Gynecomastia is a non-tumorous hyperplasia of the mammary gland. It usually affects both breasts, but can however be unitalal. What may seem paradoxical, especially when an endocrine etiology must be retained, is probably explained by differences in the sensitivity of the receptors present in the breast tissue.
The discovery mode is very variable. It may be a fortuitous discovery on clinical examination or on the contrary the very reason for consultation because of its volume or discomfort, or even pain.
In the neonatal period gynecomastia is common and is explained by the transplacental passage of estrogen. Its possible occurrence at puberty corresponds to the initiation of steroidogenesis. In the older man there is a peak frequency between 50 and 80 years when three quarters of the population are affected. The origin of these gynecomastia is often mixed but the androgen deficit is the most common cause in the elderly man.
It is a galactophoric and conjunctive proliferation of estrogenic type, without acini, but with rough pseudo-lobules. The proportion between epithelial and connective tissue depends on the age of gynecomastia.
– Type 1 corresponds to a florid aspect, quite typical of estrogen therapy. The hyperplasia of the canals is concentrically surrounded by a rather loose and edematous connective tissue where collagen fibers are scarce. The epithelium is hyperplastic.
– Type 2 shows a quiescent aspect. This is the most common type. The channels are embedded in dense collagen, without epithelial hyperplasia (Figure 1).
The appearance of gynecomastia reflects a change in estrogen / testosterone ratio. Indeed, androgens, testosterone or dihydrotestosterone are inhibitors of the proliferation of breast tissue. Endogenous estrogens, exogenous or derived from the aromatization of androgens stimulate the proliferation of breast tissue. Leydig cells secrete 15% of the circulating estradiol. The rest comes from the extragonadal conversion of an androgenic precursor. The same goes for estrone with a 5% testicular – 95% extragonadal ratio.
Hyperestrogenism can be absolute if there is a pathological increase of estrogen secretions of tumoral origin, leydigienne (stimulated by hCG) or peripheral by aromatization in adipose tissue. It may also be estrogen of exogenous origin (drugs, foods). The synthesis of SHBG is then increased and leads to a further reduction of the free fraction of androgens which further increases the estrogenic environment.
Hyperoestrogenicity may be relative if there is a decrease in plasma androgens compared to estrogen secretions that remain normal. As the affinity of SHBG is greater for androgens than for estrogens, the free fraction of androgens is further diminished.
Interrogation guides the diagnosis. Family history of the same type should be looked for, manifestations similar to puberty. The clinical examination makes it possible to specify the uni or bilateral character, the possible symmetry of the gynecomastia and the volume of the swelling. Palpation also looks for nipple discharge and possible axillary lymphadenopathy.
The main differential diagnosis to be evoked is adipomastia, which is softer, granular, noncentralized by the nipple, which tends to follow the infero-external edge of the pectoralis major muscle and is often associated with overweight. Breast tumors are rare in humans, but we must know how to evoke the diagnosis in front of a hard nodule, insensitive, accompanied by a possible flow.
Gynecomastia are most often related to hormonal imbalance. In the elderly man an iatrogenic cause must be sought first but it is most often a gynecomastia linked to hypogonadism. The following list attempts to identify iatrogenic causes in the most complete way possible, although some of the treatments mentioned are not used very frequently in older men.