
Introduction: Bronchopleural Fistula (BPF) is a rare but potentially fatal complication of pulmonary tuberculosis, whereas nontraumatic bronchial tears are even less frequently reported. In advanced cavitary disease, progressive destruction of the bronchial wall may create a communication with the pleural space, resulting in persistent air leakage, recurrent pneumothorax, and acute respiratory deterioration. This report adds to the limited literature by describing a nontraumatic bronchial tear associated with a tuberculous BPF that presented as recurrent tension pneumothorax. Case Presentation: A 33-year-old man presented with a 3-day history of hemoptysis and fever following 3 months of productive cough and weight loss. Sputum testing confirmed pulmonary tuberculosis, and drug-susceptibility testing demonstrated isoniazid resistance. Chest radiography showed cavitary and consolidative disease, while respiratory cultures yielded multiple concomitant organisms. His condition deteriorated after massive hemoptysis, cardiac arrest, and severe hypercapnic respiratory failure, requiring resuscitation, mechanical ventilation, and intensive care. On hospital day 23, a left pneumothorax was treated with chest tube drainage. On hospital day 29, persistent bubbling indicated an ongoing air leak, and chest radiography showed a massive tension pneumothorax despite the chest tube remaining in place. Emergency thoracotomy confirmed a BPF with a large bronchial tear, which was repaired by direct suturing and pleural flap reinforcement. After 43 days of multidisciplinary care, he was discharged in stable condition. Conclusion: In advanced cavitary pulmonary tuberculosis, persistent air leakage or recurrent pneumothorax despite chest tube drainage should prompt urgent evaluation for BPF and bronchial disruption. Close reassessment, serial imaging, multidisciplinary care, and timely thoracic surgical intervention may be lifesaving when respiratory deterioration persists.
Introduction: This study aimed to compare hematological indices, pulmonary function test (PFT) results, and respiratory symptoms among patients with asthma or chronic obstructive pulmonary disease (COPD), patients exposed to sulfur mustard (SM), and a control group of healthy subjects. Methods: This was a retrospective, cross-sectional, analytical study based on existing medical records collected over different time periods across the study groups. The participants were categorized into four groups: asthmatic patients (n = 48), those with COPD (n = 44), individuals with lung injuries due to SM exposure (n = 42), and healthy control subjects (n = 48). Hematological indices, respiratory symptoms—such as wheezing, cough, and exercise-induced respiratory issues—and PFT values were assessed across all groups. Results: In comparison to the control subjects, the total white blood cell count and percent of monocytes increased in COPD compared to other groups (p<0.001), the percent of eosinophils increased in asthma compared to the other groups (p<0.001), and mean corpuscular volume (MCV) was elevated in the asthma, COPD, and SM exposure groups compared to the control group. All PFT values were lower in the three patient groups than in the control group (p<0.001). Some respiratory symptom indices (cough and night-time wheeze) in the COPD and SM exposure groups were significantly higher than in the other groups. Discussion: All three groups suffer from significant pulmonary impairment; the asthma group shows a unique vulnerability in small airway mechanics, whereas the COPD and SM groups present with more pronounced upper/mid-airway irritation symptoms (cough and nocturnal wheezing). Conclusions: The respiratory and pathophysiological alterations observed in SM-induced lung injury exhibit greater phenotypic similarity to COPD than to asthma.
Introduction/Objective: Non-coding RNA (ncRNA) dysregulation has been widely investigated in Chronic Obstructive Pulmonary Disease (COPD), but interpretation of human evidence is limited by heterogeneity in smoking status, biological source, and analytical methods. This systematic review aimed to synthesize comparable evidence using explicit eligibility criteria. Methods: Scopus, Web of Science, PubMed, and SciELO were searched through April 2025. Eligible studies were original human case-control studies comparing adults with COPD with healthy nonsmoker controls with normal lung function and reporting RT-qPCR-validated ncRNA expression with quantitative fold-change data. Two reviewers independently screened studies, extracted data, and assessed methodological quality using the Newcastle-Ottawa Scale. Results: Of 1,155 records identified, 8 studies met the eligibility criteria; although the search encompassed ncRNAs broadly, all eligible studies investigated mature miRNAs. Thirteen miRNAs were significantly dysregulated in bronchoalveolar lavage fluid, alveolar macrophages, peripheral blood mononuclear cells, plasma, and serum. Seven were upregulated and six were downregulated, with log2 fold-change values ranging from -2.15 to +2.85. Methodological quality ranged from 5 to 7. Discussion: The available human evidence indicates that miRNA dysregulation is detectable in both pulmonary and circulating compartments in COPD. However, the small number of eligible studies and the remaining biological and methodological heterogeneity limit direct cross-study comparability and constrain the current strength of the biomarker evidence. Conclusion: Only a small subset of miRNAs currently meets sufficient methodological and experimental standards to support cautious consideration as exploratory biomarker candidates in COPD. PROSPERO registration: CRD420251042988.