Dietary Fiber Confers Protection against Flu by Shaping Ly6c- Patrolling Monocyte Hematopoiesis and CD8+ T Cell Metabolism.

Dietary fiber protects against chronic inflammatory diseases by dampening immune responses through short-chain fatty acids (SCFAs). Here we examined the effect of dietary fiber in viral infection, where the anti-inflammatory properties of SCFAs in principle could prevent protective immunity. Instead, we found that fermentable dietary fiber increased survival of influenza-infected mice through two complementary mechanisms. High-fiber diet (HFD)-fed mice exhibited altered bone marrow hematopoiesis, characterized by enhanced generation of Ly6c- patrolling monocytes, which led to increased numbers of alternatively activated macrophages with a limited capacity to produce the chemokine CXCL1 in the airways. Blunted CXCL1 production reduced neutrophil recruitment to the airways, thus limiting tissue immunopathology during infection. In parallel, diet-derived SCFAs boosted CD8+ T cell effector function by enhancing cellular metabolism. Hence, dietary fermentable fiber and SCFAs set an immune equilibrium, balancing innate and adaptive immunity so as to promote the resolution of influenza infection while preventing immune-associated pathology.

Microbiome-induced antigen-presenting cell recruitment coordinates skin and lung allergic inflammation.

BACKGROUND: Allergic skin inflammation often presents in early childhood; however, little is known about the events leading to its initiation and whether it is transient or long-term in nature. OBJECTIVE: We sought to determine the immunologic rules that govern skin inflammation in early life. METHODS: Neonatal and adult mice were epicutaneously sensitized with allergen followed by airway allergen challenge. Epicutaneous application of labeled allergen allowed for determination of antigen uptake and processing by antigen-presenting cells. RNAseq and microbiome analysis was performed on skin from neonatal and adult specific pathogen-free and germ-free mice. RESULTS: A mixed TH2/TH17 inflammatory response in the skin and the lungs of adult mice was observed following sensitization and challenge. Comparatively, neonatal mice did not develop overt skin inflammation, but exhibited systemic release of IL-17a and a TH2-dominated lung response. Mechanical skin barrier disruption was not sufficient to drive allergic skin inflammation, although it did promote systemic immune priming. Skin of neonatal mice and adult germ-free mice was seeded with low numbers of antigen-presenting cells and impaired chemokine and alarmin production. Enhanced chemokine and alarmin production, and seeding of the skin with antigen-presenting cells capable of instructing recruited cells to elicit their effector function, was, at least in part, dependent on formation of the microbiome, and consequently contributed to the development of overt skin disease. CONCLUSIONS: These data shed light on the principles that underlie allergic inflammation in different tissues and highlight a window of opportunity that might exist for early-life prevention of allergic diseases.

Swiss Recommendations for the Follow-Up and Treatment of Pulmonary Long COVID.

INTRODUCTION: Emerging evidence suggests that long-term pulmonary symptoms and functional impairment occurs in a proportion of individuals following SARS-CoV-2 infection. Although the proportion of affected patients remains to be determined, physicians are increasingly being confronted with patients reporting respiratory symptoms and impairment beyond the acute phase of COVID-19. In face of limited evidence, the Swiss Society for Pulmonology established a working group to address this area of unmet need and formulated diagnostic and treatment recommendations for the care of patients with pulmonary long COVID (LC). METHOD: The Swiss COVID Lung Study group and Swiss Society for Pulmonology (SSP) formulated 13 questions addressing the diagnosis and treatment of pulmonary LC. A survey within the SSP special interest groups involved in care of LC patients was conducted in Switzerland. A CORE process/Delphi-like process was used to formulate recommendations. Forty experienced pulmonologists replied to the first survey and 22 completed the second follow-up survey. Agreement of ≥70% consensus led to formulation of a recommendation. RESULTS: The participants in the survey reached consensus and formulated a strong recommendation for regarding the following points. Patients hospitalized for COVID-19 should have a pulmonary assessment including pulmonary function tests. Symptomatic subjects affected by COVID-19, including those with mild disease, should benefit from a pulmonary follow-up. Persistent respiratory symptoms after COVID-19 should be investigated by a pulmonary follow-up including plethysmography, diffusion capacity measurement, and blood gases analysis. Individuals having suffered from COVID-19 and who present with persistent respiratory symptoms should be offered a rehabilitation. Additional questions were given moderateor weak recommendations for. The panel did not reach sufficient consensus for pharmacological therapy (e.g., therapy specifically targeting lung fibrosis) to formulate recommendations for LC drug treatment. CONCLUSION: The formulated recommendations should serve as an interim guidance to facilitate diagnosis and treatment of patients with pulmonary LC. As new evidence emerges, these recommendations may need to be adapted.

