TOXIC LIVER DAMAGE IN PATIENTS WITH NORMAL AND EXCESS BODY WEIGHT RECEIVING POLYCHEMOTHERAPY: CLINICAL AND LABORATORY FEATURES
DOI:
https://doi.org/10.11603/1811-2471.2023.v.i1.13730Keywords:
toxic liver damage, polychemotherapy, liver fibrosisAbstract
SUMMARY. The article examines the problem of toxic liver damage in patients with normal and excess body weight receiving chemotherapy (PHT). Such liver damage is one of the most serious complications of PHT, so it is important to understand its clinical and laboratory features for effective treatment of patients [1,10–12]. The relevance of the study lies in the need to improve clinical approaches to the treatment of toxic liver damage and to increase the effectiveness of treatment of the underlying disease - oncological disease.
The aim – to analyze laboratory markers of liver fibrosis, evaluate their prognostic significance for the development and progression of liver function and metabolic disorders, and search for relationships between biochemical markers.
Material and Methods. The study involved women aged 35 to 79 years who were divided into three groups depending on the presence of toxic liver damage after chemotherapy. Patient examinations included general clinical laboratory and instrumental methods, which included collection and analysis of patient history and complaints, general examination with subsequent measurement of anthropometric parameters, identification of factors in the development and relationship of toxic liver damage and excess body weight.
Results. It was found that all groups included patients with increased body mass index (BMI) and obesity, except for the group without signs of non-alcoholic fatty liver disease (NAFLD), which included representatives with normal and excess body weight. As BMI increased, liver condition worsened. Standard anti-tumor therapy had a significant impact on the liver in the patients we examined. It was found that with an increase in BMI and indicators of insulin resistance, the number of manifestations of heaviness in the right hypochondrium (r=0.47, p<0.05; r=0.54, p<0.05) and cases of hepatomegaly (r=0.58, p<0.05; r=0.59, p<0.05) significantly increased. As the disease progressed, liver test indicators increased more than twice the upper limit of normal, indicating a toxic genesis of liver damage. Patients with high BMI had more pronounced changes indicating deeper liver damage. One of the reasons for this may be pre-existing NAFLD with asymptomatic course. Regularities regarding this process were identified: indicators of alanine transaminase (ALT) and aspartate transaminase (AST) were significantly dependent on BMI level (r=0.56, p<0.05; r=0.57, p<0.05). It is likely that an indisputable etiological factor in the progression of liver fibrosis in patients treated for breast cancer is a disturbance in lipid metabolism. Thus, a correlation was established between BMI and the content of low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) (r=0.884, p<0.05 and r=0.751, p<0.05, respectively), as well as a reverse dependence on high-density lipoprotein cholesterol (HDL-C) (r=-0.636, p<0.05). The content of TG correlated with the degree of liver steatosis (r=0.614, p<0.05).
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