Gynecomastia

Gynecomastia (GM) is characterized by enlargement of the male breast, caused by glandular proliferation and fat deposition. GM is common and occurs in adolescents, adults and in old age. The aim of this review is to discuss the pathophysiology, etiology, evaluation and therapy of GM. A hormonal imbalance between estrogens and androgens is the key hallmark of GM generation. The etiology of GM is attributable to physiological factors, endocrine tumors or dysfunctions, non-endocrine diseases, drug use or idiopathic causes. Clinical evaluation must address diagnostic confirmation, search for an etiological factor and classify GM into severity grades to guide the treatment. A proposal for tailored therapy is presented. Weight loss, reassurance, pharmacotherapy with tamoxifen and surgical correction are the therapeutic options. For long-standing GM, the best results are generally achieved through surgery, combining liposuction and mammary adenectomy.

ObjectivesTo evaluate the characteristics of presentation, biochemical profile, and etiology of gynecomastia in adults.MethodsMedical records of 237 men aged 18-85 years with gynecomastia were evaluated.ResultsHighest prevalence of gynecomastia was observed between 21 and 30 years (n = 74; 31.2%). The most common presenting complaints were aesthetic concerns (62.8%) and breast pain (51.2%). 25.3% of the subjects had a history of pubertal gynecomastia. 56.5% had bilateral gynecomastia. 39.9% were overweight and 22.8% were obese. The etiology could not be identified in 45.1% of the cases; the most frequent identified causes were anabolic steroids consumption (13.9%), hypogonadism (11.1%), and use of pharmaceutical drugs (7.8%). Patients with bilateral gynecomastia had a longer history of disease, higher BMI, and lower testosterone levels.ConclusionsPatients with gynecomastia presented more often with aesthetic concerns and secondarily with breast pain. The most frequent final diagnosis was idiopathic gynecomastia, whereas the most frequent identified etiologies were anabolic steroids consumption, hypogonadism, and use of pharmaceutical drugs. Despite the low frequency of etiologies such as thyroid dysfunction or adrenal carcinoma, we emphasize the importance of a thorough assessment of the patient, as gynecomastia may be the tip of the iceberg for the diagnosis of treatable diseases.

PurposeA large number of medications have been implicated in the genesis of gynecomastia. However, gynecomastia is common in men, asymptomatic, increases with age, and is considered to be due to an increased estradiol/testosterone ratio. This complicates the interpretation of medication-related gynecomastia. Therefore, we have reviewed the literature in order to assess the data relating gynecomastia onset with utilization of specific medications.MethodsThe literature was searched in PubMed and the Ovid/Medline databases from the 1946 to January 2015 with the search terminology of "gynecomastia, drugs/medications." A few other articles were found and included.ResultsOne hundred ten publications were reviewed. Sixty-three were single case reports. There were 24 population-based studies of which 8 were HIV-infected patients treated with antiretroviral agents. Among the case reports, 49 were for individual medications, and 2 were reports of antineoplastic or antiretroviral drug regimens. In the great majority, mastodynia with or without breast enlargement was present and referred to as gynecomastia. Generally, hormonal profiles could not explain the breast enlargement. The pain/tenderness and breast enlargement resolved spontaneously over time.ConclusionMany different medications have been associated with the presence of "gynecomastia." Generally, it presents as a syndrome characterized by a single painful/tender breast (mastodynia) associated with breast enlargement and is transient. We suggest that these cases be referred to as an acute gynecomastia syndrome. This syndrome also occurs independent of medication use. Thus, in an individual patient, whether it is medication induced often remains uncertain. The pathogenesis remains unknown.

International andrology guidance discusses refeeding after starvation as a clinical setting associated with gynaecomastia, based on reports from starvation-refeeding settings outside anorexia nervosa (AN). A targeted search of PubMed, PsycINFO, and Google Scholar, last conducted on 27 July 2026, identified no indexed reports in male patients recovering from AN. We therefore advance the testable hypothesis that transient glandular breast tissue may occasionally occur but remain unrecognised during nutritional recovery; the available evidence does not establish occurrence, prevalence, or clinical significance in AN. Five endocrine transitions provide biological plausibility: non-uniform recovery of the hypothalamic-pituitary-gonadal axis, expansion of the adipose tissue compartment in which aromatase is expressed, a transient leptin rise, possible preservation of adrenal androgen precursor availability, and recovery of insulin-like growth factor 1. Direct human data in male AN support parts of the endocrine trajectory, whereas the proposed link to breast tissue relies largely on indirect human evidence and preclinical studies. Potential under-recognition could arise from misclassification as pseudogynaecomastia, patient-side under-reporting, and follow-up that ends before later endocrine recovery; no clinical detection window has been established. We propose retrospective review, prospective surveillance extending beyond acute refeeding, targeted endocrine evaluation of confirmed glandular tissue, and multicentre studies of prevalence, risk factors, natural history, psychological effects, and treatment engagement.