eMedicine Specialties > Gastroenterology > Liver

Hepatitis B: Treatment & Medication

Author: Nikolaos T Pyrsopoulos, MD, PhD, FACP, Chief of Hepatology, Medical Director of Liver Transplantation, Florida Hospital; Associate Professor of Medicine, University of Central Florida College of Medicine
Coauthor(s): K Rajender Reddy, MD, FACP, FACG, Professor, Department of Medicine, Division of Hepatology, University of Miami School of Medicine
Contributor Information and Disclosures

Updated: Jun 19, 2009

Treatment

Medical Care

Therapy is currently recommended for patients with evidence of chronic active hepatitis B disease (ie, high aminotransferase levels, positive HBV DNA findings, HBeAg). Various algorithms have been proposed, such as that by Keeffe and colleagues14 and the American Association for the Study of Liver Diseases (AASLD).15 In general, for the HBeAg-positive patient population that is identified with evidence of chronic hepatitis B virus (HBV) disease, treatment is advised to be administered when the HBV DNA level is ≥20,000 IU/mL (105 copies/mL) and when serum ALT is elevated for 3-6 months.

For the HBeAg-negative chronic population with hepatitis B disease, treatment can be administered when the HBV DNA is ≥ 2000 IU/mL (104 copies/mL) and serum ALT is elevated (ALT levels >20 U/L for females and 30 U/L for males) for 3-6 months.

Medication (see also Medication, below) 
Currently, interferon alfa (IFN-a), lamivudine, telbivudine, adefovir, entecavir, and tenofovir are the main treatment drugs approved globally, although ongoing trials are investigating new types of medications, such as tenofovir disoproxil in combination with emtricitabine, clevudine (l-FMAU), and therapeutic vaccines. It appears that lamivudine and telbivudine are not recommended as first-line agents in the treatment of hepatitis B disease.16

Patients who have lost HBeAg and in whom HBV DNA is undetectable have an improved clinical outcome (ie, slower rate of disease progression, prolonged survival without complications, reduced rate of HCC, and clinical and biochemical improvement after decompensation).

Special attention must be given to patients on liver transplantation lists. Initiation of treatment with adefovir or entecavir or tenofovir or in combination with lamivudine is of cardinal importance before and after liver transplantation to achieve viral suppression and to prevent recurrence of the disease after the procedure.

