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LIVER CIRRHOSIS DISEASE AND DISEASE SYMPTOMS
Rashidova Bibixonim Zarifjon kizi
student
Jumanova Nargiza Eshmamatovna
Scientific supervisor
Abstract:
This article provides information about the disease "Liver cirrhosis". In the article,
you will get information about the symptoms and causes of the disease. Using scientific sources,
it is explained in detail about disease prevention, disease protection, different stages of disease
and disease treatment measures. The human div is a whole organism, in which every organ has
its own importance. The liver is one of the most important organs in our div. It performs many
important biological functions, such as detoxification of the div, synthesis of proteins and
biochemical substances necessary for digestion and growth. Its other metabolic roles include
carbohydrate metabolism, hormone production, conversion and storage of nutrients such as
glucose and glycogen, and breakdown of red blood cells. After all, if the liver stops working, it
causes serious problems for the whole div. Many liver diseases are insidious at a treatable stage.
Symptoms begin to be felt when the liver is already significantly damaged and serious disorders
occur. In severe cases, liver disease can lead to the death of the patient. Among the common and
dangerous pathologies of this organ, cirrhosis takes one of the leading places. But cirrhosis rarely
develops "by itself". Exceptions are primary biliary cirrhosis, in which liver cells are damaged by
the immune system. In most cases, it occurs as a result of untreated chronic problems.
Key words:
liver, cirrhosis, liver diseases, chronic disease, hepatitis, symptom, the most
important organ, gallbladder (bile), biliary cirrhosis, alcohol.
JIGAR SERROZI KASALLIGI VA KASALLIK ALOMATLARI
Bajardi:
Rashidova Bibixonim Zarifjon qizi
Ilmiy rahbar:
Jumanova Nargiza Eshmamatovna
Annotatsiya:
Ushbu maqolada “Jigar serrozi” kasalligi haqida ma’lumot berilgan. Maqolada
kasallikning alomatlari, kelib chiqish sabablari haqida ma’lumot olasiz. Bunda ilmiy
manbalardan foydalangan holda kasallikni oldini olish,kasallikdan himoyalanish,kasallikning
turli bosqichlari va kasallikni davolash chora-tadbirlari haqida batafsil yoritilgan.Inson tanasi
yaxlit organizm ,bunda har bir a’zoning o’z ahamiyati bor.Jigar-tanamizdagi eng katta
ahamiyatga ega bo’lgan organlardan biridir.
U organizmni
detoksifikatsiya
qilish, hazm qilish va
oʻsish uchun zarur boʻlgan
oqsillar
va biokimyoviy moddalarni
sintez
qilish kabi koʻplab muhim
biologik
funksiyalarni
bajaradi.
Uning
boshqa
metabolik
rollariga
uglevod
almashinuvi,
gormonlar
ishlab chiqarish,
glyukoza
va
glikogen
kabi ozuqa moddalarini
aylantirish va saqlash ,qizil qon hujayralarining parchalanishi kiradi. Mobodo,jigar ishlashdan
to’xtasa bu butun organizm uchun jiddiy muommolarni keltirib chiqaradi.
Ko’pgina jigar
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kasalliklari davolash mumkin bo’lgan bosqichida yashirin ravishda kechadi. Alomatlar jigar
allaqachon sezilarli darajada shikastlanganda va jiddiy buzilishlar yuzaga kelganida sezila
boshlaydi. O’ta murakkab holatlarda jigar kasalligi bemorning o’limiga olib kelishi mumkin.
Ushbu a’zoning keng tarqalgan va xavfli sanaladigan patologiyalari orasida sirroz yetakchi
o’rinlardan birini egallaydi. Ammo sirroz juda kamdan-kam hollarda «o’z-o’zidan» rivojlanadi.
Istisno holatlari - birlamchi biliar sirroz, bunda jigar hujayralariga immun tizimi tomonidan
shikast yetkaziladi. Aksariyat hollarda esa u davolash choralari ko’rilmagan surunkali
muammolar natijasida yuzaga keladi.
