Moan and Groan: Deficiency or Excess? A Fascinating Case of Hypercalcemia

1North Shore University Hospital, Manhasset, NY
2North Shore University Hospital, Manhasset, NY
3North Shore University Hospital, Manhasset, NY

Meeting: Hospital Medicine 2013, May 16-19, National Harbor, Md.

Abstract number: 312

Case Presentation:

A 26‐year‐old man who underwent recent resection of an ACTH‐secreting pituitary adenoma 1 month prior to admission presented to the hospital with 1 week of nausea, vomiting, and abdominal pain. Laboratory results were significant for an elevated serum calcium (14.3 mg/dL), slightly low potassium (3.2 mmol/L), and elevated creatinine (2.97 mg/dL), consistent with acute renal failure. Workup for hypercalcemia included a PTH level, which was appropriately suppressed (8 pg/mL). TSH, free T4, vitamin D‐25, vitamin D‐1,25, vitamin A, and PTH‐related peptide levels were within normal ranges. pm Cortisol level was 3.2 μg/dL (normal range, 2.3–11.9 μg/dL). On admission the patient was started on saline hydration, and his home steroid dose was doubled. On hospital day 2, because his calcium did not decrease, calcitonin and intravenous bisphosphonate was begun. On hospital day 6, his steroid was further increased to a higher dose (hydrocortisone 100 mg ever 8 hours). His hospital course was complicated by C. difficile diarrhea, which improved with oral Flagyl therapy. Soon after, the patient was discharged home with a normal calcium level (9.5 mg/dL) and improved kidney function. The patient was also discharged with a higher dose of oral steroids than he had been on at home.


In this clinical vignette, we describe a probable case of hypercalcemia caused by glucocorticoid deficiency/withdrawal. Although this is a rare phenomenon, cases of hypercalcemia have been observed in patients after an adrenalectomy despite their being on corticosteroid replacement therapy. Treatment, therefore, involves increasing a patient's steroid dose. In this patient, it is proposed that adrenal atrophy developed gradually after the onset of ACTH deficiency following pituitary surgery given that the standard workup for hypercalcemia was negative. Although a corticotropin stimulation test was not performed in this patient, it is recommended 4–6 weeks after pituitary surgery to screen for adrenal insufficiency. Thus, in patients with the above pertinent history presenting with hypercalcemia, glucocorticoid withdrawal/deficiency should be on the top differential.


This case underscores the importance of diagnosing hypercalcemia secondary to glucocorticoid deficiency/withdrawal. This condition leads to hypercalcemia with its complications if the primary pathology is not recognized. Glucocorticoids play an important, though sometimes not as prominently recognized role as PTH and vitamin D do in calcium regulation, specifically, by inhibiting calcium reabsorption from the intestines and kidneys. Hypercalcemia secondary to relative glucocorticoid deficiency and/or withdrawal is rare. It is important for the hospitalist to recognize early the cause of hypercalcemia as illustrated in this case.

To cite this abstract:

Ip M, Ahmad S, Khan M. Moan and Groan: Deficiency or Excess? A Fascinating Case of Hypercalcemia. Abstract published at Hospital Medicine 2013, May 16-19, National Harbor, Md. Abstract 312. Journal of Hospital Medicine. 2013; 8 (suppl 2). Accessed May 22, 2019.

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