A multicenter phase IIb study of a novel combination of intramuscular androgen (testosterone decanoate) and oral progestogen (etonogestrel) for male hormonal contraception.

The effect of a novel combination of oral etonogestrel (ENG) and im testosterone decanoate (TD) on suppression of gonadotropins and spermatogenesis as a potential lead for male contraception was investigated. Healthy male volunteers were randomized into two groups receiving 300 microg ENG daily and 400 mg TD every 4 (n = 55) or 6 (n = 57) wk for 48 wk. At wk 48, all men except one in the 6-wk group suppressed sperm concentration to less than 1 million/ml. Faster suppression occurred in the 4-wk group. Gonadotropins were suppressed in both groups and most consistently in the 4-wk group. During treatment, trough testosterone levels increased into the normal range in the 4-wk group but remained just below normal in the 6-wk group. All peak levels were within the normal range. After treatment cessation, recovery of sperm counts and gonadotropins to normal levels occurred in both groups. Minor effects on weight and cholesterol were noted. Fourteen subjects withdrew because of an adverse event with those possibly related to the study medication reported more frequently in the 6-wk group (nine vs. one). In conclusion, the combination of 300 microg ENG with 400 mg TD every 4 wk was superior in terms of efficacy, hormone profiles, and safety. This represents a promising approach to male hormonal contraception.

Acute urinary retention: what is the impact on patients' quality of life?

OBJECTIVE: To evaluate the impact of admission for acute urinary retention (AUR) on patients' health-related quality of life (HRQoL) compared with that on admission for elective surgery for benign prostatic hyperplasia (BPH) and emergency admission for renal colic (RC). PATIENTS AND METHODS: Over a 2-year period, three groups of men were recruited from one institution: group 1, men aged >50 years presenting to the accident and emergency (A&E) department with AUR; group 2, for comparison, men aged >50 years admitted for elective surgery for BPH; and group 3, men aged >40 years presenting to A&E with RC. A self-completed HRQoL questionnaire was administered at five visits (72 h from admission, and 1, 2, 3 and 6 months afterward) over a 6-month follow-up. RESULTS: Group 1 reported mean pain scores on admission of 7.7, compared with 5.6 for group 2 and 8.3 for group 3. Patients in group 1 had the most investigations and recurrent attendance to A&E throughout the study, compared with almost none for the other two groups. There was a substantial economic burden for group 1; 15% had extra help at home at a mean cost of 403 UK pounds for the duration of the study. For the other domains assessed (e.g. emotions, mental state, general health) groups 1 and 2 were similar. CONCLUSIONS: An episode of AUR has a measurable impact on patients' HRQoL, which often occurs in the community and therefore may not be appreciated by the urology team providing their care. Further work is therefore required to improve the "patient journey" for those with AUR, and to prevent patients developing AUR in the future.

Genetics and hypogonadotrophic hypogonadism.

Hypothalamic pulsatile gonadotrophin-releasing hormone secretion, stimulating pituitary gonadotrophin secretion, is essential for adult reproductive function. This neuroendocrine drive to the reproductive axis is critically dependent on a sequence of developmental events in utero. During early foetal life, gonadotrophin-releasing hormone neurones migrate from the nasal placode to the medial basal hypothalamus where gonadotrophin-releasing hormone can be transported down portal vessels to the anterior pituitary. Gonadotrophin-releasing hormone secretion is active fleetingly neonatally but soon becomes quiescent throughout childhood. At the time of puberty activation of gonadotrophin-releasing hormone secretion reawakens the hypothalamic pituitary-gonadal axis and secondary sexual maturation is triggered. Any disruption in gonadotrophin-releasing hormone secretion will result in hypogonadotrophic hypogonadism. The clinical manifestations of this become apparent with secondary sexual maturation. Genetic mutations have been identified in a minority of cases. These include Kallmann syndrome, adrenal hypoplasia congenital, gonadotropin-releasing hormone receptor and luteinizing hormone or follicle-stimulating hormone beta-subunit gene mutations. The importance of these discoveries is important not only in relation to the conditions that result, but also for our better understanding of normal reproductive function.