The male breast is normally vestigial but under certain hormonal and drug influences it may develop into a significant breast mound. Although gynaecomastia is a common condition, often with a physiological basis, it is important to consider the possible presence of underlying disease. Whatever the aetiology, the ultimate mechanism for breast development is usually an increase in the ratio of circulating oestrogen to androgen.

A firm disc of breast tissue at least 2 cm in diameter underlies the nipple. Approximately 90 per cent cases are bilateral, although one side may be affected several months before the other.

Histological examination will show the early stages of duct development but if gynaecomastia persists for many months fibrous tissue replaces most of the breast tissue.

Physiological gynaecomastia occurs in the majority of men at some stage in their lives. Transient breast development appears in the neonate due to maternal oestrogens and returns in 40 to 70 per cent of boys at puberty. One-third of middle-aged men have some development of their breasts and the incidence gradually increases with age to about 60 per cent in the seventh decade.

The normal testis produces testosterone and small quantities of oestrogens. The adrenal gland also produces weak androgens, the bulk of which is removed by the liver. However excess adrenal androgens and some testosterone are aromatized to oestrogens in the peripheral tissues, particularly fat. At puberty a surge of gonadotrophins induces testicular activity. Oestrogen production reaches adult levels before that of testosterone thus increasing the oestrogen to androgen ratio, sometimes enough to stimulate breast development. This usually lasts a matter of months and in almost 75 per cent of cases it subsides within 2 years. Physiological gynaecomastia later in life is due to waning testicular function with a consequent increase in pituitary gonadotrophin, which favours relatively greater oestrogen production by the testis. At the same time, increased body fat leads to greater peripheral aromatization of androgens to oestrogens.

This is the most common abnormal stimulant of breast development, especially in those over 50 years of age. Oestrogens, frequently given for prostatic carcinoma, often stimulate breast development (Fig. 1) 842. It should be remembered that unprescribed oestrogens, especially those in industrial use, can be absorbed through the skin. Other drugs may have an oestrogen-like or anti-androgen effect but in many cases the mechanism behind drug associated gynaecomastia is unknown. Drugs used in the treatment of cardiac disease or hypertension are common causes: digitalis, spironolactone, calcium channel blockers, methyldopa, and captopril have all been associated with gynaecomastia. Also associated with breast development are cimetidine in high doses, the antifungal agent ketoconazole, tricyclic antidepressants, and even diazepam. Chemotherapy and radiotherapy, especially following orchidectomy for a testicular tumour, can also cause breast development, presumably because they suppress activity in the remaining testis. Abuse of drugs such as heroin and cannabis is known to cause gynaecomastia.

Testicular tumours are an uncommon but important cause of gynaecomastia (Fig. 2) 843. Ten per cent of malignant testicular tumours, usually teratomas, are associated with gynaecomastia; this is associated with a poorer prognosis. These tumours produce human chorionic gonadotrophin which stimulates testicular production of oestrogen and testosterone. Tumour tissue also converts androgens to oestrogens. Both these factors tend to increase the oestrogen: testosterone ratio. Occasionally a benign Leydig cell tumour of the testis causes gynaecomastia by producing excess oestrogen.

Even less commonly, other tumours, such as bronchial carcinoma and occasionally pancreatic and gastric neoplasms, produce human chorionic gonadotrophin and cause breast development. Adrenal tumours cause gynaecomastia by excessive production of androgens which are then converted to oestrogens. Liver tumours sometimes contain aromatases which increase the production of oestrogens from androgens and so lead to gynaecomastia.

Cirrhosis reduces the capacity of the liver to remove adrenal androgens from the circulation, leaving more available for peripheral aromatization to oestrogens, and this often results in gynaecomastia. Alcoholism causes gynaecomastia in the absence of cirrhosis by suppressing the pituitary testicular axis and therefore reducing testosterone production. Conversion of adrenal androgen to oestrogen becomes relatively more important in this situation. In renal failure and in starvation the pituitary adrenal axis is also suppressed and breast development occasionally occurs. However, it is a much more common symptom some months after starting dialysis or refeeding, probably because of resurgent testicular activity, similar to that occurring at puberty. Thyrotoxicosis is an important cause of gynaecomastia: it affects 30 per cent of hyperthyroid males, probably because of increased aromatase activity.

The failing testis is subjected to increased stimulation by pituitary gonadotrophins and responds by producing relatively more oestrogens, sometimes sufficient to cause breast development. Common causes of primary testicular impairment are ageing, maldescent of the testes, or damage from trauma or viral infection such as mumps. Chromosomal aberrations, particularly Klinefelter's syndrome, congenital enzyme deficiencies, and congenital anorchia are less common causes. Failure of the pituitary–testicular axis as a cause of hypogonadism and subsequent gynaecomastia has already been described.

Carcinoma of the breast is considered later. Pseudogynaecomastia may occur, due to local fat deposition with no breast tissue development. The tissue lacks the firm, well-defined appearance of true gynaecomastia. It occurs in obese individuals and carries none of the implications of gynaecomastia.

If growth indices are appropriate then pubertal gynaecomastia probably requires no further investigation. Approximately 50 per cent of the remaining patients with gynaecomastia will have a pathological or iatrogenic cause. A careful drug history is essential and evidence of liver and thyroid function should be sought on history and examination. The testes should be examined for atrophy or tumour and an ultrasound examination performed to exclude a small neoplasm, particularly in the patient under 40 years of age. A chest radiograph is also important. Thyroid and liver function tests, and measurement of serum human chorionic gonadotrophin, luteinizing hormone, oestrogen, and testosterone should be performed.

