The pathophysiology of how PCP results in the formation of cysts, blebs, pneumatoceles, and eventual pneumothorax is unknown. Several mechanisms have been proposed for the cyst formation and presumed tissue destruction, including direct tissue toxicity by the organims, overdistention caused by inflamed bronchioles, and the prolonged presence of activated macrophages with the elaboration of elastase and other enzymes. Excess respiratory efforts or localized bronchiolar obstruction can lead to the development of pneumothorax. We are unaware of any reports implicating an association between pneumothorax and administration of medications commonly used to treat PCP and HIV infection, including trimethoprim-sulfamethoxazole, parenteral pentamidine, trimetho-prim-dapsone, and zidovudine. None of the patients in this study received aerosolized pentamidine; therefore, our data provide potentially useful historical information to assess whether the sadministration of aerosolized pentamidine also predisposes to pneumothorax.
That the pneumothorax resolved in all eight patients is noteworthy given the experience reported in the literature.
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