Daytime plasma melatonin levels in male hypogonadism

• Published in: The journal of clinical endocrinology and metabolism Vol. 81; no. 5; pp. 1877 - 1881
• Main Authors: OZATA, M, BULUR, M, BINGOL, N, BEYHAN, Z, CORAKCI, A, BOLU, E, GUNDOGAN, M. A
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Endocrine Society 01.05.1996
• Subjects: Adult; Biological and medical sciences; Chorionic Gonadotropin - therapeutic use; Circadian Rhythm; Dehydroepiandrosterone - analogs & derivatives; Dehydroepiandrosterone - blood; Dehydroepiandrosterone Sulfate; Endocrinopathies; Estradiol - blood; Follicle Stimulating Hormone - blood; Humans; Hypogonadism - blood; Hypogonadism - drug therapy; Hypogonadism - pathology; Hypothalamus. Hypophysis. Epiphysis (diseases); Luteinizing Hormone - blood; Male; Medical sciences; Melatonin - blood; Menotropins - therapeutic use; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Prolactin - blood; Sex Hormone-Binding Globulin - metabolism; Testis - pathology; Endocrinopathy; Human; Hypogonadotropic hypogonadism; Hypothalamic diseases; Aminoacid derivative hormone; Idiopathic; Melatonine; Genital diseases; Blood plasma; Treatment; Hormonal investigation; Day; Pineal hormone
• ISSN: 0021-972X
• DOI: 10.1210/jc.81.5.1877

It has previously been shown that increased nocturnal melatonin (MT) secretion exists in male patients with hypogonadotropic hypogonadism. However, little is known about the effects of gonadotropin and testosterone (T) treatment on early morning plasma MT levels in male hypogonadism. Also, the impact of gonadal steroids on plasma MT levels is an open question. We, therefore, determined early morning plasma MT levels at the same hour before and 3 months after treatment in 21 patients with idiopathic hypogonadotropic hypogonadism (IHH), 10 patients with primary hypogonadism, and 11 male controls. Plasma FSH, LH, PRL, T, and estradiol levels were also determined before and 3 months after treatment. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with primary hypogonadism received T treatment. Short term treatments did not achieve normal T levels, although significant increases in T were observed in both groups. Plasma MT levels were measured by a RIA with a sensitivity of 10.7 pmol/L. Mean plasma MT levels before treatment were significantly higher in IHH (41.8 +/- 24.4 pmol/L) compared with those in the controls (21.7 +/- 10.8 pmol/L; P < 0.05). However, a slight, but not significant, increase in MT (34.2 +/- 21.1 pmol/L) was found in primary hypogonadism. Mean MT levels did not change significantly 3 months after the initiation of gonadotropin (41.7 +/- 22.8 pmol/L) or T (28.4 +/- 12.6 pmol/L) treatment in either IHH or primary hypogonadism, although a tendency for MT to decrease was observed in both groups. No correlation was found between MT and circulating FSH, LH, PRL, and gonadal steroids either before or after therapy. We conclude that male patients with IHH have increased early morning MT levels, although the pathophysiological mechanism is not clear. Furthermore, our study demonstrated that mean plasma MT levels are not influenced by short term gonadotropin or T treatment in male hypogonadism, although a longer time effect of gonadotropins or T treatment may not be excluded. The lack of correlation between plasma MT and circulating gonadal steroids before and after treatment suggests that there is no classic feedback regulation between the pineal gland and the testes.