Chronic Viral Hepatitis

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Chronic Viral Hepatitis:

Chronic Viral Hepatitis De Guzman Jan Kristoper De Guzman Raquel Isabelle De Leon Gemma Rosa De Mesa Angelica Monique

Chronic Viral Hepatitis:

Chronic Viral Hepatitis HBV HCV HDV Incubation (days) 30-180 (mean 60-90) 15–160 (mean 50) 30–180 (mean 60–90) Onset Insidious or acute Insidious Insidious Age of preference Young adults (sexual and percutaneous ), babies, toddlers Any age, but more common in adults Any age (similar to HBV) Transmission Fecal-oral Percutaneous Perinatal Sexual - +++ +++ ++ - +++ ± a ± a - +++ + ++ Prognosis Worse with age, debility Moderate Poor a Primarily with HIV co-infection and high-level viremia in index case; risk ~ 5%. Adapted from Table 298-2: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., page 1939

Hepatitis B:

Hepatitis B Percutaneous inoculation has long been recognized as a major route of hepatitis B transmission Many cases of hepatitis B result from less obvious modes of nonpercutaneous or covert percutaneous transmission. oral ingestion : potential but inefficient route of exposure Intimate (especially sexual) contact and perinatal transmission considered to have greatest impact Perinatal transmission occurs primarily in infants born to HBsAg carrier mothers or mothers with acute hepatitis B during the third trimester of pregnancy or during the early postpartum period. most important mode of HBV perpetuation in the Far East and developing countries most infections occur approximately at the time of delivery and are not related to breast feeding Likelihood of perinatal transmission of HBV correlates with the presence of HBeAg Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., page 1940

Hepatitis B:

Hepatitis B The >350 million HBsAg carriers in the world constitute the main reservoir of hepatitis B in human beings A prevalence of up to 5–20% in persons with Down's syndrome, lepromatous leprosy, leukemia, Hodgkin's disease, polyarteritis nodosa ; in patients with chronic renal disease on hemodialysis ; and in injection drug users Other groups with high rates of HBV infection include spouses of acutely infected persons sexually promiscuous persons (especially promiscuous men who have sex with men) health care workers exposed to blood persons who require repeated transfusions especially with pooled blood product concentrates (e.g., hemophiliacs) residents and staff of custodial institutions for the developmentally handicapped, prisoners family members of chronically infected patients. Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., page 1940

Hepatitis B:

Hepatitis B Infection at birth is associated with clinically silent acute infection but a 90% chance of chronic infection Infection in young adulthood in immunocompetent persons is typically associated with clinically apparent acute hepatitis but a risk of chronicity of only approximately 1% Most cases of chronic hepatitis B among adults, however, occur in patients who never had a recognized episode of clinically apparent acute viral hepatitis Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., page 1956

Hepatitis C:

Hepatitis C Accounts for 40% of chronic liver disease, the most frequent indication for liver transplantation, and estimated to account for 8000–10,000 deaths per year in the United States World-wide, genotype 1 is the most common Can be transmitted via blood/blood product transfusion, other percutaneous routes such as injection drug use, and by occupational exposure to blood (with increased likelihood of infection in hemodialysis units) Ineffecient transmission occurs via sexual and perinatal routes Confined to those with multiple sexual partners and sexually transmitted diseases Breast feeding does not increase the risk of HCV infection between an infected mother and her infant Health workers are more likely to acquire HCV infection through accidental needle punctures, the efficiency of which is ~3% Other groups with an increased frequency of HCV infection include patients who require hemodialysis and organ transplantation those who require transfusions in the setting of cancer chemotherapy Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., pages 1940-1941

Hepatitis D:

Hepatitis D Infection with HDV has a worldwide distribution, with two epidemiologic patterns Endemic areas (i.e. Mediterranean) : endemic among those with hepatitis B, and is transmitted predominantly by nonpercutaneous means, especially close personal contact Non-endemic areas: confined to persons exposed frequently to blood and blood products, primarily injection drug users and hemophiliacs On a global scale, HDV infection is declining. Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., page 1940

