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. 2005 Oct 7;11(37):5834-9.
doi: 10.3748/wjg.v11.i37.5834.

Association between thrombotic risk factors and extent of fibrosis in patients with non-alcoholic fatty liver diseases

Affiliations

Association between thrombotic risk factors and extent of fibrosis in patients with non-alcoholic fatty liver diseases

N Assy et al. World J Gastroenterol. .

Abstract

Aim: To evaluate the prevalence of genetic and acquired prothrombotic risk factors and their association with the extent of fibrosis and fatty infiltration in patients with non-alcoholic fatty liver disease (NAFLD).

Methods: Forty-four patients with chronic hepatitis (28 men and 16 women, with mean age of 45+/-11 and 49+/-12 years, respectively) constituted the patient population of this study. The groups were divided as follows: 15 patients with fatty liver (FL); 15 with non-alcoholic steatohepatitis (NASH); 14 with chronic viral hepatitis (CH) diagnosed by histology and liver technetium scan or ultrasound; and 10 healthy individuals. Thrombophilic, coagulation factors and genetic mutations were diagnosed by standard hemostatic and molecular coagulation assays.

Results: Activated protein C (APC) resistance and protein S were the most prevalent thrombotic risk factors (6% and 10% in NAFLD vs 21% and 14% in CH; P<0.01 and P<0.05, respectively). One thrombotic risk factor was identified in 41% of patients (23% mild fibrosis, 18% severe fibrosis) and two thrombotic risk factors in 6% of patients with NAFLD and severe fibrosis. While no differences in APC ratio, lupus anticoagulant, fibrinogen, factor V Leiden, prothrombin, and MTHFR mutation were found. Protein S levels were significantly lower in NASH patients than in patients with FL alone (92+/-19 vs 106+/-2, P<0.01). Protein C levels were markedly higher in patients with NAFLD and mild or severe fibrosis as compared to the patients with CH, respectively (128+/-40 vs 96+/-14, P<0.001 or 129+/-36 vs 88+/-13, P<0.01).

Conclusion: Up to 46% of patients with NAFLD may have thrombotic risk factors, and the presence of thrombotic risk factors is correlated with the extent of hepatic fibrosis, suggesting a crucial role of the coagulation system in the pathogenesis of hepatic fibrosis.

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Figures

Figure 1
Figure 1
A: Protein C levels (normal 70-130%) in all study population (- median levels). B: Correlation between fat extension and protein C levels (r = 0.6, P < 0.001).
Figure 2
Figure 2
Correlation between fibrotic score and protein S levels in patients with NAFLD (r = 0.45, P < 0.01).

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