  • IFN-a17
    • Published reports indicate that after IFN-a treatment with 5 million U/d or 10 million U 3 times per week subcutaneously (SC) for 4 months, the HBV DNA levels and HBeAg become undetectable in 30-40% of patients. In addition, 10% of patients seroconvert from HBsAg to HBsAb. Unfortunately, 5-10% of patients' disease relapses after completion of treatment. A transient "flare" (ie, increased aminotransferase levels during the beginning of treatment) can be identified, and this represents the impact of the activated cytolytic T cells on the infected hepatocytes.
    • High levels of aminotransferases, a low viral load, and infection with the wild type are good prognostic factors for response to IFN-a treatment.
    • Asian patients and patients with the precore mutant virus tend to not have a clinical response to IFN-a treatment.
    • Special attention must be given to patients with HBV-decompensated cirrhosis (eg, ascites, encephalopathy) who are taking IFN-a because of the fact that, although they occasionally may have a treatment response, they can also deteriorate further.
    • The adverse effects of IFN-a treatment can sometimes be severe, even devastating. Some patients cannot complete treatment. A flulike syndrome, myelosuppression (eg, leukopenia, thrombocytopenia), nausea, diarrhea, fatigue, irritability, depression, thyroid dysfunction, and alopecia are among the adverse effects that may occur.
  • Pegylated IFN-a 2a
    • A 48-week regimen of pegylated IFN-a 2a might induce a 27% rate of HBeAg seroconversion and a 25% rate of loss of HBV DNA.18 Extension to treatment for 48 weeks resulted in an HBeAg seroconversion of 32%.
    • Placing patients that have HBeAg-negative chronic hepatitis B disease on 48 weeks of a pegylated IFN-a 2a regimen resulted in a significantly greater percentage of patients with a viral load that was nondetectable 24 weeks after the end of treatment (19%) compared with lamivudine monotherapy (7%).16
    • It appears that patients infected by hepatitis B virus (HBV) genotype A or B have a better response to IFN treatment compared with patients infected by genotype C or D, and this kind of treatment appears to be more appealing, especially for patients with increased ALT levels.
  • Lamivudine16,19,20,21
    • A nucleoside analogue that inhibits the viral polymerase, lamivudine has been associated with a 4-log reduction of the viral load. Lamivudine treatment (100 mg/d) has been associated with a 16-18% seroconversion rate from HBeAg to HBeAb, a 30-33% rate of HBeAg loss, a 40-50% normalization of the value of the aminotransferases, and a 1-2% HBsAg seroconversion rate.
    • Histologic improvement (ie, reduction of histologic activity index of >2 points) has been noticed in approximately 50% of patients taking this medication. The adverse effects are negligible.
    • Lamivudine appears to be effective for patients who do not have a treatment response to IFN-a (eg, patients infected by the precore mutant virus). A transient elevation of aminotransferases can be noticed shortly after starting treatment.
    • The HBeAg seroconversion rate has been shown to possibly increase to 27% after 2 years, 40% after 3 years, and 47% after 4 years of treatment in patients with a viral load of less than 104 pg/mL.
    • Lamivudine treatment has also been shown to dramatically improve the condition of patients with decompensated disease due to hepatitis B virus (HBV) reactivation.
    • The emergence of viral variants is the major complication in hepatitis B disease.22,23 Approximately 15-30% of patients develop a mutation of the viral polymerase gene (the YMDD variants) after 12 months of treatment, and approximately 50% develop a mutation after 3 years of treatment. However, continued treatment after the breakthrough with the variant type has been associated with lower HBV DNA levels, less aminotransferase activity, and histologic improvement. For these patients, discontinuation of treatment is accompanied by a reversion to a wild type of hepatitis B virus (HBV) and a flare of the disease.
  • Adefovir dipivoxil
    • This agent is a nucleoside analogue, a potent inhibitor of the viral polymerase. The efficacy of adefovir dipivoxil has been tested in HBeAg-positive, HBeAg-negative, and lamivudine-resistant patients with encouraging results.
    • The estimated rate of resistance to adefovir and the development of mutations (rtN236T and rtA181V) are approximately 4-6% after 3 years and approximately 30% after 5 years of treatment.24,25,26,27
    • The optimal dose seems to be 10 mg/d.28,29 Higher doses are nephrotoxic.
    • The results of 2 multicenter trials that used adefovir for 48 weeks were published. In HBeAg-positive patients who received 10 mg of adefovir daily, a median 3.52 log reduction of the viral load (HBV DNA) level was noted. In 48% of the patients, normalized aminotransferase levels were reported. Histologic improvement was noticed in 53% of the patients who received this regimen.28 The HBeAg seroconversion rate was 12%. Of the HBeAg-negative population, 64% experienced histologic improvement after receiving 10 mg of adefovir for 48 weeks, and 72% had normalized aminotransferase levels. The serum HBV DNA level was decreased in 51% of subjects.28,29 The outcomes were maintained if treatment was continued for 144 weeks, but the benefits were lost if treatment was discontinued at 44 weeks. The development of resistant mutations (rtN236T and rtA181V) has been estimated to be around 6%.29
  • Entecavir30
    • Entecavir is a potent guanosine analogue inhibitor of the viral polymerase with no resistance developed as of this writing, so far after 2 years of use, in patients who have no history of previous treatment with nucleoside analogues.
    • With regard to the HBeAg-positive population, administration of 0.5 mg of entecavir in patients who are naive to nucleoside analogues relative to patients who received 100 mg of lamivudine for a duration of 48 weeks resulted in histologic improvement in 72% of the entecavir group versus 62% of the lamivudine group (P = 0.009). Undetectable serum HBV DNA levels were reported in 67% of entecavir-treated patients compared with 36% of lamivudine-treated patients (P <0.001). Normalized ALT levels were achieved in 68% of the entecavir group versus 60% of the lamivudine group (P = 0.02). The mean reduction in serum HBV DNA from baseline to week 48 was 6.9 log copies/mL (on a base-10 scale) in the entecavir-treated patients relative to 5.4 log copies/mL in the lamivudine-treated patients (P <0.001). HBeAg seroconversion occurred in 21% of patients treated with entecavir and 18% of patients treated with lamivudine (P = 0.33).
    • With regard to the HBeAg-negative population, administration of 0.5 mg of entecavir in patients who are naive to nucleoside analogues compared with patients who received 100 mg of lamivudine for a duration of 48 weeks resulted in histologic improvement in 71% of the entecavir group versus 61% of the lamivudine group (P = 0.01). Undetectable serum HBV DNA levels were found in 90% of the entecavir-treated patients versus 72% of the lamivudine-treated patients (P <0.001). Normalized ALT levels were achieved in 78% of the entecavir group compared with 71% of the lamivudine group (P = 0.045).30 The mean reduction in serum HBV DNA levels from baseline to week 48 was 5.0 log copies/mL (on a base-10 scale) in the entecavir-treated patients versus 4.5 log copies/mL in the lamivudine-treated patients (P <0.001).30
  • Telbivudine
    • Telbivudine, a cytosine nucleoside analogue, is a potent inhibitor of the HBV DNA polymerase.
    • The results of the GLOBE Trial, a phase III study, that tested the administration of 600 mg of telbivudine versus 100 mg of lamivudine over a 2-year period were announced.31,32 In the HBeAg-positive population, therapeutic response (defined as HBV DNA <10,000 copies/mL, with either ALT normalization or HBeAg loss) was 75% for the patients treated with telbivudine compared with 67% for the patients treated with lamivudine. Of the patients receiving telbivudine, 26% lost the e antigen versus 23% of the patients receiving lamivudine.31,32 In addition, a 6.5 log reduction of the HBV DNA was noted for the patients receiving telbivudine versus a 5.5 log reduction for the patients receiving lamivudine.
    • In the HBeAg-negative patients, the response rates at 1 year were 75% for the telbivudine group and 77% in the lamivudine group, whereas 88% of the telbivudine-treated patients versus 71% of the lamivudine-treated patients were HBV DNA nondetectable. The HBV DNA log reduction was 5.2 (telbivudine group) versus 4.4 (lamivudine group).31,32
    • Because resistance is a major issue, the reported rates at 1 year were 2.6% of patients on telbivudine and 8.2% of patients on lamivudine.
  • Tenofovir
    • HBeAg-positive naive population33 : Patients were randomized in 2 arms to receive either tenofovir (300 mg once daily) or adefovir (10 mg once daily) for 48 weeks, with the adefovir-treated patients then switched to tenofovir.33

