GYNECOMASTIA

Gynecomastia is characterized by the enlargement of one or both male breasts and is due to a non tumoral proliferation of the mammary ducts and of the relative stroma-supporting tissue. It should be distinguished from the simple accumulation of adipose tissue (so-called “lipomastia” or pseudo-gynecomastia) and from the presence of inflammatory or tumoral process.

The main clinical sign/symptom is a concentric increase of the breast, which can be accompanied by pain (in about a third of the cases, linked to the “florid” phase, that is to the expansion of mammary volume) or by hypersensitivity of the area. The presence of other symptoms or clinical signs can be linked to the underlying disease which could be the actual cause of gynecomastia.

Gynecomestia often occurs in puberty, when hormonal changes can induce an attempted mammary development, limited in any case to the male genetic structure. Peripuberal gynecomastia is basically a paraphysiological phenomenon which can cause discomfort/ embarassment in the adolescent, especially if evident and considering the particularly sensitive period of a boy’s life. Besides the paraphysiological situation, a series of other causes can be involved in the pathogenesis of gynecomastia. The use of certain categories of drugs, endocrine disorders (in primis those reducing testosterone levels), testicular tumors, severe hepatic dysfunction or serious systemic diseases, genetic diseases such as Klinefelter syndrome or alterations of the androgen receptor, therapeutic use or absue of steroids (e.g. estrogens, testosterone) can be among the underlying causes of gynecomastia development. Gynecomastia can also be a sign of neoplastic disease which produces endocrine active agents (the so-called “paraneoplastic syndromes”).

When gynecomastia occurs it is always advisable to obtain specialized endocrinological-andrological assessment, in order to ascertain the origin. A mammary ecography and possible  mammography are necessary to confirm gynecomastia diagnosis and exclude other processes (e.g. male breast tumor, rare but possible). Also testicular ecography is strongly advised to exclude local processes responsible for the gynecomastia. Specific hormone evaluation and assessment  of  hepatic functionality and of the main hematochemical parameters are important as well. Case-history data about the time, onset and presentation of symptoms, possible concomitance of sexual function disorders and pharmacological history are fundamental for a good diagnosis.
The therapeutic approach is strongly affected by the pathogenesis of gynecomastia itself. The elimination or containment of possible causes is undoubtedly a rational therapy, compatibly with the clinical situations (e.g., replacement of the drug involved, if possible and without risk to the patient’s health; recovery of an adequate androgenic environment, if the patient is hypogonadal, after ascertaining the causes). The specific medical treatment also involves the use of nonsteroidal anti-inflammatory anti-edemic drugs that can reduce the discomfort of symptoms in the early stages ( the so-called “florid” phase of gynecomastia). Possible use of anti-estrogens may be useful only in the early stages of gynecomastia, when it can counteract the process of breast development.
Given that gynecomastia, at least in adolescents, is often simply a paraphysiological phenomenon, this fact should be properly explained to the patient and his family after having excluded, even in these cases, secondary causes.
Once the breast tissue has developed, possible surgical treatment is a reasonable resolutive approach, which should be considered depending on the entity of gynecomastia and on the psycho-physical implications for the patient.

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Giancarlo Balercia

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