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D Valeyre

Publications and source records attributed to D Valeyre.

At least 19 recordsLinked to original sources
PubMed2006

Mycobacterium heckeshornense: an emerging pathogen responsible for a recurrent lung infection.

Mycobacterium heckeshornense was responsible for a severe, recurrent and chronic pulmonary infection in an immunocompetent 65-year-old woman. The pathogen, initially identified as Mycobacterium xenopi and considered as a contaminant, led to a delayed adapted antimicrobial treatment. Although M. heckeshornense is phenotypically closely related to M. xenopi, its pathogenicity is noticeably higher. Accurate molecular diagnosis methods and treatment guidelines are needed to improve the management of patients infected by this uncommon pathogen.

Aged↗
PubMed2006

Use of voriconazole in a patient with aspergilloma caused by an itraconazole-resistant strain of Aspergillus fumigatus.

The case is reported of a patient with cavitary sarcoidosis complicated by an aspergilloma caused by an itraconazole-resistant strain of Aspergillus fumigatus, who was treated with voriconazole. The authors suggest that susceptibility testing of A. fumigatus strains is of value during long-term therapy with itraconazole, and that voriconazole may be a good option for treatment of patients infected with itraconazole-resistant strains of A. fumigatus.

Adult↗
PubMed2005

Pulmonary hypertension associated with sarcoidosis: mechanisms, haemodynamics and prognosis.

BACKGROUND: Pulmonary hypertension (PH) is a rare complication of sarcoidosis, although it is not uncommon in advanced disease. METHODS: A retrospective series of 22 sarcoidosis patients (16 men) of mean (SD) age 46 (13) years with PH was divided into two groups depending on the absence (stage 0: n = 2, stage II: n = 4, stage III: n = 1) or presence (n = 15) of radiographic pulmonary fibrosis at the time of PH diagnosis. RESULTS: In both groups PH was moderate to severe and there was no response to acute vasodilator challenge. In non-fibrotic cases no other cause of PH was found, suggesting a specific sarcoidosis vasculopathy, although no histological specimens were available. In cases with fibrosis there was no correlation between haemodynamics and lung volumes or arterial oxygen tensions, suggesting other mechanisms for PH in addition to pulmonary destruction and hypoxaemia. These included extrinsic arterial compression by lymphadenopathies in three cases and histologically proven pulmonary veno-occlusive disease in the five patients who underwent lung transplantation. Ten patients received high doses of oral prednisone for PH (stage 0: n = 1, stage II: n = 4 and stage IV: n = 5); three patients without pulmonary fibrosis experienced a sustained haemodynamic response. Survival of the overall population was poor (59% at 5 years). Mortality was associated with NYHA functional class IV but not with haemodynamic parameters or with lung function. CONCLUSION: Two very different phenotypes of sarcoidosis combined with PH are observed depending on the presence or absence of pulmonary fibrosis. PH is a severe complication of sarcoidosis.

Adrenal Cortex Hormones↗
PubMed2005

[Epidemiological survey of a suspected nosocomial case of tuberculosis by spoligotyping].

Transmission of tuberculosis within hospitals has been increasingly recognized as a hazard for patients and health care workers. A case of pulmonary tuberculosis was detected in September 2003 in a nursing auxiliary working at Avicenne's Hospital. This 49 year-old woman was considered infected since April 2003. During this 6 months period, she worked in 23 distinct hospital units and could have contaminated patients and hospital staffs. The epidemiological survey was comprised for 1735 individuals (701 hospital staffs and 1034 patients). It encompassed clinical, para-clinical investigations and bacteriological investigations. Furthermore, between January 2003 and September 2004, a systematic comparison of 62 Mycobacterium tuberculosis strains isolated in the hospital was conducted by spoligotyping, a molecular typing method in order to access an eventual transmission. The nursing auxiliary's strain clearly showed a distinct spoligotype from the other investigated strains. This spoligotype was unique in the international spoligotype database. In this large epidemiological survey of a case of suspected nosocomial of tuberculosis, spoligotyping appeared as an interesting, easy and rapid method of molecular typing. It allowed to demonstrate that the nursing auxiliary tuberculosis case was unrelated to the others cases of tuberculosis diagnosed in the hospital during this period.

Bacterial Typing Techniques↗
PubMed2005

[Chronic pulmonary berylliosis: a model of interaction between environment and genetic predisposition (Part 1). Mineralogy, toxicology, epidemiology and risk factors].

INTRODUCTION: The physico-chemical properties of beryllium (Be) are crucial for high technology industries. The inhalation of beryllium may cause, in certain individuals, a specific sensitisation (BeS) and lead, in some of them, to a pulmonary granulomatosis called chronic pulmonary berylliosis (CPB). BACKGROUND: Although there is no linear relationship between the level of exposure to Be and the risks of BeS and CPB, the highest exposures are associated with an increased risk. The specific influences of the chemical composition, the solubility and different types of Be on the risk of BeS an CPB are poorly understood. Insoluble particles of small diameter are probably associated with an increased risk. Many studies have reported the role of a genetic predisposition in the risk of BeS and CPB. At present the role of HLA-DPB1 Glu69 in sensitisation to Be is the best studied. CONCLUSION: Sensitisation to Be and CPB result from the combination of exposure and predisposing genetic polymorphisms. CPB is a model for the understanding of the pathology of certain ideopathic pulmonary granulomatoses such as sarcoidosis.

