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Case Study and Review of Autoimmune Hepatitis
Gloria Flamenco, MS, MLS (ASCP)CM*, Margot Hall, PhD, FAIC (CPC), FACB, FRACI (CChem A),
MRSC (CChem), and Anna K. Swann, MS, MLS (ASCP)CM
ABSTRACT
Autoimmune hepatitis (AIH) is a rare autoimmune disorder causing
chronic liver inflammation. The disorder, sometimes called lupoid
hepatitis, is not well understood because its clinical presentation is
highly variable. The liver becomes inflamed due to T-cell-mediated
activation of B cells that produce autoantibodies directed against
liver antigens. This article details the case of a 28-year-old female
patient who was diagnosed with AIH type I almost a decade ago; her
therapeutic regimen may serve as a useful model for the disorder.
An extensive interview was conducted with the patient. Herein, a
timeline of her diagnosis is discussed, and her laboratory results are
Case Study
In May 2001, a 21-year old woman was rushed to a local
emergency room in Virginia, after coming home from
college with severely jaundiced sclera. According to the
patient, her eyes had been yellow for a few days, which
she attributed to allergies. She reported feeling healthy
except for slight pruritus (ie, intense itching) on the backs
of her hands. Test results revealed extremely high serum
liver enzyme levels and elevated serum total and direct
bilirubin levels; small quantities of bilirubin were found in
her urine (Table 1).
Results of ultrasound imaging of her abdomen were
unremarkable. The patient was questioned extensively
about her lifestyle and her sexual history. She indicated
that she was not sexually active, did not have a history of
DOI: 10.1309/LML0OPQA9YD8TVGY
Abbreviations
ANA, antinuclear antibody; SMA, smooth muscle antibody; LKM1, liver/
kidney microsome 1; kidney microsome 1; LC1, liver cytosol 1(LC1); SLA,
soluble-liver antigen; AIH, autoimmune hepatitis
Department of Medical Technology, The University of Southern
Mississippi, Hattiesburg
*To whom correspondence should be addressed.
E-mail: gloria.flamenco@gmail.com
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presented. Currently, she is living a fairly healthy life despite her liver
disease. Her most recent liver function test results were completely
normal, which is unusual with AIH. The patient was prescribed the
immunosuppressive drug azathioprine to treat her AIH shortly after
diagnosis. She also began following a vegan diet with unrefined sugar
along with regular sleep and exercise. Currently, the patient is taking
no azathioprine due to consecutively normal liver function test results
over the past few years. Her continued health improvement could be
credited to her strict vegan diet.
Keywords: autoimmune, hepatitis, liver inflammation
Table 1. Laboratory Results From May 2001
Analyte Value Normal Reference Interval
PTT 36.7 s 21.5-34.0 s
Albumin 3.6 g/dL 3.9-5.0 g/dL
AST 714.0 U/L 5.0-40.0 U/L
ALT 960.0 U/L 7.0-56.0 U/L
Total bilirubin 8.4 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 7.6 mg/dL 0-0.4 mg/dL
GGT 201.0 U/L 3.0-60.0 U/L
PTT, partial thromboplastin time; AST, aspartate aminotransferase; ALT, alanine
aminotransferase; GGT, gamma-glutamyltransferase.
drug abuse, and consumed very little alcohol. She had not
recently been out of the country and denied any deviations
from her normal diet. Her medical history revealed that she
was a young adult woman who had been extremely healthy
and active before this admission to the hospital. The
patient insisted that other than the pruritus on her hands,
she felt well. She was discharged; in a few days, the
jaundice disappeared. She was given a probable diagnosis
of acute viral hepatitis.
In August 2001, the patient developed extreme joint pain.
She was evaluated for rheumatoid arthritis; the results were
negative. In December 2001, the pruritus on her hands
returned. Blood work revealed that her liver enzymes
remained extremely high but her bilirubin and albumin were
within normal limits (Table 2). A liver biopsy was ordered;
