Hypercalcemia: A Gut Feeling

Presentation Number: MON 301
Date of Presentation: April 3rd, 2017

Maria Isabel Linares*1 and Alex Manzano2
1Mount Sinai Medical Center, Miami Beach, FL, 2The Thyroid, Parathyroid and Pituitary Center for Miami, Miami, FL

Abstract

Background

Hypercalcemia is produced by primary hyperparathyroidism and malignancy in about 90% of the cases. The other 10% is caused by a variety of rare disorders including granulomatous diseases. Chron’s disease is a granulomatous disorder frequently associated with hypocalcemia due to intestinal malabsorption of vitamin D and calcium. We present a case of hypercalcemia driven by Chron’s disease activity.

Case description

38-year-old man was found to have elevated calcium levels on routine examination. His calcium was 11 mg/dL (8.7-10.2 mg/dL) and was associated with polydipsia, which had resolved. He denied polyuria, night sweats, weight loss, muscle cramps, constipation or diarrhea. His medical history was remarkable for Chron’s disease treated with mesalamine with clinically active disease three months before, and one episode of nephrolithiasis seven years earlier. On exam he had left cervical adenopathy, normal deep tendon reflexes and absence of skin lesions. Biochemical data showed calcium at 10.1 mg/dL (8.7-10.2 m/dL), albumin at 4.5 g/dL (3.2-5.6 g/dL), elevated 1,25-dihydroxyvitamin D level at 95.5 pg/mL (10-75 pg/mL), with a low 25-hydroxyvitamin D level at 23 ng/mL (30-100 ng/mL) and elevated 24-hour urine calcium at 322.8 mg (100-300 mg). Parathyroid hormone (PTH) level was normal at 34 pg/mL (16-65 pg/mL). Calcium creatinine clearance ratio was 0.017 making a diagnosis of Familial hypocalciuric hypercalcemia unlikely. US-guided FNA biopsy of the left cervical lymph node with flow cytometry did not yield features of a lymphoproliferative disorder. His hypercalcemia was deemed to be secondary to activity of Chron’s disease and he was recommended to continue its treatment. No other interventions were performed as he remained asymptomatic and his calcium was normal. On follow up exam six months after his last colitis flare, his 1,25-dihydroxyvitamin D level decreased significantly to 80.1 pg/mL and his calcium level continued to be normal.

Discussion

Granulomatous disorders such as Chron’s disease have been associated with hypercalcemia due to increased intestinal calcium absorption induced by high serum 1,25-dihydroxyvitamin D (calcitriol). Activated mononuclear cells express 1α-hydroxylase activity, able to convert 25-hydroxyvitamin D into calcitriol in a mechanism that is independent of PTH. Even though Chron’s disease is known for granuloma formation, most reports assessing calcium homeostasis describe hypocalcemia as the most common calcium abnormality due to vitamin D malabsorption in the bowel. Our patient’s hypercalcemia was likely secondary to recent Chron’s disease flare with later resolution after treatment of the flare. Treatment of hypercalcemia secondary to granulomatous disorders is based on the treatment of the underlying condition. Steroids and bisphosphonates have been used in patients not responding to these measures.

 

Nothing to Disclose: MIL, AM