      Seventy nine percent (79%) of the patients who received tenofovir were found to have a viral load below 400 copies/mL.33 In the adefovir group, 76% of patients receiving adefovir before switching to tenofovir were found to have a viral load below 400 copies/mL.

      Seventy two percent (72%) of the patients in the adefovir arm that were found to have a viral load greater than 400 copies/mL achieved viral suppression after they were switched to tenovofir, whereas for those who achieved viral suppression, the effect was maintained after they were switched to tenofovir.33 Biochemical response was reported in 77% of patients in the tenofovir arm at week 72 and in 61% of those switching from adefovir to tenofovir.

      With regard to seroconversion, 26% of patients who received tenofovir seroconverted at week 64.33 In the adefovir arm, the observed seroconversion rate was reported as 21%. It is noteworthy to mention that 5% of patients in the tenofovir arm experienced loss of the "s" antigen.
    • HBeAg-negative population34 : Patients were randomized receive either tenofovir (300 mg once daily) or adefovir (10 mg once daily). After 48 weeks, all eligible adefovir-treated patients were switched to tenofovir. 

      At 72 weeks of treatment, 91% of patients receiving tenofovir were found to have a viral load below 400 copies/mL.34 In the adefovir arm, of patients who switched to tenofovir after 48 weeks, 88% had a viral load below 400 copies/mL by week 72 of the study. All the adefovir-treated patients who had a viral load below 400 copies/mL at week 48 maintained a viral load below this level after switching to tenofovir.34 For the patient population in the adefovir arm who did not achieve optimal viral response (viral load above 400 copies/mL) at the time of switch to tenofovir, 94% had a viral load below this level by week 72.