SEROLOGY:

SEROLOGY

Antigens:

Antigens HBsAg Found on the surface of the intact virus and in serum as unattached particles Earliest detectable marker in serum indicates current Hepatitis B infection HBcAg Found within the core of the intact virus Not detectable in serum Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1933-1934

Antigens:

Antigens HBeAg Readily detectable serologic marker of HBV infection Appears shortly after HBsAg Coincides w/high levels of virus replication Indicates highly infective stage of HBV Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1935

Antibodies:

Antibodies Anti-HBs Antibody to HBsAg Becomes detectable in serum after HBsAg disappears indicates immunity to Hepatitis B infection “protective antibody” Anti-HBc Total antibody to HBcAg Only serologic evidence of recent HBV infection during the “window period” May indicate acute or chronic infection Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1933-1934

Antibodies:

Antibodies Anti-HBc IgM IGM antibody to HBcAg Seen in the 1 st 6 months after acute infection indicates recent acute Hepatitis B infection Anti-Hbc IgG -IgG antibody to HBcAg -predominates beyond 6 months - Seen in chronic HBV infection Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1934-1935

Antibodies:

Antibodies Anti-HBe - Antibody to HBeAg - Signifies low infectivity Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1935

Chronic Hepatitis B Serologic Patterns:

Chronic Hepatitis B Serologic Patterns HBs Ag Anti-HBs Anti-HBc HBeAg Anti-HBe Interpretation + - IgG + - Chronic Hepatitis B, High infectivity + - IgG - + Chronic Hepatitis B, Low infectivity Reference: 17 th Ed. Harrison’s Principles of Internal Medicine p.1943

CLINICAL and laboratory FEATURES:

CLINICAL and laboratory FEATURES CHRONIC HEPATITIS B

Progression of acute hepatitis to chronic hepatitis::

Progression of acute hepatitis to chronic hepatitis: Clinical and Laboratory features: lack of complete resolution of clinical symptoms of anorexia, weight loss, and fatigue and the persistence of hepatomegaly ; 2. the presence of bridging or multilobular hepatic necrosis on liver biopsy during protracted, severe acute viral hepatitis; failure of the serum aminotransferase , bilirubin , and globulin levels to return to normal within 6 to 12 months after the acute illness; and 4. the persistence of HBeAg beyond 3 months or HBsAg beyond 6 months after acute hepatitis. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17 th Ed., pp.1945

CHRONIC HEPATITIS B:

CHRONIC HEPATITIS B CLINICAL FEATURES Onset: insiduous Incubation period: 30-180 days (mean, 8-12 weeks) Fatigue is a common symptom Low grade fever between 38° and 39°C (100° - 102°F) when heralded with serum-sickness syndrome Reference: Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., pp.1941-1942

CHRONIC HEPATITIS B:

CHRONIC HEPATITIS B Persistent or Intermittent jaundice is a common feature in severe or advanced cases. It may lead to progressive liver injury and in cases with superimposed cirrhosis --- hepatic decompensation. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17 th Ed., p. 1957

CHRONIC HEPATITIS B:

CHRONIC HEPATITIS B LABORATORY FEATURES Aminotransferase elevations tend to be modest but may fluctuate in the range of 100-1000 units. Alanine aminotransferase (ALT) tends to be more elevated than aspartate aminotransferase (AST) When cirrhosis is established, AST tends to exceed ALT. Levels of alkaline phosphatase activity tend to be normal or only marginally elevated. Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17 th Ed., p. 1957

CHRONIC HEPATITIS B:

CHRONIC HEPATITIS B In severe cases, moderate elevations in serum bilirubin [51.3 to 171 µmol/L (3 to 10 mg/ dL )] occur. Hypoalbuminemia and prolongation of the prothrombin time occur in severe or end-stage cases. Hyperglobulinemia and detectable circulating autoantibodies are distinctly absent in chronic hepatitis B (in contrast to autoimmune hepatitis). Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 17 th Ed., p. 1957

