History

Fact Explanation
Age [1] Hepatitis B virus (HBV) and Hepatitis C virus (HCV) can cause chronic viral hepatitis. Fewer than 5 percent of adults acutely infected with HBV progress to chronic infection [1] Most patients (85 percent or more) with acute HCV infection develop chronic infection [6] Risk of chronic HBV infection is inversely related to age, with chronic infection developing in about 90 percent of infected infants, 30 percent of children younger than five years, and less than 5 percent in all other persons [1]
Chemotherapy or other immunosuppressant drugs [1] Occult infection may be reactivated by chemotherapy or other immunosuppressants [1]
Immunosuppressed conditions (eg:AIDS patients) [1] Occult infection may be reactivated by low immune conditions [1]
Intra venous drug abuse [2] Most drug abusers use the same needle to inject the drugs among several people.The risk of transmission is high as HBV and HCV can spread through blood [2]
Multiple blood transfusion [2] The risk of transmission is high as HBV and HCV can spread through blood [2]
Sex with multiple partners [2] The risk of transmission is high as HBV and HCV can spread through sex [2]
Health care and public safety workers (Specially who are not vaccinated against HBV) [1] Health care and public safety workers are at risk of exposure to blood or blood-contaminated body fluids.Thus, the risk of transmission is high as HBV and HCV can spread through blood [1]
Homosexual people [1] The risk of transmission is high in homosexual people [1]
Baby born to a mother with Hepatitis B,C [1] HBV , HCV can spread to the child during childbirth if the mother is infected from HBV [1] / HCV [5]
Symptoms of cirrhosis - yellowish discoloration of eyes, fatigue, loss of appetite, abdominal distension, leg swelling , white nails, hair loss, breast enlargement in males etc. [2] It has been estimated that 12 percent of patients with chronic HBV infection develop cirrhosis annually.The absolute lifetime risk of death from cirrhosis or hepatocellular carcinoma is 15 to 25 percent [3] Chronic HCV infection leads to cirrhosis in about 10 to 20 percent of patients [2] Mortality caused by liver disease was infrequent (range: 1.6 percent to 6 percent) [4]
Symptoms of hepatocellular carcinoma - loss of appetite, loss of weight, yelowish eyes, abdominal distension etc. [3] Smaller percentage of patients with chronic HBV infection develop hepatocellular carcinoma.The absolute lifetime risk of death from cirrhosis or hepatocellular carcinoma is 15 to 25 percent [3] Persons with HCV infection and cirrhosis have a 20-fold increased risk of hepatocellular carcinoma compared with persons without HCV infection [2] Mortality caused by liver disease was infrequent (range: 1.6 percent to 6 percent) [4]
Blistering of the skin in areas that receive higher levels of exposure to sunlight [4] Porphyria cutanea tarda is an identified extra-hepatic manifestation of chronic HCV [4]
Decrease in the amount of urine in the presence of hypertension [4] Membranoproliferative glomerulonephritis is an identified extra-hepatic manifestation of chronic HCV and HBV [4]
Excessive alcohol consumption [2] Alcohol consumption and HCV / HBV act synergistically to promote the progression of liver damage [2]
Past history of HBV / HCV infections [1] Hepatitis B virus (HBV) and Hepatitis C virus (HCV) can cause chronic viral hepatitis. Fewer than 5 percent of adults acutely infected with HBV progress to chronic infection [1] Most patients (85 percent or more) with acute HCV infection develop persistent infection.Most symptoms of chronic hepatitis C don’t appear until cirrhosis develops and the liver begins to fail. [2]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  3. LIN KW, KIRCHNER JT. Hepatitis B. Am Fam Physician [online] 2004 Jan 1, 69(1):75-82 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/14727820
  4. MOYER LA, MAST EE, ALTER MJ. Hepatitis C: Part I. Routine serologic testing and diagnosis. Am Fam Physician [online] 1999 Jan 1, 59(1):79-88, 91-2 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9917576
  5. TOSONE G, MARAOLO AE, MASCOLO S, PALMIERO G, TAMBARO O, ORLANDO R. Vertical hepatitis C virus transmission: Main questions and answers. World J Hepatol [online] 2014 Aug 27, 6(8):538-48 [viewed 25 September 2014] Available from: doi:10.4254/wjh.v6.i8.538
  6. CHEN J, ZHAO Y, ZHANG C, CHEN H, FENG J, CHI X, PAN Y, DU J, GUO M, CAO H, CHEN H, WANG Z, PEI R, WANG Q, PAN L, NIU J, CHEN X, TANG H. Persistent hepatitis C virus infections and hepatopathological manifestations in immune-competent humanized mice. Cell Res [online] 2014 Sep, 24(9):1050-66 [viewed 25 September 2014] Available from: doi:10.1038/cr.2014.116