      Normal ALT levels at week 72 were observed in 79% of patients who initiated therapy with tenofovir and in 77% of patients who switched to tenofovir drug from adefovir.34
    • In 2 double-blind, phase 3 studies, Marcellin et al evaluated tenofovir versus adefovir in the treatment of chronic hepatitis B. Patients with HBeAg-negative or HBeAg-positive chronic hepatitis B virus (HBV) infection were randomized to receive tenofovir disoproxil fumarate (DF) (300 mg) or adefovir dipivoxil (10 mg) (ratio, 2:1) once daily for 48 weeks.35 The primary efficacy end point was a plasma HBV DNA level of less than 400 copies/mL (69 IU/mL) and histologic improvement (defined as a reduction in the Knodell necroinflammation score of >2 points without worsening fibrosis) at week 48. The investigators included secondary end points such as viral suppression (HBV DNA level <400 copies/mL), histologic improvement, serologic response, normalization of ALT levels, and development of resistance mutations.35 At week 48, in both studies, a significantly higher proportion of patients receiving tenofovir than of those receiving adefovir had reached the primary end point (P <0.001), and viral suppression occurred in more HBeAg-negative patients in the tenofovir group (93%) than patients in the adefovir group (63%) (P <0.001), as well as in more HBeAg-positive patients receiving tenofovir (76%) than those receiving adefovir (13%) (P <0.001).35 In addition, significantly more HBeAg-positive patients in the tenofovir group (68%) not only had normalized ALT levels relative to those in the adefovir group (54%) (P = 0.03) but also loss of HBsAg (3% tenofovir group vs 0% adefovir group) (P = 0.02).35 At the end of 48 weeks, none the patients had developed the amino acid substitutions within HBV DNA polymerase that are associated with phenotypic resistance to tenofovir or other drugs used to treat hepatitis B virus (HBV) infection; tenofovir  produced a similar HBV DNA response in patients who had previously received lamivudine and in those who had not; and the 2 treatments in both studies had similar safety profiles.35 Marcellin et al concluded that among patients with chronic hepatitis B virus (HBV) infection, tenofovir at a daily dose of 300 mg had superior antiviral efficacy with a similar safety profile as compared with adefovir at a daily dose of 10 mg through week 48.35

Surgical Care

Orthotopic liver transplantation (OLT) is the treatment of choice for patients with fulminant hepatic failure who do not recover and for patients with end-stage liver disease. The implementation of hepatitis B immunoglobulin (HBIG) during and after the OLT period, and of lamivudine or adefovir in the pre-and post-OLT periods, dramatically improves the recurrence rate of hepatitis B virus (HBV) infection.

Diet

  • Acute and chronic hepatitis (patients without cirrhosis): No dietary restrictions
  • Decompensated cirrhosis (prominent signs of portal hypertension or encephalopathy): Low-sodium diet (1.5 g/d), high-protein diet (ie, white-meat protein [eg, pork, turkey, fish]), and, in cases of hyponatremia, fluid restriction (1.5 L/d)

Medication

The goals of pharmacotherapy in patients with hepatitis B disease are to reduce morbidity and to prevent complications.

Antivirals

Antiviral agents interfere with viral replication and weaken or abolish viral activity.


Tenofovir disoproxil fumarate (Viread)

Nucleotide analogue (adenosine monophosphate) reverse transcriptase and HBV polymerase inhibitor.

Adult

300 mg PO qd

For patients with renal impairment adjust dose as follows:

CrCl 30-49 mL/min: Administer q48h.
CrCl 10-29 mL/min Administer twice weekly.
CrCL <10 mL/min (Not on hemodialysis): Not established

Patient on hemodialysis: Administer q7d after hemodialysis or after a total of approximately 12 h of dialysis.

Pediatric

<16 years: Not established

>16 years: Administer as in adults.

Coadministration with drugs eliminated by active tubular secretion in the kidney may increase serum concentrations of either tenofovir or the coadministered drug; drugs that decrease renal function (eg, acyclovir, ganciclovir, cidofovir) may increase serum concentrations of tenofovir.

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

The CDC recommends women with AIDS not to breastfeed due to potential HIV transmission to the infant; lactic acidosis and hepatomegaly with steatosis reported with nucleoside analogues (suspend treatment if clinical or laboratory findings suggest presence of lactic acidosis or pronounced hepatotoxicity); peripheral wasting, facial wasting, breast enlargement, and "cushingoid appearance" reported with antiretroviral therapy; common adverse effects include GI complaints (eg, nausea, diarrhea, vomiting, flatulence); monitor for changes in serum creatinine and serum phosphorus in patients at risk or with history of renal dysfunction.


Lamivudine (Epivir)

Thymidine analogue that blocks viral replication by competitive inhibition of viral reverse transcriptase. There is evidence that an indirect immunomodulatory effect can be observed.

Adult

100 mg PO qd

Pediatric

Not established

TMP-SMZ increases bioavailability; increases concentration of zidovudine when administered concurrently

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust the dose in the presence of renal impairment; caution in patients with a history of pancreatitis


Adefovir dipivoxil (Hepsera)

Used to treat chronic hepatitis B disease. This agent is a prodrug that is converted to the diphosphate salt. The active drug is classified as an antiviral nucleotide reverse transcriptase inhibitor. It inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate (dATP) and by causing DNA chain termination after its incorporation into viral DNA.