Kalit so’zlar:
jigar,serroz,jigar kasalliklari,surunkali kasallik,gepatit,symptom,eng muhim
organ,o’t pufagi(safro),billiar serroz,alkagol.
ЦИРРОЗ ПЕЧЕНИ И СИМПТОМЫ ЗАБОЛЕВАНИЯ
Аннотация:
В данной статье представлена информация о заболевании «Цирроз
печени». В статье вы получите информацию о симптомах и причинах заболевания. С
использованием научных источников подробно рассказывается о профилактике
заболеваний, их защите, различных стадиях заболеваний и мерах лечения. Организм
человека представляет собой целостный организм, в котором каждый орган имеет свое
значение. Печень является одним из важнейших органов нашего организма. Она
выполняет множество важных биологических функций, таких как детоксикация организма,
синтез белков и биохимических веществ, необходимых для пищеварения и роста. Другие
его метаболические функции включают углеводный обмен, выработку гормонов,
преобразование и хранение питательных веществ, таких как глюкоза и гликоген, а также
распад эритроцитов. Ведь если печень перестает работать, это вызывает серьезные
проблемы для всего организма. Многие заболевания печени коварны на излечимой стадии.
Симптомы начинают давать о себе знать, когда печень уже значительно повреждена и
возникают серьезные нарушения. В тяжелых случаях заболевание печени может привести
к смерти больного.Среди распространенных и опасных патологий этого органа одно из
ведущих мест занимает цирроз печени. Но цирроз редко развивается «сам по себе».
Исключением является первичный билиарный цирроз печени, при котором клетки печени
повреждаются иммунной системой. В большинстве случаев это происходит в результате
невылеченных хронических проблем.
Ключевые слова:
печень, цирроз печени, заболевания печени, хронические заболевания,
гепатит, симптом, важнейший орган, желчный пузырь (желчь), билиарный цирроз печени,
алкоголь.
Cirrhosis of the liver is a chronic disease of the organ, which is characterized by the irreversible
replacement of liver parenchymatous tissue with fibrous connective tissue or stroma. Cirrhotic
liver is enlarged or reduced in size, abnormally dense, bumpy. Death occurs at the terminal stage,
depending on various circumstances, within 2-4 years, when the patient experiences severe pain
and suffering.
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Epidemiology:
In economically developed countries, cirrhosis of the liver is one of the 6 main
causes of death in patients aged 35-60 years, with 14-30 cases per 100,000 population. Every
year, 40 million people die in the world with cirrhosis of the liver and hepatocellular carcinoma
developed against the background of hepatitis B virus transport. In the CIS countries, this
disease occurs in 1% of the population. The disease is often observed in men: the ratio of sick
men to women is on average 3:1. The disease can develop in any age group, but is most often
noted after the age of 40.
Causes:
Cirrhosis of the liver often develops against the background of long-term alcohol
intoxication (from 40-50% to 70-80% according to various data), parasitic infection and viral
hepatitis B, C and D (30-40%). Less common causes of cirrhosis are diseases of the biliary tract
(inside and outside the liver), congestive heart failure, various chemicals (hepatotoxins) and
drugs. poisoning. Cirrhosis can also develop in the presence of genetic disorders of metabolism
(hemochromatosis, hepatolenticular degeneration, α1-antitrypsin deficiency) and occlusive
processes in the portal vein system (phleboportal cirrhosis).
Infectious factors:
chronic viral hepatitis, especially B and C, parasitic infections, especially
fungal and trematodes (schistosomiasis, opisthorchosis, candidiasis, aspergillosis). Primary
biliary cirrhosis of the liver usually occurs for no apparent reason. In approximately 10-35% of
patients, the etiology remains unclear.
Pathogenesis:
Over many months and years, the genome of hepatocytes changes and a clone of
pathologically changed cells is created. As a result, the immune-inflammatory process develops.
