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Describe the pathogenesis, mode of transmission, risk factors, and epidemiology for Hepatitis A, B, C, D, E, and G Accurately interpret patients serology.

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Presentation on theme: "Describe the pathogenesis, mode of transmission, risk factors, and epidemiology for Hepatitis A, B, C, D, E, and G Accurately interpret patients serology."— Presentation transcript:

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2 Describe the pathogenesis, mode of transmission, risk factors, and epidemiology for Hepatitis A, B, C, D, E, and G Accurately interpret patients serology and other appropriate markers for diagnosis of viral hepatitis Identify patients requiring treatment and formulate treatment plans for each type of viral hepatitis Identify appropriate means for prevention of viral hepatitis including vaccination or passive immunity

3 Systemic viral infection lasting 6 months Progresses through stages: incubation, hepatitis (symptoms), convalescence Acute Serologic evidence of hepatitis > 6 months Increases risk for cirrhosis, chronic liver disease and hepatocellular carcinoma Not associated with hepatitis A or E Chronic Progress quickly from hepatitis to hepatic failure due to hepatic necrosis High mortality (80%) Fulminant

4 Viruses are not directly cytopathic Host immune response to the virus causes liver inflammation and hepatitis Normal liverCirrhosis Hepatic Carcinoma

5 Identified in 1973 RNA virus Nonenveloped 7 distinct genotypes Replication in hepatocytes and gastrointestinal cells with RNA polymerase

6 Fecal – oral route Person to person Food borne or waterborne exposure Less common Sexual contact Blood transfusions IV drug use

7 Travelers to endemic countries MSM Illegal drug users Patients with clotting disorders Primate handlers Medical personnel Close contact with infected persons Day care workers Food – handlers Patients with chronic liver disease

8 Worldwide – 1.4 million cases annually US – In 2007: 92% decline since vaccine in ,979 acute cases reported Adjustment for underreporting ~ 25,000 cases Cyclic recurrences Inversely proportional to level of sanitation

9 HAV Endemicity RegionsAvg. age of patients Likely mode of transmission Very highAfrica, South America, Middle East, SE Asia Under 5 Person – person Contaminated food/water HighBrazils Amazon basin, China and Latin America 5-14 Person – person Outbreaks/ food or water IntermediateSouthern and Eastern Europe 5-24 Person – person Outbreaks/ food or water LowAustralia, USA, Western Europe 5-40 Outbreaks Very lowNorthern Europe and Japan Over 20 Exposure during travel to endemic area

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11 Patients may have an inapparent or subclinical hepatitis Children OR Patients develop anicteric or icteric hepatitis ranging from mild and transient to severe and prolonged HAV does not cause a chronic hepatitis

12 Incubation – HIGH TRANSMISSION! days while patient asymptomatic and virus replicating Prodromal Lasts several days - one week when symptoms appear Fatigue, decreased appetite, abdominal pain, nausea/vomiting/diarrhea, fever Icteric Jaundice develops and bilirubin levels mg/dL within 10 days of initial symptoms Feces still infectious for 1-2 weeks Possible fulminant hepatitis Convalescence - resolution is slow but uneventful Possible relapse in 3-20% of patients with 4-15 weeks

13 Serologic testing Anti – HAV IgM Always present in acute infection Appear 5-10 days before symptoms appear Anti – HAV IgG Persists lifelong and indicates past infection If BOTH present then ACUTE infection! Liver function assessment

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15 Self limiting disease Supportive treatment Diet, rest, fluids, avoidance of alcohol and hepatotoxic drugs Hospitalization typically not necessary INR and LFTs to identify progression to fulminant hepatitis Mortality 0.1% (children) – 2.1% (> 40 years)

16 Good hygiene Hand-washing, sanitary diaper handling, proper food preparation, travel precautions Hepatitis A vaccine Immune globulin

