PRIMARY CARE MANAGEMENT OF HEPATITIS B— QUICK

2y ago
17 Views
2 Downloads
647.22 KB
32 Pages
Last View : 2m ago
Last Download : 2m ago
Upload by : River Barajas
Transcription

PRIMARY CAREMANAGEMENT OF HEPATITIS B—QUICK REFERENCEPROTECTING CANADIANS FROM ILLNESS

TO PROMOTE AND PROTECT THE HEALTH OF CANADIANS THROUGH LEADERSHIP, PARTNERSHIP,INNOVATION AND ACTION IN PUBLIC HEALTH.—Public Health Agency of CanadaÉgalement disponible en français sous le titre :Soins primaires de l’hépatite B — Aide-mémoireTo obtain additional copies, please contact the Public Health Agency of Canada:ccdic-clmti@phac-aspc.gc.caThis publication can be made available in alternative formats upon request. Her Majesty the Queen in Right of Canada, 2013Publication date: March 2013PRINTCat.: HP40-82/2013EPDFISBN: 978-1-100-21974-5Cat.: HP40-82/2013E-PDFISBN: 978-1-100-21975-2Pub.: 120200

REPORTTITLE GOESHERE IPRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEPRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCE

II PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCE

REPORTTITLE GOESHERE IIIIIIPRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCETABLE OF CONTENTSLIST OF ABBREVIATIONS.AUTHORS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .IV. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .VCONTRIBUTORS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .VIINTRODUCTION. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1Key Facts and Figures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Epidemiology of Acute and Chronic HBV in Canada. .1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3MODULE 1: WHO SHOULD BE TESTED FOR HBV?. .Where is your patient from? .MODULE 2: APPROACH TO HBV SCREENING AND TESTING.Overview of HBV Serological Markers. . . . . . . . . . . . . . . . . . . . . . . . . . . . .4. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4Significance of HBV Serological Markers.Approach to Test Selection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5MODULE 3: INTERPRETATION OF HBV DIAGNOSTIC TEST RESULTS. . . . . . . . . . . . . . . . . . . . . . . . .MODULE 4: INITIAL MANAGEMENT OF PATIENTS WITH HBsAg-POSITIVE RESULTS.7. . . . . . . . . . . . . . . . . . . . . . .8. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Signs and Symptoms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Resolution Time and Clinical Course of Infection. .Acute HBV with Severe Presentation.8. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9. . . . . . . . . . . . . . . . . . . . . . . . .10. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11MODULE 7: NATURAL HISTORY OF CHRONIC HBV.Immune Tolerant Phase.HBeAg-positive Immune Active Chronic HBV Phase. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .HBeAg-negative Immune Active Chronic HBV Phase (anti-HBe positive).11. . . . . . . . . . . . . . . . . . . . . . .11. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .12Inactive HBsAg Phase .HBsAg Clearance.8. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .MODULE 6: INITIAL EVALUATION OF CONFIRMED CHRONIC HBV. .MODULE 8: LONG-TERM MANAGEMENT OF CONFIRMED CHRONIC HBV. . . . . . . . . . . . . . . . . . . . .MODULE 9: TREATMENT OF CHRONIC HBV AND MONITORING OF PATIENTS ON TREATMENT.13. . . . . . . . .15. . . . . . . . . . . . . . . . . . . . . . . . . . . . .16. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .18. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .20MODULE 10: PREVENTION AND VACCINATION CHECKLIST.MODULE 11: PATIENT EDUCATION AND COUNSELLING.REFERENCES.6. . . . . . . . . . . . . . . .MODULE 5: NATURAL HISTORY AND MANAGEMENT OF ACUTE HBV. .Incubation. .1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

