Factor XIII V34L polymorphism modulates the risk of chronic venous leg ulcer progression and extension

Autor:	Maria Luisa Serino, Paolo Zamboni, Monica De Mattei, Alberto Liboni, Massimiliano De Palma, Marcello Izzo, L. Fogato, Sergio Carandina, Silvia Tognazzo, Angelo Caruso, Donato Gemmati, Gian L. Scapoli, Alessia Ongaro
Rok vydání:	2004
Předmět:	Genetic Markers Male medicine.medical_specialty Pathology Genotype Dermatology Gastroenterology Venous leg ulcer Risk Assessment Severity of Illness Index NO Varicose Ulcer Pathogenesis Reference Values Internal medicine medicine Odds Ratio Humans Allele Allele frequency Aged Probability Wound Healing Chi-Square Distribution Polymorphism Genetic Factor XIII business.industry Factor V Middle Aged medicine.disease Prognosis Thrombosis Pathophysiology Case-Control Studies Chronic Disease Disease Progression Surgery Female business medicine.drug
Zdroj:	Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. 12(5)
ISSN:	1067-1927
Popis:	Low Factor XIII (FXIII) activity has been reported in the blood of patients with chronic venous leg ulcer (CVU). In vivo studies have described increased wound healing in CVU patients treated with FXIII concentrate, and in vitro studies have shown increased regenerative capacity in FXIII-treated fibroblasts. In addition, a common G-to-T polymorphism in the FXIIIA-subunit gene (V34L) significantly increases the activity and modifies the cross-linking properties of the FXIII molecule and this variant has been investigated as a protective factor against thrombosis, a recognized risk factor for CVU establishment. Therefore, the role of FXIII levels, FXIII V34L, FVR506Q, and FIIG20210A, common gene polymorphisms in the pathogenesis of CVU was investigated. Ninety-one patients with CVU and 195 healthy controls (91 of them sex- and age-matched) were PCR-genotyped for the FXIIIV34L, FVR506Q, and FIIG20210A substitutions and FXIIIA-subunit levels were determined by immuno-electrophoresis. The extent of the venous ulcer surface in patients was measured by computer software. The allele frequency and the genotype distribution of the FXIII polymorphism did not show significant differences between the whole group of cases and controls as well as prothrombin variants did. On the contrary, the FVR506Q variant (FV Leiden) allele was more frequent in patients, yielding a significant OR value of 5.93 (95 percent CI, 1.83-19.17; p= 0.003). Considering only CVU cases secondary to a post-thrombotic syndrome (n= 24), FV Leiden yielded a greater OR value of 16.08 (95 percent CI, 4.33-59.6; p < 0.0001). When the CVU cases were stratified by the three possible FXIII genotypes, a significant trend toward a lower mean value of the ulcerated area was clearly evident as the number of the polymorphic alleles (L34) increased in the genotype of patients (VV = 11.9 cm(2,)+/- 23.6; VL = 6.1 cm(2,)+/- 6.9; LL = 4.1 cm(2,)+/- 2.8; p= 0.01). On the other hand, FXIIIA antigen levels were similar between CVU cases and matched controls, but 11 percent of cases had FXIII deficiency (FXIIIA
Databáze:	OpenAIRE
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