B Housset

Université Paris-Est Créteil Val de Marne - Université Paris 12, Créteil, Île-de-France, France

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Publications (157)399.76 Total impact

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    ABSTRACT: In Europe, administration of an inhaled corticosteroid (ICS) combined with a long-acting beta2 agonist is approved in chronic obstructive pulmonary disease (COPD) patients with a pre-bronchodilator FEV1 < 60% predicted normal, a history of repeated exacerbations, and who have significant symptoms despite regular bronchodilator therapy. Minimal data are available on the use of the fluticasone propionate / salmeterol xinafoate combination (FSC) in the real-life COPD setting and prescription compliance with the licensed specifications. A French observational study was performed to describe the COPD population prescribed with FSC, prescription modalities, and the coherence of prescription practices with the market authorized population. Data were collected for patients initiating FSC treatment (500 mug fluticasone propionate, 50 mug salmeterol, dry powder inhaler) prescribed by a general practitioner (GP) or a pulmonologist, using physician and patient questionnaires. A total of 710 patients were included, 352 by GPs and 358 by pulmonologists. Mean age was over 60 years, and 70% of patients were male. More than half were retired, and overweight or obese. Approximately half were current smokers and one-third had cardiovascular comorbidities. According to both physician evaluation and GOLD 2006 classification, the majority of patients (>75%) had moderate to very severe COPD. Strict compliance by prescribing physicians with the market-approved population for dry powder inhaler SFC in COPD was low, notably in ICS-naive patients; all three conditions were fulfilled in less than a quarter of patients with prior ICS and less than 7% of ICS-naive patients. Prescription of dry powder inhaler SFC by GPs and pulmonologists has very low conformity with the three conditions defining the licensed COPD population. Prescription practices need to be improved and systematic FEV1 evaluation for COPD diagnosis and treatment management should be emphasized.
    BMC Pulmonary Medicine 04/2014; 14(1):56. · 2.76 Impact Factor
  • F. Chabot, A. Didier, B. Housset
    Revue des Maladies Respiratoires. 01/2014; 31(1):6–7.
  • F Chabot, A Didier, B Housset
    Revue des Maladies Respiratoires 01/2014; 31(1):6-7. · 0.50 Impact Factor
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    ABSTRACT: Given the interest in defining biomarkers of asbestos exposure and to provide insights into asbestos-related and cell-specific mechanisms of neoplasia, the identification of gene alterations in asbestos-related cancers can help to a better understanding of exposure risk. To understand the aetiology of asbestos-induced malignancies and to increase our knowledge of mesothelial carcinogenesis, we compared genetic alterations in relevant cancer genes between lung cancer, induced by asbestos and tobacco smoke, and malignant pleural mesothelioma (MPM), a cancer related to asbestos, but not to tobacco smoke. TP53, KRAS, EGFR and NF2 gene alteration analyses were performed in 100 non-small cell lung cancer (NSCLC) patients, 50 asbestos-exposed and 50 unexposed patients, matched for age, gender, histology and smoking habits. Detailed assessment of asbestos exposure was based on both specific questionnaires and asbestos body quantification in lung tissue. Genetic analyses were also performed in 34 MPM patients. TP53, EGFR and KRAS mutations were found in NSCLC with no link with asbestos exposure. NF2 was only altered in MPM. Significant enhancement of TP53 G:C to T:A transversions was found in NSCLC from asbestos-exposed patients when compared with unexposed patients (P = 0.037). Interestingly, TP53 polymorphisms in intron 7 (rs12947788 and rs12951053) were more frequently identified in asbestos-exposed NSCLC (P = 0.046) and MPM patients than in unexposed patients (P < 0.001 and P = 0.012, respectively). These results emphasise distinct genetic alterations between asbestos-related thoracic tumours, but identify common potential susceptibility factors, i.e. single nucleotide polymorphisms in intron 7 of TP53. While genetic changes in NSCLC are dominated by the effects of tobacco smoke, the increase of transversions in TP53 gene is consistent with a synergistic effect of asbestos. These results may help to define cell-dependent mechanisms of action of asbestos and identify susceptibility factors to asbestos.