IV PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCELIST OF ABBREVIATIONSAFPalpha-fetoproteinALPalkaline phosphataseALTalanine aminotransferaseASTaspartate aminotransferaseCBCcomplete blood countCMVcytomegalovirusCTcomputerized tomographyEBVEpstein-Barr virusHAVhepatitis A virusanti-HBchepatitis B core antibodyanti-HBehepatitis B e-antibodyanti-HBshepatitis B surface antibodyHBeAghepatitis B e-antigenHBIghepatitis B immune globulinHBVhepatitis B virusHBsAghepatitis B surface antigenHCChepatocellular carcinomaHCPhealthcare providerHCVhepatitis C virusHEVhepatitis E virusHIVhuman immunodeficiency virusHSVherpes simplex virusIgGimmunoglobulin GIgMimmunoglobulin MINRinternational normalized ratioMSMmen who have sex with menPCRpolymerase chain reactionPEPpost-exposure prophylaxisPTprothrombin timeRUQright upper quadrantSTIsexually transmitted infectionULNupper limit of normal

REPORTTITLE GOESHERE VVPRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEAUTHORSANTON ANDONOV, MD, PHDSection Head, Molecular & ImmunodiagnosticsBloodborne Pathogens and HepatitisPublic Health Agency of CanadaNational Microbiology Laboratory;Adjunct ProfessorDepartment of Medical MicrobiologyUniversity of ManitobaROSALIND LING, MDGeneral PractitionerSpecial interest in HepatitisToronto, ONJEAN-GUY BARIL, MDFamily Physician, Clinique Médicale du QuartierLatin, Montreal and Centre Hospitalier del’Université de Montréal;Assistant Clinical ProfessorDepartment of Family MedicineUniversity of MontrealROBERT MYERS, MD, MSC, FRCPCHepatologistAssociate Professor, Liver Unit, University of CalgaryDirector, Viral Hepatitis ClinicCASSANDRA BRUBACHER, BSCN, RN, CICPublic Health NurseCommunicable Disease DivisionMiddlesex-London Health UnitCARLA OSIOWY, MSC, PHDResearch ScientistBloodborne Pathogens and HepatitisPublic Health Agency of CanadaNational Microbiology Laboratory;Adjunct ProfessorDepartments of Medical Microbiology andInternal Medicine, Section of HepatologyUniversity of ManitobaGILLIAN BUTLER, RN, BNDisease Control Nurse SpecialistGovernment of Newfoundland and LabradorDepartment of Health & Community ServicesPublic Health DivisionLISA MARIE PRITCHARD, BSC, MSCResearch Support OfficerPublic Health Agency of CanadaCentre for Communicable Diseasesand Infection ControlMARGARET GALE-ROWE, MD, MPH, DABPMManager, Community Associated InfectionsPublic Health Agency of CanadaCentre for Communicable Diseasesand Infection ControlJENNIFER VERKOEYEN, RN, BSCNPublic Health NurseHealthy Sexuality & Risk Reduction ProgramOttawa Public HealthJENNY HEATHCOTE, MBBS, MD, FRCPProfessor of Medicine, University of Toronto;Head, Patient Based Clinical ResearchToronto Western Research InstituteToronto Western HospitalCOLINA YIM, RN(EC), MNNurse PractitionerToronto Western Hospital Liver CenterUniversity of TorontoCATHY LATHAM-CARMANICO, RN, BSCNNurse ConsultantPublic Health Agency of CanadaCentre for Communicable Diseasesand Infection Control

VI PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCECONTRIBUTORSPUBLIC HEALTH AGENCY OF CANADACENTRE FOR COMMUNICABLE DISEASES AND INFECTION CONTROLJane Njihia, MHScJosie Sirna, BSc, MScMaxim Trubnikov, MD, MSc, PhDHong-Xing Wu, MD, MSc, PhDCENTRE FOR IMMUNIZATION AND RESPIRATORY INFECTIOUS DISEASESMarie-Pierre Gendron, MScJulie Laroche, BSc, PhD

