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Hanyang University Hospital Seoul 133-792, South Korea
I read with great interest the article by Kang et al. [1]. The authors reported that in immunocompetent hosts who have no preexisting lesions of the lung, pulmonary aspergillosis might manifest on CT primarily as a single nodule or mass with or without an air crescent or as a localized consolidation. They termed the pattern "primary noninvasive pulmonary aspergillosis."
Unfortunately, the evidence that no preexisting underlying lesion was present is not clear in the article [1]. Did the authors draw that conclusion only because chest radiography or CT showed no other coexisting lesion? In that case, it should have been noted that diseases such as pneumonia, bronchial cyst, bulla, or lung abscess may show a single lesion, and patients who have aspergilloma that developed in such preexisting diseases may show no other lesion on radiologic studies. I think previous radiologic studies of the chest are essential to prove the absence of these preexisting diseases, but the authors did not mention previous studies. Previous CT scans showing no abnormality would be confirmatory evidence for the authors' conclusion. However, previous chest radiographs do not afford a solid basis for their conclusion because frequently a small thin-walled bronchial cyst or bulla that is visible on chest CT is not observed on chest radiographs.
As a basis for the new pattern of aspergillosis, the authors [1] presented a theory that the fungus might be implanted in a normal bronchus, which then gradually becomes dilated as a result of the pressure created by a growing colony [2]. The theory was originally from a French article [3]. I don't know how such a conclusion was drawn in the study by Monod et al. because the article was not available. I presume that in 1957 when their article was published, chest radiographs obtained before the development of aspergilloma must have been the only way to determine the absence of preexisting abnormalities. However, chest radiographs with normal findings do not exclude small thin-walled cysts absolutely. Thus, the theory does not appear to be a reliable basis for defining primary noninvasive aspergillosis.
Without evidence for the absence of preexisting diseases, the reported pathologic features [1] don't appear different from secondary noninvasive aspergillosis. It is certain that the reported findings are unusual for secondary noninvasive pulmonary aspergillosis. The article would have been better if it had reported only unusual appearances of secondary noninvasive pulmonary aspergillosis.
References
College of Medicine, Korea University Seoul, 152-050, Korea
We thank Dr. Choi for the interest in and critique of our article, "Pulmonary aspergillosis in immunocompetent hosts without underlying lesions of the lung: radiologic and pathologic findings" [1]. The letter raises two main concerns that merit further discussion.
The first issue raised was that we failed to present evidence that no preexisting underlying lesions existed. As stated in the article [1], the patients were in an immunocompetent state and had no recognized underlying lesions of the lung. It is difficult to prove that they did not have underlying lung disease, even with the help of previous chest CT scans with normal findings—and these are unavailable in the clinical setting most of the time. We agree that the process of proving that patients were without underlying lung disease was limited, and discussion of the process was further shortened during revision of the manuscript. However, the patients discussed in the article were discovered to have an abnormality on chest radiography for the first time—and it was the only abnormality detected on radiography. Subsequent CT depicted the abnormality and confirmed the absence of other underlying parenchymal abnormalities. These patients had no underlying lung disease clinically. None had a history of pulmonary disease or abnormal findings on radiography of the chest. All were in a nonneutropenic immunocompetent state and were not taking medication associated with immunosuppression. No patient had known occupational exposure to Aspergillus. No one had asthma. Therefore, we believed that the patients were in an immunocompetent state without underlying lesions of the lung.
The second major concern expressed in Choi's letter regarding our article [1] is our statement of primary noninvasive aspergillosis. Aspergillus organisms cause a variety of pulmonary diseases. Pulmonary aspergillosis can be divided into several typical patterns of disease that are mainly dependent on the patient's immune status and underlying lung architecture. Aspergilloma in immunocompetent hosts, semiinvasive aspergillosis in those in a mildly immunosuppressed state, invasive pulmonary aspergillosis in immunocompromised hosts, and allergic bronchopulmonary aspergillosis in those in a hypersensitive state are well-known manifestations. However, some patients do not fall into these patterns of aspergillosis, and occasional overlap occurs between various types of aspergillosis [2]. In our article, the absence of prior recognized lung disease separates this form from more typical secondary noninvasive aspergillosis. In addition, the absence of any recognized immunocompromised or hypersensitive states separates this form from more typical secondary invasive aspergillosis, semiinvasive aspergillosis, or allergic bronchopulmonary aspergillosis.
We used the term "primary" because the lesion was detected for the first time in an immunocompetent patient with no recognized underlying lung disease, although our study was limited in proving that no evidence of underlying lung disease was present because we had no previously obtained chest CT scans with normal findings for comparison. For probable pathogenesis explaining some nodule or mass in our article, we quoted Zimmermann and Miller [3], although we did not have the original French article that they cited [4] or the results of the experimental studies it presented. Because our patients had no recognized underlying lung disease, their aspergilloma may have been the result of the fungus having been implanted in a normal bronchus that was gradually dilated by the pressure of the growing fungus—rather than by the saprophytic growth in unrecognized preexisting lung cavity, cyst, or bulla. The histologic findings of aspergilloma in our surgical cases were the same as those of secondary invasive aspergillosis; however, these patients showed no other underlying lung disease. We used the term "noninvasive" because aspergilloma without tissue or vascular invasions was revealed histologically in surgical cases.
Aspergillus organisms are able to produce a wide spectrum of diseases, and the cases in our article [1] have differential points distinguishing them from the more typical patterns of aspergillosis. Rather than a new pattern of pulmonary aspergillosis, these cases could be characterized as less noticed or unrecognized by most radiologists.
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