Diabetes, hypertension and hyperlipidaemia.

: The predominant cause of death among diabetic patients in populations with high cholesterol levels is coronary heart disease. This effect is related to diet and both insulin dependent and non-dependent diabetes are characterized by an increase in circulating very low density lipoprotein (VLDL). Insulin deficiency or resistance accelerates the release of VLDL from the liver. However, the susceptibility to vascular disease seen among diabetics may be a particular function of their raised levels of intermediate density lipoproteins (IDL) produced when VLDL is metabolised to low density lipoprotein. The concept of hyperinsulinaemia is not helpful in explaining the diabetic patient's disturbed metabolism and is a source of confusion. The major therapeutic task in non-insulin-dependent diabetes is often to reduce the patient's weight and thus to reduce insulin resistance. In patients with coronary heart disease, this should be fully investigated at least as promptly as in non-diabetic people. Lipid lowering drugs, and particularly the fibrates, are suitable for treating diabetic patients since they lower both cholesterol and triglycerides and raise HDL. There is much more controversy about the ideal choice of antihypertensive agents, particularly for patients with only moderate increases in blood pressure. Both thiazides and beta-blockers disturb the lipid profile most markedly in many patients with diabetes or primary hyperlipidaemia. Current evidence suggests that many patients with hypertension, but no other cardiovascular risk factors, derive no benefit from receiving antihypertensive therapy. As in the management of hypercholesterolaemia, the decision to introduce drug therapy should not be determined by the blood pressure reading alone, but should take account of the whole patient risk. The combination of even "mild" hypertension with diabetes or hyperlipidaemia demands greater therapeutic activity and then there is a case for the use of antihypertensive agents which do not adversely influence the lipid profile.