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J Thromb Thrombolysis (2006) 22:51–54 DOI 10.1007/s11239-006-8322-2

The mean platelet volume in gestational diabetes
Nuray Bozkurt · Ercan Yılmaz · Aydan Biri · ¨ Zeki Taner · Ozdemir Himmeto˘ lu g

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Springer Science + Business Media, LLC 2006

Abstract Objective: To compare the platelet count and mean platelet volume (MPV) values of pregnancies diagnosed with gestational diabetes with those of healthy pregnancies. Material—method: Between June 2003 and September 2004, 100 healthy pregnancies and 100 pregnancies with gestational diabetes were studied at Gazi University, Department of Obstetrics and Gynecology. Results: While no statistically significant difference was observed in the platelet count between the two groups, the MPV of the gestational diabetes group (9.4 ± 1.6 fl) was evaluated to be significantly higher than the MPV of the healthy pregnancy group (8.3 ± 1.1 fl). Additionally, when linear regression analysis was performed an inverse relationship was observed between platelet number and MPV. Conclusion: There is a need for further research focusing on the platelet function in the observation and treatment of gestational diabetes, which can pose the risk of developing Type 2 diabetes for the mother and has negative consequences for the fetus. Keywords Mean platelet volume . Gestational diabetes

Introduction Gestational Diabetes Mellitus is defined as a carbonhydrate metabolism disorder arising during pregnancy and this
¨ N. Bozkurt . E. Yılmaz . A. Biri . Z. Taner . O. Himmeto˘ lu g Department of Gynecology and Obstetrics, Gazi University, Faculty of Medicine N. Bozkurt ( ) Tirebolu Sokak, 27/18, Yukariayranci, TR-06550, Ankara, Turkey e-mail: [email protected]

metabolism is negatively affected by the natural course of pregnancy [1]. The increased concentration of cortisone, prolactin, human placental lactogen and leptin in the circulation play an important role in the development of insulin resistance [1]. The increased insulin resistance prevents the use of glucose in peripheral tissues and increases the serum glucose concentration. 3–5% of all pregnancies are negatively affected by gestational diabetes mellitus [2]. Considering gestational diabetes mellitus’ consequences of increased perinatal morbidity and mortality, in addition to a larger frequency of long-term complications in the mother and fetus, its accurate identification and treatment is of utmost importance [3]. Women diagnosed with GDM represent approximately 90% of all cases of diabetes complicating pregnancy. More than 50% of these women will develop type 2 diabetes mellitus in their future life [2]. Placental dysfunction is assumed to be partly accountable for high frequency of perinatal impediments in diabetic women. When compared to normal pregnancy, perfused diabetic placentea transfers more arachidonic acid to prostanoids. This results in a higher TxA2 and lower PGI2 concentration in the perfusates on both the fetal and maternal side of the circulation. Platelet generated TxA2 have powerful vasoconstrictive and platelet activating functions whereas endothelial cell generated PGI2 possesses vasodilating and anti-aggregating actions. Furthermore, the hypercoagulable conditions stimulated by GDM could be correlated to the variations in TxA2 and/or PGI2 production in this disease [4]. Diabetes is a systemic disorder which affects the normal physiological function of all systems, one of which is the hematopoietic system. The micro and macro vascular pathological platelets produced in the systemic circulation of diabetic patients are the elements of the hematopoietic system causing major pathology. Platelets are the first line of defence upon loss of vascular integrity. Platelet membrane receptors’
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52 Table 1 The demographic and clinical properties of the study and control groups

J Thromb Thrombolysis (2006) 22:51–54

Gestational diabet (−) Birth weigth Age Birth week Platelet Mean platelet volume Wbc Rbc 3341 ± 418 28 ± 4 39 ± 1.3 217560 ± 53807 8.3 ± 1.1 9848 ± 2657 4.1 ± 0.5 (milyon)

