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Hypogonadism late in the course of AIDS leads to loss of libido and impotence. Half of
male AIDS patients have biochemical evidence for hypogonadism, but only 20% on
antiretroviral therapy. Gonadal dysfunction can be due to nutritional problems, infection, drugs,
and hyperprolactinemia. HIV infection reduces dopaminergic tone, leading to increased
prolactin. TNF release can inhibit steroidogenesis; IL-1 prevents LH binding to Leydig cells and
prevents steroid production.[865]
The testis in AIDS shows an atrophy somewhat like that of chronic alcoholism--there is
decreased or absent spermatogenesis, peritubular fibrosis and loss of germ cells--but
opportunistic infections and neoplasms are rare. In severely debilitated patients, there may be
marked tubular atrophy. Diffuse interstitial mononuclear cell infiltrates can occur but do not
necessarily accompany opportunistic infections, which produce more focal inflammation.[939]
Over the course of HIV infection, histologic findings in the testicular tubules can include
features of decreased spermatogenesis, spermatogenic arrest, and marked atrophy with only
Sertoli cells. The use of antiretroviral therapy with prolongation of survival leads to greater
numbers of infected males with tubular atrophy. However, even late in the course of HIV there
can still be germ cells present, and the numbers of germ cells does not correlate with the CD4
count. Thus, the potential for spread of HIV infection through the sexual route from presence of
infected testicular germ cells is variable but often present.[940]
Testicular neoplasms have peak incidence in young males and may be diagnosed in
patients with AIDS, and germ cell testicular tumors are estimated to be 50 times more common
in HIV-positive men, with two new cases per 1000 HIV-infected persons, compared with 3.5 per
100 000 of the male population. These tumors tend to be more aggressive with a greater
incidence of bilateral presentation. HIV-positive patients treated for testicular cancers have a
comparable morbidity and response to that for non-immunosuppressed patients.[919]
Orchitis and epididymitis are more common with HIV infection than the general male
population, and they can become chronic and recurrent. These infections may co-exist with
bladder infection and may be suspected when the UTI fails to clear with antibiotic therapy.
Opportunistic pathogens may include CMV, Mycobacterium avium-complex, Candida,
Toxoplasma, and Histoplasma. Gonococcal infections may occur, particularly in young men.
Infections with Salmonella may be difficult to treat, and life-long prophylaxis is needed to
prevent overwhelming sepsis.[919]
Inflammatory pseudotumor has been reported in the testis of a patient infected with HIV
and treated with antiretroviral therapy (ART) mimicking testicular cancer. The nodular lesions
on microscopic examination show a mixed chronic inflammatory infiltrate in a background of
spindle cells. The inflammatory infiltrated have a mixture of plasma cells, B lymphocytes and T
lymphocytes and the background spindle cells expressed CD68 and smooth muscle actin,
consistent with a histiocytic and fibroblastic origin. Immune reconstitution following ART may
play a role in the appearance of this lesion.[941]
The antibacterial protection of zinc, spermine and spermidine produced in the prostate
fails as HIV infection progresses, increasing the risk for prostatitis. In the general population, the
incidence of bacterial prostatitis is 1–2%, rising to 3% in asymptomatic HIV-positive patients,
and to 14% in patients with AIDS. Prostatitis may be caused by an ascending urethral infection,
by direct invasion of rectal bacteria, or by hematogenous spread to the prostate. The clinical
presentation is usually acute with severe irritative urinary symptoms, fever, and generalized
malaise. On digital rectal examination, the prostate is swollen and exquisitely tender. Prostatic
abscesses may be caused by the usual bacterial pathogens or by opportunistic fungal and