Chronic hepatitis is a long-lasting inflammatory process in the liver that can persist for years and slowly damages the liver tissue over time. It has many potential causes including viral, bacterial, parasitic, toxic, metabolic and autoimmune etiologies. The document discusses the classification, signs and symptoms, diagnostic tools and biomarkers, and treatment approaches for different types of hepatitis such as viral hepatitis B and C, autoimmune hepatitis, drug-induced liver disease, and non-alcoholic fatty liver disease. Liver biopsies and blood tests are used to evaluate liver inflammation and fibrosis to determine the severity and progression of the condition. Management involves identifying and treating the underlying cause as well as medications to suppress the immune system and reduce liver damage
3. Chronic hepatitis
• diffuse polyetiological inflammatory-destructive process in the liver
that lasts at least 6 months
• can persist for years, even decades
• does not cause significant changes in liver structure
• continued inflammation slowly damages the liver, eventually
resulting in cirrhosis, liver failure, and sometimes liver cancer
21. Biochemical Blood analysis
1.Bilirubin level (increased)
2. ALT activity, AST (more than twice increased)
3. Timol sample
4.Sulemic test
5. Level of albumins: globulins(> 25 g/l)
6. Alkaline phosphatase
7. Gamaglutamatranspeptidase
8. The level of fibrinogen, prothrombin
22. Conclusion. An increase in alkaline phosphatase and bilirubin due to conjugated (biochemical
signs of cholestasis) with normal transaminase values (absence of cytolysis), one can think of
mechanical jaundice, which can be caused by the presence of calculi in the biliary system, a tumor
or a large cyst in the pancreas, a tumor of the large duodenal papilla, etc. To clarify the diagnosis, it is
necessary to take into account the clinical manifestations and results of other laboratory (examination
of urine and feces) and instrumental (EGD, ultrasound, CT, etc.) research methods.
Parameter Result Reference ranges
Serum bilirubin 130 <20,5 mcmol/L
Conjugated bilirubin 115 <5,1 mcmol/L
Unconjugated bilirubin 15 >75% serum bilirubin
ALT 32 F <31 U/L
M <41 U/L
AST 29 F <31 U/L
M <37 U/L
Alkaline phosphatase 205 F 35-104 U/L
M 40-129 U/L
23. Parameter Result Reference range
Serum bilirubin 130 <20,5 mcmol/L
Conjugated bilirubin 32 <5,1 mcmol/L
Unconjugated bilirubin 98 75% serum bilirubin
ALT 81 F <31 U/L
M<41 U/L
AST 72 F<31 U/L
M<37 U/L
GGTP 50 F 5-36 U/L
M 8-61 U/L
Alkaline phosphatase 89 F 35-104 U/L
M 40-129 U/L
Total protein 78 66-87 g/L
Serum albumin 48 53-63 g/L
Globulins 30 23-35 g/L
α1-Globulins 3,3 3,8-6,5%
α2-Globulins 6,0 6,5-10%
β-Globulins 11,0 10-15%
γ-Globulins 18,2 14,5-19,5%
Thymol test 4 0-5 S-H
An increase in bilirubin is mainly due to unconjugated, it can be assumed that the patient
has parenchymal jaundice on the background of hepatitis with minimal activity. An increase
in the level of transaminases is less than 3 times, which reflects the presence of cytolysis and
may indicate an inflammatory process in the liver of minimal activity.
Most often, parenchymal jaundice indicates hepatitis.
Cytolytic syndrome is characterized by:
-Increasing the activity of enzymes-indicators of cytolysis and
hepatocellular necrosis - ALT, AST
-Hyperbilirubinemia with an increase in the content of mainly
direct
Levels of hepatitis activity are determined by increasing the
activity of ALT and AST serum relative to the upper limit of
normal:
-Minimum - no more than 3 times
-Moderate - 3-5 times
-Expressed - more than 5 times
24. • Considering the small (less than three-fold) increase in the level of transaminases, which indicates
minimal activity of the process in the liver, the absence of changes in protein fractions, a very
significant increase in gamma-glutamyl transpeptidase with a normal level of alkaline
phosphatase, we can assume the probability of alcoholic liver damage (alcoholic hepatitis).
Parameter Result Reference range
Serum bilirubin 20 <20,5 mcmol/L
Conjugated bilirubin 3 <5,1 mcmol/L
Unconjugated bilirubin 17 75% serum bilirubin
ALT 78 F <31 U/L
M<41 U/L
AST 108 F<31 U/L
M<37 U/L
GGTP 194 F 5-36 U/L
M 8-61 U/L
Alkaline phosphatase 91 F 35-104 U/L
M 40-129 U/L
Total protein 70 66-87 g/L
Serum albumin 44 53-63 g/L
Globulins 26 23-35 g/L
α1-Globulins 4,5 3,8-6,5%
α2-Globulins 6,8 6,5-10%
β-Globulins 9,8 10-15%
γ-Globulins 16,0 14,5-19,5%
Thymol test 3 0-5 S-H
25. Viral Hepatitis
Viral hepatitis is caused different viruses:
- Hepatitis A and E virus
- Hepatitis B virus (HBV)
- Hepatitis C virus (HCV)
- Hepatitis D virus (HDV)
- Hepatitis G, TTV, SEN viruses
- Herpes virus
- Citomegalovirus
28. Hepatitis B
• Is an infectious disease caused by the hepatitis B virus (HBV) that
affects the liver and can cause both acute and chronic liver disease
• The virus is most commonly transmitted from mother to child during
birth and delivery, as well as through contact with blood or other body
fluids, including sex with an infected partner, injection-drug use that
involves sharing needles, syringes, or drug-preparation equipment and
needle sticks or exposures to sharp instruments.