17 3 inactivated vaccines HAVRIX ®, VAQTA ®, TWINRIX ® (Hep A and B) Immunity lasts ~ 25 years Vaccine# of DosesDoseSchedule HAVRIX ® 12 mo. to 18 yr 19 years mL (720 units) 1 mL (1440 units) 0, 6-12 months VAQTA ® 12 mo. to 18 yr 19 years mL (25 units) 1 mL (50 units) 0, 6-12 months TWINRIX ® 18 years 3 or 4 1 mL (720 units) 0, 1, 6 months 0, 7, 21 days, + 1yr

18 Immune Globulin Passive immunity thru transfer of HAV antibodies For travel < 3 months: 0.02 mL/kg IM Travel 3-5 months: 0.06 mL/kg IM Alternative prophylaxis for patients who dont need long term protection IG can interfere with response to live vaccines (MMR, varicella, etc.) Prefer vaccine for prevention but can be used for children < 12 months and patients allergic to vaccine

19 Persons receiving vaccine within 2 weeks of exposure do not need post exposure prophylaxis Patients not previously vaccinated and within 2 weeks of exposure to HAV 12 months to 40 years: Single age appropriate dose of Hep A vaccine > 40 years, < 12 months, chronic liver disease, allergic to vaccine, immunocompromised Use HVIG mL/kg

20 AJ is a 47 year old white male who works as a photographer for National Geographic. His most recent expedition is scheduled in 3 weeks to take him to Mali, West Africa. Should AJ receive preventative measures for Hepatitis A? If so, what should we recommend? If AJ did not receive preventative treatment what could be done if he was exposed to HAV? Is AJ likely to have long term consequences of HAV exposure?

21 DNA virus Double-stranded, enveloped 8 major genotypes (A-H) Replicates in hepatocytes via RNA polymerase Can cause both acute and chronic hepatitis

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23 More than 2 billion people worldwide > 350 million with chronic HBV 75% in the Asian Pacific region In 2007, ~43,000 acute cases of HBV in US 800,000 – 1.4 million people in US are chronic carriers Responsible for 60-80% of primary liver cancers Mortality ~620,000 deaths worldwide each year

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25 Activities that involve percutaneous or mucosal contact with infectious blood or body fluid Sex with infected partner IV drug use Perinatal transmission Contact with open sore Needle sticks Sharing razors, toothbrushes, etc.

26 Individuals born in areas with high or intermediate prevalence rates Patients not vaccinated as children Sexual contact with HBV infected IV drug users (past or current) Patients with STDs MSM Inmates Chronic elevation of AST/ALT Persons infected with HCV or HIV Hemodialysis patients All pregnant women Patients on immunosuppressive medications

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28 AntigenMeaning HBsAg Hepatitis B Surface Antigen - Indicates the person is infectious - Found in high levels during acute and chronic infection - Used to make the HBV vaccine HBcAg Hepatitis B Core Antigen - Indicates acute or chronic infection - Not found with vaccine HBeAg Hepatitis B Envelope Antigen - Associated with the nucleocapsid gene found during acute and chronic HBV - Presence indicates replicating virus and high levels of HBV

29 AntibodyMeaning Anti-HBs Antibody to HBsAg - Indicates recovery and immunity from HBV - Develops after successful vaccination Anti-HBc - IgM - IgG Antibody to HBcAg - Appears at onset of symptoms and persists for life - Indicates a previous or ongoing infection - IgM suggests acute HBV; IgG usually chronic Anti-HBe Antibody to HBeAg - Seroconversion - Predictor of long term clearance of HBV and low levels of HBV DNA

30 HBsAg Anti-HBc Anti-HBs Negative Susceptible HBsAg Anti-HBc Anti-HBs Negative Positive Immune due to natural infection HBsAg Anti-HBc Anti-HBs Negative Positive Immune due to vaccination HBsAg Anti-HBc IgM anti-HBc Anti-HBs Positive Negative Acutely infected HBsAg Anti-HBc IgM anti-HBc Anti-HBs Positive Negative Chronic infection HBsAg Anti-HBc Anti-HBs Negative Positive Negative Unclear - resolved infection, false (+) anti- HBc, low level chronic infection, resolving acute infection

