Introduction Use of opiates/opioids is associated with hypoactive sexual desire, erectile and orgasmic dysfunction. Aim To determine prevalence and investigate etiology of sexual dysfunction in men on methadone or buprenorphine maintenance treatment (MMT, BMT). Main Outcome Measures International Index of Erectile Function (IIEF), hormone assays, Beck Depression Inventory. Methods A total of 103 men (mean age 37.6 ± 7.9) on MMT (N=84) or BMT (N=19) were evaluated using the IIEF, hormone assays, Beck Depression Inventory, body mass index (BMI), demographic, and other substance use measures. Results Mean total IIEF scores for partnered men were lower for MMT (50.4 ± 18.2; N=53) than reference groups (61.4 ± 16.8; N=415; P <0.0001) or BMT (61.4 ± 7.0; N=14; P =0.048). Among partnered men on MMT, 53% had erectile dysfunction (ED) compared with 24% of reference groups; 26% had moderate to severe ED, 12.1% in under 40s and 40.0% among those 40+ years. On multiple regression, depression, older age, and lower total testosterone were associated with lower IIEF and EF domain; on multivariate analysis, there were no significant associations between IIEF or EF and free testosterone, opioid dose, cannabis or other substance use, viral hepatitis, or BMI. Total testosterone accounted for 16% of IIEF and 15% of EF variance. Men without sexual partners had lower Desire and Erection Confidence scores and less recent sexual activity, suggesting potentially higher prevalence of sexual dysfunction in this group. Conclusion Men on MMT, but not BMT, have high prevalence of ED, related to hypogonadism and depression. Practitioners should screen for sexual dysfunction in men receiving opioid replacement treatment. Future studies of sexual dysfunction in opioid-treated men should examine the potential benefits of dose reduction, androgen replacement, treatment of depression, and choice of opioid.

The enhancement effect is consistently shown when simultaneously masked stimuli are preceded by the masker alone, with a reduction in the amount of masking relative to when that precursor is absent. One explanation for this effect proposed by Viemeister and Bacon [(1982). J. Acoust. Soc. Am. 71, 1502Am. 71, -1507 is the adaptation of inhibition, which predicts that an enhanced component (the "target") will be effectively more intense within the auditory system than one that has not been enhanced. Forward masking studies have indicated this effect of increased gain; however, other explanations of the enhancement effect have also been suggested. In order to provide an alternative measure of the amount of effective gain for an enhanced target, a subjective binaural centering task was used in which listeners matched the intensities of enhanced and unenhanced 2-kHz tones presented to opposite ears to produce a centered stimulus. The results showed that the enhancement effect produces an effective 4-5 dB increase in the level of the enhanced target. The enhancement effect was also measured using other enhancement paradigms which yielded similar results over a range of levels for the target, supporting an account based on adaptation of inhibition.

The aim of this study was to determine the prevalence and investigate the aetiology of hypogonadism in men on methadone or buprenorphine maintenance treatment (MMT, BMT). 103 men (mean age 37.6 +/- 7.9) on MMT (n = 84) or BMT (n = 19) were evaluated using hormone assays, body mass index (BMI), serological, biochemical, demographic and substance use measures. Overall 54% of men (methadone 65%; buprenorphine 28%) had total testosterone (TT) <12.0 nm; 34% (methadone 39%; buprenorphine 11%) had TT <8.0 nm. Both methadone- and buprenorphine-treated men had lower free testosterone, luteinising hormone and estradiol than age-matched reference groups. Methadone-treated men had lower TT than buprenorphine-treated men and reference groups. Prolactin did not differ between methadone, buprenorphine groups, and reference groups. Primary testicular failure was an uncommon cause of hypogonadism. Yearly percentage fall in TT by age across the patient group was 2.3%, more than twice that expected normally. There were no associations between TT and opioid dose, cannabis, alcohol and tobacco consumption, or chronic hepatitis C viraemia. On multiple regression higher TT was associated with higher alanine aminotransferase and lower TT with higher BMI. Men on MMT have high prevalence of hypogonadotrophic hypogonadism. The extent of hormonal changes associated with buprenorphine needs to be explored further in larger studies. Men receiving long term opioid replacement treatment, especially methadone treatment, should be screened for hypogonadism. Wide interindividual differences in methadone metabolism and tolerance may in a cross-sectional study obscure a methadone dose relationship to testosterone in individuals. Future studies of hypogonadism in opioid-treated men should examine the potential benefits of dose reduction, choice of opioid medication, weight loss, and androgen replacement.

Clinical characterization in a setting of high HCV prevalence has enabled the differentiation of patients into groups with no evidence of HCV viraemia, with chronic HCV infection, and those most appropriate for HCV treatment referral. These clinical assessments along with appropriate referral should be instituted in drug dependency treatment settings.

Three patients admitted to the intensive care unit after multiple injury were observed to suffer episodes of adrenocortical insufficiency suggested by clinical manifestations and confirmed by appropriately low cortisol concentrations. This prompted a prospective study of pituitary-adrenocortical function in six multiply injured patients, three ofwhom showed evidence ofadrenocortical suppression. The only factor common to the six patients with abnormally low adrenocortical function was an association between periods ofadrenocortical suppression and intravenous infusion of etomidate; when the drug was stopped adrenocortical function was restored, and renewed administration of the drug caused further inhibition. Etomidate infusions lasting only six hours were found to cause low, flat responses to short tetracosactrin tests and grossly raised plasma concentrations of adrenocorticotrophic hormone, suggesting direct suppression of the adrenal cortex. Median plasma cortisol concentrations measured at 0900 were significantly lower and median plasma concentrations of adrenocorticotrophic hormone measured at 0900 were significantly higher in the three patients studied prospectively who were receiving etomidate infusions compared with the three patients who did not receive etomidate (p= 005).