title: Elevated complement C3 is associated with early restenosis after eversion carotid endarterectomy.
abstract: Early restenosis following carotid endarterectomy (CEA) is an inflammatory process leading to myointimal hyperplasia of smooth muscle cells. The risk for restenosis is increased in homozygous carriers of the normal (A) allele of mannose-binding lectin (MBL2) gene. Our objective was to study the associations of C3 and as control three non-complement acute-phase reactants (APRs) (C-reactive protein, haptoglobin and alpha2HSglycoprotein) with early restenosis following CEA. We also considered, whether MBL2 genotype relates to C3 levels and to the risk of restenosis. Concentrations of the APRs were determined by radial immunodiffusion or immunoturbidimetric methods in 64 patients who underwent eversion CEA and were followed up with carotid duplex scan (CDS) examinations for at least one year. MBL2 genotypes were determined by a PCR-SSP method. C3 levels increased during the follow-up and correlated with the percentage of restenosis detected by CDS at 14 months postsurgery, in MBL2 A/A allele carriers. Patients with high C3 levels had nearly five-fold higher odds for the presence of significant restenosis (>50% reduction in diameter) even after adjusting for MBL2 genotype, age and gender. By contrast, no such associations were detected between the non-complement APRs and early restenosis. C3 is associated with and might have a direct role in the development of an early restenosis following CEA, which is partially related to an intact MBL lectin pathway, thus determining C3 levels might have clinical importance. On the other hand, our results indicate that the regulation of C3 differs from non-complement APRs.
authors.affiliation: 3rd Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
authors.forename: Gábor
authors.initials: G
authors.lastname: Széplaki
authors.forename: Lilian
authors.initials: L
authors.lastname: Varga
authors.forename: Judit
authors.initials: J
authors.lastname: Laki
authors.forename: Edit
authors.initials: E
authors.lastname: Dósa
authors.forename: Hans O
authors.initials: HO
authors.lastname: Madsen
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Prohászka
authors.forename: Attila
authors.initials: A
authors.lastname: Szabó
authors.forename: György
authors.initials: G
authors.lastname: Acsády
authors.forename: László
authors.initials: L
authors.lastname: Selmeci
authors.forename: Peter
authors.initials: P
authors.lastname: Garred
authors.forename: George
authors.initials: G
authors.lastname: Füst
authors.forename: László
authors.initials: L
authors.lastname: Entz
mesh_terms: D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016893:Carotid Stenosis / Q000097:blood* / Q000235:genetics / Q000517:prevention & control / Q000601:surgery; D003176:Complement C3 / Q000378:metabolism*; D016894:Endarterectomy, Carotid / Q000379:methods; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006242:Haptoglobins / Q000378:metabolism; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics; D008875:Middle Aged; D011446:Prospective Studies; D012008:Recurrence; D013997:Time Factors; D016896:Treatment Outcome; D060749:alpha-2-HS-Glycoprotein
chemical_list: C556354:AHSG protein, human; D001798:Blood Proteins; D003176:Complement C3; C485359:HP protein, human; D006242:Haptoglobins; C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin; D060749:alpha-2-HS-Glycoprotein; D002097:C-Reactive Protein