SUN-313 Unmasking Sarcoidosis as the Cause of Hypercalcemia in an Asymptomatic Patient

Abstract S. Ravi: None. K.G. Reddy: None. Background: Hypercalcemia poses a common diagnostic dilemma for endocrinologists. The vast majority of cases are precipitated by either hyperparathyroidism or malignancy, and are associated with significant symptom burden. In this abstract we present an unusual case of sarcoidosis in a patient with asymptomatic hypercalcemia and signs consistent with multiple possible etiologies. Clinical Case: A 64-year-old Hispanic male with hypothyroidism and CKD3 was referred to the hospital for hypercalcemia. He was recently diagnosed with progressive proteinuric CKD3 and elevated serum calcium (SCa) of 13.2 mg/dL. The patient denied using supplements, and endorsed feeling well overall, denying any symptoms of malaise, changes in mentation, body aches. Labs revealed calcifediol level of 22 ng/mL, calcitriol 169 pg/mL, and PTH 0.6 pg/mL. PTHrp and TSH were both within normal limits. Ultrasound of thyroid and parathyroid did not show any evidence of adenoma, only revealing a 0.3 cm hypoechoic nodule in the left lobe of the thyroid, likely representing a complex cyst. Imaging of chest and abdomen revealed mild enlargement of mediastinal, iliac and retroperitoneal lymph nodes as well as nephrolithiasis and renal cysts. Urine studies were negative for derangements of calcium excretion, but were significant for B2 microglobulin excretion. Serum Chromogranin A was elevated to 265 ng/mL as well, suggesting a malignant or neuroendocrine process. The patient was treated with aggressive IV fluid hydration which improved SCa. He was referred for lymph node biopsy and to oncology for work-up of possible lymphoma or multiple myeloma. About 4 weeks later the patient was then referred to the hospital again for SCa of 14.5 mg/dL. At this time calcitriol was elevated to >600 pg/mL. The patient was again treated with isotonic volume expansion and bisphosphonate. Biopsy results were obtained and revealed confluent nonnecrotizing granulomatous inflammation. ACE level was 145 U/L, and fungal and TB testing were negative. The patient was diagnosed with sarcoidosis and started on a protracted course of steroids with improvement. Conclusion: The pathogenesis of hypercalcemia in sarcoidosis involves dysregulated vitamin D metabolism within granulomatous lesions leading to uncontrolled production of calcitriol and increased calcium absorption. Diagnosis in this patient was complicated because he lacked typical manifestations of sarcoidosis, and his presentation included multiple red herrings pointing to exogenous vitamin D intake, as well as nephrologic, neuroendocrine, and malignant etiologies. Endocrinologists are often consulted for management of hypercalcemia. As this case illustrates, it is important to consider a broad differential including non-endocrinological etiologies when diagnosing patients. Sunday, June 2, 2024