• Over 750,000 people die of hepatitis B each year
• The infection has been preventable by vaccination since
1982. Vaccination is recommended by the World Health
Organization in the first day of life if possible. Two or three more
doses are required at a later time for full effect.
29.
30. HBV
The virus particle (virion) consists of an
outer lipid envelope and
an icosahedral nucleocapsid core composed
of core protein
The genome of HBV is made of
circular DNA
Hepatitis B virus primarily interferes with the
functions of the liver by replicating
in hepatocytes
During HBV infection, the host immune
response causes both hepatocellular damage and
viral clearance. It contributes to most of the liver
injury by killing infected cells and producing
antiviral cytokines
31. Clinical symptoms of chronic viral hepatitis:
• Fatigue
• Reduced working capacity
• Sleep disturbances
• Emotional lability
• Loss of appetite
• Discomfort in right hypochondriac region
• Bitterness in the mouth
• Sub febrile temperature
• Hepatosplenomegaly
32. HBV serum markers
Chronic hepatitis B diagnostic:
1.HBsAg in blood more than 6 month
-HBeAg;
-HBcAg;
-Anti-HBc (total) antibodies
2. Ig M anti-HBc
3. Anti-HBe antibodies
HBV DNA in blood more than 6 month
33. Treatment
- Еntecavir – 500-1000 mkg per 1 day -48 weeks
- Тenofovir - 300 мg per 2 days 1 year (can be 7 years)
- -Аdefovir– 10 mg per 1 day
Control amount of HBV DNA in blood ( treatment if more than 2000)
37. Geographical distribution of HCV subtypes
HCV genotypes Subsets Geographical distribution
Genotype 1 1a, 1b North America, Central Africa, Europe
Genotype 2 2a, 2b, 2c, 2d Western Africa
Genotype 3 3a, 3b, 3c, 3d, 3e, 3f Southeast Asia
Genotype 4 4a, 4b, 4c, 4d, 4e, 4f, 4g, 4h, 4i, 4j Central Africa
Genotype 5 5a South Africa and Asia
Genotype 6 6a Southeast Asia
38. Treatment of hepatitis C
• Without cirhosis
- Sofusbuvir velpatasvir – 12 weeks
- Glecaptovir / pibrentasvir – 8 weeks
• With cirhosis :
- Sofusbuvir velpatasvir – 24 weeks
40. Autoimmune hepatitis
• chronic necrotic-inflammatory
disease of the liver of unknown
etiology, which lasts more than
6 months, is characterized by
periportal process, the
presence of
hypergammaglobulinemia and
a high range of tissue
autoantibodies
41. AIH is more common in women
The course from asymptomatic
to severe:
• - fever
• - resistant jaundice
• - appearance of "vascular stars"
• -the appearance of devices,
bruises
Extrahepatic manifestations:
• -dermal vasculitis
• - polyarthritis, arthralgia, myalgia
• -lymphadenopathy
• pleurisy, pulmonary infiltrate
• -myocarditis
• -glomerulonephritis
• ulcerative colitis and others.
42. Diagnostic of AIH
1. Leukocytosis, increased SCE
2. Determination of blood bilirubin level
3. Determination of ALT, AST activity
7. High antibody titers depending on type: ANA, SMA, anti-LKM-1,
LKM-3, anti-SLA
8. The presence of antimitochondrial antibodies (AMA)
9. Absence of markers of viral hepatitis
10. Histological signs of inflammatory necrotic process by R.G.Knodell
11.Response to corticosteroid treatment
43. Treatment
1.Prednisolone 40-80 mg daily (two thirds dose in the morning, one
third in the evening) 1-2 weeks with a gradual reduction to 10-20 mg
2. Prednisolone 20-40 mg and azathioprine from the second week to 50
mg per day - in the first week, then reduce the dose of prednisolone to
5-10 mg per week
3. Prednisolone 10-15 mg daily in the morning - from several months to
many years
44. Treatment ( depend on severety)
1. Azathioprine 50 mg daily for 2 weeks or
2. Azathioprine 100 mg per day and prednisolone 10 mg per day or
3. Azathioprine 100 / day and budesonide 3 mg / 2-3 times a day until
complete biochemical remission - from several months to many years
Apply other cytostatics:
• Mycophenolate mofetil (Mifenax) (instead of azathioprine)
• Cyclosporine
• Tacrolimus
• Sirolimus
52. Clinical characteristics of fatty liver patients:
• Age
• 41-60 years
• Gender
• Female
• Additional diseases
• Obesity
• Diabetes mellitus
• Hyperlipidemia
• Complains
• Asymptomatic
• Discomfort in abdominal cavity
• Pain in right hypochondriac reason
• Fatigue
• Objectively
• Hepatosplenomegaly
• Laboratory changes
• Increasing AST and ALT in 2 and
more times