The function of parathyroid hormone (PTH) is to maintain extracellular fluid calcium concentration. his 84-amino acid hormone acts directly on bone and kidney and indirectly on small intestine through its efects on synthesis of vitamin D (l,25-(OH)2D) to increase serum calcium (Potts, 2015). Secretion is regulated by serum ionized calcium concentration through a negative feedback system. Cacitonin is a potent parathyroid hormone that acts as a physiological parathyroid hormone antagonist. The interrelationships between these hormones, calcium metabolism, and PTH-related protein produced by fetal tissue are discussed in Chapter 4 (p. 71).
Of fetal demands, calcium requirements reach 300 mg/d in late pregnancy and 30 g for the entire gestation. These needs and greater renal calcium loss from augmented glomerular iltration substantively raise maternal calcium demands. Pregnancy is associated with a twofold rise in serum concentrations of 1,25-dihydroxyvitamin D, which increases gastrointestinal calcium absorption. he efectuating hormone is probably of placental and decidual origin because maternal PTH levels are low normal or decreased during pregnancy (Cooper, 2011; Molitch, 2000). Total serum calcium levels decline with serum albumin concentrations, but ionized calcium levels remain unchanged. Vargas Zapata and colleagues (2004) have suggested a role for insulin-like growth factor-1 (IGF-1) in maternal calcium homeostasis and bone turnover.
Hypercalcemia is caused by hyperparathyroidism or cancer in 90 percent of cases (Potts, 2015). Because many automated laboratory systems include serum calcium measurement, hyperparathyroidism has changed from being a condition deined by symptoms to one that is discovered on routine screening (Pallan, 2012). It has a reported prevalence of 2 to 3 per 1000 women, but some have estimated the rate to be as high as 14 per 1000 when asymptomatic cases are included. Almost 80 percent are caused by a solitary adenoma, and another 15 percent by hyperfunctioning of all four glands. In the remainder, a malignancy as the cause of increased serum calcium levels is usually obvious. Of note, PTH produced by tumors is not identical to the natural hormone and may not be detected by routine assays.
In most patients, the serum calcium level is elevated to within only 1 to 1.5 mg/dL above the upper normal limit. This may help to explain why only 20 percent of those who have abnormally elevated levels are symptomatic (Bilezikian, 2004). In a fourth, however, symptoms become apparent when the serum calcium level continues to rise. Hypercacemic crisis manifests as stupor, nausea, vomiting, weakness, fatigue, and dehydration.
All women with symptomatic hyperparathyroidism should be surgically treated (Potts, 2015). Indications for parathyroidectomy include a serum calcium level 1.0 mg/dL above the upper normal range, a calculated creatinine clearance < 60 mLi min, reduced bone density, or age >50 years (Bilezikian, 2009). Those not meeting these criteria should undergo annual serum calcium and creatinine level measurement and bone density assessment every 1 to 2 years (Pallan, 2012).