Characteristics of compensated hypogonadism in patients with sexual dysfunction.
BACKGROUND
In the last few years, a view that subclinical endocrine disorders represent milder forms of the clinically overt disease has emerged. Accordingly, it has been proposed that compensated hypogonadism represents a genuine clinical subset of late-onset hypogonadism.


OBJECTIVE
The aim of the present study is to investigate the associations of compensated hypogonadism with particular clinical and psychological characteristics of male subjects complaining of sexual dysfunction.


METHODS
After excluding documented genetic causes of hypogonadism, an unselected consecutive series of 4,173 patients consulting our unit for sexual dysfunction was studied. Compensated hypogonadism was identified according to the European Male Ageing study criteria: total testosterone ≥10.5 nmol/L and luteinizing hormone >9.4 U/L.


METHODS
Several hormonal, biochemical, and instrumental (penile Doppler ultrasound) parameters were studied, along with results of the Structured Interview on Erectile Dysfunction (SIEDY) and ANDROTEST.


RESULTS
One hundred seventy (4.1%) subjects had compensated hypogonadism, whereas 827 (19.8%) had overt hypogonadism. After adjustment for confounding factors, no specific sexual symptoms were associated with compensated hypogonadism. However, compensated hypogonadism individuals more often reported psychiatric symptoms, as detected by Middlesex Hospital Questionnaire score, when compared with both eugonadal and overt hypogonadal subjects (adjusted odds ratios = 1.018 [1.005;1.031] and 1.014 [1.001;1.028], respectively; both P < 0.005). In addition, subjects with compensated or overt hypogonadism had an increased predicted risk of cardiovascular events (as assessed by Progetto Cuore risk algorithm) when compared with eugonadal individuals. Accordingly, mortality related to major adverse cardiovascular events (MACEs), but not MACE incidence, was significantly higher in subjects with both compensated and overt hypogonadism when compared with eugonadal subjects.


CONCLUSIONS
The present data do not support the concept that compensated (subclinical) hypogonadism represents a new clinical entity. The possibility that subclinical hypogonadism could be a normal response of the hypothalamus-pituitary-testis axis to somatic illness should be considered. Further studies are urgently needed to clarify this latter point.
Endocrinology Unit, Medical Department, Azienda USL Bologna Maggiore-Bellaria Hospital, Bologna, Italy.
Giovanni
G
Corona
Elisa
E
Maseroli
Giulia
G
Rastrelli
Alessandra
A
Sforza
Gianni
G
Forti
Edoardo
E
Mannucci
Mario
M
Maggi
D007172:Erectile Dysfunction / Q000000981:diagnostic imaging / Q000209:etiology*; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000150:complications*; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D013739:Testosterone / Q000097:blood; D014463:Ultrasonography
D013739:Testosterone; D007986:Luteinizing Hormone
Erectile Dysfunction; Hypogonadism; Testosterone