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Frequency of hereditary thrombophilia, anticoagulant activity, and homocysteine levels in patients with hemolysis, elevated liver functions and low thrombocyte count (HELLP) syndrome
Author(s) -
Dogan Ovgu Ozkan,
Simsek Yavuz,
Celen Sevki,
Danisman Nuri
Publication year - 2011
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/j.1447-0756.2010.01397.x
Subject(s) - hellp syndrome , medicine , antithrombin , homocysteine , thrombophilia , methylenetetrahydrofolate reductase , gastroenterology , hemolysis , factor v leiden , gene mutation , protein c , endocrinology , preeclampsia , pregnancy , heparin , mutation , thrombosis , venous thrombosis , allele , gene , genetics , biology
Aim: The purpose of this study was to investigate the correlations between thrombophilic mutations, anticoagulant activity and hemolysis, elevated liver functions and low thrombocyte count (HELLP) syndrome. Material and Methods: Twenty‐five healthy pregnant women (control group) and 34 patients with HELLP syndrome (study group) were included in the study between April 2007 and January 2008. Homocysteine levels and activities of protein C, protein S and antithrombin III of the groups were compared. Frequency of factor V Leiden mutation, prothrombin 20210A mutation and C677 T mutation of methylenetetrahydrofolate reductase gene were also compared. Results: Frequencies of thrombophilic gene mutations of the two groups were not significantly different. Homocysteine levels were significantly higher in the study group. Protein C and protein S deficiencies of the two groups were similar. Antithrombin III deficiency was statistically higher in the patients with HELLP syndrome. Conclusion: The frequency of antithrombin III deficiency and homocysteine levels were higher in the patients with HELLP syndrome; however, there was no positive relationship between hereditary thrombophilic mutations and the disease. Larger prospective studies are needed to validate our findings.