31 Presence of HBsAg and IgM anti-HBc Incubation period – 45 to 180 days If symptomatic – N/V, abdominal pain, fatigue, arthralgias, with or w/o jaundice Drastically increased LFTs – specifically ALT ~5% of adults and 90% of infants (perinatal transmission) progress to chronic infection < 1% progress to fulminant hepatic failure No specific treatment for acute HBV

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33 Persistence of HBsAg for > 6 months Active carrier – HBeAg (+), HBV DNA > 20,000 IU/mL, AST/ALT elevations Inactive carrier - Anti-HBe (seroconversion) and HBV DNA < 2,000 IU/mL, normal LFTs 67-80% of patients with seroconversion (Anti-HBe formation) will become inactive carriers ~20% progress to cirrhosis and 5% to hepatocellular carcinoma

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35 Seen in 10-20% of patients Transient serum sickness-like syndrome Fever, rash, arthritis – precedes jaundice Acute necrotizing vasculitis Arthritis, renal disease, HTN, heart disease, skin manifestations Membranous glomerulonephritis Papular acrodermatitis Skin lesions with lymphadenopathy

36 Papular Acrodermatitis Acute necrotizing vasculitis

37 Goals of treatment Suppress virus and achieve HBeAg seroconversion and undectable HBV DNA Stop or reduce hepatic inflammation Prevent development of hepatic decompensation Decrease progression to cirrhosis and HCC

38 HBsAg (+) > 6 months ALT < 1x ULN - ALT Q 3-6 mos. - HBeAg Q 6-12 mos. ALT 1-2x ULN - ALT Q 3 mo. - HBeAg Q 6 mo. - ? Biopsy (>40 yr, FHx) - * Tx as needed ALT > 2x ULN - ALT, HBeAg Q 1- 3 months - *Tx if persistent HBV DNA > 20,000 or jaundice HBeAg (+) * If HBV DNA > 20,000 IU/mL after 3-6 months of ALT 1-2x ULN consider tx

39 HBsAg (+) > 6 months ALT < 1x ULN HBV DNA < 2000 IU/mL - ALT Q 3 month x 1 yr then Q 6-12 months ALT 1-2x ULN HBV DNA 2,000-20,000 IU/mL - ALT and HBV DNA Q 3 months - ? Biopsy - * Tx as needed ALT > 2x ULN HBV DNA > 20,000 IU/mL - Tx if persistent - ? biopsy HBeAg (-) * Tx based on results of biopsy or persistent viremia

40 Available agents for HBV Interferons (non-pegylated and pegylated) Nucleoside analogs (lamivudine, entecavir, telbivudine) Nucleotide analogs (adefovir and tenofovir)

41 MOA Antiviral effects Immunomodulatory effects Antiproliferative effects Place in therapy Best response if high pretreatment ALT and low HBV DNA First line for compensated liver disease Doses INF α-2b : 5-10 MU SQ 3 times weekly HBeAg (+) for weeks HBeAg (-) for months Peg-INF α-2a : 180 mcg SQ once a week HBeAg (+) and (-) = 48 weeks

42 Side effects Flu-like syndrome (fever, chills, HA, myalgia), anorexia, hair loss, hepatitis flares, emotional lability (anxiety, irritability, depression), pancytopenia, thyroid function changes, retinal damage Contraindications Decompensated hepatic disease or autoimmune diseases (e.g. rheumatoid arthritis, lupus) ? Uncontrolled psychiatric disturbances Dose limiting toxicities – pancytopenias and flu- like syndrome

43 Advantages No drug resistance Finite treatment duration 80-90% of patients have a durable response Once weekly dosing with PEG-IFN Disadvantages Poor tolerability due to side effects Relapse is common in HBeAg (-) patients Cant use in decompensated pts Injection

