The role of the novel adipokines vaspin and omentin in chronic inflammatory diseases.

Obesity is a disease of epidemic proportions in many countries around the world. White adipose tissue is an active endocrine organ; therefore, its excess results in chronic and systemic inflammation. This inflammation is caused and maintained mostly by adipokines secreted by adipose tissue cells, mainly adipocytes and macrophages. The relatively newly discovered adipokines comprise vaspin and omentin. Their concentration in the blood, tissues, or bronchial secretion varies depending on the amount of adipose tissue and other accompanying factors, including comorbidities. The aim of this article is to demonstrate the usefulness of omentin and vaspin as biomarkers in inflammatory diseases. The Medline/PubMed database was used to search for information on obesity, inflammation, omentin, vaspin, and adipose tissue. Data from selected scientific studies, both original and review papers, are presented. Vaspin has been found to improve insulin sensitivity mainly in white adipose tissue. Omentin has an anti-inflammatory effect and, like vaspin, sensitizes tissues to insulin. The serum concentration and tissue expression of both adipokines are different in different inflammatory diseases. This review aims to present the biological functions of vaspin and omentin in the body and to indicate the possible use of these adipokines as disease markers in the future.

Pulmonary rehabilitation in interstitial lung diseases: A review of the literature.

There are more than 200 different diseases classed as interstitial lung diseases (ILDs). For epidemiological and practical purposes, ILDs are classified into diseases of known and unknown etiology. The aim of this review is to evaluate our current knowledge about the efficacy and safety of pulmonary rehabilitation (PR) in patients with ILDs. Other issues, such as ILD pathogenesis, prevalence and comorbidity, are also elaborated in the review. Pulmonary rehabilitation is an important part of comprehensive care for patients with ILDs. In comparison to PR for patients with chronic pulmonary obstructive disease (COPD), the number of clinical studies concerning PR for patients with ILDs is small. The majority of trials have been performed in relatively small groups of patients. The principles of PR in this group of patients are the same as for patients with COPD. Exercise-induced desaturation is frequently observed during PR, which is the main source of complications in patients with ILDs. Major differences between ILD and COPD patients include poorer exercise tolerance and faster development of respiratory failure in patients with ILDs.

Eradication of Helicobacter pylori, as add-on therapy, has a significant, but temporary influence on recovery in chronic idiopathic urticaria: a placebo-controlled, double blind trial in the Polish population.

INTRODUCTION: The infectious factor like Helicobacter pylori (HP) has been thought to trigger the vicious circle of chronic idiopathic urticaria (CIU), therefore its eradication could modify the course of the disease. AIM: To reveal the influence of HP eradication on CIU clinical course. MATERIAL AND METHODS: Sixty-four CIU patients, receiving fexofenadine, as the basic treatment, took part in the research, divided into 3 groups: HP patients treated by eradication, HP patients receiving placebo, and patients without bacteria. Gastroscopy, urease test and histopathology were done to detect HP. Patients with HP were randomized and received eradication treatment or placebo. The efficacy of eradication was checked after 6 weeks by means of another gastroscopy, urease test and histopathology. In the 6th week and in the 4th and 6th month after eradication, the symptoms were evaluated basing on the score symptom scale. RESULTS: Helicobacter pylori did not occur more frequently in CIU patients than in the healthy population. A statistically significant clinical improvement of CIU symptoms was observed in the 6th week after eradication as compared to the group receiving placebo (p = 0.02) and patients who were not infected (p = 0.02). Further observation in the eradicated patients group revealed the rebound phenomenon - worsening of the clinical state (p = 0.001), which in the 4th month did not differ from the patients not infected or patients receiving placebo. CONCLUSIONS: Although HP occurs as frequently in CIU patients as in the healthy population, eradication, added to basic antihistaminic treatment, has a significant influence on CIU patients' recovery parallel to the reduction of stomach inflammation features.

[Rhinitis and sinusitis: influence on asthma and COPD]. / Niezyt nosa i zapalenie zatok--wplyw na astme oskrzelowa.

