Hepatitis Types Causes Symptoms Diagnosis and Treatment

Hepatitis Types Causes Symptoms Diagnosis and Treatment

Acute Viral Hepatitis Classification Types

  • It is an acute systemic infection affecting the liver. Caused by:
  • 1. Hepatitis A virus (HAV)
  • 2. Hepatitis B virus (HBV)
  • 3. Hepatitis C virus (HCV)
  • 4. HBV associated delta hepatitis (HDV)
  • 5. Hepatitis E virus (HEV)
  • 6. Transfusion transmitted hepatitis G virus I r do not cause
  • 7. Transfusio’1 transmitted I hepatitis
  • (n virus)hepatitis J

All viruses are RNA viruses except hepatitis B virus which is a DNA virus.

  • They all produce similar clinical picture.
  • Patient may be asymptomatic or rapidly deteriorate and die.
  • There may be subclinical infection or rapidly progres­sive chronic liver disease – cirrhosis, or even hepato­cellular carcinoma (HBV, HCV and HDV).

Hepatitis

Hepatitis Types Causes Symptoms Diagnosis and Treatment


The Hepatitis Viruses Classification Types –

HAV HBV HCV HDV HEV
Viral Properties
Size, nm 27 42 ~55 ~36 ~32
Nucleic acid RNA DNA RNA RNA RNA
Genome length, kb 7.5 3.2 9.4 1.7 7.5
Classification Picornavirus Hepadnavirus Flavivirus-like Calicivirus-like or alpha-virus-like
Incubation, days 15–45 30–180 15–160 21–140 14–63
Transmission OF Hepatitis
Fecal-oral +++ +++
Percutaneous Rare +++ +++ +++
Sexual ? ++ Uncommon ++
Perinatal +++ Uncommon +
Hepatitis Clinical Features
Severity Usually mild Moderate Mild May be severe Usually mild
Chronic infection No 1–10%; up to 90% in neonates 80–90% Common No
Carrier state No Yes Yes Yes No
Fulminant hepatitis 0.1% 1% Rare Up to 20% in superinfection 10–20% in pregnant women
Hepatocellular carcinoma No Yes Yes ? No
Prophylaxis Ig; vaccine HBIg; vaccine None None (HBV vaccine for susceptibles) None

Note: HAV, hepatitis A virus; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; HEV, hepatitis E virus; Ig, immune globulin; + +, sometimes; + + +, often; ?, possibly.  

VIROLOGY AND ETIOLOGY Hepatitis A

  • It is a resistant RNA picorna virus.
  • Virus is present in liver, stools and blood during late incubation period and preicteric phase.
  • Incubation period is 4 weeks.
  • Infectivity decreases rapidly when jaundice becomes visible in patients.
  • Diagnosis is made by demonstrating anti HAV (IgM) during acute illness.

Hepatitis B

  • It is a DNA virus of Hepa DNA virus type 1.
  • HBsAg (hepatitis B surface antigen) positive serum containing HBeAg (Hepatits Be antigen) is highly in­fectious, more than HBeAg negative or anti HBe posi­tive serum. HBsAg carrier mothers who are HBeAg positive usually transmit hepatitis B to their offspring,
  • whereas HBsAg carrier mothers with anti HBe rarely infect their offspring.
  • The disappearance of HBeAg in acute hepatitis B dis­ease means a better prognosis. If HBeAg persists more than 3 months prognosis is bad.
  • After a person gets infected with HBV, first marker detectable is HBsAg in serum.

Hepatitis D

  • The delta hepatitis agent is a defective RNA virus which • requires HBV for replication and expression.
  • HDV either infects a person with HBV or after infec­tion by HBV.

Hepatitis C

  • Hepatitis C was called non A – non B hepatitis previ­ously. It is a RNA virus.

Hepatitis E

  • Previously called epidemic or non A – non B hepatitis. It is common in India and Africa.

