Rounds

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 presented. Currently, she is living a fairly healthy life despite her liver
disease. Her most recent liver function test results were completely
Autoimmune hepatitis (AIH) is a rare autoimmune disorder causing normal, which is unusual with AIH. The patient was prescribed the
chronic liver inflammation. The disorder, sometimes called lupoid immunosuppressive drug azathioprine to treat her AIH shortly after
hepatitis, is not well understood because its clinical presentation is diagnosis. She also began following a vegan diet with unrefined sugar
highly variable. The liver becomes inflamed due to T-cell-mediated along with regular sleep and exercise. Currently, the patient is taking
activation of B cells that produce autoantibodies directed against no azathioprine due to consecutively normal liver function test results
liver antigens. This article details the case of a 28-year-old female over the past few years. Her continued health improvement could be
patient who was diagnosed with AIH type I almost a decade ago; her credited to her strict vegan diet.
therapeutic regimen may serve as a useful model for the disorder.
An extensive interview was conducted with the patient. Herein, a Keywords: autoimmune, hepatitis, liver inflammation
timeline of her diagnosis is discussed, and her laboratory results are

Table 1. Laboratory Results From May 2001

Case Study
Analyte Value Normal Reference Interval
In May 2001, a 21-year old woman was rushed to a local
PTT 36.7 s 21.5-34.0 s
emergency room in Virginia, after coming home from
Albumin 3.6 g/dL 3.9-5.0 g/dL
college with severely jaundiced sclera. According to the AST 714.0 U/L 5.0-40.0 U/L
patient, her eyes had been yellow for a few days, which ALT 960.0 U/L 7.0-56.0 U/L
she attributed to allergies. She reported feeling healthy Total bilirubin 8.4 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 7.6 mg/dL 0-0.4 mg/dL
except for slight pruritus (ie, intense itching) on the backs
GGT 201.0 U/L 3.0-60.0 U/L
of her hands. Test results revealed extremely high serum
liver enzyme levels and elevated serum total and direct PTT, partial thromboplastin time; AST, aspartate aminotransferase; ALT, alanine
aminotransferase; GGT, gamma-glutamyltransferase.
bilirubin levels; small quantities of bilirubin were found in
her urine (Table 1).

Results of ultrasound imaging of her abdomen were drug abuse, and consumed very little alcohol. She had not
unremarkable. The patient was questioned extensively recently been out of the country and denied any deviations
about her lifestyle and her sexual history. She indicated from her normal diet. Her medical history revealed that she
that she was not sexually active, did not have a history of 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,
DOI: 10.1309/LML0OPQA9YD8TVGY she felt well. She was discharged; in a few days, the
jaundice disappeared. She was given a probable diagnosis
Abbreviations of acute viral hepatitis.
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 In August 2001, the patient developed extreme joint pain.
She was evaluated for rheumatoid arthritis; the results were
Department of Medical Technology, The University of Southern negative. In December 2001, the pruritus on her hands
Mississippi, Hattiesburg
returned. Blood work revealed that her liver enzymes
*To whom correspondence should be addressed. remained extremely high but her bilirubin and albumin were
E-mail: gloria.flamenco@gmail.com within normal limits (Table 2). A liver biopsy was ordered;

