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Several diseases can present with signs, symptoms, and/or [[Liver_function_tests|liver function test]] abnormalities similar to hepatitis. In severe cases of [[alpha 1-antitrypsin deficiency]] (A1AD), excess [[protein]] in liver cells causes and inflammation and cirrhosis.<ref>{{cite journal|last=Stoller|first=James K|coauthors=Aboussouan, Loutfi S|title=α1-antitrypsin deficiency|journal=The Lancet|year=2005|month=June|volume=365|issue=9478|pages=2225–2236|doi=10.1016/S0140-6736(05)66781-5|accessdate=27 November 2013}}</ref> Some [[Inborn_error_of_metabolism|metabolic disorders]] cause damage to the liver through a variety of mechanisms. In [[hemochromatosis]] and [[Wilson's disease]] toxic accumulation of [[Dietary_mineral|dietary minerals]] results in inflammation and cirrhosis.<ref>{{cite journal|last=Hansen|first=Keli|coauthors=Horslen, Simon|title=Metabolic liver disease in children|journal=Liver Transplantation|year=2008|month=May|volume=14|issue=5|pages=713–733|doi=10.1002/lt.21520}}</ref> |
Several diseases can present with signs, symptoms, and/or [[Liver_function_tests|liver function test]] abnormalities similar to hepatitis. In severe cases of [[alpha 1-antitrypsin deficiency]] (A1AD), excess [[protein]] in liver cells causes and inflammation and cirrhosis.<ref>{{cite journal|last=Stoller|first=James K|coauthors=Aboussouan, Loutfi S|title=α1-antitrypsin deficiency|journal=The Lancet|year=2005|month=June|volume=365|issue=9478|pages=2225–2236|doi=10.1016/S0140-6736(05)66781-5|accessdate=27 November 2013}}</ref> Some [[Inborn_error_of_metabolism|metabolic disorders]] cause damage to the liver through a variety of mechanisms. In [[hemochromatosis]] and [[Wilson's disease]] toxic accumulation of [[Dietary_mineral|dietary minerals]] results in inflammation and cirrhosis.<ref>{{cite journal|last=Hansen|first=Keli|coauthors=Horslen, Simon|title=Metabolic liver disease in children|journal=Liver Transplantation|year=2008|month=May|volume=14|issue=5|pages=713–733|doi=10.1002/lt.21520}}</ref> |
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== Prevention == |
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=== Vaccines === |
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[[Vaccine|Vaccines]] are available to prevent hepatitis A and B. [[Hepatitis A]] [[immunity]] is achieved in 99-100% of persons receiving the two-dose [[inactivated virus vaccine]]. The hepatitis A vaccine is not approved for children under one year of age.<ref>INSERT REFERENCE http://who.int/immunization/wer7505Hepatitis%20A_Feb00_position_paper.pdf</ref> Vaccines to prevent [[hepatitis B]] have been available since 1986 and have been incorporated into at least 177 [[national infantile immunization programs]]. Immunity is achieved in greater than 95% of infants, children and young adults receiving the three-dose [[recombinant virus vaccine]]. Vaccination of infants within 24 hours of birth can prevent transmission from an infected mother. Adults over 40 years of age have decreased immune response to the vaccine. The [[World Health Organization]] recommends vaccination of all children, particularly newborns in countries with high endemicity to prevent [[vertical transmission]].<ref>INSERT REFERENCE http://who.int/wer/2009/wer8440.pdf</ref> |
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==Screening== |
==Screening== |
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Revision as of 13:49, 8 December 2013
Diagnosis
Diagnosis is made by assessing an individual's symptoms, physical exam, and medical history, in conjunction with blood tests, liver biopsy, and imaging. Blood testing includes blood chemistry, liver enzymes, and serology. Abnormalities in blood chemistry and enzyme results are may be indicative of certain etiologies or stages of hepatitis.[1][2] Imaging can identify steatosis of the liver but liver biopsy is required to demonstrate fibrosis and cirrhosis.[3] A biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis. Furthermore, there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.[4]
| Liver chemistry test | Clinical implication of abnormality |
|---|---|
| Alanine transaminase (ALT) | Hepatocellular damage |
| Aspartate transaminase (AST) | Hepatocellular damage |
| Bilirubin | Cholestasis |
| Alkaline phosphatase | Cholestasis |
| Prothrombin time | Impaired synthetic function |
| Albumin | Impaired synthetic function |
| Gamma-glutamyl transpeptidase (GGT) | Cholestasis |
| Bile acids | Cholestasis |
| Lactate dehydrogenase | Hepatocellular damage |
Viral hepatitis
Serologic testing may be used to evaluate for viral hepatitis.
