Vascular endothelial growth factor and also angiogenin, IP-10, MCP-1, MIP-1β, and Mig may be related to the pathogenesis of age-related macular degeneration. Intravitreal bevacizumab injection increases inflammatory cytokine levels, suggesting the induction of an inflammatory process.

Objective. To investigate whether the pathogene-sis of rheumatoid arthritis (RA) is associated with the functional chemokine receptor CCR5, which is the primary CC chemokine receptor expressed by T cells in rheumatoid synovium, and its nonfunctional receptor, 32CCR5, which is generated by the homozygous 32-basepair deletion (32) in the CCR5 gene. Methods. The frequency of the CCR5 genotype was compared among 673 patients with RA, 113 patients with systemic lupus erythematosus (SLE), and 815 control subjects. The CCR5 genotype was studied by polymerase chain reaction amplification of the region flanking the 32 deletion (32CCR5). Results. Frequencies of the wild-type CCR5 alleles (0.929, 0.907, and 0.942, respectively) and 32CCR5 alleles (0.071, 0.093, and 0.058, respectively) in controls, SLE patients, and RA patients did not differ significantly. However, none of the RA patients had the homozygous 32CCR5 genotype, compared with a frequency of 0.009 in controls (P 0.014 by Fisher's exact test; 2 4.12 with Yates' correction, P 0.042) and 0.027 in SLE patients (P 0.003 by Fisher's exact test; 2 11.63 with Yates' correction, P 0.0006). Conclusion. The results suggest that the CCR5 receptor plays an important role in RA and may be a suitable target for therapy.

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The prevalence of H63D mutation in patients with PH in our region does not differ from that of the general Basque population.

HLA-B27 is strongly associated to ankylosing spondylitis (AS). The objective of our study was to analyze HLA-B27 association, B27 subtype distribution and frequency of other HLA class I and DR antigens in a group of Basque AS patients. HLA class I antigens were typed serologically and HLA-B27 and A9 subtypes were determined by DNA typing in samples from 46 patients with AS, 54 B27-positive spondyloarthropathies, 82 healthy subjects and 20 B27-positive controls. A class I HLA 9.2 kb PvuII restriction fragment length polymorphism (RFLP), previously associated with AS, was analyzed in a representative group of patients and controls. We found that HLA-B*2705 conferred a relative risk of 126 for AS in this group. HLA-A9 (A*2402) allele was significantly increased in AS patients compared with healthy controls and B27-positive control group (Pcorr<0.0001) and also increased in patients affected with peripheral arthritis. No association between class I HLA 9.2 Kb RFLP and AS was found. These results suggest that HLA-A*9 allele itself or another linked gene could act as a secondary and independent susceptibility allele to AS.

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