IMR Press / CEOG / Volume 28 / Issue 3 / pii/2001039

Clinical and Experimental Obstetrics & Gynecology (CEOG) is published by IMR Press from Volume 47 Issue 1 (2020). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Editorial

Calcium metabolism in pregnancy: Disturbed calcium homeostasis in diabetic pregnancy and preeclampsia

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1 Department of Obstetrics and Gynecology, Konan Hospital, Kobe City (Japan)
Clin. Exp. Obstet. Gynecol. 2001, 28(3), 133–141;
Published: 10 September 2001
Abstract

lα-dihydroxyvitamin D3 is a main regulator of calcium metabolism during pregnancy because this metabolite promotes the intestinal calcium absorption to meet the increased calcium demands for fetal mineralization. The mechanisms underlying the increase in la-dihydroxyvitamin D3 may be the stimulation of renal synthesis of this metabolite possibly by human pla­cental lactogen and placental synthesis. Trabecular bone mineral density may be preserved during pregnancy, but it is reduced during lactation due to hypoestrogenic state. Diabetic pregnancy is associated with altered calcium metabolism including the decrease in serum levels of calcium and la-dihydroxyvitamin D3, the impaired duodenal calcium absorption, the increase in serum PTH and hypercalciuria compared with normal pregnant women. The disturbance of transplacental calcium transfer may be a cause of neonatal hypocalcemia. Abnormal intracellular calcium handling in preeclampsia has been discussed in association with the etiology of essential hypertension. The increase in the intracellular calcium concentrations in vascular smooth muscle cells probably caused by parathyroid hormone may contribute to enhanced vascular reactivity.

Keywords
Calcium metabolism
Bone metabolism
Pregnancy
Lactation
Diabetes mellitus
Preeclampsia
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