The following stages of the pathogenesis of cirrhosis are distinguished:
1. Etiological factors: cytopathogenic effects of viruses, immune mechanisms, hepatotoxic
cytokines, chemokines, prooxidants, eicosanoids, acetaldehyde, iron, effects of lipid peroxide
oxidation products;
2. Activation of the function of Ito cells, which leads to excessive growth of connective tissue
in the perisinusoidal space and pericellular fibrosis of the liver;
3. Violation of blood supply of the liver parenchyma as a result of the narrowing of the
vascular space with the development of capillarization of sinusoids and ischemic necrosis of
hepatocytes;
4. Cytolysis of hepatocytes, activation of immune mechanisms.
In the bridging necrosis of hepatocytes, T-lymphocytes are attracted to the area of damage, and
they activate Ito cells, which acquire fibroblast-like properties: these cells synthesize type I
collagen, which in turn eventually leads to fibrosis. In addition, microscopically, false segments
without a central vein are formed in the liver parenchyma.
Influencing factors:
Alcoholic.
Stages: acute alcoholic hepatitis and hepatic dystrophy with fibrosis and
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mesenchymal reaction. The most important factor is the direct toxic effect of alcohol, as well as
necrosis of hepatocytes due to autoimmune processes.
Autoimmune.
An important factor is the sensitization of immunocytes to the div's own
tissues. The main target of autoimmune reaction is liver lipoprotein.
Congestive.
Hepatocyte necrosis is associated with hypoxia and venous damping.
Portal hypertension:
Increased pressure in the portal vein system of the liver due to internal or
external obstruction of the vessels. This leads to the formation of portocaval shunting of blood,
splenomegaly and ascites (accumulation of fluid in the abdominal cavity in cirrhosis).
Thrombocytopenia (strong deposition of platelets in the spleen), leukopenia, as well as anemia
due to high hemolysis of erythrocytes, is associated with splenomegaly. Ascites can cause the
following syndromes:
Limitation of diaphragm mobility;
Gastroesophageal reflux with peptic erosion;
Ulcers and bleeding from varicose veins of the esophagus;
Ventricular hernia;
Bacterial peritonitis;
Hepatorenal syndrome.
Primary biliary cirrhosis:
The main place belongs to genetic disorders of immunoregulation.
First, there is a violation of the biliary epithelium, and then there is a segmental necrosis of the
ducts, and then their proliferation: this is accompanied by violations of the excretion of bile. The
steps of the process are as follows:
Chronic non-purulent destructive cholangitis;
Ductular proliferation with destruction of bile ducts;
Scarring and narrowing of bile ducts;
Large nodular cirrhosis with cholestasis.
The pathologoanatomical picture of primary biliary cirrhosis includes the infiltration of the
epithelium with lymphocytes, plasma cells, macrophages. Antimitochondrial antibodies (AMA)
are detected in laboratory studies, the most characteristic of which are M2-AMA directed against
the E2 subunit of pyruvate dehydrogenase, an increase in serum IgM. In addition, extrahepatic
phenomena indirectly caused by immunity - Hashimoto's thyroiditis, Sjögren's syndrome,
fibrosing alveolitis, tubulointerstitial nephritis, celiac disease, as well as systemic scleroderma,
rheumatoid arthritis, and systemic lupus erythematosus.
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Stages:
The disease proceeds in several stages, each stage has its own clinical symptoms.
Depending on how advanced it is, not only the patient's condition, but also the therapy methods
are different.
1.
Compensated phase:
At this stage of development, the disease does not manifest itself in any
way. If the pathology is diagnosed at this stage, it is possible to compensate for the liver failure
with the help of drugs. In this phase, liver cells - hepatocytes undergo necrosis (death), and
instead of them, fibrous scar tissue begins to form. If the treatment is not started on time, soon
the organ will not be able to fully perform its functions. At this time, laboratory analyzes show
that the level of bilirubin has increased, and the prothrombin index has decreased to 60. In
general, the patient feels healthy, only sometimes the pain under the right rib is annoying.
2.