Gestational diabet (+) 3535 ± 443 31 ± 5 38.5 ± 3.3 223240 ± 48584 9.4 ± 1.6 9840 ± 2715 4.1 ± 0.9 (milyon)

p 0.002 <0.001 NS NS <0.001 NS NS

interaction with injury related factors such as collagen, microfibrils and Von Willebrand factor stimulate linkage to not only other platelets but also to the vessel wall. Moreover, comprehensive agents such as thromboxane A2 and serotonin are amalgamated and extruded from the platelet [5]. Mean platelet volume showing the platelet size is an indicator of platelet function [6]. In comparison to small platelets, larger platelets or thrombocytes with a higher MPV value produce higher amounts of the prothrombotic factor Tromboxane A2 [7]. This study aimed to compare the platelet count and mean platelet volume (MPV) values of pregnancies having gestational diabetes with those of healthy pregnancies. It also aimed to examine the change in the number of platelets and MPV values of patients with gestational diabetes as compared to those of normal pregnancies.

Statistical analysis Data were analyzed with the SPSS software version 13.0 for Windows (SPSS Inc., Chicago, Illinois). Continuous variables were presented as mean ± SD and categorical variables as frequency and percentage. Differences in baseline characteristics between groups were assessed with t tests for continuous variables and χ 2 tests for binary variables. The relationship between two continuous variables, platelet size and mean platelet volume, was assessed by linear regression analysis. All tests were two-sided with a 0.05 significance level.

Results Table 1 illustrates the clinical characteristics and laboratory test scores of the 100 GDM and 100 normal pregnancies at Gazi University, Department of Obstetrics and Gynecology. The two groups showed no significant difference between the birth week and average platelet count. As expected, the average birth weight of gestational diabetic patients’ babies was higher than those of normal pregnancies (3341 ± 418 vs. 3535 ± 443, p = 0.002). Patient in the diabetic group were on average 3 years old (28 ± 4 vs 31 ± 5, p ≤ 0.001). The platelet volume of the gestational diabetes group was significantly higher than that of the healthy pregnancy group (9.4 ± 1.6 fl vs 8.3 ± 1.1 fl, p < 0.001) (Table 1). Additionally, when linear regression analysis was performed an inverse relationship was observed between platelet number and MPV. Patients with high MPV values had a lower platelet count (Fig. 1).

Materials ve methods The study was conducted at Gazi University, Department of Obstetrics and Gynecology, between June 2003 and September 2004, and the study group consisted of 100 consecutive pregnancies with gestational diabetes and 100 healthy pregnancies. The findings were accordingly compared for these two groups. The patients and controls diagnosed with anemia, hemo globinopathy, chronic inflammatory disease, pre-existing diabetes mellitus, other chronic disease and preeclampsia excluded from the study. When plasma glucose ≥140 mg/dl was measured following the 50 gram oral glucose loading test that was administered at 24–28 gestational weeks, a 100 gr3 h oral glucose tolerance test was applied. The patients who had high values from both tests were considered to have gestational diabetes. Gestational diabetic patients whose blood glucose could be controlled through a healthy diet and exercise (Class A1) were included in this study. A fasting peripheral venous blood sample was obtained from all participants in their last trimester (32–36 weeks). All blood samples were analyzed by an auto analyzer (CellDyn 4000, Abbott) for the measurement of platelet volume. In our clinic, the MPV reference range is determined as 7–11.0 fl.
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Discussion In this study where gestational diabetic pregnancies were compared to normal pregnancies, the patients with GDM were observed to have a higher median platelet volume. Platelet volume is a marker of platelet activation and function, and is measured using MPV. In previous studies, MPV was observed to be higher in non-pregnant diabetics when compared to the normal population [8–11, 12]. Furthermore,

J Thromb Thrombolysis (2006) 22:51–54 Fig. 1 Patients with high MPV values had a lower platelet count (Fig. 1). r = 0.253; P < 0.001
400000

