Abstract: Hypercalcaemia occurring after ten weeks of immobilisation was observed in four adult patients all of whom had had prior renal failure sufficient to require renal dialysis. In all patients parathyroid hormone levels were normal or low and in three plasma 1,25(OH) 2 D 3 levels were low. These findings are consistent with immobilisation induced increases in bone calcium resorption. Renal excretion of calcium may have been impaired by renal dysfunction resulting in hypercalcaemia and suppression of plasma PTH and 1,25(OH) 2 D 3 levels. Resolution of the hypercalcaemia was associated with remobilisation. Parathyroidectomy is inappropriate treatment.
A 21-year-old man with a five-year history of recreational intravenous cocaine abuse developed chest pain within one minute and cardiopulmonary arrest within one hour following an injection. He died and, on autopsy, was found to have severe coronary obstructive lesions, as a result of chronic intimal proliferation, and acute platelet thrombosis. Secondary chronic and acute myocardial ischemic lesions also were observed. Cocaine-induced coronary artery spasm may have occurred and produced focal endothelial injury and platelet aggregation; this pathogenetic mechanism may have accounted for both the chronic and the acute coronary obstructive lesions. In addition, lymphocytic myocarditis was present and may have been related to the long-term cocaine abuse.
A new insulin regime is described, in which the primary aim is to attain normal basal plasma glucose concentrations by means of a constant insulin delivery rate from the long-acting Ultratard insulin. Additional twice daily Actrapid insulin is given to cover meals, and we have investigated this regime in 29 insulin dependent diabetics, with control assessed by admission for 24 hour profiles. Patients with low insulin requirements only need a basal insulin supplement with Ultratard insulin. With increasing insulin requirements the dose of short-acting insulin increases more than the basal insulin supplement. Thus fixed combinations of short- and long-acting insulins cannot produce good control in all patients. Twenty-one patients were deemed ‘well controlled’ in that they had no symptomatic hypoglycaemia, an overnight plasma glucose concentration of <5·5 mmol/l and a mean late post-prandial glucose concentration of <6·5 mmol/l. Their average ‘mean excess glycaemic exposure’ (mean incremental plasma glucose above 5 mmol/l) was 0·7 mmol/l (normal range 0–0·5 mmol/l), which is considerably less than that found in many maturity-onset diabetics. The distinction between basal and meal insulin requirements simplifies rules of insulin therapy.