Abstract #1401609: A Case of Vitamin D Toxicity Associated with Weight Loss During a Low Carbohydrate Diet

Abstract

Vitamin D is a commonly prescribed, fat-soluble vitamin important for calcium homeostasis and bone health. Vitamin D Toxicity (VDT) is rare and typically caused by aggressive supplementation or manufacturing errors. In epidemiologic studies, vitamin D levels correlate inversely with adiposity, and dietary weight loss is associated with increases in 25-hydroxyvitamin D [25(OH)D] level. Vitamin D is stored in adipose tissue and it is postulated that weight loss is a risk factor for the development of VDT. Here we present a case of VDT associated with weight loss during a low carbohydrate diet. A 74-year-old man with CKD stage 3a and benign prostatic hyperplasia presented to the ED with intractable emesis preceded by subacute nausea, anorexia, and constipation. He reported following a very low carbohydrate diet with intentional weight loss from 83.9kg (BMI 25.86) to 71.9kg (BMI 21.7) over five months. He reported taking Vitamin D3 250μg (10,000 IU) daily which was self-prescribed prior to admission for at least 12 months. On admission, he was mildly bradycardic and hypertensive. Laboratory evaluation in the ED revealed serum creatinine (sCr) 5.2 mg/dL (0.66-1.28, baseline 1.24 mg/dL 3 months prior), calcium 12.9 mg/dL (8.4-10.2), albumin 3.8 g/dL (3.2-4.8), and 25(OH)D >150 ng/dL (30-100). Intact PTH was suppressed at 13.2 pg/mL (14-72) and 1,25-dihydroxyvitamin D was 71 pg/mL (18-72). PTH-related protein, and serum and urine electrophoresis were within reference ranges. The patient was treated for hypercalcemia with intravenous fluids, prednisone 20mg daily, and on hospital day eight, intravenous pamidronate 30mg. Upon discharge on hospital day nine, calcium was 10.5 mg/dL. He was instructed to stop all vitamin D containing supplements. One month after discharge, sCr was 1.9 mg/dL and calcium was 8.7 mg/dL. Vitamin D is theorized to be stored in adipose tissue in clinically relevant quantities and released during weight loss. Due to the rare presentation of VDT in the setting of dietary weight loss, there are a limited number of cases described. Few clinical trials measuring serum 25(OH)D concentrations in people with obesity following weight loss have been performed. One study confirmed that patients with obesity have lower vitamin D levels that normalize after significant weight loss, supporting the hypothesis that vitamin D is stored in the adipose tissue and released following weight loss. Here we present a case of acute VDT causing symptomatic hypercalcemia after intentional dietary weight loss in the setting of chronic supratherapeutic vitamin D supplementation. As illustrated in this case, rapid weight loss in the setting of supratherapeutic doses of Vitamin D can result in VDT. Additional studies are needed to clarify the mechanisms that regulate the kinetics of vitamin D in the adipose tissue of persons with obesity.