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hepatitis profile

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  • hepatitis profile

    السادة اعضاء منتدى مختبرات العرب



    السلام عليكم ورحمة الله وبركاته

    لو سمحتم ولا عليكم امر اريد شرح وافي للتحاليل التالية

    HCV
    HbsAG
    ANT-HBs
    HIV.II
    HIV-AG
    HTLV

    وجزاكم الله خيراااااااااااااااااااا

  • #2
    Hepatitis B Virus
    Hepatitis B Virus (HBV)
    Family Hepadnaviridae
    Morphology
    A small, enveloped DNA virus (42nm)
    Icosahedral nucleocapsid
    Small, circular partially double-stranded DNA genome
    Within the core, there is DNA- dependent DNA polymerase
    HBV antigens:
    HBsAg, located in the envelope
    HBcAg, located in the core
    HBeAg, located in the core

    Hepatitis B Virus (HBV)
    Electron microscopy of a patient’s serum reveals 3 different types of particles:
    A few 42nm virions
    Many 22nm spheres and long filaments 22nm wide, both are composed of surface Ag
    These spheres and filaments are the immunogens in one form of the vaccine (the inactivated vaccine)


    Different particles in patient’s serum


    HBV : Epidemiology
    Routes of Transmission
    Contaminated blood and blood components
    Transfusion,
    Needle sharing, acupuncture
    Ear piercing,or tattooing
    Very close personal contact involving exchange of
    saliva, semen & vaginal secretions (sexual contact)
    During childbirth from mother to child
    Have 90% chance of acquiring hepatitis B infection
    HBV : Epidemiology
    Seroprevalance
    Worldwide in distribution
    Is highly endemic in the Far East, sub-Saharan Africa, the Middle East and parts of South America
    In Saudi Arabia the seropositivity rate varies with an average of 8.7%

    HBV : Epidemiology
    High risk groups
    Persons from endemic regions
    Babies of mothers with chronic HBV infection
    I.V drug abusers
    Persons with multiple sex partners
    Hemophiliacs
    Hemodialysis patients
    Health care personnel who are in contact with blood


    HBV : Clinical Features
    Incubation period
    The mean incubation period is 10-12 weeks
    Acute infection:
    Prodromal Phase
    Fever, malaise, and anorexia with nausea, vomiting, abdominal discomfort
    Classic Icteric Phase
    Has symptoms of liver damage:
    Jaundice
    Dark urine
    Pale stools
    Most patients (90%) who develop acute infection recover completely


    HBV : Clinical Features
    Fulminant Hepatitis
    In approximately 1% of patients & may be fatal
    Chronic Hepatitis
    Occurs in 5-10% of infected patients
    May be detected only by finding elevated liver
    enzymes on routine examination
    Is characterised by the presence of HBsAg in
    the blood for more than 6 months.
    HBV : Clinical Features
    Chronic Hepatitis : 4 Groups
    1. Resolution of Infection
    in 50% of patients
    2. Asymptomatic Carrier State
    Is associated with normal liver functions
    Are sero-negative for HBeAg, HBV-DNA.
    Only HBsAg is present in circulation
    HBV : Clinical Features
    3. Chronic Persistent Hepatitis
    Is characterised by mild symptoms like fatigue & discomfort over the liver region
    Liver enzymes >5 times upper limit
    4. Chronic Active Hepatitis
    Persistent elevation of serum aminotransferases
    May develop cirrhosis and liver failure
    Complication of HBV infection
    Primary Hepatocellular Carcinoma (PHC)
    80% of all cases of PHC is due to chronic HBV infections



    HBV : Infection Markers
    1. HBsAg
    Usually detectable 2-6 weeks prior to clinical and biochemical evidence of hepatitis and persists throughout the clinical course of the disease (6-12 weeks), typically disappears by the sixth month after exposure
    If >6 months = chronic infection
    serum, saliva, tears, breast milk, bile duct and urine
    All HBsAg-positive materials are potentially infectious for HBV, unless treated.

