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Biomedical subjects

C Lamblin

Publications and source records attributed to C Lamblin.

At least 19 recordsLinked to original sources
PubMed2002

Airway neutrophil inflammation in nonasthmatic patients with food allergy.

BACKGROUND: Patients with food allergy (FA) have been recently shown to develop bronchial hyperresponsiveness (BHR), despite the absence of any concomitant asthmatic manifestation. In order to explain this observation, we sought to examine the presence of a bronchial inflammation in induced sputum of nonasthmatic patients with FA. METHODS: Twelve nonasthmatic patients with FA (urticaria, digestive symptoms, anaphylaxis) were included in the study. Results were compared to these obtained from eight asthmatic patients without food allergy and eight healthy controls. Diagnosis of FA was based on double-blind placebo-controlled challenge. Sputum cells and fluid-phase eosinophil cationic protein (ECP), myeloperoxidase (MPO) and interleukin-8 (IL-8) were measured in induced sputum. BHR was evaluated using methacholine inhalation. RESULTS: Sputum from asthmatics, in comparison with the sputum of healthy subjects and patients with FA contained a higher proportion of eosinophils and higher levels of ECP (< 0.001). In marked contrast, patients with FA exhibited an increased proportion of neutrophils and IL-8 in comparison with asthmatics and controls (P < 0.05 for neutrophils and P < 0.001 for IL-8). There was a significant correlation between sputum neutrophils and IL-8 (r = 0.68, P < 0.001). MPO levels were not different between the groups. There was a trend toward higher levels of IL-8 and ECP in food allergic patients with BHR in comparison with patients with FA without BHR. CONCLUSION: Our results demonstrate that a subclinical neutrophil airway inflammation is present in patients with food allergy free of clinical respiratory symptoms and that IL-8 may be an important mediator of this neutrophilia.

Adult↗
PubMed2002

[The anti-synthetase syndrome].

The anti-synthetase syndrome comprises the association of an inflammatory myopathy (polymyositis, dermatomyositis), interstitial pneumonitis, skin lesions characteristic of "mechanics hands", Raynaud's phenomena, inflammatory polyarthritis and, at the biological level, antinuclear antibodies known as anti-synthetases. We report our observations of two patients, one with a typical anti-synthetase syndrome and one with an incomplete form. Two men aged 49 and 47 presented with increasing dyspnoea upon effort, muscular weakness, arthralgia, bilateral pulmonary crackles and, in the first case, typical hairless skin lesions. In both cases the chest x-rays and CT scans confirmed the presence of interstitial lesions, predominantly in the lower lobes. Lung function tests showed a restrictive pattern with reduced gas transfer. At the biological level both patients presented an inflammatory picture with elevated muscle enzymes and anti-Jo-1 antibodies. Immuno-suppressive treatment with cortico-steroids and cyclophosphamide lead to a symptomatic improvement, regression of the radiological changes and improvement in the measurements of pulmonary function.

Antibodies, Antinuclear↗
PubMed2001

Cell and cytokine profiles in nasal secretions from patients with nasal polyposis: effects of topical steroids and surgical treatment.

BACKGROUND: Nasal polyposis (NP), a chronic inflammatory disease of the paranasal sinus mucosa, is frequently associated with asthma. Previous reports showed that surgical treatment for nasal polyps may influence asthma evolution. We hypothesized that sinus surgery may alter the cytokine network in nasal secretions. METHODS: We evaluated the characteristics (cells and mediators) of nasal lavages in nine patients with untreated NP (group A), 17 patients treated with topical steroids (group B), 21 patients treated by nasal surgery endonasal ethmoidectomy associated with topical steroids (group C), and 12 healthy subjects (controls). RESULTS: Percentages of both eosinophils and neutrophils were higher in NP patients than in controls. Percentages of eosinophils and interleukin-5 (IL-5) level were higher in group A than in group C and controls. There was a positive correlation between IL-5 and eosinophils. In marked contrast, IL-8, IL-10, and IL-1beta levels were significantly higher in group C than in groups A and B and controls; TNF-alpha concentration was significantly lower in group C than in groups A and B and controls; and there was a negative correlation between IL-10 and TNF-alpha. The percentage of eosinophils was higher in asthmatic patients with NP than in nonasthmatic patients. In addition, in group C, asthmatic patients also had a significantly higher level of IL-10 than nonasthmatic patients. CONCLUSIONS: Our study demonstrates that percentages of eosinophils and neutrophils, and IL-5 level were increased in nasal secretions from untreated patients with NP. Topical steroid treatment is associated with a decrease of inflammatory cells and mediators. In marked contrast, nasal surgery is associated with marked changes, in cytokine profile in nasal secretions, that are clearly different from those of controls and topical steroid-treated NP patients.

