Background Pregnancy and lactation are associated with profound changes in calcium homeostasis that can complicate the management of primary hypoparathyroidism. Clinical Case A 35-year-old woman with a history of post-operative hypoparathyroidism aftertotal thyroidectomy for metastatic papillary thyroid carcinomawas found to have hypercalcemia during lactation, two months after delivery of her first pregnancy. She was taking calcitriol 0.5mcgtwo times daily prepartum, which she continued throughout pregnancy and postpartum. Two weeks prior to delivery, her serum calcium was 9.7 mg/dL (n: 8.6-10.3 mg/dL). However, testingtwo months postpartum revealed a markedly elevated serum calcium 13.7 mg/dL and ionized calcium 1.70 mmol/L (n: 1. 09-1.29 mmol/L). Subsequent workup was notable for low parathyroid hormone (PTH) 4 pg/mL (n: 11-51 pg/mL), and normal PTH-related protein (PTHrP) 0.3 pmol/L (n: <2 pmol/L), 25-hydroxy-vitamin D 60 ng/mL (n: 30-80 ng/mL), and 1,25-dihydroxy-vitamin D 38. 0 pg/mL (n: 19.9-79.3 pg/mL). Her calcitriol was reducedto 0.25mcg once daily, and her serum and ionized calcium improved to 10.2 mg/dL and 1.18 mmol/L, respectively, within 10 days. Two years later, after her second pregnancy, she again developed hypercalcemia during lactation. One month prior to delivery, her serum calcium was 8. 0 mg/dL and her ionized calcium was 1. 04 mmol/L on a regimen of calcium carbonate 1000mg three times daily and calcitriol 0.5mcg twice daily. However, two months after delivery and during lactation, her serum and ionized calcium increased to 10.4 mg/dL and 1.31 mmol/L, respectively. Evaluation of her PTHrP levels revealed an increase from 13 pg/mL (n: 14-27 pg/mL) one-year prepartum to 22 pg/mL during her third trimester, and then to17 pg/mL two months postpartum. In addition, her 1,25-dihydroxy-vitamin D increased from 60.2 pg/mL one-year prepartum to 108. 0 pg/mL during her third trimester and decreased to 70.2 pg/mL two months postpartum. Reductions in her calcium and calcitriol regimen improved her serum and ionized calcium levels. Conclusion This rare case highlights the changes in calcium physiology during pregnancy and lactation that can significantly alter calcium and calcitriol requirements in women with primary hypoparathyroidism. During pregnancy, calcium demand is met by increased placental and fetal PTHrP secretion and increased 1,25-dihydroxy-vitamin D production from placental 1-alpha-hydroxylase activity. Conversely, during lactation, this demand is met by increased net bone resorption from PTHrP produced by the mother's mammary tissue and decreased estrogen levels postpartum. As illustrated in this case, continuation of prepartum calcium and calcitriol regimens during pregnancy and lactation can result in maternal hypercalcemia. Thus, close monitoring of calcium levels during pregnancy and lactation in women with hypoparathyroidism is essential to adjust calcium and calcitriol supplementation and maintain adequate calcium homeostasis in the mother and fetus. Presentation: No date and time listed
Introduction: ACTH-dependent Cushing syndrome (CS) is associated with hypercoagulability; however, the incidence and timing of thrombosis during evaluation and management of CS is unclear. Objective: To evaluate the incidence and timing of thrombotic events in patients with ACTH-dependent CS following diagnosis and management. Methods: We performed a retrospective, longitudinal study of patients with ACTH-dependent CS seen at Stanford University Health Care from 1998 to 2020. Thrombotic events — deep vein thrombosis (DVT), pulmonary embolism (PE), cerebral vascular accident (CVA), and myocardial infarction (MI) — were recorded between diagnosis and 12 months following therapeutic intervention. Results: Of 108 patients with ACTH-dependent CS, 97 (89.8%) were women, and the mean age at diagnosis was 43.0 years (± 15.7 years). Sixty-eight (63%) patients had hypertension, 38 (35.2%) had diabetes mellitus, and 11 (10.2%) were active smokers. Of the 108 subjects, 97 (89.8%) had Cushing Disease (CD) and 11 (10.2%) had ectopic CS. Of the 97 patients with CD, 38 (39.2%) underwent inferior petrosal sinus sampling (IPSS), 59 (60.8%) underwent transsphenoidal surgery (TSS), 19 required repeat TSS (19.6%), and 15 underwent TSS and bilateral adrenalectomy (BAL) (15.4%). Of the 11 patients with ectopic CS, 3 (27.2%) underwent IPSS, 6 (54.5%) underwent BAL, and 1 (9.1%) underwent TSS and BAL. There were 10 thrombotic events among 7 (7.2%) CD patients, but no thrombotic events among ectopic CS patients. Of the thrombotic events, there were 7 (70%) DVT/PE, 2 (20%) CVA, and 1 (10%) cortical vein thrombosis. Six (60%) occurred within 30 days after TSS (range 3-25 days), 2 (20%) between 31 days and 1 year after TSS (range 59-165 days), 1 (10%) 26 days after IPSS but prior to TSS, and 1 (10%) in a patient who did not undergo IPSS or surgery. No thrombotic events were noted after BAL. Of the 8 postoperative thrombotic events, 5 (62.5%) occurred while patients received supraphysiologic glucocorticoid replacement (defined as >25mg hydrocortisone or equivalent daily) after curative surgery, 1 (12.5%) occurred after a patient was tapered to physiologic glucocorticoid replacement, and 2 (25%) occurred in patients who had persistent disease despite surgery. The degree of hypercortisolism at baseline was not associated with risk of thrombotic events. Conclusions: In this retrospective study, 6.5% of ACTH-dependent CS patients had a thrombotic event, all in patients with CD. The majority had venous thromboembolism with DVT/PE, and the highest incidence occurred up to 30 days after surgery. The degree of hypercortisolism at baseline did not correlate with subsequent thrombotic events. Therefore, it is important to monitor all patients with ACTH-dependent CS following surgical intervention for venous thromboembolism.
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