44 MOA Inhibition of DNA polymerase Premature DNA chain termination Class side effects Lactic acidosis Lipodystrophy Pancreatitis Neuropathy

45 Highest levels of drug resistance Up to 70% after 5 years tx Similar efficacy but limited use due to resistance Dose 100 mg PO QD Dose decreased in renal impairment: mL/min – 50 mg QD mL/min – 25 mg QD Duration: HBeAg (+) – 1yr (minimum) and continue for 6 months post seroconversion HBeAg (-) – usually indefinite Well tolerated – HA, fatigue, nausea

46 More potent than lamivudine but cross resistance identified Less resistance than lamivudine 25% at 2 years – limits use Dose 600 mg PO QD Renal impairment: mL/min – 600 mg Q 48 hours <30 mL/min – 600 mg Q 72 hours Duration HBeAg (+) – 1yr (minimum) and continue for 6 months post seroconversion HBeAg (-) – usually indefinite More peripheral neuropathy and myopathy

47 More potent viral suppression and histologic improvement vs. 3TC and ADF Possible use in 3TC and ADF resistant patients May cause some ETV resistance – stop 3TC Rate of ETV resistance is low (<2% at 5 yrs) Dose 0.5 mg PO QD ; 3TC-resistant: 1 mg PO QD Renal impairment: mL/min – 0.25 mg QD mL/min – 0.15 mg QD Duration HBeAg (+) – 1yr (minimum) and continue for 6 months post seroconversion HBeAg (-) – usually indefinite

48 Effective in lamivudine-resistant HBV Must continue lamivudine indefinitely with addition of adefovir Novel resistance mechanism for adefovir Up to 20% resistance at 5 years Dose 10 mg PO daily Renal impairment: mL/min – 10 mg QOD < 20 mL/min – 10 mg every third day Duration HBeAg (+) – 1yr (minimum) and continue for 6 months post seroconversion HBeAg (-) – usually indefinite Nephrotoxicity – check SCr Q 3 months

49 High potency and no resistance Significantly better viral suppression and ALT normalization vs. ADF Effective in 3TC resistant HBV Cross resistant with ADF Dose 300 mg PO QD Renal impairment: mL/min – 300 mg Q 48 hrs mL/min – 300 mg Q hrs Duration HBeAg (+) – 1yr (minimum) and continue for 6 months post seroconversion HBeAg (-) – usually indefinite Fanconi syndrome, renal insufficiency, bone density

50 Interferons Thyroid function tests every 3-6 months, CBC every week for 2 weeks then every month, depression screening every visit HBeAg, HBsAg, HBV DNA at baseline, end of therapy, and 6 months post therapy LFTs every month Nucleoside/tide Inhibitors Drug specific side effects HBeAg + patients – HBeAg and Anti-HBe at the end of 1 yr and every 3-6 months thereafter LFTs and HBV DNA every 3-6 months

51 Increase in HBV DNA > 1 log 10 after initial virologic response Elevated ALT Nucleoside analogs (lamivudine and telbivudine) highest resistance YMDD mutation in HBV Limits use No resistance with IFN or TDF

52 Treatment Resistance Action 3TC resistanceAdd Adefovir (continue 3TC) *Add Tenofovir Adefovir resistanceAdd Lamivudine *Switch or add Entecavir Entecavir resistanceSwitch to Tenofovir Telbivudine resistanceAdd Tenofovir or Adefovir

53 AdvantagesDisadvantages - IFN 5-10 MU SQ TIW - PEG-IFN 180 mcg SQ QWk - Finite tx duration - No resistance - Potent - Q week dosing - Adverse effects - Contraindications - Injection Lamivudine 100 mg QD - PO - Well tolerated - High level of resistance - Prolonged tx duration Adefovir 10 mg QD - PO - Well tolerated - Effective in 3TC resistance - Resistance rising - Nephrotoxicity - Prolonged tx duration Entecavir 0.5 mg QD - PO - More potent - Very little resistance - Well tolerated - ? Use in 3TC and ADF resistance - Prolonged tx duration Telbivudine 600 mg QD - PO - More potent than 3TC - High resistance - Neuropathy, myalgia - Prolonged tx duration Tenofovir 300 mg QD - PO - High potency - No resistance - Use in 3TC resistance - Cross resistance with ADF - Nephrotoxicity

