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PROGNOSIS OF COMPLICATIONS IN TOXIC ALCOHOLIC LIVER
LESIONS, TAKING INTO ACCOUNT BIOCHEMICAL PARAMETERS
Radjabova Gulchehra Bakhodirovna
Bukhara State Medical Institute
https://orcid.org/0009-0007-7258-3064
https://doi.org/10.5281/zenodo.15425915
Thesis
Relevance:
Toxic liver damage can manifest itself in acute and chronic
forms. Acute liver injury is characterized by necrosis and fatty degeneration of
liver cells, hemodynamic disorders, edema and protein cell degeneration. It
develops 2-3 days after exposure to the damaging agent and is accompanied by
an increase in div temperature, weakness, loss of appetite, pain in the right
hypochondrium, intense urine staining, jaundice of the sclera and skin.
Hemorrhagic and hepatorenal syndromes may develop. In contrast to acute TG,
the clinical picture of chronic toxic liver lesions is unexpressed, characterized by
a relatively benign course without a tendency to progression [5; 6]. Interleukin-
2 (IL-2) is a cytokine synthesized mainly by activated T-lymphocytes and plays a
key role in regulating the immune response. In the context of alcoholic liver
damage, IL-2 is involved in a complex cascade of immuno-inflammatory
reactions accompanying damage to hepatocytes. Studies have shown that
chronic alcohol consumption contributes to the dysregulation of IL-2, both at the
level of expression and receptor sensitivity, which affects the effectiveness of
immune surveillance and promotes the progression of the inflammatory process
in the liver [10; 13]. On the one hand, IL-2 deficiency can lead to a weakening of
the function of regulatory T cells (Treg), which disrupts the mechanism of
immune tolerance and promotes the development of autoaggression. This is
especially important in the formation of alcoholic hepatitis, where, along with
damage to hepatocytes, activation of the T-cell link and increased production of
pro-inflammatory cytokines occur. On the other hand, overexpression of IL-2
can promote hyperactivation of cytotoxic T-lymphocytes and NK cells, which
leads to direct damage to the hepatic parenchyma [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
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hepatotoxicity when patients develop nonspecific symptoms and abnormalities
in the biochemical parameters of the liver.
Goal:
Development of an algorithm for predicting complications of toxic liver
lesions of alcoholic and drug origin in young people.
The main part:
112 young patients were included in the study. The first main
group of the study consisted of 50 patients with toxic liver damage of alcoholic
origin, i.e. with alcoholic liver damage (APP), the second main group consisted of
62 patients with toxic liver damage of medicinal origin, i.e. with medicinal liver
damage (LPP), the control group consisted of 30 practically healthy young
people. The patients in the study groups were comparable in age and gender.
The research was carried out in accordance with the Helsinki Declaration. Along
with the necessary clinical studies (general blood analysis, urine, biochemical
blood analysis, coagulogram, ECG, ultrasound of the abdominal organs), all
patients underwent a study on GGTP, cytokines (IL-2 and IL-8) in blood serum.
In patients of both study groups, pronounced violations of the biochemical
parameters of liver function were revealed in comparison with the control. An
increase in AST and ALT indicates cytolytic damage to hepatocytes, an increase
in total bilirubin indicates cholestatic syndrome, and a decrease in PTI reflects a
violation of synthetic liver function. A comparative analysis of the biochemical
parameters of liver function in patients with APP and LPP revealed significant
differences both between the study groups and compared with the control
group. The ALT level was significantly higher in patients with LPP (322 ± 5.34
IU/l) compared with patients with alcohol damage (82.4 ± 1.47 IU/l), which
indicates a more pronounced necrotic damage to hepatocytes under the toxic
effects of nonsteroidal anti-inflammatory drugs. On the contrary, AST activity
was higher in patients with APP (184.1 ± 2.16 IU/l versus 198 ± 3.66 IU/L in
LPP), reflecting the predominant cytoplasmic and mitochondrial destruction of
hepatocytes characteristic of alcohol intoxication. The level of total bilirubin also
showed differences: in patients with APP, its values were higher (116.2 ± 2.09
mmol/l) compared with patients with LP (84.9 ± 1.05 mmol/L), which may
indicate a greater severity of liver conjugation function disorders in chronic
alcohol damage. The prothrombin index (PTI) was reduced in both groups
compared with the control, but the most pronounced decrease was observed in
patients with LPP (62.7 ± 0.56% versus 67.3 ± 0.98% with APP), indicating a
deeper impairment of synthetic liver function under the toxic effects of drugs
(Table 2). Thus In APP, changes characteristic of severe cholestasis and cytolytic
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syndrome predominate, while in LPP, there are more pronounced signs of acute
hepatocyte necrosis and a decrease in synthetic liver activity. Thus, patients
with toxic hepatitis, especially with alcoholic etiology, develop a pronounced
imbalance between pro-oxidant activity and antioxidant protection. This is
manifested by an increase in markers of lipid peroxidation and a decrease in the
activity of antioxidant enzymes, which correlates with the severity of structural
and functional disorders of the liver.
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