- General Drug Summary
- Drug Name
- Glucose-6-Phosphate
- Description
- An ester of glucose with phosphoric acid, made in the course of glucose metabolism by mammalian and other cells. It is a normal constituent of resting muscle and probably is in constant equilibrium with fructose-6-phosphate. (Stedman, 26th ed)
- Also Known As
- Categories
- Groups
- experimental
- Structure
- Summary In Neonatal Jaundice
- 9 record(s) for Glucose-6-Phosphate NA in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 1812331
- Glucose-6-Phosphate
- NA
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the common aetiological factors of Neonatal jaundice.
- Neonatal jaundice. A second 4-year experience in Toa Payoh Hospital (1986-1989). The Journal of the Singapore Paediatric Society, 1991 [Go to PubMed]
- A 4-year experience of neonatal jaundice, from 1982-1985, in Toa Payoh Hospital, Singapore was reported previously. The second 4-year experience (1986-1989) of neonatal jaundice is reported. The Department had a more liberal policy in the management of milder cases of neonatal jaundice since 1986, after acquisition of more phototherapy units. It is the purpose of this paper to examine the change in pattern of neonatal jaundice in the same department over these 2 study periods and a comparison is made. The reported frequency of neonatal jaundice in these 2 study periods rose from 7.9% to 10% of all babies in this hospital. Babies who have some form of treatment such as phototherapy are considered as cases of neonatal jaundice. However, the incidence of hyperbilirubinaemia (defined as serum bilirubin level of 255 umol/L or 15 mg/dl or greater) fell from 3.23% to 2.11% of all livebirths in these 2 study periods. ABO Incompatibility, glucose-6-phosphate dehydrogenase (G6PD) deficiency and low birth weights (LBW)remain as the common aetiological factors of neonatal jaundice. The indications of exchange blood transfusions have changed considerably. There were less exchange blood transfusions for severe neonatal jaundice due to G6PD deficiency. However, more LBW babies underwent exchange blood transfusion. No case of kernicterus was reported for more than 10 years.
- 20113600
- Glucose-6-Phosphate
- NA
- Clinical Trial
- Summary
- [Relationship between glucose-6-phosphate dehydrogenase gene mutations and neonatal jaundice in Naning, Guangxi]. Zhongguo dang dai er ke za zhi = Chinese journal o, 2009 Dec [Go to PubMed]
- To study the correlation between glucose-6-phosphate dehydrogenase (G-6-PD) activities and three common mutations of G-6-PD gene G1388A, G1376T and A95G and investigate the effects of G-6-PD gene mutations on neonatal jaundice in Nanning, Guangxi.
One hundred and twenty-four neonates from Nanning, Guangxi, with hyperbilirubinemia were enrolled. The ARMS-PCR and PCR/REA methods were used to determine G-6-PD gene mutations. G-6-PD activities were measured using the NBT method. The incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth were compared between the neonates with different genotypes and between the G-6-PD mutation and normal groups. The risk of blood serum bilirubin >340 mumol/L was evaluated by logistic regression analysis.
Of the 124 cases, gene mutations were found in 37 cases, including G1388A (n=20), G1376T (n=14), A95G (n=4) and G1388A+A95G (n=1). Five cases (25%) showed normal G-6-PD activities in the G1388A gene mutation group and 4 (29%) had normal G-6-PD activities in the G1376T G1388A gene mutation group. All of 4 cases of A95G G1388A gene mutation showed a deficiency of G-6-PD activities. There were no significant differences in the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between the G1388A and G1376T G1388A gene mutation groups. The incidence of acute bilirubin encephalopathy, the peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L in the G-6-PD mutation group were not different from the normal group.
G1388A, G1376T and A95G are common G-6-PD gene mutations in Nanning, Guangxi. The false negative results may be received when the NBT method is used for diagnosis of G-6-PD deficiency. There are similar effects on the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between different gene mutation groups. G-6-PD gene mutations alone may not contribute to the development of acute bilirubin encephalopathy and the changes of peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L. - 3767789
- Glucose-6-Phosphate
- NA
- NA
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficient can cause Neonatal jaundice.
- Neonatal jaundice: its prevalence in Chinese babies and associating factors. Australian paediatric journal, 1986 Aug [Go to PubMed]
- A prospective study of 1238 full-term Chinese newborn infants was conducted to determine the incidence of neonatal jaundice and associated factors. A significantly more severe degree of hyperbilirubinaemia was present in infants whose ABO blood group was incompatible with that of their mothers and those who were deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD). Among the remainder, clinical jaundice was present in 87% and 23.9% had a peak serum bilirubin (SB) concentration greater than 204 mumol/l. Factors that were found to have an association with a higher peak SB concentration included: male infants; elder siblings who had a history of neonatal jaundice; and breast-fed infants with or without supplementation with formula feed. Factors that were found to have no significant association with the peak SB concentration were: gestational age; birthweight; the mode of delivery of the infants; maternal consumption of Chinese herbs and syntocinon induction or augmentation of labour.
- 3227552
- Glucose-6-Phosphate
- NA
- NA
- Summary
- G-6-PD deficiency was found to be one cause of Neonatal jaundice
- Glucose-6-phosphate dehydrogenase deficiency in ethnic minorities in The Netherlands. Tropical and geographical medicine, 1988 Oct [Go to PubMed]
- The distribution of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in ethnic minorities in the Netherlands was studied in a random sample of 668 healthy pregnant women and 754 healthy full term neonates. The overall prevalence of G-6-PD deficiency was 6.6% in males and 5.2% in females. Highest frequencies were found in sub-Saharan blacks. The hematological data in severe deficient women of African descent suggest slight hemolysis in the first trimester of pregnancy. Mean hemoglobin concentrations in pregnant women and neonates of African descent were lower as compared to hemoglobin concentrations in persons of Asian or Mediterranean origin. G-6-PD deficiency was found to be the only cause of neonatal jaundice in 6% of the non-Caucasian neonates who underwent exchange transfusion for severe neonatal hyperbilirubinaemia. Mean bilirubin in cordblood, however, was not found to be significantly higher in severe deficient neonates of African, Asian and Mediterranean descent.
- 823756
- Glucose-6-Phosphate
- NA
- NA
- Summary
- G-6-PD deficiency was found to be one cause of Neonatal jaundice
- Glucose-6-phosphate dehydrogenase Ferrara. A new variant of g-6-PD identified in Northern Italy. Acta haematologica, 1976 [Go to PubMed]
- A new variant of glucose-6-phosphate dehydrogenase (G-6-PD) has been discovered in Northern Italy, in the district of Ferrara. This variant is characterized by high decrease of red blood cell enzyme activity (less than 5% of normal), high affinity for G-6-P and NADP, increased utilization of deamino-NADP and 2-deoxy-G-6-P, and faster electrophoretic mobility in the buffer systems commonly used for the classification of the G-6-PD variants. The new G-6-PD type was never associated with clinical manifestations in any cases except neonatal jaundice in some of the newborns with this enzyme deficiency. The frequency of the new variant in the Ferrara district indicates that it has probably appeared in this area by mutation some centuries ago. It is suggested that this variant should be named G-6-PD Ferrara.
- 16708139
- Glucose-6-Phosphate
- NA
- NA
- Summary
- G-6-PD deficiency was found to be one cause of Neonatal jaundice
- Extreme hyperbilirubinemia in newborn infants. Clinical pediatrics, 2006 Apr [Go to PubMed]
- This study was undertaken to determine the frequency and investigate the etiology of extreme hyperbilirubinemia (total serum bilirubin [TSB]>or=25 mg/dL [428 micromol/L]) in newborns admitted to a neonatal intensive care unit in southern Turkey. The charts of 93 term and near-term infants admitted with TSB levels of 25 mg/dL (428 micromol/L) or greater in the first 30 days after birth were retrospectively reviewed. During the 4.5-year study period, 774 infants were admitted to our unit with neonatal jaundice. Ninety-three (12%) of these infants had TSB levels of 25 mg/dL (428 micromol/L) or greater. The mean TSB level in the 93 cases was 30.1+/-5.7 mg/dL (514.7+/-97.5 micromol/L), and the peak levels ranged from 25.0 to 57.4 mg/dL (428-981.5 micromol/L). Thirty-three (35.5%) of the 93 babies had TSB levels of 30 mg/dL (513 micromol/L) or greater. Eighty-nine of 93 infants were being exclusively breast-fed. Nineteen babies were isoimmunized, 7 were bacteremic, 2 of the 39 babies tested for glucose-6-phosphate dehydrogenase had this enzyme deficiency, and 1 of the 71 infants tested for thyroid function had hypothyroidism. No cause for extreme hyperilirubinemia was found in 61 (65.6%) cases.
- 12208094
- Glucose-6-Phosphate
- NA
- NA
- Summary
- glucose-6-phosphate dehydrogenase deficiency is one couse of Neonatal jaundice
- Kernicterus: an international perspective. Seminars in neonatology : SN, 2002 Apr [Go to PubMed]
- Kernicterus occurs in all parts of the world. The risk is increased in countries where glucose-6-phosphate dehydrogenase-deficiency is common. In the 1990's more case reports of infants who developed kernicterus were published than in the previous decades. A combination of reduced concern for jaundice in newborns, early discharge with inadequate follow-up and a decreased awareness of the signs that may herald serious toxicity may have contributed to the apparent increase in the incidence of kernicterus. Although most jaundiced newborns do not need aggressive evaluation or treatment, physicians who deal with such infants still need to be vigilant. We lack the necessary tools to distinguish infants who may be particularly vulnerable to the effects of bilirubin on the brain from those who may tolerate high serum bilirubin levels without harm. Therefore it is imperative that each infant with significant jaundice be conscientiously evaluated and a plan for testing and, if necessary, therapy be formulated. Transcuaneous measurement of bilirubin is a simple tool that significantly reduces the need for invasive tests. Signs of possible neurotoxicity must never be disregarded or neglected. Any jaundiced infant who shows signs of possible neurotoxicity should receive intensive phototherapy as an emergency procedure while further evaluation continues. Further studies regarding bilirubin toxicity and neonatal jaundice are needed, both in the basic science as well as in the clinical arena.
- 2083201
- Glucose-6-Phosphate
- NA
- NA
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency can couse Neonatal jaundice
- Neonatal jaundice among Nigerian preterm infants. West African journal of medicine, [Go to PubMed]
- Jaundice among Nigerian preterm infants under special care was studied to determine the incidence of clinical jaundice, the predisposing factors and outcome among those with significant hyperbilirubinaemia (SBR greater than or equal to 10mg/dl). The incidence of jaundice among 292 preterm infants over an 18-month period was 71.2%. The male: female ratio was 1:1.04. Of the 74 infants with serum bilirubin 10mg/dl or more, prematurity alone was the identified cause in 44 (59.5%), Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and septicaemia were the only additional factors in 13 (17.6%) and 7 (9.5%) respectively, while multiple aetiological factors (prematurity, septicaemia and G-6-PD deficiency) were identified in six (8.1%) of the babies. Septicaemia was associated with higher mean bilirubin levels and the highest mortality. The two kernicteric infants in the study had septicaemia. Thus, the single most important cause of jaundice was prematurity. G-6-PD deficiency alone did not appear to increase theincidence and severity of hyperbilirubinaemia in this study. Septicaemia should be suspected and promptly treated in order to reduce mortality and risk of kernicterus among preterm infants with hyperbilirubinaemia.
- 19172333
- Glucose-6-Phosphate
- NA
- Review
- Summary
- Factors associated with severe NNJ in babies requiring EBT included low birthweight (<2500 g, 44.4%), ABO incompatibility (30.0%), glucose-6-phosphate dehydrogenase deficiency.
- Why we are still doing so many exchange blood transfusion for neonatal jaundice in Nigeria. World journal of pediatrics : WJP, 2009 Feb [Go to PubMed]
- Since exchange blood transfusion (EBT) is associated with serious complications, phototherapy has been made more powerful to reduce the need for EBT in the developed world. This study was undertaken to determine the indications for EBT in neonatal jaundice (NNJ) at our unit and what proportion of EBTs was possibly avoidable.
All the babies who had EBT for hyperbilirubinemia over a three-year period were included. Age, sex, weight, place of delivery, blood group of baby and mother, other investigations, management, and the outcome of the babies were recorded.
Of the 1686 babies admitted to the neonatal unit, 90 (5.3%) had EBT. Fourteen (15.6%) were inborn while 76 (84.4%) were out-born babies. Fifty-six (62.2%) babies were admitted primarily for NNJ while 34 (37.8%) developed NNJ during admission. Thirty-six (40.0%) of the babies had phototherapy for more than 24 hours prior to EBT either because they were of very low birthweight or NNJ was detected very early and therapy was so commenced. Sixty-eight (75.6%) babies had single EBT while the remaining 22 (24.4%) had two sessions of EBT. Factors associated with severe NNJ in babies requiring EBT included low birthweight (<2500 g, 44.4%), ABO incompatibility (30.0%), glucose-6-phosphate dehydrogenase deficiency (34.4%) and septicemia (26.1%). Twenty-seven (30.0%) of the neonates developed features of kernicterus: 26 before admission while 1 during admission; all except one were delivered outside the hospital.
The EBT rate in our center was high. With more effective phototherapy, EBT could be avoided in most of the babies who initially had phototherapy for more than 24 hours before EBT and repeated EBT sessions. Health education of the population at risk, especially pregnant women, and early referral at the primary health care level will reduce the burden of severe NNJ. - 77 record(s) for Glucose-6-Phosphate Effective in Inducing Remission in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 559284
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency can couse Neonatal jaundice.
- Phototherapy for neonatal jaundice in erythrocyte glucose-6-phosphate dehydrogenase-deficient infants. Pediatrics, 1977 Jun [Go to PubMed]
- The effectiveness of phototherapy in the management of neonatal hyperbilirubinemia in glucose-6-phosphate dehydrogenase (G6PD)-deficient infants was studied."
Prophylacti"
phototherapy for six continuous days commencing from the first day of life was effective in preventing a significant rise in bilirubin levels in 12 G6PD-deficient infants in the first three days, during which period a rapid rise was observed in a control group of G6PD-deficient infants. The hemoglobin levels on the first and eighth postnatal days were comparable in both groups."
Therapeuti"
phototherapy proved equally effective in reducing bilirubin levels in 24 infants with nonhemolytic hyperbilirubinemia and an equal number of infnats with hyperbilirubinemia associated with G6PD deficiency. Phototherapy was efficacious in the prevention or treatment of neonatal hyperbilirubinemia associated with G6PD deficiency; even if its use is prolonged it does not cause hemolysis in such infants. - 5697334
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD deficiency is a cause of Neonatal jaundice.
- Glucose-6-phosphate dehydrogenase deficiency in Chinese. Journal of clinical pathology, 1968 Jan [Go to PubMed]
- In a Chinese population 1,000 full-term male neonates and a further 117 jaundiced neonates of both sexes were studied in an investigation of the frequency of deficiency of erythrocyte glucose-6-phosphate dehydrogenase (G6PD). This enzyme was found to be deficient in 3.6% of male neonates. Correlation of the results with the birthplace of the 602 mothers who were known to come from Kwangtung province showed no significant differences in the frequency of the deficiency between certain parts of the province.The deficiency of G6PD in hemizygous males is profound but it is not associated with erythrocyte acid monophosphoesterase deficiency in Chinese in Hong Kong. The G6PD deficiency accounts for 15.4% of all the 117 cases of neonatal jaundice. The relative importance of G6PD deficiency as a cause of neonatal jaundice does not differ materially in male and female mutants. Neonatal jaundice can occur in all genotypes of G6PD mutation in Chinese.
- 2441650
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) is a couse of neonatal jaundice.
- Neonatal jaundice and glucose-6-phosphate dehydrogenase deficiency in Basrah. Annals of tropical paediatrics, 1987 Jun [Go to PubMed]
- In a study on a group of 186 newborn babies presenting with jaundice, erythrocyte glucose-6-phosphate dehydrogenase (G6PD) deficiency was detected in 95 (51%) of the patients. The incidence of severe hyperbilirubinaemia appeared to be much greater in G6PD-deficient infants (46%) than in infants who did not have the red cell defect (15%). No change was found in this association when ABO incompatibility was excluded. Phototherapy did not reduce the need for exchange transfusion, which was necessary in 27 babies. Eight babies developed kernicterus and one died. Early detection of G6PD deficiency and close surveillance of the affected newborns may be important in reducing the risk of severe neonatal jaundice and kernicterus associated with G6PD deficiency in Basrah.
- 1283668
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency may develop hyperbilirubinaemia.
