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IMMUNOLOGICAL PARAMETERS IN TOXIC ALCOHOLIC LIVER
LESIONS
Radjabova Gulchehra Bahodirovna
Bukhara State Medical Institute
The thesis
https://doi.org/10.5281/zenodo.15425927
Relevance:
Alcohol is one of the most common toxins that have a negative
effect on liver tissue, and young age is no exception to the risk group, given the
popularization of alcohol abuse in this age group. Alcohol metabolism in the
liver is accompanied by the formation of acetaldehyde, an active metabolite
contributing to cellular damage, inflammation, and the development of fibrosis
[1; 3]. Early diagnosis is carried out using laboratory tests, ultrasound and, in
some cases, magnetic resonance imaging, which allows you to determine the
degree of tissue damage. Treatment is based on the complete exclusion of
alcohol, the appointment of antioxidants such as vitamin E and
methylsulfonylmethane, and the use of drugs that stabilize the membrane
function of hepatocytes. Correction of metabolic disorders and the use of anti-
inflammatory drugs play an important role in slowing the progression of the
disease [1, 8]. It should be borne in mind that the residual effects of intoxication
with hepatotropic poisons in the form of functional and morphological changes
in the liver without a tendency to progression can be determined in a patient
after a long time after cessation of contact with toxic substances [2]. Chronic
toxic liver damage caused by the use of medications and alcohol abuse is quite
common, and their timely diagnosis and proper management are crucial.
Doctors should consider the possibility of hepatotoxicity when patients develop
nonspecific symptoms and abnormalities in the biochemical parameters of the
liver.
Objective:
to predict complications of toxic liver lesions of alcoholic and
drug origin in young people.
The main part:
82 young patients were included in the study.
The level of interleukin-2 (IL-2) in the first group (patients with alcoholic
liver damage, APP) was 54.1 ± 1.12 pg/ml, which was significantly higher both
compared with the control group (6.5 ± 0.09 pg/ml, p < 0.001) and compared
with the second group (patients with drug—induced liver damage, LPP - 18.2 ±
0.77 pg/ml, p < 0.001). In patients of the second group, the IL-2 level also
exceeded the values of the control group (p < 0.001), but it was significantly
lower than in patients with alcoholic liver damage. The level of interleukin-8 (IL-
8), on the contrary, was significantly higher in patients of the second group
(LPP) — 135.8 ± 1.84 pg/ml, compared with both the first group (APP — 38.3 ±
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1.08 pg/ml, p < 0.001) and the control group (15.2 ± 0.16 pg/ml, p < 0.001). In
the first group, there was a moderate increase in IL-8 levels compared with the
control (p < 0.05), but it was significantly lower than with drug-induced liver
damage.
Thus, patients with alcoholic liver damage are characterized by a marked
increase in IL-2 levels, reflecting the activation of the cellular immune response.
While for patients with drug-induced liver damage, there is a predominant
increase in IL-8 levels, which may indicate the leading role of neutrophilic
inflammation and pronounced chemotactic activity.
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