    HBV : Infection Markers
    2. HBeAg
    The second antigen that appears in circulation
    Arise during the incubation period and is present during the prodrome and early acute disease
    There is a high correlation between HBeAg and infectivity
    Specimens positive for HBeAg are considered to be highly infectious i,e., they contain high concentrations of HBV
    Infectivity is reduced, but probably not eliminated, in specimens containing anti- HBe
    Persistent positivity for HBeAg, in the absence of anti- HBe, correlates with chronic liver infection
    HBV : Infection Markers
    3. Anti-HBc
    Anti- HBc IgM is detected approximately 2-4 weeks after HBsAg appears.
    Because this Ab is directed against the internal core component of HBV, its appearance in serum indicates viral replication
    High titers of IgM-anti-HBc are detected in acute hepatitis B
    In early convalescence, HBsAg may be undetectable in serum, in that case, the IgM-anti-HBc will establish the diagnosis
    Anti- HBc of the IgG class remains detectable long after exposure to infection
    HBV : Infection Markers
    4. Anti-HBe
    Usually appears after the disappearance of HBeAg
    Its presence indicates low infectivity
    5. Anti-HBs
    Generally appears within a few weeks after HBsAg
    is cleared from circulation
    Once produced, anti-HBs persists for years
    Is the only marker for immunity against HBV infection


    HB Serological Markers
    HBV : Laboratory diagnosis
    Both ELISA and RIA assays are available
    The most important laboratory test to detect early HBV infection is the immunoassay for HBsAg.
    HBsAg appears during the incubation period and is detectable in most patients during the prodrome and acute disease. It falls to undetectable levels during convalescence. Its prolonged presence indicates carrier state
    There is a period of several weeks when HBsAg has disappeared but HBsAb is not yet detectable, this is the “window phase” at which the HBcAb is always positive and can be used to make the diagnosis
    The test for HBcAg is not readily available


    HBV : Treatment & Prevention
    IFN-alpha is currently used to treat chronic HBV infection
    Hepatitis B immune globulin (HBIG) :
    Contains a high titer of HBsAb
    Provides immediate passive protection to
    Persons exposed to HBsAg positive blood within a week of exposure, e.g, after an accidental needle- stick &
    To newborn infants of HBsAg-positive mother
    Screening donated blood for HBsAg and IgM anti-HBc
    Transmission of HBV by blood or blood products has
    been greatly reduced
    Avoiding intimate personal contact with a HBV carrier
    General hygienic measures: the use of gloves when blood or other samples are collected and the use of disposable needles and syringes.
    HBV : Treatment & Prevention
    Recommendation for neonates born to
    HBsAg & HBeAg-positive mother
    1. Hepatitis B Immunoglobulin at birth
    2. Vaccination
    The vaccine contains HBsAg produced in yeasts by genetic engineering technique
    Is administered intramuscular in 3 doses at 0, 1, and 6 months, booster is recommended every 5 years
    Prior to the advent of this vaccine, an inactivated vaccine consisting of HBsAg prepared from spherical particles purified from the serum of infected individuals was used
    Both vaccines are highly effective in preventing hepatitis B and have few side effects











    Hepatitis B vaccine produced using cloned genes
    HBsAg gene can be cloned into plasmids
    The cloned DNA can then be expressed in prokaryotic (bacteria) or eukaryotic (yeast) cells which produce the antigen in sufficient quantity
    The produced antigen is then purified giving a vaccine which contains only the immunizing protein antigen

    HBV vaccine
    The vaccine is indicated for people who are frequently exposed to blood or blood products, such as:
    Certain health care personnel e.g, laboratory personnel, medical students, surgeons, dentists
    Patients receiving multiple transfusions or dialysis
    IV drug abusers
    HB vaccine is given to all infants in Saudi Arabia
    HDV (delta agent) : Transmission & Pathogenesis
    HDV is an enveloped virus with circular ssRNA genome, the internal core protein is called delta antigen
    HDV is a defective virus, it can not replicate by itself, because it does not have the genes for its protein coat
    HDV can replicate only in cells also infected with HBV, because HDV uses the surface antigen of HBV (HBsAg) as its coat

    HDV is transmitted along with HBV
    Either at the time of first infection (co-infection) OR
    During chronic HBV infection (super-infection)
    HDV is transmitted by the same means like HBV
    More rapid & severe progression in
    super-infection than in co-infection

    HDV : Clinical syndromes
    Incubation period : 3-7 weeks
    Increases the severity of HBV infections
    Is responsible for 40% of fulminant hepatitis
    Can result in massive liver necrosis & hepatic encephalopathy


    Laboratory diagnosis, treatment and prevention of HDV
    The diagnosis is made by detecting either delta antigen or IgM antibody to delta antigen in the patient’s serum
    Alpha interferon can diminish some of the effects of the chronic hepatitis caused by HDV but does not eradicate the chronic carrier state
    There is no specific antiviral therapy against HDV
    There is no vaccine against HDV, but a person immunized against HBV will not be infected by HDV
    تذكّر أنك لست صدفة ...ولست مجرّد عنصر من منتج.... ولست ناتجاً من خط تجميع،
    بل قد خلقك الله متميزاً فثق دوماً أنك تستحق أن تعيش الحياة التي تريدها

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    • #3
      جزاكي الله خيرا اختي كروموسومه

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