- Screening for glucose-6-phosphate dehydrogenase deficiency can prevent severe neonatal jaundice. Annals of tropical paediatrics, 1992 [Go to PubMed]
- Infants with the severe variant of glucose-6-phosphate dehydrogenase (G6PD) deficiency may develop hyperbilirubinaemia sufficiently severe to cause kernicterus and death, acute haemolysis on exposure to oxidant stress, congenital non-spherocytic haemolytic anaemia and, rarely, increased susceptibility to bacterial infection. In spite of these potential problems, G6PD deficiency is often not included among screening programmes for inherited disorders. In a comprehensive screening and educational programme, we tested around 34,000 infants for G6PD deficiency. Of the total group, 18.4% (24.5% boys and 11.8% girls) were deficient. Forty-two of the 6246 (0.67%) G6PD-deficient infants required exchange transfusion. None of them developed kernicterus. By contrast, of 4755 infants who had not been screened because they were born at home, three developed kernicterus. In addition, four G6PD-deficient infants had developed kernicterus in the 20-month period prior to the screening programme. None of the hyperbilirubinaeic infants had blood group incompatibility or any other identifiable cause of hyperbilirubinaemia. To avoid this disastrous result, we believe that neonatal screening for G6PD deficiency, together with a comprehensive education programme, is advisable in those parts of the world where the severe variant of G6PD deficiency is prevalent.
- 11433050
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is a cause of Newborn jaundice.
- A single dose of Sn-mesoporphyrin prevents development of severe hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient newborns. Pediatrics, 2001 Jul [Go to PubMed]
- Severe neonatal jaundice is a common clinical manifestation of glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and the most difficult to manage; kernicterus is not an uncommon outcome. We assessed in healthy, direct Coombs test-negative Greek newborns of >/=38 weeks' gestational age 1) the current burden of G-6-PD deficiency-associated severe jaundice, and 2) the efficacy of preventive use of Sn-mesoporphyrin (SnMP), a potent inhibitor of heme oxygenase activity and thus of bilirubin production, in ameliorating jaundice in G-6-PD-deficient neonates.
The studies were conducted at Metera Maternity Hospital in Athens, Greece. Enrolled newborns had the plasma bilirubin concentration (PBC) determined in cord blood and daily thereafter until a declining level was obtained and the case was closed. Intervention with phototherapy was dictated at exact, age-specific PBC levels. In our initial study, we enrolled consecutive mature healthy G-6-PD-deficient newborns as well as a threefold excess of G-6-PD-normal neonates born at approximately the same time (control group). For the SnMP trial, G-6-PD-deficient neonates were administered SnMP as a single intramuscular dose of 6 micromol/kg birth weight within 24 +/- 12 hours of age.
SnMP was administered at 26.7 +/- 6.1 hours of age to 172 G-6-PD-deficient newborns (group A); 168 G-6-PD-normal (group B) and 58 G-6-PD-deficient (group C) newborns who were enrolled earlier provided the comparison groups. Except for the expected excess of males in the G-6-PD-deficient groups (A and C), there were no differences in the demographic characteristics among the 3 groups. The incremental changes in PBC from cord blood to 24 hours of age also were similar (group A: 4.13 +/- 1.32 mg/dL; group B: 4.05 +/- 1.34 mg/dL; group C: 4.39 +/- 1.07 mg/dL), but there were significant differences in the next period, 24 to 48 hours of age (group A: 0.63 +/- 1.44 mg/dL; group B: 1.69 +/- 1.5 mg/dL; group C: 2.45 +/- 1.72 mg/dL). Peak PBC was significantly different (group A: 7.81 +/- 3.04 mg/dL; group B: 8.68 +/- 3.1 mg/dL; group C: 11.24 +/- 3.76 mg/dL) as was the age at which peak PBC was recorded (group A: 56 +/- 29 hours of age; group B: 69 +/- 26 hours of age; group C: 83 +/- 29 hours of age). These differeces in favor of group A were observed despite the fact that phototherapy was used in 15% of the newborns in group B and 31% of those in group C, whereas none of those treated with SnMP required phototherapy. Finally, in one female, who was heterozygous for G-6-PD deficiency, in group C phototherapy failed and 2 exchange transfusions were performed.
In comparison with normal neonates, G-6-PD-deficient neonates experienced a twofold increase in the prevalence of significant hyperbilirubinemia requiring phototherapy. A single dose of SnMP administered in the 1st day of life to the G-6-PD-deficient newborns shifted the peak PBC distribution to the left (lower values) even in relation to normal neonates and entirely eliminated the need for phototherapy. Interdiction of bilirubin production by use of a heme oxygenase inhibitor such as SnMP represents a simple and highly effective means for the preventive management of jaundice in G-6-PD-deficient newborns. - 8807322
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) mutation may cause Neonatal jaundice.
- Leu): a new Chinese G6PD variant associated with neonatal jaundice. Human heredity, [Go to PubMed]
- Using a non-radioactive PCR-SSCP technique, we identified a novel glucose-6-phosphate dehydrogenase (G6PD) mutation in a Chinese newborn with neonatal jaundice. This new variant (G6PD NanKang) causes a T to C change at nucleotide position 517, producing a Phe173Leu substitution in the human G6PD protein. Since the 517 mutation does not create or remove any known restriction site, we introduced an artificially created site by adding a primer containing a mismatched base to the PCR reaction mixture. The mismatched base accompanying the nearby 517 T-->C mutation generates an XhoI site which is suitable for distinguishing normal from mutant alleles. Using this approach, the 517 mutation can be diagnosed quickly at the DNA level.
- 9332310
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Mutation of G6PD results in a deficient variant associated with Neonatal jaundice.
- Two new mutations of the glucose-6-phosphate dehydrogenase (G6PD) gene associated with haemolytic anaemia: clinical, biochemical and molecular relationships. British journal of haematology, 1997 Sep [Go to PubMed]
- In two unrelated Spanish males with glucose-6-phosphate dehydrogenase (G6PD) deficiency and haemolytic anaemia, and two different novel point mutations in the G6PD gene, have been identified. A C to T transition at nucleotide 406 resulting in a (136) Arg to Cys substitution and a C to G transition at nucleotide 1155 resulting in a (385) Cys to Trp substitution. These two molecular defects have not been described before and are designated G6PD Valladolid 406 C-->T and G6PD Madrid 1155 C-->G. In vitro biochemical characterization of both mutant enzymes showed important differences in their molecular properties according to their different clinical behaviour. In G6PD Valladolid, the mutation of which is located in exon 5, the normal in vitro heat stability may explain its mild clinical expression (low-grade haemolysis interrupted by an acute haemolytic crisis at age 70). In G6PD Madrid, the mutation, located in exon 10, results in a deficient variant associated with neonatal jaundice and life-long chronic nonspherocytic haemolytic anaemia (CNSHA). This finding further emphasizes the importance of this specific region of the G6PD gene in the stabilization of the G6PD molecule. Putative relationships between these single point mutations and the molecular properties of the mutant enzymes are also discussed.
- 11581450
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is associated with Neonatal jaundice.
- Onset of jaundice in glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics, 2001 Oct [Go to PubMed]
- We asked whether neonatal jaundice associated with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency commences either in utero or in the immediate postnatal period and whether this perinatal bilirubinemia is the precursor of the subsequent neonatal jaundice and hyperbilirubinemia.
Mandatory serum total bilirubin (STB) determinations were performed within 3 hours of birth, to reflect the in utero state (first STB), and on the third day of life (second STB), with additional determinations as clinically necessary, on healthy, term male neonates at high risk for G-6-PD deficiency. G-6-PD Mediterranean mutation was determined by molecular means. G-6-PD-deficient neonates were compared with control participants. The relationship of first STB values to second STB and subsequent hyperbilirubinemia (defined as STB >/=256 micromol/L [15.0 mg/dL]) was determined.
Both first and second STB values were significantly higher in the G-6-PD-deficient neonates (n = 52) than in control participants (n = 166; 50 +/- 12 micromol/L vs 44 +/- 10 micromol/L [2.9 +/- 0.7 mg/dL vs 2.6 +/- 0.6 mg/dL] and 174 +/- 52 micromol/L vs 152 +/- 52 micromol/L [10.2 +/- 3.1 mg/dL vs 8.9 +/- 3.0 mg/dL] for the first and second STB values, respectively). The rate of rise between these 2 points was greater in the G-6-PD-deficient neonates (2.6 +/- 0.9 micromol/L/h vs 2.2 +/- 0.9 micromol/L/h [0.15 +/- 0.05 mg/dL/h vs 0.13 +/- 0.05 mg/dL/h). Sixteen (30.8%) of the G-6-PD-deficient neonates developed hyperbilirubinemia compared with 10 (6%) of control participants (relative risk: 5.11; 95% confidence interval: 2.47-10.56). In both G-6-PD-deficient and normal populations, first STB values correlated significantly with both second STB values and with those who subsequently developed hyperbilirubinemia. Significantly more G-6-PD-deficient neonates with a first STB value greater than or equal to the man developed hyperbilirubinemia compared with those with first STB less than the mean: 13 of 28 neonates versus 3 of 24 (relative risk: 3.7; 95% confidence interval: 1.20-11.51). This difference did not reach statistical significance in the control group.
Higher first STB values, an increased risk of hyperbilirubinemia in G-6-PD-deficient neonates with first STB value greater than or equal to the mean, and significant correlation between first STB values and second STB values and hyperbilirubinemia suggest that jaundice in G-6-PD-deficient neonates commences in the immediate perinatal period, most likely in utero. - 7079890
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency contributes significantly to the severity of Neonatal jaundice in the population group.
- The effect of glucose-6-phosphate dehydrogenase deficiency on the severity of neonatal jaundice in Cape Town. South African medical journal = Suid-Afrikaanse ty, 1982 May 22 [Go to PubMed]
- A study was made of 3718 newborn infants with jaundice in excess of physiological levels. Prematurity, haemolytic disease, haematomas or infections were present in 1278 patients. Of the remaining 2440 neonates, 137 were deficient in glucose-6-phosphate dehydrogenase (G-6-PD) and 2303 had idiopathic hyperbilirubinaemia. Exchange transfusion was necessary in 59 (42,7%) of the patients with G-6-PD deficiency and in 426 (18,5%) of those with idiopathic hyperbilirubinaemia. Kernicterus occurred in 3 infants (2,2%) with G-6-PD deficiency and in 3 (0,13%) with idiopathic hyperbilirubinaemia. These findings indicate that G-6-PD deficiency contributes significantly to the severity of neonatal jaundice in the population group studied and should be regarded as a potentially dangerous condition.
- 14226101
- Glucose-6-Phosphate
- Effective in Inducing Remission
- NA
- Summary
- Red cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency contributed to severe hemolytic jaundice.
- RED CELL GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY--A NEWLY RECOGNIZED CAUSE OF NEONATAL JAUNDICE AND KERNICTERUS IN CANADA. Canadian Medical Association journal, 1964 Dec 12 [Go to PubMed]
- Seven male newborns of Chinese, Greek and Italian origin presented with severe hemolytic jaundice due to red cell glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. In five, the hemolysis was precipitated by inhalation of mothball vapours in the home. Kernicterus was evident upon admission in six infants and was fatal in four of these.G-6-PD deficiency should be suspected as a cause of jaundice in all full-term male infants of these ethnic groups. The diagnosis can be confirmed in any hospital by the methemoglobin reduction test. In areas similar to Toronto, Canada, where these high-risk ethnic groups prevail, the following measures are recommended: (1) detection of G-6-PD deficient newborns by screening cord bloods of all infants of these ethnic groups; (2) protection of affected infants from potentially hemolytic agents such as naphthalene, certain vitamin K preparations, and sulfonamides; and (3) observation of serum bilirubin levels to assess the need for exchange transfusion for hyperbilirubinemia.
- 17489836
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficient is a cause of Neonatal jaundice.
- Massive acute haemolysis and severe neonatal hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient preterm triplets. Journal of paediatrics and child health, 2007 May [Go to PubMed]
- Premature triplets (2 boys and 1 girl) were delivered at 34 weeks, with both boys identified as Glucose-6-phosphate dehydrogenase (G6PD) deficient. Despite having similar quantitative levels of G6PD in their cord blood, only one boy had severe hyperbilirubinemia and anaemia caused by acute haemolysis requiring exchange transfusion. G6PD-deficient infants with the similar genetic, demographic, maternal, clinical factors and G6PD quantification levels can have different severity of presentation of neonatal jaundice in similar environmental set up. This supports the massive acute haemolysis can occur in infant with G6PD deficiency in the absence of any obvious blood group incompatibilities, infection, or ingestion of oxidising agents known to trigger haemolysis.
- 11731664
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency contributes to Neonatal jaundice.
- Sn-Mesoporphyrin interdiction of severe hyperbilirubinemia in Jehovah's Witness newborns as an alternative to exchange transfusion. Pediatrics, 2001 Dec [Go to PubMed]
- The religious convictions of parents who are Jehovah's Witness adherents lead them to reject the use of exchange transfusions as therapy for severe hyperbilirubinemia in newborns in whom intensive phototherapy has failed to control this problem. Consequently, physicians caring for such infants may be obliged to initiate legal action to compel use of the procedure when severe hyperbilirubinemia not sufficiently responsive to phototherapy warrants an exchange transfusion. Our goal was to determine if we could use the potent inhibitor of bilirubin production, Sn-Mesoporphyrin (SnMP), to resolve the troubling medical-legal issues in such situations in 2 infants with hemolytic disease of the newborn who required exchange transfusions for severe hyperbilirubinemia but whose Jehovah's Witness parents rejected the procedure. SnMP was administered in a single dose, as in previous studies, at the time when exchange transfusion would have been initiated and plasma bilirubin levels were monitored at close intervals therafter.
SnMP is a potent inhibitor of heme oxygenase, the rate-limiting enzyme in catabolism of heme to bilirubin. We found in earlier studies that in single doses of 6 micromol/kg birth weight, SnMP is extremely effective in moderating the course of hyperbilirubinemia and in eliminating the need for supplemental phototherapy in jaundiced newborns. In the 2 cases described, a single dose of SnMP (6 micromol/kg birth weight) was administered intramuscularly to severely jaundiced infants with immune hemolysis at a time when clinical circumstances dictated the need for exchange transfusion. CASE 1: This patient was a preterm male infant (gestational age: 35 5/7 weeks; birth weight: 2790 g) whose plasma bilirubin concentration (PBC) at 1 hour after birth was 5.0 mg/dL. Despite intensive phototherapy with 3 banks of lights and 1 biliblanket, the PBC increased steadily with no diminution in the rate of increase for 75 hours. In view of the problems of immune hemolysis, and prematurity, and the inability of phototherapy tostop progression of hyperbilirubinemia, a decision to carry out an exchange transfusion was made; the decision was, however, rejected by the Jehovah's Witness parents. Pending legal action to compel use of the procedure, a request to this (Rockefeller) laboratory for SnMP was made; its use was approved by the Food and Drug Administration; and the inhibitor was delivered to the physician-in-charge (D.P.M.) in Sioux Falls, South Dakota. The single dose of SnMP was administered to the infant at 75 hours after birth; the course of hyperbilirubinemia before and after the use of the inhibitor is shown in Fig 1. [figure: see text]. CASE 2: This female term infant (gestational age: 38-39 weeks; birth weight: 4140 g) with immune hemolysis was delivered by cesarean section and because of problems related to meconium aspiration required helicopter transfer to the Special Care Nursery in Abilene, Texas, where 10 hours after birth the first PBC was determined to be 18.0 mg/dL. Double-bank phototherapy plus a biliblanket as initiated; a third bank of lights was later ordered. The PBC fluctuated in the ensuing 2 days between 13.8 to 25.8 mg/dL during which suggestive clinical signs of possible bilirubin encephalopathy became manifest. In view of the clinical circumstances and the continued severe hyperbilirubinemia, permission for a double-exchange transfusion was requested. The parents, who were Jehovah's Witness adherents, refused the procedure. While preparing legal action to compel use of the exchange, a request was made to this (Rockefeller) laboratory for use of SnMP to attempt control of hyperbilirubinemia. With FDA approval, the SnMP was delivered to the attending neonatologist (J. R. M.) in Abilene and administered in a single dose (6 micromol/kg birth weight) at 56 hours after birth when the PBC was 19.5 mg/dL. The course of bilirubinemia before and after SnMP use is shown in Fig 2. [figure: see text].
