Hepatitis – Pocket Medicine

1 In a patient presenting with hepatitis symptoms and/or abnormal liver function tests, take a focused history to assist in establishing the etiology (e.g., new drugs, alcohol, blood or body fluid exposure, viral hepatitis).

S/Sx:
  1. HAV: lasting 2mo, fulminant illness <1%, 70% children asymptomatic
    • Pre-icteric phase: abrupt onset of fever, jaundice, malaise, anorexic, n/v, abd/p, h/a, HSM, bradycardia, Cervical LN
    • Icteric phase: ↑ conjungated Bili, pale color stool, jaundice
  2. HBV:
    • Acute (subclinical 70% adult, 90% children, resolves 1-3mo)
      • N/V, anorexia, fatigue, low grade fever,
      • RUQ/epigastric pain, jaundice,
      • myalgia/joint pain, urticaria
    • Chronic: asymptomatic until cirrhosis – portal HTN,
      • hepatocellular carcinoma
  3. HCV:
    • Acute usually asymptomatic: 20% spontaneously clear
    • Chronic usually silent: fatigue, rheumatologic symptoms: myalgias, arthralgia, paresthesia
      • itching, sjogren’s syndrome (WBC destroys exocrine glands – lacrimal and salivary) – dry mouth, eye, vagina, bronchitis
      • Raynaud’s syndrome (reduce blood flow to fingers/toes due to cold/emotions)
      • chronic mild inflammation → fibrosis
Hx
  1. Hepatotoxins:
    • EtOH (>210g / wk in men or >140g/wk in women for >2 yr)
    • medications – identify all meds, amount, durations of use (include OTC, herbal, dietary supplements, and illicit drug)
  2. Viral hepatitis risks –
    • IVDU, blood transfusion (before 1992),
    • travel to endemic areas, exposure to pt with jaundice
    • Hep B/C – transmitted parenterally
    • Hep A/E – transmitted via a fecal-roal route
  3. Autoimmune conditions –
    • female, +ANA, anti-smooth muscle Ab, elevated IgG
    • IBD (primary sclerosing cholangitis, gallstones),
  4. Occupational / recreational exposures: mushroom picking, industrial chemicals
  5. Vascular dz:
    • Budd-chiari syndrome (abd pain, ascites, hepatomegaly)
    • R-sided CHF, constrictive carditis
    • Sepsis, heat stroke
    • pregnancy (gallstones),
  6. Metabolicdz:
    • hemochromatosis
    • Wilson’s dz
    • early onset emphysema (alpha 1 antitrypsin deficiency)
    • celiac dz, thyroid dz
    • DM, obesity (nonalcoholic fatty liver dz)
    • muscle disorders: polymyositis, Sz, heavy exercise
  7. Others
    1. HELLP
    2. malignant infiltration
    3. partial hepatectomy

2 In a patient with abnormal liver enzyme tests interpret the results to distinguish between obstructive and hepatocellular causes for hepatitis as the subsequent investigation differs.

  1. Hepatocellular pattern
    • AST/ALT >> ALP
    • may have ↑ bilirubin & ↓ clotting factors
  2. Cholestatic (obstructive) pattern
    • ALP >> AST / ALT
    • ↑ GGT distinguish ↑ ALP from liver disorders instead of bone disorder (if normal GGT – r/o bone dz)
    • may have ↑ bilirubin & ↓ clotting factors
  3. Isolated hyperbilirubinemia
    • ↑ bilirubin
    • normal AST/ALT & ALP
  4. Alcoholic liver dz
    • AST:ALT of 2:1 or greater
    • more suggestive if ↑ GGT
    • Most hepatocellular injury are associated with ALT>AST

3 In a patient where an obstructive pattern has been identified,
a) Promptly arrange for imaging,
b) Refer for more definitive management in a timely manner. GI referral!

DDx
  • Bile duct obstruction
  • PBC (primary biliary cirrhosis)
  • PSC Primary sclerosing cholangitis
  • Drugs: phenytoin, androgenic steroids
  • Infiltrative dz: sarcoidosis, amyloidosis, cancer
Ix in pt with ↑ ALP of hepatic origin starts with RUQ u/s to assess the hepatic parenchyma & bile ducts

1) + biliary dilatation – extrahepatic cholestasis

  • ERCP to confirm dx if acute (stone or malignancy)
  • If chronic or high risk for ERCP – MRCP or CT (then ERCP if evidence of stone, strictiue, malignancy)
  • ddx:
    • Choledocholithiasis
    • Malignant obstruction (pancreas, gallbladder, ampulla, bile duct cancer)
    • PSC (extrahepatic bile duct stricture)
    • Chronic pancreatitis with stricturing of the distal bile duct
    • AIDS cholangiopathy

2) – biliary dilatation – intrahepatic cholestasis or (extrahepatic) partial obstruction due to PSC

  • Check AMA (dx of PBC) – if +, liver biopsy to confirm dx
    • If – AMA
    • MRCP to look for evidence of PSC
    • Hep A/B/C/E / EBV / CMV testings
    • Liver biopsy to look for infiltrative dz (sarcoidosis / cancer)

4 In patients positive for Hepatitis B and/or C,
a) Assess their infectiousness,
b) Determine human immunodeficiency virus status.