    Mutagenesis 02/2013; · 3.50 Impact Factor
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    ABSTRACT: The hypothesis that asbestos exposure may have more specific associations with particular histological types of lung cancer remains controversial. The aim of this study was to analyze the relationships between asbestos exposure and pulmonary carcinoid tumors. A retrospective case-control study was conducted in 28 cases undergoing surgery for pulmonary carcinoid tumors and aged >40 years and in 56 controls with lung cancer of a different histological type, matched for gender and age, from 1994 to 1999, recruited in two hospitals in the region of Paris. Asbestos exposure was assessed via expertise of a standardized occupational questionnaire and mineralogical analysis of lung tissue, with quantification of asbestos bodies (AB). Definite asbestos exposure was identified in 25% of cases and 14% of controls (ns). Cumulative asbestos exposure was significantly higher in cases than in controls (P < 0.05), and results of the quantification of AB tended to be higher in cases than in controls (24 and 9% had >1000 AB per gram dry lung tissue, respectively, P = 0.09). Mean cumulative smoking was lower in cases than in controls (P < 0.05). This study argues in favor of a relationship between asbestos exposure and certain pulmonary carcinoid tumors.
    Annals of Occupational Hygiene 05/2012; 56(7):789-95. · 2.16 Impact Factor
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    ABSTRACT: Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.
    Revue des Maladies Respiratoires. 05/2012; 29(5):723–726.
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    ABSTRACT: Several etiologies are involved in the pathogenesis of cavitating pulmonary disease including neoplastic, infectious or inflammatory processes. Another is pulmonary infarction associated with venous thromboembolism. The lung cavities tend to be located peripherally and are the result of pulmonary embolism. We report the case of a woman with chronic thromboembolic pulmonary hypertension (CTEPH), associated with familial thrombophilia, revealed by cavitating pulmonary infarcts. CTEPH is sometimes diagnosed during an episode of recurrent pulmonary embolism following previously unnoticed lesions. Thrombophilias such as isolated elevated factor VIII are risk factors for CTEPH.
    Revue des Maladies Respiratoires 05/2012; 29(5):723-6. · 0.50 Impact Factor
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    ABSTRACT: Swallowing disorders (or dysphagia) are common in the elderly and their prevalence is often underestimated. They may result in serious complications including dehydration, malnutrition, airway obstruction, aspiration pneumonia (infectious process) or pneumonitis (chemical injury caused by the inhalation of sterile gastric contents). Moreover the repercussions of dysphagia are not only physical but also emotional and social, leading to depression, altered quality of life, and social isolation. While some changes in swallowing may be a natural result of aging, dysphagia in the elderly is mainly due to central nervous system diseases such as stroke, parkinsonism, dementia, medications, local oral and oesophageal factors. To be effective, management requires a multidisciplinary team approach and a careful assessment of the patient's oropharyngeal anatomy and physiology, medical and nutritional status, cognition, language and behaviour. Clinical evaluation can be completed by a videofluoroscopic study which enables observation of bolus movement and movements of the oral cavity, pharynx and larynx throughout the swallow. The treatment depends on the underlying cause, extent of dysphagia and prognosis. Various categories of treatment are available, including compensatory strategies (postural changes and dietary modification), direct or indirect therapy techniques (swallow manoeuvres, medication and surgical procedures).
    Revue des Maladies Respiratoires 10/2011; 28(8):e76-93. · 0.50 Impact Factor
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    ABSTRACT: Mycobacterium chelonae (M. chelonae) is rarely responsible for respiratory infection. This report concerns the case of an 81-year-old man with previously asymptomatic bronchiectasis, colonised by M. chelonae for 3 years. He was hospitalised for acute dyspnoea and fever due to a right hydro-pneumothorax with cavitated alveolar opacities of the right lung. Pleural fluid and bronchial aspiration were positive for M. chelonae and no other microorganisms were detected. The effusion was drained and the patient treated with clarythromycin and amikacin. The radiological abnormalities improved but the patient's general condition remained poor. Treatment was continued for 11 months. Because of the absence of any other bacteria, clinical deterioration following broad-spectrum antibiotics and stabilisation of the lesions after anti-mycobacterial treatment, our diagnosis was severe M. chelonae pleuro-pneumonia in an immunocompetent patient.