Examination

Fact Explanation
Tattoo marks / intra venous drug injection sites [1] Most drug abusers use the same needle to inject the drugs among several people.The risk of transmission is high as HBV and HCV can spread through blood [2]
Symptoms of cirrhosis - ascites, jaundice, gynecomastia, loss of body hair, ankle odema etc. [2] It has been estimated that 12 percent of patients with chronic HBV infection develop cirrhosis annually [3] Chronic HCV infection leads to cirrhosis in about 10 to 20 percent of patients [2]
Symptoms of hepatocellular carcinoma - mass in right hypochondriac area, cachectic appearance, jaundice, ascites, ankle odema etc. [1] Smaller percentage of patients with chronic HBV infection develop hepatocellular carcinoma [3] more than 50% of patients with HCC are HBV carriers [5] Persons with HCV infection and cirrhosis have a 20-fold increased risk of hepatocellular carcinoma compared with persons without HCV infection [2]
Skin rash - Porphyria cutanea tarda [4] Porphyria cutanea tarda is an identified extra-hepatic manifestation of chronic HCV [4]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  3. LIN KW, KIRCHNER JT. Hepatitis B. Am Fam Physician [online] 2004 Jan 1, 69(1):75-82 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/14727820
  4. MOYER LA, MAST EE, ALTER MJ. Hepatitis C: Part I. Routine serologic testing and diagnosis. Am Fam Physician [online] 1999 Jan 1, 59(1):79-88, 91-2 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9917576
  5. TAROCCHI M, POLVANI S, MARRONCINI G, GALLI A. Molecular mechanism of hepatitis B virus-induced hepatocarcinogenesis. World J Gastroenterol [online] 2014 Sep 7, 20(33):11630-11640 [viewed 25 September 2014] Available from: doi:10.3748/wjg.v20.i33.11630

Differential Diagnoses

Fact Explanation
Alcoholic hepatitis [1] Usually develops over years-long exposure to alcohol.usually with elevation of aspartate transaminase (AST) in a 2:1 ratio to alanine transaminase (ALT). liver biopsy - injury is characteristically most prominent in centrilobular (perivenular) areas [1]
Auto immune hepatitis [2] Affects women much more often than men. Other autoimmune diseases may be present. The characteristic histological feature of autoimmune hepatitis (AIH) is interface hepatitis with predominant portal lymphoplasmacytic necroinflammatory infiltration. Centrilobular necrosis (CN) [2]
Hemochromatosis [3] Iron disorder where the body simply loads too much iron. This action is genetic and the excess iron.Serum ferritin will be high. Family history may be positive. A Prussian blue iron stain demonstrates the blue granules of hemosiderin in hepatocytes and Kupffer cells [3]
Wilson's disease [4] Wilson’s disease is an inherited disorder in which defective biliary excretion of copper leads to its accumulation, particularly in liver and brain.Family history may be positive. Typically, the combination of Kayser–Fleischer rings and a low serum ceruloplasmin (<0.1 g/L) level is sufficient to establish a diagnosis. liver biopsy - In the earlier stages of the disease, the biopsy typically shows steatosis (deposition of fatty material), increased glycogen in the nucleus, and areas of necrosis (cell death). In more advanced disease, the changes observed are quite similar to those seen in autoimmune hepatitis, such as infiltration by inflammatory cells, piecemeal necrosis and fibrosis (scar tissue). In advanced disease, finally, cirrhosis is the main finding [4]
References
  1. CHAYANUPATKUL M, LIANGPUNSAKUL S. Alcoholic hepatitis: A comprehensive review of pathogenesis and treatment World J Gastroenterol [online] 2014 May 28, 20(20):6279-6286 [viewed 22 July 2014] Available from: doi:10.3748/wjg.v20.i20.6279
  2. HOFER H, OESTERREICHER C, WRBA F, FERENCI P, PENNER E. Centrilobular necrosis in autoimmune hepatitis: a histological feature associated with acute clinical presentation J Clin Pathol [online] 2006 Mar, 59(3):246-249 [viewed 22 July 2014] Available from: doi:10.1136/jcp.2005.029348
  3. BACON BR, ADAMS PC, KOWDLEY KV, POWELL LW, TAVILL AS. Diagnosis and Management of Hemochromatosis: 2011 Practice Guideline by the American Association for the Study of Liver Diseases Hepatology [online] 2011 Jul, 54(1):328-343 [viewed 22 July 2014] Available from: doi:10.1002/hep.24330
  4. EUROPEAN ASSOCIATION FOR STUDY OF LIVER. EASL Clinical Practice Guidelines: Wilson's disease. J Hepatol [online] 2012 Mar, 56(3):671-85 [viewed 22 July 2014] Available from: doi:10.1016/j.jhep.2011.11.007

