Postgrad Med J: first published as 10.1136/pgmj.61.711.47 on 1 January 1985. Downloaded from Postgraduate Medical Journal (1985) 61, 47-48

Symptomatic hypercalcaemia precipitated by magnesium therapy

Amin A. Nanji* Division ofClinical Chemistry, Vancouver General Hospital, 855 West 12th Avenue, and Department ofPathology, University ofBritish Columbia, Vancouver, B.C., Canada.

Sununary: A patient with Crohn's disease receiving vitamin D and calcium had normal serum calcium levels when serum magnesium was low. Hypercalcaemia was precipitated when supplemental magnesium was given. The reason why serum calcium was initially normal is probably related to the effect of magnesium deficiency in reducing serum calcium level.

Introduction Hypocalcaemia is a well recognized complication of ictal lateralizing neurological signs. However she was hypomagnesaemia (Rude and Singer, 1981). markedly confused. Laboratory tests showed serum Therefore the signs of hypocalcaemia frequently calcium 3.9 mmol/l, magnesium 1.0 mmol/l and serum accompany magnesium depletion. Presented below is albumin 35 g/l. Serum sodium, potassium, chloride, a patient with Crohn's disease who was bicarbonate, urea nitrogen, and receiving creatinine, arterial copyright. vitamin D and supplemental calcium in doses which blood pH and gases were normal. The patient was would normally have resulted in hypercalcaemia. treated with intravenous saline and frusemide. This However the hypercalcaemia in this patient was resulted in a decrease in serum calcium accompanied prevented by the concomitant hypomagnesaemia and by a marked improvement in the patient's mental was precipitated when magnesium was therapeutically status. The patient did not have any more seizures. The administered. dose of vitamin D and calcium were both reduced and no further magnesium supplements were given. Case report http://pmj.bmj.com/ A 69 year old female with a ten year history ofCrohn's Discussion disease and a four year history of chronic obstructive lung disease was admitted to hospital for further The above patient demonstrates an unusual manifes- evaluation of pulmonary function. Four years before tation ofmagnesium deficiency; namely that of'mask- the present admission, the patient had a partial small ing' hypercalcaemia. The dosage of vitamin D and bowel resection. Her daily medications included calcium that the patient received will in some patients 50,000 IU ofvitamin D, 1000 mg ofelemental calcium cause & hypercalcaemia (Habener Potts, 1979). on September 30, 2021 by guest. Protected and 3 g of sulphasalazine. She was not receiving any Occurrence of hypercalcaemia in this patient was corticosteroids. Physical examination at initial admis- probably initially prevented by the presence of hypo- sion was normal. On the eighth day after admission, magnesaemia; replacement ofmagnesium precipitated serum calcium and magnesium were 2.25 mmol/l hypercalcaemia. Other causes that could have con- (normal 2.1-2.7) and 0.32 mmol/l (normal 0.74-1.15) tributed to acute hypercalcaemia such as volume respectively. She was treated with intravenous mag- depletion, thiazide diuretics and immobilization were nesium sulphate l0 g over 48 h. On the I 0th day after not present. admission, the patient had a generalized grand mal There are several factors responsible for lowering type seizure which lasted 2 min. There were no post- serum calcium in magnesium deficiency. These include failure of parathyroid hormone production and re- A.A. Nanji, M.B., Ch.B., F.R.C.P. lease, hypercalciuria, altered equilibrium for calcium *Present address: Ottawa General Hospital, Ottawa, between bone and extracellular fluid and altered Ontario, Canada K1H 8L6 vitamin D metabolism (Rude & Singer, 1981; Massry, Accepted: 16 November 1983 1979). C) The Fellowship of Postgraduate Medicine, 1985 Postgrad Med J: first published as 10.1136/pgmj.61.711.47 on 1 January 1985. Downloaded from 48 CLINICAL REPORTS

The occurrence of a seizure disorder secondary to aptic nerve endings and causes seizures (Cryer and hypercalcaemia is rare (Hines & Suker, 1973). The Kissane, 1979). mechanism by which hypercalcaemia causes seizures is In summary, the above patient demonstrates that in poorly understood. It has been proposed that excess certain patients who are receiving vitamin D and calcium in the presence of decreased magnesium calcium, magnesium supplementation may precipitate concentration increases transmitter release at presyn- hypercalcaemia.

References CRYER, P.E. & KISSANE, J.M. (1979). Malignant hypercal- MASSRY, S.G. (1979). Disorders of magnesium metabolism. cemia, American Journal of Medicine, 67, 486. In Strauss and Welt's Diseases of the Kidney L.E. Earley HABENER, J.F. & POTTS, J.F. (1979). Clinical features of and C.W. Gottschalk, (eds.) p. 1639. Little Brown and primary hyperparathyroidism In Endocrinology L. De- Company: Boston, USA. Groot, (ed.) p. 708. Grune and Stratton: New York. RUDE, R.K. & SINGER, F.R. (1981). Magnesium deficiency HINES, J.R. & SUKER, J.R. (1973). Some unusual manifesta- and excess. Annual Review of Medicine, 32, 245. tions of parathyroid disease. Surgical Clinics of North America, 53, 221. copyright. http://pmj.bmj.com/ on September 30, 2021 by guest. Protected