Chronic hepatitis C virus infection is associated with more severe asthma.

BACKGROUND: Chronic hepatitis C virus (HCV) infection causes intra- and extra-hepatic complications. The elimination of HCV has been reported to be beneficial for asthmatic patients with HCV infection. Therefore, we hypothesized that chronic HCV infection might be associated with the severity of asthma. METHODS: Asthmatic patients were prospectively enrolled from 13 outpatient settings. Hepatitis B surface (HBs) antigen and HCV-RNA were measured at the time of enrollment and evaluated along with the clinical characteristics of the patients including the age, sex, duration of asthma, atopic status, smoking history, and treatment step according to the Global Initiative for Asthma guideline. RESULTS: Of 1327 asthmatic patients, 1258 patients (94.8%) were treated with inhaled corticosteroids, 18 patients were positive for HBs antigen (1.4%), and 32 patients (2.4%) were positive for HCV-RNA. When compared with HCV-RNA-negative patients, HCV-RNA-positive patients required significantly more drugs for the treatment of asthma. No such relationship was observed in patients with positive HBs antigen. A multivariate logistic regression analysis showed that the male sex, a long duration of asthma, status as a current smoker, and HCV-RNA positivity were independently associated with more severe asthma. CONCLUSIONS: These results suggest that chronic HCV infection is an independent factor that predisposes asthmatic patients to more severe asthma. The evaluation of chronic HCV infection may be helpful for the management of severe asthmatic patients without obvious factors associated with severe asthma.

Docetaxel and cisplatin as second-line chemotherapy for advanced non-small cell lung cancer.

AIMS AND BACKGROUND: Docetaxel and cisplatin are both active against non-small cell lung cancer (NSCLC). This pilot study evaluated the efficacy and toxicity of docetaxel and cisplatin as second-line chemotherapy for patients with advanced NSCLC. PATIENTS AND METHODS: Eleven patients with advanced NSCLC who had no response to platinum-based treatment or had recurrence after a partial response were enrolled (2 stage III B, 9 stage IV; 8 men, 3 women). Median age was 58 years (range, 40 to 74 years). Seven patients had an Eastern Cooperative Oncology Group performance status of 0, and four had a performance status of 1. Four weeks or more after the end of previous therapy, all 11 patients received docetaxel 60 mg/m2 and cisplatin 80 mg/m2 on day 1 every four weeks. RESULTS: Two patients (18.2%) achieved a partial response,five (45.4%) patients had stable disease, and four (36.4%) patients showed progressive disease after initiation of second-line therapy. Median survival was 277 days. Median time to disease progression was 101 days, and the one-year survival rate was 36.4%. Hematological toxicities were moderate. Grade 3 and 4 leukocytopenia and neutropenia were observed in five (45.4%) patients. Grade 3 anemia occurred in one (9 .1%) patient. No severe non-hematological toxicities were observed except grade 3 nausea in two (18.2%) patients. CONCLUSIONS: The regimen of docetaxel and cisplatin has reasonable efficacy with moderate toxicity as second-line chemotherapy for patients with previously treated, advanced NSCLC.

Pathological findings of bronchiectases caused by Mycobacterium avium intracellulare complex.

It has been argued whether bronchiectasis is truly caused by MAC infection or just a predisposed condition in which MAC colonizes. Our present study was designed to evaluate the pathological findings of bronchiectases caused by Mycobacterium avium intracellulare complex (MAC) lung infection and to demonstrate MAC in the lesion of bronchiectases. A retrospective study was performed in nine cases with positive cultures for MAC in whom lung resections were performed. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria required by the American Thoracic Society. In addition, MAC were cultured from all nine lung specimens. Pathological findings of bronchiectases were evaluated in these nine patients. Destruction of bronchial cartilage and smooth muscles layer, obstruction of airway by granulomas, and ulceration of bronchial mucosa were frequently observed. Our present study demonstrates that destruction of fundamental bronchial structure due to extensive granuloma formation throughout the airways was likely the main cause of bronchiectases in MAC infection.

Clinical features of eleven cases of Mycobacterium avium-intracellulare complex pulmonary disease associated with pneumoconiosis.

The relationship between silicosis and tuberculosis is well known. Also other mycobacteria such as Mycobacterium kansasii often occur in association with pneumoconiosis. However, there are few reports describing an association of M. avium-intracellulare complex (MAC) lung disease and pneumoconiosis. The purpose of the present study is to describe clinical features of MAC respiratory infection associated with pneumoconiosis. Eleven patients with MAC respiratory infection associated with pneumoconiosis (all men, 6 with silicosis and 5 with welders' pneumoconiosis) were collected. A determination of whether or not MAC caused pulmonary disease was made using the 1997 criteria required by the American Thoracic Society. Radiologically, cavity formation as well as upper lung field predominance of MAC disease were observed in 8 of 11 cases (72.7%). Two of 11 patients died of respiratory failure. Our present study clearly demonstrates that clinical features of MAC respiratory infection associated with pneumoconiosis were different from MAC without underlying diseases.

Pathological analysis of the cavitary wall in Mycobacterium avium intracellulare complex pulmonary infection.

OBJECTIVE: The present study was designed to evaluate the process of cavity formation in Mycobacterium avium intracellulare complex (MAC) lung infection, pathologically and clinically. METHODS: Using resected lung specimens, we first evaluated the distribution of MAC as well as the distribution of myofibroblasts in MAC lung infection according to several pathological findings classified as bronchiectasis, centrilobular nodules, cavity, nodules, bronchiolitis, or consolidation. Resected lung specimens (9 cases) were evaluated by special staining: Ziehl-Neelsen's method and immunohistochemically for CD68 (stain for monocytes and macrophages) and alpha-smooth muscle actin (stain for myofibroblasts). Chest CT findings were also examined in these 9 patients. In addition, the serial chest CT scans were reviewed in another 3 patients to evaluate the process of cavity formation, radiologically. RESULTS: Although extensive granuloma formations were observed in every pathological classification, MAC was demonstrated only in the necrotic tissue of the inner surface of the cavitary wall, which was connected to the airway. Myofibroblasts which expressed alpha-smooth muscle actin were intensely demonstrated in the cavitary wall compared with other pathological classifications. In the cavitary wall, the layer of epithelioid cells and multinucleated giant cells surrounded necrosis, and the layer of myofibroblasts surrounded the layer of epithelioid cells. Chest CT findings demonstrated that the cavitary walls were relatively thick. The evaluation of serial chest CT scans demonstrated that cavities were formed from previously existing nodules. CONCLUSIONS: Detection of mycobacteria in the cavitary wall, massive infiltration of myofibroblasts compared with other pathological classifications, and connection to the drainage bronchus, were believed to be important in the process of cavity formation in MAC pulmonary infection.