abnormal alt week 3 big group discussion 1. overview of liver function tests group d viardo-zuniga

ABNORMAL ALT

Week 3 Big Group Discussion 1

Overview of Liver Function Tests

Group DViardo-Zuniga

Evaluation of Liver FunctionTests used to:

Detect presence of liver disease

Distinguish among different types of liver disorders

Gauge the extent of known liver damage

Follow the response to treatment

Evaluation of Liver FunctionLiver tests

Can be normal in patients with serious liver disease & abnormal in patients with diseases that do not affect the liver.

Rarely suggest a specific diagnosis; they suggest a general category of liver disease.

Evaluation of Liver FunctionTo increase sensitivity and specificity of

laboratory tests in the detection of liver disease, it is best to use them as a battery.

Tests usually employed in clinical practice: Bilirubin, aminotransferases (ALT, AST), alkaline

phosphates, albumin, and PT tests.

If more than one test provides abnormal findings, or are persistently abnormal on serial determinations, the probability of liver disease is high & vice versa

Tests Based on Detoxification &

Excretory Functions

Tests That Measure Biosynthetic Function Of The Liver

Other diagnostic tests

1.Serum Bilirubin2.Urine Bilirubin3. Blood Ammonia4. Serum Enzymes - ALT - AST

1. Serum Albumin2. Serum Globulin3. Coagulation Factors

1. Percutaneous Liver Biopsy2. Ultrasonography3. Ultrasonography with Doppler Imaging

Evaluation of Liver Function

Tests Based on Detoxification & Excretory FunctionsSerum Bilirubin

Urine Bilirubin

Blood Ammonia

Serum Enzymes

Serum BilirubinUnconjugated bilirubin

Normal total serum bilirubin concentration is <17 mol/L (1 mg/dL)

Rarely due to liver disease, seen primarily in hemolytic disorders and genetic conditions such as Crigler-Najjar and Gilbert's syndromes

Urine Bilirubin

Conjugated bilirubin

(+) bilirubinuria implies the presence of liver disease

Dipstick test or Ictotest tablet used

Phenothiazines may give a false-positive reading with the Ictotest tablet

Blood Ammonia Normal protein metabolism and by intestinal

bacteria in the colon

Patients with advanced liver disease have significant muscle wasting, which contributes to hyperammonemia

Poor correlation w/ hepatic function. Ammonia can be elevated in patients with severe portal hypertension and portal blood shunting around the liver even in the presence of normal hepatic function.

Elevated arterial ammonia levels correlate with outcome in fulminant hepatic failure.

Serum EnzymesSerum enzyme tests can be grouped into three

categories: Enzymes that reflects damage to hepatocytes Enzymes that reflects cholestasis Enzyme tests that do not fit precisely into either

pattern

Enzymes that reflect hepatocyte damage

Aminotransferases Aspartate aminotransferase (AST)

Alanine aminotransferase (ALT)

Aminotransferases

Released into the blood in greater amounts when there is damage to the liver cell membrane resulting in increased permeability

Sensitive indicators of liver cell injury and most helpful in recognizing acute hepatocellular diseases (hepatitis)

Aminotransferases

Aspartate aminotransferase (AST) Found in the liver, cardiac muscle, skeletal muscle, kidneys, brain,

pancreas, lungs, leukocytes & erythrocytes ( order of concentration)

Alanine aminotransferase (ALT) Found primarily in the liver

Aminotransferase

Any type of liver cell injury can cause modest elevations in the serum aminotransferases

Levels of up to 300 U/L are nonspecific and may be found in any type of liver disorder

Striking elevations (> 1000 U/L) occurs almost exclusively in disorders associated with extensive hepatocellular injury Eg. viral hepatitis, ischemic liver injury, toxin-

induced liver injury or drug-induced liver injury

Aminotransferases In most acute hepatocellular disorders ALT is

or = to the AST

AST:ALT ratio > 2:1 is suggestive while a ratio > 3:1 is highly suggestive of alcoholic liver disease

AST in alcoholic liver disease is rarely >300 U/L and the ALT is often normal

ALT in serum is due to alcohol-induced deficiency of pyridoxal phosphate

Enzymes that Reflect CholestasisElevated in cholestasis

Alkaline Phosphatase 5'-nucleotidase Glutamyl Transpeptidase (GGT)