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the results revealed lymphocytic infiltration, eosinophils,
and plasma cells in the portal regions, with inflammatory
cells (ie, neutrophils, macrophages, monocytes, eosinophils,
and basophils) in the sinusoids. Scattered hepatic cell
necrosis was also observed. There was evidence of
scarring suggesting gradual progress of the disease. The
scarred tissue was categorized at stage 2, with some parts
categorized as stage 3 on a scale of 1 to 4. Test results
for cytomegalovirus, Epstein-Barr virus, and hepatitis A,
B, and C were negative. Antinuclear antibody (ANA) was
detected in the liver tissue extracts, with a titer of 1:160
(>1:80 indicated abnormal levels); also, a speckled ANA
pattern was observed. The biopsy and antibody screening
results indicated chronic hepatitis of autoimmune origin (oral
communication with the patient, March 2009).
Overview of the Liver
The liver is the largest internal organ in the human body1;
any substance that enters the bloodstream will pass through
the liver. The functions performed by the liver are numerous
and essential for survival. The vital functions of this organ
include synthesis of proteins such as albumin, transferrin,
and complement; the synthesis, storage, and lysis (ie,
retrieval) of fats and carbohydrates for energy production;
synthesis of bile acids and bilirubin; storage of vitamins and
minerals; and metabolism and removal of toxins.
MedicineNet.com refers to the liver as the “biochemical
factory of the body.”2 The structural organization of the liver
includes the left, right, caudate, and quadrate lobes. The
microscopic organizational unit of the liver is the acinus.1 The
acini are further divided into zones I, II, or III, with each zone
having different functions to regulate blood flow through
the liver. Microscopic tubules called canaliculi are found
throughout the liver and transport bile to the gallbladder for
storage. Bile is prepared in the individual parenchymal cells
of the liver, known as the hepatocytes. The hepatic blood
supply is delivered via 2 routes, namely, the hepatic artery
and the portal vein. The hepatic artery delivers oxygenated
blood from the lungs, and the portal vein carries nutrients
other substances absorbed from the intestine. Blood from
the hepatic artery combines with blood from the portal vein
in a network of tiny blood vessels called sinusoids.2
Liver disease results when these functions are not occurring
normally. However, the liver has substantial functional
reserve, and significant damage must occur before liver
impairment is clinically evident. Abnormally elevated levels
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Table 2. Laboratory Results From December
2001
Analyte Value Normal Reference Interval
Hemoglobin 12.9 g/dL 13.0-17.2 g/dL
Albumin 4.2 g/dL 3.9-5.0 g/dL
AST 407.0 U/L 5.0-40.0 U/L
ALT 843.0 U/L 7.0-56.0 U/L
Total bilirubin 0.7 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 0.2 mg/dL 0-0.4 mg/dL
AST, aspartate aminotransferase; ALT, alanine aminotransferase.
of liver enzymes and proteins are suggestive of liver disease.
Autoantibodies such as ANAs or smooth muscle antibodies
(SMAs) against liver antigens can reflect autoimmune liver
disease.1 The type of antibodies against the liver are used
to indicate the presence and type of autoimmune hepatitis
(AIH). For proper, accurate diagnosis of AIH, a liver biopsy
should be performed to assess the stage of hepatic tissue
necrosis and/or cirrhosis. Early diagnosis and treatment
of AIH improves the chance of the liver being able to
regenerate healthy tissue.2
Overview of Autoimmune
Disease
Autoimmune disease is a group of disorders in which
the immune system produces antibodies against healthy
organs and tissues. Currently, there are more than 80
different diseases known to be autoimmune.3 The liver
was one of the first organs recognized to be targeted
by autoantibodies.4 In 1950, Waldenström described an
inflamed liver due to an unknown cause that produced
hypergammaglobulinemia and cirrhosis; he called this
inflammation chronic active or active chronic hepatitis
