To the Editor:
We appreciate the comments and concerns raised by Rossi et al.1 regarding our report on histologic findings in a patient with coronavirus disease 2019 (COVID-19).2 As noted by Rossi et al.,1 it is possible that the coexisting tumor-related obstructive pneumonitis and comorbidities might have interfered with the interpretation of the histologic findings of patient 1; we would like to address this accordingly.
Obstructive pneumonitis is always observed in the lung parenchyma distal to the bronchial obstruction by a neoplasm. Patient 1 had squamous cell carcinoma, which was located at the posterior basal segment of the right lower lobe. As described in our report, an extensive interstitial inflammation of the lung was consistently observed on multiple sections, which were multisampled far from the tumor at other segments; obviously, these findings should not be considered as the result of the obstruction by the tumor.
Moreover, interpretation of the findings, given the background of the patient’s comorbidity, needs extra caution. Patient 1 had interstitial lung disease and presented the usual radiographic pattern of interstitial pneumonia. The most characteristic histologic feature of interstitial pneumonia is patchy interstitial fibrosis admixed with normal parenchyma, whereas infiltration by lymphocytes and plasma cells is generally sparse.3 However, the pathologic examination of patient 1 revealed interstitial inflammation with numerous plasma cell infiltrations and a large number of macrophages and foam cells in the alveoli. The histologic features were distinctively different from those of interstitial pneumonia. In a recent study, a predominantly large number of activated plasma cells with scattered alveolar macrophages were found in the bronchoalveolar lavage specimen from a patient with COVID-19.4 The findings of this study suggest that the peculiar abundance of CD138-positive plasma cells in COVID-19 may be a relevant feature.
It is definitely true that preexisting or coexisting disease might hamper the correct understanding of the morphologic changes in COVID-19, particularly in the absence of diffuse alveolar damage that has been found to be the salient feature of COVID-19 pneumonitis on microscopy.5 Nevertheless, it should be noted that, in our report, the lung specimen was taken when the patient had no symptoms, and the pathology is always consistent with the disease severity. Although there is currently lack of solid data to make an assertion, we still have reasons to speculate that the extensive interstitial inflammation with plasma cell and macrophage infiltration, and also the numerous macrophages in the alveoli might be a pathologic change related to COVID-19.
References
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