Immunotherapy-Induced Airway Disease: A New Pattern of Lung Toxicity of Immune Checkpoint Inhibitors.

Immune checkpoint inhibitors (ICIs) have been shown to improve overall and progression-free survival in various cancers but have been associated with various immune-related adverse events (IRAEs), including interstitial lung disease, especially organizing pneumonia. We report 2 cases of isolated severe airway disease attributable to ICIs, a rarely reported pattern of lung toxicity. The first patient received nivolumab with or without ipilimumab in a randomized double-blind trial for locoregional metastatic melanoma. The second patient was treated with nivolumab for lung adenocarcinoma. An IRAE was suspected in both cases due to a temporal relationship between ICI initiation and symptom onset. ICIs were stopped, and high-dose prednisone, inhaled corticosteroids, and bronchodilators were administered, allowing a rapid clinical and functional improvement in Patient 1. In Patient 2, despite prolonged high-dose prednisone, only a stabilization of forced expiratory volume in 1 s could be achieved, and the disease course was complicated by respiratory infections resulting in further loss of lung function. The patient died 1 year later due to progression of metastatic disease. These 2 cases suggest that pulmonary IRAEs secondary to ICIs may present as isolated bronchitis or bronchiolitis, with variable outcomes following ICI withdrawal and systemic corticosteroids.

Airway microbiota signals anabolic and catabolic remodeling in the transplanted lung.

BACKGROUND: Homeostatic turnover of the extracellular matrix conditions the structure and function of the healthy lung. In lung transplantation, long-term management remains limited by chronic lung allograft dysfunction, an umbrella term used for a heterogeneous entity ultimately associated with pathological airway and/or parenchyma remodeling. OBJECTIVE: This study assessed whether the local cross-talk between the pulmonary microbiota and host cells is a key determinant in the control of lower airway remodeling posttransplantation. METHODS: Microbiota DNA and host total RNA were isolated from 189 bronchoalveolar lavages obtained from 116 patients post lung transplantation. Expression of a set of 11 genes encoding either matrix components or factors involved in matrix synthesis or degradation (anabolic and catabolic remodeling, respectively) was quantified by real-time quantitative PCR. Microbiota composition was characterized using 16S ribosomal RNA gene sequencing and culture. RESULTS: We identified 4 host gene expression profiles, among which catabolic remodeling, associated with high expression of metallopeptidase-7, -9, and -12, diverged from anabolic remodeling linked to maximal thrombospondin and platelet-derived growth factor D expression. While catabolic remodeling aligned with a microbiota dominated by proinflammatory bacteria (eg, Staphylococcus, Pseudomonas, and Corynebacterium), anabolic remodeling was linked to typical members of the healthy steady state (eg, Prevotella, Streptococcus, and Veillonella). Mechanistic assays provided direct evidence that these bacteria can impact host macrophage-fibroblast activation and matrix deposition. CONCLUSIONS: Host-microbes interplay potentially determines remodeling activities in the transplanted lung, highlighting new therapeutic opportunities to ultimately improve long-term lung transplant outcome.

GLI 2012 equations define few spirometric anomalies in the general population: the PneumoLaus study.

