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Rheumatology Advance Access published online on August 19, 2008
Rheumatology, doi:10.1093/rheumatology/ken303
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Influence of inherited and acquired thrombophilic defects on the clinical manifestations of mixed cryoglobulinaemia

M. Casato1, M. Carlesimo1, A. Francia2, C. Timarco3, A. Antenucci3, M. Bove1, H. Martini1, M. Visentini1, M. Fiorilli1 and L. Conti3

1Department of Clinical Immunology 2Department of Neurological Sciences, Sapienza University of Rome and 3Department of Clinical Pathology, Hemostasis and Thrombosis Section, Istitute Regina Elena-IFO, Rome, Italy.

Correspondence to: M. Fiorilli, Department of Clinical Immunology, Sapienza University of Rome, Viale dell’Università 37, Rome 00185, Italy. E-mail: massimo.fiorilli{at}uniroma1.it


  Abstract

Objective. To investigate the contribution of inherited and acquired thrombophilic defects to the clinical manifestations of mixed cryoglobulinaemia vasculitis.

Methods. The following thrombophilic defects were investigated in 64 consecutive patients with HCV-associated mixed cryoglobulinaemia: aPLs, lupus anti-coagulant, homocysteinaemia, protein C and protein S concentrations, activated protein C resistance, plasminogen activator inhibitor-1 4G4G and 5G5G genotypes, and the presence of mutations of factor V (Leiden and H1299R), of prothrombin (G20210A) and of methyl tetrahydrofolate reductase (C677T and A1298C). Additional variables were demographic data, duration of the disease, cryocrit level and vascular risk factors (diabetes, hypertension, hypercholesterolaemia and smoking habit). The following clinical manifestations of mixed cryoglobulinaemia were analysed as dependent covariates: severity of purpura, presence of necrotic skin ulcers, presence of peripheral neuropathy and presence of kidney disease.

Results. Logistic regression analysis identified hyperhomocysteinaemia as a risk factor for severe purpura (P < 0.0001) and for the presence of skin ulcers (P < 0.0001), whereas none of the other thrombophilic defects influenced the clinical presentation of mixed cryoglobulinaemia. Purpura improved in two patients after lowering homocysteine with vitamin supplementation.

Conclusions. Hyperhomocysteinaemia may be a risk factor for severe cutaneous manifestations in mixed cryoglobulinaemia.

KEY WORDS: Vasculitis, Mixed cryoglobulinaemia, Skin ulcer, Thrombophilia, Homocysteine

Submitted 16 April 2008; revised version accepted 2 July 2008.
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