Discussion
Breast enlargement in the human immunodeficiency virus (HIV)-infected population was first described in 1987. Since then there has been an increasing number of reports in the medical literature,
suggesting that breast enlargement could present as a long-term adverse side effect of highly active antiretroviral therapy (HAART). Today breast enlargement in male HIV patients is not a rare
clinical condition. The incidence of gynecomastia in HIV male patients treated with HAART was 0.8/100 patients/year, with a prevalence of 2.8% in those treated for >2 years. After the use of
highly active antiretroviral therapy (HAART), breast enlargement is emerging as a new problem among HIV-positive male population. These patients frequently center around cosmetic problems and
sometimes have the fear of developing a breast malignancy. An evaluation of this condition helps to distinguish between true gynecomastia, pseudoangiomatous stromal hyperplasia, lipomastia,
opportunistic infections, and malignancy. The cases described in the medical literature suggest that most cases of breast enlargement in HIV-positive men are caused by gynecomastia or lipomastia.
True gynecomastia (proliferation of ducts and peripheral stroma) may have a hormonal cause, or it may be secondary to the use of medications other than those in HAART (including three to four
antiretroviral drugs belonging to the nucleoside and nonnucleoside reverse transcriptase inhibitor categories and protease inhibitors), drugs for the treatment of cardiovascular conditions and
antiulcer drugs or recreational use of marijuana, or it may reflect an underlying medical condition such as liver disease, renal failure, and the presence of certain neoplasms. The pathogenesis of
gynecomastia is unclear; PI ( protease inhibitors) and NNRTI (nonnucleoside reverse transcriptase inhibitors) may have an oestrogen-like effect on breast tissue, or may induce an elevation of the
oestrogen-androgen reaction, or the breast tissue response to hormones may have been altered. Hypogonadism, which occurs in HIV-positive men, may be partly responsible for the occurrence of
gynecomastia, in the form of many testicular tumors. True gynecomastia is nearly always unilateral with focal findings. When bilateral, it is usually asymmetric. It can develop rapidly and the
breasts may be tender. Pseudoangiomatous stromal hyperplasia (PASH) is a proliferative process that appears to have a hormonal cause. Lipomastia (increased amounts of adipose, but not ductal, in the
breast) is one of the body-shape changes that occurs due to the fat maldistribution (lipodystrophy) syndrome, associated to some extent with HAART. While the actual mechanisms underlying this
abnormality are clearly unknown, HIV-1 protease inhibitors may be the causal agents in many cases. However, the observations of lipodystrophy in patients who did not receive protease inhibitors
suggest other possible mechanism; the mitochondrial toxicity in patients treated with nucleoside reverse transcriptase inhibitors was also indicated in the pathogenesis of lipodystrophy. In this
syndrome, there is a wasting (lipoatrophy) of the peripheral body fat in the face, limbs and buttocks and a deposition of fat (lipohypertrophy) centrally in the abdomen, the breasts and the
cervicodorsal fat pad. Typically lipomastia is presented as bilateral, with more-generalized enlargement than gynecomastia. Opportunistic infections that occur in the breasts depend largely on the
geography and degree of immune depression. Generally, the most common infection is tuberculosis (TB). Nonpuerperal periductal mastitis (duct ectasia) can be the result of impaired immunity secondary
to HIV infection as well. Although most cases of breast enlargement in HIV-infected male patients have been presented as benign, there have been various reports in this population. A strong
susceptibility to male breast cancer is seen in Klinefelter’s syndrome, feminization, hypogonadism, gynecomastia and obesity. Breast adenocarcinoma in HIV-positive patients tends to occur at an
early age. Kaposis’s sarcoma (KS) can be localized to the breast in HIV-infected patients. Breast is also a recognized site of non-Hodgkin’s lymphoma (NHL) in HIV-infected patients. In
our case, infection and antiretroviral drugs could be the precipitating causes for the development of gynecomastia. In liver disease, gynecomastia is observed in advanced hepatic failure, which was
not the case in our patient, as there were no signs of decompensated cirrhosis or even portal hypertension. In our patient, the presence of microcalcifications in mammography raised the possibility
of either adenocarcinoma or KS. However, their diffuse appearance led us to attribute these findings to previous subcutaneous hematomas which had mainly occurred during the period with the
HIV-related thrombocytopenia. A biopsy was postponed and a systematic follow-up was decided. On this follow-up, three and six months after diagnosis, the mammographic findings remained stable. Until
today, little information exists, in the imaging literature, regarding breast enlargement in HIV-positive patients. HIV may directly and indirectly affect the glandular, mesenchymal, and intramammary
lymphoid tissue in these patients. Breast imaging and therapeutic challenges have not been well addressed. Ultrasonography and MR mammography should be advised in HIV-infected patients with breast
enlargement. Mammography must always be performed in order to evaluate the radiographic breast density, to reveal palpable or not palpable lesions and to identify the possible presence of
microcalcifications. Ultrasonography is a useful modality to identify the abnormality of the breast, guiding further investigations. MR mammography would seem ideally suited to breast imaging in
order to distinguish the adipose tissue from the glandular tissue. In conclusion, HIV-positive patients must have a careful evaluation, including the obtainment of a clinical history and the
performance a of physical examination, breast imaging with all the available modalities and biopsy if necessary.