53

300000

200000

PLT

100000 6 8 10 12 14

MPV

in impaired fasting glucose cases which are thought to be a pre-diabetic situation, high MPV was noted. In comparison to normal sized platelets, trombocytes with high MPV values are more reactive. Therefore, this situation may lead to an increase in production of TromboxanA2, which are specific to trombocytes and basically causes vasoconstriction and vein occlusion, a decrease in prostacylin concentration, and thus, results in vasoconstriction at vascular vein level [13–15]. It is argued that an increase in MPV sets the stage for micro and macro vascular complications in diabetic patients [11]. Increased MPV values are also reported in various cardiovascular diseases [6]. MPV values can be an effective marker reflecting blood glucose level [9]. In a study group of 22 patients with DM, MPV values were higher, but with the decrease in blood glucose, there was a significant decrease in MPV values [9]. It is suggested that insulin potentates murine megakaryocytopoiesis in vitro, in a study; therefore, due to the increased insulin in insulin resistant cases big platelets may be observed [16]. In another study, it is claimed that increased aggregation and multiplication functions occur in diabetic patients’ megakaryocyte stem-cells. It is also observed that Glycoprotein IB molecule, a marker of megakaryocyte stem-cell, is found more in platelets’ cell membrane with high MPV values in diabetic patients [10]. Our study also indicates that as the number of platelets decrease, the MPV values increase when the correlation between the number of platelets and mean platelet volume is examined. In a study, Type 2 diabetics had high MPV values while the numbers of platelets were fewer [8]. It is argued that the number of peripheral platelets may depend on variables such as platelet production rate and mean platelet survival. Some studies report that platelet survival in diabetic patients may be shorter [17]. In another study in which gestational hypertension and gestational diabetics’

platelet counts and MPV values in the last trimester were compared to healthy pregnancies, it was identified that the platelet count of women with gestational hypertension was lower than the control group whereas their MPV values were higher. Moreover, gestational diabetic women were found to have a lower platelet count on the average and a higher MPV. Nevertheless, this finding was not statistically significant [18]. So far, this is the only study which measures the MPV value of patients with gestational diabetes. However, only 21 subjects were included in this study. We were not able to track any articles printed in English on this topic. Diabetes as well as the metabolic syndrome, including insulin resistance, which lie beneath it are hyper-coagulable conditions. Increased platelet reactivity, enlarged activity of the coagulation system, and impaired fibrinolysis are typical and much is understood about them [19]. A study conducted on the placentas of diabetic patients show an increased incidence of vascular pathological changes. These lesions are embodied in obliterative endarteritis, fibromuscular sclerosis and mural thrombosis which affect the fetoplacental circulation. The changed balance between prostacyclin and thromboxane observed in these vessels might serve as an explanation for the vascular modifications mentioned [20]. As known, one of the most significant risk factors in gestational diabetic cases is intrauterine fetal loss. As with other maternal thrombophilia cases, the hypercoagubilite in diabetic patients could result in fetal loss. This risk factor arises due to the production of microthrombosis on placental bed vessels and placental infarctions. Consequently, this generates a conciliation in the fetomaternal circulatory system, that results in low placental perfusion and finally in the loss of the fetus [21]. All in all, gestational diabetes mellitus is a systemic and metabolic disorder which occurs at pregnancy and ends

