Polypoid mucosa with eosinophilia and glandular hyperplasia in chronic sinusitis: A histopathological and immunohistochemical study

Objective: To evaluate the histopathological and immunohistochemical characteristics of chronic sinusitis, with reference to the extent of sinus involvement. Study Design: A nonrandomized, retrospective, controlled qualitative and quantitative study. Methods. Twenty-nine adults with refractory chronic sinusitis underwent functional endoscopic sinus surgery. The score of computed tomography scans was used to determine the extent of disease. Six patients with normal sinus mucosae served as control subjects. Specimens underwent routine histological processing and hematoxylin-eosin and periodic acid-Schiff staining. Immunohistochemistry for T and B lymphocytes was applied. Low-magnification microscopy was designed to yield typical pathological features, and high magnification to count various inflammatory cells. Results: Patients were divided into two groups according to their dominant pathological features: 16 had polypoid mucosa and eosinophilia, and 13 had glandular hyperplasia. The number of eosinophils, T and B lymphocytes in the lamina propria was significantly higher in patients with polypoid mucosa and eosinophilia, compared with those with glandular hyperplasia and with normal control subjects, whereas the difference between patients with glandular hyperplasia and control subjects was insignificant. Although the overall inflammatory reaction was relatively modest, nasal polyposis was more prevalent in patients with polypoid mucosa and eosinophilia; likewise, computed tomography revealed a significantly more extensive disease in these patients compared with the patients with glandular hyperplasia. Conclusion: Two pathophysiological pathways, inducing prolonged obstruction to the outflow of sinus secretion and ultimately causing chronic inflammation, are suggested: 1) swollen polypoid mucosa with activation of eosinophils that damage the epithelium and 2) continued increased mucus secretion originated from hyperplastic submucosal seromucous glands.