PATHOGENESIS OF HEPATITIS

  • None of the hepatitis virus is cytopathic to hepato­cytes. The damage of liver cells occurs due to immu­nologic response of the host and can result in acute liver failure.
  • Hepatitis B
    • The virus is not directly cytopathic. The difference in T cell responsiveness and properties determines who will get mild disease and who will progress to severe fulminant HBV infection.
  • Hepatitis C
    • Liver injury is due to cell mediated immune response and T cell mediated cytokine release.
  • EXTRA HEPATIC MANIFESTATIONS Glomerulonephritis, nephritic syndrome, polyarteri­tis nodosa, vasculitis.

PATHOLOGY

  • There is pan-lobular infiltration with mononuclear cells, hepatic cell necrosis, hyperplasia of Kupffer cells and cholestasis.
  • Hepatic cell regeneration is present with mitosis, multinucleated cells and rosette or pseudoacenar for­mation. Hepatic cell regeneration and necrosis, cell drop out, ballooning of cells and acidophilic degen­eration of hepatocytes (Council man bodies or apoptotic bodies), large hepatocytes with ground glass appearance of cytoplasm is seen in chronic but not acute HBV infection. These cells contain HBsAg.
  • In hepatitis C there is less inflammation. Microvesicular steatosis is seen in Hepatitis D.
  • In Hepatitis E there is marked cholestasis.
  • Bridging hepatic necrosis or subacute or confluent necrosis is seen in acute hepatitis sometimes. Bridg­ing between the lobules is due to large areas of he­patic cell damage and collapse of the reticulin net­work. Such patients progress to cirrhosis and even death in weeks to months of chronic severe hepatitis.
  • Liver biopsies are not done routinely in acute hepati­tis.
  • In massive or fulminant hepatitis called acute yelow atrophy there is a small shrunken soft liver.
  • Biopsy if required, can be done by angiographically guided transj gular route, which permits the perfor­mance of this invasive procedure in the presence of severe coagulopathy.

EPIDEMIOLOGY

  • Viral hepatitis used to be labeled as infectious or se­rum hepatitis.

Hepatitis A

  • It is transmitted by fecao-oral route. Transmission is by contaminated food, water, milk, frozen foods.-
  • HAV infection is common in child care centers, neo­natal intensive care units and IV drug users.
  • Anti HAV which denotes previous HAV infection is com­monly found in older age groups and the poor.

Hepatitis B Infection is by :

  • 1. Skin inoculation
  • 2. Most of the hepatitis transmitted by blood trans­fusion is not caused by HBV and in 2/3’d of acute hepatitis B patients there is no history of inocu- _ lation.
  • 3. HBS Ag is found in body fluids – serum, semen and saliva, but mostly in the serum.
  • 4. Most common transmission is by sexual contact.
  • 5. Perinatal transmission occurs in infants of HBsAg carrier mothers or mothers with acute hepatitis B in third trimester of pregnancy.
  • Anti HBe positive mothers transmit HBV infec­tion to their offspring.
  • Acute infection in new born is asymptomatic but the child is HBsAg carrier.
  • Prevalence of HBsAg is common in India, Africa, Central America.
  • It is also more common in Down’s syndrome, lepro­matous leprosy, leukemia, Hodgkin’s disease, pol­yarteritis nodosa, chronic renal disease on hemodi­alysis, IV drug users, spouses of infected persons, men who have sex with men, health care workers, persons with repeated transfusions like hemophiliacs, prisoners, voluntary blood donors.

Hepatitis D

  • HDV infection is endemic in patients of hepatitis B. It is common in persons receiving blood transfusions like hemophiliacs and IV drug users.

Hepatitis C

  • Previously called non A non B hepatitis because hepa­titis A and B serology is negative.
  • It is transmitted sexually and perinatally.
  • Breast feeding does not increase risk of HCV infec­tion between infected mother and her infant.

Hepatitis E

  • This hepatitis is found in Asia, Africa, Central America. It resembles hepatitis A. It spreads through food and water. Person to person spread from close contact usually does not occur.