The use of SnMP to moderate or prevent the development of severe hyperbilirubinemia in newborns (preterm, near-term, term with high PBCs [15-18 mg/dL], ABO-incompatibility; glucose-6-phosphate dehydrogenase deficiency) has been extensively studied in carefully conducted clinical trials the results of which have been reported earlier. This inhibitor of bilirubin production has demonstrated marked efficacy in moderating the course of hyperbilirubinemia in all diagnostic groups of unconjugated neonatal jaundice. The 2 cases described in this report confirmed the efficacy of SnMP in terminating progression of hyperbilirubinemia in infants in whom phototherapy had failed to sufficiently control the problem and whose parents, for religious reasons, would not permit exchange transfusions. Interdiction of severe hyperbilirubinemia by inhibiting the production of bilirubin with SnMP can be an effective alternative to the use of exchange transfusion in the management of severe newborn jaundice that has not responded sfficiently to light treatment to ease concern about the development of bilirubin encephalopathy. - 14972648
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is related with hyperbilirubinemia and jaundice.
- An update on the prevalence of glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice in Tehran neonates. Clinical biochemistry, 2004 Mar [Go to PubMed]
- The aim of this study was to screen newborns in Tehran for glucose-6-phosphate dehydrogenase (G6PD) deficiency in relation to hyperbilirubinemia and jaundice.
We performed quantitative and qualitative red blood cell (RBC) G6PD assays in cord blood of 2000 male and female at-term neonates. Observations for jaundice and bilirubin determination were made in G6PD-deficient and normal groups. Those with severe jaundice were treated with phototherapy or exchange transfusion.
Our results showed that 2.1% (3.6% of males and 0.6% of females) was G6PD-deficient. Those with severe jaundice and hyperbilirubinemia (160 normal and 17 G6PD-deficient) were hospitalized and treated with phototherapy or exchange transfusion. Bilirubin levels in G6PD-deficient neonates were somewhat higher compared to G6PD-normal babies (18.8 +/- 2.4 mg/dl [321.5 +/- 41 micromol/l] vs. 15.7 +/- 3.2 mg/dl [268.5 +/- 54.7 micromol/l]; P < 0.05). G6PD activity was significantly lower in G6PD-deficient group than in the normal group (2.1 +/- 0.7 vs. 12.5 +/- 5.0 U/g Hb; P < 0.001).
This study shows that the incidence of G6PD deficiency in newborns of Tehran is 2.1%, which is relatively high, and also hyperbilirubinemia and jaundice are approximately 3-fold higher in G6PD-deficient group than in the G6PD-normal group (51% vs. 16%). This emphasizes the necessity of neonatal screening on cord blood samples of both sexes for G6PD deficiency and the need to watch closely for development of hyperbilirubinemia. - 9628306
- Glucose-6-Phosphate
- Effective in Inducing Remission
- NA
- Summary
- G-6-PD-deficient neonates,compared with those with either condition alone, are not at increased risk for hemolysis or hyperbilirubinemia.
- Combination of ABO blood group incompatibility and glucose-6-phosphate dehydrogenase deficiency: effect on hemolysis and neonatal hyperbilirubinemia. Acta paediatrica (Oslo, Norway : 1992), 1998 Apr [Go to PubMed]
- The incidence (%) of hyperbilirubinemia (serum bilirubin > or = 257 micromol/l) was similar in neonates with a combination of ABO incompatibility and glucose-6-phosphate dehydrogenase (G-6-PD) deficiency (45%), with ABO incompatibility (54%) or G-6-PD deficiency (37%), alone (ns). Carboxyhemoglobin values, corrected for inspired CO, were similarly elevated in all three groups (0.87 +/- 0.32%, 0.82 +/- 0.29%, 0.76 +/- 0.18%, respectively, ns), but correlated with bilirubin only in those with ABO incompatibility alone. ABO-incompatible/G-6-PD-deficient neonates, compared with those with either condition alone, are not at increased risk for hemolysis or hyperbilirubinemia.
- 8585194
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency have been shown to play a role in the etiology of Neonatal jaundice.
- The Le(a) antigen and neonatal hyperbilirubinemia in Taiwan. Vox sanguinis, 1995 [Go to PubMed]
- Neonatal jaundice is known to be more severe in Taiwanese infants than in Caucasian infants. Although ABO fetomaternal incompatibility and glucose-6-phosphate dehydrogenase deficiency have been shown to play a role in the etiology of neonatal jaundice in some Taiwanese infants, the etiology in the majority of cases is unknown. In this study we found that in Taiwanese newborn infants, the red cell Le(a) antigen appeared later in infants who were jaundiced (peak serum bilirubin levels of > 12 mg/dl during the first week of life) than in infants who were not. However, the Leb antigen, and hence the transferase encoded by the Se and Se(w) genes, did not appear to be similarly involved in the etiology of physiological jaundice. Thus it would appear that the Le gene-specified transferase is less active or has a delayed function, in jaundiced infants. The relationship between the Le gene-specified transferase and bilirubin has yet to be established.
- 19004212
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency is a cause of Neonatal jaundice.
- A research on the erupted fetal diseases caused by traditional Chinese drugs--discussion from the issue that Chinese goldthread rhizome is prohibited in Singapore. Journal of traditional Chinese medicine = Chung i , 2008 Sep [Go to PubMed]
- Chinese Goldthread Rhizome is prohibited in Singapore since it is thought to induce neonatal jaundice. In literatures of traditional Chinese medicine, this drug was never treated as a contraindicant for pregnancy, and there were no records and reports on it inducing neonatal jaundice. The results of the authors's experiments showed that Chinese Goldthread Rhizome and berberine had no induction of neonatal jaundice in pregnant rats and mice and newly born rats, and had no influence either on the activity of glucose-6-phosphate dehydrogenase of mice red blood cells. Fetal toxicity of traditional Chinese drugs including Chinese Goldthread Rhizome should be further studied in order to promote the development of traditional Chinese medicine.
- 24491445
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Single-base mutations in the glucose-6-phosphate dehydrogenase (G6PD) gene leads to Neonatal jaundice and hemolytic anemia.
- Gold nanostructures for the multiplex detection of glucose-6-phosphate dehydrogenase gene mutations. Analytical biochemistry, 2014 Apr 15 [Go to PubMed]
- We describe a gold nanoparticle-based technique for the detection of single-base mutations in the glucose-6-phosphate dehydrogenase (G6PD) gene, a condition that can lead to neonatal jaundice and hemolytic anemia. The aim of this technique is to clearly distinguish different mutations frequently described within the Asian population from their wild-type counterparts and across different mutant variants. Gold nanoparticles of different sizes were synthesized, and each was conjugated with a single-strand DNA (ssDNA) sequence specific for a particular mutation in the G6PD gene. It was found that only mutant targets presented a characteristic band on the agarose gel, indicating the successful formation of dimeric nanostructures. No such dimer bands were observed for the wild-type targets. The difference in the relative dimer band levels allowed different mutant variants to be distinguished from one another. The technique was further validated using G6PD-deficient patient samples. This simple mutation detection mthod with direct result readout is amenable for rapid and mass screening of samples.
- 22111448
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Glucose-6-phosphate dehydrogenase deficiency could cause jaundice.
- practices on care of neonatal jaundice. The Medical journal of Malaysia, 2011 Aug [Go to PubMed]
- This study aimed to determine the gaps of knowledge and practices of care of neonatal jaundice among Malaysian mothers. It was a cross sectional study of 400 mothers who attended the obstetric clinics or were admitted to the obstetric wards of a general hospital. They were surveyed with a structured set of questionnaire. The results showed that a majority (93.8%) of them knew about neonatal jaundice, and 71.7% knew that jaundice lasting more than 2 weeks was abnormal. However, only 34.3% of them were aware that jaundice appearing during the first 36 hours of life was abnormal. Less than 20% knew about glucose-6-phosphate dehydrogenase deficiency and that fetal-maternal blood group differences could cause jaundice. Although 71.7% and 69.7%, respectively, of the mothers knew that severe jaundice could cause death and brain damage, only 38.4% of them were aware that severe jaundice could result in hearing impairment. A very low proportion (27.1%) of them was aware that putting jaundiced infants under the directsun could result in dehydration and worsening of jaundice. Out of a maximum score of 15, the mean maternal knowledge score was 7.4 (95% confidence intervals: 7.1, 7.7). Majority (83.1%) of the multiparous mothers with a past history of having children developing neonatal jaundice (n = 154) practiced placing their infants under the direct sun. This study revealed that there was a wide knowledge gap among Malaysian mothers on care of neonatal jaundice. Placing infants under the direct sun was still a common practice.
- 7918083
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Mutations in the glucose-6-phosphate dehydrogenase (G6PD) gene could cause Neonatal jaundice.
- Molecular characterization of glucose-6-phosphate dehydrogenase deficiency in Chinese infants with or without severe neonatal hyperbilirubinaemia. British journal of haematology, 1994 Apr [Go to PubMed]
- To characterize mutations in the glucose-6-phosphate dehydrogenase (G6PD) gene in Chinese infants, we studied 213 G6PD-deficient infants without blood exchange transfusion (BET) therapy, and 34 patients who required BET therapy for their severe hyperbilirubinaemia after birth. Nine different oint mutations were characterized in all infants. Of these mutations, the G to T substitution at cDNA nucleotide (nt) 1376, which accounts for the mutations in 131 (53.0%) neonates, followed by G to A substitution at nt 1388 in 18 (10.5%) infants, A to G substitution at nt 493 in 17 (6.9%) infants, A to G substitution at nt 95 in 10 (4.1%) infants, C to T substitution at nt 1024 in six (2.4%) infants, and G to T substitution at nt 392 in three (1.2%) infants, G to A substitution at nt 487 in two (0.8%) infants, C to T substitution at nt 1360 in two (0.8%) infants and C to T substitution at nt 592 in two (0.8%) infants. Mutations in 48 (19.5%) G6PD-deficient infants were not characterized. Most (64.7%) mutations in the G6PD-deficient infants who required BET therapy after birth result from a G to T substitution at nt 1376. The enzyme activity of G6PD deficient infants who required BET therapy is significantly lower than for those who did not, even in a group with the same variant (as in 1376 mutation). Severeneonatal jaundice requiring BET therapy can take place with the majority of variants encountered in this area.
- 22910623
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal jaundice .
- Glucose-6-phosphate dehydrogenase screening of babies born in a tertiary care hospital in West Bengal. Indian journal of public health, [Go to PubMed]
- About 400 million individuals worldwide have been affected by the inherited disorder of glucose-6-phosphate dehydrogenase (G6PD) deficiency that predisposes individuals to neonatal jaundice or hemolytic crisis due to drugs or infections. A descriptive observational study with longitudinal design was undertaken among 109 live newborns, delivered in labor room of IPGME and R, Kolkata during the period from June to August 2009. An objective of the study was to estimate the occurrence of G6PD deficiency among newborns and its association with different socio-demographic, clinical and gestational characteristics. 14.68% newborns were found G6PD deficient. This occurrence was not significantly related to gender, religion and ethnicity, consanguineous marriage of the parents, gestational age and birth weight of the baby. Development of severe jaundice (total serum bilirubin >15 mg/dl) was found 23.8% among G6PD deficient babies and 12.5% among non-G6PD deficient. This difference was statistically not significant.
- 7393270
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal jaundice.
- Reduced chronic hemolysis during high-dose vitamin E administration in Mediterranean-type glucose-6-phosphate dehydrogenase deficiency. The New England journal of medicine, 1980 Aug 21 [Go to PubMed]
- The observation that high-dose oral vitamin E supplementation (800 IU per day) improved red-cell survival in two rare disorders associated with increased red-cell susceptibility to oxidative stress prompted a similar trial in 23 patients with Mediterranean glucose-6-phosphate dehydrogenase (G6PD) deficiency. Three months of vitamin E administration resulted in decreased chronic hemolysis as evidenced by improved red-cell life span (P less than 0.025), with an improvement in red-cell half-life from 22.9 +/- 0.7 days to 25.1 +/- 0.6 days (mean +/- S.E.M.), increased hemoglobin concentration (P less than 0.001), and decreased reticulocytosis (P less than 0.001) as compared with base-line values. Evaluation after one year of vitamin E administration demonstrated sustained improvement in all these indexes. Controlled clinical trials of vitamin E supplementation may be warranted to examine its efficacy in ameliorating acute hemolytic crises or in reducing morbidity from neonatal jaundice in this relatively common enetic disorder.
- 6209608
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Randomized Controlled Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficient can cause Neonatal jaundice.
- Cord plasma alpha-fetoprotein values and neonatal jaundice. Pediatrics, 1984 Dec [Go to PubMed]
- Umbilical cord plasma alpha-fetoprotein (AFP) values were determined in 127 infants with hyperbilirubinemia (56 glucose-6-phosphate dehydrogenase (G-6-PD) deficient and 71 G-6-PD normal) and 136 control subjects (73 G-6-PD deficient and 63 G-6-PD normal). The mean alpha-fetoprotein value of 173 +/- 35.2 (SD) mg/L for the group of infants with hyperbilirubinemia was significantly greater than that (122 +/- 21.7 mg/L) for the control infants (P less than .001). G-6-PD status and sex did not significantly affect the alpha-fetoprotein values. Using an alpha-fetoprotein level of 130 mg/L as a"
cut-of"
value, the incidence of false-positive results was 25.5% and the incidence of false-negative results was 11.8%. This test can be used as a screening procedure to detect infants at high risk for hyperbilirubinemia. - 24763104
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD deficiency frequently result in Neonatal jaundice.
- Evaluation of neonatal jaundice in the Makkah region. Scientific reports, 2014 [Go to PubMed]
- The aims of this study were to detect the frequency at which the different types of neonatal jaundice occur in Makkah and to estimate the malondialdehyde (MDA) levels. This study included 239 neonates with neonatal jaundice, 20 anemic neonates and 21 healthy neonates. ABO incompatibility was observed in 31.6% of neonates with indirect hyperbilirubinemia, in 14.3% of those with early onset jaundice, in 9.5% of those with persistent jaundice, in 8.5% of those with physiological jaundice, in 5% of anemic neonates and in 12% of all neonates. glucose-6-phosphate dehydrogenase (G6PD) deficiency was observed in 10.5% of neonates with indirect hyperbilirubinemia, in 3.9% of those with physiological jaundice, in 11.1% of those with direct hyperbilirubinemia, in 12% of those with persistent jaundice, in 10% of anemic neonates and in 6.6% of all neonates. Rh incompatibility and polycythemia were found in 2.6% of neonates with indirect hyperbilirubinemia and in 0.4% of all neonates. In comparison to control group, MDA ws significantly higher in all groups except for the anemic group. In conclusion, ABO incompatibility and G6PD deficiency frequently result in neonatal jaundice in Makkah, whereas Rh incompatibility and polycythemia are rare. The MDA level may serve as an indicator of oxidative stress.
- 1179794
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-Phosphate is related to Neonatal jaundice.
- A longitudinal study of red cell enzymes in infants of low birth weight. Zeitschrift für Kinderheilkunde, 1975 Sep 11 [Go to PubMed]
- A longitudinal study of red cell enzyme activity in newborn infants of low birth weight has been conducted over the first 2 months of life. The enzymes investigated are acetylcholinesterase (EC 3.1.3.7), an integral part of the red cell membrane and subnormal in ABO hemolytic disease of the newborn; and glucose-6-phosphate dehydrogenase (EC 1.1.1.49), an intracellularly-located, sex-linked enzyme, implicated in neonatal jaundice and of significance in drug-induced hemolytic anemias. Acetylcholinesterase activity, which is lower in normal full-term infants and in low birth weight infants than in adults, was further diminished during the initial weeks of life of the infants of low birth weight and the higher levels of activity, characteristic of adult red cells, had not appeared by 2 months of age. By contrast, red cell glucose-6-phosphate dehydrogenase activity, which is higher in full-term newborn infants and in infants of low birth weight than in adults, did not diminish as a function of age and the lower ault levels were not discernible by 2 months of life.
- 7305431
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) is related to Neonatal jaundice .
- Glucose-6-phosphate dehydrogenase status and neonatal jaundice. Archives of disease in childhood, 1981 Nov [Go to PubMed]
- Neonatal jaundice and its relationship to glucose-6-phosphate dehydrogenase (G6PD) status of healthy, term Chinese infants was evaluated in 220 G6PD-deficient infants, 26 intermediate infants who were observed for 3 weeks, and 116 normal (control) infants. Each infant was free of isoimmunisation, cephalhaematomas, or contusions. The mode of labour, method of delivery, and type of feeds had no appreciable effect on daily bilirubin levels."
Elevate"
physiological jaundice was associated with normal and G6PD-deficient status; there was no increased haemolysis. G6PD-deficient status was associated with jaundice significantly raised especially in the first week of life, and prolonged beyond that of the"
elevate"
physiological jaundice. Significantly increased though mild haemolysis was observed. Close surveillance is therefore required for G6PD-deficient infants at least for the first week of life, the period of increased risk. With G6PD-intermediate infants, only the usual measures for normal infants are required. - 12854374
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal jaundice.
