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Evaluation
The evaluation of patients suspected of hepatitis B begins with a history
and physical examination. Measure HBeAg, anti-HBe, HBV DNA, and ALTs, and
perform a liver ultrasound. HBeAg and anti-HBe are important in determining the
phase of chronic hepatitis B virus infection. HBV DNA serum level is used to
diagnose, establish the phase of the infection, decide to treat, and monitor
treatment. In HBeAg-positive chronic hepatitis B, HBV DNA level is >20,000
IU/mL while it is <20,000 IU/mL in HBeAg-negative chronic hepatitis B. Reflex HBV DNA testing may be considered in
those testing positive on HBsAg as an additional strategy to promote linkage to
care and treatment and to promote diagnosis. ALT and/or
AST levels may be normal or elevated in chronic hepatitis B.
CBC, PT, and serum albumin are also
measured to determine disease severity. Diagnosis of hepatitis D in patients with
chronic hepatitis B may be done using serological assay to detect total
anti-HDV followed by a nucleic acid testing (NAT) to detect HDV RNA and active
(viremic) infection in patients who are positive for anti-HDV.
Serological testing for anti-HDV antibodies may
be considered in patients with positive HBsAg especially in the following:
- Individuals born in HDV-endemic countries, regions and areas
- Individuals with advanced liver disease, receiving HBV treatment and with features suggestive of HDV infection (eg low HBV DNA with high ALT levels)
- Individuals with increased risk of HDV infection (eg hemodialysis recipients, people living with hepatitis C or HIV, people who inject drugs, sex workers, and MSM)
It is also essential to screen high-risk
patients for HCC every 6-12 months using ultrasound and alpha-fetoprotein.
If the patient meets the criteria for chronic hepatitis B, a liver
biopsy may be done to grade the stage of liver disease as chronic hepatitis B
may evolve into cirrhosis and HCC. A liver biopsy is essential in determining
disease activity in cases of inconclusive biochemical and HBV markers. Liver biopsy is indicated in patients with
persistently elevated ALT but persistently low HBV DNA to exclude other causes
of liver disease, and in patients who do not meet the criteria for treatment
but at risk for developing histologically active or advanced liver disease (eg
with normal or mildly elevated ALT levels [<2 times the upper limit of
normal {ULN}], persistently elevated HBV viral load [>6 months], and >40
years of age or a family history of HCC) that would benefit from treatment.
Principles of Therapy
Acute Hepatitis B
The main goal of treatment for acute hepatitis B is to prevent the
risk of acute or subacute hepatic failure. Another relevant goal of treatment
is to improve the quality of life by shortening the disease duration associated
with symptoms as well as the risk of chronicity. Supportive care should be
given as treatment with antivirals is generally not recommended. Consider
hospitalization if there is vomiting, dehydration, or signs of hepatic
decompensation. Consider treatment with nucleoside or nucleotide analogues in patients
with severe acute hepatitis.
Chronic Hepatitis B
Baseline renal function test may be performed
before initiation of antiviral therapy. Annual monitoring of renal function may
be done in patients receiving Tenofovir disoproxil fumarate. Surveillance for
HCC every 6 months using ultrasound and AFP is recommended in individuals with
cirrhosis regardless of age or other risk factors, those with a family history
of HCC, and those >40 years of age with HBV DNA level >20,000 IU/mL and without
family history of HCC or evidence of cirrhosis.
Periodic screening for HCC in high-risk carriers is likewise
essential. HCC may have a long asymptomatic stage lasting for 2 years or longer.
Carriers of hepatitis B virus at high risk for developing HCC include Asian men
>40 years, Asian women >50 years, patients with cirrhosis, coinfected with
hepatitis C virus, with hepatitis B virus genotype C, with hepatitis D virus
infection, persistent HBV DNA of >2000 IU/mL, or those with a family history
of HCC in a first-degree relative. Screening methods are ultrasound with or
without alpha-fetoprotein (AFP) determination every 6 months.
A liver biopsy may be performed to assess the degree of liver
damage, rule out other causes of liver disease, and help predict the prognosis.