Slide 22:

Reference: Braunwald, et al, Harrison’s Principles of Internal Medicine 16 th Ed., p. 1844

THERAPY:

THERAPY

Candidates for therapy:

Candidates for therapy Chronically infected individuals with: persistently elevated alanine aminotransferase a marker of liver damage HBV DNA levels Lai, CL; Yuen (2007). "The natural history and treatment of chronic hepatitis B: a critical evaluation of standard treatment criteria and end points". Annals of internal medicine 147 (1): 58–61

Candidates for therapy:

Candidates for therapy HBeAg -positive patients (w/ evidence of chronic HBV): HBV DNA level is ≥20,000 IU/ mL (10 5 copies/ mL ) Serum ALT is elevated for 3-6 months. HBeAg -negative patients(w/ evidence of chronic HBV): HBV DNA is ≥ 2000 IU/ mL (10 4 copies/ mL ) S erum ALT is elevated (ALT levels >20 U/L for females and 30 U/L for males) for 3-6 months. Pyrsopoulos , Nikolaos . Chronic Hepatitis B: treatment and medication. Emedicine.com. June 19,2009

Goals of Treatment:

Goals of Treatment to suppress HBV replication to induce remission of liver disease before development of cirrhosis and hepatocellular carcinoma

Approved Drugs for Chronic Hepatitis B treatment:

Approved Drugs for Chronic Hepatitis B treatment I nterferon (INF) α P egylated interferon Lamivudine A defovir dipivoxil Entecavir

Interferon (INF) α:

Interferon (INF) α Protein product manufactured by recombinant DNA technology Modulates host immune responses Direct antiviral activity HBeAg negative patients: 1 and ½ yr tx results in sustained remissions, with suppressed HBV DNA and aminotransferase activity, in 20%

Complications of Interferon (INF) α:

Complications of Interferon (INF) α systemic "flu-like" symptoms marrow suppression Irritability,depression /anxiety autoimmune reactions miscellaneous side effects alopecia, rashes, diarrhea , and numbness and tingling of the extremities. *With the possible exception of autoimmune thyroiditis , all these side effects are reversible upon dose lowering or cessation of therapy.

Lamivudine:

Lamivudine inhibits reverse transcriptase activity of both HIV and HBV HBeAg -reactive patients: daily doses of 100 mg for 48–52 weeks HBeAg - negative patients: 1 year of lamivudine therapy

Adefovir dipivoxil:

Adefovir dipivoxil prodrug that is converted to the diphosphate salt active drug : antiviral nucleotide reverse transcriptase inhibitor oral daily dose of 10 mg reduces HBV DNA

Pegylated interferon:

Pegylated interferon once-a-week PEG IFN was more effective than the more frequently administered, standard IFN After 6 months of therapy: HBeAg loss (30%) HBeAg seroconversion (22%–27%) undetectable HBV DNA (<400 copies/ mL by PCR) in 10–25% normal ALT in 34–39% a mean reduction in HBV DNA of 2 log 10 copies/ mL (PEG IFN-2b) to 4.5 log 10 copies/ mL (PEG IFN-2a)

Entecavir:

Entecavir Guanosine nucleoside analogue with activity against HBV polymerase Competes with natural substrate deoxyguanosine triphosphate ( dGTP ) to inhibit HBV polymerase activity Less effective for lamivudine -refractory HBV infection available as a tablet and as oral solution (0.05 mg/ mL ; 0.5 mg = 10 mL ).