and believed it to result from a previous liver infection.
However, in the 1960s it was observed that there were no
prerequisites for the contraction of chronic active hepatitis.
Then, in 1972, shortly after the discovery of the encoding of
the HLA genes that are part of the major histocompatibility
complex, it was discovered that patients with the disease
had an increased frequency of HLA-DRB1 (GenBank:
JX667743.1), a particular locus allele gene set.5 This
observation suggested that autoimmunity was a factor in
these individuals. Some of the antigens against which the
autoantibodies are produced have been identified.6 Today,
Waldenström’s chronic active hepatitis is known as AIH.
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AIH affects approximately 0.1 to 1.2 of every 100 000
individuals.7 It occurs due to a CD4+ T-cell mediated
series of events acting against a peptide expressed in
the liver. This series of events begins when a naïve CD4+
T-helper cell detects a liver peptide it does not recognize
as belonging to “self.” The T-helper cell becomes activated,
differentiating and producing cytokines.4 The T-helper
cell differentiates into several types of cells. The Th1 cells
activate macrophages, enhance HLA class I expression,
and induce HLA class II expression on the surface of
liver cells. This increases the exposure of the liver cells to
CD+8 cytotoxic attack. The Th2 cells handle autoantibody
production.8 Regulation of self-recognition is controlled by
CD+4CD+25 T cells; failure of this regulation allows for the
autoimmune response.4 It is thought that environmental
causes trigger the CD4+CD+25 T cells to fail. However, this
only becomes a problem in individuals who are genetically
predisposed toward this outcome.6 Most affected
individuals are female, with HLA-DRB1 *0301 (GenBank
Accession NM_022555) HLA-DRB1 *0401 (GenBank
Accession AF 035803), and HLA-DRB3 *0101 (GenBank
Accession AF 152844) haplotypes.7 Untreated, AIH can
result in cirrhosis and liver failure.9 AIH is a chronic, often
lifelong disease characterized by increased autoantibodies
in circulation and inflammation around the portal vein. The
disease has a variable presentation. Because of increasing
and decreasing immunological activity, it makes AIH difficult
to diagnose. The disease does not have unique histological
characteristics; it is histologically similar to other chronic
liver diseases.10 Common signs and symptoms of AIH
include fatigue, malaise, arthralgia, abdominal pain, and
pruritus of the hands. Laboratory findings include increased
levels of the serum globulins, aminotransferases, and
alkaline phosphatase, and prolonged partial thromboplastin
time, typically without hyperbilirubinemia. AIH responds to
corticosteroid and other immunosuppressive therapy, but is
not currently curable. With proper management, remission
of symptoms can be achieved, and further damage to the
liver can be halted.11
Subtypes of AIH
AIH is grouped into types I, II, and III.12 Type I is the most
common, followed by type II and type III; all 3 types mainly
affect females. Type I and III are usually diagnosed in
females in their teens to mid-thirties, whereas type II is
often diagnosed in childhood. The clinical severities of AIH
vary with each patient; however, the clinical presentations
of the 3 types are similar.
The 3 types differ only by the autoantibodies that are
present. Autoantibodies associated with type I AIH are
ANAs and SMAs. In type II AIH autoantibodies are anti–
liver/kidney microsome 1 (LKM1), and anti–liver cytosol 1
(LC1). The type III AIH autoantibodies react with the soluble
liver antigen (SLA).13 Table 3 compares the 3 types of AIH.
Diagnosis and Treatment
of the Patient
The patient was diagnosed with AIH, type I, in January
2002. Her diagnosis was based on her increased levels of
serum aminotransferases, biopsy results, and positive ANA
titer of 1:160 with a speckled pattern. She was immediately
started on corticosteroid treatment (prednisone, 50
mg per day). Corticosteroids block the synthesis of

