Endocrine Abstracts

Background: Tuberculosis rarely leads to clinically significant hypercalcemia. However, elderly patients remain predisposed due to advanced age, multiple comorbidities and polypharmacy.

Clinical Case: An 81-year-old female presented with 1 month history of bilateral weak hand grip and sluggish mastication. She was initially managed as progressive Parkinson’s Disease. After 3 weeks, she was now reported to have episodes of fall from imbalance. After few days, there was noted increased sleeping time, decreased verbal output, response lag and slurred speech. There were no pulmonary symptoms or febrile episodes. Her medical history includes hypertension, Diabetes Mellitus, previous CVD infarct, Chronic Kidney Disease, recovered Moderate COVID-19 infection and pulmonary tuberculosis that was diagnosed 30 years ago. Outpatient evaluation revealed severe hypercalcemia (15.36 mg/dl). Upon admission, Calcium (500 mg/day) and Vitamin D (1500 IU/day) supplements were discontinued. She was started on vigorous intravenous hydration and diuresis with Furosemide. Calcitonin nasal spray was administered for 2 days. Cranial CT scan showed absence of acute infarction or intracranial hemorrhage. On the 3rd hospital stay, serum calcium was still elevated (11.99 mg/dl) but decreased from baseline. Other blood tests results showed elevated 25(OH)D 119.72 ng/ml (>30 ng/ml), normal PTH 15.84 pg/dl (<67.90 pg/dl), magnesium 2.41 mg/dl (1.6–2.6 mg/dl) and phosphorous 3.6 mg/dl (2.29–4.79 mg/dl). Hence, PTH-independent causes were evaluated with high suspicion of Vitamin D intoxication. Chest imaging showed a thick walled cavitary mass with adjacent consolidation and surrounding centrilobular nodule in a tree-in-bud configuration in the right upper lobe suggestive of an infectious process. On the 10th hospital stay, CT guided biopsy of the right upper lung mass was done. Histopathology showed lung tissues with fibrosis, focal necrosis, and chronic inflammation. MTB GeneXpert was positive consistent with Tuberculosis for which she was started on Anti-Koch’s medications to be completed for 6 months. An elevated Serum 1,25(OH)₂D could have supported extrarenal 1α hydroxylation in granulomatous disease but was not readily available. On the 12th hospital stay, due to persistent hypercalcemia (11.72 mg/dl), she was started on Prednisone 10 mg/day which was up titrated to 20 mg/day after 3 days of initiation then down titrated weekly. She was discharged in a stable condition. Normocalcemia was documented upon follow up with subsequent improvement in the patient’s sensorium.

Conclusion: Granulomatous disorders as the etiology of hypercalcemia should be suspected in the setting of hypervitaminosis D and low-normal or low parathyroid hormone level. Hypercalcemic crisis is an infrequent endocrine emergency that portends excellent outcomes with prompt diagnosis and management.