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Platelet aggregation may contribute to the pathogenesis of systemic sclerosis: following activation, platelets release significant amounts of serotonin – which promotes vasoconstriction and fibrosis, and further enhances aggregation. The C+1354T polymorphism in the exonic region of the serotonin 2A receptor gene determining the His452Tyr substitution was associated with blunted intracellular responses after serotonin stimulation, and may have a role in susceptibility to scleroderma.    Methods  One hundred and fifteen consecutive systemic sclerosis patients and 140 well-matched healthy control individuals were genotyped by sequence-specific primer-PCR for the His 452 Tyr substitution of the serotonin 2A receptor gene, and associations were sought with scleroderma and its main clinical features. The functional relevance of the His 452 Tyr substitution was also assessed by evaluating the aggregation of platelet-rich plasma from His 452 /His 452  and His 452 /Tyr 452  healthy individuals after stimulation with adenosine diphosphate ± serotonin.    Results  The T allele of the C+1354T polymorphism was underrepresented in scleroderma patients compared with control individuals (5.2% versus 12.4%,  P  < 0.001, chi-square test and 1,000-fold permutation test) and its carriage reduced the risk for systemic sclerosis (odds ratio = 0.39, 95% confidence interval = 0.19 to 0.85,  P  < 0.01). Platelets from His 452 /Tyr 452  healthy subjects more weakly responded to serotonin stimulation compared with platelets from His 452 /His 452  individuals (3.2 ± 2.6-fold versus 9.6 ± 8.6-fold increase in aggregation,  P  = 0.017 by Kolmogorov–Smirnov test and  P  = 0.003 after correction for baseline adenosine diphosphate-induced aggregation values).    Conclusion  The His 452 Tyr substitution may influence susceptibility to systemic sclerosis by altering platelet aggregation in response to serotonin.

A polymorphism in the human serotonin 5-HT2A receptor gene may protect against systemic sclerosis by reducing platelet aggregation