Berylliosis↗
PubMed2005

[Chronic beryllium disease: a model of interaction between environmental exposure and genetic predisposition. Pathogenesis and clinical features (Part 2)].

INTRODUCTION: Chronic beryllium disease (CBD) is an occupational lung disease caused by the inhalation of beryllium dust, fumes or metallic salts. CURRENT DATA: Beryllium affects the lungs via particles deposited in the pulmonary alveoli. These are ingested by alveolar macrophages which act as antigen presenting cells to CD4+ T lymphocytes. T lymphocytes proliferate in response to beryllium antigens and combined with macrophages produce numerous epithelioid granulomas with the release of inflammatory cytokines (IFNgamma, IL-2, TNFalpha and IL6) and growth factors. Beryllium induces macrophage apoptosis which reduces its clearance from the lung which in turn contributes to the host's continual re-exposure and thus a chronic granulomatous disorder. Pulmonary granulomatous inflammation is the primary manifestation of CBD, but the disease occasionally involves other organs such as the liver, spleen, lymph nodes and bone marrow. The clinical, radiological, and histopathological features of CBD can be difficult to distinguish from sarcoidosis. The Beryllium lymphocyte proliferation test (BeLPT) demonstrates a beryllium specific immune response, confirms the diagnosis of CBD, and excludes sarcoidosis. CONCLUSIONS AND PERSPECTIVES: CBD provides a human model of pulmonary granulomatous disease produced by an occupational exposure, occurring more frequently in those with a genetic pre-disposition. It can be differentiated from sarcoidosis by specific immunological testing.

Berylliosis↗
PubMed2005

Pulmonary sarcoidosis.

Sarcoidosis is a multisystemic disease of unknown aetiology characterized by the formation of immune granulomas in involved organs. It is a worldwide disease that mainly affects 25-40 years old people with a lifetime incidence rate of 0.85-2.4%. Multiple clinical phenotypes are observed according to presentation, involved organs, disease duration and severity. Sarcoidosis primarily affects the lungs and the lymphatic system. The prevailing pathogenic hypothesis is that various antigens could promote sarcoidosis in genetically susceptible hosts, both these factors modulating the incidence and the clinical phenotype of sarcoidosis. So far, environmental agents have been suspected, including possible mycobacteria and propionibacteria. Interferon-gamma, tumour necrosis factor (TNF)-alpha, interleukin (IL)-12 and IL-18 play a critical role in driving the Th1 commitment in the course of granulomatous process. Evolution of sarcoidosis is often marked by spontaneous resolution within 12-36 months, but can be severe because of chronic cases with pulmonary fibrosis or involving other organs, including heart, central nervous system and eyes. Mortality, ranging between 0.5 and 5%, is most often related to pulmonary fibrosis. Corticosteroids can reverse the granulomatous process, but are only suspensive, and their long-term benefit remains under question. Corticosteroids are recommended when sarcoidosis shows unfavourable clinical tolerance and evolution. Alternative and corticosteroid-sparing therapies are of increased interest in difficult cases, while targeted new drugs such as anti-TNF-alpha are still under investigation.

Humans↗
PubMed2005

Combined pulmonary fibrosis and emphysema: a distinct underrecognised entity.

The syndrome resulting from combined pulmonary fibrosis and emphysema has not been comprehensively described. The current authors conducted a retrospective study of 61 patients with both emphysema of the upper zones and diffuse parenchymal lung disease with fibrosis of the lower zones of the lungs on chest computed tomography. Patients (all smokers) included 60 males and one female, with a mean age of 65 yrs. Dyspnoea on exertion was present in all patients. Basal crackles were found in 87% and finger clubbing in 43%. Pulmonary function tests were as follows (mean+/-sd): total lung capacity 88%+/-17, forced vital capacity (FVC) 88%+/-18, forced expiratory volume in one second (FEV1) 80%+/-21 (% predicted), FEV1/FVC 69%+/-13, carbon monoxide diffusion capacity of the lung 37%+/-16 (% predicted), carbon monoxide transfer coefficient 46%+/-19. Pulmonary hypertension was present in 47% of patients at diagnosis, and 55% during follow-up. Patients were followed for a mean of 2.1+/-2.8 yrs from diagnosis. Survival was 87.5% at 2 yrs and 54.6% at 5 yrs, with a median of 6.1 yrs. The presence of pulmonary hypertension at diagnosis was a critical determinant of prognosis. The authors hereby individualise the computer tomography-defined syndrome of combined pulmonary fibrosis and emphysema characterised by subnormal spirometry, severe impairment of gas exchange, high prevalence of pulmonary hypertension, and poor survival.

Adult↗
PubMed2005

Evolution of previous sarcoidosis under type 1 interferons given for severe associated disease.

