Pyo-pneumothorax in patients with active pulmonary tuberculosis: an analysis of 17 cases without intrapleural fibrinolytic treatment.

OBJECTIVE: To review the medical records of patients with active pulmonary tuberculosis (TB) and pyo-pneumothorax (PPT). SUBJECTS AND METHODS: Medical records of 17 patients (14 male, 3 female, mean age 23.8 years, range 20-52) with PPT and active pulmonary tuberculosis at Gulhane Military Medical Academia Haydarpasa Training Hospital, Istanbul, Turkey, were reviewed from January 1998 to December 2002. The patients were treated with chest tube drainage and chemotherapy. Intrapleural fibrinolytic agents or irrigation was not performed. RESULTS: Pleural fluid samples were available in 14 patients and the mean levels of LDH, protein and glucose in the pleural fluid were 1,767 +/- 944 U/l, 5.2 +/- 1.4 g/dl and 31.7 +/- 22.6 mg/dl, respectively. Mycobacterium tuberculosis was detected in the pleural effusion of 3 patients. The duration of chest tube drainage was longer in cases who underwent open drainage (p = 0.014). At the end of the treatment period 10 patients developed pleural thickening, 4 of them underwent decortication and pneumonectomy was also done in 1 patient. The development of pleural thickening was related to the level of pleural fluid glucose (p = 0.04). CONCLUSION: This study shows that while taking care of patients with pulmonary TB the physician must be aware of the complication of PPT and that adequate chemotherapy and drainage must be duly performed.

Investigation of Helicobacter pylori in bronchoscopic lung specimens of young male patients with bronchiectasis but without gastrointestinal symptoms.

Anti-Helicobacter pylori IgG serum levels were measured in 31 young male bronchiectasis patients without gastrointestinal symptoms, and 56 healthy males. The possible presence of H. pylori was also investigated by rapid urease tests, culture and histopathological examination of protected catheter brush and biopsy specimens from the bronchiectatic site. No serological, microbiological or histological evidence of H. pylori infection was found in the bronchiectasis patient group. H. pylori did not appear to be an agent of infection or chronic colonisation in bronchiectasis, and may not have a significant role in the progression of this disease.

The value of pleural fluid anti-A60 IgM in BCG-vaccinated tuberculous pleurisy patients.

OBJECTIVES: To determine if detection of IgM and IgG antibodies against mycobacterial antigen A60, together with the Mantoux tuberculin skin test (TST), could be used in the diagnosis of tuberculous pleurisy (TP) in BCG-vaccinated cases. METHODS: We investigated 125 BCG-vaccinated patients with pleural effusion. Of these, 88 had TP and 37 had non-tuberculous pleurisy (NTP). TST and anti-A60 IgM and IgG measurements by ELISA were performed in the sera and pleural effusions of both groups. RESULTS: Cut-off values, in optical density, for serum anti-A60 IgM, pleural fluid anti-A60 IgM, serum anti-A60 IgG and pleural fluid anti-A60 IgG were defined as 0.624, 0.614, 0.464, and 0.613, respectively. TP patients had higher IgG and IgM levels in the serum (P < 0.001 and P < 0.05, respectively) and pleural effusion (P < 0.001 and P < 0.001, respectively). Regardless of the diagnosis, IgG and IgM levels were higher in the sera (P < 0.001 and P < 0.05, respectively) and pleural effusions (P < 0.001 and P < 0.001, respectively) of TST-positive cases, and serum and pleural fluid IgM levels were higher (P < 0.001 and P < 0.001, respectively) in the TST-positive TP cases. Sensitivity and specificity of TST were 65% and 68%, respectively. As a single parameter, pleural fluid anti-A60 IgM had the highest sensitivity (77%) and specificity (94%) in patients with negative TST. CONCLUSION: We suggest that in populations where tuberculosis prevalence is high and BCG vaccination is common, pleural fluid anti-A60 IgM can facilitate the diagnosis of TP.

Hemostatic changes in active pulmonary tuberculosis.

