Abstract
More than 70 drugs are known to induce pancreatitis. The frequency, clinical manifestations, and diagnosis of drug-induced pancreatitis that occurred during tuberculosis treatment have not been studied. In addition, the literature provides information regarding the pancreatic toxicity of certain anti-tuberculosis drugs.
We examined 328 patients with pulmonary tuberculosis that occurred during drug-induced hepatitis treatment. Prior to our observation, 92 (28.0%) patients abused alcohol, so chronic hepatitis had a combined etiology, i.e., it occurred due to the toxic effect of anti-tuberculosis drugs on the liver against the background of alcoholic liver disease. However, the worsening of the course of chronic hepatitis occurred in all cases due to the intake of anti-tuberculosis drugs, so we used the term “chronic, predominantly toxic (drug-induced) hepatitis.” In these patients, we diagnosed chronic pancreatitis (CP), which had both a drug- and alcohol-induced combined etiology. Since the exacerbation of pancreatitis only occurred when anti-tuberculosis drugs were taken, the etiology was predominantly drug-induced. The comparison group included these patients with a combination of predominantly drug-induced hepatitis and drug-induced CP. The main group consisted of 236 (72.0%) patients who did not abuse alcohol, indicating that both hepatitis and CP were drug-induced.
The following conclusions were drawn as a result of our study. Pain and dyspeptic syndromes are typical of drug-induced pancreatitis: patients with pulmonary tuberculosis who do not abuse alcohol experience more intense abdominal pain, while patients with a combined etiology of CP (drug- and alcohol-induced) experience more intense dyspeptic syndrome. The phenomenon of “deviation” of pancreatic enzymes into the blood is more evident in patients with an isolated drug etiology of pancreatitis who are taking first-line anti-tuberculosis drugs at the start of treatment. Exo- and endocrine pancreatic insufficiencies are common and more severe in patients with pulmonary tuberculosis who abuse alcohol and receive pancreatic drugs. In patients with pulmonary tuberculosis who do not abuse alcohol, drug-induced CP is characterized by the following sonographic changes in the pancreas: complete or partial enlargement of the organ, decreased echogenicity, structural heterogeneity, and indistinct boundaries. In the combined etiology of CP, an increase in echogenicity, calcifications, pancreatic pseudocysts, and dilation of the Wirsungʼs duct are more prevalent. In patients with pulmonary tuberculosis who abuse alcohol, the L index is significantly higher and the histographic coefficient Kgst of the ultrasound pancreatic histogram is lower than in patients with only drug-induced CP etiology.
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