Platelet Aggregation is not Enhanced in Patients with Prediabetes

Abstract

Prediabetes [impaired glucose tolerance (IGT) and/or impaired fasting glucose (IFG)] is a major risk factor for T2DM as well as for cardiovascular disease and mortality. In the present study, the platelet aggregation and fibrinogen levels were investigated in prediabetic subjects who had no confounding factors such as hypertension, obesity or dyslipidemia. Thirty-nine subjects with prediabetes (24 IFG and 15 IGT) and age, sex and BMI matched 36 healthy controls were enrolled. Platelet aggregation, fibrinogen and hsCRP levels, HOMA-IR and HOMA-β indexes were determined. Platelet aggregation induced by collagen, epinephrine or ADP was not different (p=0.93, p=0.90 and p=0.29, respectively) between two groups, whereas fibrinogen levels were significantly higher (p=0.006) in the prediabetics when compared to controls. hsCRP levels, HOMA-IR and HOMA-β indexes in the two groups were not different. The power of the study was calculated according to the results and established as 0.97 for collagen, 0.95 for epinephrine and 0.83 for ADP. Despite the high plasma fibrinogen levels, the platelet aggregation in prediabetics was not different when compared to healthy controls. These data suggest that platelet aggregation may not be involved in the mechanism of prothrombotic state in prediabetic state.

Hubungan Lingkar Pinggang, Homeostasis Model Assessment of Insulin Resistance, dan Prostaglandin-I2 dengan Test Agregasi Trombosit pada Subyek Obesitas Sentral

“…Pada penelitian ini didapatkan korelasi positif sangat lemah yang tidak bermakna secara statistik antara HOMA-IR dan TAT dengan agregat ADP 1,0 µM (r=0,080 dan p=0,658). Hasil penelitian ini sejalan dengan penelitian Dogru et al 21 di Turki yaitu agregasi trombosit pada uji menggunakan ADP didapatkan tidak berbeda secara bermakna antara pasien dengan prediabetes dan pasien sehat (p=0,29). Hal ini dapat disebabkan karena tidak adanya resistensi insulin dan inflamasi subklinis atau faktor penyakit kardiovaskular lain.…”

“…Hal ini dapat disebabkan karena tidak adanya resistensi insulin dan inflamasi subklinis atau faktor penyakit kardiovaskular lain. 21 Selain itu korelasi negatif sangat lemah dan tidak bermakna secara statistik didapatkan antara PGI2 dengan TAT dengan agregat ADP 1,0 µM pada penelitian ini (r=-0,074; p=0,681). Menurut hasil penelitian yang dilakukan oleh Steer et al, didapatkan bahwa penambahan PGI2 pada plasma rich protein (PRP) tidak dapat mengubah agregasi trombosit.…”

“…Menurut hasil penelitian yang dilakukan oleh Steer et al, didapatkan bahwa penambahan PGI2 pada plasma rich protein (PRP) tidak dapat mengubah agregasi trombosit. 21 Hal yang agak berbeda dilaporkan oleh Russo et al 15 yaitu terdapat peningkatan bermakna dari kemampuan PGI2 dan NO untuk menginduksi sintesis nukleotida antiagregasi dengan penurunan berat badan >10%. Kemampuan NO berbanding lurus dengan kemampuan insulin untuk meningkatkan sintesis cGMP dan menghambat agregasi trombosit.…”

In vivo thromboxane‐dependent platelet activation is persistently enhanced in subjects with impaired glucose tolerance

“…Whether enhanced TXA 2 ‐dependent platelet activation occurs in the pre‐diabetic state is currently unknown. The evidence for abnormalities in platelet function in the setting of IGT is scarce and inconsistent, largely based on the measurement of indices of platelet activity/turnover, such as mean platelet volume or optical platelet aggregation . The latter suffers from large intra‐subject variability upon repeated measurements and has a poor prognostic value .…”