Factor XIII Val34Leu mutation accelerates the development of fibrosis in patients with chronic hepatitis B and C.
Summary of "Factor XIII Val34Leu mutation accelerates the development of fibrosis in patients with chronic hepatitis B and C."
Aim:  There is considerable variation in liver fibrosis stage and progression to cirrhosis among patients with chronic hepatitis B (CHB) or C (CHC). Coagulation pathway activity due to genetic variations could influence the rate of fibrosis. We investigated thrombotic risk factors and their association with the extent and progression of fibrosis in CHB or CHC patients. Methods:  In total, 194 patients with CHB (n = 88) or CHC (n = 106) were included. Data on demographic and laboratory findings were collected. Liver biopsies were evaluated according to the Ishak classification system. Fibrosis progression rate (FPR), defined as ratio of fibrosis score to duration of infection, was determined for 131 patients. Prevalence of factor V Leiden, prothrombin G20210A, plasminogen activator inhibitor type-1 (PAI-1) 4G/5G and factor XIIIA Val34Leu mutations was evaluated. Results:  Heterozygosity for factor V Leiden, prothrombin G20210A, PAI-1 4G/5G and factor XIIIA Val34Leu mutations was present in 3.1%, 2.1%, 49% and 28% of the patients, respectively. Factor XIII Val34Leu mutation was a risk for enhanced FPR (odds ratio 4.7; P = 0.01). In patients with both factor XIII Val34Leu and PAI-1 4G/5G mutations the risk of an accelerated FPR was further increased (odds ratio 5.0; P = 0.02). Mutations of the other thrombotic genes were not significantly associated with fibrosis stage and FPR. Conclusion:  Our data show that factor XIII Val34Leu mutation alone or in combination with PAI-1 4G/5G mutation is a risk factor for an increased rate of liver fibrosis development in patients with CHB or CHC.
Affiliation
Department of Internal Medicine Department of Gastroenterology and Hepatology Department of Pathology Department of Experimental Immunology Clinical Research Unit Department of Vascular Medicine Department of Experimental Vascular Medicine, Academic Medic
Journal Details
This article was published in the following journal.
Name: Hepatology research : the official journal of the Japan Society of Hepatology
ISSN: 1386-6346
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22385348
- DOI: http://dx.doi.org/10.1111/j.1872-034X.2011.00963.x
Medical and Biotech [MESH] Definitions
Factor Xiii Deficiency
A deficiency of blood coagulation FACTOR XIII or fibrin stabilizing factor (FSF) that prevents blood clot formation and results in a clinical hemorrhagic diathesis.
Factor V
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
Factor Xiiia
Activated form of FACTOR XIII, a transglutaminase, which stabilizes the formation of the fibrin polymer (clot) culminating the blood coagulation cascade.
Factor Xiii
A fibrin-stabilizing plasma enzyme (TRANSGLUTAMINASES) that is activated by THROMBIN and CALCIUM to form FACTOR XIIIA. It is important for stabilizing the formation of the fibrin polymer (clot) which culminates the coagulation cascade.
Peritoneal Fibrosis
Disorder characterized by a wide range of structural changes in PERITONEUM, resulting from fibrogenic or inflammatory processes. Peritoneal fibrosis is a common complication in patients receiving PERITONEAL DIALYSIS and contributes to its gradual decrease in efficiency.
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