Investigations - for Diagnosis

Fact Explanation
Chronic hepatitis B (HBV) - HBsAg [1] HBsAg positive for longer than six months [1]
Chronic hepatitis B (HBV) - Serum HBV DNA [1] Serum HBV DNA >100,000 copies per mL [1]
Chronic hepatitis B (HBV) - Alanine transaminase and aspartate transaminase levels [1] Persistent or intermittent elevation of alanine transaminase and aspartate transaminase levels [1]
Liver biopsy [1] Liver biopsy showing chronic hepatitis (necroinflammatory score ≥4) [1] In chronic hepatitis B, there is a varying degree of predominantly lymphocytic portal inflammation with interface hepatitis. and spotty lobular inflammation.Bridging necrosis is identified as inflammation “connecting” portal tracts to one another or to central veins [1] In patients with hepatitis C, liver biopsy provides information about fibrosis and histology.Fibrosis usually begins in the portal area in HCV [3]
Chronic hepatitis C (HCV) - HCV antibody detection by enzyme immunoassay, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR)[2] The most widely used initial assay for detecting HCV antibodies is the enzyme immunoassay. A positive enzyme immunoassay should be followed by a confirmatory test. When used in low-risk groups, an enzyme immunoassay may yield false-positive results.Recombinant immunoblot assay, a confirmatory test for a positive enzyme immunoassay, detects antibodies to individual HCV antigens and has a greater specificity [2]
Chronic hepatitis C (HCV) - viral load testing- polymerase chain reaction (PCR) assays for HCV RNA [2] Recombinant immunoblot assay used in conjunction with viral load tests to distinguish between a resolved infection and a false-positive enzyme immunoassay [2]
Chronic hepatitis C (HCV) - Alanine transaminase [4] One of the hallmarks of chronic hepatitis C is a fluctuating ALT pattern, and some patients may have prolonged periods (12 months or more) of normal ALT activity [4]
References
  1. LIN KW, KIRCHNER JT. Hepatitis B. Am Fam Physician [online] 2004 Jan 1, 69(1):75-82 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/14727820
  2. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  3. GEBO KA, BASS EB. Liver biopsy and screening for cancer in hepatitis C. Am Fam Physician [online] 2003 Nov 1, 68(9):1719, 1723, 1726, 1728 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/14620594
  4. MOYER LA, MAST EE, ALTER MJ. Hepatitis C: Part I. Routine serologic testing and diagnosis. Am Fam Physician [online] 1999 Jan 1, 59(1):79-88, 91-2 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/9917576

Investigations - Fitness for Management

Fact Explanation
Liver function tests - Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase, albumin, prothrombin time [1] Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase will be elevated in liver diseases due to liver cell destruction.Albumin will be decreased in liver diseases due to reduced production.Prothrombin time will be increased due to reduced platelet production from the liver in liver diseases [1]
Full blood count [1] Patients with liver failure has reduced platelet levels due to decreased platelet production from the liver in liver diseases [1] Variceal bleeding which is a complication of portal hypertension can give rise to low hemoglobin levels [1]
Serum creatinine [2] Important to assess as, anti viral drugs which are given for the treatment can cause nephrotoxicity [2]
References
  1. STARR SP, RAINES D. Cirrhosis: diagnosis, management, and prevention. Am Fam Physician [online] 2011 Dec 15, 84(12):1353-9 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22230269
  2. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772