Administration, Topical↗
PubMed2001

Overexpression of IL-10 mRNA in gut mucosa of patients with allergic asthma.

Because an airway-like inflammation has been reported in the gut of asthmatic patients, we sought to examine the expression of immunoregulatory cytokines like IL-4, IL-10, and IL-13 by gut mucosa. To establish this, we initiated this study to examine mRNA expressions of IL-4, IL-10, and IL-13 in duodenal mucosa from patients with asthma. Duodenal biopsy specimens were obtained from 20 asthmatic patients (10 allergic, 10 nonallergic) and 8 healthy controls. Cytokine mRNA was quantified with reverse transcriptase-competitive PCR, and results were expressed in proportion to the number of beta-actin mRNA in the same sample. IL-10 and IL-4 mRNA were detectable in all patients, whereas no IL-13 mRNA was detected. IL-10 mRNA concentrations were significantly higher in allergic subjects with asthma than in control subjects and nonallergic subjects with asthma. No significant difference was observed for IL-4. IL-10 mRNA expression was not related to asthma severity, FEV(1), blood eosinophilia, or IgE levels. Our results support the hypothesis that IL-10 overexpression may counterbalance the effects of proinflammatory cytokines and mitigate the inflammatory reaction found in gut mucosa of subjects with asthma.

Adult↗
PubMed2001

Bronchial interleukin-5 and eotaxin expression in nasal polyposis. Relationship with (a)symptomatic bronchial hyperresponsiveness.

An eosinophilic bronchial inflammation was previously demonstrated in patients with nasal polyposis (NP) and asymptomatic bronchial hyperresponsiveness (BHR) similar to that observed in asthmatic patients with NP, whereas patients with NP without BHR did not. The aim of the study was to investigate the contribution of interleukin 5 (IL-5) and eotaxin to the pathogenesis of BHR associated with NP. Eleven patients with NP without BHR (Group A), 8 patients with NP and asymptomatic BHR (Group B), and 9 patients with NP and asthma (Group C) were included. Bronchial biopsies were studied for IL-5 and eotaxin immunoreactivity and IL-5 mRNA expression. IL-5 levels were determined in bronchial lavage (BL). Compared with Groups A and B, Group C patients exhibited higher numbers of IL-5 protein(+) cells, IL-5 mRNA(+) cells, and eotaxin(+) cells in bronchial submucosa. Compared with Group A, Group B patients showed an increased number of IL-5 protein(+) cells, whereas the number of IL-5 mRNA(+) cells and eotaxin(+) cells was similar. IL-5 levels in BL were increased only in Group C. Our study provides evidence of IL-5 involvement in bronchial eosinophilia and in the pathogenesis of asymptomatic BHR associated with NP, whereas both IL-5 and eotaxin are involved in asthma associated with NP.

Adult↗
PubMed2001

[Biological manifestations of sarcoidosis].

Sarcoidosis is a multisystem granulomatous disease of unknown origin. No single biological marker allows definitive diagnosis of sarcoidosis or may accurately predict the disease prognosis. However, some biological markers are helpful tools as diagnostic aids and disease activity markers. At the blood level, lymphopenia with CD4 depletion, elevated levels of serum-angiotensin converting enzyme, lyzozyme, beta 2 microglobulin and disturbed calcium metabolism resulting in hypercalcemia and hypercalciuria can help guide diagnosis. Lymphocytic alveolitis with a high CD4/CD8 ratio in bronchoalveolar lavage fluid is highly suggestive of the disease. A wide range of new biological markers are proposed but their pronostic significance is still controversial. In clinical practice, biological markers may help in monitoring treated patients with sarcoidisis.