Gynaecomastia itself requires no treatment unless it causes serious discomfort or embarrassment to the patient. The patient with physiological gynaecomastia often needs only reassurance. Any underlying pathology must obviously be treated and responsible drugs stopped if possible, but this does not guarantee resolution of breast development if it has been present for sometime.

In general, the results of hormone treatment are disappointing, although tamoxifen has been shown to help in some cases of pubertal and middle-aged breast development.,

Surgery is the mainstay of treatment. As a cosmetic operation it is important to leave the nipple/areola in the correct position, symmetrical with the other side, with minimal obvious scarring. Most patients have relatively modest breast development and a satisfactory subcutaneous mastectomy can be performed through an incision following the inferior margin of the areola. It is important to leave a smooth contour to the breast and avoid a central crater under the areola.

Occasionally breast development is so marked that excess skin has to be removed. Several techniques have been developed to do this while preserving the areola in position with an intact blood supply.

Liposuction can be a useful adjunct to leave an acceptable chest profile, but as it removes only fat and not breast tissue it cannot be the complete surgical answer in true gynaecomastia.

This is rare. About 1 per cent of all breast cancers occur in men, slightly more in the Middle East and Africa.

Male breast cancer occurs most often in the seventh decade, slightly later than in women. Seventy-five per cent of patients present with a breast mass, the others with a bloodstained nipple discharge, nipple distortion, ulceration, or axillary lymphadenopathy. Despite the ease of examining the breast in a man in comparison to women, these tumours tend to present late, probably because of lack of concern regarding male breast symptoms. Inevitably most of these tumours arise beneath the areola, an unfavourable site for breast cancers. They are close to and often infiltrate both skin and muscle, and axillary spread is common by the time of presentation.

Most male breast cancers are ductal adenocarcinomas. Papillary tumours are uncommon, but occur more often than in women, hence the relative frequency of a nipple discharge at presentation. Over 80 per cent of these tumours are oestrogen receptor positive, a much higher percentage than in women, and this has implications for treatment. Beware the secondary deposit from tumour elsewhere, especially from prostate, which may be difficult to distinguish histologically.

There is strong evidence for a hormonal basis to the disease. Several studies, though not all, have shown significantly raised serum levels of oestrogens in men with breast carcinoma. There seems to be no increase in the incidence of breast tumours in men treated with oestrogens for carcinoma of the prostate, but the timing and duration of the hormone rise may be critical. Men who were much overweight in early adulthood have a greater chance of developing a breast tumour later in life, even if their weight subsequently falls. Obesity is linked to increased aromatase activity which increases the conversion of adrenal androgens to oestrogens. Male breast tumours are very common in patients with Klinefelter's syndrome, a condition in which there is impaired testicular function, and have also been described in association with long-standing hypopituitarism and hypogonadism, and with a history of orchitis. All these diseases would tend to increase the ratio of oestrogen: testosterone. Although similar influences have been described in the development of gynaecomastia there is no evidence that gynaecomastia itself leads to breast tumour.

A family history of male or female breast cancer is also important. Previous radiotherapy to the chest wall, certainly important in female breast tumours, has occasionally been associated with the development of male breast cancer.

The proximity of the tumour to the chest wall and the frequency of axillary spread have led to a treatment by a radical or modified radical mastectomy in most centres. Simple mastectomy with postoperative radiotherapy has been advocated by some, but the local recurrence rate appears to be higher. Unfortunately the rarity of this tumour has precluded a prospective study comparing different treatments. Over 50 per cent of patients with disseminated disease respond to orchidectomy for a median period of nearly 2 years. On recurrence a further response can still be elicited by administration of tamoxifen or antiandrogens, such as cyproterone acetate: some centres elect to use these agents as first-line treatments in preference to orchidectomy. Many patients also respond to therapy with cytotoxic agents.

Overall about 50 per cent of patients die of their diseases in the 5 years following diagnosis. Stage for stage, the prognosis is probably similar to that in women: if no axillary nodes are involved then about 80 per cent survive 5 years, but only 30 to 40 per cent of those with axillary spread survive this long. Higher grade and larger tumours have a poorer outcome.

Very rarely conditions relatively more common in the female breast such as fibroadenoma, fibrocystic disease, and phylloides tumour have been described in men.

Carlson HE. Gynecomastia. N Engl J Med, 1980; 303: 795–9.

Erlichman C, Murphy KC, Elhakim T. Male breast cancer: a 13-year review of 89 patients. J Clin Oncol, 1984; 2: 903–9.

Keddie N, Morris PJ. Male breast tumours. Surg Gynecol Obstet, 1967; 124: 332–6.

Korenman SG. The endocrinology of the abnormal male breast. Ann N Y Acad Sci, 1986; 464: 400–8.

Nuttall F. Gynecomastia as a physical finding in normal men. J Clin Endocrinol Metab, 1979; 48: 338–40.

Nydick M, Bustos J, Dale JH, Rawson RW. Gynecomastia in adolescent boys. JAMA, 1961; 178: 109–14.

Ribeiro G. Male breast carcinoma. Br J Cancer, 1985; 51: 115–9.

Wilson JD, Aiman J, MacDonald PC. The pathogenesis of gynecomastia Adv Intern Med, 1980; 25: 1–31.