- Neonatology in Singapore: the way we were, the way forward. Annals of the Academy of Medicine, Singapore, 2003 May [Go to PubMed]
- Singapore has a maternity hospital since 1924, but for many decades the newborns could only receive basic care. Neonatal and perinatal mortality rates were high. Marked improvement in neonatal care began from the 1980s when many neonatal departments were set up to provide intensive care. Improved socioeconomic status, better healthcare facilities, effective infection control, immunisation programmes and availability of potent antibiotics contributed to the decline of perinatal and neonatal mortality. Following the implementation of the glucose-6-phosphate dehydrogenase (G6PD) deficiency screening programme, severe neonatal jaundice and kernicterus were largely reduced. Exchange blood transfusions initiated in the 1960s and phototherapy in the 1970s had saved many babies. Kernicterus is almost not seen now. With more neonatal-trained staff, organised resuscitation teams, advances in respiratory management and better monitoring equipment, more babies have survived. Closer cooperation between obstetricians and eonatologists was a great leap forward towards perinatal medicine. Physicians should endeavour to reduce the incidence and prevalence of birth defects and metabolic errors. Perinatal asphyxia should be promptly detected and managed effectively, including neuroprotective strategies. There should be markers to predict the outcome of asphyxiated babies for decision-making. Neonatologists should be mindful of safe introduction of new technologies and rapid diagnostic techniques for infections, including group B streptococcal screening and chemoprophylaxis when required. Other current issues include prevention of major morbidities, preservation of brain function, improved neurodevelopmental outcome of premature babies, use of blood substitutes, optimal nutrition, fetal surgery, evidence-based medicine, better information systems, avoidance of medication errors, adequate sedation and pain relief of the baby, and the use of nitric oxide. One should bear in mind the need to enhance the neonatal intensive care enviroment, improve non-invasive monitoring and minimise invasive procedures. Physicians should prioritise neonatal care for their country and utilise less costly neonatal care. Ethical issues in neonatology that arise following advancement in neonatal care deserve attention. Advances in life sciences, such as the completion of the human genome project, cloning of tissues and organs, human stem cell research and technology, gene therapy, deoxyribonucleic acid vaccines and nanomedicine, should benefit neonatology.
- 11803427
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD deficiency can cause Neonatal jaundice .
- Neonatal jaundice--traditional Chinese medicine approach. Journal of perinatology : official journal of the , 2001 Dec [Go to PubMed]
- Herbal treatment of neonatal jaundice (NNJ) has been practiced in China for a long time. Even to-date, a variety of herbal items, including"
Yin-chi"
(Artemisia),"
Huang-qi"
(Scutellaria),"
Da-huan"
(Rheum officinale),"
Gan-ca"
(Glycyrrhiza), and"
Huang-li"
(Coptis chinesis), are still being prescribed to jaundiced infants, often in combination with modern treatment such as phototherapy and exchange transfusion. Their efficacy has, however, not been tested by properly conducted randomised controlled trial. On the other hand, exposure to herbs either before or after birth has been suspected to be a cause of hemolysis and jaundice in the newborns. It is also widely believed in the Chinese community that a number of herbal items are hemolytic agents in infants deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD). The belief is so deep rooted that each infant detected to have G6PD deficiency by neonatal cord blood screening is given a G6PD deficiency alert card, which states that the child must avoid these herb items for life. In a cohort of 1008 mother-infant pairs, however, we have previously shown that there was no association between maternal herb consumption during pregnancy and the incidence or severity of neonatal hyperbilirubinemia in their offprings, including those who were deficient in G6PD. A thorough search of medical literature also fails to detect any evidence that any of the herbs stated in the G6PD deficiency alert card causes hemolysis in G6PD-deficient subjects. Thus, there are many misunderstandings and unsubstantiated beliefs about the relationship between herbal medicine and NNJ. Given the potential usefulness of Chinese traditional medicine, which has been practiced for almost 3000 years and is still gaining momentum in the modern days, extensive scientific studies to determine the therapeutic efficacy and potential harmful effects of the various herbal items are warranted. - 8861278
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Genetic variability of G6PD has played an important role in the understanding of a variety of developmental processes.
- G6PD: population genetics and clinical manifestations. Blood reviews, 1996 Mar [Go to PubMed]
- The glucose-6-phosphate dehydrogenase (G6PD) gene is X-linked. There are numerous mutations that cause a deficiency of this enzyme in erythrocytes. G6PD deficiency can produce anemia, both when drugs are administered and under the stress induced by infection. Functionally severe variants cause hereditary non-spherocytic hemolytic anemia, i.e. anemia even in the absence of stress. Neonatal jaundice occurs in G6PD deficiency, but it is likely that it is largely due to impairment of liver function, rather than to hemolysis. It has been suggested that there are clinical manifestations of G6PD deficiency that are related to other tissues, but the existence of these is not well documented. Some mutations that produce G6PD deficiency in red cells exist at polymorphic frequencies. Individuals with such mutations seem to have enjoyed a selective advantage because of resistance to falciparum malaria. Different mutations, each characteristic of certain populations, are found, and have been characterized at the deoxyribnucleic acid (DNA) level. G6PD A-(202A376G) is the most common African mutation. G6PD Mediterranean(563T) is found in Southern Europe, the Middle East and in the Indian subcontinent. Several other mutations are common in Asia. Genetic variability of G6PD has played an important role in the understanding of a variety of developmental processes.
- 24774506
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause severe Neonatal jaundice.
- Pattern and predictors of maternal care-seeking practices for severe neonatal jaundice in Nigeria: a multi-centre survey. BMC health services research, 2014 [Go to PubMed]
- Nigeria is frequently associated with disproportionately high rates of severe neonatal jaundice (NNJ) underpinned by widespread Glucose-6-phosphate dehydrogenase (G6PD) deficiency. Timely and appropriate treatment of NNJ is crucial for preventing the associated morbidity and neuro-developmental sequelae. Since mothers are likely to be the first mostly to observe the onset of severe illness in their newborns, we set out to identify the pattern and predictors of maternal care-seeking practices for NNJ in three culturally-distinct settings in Nigeria.
A multi-centre study was conducted among women attending antenatal clinics in Abuja, Lagos and Port Harcourt from October 2011 to April 2012 using a pretested questionnaire. Predictors of awareness of NNJ, accurate recognition of NNJ, use of potentially harmful therapies and preference for future hospital treatment were determined with multivariate logistic regressions.
Of the 488 participants drawn from the three locations, 431 (88.3%) reported awareness of NNJ, predominantly (57.8%) attributable to professional health workers. A total of 309 (63.3%) mothers with prior knowledge of NNJ claimed they could recognise NNJ, but 270 (87.4%) from this group accurately identified the features of NNJ. Multiparous mothers (Adjusted odds ratio, AOR:4.05; 95% CI:1.75-9.36), those with tertiary education (AOR:1.91; CI:1.01-3.61), and those residing in Lagos (AOR:2.96; CI:1.10-7.97) were more likely to have had prior knowledge of NNJ. Similarly, multiparous mothers (AOR:2.38; CI:1.27-4.46) and those with tertiary education (AOR:1.92; CI:1.21-3.05) were more likely to recognise an infant with jaundice accurately. Mothers educated by health workers were 40% less likely to resort to potentially harmful treatment for NNJ (AOR:0.60; CI:0.39-0.92) but more likely to seek hospital treatment in future for an infant suspected with jaundice (AOR:1.88; CI:1.20-2.95).
Women with tertiary education and multiparous mothers who attend routine antenatal clinics are more likely than less educated women, to be associated with appropriate care-seeking practices for infants with NNJ regardless of the socio-cultural setting. Systematic efforts by professional health workers are warranted, as part of routine antenatal care, to engage other groups of mothers especially those likely to indulge in self-use of potentially harmful therapies. - 16753852
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal jaundice.
- G6PD deficiency with hemolytic anemia due to a rare gene deletion--a report of the first case in Malaysia. Hematology (Amsterdam, Netherlands), 2006 Apr [Go to PubMed]
- A 2-year-old Chinese boy was referred to Hospital UKM for investigation of recurrent episodes of dark-coloured urine and pallor since birth. He was born prematurely at 34 weeks gestation and developed severe early-onset neonatal jaundice requiring exchange blood transfusion. Screening at birth showed Glucose-6-phosphate dehydrogenase (G6PD) deficiency. On admission, physical examination revealed pallor, jaundice and mild hepatomegaly. Results of laboratory investigations showed a hemoglobin level of 11.0 g/dl with a hemolytic blood picture, reticulocytosis of 20% and red cell G6PD activity reported as undetectable. The patient's DNA was analysed for G6PD mutations by PCR-based techniques and DNA sequencing and results showed a 24 bp deletion of nucleotide 953-976 in the exon 9 of the G6PD gene. DNA analysis was also performed on blood samples of the patient's mother and female sibling confirming their heterozygous status, although both showed normal red cell G6PD activity levels. The patient was discharged wll and his parents were appropriately advised on the condition and the importance of taking folic acid regularly. This is a first case report in Malaysia of G6PD deficiency causing chronic-hemolytic anemia. The rare 24 bp deletion causes the G6PD Nara variant, previously reported only in two other unrelated males, a Japanese and a Portuguese both with chronic hemolytic anemia.
- 12476860
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause hemolytic anemia and Neonatal jaundice.
- Frequency of glucose 6 phosphate dehydrogenase deficiency and related hemolytic anemia in Riyadh, Saudi Arabia. Journal of Ayub Medical College, Abbottabad : JAMC, [Go to PubMed]
- Glucose 6 Phosphate dehydrogenase deficiency is present in over 400 million people world wide. It is more common iin tropical and subtropical countries and is one of the important causes of hemolytic anemia and neonatal jaundice. We studied the frequency of glucose-6-phosphate dehydrogenase deficiency and associated complications in Central Region (Riyadh) of Saudi Arabia.
A total of 1740 subjects referred by Ministry of Interior and different hospitals in Riyadh were investigated for glucose-6-phosphate dehydrogenase deficiency. Glucose 6 phosphate dehydrogenase activity was determined by a screening test described by Beutler.
Out of these, 106 (6.09%) subjects were deficient. The subjects were divided into marriage and hospital groups. In marriage group deficiency was 4.1% while in hospital group it was 13.3%. In 54 glucose-6-phosphate dehydrogenase deficient patients red blood cell count and haemoglobin levels were determined to see the degree of anaemia. Sixty one percent (61%) had anaemia. In hospital patients 8% patients had severe anaemia while in marriage group no patients had severe anaemia. However mild anaemia was seen in 25% subjects in marriage group.
In conclusion the study indicates that glucose-6-phosphate dehydrogenase deficiency is common in the central region of Saudi Arabia and a lot of patients present with haemolytic episodes. The haemolytic crisis however is not related to the intake of fava beans. The type of variant causing anaemia and suggestions for prevention in marriage group are outlined. - 10914965
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause Neonatal jaundice.
- Investigation of prolonged neonatal jaundice. Acta paediatrica (Oslo, Norway : 1992), 2000 Jun [Go to PubMed]
- Jaundice persisting beyond 14 d of age (prolonged jaundice) can be a sign of serious underlying liver disease. Protocols for investigating prolonged jaundice vary in complexity and the yield from screening has not been assessed. In order to address these issues, we carried out a prospective study of term infants referred to our neonatal unit with prolonged jaundice over an 18 mo period. Infants were examined by a paediatrician and had the following investigations: a total and conjugated serum bilirubin, liver function tests, full blood count, packed cell volume, group and Coombs' test, thyroid function tests, glucose-6-phosphate dehydrogenase levels and urine for culture. One-hundred-and-fifty-four infants were referred with prolonged jaundice out of 7,139 live births during the study period. Nine infants were referred to other paediatric specialties. One infant had a conjugated hyperbilirubinaemia, giving an incidence of conjugated hyperbilirubinaemia of 0.14 per 1,000 live births. Diagnoses included: giantcell hepatitis (n = 1), hepatoblastoma (n = 1), trisomy 9p (n = 1), urinary tract infections (n = 2), glucose-6-phosphate dehydrogenase deficiency (n = 3) and failure to regain birthweight (n = 1).
In conclusion, a large number of infants referred to hospital for prolonged jaundice screening had detectable problems. The number of investigations may safely be reduced to: a total and conjugated bilirubin, packed cell volume, glucose-6-phosphate dehydrogenase level (where appropriate), a urine for culture and inspection of a recent stool sample for bile pigmentation. Clinical examination by a paediatrician has a vital role in the screening process. - 17909678
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause Neonatal jaundice .
- A review of Orang Asli newborns admitted to a neonatal unit in a Malaysian general hospital. Singapore medical journal, 2007 Oct [Go to PubMed]
- The Orang Asli are the indigenous population in peninsular Malaysia and are in fact a diverse sub-ethnic group with different languages. Our aim was to collect data on Orang Asli newborns, from western and central Pahang, that were admitted to a general hospital with paediatric specialist services.
This is a retrospective study of all Orang Asli neonates admitted to the Neonatal Unit in Temerloh Hospital over a one-year period (2003).
There were 65 Orang Asli admissions out of a total of 1,543 admissions to our Neonatal Unit. The average birth weight was 2,569 g. The commonest indication for admission was neonatal jaundice secondary to glucose-6-phosphate dehydrogenase deficiency. Ten babies were ventilated, seven for prematurity and three for mild-moderate perinatal asphyxia. There were three deaths: a baby with a lethal congenital abnormality, one with congenital rubella syndrome with cardiac failure, and a preterm baby delivered at 28 weeks gestation, with late neonatal sepsis.
This is the first attempt to assess the health status of Orang Asli neonates in peninsular Malaysia. There are no published reports on the health status of this group of neonates. A larger multicentre study is needed to determine the exact health status of Malaysian Orang Asli newborns. - 16205054
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause hyperbilirubinemia and Neonatal jaundice.
- The effectiveness of oral tin mesoporphyrin prophylaxis in reducing bilirubin production after an oral heme load in a transgenic mouse model. Biology of the neonate, 2006 [Go to PubMed]
- Neonatal jaundice is commonly encountered and rarely associated with morbidity and mortality. Nonetheless, infants with glucose-6-phosphate dehydrogenase deficiency often have hemolysis (a heme load) caused by an environmental oxidant trigger, thus increasing their risk for serious morbidity. The use of tin mesoporphyrin (SnMP) has been proposed for interdicting the development of severe hyperbilirubinemia in a variety of conditions.
We studied the in vivo effects of prophylactic oral SnMP on heme oxygenase (HO) activity and bilirubin production, as indexed by the excretion rate of carbon monoxide (VeCO), following a subsequent oral heme load.
Adult mice were exposed serially to heme and assessed for in vivo bilirubin production rates, HO-1 transcription and protein, and HO activity. The effect of prophylaxis with a single oral dose of SnMP prior to an oral heme load was assessed by measuring VeCOand tissue HO activities.
After serial heme exposures, VeCO, HO-1 transcription and protein, and liver and spleen HO activities increased incrementally. After pretreatment with oral SnMP, bilirubin production decreased in response to an oral heme load. Also, heme-mediated increases in liver, spleen, and intestine HO activities were significantly dampened.
A single oral dose of SnMP results in durable inhibition of bilirubin production and HO activity for at least 24 h in a mouse model of oral heme loading. Further studies are needed to fully elucidate the duration of this protection against hyperbilirubinemia due to a delayed heme load and any long-term consequences of prophylaxis with SnMP on HO-1 transcription and HO-1 protein. - 23616073
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal jaundice and Neonatal hyperbilirubinemia .
- Influence of changes in the evaluation of neonatal jaundice. American journal of perinatology, 2014 Mar [Go to PubMed]
- To study the influence of policy changes in the evaluation of neonatal hyperbilirubinemia on discharge process from the nursery. Changes included early assessment of risk factors by universal umbilical blood sampling for blood type, Coombs test, and glucose-6-phosphate dehydrogenase (G6PD) and universal noninvasive transcutaneous bilirubinometry at discharge.
The 1,569 newborns (≥ 36 weeks' gestation) admitted after the implementation of changes were compared with the 1,822 born before.
Policy changes improved the diagnosis of G6PD deficiency and ABO incompatibility and decreased the number of referrals from the community for jaundice follow-up. The average number of needlesticks per baby as well as the time required for the analysis of serum bilirubin levels on discharge day decreased. Changes did not significantly increase costs.
Changes seem to have improved the quality of medical care, including early identification of risk factors and better follow-up of neonatal hyperbilirubinemia with reduction of pain and increased efficiency. - 15319464
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency can cause Neonatal hyperbilirubinemia .
