M. Farrer et al., SIMVASTATIN IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS - EFFECT ON SERUM-LIPIDS, LIPOPROTEINS AND HEMOSTATIC MEASURES, Diabetes research and clinical practice, 23(2), 1994, pp. 111-119
The clinical efficacy of the 3-hydroxy-3-methyl-glutaryl-coenzyme A (H
MGCoA) reductase inhibitor simvastatin in the treatment of hypercholes
terolaemia in non-insulin-dependent diabetes (NIDDM), was examined in
a double-blind placebo-controlled study of 6 months in 70 patients wit
h NIDDM (age 25-70 years), of whom 57 were randomised to placebo (29 p
atients) or simvastatin for 6 months, following a 3-month run-in on di
et. Patients were hypercholesterolaemic (7.8 (7.6-8.0) (mean (95% conf
idence intervals)) mmol/l simvastatin vs. 8.0 (7.7-8.5) mmol/l placebo
) and mildly hypertriglyceridaemic (2.6 (2.2-3.0) simvastatin vs. 2.9
(2.3-3.5) placebo). Other lipid measures and estimates of glycaemic co
ntrol and haemostasis were similar in both groups. There were no signi
ficant changes in lipids, haemostatic factors, or measures of glycaemi
c control in the placebo treatment group. Conversely by the end of 24
weeks, simvastatin produced a 28% reduction in cholesterol (to 5.6 (5.
0-6.2) mmol/l (P < 0.001)), a 38% reduction in LDL cholesterol (from 5
.5 (5.4-5.6) mmol/l to 3.4 (2.8-4.0) mmol/l, P < 0.001), a 15% reducti
on in triglyceride (to 2.2 (1.8-2.6) mmol/l, P < 0.05, and a 9% rise i
n HDL (from 1.16 (1.07-1.25) to 1.23 (1.14-1.32) mmol/l, P < 0.05). Im
provements in apolipoprotein B (ape B) (-28%, P < 0.001), the LDL chol
esterol to apo B ratio (-20%, P < 0.001), and apo Al (+15%, P < 0.001)
were recorded. There were no effects upon fibrinogen, factor VII acti
vity, factor VIII activity, or measures of glycaemic control (fasting
glucose, insulin, C-peptide, or HbA(1)). Simvastatin is an effective t
reatment for hypercholesterolaemia in NIDDM with normal or mildly elev
ated triglycerides, which is well tolerated and has no adverse effect
upon glycaemic control. Simvastatin may additionally reduce triglyceri
des and improve the abnormality of LDL composition which is characteri
stic of hyperlipidaemic NIDDM.