Table 3. Characteristics of Autoimmune Hepatitis, Types I to III6,7

Variable Type I Type II Type III

Autoantibodies ANA, SMA, anti-actin, anti-FLAG, L-PAG Anti-LKM1, anti-LC1 Anti-SLA  

Epidemiologic occurrence Most common in United States Rare in adults in United States Rare (<3% of patients)
   and worldwide  and worldwide
Sex of patients 75% female 95% girls Typically young, female
Clinical severity Broad Generally severe Broad-severe; usually present
  with another AID
Treatment failure Infrequent Frequent Infrequent
Cirrhosis 45% 80% 75%
Need for long-term management Variable Approximately 100% Variable
Relapse after drug withdrawal Variable Common Variable

ANA, antinuclear antibody; SMA, smooth muscle antibody; anti-FLAG, anti–epitope DYKDDDDK; L-PAG; anti-LKM1, anti–liver/kidney microsome 1; anti-LC1, anti–liver cytosol
1; anti-SLA, anti–soluble-liver antigen; AID, autoimmune disorder.

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lymphokines and cytokines, inhibiting the T-cell response
and decreasing the numbers of T and B cells in circulation.
The immmunosuppressive drug azathioprine was added to
the patient’s regimen (100 mg/d); the drug inhibits purine
synthesis, suppressing DNA, RNA and protein synthesis.1
After one month on this regimen, her liver function test
results (Table 4) were close to normal. When an individual
is taking azathioprine, the white-blood-cell count should
be monitored on a regular basis to prevent possible bone
marrow malfunction.1 After having taken azathioprine for 1
month, the patient’s white blood cell count was 9.30 × 109
cells/mL (normal range, 4.00-11.00 × 109 cells/mL).
Although the patient was advised that a change in diet
was unnecessary, the patient began a vegetarian diet. The
patient’s health seemed to be improving until she began
feeling adverse effects from the prednisone. The adverse
effects of this drug include loss of appetite, menstrual
period irregularities, gastrointestinal upset, sore throat,
malaise, headache, fever, depression, dizziness, lethargy,
exaggerated sense of well-being, mood swings, personality
changes, thinning of bones, thinning of hair and skin, puffing
of the face, swelling of feet and/or legs, weight gain, or
weight loss.9 The patient experienced moderate-to-severe
side effects ranging from loss of appetite to chronic sore
throat and swelling of the extremities.
Following the cessation of prednisone therapy, the patient’s
immune system became hyperactive; small cuts and
mosquito bites would swell to abnormal sizes and would
not heal. In July 2003, the patient began relapsing into AIH
symptoms. Her laboratory results indicated normal values
except for a high eosinophil count and a low neutrophil
count. These abnormal cell counts could be responsible for
her exaggerated immune reactions to the small cuts and
mosquito bites. Eosinophils are released during allergic
reactions. What triggered the release of eosinophils in the
patient is unknown. The low neutrophil count might have
been due to immunosuppressive therapy. After the patient’s
relapse, she was diagnosed with depression. Bupropion
hydrochloride (Wellbutrin, GlaxoSmithKline, London,
England) was prescribed to treat her depression.
In August 2003, the patient suffered an anaphylactic-like
reaction in which her throat and tongue swelled enough
to hinder breathing; the reaction was attributed to the
bupropion hydrochloride. The patient was switched to
sertraline hydrochloride (Zoloft, Pfizer Inc, New York, NY)
for treatment of her depression. Within the next year, she
suffered 2 more episodes of this anaphylactic-like reaction;
the cause of these episodes was never confirmed. Through
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Table 4. Laboratory Results From January 2002
Analyte Value Normal Reference Interval
Hemoglobin 13.3 g/dL 13.0-17.2 g/dL
Albumin 4.0 g/dL 3.9-5.0 g/dL
AST 35.0 U/L 5.0-40.0 U/L
ALT 78.0 U/L 7.0-56.0 U/L
Total bilirubin 0.7 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 0.2 mg/dL 0-0.4 mg/dL
the end of 2003 and the year 2004, the patient experienced
poor health. She reported feeling very tired, experiencing
lethargy, and becoming more depressed. She was still
suffering adverse effects of prednisone and azathioprine.
The adverse effects of azathiopurine, namely, occasional
hoarseness and a sore throat were not as severe as those
from prednisone. The patient converted to a vegan diet,
which does not contain meat, poultry, eggs, fish, or dairy.14
this change was made without recommendation from a
physician. Another dietary change she made was a switch
to unrefined sugar. The patient stated that she wanted to
give her liver the simplest nourishment to process so that
it had a chance to recover (oral communication with the
patient, March 2009).
At the beginning of 2005, the patient’s health showed
improvement. Her liver-function test results were within
the normal range. She had a second biopsy performed in
February 2006, the results of which showed inflammatory
cell infiltrates composed of lymphocytes but few plasma cells
or eosinophils. The sinusoids were slightly dilated, and no
cellular necrosis was observed; mild fibrosis was observed.
ANA results remained positive at a titer of 1:80, rather than
1:160, as had been the case 2 years earlier. Results of the
patient’s liver function test are shown in Table 5.
Table 5. Laboratory Results from February 2006
Analyte Value Normal Reference Interval
Albumin 4.6 g/dL 3.9-5.0 g/dL
AST 14.0 U/L 5.0-40.0 U/L
ALT 10.0 U/L 7.0-56.0 U/L
Total bilirubin 0.4 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 0.1 mg/dL 0-0.4 mg/dL
GGT 10.0 U/L 3.0-60.0 U/L
AST, aspartate aminotransferase; ALT, alanine aminotransferase, GGT, gamma-
glutamyltransferase.
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 Rounds

2002 Exaggerated sense of well-being, appetite loss, and changes

Figure 1

Adverse effects of prednisone (50 mg/
day) experienced by the patient between
January 2002 and December 2004.
↓
  in menstrual periods
General body discomfort, prolonged sore throat, and mood swings
2004 Weight gain, facial puffiness, and depression

AST values
800
Figure 2
700
Aspartate aminotransferase values for the patient between 2001

