Gastroenterology and Hepatology - Abnormal LFTs

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    Evaluation of Liver

    FunctionAbnormalities

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    Goals:

    Know the treatable causes of liver disease. Understand the 3 patterns of abnormal LFTs. Know the differential diagnosis of LFT

    abnormalities. Be able to select appropriate diagnostic tests.

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    TreatableChronic Liver Diseases

    Hemochromatosis

    Wilsons disease

    Autoimmune hepatitis Hepatitis C

    Chronic hepatitis B

    Drug hepatotoxicity NAFLD/NASH

    Celiac sprue

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    Abnormal LFTs:

    3 Patterns

    1. Hepatocellular:

    AST and ALT > 2x normal.2. Hepatocanalicular: mixed

    transaminases and alk phos elevated > 2x

    normal.3. Canalicular/Cholestatic:alk phos and bilirubin elevated > 2x normal.

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    Hepatocellular

    AST and ALT levels:1.5-3 x normal

    80-180

    4-7 x normal

    200-400

    > 10 x normal

    800-10,000

    Alcohol

    NAFLD/NASH

    Medications

    Chronic Hepatitis C, BHemochromatosis

    Autoimmune CAH

    A1AT deficiency

    Celiac sprue

    Alcohol

    Alcoholic Hepatitis

    NASH

    MedicationsChronic Hepatitis C, B

    Autoimmune CAH

    Wilsons disease

    Tylenol

    Alcohol + Tylenol

    Acute Hepatitis:

    A, B, CAutoimmune CAH

    Ischemia

    Medications

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    Alcoholic Hepatitis

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    Alcoholic Hepatitis: Lab

    AST, ALT and alk phos are elevated.

    AST and ALT < 500.

    AST two-fold higher than ALT.

    Leukocytosis.

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    Alcoholic Hepatitis:

    Prognosis

    Maddrey discriminant function:

    (4.6 x [PT control PT]) + (serum bilirubin). DF > 32 high short-term mortality 35% one month mortality without encephalopathy

    45% with encephalopathy

    MELD score. MELD > 11 performs as well as DF. MELD > 21 predicts a 75% 90-day mortality.

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    Alcoholic Hepatitis:

    Treatment

    Enteral feeding can improve survival. 12 vs. 47% mortality (Cabre, et al. 1990)

    Treat alcohol withdrawal.

    Fluids, calories and vitamins (thiamine, folate, pyridoxine).

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    Alcoholic Hepatitis:Steroids

    12 controlled trials: 5 showing reduced mortality and 7 with no

    difference.

    2/3 meta-analysis show benefit.

    Benefit most evident in severe disease,especially with encephalopathy.

    DF > 32 Prednisolone 40 mg daily forfour weeks, then taper.

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    Mortality about 40%, even with steroids. About 7 patients need to be treated to

    prevent one death.

    Alcoholic Hepatitis:Steroids

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    Inhibits TNF synthesis.

    400 mg po tid. Four week mortality 25% vs. 46%.

    Benefit related to decreased HRS.

    Alcoholic Hepatitis:

    Pentoxifylline

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    NON-ALCOHOLIC FATTY

    LIVER DISEASE (NAFLD)and

    STEATOHEPATITIS (NASH

    )

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    Key Concepts

    NAFLD is the most common cause of chronic liverdisease.

    NAFLD is caused by insulin resistance (IR).

    Spectrum: simple steatosis steatohepatitis.

    NASH: necroinflammation and fibrosis.

    Two-hit hypothesis: IR + oxidative stress.

    TNF-a + adiponectin: central roles in pathogenesis of IR. Treatment: reversal of IR, TNF-a inhibition?

    NAFLD and NASHNAFLD and NASH

    NAFLD: Spectrum of Hepatic Pathology

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    Steatosis

    Steatohepatitis

    Cirrhosis

    Hepatocellular

    carcinoma

    NAFLDSpectrum of Hepatic Pathology

    p p gy

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    NAFLD and the Metabolic Syndrome

    Knobler, et al. Fatty liver-an additional and treatable feature of the

    insulin resistance syndrome. Q. J. Med. 1999;9273-9.

    Marceau, et al. Liver pathology and the metabolic syndrome X in severe

    obesity. J. Clin. Endocrinol. Metab. 1999;84:1513-17.