REPORTTITLE GOESHERE 11PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEINTRODUCTION*KEY FACTS AND FIGURES HBV is a vaccine-preventable disease that is highlyinfectious—far more so than either HIV or HCV.It is transmitted through perinatal, percutaneous,or sexual exposure to an infected person’s blood/body fluids; household contacts exposed to aninfected person are also at risk of infection.Acute and chronic HBV infections are frequentlyasymptomatic or present with nonspecificsymptoms; about two-thirds of chronically infectedpeople are unaware of their status, and mostwill only be detected through proactive screening. Of those infected as adults, 5% will becomechronically infected; in contrast, about 90%of infants infected at birth will developchronic infection.(1) Without intervention, 15%–40% of chronicallyinfected people will go on to develop cirrhosis,end-stage liver disease, and/or HCC.HBV is a notifiable disease in all provinces and territories in Canada.As such, it must be reported to the regional/local Medical Officer of Health.EPIDEMIOLOGY OF ACUTE AND CHRONIC HBV IN CANADAAcute HBV: Canada is a region of low endemicity;however, certain vulnerable populations aredisproportionately affected. These include Aboriginalpeoples, MSM, street-involved youth, and peoplewho are or have been incarcerated.(2) Peak incidenceis among those aged 30–39 years. The mostcommonly identified risk factors are high-risksexual activities and injection drug use.Canada has had universal HBV immunizationprograms in place since the mid-1990s. All provincesand territories have programs that target childrenaged 9–13 years, and some have also implementeda neonatal immunization program.(3) In addition, someprovinces/territories provide coverage for high-riskindividuals, but eligibility varies across jurisdictions(see Module 10). Despite the success of theseprograms, there may be many who remain at riskof acquiring HBV.Immunization contributes to disease control by interrupting disease transmissionand decreasing the pool of susceptible people. It is essential to identifythose at risk who would benefit from receiving the HBV vaccine.Chronic HBV: It is estimated that less than 1% ofCanadians are chronically infected with HBV; innorthern regions, serosurveys have documented theprevalence of chronic HBV at 3%–4%.(4, 5) Althoughthe number of studies is limited, data suggest thatup to 70% of chronically infected Canadians areimmigrants from regions of high endemicity.Screening immigrants from these regions will identifychronically infected individuals who can benefit frommonitoring and medical management (secondaryprevention); doing so will also permit vaccination ofsusceptible contacts, particularly infants and youngchildren who are at risk of developing chronicinfection (primary prevention).There is an urgent need to screen, diagnose, and treat (where appropriate) chronic HBV infectionso as to reduce associated morbidity and mortality and to prevent further transmission.*This Quick Reference does not supersede any provincial/territorial legislative, regulatory, policy and practice requirements or professionalguidelines that govern and inform the practice of care providers in their respective jurisdictions.

2 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEMODULE 1: WHO SHOULD BE TESTED FOR HBV?In low-risk populations, routine screening for chronic infection or immunity is not recommended. Testingto determine immune status and/or to detect chronic infection is indicated for those at risk of exposure;susceptible people should be immunized.Clinicians should maintain a high index of suspicion for HBV as infection isfrequently asymptomatic; 30% of infections have no identified risk factors.(6)The decision to screen and the selection of tests should be based on a thorough review of the following: Self-reported HBV immunization historyand/or documentation Results of previous testing Presence of risk factors for HBV infectionRisk factors for HBV infection (current or past)—screen routinely at first visit:(3,6,7) Birth in a region with intermediate orhigh endemicity†Canada before 1970† Infant of HBsAg-positive mother† Exposure before 7 years of age (e.g., child’simmediate and/or extended family immigratedfrom a region of intermediate/high endemicityand/or child visited such a region)†WHO TO SCREEN Transfusion recipient/medical procedure in Family history of hepatitis B or hepatoma† Exposure to HBsAg-positive person (e.g.,percutaneous, sexual/household contact)‡ High-risk sexual activities (e.g., unprotected sex,multiple sexual partners)‡ Substance use with sharing of equipment(e.g., injection/inhalation drug use)‡ Exposure to blood/blood products in endemic Use of shared/contaminated materials orequipment (e.g., instruments/tools used forpersonal services procedures such as tattooing/piercing/body modifications, or any alternativehealth care that has the potential to break the skin)‡ Use of shared/contaminated medical devices(e.g., glucometers)‡ Occupational exposure to blood/body fluids‡ Travel to/residence in a region of intermediate/high endemicity‡ Incarceration‡ Institutionalization (particularly in institutions forthe developmentally challenged)‡regions without routine precautions/screening†Special clinical considerations—screen routinely: Pregnancy Planned therapy with immunosuppressive/ HIV or HCV infection Immunocompromisedimmunoregulatory agents (e.g., rituximab—increased risk of hepatic flares or reactivationof hepatitis B)Identification of any risk factor is an indication for screening.†Most commonly identified risk factors for chronic HBV infection.‡Most commonly identified risk factors for acute HBV infection in susceptible individuals; indications for vaccination; consider screeningfor HIV/STI in select cases.MODULE 1