Alkaline PhosphataseNormal serum levels consists of distinct

isoenzymes found in the liver, bone, placenta

Normal non-pathologic found in: Over age 60 (1–1½ times normal) Blood types O and B: after eating a fatty meal Children and adolescents undergoing rapid bone

growth Late in normal pregnancies: influx of placental

alkaline phosphatase

Alkaline Phosphatase• > four times normal occur in:

– Cholestatic liver disorders

– Infiltrative liver diseases (cancer and amyloidosis)

– Bone conditions characterized by rapid bone turnover (Paget's disease)

• In the absence of jaundice or elevated aminotransferases, an elevated alkaline phosphatase of liver origin often, but not always, suggests early cholestasis

Alkaline PhosphataseOther conditions that cause isolated elevations

of the alkaline phosphatase include Hodgkin's disease, diabetes, hyperthyroidism, congestive heart failure, amyloidosis, and inflammatory bowel disease

5'-nucleotidase or GGT

Rarely elevated in conditions other than liver disease

GGT Good:

more sensitive marker for cholestatic damage than ALP. Helpful in identifying cause of isolated elevation in ALP

Raised in alcohol toxicity (acute and chronic). Bad:

elevated with even minor, sub-clinical levels of liver dysfunction

5'-nucleotidase Specific for cholestasis or damage to the intra or extrahepatic

biliary system


Excretory Functions







Serum Albumin

Serum Globulins

Coagulation Factors

TESTS THAT MEASURE BIOSYNTHETIC FUNCTION OF THE

LIVER

Serum Albumin synthesized exclusively by hepatocytes has a long half-life: 18 to 20 days, with

approximately 4% degraded per day not a good indicator of acute or mild hepatic

dysfunction In hepatitis, albumin levels <3 g/dL = possible

chronic liver disease hypoalbuminemia is common in cirrhosis and

reflects severe liver damage and decreased albumin synthesis

In ascites, synthesis may be normal or increased, but in low levels =increased volume of distribution

hypoalbuminemia may occur in protein malnutrition of any cause, as well as protein-losing enteropathies, nephrotic syndrome, and chronic infections

Harrison’s Principle of Internal Medicine, 17th ed.

Serum Globulins Made up of:

gamma globulins (immunoglobulins) produced by B lymphocytes and alpha and beta globulins produced primarily in hepatocytes.

Gamma globulins are increased in chronic hepatitis and cirrhosis.

In cirrhosis, the increased serum gamma globulin concentration is due to increased synthesis of antibodies

Diffuse polyclonal increases (increases > 100%) in IgG

levels are common in autoimmune hepatitis.

Increases in the IgM levels are common in primary biliary cirrhosis.

Increases in the IgA levels occur in alcoholic liver disease Harrison’s Principle of Internal Medicine,

17th ed.

Coagulation Factors • With the exception of factor VIII, the blood clotting factors

are made exclusively in hepatocytes

• Their serum half-lives range from 6 h for factor VII to 5 days for fibrinogen

• Measurement of the clotting factors is the single best acute measure of hepatic synthetic function and helpful in both the diagnosis and assessing the prognosis of acute parenchymal liver disease

• Useful for this purpose is the serum prothrombin time, which measures factors II, V, VII, and X.

• Biosynthesis of factors II, VII, IX, and X depends on vitamin K.

• Prothrombin time is elevated in hepatitis and cirrhosis as well as in obstructive jaundice or fat malabsorption of any kind.

• Marked prolongation of the prothrombin time, >5 s above control and not corrected by parenteral vitamin K administration, is a poor prognostic sign in acute viral hepatitis and other acute and chronic liver diseases.



Excretory Functions







Other diagnostic testsPreviously discussed tests direct the physician

to the category of the liver disease

Other radiologic testing and procedures are often necessary to make the proper diagnos

Percutaneous Liver BiopsySafe, bedside procedure

Most accurate in disorders causing diffuse changes in the liver

Of proven value in the following situationsHepatocellular disease of uncertain causeProlonged hepatitis with the possibility of chronic

active hepatitisUnexplained hepatomegalyUnexplained SplenomegalyHepatic filling defects by radiologic imagingFUOStaging of malignant lymphoma

Percutaneous Liver Biopsy

Contraindications

Significant ascites

Prolonged INR

Ultrasonography

First diagnostic test to use in patients whose liver tests suggest cholestasis

Determine presence of a dilated intrahepatic or extrahepatic biliary tree

Identification of gallstones

Space occupying lesion

Distinguish between solid and cystic masses

Helps direct percutaneous biopsies

Ultrasonography with Doppler ImagingFirst test ordered in patients suspected of

having Budd-Chiari syndrome

Detect patency of portal vein, hepatic artery, hepatic veins and determination of direction of blood flow

