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Kardos P.,Respiratory
Breathe | Year: 2010

Cough is highly prevalent as a cumbersome presenting complaint for many patients. The symptom cough is elicited by a myriad of very different respiratory and nonrespiratory diseases. Symptomatic pharmacological treatment is of very limited efficacy. Presently, no new drug for cough in the pipeline has completed phase II development. Therefore, treating cough requires exact diagnosis for causal treatment. Cough is often the first (but not necessarily an early) symptom of life-threatening diseases, such as lung tumours or recurrent pulmonary embolism. Thus, in 2004, the German Respiratory Society published evidence-based guidelines on the management of cough. Acute and chronic cough were defined, and algorithms were provided for diagnostic workup. In 2010, the guidelines were updated (http://leitlinien.net). An abridged english version is also now available [1]. In this review, evidence-based recommendations (mostly weak evidence or consensus) from these guidelines are adapted into learning points. Source

Pescosolido N.,Respiratory | Buomprisco G.,University of Rome La Sapienza
European Endocrinology | Year: 2014

Retinopathy is a serious and common complication of diabetes that represents the leading cause of blindness, among people of working age, in developed countries. It is estimated that the number of people with diabetic retinopathy (DR) will increase from 126.6 million in 2011 to 191 million by 2030. The visual function that seems to be affected first in the course of DR is probably the contrast sensitivity; in addition, being mainly a macular function, the perception of colour is also compromised. Moreover, the duration of the disease, the levels of glycated haemoglobin (HbA1c) and the presence of cystoid macular oedema are strongly associated with the impairment of fixation stability in patients with diabetes with clinically significant macular oedema, suggesting the possible diagnostic role of microperimetry. The test of contrast sensitivity and the microperimetry and the chromatic sensitivity tests have proved to be useful, safe, reproducible and inexpensive tools to diagnose the disease early. © Touch Medical Media 2014. Source

Price D.B.,University of Aberdeen | Price D.B.,Research in Real Life | Rigazio A.,Research in Real Life | Campbell J.D.,Aurora Pharmaceutical | And 12 more authors.
The Lancet Respiratory Medicine | Year: 2015

Background: Elevated sputum eosinophil counts predict asthma exacerbations and responsiveness to inhaled corticosteroids but are impractical to measure in primary care. We investigated the relation between blood eosinophil count and prospective annual asthma outcomes for a large UK cohort. Methods: This historical cohort study used anonymised medical record data to identify primary care patients with asthma aged 12-80 years with 2 years of continuous records, including 1 year before (baseline) and 1 year after (outcome) their most recent eosinophil count. Negative binomial regression was used to compare outcome exacerbation rates and logistic regression to compare odds of asthma control for patients with blood eosinophil counts of 400 cells per μL or less versus greater than 400 cells per μL, adjusting for age, sex, body-mass index, smoking status, and Charlson comorbidity index. The study is registered at ClinicalTrials.gov, number NCT02140541. Findings: Overall, 20 929 (16%) of 130 248 patients had blood eosinophil counts greater than 400 cells per μL. During the outcome year, these patients experienced significantly more severe exacerbations (adjusted rate ratio [RR] 1·42, 95% CI 1·36-1·47) and acute respiratory events (RR 1·28, 1·24-1·33) than those with counts of 400 cells per μL or less. They also had significantly lower odds of achieving overall asthma control (OR 0·74, 95% CI 0·72-0·77), defined as limited reliever use and no asthma-related hospital attendance or admission, acute course of oral corticosteroids, or prescription for antibiotics. Exacerbation rates increased progressively with nine ascending categories of blood eosinophil count as compared with a reference category of 200 cells per μL or less. Interpretation: Patients with asthma and blood eosinophil counts greater than 400 cells per μL experience more severe exacerbations and have poorer asthma control. Furthermore, a count-response relation exists between blood eosinophil counts and asthma-related outcomes. Blood eosinophil counts could add predictive value to Global Initiative for Asthma control-based risk assessment. Funding: Teva Pharmaceuticals. © 2015 Elsevier Ltd. Source