REPORTTITLE GOESHERE 33PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEIndividuals born in regions with intermediate or high endemicityare at particular risk of having chronic HBV infection.WHERE IS YOUR PATIENT FROM?Reproduced with permission from NEJM 359:14 October 2008(8)Screening populations at high risk of chronic HBV infection is essentialto identify anyone who can benefit from monitoring and treatment.WHO TO TESTIn the absence of any identified risk factors, clinicians should test anyone who presents with anyof the following: Clinical and laboratory findings suggestive ofchronic liver disease: Signs and symptoms of acute hepatitis:»» RUQ abdominal discomfort, fatigue,»» Abnormal liver biochemistry is usually thefever, nausea, vomiting, malaise, abnormalliver biochemistry, jaundice, dark urine,rash, arthralgiaonly finding»» Hepatomegaly, splenomegaly, and jaundiceare late findings Diagnosis of HCC»» Thrombocytopenia Previous diagnosis of other liver diseaseMODULE 1

4 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEMODULE 2: APPROACH TO HBV SCREENINGAND TESTINGOVERVIEW OF HBV SEROLOGICAL MARKERSAcute HBV with recovery(9)Chronic HBV(10)SymptomsHBeAgAcute(6 months)anti-HBeChronic(Years)HBeAgTitreTotal anti-HBcanti-HBeHBsAganti-HBc IgMHBsAganti-HBsTitreTotal anti-HBcanti-HBc IgM*0481216202428323652100048Weeks after Exposure1216202428323652YrsWeeks after Exposure* May reappear during flares of activitySIGNIFICANCE OF HBV SEROLOGICAL MARKERSHBsAg (surface antigen) indicates infection.Persistence of HBsAg for 6 months or more indicateschronic infection. However, up to 50% of peoplewith extended chronic infection will eventually clearHBsAg. By contrast, those with resolving acute HBVwill clear HBsAg several months after initial infection.Anti-HBs (surface antibody) is a protective antibodyproduced with recovery from infection or in responseto immunization. Over time, titre may decline toundetectable levels. NOTE: There is a gap of severalweeks to months between the disappearance ofHBsAg and the appearance of anti-HBs; during thisperiod, anti-HBc total is detectable as a marker ofHBV infection.Anti-HBc IgM (core antibody—IgM) appears early inacute HBV infection and persists for about 6 months.It may also be seen in chronic infection during flaresof activity, so clinical/epidemiological correlation isrequired for interpretation.MODULE 2Anti-HBc total (total core antibody—IgM and IgG)is a marker of past exposure or current infection. IgGusually persists for life. In low prevalence populations,a finding of isolated anti-HBc may signify a falsepositive result.HBeAg (e-antigen) is a marker of viral replication;its presence indicates high infectivity. Implications forliver injury vary with stage of infection (see Module 7for significance).Anti-HBe (e-antibody) appears with recovery fromacute infection. In chronic infection, the presenceof anti-HBe is generally a marker of reduced viralreplication, indicating a less infectious state. Theimplications for liver injury vary with stage of infection(see Module 7 for significance).