CLINICAL FEATURES of  Hepatitis  – Signs and Symptoms

History

  • •Determine exposure: Obtaining complete social history is key.
  • •Chronic HCV: Vast majority of cases present as mildly symptomatic (nonspecific fatigue) or asymptomatic elevated ALT/aspartate aminotransferase (AST)
  • Acute HCV: If symptoms develop (rare):
    • Onset 2+ weeks postexposure
    • Persist 2–12 weeks
    • Spontaneous clearance more likely
    • Fever
    • Malaise/fatigue
    • Nausea/vomiting
    • Anorexia
    • Jaundice/icterus
    • Dark urine
    • Pale stools
    • Pruritus
    • Right upper quadrant (RUQ) pain
    • Arthralgias/myalgias

Physical Exam

  • Typically normal unless advanced fibrosis/cirrhosis
  • May have RUQ tenderness/hepatomegaly

Incubation period for:

  • Hepatitis A 15 – 45 days
  • Hepatitis Band D 30 – 180 days
  • Hepatitis C 15 – 160 days
  • Hepatitis E 14 – 60 days
  • Symptoms are anorexia, nausea, vomiting, fatigue, malaise, arthralgias, myalgias, headache, photopho­bia, pharyngitis, cough, coryza and jaundice.
  • There is change in taste.
  • Low grade fever 100 – 1020 F in hepatitis A and E. Urine is dark and stool clay coloured from 1 – 5 days before jaundice.
  • When jaundice is seen, constitutional symptoms like nausea, vomiting and fever subside.
  • Liver is enlarged and tender. There is extra hepptic biliary obstruction giving rise to itching.
  • There is spleenomegaly and cervical lymphadenopa­thy.
  • There may be spider angiomas.
  • Jaundice persists for few days and then patient re­mains ill for 2 – 12 wks and even more in hepatitis B and C.
  • Some patients of viral hepatitis never become icteric (jaundiced).
  • Infection with HDV occurs with HBV infection.
  • Acute HDV infection becomes chronic when there is underlying HBV infection.
  • There is clinical deterioration of hepatitis B patients when HDV super infection occurs.

LABORATORY FEATURES in Hepatitis

  • The serum amino transferases – aspartate amino transferase (AST) and alanine amino transferase (ALT) also called SGOT and SGPT respectively increase dur­ing prodromal phase of acute viral hepatitis before jaundice occurs.
  • The SGOT, SGPT levels do not correlate with liver damage.
  • Peak levels may be 400 – 4000 IU and gradually di­minish during recovery.
  • Jaundice is seen in sclera, skin when serum bilirubin value is more than 2.5 mg/dl. Serum bilirubin rises to 5 – 20 mg/dl. The conjugated and unconjugated frac­tions of bilirubin are equal. Bilirubin level more than 20 mg/dl leads to severe liver disease. In case of hemolytic anaemi or sickle cell anaemia high biliru­bin levels are common.
  • There may be neutropenia, lymphopenia with atypi­cal lymphocytes.
  • Prothrombin time (PT) is prolonged in acute viral hepa­titis.
  • Serum alkaline phosphatase may be increased but serum albumin is normal.
  • Serum IgG and IgM may be increased.

Hepatitis Treatment

  • Acute HCV: Antiviral therapy highly effective if given within 12 weeks of infection
  • Pegylated interferon (IFN) alone or in combination with low-dose ribavirin, for 12–24 weeks
  • Chronic HCV: Variably effective:
  • Peg-IFN/ribavirin combined therapy
  • Peg-IFN 2b 1.5 µg/kg SC weekly OR
  • Peg-IFN 2a 180 mcg SC weekly WITH
  • Ribavirin 800–1,400 mg PO b.i.d, weight-based
  • Duration of therapy: 12–72 weeks based on genotype, presence of cirrhosis, HIV coinfection, and rate plus degree of viral response (levels at 4, 12, and 24 weeks)
  • 32–36 weeks of HCV RNA undetectability optimal duration for genotype 1 patients
  • 24 weeks sufficient for genotype 2/3 if early viral response (EVR):
  • Cirrhosis lowers sustained viral response (SVR) by 50% in all genotypes.
  • Dose-reduced ribavirin/therapy interruption, especially before RNA negative, reduces SVR
  • Hepatitis PROPHYLAXIS and Hepatitis TREATMENT and Management

  • Complete article for Treatment and management
  • http://medicscientist.com/hepatitis-prophylaxis-and-hepatitis-treatment-and-management
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