01OverviewDefinition, clinical context and the essential points that orientate the chapter.
HAV and HEV are RNA viruses that usually produce an acute hepatitic syndrome with malaise, anorexia, nausea, fever, right-upper-quadrant discomfort, dark urine, pale stools, pruritus and jaundice. Children with HAV may have few symptoms, whereas symptomatic and severe disease is more likely with increasing age or pre-existing liver disease. Incubation means exposure can be remote and patients may be infectious before jaundice. HAV is transmitted through contaminated food or water and close contact; outbreaks also occur within sexual networks and other settings where faeco-oral exposure is facilitated.
HEV is not merely travel-related. Genotypes circulating in the UK are zoonotic, with undercooked pork, pork products, wild boar and venison relevant exposures; transfusion or transplantation transmission is rare but important. In immunocompetent people infection is usually self-limited. In solid-organ recipients and some other immunosuppressed people, HEV RNA can persist and cause chronic hepatitis, fibrosis and cirrhosis. Pregnancy-associated severe HEV is particularly described with genotypes prevalent in endemic regions, so a pregnant patient with compatible acute hepatitis deserves urgent specialist assessment regardless of where she lives.
Diagnosis must reflect timing. HAV IgM supports recent infection in a compatible syndrome, while total or IgG HAV antibody indicates immunity or prior exposure. HEV IgM can support recent infection but false-positive and false-negative results occur; HEV RNA confirms viraemia and is crucial when immunosuppression blunts antibody responses or persistence is suspected. Management is supportive unless acute liver failure develops. Public-health teams advise hygiene, exclusion from high-risk work, outbreak control, vaccination or human normal immunoglobulin for selected HAV contacts. Persistent HEV is managed by the transplant or hepatology service, often beginning with carefully judged reduction of immunosuppression and considering specialist antiviral therapy.
Key points
- Hepatitis A spreads mainly by the faeco-oral route and does not become chronic, although cholestatic or relapsing illness can prolong recovery.
- Hepatitis E in the UK is often zoonotic and linked to undercooked pork or game; absence of foreign travel does not exclude it.
- Test for HAV IgM in compatible acute illness and request HEV serology with RNA testing according to timing and immune status.
- An isolated positive total HAV antibody usually indicates past infection or vaccination and does not diagnose current acute hepatitis.
- Most immunocompetent patients receive supportive care, avoidance of alcohol and careful review of prescribed and non-prescribed hepatotoxic exposure.
- HEV can persist after solid-organ transplantation or other immunosuppression; chronicity requires viral RNA follow-up and specialist management.
- Acute infectious hepatitis is notifiable in the UK jurisdictional framework; contact the local health-protection team for case and contact measures.
- HAV vaccination and post-exposure prophylaxis follow current Green Book and UKHSA risk assessment; there is no routinely available UK HEV vaccine.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Faeco-oral hepatitis A
HAV spreads through contaminated food, water or close contact, with travel, household and outbreak exposure informing public-health action.
Zoonotic hepatitis E
UK HEV infection is often acquired from undercooked pork or game and should not be excluded solely because there was no foreign travel.
Immune-status susceptibility
Pregnancy, pre-existing liver disease and immunosuppression modify severity, while persistent HEV infection is chiefly a concern in immunocompromised patients.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Enteric acquisition and viraemia
Virus enters through the gastrointestinal tract, replicates and reaches hepatocytes via the bloodstream before jaundice becomes apparent.
- 2Immune-mediated hepatocyte injury
The host response clears infected cells but causes hepatocellular inflammation, aminotransferase release and impaired bilirubin handling.
- 3Resolution or severe failure
Most immunocompetent infection resolves, but extensive injury can cause cholestasis or acute synthetic and neurological failure.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Fatigue, anorexia, nausea, myalgia or fever may precede dark urine and jaundice. Ask about household illness, food, water, sex, travel and occupational exposures.
