Faculty of Medicine

Medicine & Surgery Program

Hepatitis
Dr. : Mohamed Basyouni Date: 25/ 10 /2023
Acute Hepatitis
Viral Hepatitis
HAV
HBV HCV

HDV
Pathology: Centri-lobular hepatic necrosis

 Diffuse lobular infiltration by mononuclear cells

(lymphocytes and plasma cells), histocytes with kuppfer
cells hyperplasia.
 Hepatocytes degeneration (ballooning) and apoptosis
(acidophilic bodies called the Councilman body)
 More severe cases demonstrate bridging necrosis.
 There is preservation of the reticular framework &
hepatocyte regeneration. the liver completely restores its
normal structure & function within 3-6 months.
 In severe fulminant cases, there is massive necrosis with
marked reduction of liver size.
Central vein
Complications of acute hepatitis
 Hepatic complications:
 Relapsing hepatitis:
 Clinical relapse: recurrence of clinical features of acute hepatitis
 Biochemical relapse: re-elevation of serum ALT, AST & bilirubin levels with
or without clinical relapse

 Carrier state: mainly with HAV

 Post-hepatitis cholestasis (Watson syndrome):

 Persistent jaundice & pruritus with elevation of direct bilirubin and ALP for
more than 6 months after resolution of all other features of hepatitis.
 It is common with HAV infection due to edema of hepatocytes compressing
adjacent bile canaliculi.
 It is self-limited condition (never cause chronic hepatitis)
 Fulminant hepatitis:
 The most severe complication of acute hepatitis (90-95% mortality rate)
 It is most common with HBV, combined HBV & HDV, 5% of HAV cases, 20%
of cases of HEV infection in pregnant women but very rare with HCV.
 Characterised pathologically by massive hepatic necrosis
 Clinical features : rapid deterioration of conscious level (hepatic
encephalopathy), coagulopathy & jaundice
 The most common causes of death are GIT bleeding, renal failure,
hypoglycemia, sepsis or massive cerebral edema
 Liver transplantation is the only curative treatment

 Chronic complications: don’t occur with HAV or HEV infection

 Chronic hepatitis
 Liver cirrhosis
 Hepatocellular carcinoma
 Extra-hepatic complications:
 They represent autoimmune reactions against HBV & HCV affecting many parts
of the body other than the liver.
 HCV can be complicated by essential mixed cryoglobulinemia (EMC), porphyria
cutanea tarda, lichen planus and membrano-proliferative glomerulonephritis
 HCV may be complicated by lympho-proliferative disorder that may progress to
lymphoma
 HCV may be also complicated by metabolic syndrome (fatty liver disease, insulin
resistance, type 2 diabetes, dyslipidemia, hypertension)
 HBV may be complicated by Polyarteritis nodosa (PAN) and membranous
glomerulonephritis
 Pancreatitis, myocarditis, aplastic anemia, Guillian-Barre syndrome, urticaria and
arthritis may occur with HAV, HBV or HCV
Investigations of acute hepatitis:
1. Liver function tests: high liver enzymes (ALT, AST, ALP) with increased
serum bilirubin. PT & INR are increased in severe cases indicating poor
prognosis.
2. Hepatitis markers:
 HAV-IgM: in Acute infection, HAV-IgG in Vaccination & previous infection
 HCV: HCV–Ab (by ELISA) & confirmed by HCV-RNA (by PCR)
 HBV:
 HBs Ag: Indicates acute infection & if persists > 6 months, indicates chronic
infection
 HBs Ab: indicates vaccination or convalescence from infection
 HBcAg: not present in blood (detected only by liver biopsy in hepatocytes)
 HBcAb: the only marker present in window period of acute hepatitis
 HBe Ag: Indicates high infectivity & high viral replication
 HBe Ab: Indicates low viral replication
 HBV-DNA PCR: The best diagnostic test for HBV infection
Treatment of acute hepatitis:
 Prevention: the most important
 HAV:
 Public hygienic measures for sanitary food & water handling
 HAV vaccine: for high risk populations (food handlers, travelers to endemic
areas & during outbreaks)
 HBV:
 Safe handling & proper sterilization of blood products, needles & surgical
equipments
 HBV vaccine: for high risk population ( all neonates, medical staff, babies of
infected mothers, hemodialysis & hemophilic patients)

 Treatment of acute infection:

 Bed rest: till disappearance of symptoms & normal serum bilirubin
 Diet: plenty of fluids with high carbohydrate & protein but low-fat
 Symptomatic treatment: for pain, fever, vomiting, diarrhea
Chronic Hepatitis
 Definition: persistence of clinical &/or biochemical evidence of hepatic
inflammation for > 6 months
 Clinically: persistent anorexia, weight loss, fatigue, and hepatomegaly
 Presence of bridging/interface hepatic necrosis on liver biopsy
 Persistence of elevated ALT & AST, bilirubin > 6 months
 Persistence of HBeAg for >3 months or HBsAg for >6 months
 Causes::
 Hepatotropic viruses: only with HCV, HBV & HDV: 85-90% , 10-15% & 4% of
cases of acute hepatitis progress to chronic hepatitis respectively.
 Chronic alcoholism
 Metabolic disorders: Wilson disease, hemochromatosis, alpha-1 anti-trypsin
deficiency
 Autoimmune hepatitis
 Pathology of chronic hepatitis & Liver cirrhosis
Chronic hepatitis Liver cirrhosis
 Clinical picture:
 The patient may remain asymptomatic for years till complicated by liver
cirrhosis & liver cell failure
 Patients may show chronic unexplained fatigue with jaundice & hepatomegaly
 Investigations:
 Liver functions tests: high ALT, AST, bilirubin & may be decreased albumin
 Viral markers: for chronic viral hepatitis (HBV, HCV, HDV).. Describe
 Autoimmune markers: in autoimmune hepatitis
 High ESR (>100) & high immunoglobulins mainly IgG
 In type I: increased ANA & anti-smooth muscle antibodies (ASMA)
 In type II: increased liver-kidney microsomal antibody (LKMA)
 In type III: increased soluble liver antigen antibody (SLA)
 Treatment:
- Chronic HBV: Interferon SC or oral antiviral drugs (e.g: Entecavir, Tenofovir)
- Chronic HCV: Interferon SC or Direct-acting antivirals (DAAs) drugs e.g
Sofosbuvir, Velpatasvir, Ledipasvir, Daclatasvir
- Autoimmune hepatitis: corticosteroids, azathioprine