PubMed · 14377183
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M MESITI, N D'AGOSTINO, G DE RITIS. 1954. [Bronchiectasis and tuberculosis].. https://pubmed.ncbi.nlm.nih.gov/14377183/
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BACKGROUND: Bronchiectasis is a condition that is characterized by the permanent dilation of bronchi with destruction of elastic and muscular components of their walls, usually due to acute or chronic infection. The cardinal symptom is a chronic productive cough. METHODS: Review of articles cited in the systematic literature search, along with others found in Ovid MEDLINE and the Cochrane Library (including the Cochrane Database of Systematic Reviews, the Cochrane Controlled Trial Register, and the Database of Abstracts of Reviews of Effectiveness) from 1966 through 2003. RESULTS/CONCLUSIONS: High-resolution CT scanning of the chest is the preferred means of establishing the diagnosis of bronchiectasis. With the increasing use of antibiotics in the treatment of childhood infection in the last several decades, an increasing percentage of patients with bronchiectasis now have an underlying disorder that predisposes them to chronic or recurrent infection. These include cystic fibrosis, common variable immunodeficiency, HIV infection, primary ciliary dyskinesia, allergic bronchopulmonary aspergillosis, and chronic Mycobacterium avium complex infection. A variety of agents have been used to improve cough effectiveness and prevent infectious exacerbations in patients with bronchiectasis, with variable results. Chest physiotherapy offers a modest benefit in increasing sputum volume, but its long-term effectiveness is unknown. Selected patients with localized idiopathic bronchiectasis that causes intolerable symptoms despite maximal medical therapy should be offered treatment with surgery. Patients with exacerbations of bronchiectasis should be given antibiotics, with the choice of agents depending on the likely causative pathogens.
RATIONALE: In idiopathic bronchiectasis, lung inflammation and chronic bacterial infection lead to progressive lung damage. A possible role for natural killer (NK) cells is suggested by the observation that familial bronchiectasis occurs in a rare group of individuals with impaired HLA class I expression and consequent NK cell dysfunction. OBJECTIVE: Because the HLA-C locus and killer cell immunoglobulin-like receptors (KIRs) are of key importance for NK cell recognition, we analyzed HLA-C/KIR combinations by genotyping patients with idiopathic bronchiectasis. METHODS: Genomic DNA from 96 individuals with idiopathic bronchiectasis and 101 control subjects was analyzed by polymerase chain reaction with sequence-specific primers. High-resolution HLA-C genotyping was performed in addition to KIR analysis. RESULTS: HLA-Cw*03 alleles and, in particular, HLA-C group 1 homozygosity are associated with the presence of bronchiectasis. Analysis of the relationship between HLA-C and KIR genes suggests a shift to activatory NK cell function. CONCLUSION: This is the first demonstration of genetic susceptibility in idiopathic bronchiectasis. The association with HLA-C group 1 homozygosity, and the interplay between HLA-C and KIR genes, argue for a role for NK cells in the progressive lung damage seen in this disease. This will require further investigation using functional studies.
The occurrence of follicular bronchiolitis (FB), lymphoid hyperplasia of the bronchus-associated lymphoid tissue, is reported in association with several systemic rheumatic diseases. However, the occurrence of FB in patients with giant cell arteritis (GCA) is not described. A 64-year-old man with long-standing GCA subsequently presented with haemoptysis. A mass in the lower lobe of the left lung was seen on chest x-ray and computed tomography. A wedge resection was performed, and histological examination revealed bronchiectasis, granulation tissue and hyperplasia of peribronchiolar lymphoid aggregates, consistent with FB. FB should be included in the differential diagnosis of haemoptysis in patients with systemic rheumatic diseases.