Maternal serum amyloid A levels in pregnancies complicated with preterm prelabour rupture of membranes
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(4) 3%&'4( )* 5 1 2 3 4 5. Dr Zekai Tahir Burak Women’s Health Education and Research Hospital, Division of Gynecology, Ankara, Turkey Muğla Sıtkı Koçman University, Department of Gynecology, Muğla, Turkey Bozok University, Department of Gynecology, Yozgat, Turkey Hacettepe University, Department of Biology, Department of Moleculer Biology, Ankara, Turkey Dr Zekai Tahir Burak Women’s Health Education and Research Hospital, Division of High Risk Preganancy, Ankara, Turkey. Abstract Objective: The aim of the study was to investigate a possible association between maternal serum amyloid A levels (SAA) and maternal and fetal parameters in pregnancies complicated with preterm prelabor rupture of membranes (PPROM). Material and methods: A total of 88 pregnant women (PPROM group, n=44 and control group, n=44) were included into this prospective case control study. Serum blood samples for SAA were obtained from both groups within 1h since the rupture of the membranes and before administration of any medicine. The samples were kept frozen at -70°C until the analysis. The recorded risk factors were: age, gravidity, parity, delivery mode, gender, fetal birth weight, APGAR scores, white blood cell count, microCRP, neutrophil/lymphocyte ratio (NLR), and maternal serum SAA levels. Results: Demographic characteristics showed no statistically significant differences between the groups (p>0.05). The mode of delivery mode was cesarean section: 41% and 43.2% in the study and the control group, respectively, and this difference was statistically significant between the groups (p<0.05). Fetal parameters also showed statistically significant differences (p<0.05). There was a statistically significant difference between the groups in terms of micro CRP, NLR and SAA. SAA levels were higher in the PPROM group (p<0.005). SAA levels at a cut-off 95.63 ng/ml. Conclusion: We are of the opinion that second trimester maternal serum SAA level may be a predictive marker for PPROM. However, further studies with more participants are required.. Keywords: preterm prelabour rupture of membranes / maternal / / serum amyloid A protein /. Corresponding author: Ali İrfan Güzel Dr Zekai Tahir Burak Women’s Health Education and Research Hospital, Division of Gynecology, Ankara, Turkey Tel: +90 532 293 71 31, Fax: +90 312 306 59 17 E mail: alijnk@hotmail.com. 516. © Polskie Towarzystwo Ginekologiczne. Otrzymano: 15.01.2014 Zaakceptowano do druku: 15.03.2014. Nr 7/2014.
(5) Ginekol Pol. 2014, 85, 516-520. P R A C E. O R Y G I N A L N E po ł o ż n i c t wo. Sezen Bozkurt Köseoğlu et al. Maternal serum amyloid A levels in pregnancies complicated with preterm prelabour rupture of membranes.. Streszczenie Cel pracy: Celem badania jest ocena związku pomiędzy matczynym poziomem amyloidu A (SAA) a parametrami matczynymi i płodowymi w ciąży powikłanej przedwczesnym pęknięciem błon płodowych (PPROM). Materiał i metoda: Do badania prospektywnego z grupą kontrolną włączono 88 kobiet ciężarnych (grupa z PPROM – 44 pacjentki, grupa kontrolna – 44 pacjentki). Próbki krwi do badania na SAA pobierano w ciągu godziny od pęknięcia błon płodowych i przed podaniem jakichkolwiek leków. Próbki były utrzymywane w temp.