In their review, Schnatz and Thaxton (2005) found fewer than 200 reported cases of hyperparathyroidism complicating pregnancy. As in nonpregnant patients, parathyroid adenoma is the most common etiology. Ectopic parathyroid hormone production and rare cases of parathyroid carcinoma have been reported in pregnancy (Montoro, 2000; Saad, 2014). Symptoms include hyperemesis, generalized weakness, renal calculi, and psychiatric disorders. Occasionally, pancreatitis is the presenting disorder (Cooper, 2011; Hirsch, 2015).
Pregnancy theoretically improves hyperparathyroidism because of signiicant calcium shunting to the fetus and augmented renal excretion (Power, 1999). When the "protective efects" of pregnancy are withdrawn, however, postpartum hypercalcemic crisis is a significant danger. his life-threatening complication can be seen with serum calcium levels greater than 14 mgl dL and is characterized by nausea, vomiting, tremors, dehydration, and mental status changes (Malekar-Raikar, 2011).
ism. More recent reports, however, described lower rates of stillbirth, neonatal death, and neonatal tetany (Kovacs, 201r1).
Other fetal complications include miscarriage,r· fetal-growth restriction, and low birthweight (Chamarthi, 2011). Schnatz (2005) reported a 25-percent incidence of preeclampsia.
Management in Pregnancy. Surgical removal of a symptomatic parathyroid adenoma is preferable. This should prevent fetal and neonatal morbidities and postpartum parathyroid crises (Kovacs, 2011). Elective neck exploration during pregnancy is usually well tolerated, even in the third trimester (Hirsch, 2015; Schnatz, 2005; Stringer, 2017). In at least two cases, a mediastinal adenoma was removed at midpregnancy (Rooney, 1998; Saad, 2014).
Medical management may be appropriate in asymptomatic pregnant women with mild hypercalcemia (Hirsch, 2015). If so, patients are careully monitored in the puerperium for hypercalcemic crisis. Initial medical management might include cacitonin to decrease skeletal calcium release, or oral phosphate, 1 to 1.5 g daily in divided doses, to bind excess calcium. For women with dangerously elevated serum calcium levels or those who are mentally obtunded with hypercacemic crisis, emergency treatment is instituted. Diuresis with intravenous normal saline is begun so that urine low exceeds 150 mLlhr. Furosemie is given in conventional doses to block tubular calcium reabsorption. Importantly, hypokalemia and hypomagnesemia should be prevented. Adjunctive therapy includes mithramycin, which inhibits bone resorption.