Drug-induced liver injury (DILI) is one of the main reasons for drug withdrawal from the market, and a cause of worldwide morbidity. Although several issues on DILI are still unsolved, there have been significant advances in new definitions and diagnosis tools. DILI is the result of a complex interaction between genetic and environmental factors, and constitutes an expanding area of investigation. DILI can mimic virtually all known hepatopathies, including vascular disorders and liver tumours. As part of this broad spectrum of clinical presentations, DILI severity ranges from asymptomatic elevations of aminotransferases to acute liver failure. Although biomarkers are emerging as valuable diagnostic tools, they are not available in clinical practice. Accurate DILI diagnosis is a challenging issue, particularly the establishing of causal relationships with the culprit agent and the exclusion of competing causes of liver injury. Given that the understanding of the mechanisms inducing DILI is growing, and both DILI causality assessment scales and the performance of international DILI networks have been improved, hepatotoxicity may be recognised earlier in clinical practice. In this review, advances and results obtained by DILI registries around the world, case characterisations, particularly those relevant to newer definitions in DILI, and the behaviour of chronic liver disease induced by drugs will be updated. In addition, recently published data on herbal and dietary supplements and new predictive scores for acute liver failure assessment will also be discussed.

El consumo ilícito de esteroides anabólicos androgénicos con fi nes estéticos ha aumentado en los últimos años y, aunque raro, es causa de hepatotoxicidad. Los casos con daño hepatocelular son más frecuentes, pero los colestásicos son más graves y pueden asociarse a falla renal. Salvo por la suspensión del fármaco, la hepatotoxicidad por anabólicos no tiene tratamiento específi co. Se describe y discuten las historias clínicas de dos hombres jóvenes, deportistas afi cionados que consultaron por ictericia y presentaron colestasis e insufi ciencia renal. El reporte de casos, en patologías poco frecuentes, resulta fundamental para difundir y ampliar la información que ayude al clínico a considerar con fi rmeza este diagnóstico, incluso ante la falta de reconocimiento inicial del consumo por parte del paciente. Palabras clave:Esteroides anabólicos androgénicos, hepatotoxicidad. Abstract:Illicit consumption of anabolic-androgenic steroids for aesthetic purposes has increased in recent years. Hepatocellular damage is more frequent, but cholestasis is more dangerous and may be associated with renal failure. The clinical records of two young men, amateur athletes who consulted for jaundice in the last year and denied its consumption at the beginning, are described. Except for the drug interruption, hepatotoxicity by anabolics has no specifi c treatment. Usually presented as cholestatic liver disease and renal failure, case reports are fundamental to characterize its clinical-evolutionary presentation. This may also allow clinicians to fi rmly consider diagnosis even when the patient denies consumption. Resumo:O uso ilícito de esteróides androgênicos anabólicos para fi ns estéticos tem aumentado nos últimos anos e, apesar de raro, é causa de hepatotoxicidade. Casos com dano hepatocelular são mais freqüentes, mas colestesia é mais grave e pode estar associada à insufi ciência renal. Com exceção da suspensão do medicamento, a hepatotoxicidade anabólica não possui tratamento específi co. As histórias clínicas de dois homens jovens, atletas amadores que consultaram para icterícia e apresentaram colestase e insufi ciência renal, são descritos e discutidos. O relato de casos, em patologias pouco freqüentes, é fundamental para disseminar e ampliar as informações que auxiliam o clínico a considerar com fi rmeza esse diagnóstico antes mesmo do não reconhecimento inicial do consumo pelo paciente.

Background: Evidence indicates that low-grade inflammation can alter gastrointestinal motor and sensory function and might contribute to the genesis of symptoms in IBS. Objective: To examine relationships between IBS, disease antibodies and cytokine titers in celiac patients and a control group. Materials and methods: IBS, CD activity and serum levels of IL-6, IL-8 and IL12/23p40 were determined in celiac patients and controls. Results: 123 celiac patients were included, 89% were female. 59% demonstrated disease activity and 32% met IBS criteria. Prevalence of IBS was not different between patients who adhered or did not adhere to GFD as well as between patients with or without positive antibodies. Celiac patients had increased levels of IL-6, IL-8 and IL12/23p40 as compared to controls. Higher levels of cytokines were found in celiac patients with IBS than in those without IBS. No difference in levels of cytokines was found between patients with and without CD positive antibodies. A significant negative correlation between the mental component of QoL and IL-6 and IL12/23p40 levels was found, but not with IL-8. Conclusion: Higher levels of inflammatory cytokines were found in CD patients with IBS than in either those without IBS or controls, indicating that IBS symptoms are associated with an increase in the inflammatory response s. These differences in cytokine levels were not related to CD antibodies status gesting that IBS, in CD, is related to a different inflammatory process than that which is relevant to CD.

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Enfermedad de Wilson: presentación hepática y revisión bibliográfica Wilson's disease: liver presentation and literature review Doença de Wilson: apresentação hepática e revisão de literatura Resumen: La Enfermedad de Wilson es un trastorno genético raro que puede presentarse a cualquier edad y se caracteriza por el depósito de cobre a nivel hepático y cerebral. La afectación hepática abarca desde formas asintomática hasta falla hepática fulminante o cirrosis. Su diagnóstico precoz tiene implicancias pronósticas ya que el tratamiento puede lograr un balance negativo de cobre, permitir el control sintomático y prevenir la progresión de la enfermedad. Se presenta el caso de un hombre de 27 años, con dolor abdominal, en el que se hizo el diagnóstico de Enfermedad de Wilson a partir de una hipertransaminasemia leve. Los hallazgos que orientaron al diagnóstico fueron una cupruria aumentada por inducción con D-penicilamina y una cuantificación de cobre en tejido hepático seco elevada. Con un estadio de fibrosis leve, se comenzó tratamiento con D-penicilamina con buena tolerancia y la normalización de las alteraciones bioquímicas.