Magnesium metabolism in primary hyperparathyroidism.

1. Magnesium metabolism has been studied in forty-eight patients with primary hyperparathyroidism. Metabolic balance studies were undertaken in forty-three untreated patients and in fifteen patients after parathyroidectomy. The data obtained are compared with the pattern of magnesium metabolism in healthy adults, as established by analysis of collected nutritional studies. The renal handling of magnesium was assessed from measurements of 24-h renal clearances. 2. The mean serum magnesium in primary hyperparathyroidism was normal but low levels were present in nine of the forty-eight patients. There was a significant inverse correlation between serum levels of calcium and magnesium. 3. The magnesium balance was negative by amounts >5% of the dietary intake in eleven patients, and positive to a similar degree in twenty-one. Patients in negative balance ingested and consequently absorbed less magnesium than those in positive balance ; the negative balance was apparently due to inadequate renal conservation of magnesium in the face of this lower intake and, in some cases, despite a low serum magnesium. When related to the level of dietary intake, intestinal net absorption of magnesium tended to be greater than normal. 4. In eleven of twelve patients studied, the urinary output of magnesium was lower after parathyroidectomy irrespective of changes in the serum level of magnesium. This fall in output appeared to depend mainly on reduction in the serum calcium. In untreated patients without advanced secondary renal disease there was a positive correlation between the serum calcium and the clearance ratio CMg/Ccreatinine. Additional mechanisms may contribute to renal loss of magnesium when renal failure is advanced. 5. The tendency to develop a negative magnesium balance and hypomagnesaemia in untreated patients of this series thus appeared related to the height of the serum calcium, the presence of advanced secondary renal disease and inadequate dietary intake. * Present address : Prince Henry’s Hospital, Melbourne, Australia. Correspondence: Professor S. W. Stanbury, Division of Metabolism, University Department of Medicine, The Royal Infirmary, Manchester M13 9WL.