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studies, i.e. magnetic resonance cholangiography. The treatment is comprised of
immunosuppression, which is associated with a good response in the hepatocellu-
lar injury component of the disease. In contrast, the injurious process of the bile
duct is not halted by this type of therapy in approximately half of the affected
patients. The need for liver transplantation in this type of liver disease is increased
in the PSE AIH variant, as is the disease's recurrence in the liver graft post trans-
plantation [144].
The treatment for AIH in children is prednisone (or prednisolone) in combina-
tion with azathioprine; as in adults, treatment should be individualized. A proposed
treatment for AIH consists of prednisolone per body weight, orally, daily of 2 to a
maximum dose of 60 mg during the rst week of treatment, with subsequent
decreases by 0.25mg/kg/day until completion of the seventh week of treatment, to
0.25 during the eighth and ninth weeks, and to 0.1–0.2 during the tenth and elev-
enth weeks. Evaluation with hepatic panel is recommended weekly prior to decreas-
ing the dose of steroids; if the decrease in AST and ATL activity stops, it is
recommended to add AZA at a dose of 0.5mg/day with increases to 2–2.5mg/kg/
day, until the goal is achieved. The dose of steroids should be decreased to 2–2.5mg/
kg/day over 2weeks and then discontinued if serious side effects arise during their
use [145]. The use of AZA as rst-line treatment is not recommended because of
potential toxicity, especially in patients with hyperbilirubinemia; however, most
patients have been reported to require the addition of this drug to achieve remis-
sion. Testing for TPMT is also applied in children, as is the monitoring of AZA
metabolites, 6-thioguanine, and 6-methylmercaptopurine, to identify the optimal
therapeutic level of AZA, as reported in a prospective study that included 20 chil-
dren with AIH [146], and as done in the treatment of inammatory bowel disease.
The optimal levels of these metabolites in relation to AZA's salutary effect have not
been clearly established [147]. A recent report documented that a majority of chil-
dren on AZA therapy maintained biochemical remissions at 6-TGN levels ranging
from 50 to 250pmol/8×10
8
RBC, in association with the lowest doses of the drug,
suggesting that AZA can be used as a steroid sparing agent in children with AIH
[148], as it is done in adult subjects. This information can be used as doses are
adjusted [106].
The goal of treatment is remission, dened as: (i) no symptoms, (ii) normal
serum activity of AST and ALT, and (iii) normal serum concentrations of IgG.In
addition, low or absent titers for ANA and ASMA, and anti-LKM are included in the
criteria for remission [149].
In general, the duration of standard therapy is 24months in patients aged 60 or
beyond and 36months in patients up to 40years of age. Remission of AIH has been
dened as normal AST activity in two consecutive months and absence of symp-
toms. Discontinuation of immunosuppression therapy can be considered after docu-
mented normal AST and ALT serum activity every 3months for at least 1year and
the absence of necroinammatory activity on liver histology. Serum AST activity
was reported to correlate with serum concentrations of IgG in types 1 and 2 AIH and
with titers of ASMA in type 1, suggesting that these markers can be included as
measures of response to treatment [150].
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From a retrospective study that included 20years of experience in the treatment
of children with AIH, it was reported that discontinuation of therapy was possible in
19% of ANA and ASMA positive patients after treatment for a median of 3years;
however, in this series, none of the patients who had anti-LKM antibodies were able
to have therapy discontinued [151]. Close monitoring of patients and their labora-
tory exams are required to identify and treat relapse of disease, dened as an increase
in AST activity by two fold from baseline. Relapses of AIH are treated with pred-
nisolone (or prednisone) at 1–2mg/kg/day, a dose that can be increased to 2–2.5mg/
kg/day untilthetherapeutic goal is achieved (see above).
Penicillamine, cyclosporin A, and mycophenolic mofetil have been used in chil-
dren who do not respond to standard therapy [152]; however, alternate treatments
have not been tested in randomized clinical trials. The reader is referred to clinical-
trials.gov for information on available clinical studies.
Liver Transplantation
Liver transplantation is the alternative to the treatment of AIH not responsive to
immunosuppressant therapy. Prospectively studied, it was documented that from a
group of 1429 patients, 55 (3.8%) were transplanted for AIH, the majority of whom
were women, and tended to exhibit episodes of rejection within the rst 3, 6, and
12 months; however, the patient and graft survivals were similar to those trans-
planted for other indications [153]. The survival rate of patients with AIH who
undergo liver transplantation is reported as 87% at 1year and from 80% to 90% at
ve, and the survival rates of liver grafts are 84% at 1 year and 74–76% at ve
[154, 155].
AIH recurs in the liver graft. A large prospective study reported that 20% of
patients sustained a recurrence of disease, most within the rst year after transplan-
tation. However, none of these patients required retransplantation because of dis-
ease recurrence [153]. The literature reports the clinical presentation of AIH
recurrence from 1month to 5years post transplant [155]; recurrences after 15years
have been documented [156] and also, with histological ndings in the graft at least
5years before a clinical presentation suggestive of recurrence in 24% of patients in
a published series [156]. A retrospective review did not report any recurrence,
though, in the six out of 32 patients who were transplanted for acute liver failure at
presentation [157]. The criteria that dene recurrent AIH can be summarized as fol-
lows: (1) indication of AIH for transplant, (2) autoantibodies at high titers, (3) per-
sistently increase in the activity of ALT over twice the upper limit of normal, (4)
high serum immunoglobulin concentration, (5) liver histology compatible for AIH,
(6) dependency on corticosteroid to maintain normal liver prole or need to increase
steroid dose, and (7) exclusion of other causes of post transplant hepatitis or graft-
dysfunction [155, 158].
Post transplant de novo AIH occurs in patients who have received a liver trans-
plant for diseases other than AIH [159]. It was initially reported in children, with
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4% of patients from 180 developing the disease over 5years [160]. Histologically
this condition is characterized by interface hepatitis, and an inammatory inltrate
highly comprised of plasma cells. The factors that have been identied as predispos-
ing to de novo AIH are HLA-DR3 or HLA-DR4 recipient or donor, previous epi-
sodes of acute cellular rejection, steroid dependence, female donor, aged donor, and
tacrolimus-based immunosuppression [159]. The treatment of post transplant de
novo AIH is the standard therapy for AIH, emphasizing the importance of making
the diagnosis of de novo post transplant AIH promptly not to deviate treatment
efforts to a presumed diagnosis of rejection, to preserve the life of the graft [161].
The importance of treatment with steroids was documented in a case series in which
ve non-treated patients lost the graft a few months after diagnosis of de novo AIH
in contrast to the seven who were treated, none of whom lost their graft after a fol-
low- up period of a mean of 4years; also, the tapering of steroids was associated
with relapse [162]. A long-term study has found that de novo AIH does respond to
treatment, but relapse and progression to cirrhosis were documented [163].
Acknowledgments The author acknowledges Dr. Cesar del Rosario for having contributed
Figures4.1, 4.2, and 4.3.
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