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 Zambia HIV National Guidelines
 


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 Guide Editors
 Editor In Chief
    Joel E. Gallant, MD, MPH

Pharmacology Editor
    Paul Pham, PharmD, BCPS

Zambia Guideline Team
   Peter Mwaba MMed PhD FRCP
   Alywn Mwinga MMed
   Isaac Zulu MMed MPH
   Velepie Mtonga MMed
   Albert Mwango MBChB
   Jabbin Mulwanda MMed FCS
 

 

 

Diagnosis>Opportunistic Infections>
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Hepatitis C

Joel E. Gallant, MD, MPH and Christopher Hoffmann, MD, MPH
06-04-2009

Zambia Specific Information

  • Prevalence of HCV unknown in Zambia, but likely to be low (1-5%) based on limited studies and data from other southern African countries
  • HCV-antibody testing more commonly associated with HIV cross-reactivity and false positives in Africa than elsewhere; positive HCV Ab ideally should be confirmed with antigen or HCV RNA testing (not generally available in Zambia)
  • Treatment for HCV (peg-IFN & RBV) not available in Zambia
  • General screening for HCV not recommended because of limitations of available tests and no change in overall management
  • HCV infection should not change management of HIV
  • Infection control is most important intervention for HCV+ pts: use of universal precautions in clinic & advice to not share razors or toothbrushes & not to donate blood. Sexual transmission of HCV extremely rare.

REFERENCES

Zambia Information Author: Christopher Hoffmann MD, MPH

PATHOGENS

  • Hepatitis C virus (HCV): small, enveloped, single-stranded RNA virus of the family Flaviviridae spread primarily by contact with blood and blood products

CLINICAL

  • HIV/HCV coinfection common in US & Europe due to shared routes of transmission. In U.S. 30% of HIV+ pts are coinfected, with highest rates among IDUs. HCV is 10x more infectious from needlestick than HIV. Co-infection uncommon in most of Africa.
  • After exposure, HIV+ pts more likely to progress to chronic HCV infection (>80%) especially pts with low CD4 counts. They also ave higher HCV RNA levels and are more likely to progress to liver disease fibrosis (7-26 vs 23-38 yrs) & cirrhosis than with HCV alone. Lower CD4 count associated with increased fibrosis.
  • ESLD is common cause of mortality in HIV+ pts, especially HCV co-infected. Sustained virologic response (SVR) to HCV therapy lower than with HCV infection alone.
  • Effect of HCV on HIV progression unclear.
  • Extra-hepatic manifestations of HCV: porphyria cutanea tarda, lichen planus, arthralgias, fatigue, mixed cryoglobulinemia (cutaneous & renal disease), & splenic lymphoma

DIAGNOSIS

  • HCV EIA (Ab) for screening; sensitivity & specificity 99% with 3rd generation assay. All HIV+ pts should be tested in high HCV prevalence regions (such as U.S).
  • False negatives (1-5% among all HIV+ pts, 15% among IDUs) justify RNA testing in high risk pts with negative EIA (IDU, low CD4, unexplained high ALT). False negatives also occur during acute infection before seroconversion.
  • False positives common in Africa, where prevalence of HCV generally very low.
  • Positive EIA should be followed with HCV RNA, which indicates current infection.
  • If HCV RNA+, check  HCV genotype to predict treatment response.
  • Liver Bx useful to determine stage of disease and to assess need for therapy. Serum tests (e.g. FibroSure) may be useful if they suggest either cirrhosis or no liver disease; intermediate results less informative. Imaging can help to assess for cirrhosis but has limited sensitivity. Pts not candidates for treatment because of minimal fibrosis should be re-evaluated q 2-3 yrs (with Bx or non-invasive means).
  • ALT fluctuates during natural Hx & does not reflect disease activity or prognosis.

