The optimal management of postintubation tracheal stenosis is not well defined.A therapeutic algorithm was designed by thoracic surgeons, ear, nose and throat (ENT) surgeons, anaesthetists and pulmonologists. Rigid bronchoscopy with neodymium±yttrium aluminium garnet (Nd-YAG) laser resection or stent implantation (removable stent) was proposed as first-line treatment, depending on the type of stenosis (web-like versus complex stenosis). In patients with web-like stenoses, sleeve resection was proposed when laser treatment (up to three sessions) failed. In patients with complex stenoses, operability was assessed 6 months after stent implantation. If the patient was judged operable, the stent was removed and the patient underwent surgery if the stenosis recurred.This algorithm was validated prospectively in a series of 32 consecutive patients. Three patients died from severe coexistent illness shortly after the first bronchoscopy. Of the 15 patients with web-like stenosis, laser resection was curative in 10 (66%). Among the 17 patients with complex stenoses, three remained symptom-free after stent removal. Bronchoscopy alone was thus curative in more than one-third of the patients. Six patients underwent surgery, two after failure of laser resection and four after failure of temporary stenting. Surgery was always performed with the patient in good operative condition. Palliative stenting was the definitive treatment in nine cases. Tracheostomy was the definitive solution in two cases.This approach, including an initial conservative treatment, depending on the type of the stenosis, appears to be applicable to almost all patients and allows secondary surgery to be performed with the patient in good condition. Eur Respir J 1999; 13: 888±893.

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Status asthmaticus (SA) is an acute respiratory failure combining an acute bronchospastic reaction with a severe airway inflammation. We previously reported an important influx of neutrophils and an increased secretion of interleukin-8 (IL-8) in patients with SA. The aim of this prospective study was to evaluate in bronchial lavage (BL) of patients with SA (n = 9) under mechanical ventilation (MV) the concentrations of cytokines and related mediators which have the ability to modulate inflammation, either proinflammatory (interleukin-1beta [IL-1beta], IL-6, tumor necrosis factor-alpha [TNF-alpha]), or anti-inflammatory mediators (IL-10, transforming growth factor-beta1 [TGF-beta1]), interleukin-1 receptor antagonist [IL-1Ra], soluble TNF receptor I and II [sTNFRI and II]). To determine the relative importance of both pro- and anti-inflammatory mediators, the net inflammatory activity was analyzed by the capacity of BL fluids (BLF) to increase intercellular adhesion molecule-1 (ICAM-1) expression in the human lung A549 epithelial cell line. These data were compared with those obtained from patients who required MV without respiratory disease (V, n = 4), controlled asthma (A, n = 11), and nonsmoking healthy volunteers (C, n = 8). Levels of IL-1, IL-6, TNF-alpha, and of the active form of TGF-beta1 were significantly higher in SA compared with the other groups. The concentrations of IL-1Ra, IL-10, the latent form of TGF-beta1, and of the sTNFRI and II were not significantly different between SA and V, albeit higher in SA than in A and C. The ratio between IL-1Ra and IL-1beta was significantly higher in patients with SA compared with the other groups, whereas there was no difference for the ratio between both types of sTNFR and TNF-alpha. Despite a marked increase of anti-inflammatory mediators in BL from patients with SA, the net inflammatory activity was found to be proinflammatory and mainly due to the presence of bioactive IL-1beta (79% inhibition of ICAM-1 expression with anti-IL-1beta antibodies) and to a lesser extent TNF-alpha (32% inhibition with anti-TNF-alpha antibodies).

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Background The etiology of Dupuytren's disease is unknown, and the role of occupational exposure is still debated. Our objective was to study the association between occupational exposures, personal risk factors and Dupuytren's disease. Methods In this cross‐sectional survey, nine occupational physicians performed clinical examinations, focused on Dupuytren's disease, of 2,406 French male civil servants employed at the Equipment Ministry in 1998 and interviewed them about medical history, leisure manual exposure and occupational biomechanical exposure to vibrations and manual work. A cumulative occupational exposure score was defined, with three levels of exposure. Results Dupuytren's disease was diagnosed in 212 men (8.8%). The occupational exposure score was significantly higher in this group of cases than in the rest of the sample (377 (SD280) vs. 223 (SD250), respectively; P < 0.0001). Occupational exposure was associated with Dupuytren's disease (adjusted Odds Ratio = 2.20 [1.39–3.45] for the intermediate and 3.10 [1.99–4.84] for the high exposure groups), with adjustment for age, leisure physical activities, alcohol consumption (≥5 servings per day), history of diabetes, epilepsy, hand trauma, and familial history of Dupuytren's disease. Conclusion Manual work exposure was associated with Dupuytren's disease after adjustment for personal risk factors. Longitudinal studies are needed to confirm these results. Am. J. Ind. Med. 51:9–15, 2008. © 2007 Wiley‐Liss, Inc.