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J Thromb Thrombolysis (2006) 22:51–54 7. Martin JF, Trowbridge EA, Salmon G, Plumb J (1983) The biological significance of platelet volume: its relationship to bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration. Thrombosis Research 1(32):443–460 ¨ 8. Hekimsoy Z, Payzin B, Ornek T, Kando˘ an G (2004) Mean platelet g volume in type 2 diabetic patients. J Diabet Complications 18:173– 176 9. Saigo K, Yasunaga M, Ryo R (1992) Mean platelet volume in diabetics. Rinsha Byar 40(2):215–217 (Abstract) 10. Tschope D, Langer E, Schauseil S, Rosen P, Kaufmann L, Gries FA (1989) Increased platelet volume sign of impaired thrombopoiesis in diabetes mellitus. Klin Wochenschr 67(4):253–259 11. Sharpe PC, Trinick T (1993) Mean platelet volume in diabetes mellitus. Q J Med 86(11):739–742 12. Coban E, Bostan F, Ozdogan M (2006) The mean platelet volume in subjects with impaired fasting glucose. Platelets 17(1):67–69 13. Greer IA, et al (1988) Increased platelet reactivity in pregnancy induced hypertension and uncomplicated diabetic pregnancy indication for antiplatelet therapy. BJOG. 95:1204–1206 14. Dadak C, Kefalides A, Sinzinger H, Weber G (1982) Reduced umbilical artery prostacyclin formation in complicated pregnancies. Am J Obstet Gynecol 144:792–795 15. Ylikorkola O, Maluka UM (1985) Prostacyclin and thromboxane in gynecology and obstetrics. Am J Obstet Gynecol 152:318–329 16. Watanabe Y, Kawada M, Kobayashi B (1987) Effect of insulin on murine megakaryocytopoiesis in a liquid culture system. Cell Struct Funct 12(3):311–316 17. Jones RL, Paradise C, Peterson CM (1981) Platelet survival in patients with diabetes mellitus. Diabetes 30(6):486–489 18. Yin SM, Li YQ, Xie SF, Ma LP, Wu YD, Nie DN, Feng JH, Xu LZ (2005) Study on the variation of platelet function in pregnancy induced hypertension and gestational diabetes mellitus. Zhongua Fu Chan Ke Za Zhi 40(1):25–28 (Abstract) 19. Sobel BE, Schneider DJ (2004) Platelet function, coagulopathy, and impaired fibrinolysis in diabetes Cardiol Clin 22(4):511–526 20. Saldeen P, Olofsson P, Laurini RN (2002) Structural, functional and circulatory placental changes associated with impaired glucose metabolism. Eur J Obstet Gynecol Reprod Biol 105(2):136–142 21. Alonso A, Soto I, Urgelles MF, Corte JR, Rodriguez MJ, Pinto CR (2002) Acquired and inherited thrombophilia in women with unexplained fetal losses. Am J Obstet Gynecol 187(5):1337– 1342

postpartum, but has a high possibility of developing into Type 2 diabetes. Patients diagnosed with gestational diabetes need to be closely observed in their antenatal check ups. Close observation is a must in order to prevent complications of diabetic illnesses characterized with hyperglycemia negatively influencing all maternal systems and fetal homeostasis. Further research may indicate higher MPV values in gestational diabetic patients whose diabetes cannot be regulated with a healthy diet, but with insulin (Class A2), who had preconceptional overt diabetes before falling pregnant and whose diabetes is difficulty regulated with insulin treatment. As studies related to platelet functions in gestational diabetes increase, we strongly believe that there will be improvements in prenatal and postnatal observation and treatment, and thus a decrease in the complications for both the fetus and the mother.

References
1. Hyer SL, Shehata HA (2005) Gestational diabetes mellitus. Current Obstet Gynecol 15:368–374 2. Gabbe SG, Graves CR (2003) Management of diabetes mellitus complicating pregnancy. Obstet Gynecol 102(4):857–868 3. Jimenez-Moleon JJ, Bueno-Cavanillas A, Luna-Del-Castillo JD, Garcia-Martin M, Lardelli-Claret P, Galvez-Vargas R (2002) Prevalence of gestational diabetes mellitus: Variations related to screening strategy used. Eur J Endocrinol 146(6):831–837 4. Hishinuma T, Tsukamoto H, Suzuki K, Mizugaki M (2001) Relationship between thromboxane/prostacyclin ratio and diabetic vascular complications. Prostaglandins Leukot Essent Fatty Acids 65(4):191–196 5. Mazzanfi L, Mutus B (1997) Diabetes-induced alterations in platelet metabolism. Clinical Biochemistry 30(7):509–515 6. Cay S, Bıyıkoglu F, Cihan G, Korkmaz S (2005) Mean platelet volume in the patients with cardiac syndrome X. Journal of Thrombosis and Thrombolysis 20:175–178

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