| Marker | Detection Time | Description | Significance |
|---|---|---|---|
| Faecal HAV | 2–4 weeks or 28days | - | Early detection |
| IgM anti HAV | 4–12 weeks | Enzyme immunoassay for antibodies | During Acute Illness |
| IgG anti HAV | 5 weeks - persistent | Enzyme immunoassay for antibodies | Old infection or Reinfection |
| Marker | Detection Time | Description |
|---|---|---|
| Hepatitis B surface antigen (HBsAg) | Present in acute and chronic disease | Surface protein of Hepatitis B virus, presence indicates individual is infectious |
| Hepatitis B e antigen (HBeAg) | Early infection | Indicates individual is highly infectious |
| Hepatitis B surface antibody (anti-HBs) | timeframe | Indicates recovery or immunity from Hepatitis B |
| Hepatitis B core antibody (anti-HBc) | timeframe | Indicates previous or ongoing Hepatitis B infection |
| IgM antibody to Hepatitis B core antigen (IgM anti-HBc) | timeframe | Indicates recent Hepatitis B infection |
INSERT HEP BE SEROLOGY INTERPRETATION TABLE
| Marker | Detection Time | Description | Significance | Note |
|---|---|---|---|---|
| HCV-RNA | 1–3 weeks or 21 days | PCR | Demonstrates presence or absence of virus | Results may be intermittent during course of infection. Negative result is not indicative of absence. |
| anti-HCV | 5–6 weeks | Enzyme Immunoassay for antibodies | Demonstrates past or present infection | High false positive in those with autoimmune disorders and populations with low virus prevalence. |
| ALT | 5–6 weeks | - | Peak in ALT coincides with peak in anti-HCV | Fluctuating ALT levels is an indication of active liver disease. |
Differential diagnosis
Several diseases can present with signs, symptoms, and/or liver function test abnormalities similar to hepatitis. In severe cases of alpha 1-antitrypsin deficiency (A1AD), excess protein in liver cells causes and inflammation and cirrhosis.[9] Some metabolic disorders cause damage to the liver through a variety of mechanisms. In hemochromatosis and Wilson's disease toxic accumulation of dietary minerals results in inflammation and cirrhosis.[10]
Prevention
Vaccines
Vaccines are available to prevent hepatitis A and B. Hepatitis A immunity is achieved in 99-100% of persons receiving the two-dose inactivated virus vaccine. The hepatitis A vaccine is not approved for children under one year of age.[11] Vaccines to prevent hepatitis B have been available since 1986 and have been incorporated into at least 177 national infantile immunization programs. Immunity is achieved in greater than 95% of infants, children and young adults receiving the three-dose recombinant virus vaccine. Vaccination of infants within 24 hours of birth can prevent transmission from an infected mother. Adults over 40 years of age have decreased immune response to the vaccine. The World Health Organization recommends vaccination of all children, particularly newborns in countries with high endemicity to prevent vertical transmission.[12]
Screening
A recently completed high-quality study evaluating the utility of these tests found that [13]
- ^ Green, RM (2002 Oct). "AGA technical review on the evaluation of liver chemistry tests". Gastroenterology. 123 (4): 1367–84. PMID 12360498.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Pratt, DS (2000 Apr 27). "Evaluation of abnormal liver-enzyme results in asymptomatic patients". The New England journal of medicine. 342 (17): 1266–71. PMID 10781624.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Masuoka, Howard C. (2013). "Nonalcoholic fatty liver disease: an emerging threat to obese and diabetic individuals". Annals of the New York Academy of Sciences. 1281 (1): 106–122. doi:10.1111/nyas.12016.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ Grant, A (1999). "Guidelines on the use of liver biopsy in clinical practice". Gut. 45 (Suppl 4): 1–11. doi:10.1136/gut.45.2008.iv1. PMC 1766696. PMID 10485854.
The main cause of mortality after percutaneous liver biopsy is intraperitoneal haemorrhage as shown in a retrospective Italian study of 68 000 percutaneous liver biopsies in which all six patients who died did so from intraperitoneal haemorrhage. Three of these patients had had a laparotomy, and all had either cirrhosis or malignant disease, both of which are risk factors for bleeding.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ "Acute Viral Hepatitis : Introduction Harrison's Principle of Internal Medicine, 17 Edition".
- ^ A Comprehensive Immunization Strategy to Eliminate Transmission of Hepatitis B Virus Infection in the United States: Recommendations of the Advisory Committee on Immunization Practices. Part I: Immunization of Infants, Children, and Adolescents. MMWR 2005;54(No. RR-16).
- ^ WHO Document http://who.int/wer/2009/wer8440.pdf
- ^ "WHO | Hepatitis C". Who.int. 2010-12-08. Retrieved 2012-08-26.
- ^ Stoller, James K (2005). "α1-antitrypsin deficiency". The Lancet. 365 (9478): 2225–2236. doi:10.1016/S0140-6736(05)66781-5.
{{cite journal}}:|access-date=requires|url=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ Hansen, Keli (2008). "Metabolic liver disease in children". Liver Transplantation. 14 (5): 713–733. doi:10.1002/lt.21520.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help) - ^ INSERT REFERENCE http://who.int/immunization/wer7505Hepatitis%20A_Feb00_position_paper.pdf
- ^ INSERT REFERENCE http://who.int/wer/2009/wer8440.pdf
- ^ Lilford, RJ (2013 Jul). "Birmingham and Lambeth Liver Evaluation Testing Strategies (BALLETS): a prospective cohort study". Health technology assessment (Winchester, England). 17 (28): i–xiv, 1–307. PMID 23834998.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help)