Acute hepatitis B virus infection:
Thirty percent of patients with acute hepatitis B develop icteric hepatitis, while roughly seventy percent have subclinical or anicteric hepatitis. Patients with underlying liver disease or other hepatitis viruses may have a more severe case of the disease.
One to six months pass during the incubation phase. During the prodromal stage, a syndrome resembling serum sickness may appear, followed by constitutional symptoms, anorexia, nausea, jaundice, and discomfort in the right upper quadrant. In most cases, the symptoms and jaundice go away after one to three months. A rare condition, cute liver failure affects 0.1 to 0.5 percent of patients.
Acute hepatitis with HBsAg positivity can also be diagnosed as:
(1) Acute hepatitis B
(2) Chronic hepatitis B exacerbations, such as acute hepatitis brought on by drugs and other toxins in a chronic hepatitis B infected person, reactivation of chronic hepatitis B, or superinfection of a chronic hepatitis B infection with hepatitis C, A, E, or D virus.
Alanine and aspartate aminotransferase levels (ALT and AST) are elevated during the acute phase of acute hepatitis B; values up to 1,000 to 2,000 IU/L are typically seen during this phase, with ALT being higher than AST. The serum levels of lactic dehydrogenase and alkaline phosphatase are typically only slightly elevated (less than threefold). Both the direct and indirect fractions of the bilirubin are variablely elevated. Patients with an-icteric hepatitis may have normal serum bilirubin levels. Except in cases of chronic, severe disease, serum albumin rarely decreases. The best prognosis predictor is the prothrombin time.
Normalisation of serum aminotransferases takes one to four months to happen in patients who make a full recovery. Persistent elevation of serum ALT for more than six months may indicate progression to chronic hepatitis.
- Precore mutants have mutations in the precore region, which abolishes HBeAg production, or in the core promoter region, which downregulates HBeAg production. Despite possibly producing anti-HBe and anti-HBc antibodies, these patients do not produce HBeAg.
- The second group of so-called escape mutants (due to mutations in a determinant of S gene preventing them from being neutralised by the anti-HBs) is seen in some infants born to HBeAg positive mothers and in liver transplant patients who have received combined immunisation with anti-HBV immunoglobulin and vaccine. This has no effect on viral replication; in fact, such cases are more difficult to treat and have a higher risk of turning into cirrhosis.
- HBeAg and HBsAg may both be suppressed by co-infection with HCV.
- HBcAb is occasionally the only serological marker that can be found. This could be either because of Co-infection with HCV or HIV, Remote infection, "Window" period between HBsAg and HBsAb, False positive test result - HBcAb is marker most prone to false positives or Resolved HBV with diminishing anti-HBs levels.
- Regardless of ALT levels, HBeAg status, or HBV DNA levels, treatment for all adults, adolescents, and kids with CHB and signs of compensated or decompensated cirrhosis should be prioritised.
- Regardless of HBeAg status, treatment is advised for adults with CHB who do not have cirrhosis but are older than 30 (in particular), have persistently abnormal ALT levels, and show evidence of high-level HBV replication (HBV DNA >20 000 IU/mL).
- In people without signs of cirrhosis, with persistently normal ALT levels, and with low levels of HBV replication (HBV DNA 2000 IU/mL), regardless of HBeAg status or age, antiviral therapy is not advised and can be postponed.
- In the absence of HBV DNA testing, treatment can be postponed in HBeAg-positive people 30 years of age or younger with persistently normal ALT levels.
- All CHB patients need to be monitored regularly, but it's especially important for those who don't currently fit the guidelines for whether or not to receive treatment, to find out if antiviral therapy will ever be necessary to stop the progression of liver disease. These people include those under 30 years old without cirrhosis who have HBV DNA levels greater than 20,000 IU/mL but persistently normal ALT.
- The NAs with a high barrier to drug resistance (tenofovir or entecavir) are advised for all adults, adolescents, and children aged 12 years or older for whom antiviral therapy is indicated.
- Tenofovir may be preferred as the medication of choice in women of childbearing age in the event of pregnancy. Pregnancy is not advised when using entecavir.
- Patients with a risk of developing Entecavir resistance who have taken lamivudine are advised to use tenofovir instead.
- Children between the ages of 2 and 11 should not take entecavir.
- Entecavir may be preferred over Tenofovir in Age > 60, history of fragility fractures or osteoporosis; use of other drugs that worsen bone density, altered renal function (eGFR 60 mL/min/1.73 m2, albuminuria > 30 mg/24 hr, moderate dipstick proteinuria, Low phosphate (2.5 mg/dL) or in patients receiving hemodialysis.
- Drugs with a low barrier to resistance (lamivudine, adefovir, or telbivudine) are available but not advised as they promote drug resistance. Tenofovir alafenamide fumarate (TAF) is the drug of choice in patients with reduced renal function or bone disease bone toxicities, where entecavir is contraindicated.
- HBV DNA levels (where HBV DNA testing is available), HBsAg, HBeAg, and ALT levels (and AST for APRI)
- Non-invasive tests (APRI score, FIB-4, or FibroScan) to determine whether fibrosis has gotten worse or whether cirrhosis has developed in people who didn't have it at the start.
- If receiving treatment, adherence needs to be checked frequently and at each appointment.