Investigations - Followup

Fact Explanation
α-fetoprotein levels [1] α-fetoprotein levels will be increased in hepatocellular carcinoma ( HCC ). HCC surveillance in patients with chronic HBV infection is often performed every six to 12 months using α-fetoprotein levels and abdominal ultrasonography.A systematic review found that the sensitivity was 60 percent (95% CI 44-76%) and specificity was 97 percent (95% CI 95-98%) [1] The relative risk of HCC in HBsAg-positive persons compared to HBsAg-negative controls was 18.8 for men and 33.2 for women. [2] Risk Factors for Developing HCC with Chronic HBV Infection- Alcohol abuse Asian or African race Cirrhosis Coinfection with hepatitis C and D virus Exposure to aflatoxin Family history of HCC HBV DNA viral load >10,000 IU per mL HBV genotype C Longer duration of infection Male sex Older age Presence of hepatitis B e antigen Smoking [1] The average annual risk of HCC in patients with cirrhosis from HCV is 3.2% [3]
Ultrasound (US) abdomen [3] To detect HCC - On US, HCC often appears as a small hypo-echoic lesion with poorly defined margins and coarse irregular internal echoes. When the tumor grows, it can sometimes appear heterogeneous with fibrosis, fatty change, and calcifications.ultrasonography was less effective for detecting early hepatocellular carcinoma, with a sensitivity of only 63 percent [3] To detect cirrhosis - surface nodularity, overall coarse and heterogeneous echotexture, fatty change (variable) segmental hypertrophy / atrophy, signs of portal hypertension- doppler flow changes enlarged portal vein [4]
Computed tomography (CT) [1] To detection of hepatocellular carcinoma- On CT, HCC can have three distinct patterns of growth: A single large tumor Multiple tumors Poorly defined tumor with an infiltrative growth pattern [1]
Liver function tests - Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase, albumin, prothrombin time [4] Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase will be elevated in liver diseases due to liver cell destruction.Albumin will be decreased in liver diseases due to reduced production.Prothrombin time will be increased due to reduced platelet production from the liver in liver diseases [4]
Serum cretinine levels [1] Important to assess as, anti viral drugs which are given for the treatment can cause nephrotoxicity [1]
HBV viral load (PCR) [5] high HBV viral load has an adverse effect on overall survival, and it is associated with the rapid progression of HCC after initial treatment [5]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. DI BISCEGLIE AM. Hepatitis B And Hepatocellular Carcinoma Hepatology [online] 2009 May, 49(5 Suppl):S56-S60 [viewed 22 July 2014] Available from: doi:10.1002/hep.22962
  3. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  4. STARR SP, RAINES D. Cirrhosis: diagnosis, management, and prevention. Am Fam Physician [online] 2011 Dec 15, 84(12):1353-9 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22230269
  5. YU SJ, KIM YJ. Hepatitis B viral load affects prognosis of hepatocellular carcinoma. World J Gastroenterol [online] 2014 Sep 14, 20(34):12039-12044 [viewed 25 September 2014] Available from: doi:10.3748/wjg.v20.i34.12039

Investigations - Screening/Staging

Fact Explanation
α-fetoprotein levels [1] α-fetoprotein levels will be increased in hepatocellular carcinoma ( HCC ).HCC surveillance in patients with chronic HBV infection is often performed every six to 12 months using α-fetoprotein levels and abdominal ultrasonography.A systematic review found that the sensitivity was 60 percent (95% CI 44-76%) and specificity was 97 percent (95% CI 95-98%) [1] Cirrhosis proved to be the primary risk factor for HCC. At the time of presentation, liver cirrhosis (LC) was present in 10% associated viral B hepatitis (HBV) and 6% viral C hepatitis (HCV), with no signs of LC . Thus a similar percentage may have HCC [2]
Ultrasound (US) abdomen [3] To detect HCC - On US, HCC often appears as a small hypo-echoic lesion with poorly defined margins and coarse irregular internal echoes. When the tumor grows, it can sometimes appear heterogeneous with fibrosis, fatty change, and calcifications.ultrasonography was less effective for detecting early hepatocellular carcinoma, with a sensitivity of only 63 percent [3] To detect cirrhosis - surface nodularity, overall coarse and heterogeneous echotexture, fatty change (variable) segmental hypertrophy / atrophy, signs of portal hypertension- doppler flow changes enlarged portal vein [4]
Computed tomography (CT) [1] To detection of hepatocellular carcinoma- On CT, HCC can have three distinct patterns of growth: A single large tumor Multiple tumors Poorly defined tumor with an infiltrative growth pattern [1]
Liver function tests - Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase, albumin, prothrombin time [4] Alanine transaminase , aspartate aminotransferase, Gamma-glutamyl transpeptidase will be elevated in liver diseases due to liver cell destruction.Albumin will be decreased in liver diseases due to reduced production.Prothrombin time will be increased due to reduced platelet production from the liver in liver diseases [4]
Chronic hepatitis B (HBV) - HBsAg [1] HBsAg positive for longer than six months in chronic HBV infected patients [1]
Chronic hepatitis C (HCV) - HCV antibody detection by enzyme immunoassay, recombinant immunoblot assay, and quantitative HCV RNA polymerase chain reaction (PCR)[3] The most widely used initial assay for detecting HCV antibodies is the enzyme immunoassay. A positive enzyme immunoassay should be followed by a confirmatory test. When used in low-risk groups, an enzyme immunoassay may yield false-positive results.Recombinant immunoblot assay, a confirmatory test for a positive enzyme immunoassay, detects antibodies to individual HCV antigens and has a greater specificity [3]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. CONSTANTIN CV, STREBA CT, ROGOVEANU I, NITA-STEFANESCU L, IONESCU AG. Cirrhosis and Chronic Viral Hepatitis as Risk Factors for Hepatocellular Carcinoma: Romanian Single-clinic Experience Maedica (Buchar) [online] 2010 Dec, 5(4):265-270 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3152834
  3. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  4. STARR SP, RAINES D. Cirrhosis: diagnosis, management, and prevention. Am Fam Physician [online] 2011 Dec 15, 84(12):1353-9 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/22230269

