Influence of allergy on the immunomodulatory and clinical effects of long-term low-dose macrolide treatment of nasal polyposis (original) (raw)

Aims. Cytokine levels in nasal secretions reflect the inflammatory status of the nasal and paranasal sinus mucosa and the development of mucosal disease. The results of previous investigations suggest that macrolide antibiotics can be effective in treatment of chronic rhinosinusitis and nasal polyposis. The aim of this prospective study was to compare the immunomodulatory and clinical effects of long-term low-dose macrolide treatment of nonatopic and atopic patients with nasal polyposis. Methods. Forty (n = 40) patients with nasal polyposis, 22 allergic and 18 nonallergic were administered clarithromycin (CAM) 500 mg/day single oral dose for eight weeks. We measured the levels of proinflammatory Th1 cytokines TNF-α and IL-1β, Th2 cytokines IL-4, IL-5 and IL-6, and chemokine IL-8 in the nasal fluid samples, before and after treatment, using flow cytometric method. We also scored each of the 40 patients before and after therapy according to nasal symptom score and endoscopic score. Results. Following treatment, we found significantly reduced levels of IL-8 (p<0.01) and TNF-α (p<0.01) in nasal secretions in nonallergic patients. In subjects with nasal polyposis and allergy, we found decreased levels of IL-8 (p<0.01), IL-6 (p<0.05) and IL-1β (p<0.01). Macrolide therapy decreased the size of polyps in 45.45% of nonatopic and in 50% of atopic patients. After macrolide treatment, we found 67.83% patients in nonallergic group and 55.55% patients in allergic group with improved nasal symptoms. Conclusions. Long-term low-dose treatment with CAM was effective in the management of nasal polyposis. Our results showed that macrolide treatment of nasal polyposis have different immunomodulatory and similar clinical effects in allergic and nonallergic patients. tegrated process of mucosal epithelium, lamina propria and inflammatory cells, which, in turn, may be initiated by both infectious and noninfectious inflammation 1. Nasal polyposis is an example of an extreme immune dysregulation 2. The mechanisms responsible for selective accumulation of eosinophils and neutrophils in polyps are unknown. Nasal polyp fibroblasts could play a role in the recruitment of eosinophils and neutrophils through the release of RANTES (regulated on activation, normal T cell expressed and secreted) and GM-CSF (granulocytemacrophage colony-stimulating factor) 3. Several cytokines (interleukin (IL)-4, IL-5, IL-6, IL-8, tumor necrosis factoralpha (TNF-α), RANTES, GM-CSF) have been shown to be upregulated in nasal polyposis, suggesting that resident structural cells can produce a number of molecules to attract inflammatory cells and prolong their survival. These inflammatory cells themselves can also produce cytokines which recruit more inflammatory cells in an autocrine fashion 3. Although surgery has been the preferred treatment for nasal polyposis for a long time, a change in the treatment strategy in recent years has lead to greater use of medica-ABBREVIATIONS IL-Interleukin TNF-Tumor necrosis factor