Use of Liver Tests

To increase the sensitivity and specificity of lab tests in the detection of liver disease a battery of tests is used

No single set of liver tests will necessarily provide a diagnosis

Necessary to repeat liver tests to a diagnostic pattern to emmerge

Hepatitis BHepatitis CHepatitis D

HBV HCV HDVIncubation

(days)30-180, mean

60-9015-160, mean

5030-180, mean

60-90

Onset Insidious or acute

insidious Insidious or acute

Age preference

Young adults, babies, toddlers

Any age, more common in

adults

Any age (same as HBV)

Transmission Percutaneous, perinatal, sexual

Percutaneous Percutaneous, non-

percutaneous

Severity Occasionally severe

moderate Occasionally severe

Fulminant 0.1-1% 0.1% 5-20%

Progression to chronicity

Occasional (1-10%) (90% of

neonates)

Common (85%) Common

Carrier 0.1-30% 1.5-3.2% Variable

Cancer + + +/-

Prognosis Worse with age Moderate Chronic - poor

Likelihood of chronicity after acute infection varies as a function of age.

More common in those who present with chronic infection without having experienced an acute illness neonatal infection infection in immunocompromised host

Most cases of chronic Hepatitis B among adults occur in patients who never had a recognized episode of clinically apparent acute viral hepatitis

HBV HCV HDV

Incubation (days)

30-180, mean 60-90 15-160, mean 50 30-180, mean 60-90

Onset Insidious or acute insidious Insidious or acute

Age preference Young adults, babies, toddlers

Any age, more common in adults



Percutaneous Percutaneous, non-percutaneous

Severity Occasionally severe moderate Occasionally severe

Fulminant 0.1-1% 0.1% 5-20%


Occasional (1-10%) (90% of neonates)

Common (85%) Common


Cancer + + +/-


A very slow and insidious process

Common even in those with a return to normal in aminotransferase levels after acute hepatitis C

Hepatitis C accounts for 40% of chronic liver disease (the most frequent indication for liver transplantation)

20-30% of patients with chronic hepatitis C will develop cirrhosis over 20-30 years

However, long term prognosis for majority is benign (asymptomatic & well compensated)

HBV HCV HDV

Incubation (days)

30-180, mean 60-90

15-160, mean 50 30-180, mean 60-90

Onset Insidious or acute insidious Insidious or acute

Age preference

Young adults, babies, toddlers

Any age, more common in adults



Percutaneous Percutaneous, non-percutaneous

Severity Occasionally severe

moderate Occasionally severe

Fulminant 0.1-1% 0.1% 5-20%


Occasional (1-10%) (90% of

neonates)

Common (85%) Common


Cancer + + +/-


Delta hepatitis agent, HDV – a defective RNA virus that co-infects and requires the helper function of HBV for its replication and expression

Co-infection can increase severity of acute hepatitis B but does not increase the likelihood of progression to chronic hepatitis

Superinfection occurs in patients who is already chronically infected with HBV (more severe liver disease versus co-infection)

90% chance of chronic infection if infected at birth despite being clinically silent

1% risk of chronicity if infection occurs in young adulthood and immunocompetent persons wherein clinical signs and symptoms are often present

broad, ranging from asymptomatic infection to debilitating disease or even end-stage, fatal hepatic failure

Fatigue- most common

persistent or intermittent jaundice

malaise and anorexia

progressive liver injury

hepatic decompensation (when superimposed on well-established cirrhosis)

do not distinguish adequately between histologically mild and severe hepatitis.

Aminotransferase elevations tend to be modest for chronic hepatitis B but may fluctuate in the range of 100–1,000 units.

alanine aminotransferase (ALT) tends to be more elevated than aspartate aminotransferase (AST); however, once cirrhosis is established, AST tends to exceed ALT

Levels of alkaline phosphatase activity tend to be normal or only marginally elevated.

In Severe Cases

moderate elevations in serum bilirubin [51.3–171 mol/L (3–10 mg/dL)] occur.

Hypoalbuminemia and prolongation of the prothrombin time

Hyperglobulinemia and detectable circulating autoantibodies are distinctly absent in chronic hepatitis B (in contrast to autoimmune hepatitis).

