Endocrine Abstracts

JOINT1135

Although signs and symptoms associated with male hypogonadism are commonly encountered in endocrinology outpatient clinics, their clinical implications are not well characterized. In present study, we aimed to describe the etiologic distribution, as well as the anthropometric and biochemical features of adult-onset male hypogonadism, using electronic health record data of individuals referred for an endocrine evaluation between 2020-2022 due to low testosterone and hypogonadal symptoms. Of the total of 119 individuals referred, 88 patients who had low testosterone (i.e., less than 10 nmol/l)on repeated measurements constituted the study population. Patients were grouped into four categories according to the etiology of hypogonadism: primary hypogonadism (n=13), morbid obesity-associated secondary hypogonadism (MOSH) (n=49), prior anabolic-androgenic steroid use (AAS) (n=5), and hypogonadotropic hypogonadism (HGHG) (n=21). The latter group included patients with a specific disease of the pituitary gland (n=6), as well as patients with prior and/or current opioid/glucocorticoid use (n=8), patients with obstructive sleep apnea without morbid obesity or other sleep disorders (n=3) and patients with miscellaneous etiology of HGHG (n=4). The median serum testosterone levels were 6.7 [5.0-9.4], 7.3 [5.9-8.6], 6.3 [2.8-8.0] and 6.9 [3.9-8.2] nmol/lin primary, MOSH, AAS and HGHG groups, respectively (NS in Kruskal-Wallis test) and symptoms distribution (NS in chi-square test) were comparable among the groups whereas luteinizing hormone (LH) levels were higher in patients with primary hypogonadism (10.8 [5.0-21.2] U/l)than other groups (4.1 [2.2-5.4], 1.3 [0.0-2.5] and 2.9 [0.3-4.5] U/lin MOSH, AAS and HGHG groups, respectively, P < 0.001). Prevalence of hypertension and obstructive sleep apnea (both P < 0.01) were higher in MOSH compared to the rest of the groups although glucose and lipid profiles were comparable among the groups. Surprisingly, serum testosterone levels in the MOSH group were inversely correlated with gonadotropin levels (LH: r=-0.42, P<0.01; FSH: r=-0.41, P<0.01); this was not observed in HGHG group. In summary, morbid obesity is the leading cause of adult-onset male hypogonadism whereas cases due to specific conditions affecting HPT axis, such as prolactinoma or testicular failure, are rare. Although negative feedback of testosterone on gonadotropins is preserved in hypogonadal men with morbid obesity, gonadotropin secretion is insufficient for maintaining adequate testosterone levels. This is in contrast with hypogonadotropic hypogonadism, which is characterized by a total disruption of HPT axis regulation.