-70 C do czasu przeprowadzenia analizy. Analizowano następujące czynniki ryzyka: wiek, liczba ciąż, liczba porodów, sposób porodu, płeć płodu, masa urodzeniowa, APGAR, liczba leukocytów, wskaźnik neutrofili/limfocytów (NLR) i poziom matczynego amyloidu A w surowicy. Wyniki: Czynniki demograficzne nie różniły się istotnie pomiędzy badanymi grupami (p>0,05). Odsetek porodów przez cięcie cesarskie: 41% i 43,2% odpowiednio w grupie badanej i w grupie kontrolnej różnił się istotnie (p<0,05). Parametry płodowe różniły się istotnie statystycznie pomiędzy obiema grupami (p<0,05). Znaleziono istotną statystycznie różnicę pomiędzy grupami w odniesieniu do CRP, NLR i SAA. Poziom SAA był istotnie wyższy w grupie z PPROM (p<0,005). Poziom odcięcia dla SAA wynosił 95,63ng/ml. Wnioski: Wydaje się, że poziom matczynego SAA w surowicy może być markerem predykcyjnym dla PPROM. Konieczne są dalsze badania na większej grupie pacjentek.. Słowa kluczowe:
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(262) >1. 29(%65,9) 15(%34,1). 37(%84) 17(%16). 0,720. Age (years) *. *. *Smokers (%). 6(%13,6). 5(%11,3). 0,980. Income (TL/month). 1260±576. 1146±389. 0,103. 905.16±2652.79. 72,71±100.09. 0.041. MicroCRP. 15,88±15,9. 6,99±10,1. 0,003. NLR. 5,79±3,27. 4,27±1,65. 0,024. SAA. * Data was presented as % and p calculated by (c2) test, TL: Turkish lira, SAA: serum amyloid A. Table II. The clinical characteristics of the newborns. PPROM group (n=44). Control group (n=44). p. 1960.68±382.18. 3160.23±435.79. <0.001. 31,3±1,99. 38,8±1.47. 0,043. Delivery type Vaginal (%) C/S (%). 26(%59) 18(%41). 25(%56,8) 19(%43,2). 0,903. Gender Female(%) Male(%). 17(%38,6) 34(%61,4). 23(%52,2) 21(%47,8). 0,286. 4(%) 5(%) 6(%) 7(%). 1(%2,2) 2(% 2,2) 2(%4,5) 39(%88,6). 1(%2,2) 43(%97,7). 7(%) 8(%) 9(%). 3(%6,8) 1(%2,2) 40(%91). 1(%2,2) 43(%97,8). Birth weights (grams) Gestational age at delivery (weeks). Apgar 1. Apgar 5. 0,220. 0,369. Apgar 1: 1.minute APGAR score, Apgar 5: 5. minute APGAR score. Table III. Odds ratio calculated by binary logistic regression method. . Wald. Odds ratio. SE. MicroCRP. -,063. 9,145. ,939. ,021. NLR. -,363. 7,713. ,695. ,131. SAA. -,002. 1,055. ,998. ,002. Table IV. Pearson correlation analysis between microCRP, NLR and SAA levels. MicroCRP. Serum amyloid A. 518. NLR. R. p. r. P. -0.265. 0.017. -0.334. 0.023. © Polskie Towarzystwo Ginekologiczne. Nr 7/2014.
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(831) 9. 520. Acknowledgement :HWKDQNWR0UV,]DEHOOD0UXJDOVNDIRU(QJOLVKUHYLVLRQ Authors’ Contribution 1. Sezen Bozkurt Köseoğlu – concept, analysis and interpretation of data. 2. Ali Irfan Guzel – corresp;onding author, concept, assumptions, study design, revised article critically. 3. Ruya Deveer – revised article critically. 4. Aytekin Tokmak – acquisition of data, analysis and interpretation of data. 5. Yaprak Engin-Ustun – revised article critically. 6. Sibel Özdas – revised article critically and edited the laboratory studies. 7. Nuri Danışman – revised article critically. Authors’ statement ³ >RS] S] ^Y MO\^SPc ^RK^ ^RO Z_LVSMK^SYX aSVV XY^ `SYVK^O ^RO MYZc\SQR^] YP K ^RS\N. party, as understood according to the Act in the matter of copyright and related rights of 14 February 1994, Official Journal 2006, No. 90, Clause 63, with respect to the text, data, tables and illustrations (graphs, figures, photographs); ³ ^RO\O S] XY mMYX»SM^ YP SX^O\O]^]p aRSMR YMM_\] aROX ^RO K_^RY\ \OWKSX] SX. a financial or personal relationship which unjustly affects his/her actions associated with the publication of the manuscript; ³ KXc ZY]]SLVO \OVK^SYX]RSZ] YP ^RO K_^RY\] aS^R ^RO ZK\^cZK\^SO] SX^O\O]^ON. in the publication of the manuscript are revealed in the text of the article; ³ ^RO WKX_]M\SZ^ RK] XY^ LOOX Z_LVS]RON SX Y\ ]_LWS^^ON ^Y KXc Y^RO\ TY_\XKV. ³ =Y_\MO YP ºXKXMSXQ$ We have not conflict od interest.. References: 1. Goldenberg RL, Culhane JF, Iams JD, Romero R. Epidemiology and causes of preterm birth. Lancet. 