REPORTTITLE GOESHERE 55PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEAPPROACH TO TEST SELECTIONThe choice of tests should be based on patient history and clinical presentation.Screening to detect infection or determineimmune status§ in asymptomatic patientsat risk of acute or chronic infection: HBsAg, anti-HBs anti-HBc IgM—in case of recent knownor suspected exposureBaseline screening to assess need for PEP(i.e., immune status unknown and recenthigh-risk exposure):** HBsAg, anti-HBsScreening in patients with definedclinical conditions: HBsAg, anti-HBsPost-immunization screening§ for thosewith ongoing exposure or risk of exposure(e.g., HBV-positive sexual partner, injectiondrug use): anti-HBsTesting to confirm diagnosis in patients withclinical or laboratory findings consistentwith acute hepatitis: HBsAg, anti-HCV, anti-HAV IgMIf these are negative, test for:»» HBsAg at first prenatal visit or at delivery»» HEV, HCV-RNA»» Consider other infectious causes (e.g.,Before starting immunosuppressive therapy(e.g., prednisone, azathioprine, chemotherapy,infliximab, rituximab)»» HBsAg (plus anti-HBc if to receive rituximab) Pregnancy (in the absence of identified risk factors)if there is no documented result on file Pre-immunization screening of high-riskpopulation:§CMV, EBV, HSV) or non-infectious causes(e.g., hepatotoxic drugs, autoimmunehepatitis, Wilson’s disease, vascular causes,or other pre-existing chronic liver diseases)Known HIV or HCV infection(3,11)»» HBsAg, anti-HBs, anti-HBc (total) Immunocompromised»» HBsAg, anti-HBc (total)§Refer to the Canadian Immunization Guide (CIG) or to your provincial/territorial guidelines for a discussion of pre- and post-immunizationtesting for HBV serologic markers.**Refer to the Canadian Immunization Guide (CIG) or to your provincial/territorial guidelines for recommendations for managementand follow-up including PEP.MODULE 2

6 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEMODULE 3: INTERPRETATION OF HBV DIAGNOSTICTEST RESULTSHBV SEROLOGICAL MARKERSHBsAganti-HBsanti-HBc(total)anti-HBc IgMInterpretation and recommended nateNegativePositive*,†NegativeN/AImmune due to vaccinationCounsel as outlined in Module 11NegativePositive‡PositiveN/AImmune due to previous infectionCounsel as outlined in Module te infectionRefer to Module 4 and counsel as outlined in Module chronic infectionRefer to Module 4 and counsel as outlined in Module 11NegativeNegativePositive NegativeFour possible interpretations(12)See below and counsel as outlined in Module 11*About 5%–10% of people will not respond to the vaccine or else do not produce protective levels of antibody post-vaccination(i.e., 10 IU/ml).†Levels of anti-HBs may decline over time and become undetectable.‡A small percentage of people with chronic infection will have both HBsAg and anti-HBs markers present.§Since anti-HBc IgM can be detected in acute HBV, this test may be helpful when acute infection is suspected. It may also reappearin a flare of chronic infection. On rare occasions, an isolated anti-HBc total will be the only detectable marker. Although there are four possible interpretationsfor this finding, it is more common in immunocompromised people and in those who are co-infected with HIV or HCV. In low prevalence populations this finding is most often a false positive result or due to lab error. Repeat test if lab error is suspected. Less frequently this finding may reflect» resolving acute infection before the appearance of anti-HBs» natural immunity with undetectable anti-HBs due to a decline in antibody titre over time Rarely, this finding may represent a chronic infection with undetectable HBsAg.» Consult a specialist for guidance.MODULE 3

