Imaging in gynecomastia.

BACKGROUND: Gynecomastia (GM) is the benign proliferation of glandular tissue in the male breast. It is a common condition, which may occur physiologically and shows three age peaks during a male's lifespan: infancy, puberty, and senescence. An underlying pathology may be revealed in 45%-50% of adult men with GM, such as aggravating medications, systemic diseases, obesity, endocrinopathies, or malignancy. OBJECTIVE: To discuss the role of imaging in the evaluation of GM and its contribution to therapeutic decision-making. MATERIALS/METHODS: The current literature was reviewed through PubMed, Scopus, and CENTRAL electronic databases to identify the best available evidence concerning imaging modalities in patients with GM. RESULTS: Most male breast lesions can be diagnosed on clinical grounds; however, in certain cases, when physical examination is inconclusive, imaging may be helpful. DISCUSSION: The main purpose of evaluating a patient with GM is to establish the diagnosis and differentiate true GM from pseudogynecomastia, exclude breast cancer, and detect the possible cause. GM is seen in mammography as a subareolar opacity and three mammographic patterns of GM are described: nodular, dendritic, and diffuse, corresponding to florid GM of early onset, fibrous persistent GM, and GM due to exogenous estrogen administration, respectively. In ultrasound (US), florid GM is depicted as a disk-shaped, hypoechoic area underlying the areola, whereas echogenicity of the lesions increases as fibrosis develops. Data on the use of MRI in the evaluation of the male breast and GM are still limited. Imaging findings can be classified according to the BIRADS (breast imaging reporting and data system) based on their malignant potential. CONCLUSION: Both mammography and US are sensitive and specific to diagnose GM and distinguish it from breast cancer. When clinical findings are suggestive of malignancy or imaging findings are inconclusive, a histological confirmation should be sought.

Endocrine Follow-Up of Men with Non-Obstructive Azoospermia Following Testicular Sperm Extraction.

Testicular sperm extraction (TESE) is a surgical procedure which, combined with intracytoplasmic sperm injection, constitutes the main treatment for achieving biological parenthood for patients with infertility due to non-obstructive azoospermia (NOA). Although it is effective, TESE procedures might cause structural testicular damage leading to Leydig cell dysfunction and, consequently, temporary or even permanent hypogonadism with long-term health consequences. To a lesser extent, the same complications have been reported for microdissection TESE, which is considered less invasive. The resulting hypogonadism is more profound and of longer duration in patients with Klinefelter syndrome compared with other NOA causes. Most studies on serum follicle-stimulating hormone and luteinizing hormone concentrations negatively correlate with total testosterone concentrations, which depends on the underlying histology. As hypogonadism is usually temporary, and a watchful waiting approach for about 12 months postoperative is suggested. In cases where replacement therapy with testosterone is indicated, temporary discontinuation of treatment may promote the expected recovery of testosterone secretion and revise the decision for long-term treatment.

Metformin administration was associated with a modification of LH, prolactin and insulin secretion dynamics in women with polycystic ovarian syndrome.

UNLABELLED: AIM. To elucidate the dynamics of FSH, LH, prolactin (PRL), TSH and insulin secretion in women with polycystic ovarian syndrome (PCOS) treated with metformin (MET). PATIENTS AND METHODS: In a prospective, controlled and randomised trial, 32 women with PCOS and 32 with normal cycle were recruited to receive MET (850 mg b.i.d.) or placebo (n: 16 for each subgroup) for an average of 40 days. Pituitary function and insulin secretion were assessed before and after intervention by GnRH-TRH tests and oral glucose tolerance test induced insulin response. RESULTS: Basal and area under the response curve (AURC) LH values were higher in PCOS than in normal controls before MET and declined following treatment in the former group (P < 0.05). Ovulatory PCOS responders had lower basal LH, AURC(LH) and AURC(PRL) values during MET than anovulatory cases (P < 0.05 for all) and AURCins was lower in ovulatory than anovulatory PCOS before and on MET (P < 0.02-P < 0.05), with a rise of QUICKY index in the former group during MET treatment (P < 0.05). FSH and TSH were similar. CONCLUSIONS: MET administration lowered LH activity in all PCOS women and in ovulatory responders and also compromised PRL stimulated secretion in the latter cases. These findings were indicative of an effect of MET on pituitary activity.

Association of carotene rich diet with hypogonadism in a male athlete.

AIM: To report on a unique case of hypogonadism associated with excessive carotene intake in a young male athlete. CASE REPORT: A 20-year-old patient presented with a gradual decline in muscular and physical activity, sexual interest and erectile ability associated with a high in carotene and low in animal fat diet of his own design a year prior to the clinical manifestations. Clinically, he presented with very overt signs of carotene excess: his palms and soles were yellow. Moreover, 2 weeks after normalization of his diet, carotene B levels were at the upper end of the normal range. METHODS: Repeated stimulation tests of hypothalamic, pituitary and testicular function were performed before and at 3, 6 and 12 months after the introduction of a balanced diet. RESULTS: Very low basal and stimulated values for gonadotropins and gonadal steroids were found at the initial evaluation with a progressive recovery shown after months of a balanced diet and carotene B restoration. Complete androgen secretion and sexual response recovery were observed only after 9-12 months from diagnosis. CONCLUSION: This is the first report associating excessive carotene intake with a hypothalamic form of hypogonadism in a young man.

Effectiveness of combined tamoxifen citrate and testosterone undecanoate treatment in men with idiopathic oligozoospermia.

OBJECTIVE: To assess the effect of treatment with a combination of the antiestrogen tamoxifen citrate and the androgen testosterone undecanoate on sperm variables and pregnancy incidence in men with idiopathic oligozoospermia and couple subfertility. DESIGN: Prospective, randomized, placebo-controlled trial. SETTING: Clinical research in a tertiary care academic hospital. PATIENT(S): Two hundred twelve men with idiopathic oligozoospermia and 82 normozoospermic men with female factor subfertility. INTERVENTION(S): Oligozoospermic patients were randomly assigned to two treatment groups with tamoxifen citrate, 20 mg/d, and testosterone undecanoate, 120 mg/d (n = 106) or placebo treatment (n = 106) for 6 months. Normozoospermic men were followed for the same period. Couple counseling was part of the intervention in all groups. MAIN OUTCOME MEASURE(S): Pregnancy incidence and sperm characteristics after 3 and 6 months on medication and 3 months after the end of the trial. RESULT(S): In the active treatment group, total sperm count (median [25th, 75th percentile], 27.1 x 10(6) cells/mL [9.4, 54.0 x 10(6) cells/mL] at baseline and 61.5 x 10(6) cells/mL [28.2, 119.6 x 10(6) cells/mL] at 6 months), progressive motility (mean [+/-SD], 29.7% +/- 12.0% at baseline and 41.6% +/- 13.1% at 6 months), and normal morphology (mean, 41.2% +/- 14.0% at baseline and 56.6% +/- 11.5% at 6 months) were noted. No marked changes were observed in placebo recipients or normozoospermic men. The incidence of spontaneous pregnancy was 33.9% in the active treatment group and 10.3% in the placebo group (36 vs. 11 pregnancies), with a relative risk of 3.195 (95% CI, 2.615 to 3.765). CONCLUSION(S): Treatment with tamoxifen citrate and testosterone undecanoate improved sperm variables and led to a higher incidence of pregnancy in couples with subfertility related to idiopathic oligozoospermia.