Basing on epidemiology, pathophysiology and clinical manifestations we can show an important correlation between rhinitis and bronchial asthma. Prevalence of allergic rhinitis in childhood is an early manifestation of atopy. It is estimated that allergic rhinitis occurs in about 60% of patients before the onset or simultaneously with bronchial asthma. The epidemiologic, etiopathogenetic and clinical data demonstrate that the upper and lower airways are one system, which, in the case of allergic inflammation induces common mechanisms intensifying and maintaining this process. There is no doubt that allergic rhinitis is a risk factor of asthma development. Early diagnosis, treatment and prophylaxis should involve both the upper and lower airways. Coexistence of sinusitis and nasal polyps is another factor causing bronchial hyperreactivity and asthma symptoms.

[Blood and tissue eosinophilia in patient with angioedema caused by inhibitor of angiotensin converting enzyme (ACE)--case report and a view of literature]. / Eozynofilia obwodowa i tkankowa u pacjenta z obrzekiem naczynioruchowym wywolanym inhibitorem enzymu konwertujacego angiotensyne (ACE)--opis przypadku i przeglad pismiennictwa.

A case of angioedema caused by enalapril, undiagnosed for 5 years was presented. Enhanced blood and tissue eosinophilia shown in nasal smear was observed. In addition increased activity of coagulation system was shown manifested by enhance of concentration of Hageman factor and cardiolipin antibodies IgM and IgA isotype. The role of coagulation, complement and fibrinolysis systems in pathogenesis of ACE-inhibitors induced angioedema was discussed. The influence of bradykinin on activity of eosinophils was analyzed.

[Histamine receptors expression on lymphocytes and neutrophils in glucocorticosteroid sensitive and resistant asthma patients]. / Ekspresja receptorów histaminowych na limfocytach i neutrofilach u chorych na astme wrazliwa i oporna na glikokortykosteroidy.

Histamine is a physiological mediator which exerts both, effector and regulatory influence through its receptors on various cells. In the study we evaluated the expression of histamine receptors (HR) on inflammatory cells (lymphocytes and neutrophils) in glucocorticosteroid sensitive (n. = 17) and resistant (n. = 19) asthmatic patients and healthy subjects (n = 14). Moreover, we examined in vitro the influence of cortisol on HR expression in both studied groups with asthma and in a control group. We concluded that HR expression on lymphocytes was similar in all studied subjects. However, HR expression on neutrophils in both groups of asthmatic patients was significantly decreased compared to the control group. After the in vitro incubation with cortisol, we observed a significant decrease in HR expression on neutrophils (10(-8)-10(-5) M) and lymphocytes (10(-8)-10(-4) M) only in healthy subjects. Taking into consideration that histamine proinflammatory action is mediated by H1 receptor, and that in patients treated with long-time systemic GCS therapy we did not observe any decrease in HR expression in vitro, we suggest additional therapy with the second-generation antihistamines. These drugs not only block H1 receptors, but also have an anti-inflammatory effect.

[Non-compliance resulting in fatal asthmatic attack in a 27-year-old woman]. / Trudna, ciezka astma: zgon w stanie astmatycznym u 27-letniej kobiety wczesniej odmawiajacej przewleklego leczenia przeciwzapalnego.

We describe a case of fatal asthmatic attack in 27-year-old woman with type II brittle asthma and pollinosis. Despite recurrent episodes of severe asthmatic attacks she refused prolonged therapy with the exception of beta 2-agonists used when needed. The day prior to the fatal attack she was intensively exposed to pollens. She ineffectively tried to manage the attack with high doses of beta 2-agonists administered by MDI and jet nebulizer. After being intubated and transferred to the hospital, she was ventilated mechanically and treated intensively with high doses of corticosteroids, beta 2-agonists, both intravenously and in nebulisation, and nebulised with anticholinergics, but remained unresponsive to the therapy. She gradually deteriorated and died after nine hours of treatment. We conclude that the unresponsiveness to the treatment was mainly due to down-regulation of beta 2-receptors and point out the necessity of regular treatment with inhaled corticosteroids in patients with brittle asthma type II, even in the absence of symptoms.