Abstract
Extract: Coproporphyrin analysis was performed on urine from 17 male and 7 female premature infants (birth wt 1.5–4.5 kg, average 1.7 kg). Six specimens of amniotic fluid obtained before elective abortion induced by saline solution infusion were also examined. Normal adult control subjects excreted 24.6% ± 5.6% of total coproporphyrin as coproporphyrin I. Twenty-three premature infants excreted 59.4% ± 17.3% as coproporphyrin I, significantly higher amounts than control subjects (P < 0.001). Coproporphyrin I excretion in six specimens of amniotic fluid was 84.9% ± 10.4%, significantly higher than in urine from adults and premature infants (P < 0.001).
Speculation: These results raise the possibility of a similar hepatic excretory defect in porphyrin metabolism in the developing fetus and in the Dubin-Johnson syndrome. In the former, the defect is developmental; in the latter, it is lifelong and is present in obligate heterozygotes. Uroporphyrinogen III cosynthetase normally catalyzes conversion of porphobilinogen to isomer III rather than isomer I porphyrins. Developmental deficiency of this enzyme may be responsible for the observed pattern of coproporphyrin isomers seen in the fetus and neonate.
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Wolkoff, A., Arias, I. Coproporphyrin Excretion in Amniotic Fluid and Urine from Premature Infants: A Possible Maturation Defect. Pediatr Res 8, 591–593 (1974). https://doi.org/10.1203/00006450-197405000-00007
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DOI: https://doi.org/10.1203/00006450-197405000-00007