Acute and Chronic Hepatitis(A,B,C,D,E ,)

Acute and Chronic Hepatitis
DR ASAD ULLAH
Senior Registrar Endocrinology and Diabetes

Acute Hepatitis
 Acute hepatitis occurs when the liver suffers an injury resulting in an inflammatory reaction
 Clinical presentation
 Patients often present with fever, abdominal pain, and jaundice. Multiple serum lab values are often elevated,
including AST, ALT, and GGT.
ETIOLOGY : Hepatotropic viruses (e.g. HAV, HBV, HCV,HDV,HEV)
 non-hepatotropic viruses (e.g. EBV, CMV, HSV, etc.)
 other infections (e.g. parasites)
 drug/toxin-induced hepatitis (e.g. acetaminophen toxicity, alcohol)
 autoimmune hepatitis, acute fatty liver of pregnancy,HELLP syndrome
 metabolic disease (e.g. nonalcoholic fatty liver disease, Wilson disease, hemochromatosis)
 ischemic (e.g. systemic shock, Budd-Chiari syndrome)

ACUTE HEPATITIS A VIRUS
 Hepatis A virus(HAV) is a 27 nm RNA virus, which causes
epidemics and sporadic cases. Globally over 1.5 million
people are infected annually.
 The virus is transmitted by fecal-oral route by either person
to person contact or ingestion of contaminated food or
water.
 Common source outbreak resulting from contaminated food,
untreated ground water from wells.
 The incubation period averages 30 days.HAV is excreted in
faces for up to 2 weeks before clinical illness but rarely after
the first week of illness.
 There is no chronic carrier state.

Clinical Presentation of HAV
Malaise,myalgias,arthralgias,easy fatigability,anorexia,nausea,vomiting
Jaundice occurs 5-10 days after symptoms
The acute illness usually subsides over 2-3 weeks with complete clinical and laboratory recovery by 9 weeks.
LABORATORY Findings
ALT and AST levels are strikingly high followed by elevations of bilirubin.
Anti body to hepatitis A(Anti-HAV) appears early in the course of the illness. Both IgM and IgG anti HAV are
detectable in serum soon after the onset.
PREVENTION
Unvaccinated persons who are exposed to HAV are advised to receive post exposure prophylaxis with a single
dose of HAV vaccine or immune globulin or both.

Vaccination for HAV
 Vaccination with one of the two effective inactivated hepatitis A vaccines are available.
 Vaccination is recommended for persons living in or travelling to endemic areas, persons aged above 40,Persons
with HIV,animal handlers, injection drug users,incarcerated,homelesness,.
 For travelers, a single dose of vaccine at any time before departure can provide adequate protection.
 Treatment
 Symptomatic(anti emetics, dextrose)

Acute Hepatitis B
 Hepatitis B is DNA virus
 HBV is usually transmitted by inoculation of infected blood or blood products or by sexual contact and it is
present in saliva,semen,and vaginal secretion,HBsAg positive mothers may transmit HBV at delivery.
 HBV is prevalent in homosexual people and those who inject drugs, but the greatest number of cases result from
heterosexual transmission. Other groups at risk are physicians,dentists,nurses,laboratory technicians
 Incubation period is 6 weeks to 6 months.
 Symptoms and signs
 Similar to Hepatitis A
 Laboratory Findings
 HBsAg. First evidence of infection, persistence for more than 6 months signifies chronic hepatitis B.
 Anti-HBs. appears in most individuals after clearance of HBsAg and after successful vaccination,
 Disappearance of HBsAg and appearance of Anti-HBs signal recovery.

 Anti-HBc -IgM anti-HBc appears shortly after HBsAg is detected. It indicates a diagnosis of acute hepatitis B.
 HBeAg.IT indicates viral replication and infectivity
 HBV DNA. It is a more sensitive and precise marker of viral replication and infectivity.
 Treatment of acute HBV
 Same as acute HAV.

