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Abstract
Aim. To study the frequency, clinical and diagnostic features, and characteristics of the course of drug-induced pancreatitis (DIP) that developed during treatment for pulmonary tuberculosis, depending on the anti-tuberculosis drugs used and the influence of alcohol consumption.
Materials and methods. We examined 328 patients with pulmonary tuberculosis who developed signs of liver and pancreas damage during anti-tuberculosis therapy. Patients were divided into groups according to the type of drugs used (first or second line) and the presence of alcohol abuse. Clinical assessment of symptoms, biochemical studies of α-amylase, pancreatic isoamylase and lipase activity, determination of faecal elastase-1, coproscopy and sonographic examination of the pancreas with histographic assessment of the structure were performed.
Results. It was found that DIP developed more often with the use of isoniazid, rifampicin, and erythromycin. Patients without alcohol consumption had more severe abdominal pain (average severity 2.06), significant hyperfermentemia, and characteristic ultrasound signs — enlargement of the gland, decreased echogenicity, and blurred contours. In patients with combined (drug-alcohol) damage, dyspeptic disorders, exocrine insufficiency, calcifications, pseudocysts, and dilation of the Wirsung duct prevailed. An increase in pancreatic enzymes was most often recorded in the initial phase of therapy and when using first-line drugs.
Conclusions. DIP in the treatment of pulmonary tuberculosis is characterized by pronounced pain and dyspeptic syndromes, hyperfermentemia, and typical sonographic changes in the pancreas. Alcohol aggravates the course of the disease, contributing to the development of exocrine and endocrine insufficiency. Prospects for further research are related to the development of differentiated approaches to the prevention and treatment of DIP in patients with tuberculosis.
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