Subcompensated phase:
In this phase, the symptoms of the disease begin to be felt more
clearly. This indicates an increase in the number of dead hepatocytes. At this stage, the patient
has symptoms such as weakness, apathy (indifference), reduced work capacity, nausea, and
weight loss. In men, the first signs of gynecomastia can be noted. In laboratory indicators, it is
noted that the level of albumin decreases and the prothrombin index reaches 40. If the treatment
is started on time, the disease can be brought to the compensated stage.
3.
Decompensated phase:
in the 3rd phase, the number of normally functioning hepatocytes is
greatly reduced. This leads to the development of liver failure and increased symptoms of the
disease. The patient's skin turns yellow, pains in the abdomen begin to be felt. At this stage,
astitis (accumulation of fluid in the abdominal cavity) often develops. Laboratory analysis
reveals that the level of albumin and the prothrombin index have decreased significantly.
Treatment is ineffective and there is a risk of complications (especially liver coma, cancer,
internal bleeding, peritonitis and pneumonia). The patient must be hospitalized under the
supervision of a doctor.
4.
Terminal phase:
In the final stage of the disease, the organ is unable to perform its function
due to severe damage. The patient suffers from severe pain, because of which he is prescribed
strong painkillers. At this stage, there is no way to stop the development of the pathology. The
prognosis is generally negative. If a new liver is not transplanted, death will occur due to severe
complications of the disease.
Symptoms of cirrhosis of the liver: Many non-hepatic symptoms are associated with increased
pressure in the sinusoids, which leads to increased pressure in the portal venous system. Another
characteristic symptom of the disease - "Medusa's head" - is the filling of the veins of the
anterior abdominal wall with blood.
Common symptoms of cirrhosis include:
Weakness, reduced working capacity;
Unpleasant feelings in the abdomen;
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Dyspeptic disorders;
Increase in div temperature;
Pain in the joints;
Flatulence, pain and heaviness in the upper half of the abdomen;
Weight loss;
Asthenia.
During the examination, it is determined that the liver is enlarged, its surface is thickened and
deformed, and its edges are sharpened. At first, uniform, moderate enlargement of both lobes of
the liver is noted, and later, as a rule, enlargement of the left lobe is more dominant. Portal
hypertension is manifested by a slight enlargement of the spleen. A common clinical picture is
manifested by liver-cellular failure and portal hypertension syndromes. Abdominal discomfort,
intolerance to fatty food and alcohol, nausea, vomiting, diarrhea, heaviness and abdominal pain
(mainly under the right rib) are also observed. In 70% of cases, hepatomegaly is detected, the
liver is thickened, and its edges are sharp. In 30% of patients, palpation of the surface of the
liver is nodular, and in 50%, splenomegaly is noted. Subfebrile fever may be associated with the
passage of intestinal bacterial pyrogens that cannot be neutralized by the liver. The fever is
resistant to antibiotics and passes only when the liver function improves.
External symptoms observed in liver cirrhosis:
Palmar (palm) or plantar erythema;
Veined asterisks;
Lack of hair in the armpit and groin area;
Whiteness of nails;
Development of gynecomastia due to hyperestrogenemia in men.
Similarity of fingers to "drumsticks".
In the terminal stage of the disease, 25% of cases show a decrease in the size of the liver. Also,
due to jaundice, ascites, hyperhydration, peripheral edema (first of all, swelling of the legs),
external venous collaterals (varicose dilatation of the esophagus, stomach, intestinal veins) also
occur. Bleeding from the veins often leads to death. Sometimes hemorrhoidal bleeding is
observed, but their intensity is less. Encephalopathy can be the result of both hepatocellular and
portal liver failure.
Complications:
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Hepatic coma;
Bleeding from varicose veins of the esophagus;
Thrombosis in the portal vein system;
Hepatorenal syndrome;
Liver cancer — formation of hepatocellular carcinoma;
Infectious complications — pneumonia, "spontaneous" peritonitis in ascites, sepsis.