The laboratory abnormalities consist of : elevation of the ALT (normal to 200 IU/l) in up to 90% of patients. Transaminases, serum bilirubin, albumin, and gammaglobulin values

are mild to markedly elevated. autoimmune antibodies such as antinuclear antibody, anti-smooth

muscle antibody and antimitochondrial antibody may be present.

Sustained increases in the concentrations of the aminotransferases together with the presence of HBsAg for >6 months is regarded as indicative of chronic hepatitis.

http://www.who.int/csr/disease/hepatitis/whocdscsrlyo20022/en/index3.html#features

HBs Ag

AntiHBs

AntiHBc

HBe Ag

AntiHBe Interpretation

+ - IgM + -Acute Hepatitis BHighly infectivity

+ - IgG + -Chronic Hepatitis

BHighly Infectivity

HBs Ag

AntiHBs

AntiHBc

Hbe Ag

AntiHbe

Interpretation

+ - IgG - +

1. Late Acute or Chronic Hepatitis BLow infectivity

2. HBeAg negative(precore-mutant)Hepatitis B (chronic or rarely acute)

+ + + -/+ -/+

1. HbsAg of one subtype and heterotupic anti-HBs (common)

2. Process of seroconversion from HBsAg to anti HBs (rare)

HBsAg

AntiHBs

AntiHBc

HBe Ag

AntiHBe

Interpretation

- - IgM -/+ -/+1. Acute Hepatitis B2. Anti-HBc

“window”

- - IgG - -/+

1. Low levels Hepatitis B Carrier

2. Hepatitis B in remote past

HBsAg

AntiHBs

AntiHBc

HBeAg

AntiHBe

Interpretation

- + IgG - -/+ Recovery from Hepatitis B

- + - - -

1. Immunization with HBsAg (after vaccination)

2. Hepatitis B in remote past

3. False positive

Occurs in the end-stage of chronic hepatitis

Includes:AscitesEdema bleeding gastroesophageal variceshepatic encephalopathycoagulopathy hypersplenism

Associated with deposition of circulating hepatitis B antigen-antibody immune complexes

Common arthralgias arthritis

Rarepurpuric cutaneous lesions (leukocytoclastic

vasculitis)immune-complex glumerulonephritisgeneralized vasculitis (polyarteritis nodosa)

Management of chronic hepatitis B is directed at suppressing the level of virus replication

Treatment is suppressive rather than curative

3 drugs have been proven effective: Interferon (INF) α Lamivudine Adefovir dipivoxil

Mechanism of Action

Interferon

•induction of intracellular signals following binding to specific cell membrane receptors, resulting in inhibition of viral penetration, translation, transcription, protein processing, maturation, and release.•It also exerts immunomodulatory and antiproliferative activities

Lamivudine

inhibits HBV DNA polymerase by competing with deoxycytidine triphosphate for incorporation into the viral DNA, resulting in chain termination

Adefovir

a diester prodrug of adefovir, phosphorylated by cellular kinases to active diphosphate metabolite and then competitively inhibits HBV DNA polymerase to result in chain termination

Patients with Chronic Hepatitis B who are candidates for Antiviral Therapy

Clinical Feature Interferon

Lamivudine

Adefovir

Detectable markers of HBV replication

Yes Yes Yes

Normal ALT activity No No No

ALT <2 x upper limit of normal No No No

ALT >2 x upper limit of normal Yes Yes Yes

Immunocompetent Yes Yes Yes

Immunocompromised No Yes Yes

Adult acquisition (western) Yes Yes Yes

Childhood acquisition (asian) No Yes Yes

Compensated liver disease Yes Yes Yes

Decompensated liver disease No Yes Yes

“wild-type” HBeAg-reactive Yes Yes Yes

HBeAg-negative chronic hapatitis

Yes Yes Yes

Interferon refractory No Yes Yes

Comparison of the three drugs

Feature Interferon Lamivudine AdefovirRoute Injection Oral Oral

Duration of therapy 4 months ≥52 weeks ≥48 weeks

Tolerability poor good good

Nephrotoxicity none none Crea monitoring

HBeAg loss 33% 32-33% 23%

HBeAg seroconversion 18-20% 16-20% 12%

HBV DNA PCR negative

unlikely ~30% HBeAg +39% HBeAg -

21% HBeAg +52% HBeAg -

ALT normalization Confined to HBeAg responders

>40% HBeAg +>70% HBeAg -

50% HBeAg +72% HBeAg -

HBsAg loss during Rx 3-8% 2-4% Unlikely

HBsAg loss after Rx 80% over 9 yrs 23% over 2 yrs To be determined

Viral resistance None 15-30% @ 1 yr70% @ 5 yrs

None @ 1 yr2.5% @ 2 yrs

Natural History Reduced mortality, decompensation, HCC

To be determined To be determined

NONALCOHOLIC LIVER DISEASE

Group BTan, Genevieve - Tongo

Definitionrefers to a wide spectrum

of liver disease that include simple hepatic steatosis which over time can progress to NASH, with the subsequent development of fibrosis and cirrhosis

