Eatures of the clinical course and therapeutic tactics in a smoking patient with widespread destructive pulmonary tuberculosis in combination with COPD and pneumoconiosis: clinical observation

Background. An urgent problem in modern phthisiology is the increasing number of patients with pulmonary tuberculosis accompanied by concomitant diseases and significant risk factors. Chronic obstructive pulmonary disease (COPD) and tobacco smoking are among the five most significant risk factors for tuberculosis development. Pneumoconioses, including pulmonary silicosis, are also important occupational risk factors, with tuberculosis infection occurring in almost 40% of cases. The combination of these factors creates significant difficulties in the diagnosis and treatment of pulmonary tuberculosis.

Objective. To demonstrate the clinical course features and effectiveness of comprehensive treatment in a smoking patient with widespread destructive pulmonary tuberculosis combined with COPD and pneumoconiosis.

Materials and methods. A clinical case of a 54-year-old male patient, a miner by profession, with a long history of tobacco smoking (30 years, smoking index 60) is presented. Retrospective observation, clinical analysis, radiography, MSCT of the chest, microbiological sputum examination, bronchoscopy, and spirometry were utilized. The diagnosis was established as infiltrative pulmonary tuberculosis in the phase of cavitation and dissemination with multidrug resistance (HR) combined with COPD and bullous pulmonary emphysema. Treatment included anti-tuberculosis chemotherapy for MDR-TB, COPD therapy, nicotine replacement therapy, and surgical intervention (combined resection of the left lung).

Results. Through a comprehensive approach, positive clinical, laboratory, and radiological dynamics were achieved after 2 months of treatment: cessation of bacterial excretion, normalization of inflammatory markers, and partial resolution of infiltrative changes. The patient completely quit smoking. After 3 months, successful surgery was performed. Pathohistological examination confirmed tuberculous etiology with signs of pneumoconiosis (multiple coniotic nodules in the lung and lymph nodes). The postoperative period was uncomplicated, and clinical cure was achieved.

Conclusion. A comprehensive treatment approach including correction of concomitant pathology (COPD, tobacco smoking), properly selected antituberculosis therapy, and timely surgical treatment enabled clinical cure of a patient with widespread destructive tuberculosis combined with COPD and pneumoconiosis in the shortest possible time.

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