[Chronic bronchitis].

The spectrum of radiographic findings in pulmonary infections due to M. tuberculosis (TB) and non-tuberculous mycobacteria (NTM) are being increasingly discussed, primarily as a result of the increasing prevalence of these infections. The NTM organisms are often overlooked as potential infecting organisms, diagnosis is often delayed and radiologists tend not to include NTM in their differential diagnosis. The literature on the imaging appearances of NTM pulmonary infections is now sufficiently large as to identify some features that would help to distinguish an NTM infection from conventional pulmonary tuberculosis, allowing the radiologist at least to raise the possibility of NTM infection. This review article is intended to describe the radiological features, in the immunocompetent host, that accompany TB and NTM pulmonary infections and highlight the imaging features that would favour an NTM as the causative organism.

Bronchitis↗

PubMed2004

Mechanisms of chronic airway obstruction in smokers.

Studies over the past few decades have showed a clear association between cigarette smoking and the development of chronic airway obstruction. Yet, only a minority of smokers is affected so that in many, even heavy, smokers, pulmonary function remains within normal limits. While carcinogens have been well characterized, there is only limited information about the constituents of cigarette smoke responsible for inducing chronic airway obstruction. In addition, the associated risks factors for airway obstruction in smokers have not been totally identified. The present paper is a review of the recently accumulated facts concerning the intimate action of cigarette smoke at the level of large and small airways and lung parenchyma. The role of classical inflammatory cells such as neutrophils and alveolar macrophages is reviewed, but emphasis is put on recent evidence indicating the involvement of CD8 + T-lymphocytes and possibly eosinophils in the genesis of the structural changes leading to airways obstruction. The mechanisms by which airway inflammation and remodelling cause airway narrowing and airflow limitation are discussed, along with the associated loss of lung elasticity secondary to destructive emphysema. Other biological, epidemiological, physiopathological, and clinical aspects are analyzed, stressing such fundamental aspects as the defence mechanisms, the morpho-functional correlations, the identification of susceptible smokers, and the early detection of airway obstruction, both in specialized laboratories and in primary care.

Bronchitis↗