54 Patient Specific CircumstancePreferred Agents HBeAg (+) or HBeAg ( - )Peg-IFN, Entecavir, Tenofovir Decompensated liver disease Tenofovir or Entecavir (lack of data) Lamivudine/Telbivudine + Adefovir/Tenofovir NO INTERFERON! Compensated CirrhosisTenofovir or Entecavir PregnancyTenofovir or Telbivudine (Category B) HIV Co-infection If desire to tx HIV – use combination of 2 HIV/HBV active drugs (3TC + TDF) If not desiring HIV tx – use IFN or ADF

55 All infants Children < 19 yrs not previously vaccinated Susceptible sex partners Person getting treated for any STD MSM IV drug users Health care workers Dialysis patients Travelers to high risk areas Persons with chronic liver disease HIV infected persons Do not have to have any risk factor to be vaccinated

56 Single Antigen Hepatitis B Vaccines AgeDoseSchedule Engerix-B Infant – AdultInfant – 19yrs: 10 mcg >20 yr: 20 mcg HD and IC: 40 mcg 0, 1, 6 months (40 mcg – 0,1,2,6) Recombivax HB Infant – AdultInfants – 19 yrs: 5 mcg >20 yr: 10 mcg HD and IC: 40 mcg 0, 1, 6 months (40 mcg – 0,1,2,6) Combination Hepatitis Vaccines Comvax (HBV& Hib conjugate) 6 wks – 71 months 5 mcg2, 4, months Pediarix (HBV, DTaP, IPV) 6 wks – 7 yrs10 mcg6 wk, 10 wk, 6 months Twinrix (HAV& HBV) > 18 yrs20 mcg0, 1, 6 months ** Single antigen vaccines composed of HBsAg subunits derived from bakers yeast

57 Passive immunity – immediate with 3-6 month duration Should be administered within 48 hours of exposure Administer in conjunction with HBV vaccine Recommendations Neonate born to HBsAg (+) mothers within hours Sexual exposure Susceptible healthcare workers post-exposure Liver transplant patients

58 JM is a 54 year old Asian female who presents to her family physician complaining of unusual fatigue, N/V, and abdominal pain. Since the patient takes care of her mother, who is chronically infected with HBV, the physician decides to do a complete HBV workup along with the routine labs. PMH: Rheumatoid arthritis, hypothyroidism, IBS, dysthymia HBV Panel: HBsAg +, Anti-HBc IgM +, HBeAg +, Anti-HBs – ALT = 29 AST = 18 WBC = 8.9 x 10 3 RBC = 3.2 HGB = 12.4 g/dL CrCL = 89 mL/min What is JMs diagnosis? Does she require therapy?

59 JMs symptoms resolve over the next month and she feels back to normal. Her physician asked her to follow-up with him in 6 months to recheck her lab work. Upon recheck her labs are as follows: HBsAg +, Anti-HBc IgM -, HBeAg +, Anti-HBs – AST = 42 ALT = 63 WBC = 4.2 x 10 3 RBC = 3.1 HGB = 11.9 g/dL What is JMs diagnosis? Should JM be treated? If so, what agent should we recommend?

60 The physician ignores your recommendation (punk!) and starts the patient on lamivudine (3TC) 100 mg daily. After 3 months of therapy JMs HBV DNA=2,100 and ALT=18. How long should therapy be continued? At JMs 6 month visit her HBV DNA=32,000 and ALT=54. What happened? What should you recommend? What adverse effects should you counsel the patient/physician to look out for?