BACKGROUND: Reduced lung function predicts increased mortality, but its prevalence may vary depending on definition considered, use of bronchodilation and applied reference values. We aimed to assess lung function abnormalities in Lausanne, Switzerland, and their association with clinical history. METHODS: In a general population sample, spirometry was performed and bronchodilation applied if the ratio forced expiratory volume in 1 s (FEV1) / forced vital capacity (FVC) or the FVC was below the lower limit of normal (LLN) according to Global Lung Function Initiative 2012 references. Results for FEV1/FVC according to the LLN were compared to the 0.7 fixed ratio. Respiratory risk factors, symptoms and self-reported respiratory diagnoses were recorded through a questionnaire. RESULTS: Out of the 3342 included subjects, 3.8% had chronic obstruction and 2.5% reversible obstruction when using the LLN; possible lung restriction alone was present in 1.8%, and associated with chronic obstruction in 0.4%. Ever smokers had a higher prevalence of abnormal spirometry, chronic obstruction and reversible obstruction; there was no difference with regard to possible restriction. Overall, chronic airway obstruction was found in 8.9% of current smokers, 4.6% of former smokers and 1.5% of never smokers. Only one third of participants with chronic obstruction were aware of a respiratory disease. CONCLUSION: Prevalence of abnormal lung function in the population of Lausanne is low. This may be due to a low rate of ever-smokers, the application of a full bronchodilation dose, but also to inherent characteristics of this population.

Diagnosis and Management of Asthma - The Swiss Guidelines.

The Global Initiative for Asthma (GINA) is a network of individuals, organizations, and public health officials that was established to disseminate information about the care of patients with asthma and to improve asthma care. The GINA ("Global Strategy for Asthma Management and Prevention") report has been updated annually since 2002. Due to new knowledge and therapeutic development in the field, the Swiss Respiratory Society felt the need to provide a new document that is based on both the available literature and the recommendations of the 2016 GINA report. Key new features of the 2016 GINA report include a "new" definition of asthma, underscoring its heterogeneous nature, and the core elements of variable symptoms and variable expiratory airflow limitation; the importance of confirming the diagnosis of asthma in order to minimize both under- and overtreatment; practical tools for the assessment of symptom control and risk factors for adverse outcomes; a comprehensive approach to asthma management that acknowledges the foundational role of inhaled corticosteroid therapy, but also provides a framework for individualizing patient care; an emphasis on maximizing the benefit of available medications by addressing common problems such as incorrect inhaler technique and poor adherence; a continuum of care for worsening asthma, starting with early self-management and progressing to primary care or acute care management; and diagnosis of the asthma/chronic obstructive pulmonary disease overlap syndrome. This document is meant to advice the key stakeholders on the diagnosis and management of asthma and highlights the need to individualize the care of each and every asthmatic patient.

[When home become breathtaking]. / Quand la maison nous coupe le souffle.

We spend most of our time indoor and mainly at home. Thermal insulation has greatly improved in the last decades, thus leading to deficiency in ventilation and poor indoor air quality. Many studies suggest that there is a link between respiratory diseases and various indoor air pollutants such as moulds, allergens, volatile organic compounds, combustible smoke, house dust mite, radon or asbestos. This article reviews the most common pathogenic pollutants at home as well as their sources and related respiratory diseases. Preventive measures are further presented for every category of contaminant.

Nous passons la plupart de notre temps à l'intérieur et le plus souvent à notre domicile. Durant les dernières décennies, l'amélioration de l'isolation thermique des habitats a entraîné une diminution de la ventilation des espaces clos et un appauvrissement de la qualité de l'air intérieur. Plusieurs études suggèrent une association entre des symptômes ou pathologies respiratoires et différents contaminants de l'air intérieur comme les moisissures, les animaux domestiques, les composés organiques volatiles, les produits de combustion, les acariens, le radon ou l'amiante. Cet article passe en revue les substances pathogènes les plus fréquentes dans le milieu domestique, ainsi que leurs sources et les pathologies respiratoires associées. Des recommandations sont proposées pour chaque catégorie de contaminant.

