Calcium homeostasis in pregnancy

Abstract

The demands of fetal growth lead to an adaptation of maternal homeostasis in order to provide the required calcium from enhanced intestinal absorption rather than from mobilization of maternal skeletal reserves. In large part this adaptive process depends on the interrelationship between PTH and 1,25(OH)2D which shows quantitative rather than qualitative changes from the non-pregnant state. In contrast the maintenance of fetal mineral homeostasis largely depends on PTHrP which regulates active placental calcium transfer and the calcium fluxes across the kidney and bone. The major source of PTHrP is the fetal parathyroid gland although some is provided by the placenta. It may be this latter component which passes into the maternal circulation where it may play a role in calcium homeostasis by acting through the PTH receptor.

Primary Hyperparathyroidism in Pregnancy—A Rare Cause of Life-Threatening Hypercalcemia: Case Report and Literature Review

“…The increased calcium demands during pregnancy are primarily meet via the enhanced maternal intestinal calcium absorption [21] related to increased Vit D1,25OH production [17], with a 2-fold increase in intestinal calcium absorption occurring during pregnancy [22]. In our patient, 1,25-dihydroxycholecalciferol levels were nearly twice the upper limit of the healthy subject range.…”

Changes in serum markers of bone turnover during normal pregnancy

“…The temporal changes in their concentrations are consistent with our current understanding of the way in which maternal calcium homeostasis adapts to provide calcium for the fetus. 12,28 The increase in bone turnover later in pregnancy would suggest that the body has an apparent lack of capacity to obtain the necessary calcium for fetal skeleton formation from dietary sources. It has been suggested that the gastrointestinal tract may not be able to increase calcium absorption adequately enough to provide this response.…”

Calcium economy in human pregnancy and lactation

“…However, because PTH concentration is lowered or unchanged in pregnant women, it is unlikely to be primarily responsible for the increase in 1,25(OH) 2 D seen in pregnancy (3) , although it remains responsive to changes in Ca load (147) . Although hormones, such as oestrogen, prolactin, growth hormone and insulin-like growth factor-I, have the ability to induce 1-a-hydroxylase activity (174,175,181) , it is likely that PTHrP has a key role (3,179,182) . This activates the PTH/PTHrP receptor and therefore exhibits PTH-like effects, including stimulation of renal 1,25(OH) 2 D production (182,183) .…”

“…Although hormones, such as oestrogen, prolactin, growth hormone and insulin-like growth factor-I, have the ability to induce 1-a-hydroxylase activity (174,175,181) , it is likely that PTHrP has a key role (3,179,182) . This activates the PTH/PTHrP receptor and therefore exhibits PTH-like effects, including stimulation of renal 1,25(OH) 2 D production (182,183) . Increased concentrations of PTHrP are detected in the plasma of pregnant women, probably originating from fetal, placental and mammary tissues (4) , and its concentration rises by about two-fold from early to late pregnancy (110,176) .…”