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.

Acute hypoglycaemia is a pathological state induced by low plasma glucose concentration that results in a combination of early adrenergic symptoms due to catecholamine release and neuroglycopenic manifestations secondary to a deficient glucose influx to the brain. The initial adrenergic symptom acts as an early warning system so that hypoglycaemia can be corrected. However, subacute or chronic hypoglycaemia can be insidious and symptoms are not apparent. In chronic recurrent hypoglycaemia, sympathetic activity is reduced or delayed until profound hypoglycaemia develops and this can lead to increased confusion, behavioural changes and life-threatening complications such as convulsions, coma and death.In patients with diabetes, hypoglycaemia is commonly the result of excess insulin, oral hypoglycaemic medication or due to impairment of glucose counterregulation. Other conditions associated with subacute/chronic hypoglycaemia include ethanol consumption, congenital or acquired insulin excess, starvation, hormone deficiencies (hypoadrenalism, hypopituitarism, GH or isolated adrenocorticotropic hormone deficiency), critical illness and major organ failure. Hypoglycaemia in people without diabetes is uncommon. Rarely, symptomatic fasting hypoglycaemia can be induced by solid tumours and can present a diagnostic challenge as illustrated in this case report.A 70-year-old man presented with an intermittent history of violent, inappropriate behaviour, confusion, impaired consciousness and progressive memory and cognitive decline over a period of two years. He was periodically brought to the accident and emergency department with low blood glucose readings ranging between 1.9 mmol/L and 3.5 mmol/L. His symptoms rapidly resolved with intravenous dextrose. Hypoglycaemia was presumed to be secondary to reduced food intake. After correction of hypoglycaemia, he was discharged home from the emergency department. There was no past medical or family history of note. He was not on any regular medication, his alcohol intake was minimal and he was an ex-smoker. None of his family members was on hypoglycaemic agents. The physical examination was unremarkable. However, in view of his recurrent hypoglycaemic episodes, gradual weight loss and worsening cognition, he was admitted to hospital.The results of initial investigations, including full blood count, bone profile, renal, liver and thyroid function tests, prostate specific antigen, tumour markers and myeloma screening, were all within a normal range. Short synacthen and pituitary function tests were also normal. A supervised 24-h fast, which induced symptomatic hypoglycaemia yielded normal insulin (< 10 mU/L) and C-peptide concentrations (< 94 ng/ml). IGF-I and IGF-II were measured and found to be abnormal with a high IGF-II:IGF-I ratio at 15.6 (reference range < 10). Abdominal and pelvic MRI scan revealed a large pelvic tumour (figure 1) and histological features were consistent with retroperitoneal sarcoma. However, surgical excision was thought to be high risk because the patient...