It is also recommended for chronic hepatitis B patients who are candidates for
antiviral therapy.
Hepatitis D
The aim of treatment in patients with hepatitis D is to eradicate
or to achieve long-term suppression of both hepatitis D virus and hepatitis B
virus. Supportive care should be given, and hospitalization should be
considered if there is vomiting, dehydration, or signs of hepatic
decompensation. It is essential to screen the patient for other sexually
transmitted diseases (STDs) in cases of sexually acquired hepatitis or if otherwise
appropriate. Consideration of an expert referral is also important. Screening for HCC every 6
months with ultrasound is recommended in patients with chronic HDV and advanced
fibrosis or cirrhosis is also recommended.
Pharmacological therapy
Severe Acute Hepatitis B
Severe acute hepatitis B is characterized by
coagulopathy, persistent jaundice for >4 weeks, or signs of acute hepatic
failure. More than 95% of immunocompetent individuals with symptomatic acute
hepatitis B would recover spontaneously without antiviral therapy. Antiviral
therapy is given only to patients with acute liver failure or with a protracted
severe course (ie total bilirubin >3 mg/dL, international normalized ratio
of >1.5, presence of ascites or encephalopathy).
Entecavir, Tenofovir alafenamide, or Tenofovir disoproxil fumarate
may be used in these patients, while Peginterferon is contraindicated. Observational
data have shown that early nucleos(t)ide analogue treatment can reduce rates of
chronicity if treatment is initiated within 8 weeks of acute hepatitis B. Continue
treatment until HBsAg is cleared, or at least 12 months after anti-HBe
seroconversion without HBsAg loss, or indefinitely if to undergo liver
transplantation.
Chronic Hepatitis B
In patients without clinical evidence of cirrhosis, with
persistently normal ALT, HBV DNA of <2,000 IU/mL, regardless of HBeAg status
or age, treatment is not recommended.
Treatment is recommended in adults and adolescents ≥12 years of age with
chronic hepatitis B including pregnant and nonpregnant women of reproductive
age with:
- Significant fibrosis based on APRI score >0.5 or transient elastography value of >7.0 kPa or evidence of cirrhosis which is based on clinical criteria or an APRI score of >1.0 or a transient elastography value of >12.5 kPa regardless of HBV DNA or ALT levels, or
- HBV DNA >2,000 IU/mL and an ALT level above ULN (30 U/L for males and 19 U/L for females), measured on at least 2 occasions for adolescents in a 6- to 12-month period, or
- Presence of coinfections (eg HIV, hepatitis D, or hepatitis C), family history of liver cancer or cirrhosis, immune suppression (eg long-term steroids, solid organ or stem cell transplant), comorbidities (eg diabetes or metabolic dysfunction-associated steatotic liver disease), extrahepatic manifestations (eg glomerulonephritis, vasculitis) regardless of APRI score or HBV DNA or ALT levels, or
- Persistently abnormal ALT levels which is defined as 2 ALT values above ULN at unspecified intervals during a 6- to 12-month period regardless of APRI score in the absence of access to HBV DNA assay
The primary goal of treatment in chronic hepatitis B treatment is
to permanently suppress hepatitis B virus or to eliminate it. It is necessary
to achieve continued viral suppression to reduce or prevent hepatic disease and
disease progression. The short-term goals are to sustain the suppression of HBV
DNA, ALT normalization, to prevent decompensation, and to decrease hepatic
necroinflammation and fibrosis during and after therapy. The long-term goals of
therapy are to avoid hepatic decompensation, reduce or prevent progression to
cirrhosis and/or HCC, and prolong survival.
Endpoints used to assess response include the following:
- Biochemical response: Normalization of serum ALT
- Virological response: HBV DNA of <104 copies/mL and sustained seroconversion from HBeAg to anti-HBe
- Histological response: Decrease in histology activity compared to pretreatment liver biopsy or a reduction of at least 1 point in fibrosis by Metavir staging
- Complete response: Fulfill criteria of biochemical and virological response and loss of HBsAg
Considerations Prior to Initiation of
Treatment
Prior to initiation of treatment, it is important to consider the
age of the patient, the severity of the liver disease, the likelihood of
response, potential adverse events, and complications. HBeAg-positive patients
with elevated ALT levels and compensated liver disease should be observed for 3
to 6 months for spontaneous seroconversion from HBeAg to anti-HBe prior to
initiation of treatment. The choice of therapy will depend on the availability,
cost of medication, the necessary number of clinic visits, the expected duration
of treatment, and patient or clinician preference.
