Hypervitaminosis D and Cortical Venous Thrombosis; An Unusua
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There is considerable interest in the role vitamin D plays in human health. It has been shown that 1,25-dihydroxyvitamin D exert anticoagulant effects in patients with leukemia through the upregulation of thrombomodulin and downregulation of tissue factors (TFs) in monocytes and myelogenous cells. It has also been demonstrated that vitamin D receptors may play an important role in thrombosis. Despite of protective role in thrombosis, occurrence of Cortical Venous thrombosis in setting of hypervitaminosis D is an unusual presentation.

A 65 year old male presented with complaints of altered sensorium since 1 day, nausea, giddiness and persistent vomiting since 15 days. On examination, he was drowsy, disoriented in time, place and person. He was moving all 4 limbs. His pulse was 88 beats minute and blood pressure was 120/80 mm of Hg. Respiratory rate was 16 per minute. Oral mucosa was dry. His laboratory investigations revealed hemoglobin of 9.1 g/dl with normal WBC and platelet counts. His blood urea nitrogen was 64mg/dl and creatinine of 4.4 mg/dl. Sodium was 136 mEq/L, potassium was 3.8 mEq/L, serum calcium of 14.4mEq/L and phosphorus 3.0 mEq/L. Alkaline phosphatase 35 IU/L.

MRI brain with venography showed loss of flow in left transverse sigmoid sinus suggestive of cortical venous thrombosis (CVT) and left acute mastoiditis. To search for cause of hypercalcemia, his urine for Bence Jones protein was sent which was positive, but his protein electrophoresis and bone marrow examination was normal. His vitamin D levels were done which was >150 ng/mL and whole body CT scan was normal.

A detailed history of patient after regaining consciousness on day 3 revealed that he had persistent backache for which he had taken 15 injections of Arachitol (vitamin D) 6 Lacs IU intramuscularly along with once week chewable cholecalciferol tablets since 6 months. So he was diagnosed as CVT with acute renal failure with hypercalcemia secondary to iatrogenic hypervitaminosis D. His CVT was managed with anticoagulation. His hypercalcemia was treated with hydration, calcitonin, steroids and Zolendronate.

This case highlights the necessity of taking a diligent history in cases presenting with hypercalcemia and acute kidney injury to unveil a treatable cause especially in elderly patients with altered sensorium.

Source: https://www.japi.org/x26474c4/hypervitaminosis-d-and-cortical-venous-thrombosis-an-unusual-presentation
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