Background Behcet's Disease (BD) has the hallmarks of complex genetic disorder. The most established genetic marker-HLA B51 does not account for more than 20% of the relative risk in siblings of affected individuals. Heat shock proteins (HSP) might stimulate both innate and adaptive immune mechanisms in BD. They might be linked to the chemoattraction of inflammatory cells. HSP gene polymorphisms could explain the clinical diversity of the BD.
Methods Case patients were 110 consecutive Turkish patients with BD, 100 healthy controls and 93 connective tissue disease patients rather then BD (rheumatoid arthritis, n: 29; primer systemic vasculiitis, n:18; ankylosing spondiliitis, n:15; systemic sclerosis, n:11; systemic lupus erythematosus, n:8; primary Raynoud's syndrome, n:7; Sjögren's syndrome, n:3; dermatomyositis, n:1; recurrent oral ulceration, n: 1) were involved in this study. All BD patients and controls were genotyped by polymerase chain reaction for HSP60 polymorphism at codon 136-1 and 2, 178, 244, and 336.
Results The frequency of GAT/GAA single nucleotide polymorphism in codon 136-2 was found in three BD patients with vascular clinical manifestation, but none of the any subject in control groups (p<0.001).
Conclusions Our findings show that GAT/GAA 136-2 polymorphism of HSP60 might be associated the severity of the BD mainly with vascular manifestations susceptibility. But this association is difficult to be accepted as SNP that causes the disease susceptibility or severity.
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Disclosure of Interest None declared
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