Adult

CrCl >50 mL/min: 10 mg PO qd
CrCl 20-49 mL/min: 10 mg PO q48h
CrCl 10-19 mL/min: 10 mg PO q72h

Hemodialysis: 10 mg PO qwk following hemodialysis

Pediatric

Not established

Coadministration with ibuprofen increases the bioavailability of adefovir; drugs that alter renal tubular secretion may affect adefovir renal elimination.

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hepatitis exacerbation may occur following drug discontinuation; may increase the risk of renal dysfunction; HIV resistance may emerge in patients with untreated or unrecognized HIV; lactic acidosis and hepatomegaly with steatosis have been reported with other nucleoside analogues


Entecavir (Baraclude)

Guanosine nucleoside analogue with activity against HBV polymerase. Competes with natural substrate deoxyguanosine triphosphate (dGTP) to inhibit HBV polymerase activity (ie, reverse transcriptase). Less effective for lamivudine-refractory HBV infection. Indicated for treatment of chronic HBV infection. Available as a tablet and as oral solution (0.05 mg/mL; 0.5 mg = 10 mL).

Adult

Treatment for nucleoside naive: 0.5 mg PO qd 2 h ac or 2 h pc

CrCl 30-49 mL/min: 0.25 mg PO qd
CrCl 10-29 mL/min: 0.15 mg PO qd
CrCl <10 mL/min: 0.05 mg PO qd

Receiving lamivudine or lamivudine resistance: 1 mg PO qd 2 h ac or 2 h pc

CrCl 30-49 mL/min: 0.5 mg PO qd
CrCl 10-29 mL/min: 0.3 mg PO qd
CrCl <10 mL/min: 0.1 mg PO qd

Pediatric

<16 years: Not established

>16 years: Administer as in adults.

Not a substrate, inhibitor, or inducer of cytochrome P450; coadministration with drugs that reduce renal function (eg, aminoglycosides, cidofovir, cyclosporine) or that compete for active tubular secretion (eg, probenecid, salicylates) may increase serum concentration of either entecavir or coadministered drug

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Reduce the dose in patients with renal impairment; if on hemodialysis, administer afterward; common adverse effects include headache, fatigue, dizziness, and nausea; may elevate liver enzyme levels; may cause lactic acidosis; severe acute exacerbations of HBV infection may occur in patients who discontinue anti-HBV therapy


Telbivudine (Tyzeka)

Nucleoside analogue approved by the FDA for chronic hepatitis B treatment. Inhibits hepatitis B viral DNA polymerase. Indicated for patients with evidence of ongoing hepatitis B viral replication and either persistent elevated aminotransferase activity or histologic evidence of active liver disease. Consider for patients whose condition did not or is unlikely to respond to interferon or for patients who cannot tolerate interferon. Emergence of resistance is a major drawback of nucleoside analogue monotherapy.

Adult

CrCl >50 mL/min: 600 mg PO qd
CrCl 30-49 mL/min: 600 mg PO q48h or 400 mg PO qd
CrCl <30 mL/min (not requiring dialysis): 600 mg PO q72h or 200 mg PO qd

ESRD: 600 mg PO q96h

Optimal treatment duration not established

Pediatric

<16 years: Not established

>16 years: Administer as in adults.

Toxicity may increase when administered concurrently with drugs that decrease renal excretion (eg, acyclovir, aminoglycosides, amphotericin B, cisplatin, cyclosporine, metformin, tacrolimus); may increase the risk of myopathy when coadministered with HMG-CoA reductase inhibitors (statins)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues alone or in combination with antiretrovirals; severe acute hepatitis B exacerbations have been reported when anti-hepatitis B therapy (including telbivudine) is discontinued (closely monitor hepatic function with both clinical and laboratory follow-up for at least several months following discontinuation of anti-hepatitis B therapy, and resume therapy, if necessary); myopathy has been reported; common adverse effects include upper respiratory tract infection, fatigue, malaise, abdominal pain, nasopharyngitis, headache, increased CK level, cough, nausea, vomiting, flulike symptoms, diarrhea, pyrexia, arthralgia, rash, back pain, dizziness, and dyspepsia.

Interferons

Interferon agents are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions.


Peginterferon alfa 2a (Pegasys)

Binds to cell surface receptors in a cascade of protein interactions resulting in gene transcription. These stimulated genes inhibit viral replication in infected cells, cell proliferation, and immunomodulation. Indicated for adults with HBeAg-positive and HBeAg-negative chronic hepatitis B disease with compensated liver disease and evidence of viral replication and liver inflammation.

