The Role of Fibrinolytic and Antifibrinolytic Activities in the Pathophysiology of HELLP Syndrome


GÜVEN S. , Sonmez M. , KARAHAN S. C.

HYPERTENSION IN PREGNANCY, vol.30, no.3, pp.275-286, 2011 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 30 Issue: 3
  • Publication Date: 2011
  • Doi Number: 10.3109/10641950902968718
  • Title of Journal : HYPERTENSION IN PREGNANCY
  • Page Numbers: pp.275-286

Abstract

Objective. To determine the role of the fibrinolytic and antifibrinolytic systems in HELLP syndrome. Methods. This study consisted of patients with HELLP Syndrome (study group, n = 17), women who were admitted for routine prenatal care (pregnant control group, n = 21) and those presenting for routine gynecologic examination (nonpregnant control group, n = 21). Plasma tissue-type plasminogen activator (tPA), thrombin-activatable fibrinolysis inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1), thrombin-antithrombin complex (TAT) and thrombomodulin (TM) were measured at admission for all groups. They were again measured after 7 days of biochemical improvement in HELLP Syndrome group. Results. The mean ages of women in the study, pregnant, and non-pregnant control groups were 29.82 +/- 4.98, 29.71 +/- 5.64, and 27.60 +/- 4.21, respectively. Demographically, the patients in all three groups were similar with regard to maternal age, race, and body mass index. Compared to the control groups, the mean tPA, PAI-1, TAFI, TAT, and TM levels were significantly increased in HELLP Syndrome. The mean plasma TAFI antigen concentration 7 days after delivery was significantly lower compared to the baseline (5.84 +/- 7.14 % change, p < 0.01). Significant decreases in the mean plasma concentrations were also found in tPA (21.78 +/- 20.93 ng/mL mean difference, p < 0.01), PAI-1 (14.22 +/- 10.38 ng/mL mean difference, p < 0.001), TAT (0.93 +/- 1.19 ng/mL mean difference, p < 0.01), and TM (0.54 +/- 0.94 ng/mL mean difference, p < 0.05). Conclusion. It is likely that the impaired fibrinolytic and antifibrinolytic systems, in response to thrombus formation, affect the pathophysiology of HELLP syndrome.