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Gestational diabetes: Is it linked to platelets hyperactivity?

Pregnancy is characterized by a hyperinsulinemic state and a decrease of tissues receptors to insulin. Some women develop glucose intolerance resulting in gestational diabetes or impaired glucose tolerance which affects between 3 and 6% of all pregnancies [1]. When compared to normal pregnancy, perfused diabetic placenta transfers more arachidonic acid to prostanoids, resulting in higher TxA2 and lower PGI2 [2]. Platelet generated TxA2 has powerful vasoconstrictive and platelet activating functions leading to the occurrence of microthrombosis on placental bed vessels and placental infarctions. Considering the former biochemical changes in pregnancy, we aimed to investigate the platelet count and function in cases with gestational diabetes mellitus (GDM). This prospective multi-centre case-control study included third trimester single pregnancies monitored at outpatient services from three third level hospitals, recruiting cases in the period from September 2003 to November 2007. One hundred and twelve women affected by gestational diabetes, and the same number of healthy pregnant women were included in order to compare parameters randomly in a paired fashion regarding gestational age. GDM was diagnosed by the standard oral glucose tolerance test (OGTT, 100 g) performed between 26 and 30 weeks of gestation. From all pregnant women, whole venous blood was obtained from the antecubital vein into citrate tubes as previously described [3] and analysed for different blood parameters among which platelet count (PLT) and mean platelet volume (MPV). An automated commercial Coulter counter (Coulter counter, Max Instruments Laboratory, Milan, Italy) was utilized for analysing PTL, red blood cells (RBC) and granulocyte count analysing the blood. All pregnant women signed an informed consent as stated by the ethical committees from every Institution were cases were recruited. Platelet count values did not differ significantly between cases and control group Conversely, MPV was significantly higher in GDM group respect to controls (8.9þ/ 1.9 vs. 8.0þ/ 1.3 fl, p50.001). Interestingly also RBC number was higher in cases respect to controls (p50.001). Nevertheless, mean corpuscular volume (MCV) did not show any difference between groups (Table I). Platelet count and function are the most important platelet characteristics and MPV is the indicator for its function. Increase in MPV has been documented in patients with metabolic syndrome, stroke and diabetes mellitus. It has been observed that diabetic patients presenting different complications have a significantly higher MPV than those without complications [4, 5]. Since, we have hypothesised that platelets hyperactivity could be the cause of fetal loss