- Risk factors for severe hyperbilirubinemia in neonates. Pediatric research, 2004 Nov [Go to PubMed]
- The incidence of severe neonatal hyperbilirubinemia is higher in Asians than in whites. A case-control study was designed to investigate the effects of eight known risk factors [breast feeding, ABO incompatibility, premature birth, infection, cephalohematoma, asphyxia, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and variant UDP-glucuronosyltransferase 1A1 (UGT1A1) gene] and a suspicious analog [organic anion transporter 2 (OATP 2) gene] on severe hyperbilirubinemia in Taiwanese neonates. The 72 study subjects and 100 hospital control subjects consisted of neonates with peak serum bilirubin levels > or =342 microM and <256.5 microM, respectively. The PCR-restriction fragment length polymorphism method was applied to detect the UGT1A1, OATP 2, and G6PD genes. The results of multivariate logistic regressions, adjusted for covariates, revealed odds ratios (ORs) of 4.64 [95% confidence interval (CI): 2.25-9.57; p < 0.001], 3.36 (95% CI: 1.54-7.35; p=0.002), and 3.02 (95% CI: 1.30-6.99; p=0.010) for neonates who were fed with breast milk, and carry the variant UGT1A1 gene at nucleotide 211 and the variant OATP 2 gene at nucleotide 388, respectively. The ORs, adjusted for covariates, for the other six risk factors were not statistically significant. The ORs in neonates who had one, two, and three significant risk factors were 8.46 (95% CI: 2.75-34.48; p < 0.001), 22.0 (95% CI: 5.50-88.0; p < 0.001), and 88.0 (95% CI: 12.50-642.50; p < 0.001), respectively. In conclusion, neonates who carry the 211 and 388 variants in the UGT1A1 and OATP 2 genes, respectively, as well as feed with breast milk are at high risk to develop severe hyperbilirubinemia.
- 1160703
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase-deficient can cause Neonatal jaundice .
- Neonatal jaundice and glucose-6-phosphate dehydrogenase deficiency in Papua New Guinea. The Medical journal of Australia, 1975 Apr 5 [Go to PubMed]
- Of 50 jaundiced neonatal patients studied at the Port Moresby General Hospital, 11 (22%) were found to be glucose-6-phosphate dehydrogenase-deficient. No apparent exogenous precipitating causes for the jaundice were noted. Serum bilirubin levels exceeded 20 mg/100 ml in seven of these glucose-6-phosphate dehydrogenase-deficient infants, and exchange transfusions were required for three subjects. Glucose-6-phosphate dehydrogenase deficiency must be considered in the differential diagnosis of neonatal jaundice in Papua New Guinea.
- 12737938
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD Sumaré is a variant causing chronic nonspherocytic hemolytic anemia.
- Mild hemolysis in a girl with G6PD Sumaré (class I variant) associated with G6PD A-. diseases, [Go to PubMed]
- In the present study we describe the clinical and laboratory features of a female child, a compound heterozygote for glucose-6-phosphate dehydrogenase (G6PD) Sumaré (1292T-->G) and African variants (202G-->A). G6PD Sumaré is a variant causing chronic nonspherocytic hemolytic anemia. The child had neonatal jaundice 2 days after birth and needed phototherapy for 8 days. Since then, she has not had episodes of dark urine or new episodes of jaundice. She has not had hemolytic crises in spite of five respiratory infections and antibiotics administration. Laboratory data showed a reticulocytosis (5.6%) without anemia and serum unconjugated bilirubin at the upper limit of the normalcy. No hemoglobin and hemosiderin in the urine were detected. G6PD activity at 37 degrees C was 1.15 UI/g Hb and G6PD cellulose acetate electrophoresis at pH 9.0 revealed two bands, in equal amounts, with normal and faster migration, respectively. She was homozygous for the normal (TA)6(TA)6 repeat in the UGT1A1 promoter. We conclude that the association of G6PD Sumaré and G6PD A- gave rise to a very mild chronic hemolysis, and the red cell population containing G6PD A- is probably enough to protect against severe chronic hemolysis.
- 18165833
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause severe Neonatal jaundice.
- Clostridium difficile infection precipitating hemolysis in glucose-6-phosphate dehydrogenase-deficient preterm twins causing severe neonatal jaundice. Journal of perinatology : official journal of the , 2008 Jan [Go to PubMed]
- The incidence of glucose-6-phosphate dehydrogenase deficiency in neonates of immigrant mothers in Canada is increasing. Newborn screening programs in Canada do not screen for this disorder. Infants with G-6-PD deficiency may develop jaundice resulting in kernicterus with devastating sequelae. In this case report, we speculate that Clostridium difficile infection may have triggered severe jaundice in G-6-PD-deficient neonates.
- 12093957
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficiency can couse neonatal jaundice
- Isoimmunization is unlikely to be the cause of hemolysis in ABO-incompatible but direct antiglobulin test-negative neonates. Pediatrics, 2002 Jul [Go to PubMed]
- It is stated that the direct antiglobulin (Coombs') test (DAT) may be negative in ABO hemolytic disease of the newborn. Thus, significant jaundice in neonates who are A-B incompatible with their mothers but DAT test negative is often attributed to isoimmunization and another diagnosis is not sought. We wished to determine the rate of bilirubin production, as an objective measure of hemolysis, in 2 groups of DAT-negative neonates--ABO-compatible and ABO-incompatible--and in DAT-positive ABO-incompatible neonates.
In consecutive, term, healthy newborns who were admitted to the general care nursery, we measured the level in parts per million (ppm) of end-tidal breath carbon monoxide (CO), corrected for inspired CO (ETCOc), an index of the rate of bilirubin production. We compared the levels in DAT-negative ABO-incompatible neonates with those in ABO-compatible neonates and with the levels in DAT-positive ABO-incompatible neonates. Statistical analysis was performed using 2-sample t and chi(2) tests.
There was no significant difference between the mean 12-hour ETCOc levels in DAT-negative ABO-incompatible neonates (n = 60, 2.2 +/- 0.6 ppm) versus DAT-negative ABO-compatible neonates (n = 171, 2.1 +/- 0.6 ppm), although there was a difference between the mean levels in DAT-positive ABO-incompatible neonates (n = 14, 3.4 +/- 1.8 ppm) and the DAT-negative groups. Four DAT-negative ABO-incompatible neonates had elevated ETCOc levels; in 2, we diagnosed a specific hematologic abnormality, namely, glucose-6-phosphate dehydrogenase deficiency in 1 and elliptocytosis in the other.
In DAT-negative newborns with significant jaundice or increased bilirubin production, even if ABO-incompatible, a cause other than isoimmunization should be sought. - 9099326
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD)-deficient is one couse of neotanal jaundice
- Photooxidant injury to glucose-6-phosphate dehydrogenase-deficient erythrocytes with bilirubin as the sensitizer--an in vitro study. Acta paediatrica (Oslo, Norway : 1992), 1997 Mar [Go to PubMed]
- To evaluate the hypothesis that glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes are more prone to photooxidant injury with bilirubin as the sensitizer, we compared the malonyl dialdehyde (MDA) levels and haematocrit values in 11 G6PD-deficient samples with a bilirubin: albumin molar ratio of 1:2 (10 mg% bilirubin, 2.5 g % albumin) photoexposed at 6 microW cm-2 nm-2 (420-460 nm), with 11 of control samples. Twelve hours after photoexposure the incremental changes in MDA levels (OD units) were higher in G6PD-deficient samples [mean (SE) = 0.230 (0.171) vs 0.075 (0.043), p < 0.01]. Antioxidant drugs may have a protective role while G6PD-deficient neonates undergo phototherapy.
- 933922
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficiency may cause jaundice
- The mortality of exchange transfusions. The Medical journal of Australia, 1976 Apr 3 [Go to PubMed]
- A prospective study of the effect and mortality of exchange transfusion was carried out in the Kandang Kerbau Hospital, Singapore. Altogether 140 exchange transfusions were performed on 122 infants. The exchanges were done for hyperbilirubinaemia due to"
idiopathi"
jaundice, ABO haemolytic disease, and glucose-6-phosphate dehydrogenase deficiency. Eight infants deteriorated during the exchange, in three of whom the procedure had to be terminated prematurely. Two deaths occurred two days after the exchange--the procedure being partly responsible in one case; necrotizing enterocolitis was present in addition to the kernicterus. Exchange transfusion is not without hazards, and should be performed carefully with close monitoring of the clinical status of the infant during and immediately after the procedure. - 12777545
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficiency may cause neonatal jaundice
- Infants with bilirubin levels of 30 mg/dL or more in a large managed care organization. Pediatrics, 2003 Jun [Go to PubMed]
- To describe the incidence, etiology, treatment, and outcome of newborns with total serum bilirubin (TSB) levels >or=30 mg/dL (513 micro mol/L).
Population-based case series.
Eleven Northern California Kaiser Permanente Medical Care Program hospitals and 1 affiliated hospital.
Eleven infants with TSB levels of >or=30 mg/dL in the first 30 days after birth, identified using computer databases from a cohort of 111,009 infants born 1995-1998.
Clinical data from the birth hospitalization, rehospitalization, and outpatient visits in all infants; psychometric testing at age 5 (N = 3), neurologic examinations by child neurologists at age 5 (N = 3), or primary care providers (N = 7; mean age: 2.2 years); Parent Evaluation of Developmental Status (N = 8; mean age: 4.2 years).
Maximum TSB levels of the 11 infants ranged from 30.7 to 45.5 mg/dL (525 micro mol/L to 778 micro mol/L; mean: 34.9 mg/dL [597 micro mol/L]). Four were born at 35 to 36 weeks gestation, and 7 were exclusively breastfed. Two had apparent isoimmunization; the etiology for the other 9 remained obscure, although only 4 were tested for glucose-6-phosphate dehydrogenase deficiency and 1 was bacteremic. None had acute neurologic symptoms. All received phototherapy and 5 received exchange transfusions. One infant died of sudden infant death syndrome; there was no kernicterus at autopsy. Two were lost to follow-up but were neurologically normal when last seen for checkups at 18 and 43 months. One child was receiving speech therapy at age 3. There were no significant parental concerns or abnormalities in the other children.
In this setting, TSB levels >or=30 mg/dL were rare and generally unaccompanied by acute symptoms. Although we did not observe serious neurodevelopmental sequelae in this small sample, additional studies are required to quantify the known, significant risk of kernicterus in infants with very high TSB levels. - 23719252
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice
- Nonimmune hydrops fetalis caused by G6PD deficiency hemolytic crisis and congenital dyserythropoietic anemia. Journal of perinatology : official journal of the , 2013 Jun [Go to PubMed]
- We present a case of a female neonate who had a nonimmune hydrops fetalis and severe hemolytic anemia due to a rare combination of glucose-6-phosphate dehydrogenase (G6PD) deficiency and congenital dyserythropoietic anemia. We conclude that in severe cases with persistent anemia one should search after delivery for a second reason other than G6PD deficiency alone.
- 16493435
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice
- Glucose-6-phosphate dehydrogenase deficiency in triplets of African-American descent. Journal of perinatology : official journal of the , 2006 Mar [Go to PubMed]
- Despite the prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency in African Americans, the disorder maybe often overlooked as a diagnosis in the absence of overt signs of hemolysis in neonates with hyperbilirubinemia. We present a case report of anemia and prolonged hyperbilirubinemia due to G6PD deficiency in the absence of hemolysis in dichorionic, triamniotic, preterm triplets of African-American descent.
- 12369486
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Randomized Controlled Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice
- Serum bilirubin levels in 1-month-old, healthy, term infants from southern Turkey. Annals of tropical paediatrics, 2002 Sep [Go to PubMed]
- This study investigated bilirubin levels in 282 1-month-old, healthy, term infants from the Adana region in southern Turkey. Total bilirubin was > 5 mg/dl in 20.2% of the infants and > 10 mg/dl in 6% of the group. Thyroid function and levels of alanine aminotransferase, aspartate aminotransferase and glucose-6-phosphate dehydrogenase were determined in babies with bilirubin levels > 5 mg/dl. The results were normal in all but one case, an infant with a bilirubin level of > 10 mg/dl and glucose-6-phosphate dehydrogenase deficiency. The results indicate that in this population a 5-mg/dl cut-off level for further investigation would mean that 20% of all infants would require further evaluation. This is not cost-effective. Based on our findings, we suggest that the cut-off level for investigating prolonged jaundice in term, 1-month-old, healthy infants in the Turkish population should be > 5 mg/dl.
- 6882560
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficiency may cause jaundice
- [Kinetics of erythrocyte populations in newborn infants with hyperbilirubinemia]. Bollettino della Società italiana di biologia spe, 1983 May 30 [Go to PubMed]
- Determinations of erythrocyte glucose-6-phosphate dehydrogenase, pyruvate kinase and glucose-phosphate isomerase activities have been carried out in jaundiced and non-jaundiced newborn infants at birth and after 5 days of life. Only hyperbilirubinemias of unknown etiology have been considered. Previous investigations have demonstrated that erythrocyte age dependent enzyme activities decrease in the healthy newborn during the first week of life. Following the results of the present paper, jaundiced newborns do not show such a decrease, since a statistically significant difference between paired data of glucose-6-phosphate dehydrogenase and pyruvate kinase in jaundiced and non-jaundiced newborns have been found. It is likely that the lack of decrease of enzyme activities in the jaundiced infants depend upon the loss of oldest red cells with low glucose-6-phosphate dehydrogenase and pyruvate kinase. Our observation suggests the occurrence of a slight hemolysis in newborn infants with hyperbilirubinemia of unknon etiology.
- 20497361
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD deficiency were independent predictors for PUJ while using of oxytocin during labor.
- Natural history and predictive risk factors of prolonged unconjugated jaundice in the newborn. Pediatrics international : official journal of the, 2010 Oct [Go to PubMed]
- This study aimed to investigate the natural course and risk factors for prolonged unconjugated jaundice (PUJ) in neonates.
This was a prospective descriptive study conducted in a tertiary care referral hospital of Northern India. The study included neonates who presented with clinical jaundice beyond 14 days of age. A detailed history, clinical examination and investigations were performed in all. All were followed till the normalization of clinical jaundice or up to 8 weeks of age, whichever was earlier. The key outcome measure was time to normalization of PUJ. Predictive risk factors for PUJ were analyzed by comparing with matched controls. Regression analysis was done for independent predictive risk factors of PUJ.
A total of 71 infants presented with prolonged jaundice (PJ). Out of these, 66 infants (93%) had PUJ. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was the most commonly identified association of PUJ (24%). The median duration of jaundice in infants with PUJ was 5 weeks (range: 5-8). PJ in siblings (OR 2.9 [1.1-7.6]), oxytocin use during labor (OR 3.4 [1.1-10.4]) and G6PD deficiency (OR 4.0 [1.1-14.1]) were independent predictors of PUJ.
Irrespective of the etiology, by 8 weeks, PUJ disappeared in all infants. G6PD deficiency was the most common association of PUJ. A history of PJ in siblings, use of oxytocin during labor and G6PD deficiency were independent predictors for PUJ. - 1445122
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice.
- Jaundice: clinical practice in 88,000 liveborn infants. gynaecology, 1992 Aug [Go to PubMed]
- We reviewed jaundiced infants born between 1971 and 1989. Jaundice was diagnosed in infants whose serum bilirubin level was found to be 154 umol/l or greater. Of 88,137 livebirths, 10,944 (12.4%) were jaundiced. The most common aetiological factor was prematurity (20.3%), followed by ABO erythroblastosis (5.5%), sepsis (1.8%), Rh erythroblastosis (1.8%), bruising (1.3%), multifactorial (1.0%) and glucose-6-phosphate dehydrogenase deficiency (0.5%). In the remainder (67.8%) no cause was found or inadequate investigations were performed to determine a cause. During the period under review there was a significant increase (r = 0.91) in the proportion of newborn infants with jaundice of prematurity, in those not investigated (r = 0.92) and a decrease in the proportion with bruising (r = -0.90) as the cause. Phototherapy was used on 4,126 (37.7%) infants and exchange transfusion performed on 248 (2.3%). Causes of jaundice in infants requiring exchange transfusion were Rh erythroblastosis (108, 43.6%), ABO erythrolastosis (58, 23.4%), jaundice of prematurity (44, 17.7%) and a variety of causes in the remaining 38 (15.3%). Death occurred in 164 (1.5%) infants. In only 7 (4.3%), however, was the death possibly related to hyperbilirubinaemia or its treatment (Rh erythroblastosis (4), necrotizing enterocolitis following exchange transfusion (2) and pulmonary haemorrhage following exchange transfusion (1)). Phototherapy proved safe with no deaths attributable to its use.