OBJECTIVE: Severe pulmonary tuberculosis (PTB) is sometimes complicated by deep vein thrombosis (DVT). We have searched for possible hemostatic disturbances that are predisposing factors for venous thrombosis in patients with PTB. DESIGN: Coagulation and platelet function tests were studied in 45 patients with active PTB and 20 healthy control volunteers before therapy. Findings were compared with results at 30 days. RESULTS: Analysis in patients with active PTB showed anemia, leucocytosis, thrombocytosis, elevation in plasma fibrinogen, factor VIII, plasminogen activator inhibitor 1 (PAI-1) with depressed antithrombin III (AT III) and protein C (PC) levels. On the 30th day of treatment, anemia, leucocytosis and thrombocytosis were improved. Fibrinogen and factor VIII levels had decreased to normal levels, PC and AT III levels had increased to normal levels, and there was no difference in PAI-1 levels. We found no activated protein C resistance. Platelet aggregation studies demonstrated increased platelet activation. However, DVT was not detected in patients during the follow-up period. CONCLUSION: Decreased AT III, PC and elevated plasma fibrinogen levels and increased platelet aggregation appear to induce a hypercoagulable state seen in PTB and improve with treatment.

The effect of pleural fluid content on the development of pleural thickness.

SETTING: Residual pleural thickness (RPT) is a common complication of tuberculous pleurisy (TP), and the degree of RPT cannot be predicted in advance. OBJECTIVES: To determine whether pleural fluid content has an effect on the development of RPT. DESIGN: Forty-seven patients with TP were enrolled in the study. A set of biochemical tests: lactate dehydrogenase, glucose, total proteins, adenosine deaminase, tumour necrosis factor alpha (TNF-alpha), alpha-1 acid glycoprotein (AAG), alpha-2 macroglobulin, C-reactive protein (CRP), complement 3 and complement 4 were studied in the pleural fluid samples. After 6 months of anti-tuberculosis treatment, patients were re-evaluated for RPT. RPT was defined in a posteroanterior chest radiograph as a pleural space of >2 mm or >10 mm measured in the lower lateral chest at the level of an imaginary horizontal line intersecting the diaphragmatic dome. RESULTS: Seventeen patients (36.17%) had an RPT of <2 mm, 18 (38.29%) had an RPT of 2-10 mm, and 12 (25.53%) had an RPT of >10 mm. TNF-alpha levels were lower in patients with an RPT of <2 mm than in patients with an RPT of 2-10 mm or >10 mm (P < 0.05 and P < 0.01, respectively). The level of TNF-alpha was higher in patients with an RPT of >10 mm compared to the 2-10 mm group (P < 0.05). Meanwhile, pleural fluid glucose, AAG and CRP concentrations were significantly higher in patients with an RPT of >10 mm than in patients with <2 mm RPT (P < 0.05, P < 0.01, and P < 0.05, respectively). CONCLUSION: In TP, the development and degree of RPT are significantly correlated to the glucose, CRP, AAG, and TNF-alpha levels in the pleural fluid.

The Hemostatic Changes in Active Pulmonary Tuberculosis.

Severe pulmonary tuberculosis (PTB) is sometimes complicated with deep venous thrombosis (DVT). We have examined the role of possible hemostat>c disturbance, which are predisposing factors for venous thrombosis in patients with PTB. Coagulation and platelet function tests have been studied in 40 patients with severe PTB and 40 healthy control volunteers before therapy and they were compared with 30th day results and controls. Analysis in patients with active PTB showed anemia, leucocytosis, thrombocytosis, elevation in plasma fibrinogen, factor VIII, plasminogen activator inhibitor 1 (PAI-1) with depressed antithrombin III (ATIII) and protein C (PC) levels. On the 30th day of treatment, anemia, leucocytosis and thrombocytsis were improved. Fibrinogen and factor VIII levels decreased to normal levels, PC and AT III levels increased to normal levels whereas there was no difference in PAI-1 levels. Platelet aggregation studies demonstrated increased platelet activation. Activated protein C resistance was not determined. DVT was not detected in patients during the follow up period. Decreased AT III, PC and elevated plasma fibrinogen levels and increased platelet aggregation appear to induce hypercoagilable state seen in PTB and improves with tretament.

Determination of the etiological organism during acute exacerbations of COPD and efficacy of azithromycin, ampicillin-sulbactam, ciprofloxacin and cefaclor. Turkish Thoracic Society COPD Working Group.

Acute exacerbations, most of which are due to lower respiratory tract infections, cause great morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD) and most of these are due to lower respiratory tract infections. The aim of this study was to determine the causative organism and the effects of azithromycin, ampicillin sulbactam (sultamicillin), ciprofloxacin and cefaclor monohydrate therapy in COPD. One hundred and six patients with COPD in acute exacerbation were randomized into four groups for empiric antibiotic treatment following lung function tests and sputum examination. The most common strains isolated from sputum were Haemophilus influenzae (30.8%), Streptoccocus pneumoniae (12%) and Moraxella catarrhalis (7.7%). Azithromycin, sultamicillin, ciprofloxacin and cefaclor monohydrate were found to be effective in treating COPD exacerbations.