61 CSO6iJDM CSO6iJDM

62 Identified in 1989 RNA virus Enveloped 11 genotypes and > 50 subtypes identified 6 major genotypes Vary in responsiveness to treatment Prohibits vaccine development Can cause both acute and chronic disease

63 Genotype 1a & 1b most common 60% of global infection Type 3 endemic to SE Asia Type 5 exclusive to South Africa Type 6-11 in Asia

64 About 3% of worlds population has HCV Leading cause for liver transplantation Most common chronic blood borne infection in the US 3.2 million persons in US have chronic Hep C Most prevalent in people years old 849 cases of acute hepatitis in US in 2007 Approximately 17,000 adjusted for under reporting

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66 Contact with infected blood or blood products Sharing needles and blood transfusions (prior to 1992) Less commonly spread through sexual contact Monogamous sexual transmission is rare Perinatal transmission less common < 5% of babies born to HCV + mothers are infected

67 Injection drug users Blood transfusions or solid organ transplants prior to 1992 Recipients of clotting factors prior to 1987 Chronic hemodialysis Known exposure to HCV Healthcare workers Recipients of blood or organs from HCV (+) donors HIV infected persons Children with HCV (+) mothers

68 Acute Hepatitis Incubation period 6 – 10 weeks 80% of patients have are asymptomatic Insidious onset of fatigue, N/V, jaundice, abd. pain Chronic Hepatitis 60 – 80 % are asymptomatic Liver biopsy only way to assess progression Cirrhosis Symptoms appear up to 20 years after acute phase – hepatomegaly, splenomegaly, ascites Hepatocellular Carcinoma 70 – 90 % 10 – 20 % 3-5% ~25%

69 Extrahepatic manifestations (1-2% of patients) Cryoglobulinemia Cutaneous vasculitis Renal disease Neuropathy Lymphoma Sjogrens syndrome

70 Cryoglobulinemia and Cutaneous vasculitis

71 Liver function tests: AST, ALT, alk phos, bilirubin, PT/INR, albumin, CBC Initial screening test: Anti-HCV using enzyme immunoassay May not be (+) for up to 6-9 months after onset False negatives common Confirmation test: HCV RNA Present within 1 week of infection IgG and IgM unreliable for diagnosis of acute vs. chronic disease

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73 Determine patients HCV genotype first! Influences treatment regimen and duration Treatment goals – reduce inflammation, prevent progression to fibrosis, cirrhosis, and HCC Responses Early virologic response (EVR): 2-log drop or loss of HCV RNA 12 weeks into therapy Sustained virologic response (SVR): absence of HCV RNA in serum at end of treatment and 6 months later Nonresponders: HCV RNA levels remain stable on tx

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75 > 18 years Abnormal ALT Normal ALT?? Liver biopsy with fibrosis Compensated liver disease Hgb > 13 g/dL for men > 12 g/dL for women Previously treated HCV Transplant recipients Autoimmune hepatitis Untreated hyperthyroidism Pregnant Severe HTN, HF, CAD < 3 years old

76 Predictors of good response Genotype is strongest predictor SVR higher in genotype 2 and 3 (76-82% vs. 42 to 46% of genotype 1) Lower pretreatment HCV RNA Younger age (< 40 yrs) Lower body weight (< 75 kg) Absence of cirrhosis and fibrosis

77 Genotypes 1 & 4 Interferon alfa – 2a or 2b 3 million units SQ three times a week - Or - **Peginterferon alfa-2a (Pegasys) 180 mcg SQ weekly - Or - **Peginterferon alfa-2b (Peg-Intron) 1.5 mcg/kg SQ weekly PLUS Ribavirin 1,000 mg (if 75 kg) PO divided BID HCV RNA at 12 weeks No EVR consider D/CEVR– 48 weeks total tx HCV RNA 24 weeks post tx

78 Genotypes 2 & 3 Interferon alfa – 2a or 2b 3 million units SQ three times a week - Or - **Peginterferon alfa-2a (Pegasys) 180 mcg SQ weekly - Or - **Peginterferon alfa-2b (Peg-Intron) 1.5 mcg/kg SQ weekly PLUS Ribavirin 800 mg PO divided BID Continue tx for 24 weeks HCV RNA at 24 weeks post tx

