AIDS-Related Alveolar Hemorrhage: Discussion
This analysis of 273 consecutive BAL specimens from HIV-infected patients showed the following: (1) that AH was present in about one third of patients but was usually clinically occult and cytolog-ically mild; (2) AH was clearly associated with specific underlying AIDS-associated pulmonary disorders, namely, pulmonary KS, CMV pneumonia, and hydrostatic pulmonary edema; and (3) AH was favored by triggering factors, especially thrombocytopenia. The high frequency of AH in this series is in keeping with that in a previous study.
As HIV infection indirectly causes nonspecific lesions of the pulmonary artery,2 it might also lead to inflammatory lesions of the alveolar capillaries similar to those described in some immunologic disorders and referred to as capillaritis. However, although HIV-related vasculitis has been described, to our knowledge, capillaritis has never been reported in the lungs of patients with AIDS. Several findings in the present study suggest that HIV-related pulmonary vasculitis was not responsible for AH. First, AH was never found in the 17 subjects who had no underlying pulmonary disorders. Second, all the patients with AH had at least one AIDS-related pulmonary disorder. Patients with AH were more profoundly immunodeficient (Table 1), raising the possibility of an indirect contribution of HIV to the onset of AH. Indeed, HIV disease progression is associated with an increase in alveolar permeability and a rising incidence of AH risk factors, such as pulmonary KS, CMV pneumonia, and clotting disorders. buy flovent inhaler
Even if AH should be observed in all patients with AIDS-related pulmonary disorders, only three of the latter (ie, pulmonary KS [OR, 5.3], CMV pneumonia [OR, 10], and hydrostatic pulmonary edema [OR, 16.4]) were identified as independent risk factors for AH in a stepwise forward logistic regression model (Table 3). Interestingly, these disorders are also known to interact with the vascular or blood flow pulmonary system through pulmonary vascular an-giogenesis, capillary endothelial lesions, and a rise in capillary hydrostatic pressure, respectively. This larger series confirms the high rate of AH (75%) that we observed in a previous study of patients with pulmonary KS.