Endocrine complications of human immunodeficiency virus infection: hypogonadism, bone disease and tenofovir-related toxicity.

Treatment with highly active antiretroviral therapy (HAART) has revolutionized care of patients with HIV infection. The cost of increased survival has been antiretroviral toxicity and increasing age-related co-morbidities that include significant metabolic issues. Hypogonadism was first described in the setting of advanced AIDS and can be primary or secondary. Data regarding treatment largely concern patients with wasting. Varied syndromes involving bone have been described in patients with HIV including osteonecrosis, low bone mineral density (BMD) and osteoporosis, and rarely osteomalacia. Low BMD leading to osteoporosis is the most common bone pathology and may be as a result of HIV infection, drug toxicity or co-morbidities. However, increasingly fragility fractures are reported in HIV-infected patients, suggesting bone demineralization in this population is of clinical relevance. Further research is required to understand its pathogenesis and determine effective management; however, initiation of antiretroviral therapy seems to accelerate (in the short-term) bone demineralization. One particular antiretroviral agent, tenofovir is widely used and is potentially implicated as having a greater role in long-term bone and renal dysfunction. As this population ages, screening for low BMD will become increasingly more important.