    NAFLD

    Obesity

    Diabetes Hyperlipidemia

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    Hispanics Whites Blacks

    45%

    33%24%

    Fatty liver

    Prevalence of Hepatic SteatosisVaries with Ethnicity

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    NAFLD PrevalenceGeneral US Adult Population

    Dallas Heart Study (2,200 adults)

    Assessed NAFLD with l iver imaging

    General prevalence of fatty liver 31%(range 24% - 45%)

    Most in div iduals (79%) w ith fatty l iver do no t

    exhibi t am ino transferase elevations

    NHANES III (15, 700 adults)Assessed NAFLD with aminotransferases

    General prevalence of NAFLD 5.5%

    NAFLD Prevalence

    5.5-31%

    3-10 x more

    prevalent than

    Hepatit is C

    Risk Factors for Cirrhosis

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    Risk Factors for Cirrhosis

    Age > 45-50 years

    Obesity Diabetes

    66% p revalence of b r idging f ibrosis

    i f age > 50 years and patient obese

    or diabetic

    s acto s o C os s

    Prevalence of F3-F4 Fibrosis in Common Liver Diseases

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    Prevalence of F3-F4 Fibrosisin Common Liver Diseases

    %

    NAFLD Other

    ObeseGastric bypass

    patients

    OlderDiabetics

    AlcoholAbusers

    ChronicHCV

    0

    50

    75

    100

    25

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    Types of NAFLD:

    Type 1: Fat alone Type 2: Fat + inflammation Type 3: Fat + ballooning degeneration

    cirrhosis 21% Type 4: Fat + fibrosis and/or Mallory

    bodies cirrhosis 28%

    Retrospective study, 136 patients, 98 followed 10 years.

    Matteoni, et al. Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity.

    Gastroenterology 1999;116:1413-9.

    Prognostic Implications of NASH + Fibrosis

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    More consistent and rapidprogression to cirrhosis than NAFL

    NAFL Cirrhosis

    3%

    NASH +fibrosis

    Cirrhosis30%

    > 10 years

    5-10 years

    Matteon i et al. Gastro entero log y 1999; 116:1413

    Prognostic Implications ofNASH + Fibrosis

    g p

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    Treatment of NAFLD

    Diet

    Exercise

    Weight loss

    NAFLD - What can we do?

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    NAFLDWhat can we do?

    Other approaches unproven

    Specific pharmacotherapy for NAFLD

    Beneficial in preliminary studiesInsulin sensitizers: TZDs > metformin

    Benefit still unproven by preliminary studiesLipid lowering agents: Statins, fibratesAntioxidants: Betaine, SAMe, vitamin E

    Probiotics

    Not beneficialUrsodeoxycholic acid

    NAFLD: Therapeutic Approach

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    Steatosis CirrhosisSteatohepatitis

    Overt Metabolic Syndrome (MS)

    Yes No

    Treat MS

    Rx DMAnti-HTN

    Lower lipids

    Treat NAFLD

    Monitor for NAFLD ProgressionPhysical exams (portal HTN)

    Blood tests (platelets, AST/ALT; fibrotest?)

    Reduced kcals

    Exercise

    Enroll in trial Rx portal HTN

    Screen for HCC

    OLT *

    *Decompensated pat ients without s urgical contra indicat ions

    NAFLD: Therapeutic Approach

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    Drug Hepatotoxicity

    Sulfonamides, PCN, TCN, fluconazole,

    phenytoin, anti-emetics, NSAIDs. Occurs within 2 weeks 12 months ofexposure.

    Fever, pruritus, skin rash, arthralgias,eosinophilia.

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    Viral Hepatitis

    Hepatitis A: IgM ab.

    Hepatitis B: HBsAg.

    Hepatitis C: antibody and PCR.

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    Hemochromatosis

    Affects 1 in 200 people.

    Transferrin saturation > 50%. Ferriten > 1000.

    HFE gene analysis. Biopsy with hepatic iron index.

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    Autoimmune Chronic

    Active Hepatitis Young women. Type 1: ANA, ASMA, aSLA.

    Type 2: aLKM. Increased IgG level.

    Increased g-fraction on SPEP. Liver biopsy: inflammation.

    Response to steroids.

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    Alpha-1 Antitrypsin

    Deficiency A1AT level.

    A1AT phenotype. Liver biopsy:PAS positive- diastase

    resistant hepatocellulargranules.

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    Celiac Disease

    Affects 1/100 people.

    A cause of abnormal LFTs.

    A cause of liver failure.

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    Wilsons Disease

    Age < 55.

    Hemolytic anemia, movementdisorder, coma.

    Diagnosis: low ceruloplasmin,high 24 h urine copper, KFrings, liver biopsy.

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    Hepatocanalicular

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    Hepatocanalicular

    Mixed pattern: elevated transaminasesand alk phos.

    Medications: ASA, NSAIDs,antibiotics.