Other Considerations in Pharmacologic Therapy
There
is no evidence that combination therapy of two direct antiviral agents result
in better viral suppression compared to a single agent. Antiviral therapy does
not remove the risk of HCC, thus HCC surveillance must continue. In treating
concurrent infections such as hepatitis C virus, hepatitis D virus, and HIV
infection, it is important to identify the dominant virus as this will
determine the therapeutic regimen. Concurrent hepatitis C infection may be
treated with the same antiviral therapy for hepatitis C virus monoinfection.
Lifetime treatment with nucleos(t)ide analogues
is recommended in all patients with cirrhosis (based on clinical evidence, APRI
score, or transient elastography score) to prevent risk of reactivation which
can cause an acute hepatitis flare. HBV reactivation may be induced by
immunosuppressive agents (eg cancer chemotherapy, checkpoint inhibitors, bone
marrow and stem cell treatment, anti-tumor necrosis factor, novel
immunobiologics [eg tyrosine kinase inhibitors, chimeric antigen receptor
T-cell treatment] and therapy for HCV).
Lifetime treatment of chronic hepatitis is
recommended but discontinuation of nucleos(t)ide analogue therapy may be
considered in the following:
- Individuals without clinical evidence of cirrhosis
- Individuals who can be followed up carefully after discontinuation and long term for reactivation
- Evidence of HBsAg loss and seroconversion to anti-HBe (for patients who were initially HBeAg-positive) and after completion of at least 1 additional year of treatment
- Individuals with persistently normal ALT levels and persistently undetectable HBV DNA levels
Retreatment is recommended in patients who
discontinued nucleos(t)ide analogue therapy showing consistent signs of
reactivation (HBsAg or HBeAg becomes positive, increase in ALT levels or
detection of HBV DNA). Treatment should be restarted if HBV DNA concentrations
rise to >4 log 10 IU/mL before any elevation in serum aminotransferases to
avoid immune-mediated flare.
Relapse and Flare
Independent risk factors
associated with increased risk of relapse include the presence of cirrhosis,
older age, shorter nucleos(t)ide analogue treatment duration, and higher
pretreatment HBV DNA levels. Biochemical relapse is defined as an increase in ALT
levels >2 times the ULN. Hepatitis flare is defined as an increase in ALT
levels >5 times the ULN. Severe hepatitis flare is defined as an ALT level
>1,000 U/L or ALT <1,000 U/L with a total bilirubin ≥3.5 mg/dL or an INR
≥1.5. Viral relapse is defined as HBV DNA >2,000 IU/mL.
Preferred Agents
Entecavir
Entecavir is considered a first-line agent for the treatment of
chronic hepatitis B virus infection. Recommended for the treatment of patients with
chronic HBV infection with established osteoporosis and/or impaired renal
function, and as an alternative for children ≥2 years old and adolescents with
chronic HBV infection. It is approved for the treatment of
chronic hepatitis B virus infection in adults with evidence of active viral
replication and either evidence of persistent elevations in ALT or AST or
histologically active disease. Its use is based on histologic, virologic, biochemical,
and serologic responses in nucleoside-treatment-naive and Lamivudine-resistant
adult patients with HBeAg-positive or HBeAg-negative chronic hepatitis B virus
infection with compensated liver disease after 1 year of treatment.
It appears to be superior to Lamivudine based on histologic
improvement, reduction in viral load, and ALT normalization. It is also effective
in the treatment of patients with Adefovir and Tenofovir resistance. It inhibits
hepatitis B virus polymerase activities such as base priming, reverse
transcription of the negative strand from the pregenomic messenger RNA, and
synthesis of the positive strand of HBV DNA.