Although, histologically NAFLD resembles alcohol-induced liver disease, by definition NAFLD develops in patients who consume little or no alcohol.

Fauci et al. Harrison’s Principles of Internal Medicine 17 th ed. vol2. 2008.

Epidemiology

US and Europe

14-20% prevalence

US

NASH = 3%

Fibrosis due to NASH >40% of obese patients


Aminotransferases are mildly elevated 1.5 – 2x the upper limit of normal ALT > AST

Fatigue

Vague right upper quadrant discomfort

Clinical Features


Clinical Features

NASH is frequently seen in conjunction with other components of the metabolic syndromeHypertensionDMElevated lipidsObesity

Insulin resistanceMarker: Elevated ferritin levels


DiagnosisExclude alcoholic liver disease

< 20 g/d of alcohol be consumed

Lab TestLiver enzymes (ALT > AST)Hepatitis B and CIron studiesAutoimmune serology

Liver Biopsy

UltrasoundFauci et al. Harrison’s Principles of Internal Medicine 17 th ed. vol2. 2008.

Ultrasound

A sonogram of a fatty liver showing increased echotexture compared with the adjacent kidney (bright liver).

Liver Biopsy

Macrovesicular & Microvesicular Steatosis

Two patterns of hepatic steatosis are recognized:

(1) microvesicular steatosis: the cytoplasm is replaced by bubbles of fat that do not displace the nucleus; and

(2) macrovesicular steatosis: the cytoplasm is replaced by a large bubble of fat that displaces the nucleus to the edge of the cell.

Steatohepatitis

The histologic findings shown include macrovesicular steatosis, cytologic ballooning, Mallory bodies, and scattered lobular inflammation.

Mallory Body

Mallory body is shown within a ballooned hepatocyte

Pericellular Fibrosis

Pericellular fibrosis is shown (Masson's trichrome stain). The collagenous tissue (shown in blue) surrounds individual hepatocytes, producing a chicken-wire appearance.

Treatment


Treatment

Orlistat (Xenical) – reversible inhibitor of gastric and pancreatic lipase

Lipase break down fat in food so that it can be absorbed into the body.

So if Orlistat blocks this, then the fat can’t be absorbed. The Unabsorbed fat is excreted in the stool. Aid to weight loss.

Treatment

Thiazolidinedione – peroxisome proliferator-activated receptor (PPAR) gamma inhibitor

Improves insulin sensitivity within the adipocyte and skeletal muscle by upregulating specific protein kinases involved in decreasing fatty acid synthesis

Antioxidants – Vitamin E supplementation

Bariatric Surgery


Efforts should be directed to

encouraging the patient to

exercise and lose weight.

Treatment


AUTOIMMUNE HEPATITIS

Group CTorres - Ventura

Autoimmune HepatitisChronic disorder characterized by continuing hepatocellular necrosis and inflammation, usually with fibrosis

Capable of progressing to cirrhosis and liver failure

Prominent extrahepatic features of autoimmunity and seroimmunologic abnormalities

Autoimmune Hepatitis

Cell-mediated immunologic attack against liver cells progressive liver injury

Humoral immune mechanism extrahepatic manifestations of AIH

Predisposition is inherited

Liver specificity of the injury is triggered by environmental factors (chemical/viral)

Clinical Features insidious/abrupt onset

Young to middle-aged women

Marked hyperglobulinemia

High-titer circulating ANAs

Fatigue, malaise, anorexia, amenorrhea, acne, arthralgia, jaundice

Arthritis, maculopapular eruptions, erythema nodosum, colitis, pleurisy, pericarditis, anemia, azotemia, sicca syndrome

Ascites and edema, encephalopathy, hypersplenism, coagulopathy, variceal bleeding complications of cirrhosis

Laboratory FeaturesParameter

Values

ALT ↑ (100 – 1000 units)

