OBJECTIVE: It has been hypothesised, mainly on the basis of indirect evidence, that low serum concentrations of androgen-anabolic hormones would play a causal part in the aetiology of rheumatoid arthritis (RA). METHODS: A case-control study was nested with a Finnish cohort of 19,072 adults who had neither arthritis nor a history of it at the baseline examination during 1973-1977. Pre-illness serum specimens for the assay of testosterone and dehydroepiandrosterone sulphate (DHEAS) were available from 116 cases who had developed RA by late 1989. Three controls per each incident case were individually matched for sex, age, and municipality. RESULTS: The mean testosterone concentration was 1.4 nmol/l in those 84 women who developed RA and 1.4 nmol/l in their controls; the corresponding figures for DHEAS were 5.2 mumol/l and 5.5 mumol/l, respectively. Mean testosterone concentration in the 32 male cases was 26.1 nmol/l and 26.4 nmol/l in their controls; the corresponding figures for DHEAS were 11.2 mumol/l and 10.1 mumol/l, respectively. Analysis by subgroups (rheumatoid factor positive and negative disease, pre-menopausal and postmenopausal women) and by hormone distributions showed no differences. CONCLUSION: The findings are not in line with the contention that low concentrations of testosterone and DHEAS play a part in the aetiology of RA.
OBJECTIVE: It has been hypothesised, mainly on the basis of indirect evidence, that low serum concentrations of androgen-anabolic hormones would play a causal part in the aetiology of rheumatoid arthritis (RA). METHODS: A case-control study was nested with a Finnish cohort of 19,072 adults who had neither arthritis nor a history of it at the baseline examination during 1973-1977. Pre-illness serum specimens for the assay of testosterone and dehydroepiandrosterone sulphate (DHEAS) were available from 116 cases who had developed RA by late 1989. Three controls per each incident case were individually matched for sex, age, and municipality. RESULTS: The mean testosterone concentration was 1.4 nmol/l in those 84 women who developed RA and 1.4 nmol/l in their controls; the corresponding figures for DHEAS were 5.2 mumol/l and 5.5 mumol/l, respectively. Mean testosterone concentration in the 32 male cases was 26.1 nmol/l and 26.4 nmol/l in their controls; the corresponding figures for DHEAS were 11.2 mumol/l and 10.1 mumol/l, respectively. Analysis by subgroups (rheumatoid factor positive and negative disease, pre-menopausal and postmenopausal women) and by hormone distributions showed no differences. CONCLUSION: The findings are not in line with the contention that low concentrations of testosterone and DHEAS play a part in the aetiology of RA.
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