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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
Turio E., Avvenente A., Evangelisti L. *, Panicucci E. *, Giordani R. *, Sagripanti A. **, Barachini P.
Dipartimento di Patologia Sperimentale, Biotecnologie Mediche, Infettivologia ed Epidemiologia Sezione di Dermatologia e Venereologia
*Laboratorio di Analisi Chimico-Cliniche
**Dipartimento di Medicina Interna, Clinica Medica I
Background. Abnormalities of blood coagulation and fibrinolysis can play a role in the pathogenesis and development of venous ulcers of the lower limbs. To gain a deep insight into the haemostatic disorders contributing to these cutaneous lesions we have carried out an evaluation of laboratory parameters of coagulation and fibrinolysis.
Methods. We have measured in the plasma of 30 patients affected by leg venous ulcer (15 patients with post-phlebitic ulcer and 15 patients with non post-phlebitic ulcer) the following parameters: fibrinogen, prothrombin fragments (F1+2), thrombin-antithrombin complex (TAT), D-dimer, antithrombin, protein C, protein S, activated protein C resistance, plasminogen, a2 antiplasmin, tissue-type plasminogen activator (tPA) basal and after venous occlusion, plasminogen activator inhibitor type 1 (PAI-1) basal and after venous occlusion, lipoprotein (a). Fifteen healthy subjects, matched with the patients for age and sex, served as controls. All the patients have been followed up at our outpatient department and data about venous ulcer were evaluated.
Results. All patients presented abnormalities in one or more plasmatic parameters, namely: tapered tPA increase after venous occlusion, hyperfibrinogenemia, high lipoprotein (a), elevated D-dimer, high basal PAI-1, elevated F1+2 and TAT, increased resistance to activated protein C.
Conclusions. The results obtained show an accelerated fibrin in vivo formation and depressed fibrinolytic response in a considerable number of patients affected with venous ulcer, either post-phlebitic or non post-phlebitic. Increased fibrin deposition and decreased fibrin clot lysis may be due to reduced tPA vascular secretion and/or increased PAI-1 level. PAI-1 appears to have a prognostic value, as it is significantly more elevated in patients who do not heal