Early complement activation follows eversion carotid endarterectomy and correlates with the time of clamping of the carotid artery
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Early complement activation follows eversion carotid endarterectomy and correlates with the time of clamping of the carotid artery. / Széplaki, Gábor; Hirschberg, Kristóf; Gombos, Tímea; Varga, Lilian; Prohászka, Zoltán; Dósa, Edit; Acsády, György; Karádi, István; Garred, Peter; Entz, László; Füst, George.
I: Molecular Immunology, Bind 45, Nr. 11, 2008, s. 3289-3294.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - Early complement activation follows eversion carotid endarterectomy and correlates with the time of clamping of the carotid artery
AU - Széplaki, Gábor
AU - Hirschberg, Kristóf
AU - Gombos, Tímea
AU - Varga, Lilian
AU - Prohászka, Zoltán
AU - Dósa, Edit
AU - Acsády, György
AU - Karádi, István
AU - Garred, Peter
AU - Entz, László
AU - Füst, George
N1 - Keywords: Adult; Aged; Aged, 80 and over; C-Reactive Protein; Carotid Arteries; Complement Activation; Complement C3a; Constriction; Endarterectomy, Carotid; Female; Genotype; Humans; Male; Mannose-Binding Lectin; Middle Aged; Reperfusion Injury; Stents; Time Factors
PY - 2008
Y1 - 2008
N2 - BACKGROUND: Complement activation plays an important role in ischemia/reperfusion (I/R) injury. The objective of the present study was to detect the presence and mechanism of complement activation in patients who underwent carotid endarterectomy (CEA). METHODS: Complement activation products C1rsC1-inhibitor, C4d, C3a and SC5b-9 and concentrations of C-reactive protein (CRP) were measured in samples serially taken from 16 patients with eversion CEA and 10 with carotid artery stenting (CAS) in the first 24h post-surgery/intervention. MBL2 genotypes were also determined. RESULTS: In patients with CEA an intense increase in C3a levels were observed immediately after surgery (p<0.001), accompanied by a slight elevation in SC5b-9 levels (p<0.05). C3a levels remained elevated until 4h post-surgery, compared with the baseline values and with CAS patients. Peak C3a levels correlated with the time of carotid clamping (r=0.5921, p=0.02). No significant changes were detected in C1rsC1-inhibitor or C4d levels following CEA, and we found no association between the generation of C3a and MBL2 genotypes or CRP levels. Complement activation was not present in patients with CAS. CONCLUSIONS: Early complement activation follows CEA and correlates with the time of I/R injury. The lack of C4d generation suggests the role of the alternative and not the lectin pathway in the process Udgivelsesdato: 2008/6
AB - BACKGROUND: Complement activation plays an important role in ischemia/reperfusion (I/R) injury. The objective of the present study was to detect the presence and mechanism of complement activation in patients who underwent carotid endarterectomy (CEA). METHODS: Complement activation products C1rsC1-inhibitor, C4d, C3a and SC5b-9 and concentrations of C-reactive protein (CRP) were measured in samples serially taken from 16 patients with eversion CEA and 10 with carotid artery stenting (CAS) in the first 24h post-surgery/intervention. MBL2 genotypes were also determined. RESULTS: In patients with CEA an intense increase in C3a levels were observed immediately after surgery (p<0.001), accompanied by a slight elevation in SC5b-9 levels (p<0.05). C3a levels remained elevated until 4h post-surgery, compared with the baseline values and with CAS patients. Peak C3a levels correlated with the time of carotid clamping (r=0.5921, p=0.02). No significant changes were detected in C1rsC1-inhibitor or C4d levels following CEA, and we found no association between the generation of C3a and MBL2 genotypes or CRP levels. Complement activation was not present in patients with CAS. CONCLUSIONS: Early complement activation follows CEA and correlates with the time of I/R injury. The lack of C4d generation suggests the role of the alternative and not the lectin pathway in the process Udgivelsesdato: 2008/6
U2 - 10.1016/j.molimm.2008.02.011
DO - 10.1016/j.molimm.2008.02.011
M3 - Journal article
C2 - 18374983
VL - 45
SP - 3289
EP - 3294
JO - Molecular Immunology
JF - Molecular Immunology
SN - 0161-5890
IS - 11
ER -
ID: 10209332