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 Rounds

the results revealed lymphocytic infiltration, eosinophils,

Table 2. Laboratory Results From December
and plasma cells in the portal regions, with inflammatory 2001
cells (ie, neutrophils, macrophages, monocytes, eosinophils,
and basophils) in the sinusoids. Scattered hepatic cell Analyte Value Normal Reference Interval
necrosis was also observed. There was evidence of
Hemoglobin 12.9 g/dL 13.0-17.2 g/dL
scarring suggesting gradual progress of the disease. The
Albumin 4.2 g/dL 3.9-5.0 g/dL
scarred tissue was categorized at stage 2, with some parts AST 407.0 U/L 5.0-40.0 U/L
categorized as stage 3 on a scale of 1 to 4. Test results ALT 843.0 U/L 7.0-56.0 U/L
for cytomegalovirus, Epstein-Barr virus, and hepatitis A, Total bilirubin 0.7 mg/dL 0.2-1.3 mg/dL
B, and C were negative. Antinuclear antibody (ANA) was Direct bilirubin 0.2 mg/dL 0-0.4 mg/dL
detected in the liver tissue extracts, with a titer of 1:160 AST, aspartate aminotransferase; ALT, alanine aminotransferase.
(>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). 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
Overview of the Liver to indicate the presence and type of autoimmune hepatitis
(AIH). For proper, accurate diagnosis of AIH, a liver biopsy
The liver is the largest internal organ in the human body1; should be performed to assess the stage of hepatic tissue
any substance that enters the bloodstream will pass through necrosis and/or cirrhosis. Early diagnosis and treatment
the liver. The functions performed by the liver are numerous of AIH improves the chance of the liver being able to
and essential for survival. The vital functions of this organ regenerate healthy tissue.2
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 Overview of Autoimmune
minerals; and metabolism and removal of toxins.
Disease
MedicineNet.com refers to the liver as the “biochemical Autoimmune disease is a group of disorders in which
factory of the body.”2 The structural organization of the liver the immune system produces antibodies against healthy
includes the left, right, caudate, and quadrate lobes. The organs and tissues. Currently, there are more than 80
microscopic organizational unit of the liver is the acinus.1 The different diseases known to be autoimmune.3 The liver
acini are further divided into zones I, II, or III, with each zone was one of the first organs recognized to be targeted
having different functions to regulate blood flow through by autoantibodies.4 In 1950, Waldenström described an
the liver. Microscopic tubules called canaliculi are found inflamed liver due to an unknown cause that produced
throughout the liver and transport bile to the gallbladder for hypergammaglobulinemia and cirrhosis; he called this
storage. Bile is prepared in the individual parenchymal cells inflammation chronic active or active chronic hepatitis
of the liver, known as the hepatocytes. The hepatic blood and believed it to result from a previous liver infection.
supply is delivered via 2 routes, namely, the hepatic artery However, in the 1960s it was observed that there were no
and the portal vein. The hepatic artery delivers oxygenated prerequisites for the contraction of chronic active hepatitis.
blood from the lungs, and the portal vein carries nutrients Then, in 1972, shortly after the discovery of the encoding of
other substances absorbed from the intestine. Blood from the HLA genes that are part of the major histocompatibility
the hepatic artery combines with blood from the portal vein complex, it was discovered that patients with the disease
in a network of tiny blood vessels called sinusoids.2 had an increased frequency of HLA-DRB1 (GenBank:
JX667743.1), a particular locus allele gene set.5 This
Liver disease results when these functions are not occurring observation suggested that autoimmunity was a factor in
normally. However, the liver has substantial functional these individuals. Some of the antigens against which the
reserve, and significant damage must occur before liver autoantibodies are produced have been identified.6 Today,
impairment is clinically evident. Abnormally elevated levels 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 corticosteroid and other immunosuppressive therapy, but is
individuals.7 It occurs due to a CD4+ T-cell mediated not currently curable. With proper management, remission
series of events acting against a peptide expressed in of symptoms can be achieved, and further damage to the
the liver. This series of events begins when a naïve CD4+ liver can be halted.11
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 Subtypes of AIH
activate macrophages, enhance HLA class I expression,
and induce HLA class II expression on the surface of AIH is grouped into types I, II, and III.12 Type I is the most
liver cells. This increases the exposure of the liver cells to common, followed by type II and type III; all 3 types mainly
CD+8 cytotoxic attack. The Th2 cells handle autoantibody affect females. Type I and III are usually diagnosed in
production.8 Regulation of self-recognition is controlled by females in their teens to mid-thirties, whereas type II is
CD+4CD+25 T cells; failure of this regulation allows for the often diagnosed in childhood. The clinical severities of AIH
autoimmune response.4 It is thought that environmental vary with each patient; however, the clinical presentations
causes trigger the CD4+CD+25 T cells to fail. However, this of the 3 types are similar.
only becomes a problem in individuals who are genetically
predisposed toward this outcome.6 Most affected The 3 types differ only by the autoantibodies that are
individuals are female, with HLA-DRB1 *0301 (GenBank present. Autoantibodies associated with type I AIH are
Accession NM_022555) HLA-DRB1 *0401 (GenBank ANAs and SMAs. In type II AIH autoantibodies are anti–
Accession AF 035803), and HLA-DRB3 *0101 (GenBank liver/kidney microsome 1 (LKM1), and anti–liver cytosol 1
Accession AF 152844) haplotypes.7 Untreated, AIH can (LC1). The type III AIH autoantibodies react with the soluble
result in cirrhosis and liver failure.9 AIH is a chronic, often liver antigen (SLA).13 Table 3 compares the 3 types of AIH.
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 Diagnosis and Treatment
to diagnose. The disease does not have unique histological
characteristics; it is histologically similar to other chronic
of the Patient
liver diseases.10 Common signs and symptoms of AIH The patient was diagnosed with AIH, type I, in January
include fatigue, malaise, arthralgia, abdominal pain, and 2002. Her diagnosis was based on her increased levels of
pruritus of the hands. Laboratory findings include increased serum aminotransferases, biopsy results, and positive ANA
levels of the serum globulins, aminotransferases, and titer of 1:160 with a speckled pattern. She was immediately
alkaline phosphatase, and prolonged partial thromboplastin started on corticosteroid treatment (prednisone, 50
time, typically without hyperbilirubinemia. AIH responds to 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

