Primary Hyperparathyroidism Discovered in the Pregnant Patient

Presentation Number: MON 311
Date of Presentation: April 3rd, 2017

Kimberly Kochersperger Lessard*1, Linda Nguyen1, Arthur Chernoff2 and Naureen Jessani3
1Albert Einstein Medical Center, Philadelphia, PA, 2Albert Einstein Med Ctr, Philadelphia, PA, 3Albert Einstein Medical Center, Elkins Park, PA

Abstract

Background: Primary hyperparathyroidism (PHP) discovered in pregnancy is a rare entity with substantial risk to both mother and fetus. With marked changes in hormonal and calcium homeostasis, PHP in pregnancy poses diagnostic and therapeutic challenges and requires time-sensitive clinical decision making.

Case: A 44-year-old female presented at 21 weeks gestation for evaluation of refractory nausea, vomiting, and abdominal pain. Laboratory evaluation revealed a total calcium level of 12.2 mg/dL (8.4 – 10.3mg/dL), corrected to 13.0mg/dL for a decreased albumin level of 3.0 gm/dL (3.5 – 5.0 gm/dL). A corresponding iPTH level was significant at 105.9 pg/ml (9-73 pg/ml). With the exception of abdominal pain, she had no previous or current symptoms of hypercalcemia. Ultrasound revealed a hypoechoic nodule posterior to the mid-lower pole of the right thyroid lobe consistent with a parathyroid adenoma. She was recommended a low calcium diet with increased hydration. Unfortunately, total calcium remained elevated at 11.6 mg/dL at 22 weeks, 10.7 mg/dL at 28 weeks for which she was then referred for surgical evaluation. She underwent adenoma removal at 32.5 weeks without issue. Subsequent serologies showed appropriate normalization of iPTH and calcium levels. Cesarean section was performed at 36 weeks with delivery of a healthy female neonate.

Discussion: While pregnant women are at no greater risk for development of PHP, they have a substantially increased risk of complications. Increased estrogen, renal excretion of calcium, placental calcium transport, and hypoalbuminemia contribute to the appearance of lower, seemingly normal, levels of calcium in pregnancy in PHP. The fetus can inherently tolerate mild hypercalcemia during bone mineralization, however significant maternal hypercalcemia can cause fetal PTH suppression leading to post-partum hypocalcemia. The duration of neonatal hypocalcemia is variable and, in rare cases, permanent due to disrupted brachial cleft development. Calcium >11.5mg/dL is also associated with hyperemesis, preeclampsia, IUGR, and a three-to-fivefold increased risk of miscarriage. Without treatment, fetal complications are seen in up to 80% of cases. Once PHP is diagnosed, consideration must be given to severity and gestational age. Conservative approaches, including low-calciumdiet, hydration and loop diuretics are generally first line. Subcutaneous calcitonin and cinacalcet, used to reduce PTH levels, are both considered Category C. Limited data exists regarding indications for surgical intervention for PHP in the pregnant patient. Adenoma removal is curative with the second trimester of pregnancy considered the safest. Surgery during the first and third trimester imparts risks of teratogenic effects and preterm labor, respectively. Consequently, early detection and individualized treatment of PHP in the pregnant patient is critical.

 

Nothing to Disclose: KKL, LN, AC, NJ