Endocrine Abstracts

A 53 year old man with ANCA-positive glomerulonephritis was referred with a 3-month history of hypercalcaemia. There was no significant family history and treatment consisted of Maxepa concentrated fish oils 5g/day for glomerulonephritis and lansoprazole plus Bisodol (proprietary indigestion preparation containing calcium, magnesium and sodium bicarbonate) for a hiatus hernia. Investigations revealed a corrected calcium concentration of 3.06 mmol/l, phosphate 1.27 mmol/l, creatinine 180 micromol/l, albumin 32 g/l, PTH 0.8 pmol/l (1.1-6.8), and 25-hydroxyvitamin D 25.3 nmol/l (7-50). Serum and urinary electrophoresis and serum ACE levels were normal. A 24-hour urinary calcium to creatinine clearance ratio of 0.021 excluded familial hypocalciuric hypercalcaemia. Renal ultrasound revealed nephrocalcinosis. Maxepa and Bisodol therapy was considered as a cause of his hypercalcaemia and treatment was discontinued. Serum calcium concentrations returned to normal within six weeks and have remained so. Maxepa contains the omega-3 marine triglycerides eicosapentaenoic acid 170 mg/g and docosahexenoic acid 115mg/g, together with vitamin A < 100units/g and vitamin D < 10 units/g. Therapeutic interest in fish oil dates from 1970 when Danish physicians observed that Eskimos and Greenlanders had a low incidence of heart disease and arthritis despite a high-fat diet. Maxepa therapy reduces plasma triglyceride concentrations but does not affect total cholesterol concentration. Used as an antioxidant in cardiovascular disease, it retards atheromatous plaque progression by inhibiting monocyte migration and growth factor production. Maxepa also promotes NO synthesis in vascular endothelium. There are 4 reports describing Maxepa treatment in glomerulonephritis: in two a beneficial effect on renal function was demonstrated but no effect was identified in the others. Maxepa has not been described previously to cause hypercalcaemia. Thus, in combination with antacids such as Bisodol, Maxepa may induce hypercalcaemia and should be considered as a novel cause of the milk-alkali syndrome.