Table 4. Laboratory Results From January 2002
and decreasing the numbers of T and B cells in circulation.
The immmunosuppressive drug azathioprine was added to Analyte Value Normal Reference Interval
the patient’s regimen (100 mg/d); the drug inhibits purine
synthesis, suppressing DNA, RNA and protein synthesis.1 Hemoglobin 13.3 g/dL 13.0-17.2 g/dL
Albumin 4.0 g/dL 3.9-5.0 g/dL
After one month on this regimen, her liver function test AST 35.0 U/L 5.0-40.0 U/L
results (Table 4) were close to normal. When an individual ALT 78.0 U/L 7.0-56.0 U/L
is taking azathioprine, the white-blood-cell count should Total bilirubin 0.7 mg/dL 0.2-1.3 mg/dL
be monitored on a regular basis to prevent possible bone Direct bilirubin 0.2 mg/dL 0-0.4 mg/dL
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).
the end of 2003 and the year 2004, the patient experienced
Although the patient was advised that a change in diet poor health. She reported feeling very tired, experiencing
was unnecessary, the patient began a vegetarian diet. The lethargy, and becoming more depressed. She was still
patient’s health seemed to be improving until she began suffering adverse effects of prednisone and azathioprine.
feeling adverse effects from the prednisone. The adverse The adverse effects of azathiopurine, namely, occasional
effects of this drug include loss of appetite, menstrual hoarseness and a sore throat were not as severe as those
period irregularities, gastrointestinal upset, sore throat, from prednisone. The patient converted to a vegan diet,
malaise, headache, fever, depression, dizziness, lethargy, which does not contain meat, poultry, eggs, fish, or dairy.14
exaggerated sense of well-being, mood swings, personality this change was made without recommendation from a
changes, thinning of bones, thinning of hair and skin, puffing physician. Another dietary change she made was a switch
of the face, swelling of feet and/or legs, weight gain, or to unrefined sugar. The patient stated that she wanted to
weight loss.9 The patient experienced moderate-to-severe give her liver the simplest nourishment to process so that
side effects ranging from loss of appetite to chronic sore it had a chance to recover (oral communication with the
throat and swelling of the extremities. patient, March 2009).