REPORTTITLE GOESHERE 77PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEMODULE 4: INITIAL MANAGEMENT OF PATIENTSWITH HBsAg-POSITIVE RESULTSLaboratory reports HBsAg-positive resultLocal public health department asper provincial/territorial legislationPrimary care provider Advises patient of positive result Advises patient that HBV is reportableto public health; reports to local publichealth department if not reported bylaboratory staff Reviews history (including family history)and risk factors (see Module 1) Conducts physical assessmentand follow-up testing Initiates contact investigation andfollow-up where possible Screens contacts (see Module 2for test selection) and vaccinatessusceptible individuals Assesses need for/initiates PEP Conducts source caseOngoingcommunicationfor casemanagementand follow-upinvestigation Assists with contact notificationand follow-up (all contactsshould be located and offeredvaccine /- HBIg if they do notshow evidence of past exposure/immunity (see Module 10) Vaccinates contacts throughpublic health clinics or facilitatesprimary care providers’ accessto free vaccine Provides patient and HCPeducational materials(see Module 11)for contacts with acute exposures(see Module 10) Provides education and counsellingbased on identified risk factors andprovisional diagnosis (see Module 11)Suspectedacute HBV(see Module 5)Suspectedor confirmedchronic HBV(see Module 6)MODULE 4

8 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEMODULE 5: NATURAL HISTORY AND MANAGEMENTOF ACUTE HBVINCUBATIONThe incubation period ranges from 45–180 days (average is 60–90 days).(1)SIGNS AND SYMPTOMSWhereas infants and children rarely have symptoms, 30%–50% of adults are symptomatic.(1) Symptoms tendto be insidious and can include fatigue, malaise, fever, nausea, vomiting, anorexia, rash, arthralgia, dark urine,and abdominal discomfort. Most will have elevated ALT/AST; a small proportion will develop acute ictericviral hepatitis.A flare of chronic HBV may present like acute HBV, and should be included in the differential diagnosis.RESOLUTION TIME AND CLINICAL COURSE OF INFECTIONThe majority (95%) of immunocompetent adults will recover within 6 months and develop lifelong immunity;the remainder will be chronically infected. Immunocompromised adults are at particular risk of developing chronicinfection. The risk of developing chronic infection is also much higher for those who acquired the infection ininfancy (70%–90%) or before 7 years of age (10%–30%).(3,13,14)Acute HBV does not require antiviral treatment. Management should focus on relief of symptoms, monitoringand prevention of hepatic complications, as well as counselling aimed at preventing transmission. Persistenceof HBsAg for 6 months indicates chronic infection.Baseline laboratory testing to assess liver function and screen for other infections: Bilirubin (total and direct), albumin, INR (PT), creatinine ALT, AST, ALP CBC anti-HBc IgM (if not already done) Testing for STIs, including HIV, and for HCV, where appropriate Repeat HBsAg at least 6 months after baseline, to confirm/rule out chronic infection.(NOTE: symptomatic patients may demonstrate seroconversion and recovery from acute infectionat 3 months from baseline). See Module 6 for additional testing recommendations for those withconfirmed chronic HBV.MODULE 5

REPORTTITLE GOESHERE 99PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCEACUTE HBV WITH SEVERE PRESENTATIONPresentation of acute HBV as fulminant hepatitis is uncommon but can nevertheless be life threatening.Those most at risk include patients with pre-existing chronic liver disease of any etiology. Manifestationsinclude fatigue, jaundice, altered mental status (encephalopathy), and abdominal swelling (ascites).In patients with chronic HBV infection, spontaneous flares of disease or flares precipitated by withdrawalfrom immuno suppressive therapy can result in fulminant hepatitis. It is important to maintain a high indexof suspicion and watch for signs of impending liver failure (see below).Indications for urgent and immediate referral to a specialist: Worsening symptoms/signs of liver failure (e.g., encephalopathy) Laboratory tests indicating deteriorating liver function or liver failure»» Elevated or rising INR»» Elevated or rising bilirubin»» Low or falling platelet countMODULE 5

