DISCUSSION
AIH is characterized by an immune reaction directed towards liver tissue
with autoantibodies being the culprit that not only commence, but also
sustain the harm [2]. Clinically, it can have a variable
presentation. There can be silent cases with no symptoms, but also there
can be patients with significant symptoms related to hepatitis, which
can rarely lead to acute liver failure as well.
AIH type 1, also known as Classical AIH, is known for the presence of
ANA and/or smooth muscle autoantibodies (AMSA) and autoantibodies
against actin and atypical perinuclear anti neutrophilic cytoplasmic
antibodies (p-ANCA). Type 2 AIH shows the occurrence of specific
antibodies which are targeted against liver and kidney microsomal
antigens (anti-LKM Ab) and/or liver cytosol type 1 antibody (ALC-1). For
making a diagnosis, we need to rule out extrinsic causes of hepatitis
such as drugs, alcohol, and viruses. Also, there should be satisfying
inclusive criteria such as hyperglobulinemia, the presence of
autoantibodies, and characteristic histologic features including
interface hepatitis, plasma cells and rosettes. In about 70-80% of AIH
cases, both ANA and ASMA can be found. Only in approximately 10% of
patients of AIH, there are no circulating autoantibodies. Apart from a
negative panel of autoantibodies, patients with SAIH are very similar to
those of classical AIH in terms of their demographic, biochemical, and
histological features. That is why they can be treated very successfully
like classical AIH with corticosteroids. Also, they have similar
prognosis after steroid therapy. SAIH has a favorable prognosis for
patients who respond to
treatment. Most of the patients who receive appropriate treatment
undergo remission, and the 10-year survival rate has approached from
83.8% to 94%. MIn the majority of cases we need to institute a
maintenance therapy for their entire life, since discontinuation of the
treatment can cause a reappearance of the disease in about 80% patients
out of 100, over a term of 3 years.
In the past, there has been a case of seronegative autoimmune hepatitis
reported by J.M. Sherigar et al. where a 58 y/o female patient came to
the emergency department due to pain in her epigastrium along with
nausea and vomiting, all the symptoms being there only for a day. That
being an acute presentation of Seronegative autoimmune hepatitis is
different from our patient who had chronic manifestations of fever and
yellowish discoloration for 2 months. Also, in their case, the patient
underwent a core liver biopsy which revealed that the portal tracts were
penetrated with lymphocytes, plasma cells, and eosinophils. It also
showed a severe grade 4 circumferential interface hepatitis, and steroid
therapy was started after biopsy findings were confirmed, while in our
case biopsy could not be performed as the patient was too unstable, so
steroid therapy was started early based on clinical suspicion, showing
how sometimes we have to start the therapy even in the absence of
definitive diagnosis.