Following the cessation of prednisone therapy, the patient’s At the beginning of 2005, the patient’s health showed
immune system became hyperactive; small cuts and improvement. Her liver-function test results were within
mosquito bites would swell to abnormal sizes and would the normal range. She had a second biopsy performed in
not heal. In July 2003, the patient began relapsing into AIH February 2006, the results of which showed inflammatory
symptoms. Her laboratory results indicated normal values cell infiltrates composed of lymphocytes but few plasma cells
except for a high eosinophil count and a low neutrophil or eosinophils. The sinusoids were slightly dilated, and no
count. These abnormal cell counts could be responsible for cellular necrosis was observed; mild fibrosis was observed.
her exaggerated immune reactions to the small cuts and ANA results remained positive at a titer of 1:80, rather than
mosquito bites. Eosinophils are released during allergic 1:160, as had been the case 2 years earlier. Results of the
reactions. What triggered the release of eosinophils in the patient’s liver function test are shown in Table 5.
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, Table 5. Laboratory Results from February 2006
England) was prescribed to treat her depression.
Analyte Value Normal Reference Interval
In August 2003, the patient suffered an anaphylactic-like
Albumin 4.6 g/dL 3.9-5.0 g/dL
reaction in which her throat and tongue swelled enough AST 14.0 U/L 5.0-40.0 U/L
to hinder breathing; the reaction was attributed to the ALT 10.0 U/L 7.0-56.0 U/L
bupropion hydrochloride. The patient was switched to Total bilirubin 0.4 mg/dL 0.2-1.3 mg/dL
Direct bilirubin 0.1 mg/dL 0-0.4 mg/dL
sertraline hydrochloride (Zoloft, Pfizer Inc, New York, NY) GGT 10.0 U/L 3.0-60.0 U/L
for treatment of her depression. Within the next year, she
AST, aspartate aminotransferase; ALT, alanine aminotransferase, GGT, gamma-
suffered 2 more episodes of this anaphylactic-like reaction; glutamyltransferase.
the cause of these episodes was never confirmed. Through

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

Figure 1

↓
  in menstrual periods
Adverse effects of prednisone (50 mg/
day) experienced by the patient between General body discomfort, prolonged sore throat, and mood swings
January 2002 and December 2004. 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
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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
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–200
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Vegan diets are typically higher in vitamins C and E, folic taken the anti-inflammatory drug on several previous
acid, fiber, magnesium, potassium, phytochemicals, and occasions without adverse effects. Her case of hives was
unsaturated fats than typical non-vegan diets. Vegan diets attributed to the unstable functioning of her immune system.
are low in vitamin D, protein, retinol, vitamin B12, calcium,
and zinc. Many foods are fortified with these nutrients; In May 2008, the patient was assessed as being in
however, supplements must often be taken to achieve a remission from her disease. Results of her liver function
healthy, balanced diet.15 test for an 8-year period can be seen in Figure 1, Figure
2, and Figure 3).
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 Patient Outlook
urticaria. A brief course of prednisone was prescribed,
which cleared up the rash. The patient had taken naproxen In June 2010, the patient had a checkup in which her
sodium before the urticaria occurred; however, she had 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
40
20
0

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negative. After 3 years of normal values on her laboratory

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

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8. Stevens, CD. Clinical Immunology and Serology: A Laboratory

Perspective. 3rd edn. Philadelphia: F.A. Davis Company; 2003.
To read this article online, scan
9. U.S. Department of Health and Human Services, National Institute of
the QR code, http://labmed.
Diabetes and Digestive and Kidney Diseases. Autoimmune Hepatitis.
ascpjournals.org/content/44/1/79. National Digestive Diseases Information Clearinghouse Web site.
full.pdf+html http://digestive .niddk.nih.gov/ddiseases/pubs/autoimmunehep/.
Accessed November 15, 2012.
10. Alvarez F, Berg PA, Bianchi FB, et al. International Autoimmune
Hepatitis Group Report: review of criteria for diagnosis of
autoimmune hepatitis. J Hepatol. 1999;31:929-938.

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