III型高リボ蛋白血症, 心筋梗塞を合併した糖尿病の1例

The incidence and pathogenesis of type III hyperlipoproteinemia in diabetes mellitus are not known. A higher incidence of atherosclerotic vascular complications in type hyperlipoproteinemia and in diabetes mellitus has been reported. A case of diabetes mellitus having type II hyperlipoproteinemia, acute myocardial infarction and a history of cerebral infarction, is described here, and the relationships between diabetes mellitus, type la hyperlipoproteinemia and atherosclerotic vascular disease are discussed. The 55-yr-old male diabetic patient suffered cerebral infarction with r-hemiparesis and speech disturbance five years ago but recovered almost completely. He later complained of chest oppression and pain on Oct. 31, 1976. ECG showed a QS pattern and ST elevation in a V L, V₁ and V₂, ST depression in TI, 1ff and aVF, and negative T in V_{4, 5, 6}. He was diagnosed as having acute lateral and old anteroseptal myocardial infarction. Coronary angiography revealed marked atherosclerotic changes in all three main coronary arteries and their branches. Diabetes mellitus had been pointed out five years previously and the patient had received acetohexamide (500 mg/day) for a year. His blood glucose levels after 50 g glucose ingestion on Nov. 11, 1976 were 191 (0'), 295 (60') and 229 (120') mg/dl. His insulin responses to 50 g glucose ingestion, intravenous injection of tolbutamide (1 g) and glucagon (1 mg) were very weak. Eye fundus showed Scott 11 a and Scheie Si, H1 changes. Persistent proteinuria was found (0.51 g/day) and nodular diabetic glomerulosclerosis was observed in the kidney. However, no mesangial foam cells in the renal glomeruli, as reported by Amatruda, J.M., were noticed. Renal function was normal. The levels of plasma cholesterol and triglycerides on Nov. 16, 1976 were 318 and 441 mg/dl, respectively. Agarose gel electrophoresis showed floating β(broad β) lipoproteins. The values of cholesterol in VLDL (d<1.006 g/dl), VLDL cholesterol/VLDL triglycerides and VLDL cholesterol/plasma triglycerides were 107 mg/dl, O.38 and O.243, respectively. This abnormal lipoprotein pattern was considered to represent type III hyperlipoproteinemia, fulfilling the chemical indices of Vessby, Mishkel and Albers et al. The type III hyperlipoproteinemia changed to a type 11 a pattern after combined treatment by diet, clofibrate (2.0 g/day) and acetohexamide (250 mg/day). The hepatic and extrahepatic triglyceride lipase activities after intravenous injection of heparin (100 U/kg) were decreased to about half the activities of control subjects. All endocrinological tests including those of pituitary and thyroid function were normal. The patient had no xanthomas such as palmar, tendinous, tuberous, eruptive xanthomas or xanthelasma. No hepatosplenomegaly was observed. Stern. M.P. has described transient type hyperlipoproteinemia in a patient with diabetic ketoacidosis, but the present case is the first known report of transient type hyperlipoproteinemia associated with diabetes mellitus without ketoacidosis. It is considered that abnormal lipoprotein metabolism in the present diabetic patient may have played a significant etiological role in the development of atherosclerotic vascular disease.