    Revue des Maladies Respiratoires 03/2011; 28(3):348-51. · 0.50 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a major risk factor for cardiovascular disease. Polycythemia, a common complication of hypoxic COPD, may affect systemic vascular function by altering blood viscosity, vessel wall shear stress (WSS), and endothelium-derived nitric oxide (NO) release. Here, we evaluated the effects of hypoxia-related polycythemia on systemic endothelial function in patients with COPD. We investigated blood viscosity, WSS, and endothelial function in 15 polycythemic and 13 normocythemic patients with COPD of equal severity, by recording brachial artery diameter variations in response to hyperemia and by using venous occlusion plethysmography (VOP) to measure forearm blood flow (FBF) responses to a brachial artery infusion of acetylcholine (ACh), bradykinin (BK), sodium nitroprusside (SNP), substance P (SP), isoptin, and N-monomethyl-L-arginine (L-NMMA). At baseline, polycythemic patients had higher blood viscosity and larger brachial artery diameter than normocythemic patients but similar calculated WSS. Flow-mediated brachial artery vasodilation was increased in the polycythemic patients, in proportion to the hemoglobin levels. ACh-induced vasodilation was markedly impaired in the polycythemic patients and negatively correlated with hemoglobin levels. FBF responses to endothelium- (BK, SP) and non-endothelium-dependent (SNP, isoptin) vasodilators were not significantly different between the two groups. L-NMMA infusion induced a similar vasoconstrictor response in both groups, in accordance with their similar baseline WSS. In conclusion, systemic arteries in polycythemic patients adjust appropriately to chronic or acute WSS elevations by appropriate basal and stimulated NO release. Overall, our results suggest that moderate polycythemia has no adverse effect on vascular function in COPD.
    Journal of Applied Physiology 01/2011; 110(5):1196-203. · 3.48 Impact Factor
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    ABSTRACT: To evaluate the possible involvement of obstructive sleep apnea (OSA) in retinal vein occlusion (RVO). From the medical records of 63 consecutive patients with RVO, 30 patients with 2 of the 3 following risk factors for OSA were selected for further screening from February 1, 2008, through March 31, 2009: associated cardiovascular disease, snoring, or daytime sleepiness. Of the 30 selected patients, 23 (77%) had OSA. If all 33 of the unscreened patients did not have OSA, the OSA prevalence would have been 37%. Among the patients with OSA, the mean apnea-hypopnea index (AHI) was 21; OSA was mild (AHI <15) in 13 patients, moderate in 5 patients (AHI 15-30), and severe (AHI >30) in 5 patients. The AHI was correlated with body mass index (P = .02). We found a higher than expected prevalence of OSA in a series of patients with RVO. Our findings suggest that OSA could be an additional risk factor that plays an important role in the pathogenesis of RVO or at least that it is a frequently associated condition that could be a triggering factor. This association may explain why most patients discover visual loss on awakening. It is too early to assess whether OSA treatment could improve visual outcome of RVO, but it seems vital to recognize OSA in RVO for the general health of the patient.
    Archives of ophthalmology 12/2010; 128(12):1533-8. · 3.86 Impact Factor
  • B Housset
    Revue des Maladies Respiratoires 11/2010; 27(9):991-2. · 0.50 Impact Factor
  • B. Housset
    Revue Des Maladies Respiratoires - REV MAL RESPIR. 01/2010; 27(9):991-992.
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    ABSTRACT: Obstructive sleep apnea syndrome (OSAS) is a very common disease and has recently been increasingly incriminated in the initiation and progression of numerous cardiovascular, neurologic, and ophthalmologic diseases. In ophthalmologic practice, it may be related to glaucoma, nonarteritic anterior ischemic optic neuropathy, visual field defects, papilledema, central serous chorioretinopathy, and floppy eyelid syndrome. Because of personal observations, we investigated its link with retinal vein occlusion (RVO). We report the observations on three patients who presented with retinal vein occlusion and who were investigated positively for OSAS, including patients with no conventional vascular risk factors. The local and systemic effects of OSAS could explain, in some patients, the occurrence and/or the aggravation of RVO. The first-stage effects of OSAS are nocturnal hypoxemia, hypercapnia, intrathoracic pressure changes, arousals, and sleep fragmentation. RVO could be a consequence of a slow-down of blood flow circulation secondary to hypoxemia and elevated nocturnal intracranial pressure. The arousals cause an additional acute increase in arterial blood pressure. Ancillary effects include increased platelet aggregability, increased sympathic activation, oxidative stress, vascular endothelial dysfunction, inflammation, and metabolic dysregulation. This short series for the first time reports RVO patients presenting with OSAS. This suggests that OSAS, by acting on retinal microcirculation, could be an additional risk factor for the occurrence or the aggravation of RVO. Further studies are needed to confirm this possible relationship.
