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.

Prophylactic treatment with barbituric acid has been made for preventing severe hyperbilirubinemia in G-6-PD deficient newborn infants. In 17 out of 46 untreated and in 7 out of 171 treated cases exchange transfusions were needed since the biliriibin serum level exceeded 18 mg/100 ml. These data show that this prevention can be useful in areas, such as Sardinia, where the incidence of G-6-PD deficiency is very high. It has been further demonstrated that this particular form of neonatal hyperbilirubinemia is not due to increased red cell destruction.

No abstract

Salicylamide-glucuronide formation has been determined in 27 children who underwent a favism crisis, 25 parents, and in 25 normal children who served as controls. A highly significant mean lower glucuronide formation was observed in the favism group in respect to the controls. The difference between fabic children and their parents was significant, and between parents and controls there was no significant difference.

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(l 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.