title: Thrombophilic risk factors and peripheral arterial disease severity.
abstract: Few data are available on thrombophilic risk factors and progression of atherosclerotic peripheral arterial disease (PAD). Thrombophilic alterations can be an aggravating factor when arterial stenoses are present. In a cross-sectional study, we evaluated the presence of the thrombophilic factors fibrinogen, homocysteine, factor (F)VIII, lupus anticoagulant (LAC), FII G20210A, and FV R506Q mutations in 181 patients with PAD at Fontaine's stage II (claudication), in 110 patients with critical limb ischaemia (CLI), and in 210 controls. Fibrinogen was higher in patients with CLI vs. those with claudication and controls (427.9 +/- 10.5 vs. 373.1 +/- 5.2 vs. 348.9 +/- 7.0 p=0.001, respectively). Homocysteine and FVIII were higher in patients with PAD than in controls, but were similar in patients with CLI and claudication. The prevalence of LAC increased in patients with CLI vs. those with claudication and controls (21.4% vs. 7.8% vs. 5.2% p<0.001, respectively). The prevalence of FII 20210A allele was higher in patients with CLI vs. those with claudication and controls. Using a logistic model, FII G20210A mutation (odds ratio [OR] 19.8, confidence interval [CI] 4.5-87.1, p=0.001), LAC (OR 2.7, CI1.1-6.5, p=0.032), and fibrinogen (OR 1.01, CI 1.00-1.01, p=0.001) were associated with CLI, whereas homocysteine, FVIII, and FV R506Q mutation were not. CLI risk increased according to the number of thrombophilic alterations. In conclusion, altered levels of some important thrombophilic risk factors are independently associated with PAD severity. These data suggest that the presence of two or more thrombophilic risk factors raise the likelihood of PAD being more severe, justifying the need for larger longitudinal studies.
authors.affiliation: U.O. di Angiologia e Malattie della Coagulazione Marino Golinelli, Azienda Ospedaliera di Bologna, Policlinico Sant'Orsola Malpighi, Pad. 2, Via Albertoni 15, Bologna, Italy. michelangelo.sartori@aosp.bo.it
authors.forename: Michelangelo
authors.initials: M
authors.lastname: Sartori
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Favaretto
authors.forename: Cristina
authors.initials: C
authors.lastname: Legnani
authors.forename: Michela
authors.initials: M
authors.lastname: Cini
authors.forename: Eleonora
authors.initials: E
authors.lastname: Conti
authors.forename: Alfio
authors.initials: A
authors.lastname: Amato
authors.forename: Gualtiero
authors.initials: G
authors.lastname: Palareti
mesh_terms: D000368:Aged; D003251:Constriction, Pathologic; D004252:DNA Mutational Analysis; D018450:Disease Progression; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000235:genetics / Q000378:metabolism*; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D007511:Ischemia; D016682:Lupus Coagulation Inhibitor / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008297:Male; D009154:Mutation / Q000235:genetics; D058729:Peripheral Arterial Disease / Q000097:blood / Q000235:genetics* / Q000503:physiopathology*; D011110:Polymorphism, Genetic; D011516:Prothrombin / Q000235:genetics*; D012307:Risk Factors; D019851:Thrombophilia
chemical_list: D016682:Lupus Coagulation Inhibitor; D006710:Homocysteine; D011516:Prothrombin; D005169:Factor VIII; D005340:Fibrinogen