    Journal francais d'ophtalmologie 07/2009; 32(6):420-4. · 0.51 Impact Factor
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    ABSTRACT: Epidemiological studies have shown that asbestos fibers constitute the major occupational risk factor and that asbestos acts synergistically with tobacco smoking to induce lung cancer. Although some somatic gene alterations in lung cancer have been linked to tobacco smoke, few data are available on the role of asbestos fibers. P16/CDKN2A is an important tumor suppressor gene that is frequently altered in lung cancer via promoter 5'-CpG island hypermethylation and homozygous deletion, and rarely via point mutation. Many studies suggest that tobacco smoking produces P16/CDKN2A promoter hypermethylation in lung cancer, but the status of this gene in relation to asbestos exposure has yet to be determined. The purpose of this study was to investigate the mechanism of P16/CDKN2A alterations in lung cancer in asbestos-exposed patients. P16/CDKN2A gene status was studied in 75 human non-small-cell lung cancer (NSCLC) cases with well-defined smoking habits, and detailed assessment of asbestos exposure, based on occupational questionnaire and determination of asbestos bodies in lung tissue. The results of this study confirm published data on the effect of tobacco smoke on P16/CDKN2A gene alterations, characterized by significantly higher P16/CDKN2A promoter hypermethylation in heavy smokers (more than 40 pack-years (P-Y)) than in smokers of less than 40 P-Y. These results also demonstrate a higher incidence of loss of heterozygosity and homozygous deletion in asbestos-exposed cases, after adjustment for age and cumulative tobacco consumption, than in unexposed cases (P=0.0062). This study suggests that P16/CDKN2A gene inactivation in asbestos-exposed NSCLC cases mainly occurs via deletion, a feature also found in malignant mesothelioma, a tumor independent of tobacco smoking but associated with asbestos exposure, suggesting a possible relationship with an effect of asbestos fibers.
    Lung cancer (Amsterdam, Netherlands) 05/2009; 67(1):23-30. · 3.14 Impact Factor
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    ABSTRACT: Pulmonary artery remodeling triggered by alveolar hypoxia is considered the main mechanism of pulmonary hypertension (PH) in COPD patients. We hypothesized that the risk for PH in COPD is increased by an elevation in the proinflammatory cytokines interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and IL-1beta, as well as by specific genetic polymorphisms of these cytokines. We assessed cytokine plasma levels and the polymorphisms G(-174)C IL-6, C(-511)T IL-1beta, and A(-2518)G MCP-1 in 148 COPD patients (recruited at two centers) with right heart catheterization data and 180 control subjects including smokers and nonsmokers. Human pulmonary artery smooth muscle cells (PA-SMCs) were cultured for IL-6 messenger RNA assays under normoxic and hypoxic conditions. Patients with PH (mean pulmonary artery pressure [PAP], >or= 25 mm Hg) had lower Pao(2) and higher plasma IL-6 values than those without PH; there were no differences in terms of pulmonary function test results or CT scan emphysema scores. Plasma IL-6 correlated with mean PAP (r = 0.39; p < 0.001) and was included in a multiple stepwise regression analysis, with mean PAP as the dependent variable. In patients with the IL-6 GG genotype, the mean PAP value was significantly higher and PH was more common than in CG or CC patients (adjusted odds ratio, 4.32; 95% confidence interval, 1.96 to 9.54). Exposure to 4 h of hypoxia led to an about twofold increase in IL-6 messenger RNA in cultured human PA-SMCs. Inflammation, most likely involving IL-6, may contribute substantially to PH complicating COPD.
    Chest 04/2009; 136(3):678-87. · 5.85 Impact Factor
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    ABSTRACT: Swallowing disorders (or dysphagia) are common in the elderly and their prevalence is often underestimated. They may result in serious complications including dehydration, malnutrition, airway obstruction, aspiration pneumonia (infectious process) or pneumonitis (chemical injury caused by the inhalation of sterile gastric contents). Moreover the repercussions of dysphagia are not only physical but also emotional and social, leading to depression, altered quality of life, and social isolation. While some changes in swallowing may be a natural result of aging, dysphagia in the elderly is mainly due to central nervous system diseases such as stroke, parkinsonism, dementia, medications, local oral and oesophageal factors.To be effective, management requires a multidisciplinary team approach and a careful assessment of the patient's oropharyngeal anatomy and physiology, medical and nutritional status, cognition, language and behaviour. Clinical evaluation can be completed by a videofluoroscopic study which enables observation of bolus movement and movements of the oral cavity, pharynx and larynx throughout the swallow. The treatment depends on the underlying cause, extent of dysphagia and prognosis. Various categories of treatment are available, including compensatory strategies (postural changes and dietary modification), direct or indirect therapy techniques (swallow manoeuvres, medication and surgical procedures).