[Noninvasive ventilation for chronic hypercapnic respiratory failure]. / Rôle de la ventilation non invasive dans l'insuffisance respiratoire hypercapnique chronique.

Chronic hypercapnic respiratory failure is essentially a ventilatory failure. Noninvasive ventilation (NIV ) reduces the work of breathing, improves pulmonary compliance and alveolar ventilation, corrects gas exchange disorders and improves dyspnoea. However, treatment efficacy depends on the underlying pathology, on correct timing and on patient compliance. In this context, the principal role of the primary care physician is to search for, at every visit of at risk patients, signs and symptoms of ventilatory failure and to refer the patient to a respiratory care specialist. He also plays a role in the follow up of patients under noninvasive ventilation for the detection of clinical parameters suggesting NIV failure.

L'insuffisance respiratoire hypercapnique chronique est essentiellement une défaillance ventilatoire. La ventilation non invasive (VNI) diminue le travail des muscles respiratoires, augmente la compliance thoracique, améliorant ainsi la dyspnée et les troubles des échanges gazeux. Toutefois, l'efficacité du traitement dépend de la pathologie sous-jacente, du bon timing d'initiation et de la compliance du patient. Dans ce contexte, le rôle principal du médecin de premier recours consiste à rechercher, lors de chaque visite médicale de patients à risque, des signes et symptômes de défaillance ventilatoire qui nécessitent de référer le patient à un pneumologue. Son rôle est aussi important dans le suivi des patients ventilés pour la détection précoce des paramètres cliniques suggérant un échec de VNI.

[Systemic biomarkers in respiratory tract infections]. / Biomarqueurs systèmiques pour les infections respiratoires.

Respiratory tract infections represent a major cause of morbidity and mortality despite the progress made in their diagnosis and treatment. Since the clinical presentation of a viral or bacterial infection is often similar, the identification of a biomarker that could guide the clinician whether or not to introduce an antibiotic therapy is crucial. C-reactive protein and procalcitonin are the most commonly used biomarkers as a diagnostic tool for respiratory tract infections. New biomarkers show promising results for assessing the severity of infection and identifying patients at risk for complications. However, the use of biomarkers has limitations and the diagnosis of a bacterial infection should not be based solely on the measurement of a biomarker.

Malgré le progrès effectué pour le diagnostic et le traitement des infections respiratoires, ces dernières représentent une cause de morbidité et mortalité importante. La présentation clinique d'une infection virale ou bactérienne étant souvent identique, l'identification d'un biomarqueur qui pourrait aider le clinicien à la décision d'introduire ou pas un traitement antibiotique est cruciale. La protéine C-réactive et la procalcitonine sont les biomarqueurs les plus fréquemment utilisés comme aide au diagnostic. Des nouveaux biomarqueurs montrent des résultats prometteurs pour évaluer la sévérité de l'infection et les patients à risque de complication. Toutefois, l'utilisation des biomarqueurs présente des limitations et le diagnostic d'une infection bactérienne ne doit en aucun cas être basé uniquement sur la mesure d'un biomarqueur.

Cystic Lung Disease in Genetic Syndromes with Deficient Tumor Suppressor Gene Function.

Cystic lung diseases constitute a distinct group of rare lung disorders, among which two result from monogenic defects affecting tumor suppressor genes: lymphangioleiomyomatosis, either sporadic or associated with tuberous sclerosis complex, and Birt-Hogg-Dubé syndrome. These disorders have similarities in their clinical expression, including occurrence in young adults, multiple pulmonary cysts, recurrent pneumothorax, skin hamartomas, and renal tumors. However, they markedly differ in their gender distribution, pathogenesis, disease course, and prognosis. Our knowledge on these two rare conditions is rapidly expanding. Management of lymphangioleiomyomatosis has substantially improved in the past decade with the understanding of its pathogenic mechanisms, the discovery of an effective therapy, and development of large cohorts and international guidelines. Birt-Hogg-Dubé syndrome has been described more recently and still awaits deeper understanding of its pathophysiology.

