Differentiating drug-induced liver injury from autimune hepatitis is a challenging task. Especially the indiosyncratic form (no clear dose-depence, long latency to onset) may be indistiguishable from autoimmune hepatitis: http://www.ncbi.nlm.nih.gov/pubmed/20512992
In the manuscript above, there is evidence that patients that suffered autoimmune-like DILI may not need long term immunosuppression.
I would appreciate comments on how to deal with this difficult differential diagnoses: What in your opinion are criteria to risk cessation of immunosuppressive treatment in cases where DILI or AIH cannot be reliably differentiated? (perhaps this could save patients from side-effects of long term immunosuppression)
Often in Medicine, we cannot give an immediate answer to a question. In this case, only the follow-up of the clinical pattern may help the doctor and the patient. When serological markers of autoimmune hepatitis are negative and the clinical course is not very severe, a challange with immunosuppresant withdrawal could be attempted and its effect clarify the problem. At the moment I do not have any other strategy to suggest.
I think on going communication with the patient and their GP is essential, and severity of liver injury and presence or absence of underlying cirrhosis will also inform decision. I try to provide as such information as possible to the patient - highlighting the possible differential diagnosis of AIH vs. AIH like form of DILI (drug induced liver injury) if the history of patient is suggestive of DILI with an AIH like clinical and histological picture. I tend to start immunosuppression (steroids) and monitor blood frequently for response, once LFT normalised for a couple of month I offer withdrawal of steroids with ongoing frequent monitoring - if LFTs remain normal no further treatment and eventually monitoring in primary with early referral back if problems; if LFTs flare after withdrawal - I treat it as AIH and reintroduce steroids and discuss introduction of Azathioprine.
1) drug-induced liver disease and autoimmune hepatitis are not mutually exclusive!
2) sometimes the drug (like nitrofurantoine) may initially thought to be the "cause" but features of chronicity etc. may suggest that the top of the iceberg showed up and a disease / symptom provoked to give a drug that subsequently is given and deemed the culprit although it is wasn't .....
3) if in doubt I am inclined to treat as AIH but the less classical (high titers of AI markers) the more I may attempt to much earlier reduce immunosuppression compared to classical AIH. Also, unless advanced disease, budesonide may be safer than traditional steroids
DILI may resemble AIH in 2 ways;- [a] autoantibodies in blood, [b] histology. I feel the best way is to elicit history of culprit drug intake or using some measure like RUCAM scale to elicit whether really a drug is the culprit. In positive cases the best way is to stop the drug and follow LFT to check improvement. In most cases of DILI this improves which is not the case with AIH. I feel this is better than exposing patient to immunosuppressives which are anyway not the SOC for DILI and more harmful. On the contrary If AIH is suspected but the antibodies are negative or low titre, additional antibodies like LCA, LPA may be checked in addition to history of other autoimmune diseases. All these however needs discussion with patient relatives.
I think that the below publication may help to understand this difficult diferential diagnosis and treatment.
Article Drug-induced autoimmune liver disease: A diagnostic dilemma ...
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