Studies in rodents exposed to high doses (ie 3-40
times that given to humans) of Entecavir showed an increased incidence of lung
adenomas, brain gliomas, and HCC.
Tenofovir alafenamide
Tenofovir alafenamide is
used as a first-line agent for the treatment of immune-active chronic hepatitis
B virus infection in adults with compensated liver disease. It is recommended for the treatment of patients with chronic
HBV infection with established osteoporosis and/or impaired renal function
(eGFR >15 mL/min), and as an alternative for adolescents ≥12 years old with
chronic HBV infection. It may be considered as an alternative agent in patients
with treatment failure due to suspected or confirmed resistance to Adefovir,
Entecavir, Lamivudine, and Telbivudine. It is equally effective as
Tenofovir disoproxil fumarate but uses a lower dose, thus it has fewer systemic
adverse effects. It should be considered in patients with or at risk of bone
disease or renal dysfunction. It is approved for use in patients with HIV in
combination with Emtricitabine with or without other HIV drugs. Clinical trials
with follow-up at 2 years reported no resistance to Tenofovir alafenamide
therapy.
Tenofovir
alafenamide is a phosphonamidite prodrug of Tenofovir that inhibits hepatitis B
virus replication through incorporation into the viral DNA by hepatitis B virus
reverse transcriptase resulting in DNA chain termination. Its potential
significant side effect includes lactic acidosis; hence, it is essential to
perform HIV testing prior to initiating therapy and to monitor lactic acid
levels.
Tenofovir disoproxil fumarate
Tenofovir disoproxil fumarate is used
as a first-line agent for the treatment of chronic hepatitis B virus infection and
as an alternative agent in patients with treatment
failure due to suspected or confirmed resistance to Adefovir, Entecavir,
Lamivudine, and Telbivudine. It is recommended to be
used in combination with Lamivudine or Emtricitabine as an alternative agent
regimen for the treatment of chronic HBV infection if monotherapy with
Tenofovir disoproxil fumarate is not available. It is an effective
antiviral agent for hepatitis B (chronic HBeAg positive or HBeAg negative) that
so far has no resistance detected. It is also a
recommended prophylaxis for pregnant women and adolescent females who are
HBV-positive (HBsAg-positive) with HBV DNA ≥200,000 IU/mL or positive HBeAg
(preferably in the second trimester of pregnancy until at least delivery or
completion of the infant HBV vaccination series) to prevent mother-to-child
transmission of HBV.
Tenofovir disoproxil fumarateIt is a
prodrug of Tenofovir and it inhibits hepatitis B virus polymerase resulting in
the inhibition of viral replication. Its potential significant side effects
include lactic acidosis, nephropathy, Fanconi syndrome, and osteomalacia. It is
essential to perform HIV testing prior to initiating therapy and to monitor
renal function at baseline, within the first 4 weeks of treatment, after 3
months of treatment, and every 3-6 months thereafter; bone density at baseline
and during treatment; and lactic acid levels if with clinical concern.
Hepatitis B_ManagementPeginterferon alfa
Peginterferon alfa is approved in several countries as first-line agent for chronic hepatitis B for both HBeAg-positive and HBeAg-negative chronic hepatitis in adult patients with compensated liver disease, evidence of viral replication, and liver inflammation. In many countries in Asia, Peginterferon alfa 2b is approved for use in the treatment of chronic hepatitis B.
It appears to have superior efficacy compared to nucleos(t)ide analogues based on HBeAg seroconversion, HBV DNA suppression and HBsAg seroconversion. It has a longer half-life compared to Interferon alfa and it appears to impart a clinical benefit over conventional Interferon alfa. Treatment with Peginterferon is more likely to achieve loss of HBeAg and HBsAg in genotypes A and B than in other genotypes.
An inert polyethylene glycol is added to Interferon, decreasing the drug’s renal clearance and increasing its half-life. It provides sustained viral suppression with efficacy similar to or better than the standard Interferon alfa. It has a finite duration of therapy with no reported resistance. It is contraindicated in patients with decompensated cirrhosis, autoimmune disease, uncontrolled epilepsy, severe infection, retinal disease, heart failure, chronic obstructive pulmonary disease, pregnancy, history of mental illness, and other underlying diseases. Its side effects include mood swings and depression; hence, the patient’s mental health should be closely monitored by the clinician.