Adult

180 mcg SC once weekly for 48 wk; administer in abdomen or thigh

Pediatric

Not established

Theophylline may increase toxicity by reducing clearance; cimetidine may increase the antitumor effects; zidovudine and vinblastine may increase toxicity.

Documented hypersensitivity; decompensated liver disease; significant preexisting psychiatric disease; ongoing or recent alcohol use; platelet count <70,000/mm3

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

X - Contraindicated; benefit does not outweigh risk

Precautions

Insomnia; mental dysfunction (eg, mood dysfunction, depression, psychosis, aggressive behavior, hallucinations, violent behavior, suicidal ideation, suicide attempt, suicide, homicidal ideation [rare]), even without previous history of psychiatric illness; flulike symptoms; rash and pruritus; anorexia; neutropenia; thrombocytopenia; thyroid dysfunction; retinal abnormalities


Interferon alfa-2b (Intron A) or alfa-2a (Roferon-A)

Protein product manufactured by recombinant DNA technology. Mechanism of antiviral activity is not clearly understood. However, modulation of host immune responses enhances cytolytic T-cell activity; stimulates natural killer cell activity and amplifies HLA class I protein on infected cells. Direct antiviral activity activates viral ribonucleases, inhibits viral entry to cells, and inhibits viral replication. Direct antifibrotic effect has been postulated.

Before initiation of therapy, perform tests to quantitate peripheral blood hemoglobin, platelets, granulocytes, hairy cells, and bone marrow hairy cells; monitor periodically (eg, monthly) during treatment to determine response to treatment; if patient's condition does not respond within 4 months, discontinue treatment. If a response occurs, continue treatment until no further improvement is observed. Whether continued treatment is beneficial after that time remains unknown.

Adult

5 million U IM/SC qd for 16 wk; alternatively, 10 million U IM/SC 3 times per wk for 16 wk

Reduce dose by 50% if severe reactions occur or temporarily discontinue therapy until symptoms from adverse reactions improve.

Pediatric

Not established

Theophylline may increase toxicity; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity.

Documented hypersensitivity; autoimmune hepatitis, other autoimmune disorders

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with brain metastases, severe hepatic or renal insufficiencies, seizure disorders, multiple sclerosis, or compromised CNS; associated with depression and suicidal ideation and severe or fatal GI hemorrhage

More on Hepatitis B

Overview: Hepatitis B
Differential Diagnoses & Workup: Hepatitis B
Treatment & Medication: Hepatitis B
Follow-up: Hepatitis B
Multimedia: Hepatitis B
References
Further Reading
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Further Reading

Additional resources on hepatitis B are available at Medscape’s Hepatitis B Resource Center.

Related eMedicine Topics

Clinical Trials

National Guideline Clearinghouse

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Keywords

hepatitis B, hepatitis, HBV, hepatitis B infection, viral hepatitis, hepatitis B virus, chronic hepatitis, acute hepatitis, cirrhosis, fulminant hepatitis, hepatocellular carcinoma, HCC, extrahepatic manifestations, hepatitis D virus, HDV, delta virus, hepatitis C virus, HCV, hepatitis B surface antigen, HBsAg, Australia antigen, hepatitis B surface antibody, HBsAb, orthohepadnavirus, hepadnaviridae infection,

liver transplantation, liver transplant, OLT, interferon-alpha, IFN-a, peginterferon-alfa 2a, pegylated IFN-a 2a, lamivudine, adefovir dipivoxil, entecavir, telbivudine, tenofovir

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Contributor Information and Disclosures

Author

Nikolaos T Pyrsopoulos, MD, PhD, FACP, Chief of Hepatology, Medical Director of Liver Transplantation, Florida Hospital; Associate Professor of Medicine, University of Central Florida College of Medicine
Nikolaos T Pyrsopoulos, MD, PhD, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Liver Foundation, American Medical Association, American Society of Gastrointestinal Endoscopy, American Society of Transplantation, International Liver Transplantation Society, and Transplantation Society
Disclosure: Gilead Sciences Honoraria Speaking and teaching; Schering-Plough Honoraria Speaking and teaching; Roche Honoraria Speaking and teaching

Coauthor(s)

K Rajender Reddy, MD, FACP, FACG, Professor, Department of Medicine, Division of Hepatology, University of Miami School of Medicine
K Rajender Reddy, MD, FACP, FACG is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and Florida Medical Association
Disclosure: Nothing to disclose.

Medical Editor

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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