Diagnosis:
The disease is characterized by increased activity of alkaline phosphatase, ALT, AST,
and leukocytosis. This is determined by biochemical analysis of blood. Hepatolienal syndrome
can develop leukopenia, thrombocytopenia, anemia, and hypersplenism, which is manifested by
an increase in cellular elements in the bone marrow. Expanded and branched venous collaterals
are visible during angiography, computer tomography, ultrasound examination or surgical
intervention. If necessary, MRI of the liver and dopplerometry of the liver vessels can be
performed.
Child-Pugh liver failure severity rating scale
Liver cell function in liver cirrhosis is evaluated according to Child-Pugh.
Parameter
Points
1
2
3
Ascites
No
Mild,
treatable
Advanced, difficult to treat
Encephalopathy
No
Light (I-II)
Severe (III-IV)
Bilirubin, μmol/l (mg%)
less than 34
(2.0)
34-51
(2.0-
3.0)
over 51 (3.0)
Albumin, g
More than 3.5
2,8-3,5
less than 2.8
PTV, (seconds) or PTI (%)
1-4 (over 60)
4-6 (40-60)
More than 6 (less than 40)
The class of cirrhosis is determined based on the sum of points for all indicators. When the sum
of points is 5-6, it is class A, when it is 7-9 it is class B, and when it is 10-15 it is class C.
1. Class A patients' life expectancy is expected to be 15-20 years. The postoperative mortality
rate in abdominal surgery is 10%.
2. Class B is an indication for liver transplantation. The rate of postoperative death in
abdominal surgery is 30 percent.
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3. The life expectancy of C-class patients is expected to be 1-3 years, and the postoperative
mortality rate in abdominal surgery is 82%.
The need for a liver transplant is also assessed based on the Child-Pugh criteria: for class C
patients, it is extremely necessary, for class B - moderate, and for class A - low.
SAPS criteria system:
In recent years, the SAPS (Simplified Acute Physiology Score) criteria
system, which includes basic physiological parameters, has been used to determine the prognosis
of patients during the development of gastrointestinal bleeding, coma, sepsis, and other
complications. The patient's age, number of heart contractions (HRC), respiratory rate, systolic
arterial pressure, div temperature, diuresis, hematocrit, blood leukocytes, urea, potassium,
sodium, and plasma are used for classification. The amount of bicarbonates, as well as the stage
of liver coma, have a value.
SAPS evaluation criteria:
Unit
of
assessment
Points
4
3
2
1
0
1
2
3
4
Age, in years
≤45
46-55 56-65 66-75
>75
YQS,
per
minute
≥180
140-
179
110-
139
70-
109
55-69 40-54
<40
Systolic
arterial
pressure, mm.
sim. above
.
≥190
150-
189
80-
149
55-79
<55
Body
temperature,
ºС
≥41
39,0-
40,9
38,5-
38,9
36,0-
38,4
34,0-
35,9
32,0-
33,9
30,0-
31,9
<30
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Breathing
rate,
per
minute
≥50
35-49
25-34 12-24 10-11 6-9
*O'SV
or
HDMB
<6
Urine volume,
l/milk
≥5,00
3,50-
4,99
0,70-
3,49
0,50-
0,69
0,20-
0,49
<0,2
Blood
urea,
mmol/l
≥55
36
−54,9
29
−35,9
7,5
−28,9
3,5
−7,4
<3,5
Hematocrit, % ≥60,0
50,0-
59,9
46,0-
49,9
30,0-
45,9
20,0-
29,9
<20,0
The number
of leukocytes,
×109/l
≥40
20,0-
39,9
15,0-
19,9
3,0-
14,9
1,0-
2,9
<1
Blood
glucose,
mmol/l
≥44,4 27,8-
44,3
13,9-
27,7
3,9-
13,8
2,8-
3,8
1,6-2,7
<1,6
Blood
potassium,
mEq/l
≥7,0
6,0-6,9
5,5-
5,9
3,5-
5,4
3,0-
3,4
2,5-
2,9
<2,5
Sodium
in
blood, mEq/l
≥180
161-
179
156-
160
151-
155
130-
150
120-
129
110-119 <110
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HCO3, mEq/l
≥40
30,0-
39,9
20,0-
29,9
10,0-
19,9
5,0-9,9
<5,0
Glasgow
scale, scores
13-15 10-12 7-9
4-6
3
HDMB — constant positive air pressure, O'SV — artificial lung ventilation.