2008, 371, 75–84. 2. Porreco RP, Heyborne KD, Shapiro H. Amniocentesis in the management of preterm premature rupture of the membranes: a retrospective cohort analysis. J Matern Fetal Neonatal Med. 2008, 21, 573–579. 3. Harger JH, Hsing AW, Tuomala RE, [et al.]. Risk factors for preterm premature rupture of fetal membranes: a multicenter case-control study. Am J Obstet Gynecol. 1990, 163, 130–137. 4. Melamed N, Ben-Haroush A, Pardo J, [et al.]. Expectant management of preterm premature rupture of membranes: is it all about gestational age? Am J Obstet Gynecol. 2011, 204, 48.e1– 8. 5. Ernest JM. Neonatal consequences of preterm PPROM. Clin Obstet Gynecol. 1998, 41, 827– 831. 6. French JI, McGregor JA. The pathobiology of premature rupture of membranes. Semin Perinatol. 1996, 20, 344-368. 7. Flídrová E, Krejsek J. Innate immunity in pathogenesis of intraamniotic inflammation in pregnancies complicated by preterm premature rupture of membranes Ceska Gynekol. 2011, 76, 46-50. 8. Uhlar CM, Whitehead AS. Serum amyloid A, the major vertebrate acute-phase reactant. Eur J Biochem. 1999, 265, 501-523. 9. Lannergård A, Larsson A, Kragsbjerg P, Friman G. Correlations between serum amyloid A protein and C-reactive protein in infectious diseases. Scand J Clin Lab Invest. 2003, 63, 267272. 10. Cekmez Y, Cekmez F, Ozkaya E, [et al.]. Proadrenomedullin and Serum Amyloid A as a Predictor of Subclinical Chorioamnionitis in Preterm Premature Rupture of Membranes. J Interferon Cytokine Res. 2013, 33 (11), 694-699. 11. Celik Y. Biostatistics, principles of research. Diyarbakir: Dicle University Press, 2007. 12. Mc Parland PC, Bell SC. The fetal membranes and mechanisms underlying their labour associated and pre-labour rupture during pregnancy. Fetal Matern Med Rev. 2004, 15, 73–108. 13. Murtha AP, Sinclair T, Hauser ER, [et al.]. Maternal serum cytokines in preterm premature rupture of membranes. Obstet Gynecol. 2007, 109, 121–127. 14. Popowski T, Goffinet F, Maillard F, [et al.]. Maternal markers for detecting early-onset neonatal infection and chorioamnionitis in cases of premature rupture of membranes at or after 34 weeks of gestation: a two-center prospective study. BMC Pregnancy Childbirth. 2011, 7, 11-26. 15. Gulati S, Agrawal S, Raghunandan C, [et al.]. Maternal serum interleukin-6 and its association with clinicopathological infectious morbidity inpreterm premature rupture of membranes: a prospective cohort study. J Matern Fetal Neonatal Med. 2012, 25, 1428-1432. 16. Kuyumcuoglu U, Kangal K, Guzel AI, Celik Y. Clinical significance of procalcitonin in cervicovaginal secretions of women with preterm rupture of membranes. Clin Exp Obstet Gynecol. 2010, 37, 319-321. 17. Terradas R, Grau S, Blanch J, [et al.]. Eosinophil count and neutrophil-lymphocyte count ratio as prognostic markers in patients with bacteremia: a retrospective cohort study. PLoS One. 2012, 7, e42860.. © Polskie Towarzystwo Ginekologiczne. Nr 7/2014.
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