Idiopathic Pulmonary Fibrosis in Switzerland: Diagnosis and Treatment.

Idiopathic pulmonary fibrosis (IPF) is a severe progressive and irreversible lung disease. Novel antifibrotic drugs that slow disease progression are now available. However, many issues regarding patient management remain unanswered, such as the choice between available drugs, their use in particular subgroups and clinical situations, time of treatment onset, termination, combination or switch, or nonpharmacologic management. To guide Swiss respiratory physicians in this evolving field still characterized by numerous areas of uncertainty, the Swiss Working Group for interstitial and rare lung diseases of the Swiss Respiratory Society provides a position paper on the diagnosis and treatment of IPF.

Microbiota Promotes Chronic Pulmonary Inflammation by Enhancing IL-17A and Autoantibodies.

RATIONALE: Changes in the pulmonary microbiota are associated with progressive respiratory diseases including chronic obstructive pulmonary disease (COPD). Whether there is a causal relationship between these changes and disease progression remains unknown. OBJECTIVES: To investigate the link between an altered microbiota and disease, we used a murine model of chronic lung inflammation that is characterized by key pathological features found in COPD and compared responses in specific pathogen-free (SPF) mice and mice depleted of microbiota by antibiotic treatment or devoid of a microbiota (axenic). METHODS: Mice were challenged with LPS/elastase intranasally over 4 weeks, resulting in a chronically inflamed and damaged lung. The ensuing cellular infiltration, histological damage, and decline in lung function were quantified. MEASUREMENTS AND MAIN RESULTS: Similar to human disease, the composition of the pulmonary microbiota was altered in diseased animals. We found that the microbiota richness and diversity were decreased in LPS/elastase-treated mice, with an increased representation of the genera Pseudomonas and Lactobacillus and a reduction in Prevotella. Moreover, the microbiota was implicated in disease development as mice depleted, or devoid, of microbiota exhibited an improvement in lung function, reduced inflammation, and lymphoid neogenesis. The absence of microbial cues markedly decreased the production of IL-17A, whereas intranasal transfer of fluid enriched with the pulmonary microbiota isolated from diseased mice enhanced IL-17A production in the lungs of antibiotic-treated or axenic recipients. Finally, in mice harboring a microbiota, neutralizing IL-17A dampened inflammation and restored lung function. CONCLUSIONS: Collectively, our data indicate that host-microbial cross-talk promotes inflammation and could underlie the chronicity of inflammatory lung diseases.

Airway Microbiota Determines Innate Cell Inflammatory or Tissue Remodeling Profiles in Lung Transplantation.

RATIONALE: In lung transplant recipients, long-term graft survival relies on the control of inflammation and tissue remodeling to maintain graft functionality and avoid chronic lung allograft dysfunction. Although advances in clinical practice have improved transplant success, the mechanisms by which the balance between inflammation and remodeling is maintained are largely unknown. OBJECTIVES: To assess whether host-microbe interactions in the transplanted lung determine the immunologic tone of the airways, and consequently could impact graft survival. METHODS: Microbiota DNA and host total RNA were isolated from 203 bronchoalveolar lavages obtained from 112 patients post-lung transplantation. Microbiota composition was determined using 16S ribosomal RNA analysis, and expression of a set of genes involved in prototypic macrophage functions was quantified using real-time quantitative polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS: We show that the characteristics of the pulmonary microbiota aligned with distinct innate cell gene expression profiles. Although a nonpolarized activation was associated with bacterial communities consisting of a balance between proinflammatory (e.g., Staphylococcus and Pseudomonas) and low stimulatory (e.g., Prevotella and Streptococcus) bacteria, "inflammatory" and "remodeling" profiles were linked to bacterial dysbiosis. Mechanistic assays provided direct evidence that bacterial dysbiosis could lead to inflammatory or remodeling profiles in macrophages, whereas a balanced microbial community maintained homeostasis. CONCLUSIONS: The crosstalk between bacterial communities and innate immune cells potentially determines the function of the transplanted lung offering novel pathways for intervention strategies.

