GH deficiency is associated with increased cardiovascular morbidity, which may be determined by alterations in vascular risk factors. We report the effect of partially treated hypopituitarism and subsequent GH replacement (mean dose, 0.2 IU/kg.week) on putative cardiovascular risk factors in 22 nondiabetic hypopituitary subjects in a 6-month, double blind, controlled study (active/placebo ratio, 11:11). All patients were subsequently treated with GH for a further 6 months. Total fat, percent body fat, and central fat were measured by dual energy x-ray absorptiometry. The hypopituitary patients had increased percent fat (P = 0.03) and central fat (P < 0.01) compared with body mass index-matched controls. Before GH treatment, fasting (total) and specific insulin positively correlated with body mass index (P = 0.02 and P < 0.001, respectively), waist/hip ratio (P = 0.05 and P = 0.01), and central fat (P = 0.03 and P = 0.003). Specific insulin and insulin sensitivity (IS), calculated by homeostatic model of assessment, were related to total fat (P < 0.001 and P = 0.02). GH treatment for 6 months led to a reduction in total fat (P < 0.02), percent fat (P = 0.002), central fat (P = 0.012), waist/hip ratio (P < 0.05), total cholesterol (P = 0.03), and apolipoprotein-B (P = 00001), as well as a decrease in the IS from 36.9% (range, 12-100%) to 25% (range, 2.5-55%; P = 0.0002). This was paralleled by a rise in fasting (total) and specific insulin (P = 0.016 and P = 0.002). The degree of correlation among indices of IS, body composition, and fat distribution increased after GH treatment. Fasting plasma glucose rose significantly, but was within the reference range. During 12 months of GH therapy, a significant increase in serum lipoprotein-(a) was observed (P < 0.05). Although GH has beneficial effects on central adiposity and lipid fractions, it is also associated with a decrease in IS; these effects may vary between individuals.

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A cross-sectional study of testosterone levels in 276 males was undertaken. Of these 87 were RA patients, 48 males with AS and 141 were healthy controls. Free and serum testosterone levels were significantly lower in the RA males than in either the AS group or the healthy controls (p less than 0.001). This difference was unaffected by age. No differences were seen in testosterone levels between DR1 or DR4 RA patients compared to those without these antigens. No evidence of hyperandrogenicity was seen in the AS group. The finding that males with RA have lower androgen levels than both normal controls and a disease group with inflammatory spondarthritis supports the hypothesis that male sex hormones may be a protective factor against the development of RA.

A 3-year placebo-controlled trial of sulphasalazine (SASP) in 89 patients with established AS (including radiological sacroiliitis) showed a reduced frequency of peripheral arthritis in the treated group but did not show any definite benefit in the maintenance of spinal mobility. Adverse effects causing treatment withdrawal occurred in five placebo-treated patients and eight SASP-treated patients, but 22 patients preferred to stop taking daily medication of unproven benefit for the full 3 years. The natural history of established AS suggested two groups of patients: the majority with principally spinal symptoms and infrequent peripheral arthritis or iritis, and a minority who tend to have recurrent extra-spinal problems.

Prevention of postmenopausal osteoporosis is now possible with current therapy, if initiated soon after the menopause and continued for at least 10 years. Simple ways of detecting those at risk of subsequent osteoporosis are urgently needed. This study investigated the hypothesis that certain serum sex hormones could predict bone mineral content (BMC) as measured by dual photon densitometry, soon after the menopause. The subjects included 136 healthy white females within 30 months of their last menstrual period with a mean age of 52 years. Of the sex hormones, the adrenal androgen dehydroepiandrosterone sulphate (DHEAS) correlated best with spinal BMC, a relationship which was significant using multiple regression (P = 0.02), although the correlation was weak (r = +0.19). A direct physiological role for DHEAS has yet to be found, despite being present in large quantities in serum, although it may act as a marker for other processes. No association was seen between testosterone, sex hormone binding globulin, oestradiol, oestrone and oestrone sulphate and spinal BMC. No significant correlations with any hormones were seen with femoral BMC. The data suggest that serum sex hormones are not useful markers of current bone mineral status soon after the menopause, although further work is needed to explore the relationship with DHEAS.