Regular Article Haemostatic profile of healthy premature small for gestational age neonates George Mitsiakos a, ⁎, Evaggelia Giougi a , Ilias Chatziioannidis a , Paraskevi Karagianni a , Emmanouil Papadakis b , Christos Tsakalidis a , Georgia Papaioannou b , Pavlos Malindretos a , Nikolaos Nikolaidis a a 2nd NICU and Νeonatology Department of Aristotle University of Thessaloniki, G.P.N. Papageorgiou, Ring Road Nea Efkarpia, T.K. 56403 Thessaloniki, Greece b Hematology Department, G.P.N. Papageorgiou, Thessaloniki, Greece abstract article info Article history: Received 9 September 2009 Received in revised form 1 May 2010 Accepted 13 May 2010 Available online 9 June 2010 Keywords: SGA newborn prematurity coagulation fibrinolysis Background: The pathogenetic profile of premature Small for Gestational Age (SGA) neonates is strongly related to their haemostatic equilibrium, which is inadequately understood. Objective: To evaluate coagulation and fibrinolysis in premature SGA neonates before intervening with Vitamin K administration. Study design: We performed a comparison of coagulation, natural inhibitors and fibrinolysis between SGA and Appropriate for Gestational Age (AGA) infants born prematurely [gestational age (G.A.) b 37 weeks]. Study population consisted of 139 preterm newborns, 68 of whom were SGA (25 males and 43 females), while 71 were AGA (37 males and 34 females) that consisted the control group. Blood samples were obtained within 30 minutes following birth and before the administration of vitamin K. Investigation included: PT, INR, APTT, fibrinogen, coagulation factors II, V, VII, VIII, IX, X, XI, XII, vWillebrand factor, protein C and free protein S, antithrombin (AT), APCR, tPA and PAI-1. The independent t-test and the Mann-Whitney U test were used to compare the differences between the values of haemostatic parameters. Results: Premature SGA infants presented significantly lower levels of fibrinogen (p b 0.029) and higher levels of VIIIc factor, APCR, tPA and PAI-1 (p b 0.041, 0.017, 0.021 and 0.019 respectively). The two groups had similar demographic characteristics (except from birth weight), without significant differences in the values of other haemostatic parameters. Conclusions: Despite the statistically significant differentiation in the levels of fibrinogen, VIIIc factor, APCR, tPA and PAI-1, the rest of haemostatic parameters have similar values between SGA and AGA preterms. © 2010 Elsevier Ltd. All rights reserved. Introduction Small for gestational age (SGA) neonates account for a large proportion of the neonatal population and constitute the 30-50% of the extremely low birth weight (ELBW) infants. Premature SGA infants present higher morbidity and mortality rates compared to appropriate for gestational age (AGA) premature infants, possibly due to the unfavorable in utero environment [1–5]. As a result of high morbidity, requirement for catheterization of central vessels is increased, predisposing to thromboembolic complications that are usually secondary to the use of intra-arterial and intravenous catheters [6,7]. The pathogenetic profile of SGA neonates has been extensively studied; premature SGA present a higher risk for thromboembolic events [8–10] and necrotizing enterocolitis (NEC) compared to premature AGA infants; NEC is triggered by hypoxia that leads to ischemic thrombosis of the enteric capillary bed as a result of blood redistribution to the vital organs. Massive pulmonary hemor- rhage has been reported as the cause of sudden death in an SGA infant [8]. SGA neonates present an increased incidence for vascular cerebral stroke [11]. Moreover, premature infants are at high risk for hemorrhagic complications [7,12]. The incidence of complications is inversely proportional to gestational age and is clearly elevated in SGA in comparison to AGA infants [8]. Physiology of neonatal hemostasis is inadequately understood in comparison to the adult model. Ιn healthy preterm neonates the coagulation system is more immature at birth compared to full-terms and gradually evolves toward the mature adult system [13–18]. Besides the fact that pathophysiology of SGA premature infants is strongly related to their hemostatic status, there is insufficient literature data regarding hemostasis in this neonatal population; there is only one published report on hemostasis of full-term SGA infants [19]. Moreover, laboratories that work out on large amounts of neonatal samples should establish their own reference values, since results are strongly related to the specific analyzer device and the reagents that are being utilized; it is well known that there are many pitfalls and dilemmas in the evaluation of neonatal hemostasis [7,20,21]. Thrombosis Research 126 (2010) 103–106 ⁎ Corresponding author. Tel.: +30 2310693354; Fax: +30 2310693360. E-mail addresses: mga@otenet.gr, mitsiakg@med.auth.gr (G. Mitsiakos). 0049-3848/$ – see front matter © 2010 Elsevier Ltd. All rights reserved. doi:10.1016/j.thromres.2010.05.010 Contents lists available at ScienceDirect Thrombosis Research journal homepage: www.elsevier.com/locate/thromres