Phenobarbital for prevention of hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient newborn infants

Meloni, T; Cagnazzo, G; Dore, Angelo; Cutillo, S

doi:10.1016/s0022-3476(73)80442-1

Cited by 41 publications

(16 citation statements)

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“…The findings support the theory we previously enunciated [9] and which has been confirmed by Greek authors [6] that neonatal hyperbiliru binemia encountered in erythrocyte G-6-PD deficiency is not depending on hemolysis and bears a close resemblance to jaundice due to transiently impaired liver function as in premature babies. This assumption does not agree with many reports in the literature which have contributed to the statement that severe jaundice in G-6-PD-deficient newborn babies is the consequence of a severe reduction of the red cell mass.…”

Section: Discussionsupporting

confidence: 91%

“…Hemoglobin, hematocrit, hemopexin and haptoglobin showed no or little differences between either of the two groups and the controls. The findings confirm the authors' assumption ex pressed elsewhere that this form of hyperbilirubinemia is not hemolytic in nature.In previous reports we illustrated the results obtained with phénobar bital [9] and with orotic acid [1] in preventing severe hyperbilirubinemia which often affects newborns with erythrocyte glucose-6-phosphate dehy drogenase (G-6-PD) deficiency. In all the cases studied, no sign of marked hemolysis, independent of the bilirubin level, was observed.…”

mentioning

confidence: 99%

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Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

Meloni¹,

Costa²,

Cutillo³

1975

Acta Haematol

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Hemolysís was studied in 40 G-6-PD-deficient newborn infants, half of whom had bilirubin blood levels within the normal range whereas the others, who were hyperbilirubinemic, underwent exchange transfusion. Hemoglobin, hematocrit, hemopexin and haptoglobin showed no or little differences between either of the two groups and the controls. The findings confirm the authors’ assumption expressed elsewhere that this form of hyperbilirubinemia is not hemolytic in nature.

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

Meloni¹,

Costa²,

Cutillo³

1975

Acta Haematol

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“…7 This study design with its limitations could not eliminate the effects of selection bias and measurement bias. The favorable results in Meloni's study cannot be attributed simply to the higher dose (7 mg/kg day) and duration of Phenobarbital, because work in the early 1980's had clearly showed that phenobarbital in the dose of 5 to 10 mg/kg day for 2 days is as effective as more prolonged treatment.…”

Section: Discussionmentioning

confidence: 97%

“…A couple of small, nonrandomized, unblinded trials evaluated prophylactic oral phenobarbital in preventing severe hyperbilirubinemia in G6PD-deficient neonates. 7,8 These studies carried out in the early 1980s suggested a role of Phenobarbital in preventing jaundice in G6PD deficient neonates. However, due to the methodological weaknesses of these trials, the use of prophylactic phenobarbital did not gain acceptance.…”

Section: Introductionmentioning

confidence: 99%

A Randomized, Triple-Blind, Placebo-Controlled Trial of Prophylactic Oral Phenobarbital to Reduce the Need for Phototherapy in G6PD-Deficient Neonates

et al. 2005

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Decreased conjugation is probably more important than hemolysis for causing jaundice in G6PD-deficient neonates. The role of enzyme inducers, like phenobarbital, in G6PD deficiency is unclear. This randomized controlled trial was performed to evaluate Phenobarbital's role in reducing the need for phototherapy among G6PD-deficient neonates. STUDY DESIGN:This stratified, randomized, triple-blinded, placebo-controlled trial was conducted in a level III NICU. Consecutive babies with gestation Z34 weeks and birth weight Z1800 g were screened from cord blood. G6PD-deficient neonates, who were otherwise healthy, were enrolled. Rh isoimmunization, maternal Phenobarbital use and lack of parental consent were exclusion criteria. Subjects were randomly allocated to receive 5 mg/kg day of oral phenobarbital/ placebo for first 3 days. They were monitored daily for total serum bilirubin (TSB) until declining TSB was documented twice. The primary outcome was requirement for phototherapy and secondary outcomes were duration of phototherapy, need for exchange transfusion, peak TSB and adverse effects. Sample size of 56 could detect a decline in phototherapy requirement from 40 to 5% with 80% power and 5% error. RESULTS:Of 2370 babies screened, 63 were G6PD-deficient. Of them, 56 eligible babies were allocated to phenobarbital (n ¼ 27) or placebo (n ¼ 29).The mean age of administration of the first dose was 18.55±7.3 h. In total, 44% in phenobarbital group and 41% in placebo group required phototherapy (p ¼ 1.0). There was no significant difference in exchange transfusion rates (18.5 vs 10%, p ¼ 0.46). No baby had adverse reactions. CONCLUSION:Prophylactic oral phenobarbital does not decrease the need for phototherapy or exchange transfusions in G6PD-deficient neonates.

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“…However, because its effects are only noted after 3 -4 days, phénobarbital appears less effective than phototherapy in the treatment of neonatal jaundice (117,122). In hemolytic jaundice o f the newborn, either due to feto-maternal incompatibility (65) or to red cell enzyme abnormalities (66,69), phénobarbital likewise decreases bilirubinemia.…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

Barbiturates and Biliary Function

Capron

Erlinger²

1975

Digestion

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This paper reviews the principal effects of phenobarbital on biliary function. Phenobarbital administration is followed by an increase in bile flow. This is mainly due to an increase in the bile salt-independent fraction of canalicular bile flow possibly through an increase in canalicular Na⁺-K⁺ ATPase activity. In addition, bile salt excretion may be increased. This effect of barbiturates on choleresis appears to be independent of microsomal enzyme induction. Barbiturates increase the uptake, storage and excretion of various dyes, for example sulfobromophthalein. Phenobarbital increases bilirubin clearance by the liver; it enhances bilirubin-UDP-glucuronyl transferase activity; whether the influence on bilirubin clearance is related to the effect on the enzyme is unknown. The influence of phenobarbital on biliary lipids is markedly different from one species to the other. In the rhesus monkey and in the rat, the relative concentration of cholesterol is decreased; in the hamster it is increased, and in man it appears largely unaffected. These effects of phenobarbital have been utilized in the treatment of chronic unconjugated hyperbilirubinemia and of certain cholestatic syndromes. Phenobarbital alone has not been useful, so far, in the treatment of cholesterol gallstones.

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Phenobarbital for prevention of hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient newborn infants

Cited by 41 publications

References 2 publications

Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

Haptoglobin, Hemopexin, Hemoglobin and Hematocrit in Newborns with Erythrocyte Glucose-6-Phosphate Dehydrogenase Deficiency

A Randomized, Triple-Blind, Placebo-Controlled Trial of Prophylactic Oral Phenobarbital to Reduce the Need for Phototherapy in G6PD-Deficient Neonates

Barbiturates and Biliary Function

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