Review
Copyright ©The Author(s) 2016.
World J Gastroenterol. Mar 14, 2016; 22(10): 2906-2914
Published online Mar 14, 2016. doi: 10.3748/wjg.v22.i10.2906
Table 1 Differential features of de novo autoimmune hepatitis from other resembling etiologies of late graft dysfunction[1,2,7,8,58]
de novo AIHHCV recurrenceAcute rejectionChronic rejection
Laboratory onsetHBV/HCV/HIV/CMV/EBV negativeHCV-RNA positiveTransaminases elevationTransaminases normal/slightly increased
Moderate liver enzymes increaseLow-moderate liver enzymes increaseImmunosuppressants levels under protective limitsImmunosuppressants levels under protective limits
High IgG concentrationsANA frequently positiveAutoantibodies negative or mild positiveAutoantibodies negative/mild positive
Positivity for ANA, SMA, LKM, atypical LKM (anti-GSTT1), and/or AMASMA, AMA, LKM rarely positive
Clinical presentationOnset variable from indolent to overt, may follow an antiviral treatment for HCV recurrence, especially when viral clearance is obtainedGradual progression to cirrhosis except severe formsRapidly progressive deterioration of liver function scoresSilent onset
Slow progression to deterioration of liver function scores
IAHG probable/definite diagnosis
HistologyPortal tract infiltrate rich in plasma-cellsChronic logistic infiltrateCentral perivenulitisBiliary inflammatory and ischemic pattern: bile ductopenia and inflammation, artheriolar/capillary obliterative features or loss
Interface hepatitisPossible interface hepatitisHepatic venous endothelitis
RosetteConfluent/bridging necrosisMononuclear/mixed portal infiltrate
Lobular inflammation ± bridging/confluent necrotic fociProgression to cirrhosis
Possible fibrosing cholestatic hepatitisBile ducts inflammation
TreatmentPrednis(ol)one ± MMF/azathioprineAntiviral treatmentSteroids bolusSteroids bolus
Immunosuppression levels monitoringAdjustment of immunosuppressive regimenSwitch to/addition of a new immunosuppressant and/or optimization of current regimen)