- 6674910
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Human essential enzyme,alternatively known as phosphoglucose isomerase or phosphohexose isomerase.
- Effect of phenobarbital treatment on erythrocyte glucose-6-phosphate dehydrogenase in human newborns. Pediatric pharmacology (New York, N.Y.), 1983 [Go to PubMed]
- The effect of phenobarbital (PB) treatment on erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) levels was studied in normal and G-6-PD-deficient human newborns. An increase of erythrocyte G-6-PD levels was observed in normal G-6-PD patients, while increase in the enzymatic activity was not observed in G-6-PD-deficient neonates.
- 367457
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency was found to be one cause of hyperbilirubinemia in newborn infants .
- Agar in control of hyperbilirubinemia of full-term newborn infants with erythrocyte G-6-PD deficiency. Biology of the neonate, 1978 [Go to PubMed]
- 40 full-term newborn infants with erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) deficiency were used for a study concerning the effectiveness of agar per os in preventing severe hyperbilirubinemia. 20 randomly selected neonates were given agar (1 g/kg/day) orally in 4 daily doses from their 1st to their 5th day of life. 20 infants were not treated and served as controls. Three exchange transfusions were performed in the experimental as well as in the control group. According to these results, agar does not seem to be effective in preventing severe hyperbilirubinemia, which frequently occurs in newborn infants with erythrocyte G-6-PD deficiency.
- 12368976
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency was considered related with unexplained hemolysis or hyperbilirubinemia in newborn infants.
- Hemolysis and hyperbilirubinemia in an African American neonate heterozygous for glucose-6-phosphate dehydrogenase deficiency. Journal of perinatology : official journal of the , [Go to PubMed]
- Despite recent case reports of bilirubin encephalopathy in African American glucose-6-phosphate dehydrogenase (G6PD)-deficient neonates, there is a misconception that, in African Americans, G6PD deficiency need not be considered in the differential diagnosis of hyperbilirubinemia. We present a case of a hyperbilirubinemic African American female neonate in whom coexisting G6PD deficiency in the heterozygous state, and Gilbert's syndrome, were confirmed by DNA analysis. Hemolysis, predictive of the subsequent icterus, was documented by end-tidal carbon monoxide determinations at two time periods within the first 25 hours of life. A diagnosis of G6PD deficiency should be considered in African American neonates, females as well as males, with unexplained hemolysis or hyperbilirubinemia.
- 6414449
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- Summary
- Glucose-6-phosphate dehydrogenase deficiency may cause Neonatal jaundice.
- Jaundice: a 10 year review of 41,000 live born infants. Australian paediatric journal, 1983 Jun [Go to PubMed]
- A review is presented of jaundiced newborn infants during the 10-year period to 1980. Included are those whose serum bilirubin level was 154 mumol/l or more. Of 41,057 live births, 4,406 (10.7%) infants had hyperbilirubinaemia. The most common (19.9;%) aetiological factor was prematurity, followed by ABO erythroblastosis 7.1%; sepsis 3.4%; Rhesus erythroblastosis 2.7%; bruising 2.2%; multifactorial 1.0% and glucose-6-phosphate dehydrogenase deficiency 0.5%. Treatment was not undertaken in 2,855 (64.7%) infants, but 1,419 (32.2%) received phototherapy alone, 122 (2.7%) infants received both exchange transfusion and phototherapy and 10 (0.2%) infants received exchange transfusion alone. Of the infants requiring exchange transfusion 50.0% had Rhesus erythroblastosis, 28.0% ABO erythroblastosis, 10.6% jaundice of prematurity and the remainder were due to a variety of causes. Sixty-three (1.4%) infants died, with two deaths being related to the hyperbilirubinaemia, as their death was due to necrotizing enterocoliis following exchange transfusion. Phototherapy proved safe with no deaths directly attributable to its use.
- 9848766
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- Summary
- Glucose-6-phosphate dehydrogenase deficient may cause hyperbilirubinemia.
- Favism by proxy in nursing glucose-6-phosphate dehydrogenase-deficient neonates. Journal of perinatology : official journal of the , [Go to PubMed]
- Two nursing neonates deficient in glucose-6-phosphate dehydrogenase developed severe hyperbilirubinemia despite phototherapy. Mothers of both the infants had recently eaten fava beans. The hemolytic triggers found in fava beans may have been absorbed by the mothers and excreted in their breast milk. Carboxyhemoglobin determination performed on one of the infants reflected ongoing hemolysis.
- 1468858
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency effects the PSB level and the incidence rate of severe Neonatal jaundice.
- Association between glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice: interaction with multiple risk factors. International journal of epidemiology, 1992 Oct [Go to PubMed]
- This nonconcurrent cohort study was carried out to evaluate the association of neonatal jaundice with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and its interactions with other risk factors. The G-6-PD enzyme activity of 12,379 neonates was screened by a semi-quantitative fluorometric assay and double-checked by a quantitative method to identify a G-6-PD deficient cohort of 333 neonates. Matched with these on birth date, sex and delivery hospital were a G-6-PD normal cohort of 653 neonates. Neonatal jaundice was defined by a peak serum bilirubin (PSB) level of > or = 15 mg/dl. A significant association between G-6-PD deficiency and neonatal jaundice was observed in male but not female neonates. There was an inverse dose-response relation between G-6-PD activity and neonatal jaundice among male neonates. Both hypoxia/asphyxia and maternal hepatitis B surface antigen (HBsAg) carrier status were associated with an increased risk of neonatal jaundice among G-6-PD deficient but not G-6-PD normal male neonates. Based on multiple regression analyses, an additively synergistic effect on PSB level and severe jaundice (PSB > or = 20 mg/dl) was observed for G-6-PD deficiency and maternal HBsAg carrier status.
Researchers compared data on 333 newborns with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency at 5 public and 5 private hospitals in Taiwan with data on 653 birth date, sex, and delivery hospital matched newborns to examine the peak serum bilirubin (PSB) level and incidence of neonatal jaundice of both G-6-PD deficient and G-6-PD normal newborns. They also wanted to determine whether an association exists between G-6-PD activity level and incidence of neonatal jaundice and associations between G-6-PD deficiency and other likely risk factors of neonatal jaundice. A significant association between G-6-PD deficiency and neonatal jaundice existed among male neonates but not female neonates. Male neonates had a considerably higher incidence of neonatal jaundice than did female neonates (11.6% vs. 6.2%). There was a significant inverse dose-response relationship between G-6-PD activity and neonatal jaundice among the male neonates (p.01). For example, the relative risk was 1.78 for 20.1-29.9 relative intensty, 2.01 for 15.1-20, 2.61 for 10.1-15, and 4.07 for 10. Maternal hepatitis B surface antigen (HBsAg) carrier status and hypoxia/asphyxia significantly increased the risk for G-6-PD deficiency in male neonates (p.05). The multiple regression analysis indicated a significant effect of G-6-PD deficiency on the PSB level and the incidence rate of severe neonatal jaundice. There was a similar significant interaction between G-6-PD deficiency and maternal HBsAg carrier status. - 8571933
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- The nucleotide substitution at 1376 is the most common and important mutation for G6PD deficiency in Chinese neonates in Taiwan.
- Neonatal jaundice and molecular mutations in glucose-6-phosphate dehydrogenase deficient newborn infants. American journal of hematology, 1996 Jan [Go to PubMed]
- Molecular mutations of the glucose-6-phosphate dehydrogenase (G6PD) gene and clinical manifestations of neonatal jaundice in 112 male and 50 female Chinese neonates with G6PD deficiency were studied. In the 112 males, the nucleotide (nt) 1376 (G-->T) mutation was the dominant type (50.0%), followed by nt 1388 (G-->A) (16.1%), nt 493 (A-->G) (8.0%), nt 1024 (C-->T) (6.2%), nt 95 (A-->G) (5.4%), nt 392 (G-->T) (1.8%), nt 487 (G-->A) (1.8%), nt 871 (G-->A) (0.9%), and nt 1360 (C-->T) (0.9%). The nt 871 variant has not been reported in Taiwan before. The occurrence rates for nt 1376, nt 1388, nt 493, nt 95, and nt 1024 mutations in the 50 females were 44.0%, 18.0%, 12.0%, 6.0%, and 6.0%, respectively. The type of G6PD mutation in 10 male and 7 female neonates has not been identified yet. Although G6PD deficient neonates had higher frequency of phototherapy than G6PD normal neonates in both sexes, a significant difference in the prevalence of hyperbilirubinemia (peak bilirubin > or = 15.0 mg/dl) between G6PD deficient and normal neonates was found only in males. Further analysis showed that duration of phototherapy was longer in G6PD deficient male neonates than in the control group, while the outcome of phototherapy was better in subjects with non-nt 1376 mutations than subjects with the nt 1376 mutation. Most (78.3%) of the 23 G6PD deficient neonates who subsequently suffered from neonatal hyperbilirubinemia carried the nt 1376 mutation. The results of this study indicate that the nucleotide substitution at 1376 is the most common and important mutation for G6PD deficiency in Chinese neonates in Taiwan.
- 12680285
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency can couse Neonatal jaundice.
- [Glucose-6-phosphate dehydrogenase deficiency, neonatal hyperbilirubinemia and Gilbert syndrome]. Acta médica portuguesa, [Go to PubMed]
- The aim of this work was to evaluate the influence of abnormal UDP-glucoronosyltransferase-1 (UGT1A1) gene variant, on the incidence and severity of neonatal hyperbilirubinemia, in glucose-6-phosphate dehydrogenase (G6PD) deficient newborns. The A(TA)nTAA region in the promoter of the UGT1A1 gene was analysed in 20 children with G6PD deficiency. Fourteen of these children had the African type variant (G6PDA-) and 6 had different variants (G6PDNara, G6PDGuadalajara, G6PDDurham, G6PDTomah, G6PDAveiro e G6PDNashville) related to chronic nonspherocytic haemolytic anaemia (CNSHA). The existence of a positive history of neonatal hyperbilirubinemia, as well as its severity was registered. The incidence of neonatal hyperbilirubinemia was increased in this group of children (90%) and was not associated with abnormal alleles of the UGT1A1 gene. It was not possible to assess the influence of abnormal alleles in the severity of the neonatal hyperbilirubinemia. However, these abnormal alleles did not account for the seveity of jaundice in children who presented variants related to CNSHA, since 5 were treated with an exchange transfusion and none presented abnormal alleles.
- 7919613
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency can couse Neonatal jaundice.
- Severe neonatal jaundice associated with glucose-6-phosphate dehydrogenase deficiency: pathogenesis and global epidemiology. Acta paediatrica (Oslo, Norway : 1992). Supplement, 1994 Mar [Go to PubMed]
- The association of glucose-6-phosphate dehydrogenase deficiency (G6PD def) with severe neonatal jaundice (NJ) and Kernicterus was described just over 30 years ago in reports from Sardinia (1-4) Singapore (5,6) and Greece (7,8). In this review we will examine the progress made since that time in our understanding of the pathophysiology of severe NJ associated with G6PD def, its global epidemiology, and its role in the balanced polymorphism of the G6PD def gene (Gd). Including this review in the Festschrift to Spyros Doxiadis should highlight his contribution to the field. In Greece the search for a new cause of severe NJ and Kernicterus was triggered by his realization that the recognized at the time, causes of severe NJ were absent in a large proportion of the neonates treated at the"
Alexandr"
Maternity Hospital in Athens (9). - 12105841
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G6PD deficiency is one cause to Neonatal hyperbilirubinemia.
- Glucose-6-phosphate dehydrogenase deficiency, the UDP-glucuronosyl transferase 1A1 gene, and neonatal hyperbilirubinemia. Gastroenterology, 2002 Jul [Go to PubMed]
- Coinheritance of the A(TA)7TAA promoter variant in the uridine 5'-diphosphate-glucuronosyl transferase 1A1 (UGT1A1) gene and glucose-6-phosphate dehydrogenase (G6PD) deficiency is crucial to hyperbilirubinemia in white male neonates. A variation rate of 29.3% was determined within the coding region of the UGT1A1 gene in Taiwanese subjects, suggesting the hypothesis that this variation may influence incidence of hyperbilirubinemia in male neonates with G6PD deficiency.
The full sequence of the UGT1A1 gene was identified for 212 G6PD-deficient and 232 control male neonates by using polymerase chain reaction (PCR).
Both study and control groups were divided into 5 subgroups according to their UGT1A1 genotypes. Most subjects carried G to A variation at nucleotide 211 for both genotypes of heterozygous variation within coding region and homozygous variation. No significant differences were noted for the frequencies of the 5 UGT1A1 genotypes, gestation age, and birth weight comparing the G6PD-deficient and control groups. The incidence of hyperbilirubinemia, however, was significantly higher for the study group than for the controls. This difference was noted only for the subgroup bearing the homozygous variant of the UGT1A1 gene. In the subgroup of homozygous variation, the serum bilirubin value was significantly higher for G6PD-deficient neonates than for controls. All 11 G6PD-deficient neonates with the homozygous 211 G to A variation suffered from hyperbilirubinemia.
The results indicate that carriage of the homozygous 211 G to A variation within the coding region in the UGT1A1 gene is an additive risk factor for neonatal hyperbilirubinemia in G6PD-deficient Taiwanese male neonates. - 12663150
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- The lower G6PD enzyme activity was associated with the Neonatal hyperbilirubinemia in G6PD-deficient male neonates.
- Hyperbilirubinemia in healthy neonates with glucose-6-phosphate dehydrogenase deficiency. Early human development, 2003 Apr [Go to PubMed]
- A cohort study was carried out to assess the association between glucose-6-phosphate dehydrogenase (G6PD) deficiency, diagnosed by quantitative enzyme assay, and neonatal hyperbilirubinemia, defined as serum total bilirubin >/=15 mg/dl, in the well-baby nursery of Chang Gung Children's Hospital. Among 42,110 inborn infants, 757 male (3.54%) and 326 female (1.57%) newborns were G6PD-deficient. Compared to the occurrence of hyperbilirubinemia in G6PD-normal newborns (1.41% in male, 1.44% in female) in the well-baby nursery, a significantly higher incidence was observed in both G6PD-deficient male (11.36%) and female (7.06%) newborns. Further analyses demonstrated that the enzyme activity of G6PD in G6PD-deficient male newborns with hyperbilirubinemia (1.56+/-1.37 U/g Hb) were significantly lower than the subjects without hyperbilirubinemia (2.01+/-1.7 U/g Hb). No significant difference was observed in G6PD-deficient female newborns with hyperbilirubinemia (6.91+/-2.76 U/g Hb) compared to those without hyperbilirubinemia (7.81+/-2.84 U/g Hb). These data suggest that the G6PD-deficient neonates are at increased risk for hyperbilirubinemia even in the nursery free from agents that can potentially cause hemolysis to G6PD-deficient redcells. The lower G6PD enzyme activity was associated with the neonatal hyperbilirubinemia in G6PD-deficient male neonates.
- 8942026
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Neonatal screening programs for G-6-PDD is effectiveness to prevent severe Neonatal jaundice(NJ).
- Can severe neonatal jaundice be prevented by neonatal screening for glucose-6-phosphate dehydrogenase deficiency?--a review of evidence. Zhonghua Minguo xiao er ke yi xue hui za zhi [Jour, [Go to PubMed]
- An evidence-based approach is used to evaluate the neonatal screening program for glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. The primary consideration to include G-6-PD deficiency (G-6-PDD) in neonatal screening program was the public health burden of G-6-PDD-associated neonatal jaundice (G-6-PDDANJ) in the target population. However, the prevalence of G-6-PDD per se cannot be the sole index of the public health burden of G-6-PDDANJ. In more developed areas, G-6-PDDANJ is no longer a major public health problem. Further, most cases with G-6-PDDANJ in more developed areas are not precipitated by any identifiable icterogenic agents, and therefore not preventable by avoidance education. In less developed areas, however, G-6-PDDANJ is still a big public health burden and requires intervention. In this study, the effectiveness of neonatal screening programs for G-6-PDD to prevent severe neonatal jaundice(NJ) has been shown based on historical comparison, but the results may be confounded by other tempral factors. G-6-PDDANJ usually occurs in the first week after birth. Prompt need for G-6-PD screening results precludes it from incorporation into other existent neonatal screening programs (i.e., for PKU), and from centralization of laboratory work. The efficacy, adverse effects and cost-effectiveness of this mass screening program need further study.
- 1977848
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with Neonatal hyperbilirubinemia.