Management - General Measures

Fact Explanation
Pregnancy [1] Every pregnant woman should be tested for HBsAg at her first prenatal visit. The risk of an infant acquiring HBV from an HBsAg- or HBeAg-positive mother is 80 to 90 percent if the infant is not given an intramuscular injection of 0.5 mg of hepatitis B immune globulin within 12 hours of birth, followed by three timed doses of hepatitis B vaccine [1]
Hepatitis B vaccination [1] Health care professionals should receive hepatitis B vaccination. Following the primary course of 3 vaccinations ( Time of first injection and then at one to two, and four to six months) , a blood test may be taken after an interval of 1–4 months to establish if there has been an adequate response, which is defined as an anti-hepatitis B surface antigen (anti-Hbs) antibody level above 100 mIU/ml. Such a full response occurs in about 85–90% of individuals [1]
Hepatitis A vaccine [1] Persons with chronic HBV / HCV infection who are not immune to hepatitis A should receive two doses of hepatitis A vaccine at least six months apart [1]
Regular monitoring [1] Patients in the inactive or immune tolerant phases of chronic HBV infection should be monitored on a regular basis assessing the serum viral load, (every six to 12 months) for reactivation of their infection [1]
Abstain from alcohol [2] Persons with chronic HCV infection should abstain from alcohol consumption as alcohol together with the infection causes more liver damage [2]
Avoidance of hepatotoxic drugs [2] Hepatotoxic drugs should be avoided in persons with chronic HCV / HBV infection and cirrhosis as it causes more liver damage [2]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755

Management - Specific Treatments

Fact Explanation
Chronic HBV treatment - Pegylated interferon alfa-2a [1] Administered subcutaneously in well-compensated patients once weekly for six to 12 months. More than 50 percent of patients with HBeAg-positive genotype A infections will achieve seroconversion.Serum HBV DNA level, HBeAg, and HBeAb should be measured at the end of treatment, and at three and six months after treatment [1]
Chronic HBV treatment - Oral antiviral drugs ( Adefovir , Entecavir , Lamivudine , Telbivudine , Tenofovir ) [1] Five oral nucleotide reverse transcriptase inhibitors are approved for the treatment of HBV infection. If HBV DNA levels do not become undetectable within six to 12 months, a second antiviral agent should be used. The incidence of seroconversion increases in a stepwise fashion with ongoing treatment and with the duration of undetectable HBV DNA levels. [1]
Chronic HCV treatment - Pegylated interferon alfa-2a [2] Peginterferon alfa-2a is a long acting interferon. Interferons are proteins released in the body in response to viral infections. Interferons are important for fighting viruses in the body, for regulating reproduction of cells, and for regulating the immune system [2]
Chronic HCV treatment - Ribavarin [3] Analog used to stop viral RNA synthesis and viral mRNA capping, thus, it is a nucleoside inhibitor [2]
References
  1. WILKINS T, ZIMMERMAN D, SCHADE RR. Hepatitis B: diagnosis and treatment. Am Fam Physician [online] 2010 Apr 15, 81(8):965-72 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20387772
  2. WILKINS T, MALCOLM JK, RAINA D, SCHADE RR. Hepatitis C: diagnosis and treatment. Am Fam Physician [online] 2010 Jun 1, 81(11):1351-7 [viewed 22 July 2014] Available from: http://www.ncbi.nlm.nih.gov/pubmed/20521755
  3. KAYVANJOO AH, EBRAHIMI M, HAQSHENAS G. Prediction of hepatitis C virus interferon/ribavirin therapy outcome based on viral nucleotide attributes using machine learning algorithms. BMC Res Notes [online] 2014 Aug 23, 7(1):565 [viewed 25 September 2014] Available from: doi:10.1186/1756-0500-7-565