Life threatening hypocalcaemia resulting from hypoparathyroidism and coeliac disease.

Dr I Talapatra and Dr D J Tymms

Department of Medicine and Endocrinology
Royal Albert Edward Infirmary
Wigan lane, Wigan, UK


We describe below a patient who was admitted with severe hypocalcaemia. His serum calcium was 0.64 mmol/l. His serum magnesium level was also quite low (0.4 mmol/l) and needed intravenous calcium and magnesium supplements initially before being maintained on oral supplemental therapy alone. The patient had ECG changes mimicking myocardial infarction which resolved following improvement in serum calcium level. He probably had hypocalcaemic cardiomyopathy. The patient diagnosed with hypoparathyroidism initially was later on found to have coeliac disease as well and was put on gluten free diet. With proper dietary treatment and hydoxylated Vitamin D supplements, the patient continued to remain well both clinically as well as biochemically.
Key words: Hypocalcaemia, Hypomagnesemia, Hypoparathyroidism, Coeliac disease, Hypocalcaemic Cardiomyopathy.

Case Report:

A 62 year old gentleman was admitted with multiple problems together with life threatening hypocalcaemia. He had difficulty in swallowing and tingling sensation in his extremities. There was a history of weight loss of 2 ½ stones over past 15 months. He had a background history of Non Hodgkin’s lymphoma of right maxillary antrum 12 years ago treated with radiotherapy to the jaw and chemotherapy. On examination his BP was 139/70 mmHg and pulse 99/min. His blood results showed normal urea and creatinine, adjusted calcium 0.64 mmol/l (normal 2.05-2.60), Albumin 40 g/l, ionised calcium 0.46 mmol/l, phosphate 1.67 mmol/l (normal 0.8-1.45), normal alkaline phosphatase, PTH <0.7 pmol/l (normal 1.1-6.9), magnesium 0.40 mmol/l (normal 0.7-1.0) and haemoglobin 10.8 g/l (normal 13-17) with normal MCV (mean corpuscular volume), normal white cell count and platelet count. ECG showed ST segment elevation in anterior and inferior wall leads with a prolonged QTc of 492 ms. Three estimations of CK were 1927, 3656 and 7442 U/l (normal 24-190), Troponin I was >50 ug/l (normal <2). The patient had no chest pain and was not thrombolysed. The ECG changes reverted after correction of his hypocalcaemia. His echocardiogram showed impaired (moderate to poor) left ventricular function with diastolic dysfunction. His left ventricular function improved after correction of his hypocalcaemia. Other investigation results showed normal ferritin, normal serum Vitamin B12, normal red cell folate, normal reticulocyte count, negative Coomb’s test, serum iron was 2umol/l (normal 11-32), transferrin 1.4 g/l (normal 2-32), transferrin saturation 5.7% (normal 23-32). The patient had anaemia of chronic disease. The patient was treated with IV Calcium gluconate infusion 10% 100 ml/24 hours and IV Magnesium sulphate 5 gm or 20 mmol of Mg2+/24 hours for three days.Corrected calcium level was 0.75 mmol/l and 0.81 mmol/l on the 2nd and 3rd day with a phosphate level around 1.50 mmol/l and normal alkaline phosphatase; serum magnesium was ranging between 0.50-0.60 mmol/l. The patient was also put on Alfacalcidol (one alpha hydroxyl cholecalciferol) 2 mcg, Calcichew 4 tablets (each containing 1.25 gm of calcium carbonate or 500 mg of calcium) and Magnesium glycerophosphate 6 tablets (24 mmol Mg2+) daily. His echocardiogram was repeated after a week. It showed hypertrophied left ventricle with normal internal dimensions. There was some degree of diastolic dysfunction ; the apical region was hypokinetic with moderate left ventricular function overall. The right heart was within normal dimensions with trivial TR (tricuspid regurgitation) and mild PR (pulmonary regurgitation) on colour Doppler.

The patient was discharged with a serum calcium level of 1.8 mmol/l and magnesium of 0.72 mmol/l. The patient continued to have normocytic anaemia. His bone marrow biopsy showed a normocellular bone marrow. His calcium control was difficult and in view of his persistent anaemia he was further investigated. The antiendomyseal antibody was 100 (normal: negative). Oral gastro duodenoscopy showed Barrett’s oesophagus, pangastritis with +ve CLO test (test for Helicobacter pylori) and biopsy of duodenal mucosa showed villous blunting associated with mild rise of chronic inflammatory cells in the lamina propria and a focal rise in the number of intraepithelial lymphocytes with crypt hyperplasia suggestive of coeliac disease. The patient’s Vitamin D level was measured later on. It was low (estimated in April): Vitamin D3 was <4.0 ng/ml (normal : 10- 60 in summer; 5-25 in winter). The patient was put on a gluten free diet.

