Pulmonary Hypertension Associated With HIV Infection
Pulmonary Hypertension Associated With HIV Infection
Pulmonary hypertension occurs with increased frequency among patients with human immunodeficiency virus (HIV) infection. Although the pathogenesis of HIV-associated pulmonary hypertension remains unknown, it appears to occur independently of other risk factors associated with pulmonary vasculopathy, such as chronic hepatitis C infection and intravenous drug use. Signs and symptoms are typical of those immunocompetent patients with primary pulmonary hypertension, but because many HIV-infected patients are receiving intensive medical supervision, the diagnosis of pulmonary hypertension is often made at an earlier stage. Acute responses to epoprostenol are similar to those among non-HIV-infected individuals, but the benefits of long-term, intravenous treatment with epoprostenol in HIV-infected patients is unknown. Future investigations should define the true incidence of pulmonary hypertension and the long-term effects of epoprostenol on survival among HIV-infected individuals. Physicians should be alert to possible pulmonary hypertension in persons infected with HIV.
Human immunodeficiency virus has been associated with multiple infectious and noninfectious pulmonary diseases. As a result of better prophylaxis against opportunistic infections and longer survival, noninfectious complications, such as lymphocytic interstitial pneumonia, non-Hodgkin's lymphoma, and pulmonary hypertension, are becoming more prominent. We review the literature concerning HIV-associated pulmonary hypertension, and we suggest therapeutic options and future areas of study.
Kim and Factor first reported pulmonary hypertension associated with HIV infection in a hemophiliac with membranoproliferative glomerulonephritis. Other cases of pulmonary hypertension were described among HIV-infected hemophiliacs, suggesting a causative role of treatment with low-purity factor VIII. However, as subsequent nonhemophilia cases were described, suspicion rose that the pulmonary hypertension might be directly related to HIV infection.
Many patients with HIV-associated pulmonary hypertension have other known risk factors for pulmonary hypertension, such as intravenous drug abuse or chronic liver disease. This initially cast doubt on an HIV-mediated pathogenesis. Illicit intravenous drugs derived from tablets or pills contain insoluble microcrystals that can cause angiocentric foreign body granulomatous inflammation, thrombosis, and pulmonary hypertension when injected long-term. However, fewer than 5% of intravenous drug abusers inject tablet derivatives, making this explanation for most cases of HIV-associated pulmonary hypertension unlikely. Furthermore, in a recent review of HIV-associated pulmonary hypertension by Mesa et al, none of the 33 reported cases with known histology had pathologic evidence of foreign body granulomatosis.
Portal hypertension and cirrhosis have also been associated with pulmonary hypertension. In a prospective study of 507 patients with portal hypertension, prevalence of pulmonary hypertension was 2%, with the majority of patients having plexogenic pulmonary arteriopathy on biopsy or autopsy. Liver disease could account for only a minority of cases of HIV-associated pulmonary hypertension, since only 15% of patients in whom HIV-associated pulmonary hypertension has been reported have a history of hepatitis, evidence of cirrhosis, or portal hypertension.
Pulmonary hypertension occurs with increased frequency among patients with human immunodeficiency virus (HIV) infection. Although the pathogenesis of HIV-associated pulmonary hypertension remains unknown, it appears to occur independently of other risk factors associated with pulmonary vasculopathy, such as chronic hepatitis C infection and intravenous drug use. Signs and symptoms are typical of those immunocompetent patients with primary pulmonary hypertension, but because many HIV-infected patients are receiving intensive medical supervision, the diagnosis of pulmonary hypertension is often made at an earlier stage. Acute responses to epoprostenol are similar to those among non-HIV-infected individuals, but the benefits of long-term, intravenous treatment with epoprostenol in HIV-infected patients is unknown. Future investigations should define the true incidence of pulmonary hypertension and the long-term effects of epoprostenol on survival among HIV-infected individuals. Physicians should be alert to possible pulmonary hypertension in persons infected with HIV.
Human immunodeficiency virus has been associated with multiple infectious and noninfectious pulmonary diseases. As a result of better prophylaxis against opportunistic infections and longer survival, noninfectious complications, such as lymphocytic interstitial pneumonia, non-Hodgkin's lymphoma, and pulmonary hypertension, are becoming more prominent. We review the literature concerning HIV-associated pulmonary hypertension, and we suggest therapeutic options and future areas of study.
Kim and Factor first reported pulmonary hypertension associated with HIV infection in a hemophiliac with membranoproliferative glomerulonephritis. Other cases of pulmonary hypertension were described among HIV-infected hemophiliacs, suggesting a causative role of treatment with low-purity factor VIII. However, as subsequent nonhemophilia cases were described, suspicion rose that the pulmonary hypertension might be directly related to HIV infection.
Many patients with HIV-associated pulmonary hypertension have other known risk factors for pulmonary hypertension, such as intravenous drug abuse or chronic liver disease. This initially cast doubt on an HIV-mediated pathogenesis. Illicit intravenous drugs derived from tablets or pills contain insoluble microcrystals that can cause angiocentric foreign body granulomatous inflammation, thrombosis, and pulmonary hypertension when injected long-term. However, fewer than 5% of intravenous drug abusers inject tablet derivatives, making this explanation for most cases of HIV-associated pulmonary hypertension unlikely. Furthermore, in a recent review of HIV-associated pulmonary hypertension by Mesa et al, none of the 33 reported cases with known histology had pathologic evidence of foreign body granulomatosis.
Portal hypertension and cirrhosis have also been associated with pulmonary hypertension. In a prospective study of 507 patients with portal hypertension, prevalence of pulmonary hypertension was 2%, with the majority of patients having plexogenic pulmonary arteriopathy on biopsy or autopsy. Liver disease could account for only a minority of cases of HIV-associated pulmonary hypertension, since only 15% of patients in whom HIV-associated pulmonary hypertension has been reported have a history of hepatitis, evidence of cirrhosis, or portal hypertension.
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