- Alpha-thalassemia minor and neonatal hyperbilirubinemia. Journal of the Formosan Medical Association = Taiw, 1990 May [Go to PubMed]
- Infants on this island are known to have higher incidences of neonatal hyperbilirubinemia and alpha-thalassemia minor than Caucasians. In order to investigate the correlation between these two conditions, we collected a total of 110 newborns with alpha-thalassemia minor delivered at the National Taiwan University Hospital during the period from January 1985 through February 1988 for this retrospective study. The infants in the study group were ascertained to have the condition by the presence of Hb Bart's with a concentration from 3% to 13%, in the cord blood. None of them had glucose-6-phosphate dehydrogenase (G6PD) deficiency. For each study infant, two control infants were selected. Criteria for enrollment in the control group were: (1) same sex; (2) absence of G6PD deficiency; and (3) birth time as close as possible to that of the study infant, with the 1st control born before the study infant and the 2nd control after. The timing of bilirubin quantitation was based on clinical judgement of jaundice by te pediatricians and phototherapy was started as indicated. Gestational age, birth weight, and rates of preterm delivery, low birth weight infants and low Apgar scores were comparable between the study and control groups. On day 3 after birth, the incidence of hyperbilirubinemia (bilirubin level over 10 mg/dl) was significantly lower in the study group than in the control group (0.9% vs 9.5%, Fisher's exact probability = 0.0012). However, the difference was not significant later. The incidence of phototherapy was also significantly lower in the study group (20%) than in the control group (31%).(ABSTRACT TRUNCATED AT 250 WORDS)
- 18185880
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficient may cause neonatal jaundice
- Identifying risk of neonatal hyperbilirubinaemia and early discharge for glucose-6-phosphate dehydrogenase deficient newborns in Singapore. Annals of the Academy of Medicine, Singapore, 2007 Dec [Go to PubMed]
- This study aims to compare and assess usefulness of day 3 and 4 (49 to 96 hours) pre-phototherapy total serum bilirubin (TSB) in predicting subsequent significant hyperbilirubinaemia (SHB) in glucose-6-phosphate dehydrogenase (G6PD) deficient neonates.
This prospective study was on all the G6PD deficient newborns weighing >2500 g. Day 3 and 4 pre-phototherapy TSB and phototherapy requirements in their first 2 weeks of life were analysed for its value in predicting subsequent SHB.
The frequency of G6PD deficiency was 2.4%, 1 per 42 live births (1.3% in males and 1.1% in females). Phototherapy was required in 51% of G6PD deficient infants, all within the first week of life. In the absence of SHB in the first week, the probability of its development in the second week was zero (95% confidence interval, 0 to 0.051). The day 4 pre-phototherapy TSB of <160 micromol/L predicted no measurable risk of subsequent SHB (sensitivity, 94%; 95% confidence interval, 83.5% to 97.9%; specificity 82.8%; 95% confidence interval, 71.1% to 90.4%).
G6PD deficient newborns without SHB in their first week of life were at no measurable risk of its development in the second week. Day 4 pre-phototherapy has better sensitivity and specificity compared to day 3 pre-phototherapy TSB in predicting the risk of subsequent SHB. Low-risk infants, thus identified, may be eligible for discharge on or before day 7 of life. Infants with Day 4 TSB <160 can be even discharge on day 4 with follow-up appointment. Evidence-based early discharge can decrease the social, emotional and financial burden of G6PD deficiency in Singapore. - 8354322
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Phototherapy would therefore seem to be a simple and effective method for the management of severe jaundice associated with G6PD deficiency.
- Efficacy of phototherapy in neonatal hyperbilirubinaemia associated with glucose-6-phosphate dehydrogenase deficient status. European journal of pediatrics, 1993 Jul [Go to PubMed]
- The efficacy of phototherapy in a group of 427 infants with hyperbilirubinaemia associated with glucose-6-phosphate dehydrogenase (G6PD) deficiency and a comparable group of 3924 G6PD normal infants with non-haemolytic hyperbilirubinaemia was evaluated. Phototherapy was highly effective in reducing bilirubin levels in both groups of infants, being significantly more effective in the group with normal G6PD status. Failure rate was very low (2.03/1000) in the group with normal G6PD status and nil in the G6PD deficient group. Bilirubin rebound after phototherapy was unremarkable with very few infants requiring a second exposure--4.68/1000 in the G6PD deficient group and 6.37/1000 in the G6PD normal group. All the babies tolerated phototherapy well. Phototherapy would therefore seem to be a simple and effective method for the management of severe jaundice associated with G6PD deficiency.
- 8628611
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- G-6-PD deficiency was considered related with unexplained hemolysis or hyperbilirubinemia in newborn infants.
- Henna: a potential cause of oxidative hemolysis and neonatal hyperbilirubinemia. Pediatrics, 1996 May [Go to PubMed]
- To evaluate the in vitro oxidation potential of lawsone (2-hydroxy-1,4 naphthoquinone). Lawsone is a chemical present in henna, the crushed leaves of which are used worldwide as a cosmetic agent to stain the hair, skin, and nails.
Venous blood from glucose-6-phosphate dehydrogenase (G6PD)-normal and G6PD A- subjects were incubated with various amounts of lawsone for 2 hours at 37 degrees C. Reduced glutathione and methemoglobin (MHb) levels were measured before and after incubation.
Final molar concentrations of lawsone in normal blood of 1.4, 2.8, 5.7, and 8.6 x 10-3 mol/L increased MHb percentages from 0.5% to 2.2%, 8.3%, 9.5% and 12.5%, respectively. In a C6PD A- blood, MHb percentages were 19.8%, 32.2%, 44.9%, and 53.9%. At a lawsone concentration of 2.8 x 10-3 mol/L, blood from 15 healthy adults formed MHb percentages of 7.4% +/- 3.3% (+/- 1 SD); in blood from 4 G6PD A- adults, percentages were 44.5%, 40.6%, 41.3%, and 42.8%. Simultaneous measurements of reduced glutathione revealed preincubation values of greater than 40 mg/100 mL of red cells in blood of healthy and G6PD A- subjects. Postincubation values were greater than 40 in blood of healthy subjects and less than 40 in blood of G6PD A- subjects.
These in vitro observations indicate that lawsone is an agent capable of causing oxidative hemolysis. In regions of the world where there is a high incidence of G6PD deficiency and unexplained hyperbilirubinemia, oxidative hemolysis secondary to the cutaneous application of henna could be the initiating event. - 807541
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency can cause neonatal jaundice.
- D-Glucaric acid excretion in newborns with severe jaundice of unknown etiology and due to glucose-6-phosphate dehydrogenase deficiency in Greece. Helvetica paediatrica acta, 1975 Jul [Go to PubMed]
- The urinary D-glucaric acid of 86 full-term newborns was determined on the 10th day of life. Of these, 28 had jaundice due to glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, 24 jaundice of unknown etiology and 18 Rhesus incompatibility. Practically all the cases of the first two groups had a greatly decreased D-glucaric acid excretion whereas this was not a constant finding in the 18 cases with Rh-incompatibility. Normal values were found in 16 healthy controls of the same age. These findings suggest that in severe neonatal jaundice due to G-6-PD deficiency and in jaundice of unknown etiology, there is a greatly reduced excretion of endogenously formed D-glucaric acid, due probably to decreased activity of liver enzymes involved in the metabolism of glucuronic acid. This defect probably contributes to the unconjugated hyperbilirubinemia in these newborns.
- 10699105
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency was considered related with unexplained hemolysis or hyperbilirubinemia in newborn infants.
- Predischarge bilirubin screening in glucose-6-phosphate dehydrogenase-deficient neonates. Pediatrics, 2000 Mar [Go to PubMed]
- To assess the validity of predischarge serum bilirubin values in determining or predicting hyperbilirubinemia in glucose-6-phosphate dehydrogenase (G-6-PD)-deficient neonates, and to facilitate appropriate discharge planning.
Serum total bilirubin values were determined between 44 and 72 hours of life in a cohort of term, healthy neonates at high-risk for G-6-PD deficiency but with no other risk factors for hyperbilirubinemia. Percentile-based bilirubin nomograms were constructed for G-6-PD-deficient infants and normal infants according to age at sampling. The incidence of hyperbilirubinemia (serum bilirubin value > or =256 micromol/L [15 mg/dL]) for each group was determined according to the percentiles for that group.
In both G-6-PD-deficient neonates (n = 108) and control neonates (n = 215) with serum bilirubin values <50th percentile for age, the incidence of hyperbilirubinemia was low in the G-6-PD-deficient neonates, with no measurable incidence in the controls. The incidence of hyperbilirubinemia became clinically consequential, and significantly higher in the G-6-PD-deficient groups, when the percentiles were > or =50: for those in the 50% to 74% range the incidence was moderate (23%) for the G-6-PD-deficient and small (7%) for the control infants (relative risk, 3.29; 95% confidence interval, 1.01-10.67). Among those infants > or =75th percentile, 82% of the G-6-PD-deficient infants, compared with 25% of the control infants, were either already hyperbilirubinemic at the time of screening or subsequently developed hyperbilirubinemia (relative risk, 3.23; 95% confidence interval, 1.99-5.24).
Timed, predischarge serum bilirubin screening can be used to identify G-6-PD-deficient neonates at low, intermediate, or high-risk of developing severe neonatal hyperbilirubinemia, and thus offer a selective approach to the discharge and follow-up surveillance of these infants. - 7567338
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency is one couse of Neonatal jaundice.
- Hospital readmission due to neonatal hyperbilirubinemia. Pediatrics, 1995 Oct [Go to PubMed]
- Severe neonatal hyperbilirubinemia can occur without apparent reason in term healthy breast-fed infants and some develop kernicterus. The aim of our study was to assess the incidence of severe hyperbilirubinemia in term healthy newborns discharged from the hospital. From January 1 through December 31, 1994, 6705 infants were delivered at Bikur-Cholim and Misgav-Ladach Community Hospitals. All 1448 newborns discharged with a serum bilirubin level > 10.0 mg/dL were instructed to return to the hospital within 3 days for follow-up, as well as bilirubin determination. Twenty-one newborns with a bilirubin level > 18.0 mg/dL were identified and readmitted at mean +/- standard deviation (SD) 5.5 +/- 1.8 (range, 5 to 10 days of life). This represents 1.7% of the 1220 infants who returned for follow-up examination. Mean +/- SD serum bilirubin levels at readmission were 19.6 +/- 2.5 mg/dL. All but one of the infants were breast-fed. No cases of ABO incompatibility were found and two newborns were glucose-6-phosphate dehydrogenase (G6PD)-deficient. Sepsis work-up and direct Coomb's tests were negative in all cases. None had hemolysis or were found to have any cause for hyperbilirubinemia other than breast-feeding. Phototherapy was provided in all but two cases, and an exchange transfusion was performed in one case. Three additional infants, with bilirubin levels < 10 mg/dL at discharge, were readmitted due to hyperbilirubinemia. One was diagnosed with neonatal hepatitis. We conclude that, based on our study population, 0.36% of term infants may subsequently develop severe neonatal hyperbilirubinemia in the first postnatal week.(ABSTRACT TRUNCATED AT 250 WORDS)
- 7472840
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- glucose-6 phosphate dehydrogenase deficiency may cause Neonatal jaundice. hemolysis is not a sufficient explanation for jaundice in G6PD-deficient newborn infants in the transitional period.
- Role of hemolysis in neonatal jaundice associated with glucose-6 phosphate dehydrogenase deficiency. The Journal of pediatrics, 1995 Nov [Go to PubMed]
- End-tidal carbon monoxide was measured in 108 newborn infants who had been screened for glucose-6-phosphate dehydrogenase (G6PD) deficiency. The mean +/- SD end-tidal carbon monoxide did not differ significantly between the G6PD-deficient and the normal neonates, 2.1 +/- 0.6 microliters/L and 2.0 +/- 0.5 microliters/L, respectively, within 12 hours of birth and 1.9 +/- 1.4 microliters/L and 1.5 +/- 0.7 microliters/L, respectively, at 48 to 72 hours after birth. On the basis of these measurements, hemolysis is not a sufficient explanation for jaundice in G6PD-deficient newborn infants in the transitional period.
- 9664196
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice.
- Current drug treatment options in neonatal hyperbilirubinaemia and the prevention of kernicterus. Drugs, 1998 Jul [Go to PubMed]
- Neonatal jaundice is a frequent problem in neonatology, but the advent of phototherapy which has simplified its treatment, it no longer represents a major concern. Early hospital discharge of neonates has now resulted in a re-emergence of kernicterus. Neonatal jaundice is principally the result of a transient deficiency of bilirubin conjugation, of a partial deficiency of hepatic bilirubin uptake and intracellular transport and of an increased enterohepatic circulation of the pigment. The fact that bilirubin production in the neonate is 2 or more times greater than in the adult per kilogram of bodyweight represents the mainstay of this condition. Prevention of kernicterus in full term infants is based on the detection of neonates at risk for developing hyperbilirubinaemia, and can be accomplished with simple tests performed on umbilical cord blood such as blood type, Rh, Coombs' test and glucose-6-phosphate dehydrogenase, in order to detect haemolytic diseases. The daily evaluation of transcutaneous bilirubi measurement gives additional information on the rise of serum bilirubin level, and can help to distinguish physiological from nonphysiological hyperbilirubinaemia. A significant hyperbilirubinaemia is more frequent in infants born before term, and in neonates who do not feed well and lose more than 10% of bodyweight. In preterm infants the typical clinical feature of kernicterus is seen very rarely, and kernicterus is now a very infrequent postmortem observation. Since it is very difficult to distinguish the effects of bilirubin from other potentially toxic factors, it is difficult to give guidelines for the treatment of jaundice in very low birthweight infants other than to keep the serum bilirubin levels to a lower level than in full term infant (e.g. 10 mg/dl lower than in full term babies). The intramuscular administration of a single dose of Sn-mesoporphyrin (6 mumol/kg bodyweight) in healthy term or near-term infants seems to be a promising treatment modality for controlling hyperbilirubinaemia.
- 22028581
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is an X-linked recessive disease, which leads to hemolytic anemia and jaundice.
- Hypohidrotic ectodermal dysplasia associated with glucose-6-phosphate dehydrogenase deficiency. Annals of dermatology, 2011 Sep [Go to PubMed]
- Hypohidrotic ectodermal dysplasia (HED) is a syndrome characterized by hypodontia, hypotrichosis, and partial or total ecrine sweat gland deficiency. The most prevalent form of HED is inherited as an X linked pattern. Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency is an X-linked recessive disease, which leads to hemolytic anemia and jaundice. It is expressed in males, while heterozygous females are usually clinically normal. A 12-year-old boy with the complaints of hair and eyebrow disturbances, teeth disfigurement, decreased sweating, and xerosis presented to the outpatient clinic. Dermatological examination revealed sparse hair and eyebrows, conical-shaped teeth, xerosis, syndactylia, transverse grooves, and discoloration of nails. Laboratory findings indicated anemia. His 3-year-old sister also had sparse hair and eyebrows, xerosis, and syndactylia. We learned that the patient had a previous history of neonatal jaundice and a diagnosis of G-6-PD deficiency. Although it has been shown that loci of etodermal dysplasia and G-6-PD deficiency genes are near to one another, we did not find any case study reporting on occurrence of these two genetic diseases together. With the aspect of this rare and interesting case, the relationship between HED and G-6-PD deficiency was defined.
- 11275655
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice.
- Prevention of bilirubin encephalopathy. Biology of the neonate, 2001 [Go to PubMed]
- Prevention of bilirubin encephalopathy is based on the detection of infants at risk of developing a significant hyperbilirubinemia. This task can be accomplished by performing a simple umbilical cord blood test, such as blood group, Rh, Coombs' test and glucose-6-phosphate dehydrogenase, in order to detect hemolytic diseases. In preterm infants, the prevention of hyperbilirubinemia with phototherapy is a relatively simple task, since these infants are cared for in hospital. Early hospital discharge of full-term neonates represents a major concern. The management of neonatal jaundice requires that therapy begins when total serum bilirubin levels are significantly below the levels at which kernicterus is considered an immediate threat. Unfortunately, determination of serum bilirubin is a painful procedure, and is not very accurate since there is a high variability in laboratory measurements. The accuracy and precision of a new transcutaneous bilirubin measurement, comparable to the standard of care laboratory est, makes the daily evaluation of transcutaneous bilirubin measurement a useful tool in distinguishing physiological from nonphysiological hyperbilirubinemia, and determining the bilirubin increment in the first days of life. Full-term neonates who lose a significant amount of weight are especially at risk of significant hyperbilirubinemia and must be treated with ad libitum feeding and intensive phototherapy.
- 6626633
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficient may cause hyperbilirubinemia.