Biomarkers↗
PubMed2001

[Respiratory bronchiolitis with diffuse interstitial lung disease].

Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) is a disease that exclusively affects cigarette smokers. Long-term prognosis is good with cessation of smoking, in combination or not with corticosteroid therapy. We report here the case of a 50-year-old patient with RB-IL diagnosed on lung biopsy. Despite corticosteroid and cyclophosphamide therapy, no functional or radiological improvement was obtained. In contrast, cessation of smoking was associated with the disappearance of the infiltrative opacities. Clinical and radiological parameters remained stable during follow-up (13 years) while a moderate obstructive pattern appeared.

Adrenal Cortex Hormones↗
PubMed2001

Interstitial lung diseases in collagen vascular diseases.

In this review, a clinical update is presented of the most important collagen vascular diseases (CVDs) and the different types of interstitial lung disease (ILD) encountered in these CVDs. These CVDs represent a heterogenous group of immunologically mediated inflammatory disorders with a large variety of affected organs besides the lungs. The frequency, clinical presentation, prognosis and response to therapy vary depending on the histological pattern (usual interstitial pneumonia, desquamative interstitial pneumonia, organising pneumonia, diffuse alveolar damage, nodular lesions, etc.), as well as on the underlying CVD (scleroderma, rheumatoid arthritis, systemic lupus erythematosus, dermatopolymyositis, Sjogren's syndrome or mixed connective tissue disease). The diagnosis of most of these CVDs is based on a number of criteria; in several of these, however, lung involvement is not part of the diagnostic criteria. In addition, there may be overlaps between several of these CVDs. Optimal treatment varies depending on the type of collagen vascular disease and the presence of interstitial lung disease, although in many cases, a combination of corticosteroids and cytostatic drugs are given.

Arthritis, Rheumatoid↗
PubMed2000

[Idiopathic pulmonary fibrosis: from biopathology to treatment].

Alveolitis, accumulation of immune and inflammatory cells within the lower respiratory tract, is the key to the development of pulmonary fibrosis. Alveolitis is responsible for lung injury (due to release of oxidant and proteolytic enzymes) and exaggerated lung repair (due to proliferation of mesenchymal cells and imbalance of collagen synthesis). Rationale for the treatment of pulmonary fibrosis implies the knowledge of pathophysiology of the different steps of the fibrotic process.

Cell Division↗
PubMed2000

Increased frequency of asymptomatic bronchial hyperresponsiveness in nonasthmatic patients with food allergy.

Subclinical inflammation in gut mucosa has been demonstrated in bronchial asthma suggesting the whole mucosal system is involved in allergic diseases. The presence of subclinical bronchial involvement was assessed by nonspecific bronchial hyperresponsiveness (BHR) in nonasthmatic patients with food allergy (FA). BHR was studied in 35 patients with various manifestations of FA without food-induced asthma. Sixteen had a previous history of asthma and/or rhinitis to aeroallergens (group A), whereas 19 patients (group B) did not. BHR was defined by a provocative dose causing a 20% fall in forced expiratory volume in one second of (PC20) <8 mg.mL(-1) of methacholine. Asymptomatic BHR occurred frequently in nonasthmatic patients with FA (10 of 19, 53%); this did not significantly differ from patients with FA and a previous history of asthma and/or rhinitis to aeroallergens (13 of 16, 81%). PC20 was significantly lower in group A (1.84+/-0.53 mg.mL(-1)) than in group B (3.35+/-0.74 mg.mL(-1); p<0.05). The number of patients with positive skin tests to aeroallergens was similar between groups. Sequential evaluation, performed 1 year after initial evaluation, in 7 nonasthmatic patients (group B) demonstrated a similar level of BHR. The present study demonstrated that BHR is a frequent finding in nonasthmatic patients with food allergy which may be due, at least in part, to a subclinical inflammatory process in the bronchi.