Prominent pruritus, pale stools and prolonged jaundice can occur even when the initial systemic illness is improving; exclude obstruction and monitor synthetic function.
Encephalopathy with coagulopathy in a person without established cirrhosis is a transplant emergency, even before bilirubin becomes extreme or a viral result returns.
Unexplained transaminitis in a transplant recipient or other immunosuppressed patient warrants HEV RNA testing because antibody testing alone can miss active infection.
Acute jaundice after travel or relevant exposure during pregnancy requires immediate obstetric and liver assessment because severe HEV-associated liver failure is possible.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Liver profile and coagulationFirst step - Why
- Confirm hepatocellular injury, assess cholestasis and detect failing synthetic function.
- Interpretation and limitations
- ALT can be very high in acute viral hepatitis but does not measure liver function. Rising INR, hypoglycaemia or encephalopathy signals severity even if aminotransferases begin to fall.
- 02
HAV IgM and total antibody - Why
- Distinguish recent hepatitis A from prior infection or vaccine-derived immunity.
- Interpretation and limitations
- HAV IgM in a compatible illness supports acute infection. Total antibody without IgM generally reflects past exposure or vaccination; interpret unexpected IgM with clinical and laboratory advice.
- 03
HEV IgM, IgG and HEV RNA - Why
- Diagnose recent HEV and identify ongoing viraemia or chronic infection.
- Interpretation and limitations
- Use local reference-laboratory algorithms. RNA is particularly important early, in immunosuppression and when persistence is suspected; serial RNA rather than ALT alone determines virological clearance.
- 04
Broader acute hepatitis screen - Why
- Find coexisting or alternative viral, drug-induced, autoimmune, vascular or biliary causes.
- Interpretation and limitations
- Select HBV, HCV, EBV, CMV, autoimmune tests, paracetamol concentration and pregnancy-related studies by presentation. One positive viral antibody should not end causal assessment automatically.
- 05
Abdominal ultrasound - Why
- Exclude biliary obstruction and assess liver, portal vessels and gallbladder when jaundice is substantial or atypical.
- Interpretation and limitations
- Gallbladder-wall thickening can accompany acute hepatitis and need not indicate cholecystitis. Dilated ducts or vascular abnormality redirects urgent management.
- 06
Glucose, renal function and serial clinical observations - Why
- Detect systemic complications and evolving acute liver failure.
- Interpretation and limitations
- Hypoglycaemia, AKI, acidosis, worsening INR or cognitive change requires higher-acuity monitoring and early transplant-centre discussion, not reassurance from falling ALT.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute hepatitis B or C
Blood, sexual or injecting exposure and virus-specific serology or RNA distinguish parenteral hepatitis from enterically acquired HAV or HEV.
Drug-induced liver injury
A compatible medicine, supplement or toxin timeline with exclusion of viral disease supports DILI; clinical patterns may otherwise be indistinguishable.
Acute biliary obstruction
Colicky pain, duct dilatation and a cholestatic trajectory suggest obstruction, though viral hepatitis can also produce jaundice and pruritus.
Additional chapter-specific clues
Paracetamol exposure, autoimmune markers, biliary pain, shock, pregnancy-specific liver disease or another viral risk may identify a different or additional cause of hepatitis.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01DiagnoseInvestigate acute jaundiceFirst stepA patient has a hepatitic liver profile, dark urine, jaundice or a compatible exposure history.+
- 1Assess physiological stability, cognition, glucose, INR and medication or toxin exposure before awaiting pathogen tests, and arrange emergency liver-centre discussion if failure features appear.
- 2Request HAV IgM and HEV testing alongside a broader cause-directed acute-hepatitis screen, explicitly telling the laboratory about immunosuppression, pregnancy, onset and relevant food or travel exposures.
- 3Use ultrasound when obstruction or another structural cause is possible, then interpret serology and RNA with timing rather than accepting any isolated antibody result uncritically.
