Peipsimaa vanausulised läbi aegade – rahvakultuur ja elu

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Caplani sündroom. Haigusjuhu kirjeldus

Caplani sündroomi ehk reumatoidse pneumokonioosi patognoomiline tunnus on iseloomulik radioloogiline leid kopsudes reumatoidartriidi ja pneumokonioosiga patsientidel. Diferentsiaaldiagnoosideks on pahaloomulised kasvajad ja tuberkuloos. Caplani sündroomi ravi on sümptomaatiline, haigusspetsiifiline ravi puudub. Seetõttu jääb kõige olulisemaks haiguse profülaktika. Artiklis on kirjeldatud haigusjuhtu Caplani sündroomiga patsiendil, kellel iseloomulikud muutused kopsudes avastati rutiinse radioloogilise uuringu käigus. Diagnoosi õige hüpotees tekkis tänu põhjalikult võetud anamneesile, eelkõige tööanamneesile. Eesti Arst 2012; 91(7):361–36

Allergy in severe asthma

It is well recognized that atopic sensitisation is an important risk factor for asthma, both in adults and in children. However, the role of allergy in severe asthma is still under debate. The term "Severe Asthma" encompasses a highly heterogeneous group of patients who require treatment on steps 4-5 of GINA guidelines to prevent their asthma from becoming "uncontrolled", or whose disease remains "uncontrolled" despite this therapy. Epidemiological studies on emergency room visits and hospital admissions for asthma suggest the important role of allergy in asthma exacerbations. In addition, allergic asthma in childhood is often associated with severe asthma in adulthood. A strong association exists between asthma exacerbations and respiratory viral infections, and interaction between viruses and allergy further increases the risk of asthma exacerbations. Furthermore, fungal allergy has been shown to play an important role in severe asthma. Other contributing factors include smoking, pollution and work-related exposures. The "Allergy and Asthma Severity" EAACI Task Force examined the current evidence and produced this position document on the role of allergy in severe asthma. This article is protected by copyright. All rights reserved

Research needs in allergy: an EAACI position paper, in collaboration with EFA

Abstract In less than half a century, allergy, originally perceived as a rare disease, has become a major public health threat, today affecting the lives of more than 60 million people in Europe, and probably close to one billion worldwide, thereby heavily impacting the budgets of public health systems. More disturbingly, its prevalence and impact are on the rise, a development that has been associated with environmental and lifestyle changes accompanying the continuous process of urbanization and globalization. Therefore, there is an urgent need to prioritize and concert research efforts in the field of allergy, in order to achieve sustainable results on prevention, diagnosis and treatment of this most prevalent chronic disease of the 21 st century. The European Academy of Allergy and Clinical Immunology (EAACI) is the leading professional organization in the field of allergy, promoting excellence in clinical care, education, training and basic and translational research, all with the ultimate goal of improving the health of allergic patients. The European Federation of Allergy and Airways Diseases Patients' Associations (EFA) is a non-profit network of allergy, asthma and Chronic Obstructive Pulmonary Disorder (COPD) patients' organizations. In support of their missions, the present EAACI Position Paper, in collaboration with EFA, highlights the most important research needs in the field of allergy to serve as key recommendations for future research funding at the national and European levels. Although allergies may involve almost every organ of the body and an array of diverse external factors act as triggers, there are several common themes that need to be prioritized in research efforts. As in many other chronic diseases, effective prevention, curative treatment and accurate, rapid diagnosis represent major unmet needs. Detailed phenotyping/endotyping stands out as widely required in order to arrange or re-categorize clinical syndromes into more coherent, uniform and treatment-responsive groups. Research efforts to unveil the basic pathophysiologic pathways and mechanisms, thus leading to the comprehension and resolution of the pathophysiologic complexity of allergies will allow for the design of novel patient-oriented diagnostic and treatment protocols. Several allergic diseases require well-controlled epidemiological description and surveillance, using disease registries, pharmacoeconomic evaluation, as well as large biobanks. Additionally, there is a need for extensive studies to bring promising new biotechnological innovations, such as biological agents, vaccines of modified allergen molecules and engineered components for allergy diagnosis, closer to clinical practice. Finally, particular attention should be paid to the difficult-to-manage, precarious and costly severe disease forms and/or exacerbations. Nonetheless, currently arising treatments, mainly in the fields of immunotherapy and biologicals, hold great promise for targeted and causal management of allergic conditions. Active involvement of all stakeholders, including Patient Organizations and policy makers are necessary to achieve the aims emphasized herein