Gordon C.L.,Austin Hospital | Johnson P.D.R.,Austin Hospital | Johnson P.D.R.,University of Melbourne | Permezel M.,Mercy Hospital for Women | And 15 more authors.
Clinical Infectious Diseases | Year: 2010

Background. Severe pandemic 2009 influenza A virus (H1N1) infection is associated with risk factors that include pregnancy, obesity, and immunosuppression. After identification of immunoglobulin G2 (IgG2) deficiency in 1 severe case, we assessed IgG subclass levels in a cohort of patients with H1N1 infection. Methods. Patient features, including levels of serum IgG and IgG subclasses, were assessed in patients with acute severe H1N1 infection (defined as infection requiring respiratory support in an intensive care unit), patients with moderate H1N1 infection (defined as inpatients not hospitalized in an intensive care unit), and a random sample of healthy pregnant women. Results. Among the 39 patients with H1N1 infection (19 with severe infection, 7 of whom were pregnant; 20 with moderate infection, 2 of whom were pregnant), hypoabuminemia (P< .001 ), anemia (P < .001), and low levels of total IgG (P = .01), IgG1 (P = .022), and IgG 2 (15 of 19 vs 5 of 20; P = .001; mean value ± standard deviation [SD], 1.8 ± 1.7 g/L vs 3.4 ± 1.4 g/L; P = .003) were all statistically significantly associated with severe H1N1 infection, but only hypoalbuminemia (P = .02) and low mean IgG2 levels (P = .043) remained significant after multivariate analysis. Follow-up of 15 (79%) surviving IgG2-deficient patients at a mean (±SD) of 90 ± 23 days (R, 38-126) after the initial acute specimen was obtained found that hypoalbuminemia had resolved in most cases, but 11 (73%) of 15 patients remained IgG2 deficient. Among 17 healthy pregnant control subjects, mildly low IgG1 and/or IgG2 levels were noted in 10, but pregnant patients with H1N1 infection had significantly lower levels of IgG 2 (P = .001). Conclusions. Severe H1N1 infection is associated with IgG2 deficiency, which appears to persist in a majority of patients. Pregnancy-related reductions in IgG2 level may explain the increased severity of H1N1 infection in some but not all pregnant patients. The role of IgG2 deficiency in the pathogenesis of H1N1 infection requires further investigation, because it may have therapeutic implications. © 2010 by the Infectious Diseases Society of America. All rights reserved. Source

Henault J.,Respiratory | Martinez J.,St Jude Childrens Research Institute | Riggs J.M.,Respiratory | Tian J.,Respiratory | And 11 more authors.
Immunity | Year: 2012

Toll-like receptor-9 (TLR9) is largely responsible for discriminating self from pathogenic DNA. However, association of host DNA with autoantibodies activates TLR9, inducing the pathogenic secretion of type I interferons (IFNs) from plasmacytoid dendritic cells (pDCs). Here, we found that in response to DNA-containing immune complexes (DNA-IC), but not to soluble ligands, IFN-α production depended upon the convergence of the phagocytic and autophagic pathways, a process called microtubule-associated protein 1A/1B-light chain 3 (LC3)-associated phagocytosis (LAP). LAP was required for TLR9 trafficking into a specialized interferon signaling compartment by a mechanism that involved autophagy-related proteins, but not the conventional autophagic preinitiation complex, or adaptor protein-3 (AP-3). Our findings unveil a new role for nonconventional autophagy in inflammation and provide one mechanism by which anti-DNA autoantibodies, such as those found in several autoimmune disorders, bypass the controls that normally restrict the apportionment of pathogenic DNA and TLR9 to the interferon signaling compartment. © 2012 Elsevier Inc. Source

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