This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Cimminiello, C. Articles by Bonfardeci, G. Search for Related Content PubMed PubMed Citation Articles by Cimminiello, C. Articles by Bonfardeci, G. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Raynaud's Disease Social Bookmarking                         What's this?

t-PA, PAI, and Protein C Before and After Vascular Occlusion of the Upper Limb in Patients with Raynaud's Phenomenon

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Massimo Milani

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Tiziano Uberti

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Guido Arpaia

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Adele Motta

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Giuseppe Bonfardeci

he Fourth Medical Department, Vascular and Thrombotic Pathology, S. Carlo Borromeo General Hospital, Milan, Italy

Tissue plasminogen activator (t-PA) and its inhibitor (PAI) were assessed in venous blood drawn before and after venous occlusion (bvo, avo) for 33 patients with Raynaud's phenomenon (RP), 14 with primary RP (PRP), 9 with suspected secondary RP (SSRP), and 10 with definite collagen disease and secondary RP (SRP). There were significant differences in PAI values avo between PRP (and controls), SSRP, and SRP. PAI activity decreased significantly avo only in controls and in PRP, and there was significant t-PA antigen elevation avo in the same groups. In addition, since PAI is neutralized by activated protein C (PC), both PC antigen and PC activity were assessed avo and bvo. PC Ag remained unchanged in all groups, with PC activity significantly lower than controls in SRP and SSRP. Finally the authors looked for interference of anticardiolipin antibod ies (ACA) and lupus-like anticoagulant (LAC) with the PC system in collagen disease-associated RP. Specific IgG ACA were found in only 1 patient with SRP. In conclusion, there is an endothelial derangement, involving t-PA release and PAI, in SSRP and SRP patients. The reduced PC activity in these latter groups appears to be due to increased PAI influence rather than to ACA/LAC.

Angiology, Vol. 42, No. 3, 231-238 (1991)
DOI: 10.1177/000331979104200308


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?