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  • Factors Associated with Fatal Hemoptysis in Cancer Patients: Discussion

Unfortunately, diagnosis of fungal infections is difficult in immunocompromised patients. An antemor-tem diagnosis of fungal pneumonia was achieved in seven of eight patients in our study, but in two patients this diagnosis was made only from a sputum culture relatively late in the clinical course. Further, autopsies were not performed on all of our patients, and hence, cases of fungal pneumonia might have been undetected. Recent studies, however, have shown that bron-choalveolar lavage is superior to conventional bron-choscopic techniques in identifying fungal infections. The presence of pulmonary hemorrhage in immunocompromised patients with undiagnosed pulmonary infiltrates may also serve as a clue to the presence of a fungal infection, as 33 percent of our patients with a hematologic malignancy and hemoptysis had a fungal pneumonia. Similarly, Kahn and colleagues observed with bronchoalveolar lavage that 50 percent of patients with significant occult pulmonary hemorrhage had an Aspergillus pneumonia.

Our investigation might have overestimated the true incidence of fatal hemoptysis in immunocompromised patients with a fungal pneumonia, as less severe cases of hemoptysis might have been omitted owing to methodologic constraints. However, in another study, in which all patients with a hematologic malignancy and a fungal pneumonia were identified, a 40 percent incidence of massive pulmonary bleeding was observed in those patients with hemoptysis, confirming the frequent occurrence of fatal hemoptysis in these patients. diabet glucotror
The histopathologic data showed that fungal organisms cause pulmonary hemorrhage by vascular invasion, resulting in thrombosis, distal ischemic necosis, and hemorrhagic infarction. An additional finding was that granulocytes are not necessary for the vascular injury and consequent necrosis associated with fungal pathogens. Other investigators have observed tissue necrosis associated with fungal vascular invasion in the absence of a granulocytic infiltrate on pathologic specimens from similar patients. Release of a proteolytic enzyme by Aspergillus spp may play a role in this destructive process. This conclusion differs from that of Albelda and coworkers, who observed an association between bone marrow recovery and the appearance of cavitary lesions on chest x-ray film in leukemic patients with invasive pulmonary aspergillosis, some of whom developed massive hemoptysis. However, this association may be questionable, because cavities have been observed on chest roentgenograms in leukemic patients with granulocytopenia, and chest roentgenography may not be a sensitive technique for the detection of fungus-associated necrotic lung tissue.

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