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Data about the clinical presentation of chronic obstructive pulmonary disease (COPD) have resulted in a new classification of the disease. The degree of airflow limitation has been amended by symptoms and exacerbation rate. The standard pharmacotherapy of stable COPD is in transition, as fixed combinations of long acting beta agonists and long acting anticholinergics are in the late stages of clinical development. On this background inhaled corticosteroids will need to be re-evaluated. Roflumilast is a recently approved therapeutic option that primarily diminishes exacerbation frequency in patients with chronic bronchitis and severe airflow obstruction (FEV(1) < 50%). In COPD patients with acute exacerbations procalcitonin levels can be used to guide antibiotic therapy. Comparable clinical outcomes can be achieved while using significantly less amounts of antibiotics.

Allergic diseases of the lungs may affect the airways, the pulmonary parenchyma and the pulmonary vessels. The most relevant representatives are allergic asthma, hypersensitivity pneumonitis, bronchopulmonary aspergillosis and the Churg-Strauss syndrome. The type of allergic reaction and the pathophysiological consequences vary considerably between these entities. New drugs target specific mechanisms based on new insights into the pathogenetic processes of the underlying disease.

Acute respiratory failure and the "acute respiratory distress syndrome" (ARDS) are frequent medical conditions in critically ill patients. Various causes can potentially result in the development of ARDS. Two cases are presented, in which malignant diseases were identified as causes of the respiratory failure. The first patient was diagnosed with an acute myeloic leukemia M5 (FAB). In the second patient, lung histology revealed an adenocarcinoma of the lung. These case reports show that in addition to the classical causes of ARDS, specific disease entities can mimic this form of respiratory failure. Beside solid cancers and lymphomas, acute and progressive forms of inflammatory, parenchymal lung diseases (such as acute interstitial pneumonitis, acute eosinophilic pneumonia, diffuse alveolar hemorrhagia, and acute hypersensitivity pneumonitis) can manifest with this picture. As a consequence, the diagnostic workup of respiratory failure of unknown cause should include these entities.

Dyspnoea is a very subjective phenomenon based on the variation in severity for a given degree of functional impairment. It is difficult to grade dyspnoea. Dyspnoea is caused by a variety of physiological, pathophysiological, psychological and environmental factors. The mechanisms leading to dyspnoea are not completely understood. It is known that mechanical reasons like ventilation disturbances (obstruction, restriction), impairment of the ventilation muscles, skeletal deformation and many other reasons can cause dyspnoea. Every pulmonary or cardiac disease may induce dyspnoea depending on the progression of the underlying disease. The aim of this article is to give an overview of basic pathophysiological mechanisms, diagnostic procedures and considerations with regard to possible differential diagnoses.

It is currently believed that the most important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD) is inflammation of the small airways caused by inhaled particles and gases. In this context, a disturbance of the physiological balance between proteases and antiproteases develops that may cause lung emphysema. Moreover, oxidative stress seems to be important, as it may enhance the inflammatory reaction. The development of emphysema may also involve a loss of alveolar cells by apoptosis. Finally, several studies have indicated that a systemic inflammation is induced by COPD that may be of relevance to the development of systemic components that are observed in COPD patients.

Asthma, chronic obstructive pulmonary diseases, interstitial lung diseases and myocardial dysfunction are the leading diagnoses of patients with dyspnoea. Acute dyspnoea appears suddenly or within a few hours and is caused by a relatively limited number of conditions some of which can be life-threatening. Therefore, it is of utmost importance to identify the cause of dyspnoea immediately. Once found, the disorder is treated according to the guidelines for the underlying disease.

The chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality worldwide. Recently, international guidelines for diagnosis, prevention and therapy have been published. Now also a modified German version of these guidelines is available. The diagnosis and the severity of the disease is established on the basis of spirometric findings. All stages of COPD are treated with bronchodilators (beta 2-sympathomimetics and anticholinergics). In addition, in stage II and III theophylline and inhaled corticosteroids may be used. Systemic steroids should be restricted to acute exacerbations. For patients with advanced COPD long-term oxygen therapy and in selected cases surgical procedures may be indicated. Rehabilitation measures are of high value. Strategies for primary prevention and smoking cessation programs are extremely important. To get to the diagnosis of COPD as early as possible, all smokers with cough and phlegm should undergo spirometry.

