Abstract
Elevated fetal plasma total calcium (Ca), ionized calcium (Cai) and inorganic phosphorus (P) decline during the first 2-3 days of life. 1/3 to 1/2 of preterm infants will exhibit an exaggerated early neonatal hypocalcemia (ENH). Previous studies of immunoreactive PTH (iPTH) in ENH have yielded inconclusive results since some antisera are directed against biologically inactive forms of hormone. We used a sensitive cytochemical bioassay to measure circulating levels of bioPTH as well as iPTH. Assays were carried out in umbilical cord plasma (n=60) and plasma from normo- and hypocalcemic neonates from 25-42 weeks gestation (n=10). The bioassay is based on PTH mediated stimulation of glucose 6-phosphate dehydrogenase activity in distal convoluted tubules of guinea pig kidney. Cord plasma bioPTH was elevated (30.7±10.1 (SEM) pg/ml) compared to normal adults (9.2 ±1.0 pg/ml). Addition of antihuman PTH antibody to plasma extinguished bioactivity. Postnatal decline in Ca (7.2±0.2 mg/dl) and Cai (1.05±0.05 mM/l), even in extremely preterm infants, resulted in increased bioPTH levels (61.8±11.3 pg/ml). When Ca increased after day 3, bioPTH was suppressed to levels below those obtained from paired cord samples. iPTH also rose and fell inversely with Ca. Biologically active PTH is produced by the fetus and newborn infant, and circulating levels of hormone respond to physiological changes in Ca and Cai.
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