Quality of life in nasal polyposis.

BACKGROUND: Nasal polyposis (NP) is a frequent inflammatory chronic disease of the upper respiratory tract, which may impair quality of life (QOL). The NP impact, which is frequently associated with lower respiratory disorders, has never before been studied. OBJECTIVE: We initiated this prospective study to establish internal validity and reliability of the generic SF-36 questionnaire in NP and to determine to what level daily functioning becomes impaired as a result of NP. METHODS: Forty-nine consecutive patients with NP were included. They were assessed for the severity of nasal symptoms and underwent pulmonary function tests. The QOL profiles in patients with NP were compared with those of patients with perennial rhinitis (n = 111) and healthy subjects (n = 116). RESULTS: Cronbach's coefficient alpha demonstrated the high reliability and validity of the SF-36 questionnaire for patients with NP (alpha =.89). NP impaired QOL more than perennial allergic rhinitis (P <.05). The impairment of QOL was greater when NP was associated with asthma (P <.05). SF-36 scores appeared highly correlated to pulmonary function (FEV1, maximal midexpiratory flow, forced vital capacity), suggesting relationships between QOL in NP and associated bronchial obstruction. Severity of nasal symptoms were not related to QOL scales. In addition, sequential evaluations of QOL, nasal symptoms, and pulmonary function were performed 10 months after the first evaluation in 28 patients with NP. These evaluations demonstrated that NP treatment either with nasal steroids or endonasal ethmoidectomy significantly improved both nasal symptoms and QOL without significant change of pulmonary function. CONCLUSION: Our study clearly demonstrated that the SF-36 questionnaire presented a high internal validity and reliability in patients with NP. NP impaired QOL to a greater degree than perennial allergic rhinitis. QOL improvement after NP treatment is related to nasal symptoms improvement.

Eosinophilic airway inflammation in nasal polyposis.

BACKGROUND: Asthma and asymptomatic bronchial hyperresponsiveness (BHR) are frequent findings in patients with nasal polyposis (NP). OBJECTIVE: To elucidate mechanisms responsible for the development of BHR, we initiated a prospective study of bronchial inflammation as assessed by bronchial lavage (BL) and bronchial biopsy specimens in 35 patients with noninfectious NP. METHODS: BHR was determined with methacholine provocation testing. Differential cell count, ECP, and histamine and tryptase levels were determined in BLs. Pathologic examination of bronchial biopsy specimens was performed with May-Grünwald-Giemsa stain to assess the number of lymphocytes. Indirect immunoenzymatic methods were used to identify eosinophils and mast cells. RESULTS: Fourteen patients did not exhibit BHR (group A); 7 patients had asymptomatic BHR (group B); and 14 patients had BHR associated with asthma (group C). Patients of group C tended to have a longer duration of nasal symptoms than those of groups A and B. FEV1 (L) was significantly lower in group C than in groups A and B. The number and percentage of eosinophils were significantly higher in BLs in groups B and C than in group A (P <. 05). Patients of groups B and C had a significantly higher number of eosinophils in bronchial submucosa (14.0 +/- 1.5/mm2 and 19.0 +/- 1. 9/mm2, respectively) than patients of group A (0.1 +/- 0.1/mm2). The number of lymphocytes was also higher in groups B and C than in group A. FEV1 (percent of predicted value) and eosinophil number within bronchial mucosa correlated negatively. CONCLUSION: Our results demonstrate that patients with NP and asymptomatic BHR had an eosinophilic bronchial inflammation similar to that observed in asthmatic patients with NP, whereas patients with NP without BHR do not feature eosinophilic lower airways inflammation. The clinical relevance of these results requires careful follow-up to determine whether eosinophilic inflammation in these patients precedes and is responsible for the development of obvious asthma.

Interleukin-5 immunoreactivity and mRNA expression in gut mucosa from patients with food allergy.

BACKGROUND AND AIMS: Eosinophils, mast cells and T lymphocytes are important cells in the allergic inflammatory process. These cells produce and are regulated by cytokines such as interleukin-3 (IL-3), interleukin-5 (IL-5) and granulocyte macrophage-colony stimulating factor (GM-CSF). We initiated this study to evaluate pathological abnormalities and to detect IL-5 in the duodenal mucosa from patients with food allergy. METHODS: Endoscopy duodenal biopsy specimens were obtained from seven food-allergic patients, six atopic healthy controls and six nonatopic healthy controls. IL-5 protein was evaluated by immunohistochemistry. Electron microscopy as well as double immunofluorescent staining were used to identify the labelled cells and to localize IL-5. IL-5 mRNA expression was evaluated by qualitative polymerase chain reaction. RESULTS: A significantly increased number of lymphocytes, mast cells and eosinophils was detected in the lamina propria in food-allergic patients and, in lower number, in atopic controls. Immunostaining for IL-5 was markedly positive in food-allergic patients, slightly increased in atopic controls and negative in nonatopic controls. Ultrastructurally, in food-allergic patients and in atopic controls, IL-5 was localized in eosinophil granules, in the matrix of intact granules and at the periphery of altered granules. Double immunofluorescent staining was performed in food-allergic patients and showed that 86.7% of IL-5+ cells were eosinophils, and that IL-5 was expressed by 24% of eosinophils. IL-5 mRNA was expressed in food-allergic patients but was not detected in atopic and nonatopic controls. CONCLUSION: Activated eosinophils are involved in gut atopic reactions occurring in food allergy and are probably in part upregulated by their own local production of IL-5.

[Interstitial lung disease induced by timolol eye solution]. / Pneumopathie interstitielle induite par un collyre de timolol.

Timolol maleate is a beta-blocker widely used in topical administration for open angle glaucoma. We report a case of interstitial pneumopathy which developed in a 58-year-old patient who was given timolol eyedrops (2 drops b.i.d. since 1986). The patient presented with cough and dyspnea and was found to have a restrictive disorder leading to hypoxemia (68 mmHg at rest and 51 mmHg during exercise). Bronchial lavage fluid had high lymphocyte (28%) and neutrophil (7%) counts. Transbronchial biopsies demonstrated moderate fibrous thickening of the interalveolar walls. Timolol eyedrops were stopped. Three months later, the patient was asymptomatic with normal lung function, chest x-ray and thoracic CT-scan.

[Interstitial lung disease linked to fluoxetine]. / Pneumopathie interstitielle liée à la prise de fluoxétine.

Fluoxetine (Prozac) is a new anti-depressant introduced on the marked in France since 1989. We report a case of a patient who developed progressive dyspnea without any other symptoms who had been treated with Prozac for nine months. Clinical examination found bilateral basal crepitations. Laboratory assessments showed evidence of inflammation (ESR: 50 mm per hour; CRP 8.9 mg/l), the pulmonary radiograph and thoracic CT scan showed evidence of bilateral diffused interstitial disease. There was also a restrictive ventilatory defect (TLC 59 per cent predicted; FEV1 79 per cent predicted; FVC 70 per cent predicted), effort hypoxaemia and alveolar hyperlymphocytosis (35 per cent). The clinical, radiological and pulmonary function improved and the bronchoalveolar lavage became normal three months after stopping Prozac suggesting a role for this drug in the genesis of this interstitial pneumonia.