Difference of concentration of placental soluble fms-like tyrosine kinase-1(sFlt-1), placental growth factor (PlGF), and sFlt-1/PlGF ratio in severe preeclampsia and normal pregnancy

BMC Research Notes

Dwi Davidson Rihibiha²  A. Yogi Pramatirta¹  Prima Nanda Fauziah³  Anita Deborah Anwar¹  Mieke H. Satari⁴  Budi Handono¹  Johannes Mose¹  Jeffry Iman Gurnadi¹ 

[1] Department of Obstetrics and Gynecology, Faculty of Medicine, Padjadjaran University, Bandung, Indonesia;Department of Biotechnology, School of Life Sciences and Technology, Bandung Institute of Technology, Bandung, Indonesia;Department of Biology, School of Life Sciences and Technology, Bandung Institute of Technology, Bandung, Indonesia;Department of Microbiology, Faculty of Dentistry, Padjadjaran University, Bandung, Indonesia

关键词: sFlt-1;    PlGF;    Severe preeclampsia;    Normal pregnancy;   

Others  :  1229862
DOI  :  10.1186/s13104-015-1506-0

 received in 2014-10-21, accepted in 2015-09-21,  发布年份 2015

【 摘 要 】

Background

Placental soluble fms-like tyrosine kinase-1 (sFlt-1) which is an antagonist of vascular endothelial growth factor and placental growth factor (PIGF), is considered as one of etiology factors cause endothelial damage in preeclampsia due to increase of sFlt-1 level that change vascular endothelial integrity. This study aims to analyze the difference of sFlt-1 and PlGF concentration in severe preeclampsia and normal pregnancy, and the correlation between both in occurrence of severe preeclampsia.

Method

This is case control study involving 18 subjects with severe preeclampsia and 19 subjects with normal pregnancy as controls who met inclusion and exclusion criteria. Concentration of sFlt-1 and PlGF are measured with ELISA. Statistical analysis is performed with Chi square test, Fisher’s exact test, T test, Mann–Whitney test, and Spearman’s rank correlation test.

Results

This study results in no significant difference in characteristics of gestational age, and parity in both study groups. Median concentration of sFlt-1 in severe preeclampsia is higher (20,524.75 pg/mL) compared with normal pregnancy (6820.4 pg/mL). Concentration of PlGF is lower in severe preeclampsia (47 pg/mL) compared with normal pregnancy (337 pg/mL). sFlt-1 concentration is higher in severe preeclampsia compared to normal pregnancy. PlGF concentration is lower in severe preeclampsia compared to normal pregnancy. Ratio of sFlt-1 and PlGF concentration is significantly correlated in both severe preeclampsia and normal pregnancy.

Conclusions

There is a significant negative correlation between the concentration of sFLt-1 and PlGF in normal pregnancy.

