By G. B. E. Jemec and J. H. Sindrup
Summary
The excretion of collagen metabolites and circulating androgens was measured in ten males suffering from progressive systemic sclerosis. Significantly higher levels of sex hormone-binding globuline, total testosterone and dihydrotestosterone (DHT) (P
<0.01), and total oestradiol (P
<0.05), were found in patients when compared with age-matched controls.
Urinary excretion of hydroxyproline in patients was found to correlate significantly with total testosterone (P=0.035), with DHT (P=0.005) and dehydroepiandrosteronsulphate (DHEAS) (P=0.034). Similarly the hydroxyproline peptide fraction was found to correlate significantly with total testosterone (P=0.037), with DHT (P=0.005) and with DHEAS (P=0.008).
Hydroxylysine peptide in the urine correlated significantly with free testosterone (P=0.035) and DHT (P=0.040). Oestrogens did not correlate with urinary excretion of collagen metabolites. These findings suggest that androgens may play a role in the pathogenesis of scleroderma in male patients.
By G. B. E. Jemec and J. H. Sindrup
Summary
The excretion of collagen metabolites and circulating androgens was measured in ten males suffering from progressive systemic sclerosis. Significantly higher levels of sex hormone-binding globuline, total testosterone and dihydrotestosterone (DHT) (P <0.01), and total oestradiol (P <0.05), were found in patients when compared with age-matched controls.
Urinary excretion of hydroxyproline in patients was found to correlate significantly with total testosterone (P=0.035), with DHT (P=0.005) and dehydroepiandrosteronsulphate (DHEAS) (P=0.034). Similarly the hydroxyproline peptide fraction was found to correlate significantly with total testosterone (P=0.037), with DHT (P=0.005) and with DHEAS (P=0.008).
Hydroxylysine peptide in the urine correlated significantly with free testosterone (P=0.035) and DHT (P=0.040). Oestrogens did not correlate with urinary excretion of collagen metabolites. These findings suggest that androgens may play a role in the pathogenesis of scleroderma in male patients.