Guidelines of the German Respiratory Society for diagnosis and treatment of adults suffering from acute or chronic cough.

The first set of German guidelines for diagnosis and treatment of patients suffering from acute or chronic cough was published in 2004. Scientific developments over the past five years necessitate an update. The purpose of this document is to assist in ascertaining underlying causes and treating cough, in order to eliminate or minimize impairments of patients' health. The guidelines aim to introduce scientifically founded, evidence-based steps for the diagnosis and treatment of cough and optimize cost-effectiveness. Recommendations are assessed through the GRADE system (The Grades of Recommendation, Assessment, Development and Evaluation). Cough as a symptom is categorized as either acute (lasting up to 8 weeks) or chronic (lasting more than 8 weeks) and attributed to distinct diseases. For acute and chronic cough the diagnostic algorithms are updated; cost effectiveness is also taken into account. Additionally, the most frequent diagnostic errors are highlighted. Finally, available therapeutic options are discussed.

[COPD and infection]. / COPD und Infektion.

Infections are frequent and important causes of exacerbations in patients with COPD. This article reviews underlying mechanisms and therapeutic consequences. A complex interaction exists between COPD, co-morbidities, physical inactivity and systemic inflammation. The components of the postulated chronic inflammatory systemic syndrome need to be identified in more detail; physical inactivity seems to be the least common denominator. The patient's adaptive and innate immune systems play a role for the pathogenesis of infections. When interpreting positive bacterial cultures, it is important to differentiate between colonisation and infection. The impact of viral infections in COPD exacerbation needs further clarification, including the task to distinguish acute infection from viral persistence. Community acquired pneumonias pose a special risk for patients with COPD. Clinical scores and procalcitonin serum concentrations can support decisions on whether or not to start antibiotic treatment. Antibiotics probably do not need to be taken for longer than 5 days, since their efficacy does not increase after longer treatment, while adverse events rise in frequency. Hospitalisations for respiratory exacerbations are associated with increased mortality in COPD.

[Assessment and outcome parameters in COPD]. / Beurteilungs- und Prognosekriterien bei COPD1.

BACKGROUND: A standard outcome parameter for pharmacological trials in COPD has not yet been defined. Therefore, it is the aim of this review to evaluate frequently used parameters for their eligibility as assessment and outcome parameters in COPD. METHODS: A review of the actual scientific literature was performed. RESULTS: It is recommended to continue to rely primarily on the FEV (1), which has been used as a primary variable in the vast majority of trials. In addition, further parameters, such as FVC and IC/TLC should be determined. If available, additional information is provided by RV/TLC, K (co), PaO (2) and PaCO (2). FEV (1) is not a surrogate parameter for dyspnoea, quality of life, and exercise tolerance, which should therefore be assessed separately. Frequency and severity of exacerbations and mortality are important outcome parameters in long-term trials. Complex indices, such as the BODE index, may be superior to single variables. CONCLUSIONS: No single additional parameter has been evaluated sufficiently in order to substitute FEV (1) as the standard parameter for the assessment and outcome in COPD.

Safety and tolerability of bosentan in idiopathic pulmonary fibrosis: an open label study.

Idiopathic pulmonary fibrosis (IPF) is a fatal disease for which no effective treatment exists. In the present study, 12 IPF patients underwent analysis of gas exchange properties using the multiple inert gas elimination technique on day 1 before and after the administration of 125 mg bosentan, a dual endothelin antagonist. Following this, patients received chronic administration for 12 weeks (62.5 mg b.i.d. in week 1, 125 mg b.i.d. thereafter). The primary objective was to determine the effect of bosentan on gas exchange (day 1) and on oxygen saturation and minute ventilation (week 2). With one exception, where redistribution of total pulmonary blood flow from normal ventilation/perfusion (V'/Q') areas (93% before, 72% after bosentan) to low V'/Q' areas (0% before, 22.2% after) was encountered, no patient showed any change in gas exchange (mean+/-SD shunt flow (% of cardiac output) 8.5+/-3.4% before, 6.1+/-2.3% after bosentan; day 1) or oxygen saturation and minute ventilation (week 2). Similarly, none of the secondary parameters was significantly changed either at week 2 or at the end of the study period (week 12). Five patients developed respiratory infections and two died because of pneumonia; this was judged as being unrelated to bosentan intake. In conclusion, bosentan administration does not seem to induce clinically relevant gas exchange abnormalities in idiopathic pulmonary fibrosis patients.

