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dyspnea/inflammation

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OBJECTIVE Dyspnea perception in asthmatics differs between subjects. Poor perception is usually associated with increased risk of asthma attack/exacerbation. The advanced stage of the disease and the presence of eosinophilic airways inflammation have been recently recognized as being responsible for

Shortness of breath in a patient with inflammatory bowel disease.

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Cytomegalovirus (CMV) is an important cause of morbidity and mortality in immunocompromised patients. Although immunosuppressive therapy is the mainstay of medical treatment for patients with inflammatory bowel disease, the importance of CMV as a cause of pneumonia in this group is less well
Evaluation of the state of respiratory muscles during lung hyperinflation and their role in the development of dyspnea in severe chronic obstructive pulmonary disease involved 18 patients with stage III-IV disease (mean age 66.1 +/- 6.5 yr; mean duration of the disease 16.7 +/- 8.4 yr). It included
BACKGROUND There are a variable number of obese subjects with self-reported diagnosis of asthma but without current or previous evidence of airflow limitation, bronchial reversibility, or airway hyperresponsiveness (misdiagnosed asthma). However, the mechanisms of asthma-like symptoms in obesity

Airway nerves and dyspnea associated with inflammatory airway disease.

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The neurobiology of dyspnea is varied and complex, but there is little doubt that vagal nerves within the airways are capable of causing or modulating some dyspneic sensations, especially those associated with inflammatory airway diseases. A major contributor to the dyspnea associated with

Breathlessness and inflammation: potential relationships and implications.

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Breathlessness and chronic inflammation both span a wide range of disease contexts and hold prognostic significance. The possibility of a causal relationship between the two has been hypothesized. The aims of this article are to review the intersections between breathlessness and inflammation in the

Inflammatory biomarkers predicting prognosis in patients with acute dyspnea.

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OBJECTIVE The objective was to identify inflammatory biomarkers that predict risk of 90-day mortality in patients with acute dyspnea. METHODS We analyzed 25 inflammatory biomarkers, in plasma, in 407 adult patients admitted to the emergency department (ED) with acute dyspnea and related them to risk
Inflammatory bowel disease complications can be related to inflammatory bowel disease-related pulmonary diseases or a form of hypersensitivity pneumonitis secondary to the immunosuppressive medications. We present a patient with intermittent chest pain and hypoxic respiratory failure who was found

[Dyspnea and inflammatory syndrome].

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[An atypical cause of asthmatic dyspnea - an inflammatory bronchial polyp].

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Poor dyspnea perception might be a risk factor for developing asthma exacerbations. We investigated whether severe asthmatics with recurrent exacerbations (brittle asthma) have different dyspnea perception and sputum cells compared with equally severe, but stable asthmatics, or patients with mild
We studied the perception of bronchoconstriction in asthmatic subjects who were randomly treated with inhaled beta 2 agonist given either alone (n = 9) or associated with inhaled corticosteroids (n = 9). Methacholine and bradykinin challenges, bronchoalveolar lavage, and bronchial biopsies were

Pathophysiology of dyspnea.

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Dyspnea may be defined as an uncomfortable sensation of breathing. The sense of respiratory effort, chemoreceptor stimulation, mechanical stimuli arising in lung and chest wall receptors, and neuroventilatory dissociation may all contribute to the sensation of dyspnea. Different mechanisms likely
A young woman presented with gradually progressive breathlessness, cough and muscle weakness for one and a half year. Her chest radiograph showed multiple, bilateral thin-walled cavitary lesions. Her serum was found to be positive for anti-Jo1 antibodies on serology. Histopathology of lung lesions
Six 3-month-old BALB/c Rag2-/- mice developed dyspnea 10 days after intravenous injection of wild type BALB/c CD45RB(high) lymphocytes to induce colitis as a model of inflammatory bowel disease. The lungs of all 6 mice were diffusely gray-purple and did not collapse completely. Microscopic findings
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