Other Agents
Adefovir dipivoxil
Adefovir dipivoxil is used as an alternative treatment in patients with HBeAg-positive chronic hepatitis B infection. It may be a preferred agent for patients with negative HBeAg, HBV DNA >105 copies/mL, and elevated ALT. It is effective as an add-on agent in suppressing Lamivudine-resistant hepatitis B virus; resulted in HBV DNA suppression of 82-87% and lower risk of Adefovir resistance of 4-8% in 3-4 years. The 10-mg dose has a more favorable risk-benefit profile compared to the 30-mg dose.
HBeAg-positive chronic hepatitis patients may discontinue therapy after 1 year and with confirmed HBeAg seroconversion, but the durability of response is unknown. Therapy may be continued in those who did not achieve HBeAg seroconversion, but safety and efficacy have not been established. HBeAg-negative chronic hepatitis may need extended treatment (>1 year) to maintain response. Further studies are needed to determine the optimal duration of therapy.
It works by inhibiting the reverse transcriptase and DNA polymerase activity and is incorporated into hepatitis B virus DNA causing chain termination; however, its barrier to resistance is low and can lead to drug resistance. Renal function and bone profile must be monitored every 3 months for patients with predisposition to renal insufficiency and for patients on Adefovir dipivoxil for >1 year.
Clevudine
A daily dose of 30 mg for 24 weeks of Clevudine has been shown in two randomized, double-blind, placebo-controlled studies to be associated with serum HBV DNA levels of <300 copies/mL in the Amplicor PCR assay in 59% of HBeAg-positive patients and in 92% of HBeAg-negative patients. It is essential to monitor for muscle symptoms and muscle weakness during therapy. This drug is already discontinued in some countries due to cases of serious myopathy leading to myonecrosis.
Interferon alfa
Interferons have antiviral, antiproliferative, and immunomodulatory effects. Interferon alfa may be a preferred agent in the treatment of HBeAg-negative chronic hepatitis B and HBeAg-positive chronic hepatitis with elevated ALT. It suppresses hepatitis B virus replication and induces remission of liver disease. Its efficacy is limited to a small percentage of highly selected patients and relapse is a major problem in HBeAg-negative chronic hepatitis B. It also has a finite duration of therapy. For HBeAg-positive chronic hepatitis B, important predictors of response to therapy are high pretreatment ALT and lower levels of serum HBV DNA.
Prednisone priming prior to Interferon alfa therapy is not recommended. Interferon alfa is contraindicated in patients with decompensated cirrhosis and coexisting autoimmune diseases. It is not recommended for patients with compensated cirrhosis because of risk of hepatic decompensation associated with Interferon alfa-related flares of hepatitis. Side effects include mood swings and depression; hence, the patient’s mental health should be closely monitored by the clinician. Pregnancy is discouraged during Interferon therapy and if the patient becomes pregnant during therapy, Interferon should be replaced with another drug.
Lamivudine
Lamivudine is used in patients with HBeAg-positive chronic hepatitis with elevated ALT but has a high rate of drug resistance during long-term treatment. It is recommended in viremic patients (HBeAg-positive and HBeAg-negative patients) with an ALT of >5x the upper limit normal especially if there is concern regarding decompensation.
Its good safety profile and ease of administration are its advantages over Interferon alfa. Pretreatment ALT is the most important predictor of response and response is greatest in patients with an ALT that is 2-5x the normal value. Treatment with Lamivudine may be discontinued in patients who have completed 1 year of treatment and have persistent HBeAg seroconversion to anti-HBe and undetectable HBV DNA by PCR assay. Treatment may be continued in patients who have not achieved HBeAg seroconversion and have no evidence of breakthrough infection because HBeAg seroconversion may occur with continued treatment.
It causes premature termination of the viral DNA chain termination thereby inhibiting hepatitis B virus DNA synthesis. It induces histologic improvement and reduction in rate of development of hepatic fibrosis. While on therapy, it is essential to monitor liver function tests, HBeAg, and anti-HBe every 3 months. Test for HBV DNA at 3 and 6 months of therapy and every 3-6 months thereafter.
