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Normal Intrauterine Development of the Fetus of a Woman Receiving Extraordinarily High Doses of 1,25-Dihydroxyvitamin D₃^*

Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases Bethesda, Maryland 20205
Internal Medicine Group of Cleveland Cleveland, Tennessee 37311;
Department of Biochemistry, University of Wisconsin Madison,Wisconsin 53141

Address requests for reprints to: Dr. Stephen J. Marx, Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, Building 10, Room 9D20, National Institutes of Health, Bethesda, Maryland 20205.

We monitored the course of pregnancy in a 28-yr-old patient with hereditary insensitivity to 1,25-dihydroxyvitamin D (1,25-(OH)₂D). During pregnancy, she received 1,25- (OH)2D3 in doses of 17–36 µg/day (usual dose for hypocalcemia, 0.25–1.0 µg/day). We separately measured 25-hydroxyvitamin D3 (25OHD3), 25OHD2, 1,25-(OH)₂D₃, and 1,25-(OH)₂D₂ to as sess contributions to total 1,25-(OH)₂D from endogenous biosynthesis (l-hydroxylation of 25OHD₂ or 25OHD₃) vs. contributions from exogenously administered 1,25-(OH)₂D₃. Serum concentrations of 1,25-(OH)₂D were extraordinarily high throughout gestation. The evaluations of total 1,25-(OH)₂D in maternal plasma reflected large amounts from both l-hydroxylation of 25OHD and oral intake of 1,25-(OH)₂D₃. At parturition, the calcium concentration was 9.6 mg/dl in maternal serum and 10.2 mg/dl in cord serum. The concentration of total 1,25-(OH)₂D in cord serum was high (470 pg/ml; normal mean for placental venous serum, 19 pg/ml); most derived from transplacental passage of maternal 1,25-(OH)₂D₃ and not from fetoplacental biosynthesis. The child manifested mild hypercalcemia in the first 2 days of life, indicating that the 1,25-(OH)2D3 measured in cord serum was active in vivo. The child showed no somatic features of the syndrome of elfin facies and supravalvular aortic stenosis. We conclude that an extraordinarily high concentration of 1,25-(OH)₂D in maternal serum throughout gestation was not apparently toxic to the fetoplacental unit, though the maternal metabolite entered the fetal circulation.

^* This work was supported in part by NIH Grant AM-14881 and NASA Grant NAS 9-15580.

Received April 21, 1980.

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