- Moderately increased hemolysis in newborn infants with hyperbilirubinemia of unknown etiology. Biology of the neonate, 1983 [Go to PubMed]
- Serial determinations of carboxyhemoglobin (COHb) levels were performed in full-term newborn infants during the first few days of life and their mothers. A close correlation was found between COHb in the mother and that determined in the cord blood. The correlation between COHb in the mother at delivery and that found in the neonate disappeared after 48 h of life. The determination of COHb after this period demonstrated significantly higher values of COHb levels in jaundiced neonates compared with normal infants. Determinations of erythrocyte age-dependent enzyme activities carried out at birth and after 5 days of life did not demonstrate any significant difference between the mean values in jaundiced and normal infants. However, the normal infants demonstrated a decrease of glucose-6-phosphate dehydrogenase and pyruvate-kinase activities from birth to the 5th day which is not appreciable in neonates with hyperbilirubinemia of unknown etiology. The results are discussed in relation to the role of hemolysis i neonatal hyperbilirubinemia.
- 22002596
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency can cause neonate jaundice.
- Berberine-induced haemolysis revisited: safety of Rhizoma coptidis and Cortex phellodendri in chronic haematological diseases. Phytotherapy research : PTR, 2012 May [Go to PubMed]
- Two commonly used berberine-containing Chinese herbs, Rhizoma coptidis (RC) and Cortex phellodendri (CP), have been banned in Singapore for the past three decades due to implication of berberine in aggravating jaundice and kernicterus in neonates with glucose-6-phosphate dehydrogenase deficiency. Here we conducted a single arm, phase I/II clinical study on Chinese herbal medicine for patients with chronic cytopenic haematological conditions and we analysed a subset of 20 patients who also had RC, CP or both in their herbal concoction. We found no organ toxicity or electrolyte imbalance in these 20 patients where RC was administered for 1055 patient-days and CP for 1252 patient-days. In three patients with thalassemia intermedia, transient elevation in serum bilirubin level was observed but this was not associated with any aggravation of anaemia or liver dysfunction. A review of the literature found conflicting evidence of varying levels either supporting or refuting the allegation of neonatal jaundice and kenicterus caused by berberine. There were, however, very few clinical reports of adverse reaction attributable to RC or CP in oral TCM concoction. We conclude that based on traditional dosage and indication, the use of RC and CP in oral concoction is safe.
- 12772532
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- G-6-PD deficiency was considered related with unexplained hemolysis or hyperbilirubinemia in newborn infants.
- Predicting significant hyperbilirubinaemia and early discharge for glucose-6-phosphate dehydrogenase deficient newborns. Annals of the Academy of Medicine, Singapore, 2003 Mar [Go to PubMed]
- This study aims to assess the usefulness of day 3 (49 to 72 hours) pre-phototherapy total serum bilirubin (TSB) in predicting subsequent significant hyperbilirubinaemia (SHB) and the feasibility of early discharge for term and near-term glucose-6-phosphate dehydrogenase (G6PD) deficient newborns.
This prospective cohort study involved in born G6PD deficient neonates who were > or = 35 weeks and weighted > or = 2000 g at birth. TSB levels and phototherapy requirements in their first two weeks of life were studied. Day 3 pre-phototherapy TSB in the subgroup weighing > or = 2500 g at birth was analysed for its value in predicting subsequent SHB.
Of the 129 neonates, 58 (45%) required phototherapy in the first week. Of these, only 4 patients (3.1%) needed phototherapy to be restarted in the second week. Seventy-one (55%) neonates did not require phototherapy at all. In the absence of SHB in the first week, the probability of its development in the second week was zero (95% confidence interval, 0 to 0.057). In the subgroup weighing > or = 2500 g at birth, day 3 pre-phototherapy TSB < or = 154 umol/L predicted no measurable risk of subsequent SHB (sensitivity, 100%; 95% confidence interval, 91.4% to 100%; negative predictive value, 100%; 95% confidence interval, 86.7% to 100%).
G6PD deficient newborns without SHB in their first week of life were at no measurable risk of its development in the second week. Day 3 pre-phototherapy TSB in the subgroup weighing > or = 2500 g was useful for predicting the risk of subsequent SHB. Low-risk infants, thus identified, may be eligible for discharge on or before day 7 of life. Evidence-based early discharge can decrease the social and financial burden of G6PD deficiency in Singapore. - 8157034
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- Summary
- Glucose-6-phosphate dehydrogenase deficiency may cause hyperbilirubinaemia.
- Acute intravascular haemolysis following exchange transfusion with G-6-PD deficient blood. European journal of pediatrics, 1994 Feb [Go to PubMed]
- A neonate with hyperbilirubinaemia who developed massive intravascular haemolysis following exchange transfusion with glucose-6-phosphate dehydrogenase deficient blood is described. It is recommended that in areas endemic for this enzyme deficiency the donor blood should be screened before being used for exchange transfusion.
- 16207591
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficient may cause hyperbilirubinemia.
- Neonatal anemia associated with Southeast Asian ovalocytosis. International journal of hematology, 2005 Oct [Go to PubMed]
- The purposes of this study were to evaluate the reliability of the previously described diagnostic criteria for Southeast Asian ovalocytosis (SAO) in adults in the diagnosis of SAO in newborns and to describe the role of SAO in newborn infants presenting with pallor and jaundice. The inclusion criteria in this retrospective descriptive study were that the patient be a newborn with pallor or jaundice and with ovalocytes in the peripheral blood smear (PBS). The exclusion criteria were newborn status with other causes of neonatal hemolysis or anemia. Controls were age-matched newborn infants who did not have SAO or other causes of neonatal anemia or hemolysis. Hematological data were assessed with a hematology analyzer. DNA analysis for SAO band 3 was done by polyerase chain reaction. Among 107 newborn infants with SAO, 30 infants were excluded from the study. The exclusions were premature infants, an infant with congenital syphilis, low-birth-weight infants, infants with ABO blood group incompatibility, infants with 3-thalassemia, infants with hemoglobin E heterozygote or homozygotes, glucose-6-phosphate dehydrogenase-deficient infants, and infants with fetomaternal hemorrhage. The DNA analysis for SAO band 3 was done in 56 newborns, and 54 had positive results for SAO band 3 gene deletion. Approximately one half of the 54 newborn infants with SAO had hyperbilirubinemia, and 3 had severe hyperbilirubinemia. The mean hemoglobin concentration, packed cell volume, and red blood cell (RBC) count in the infants with SAO in the first week of life were significantly lower than those in control infants. The mean absolute number of reticulocytes, mean corpuscular hemoglobin, and red cell volume distribution width in infants with SAO band 3 in the first week of life were signficantly higher than those in control infants. The neonatal diagnosis of SAO can be made by examination of RBC morphology in the PBS with the presence of stomatocytes, theta cells, and > or = 25% ovalocytes. SAO plays a role in anemia and hyperbilirubinemia in newborn infants.
- 3 record(s) for Glucose-6-Phosphate Adverse Event in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 6662695
- Glucose-6-Phosphate
- Adverse Event
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase deficiency may cause Neonatal jaundice
- Neonatal bilirubin levels and glucose-6-phosphate dehydrogenase deficiency in preterm and low-birth-weight infants in Israel. Israel journal of medical sciences, 1983 Dec [Go to PubMed]
- Eight hundred preterm (PT) and low-birth-weight (LBW) infants, born during a period of 33 months, were examined for erythrocyte glucose-6-phosphate dehydrogenase (G6PD) activity. Each of 17 infants with G6PD deficiency was compared with the next PT or LBW infant born with normal enzyme activity. The groups were similar with respect to gestational age, birth weight, maximal weight loss, breast or formula feeding and the use of oxytocin during labor. Peak bilirubin levels were significantly higher in G6PD-deficient PT and LBW infants (11.7 +/- 1.4 vs. 9.5 +/- 2.1 mg/dl, P less than 0.001). There were no signs of frank hemolysis, and none of the patients underwent exchange transfusion. Early jaundice and the use of phototherapy were somewhat more frequent among the G6PD-deficient group, but not significantly so. It is suggested that PT and LBW infants born to parents of Asian or North African origin be routinely screened for erythrocyte G6PD activity and monitored for possible jaundice.
- 16417692
- Glucose-6-Phosphate
- Adverse Event
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency is associated with Neonatal jaundice in newborns.
- Neonatal screening of glucose-6-phosphate dehydrogenase deficiency in Yanbu, Saudi Arabia. Journal of medical screening, 2005 [Go to PubMed]
- To determine the prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency in the population tested, and to evaluate the prevalence of neonatal jaundice in newborns with G6PD deficiency.
Cord blood of all babies born between October 1996 and October 1998 at the Royal Commission Medical Center in Yanbu, Saudi Arabia, was screened for G6PD deficiency by fluorescent spot test. The results of screening of cord blood samples were reported to the physician in charge, and also placed on the files of the babies and their mothers. These babies were observed for 72 h and discharged if no jaundice developed.
During this two-year period, 2,505 neonatal cord blood samples from 1,278 boys and 1,227 girls were screened for G6PD. There were 50 positive results for G6PD deficiency (39 boys and 11 girls), and the prevalence was estimated to be around 2%. The sex-specific prevalence for boys was 3.05%, and for girls 0.9%. Male to female ratio was 3:1. Neonatal jaundice developed in six (12%) babies, five male and one female. All were treated with phototherapy and discharged within one week of birth.
The prevalence of G6PD is relatively high in Yanbu. Routine neonatal screening in areas with a high prevalence of G6PD in Saudi Arabia is justifiable. - 21063220
- Glucose-6-Phosphate
- Adverse Event
- Case Report
- Summary
- A new glucose-6-phosphate dehydrogenase deficiency variant, G6PD Mizushima, showing increases in serum ferritin and cytosol leucine aminopeptidase levels.
- A new glucose-6-phosphate dehydrogenase deficiency variant, G6PD Mizushima, showing increases in serum ferritin and cytosol leucine aminopeptidase levels. Journal of pediatric hematology/oncology, 2011 Jan [Go to PubMed]
- We made a diagnosis of glucose-6-phosphate dehydrogenase (G6PD) deficiency with a new mutation of 848A→G (exon 8) in a 16-year-old male patient presenting with severe hemolysis. He was administered a diclofenac sodium suppository (50 mg) at the time of first visit to our hospital because of pyrexia. In the acute phase, pyrexia, severe general fatigue, lumbar back pain, hemoglobinuria, and jaundice developed. Laboratory blood examinations showed hemolysis, and remarkable increases in serum ferritin and cytosol leucine aminopeptidase levels. Serum interleukin-6 and interferon-γ levels were also increased. No liver injury was found. He had neonatal jaundice persisting over 3 weeks. He did not have a history of chronic hemolysis or hyperbilirubinemia. Increases in serum ferritin or cytosol leucine aminopeptidase levels in G6PD-deficient patients were not reported earlier. In this case, it is presumed that infection and administration of anti-inflammatory agents induce the hemolytic episode and that hyperytokinemia deteriorates the disease condition.
- 2 record(s) for Glucose-6-Phosphate Effective in Maintaining Remission in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 830875
- Glucose-6-Phosphate
- Effective in Maintaining Remission
- Clinical Trial
- Summary
- glucose-6-phosphate dehydrogenase (G6PD) deficiency may cause neonatal jaundice
- Light (phototherapy)--induced riboflavin deficiency in the neonate. The Journal of pediatrics, 1977 Jan [Go to PubMed]
- Phototherapy with blue light decomposes riboflavin, which has a maximum absorption at 450 nm. A study was designed to determine whether riboflavin deficiency developed in neonates who received phototherapy for moderate hyperbilirubinemia. Twenty-one infants with normal erythrocyte glucose-6-phosphate dehydrogenase activity were investigated. Five infants with moderate hyperbilirubinemia who did not require phototherapy served as the controls. Riboflavin deficiency was determined from the degree of saturation of erythrocyte glutathione reductase, a method shown to reflect riboflavin nutritional status in the neonate. Sixteen of 21 infants who were exposed to phototherapy developed riboflavin deficiency; all who had phototherapy for 49 hours or more developed the deficiency. That the concentration of serum bilirubin or the duration of hyperbilirubinemia was not a factor is supported by the fact that none of the controls became deficient. This observation may have important metabolic and clinical consequences fr the neonate.
- 17611006
- Glucose-6-Phosphate
- Effective in Maintaining Remission
- Review
- Summary
- Deficiency of glucose-6-phosphate dehydrogenase is a common disorder,and is susceptible to Neonatal jaundice, and acute hemolytic anemia.
- G6PD deficiency: the genotype-phenotype association. Blood reviews, 2007 Sep [Go to PubMed]
- Deficiency of glucose-6-phosphate dehydrogenase is a very common X-linked genetic disorder though most deficient people are asymptomatic. A number of different G6PD variants have reached polymorphic frequencies in different parts of the world due to the relative protection they confer against malaria infection. People, usually males, with deficient alleles are susceptible to neonatal jaundice, and acute hemolytic anemia, usually during infection, after treatment with certain drugs or after eating fava beans. Very rarely de novo mutations can arise causing the more severe condition of chronic nonspherocytic hemolytic anemia. Altogether 160 different mutations have been described. The majority of mutations cause red cell enzyme deficiency by decreasing enzyme stability. The polymorphic mutations affect amino acid residues throughout the enzyme and decrease the stability of the enzyme in the red cell, possibly by disturbing protein folding. The severe mutations mostly affect residues at the dimer interface or tose that interact with a structural NADP molecule that stabilizes the enzyme.
- General Drug Summary
- Drug Name
- Glucose-6-Phosphate
- Description
- An ester of glucose with phosphoric acid, made in the course of glucose metabolism by mammalian and other cells. It is a normal constituent of resting muscle and probably is in constant equilibrium with fructose-6-phosphate. (Stedman, 26th ed)
- Also Known As
- Categories
- Groups
- experimental
- Structure
- Summary In Neonatal Jaundice
- 9 record(s) for Glucose-6-Phosphate NA in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 1812331
- Glucose-6-Phosphate
- NA
- Clinical Trial
- 20113600
- Glucose-6-Phosphate
- NA
- Clinical Trial
- 3767789
- Glucose-6-Phosphate
- NA
- NA
- 3227552
- Glucose-6-Phosphate
- NA
- NA
- 823756
- Glucose-6-Phosphate
- NA
- NA
- 16708139
- Glucose-6-Phosphate
- NA
- NA
- 12208094
- Glucose-6-Phosphate
- NA
- NA
- 2083201
- Glucose-6-Phosphate
- NA
- NA
- 19172333
- Glucose-6-Phosphate
- NA
- Review
- 77 record(s) for Glucose-6-Phosphate Effective in Inducing Remission in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 559284
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 5697334
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 2441650
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 1283668
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 11433050
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8807322
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 9332310
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 11581450
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 7079890
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 14226101
- Glucose-6-Phosphate
- Effective in Inducing Remission
- NA
- 17489836
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 11731664
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 14972648
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 9628306
- Glucose-6-Phosphate
- Effective in Inducing Remission
- NA
- 8585194
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 19004212
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 24491445
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 22111448
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 7918083
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 22910623
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 7393270
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 6209608
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Randomized Controlled Trial
- 24763104
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 1179794
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 7305431
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12854374
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 11803427
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8861278
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 24774506
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 16753852
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12476860
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 10914965
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 17909678
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 16205054
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 23616073
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 15319464
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 1160703
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12737938
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 18165833
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- 12093957
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 9099326
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 933922
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12777545
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 23719252
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 16493435
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12369486
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Randomized Controlled Trial
- 6882560
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 20497361
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 1445122
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 6674910
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 367457
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12368976
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 6414449
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- 9848766
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Case Report
- 1468858
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8571933
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12680285
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 7919613
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 12105841
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12663150
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8942026
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 1977848
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 18185880
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8354322
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8628611
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 807541
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 10699105
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 7567338
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 7472840
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 9664196
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 22028581
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 11275655
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 6626633
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 22002596
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 12772532
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 8157034
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Review
- 16207591
- Glucose-6-Phosphate
- Effective in Inducing Remission
- Clinical Trial
- 3 record(s) for Glucose-6-Phosphate Adverse Event in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 6662695
- Glucose-6-Phosphate
- Adverse Event
- Clinical Trial
- 16417692
- Glucose-6-Phosphate
- Adverse Event
- Clinical Trial
- 21063220
- Glucose-6-Phosphate
- Adverse Event
- Case Report
- 2 record(s) for Glucose-6-Phosphate Effective in Maintaining Remission in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- 830875
- Glucose-6-Phosphate
- Effective in Maintaining Remission
- Clinical Trial
- 17611006
- Glucose-6-Phosphate
- Effective in Maintaining Remission
- Review
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