REPORT: PATHOGENESIS, DIAGNOSTICS, TREATMENT AND PRINCIPLES OF PROPHYLAXIS OF PARENTARAL VIRAL HEPATITIS (B-C-D-GB-TT) Sajid Mehmood
Adnan Akram
Aftab Ahmed
Accident & Emergency Department. Royal Infirmary Liverpool. United Kingdom
Department of Infectious Diseases. University Hospital Riga. Latvia
Department of Infectious Diseases. Kaunas Medical University Hospital. Kaunas. Lithuania
sajid@infekcijas.eu
adnan@infekcijas.eu
aftab@infekcijas.eu
HBV- virus DNA (Hepadna group) Can occur at any age Transmission-parantaral by intravenous rout, infected blood,mainly in homosexuals, Vertical transmission. I.p- 1 to 6 months. Clinics- Prodromal period 1 month generally 1-2 wks, during this time occur arthralgia mostly in large joints and influenza like symptoms. -May fallow serum sickness like immunological syndrome (other constitutional symptoms of anorexia, fever law grade, malaise, vomiting, head ache). Serum sickness like symptoms may consist of rashes eg- urticaria and macular papular rash. -With the onset of jaundice clinical symptoms decrease. -urine becomes dark and stools become pale. -Liver may be enlarged, spleen may be palpable (cytolitic syndrome). Complications – extra hepatic immune complex mediated conditions such as arthritis or glomerular nephritis seen. Investigations – (1) liver biochemical analysis- [A] in prodromal stage-serum bilirubin is normal, Bilirubin urea ,urobilinogen in urine, amino transferases, ASAT and ALAT are all increased ( ALAT >ASAT). [b] Icteric stage- serum bilirubin reflect the level of jaundice, serum ASAT reaches max 1-2 days after the appearance of jaundice, Alkaline phosphatase in serum mildly elevated. (2) Blood analysis- Leukopenia and relative Lyphocytosis, prolonged PT, increased ESR (3) Viral markers Structure of hepatitis B virus- complete infective virion (dane particle) consist os circular double stranded DNA, specific DNA polymarase and structural proteins, surrounded by an outer envelop of surface proteins which is recognized serologically as HBV surface antigen (HBS antigen). Nucleo capcid contains 2 serologically distinct antigens the Core and E antigen ( HBC ag, HBE ag),
a. HBS antigen- associated with the viral surface coat, it is found in serum during the 1st acute infection, Appears usually 1-6 wks before clinical or biochemical illness develops (I.P) , and disappears in recovery period. Corresponding Anti HBS ab- Appears wks or months later after clinical recovery and usually persist for life its detection indicates past HBV infection and relative immunity. (vaccination). In chronic state or carrier state usually HBS ag persist and Anti HBS does not develop. b. Hbc ag – Associated with viral core found in infected liver cells not in serum, corresponding anti Hbc- appears at the onset of symptoms nearly 2 months also found in acute infections (HBS ag +, Anti Hbc IgM+), chronic hepatitis (HBS ag +, Anti Hbc IgM negative but Anti Hbc IgG +), Carrier state (HBS ag+, Anti Hbc IgM negative and Anti Hbc IgG+). Therefore Anti Hbc- (IgM-Acute),(IgG-Chronic carrier state) c. Hbe ag – viral core ag found only in HBS ag positive serum, It tends to produce viral DNA polymerase does its presence reflects more active viral replication and associated with greater infectivity of the blood and progress to chroni liver disease. Corresponding Anti Hbe- points to relatively law infectivity, (Anti Hbe+, Hbe ag negativecarrier ),(Anti Hbe negative ,Hbe ag +-chronic). ACUTE HBS ag + Hbc Anti, IgM + Hbc Anti IgG negative
TOTALLY RECOVERED HBS ag Hbc anti IgM negative HBC anti IgG +
CHRONIC
CARRIER
HB sag + Hbc anti IgM negative Hbc anti IgG +
Hbs ag + Hbc anti IgM negative Hbc anti IgG +
Hbe ag + Anti Hbc negative
Hbe ag negative Anti Hbe +
Treatment – symptomatic Prevention and profilaxis1.Avoid risk factors shared needles, homosexuals, multiple partners 2. Passive and active immunity- Vaccination should be given to all persons at risk COMBINATION PRFILAXIS (vaccination + immunoglobulins) should be given to accidental injury- needle stick, new born with HBS ag + mothers, Rgular sexual partners of Hbs ag + who have been found HBV negative. (500 Iu adults, 200 Iu new born i.m ) 3. Chronic Hbv carriers treatment- patients who are Hbe ag+, HBS ag +, Anti Hbe negative. Chronic state can be treated with alfa INF. VHD - Delta virus Incomplete RNA virus, enclosed in shel of HB ag It is unable to replicate on its own ,and activated by presence of HBV Route of transmission- mainly in drug users IP- 1-2mo Any age, prodromal period nearly 1mo
During this period artharalgia, influenza like symptoms. Clinic similar to HBV HDV infection can occur either as a coinfection with HBV or as a superinfection in an HB sag+ patients Coinfection of HDV and HBV clinically indistinguishable, Dg is confirmed by anti HDV IgM+, anti HBC IgM+ Anti HDV Igm appears at 1 week and dissappear by 5-6 weeks when anti HDV IgG = Increase serum ASAT HDV RNA in serum and liver can be messured and is found in acute and chronic HDV infection.chronic HDV is a severe form of liver disease 15 of dis. Progress in dev. Of cirrhosis Treatment - alfa INF produces remission and relapses is common. VHC RNA virus 6 subtypes are seen Route of transmission-parenteral, post transfusion hep(blood) Sexual contact Mother- child IP-1-2 mo Clinical features-prodromal period nearly 1 mo,in acute phase flue like symptoms increase in serum transferaces, Extra hepatic manifestations-artheritis,agranulocytosis,aplastic anemia,diffuse neurological problems/ In HCV- acute form, chronic,Hepatic cirrhosis dev within 15-30 yrs, Hepatocellular carcinoma dev Diagnosis- (1)anti HCV IgM in serum (1st gen.test) (2) 2nd gen.testa. ELISA, b. RIBA(recombinant immunoblotassy),c. PCR-to check viral RNA .if + then do liver biopsy to detect chronic hepatitis and cirrhosis/ Treatment- no clear guide line, INF been used in acute phases/ VH-GB(HGBV) RNA virus,flavi vir Parenteral-sexual contact,blood IP-180 days Characteristic chronic forms Can occur fulfilmant form DG-HGB ag+, Anti HGBV, PCR VH-TT Recently detected ,parenteral route Mainly blood.similar to HCV and HGBV in clinics and in investigations Viral hepatitis dg. Is based on 4 steps. 1.epidermiological 2.pre icteric( prodromal) variation 3.clinics 4. lab Data