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Adverse drug reactions are among the most frequent side effects of synthetic and complementary alternative drugs and represent the premier causes of license revocations and acute liver failure. Drug-induced liver injury can resemble literally any other genuine liver disease and usually responds well to drug dechallenge. However, in some cases autoimmune-like hepatitis can evolve, requiring short- and sometimes long-term immunosuppression. Here, we present the hitherto first case of autoimmune-like hepatitis following treatment with zoledronic acid.

Abstract: Background: Although very rare, pantoprazole can result in acute hepatitis. It has yet to be reported, however, that it can also cause chronic autoimmune hepatitis. Aim, method and results: We report the case of a patient in whom pantoprazole administration for 2 months was followed by acute liver injury with severe jaundice and features of autoimmunity. A liver biopsy revealed acute hepatocellular lesions associated with cholestasis, acute cholangitis and polymorphous inflammatory infiltration suggestive of drug‐induced liver injury. The jaundice disappeared following discontinuation of the pantoprazole. There was, however, chronic autoimmune liver injury, with the occurrence of extensive liver fibrosis within a few months. This led to the administration of immunosuppressive agents, which led to progressive and complete recovery associated with the disappearance of autoantibodies. Conclusion: This observation further supports the notion that pantoprazole can induce acute hepatocellular hepatitis, and it strongly suggests that it may trigger acute cholangitis and autoimmune liver injury. This case also helps document that some drugs can induce chronic autoimmune hepatitis that can resolve with immunosuppressive treatment. [ABSTRACT FROM AUTHOR]

Drug-induced autoimmunity (DIA) refers to a group of adverse drug reactions, and they remain unpredictable largely due to the limited understanding of the mechanisms involved. There is evidence that procainamide can cause autoimmune reactions in humans but the mechanisms involved remain unclear. To examine the cellular and genetic factors involved in the procainamide-induced autoimmune response, we compared rats that are genetically T-helper (Th)2-predisposed (Brown Norway (BN)), Th1-predisposed (Lewis (LEW)) or not genetically predisposed (Sprague Dawley (SD)). We revealed significant differences in response to autoimmunity induced by procainamide among three strains rats, BN was the most sensitive one, SD exhibited less sensitive, while LEW resistance to procainamide. Much more pronounced of Th2-type responses and more complex differentially expressed genes involved in immune regulation and response in BN might contribute to its susceptibleness to DIA. Moreover, similar immune mechanisms were found between BN and SD, which suggesting that these changes would serve as the potential bridge biomarkers to predict DIA among species. This study may also benefit to further understand the toxicological mechanism of drug-induced autoimmune reactions. [ABSTRACT FROM AUTHOR]

Drugs are special products designed to prevent, treat and cure diseases, and are produced under strict control to high theirs specifications. Despite their therapeutic efficacy, there is no way to guarantee absolute safety in medication use that, eventually, may cause unexpected and unpredictable adverse events. Factors such as age, gender, polypharmacy, and individual susceptibility may contribute to the development of drug-induced diseases. The diagnosis of these conditions is difficult, affecting directly on the patient health and on health system's costs. Almost all pharmaceutical classes have been associated with the development of diseases, and all organs and systems can be affected. The disclosure of information about the drug-induced diseases is relevant and necessary, since new drugs has been constantly introduced into the market, and may have important adverse events. Among the drug-induced diseases, this review article highlighted drug-induced autoimmune diseases, and drug-induced lung and movement disease as well. [ABSTRACT FROM AUTHOR]

The effect of cadralazine and its active metabolite CGP 22639 on the covalent binding reaction of C4 and C3 has been studied. Trypsin-Sepharose was used to activate radio-labelled C3 and C4 and binding of the radio-labelled protein to the trypsin-Sepharose was measured. Cadralazine inhibited 50% of the binding of C3 and C4 at concentrations of 19 mmol/l and 15 mmol/l, respectively. Its active metabolite was more potent and inhibited 50% of the C3 and C4 binding at concentrations of 8 and 3.5 mmol/l, respectively. These concentrations are much higher than those found in plasma during therapy. This is consistent with the clinical observation that in patients with normal kidney function cadralazine is not an inducer of SLE. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented that relates a study that discusses simvastatin-induced amyopathic dermatomysitis.

Methotrexate (MTX) is one of the most commonly used medicines in the treatment of psoriatic arthritis. The drug can produce steatosis and cirrhosis. Autoimmune hepatitis is a rare and serious adverse effect. We describe the case of a 53-year-old woman who developed autoimmune hepatitis after a long-term use of MTX for psoriatic arthritis. Hepatitis was completely resolved 4 months after stopping this drug. The pathophysiologic mechanisms of a drug-induced autoimmunity are unclear and complex. This report confirms the need to monitor liver enzymes carefully in patients using long-term treatment with MTX for psoriasis or rheumatoid arthritis. [ABSTRACT FROM AUTHOR]