Previous studies have shown the implication of beta-defensins in host defense of the human body. The human beta-defensins 1 and 2 (hBD-1, hBD-2) have been isolated by biochemical methods. Here we report the identification of a third human beta-defensin, called human beta-defensin 3 (hBD-3; cDNA sequence, Genbank accession no. AF295370), based on bioinformatics and functional genomic analysis. Expression of hBD-3 is detected throughout epithelia of many organs and in non-epithelial tissues. In contrast to hBD-2, which is upregulated by microorganisms or tumor necrosis factor-alpha (TNF-alpha), hBD-3 expression is increased particularly after stimulation by interferon-gamma. Synthetic hBD-3 exhibits a strong antimicrobial activity against gram-negative and gram-positive bacteria and fungi, including Burkholderia cepacia. In addition, hBD-3 activates monocytes and elicits ion channel activity in biomembranes, specifically in oocytes of Xenopus laevis. This paper also shows that screening of genomic sequences is a valuable tool with which to identify novel regulatory peptides. Human beta-defensins represent a family of antimicrobial peptides differentially expressed in most tissues, regulated by specific mechanisms, and exerting physiological functions not only related to direct host defense.

Study Objective: To analyze the extent to which the clinical diagnosis of bleach-induced asthma can be confirmed by laboratory tests and to determine the role of work-related exposure to bleaching powder in a group of hairdressers with respiratory complaints., Methods: The study population consisted of 55 female hairdressers who had regular contact with various hair products and a clinical history of job-related rhinitic and/or asthmatic symptoms. We divided the individuals into two groups: group I, with asthmatic symptoms (n = 38), and group II, without asthmatic symptoms (control group, n = 17). All subjects underwent immunological, pulmonary-function, and nonspecific bronchial provocation tests, and 46 study participants were subjected to a standardized bleaching-powder test in a designated chamber., Results: There were 13 positive responses to bleaching powder in the skin test, and 32 individuals showed positive bronchial responsiveness to acetylcholine; positive responses to the challenge with bleaching powder occurred in 9 women (22% of those tested). None of the women in group II reacted to bleaching powder. There was no significant difference between persons with a positive or a negative bronchial provocation test with regard to the evaluated parameters., Conclusions: In the diagnostic workup of hairdressers with work-related respiratory symptoms, bleaching powder is one of the products that need to be tested. As not every patient with an asthmatic response to bleaching powder shows a positive response to the acetylcholine challenge test, in doubtful cases a specific exposure test may be recommendable.

We performed diisocyanate inhalation tests (maximal concentration, 20 ppb; exposure time, 1-2 h) using toluene diisocyanate (TDI, n = 15) and diphenylmethane diisocyanate (MDI, n = 7) as well as methacholine challenges in 19 workers who had a clinical history of TDI/MDI-induced asthma. Additionally we tested volunteers who had no previous contact with diisocyanates: 10 healthy individuals with a negative methacholine test and 14 patients with asthma and a positive methacholine test were exposed to TDI. In all, 1 of the normal volunteers and 3 of the patients with asthma unrelated to diisocyanates showed a positive airway reaction to TDI, and 13 of the 19 diisocyanate workers displayed a positive result in the TDI/MDI inhalation test; however, only 6 of these 13 individuals reacted to methacholine. Furthermore, 3 of the 6 patients with a negative TDI/MDI challenge test demonstrated a significant response to methacholine. We conclude that bronchial hyperreactivity as evaluated by the methacholine challenge test is not closely related to isocyanate-induced bronchoconstriction and, therefore, the metacholine challenge is only of limited diagnostic value in patients with suspected isocyanate-induced asthma.