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Abstract: PO1190

Systemic Sarcoidosis Presenting with Hypercalcemia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Mahmood, Salman Bin, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
  • Junghare, Milind Y., University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
  • Mettler, Tetyana, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States

Sarcoidosis is an idiopathic autoimmune illness that typically presents with pulmonary involvement but can affect virtually any organ. This often makes it challenging to diagnose as its manifestations can be quite varied. We report an interesting case of systemic sarcoidosis presenting with hypercalcemia of unclear mechanism.

Case Description

A 53-year-old Caucasian male presented to the clinic with polyuria, forgetfulness and weight loss. Medical history included hypercalciuria with recurrent nephrolithiasis, diabetes and positive ANA (titer 1:160) without any prior history of constitutional, respiratory or joint symptoms. Serum calcium returned 13 mg/dl. The patient also had an AKI and an elevated ALP. Further workup revealed a suppressed PTH, normal 25-OH and 1,25-OH vitamin D, but a borderline elevated PTHrP (2.5 pmol/L [0-2.3 pmol/L]). This prompted a CT CAP with contrast to rule out malignancy that instead showed mediastinal lymphadenopathy, heterogeneous liver enhancement suggestive of cirrhosis and an enlarged, nodular spleen. Transbronchial lymph node biopsies were normal and an extensive infectious and malignancy workup remained negative. The patient was given fluids followed by zoledronate with resolution of hypercalcemia and AKI. A liver biopsy was ultimately pursued which showed non-caseating granulomas. The patient was prescribed steroids with improvement in symptoms and normalization of ALP.


In patients with sarcoidosis, the development of hypercalcemia is thought to be mediated via aberrant activation of vitamin D leading to calcitriol excess. Our patient's calcitriol level was normal and hypercalcemia may also occur in the absence of elevated levels. Possible described mechanisms include "inadequate normal" calcitriol concentration without elevation in systemic levels, elevated PTHrP and direct action of pro-inflammatory cytokines causing osteolysis.

CT with contrast showing heterogenous liver enhacement and a nodular spleen.