[Exercise-induced bronchoconstriction: epidemiology, physiopathology and management]. / Bronchoconstriction induite par l'effort : épidémiologie, physiopathologie et prise en charge.

Exercise-induced bronchoconstriction, associated or not with asthma, describes a transient limitation of airflow in the airways occurring during or after physical activity, regardless of age or training. Bronchoconstriction on exertion is principally induced by thermal and fluid losses of the bronchial mucosa by hyperventilation of large air volumes. Respiratory symptoms are variable and not specific. Among bronchial provocation test, eucapnic voluntary hyperventilation owns the best sensitivity and specificity in the diagnosis of exercise-induced bronchoconstriction. Therapeutic management consists in an adjustment of the environment and training, as well as bronchodilators.

La bronchoconstriction induite par l'effort, associée ou non à un asthme, décrit une limitation transitoire des débits d'air dans les voies aériennes survenant au cours ou au décours d'une activité physique, quels que soient l'âge ou le niveau d'entraînement. Des pertes thermiques et hydriques au niveau de la muqueuse bronchique par l'hyperventilation de grands volumes d'air jouent un rôle prépondérant dans la genèse d'une bronchoconstriction à l'effort. La symptomatologie respiratoire est variable et peu spécifique. Parmi les tests de provocation bronchique, l'hyperventilation eucapnique présente les meilleures sensibilité et spécificité dans le diagnostic d'une bronchoconstriction induite par l'effort. La prise en charge thérapeutique consiste en une adaptation de l'environnement et de l'entraînement, ainsi que des bronchodilatateurs.

[Lung and pleural space ultrasonography for pulmonologist]. / L'échographie pleuro-pulmonaire pour le pneumologue.

In the past twenty years ultrasound has been the subject of renewed interest in lung exploration in the broad sense. The necessity of accessing a means of rapid exploration at the bed of the patient in a critical situation has led to the development of a pleuro-pulmonary ultrasound semiology to make it a diagnostic tool of choice which exceeds the strict framework intensive care units and emergency services. With the diagnosis of thoracic tumors or the exploration of interstitial syndromes, it tends to integrate more into the daily practice of the pulmonologist. This article is a review of the possibilities offered by ultrasound in the field with its advantages and limitations.

Depuis une vingtaine d'années, l'échographie fait l'objet d'un regain d'intérêt pour l'exploration pulmonaire au sens large. La nécessité d'accéder à un moyen d'exploration rapide au lit du malade en situation critique a mené au développement d'une sémiologie échographique pleuro-pulmonaire jusqu'à en faire un outil diagnostique de choix dont l'utilisation dépasse désormais le cadre strict des unités de soins intensifs et des services d'urgence. Avec le diagnostic des tumeurs thoraciques ou encore l'exploration des syndromes interstitiels, elle tend à s'intégrer davantage dans la pratique quotidienne du pneumologue. Cet article est une revue des possibilités qu'offre l'échographie dans ce domaine avec ses avantages et ses limites.

[Pulmonary hypertension and pregnancy]. / Hypertension artérielle pulmonaire et grossesse.

Pregnancy in the context of pulmonary hypertension is characterised by high mortality for the mother and the foetus and is therefore strongly discouraged ; contraception has to be prescribed to patients in reproductive age. Women who decide to continue their pregnancy should be followed by multidisciplinary teams in specialised centres. A specific treatment should be defined with no delay. In case of clinical deterioration, the early, intravenous administration of prostacyclin should be considered. The ideal time and method of delivery are still disputed.