【 授权许可】

   
2015 Gurnadi et al.

【 参考文献 】

• [1]Cunningham FG, Norman FG, Kenneth JL, Larry CG, John CH, Katharine DW: Williams obstetrics. 22nd edition. Williams and Wilkins, New York; 2005.
• [2]Lindheimer , Marshall D, Sandra J, Taler , Gary Cunningham F: Hypertension in Pregnancy. J Am Soc Hypertens. 2008, 2((6)):484-494.
• [3]Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rause DJ, Spancy CY: Wiliams obstetrics. 23rd edition. Mc Graw Hill, New York; 2010.
• [4]Effendi JS, Permadi W, Hidayat D, Tjahyadi D, Mulyakusumah A, Hermawan M, et al. Annual Report 2010. Bandung: Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University/Perjan Dr.Hasan Sadikin Hospital 2011.
• [5]Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University/Perjan Dr.Hasan Sadikin Hospital. Annual Report 2003. Bandung: Department Obstetric and Gynecology Faculty of Medicine, Padjadjaran University, Perjan Dr.Hasan Sadikin Hospital Bandung; 2004.
• [6]Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University Dr.Hasan Sadikin Hospital Annual Report 2004. Bandung: Departement of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University/Perjan Dr.Hasan Sadikin Hospital; 2005.
• [7]Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University Dr.Hasan Sadikin Hospital. Annual Report 2005. Bandung: Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University/Perjan Dr.Hasan Sadikin Hospital; 2006.
• [8]Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University Dr.Hasan Sadikin Hospital. Annual Report 2006. Bandung: Department of Obstetric and Gynecology Faculty of Medicine, Padjadjaran University/Perjan Dr.Hasan Sadikin Hospital; 2007.
• [9]Indonesia Survey of Demography and Health (SKDI). Number of Ibu Maternal Mortality. In: Ri D, editor. Jakarta; 2007. p. 1–6.
• [10]Roeshadi RH. Hypertension in Pregnancy. In: Hariadi R, editors Fetomaternal Medical Science. 1 edn. Surabaya: Fetomaternal Medical Community, Indonesia Obstetric and Gynecology Association; 2004. p. 494–99.
• [11]Robert J: Pregnancy-related hypertension. In Maternal fetal medicine principle and practice. Edited by Creasy R, Iams J. WB Saunders, Philadelphia; 2004:859-880.
• [12]Park M, Brewster UC: Management of preeclampsia. Hosp Phys. 2007, 43(11):25.
• [13]Yuan HT, Haig D, Krumanchi SA: Angiogenic factors in the pathogenesis of preeclampsia. Curr Top Dev Biol 2005, 71:297-312.
• [14]Ahmad S, Ahmed A: Elevated placental soluble vascular endothelial growth factor receptor-1 inhibits angiogenesis in preeclampsia. Circ Res 2004, 95(9):884-891.
• [15]Stepan H, Faber R, Dornhofer N, Huppertz B, Robitzki A, Walther T: New insight onto biology of preeclampsia. Biol Reprod 2006, 74(5):772-776.
• [16]Aggarwal PK, Chandel N, Jain V, Jha V: The relationship between circulating endothelin-1, soluble fms-like tyrosine kinase-1 and soluble endoglin in preeclampsia. J hum Hypertens 2012, 26(4):236-241.
• [17]Lam C, Lim KH, Karumanchi SA: Circulating angiogenic factors in the pathogenesis and prediction of preeclampsia. Hypertension 2005, 46:1077-1085.
• [18]Stepan H, Geide A, Faber R: Soluble fms-like tyrosine kinase 1. New Eng J Med. 2004, 351(21):2241-2242.
• [19]Levine RJ, Qian C, Maynard SE, Yu KF, Epstein FH, Karumanchi SA: Serum sFlt1 concentration during preeclampsia and mid trimester blood pressure in healthy nulliparous women. Am J Obstet Gynecol 2006, 194:1034-1041.
• [20]Purwosunu Y, Sekizawa A, Farina A, Wibowo N, Koide K, Okazaki S, et al.: Evaluation of physiological alterations of placenta through analysis of cell free messenger ribonucleic acid concentrations of angiogenic factor. Am J Obstet Gynecol 2008, 198(1):124el-124e7.
• [21]Thana NG, Romerob R, Hillermannd R, Cozzie V, Nief G, Huppertzg B: Prediction of Preeclampsia—A Workshop Report. Placenta. 2008, 29(Suppl A):83-85.
• [22]Mutter WP, Karumanchi SA: Molecular mechanisms of preeclampsia. Microvasc Res 2008, 75(1):1-8.
• [23]Grill S, Rusterholz C, Zanetti-Dällenbach R, Tercanli S, Holzgreve W, Hahn S, et al.: Potential markers of preeclampsia—a review. Reprod Biol Endocrinol. 2009, 7(70):10-1186.
• [24]Dechend RLF, Luft FC: Angiogenesis factors and preeclampsia. Nat Med 2008, 14(11):1187-1188.
• [25]Tsatsaris V, Goffin F, Munaut C, Brichant J, Pignon M, Noel A, et al.: Overexpression of the soluble vascular endothelial growth factor receptor in preeclamptic patients: pathophysiological consequences. J Clin Endocrinol Metab 2008, 88:5555-5563.
• [26]Chen Yu: Novel angiogenic factors for predicting preeclampsia: sFlt-1, PlGF, and soluble endoglin. Open Clin Chem J 2009, 2:1-6.
• [27]Yang Gu, Lewis David F, Wang Yuping: Placental productions and expressions of soluble endoglin, soluble fms-like tyrosine kinase receptor-1, and placental growth factor in normal and preeclamptic pregnancies. J Clin Endocrinol Metab 2008, 93:260-266.
• [28]Kopcow Hernan D, Karumanchi Ananth: Angiogenic factors and natural killer (NK) cells in the pathogenesis of preeclampsia. J Reprod Immunol 2007, 76(1–2):23-29.
• [29]Levine Richard J, Lam Chun, Cong Qian MS, Yu Kai F, Maynard Sharon E, Sachs Benjamin P, et al.: Soluble endoglin and other circulating antiangiogenic factors in preeclampsia. N Engl J Med 2006, 355:992-1005.
• [30]Creasy RK, Resnik R, Iams J: Maternal fetal medicine principles and practice. 6th edition. WB Saunders Co., Philadelphia; 2009.