Hepatitis E laboratory tests
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [2] João André Alves Silva, M.D. [3]
Overview
Laboratory Findings
Every patient with acute or chronic hepatitis, which cannot be explained by other causes, should be tested for hepatitis E.[1] Unfortunately, the different available assays show different specificity and sensitivity, and are only available at certain centers.[2]
Throughout the course of infection, serologic markers will vary according to the stage of the disease:[2]
- Incubation period
- Symptom onset
- IgM and IgG antibody detection
- Elevations on serum aminotransferase and symptom onset
- HEV detected in stool
- Recovery
The detection of increased levels of anti-HEV IgG may therefore indicate recent HEV infection.[1] Several assays are based on the HEV genotype, therefore, even though the specificity may be high, sensitivity of different tests for the remaining genotypes may be lower.[1]
Immunocompromised patients may have a delayed immune response to HEV, and hence delayed seroconversion. Therefore, these patients should be tested for HEV RNA.[3] The RNA of the virus may be detected in blood and stool for several weeks, and quantified in order to evaluate response to treatment[1][4]
The table below displays nonspecific laboratory abnormalities associated with Hepatitis E, including:[5][6][7][8][9]
| Test | Findings |
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| Complete Blood Count |
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| Electrolytes |
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| Inflammatory Markers |
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| Blood cultures |
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| Urinalysis |
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The following tests are done to identify and monitor liver damage from hepatitis B:
- Albumin level
- Liver function tests
- Prothrombin time
- Antibody test
Since cases of hepatitis E are not clinically distinguishable from other types of acute viral hepatitis, diagnosis is made by blood tests which detect elevated antibody levels of specific antibodies to hepatitis E in the body or by reverse transcriptase polymerase chain reaction (RT-PCR). Unfortunately, such tests are not widely available.
Hepatitis E should be suspected in outbreaks of waterborne hepatitis occurring in developing countries, especially if the disease is more severe in pregnant women, or if hepatitis A has been excluded. If laboratory tests are not available, epidemiologic evidence can help in establishing a diagnosis.
References
- ↑ 1.0 1.1 1.2 1.3 Wedemeyer H, Pischke S, Manns MP (2012). "Pathogenesis and treatment of hepatitis e virus infection". Gastroenterology. 142 (6): 1388–1397.e1. doi:10.1053/j.gastro.2012.02.014. PMID 22537448.
- ↑ 2.0 2.1 Hoofnagle JH, Nelson KE, Purcell RH (2012). "Hepatitis E." N Engl J Med. 367 (13): 1237–44. doi:10.1056/NEJMra1204512. PMID 23013075.
- ↑ Pischke S, Suneetha PV, Baechlein C, Barg-Hock H, Heim A, Kamar N; et al. (2010). "Hepatitis E virus infection as a cause of graft hepatitis in liver transplant recipients". Liver Transpl. 16 (1): 74–82. doi:10.1002/lt.21958. PMID 19866448.
- ↑ Baylis SA, Hanschmann KM, Blümel J, Nübling CM, HEV Collaborative Study Group (2011). "Standardization of hepatitis E virus (HEV) nucleic acid amplification technique-based assays: an initial study to evaluate a panel of HEV strains and investigate laboratory performance". J Clin Microbiol. 49 (4): 1234–9. doi:10.1128/JCM.02578-10. PMC 3122834. PMID 21307208.
- ↑ "Diarrhoea and Vomiting Caused by Gastroenteritis".
- ↑ Agarwal R, Afzalpurkar R, Fordtran JS (1994). "Pathophysiology of potassium absorption and secretion by the human intestine". Gastroenterology. 107 (2): 548–71. PMID 8039632.
- ↑ Wang F, Butler T, Rabbani GH, Jones PK (1986). "The acidosis of cholera. Contributions of hyperproteinemia, lactic acidemia, and hyperphosphatemia to an increased serum anion gap". N Engl J Med. 315 (25): 1591–5. doi:10.1056/NEJM198612183152506. PMID 3785323.
- ↑ Welbourne T, Weber M, Bank N (1972). "The effect of glutamine administration on urinary ammonium excretion in normal subjects and patients with renal disease". J Clin Invest. 51 (7): 1852–60. doi:10.1172/JCI106987. PMC 292333. PMID 4555786.
- ↑ Batlle DC, von Riotte A, Schlueter W (1987). "Urinary sodium in the evaluation of hyperchloremic metabolic acidosis". N Engl J Med. 316 (3): 140–4. doi:10.1056/NEJM198701153160305. PMID 3796685.