AST

ALP Normal/↑

Serum Albumin

Normal/↓ in very active or advanced disease

Serum Globulin

N/↑ (>2.5 g/dL)

Bilirubin ↑ (51-171 µmol /L [3-10 mg/dL])

PT Prolonged (active or late phase)

RF present

ANA Homogenous stain

Liver BiopsySimilar to chronic viral hepatitisInterface hepatitis or piecemeal necrosis

Expanding portal tracts and mononuclear cell infiltrates (plasma cells) extending beyond the plate of periportal hepatocytes into the parenchyma

necroinflammatory activity characterizes the lobular parenchyma

“rosette” formation, thickened liver cell plates, regenerative “pseudolobules” hepatocellular regeneration

Common are septal fibrosis, bridging fibrosis and cirrhosis

Alvarez F, et al. International Autoimmune Hepatitis Report: review of criteria for diagnosis of autoimmune hepatitis. Journal of Hepatology. 1999; 31:929-38.

Hennes. E, et al. Simplified Criteria for the Diagnosis of Autoimmune Hepatitis. Hepatology. 2008; 48:169-176

Treatment

• initiated at 20 mg/d• in the US: initiation dose of 60 mg/d, tapered successively over the course of a month down to a maintenance level of 20 mg/d

Features found in AIH

Features found in the patient

Age and Gender Young to middle-aged females

50 year old female

Transaminases Elevated (100-1000 units)

Elevated

Clinical features arthralgia Joint pains

ANALYSIS

Group DViardo-Zuniga

BRIEF ReviewNORMAL VALUES (Widmann's Clinical Interpretation of

Laboratory Tests) ALT = 10-40 IU/L AST = 10-37 IU/L

Our case patient’s ALT = 90 IU/L

SALIENT FEATURES50 years old

Dialysis nurse

Elevated transaminase (ALT – 90 IU/L)

Rises in BP since 2003

Blood sugar elevated 2 years ago

joint pains

Body Mass Index = 30.47 OBESE CLASS

BP = 160/100

PR = 75/min regular

RR = 21/min

• Afebrile• Pink palpebral

conjunctivae, neck veins not distended

• Adynamic precordium, apex beat at 5th LICS MCL, *sustained, not diffuse, normal heart sounds, no murmurs

• Lungs/abdomen unremarkable. No pedal edema.

Differential DiagnosisChronic Viral Hepatitis

Autoimmune Hepatitis

Non-alcoholic liver disease

Chronic Viral Hepatitis

Strongest Risk Factor: Dialysis nurse (occupation)

High rates of HBV infection include health care workers exposed to blood.

Extrahepatic complications of chronic hepatitis B are associated with deposition of circulating hepatitis B Ag-Ab immune complexes. These include arthralgias and arthritis, which are common.“She occasionally takes Celecoxib for her joint pains”

Chronic Viral HepatitisAminotransferase elevations tend to be modest

for chronic hepatitis, may fluctuate in the range of 100-1000 units. Patient’s ALT is ALT = 90 IU/L, relatively near the

range for chronic hepatitis.

Autoimmune HepatitisMinimal aminotransferase elevations, serum

AST & ALT fluctuate in the range of 100-1000 units Patient’s ALT is ALT = 90 IU/L, relatively near the

range for chronic hepatitis.

Clinical features similar to chronic viral hepatitis. Fatigue, malaise, anorexia, acne, arthralgias, and jaundice are common. Patient did not manifest these symptoms.

PATIENTNON ALCOHOLIC FATTY

LIVER DISEASEelevated ALT noted on HPN work-

up (asymptomatic for liver disease)

incidentally discovered elevated liver enzymes

BMI = 30.47Obese, diabetic, non-alcoholic

patients

ALT = 90 IU/L (Normal: 10-40 IU/L)aminotransferases are only mildly

elevated(1.5-2 times upper limit of normal)

rises in BP since 2003, elevated blood sugar 2 years ago

frequently seen with other components of the metabolic syndrome (HPN, DM, elevated

lipids, and obesity), insulin resistance in virtually all patients

alcohol intake not noted< 20 grams per day alcohol to exclude alcohol liver disease

Most Likely DiagnosisNon-Alcoholic Fatty Liver Disease

“Minimal ALT elevations in asymptomatic blood donors rarely indicate severe liver disease; studies have shown that fatty liver disease is the most likely explanation.”

abnormal alt week 3 big group discussion 1. overview of liver function tests group d viardo-zuniga

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