SUN-515 A Case report of Severe Persistent Hypocalcaemia due to Functional Hypoparathyroidism

Abstract

Introduction: Severe Hypocalcaemia is generally seen in clinical practice in patients following thyroid or parathyroid surgery .We report a case of severe hypocalcaemia with unusual presentation and etiology with challenging management. Case report: A 49 year old gentleman presented to hospital with unexpected, unintentional severe weight loss (20kg over 2 months), vomiting, diarrhoea, muscle cramps and pins & needles in both hands. His past medical history included beta thalassemia trait. He had a recent bereavement in his family and therefore had attributed his symptoms to the grieving process. He had no significant or relevant family history of note.Physical examination revealed positive Chvostek and Trousseau’s signs. His initial biochemistry showed corrected calcium of 0.86 (Normal range:2.20-2.60 mmol/l), Magnesium 0.58 (Normal range:0.7-1.0mmol/l), K+:3.3(Normal range:3.5-5.3mmol/l),Parathyroid hormone(PTH) suppressed at 0.7(Normal range:1.1-4.7pmol/l) and 25 OH Vitamin D 25(Normal range:50-250nmol/l).ECG showed long QTc.He wasn’t taking any proton pump inhibitor. He was started on intravenous magnesium infusion (6g of MgSO4 in 500 ml Normal saline), Calcium Gluconate infusion (100ml of 10% Ca. Gluconate in 1000mls of Normal saline at 50-100 ml/hr), Calcium carbonate tablets and Cholecalciferol 20,000 units daily(for 10 days). His corrected calcium gradually improved and he noticed immediate resolution of his symptoms. His CT chest,Abdomen,Pelvis did not show any evidence of malignancy and Gastroscopy showed mild erosive gastritis.He was reviewed by Gastroenterology but no other cause for significant weight loss and gastrointestinal symptoms was found. He was thought to be having Severe Hypocalcaemia due to Functional Hypoparathyroidism caused by Magnesium and Vitamin D deficiency. He was discharged on oral calcium and cholecalciferol tablets. He represented to hospital a month later with corr. Ca+ of 1.57mmol/l. Vitamin D had improved to 90nmol/l, however, PTH was still suppressed at 0.8pmol/l.His calcium carbonate tablets were increased to daily dose of 3g per day and he was also started on 1-alfacalcidol 250 nanograms BD. Subsequent review in ambulatory clinic revealed that he was still hypocalcaemic at 1.75mmol/l. His 1-alfacalcidol was increased to 500 nanograms BD. He continues to be on this treatment, has gained weight and is asymptomatic. Conclusion: Although calcium abnormalities are commonly treated on medical wards, it is very rare to see such severe hypocalcaemia in the absence of any significant pathology. Understanding the physiology of calcium homeostasis is vital to guide appropriate management, especially in situations of clinical emergency which can be very challenging, as we have highlighted in our case.