10 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEMODULE 6: INITIAL EVALUATION OF CONFIRMEDCHRONIC HBV(2)Baseline clinical evaluation includes: History, particularly risk factors for hepatitis acquisition, and family history of liver disease including HCC Physical examination to look for signs of liver failure (e.g., jaundice, ascites, encephalopathy)Initial laboratory evaluation HBeAg/anti-HBe,* quantitative HBV DNA (viral load)* ALT,*† AST, ALP, bilirubin (total and direct) CBC, albumin, INR (PT)‡ Creatinine anti-HAV (IgG) (vaccinate if negative) HIV-antibody testing, if not already done HCV-antibody testing, if not already doneImaging Abdominal ultrasoundAll patients with chronic HBV should be referred to a specialist at some point.There are certain situations where referrals should be expedited.Indications for urgent referral to a hepatologist: Signs of liver failure—acute or chronic Pregnant patients (HBV DNA detected during pregnancy) Imaging results suggestive of HCCIndications for semi-urgent referral: Co-infection with HCV or HIV (refer to a hepatologist or an infectious disease specialist/primary carephysician experienced in HIV and hepatitis care) Suspected cirrhosis‡ (provide counselling as outlined in Module 11)*HBeAg status, ALT, and viral load will determine long-term management (i.e., monitoring/consulting versus referral to a specialistfor treatment—see Module 8).†The ULN of ALT for men is 30 U/L; for women, 20 U/L. NOTE: liver injury may be present despite normal ALT.‡IMPORTANT NOTE: Decreased platelet count ( 150 x 109/L) is highly suspicious for cirrhosis even if liver biochemistry is normal.MODULE 6

REPORTTITLE GOESHERE 11PRIMARY CARE MANAGEMENT OF HEPATITISB—QUICKREFERENCE 11MODULE 7: NATURAL HISTORY OF CHRONIC HBV(15,16)The natural history and progression of chronic HBV is complex and non-linear,and varies from person to person. Familiarity with the natural historycan help guide decisions related to treatment and monitoring.IMMUNE TOLERANT PHASEThe immune tolerant phase is mainly seen in people infected at birth or in early childhood. During this phase,the body does not recognize the virus as foreign. HBeAg is present; HBV DNA levels are high; ALT levels arenormal; and hepatic fibrosis is minimal or non-existent. Immune tolerant individuals may stay in this phasefor up to 40 years or more before eventually progressing to the immune active phase.HBeAg-POSITIVE IMMUNE ACTIVE CHRONIC HBV PHASEProgression to the HBeAg-positive immune active chronic HBV phase occurs when the host immunesystem recognizes the virus as foreign. During this phase, ALT levels are elevated (sometimes only intermittently);HBV DNA levels are also elevated but not as high as in the immune tolerant phase; and mild to severe liverinflammation with/without fibrosis is found on biopsy. This phase can be prolonged, which may result insevere liver injury. Over 5–25 years, 90% of cases seroconvert to e-antibody-positive, which generally representsa transition to the inactive HBsAg phase.(15) Of these, approximately 4% are at risk of seroreversion (i.e., becomeHBeAg-positive again) with associated flares of activity.(14)HBeAg-NEGATIVE IMMUNE ACTIVE CHRONIC HBV PHASE (anti-HBe POSITIVE)Even after seroconversion to anti-HBe, approximately 20% of people remain in the immune active phase dueto a mutant form of the virus. Their HBV DNA levels are elevated, although these are not as high as in theHBeAg-positive immune active phase, and ALT is elevated (this may be intermittent). Depending on the hostimmune response during this phase, liver injury may occur, increasing the risk of progression to cirrhosis and HCC.INACTIVE HBsAg PHASEMost people enter the inactive HBsAg phase after they undergo seroconversion to anti-HBe positive. This phaseis characterized by an HBeAg-negative status, normal ALT, and low levels of HBV DNA (often undetectable byPCR). Most individuals (70%–80%) remain in this inactive phase for life. An estimated 20% risk reactivating to the HBeAg-negative or returning to the HBeAg-positive immuneactive phase. They can have hepatitis flares over their lifetime, which in turn can lead to cirrhosis or HCC.Either initiation of, or withdrawal from, immunosuppressive therapy may precipitate reactivation. Increasing ALT and HBV DNA levels are a sign of reactivation.(17)MODULE 7