The outcome of asthma and/or nonspecific bronchial hyperresponsiveness (BHR) associated with nasal polyposis (NP) is uncertain. Over a 4-yr period, we investigated the long-term changes of pulmonary function and BHR in 46 patients with NP. Each subject was assessed for nasal symptoms and tested for allergy skin prick tests, serum total IgE, spirometry, and carbachol challenge at baseline before initiating any treatment (T0). Nasal symptoms evaluation, spirometric measurements, and carbachol challenge were repeated at T1 and at T2 (respectively, 12.7 +/- 0.9 and 47.9 +/- 2. 2 mo after T0). In addition, bronchodilator response was measured at T2. At T0, 25 patients exhibited BHR and 16 of 25 were asthmatic. All patients were treated first with topical steroids for 6 wk (beclomethasone 600 microg/d). Eighteen patients were successfully treated with topical steroids (topical steroids responders). Intranasal ethmoidectomy was performed in 28 patients who did not improve with topical steroids alone (topical steroids nonresponders). Nasal score improved at T1 and remained improved at T2 as compared with T0 in both groups (p < 0.005). Topical steroids nonresponders demonstrated a significant decrease of FEV(1), FEV(1)/FVC ratio, and FEF(25-75) at T1 (p < 0.05) and at T2 (p < 0.0005), whereas no significant change was observed in FEV(1) and FEV(1)/FVC ratio in responders. DeltaFEV(1) (%) between T2 and T0 was not related to the presence of asthma, BHR, or atopy. Bronchodilator response at T2 was similar in the two groups. BHR did not significantly change over the 4-yr follow-up period in the two groups. No change in pulmonary symptoms and/or asthma severity occurred. Our results show that nonreversible airflow obstruction appears over a 4-yr follow-up period in topical steroids nonresponders patients with NP requiring nasal surgery. The long-term contribution of these changes to the development of respiratory symptoms in patients with NP remains to be documented.

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Aside from its mechanical barrier function, bronchial epithelium plays an important role both in the host defense and in the pathogenesis of inflammatory airway disorders. To investigate its role in lung defense, the effect of a bacterial cell wall protein, the outer membrane protein A from Klebsiella pneumoniae (kpOmpA) on bronchial epithelial cells (BEC) was evaluated on adhesion molecule expression and cytokine production. Moreover, the potential implication of this mechanism in kpOmpA-induced lung inflammation was also determined. Our in vitro studies demonstrated that kpOmpA strongly bound to BEAS-2B cells, a human BEC line, and to BEC primary cultures, resulting in NF-κB signaling pathway activation. Exposure to kpOmpA increased ICAM-1 mRNA and cell surface expression, as well as the secretion of IL-6, CXC chemokine ligand (CXCL)1, CXCL8, C-C chemokine ligand 2, CXCL10 by BEAS-2B cells, and BEC primary cultures (p &lt; 0.005). We analyzed in vivo the consequences of intratracheal injection of kpOmpA to BALB/c mice. In kpOmpA-treated mice, a transient neutrophilia (with a maximum at 24 h) was observed in bronchoalveolar lavage and lung sections. In vivo kpOmpA priming induced bronchial epithelium activation as evaluated by ICAM-1 and CXCL1 expression, associated with the secretion of CXCL1 and CXCL5 in bronchoalveolar lavage fluids. In the lung, an increased level of the IL-6, CXCL1, CXCL5, CXCL10 mRNA was observed with a maximum at 6 h. These data showed that kpOmpA is involved in host defense mechanism by its ability to activate not only APC but also BEC, resulting in a lung neutrophilia.