Sarcoidosis is a granulomatous disorder with a well-known T helper (Th) type 1 cell commitment and a key pathogenic role of interferon (IFN)-gamma. However, little is known about the influence of type 1 IFNs, such as IFN-alpha and IFN-beta, on the course of previous sarcoidosis. The aim of this study was to determine whether type 1 IFNs can safely be used in patients with sarcoidosis for severe associated disease. The present study examined a series of four patients with sarcoidosis, treated by IFN-alpha or IFN-beta for viral hepatitis (three cases) or multiple sclerosis (one case). IFN was initiated soon after apparent recovery (three cases) or during a worsening phase of sarcoidosis (one case). Hydroxychloroquine was added in the case with active disease. Patients received interferon for 6-24 months and had close monitoring during and after IFN therapy. Interestingly, no recurrence or exacerbation of sarcoidosis had occurred at 4 yrs of follow up. Two patients were cured from viral hepatitis, whilst treatment for another failed. No neurological progression was observed in the remaining patient. This series suggests that, despite the T helper type 1 phenotype of sarcoid granulomatous reaction, type 1 interferons do not exacerbate sarcoidosis in remission and this makes their use possible if indicated. However, their effect in persistent forms of the disease needs further evaluation.

Adult↗
PubMed2004

Chemokine receptor CXCR4 and early-stage non-small cell lung cancer: pattern of expression and correlation with outcome.

BACKGROUND: The expression of CXCR4 has been implicated in metastatic dissemination in different models of breast cancer and melanoma. In the present study, we evaluated CXCR4 expression in non-small-cell lung cancer (NSCLC) and the relationship between CXCR4 expression and the prognosis of stage I disease. PATIENTS AND METHODS: Using immunohistochemical analysis, we retrospectively analyzed CXCR4 expression in specimens from 61 patients with completely resected pathologically confirmed stage I NSCLC for whom clinical follow-up data were available. RESULTS: In the present study, we have shown that: CXCR4 is expressed by tumor cells in stage I NSCLC; CXCR4 is located in the nucleus and/or in the cytoplasm of tumor cells; strong nuclear staining was observed in 17 cases (29.8%); patients whose tumors had CXCR4-positive nuclear staining had a significantly longer duration of survival than patients whose tumors had no nuclear expression (P = 0.039, log-rank test). Interestingly, the 5-year metastasis rates were 23.5% and 34.1% in patients with CXCR4-positive and CXCR4-negative nuclear expression, respectively (P = 0.2). CONCLUSION: Strong CXCR4-positive nuclear staining was associated with a significantly better outcome in early-stage NSCLC. The mechanisms underlying this clinically and biologically important finding need to be further explored.

Adult↗
PubMed2004

Expression of apoptosis-regulatory proteins in lesions of pulmonary Langerhans cell histiocytosis.

AIMS: Pulmonary Langerhans cell histiocytosis (PLCH) is characterized by the presence of lesions containing numerous activated Langerhans cells (LCs). An uncontrolled immune response sustained by activated LCs seems to be involved in the pathogenesis of the disease. The aim of this study was to establish whether disruption of LC apoptosis related to the expression of the Bcl-2 family proteins is implicated in the maintenance of PLCH lesions. METHODS: Six patients with PLCH were evaluated by morphological and immunohistochemical techniques to explore the incidence of apoptosis in pathological LCs and to characterize the expression of Bcl-2-related proteins by these cells. RESULTS: Very few LCs present in PLCH lesions exhibited nuclear apoptotic changes or expressed cleaved caspase-3, whereas they all strongly expressed the anti-apoptotic molecule Bcl-x(L). Interestingly, pulmonary LCs present in intervening lung tissue not involved by the pathological process and known to be immature dendritic cells did not express Bcl-2 family proteins. CONCLUSIONS: These findings suggest that activated LCs present within PLCH lesions are poorly susceptible to apoptosis and, thus, are able to sustain the pathological process by causing continuous local stimulation of T cells. Functional studies are needed, however, to demonstrate that they are actually resistant to programmed cell death.

Adult↗
PubMed2004

Tuberculosis in HIV-infected patients: a comprehensive review.

The incidence of tuberculosis (TB) is currently increasing in HIV-infected patients living in Africa and Asia, where TB endemicity is high, reflecting the susceptibility of this group of patients to mycobacteria belonging to the TB group. In this population, extension of multiple resistance to anti-tuberculous drugs is also a matter of anxiety. HIV-induced immunosuppression modifies the clinical presentation of TB, resulting in atypical signs and symptoms, and more frequent extrapulmonary dissemination. The treatment of TB is also more difficult to manage in HIV-infected patients, particularly with regard to pharmacological interactions secondary to inhibition or induction of cytochrome P450 enzymes by protease inhibitors with rifampicin or rifabutin, respectively. Finally, immune restoration induced by highly active anti-retroviral therapy (HAART) in developed countries may be responsible for a paradoxical worsening of TB manifestations.

AIDS-Related Opportunistic Infections↗