12 PRIMARY CARE MANAGEMENT OF HEPATITIS B—QUICK REFERENCEHBsAg CLEARANCEOver many years, 50% of chronically infected individuals who are in the inactive phase will clear HBsAg; of those,most—but not all—will develop anti-HBs. During this phase, individuals who developed cirrhosis pre-clearanceand those who do not develop anti-HBs are at increased risk of HCC. Reactivation (seroreversion to HBsAg-positive) is possible, although rare. Continued monitoring forreactivation is important for patients who remain anti-HBs negative

HAV hepatitis A virus anti-HBc hepatitis B core antibody anti-HBe hepatitis B e-antibody anti-HBs hepatitis B surface antibody HBeAg hepatitis B e-antigen HBIg hepatitis B immune globulin HBV hepatitis B virus HBsAg hepatitis B surface antigen HCC hepatocellular carcinoma HCP healthcare provider HCV hepatiti

Related Documents:

Hepatitis C 2 What is hepatitis C? Hepatitis C is a disease caused by a virus that infects the liver. This virus, called the hepatitis C virus or HCV for short, is just one of the hepatitis viruses. The other common hepatitis viruses are A and B, which differ somewhat from hepatitis C in the way they are spread and treated.

Mar 22, 2010 · with hepatitis B and hepatitis C can vary considerably between, and within, countries and therefore, even in areas of low overall prevalence, rates in certain sub-populations can be very high.3 Both hepatitis B and hepatitis C are efficiently transmitted through contact with infected bloo

atitis B, the hepatitis B surface antigen (HBsAg).1 According to a recent report from the Institute of Medicine (IOM), most obstetrical care providers do screen pregnant women for hepatitis B and ad-vise that newborns of HBsAg-positive mothers receive both hepatitis B im-mune globulin and hepatitis

Hepatitis B and D by Robert Perrillo and Satheesh Nair, pp. 1647-1679. Sources of Infection for Persons with Hepatitis C (CDC) US.png Wedemeyer, H. Hepatitis C. Gastrointestinal and Liver Disease. 2016 Vol 2, 10th edition, 1309-1321. Wells J and Perillo R. Hepatitis B. Gastroi

HBeAg Hepatitis B Virus Early Antigen HBIg Hepatitis B Immune globulin HBs Ag Hepatitis B surface Antigen HBV Hepatitis B Virus HCC Hepatocellular Carcinoma Y _ 3DJH 9LUDO HSDWLWLV % DQG & *XLGHOLQHV HCV Hepatitis C Virus HCWs Community Health Workers HIV Human immunode

Hepatitis B virus (HBV) and hepatitis C virus (HCV) can cause acute and chronic hepatitis and potentially lead to the development of cirrhosis, liver cancer and death. In the EU/EFTA, an estimated 4.7 million people have a chronic hepatitis B virus infection, and 3.9 million people have chronic

Federal Bureau of Prisons Prevention and Treatment of Hepatitis A Clinical Guidance November 2018 2 4. NATURAL HISTORY The INCUBATION PERIOD is the period of time from infection with HAV until the onset of hepatitis symptoms. The average INCUBATION PERIOD for hepatitis A is 28 days (ranging from 15—50 days). Hepatitis A dise

President Judy Harris president.sydneyu3a@gmail.com VP Education Anne Richardson vpeducation.sydneyu3a@gmail.com VP Public Relations TBA Treasurer Ivona Kadlec sydu3a.treasurer@gmail.com Secretary Pamela Frei secretary.sydneyu3a@gmail.com Admin Manager Lynda Cronshaw officemgr.sydneyu3a@gmail.com Course Listing Order Course Delivery Booking a Course Insurance Principal Officers . 5. REGIONAL .