Hep B – DNA virus
  1. Immunization: + Anti-HBonly (negative Anti-HBc – requires actual infection)
  2. Resolved infection: – HBsAg & IgG for anti-HB± Anti-HBs / Anti-HBe
  3. Acute infection: + HBsAg (infectious) & HBeAg, IgM for anti-HBc
  4. Chronic infection: + HBsAg & IgG for anti-HBc, if + HBeAg (high HBV DNA)
Hep C – RNA virus
  • dx by HCV-RNA in serum

5 In patients who are Hepatitis C antibody positive determine those patients who are chronically infected with Hepatitis C, because they are at greater risk for cirrhosis and hepatocellular cancer.

  1. HCV RNA – + within 2 wks, marker of active infection
  2. Resolved hepatitis: HCV RNA ± anti-HCV ( + in 6 weeks, doesn’t = recovery / immunity)
  3. Chronic hepatitis: + HCV RNA, + anti-HCV

6 In patients who are chronically infected with Hepatitis C, refer for further assessment and possible treatment.

Tx of Hep C – always refer
  • blood-borne precautions; HepB/A vaccines if serology negative, avoid EtOH
  • Clinically significant liver dz:
    • persistently elevated transaminases,
    • liver biopsy shows fibrosis / cirrhosis,
    • moderately necrosis / inflammation
  • Tx with interferon-a & ribavirin (50-80% success rate)
    • Length of Tx based on time required for HCV-RNA to fall
    • measure HCV-RNA at 1 & 3 mo after Tx
    • Adverse effects:
      • depression / fatigue,
      • hemolysis, bone marrow suppression,
      • fever / myalgia, skin rashes
  • Poor response:
    • cirrhosis,
    • genotype 1, high HCV-RNA,
    • co-infection with HIV,
    • African-American race

7 In patients who are at risk for Hepatitis B and/or Hepatitis C exposure,
a) Counsel about harm reduction strategies, risk of other blood borne diseases,
b) Vaccinate accordingly.

  • HAV / HEV – fecal-oral through close contact andfood-borne & rarely through blood products
    • Risk Factors
      • Travelers
      • MSM
      • Drug abusers
      • Recipients of clotting factor replacement
  • HBV – parenteral (incubation for days) / sexual: body fluids – semen, saliva (incubation 4-8 weeks)
    • Anal > vaginal > oral
    • Horizontal: household contacts
    • Vertical: Mother to neonate
    • Parenteral: IVDU
    • Risk factors:
      • STI Hx, MSM, >1 sexual partner in past 6months
      • Household contact, infant born to HBV infected mother
      • Healthcare worker
      • Hemodialysis; IVDU
  • HCV – parenteral (transfusion, IVDU) > sexual; 40% with unknown risk factors
    • Risk factors
      • Blood transfusion before 1992
      • Incarceration / imprisonment
      • Unhygienic tattoos or body piercing
      • Sharing sharp personal items
      • High risk sexual activity
    • Pregnancy is not C/I & not transmit through coughing, kissing, shaking hands, sharing utensils / food/water
Prevention:
  1. vaccinate high-risk pt for HepB (3 doses, 0, 1, 6 months)
  2. Vaccine all chronic HCV pt against HBV & HAV if not immune
  3. Hep A – vaccinate children & pts with chronic HBV, HCV or other liver dz

8 Offer post-exposure prophylaxis to patients who are exposed or possibly exposed to Hepatitis A or B.

Post-exposure – Hep B
  • risk infxn ~ 30%
  • Tx: HBIG & vaccine (if unvac or known nonresponder)
Post-Exposure – Hep A
  • Vaccine age <1 or > 40yo or immunosupp
Post-exposure – Hep C (needle stick injury)
  • If HCV RNA +, consider Rx within 3 months

9 Periodically look for complications (e.g., cirrhosis, hepatocellular cancer) in patients with chronic viral hepatitis, especially hepatitis C infection.

Prognosis of Hep C
  1. 80% acute Hep C become chronic and 20% evolve to cirrhosis
  2. ↑ hepatocellular carcinoma risk if cirrhotic
  3. ↑ risk of B-cell non-Hodgkin lymphoma
  4. Can cause cryoglobulinemia: ↑ membranoproliferative glomerulonephritis, lymphoma

HBV & HCV are oncogenic – hepatocellular carcinoma secondary to cirrhosis
EBV – associated with Burkitt’s lymphoma & nasopharyngeal carcinoma


References:
  • TN2014
  • UpToDate 2015
  • Pocket Medicine 4th edition

 

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Posted in 45 Hepatitis, 99 Priority Topics, FM 99 priority topics, GI

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