Slide 34:

Table 300-4 Recommendations for Treatment of Chronic Hepatitis B HBeAg Status Clinical HBV DNA (copies/mL) ALT Recommendation HBeAg -reactive Mild or inactive clinically <10 5 Normal (2 x ULN) b No treatment; monitor Chronic hepatitis 10 5 Normal (2 x ULN) b, c No treatment; current treatment of limited benefit (Some suggest liver biopsy and treating if abnormal) Chronic hepatitis 10 5 Elevated (>2 x ULN) b Treat d Cirrhosis compensated + or – e Normal or elevated Treat e with oral agents, f not PEG IFN Cirrhosis decompensated + or – e Normal or elevated Treat e with oral agents, g not PEG IFN; refer for liver transplantation Harrison’s Principles of Internal Medicine, 17 edition

Slide 35:

HBeAg -negative a <10 4 or 10 5 h Normal (2 x ULN) b Inactive carrier; treatment not necessary Chronic hepatitis 10 4 or 10 5 h Normal Consider liver biopsy; treat if biopsy abnormal Chronic hepatitis 10 4 or 10 5 h (>2 x ULN) b Elevated Treat i Cirrhosis compensated + or – Elevated or normal Treat with oral agents, j not PEG IFN (some authorites recommend either following or treating for HBV DNA <10 4 copies/ mL ) Cirrhosis decompensated + or – Elevated or normal Treat with oral agents, j not PEG IFN (some authorities would follow without therapy for undetectable HBV DNA; refer for liver transplantation) Table 300-4 Recommendations for Treatment of Chronic Hepatitis B HBeAg Status Clinical HBV DNA (copies/mL) ALT Recommendation Harrison’s Principles of Internal Medicine, 17 edition

SEQUELAE:

SEQUELAE

Sequelae:

Sequelae patients may (1) be inactive carriers; (2) have low-grade, mild chronic hepatitis; or (3) have moderate to severe chronic hepatitis with or without cirrhosis The most feared complication of viral hepatitis is fulminant hepatitis (massive hepatic necrosis) Hepatitis B accounts for >50% of fulminant cases of viral hepatitis Fulminant hepatitis is hardly ever seen in hepatitis C The liver is usually small and the PT excessively prolonged Hepatic failure + encephalopathy rapidly shrinking liver size, rapidly rising bilirubin level, marked prolongation of the PT clinical signs of confusion, disorientation, somnolence, ascites , and edema cerebral edema is common brainstem compression, gastrointestinal bleeding, sepsis, respiratory failure, cardiovascular collapse, and renal failure are terminal events The mortality rate >80% in patients with deep coma Liver transplantation may be life-saving in patients with fulminant hepatitis if donor liver can be located on time Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., pp 1944-1945

Sequelae:

Sequelae Hepatitis D has the potential for contributing to the severity of chronic hepatitis B can transform inactive or mild chronic hepatitis B into severe, progressive chronic hepatitis and cirrhosis can also accelerate the course of chronic hepatitis B HDV superinfections in patients with chronic hepatitis B can sometimes lead to fulminant Cirrhosis has been reported in as many as 50% of patients with chronic hepatitis C. Progression of chronic hepatitis C may be influenced by age of acquisition, duration of infection, immunosuppression , coexisting excessive alcohol use, concomitant hepatic steatosis , other hepatitis virus infection, or HIV co-infection. Instances of severe and rapidly progressive chronic hepatitis B and C are being recognized with increasing frequency in patients with HIV infection Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., pp 1944-1945

Sequelae:

Sequelae Hepatocellular carcinoma Enhanced risk in patients with chronic hepatitis B, particularly those infected in infancy or early childhood, especially those with HBeAg and/or high-level HBV DNA Increased risk also in patients with chronic hepatitis C, almost exclusively in patients with cirrhosis, and almost always after at least several decades, usually after three decades of disease EMC is an immune-complex disease that can complicate chronic hepatitis C and is part of a spectrum of B cell lymphoproliferative disorders, which, in rare instances, can evolve to B cell lymphoma Braunwald , et al, Harrison’s Principles of Internal Medicine 17 th Ed., pp 1944-1945

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