    Revue des Maladies Respiratoires. 01/2009; 26(6):587-605.
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    ABSTRACT: Telomere length is considered a marker for biological aging. Chronic obstructive pulmonary disease (COPD) may be associated with premature aging. To test the hypothesis that patients with COPD experience accelerated telomere shortening and that inflammation is linked to this process. We measured telomere length, using a quantitative polymerase chain reaction-based method, and plasma levels of various cytokines in 136 patients with COPD, 113 age- and sex-matched smokers, and 42 nonsmokers with normal lung function. Median (range) telomere length ratio was significantly lower in patients with COPD (0.57 [0.23-1.18]) than in control smokers (0.79 [0.34-1.58]) or nonsmokers (0.85 [0.38-1.55]) (P < 0.001). The difference remained highly significant when using logistic regression analysis adjusted for age, sex, and tobacco exposure. Both females and males with COPD had shorter telomere length than same-sex control subjects. Telomere length was related to age in patients and control subjects but was shorter in patients than in control subjects in all age groups. No relationship was found between telomere length and tobacco exposure in patients or control subjects, with no difference between control smokers and nonsmokers. In patients with COPD, telomere length was related to PaO2 (P < 0.001) and PaCO2 (P < 0.001) but not to lung function parameters or the BODE Index. Patients with COPD also had elevated plasma levels of various cytokines, interleukin-6 correlating negatively with telomere length (P < 0.001). Given that in vivo telomere length reflects cellular turnover and exposure to oxidative and inflammatory damage, our data support accelerated aging in COPD.
    American Journal of Respiratory and Critical Care Medicine 01/2009; 179(7):566-71. · 11.04 Impact Factor
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    ABSTRACT: PurposeObstructive sleep apnea syndrome (OSAS) is a very common disease and has recently been increasingly incriminated in the initiation and progression of numerous cardiovascular, neurologic, and ophthalmologic diseases. In ophthalmologic practice, it may be related to glaucoma, nonarteritic anterior ischemic optic neuropathy, visual field defects, papilledema, central serous chorioretinopathy, and floppy eyelid syndrome. Because of personal observations, we investigated its link with retinal vein occlusion (RVO).ObservationWe report the observations on three patients who presented with retinal vein occlusion and who were investigated positively for OSAS, including patients with no conventional vascular risk factors.DiscussionThe local and systemic effects of OSAS could explain, in some patients, the occurrence and/or the aggravation of RVO. The first-stage effects of OSAS are nocturnal hypoxemia, hypercapnia, intrathoracic pressure changes, arousals, and sleep fragmentation. RVO could be a consequence of a slow-down of blood flow circulation secondary to hypoxemia and elevated nocturnal intracranial pressure. The arousals cause an additional acute increase in arterial blood pressure. Ancillary effects include increased platelet aggregability, increased sympathic activation, oxidative stress, vascular endothelial dysfunction, inflammation, and metabolic dysregulation.Conclusion This short series for the first time reports RVO patients presenting with OSAS. This suggests that OSAS, by acting on retinal microcirculation, could be an additional risk factor for the occurrence or the aggravation of RVO. Further studies are needed to confirm this possible relationship.
    Journal francais d'ophtalmologie 01/2009; 32(6):420-424. · 0.51 Impact Factor
  • Journal Francais D Ophtalmologie - J FR OPHTALMOL. 01/2009; 32.

Publication Stats

1k Citations
399.76 Total Impact Points

Institutions

  • 2009–2011
    • Université Paris-Est Créteil Val de Marne - Université Paris 12
      • Faculty of medicine
      Créteil, Île-de-France, France
    • Centre Hospitalier Universitaire de Nancy
      Nancy, Lorraine, France
  • 2010
    • Assistance Publique – Hôpitaux de Paris
      • Department of Ophthalmology
      Paris, Ile-de-France, France
  • 1995–2010
    • Centre Hospitalier Intercommunal Creteil
      Créteil, Île-de-France, France
  • 2006
    • Société Française de Cardiologie
      Lutetia Parisorum, Île-de-France, France
    • Université René Descartes - Paris 5
      Lutetia Parisorum, Île-de-France, France
  • 1998
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 1990–1994
    • Hôpital La Pitié Salpêtrière (Groupe Hospitalier "La Pitié Salpêtrière - Charles Foix")
      • Service de Pneumologie
      Paris, Ile-de-France, France
  • 1993
    • Hôpital Henri Mondor (Hôpitaux Universitaires Henri Mondor)
      Créteil, Île-de-France, France