Adult↗
PubMed2000

Cytokine profile in minor salivary glands from patients with bronchial asthma.

BACKGROUND: T lymphocytes are important components of the bronchial inflammatory cell infiltrate in asthma. Because lymphocytes activated in the respiratory tract recirculate to remote glandular and mucosal sites, we previously studied the histologic features of minor salivary glands (MSGs) in bronchial asthma and found an airway-like inflammation with T-lymphocyte infiltration, the presence of mast cells that were often degranulated, and basement membrane thickening but no eosinophil infiltration. OBJECTIVE: We sought to investigate the cellular infiltration and cytokine profile in MSGs from untreated asthmatic subjects, steroid-treated asthmatic subjects, and control subjects and to compare these values with those found in bronchial biopsy specimens. METHODS: The cellular infiltration was studied by using immunohistochemistry. Cytokine messenger (m)RNA expression for IL-4, IL-5, and IFN-gamma was determined by using in situ hybridization and cytokine immunoreactivity with immunohistochemistry. RESULTS: A significant increase in CD4 and IL-4 mRNA(+) cells was observed in MSGs from asthmatic patients (both untreated and steroid-treated subjects) when compared with control subjects, which correlated with the clinical severity of asthma (FEV(1) and Aas score). In contrast to the bronchi, no IL-5 mRNA expression was observed in MSGs, and no difference was observed for MSG IFN-gamma mRNA between the groups. At the level of MSG protein expression, the 3 cytokines were seen, with a significant increase in IL-4 protein expression in steroid-treated asthmatic subjects compared with untreated asthmatic subjects and control subjects, but there were no differences between the groups in IL-5 and IFN-gamma protein expression. CONCLUSION: The cytokine mRNA expression pattern observed in the MSGs of asthmatic subjects was different from that found in the bronchi, suggesting a different local immune regulation.

Adult↗
PubMed2000

Long-term follow-up of pulmonary function in patients with nasal polyposis.

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.

Administration, Intranasal↗
PubMed2000

[Allergic bronchopulmonary aspergillosis].

Allergic bronchopulmonary aspergillosis (ABPA) is an immunologic bronchopulmonary inflammation due to an immune response of the lower respiratory tract against Aspergillus fumigatus. The major clinical features of ABPA include asthma, recurrent pulmonary infiltrates, immediate wheal and flare skin reactivity to A. fumigatus, elevated total serum IgE levels, detectable serum precipitating antibodies to A. fumigatus, peripheral blood eosinophilia, elevated levels of Aspergillus-specific serum IgE and central bronchiectasis with normal distal structures. The diagnosis of ABPA should be considered in asthmatics of all ages. Evolution of the disease comprises five stages from the acute to the fibrotic stage including pulmonary fibrosis and respiratory insufficiency. The goals of ABPA treatment are to control patient's asthma and prevent exacerbations of ABPA. During the acute stage, prednisone should be administered. Antifungals agents (itraconazole) may be useful to prevent exacerbations of the disease.

Aspergillosis, Allergic Bronchopulmonary↗
PubMed2000

[The common mucosal immune system in respiratory disease].

The principal function of the mucosal immune system is to protect the mucosa from exogenous aggression. It also involves a lymphocyte recirculation phenomenon allowing activated lymphocytes to migrate to the aggressed site, for example the bronchi, and to recirculate and colonize other sites of the mucosal immune system. In asthma, analysis of the other sites of the common mucosal immune system demonstrates asthma-like inflammatory reactions in the accessory salivary glands and the gut: lymphocyte infiltrate, mast cell activation, thickening of the basal membrane, accumulation and activation of eosinophils (gut), activation of endothelial cells expressing ICAM-1. Lymphocyte, eosinophil and mast cell infiltration is observed in the digestive tract as well as increased expression of IL-3, IL-5 and GM-CSF. The similarity of the anomalies observed in BALT and GALT tissues would suggest the entire mucosal immune system is implicated in asthma.

Asthma↗
PubMed1999

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.

Adult↗
PubMed1999

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.

Adult↗