Mechanisms of allergic airway inflammation. Role of bone marrow

Allergic airway (AW) inflammation is characterized by accumulation of inflammatory cells within the AW. It is likely that the accumulation of cells within AW is a combination of increased production, migration and prolonged survival of the cells. Inflammatory cells develop from CD34+hematopoietic progenitor cells. Importantly, allergic subjects have increased numbers of CD34+progenitors in bone marrow (BM) and AW. The aims of this thesis were to determine the mechanisms underlining the allergen-induced accumulation of eosinophils and neutrophils in the AW. With reference to allergen-induced AW eosinophilia, the contribution of eosinophilopoiesis in different compartments was studied. In addition, the contribution of the pro-inflammatory cytokine IL-17 in accumulation of eosinophils and neutrophils within the AW was evaluated. The effect of local corticosteroids and systemic blockage of IL-17 cytokine, respectively, were determined. For that purpose, mice models of allergen exposure-induced allergic inflammation and nasal biopsies from allergic rhinitis patients were used. Repeated allergen exposure of sensitized mice resulted in an increase in the number of primitive myeloid progenitors within the BM CD34+cell population. The earliest eosinophil-committed CD34+cells were restricted to the BM compartment. After the allergen exposure, a substantial part of CD34+progenitor cells was de novo produced. In the BM, allergen exposure increased the number of CD34+eosinophilic cells and CD34-mature eosinophils. In blood and AW, allergen exposure induced an increase in the number of CD34+eosinophilic cells, CD34- mature eosinophils and also in newly produced CD34+cells. Furthermore, allergen exposure induced a shift in differentiation of BM, blood and BALf eosinophil-committed CD34+cells towards more mature eosinophils. Importantly, AW CD34+cells from allergen-exposed mice expressed stem cell antigen (Sca-1), produced eosinophil colonies and in response to stimulation with IL-5 expressed IL-5 receptor a chain (IL-5Ra). Moreover, AW CD34+eosinophilic cells themselves released high amounts of IL-5 after unspecific stimulation. In the mouse model of repeated allergen exposure, administration of an intranasal corticosteroid, fluticasone propionate (FP), significantly reduced the allergen-induced elevation of BM eosinophil number, without substantial effect on the number of AW eosinophils. In subjects with allergic rhinitis, the exposure to allergen increased the number of nasal mucosal CD34+hematopoietic cells concomitantly with up-regulation of CXCR4 expression within the CD34+cell population. Furthermore, also the number of CD34+eosinophils in nasal mucosa was increased following exposure to allergen. A local corticosteroid, FP, provided protection against this pollen-induced increase in tissue CD34+cells. The systemic pre-treatment with an anti-IL-17 antibody in allergen-exposed mice reduced the number of AW neutrophils, but not eosinophils, without any significant changes in BM granulocyte counts. In addition, the expression of matrix metalloproteinase-9 (MMP-9) by AW neutrophils but not eosinophils was downregulated by the pre-treatment with anti-IL-17 antibody. In conclusion, this thesis demonstrates the exclusive role of BM in the first-line commitment of hematopoietic progenitors into the eosinophilic lineage. Importantly, allergen exposure induces not only a shift in the differentiation of eosinophil-committed progenitors towards mature cells, but also increases in the number of primitive myeloid progenitors in BM. In response to allergen exposure, CD34+progenitor cells are mobilized into the airways with one mechanism being CXCR4-mediated cell recruitment. The AW CD34+cells maintain a phenotype of a true hematopoietic progenitor cells and retain the ability to multiply likely via autocrine IL-5 release and IL-5-induced up-regulation of IL-5Ra. Local corticosteroids inhibit the allergen-induced BM and AW eosinophilopoiesis as well as allergen-induced CXCR4-mediated recruitment of CD34+cells into AW. Endogenous IL-17 increases the number of MMP-9+ neutrophils in allergic AW inflammation, without substantial effect on the number of eosinophils

Toward Clinically Applicable Biomarkers For Asthma: An Eaaci Position Paper

Inflammation, structural, and functional abnormalities within the airways are key features of asthma. Although these processes are well documented, their expression varies across the heterogeneous spectrum of asthma. Type 2 inflammatory responses are characterized by increased levels of eosinophils, FeNO, and type 2 cytokines in blood and/or airways. Presently, type 2 asthma is the best-defined endotype, typically found in patients with allergic asthma, but surprisingly also in nonallergic patients with (severe) asthma. The etiology of asthma with non-type 2 inflammation is less clear. During the past decade, targeted therapies, including biologicals and small molecules, have been increasingly integrated into treatment strategies of severe asthma. These treatments block specific inflammatory pathways or single mediators. Single or composite biomarkers help to identify patients who will benefit from these treatments. So far, only a few inflammatory biomarkers have been validated for clinical application. The European Academy of Allergy & Clinical Immunology Task Force on Biomarkers in Asthma was initiated to review different biomarker sampling methods and to investigate clinical applicability of new and existing inflammatory biomarkers (point-of-care) to support diagnosis, targeted treatment, and monitoring of severe asthma. Subsequently, we discuss existing and novel targeted therapies for asthma as well as applicable biomarkers.WoSScopu

Heterogeneity in the use of biologics for severe asthma in Europe: a SHARP ERS study

International audienceIntroduction Treatment with biologics for severe asthma is informed by international and national guidelines and defined by national regulating bodies, but how these drugs are used in real-life is unknown. Materials and methods The ERS SHARP clinical research collaboration conducted a 3-step survey collecting information on asthma biologics use in Europe. Five geographically distant countries defined the survey questions, focusing on 7 endpoints: biologics availability and financial issues, prescription and administration modalities, inclusion criteria, continuation criteria, switching biologics, combining biologics, and evaluation of corticosteroid toxicity. The survey was then sent to SHARP National Leads of 28 European countries. Finally, selected questions were submitted to a broad group of 263 asthma experts identified by national societies. Results Availability of biologics varied between countries, with 17/28 countries having all 5 existing biologics. Authorised prescribers (pulmonologists and other specialists) also differed. In-hospital administration was the preferred deliverance modality. While exacerbation rate was used as an inclusion criterion in all countries, FEV 1 was used in 46%. Blood eosinophils were an inclusion criterion in all countries for IL5- and IL4/IL13- targeted biologics, with varying thresholds. There were no formally established criteria for continuing biologics. Reduction in exacerbations represented the most important benchmark, followed by improvement in asthma control and quality of life. Only 73% (191/263) of surveyed clinicians assessed their patients for corticosteroid-induced toxicity. Conclusion Our study reveals important heterogeneity in the use of asthma biologics across Europe. To what extent this impacts on clinical outcomes relevant to patients and healthcare services needs further investigation