Expiratory central airway collapse - an overlooked entity?: Two case reports.

INTRODUCTION: Expiratory central airway collapse is defined by excessive inward bulging of either tracheobronchial posterior membrane or cartilage. The former is called excessive dynamic airway collapse (EDAC), and the latter, depending on the site of collapse, tracheomalacia, bronchomalacia or tracheobronchomalacia. Due to their non-specific symptoms and lack of awareness amongst clinicians they tend to be mislabeled as common obstructive lung disorders, or complicate their course undetected. Particular controversies refer to EDAC sometimes considered just as a symptom of obstructive lung disease and not a separate entity. Nonetheless, a growing body of evidence indicates that EDAC might be present in patients without apparent obstructive lung disease or it might be an independent risk factor in chronic obstructive pulmonary disease or asthma patients. PATIENT CONCERNS: Patient #1 was admitted because of idiopathic chronic cough whereas patient #2 was admitted for differential diagnosis of dyspnea of uncertain etiology. In both patients symptoms were unresponsive to bronchodilators and inhaled corticosteroids. FINDINGS AND DIAGNOSIS: In both patients an excess collapse of tracheobronchial posterior membrane was detected during bronchoscopy; in patient #1, of right main bronchus and right upper lobe bronchus and in patient #2 of right upper lobe bronchus and both main bronchi. Excess central airway collapse in patient #2 was also visualized on expiratory chest CT. In patient #1 spirometry did not reveal obturation, whereas in patient #2 only mild, irreversible, obstruction was revealed, disproportionate to patients significant breathlessness. INTERVENTIONS: Both patients were treated with N-acetylcysteine and adjustable positive expiratory pressure valves. OUTCOMES: Due to aforementioned treatment chronic cough in patient #1 subsided almost completely whereas patient's #2 dyspnea improved significantly. CONCLUSIONS: In presented cases EDAC was an unexpected finding, even though, it firmly corresponded with reported symptoms. Treatment modification led to improvement of patients quality of life.

Usefulness of lung ultrasound in diagnosing causes of exacerbation in patients with chronic dyspnea.

Dyspnea is a non-specific symptom that requires fast diagnostics, accurate diagnosis and proper treatment. The most common causes of dyspnea include exacerbation of chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF). Distinction between these two medical conditions seems to be critical in diagnostics of emergencies. At the same time, basic diagnostic tools available in emergency room, such as classic radiography (X-ray) of the chest, electrocardiography (ECG) or b-type natriuretic peptide test, are sometimes ambiguous. Therefore looking for additional diagnostic tool seems to be justified and necessary. Transthoracic lung ultrasound assessment is a simple and easily accessible examination, enabling the early and explicit diagnostics of pulmonary oedema and its distinction from other, non-cardiac causes of dyspnea. This review outlines the current knowledge on the subject of transthoracic lung ultrasound (TLUS), particularly in respect of its clinical usefulness in distinction of causes of dyspnea exacerbation.

Changed phagocytic activity and pattern of Fcγ and complement receptors on blood monocytes in sarcoidosis.

We have recently revealed that mycobacterial heat shock proteins (Mtb-hsp), involved in forming of immune complexes (CIs), can induce immune response in sarcoidosis (SA). The complexemia may result from inappropriate phagocytosis and clearance of CIs by monocytes with following persistent antigenemia and granuloma formation. Because an aberrant expression of receptors for Fc fragment of immunoglobulin G (FcγR) and complement receptors (CR) on monocytes can be involved in this process, we have evaluated the expression of FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16) and CR1 (CD35), CR3 (CD11b), CR4 (CD11c) receptors on blood CD14(+) monocytes and its phagocytic activity in 24 patients with SA and 20 healthy volunteers using flow cytometry. We found significantly increased expression of all examined FcγR and decreased expression of CD35 and CD11c on CD14(+) monocytes in SA patients vs controls. Significantly increased percentage of CD14(+)CD16(+)CD35(-), CD14(+)CD64(+)CD35(+), CD14(+)CD64(+)CD11b(+), CD14(+)CD64(+)CD11c(+) and decreased of CD14(+)CD32(-)CD35(+), CD14(+)CD32(-)CD11b(+), CD14(+)CD32(-)CD11c(+) monocytes' phenotypes was revealed in SA. The total number and percentage of phagocyting monocytes was significantly increased in SA as compared with controls. In conclusion, altered expression of FcγR and CR on CD14(+) monocytes and its increased phagocytic activity may be responsible for high antigen load, persistent antigenemia and immunocomplexemia in SA patients.