J. Kramer et al., Frequencies of certain complement protein alleles and serum levels of anti-heat-shock protein antibodies in cerebrovascular diseases, STROKE, 31(11), 2000, pp. 2648-2652
Background and Purpose-A strong correlation exists between the intensity of
atherosclerotic alterations in different arteries. Marked differences exis
t, however, in the age and sex distribution and risk factors for coronary h
eart disease (CHD) and cerebrovascular disease (CVD). We therefore performe
d genetic and immunologic studies in patients with CVD.
Methods-We studied 292 patients with CVD (stroke or transient ischemic atta
ck) and as control either 198 healthy blood donors and 485 healthy elderly
(aged >60 years) people (genetic study) or 94 blood donors aged 45 to 60 ye
ars and 49 healthy elderly (aged >60 years) people (anti-heat-shock protein
[hsp] measurements). Allele frequencies of 3 genes (C4A, C4B, and C3) enco
ding proteins of the complement system were determined by electrophoresis a
nd immunofixation. Serum concentration of autoantibodies against 60-kDa hea
t-shock protein (anti-hsp60) was measured by the enzyme-linked immunosorben
t assay method.
Results-Marked differences were observed between CVD patients and controls
in the genetic studies. In the CVD patients aged >60 years, the frequency (
11.3%) of the deficient allele of the C4B gene (C4B*Q0) was significantly (
P=0.0003) higher than that of the healthy controls (5.4%). By contrast, in
the group aged 45 to 60 years, the frequency of the C4B*Q0 allele was lower
in patients than in controls. Serum concentration of anti-hsp60 in the CVD
patients did not differ from control values.
Conclusions-In previous studies C4B*Q0 frequency was reported to be higher
in CHD patients aged 45 to 60 years than in aged-matched controls. Moreover
, high anti-hsp60 levels were found in CHD patients. These findings contras
t with our present report of lower frequency of C4B*Q0 in CVD patients. The
refore, genetic and immunologic factors may at least partly explain the dif
ferences between the natural history and risk factors of CHD and CVD.