Extrinsic allergic alveolitis with IgA deficiency.

Up to now only 3 cases of extrinsic allergic alveolitis (hypersensitivity pneumonitis) with IgA deficiency have been published worldwide. We had the opportunity to detect two additional cases which will be presented here. Summarizing all cases IgA deficiency is a risk factor for a severe course of the disease and an increased susceptibility to acquire allergic alveolitis by low dose antigen exposure.

Fuzzy logic-based tumor marker profiles improved sensitivity of the detection of progression in small-cell lung cancer patients.

Tumor markers were used for disease monitoring in small-cell lung cancer patients. The aim of this study was to improve diagnostic efficiency in the detection of tumor progression in small-cell lung cancer patients by using fuzzy logic modeling in combination with a tumor marker panel (NSE, ProGRP, Tumor M2-PK, CYFRA 21-1, and CEA). Thirty-three consecutive small-cell lung cancer patients were included in a prospective study. The changes in blood levels of tumor markers and their analysis by fuzzy logic modeling were compared with the clinical evaluation of response versus non-response to therapy. Clinical monitoring was performed according to the standard criteria of the WHO. Tumor M2-PK was measured in plasma with an ELISA, all other markers were measured in sera. At 90% specificity, clinically detected tumor progression was found by the best single marker, NSE, in 32% of all cases. A fuzzy logic rule-based system employing a tumor marker panel increased the sensitivity significantly (P>0.0001) in small-cell carcinomas to 67% with the threemarker combination NSE/ProGRP/Tumor M2-PK and to 56% with the best two-marker combination ProGRP/Tumor M2-PK, respectively. An improvement of sensitivity was also observed using the two-marker combination of ProGRP/NSE (sensitivity 49%) or NSE/Tumor M2-PK (sensitivity 52%). The fuzzy classifier was able to detect a higher rate of progression in small-cell lung cancer patients compared with the multiple logistic regression analysis using the marker combination NSE/ProGRP/Tumor M2-PK (sensitivity 44%; AUC=0.76). With the fuzzy logic method and different tumor marker panels (NSE, ProGRP and Tumor M2-PK), a new diagnostic tool for the detection of progression in patients with small-cell lung cancer is available.

Altered fatty acid composition of lung surfactant phospholipids in interstitial lung disease.

Deterioration of pulmonary surfactant function has been reported in interstitial lung disease; however, the molecular basis is presently unclear. We analyzed fatty acid (FA) profiles of several surfactant phospholipid classes isolated from large-surfactant aggregates of patients with idiopathic pulmonary fibrosis (IPF; n = 12), hypersensitivity pneumonitis (n = 5), and sarcoidosis (n = 12). Eight healthy individuals served as controls. The relative content of palmitic acid in phosphatidylcholine was significantly reduced in IPF (66.8 +/- 2.5%; means +/- SE; P < 0.01) but not in hypersensitivity pneumonitis (78.5 +/- 1.8%) and sarcoidosis (78.2 +/- 3.1%; control 80.1 +/- 0.7%). In addition, the phosphatidylglycerol FA profile was significantly altered in the IPF patients, with a lower relative content of its major FA, oleic acid, at the expense of saturated FA. In the phosphatidylcholine class, a significant correlation between the impairment of biophysical surfactant function and decreased percentages of palmitic acid was noted. We conclude that significant alterations in the FA profile of pulmonary surfactant phospholipids occur predominantly in IPF and may contribute to the disturbances of alveolar surface activity in this disease.