La grossesse dans un contexte d'hypertension pulmonaire est caractérisée par une mortalité élevée pour la mère et le fœtus et fortement découragée ; une contraception doit être prescrite aux patientes dès l'âge de procréer. Les femmes qui décident de poursuivre leur grossesse doivent être suivies par des équipes multidisciplinaires dans des centres spécialisés. Le traitement spécifique doit être adapté sans tarder. En cas de dégradation clinique, l'introduction précoce de prostacycline intraveineuse est envisagée. Le timing et le mode idéaux d'accouchement restent sujets à débat.

Diagnostic Value of the CD103+CD4+/CD4+ Ratio to Differentiate Sarcoidosis from Other Causes of Lymphocytic Alveolitis.

BACKGROUND: The CD103 integrin is present on CD4+ lymphocytes of the bronchial mucosa, but not on peripheral blood CD4+ lymphocytes. It has been hypothesized that CD4+ lymphocytes in pulmonary sarcoidosis originate from redistribution from the peripheral blood to the lung, and therefore do not bear the CD103 integrin. Some data suggest that a low CD103+ percentage among bronchoalveolar lavage fluid (BALF) CD4+ lymphocytes discriminates between sarcoidosis and other diagnoses. OBJECTIVE: To determine the diagnostic value of BALF CD103+ to identify sarcoidosis among other causes of alveolar lymphocytosis in a large retrospective case series. METHODS: Among 391 consecutive bronchoalveolar lavages performed at our institution and analyzed by flow cytometry, we identified 207 cases, which were grouped into nine diagnostic categories: sarcoidosis, tuberculosis, non-tuberculous infections, hypersensitivity pneumonitis, non-specific interstitial pneumonia, organizing pneumonia, drug-induced lung diseases, other interstitial lung diseases (ILDs), and other diagnoses. To assess the discriminative value of the CD103+CD4+/CD4+ ratio to distinguish sarcoidosis from other entities, areas under ROC curves (AUC) were calculated. RESULTS: Sarcoidosis patients (n = 53) had significantly lower CD103+CD4+/CD4+ ratios than patients in other diagnostic categories. The AUC was 62% for sarcoidosis compared to all other diagnoses, and 69% for sarcoidosis compared to other ILDs. When combining CD103+CD4+/CD4+ and CD4+/CD8+ ratios, the AUC increased to 76 and 78%, respectively. When applying previously published cut-offs to our population, the AUC varied between 54 and 73%. CONCLUSIONS: The CD103+CD4+/CD4+ ratio does not accurately discriminate between sarcoidosis and other causes of lymphocytic alveolitis, neither alone nor in combination with the CD4+/CD8+ ratio, and is not a powerful marker for the diagnosis of sarcoidosis.

Radial Ultrasound-Assisted Transbronchial Biopsy: A New Diagnostic Approach for Non-Resolving Pulmonary Infiltrates in Neutropenic Hemato-Oncological Patients.

The role of radial-endobronchial ultrasound (R-EBUS) assisted transbronchial biopsy (TBB) for the diagnosis of peripheral pulmonary lesions is well established. However, no study has addressed its safety and value in hemato-oncological patients presenting with non-resolving infiltrates during persistent febrile neutropenia. To assess safety and feasibility of R-EBUS assisted TBB in severe thrombocytopenic and neutropenic patients. Over a period of 18 months, eight patients were assessed with R-EBUS assisted TBB after adequate platelet transfusion. This technique allowed precise localisation and sampling of the pulmonary lesions in seven of eight patients. In the seven patients, R-EBUS assisted TBB enabled treatment optimization. Invasive fungal infection was diagnosed in four patients, idiopathic acute fibrinous and organising pneumonia in three patients, and a granulomatous inflammation of undetermined origin in one patient. Importantly, no complications, such as bleeding, were observed. R-EBUS assisted TBB is a promising and safe procedure for the evaluation of nonresolving pulmonary infiltrates in febrile neutropenic hemato-oncological patients.