79 Retreatment Relapsed patients – initial SVR but subsequent increase in HCV RNA Re-treat with peg-IFN + ribavirin if initially treated with IFN Try second round if already used peg-IFN + ribavirin Nonresponders – no initial SVR Try peg-IFN if previously on IFN Do not re-treat with peg-IFN if already tried Decompensated cirrhosis Liver transplantation Low doses of antiviral therapy

80 MOA: Synthetic nucleoside analog which inhibits HCV DNA polymerase Dose: Based on weight and genotype (refer to algorithm) AEs: Hemolytic anemia, neutropenia, decreased Hgb, fatigue, itching, rash, sinusitis, hyperuricemia, insomnia, depression, myalgias

81 CI: Pregnancy, CrCL < 50 ml/min, severe heart disease, bone marrow suppression Monitoring: CBC, LFTs, uric acid at initiation and every 2 weeks for 8 weeks then every 4 weeks, TSH every 12 weeks Pregnancy test at initiation & Q month until 6 months after D/C Toxicity: Dose decreased for Hgb < 10 D/C if Hgb drop to < 8.5 in patients w/o cardiac history or if Hgb < 12 after dose adjustment

82 There is no vaccine or IG for HCV No post exposure prophylaxis Screening and treatment of blood products Safe injection practices Monogamy Adequate sterilization of reusable instruments (dental equipment)

83 NK is a 34 year old, 65 kg, white female who is a single mom of 2 working as a high school chemistry teacher. During her college days at LA Tech, NK experimented a few times with IV heroin. She says she was young and stupid and always thought her friends were healthy so she didnt mind sharing needles. She says she only used heroin about 5 times and 15 years ago. Today she presents to her physician with generalized fatigue (which she attributes to her busy schedule as a single mom) and some abdominal pain. Her physician performs a full work-up. PMH: Appendectomy at 15 yr, allergic rhinitis, hypertension WBC = 5.4 x 10 3 RBC = 2.9 HGB = 13.1 g/dL AST = 25 ALT = 29 CrCL = 100 mL/min Anti-HBs +, Anti-HBc -, HBeAg – Anti-HCV +, HCV RNA 5.8 log 10 IU/mL

84 What is NKs diagnosis? Does she need treatment? If so, what information do you need before recommending a treatment regimen? What treatment regimen do you recommend? What drug specific problems should we monitor for? When does NK need to return for monitoring for response?

85 NK returns to the office for her follow-up labs. WBC = 4.4 x 10 3 RBC = 3.1 HGB = 11 g/dL AST = 21 ALT = 23 Anti-HCV +, HCV-RNA = 2.5 log 10 IU/mL Is NK responding to therapy? How much longer should she be treated? What should be done after NK finishes treatment?

86 RNA virus Requires HBV to replicate Prevalence similar to HBV Blood borne or sexual transmission Either a coinfection or superinfection with HBV Coinfection usually acute and self limiting with <5% progressing to chronic HDV Superinfection severe acute hepatitis and 80% progress to chronic HDV 60-70% will develop cirrhosis

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88 Persons at risk: Anyone with chronic HBV infection Same risks for HBV (IV drug use, sexual promiscuity, blood products, etc.) Patients not vaccinated against HBV Prevention & Treatment No vaccine specifically for HDV HBV vaccination prevents HDV No IG for HDV Treatment not currently recommended

89 RNA virus Transmission via fecal-oral route Waterborne spread Causes an acute hepatitis similar to HAV Not associated with chronic inflammation or HCC High mortality rate in pregnancy (~20% in 3 rd trimester) No vaccine or IG Treatment not usually required

90 RNA virus Transmitted via infected blood products, sexually, perinatally Usually presents as a coinfection with HBV, HCV, or HIV Patients dont display typical hepatitis symptoms ? If this is a true hepatitis virus No vaccine or prophylaxis


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