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epoprostenol, bosentan, iloprost, and sildenafil. The course is slightly more fulminant than in
patients with primary PAH, with a third of patients dying in within 5 years.[649,650]
Chronic obstructive pulmonary disease (COPD), including pulmonary emphysema and
chronic bronchitis, are found with increased prevalence because HIV-infected persons are more
likely to have been smokers or to be current smokers than non-infected persons. However,
COPD occurs in association with HIV infection independently of other risk factors such as
smoking.. The pathogenesis of parenchymal destruction of distal airways may begin with
cytotoxic lymphocyte (CTL) activation, followed by capillary endothelial cell injury, then CTL-
induced apoptosis. HIV proteins tat and nef enhance endothelial cell apoptosis. Small airway
hyperreactivity, sphingolipid imbalance and oxidative stress may also contribute to ongoing lung
injury. Pneumocystis jiroveci infection and colonization may also be implicated in development
of COPD. The initiation of antiretroviral therapy can lead to immune reconstitution
inflammatory syndrome that enhances pulmonary injury.[651,652]
Pleural effusions are relatively common in association with a variety of infectious
pulmonary complications of HIV infection. The most common infectious cause of AIDS-
associated pleural effusions is bacterial pneumonia. Sometimes, the pneumonia may be severe
enough to result in empyema. Mycobacterium tuberculosis is another frequent cause for pleural
effusion. Of neoplasms seen with AIDS, Kaposi’s sarcoma is most likely to result in the finding
of pleural effusion, particularly with bilateral effusions. Though P jiroveci (carinii) is frequent
in AIDS, it is less likely to result in effusions; however, it is the most likely cause for
spontaneous pneumothorax, which complicates the course in 1 to 2% of hospitalized patients
with HIV infection. Radiographic evidence for cysts, bulla, or pneumatoceles suggests a risk for
pneumothorax. A third of these patients may die.[653,654]
There is an increased risk for development of chronic obstructive pulmonary disease in
HIV-positive patients (odds ratio 1.47). Thus, COPD will increase as persons with HIV live
longer. The cause for this association is unclear.[655]

UPPER RESPIRATORY TRACT IN AIDS.-- The epiglottis, pharynx, larynx, and
trachea can also be affected by AIDS-diagnostic diseases. The commonest are invasive
candidiasis and Kaposi's sarcoma. Kaposi's sarcoma has a predilection for the epiglottis.
Clinical findings of stridor and hoarseness may suggest KS involvement of the upper airway.
Biopsy can be done, but granulation tissue formed with long-standing intubation or ulceration
from infectious agents may be difficult to distinguish from KS. In order for the presence of
Candida to be diagnostic of AIDS, it must be demonstratably invasive (most commonly in
trachea) and not be found just in secretions.[547]

CLINICAL DIAGNOSTIC TECHNIQUES.-- Roentgenographic imaging procedures are
often employed. Contrast enhanced CT imaging provides the best sensitivity, including disease-
specific sensitivity, for diagnosis of HIV-related conditions.[656] with Gallium scintigraphy
may be performed to aid pulmonary diagnosis. Diffuse bilateral parenchymal uptake is most
often associated with PCP, particularly if uptake is intense and heterogenous. A negative
Gallium scan in a patient with Kaposi’s sarcoma and an abnormal chest radiograph suggests
respiratory disease due to Kaposi’s sarcoma. Lymph node uptake of Gallium is typically
associated with mycobacterial infection (MAC or MTB) and lymphoma. Gallium positive with
thallium negative studies suggest mycobacterial disease.[657]