AST Levels in U/L

600
and 2008. 500
400
300
200
100
0
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ALT values
1,200
Figure 3
ALT Levels in U/L

1,000
Alanine aminotransferase levels for the patient between 2001 and 800
600
2008.
400
200
0
–200
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Vegan diets are typically higher in vitamins C and E, folic
acid, fiber, magnesium, potassium, phytochemicals, and
unsaturated fats than typical non-vegan diets. Vegan diets
are low in vitamin D, protein, retinol, vitamin B12, calcium,
and zinc. Many foods are fortified with these nutrients;
however, supplements must often be taken to achieve a
healthy, balanced diet.15
During the next year, the patient’s overall health improved.
Her laboratory results returned to normal. She continued
to follow her vegan diet strictly. In June 2007, the patient
experienced another anaphylactic-like reaction along with
urticaria. A brief course of prednisone was prescribed,
which cleared up the rash. The patient had taken naproxen
sodium before the urticaria occurred; however, she had
taken the anti-inflammatory drug on several previous
occasions without adverse effects. Her case of hives was
attributed to the unstable functioning of her immune system.
In May 2008, the patient was assessed as being in
remission from her disease. Results of her liver function
test for an 8-year period can be seen in Figure 1, Figure
2, and Figure 3).
Patient Outlook
In June 2010, the patient had a checkup in which her
laboratory results were normal and her ANA test results were

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Alkaline Phosphate Levels in U/L

ALP values
Figure 4
180
Alkaline phosphatase levels for the patient between 2001 and 160
2008. 140
120
100
80
60
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negative. After 3 years of normal values on her laboratory

tests, her physicians decided to begin withdrawal of her
azathioprine in stages. Her dosage would be lowered by 25
mg every 3 to 6 months until the medicine was completely
discontinued. If her liver function test results remained
normal, the patient would cease use of the drug within 2
years. By October 2011, the patient was no longer taking
azathioprine. The patient continued to have normal liver
function test results throughout 2011 and 2012. Remarkably,
the patient has been in total remission of AIH with no
immunosuppressive drugs for over a year.
There is no cure for AIH; management of the disease must
be individualized to each patient. Proper management of
AIH can alleviate the inflammation of liver tissue, slow the
disease development prolonging the life of the patient,
and avoid the need for a liver transplant.11 The typical
treatment of AIH involves corticosteroids with or without
an immunosuppressive drug, regardless of the type of
AIH. Successful treatment of the disease is more likely
with early diagnosis, which is difficult because diagnostic
criteria are not widely agreed on. Typically, if the patient
responds to treatment for a period of approximately
5 years, withdrawal from or decreasing the dosage
of medicines is possible.16 Remission is achieved in
approximately 7 of 10 individuals with AIH. Remission
usually is not permanent; symptoms of the disease often
return within a year. However, about 1 in 3 patients with
AIH are successful enough with treatment to discontinue
the drugs at some point in their therapy.12 There have been
reports of patients who have been off treatment for as
long as 11 years whose disease has suddenly relapsed.16
Treatment of AIH requires constant surveillance.
Discussion and Conclusion
The patient described herein has been living with type I
AIH for nearly a decade. She has been in remission for
the past 5 years. She began her steroid and immunosup-
pressive medical regimen in early 2002. Figures 2, 3,
and 4 show serum aspartate aminotransferase, alanine
aminotransferase, and alkaline phosphatase values during
the 9-year period when the patient had active AIH. These
laboratory values decreased significantly when she first
began anti-inflammatory and immunosuppressive ther-
apy. Subsequently, her test values remained in the normal
range after the vegan diet had been implemented in late
2002 and early 2003.
The patient has been successfully off of the
immunosuppressive drug since October 2011. Since the
patient is in the beginning stages of remission with no
immunosuppressive drug therapy, it cannot yet be safely
stated that a vegan diet is effective in the treatment
of AIH. However, it is possible that liver damage
may be attenuated or halted by merely changing the
patient’s diet. This patient demonstrated considerable
improvement after a course of immunosuppressive
drugs even before starting the dietary regimen. Studies
assessing the effect of diet on this disease may lead to
improved prevention and treatment of AIH. Nonetheless,
diet should be incorporated more into the management
of this rare autoimmune disorder. Has this patient found
a way to properly manage autoimmune hepatitis without
harsh, costly drugs through the vegan diet? With this
case, only time will tell. LM

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