    Alcohol

    Overlap syndrome: PBC + AI-CAH

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    Canalicular/Cholestatic

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    Canalicular/Cholestatic

    Elevated alk phos and bilirubin

    Sepsis

    Drug-induced cholestasis

    Post-operative jaundice Genetic disorders: Gilberts syndrome

    TPN

    Primary Biliary Cirrhosis (PBC) Primary Sclerosing Cholangitis (PSC)

    Biliary obstruction

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    60 yo man with history of alcohol abuse andhepatitis C sustained multiple trauma in

    MVA requiring exploratory laparotomy.

    Received multiple units of PRBCs. Required

    intubation/PEEP, antibiotics for pneumonia,

    blood cultures positive, on TPN.

    You are consulted for evaluation of abnormalLFTs. Bilirubin 26, alk phos 350, ALT 150,

    INR 1.6

    CASE #1

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    Multifactorial

    Postoperative jaundice Sepsis

    Medications

    TPN

    Increased pigment load:hemolysis of transfused cells,

    resorption of hematomas.

    Ventilator/PEEP

    Underlying liver disease

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    Postoperative Jaundice

    25-75% of pts develop abnl LFTs

    post-op. 47% of cirrhotics become jaundiced.

    History:type of surgery, blood products,

    hypoxia, hemodynamics, anesthetic, meds, TPN,rule-out infection.

    Postoperative Jaundice

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    Isolated unconjugated hyperbilirubinemia.

    Hemolytic disorders: G-6PD def,SS dz, thallasemias, autoimmune, meds,

    infection, DIC. Hemolysis of transfusedPRBCs.

    Resorption of hematomas. Gilberts syndrome.

    Postoperative Jaundice

    Postoperative Jaundice

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    Hemolysis Increased reticulocytes

    Unconjugatedhyperbilirubinemia (bili < 5 mg/dl)

    Increased AST and LDH

    Decreased haptoglobin Schistocytes

    Normal alk phos and ALT

    Postoperative Jaundice

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    Sepsisand cholestasis.

    Endotoxins (LPS) induceinflammatory cytokines.

    Impaired transport of bile acidsand bilirubin; decreased bile flow.

    100 consecutive septic pts:54% elevated bili (34% > 2), worse with liver dz,preceded bacteremia in 1/3 by 1 to 9 days, 61%mortality, 100% mortality with persistent jaundice.

    Postoperative Jaundice

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    TPN 2 weeks fatty livermoderate

    increases in ALT and alk phos. > 3 weeks cholestasis.

    Treatment: avoid excess non-protein

    calories, cycle TPN (10-12 hrs), add lipids,r/o acalculous cholecystitis.

    Postoperative Jaundice

    Postoperative Jaundice

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    Acalculous Cholecystitis

    Risks:male, major surgery, trauma, burns, long-termTPN, mech vent with PEEP, narcotics, renal failure.

    Fever, pain, leukocytosis, non-specific

    LFTs. CT and US:pericholecystic fluid, thickened

    wall. (HIDA, too many false +/-.)

    Treatment: cholecystectomy, -cystostomy. Mortality: 70%.

    Postoperative Jaundice

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    30 yo male GI fellow was told by hisattending that he is jaundiced, especially

    prominent on the day after weekend

    call. Complains of fatigue and

    irritability. Drinks an occasional

    margarita.

    Physical exam with mild icterus.Bili 3.9 (all indirect), LFTs o/w normal.

    Case #2

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    Gilberts Syndrome

    Decreased UDP glucuronyl

    transferase levels. Unconjugated hyperbilirubinemia.

    Total bilirubin < 4 mg/dl.

    Rule-out hemolysis.

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    51 yo woman with pruritus, fatigue and

    jaundice, worsening over several years.

    Past history of hypothyroidism, sicca

    syndrome and hypercholesterolemia.

    PE: jaundice, splenomegaly, xanthoma,

    bruising.

    Lab: bili 10.5, alk phos 650, ALT 95,

    INR 2.5, plts 65k.

    Case #3

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    AMA + 1/640

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    Primary Biliary Cirrhosis

    (PBC)

    A chronic autoimmune hepatobiliarydisease resulting from T cell-mediatedapoptotic destruction of biliaryepithelial cells lining interlobular to

    septal caliber intrahepatic bile ducts.

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    PBC: Florid Duct Sign

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    PBC:Clinical Features

    Female 82%.

    Age at diagnosis: 51 (middle age).

    AMA + in 92-95%. Symptoms: fatigue, pruritus, arthralgias.

    Signs: jaundice, hypothyroid, sicca, Raynauds.

    Prognosis: (Mayo Risk Score) age, bili, alb, PT,edema.

    A progressive disease ending in liver failure.

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    24 yo man with chronic bloody

    diarrhea. Also c/o pruritus.

