The effect of metformin on mean platelet volume in diabetic patients


Dolasik I., Sener S. Y., Celebi K., Aydin Z. M., Korkmaz U., CANTÜRK Z.

PLATELETS, sa.2, ss.118-121, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2013
  • Doi Numarası: 10.3109/09537104.2012.674165
  • Dergi Adı: PLATELETS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.118-121
  • Kocaeli Üniversitesi Adresli: Evet

Özet

Diabetes mellitus (DM) is an independent risk factor for cardiovascular diseases. Metformin, the most commonly used antidiabetic, also has an antiatherogenic effect. Mean platelet volume (MPV) is increased in patients with high thrombogenic activation and also at risk for atherosclerosis. The purpose of this study was to examine the effects of metformin on MPV values in newly diagnosed type II DM patients on metformin monotherapy. In this study, 60 newly diagnosed type II DM patients (45 females, 15 males), who had applied to the Kocaeli University School of Medicine Endocrinology outpatient clinic, and 47 healthy individuals (35 females, 12 males) were included. The two groups have similarity for age, sex and body mass index. The patients with additional disease, nephropathy, smoking and using drugs that may affect the MPV were excluded. At baseline and 6 months after metformin treatment, patient demographics and laboratory values were compared. MPV was higher among type II DM patients than the control group (p < 0.001). After 6 months of metformin treatment, MPV values were significantly decreased (p < 0.001). HbA1c and mean platelet mass were also significantly decreased (p = 0.022 and 0.001, respectively). There was no correlation between MPV and HbA1c values (r = -0.13, p = 0.926). Metformin, which has been shown to exhibit antiatherogenic effect through positive effects on cholesterol levels, inflammatory markers and vascular adhesion molecules, decreased MPV values that appear to play a crucial role at the beginning of atherosclerosis development. We conclude that our result may contribute to the explanation for antiatherogenic effect of metformin.