Pulmonary Excretion of Carbon Monoxide in the Human Infant as an Index of Bilirubin Production

ABSTRACT

A total of 20 infants who had levels of erythropoietin (Ep), the major hormone regulating erythropoiesis, measured in their cord blood also had determinations of the pulmonary excretion rate of CO (Ve_co) performed, as an index of total bilirubin production. They were either infants of normal mothers or those of mothers with diabetes, gestational diabetes, and missed abnormalities of gestational glucose metabolism. The mean Ve_co (13.0 ± 3.5 μ1/kg/hr) and the mean Ep (20.0 ± 9.7 SD mU/ml) of the infants with normal mothers (n=9) were not different from the means previously established by our laboratories (13.9 ± 3.5 SD μ1 /kg/hr, n = 20; and 23.7 ± 12.8 SD mU/ml, n = 30, respectively); they were significantly lower than those of the infants of the abnormal mothers in this study. The 5 infants who had a cord blood Ep level greater than 50 mU/ml had a higher mean Ve_co, 27.8 ± 7.1 μ1/kg/hr, compared with 17.2 ± 4.9 SD μ1/kg/hr, of the six infants with cord blood Ep levels that were within 2 SD of the previously established normal mean cord blood Ep level (p < .025). These data suggest that increased cord blood Ep levels and postnatal bilirubin production in infants whose mothers had abnormalities of gestational glucose metabolism are associated phenomena. Since polycythemia did not occur in these infants, ineffective erythropoiesis or mild, compensated hemolysis remains a likely cause of the increased total bilirubin production. In some cases, perinatal hypoxic stress may have affected the Ep response. Elevations in Ep may have an adverse effect on postnatal heme catabolism related to stimulated erythropoiesis, which could result in relatively greater increases in bilirubin production among infants who are already predisposed to accelerated heme catabolism.