The emergence of Lamivudine-resistant hepatitis B virus is increasingly common with prolonged treatment, together with a decreasing rate of remission. It is associated with the development of Lamivudine-resistant YMDD viral mutants, which appear to be less virulent than wild-type hepatitis B virus but have been associated with rapidly progressive liver disease in some patients. Lamivudine resistance is usually manifested as a breakthrough infection with the reappearance of hepatitis B virus DNA in the serum. The benefits of continued treatment must be balanced against the risk of resistant mutants.
Telbivudine
Telbivudine is an orally bioavailable drug with potent and specific anti-hepatitis B virus activity. Clinical trials show that Telbivudine gave more potent hepatitis B virus suppression than Lamivudine or Adefovir in both HBeAg-positive and negative patients. It also showed equal potency to Entecavir when it comes to hepatitis B virus suppression in HBeAg-positive patients but has a high rate of resistance.
It works by competitively inhibiting the viral reverse transcriptase, thereby blocking the DNA polymerase activity. It is essential to monitor for muscle symptoms and muscle weakness during therapy.
Hepatitis D
Patients for whom treatment is recommended include those without advanced fibrosis or cirrhosis but with increased levels of ALT and/or chronic hepatitis on liver biopsy, and those patients with HBV/HDV and advanced fibrosis or cirrhosis regardless of HBV DNA, HDV RNA, or ALT level.
Bulevirtide
Bulevirtide is approved by the European Medicines Agency (EMA) for the therapy of chronic HDV infection in plasma or serum HDV RNA-positive adult patients with compensated liver disease. It acts by blocking the entry of HBV and HDV into the hepatocytes through binding to and inactivation of the sodium taurochlolate cotransporting polypeptice (NCTP), a bile salt liver transporter which serves as essential HBV/HDV entry receptor. The endpoint in therapy is the persistent decline of serum HDV RNA by ≥2 log 10 IU/mL (100-fold).
Pegylated Interferon alfa-2a (Peginterferon alfa-2a)
Interferon alfa is the only approved chronic hepatitis D treatment and Peginterferon is the drug of choice. Peginterferon alfa is recommended to be given for 48 weeks in patients with elevated ALT and HDV RNA levels. The endpoint of therapy is the achievement of a complete virological response (ie undetectable HBsAg with sustained suppression of HDV RNA accompanied by normalization of ALT level).
Hepatitis B_Management 2Nonpharmacological
Patient Education
Acute Hepatitis B
Partner notification for at-risk contacts is essential. Contact
tracing should include any sexual contact (penetrative vaginal or anal or
oral/anal) or needle-sharing partners within 2 weeks before the onset of
jaundice until the patient becomes negative for HBsAg. All non-immune sexual and
household contacts must be vaccinated.
Provide the patients with a detailed explanation of
their condition and emphasize the disease’s long-term implications (eg
long-term medical therapy, continuous monitoring) for their and their partners’
health. Provide clear and accurate written information for easier
understanding. Advise the patients to avoid unprotected sexual intercourse and
emphasize condom use. Screen patients for other sexually transmitted diseases
in cases of sexually acquired hepatitis or if otherwise appropriate.
Chronic Hepatitis B
Partner notification is essential. Trace contacts as far back as
any episode of jaundice or to the time when the infection is thought to have
been acquired. All non-immune sexual and household contacts must be vaccinated.
Provide the patients with a detailed explanation of
their condition and emphasize the disease’s long-term implications (eg
long-term medical therapy, continuous monitoring) for their and their partners’
health. Provide clear and accurate written information for easier
understanding. Advise patients to observe abstinence or limited use of alcohol
to prevent further liver injury.
Counseling regarding the prevention of transmission of hepatitis B
virus is also important. To prevent sexual transmission, protected sexual
intercourse like condom use may be done. To prevent perinatal transmission, hepatitis
B immune globulin (HBIg) and hepatitis B vaccine at delivery for babies of hepatitis
B virus-infected mothers may be given. Counseling to prevent inadvertent
transmission via environmental contamination from a blood spill may also be done.