Two months later his echocardiogram showed mild left ventricular hypertrophy with mild global systolic dysfunction. The left atrium was within normal dimensions and the right heart was also normal with no significant tricuspid regurtitation..
The patient currently is on Calcitriol (1,25 dihyroxy cholecalciferol 0.25 mcg per tablet) 8 tablets a week, Calcichew 2 tablets, Bendrofluazide 2.5 mg and Omeprazole 20 mg daily and on no magnesium supplement. His latest calcium level is 2.05 mmol/l with normal magnesium. Latest echocardiogram report showed good LV function with no mitral regurgitation or aortic regurgitation. Right ventricle appeared mildly hypertrophied with trivial tricuspid and pulmonary regurgitation.

Discussion :

Our patient presented with severe hypocalcaemia dueto multiple pathologies. He had parathyroid hormone deficiency (1) together with coeliac disease (2) and Vitamin D deficiency (3). He could well have two co-existing autoimmune diseases in the form of hypoparathyroidism and coeliac disease or his hypoparathyroidism could have been caused by previous radiotherapy treatment. Interestingly enough there has been a case report of coeliac disease and hypoparathyroidism where the endomyseal antibodies cross reacted with parathyroid tissue (4). The patient recovered well from life threatening hypocalcaemia (5). His initial hypomagnaesemia needed to be corrected together with administration of calcium and hydroxylated Vitamin D supplements for the calcium level to improve. Following the diagnosis of coeliac disease, with proper dietary treatment magnesium deficiency (6) was corrected. There have been a few case reports (7,8,9) of hypocalcaemia and ECG changes mimicking MI and poor left ventricular function related to hypocalcaemia (Hypocalcaemic cardiomyopathy). With improvement in the patient’s calcium level the ST segment elevation in the patient’s ECG also resolved. Since being on gluten free diet and on hydroxylated Vitamin D derivatives the patient’s calcium level has been maintained at the desired lower limit of normal with stable renal function. There has been a case report (10) where coeliac disease co-existed with hyperthyroidism and hypoparathyroidism but we have not come across any case report where a patient presented with such severe hypocalcaemia resulting from multiple causes. Our case report therefore emphasizes the need to consider more than one cause for severe hypocalcaemia.
1,25 dihydroxy cholecalciferol (calcitriol) is the active form of Vitamin D which is synthesized in the kidney from 25 hydroxy cholecalciferol under the influence of the enzyme one alpha hydroxylase which is induced by parathyroid hormone (and also low phosphate level in the serum). Vitamin D plays an important role in calcium absorption.




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(2) Diagnosis of Celiac Disease- Celiac Sprue Association USA, Inc. Updated Jan 1 2004.
(3) Basha B, Rao S, Han ZH, Parfitt AM. Osteomalacia dueto Vitamin D depletion: neglected consequence of Intestinal Malabsorption; Am J Med 2000; 08(4): 291-300
(4)) Kumar V, Valeski JE, Wortsman J. Coeliac disease and hypoparathyroidism: cross- reaction of endomyseal antibodies with parathyroid tissue. Clin Diagn Lab Immunol, 1996 March, 3:2:143-6
(5) Tohme JF, Bilezikian JP. Hypocalcemic emergencies. Endocrinol Metab Clin North Am 1993 June; 22(2): 363-75
(6) Goldman AS, Van Fossan DD, Baird EE .Magnesium deficiency in celiac disease; Pediatrics 1962 Jun; 29: 948-52
(7) Hasan A, Mustafa K B, Gökhan Y, Ender S, Gülay Ö, Ümit K. Hypocalcemic Cardiomyopathy due to Untreated Hypoparathyroidism; Hormone Research 2003;59:201-204
(8)Bashour T, Basha HS and Cheng TO. Hypocalcemic cardiomyopathy; Chest, Vol 78, 663-665
(9)) Azzoug S, Chentli F. Hypocalcaemic cardiomyopathy in a patient with primary hypoparathyroidism and Fahr’s disease; Endocrine Abstracts (2006) 11 P98
(10) Khandwala HM, Chibbar R, Bedi A. Coeliac disease occurring in a patient with Hypoparathyroidism and Autoimmune Thyroid disease; Southern Medical Journal. March 2006; 99(3): 290.


First Published August 2006

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