Based on a possible involvement of serotonergic dysfunction in the pathophy
siology of fibromyalgia (FM) and on preliminary reports of a possible genet
ically driven vulnerability for this disorder we investigated the silent T1
02C polymorphism of the 5-HT2A-receptor gene in 168 FM patients and 115 hea
lthy controls. Our results showed a significantly different genotype distri
bution in FM patients with a decrease in T/T and an increase in both T/C an
d C/C genotypes as compared to the control population (Fisher's Exact test,
two-sided, P = 0.008). However, the increase in allele-C102 frequency felt
short of significance (P = 0.07). Correlation of genotypes to clinical par
ameters revealed no influences on age of onset, duration of disease or psyc
hopathological symptoms, measured with the Beck Depression Inventory and th
e symptom checklist SCL-90-R. In contrast to that the pain score, being a s
elf reported information on pain severity, was significantly higher in pati
ents of the T/T genotype (Mann-Whitney U test, P = 0.028). This suggests th
at the T102-allele might be involved in the complex circuits of nociception
. However, the T102C polymorphism is not directly involved in the aetiology
of FM but might be in linkage dysequilibrium with the true functional vari
ant, which has to be unravelled. (C) 1999 Academic Press.