Liver Cirrhosis Treatment:
Liver cirrhosis is treated with medication and a strict diet, but
once it develops, it is irreversible. In this case, the liver cannot be treated, the only way to save
the patient's life is liver transplantation. In severe ascites, fluid can be removed from the
abdomen.
Diet:
The diet in liver cirrhosis should be complete, containing 70-100 g of protein (1-1.5 g per
1 kg of div mass), 80-90 g of fats (50 percent of which are plant-based), and 400-500 g of
carbohydrates. It is necessary to take into account the patient's habits, tolerance to food and the
presence of other diseases of the digestive system. Chemical additives, preservatives and toxic
ingredients are excluded from the recipe. The diet changes when there are complications of
portal hypertension. Contraindicated products include:
Any chemical food additives, including preserves;
Fried, salted, marinated, smoked;
Confectionery, chocolate, ice cream;
Animal fats, margarine, fatty meat and meat broths;
Salty cheeses, dairy products with a high percentage of fat;
Legumes, radish, spinach, radish, corn, garlic, onion;
Sour fruits and berries;
Sweet carbonated drinks, spicy tea and coffee.
Ursodeoxycholic acid:
Use of ursodeoxycholic acid (UDXK) is appropriate to replace bile acid
deficiency in the intestine caused by biliary insufficiency. Dosage — 1 time a day, in the
evening, 10-15 mg per 1 kg of the patient's weight, which helps to restore digestive processes.
The impact of UDXK includes the following:
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1. An increase in the amount of pancreatic and bile fluid entering the intestine;
2. Completion of intrahepatic cholestasis;
3. Increased contraction of the gallbladder;
4. Saponification of fats and increase in lipase activity;
5. Improvement of intestinal motility, which improves mixing of enzymes with chyme;
6. Normalization of the immune response.
Homeopathic medicines:
The most popular remedies for liver diseases are:
Phosphorus 6, 12;
Magnesia Muriatica 6;
Lycopodium 6;
Nux Vomica 6;
Mercur dulcis 6 and others.
However, it should not be forgotten that homeopathy is not recognized by official evidence-
based medicine, and its methods are not subjected to serious clinical trials. Today, it has not
been confirmed that such preparations have a therapeutic effect due to their components.
Medicinal therapy:
It should be noted that there is no specific treatment method for cirrhosis.
In compensated or subcompensated cirrhosis, supportive therapy is prescribed - a strict diet and
hepatoprotectors (glycyrrhizic acid, phospholipids, amino acids, milk thistle (Silybum marianum)
and other components that contribute to the restoration of liver function). In the decompensated
stage of the disease, the effectiveness of drug therapy is low, and the issue of liver
transplantation should be considered. If the cause of liver cirrhosis is viral in the case of primary
disease such as hepatitis C and B, therapy includes anti-viral, as well as anti-fibrosis and
cirrhotic treatments.
Cellular therapy:
Conventional treatment mainly consists of using pharmaceutical agents to
protect liver cells from damage, stimulate bile secretion, and correct metabolic disorders.
Undoubtedly, this improves the patient's condition, but cannot stop the development of the
disease. If the above treatments do not help, liver transplantation (transplantation) is performed.
Any approach aimed at preventing hepatitis can be included in the preventive measures of
liver cirrhosis. In addition, it is recommended to follow the following: treatment of hepatitis
with the help of a qualified hepatologist and compliance with the prescribed therapeutic regimen;
limit arbitrary intake of drugs, avoid working in harmful industrial enterprises. Take vitamin and
mineral complexes according to the doctor's recommendation; do not eat fatty, fried and bitter-
tasting, canned and semi-finished products; refrain from bad habits, especially the abuse of
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alcoholic beverages; annual endoscopic examination of the digestive system it is also
recommended to take a vaccine against viral hepatitis B.
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