ACUTE HEPATITIS C
 HCV is RNA virus, seven major genotypes of HCV have been identified.
 Transmitted by blood transfusion, injection drug use, body piercing,tattoos,hemodialysis.Risk of sexual and
maternal-neonatal is low
 Incubation period 6-7 weeks, usually asymptomatic
 Laboratory Diagnosis.
 Enzyme immunoassay(EIA) that detects antibodies to HCV.
 Treatment.
 A 6 Week course of ledipasvir and sofosbuvir has been shown to prevent chronic hepatitis in patients with acute
genotype 1 hepatitis C and lack of spontaneous clearance after 3 months.
.

HEPATITIS D
 HDV is RNA virus that causes hepatitis only in association with HBV infection
 HDV may coinfect with HBV or may superinfect a person with chronic hepatitis B.in chronic hepatitis
Superinfection by HDV appears to carry a worse short term prognosis often resulting in acute liver failure.
 Diagnosis is by detection of antibody to hepatitis D antigen(anti-HDV) or HDV RNA in serum.

HEPATITIS E
 HEV is RNA virus
 Transmission is by feco-oral route
 Most common in central and southeast Asia.
 3 month course of Ribavirin has been reported to induce sustained clearance of HEV RNA infection.

CHRONIC VIRAL HEPATITIS
 It is defined as chronic necroinflammation of the liver of more than 3-6 months duration,demonstrated by
persistently elevated serum aminotransferase level or characteristic histologic findings often in the absence of
symptoms.
 Causes of chronic hepatitis is include viruses(HBV,HCV,HDV),Autoimmune hepatitis, alcohol associated and non
alcoholic steatohepatitis, certain medications such as isoniazid,nitrofurantoin,Wilson disease,alpha-1 antitrypsin
deficiency, Haemochromatosis and rarely coeliac disease.
 Chronic Hepatitis B and chronic hepatitis D
 Chronic HBV afflicts 316 million people worldwide.
 Five phases of chronic hepatitis B infection are recognized
 1.Immune tolerant phase(HBeAg positive chronic HBV infection)HBeAg and HBV DNA are present in serum and
are indicative of active viral replication, and serum aminotransferase level are normal with little necroinflammation
in the liver, This phase is common in infants and young children whose immune system fails to mount an immune
response to HBV.

 Persons in the immune tolerant phase and those who acquire HBV later in life may enter an immune active
phase(HBeAg positive chronic HBV)in which aminotransferase and HBV DNA levels are elevated and
necroinflammation is present in the liver with a risk of progression to cirrhosis and HCC;Low level IgM Anti-
HBC is present in serum in about 70%.
 Patents enter the inactive HBs carrier state(HBeAg negative chronic HBV infection) when biochemical
improvement follows immune clearance, This improvement coincides with the disappearance of HBeAg and
reduced HBV DNA levels(less the 10 5copies/ml or less than 20,000 iu/ml in serum, appearance of anti Hbe
and integration of the HBV genome into the host genome in infected hepatocytes. Patients in this phase are at
low risk of cirrhosis.
 The reactivated chronic hepatitis B phase (HBeAg negative chronic hepatitis B)may result from infection by
pre core mutant of HBV or from spontaneous mutation of the pre core or core promoter region of the HBV
genome during the course of chronic hepatitis caused by wild type HBV.HBeAg negative chronic hepatitis B
accounts for less than 10% of cases of chronic HBV .
 In reactivated chronic HBV,there is rise in serum HBV DNA levels and possible progression to cirrhosis.
 Only 1% of treated and untreated patients per year reach the HBsAg negative phase ,in which anti-Hbe may
remain detectable ,serum ALT are normal and HBV DNA is undetectable in serum but remains present in liver.
This is called Functional cure.