TREATMENT

General considerations

  • Reduce hepatic risks: vaccinate against HAV & HBV if non-immune, counsel on abstinence from alcohol and IDU, enroll in IDU treatment and/or methadone maintenance when appropriate, manage psychiatric co-morbidities, start ART if pt meets criteria for therapy. 
  • Educate on HCV transmission modes: blood, shared IDU needles & 'works'; anal sex
  • If HCV untreated, screen annually for HCC in high risk (men, age >45, cirrhotics, pts with HBV coinfection) with AFP & U/S or CT if high risk.
  • Treatment indications: detectable HCV RNA, stable HIV infection, portal or bridging fibrosis or worse liver histology. Contraindications: decompensated liver disease, pregnancy (if on treatment, use contraceptives & 2 forms of birth control until 6 mos after completion of therapy due to risk of fetal loss and teratogenicity). Drug use and psychiatric disease not contraindications, but pts need to be carefully evaluated & may need extra support.
  • Lower response with genotypes 1 & 4 (14-29% SVR) vs. 2 & 3 (44-73% SVR), HCV RNA > 800,000 (response with <800,000 similar to HIV-negative), & African-American & Latino vs. Caucasian. CD4 not predictive of outcome.
  • Decompensated liver disease (portal hypertension, coagulopathy, ascites, encephalopathy) increase mortality with PEG-IFN. Consider evaluation for orthotopic liver transplantation.
  • Liver fibrosis score improves with SVR.
Acute Infection

  • If acute HCV Dx'd, repeat HCV RNA assay at 8-12 wks post exposure. If HCV RNA persistently detectable, treat with PEG-IFN alfa for 24 wks (see below for dosing). Early treatment after acute infection increases probability of SVR
Treatment Naive

  • PEG-IFN alfa-2a 180 mcg SQ q wk + RBV 800-1200* mg/d PO in divided doses.
  • PEG-IFN alfa-2b 1.5 mcg/kgSQ q wk + RBV 800-1200 mg/d PO in divided doses. RBV dose based on HIV-negative studies for genotype 1: 1000 mg/d (<75 kg) or 1200 mg/d (>75 kg). For genotype 2 and 3 or weight <40kg: RBV 800 mg/d.
  • PEG-IFN alfa-2a & alfa-2b have similar efficacy in HIV.
  • Duration 48 wks for all genotypes in HIV+ pts, who may have slower response 
  • If no evidence of response at 12 wks (HCV RNA decrease <2 log10), discontinue treatment
  • Clinical trials of HCV protease & polymerase inhibitors in combination with PEG-IFN are ongoing.
Treatment-Experienced Pts without SVR

  • Past failure of conventional (3x/wk) IFN (+/- RBV) does not preclude response to PEG-IFN + RBV (retreat with PEG-IFN + RBV)
  • Among HIV-negative non-responders, prolonged low-dose IFN does not slow fibrosis.
Use of HAART during HCV Therapy

  • HAART- associated hepatotoxicity may be reduced by treating HCV first.
  • NVP has high risk of hepatotoxicity, consider alternative
  • RBV increases toxicity of ddI: avoid combination
  • Anemia common with RBV + AZT: avoid AZT or use with careful monitoring and erythropoietin if necessary
  • ABC may decrease SVR, especially with higher HCV RNA & lower RBV dose, consider another agent.
Laboratory monitoring

  • HCV RNA testing: 1) 12 wks: if <2 log decline, low likelihood of SVR (<2%), D/C therapy. 2) 24 wks: if detectable, low likelihood of SVR; D/C therapy. 3) 48 wks: assess response. 4) 6 mos after completing therapy (if was neg at 48 wks): undetectable HCV RNA 24 wks after treatment = SVR.
  • CBC, ALT at 2, 4 wks, & q month. TSH q3-6 mos. Neuropsych eval q month.
  • HCG q month in women.
  • CD4 q12 wks. Absolute CD4 usually declines approximately 60% or 100-200 cells while CD4% often rises 3%. Decline in CD4 count does not appear to affect OI risk & should not prompt change in therapy.
Management of Adverse Events

  • Anemia (from RBV or PEG-IFN): if Hgb < 10 g/dL, decrease RBV (by 200 mg at a time); stop RBV if Hgb < 8.5 & support with epoeitin alfa (40K IU SQ qwk)
  • Severe neutropenia (from PEG-IFN): support with G-CSF (5 mcg/d sq until ANC>1000)
  • Depression: consider SSRI (optimally start before starting HCV therapy)

Drug Comments

DrugRecommendations/Comments
Peginterferon alfa Treatment of choice (with RBV) due to weekly dosing, increased efficacy, and better tolerability (vs. IFN + RBV or IFN alone).
Ribavirin Treatment of choice (with PEG-IFN).
Interferon alpha No longer recommended because of superiority of PEG-IFN

Pathogen Specific Therapy

REFERENCES

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