    Lab: bili 8.5, alk phos 800, INR 2.7,

    plts 95 k, Ca++ 6.5

    Case #4

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    Primary Sclerosing Cholangitis(PSC)

    A chronic cholestatic liver disease ofunknown pathogenesis that is stronglyassociated with chronic ulcerative colitis.

    Characterized by progressive

    destruction of bile ducts, resulting in thedevelopment of biliary cirrhosis.

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    PSC:Clinical Features

    Prevalence 6-8 cases/100 k

    M/F = 3/1

    Presents ~ age 20-30

    80% of PSC patients have IBD.

    4% of IBD patients have PSC. Median survival ~ 12 yrs.

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    PSC:Symptoms

    Pruritus

    Jaundice

    Abdominal pain Fatigue

    Complications of cirrhosis and portal HTN.

    Bacterial cholangitis Cholangiocarcinoma: lifetime prevalence 10-30%.

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    PSC: Diagnosis

    Clinical, biochemical, histologic findings.

    ERCP multifocal strictures and dilationsinvolving intra- and extrahepatic ducts.

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    Liver Imaging

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    Imaging US and CT: useful for fatty liver, r/o dilated

    ducts, screening for hepatoma, patency ofhepatic and portal veins, cholecystitis,pancreatic mass.

    MR/MRCP: useful for ductal disease,choledocholithiasis, iron overload, hepatoma vshemangioma.

    ERCP/EUS: rule out PSC, PBC,

    cholangiocarcinoma, pancreatic neoplasm,choledocholithiasis, ampullary neoplasm,adenopathy.

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    Liver Biopsy

    Grade and stage viral hepatitis. Unknown cause of liver disease

    (rule out fatty liver, granulomatoushepatitis).

    Rule outAI-CAHIron overloadWilsonsA1AT deficiency

    Cirrhosis?

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    Goals:

    Know the treatable causes of liver disease. Understand the 3 patterns of abnormal LFTs. Know the differential diagnosis of LFT abnormalities.

    Be able to select appropriate diagnostic tests.

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    Staging Liver Disease

    Severity of Liver Disease:

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    Severity of Liver Disease:

    Child-Turcotte-Pugh Class

    Ascites None Slight Mod/severe

    Encephalopathy None Slight/mod Mod/severe

    Bilirubin 3.0

    Albumin >3.5 2.8-3.5 6

    Parameter 1 2 3

    Total numerical score

    5-6

    7-9

    10-15

    Child-Turcotte-Pugh class

    C

    B

    A

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    Model for End-Stage LiverDisease (MELD)

    Mathematical survival model created fromdata on patients undergoing TIPS

    MELD score estimates risk of 3-monthmortality

    Uses 3 laboratory values

    - Serum total bilirubin- Serum creatinine

    - INR

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    Calculating MELD Scores

    The hard way6.4 + 9.8 x log (INR) + 11.2 x log (Cr) +

    3.8 x log (Bilirubin)

    The easy way

    www.unos.org/resources/

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    Ascites and Prognosis

    Ascites occurs in of cirrhoticpatients within 10 yrs.

    50% 2 year mortality.

    75% 1 year mortality withrefractory ascites.

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    SBP Treatment

    IV albumin: 1.5 g/kg on day 1 and 1

    g/kg on day 3. Reduced risk of renalfailure and improved survival.

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    Hepatorenal Syndrome

    HRS: functional renal failure in the

    setting of cirrhosis and in the absence

    of intrinsic renal disease.

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    HRS: Treatment Midodrine: an alpha agonist that improves

    systemic blood pressure, thereby improvingrenal perfusion.

    Octreotide: antagonizes the action ofvarious splanchnic vasodilators.

    Albumin: increases circulatory volume.

    Combined: improved systemic hemodynamics improved renal circulation.

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    HRS: MOA

    Midodrine, octreotide and albumin (5pts) vs dopamine and albumin (8 pts)for 20 days.

    Improvement in renal function with noside-effects in all 5 on MOA (1/8 ondopamine improved).

    Angeli, et al. Reversal of type 1 hepatorenal

    syndrome with the administration of midodrine

    and octreotide. Hepatology, 19:1690, 1999.

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    HRS:midodrine, octreotide, albumin.

    14 ascitic cirrhotic pts with type 1 HRS.

    Midodrine 2.5 mg/d, octreotide 25 mg/h and albumin50 g/d for 14 days reversed HRS in 10 of 14 pts.

    Subsequent TIPS in 5 pts maintained normal renalfunction at 1 y.

    2 responders transplanted.

    Wong, et al. Midodrine, octreotide, albumin and

    TIPS in selected patients with cirrhosis and type 1

    hepatorenal syndrome. Hepatology 40:55, 2004.

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