TREATMENT
 Patients with active viral replication (HBeAg and HDV DNA [10 5 copies/ml or more or 20,000 iu/ml or more in
serum and elevated aminotransferase levels may be treated with a nucleoside or nucleotide analogs or with
PEGylated interferons.
 For patients who are HBeAg negative, the threshold for treatment is serum HBV DNA level of10 4 copies/ml or
2000 iu/ml the threshold HBV DNA levels for treatment is met but the serum ALT levels is normal, treatment
may still be considered in patients over age 3-40 if liver biopsy or a noninvasive assessment of liver fibrosis
demonstrates a fibrosis stage of 2 of 4(moderate or higher.
 AIMS (Reducing and maintaining HBV DNA to the lowest level, normalization of ALT,IN HBeAg positive
patients seroconversion to ant-Hbe and clearance of HBsAg.
 Therapy should continue for 6-12 months after HBeAg to anti- Hbe seroconversion.
 Preferred first line oral agents are entecavir and tenofovir.

CHRONIC HEPATITIS C
 Chronic hepatitis c develops in 85% of patients with acute hepatitis c.
 Worldwide,8 million people are infected with HCV.It is diagnosed by Anti-HCV.In rare cases of suspected HCV
but a negative EIA,HCV RNA is detected by PCR testing.
 TREATMENT
 Sofosbuvir-Velpatasvir(Hilvel,Epclusa)
 1 tablet daily for 12 weeks
 Glecapriver-Pibrentasvir
 3 tablets daily for 8 weeks

AUTOIMMUNE HEPATITIS
 Usually seen in young women
 Insidious,25% with acute severe hepatitis
 Exacerbation may occur postpartum, amenorrhea may be the presenting feature
 Laboratory findings
 Aminotransferase levels may be greater then 1000u/l and total bilirubin is usually increased.
 It has classified as type ɪ or type ɪɪ.
 In type ɪ,ANA or smooth muscle antibodies are usually detected.
 Anti bodies to soluble liver antigen (anti-SLA) characterize a variant of type that is marked by severe disease ,high
relapse rate after treatment and absence of ANA,ASMA
 Type ɪɪ is seen more often in girls under age 14 is characterized by Liver kidney micro some type ɪ(anti-LKM1)
 TREATMENT
 (Prednisolone with or without azathioprine)..cilosporin,tacrolimus,methotrexate,Mycophenoalte mofetil

OTHER CAUSES OF CHRONIC HEPATITIS
 Alcohol associated liver disease
 Excessive alcohol intake can lead to fatty liver,hepatitis and cirrhosis.
 Frequency is 10-15% among persons ho consume over 0gm of alcohol(4 oz of 100-proof whiskey,1 oz of wines, or
four 12 oz cans of beer daily for more than 10 years.
 From hepatomegaly to acute liver failure
 Laboratory
 Anemia(macrocytic),AST is usually elevated than ALT by a factor of 2 or more.
 Liver biopsy ;macro vesicular fat,polymorphonuclear infiltration with hepatic necrosis, Mallory bodies,pervenular
and per sinusoidal fibrosis.
 Treatment
 Abstinance,naltrexone,topiramate,gabapentin,methyprednisolone

NON ALCOHOLIC FATTY LIVER DISEASE
Mostly asymptomatic, hepatomegaly present in 75% of patients
Laboratory
Mild elevated aminotransferses,ALP
The ratio of ALT to AST is almost always greater then 1.0 in NALD.
Imaging
Steatosis may be demonstrated on USG,CT or MRI.
Liver Biopsy and risk scores
Percutaneous liver biopsy is the gold standard.
Treatment
Lifestyles changes(wt loss,exercise,fructose restriction,dietry fiber
DRUGS(vitamin E,Thioolidinediones,obeticholic acid,semaglutide,liraglutide)
Bariatric surgery, Liver transplantation

Acute and Chronic Hepatitis(A,B,C,D,E ,)

More Related Content

Similar to Acute and Chronic Hepatitis(A,B,C,D,E ,) (20)

Recently uploaded (20)

Acute and Chronic Hepatitis(A,B,C,D,E ,)