PSAT049 A Case of Hypercalcemia as the First Presentation of Addison's Disease
Authors: Horani Mohamad , Kanaan Zahi 
Published: November 2022

Abstract

Introduction
Hypercalcemia is stratified into mild, moderate, and severe. This stratification is determined by serum ionized calcium and total calcium. For example, mild hypercalcemia is defined as a serum ionized calcium of 5.6 - 8. 0 mg/dL [1.4 - 2 mmol/L] or a total calcium of 10 - 12 mg/dL [2.5 - 3 mmol/L]. Hypercalcemia is commonly caused by primary hyperparathyroidism and malignancy. Other causes include vitamin D excess or immobilization. An uncommon cause that is pertinent to the patient is primary adrenal insufficiency. A patient with hypercalcemia can either be asymptomatic or have a wide array of symptoms, such as musculoskeletal pain, nausea/vomiting or constipation, and altered mental status.

Case Presentation
The patient is a 36 year old female who came to the ED due to sharp upper quadrant abdominal pain that waxed and waned for about 8 weeks in duration. During her visit in the ED, the patient was hypotensive and tachycardic, which improved with IVF. The patient was also experiencing loss of appetite, nausea/vomiting, diarrhea. She also reported to have lost 38 lbs unintentionally dating back to 07/2021. The patient had undergone an EGD and colonoscopy, however the results were unremarkable. She also required further evaluation of her hypercalcemia of 12.7. She reported to take an unknown amount of vitamin D on a daily basis. She stopped taking her calcium supplementation a few weeks prior to her visit. The patient was afebrile, moderately tachycardic, tachypneic, and hypotensive. The physical exam was remarkable for tenderness to palpation in the epigastric region and skin hyperpigmentation. CT chest, abdomen, pelvis with contrast revealed intralobular septal thickening, diffuse mild colitis, some reactive mesenteric and retroperitoneal lymph nodes. Bone survey, CT head without contrast, gastric emptying study and hepatobiliary scan were unremarkable. Labs revealed: Ca 12.7, Na 132, K 4.4. PTH 6.3, ACTH 2,400, Cortisol base &lt;1. 0, Serum Aldosterone &lt;3. 0, Positive 21-Hydroxylase Autoantibody, DHEA 0. 099, DHEA sulfate 8. 0. Total 25-Hydroxyvitamin D 34. 0, 1,25-Dihydroxyvitamin D 5.6. After hydrocortisone and florinef administration, the patient's hypercalcemia normalized. As a result, the patient's hypercalcemia was secondary to primary adrenal insufficiency.

Discussion
Primary adrenal insufficiency is an uncommon cause of hypercalcemia. This can be attributed to a hypovolemic state that arises from a reduction in mineralocorticoids. As a result, there is a reduction in the GFR, which reduces glomerular filtration of calcium and increases reabsorption of calcium in the proximal tubule. Another proposed mechanism is the increase in 1-alpha-hydroxylase due to a reduction in glucocorticoids. Consequently, an increase in 1-alpha-hydroxylase will increase calcitriol production, which subsequently increases intestinal calcium absorption. These proposed mechanisms highlight the importance of adrenal function on calcium regulation and homeostasis.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.