Hepatitis D
Partner notification for at-risk contacts is
essential. Provide the patient with a detailed explanation of his condition and
emphasize the disease's long-term implications (eg long-term medical therapy, continuous
monitoring) for their and their partner’s health. Provide clear and accurate
written information for easier understanding. Advise patients to avoid
unprotected sexual intercourse.
Hepatitis B_Management 3Surgery
Liver Transplantation
Liver transplantation is indicated in patients with end-stage
liver disease (cirrhosis), HCC, and acute liver failure (ie caused by viruses, drugs,
and toxic agents). It is considered in patients with expected survival of ≤1
year without transplantation or if the quality of life is unsatisfactory due to
liver disease. Patients with hepatitis B virus infection should be evaluated
for liver transplantation despite antiviral therapy as the development of liver
failure cannot be predicted.
The
combination therapy with hepatitis B immunoglobulin and nucleos(t)ide analogues
helps prevent hepatitis B virus recurrence in these patients undergoing liver
transplantation. Recipient patients without anti-HBs should receive prophylaxis
for hepatitis B virus recurrence if transplanted liver is anti-HBc positive.
Hepatitis D virus replication is not a contraindication for liver
transplantation.
Prevention
Prevention and Post-exposure Prophylaxis of Hepatitis B
| Patient Group for Whom Prevention or Post-exposure Prophylaxis is Recommended | Recommended Prevention or Post-exposure Prophylaxis Regimen |
| Prevention | |
| Unvaccinated medically-stable infants, children, adolescents and adults Premature infants with immediate risk of HBV infection Unvaccinated persons who attend STD clinics, including pregnant women Persons with any of the following sexual risk factors: History of STD and HIV, multiple sex partners, sex with an injection drug user, sexual partner of HBsAg-positive individuals, MSM, victims of sexual assault Illegal IV drug users Household members, sex partners and drug-sharing partners of a person with chronic HBV infection1 Residents or staff of facilities for developmentally disabled individuals Persons on hemodialysis, are receiving clotting factor concentrates, who have occupational exposure to blood, or are needing immunosuppressive therapy Healthcare personnel in treatment facilities Inmates of correctional facilities Patients with diabetes mellitus, HCV infection, chronic liver disease, HIV infection Travelers to places with endemic HBV infection (≥2% HBsAg prevalence) Individuals seeking protection from HBV infection |
Hepatitis B Vaccine |
| Post-exposure Prophylaxis | |
| Unvaccinated or non-immune sex partners of persons with acute hepatitis B |
Administer hepatitis B immune globulin (HBIg) within 14 days after the most recent sexual contact and begin hepatitis B vaccination series (if not contraindicated) For individuals or healthcare personnel with percutaneous or mucous membrane exposure2 to blood or body fluids from patients with HBV, HBIg is recommended if unvaccinated, unresponsive to previous vaccination or with unknown response to immunization |
1Vaccination
of household contacts (especially children and adolescents) of persons with
acute hepatitis B virus infection is also encouraged. Consider postvaccination
testing (anti-HBs) for sexual partners of persons with chronic hepatitis B virus
infection. Those found to be antibody negative should receive a second,
complete, vaccination series.
2Skin
and wound sites exposed to blood or body fluids with hepatitis B virus
infection should be washed with soap and water immediately following contact;
exposed mucous membranes should be flushed with water.
Revaccination is recommended for infants born to HBsAg-positive
mothers, healthcare practitioners, hemodialysis patients, and immunocompromised
individuals when anti-HBs is <10 mIU/mL. Postvaccination serologic testing
is recommended only for infants born to HBsAg-positive mothers, healthcare practitioners,
hemodialysis patients, immunocompromised individuals (eg HIV-positive patients,
stem-cell transplant recipients, cancer patients receiving chemotherapy), and
sexual partners of HBsAg-positive individuals.
Hepatitis B_Follow upHepatitis D
Vaccination and safety measures against hepatitis B virus infection are the best protection against hepatitis D virus infection. Immunization does not apply to patients already positive for hepatitis B virus infection.