02SupportManage uncomplicated infectionHAV or acute HEV is confirmed and there is no acute liver failure or uncontrolled vomiting.+
- 1Provide hydration and antiemetic support as needed, avoid alcohol and non-essential hepatotoxic medicines, and give clear return advice for confusion, bleeding, poor intake or rapidly worsening jaundice.
- 2Notify the appropriate public-health route and follow health-protection advice on hand hygiene, work or school exclusion, food handling, contacts and possible outbreak investigation.
- 3Repeat clinical assessment, liver tests and INR at an interval matched to severity, comorbidity and trajectory rather than discharging every jaundiced patient without follow-up.
03PreventInterrupt transmission and persistenceA HAV case, exposure or risk indication is identified, or HEV remains detectable in an immunosuppressed person.+
- 1For HAV, let the health-protection team apply current Green Book timing and risk criteria for vaccine and, in selected vulnerable contacts, human normal immunoglobulin.
- 2For HEV prevention, advise thorough cooking of pork, offal, game and processed meat products, especially for immunosuppressed patients, and reinforce general food hygiene.
- 3Refer persistent HEV viraemia to the relevant transplant or hepatology specialist for fibrosis assessment, cautious immunosuppression adjustment and any antiviral decision with reproductive safeguards.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Acute liver failure
Severe injury causes coagulopathy, hypoglycaemia and encephalopathy, with greater concern in pregnancy, older age or pre-existing liver disease depending on virus.
Prolonged cholestatic or relapsing illness
Jaundice and pruritus can persist or recur after apparent improvement, prolonging incapacity despite eventual viral clearance.
Chronic hepatitis E
Immunosuppressed patients may fail to clear HEV, developing persistent inflammation, progressive fibrosis and a need for specialist antiviral and immunosuppression review.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Trend symptoms, hydration, bilirubin, aminotransferases, INR, glucose and renal function according to initial severity and speed of change.
- Escalate immediately for new confusion, falling glucose, rising INR, bleeding, oliguria or inability to maintain oral intake.
- In persistent or immunosuppressed HEV, follow HEV RNA and liver fibrosis through the specialist protocol; aminotransferase normalisation alone does not prove clearance.
- Confirm completion of indicated HAV vaccination or post-exposure measures and document advice issued by the health-protection team.
- Review food and occupational risk, household or sexual contacts and potential outbreak links without attaching blame to infection.
- After recovery, re-evaluate alcohol, medicines and underlying chronic liver disease because residual vulnerability may affect future prognosis.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Travel absence misleads
Autochthonous HEV is well established in the UK, so unexplained acute hepatitis deserves HEV testing even when the patient has not travelled.
ALT is injury
Aminotransferases mark hepatocyte injury, not remaining functional mass; falling values alongside worsening INR and encephalopathy can indicate catastrophic loss rather than recovery.
HAV leaves no chronic infection
Prolonged cholestasis or relapsing symptoms can follow hepatitis A, but persistent viral carriage is not the explanation and chronic hepatitis needs another cause.
Immunosuppression changes tests
An impaired antibody response can make HEV serology falsely reassuring, which is why RNA detection is central in transplant recipients with unexplained liver-test abnormalities.
Prevention is time-sensitive
HAV post-exposure intervention depends on interval, age, immune status and liver disease, so prompt health-protection contact is more reliable than a universal clinic rule.
11Common pitfallsFrequent interpretation and management errors.
- 01
Excluding hepatitis E solely because the patient has never travelled outside the United Kingdom.
- 02
Calling total HAV antibody evidence of acute infection without checking the IgM result and clinical timing.
- 03
Reassuring from a falling ALT despite a rising INR, hypoglycaemia or new cognitive change.
- 04
Relying on negative HEV antibody tests in an immunosuppressed patient without requesting RNA.
- 05
Giving generic contact advice instead of notifying and involving the health-protection team promptly.
- 06
Starting ribavirin for persistent HEV without transplant-hepatology oversight, interaction review and strict pregnancy safeguards.