Acute liver toxicity due to methylprednisolone: consider this diagnosis in the context of autoimmunity.

The occurrence of corticosteroid-induced hepatitis is a rare event that has been recently described in the literature. We report the case of an acute cytolytic hepatitis in a patient treated with methylprednisolone for multiple sclerosis associated with an autoimmune thyroid dysfunction. After ruling out other etiologies, we concluded that the acute liver injury was due to steroids, and we analyzed the specific circumstances in the literature where methylprednisolone may have been responsible for acute hepatitis.

[Latency and reactivation of HSV: role of LAT and ICP0]. / Latence et réactivation de HSV1, LAT et ICP0 : les deux faces d'une seule médaille.

The virus herpes simplex type 1 (HSV1) is characterized by its ability to become latent within the nervous system after a primary infection that is almost always located into the oral mucosa. Several factors may trigger HSV1 reactivation, thus inducing recurrences, which are mostly located on the lips (cold sore), sometimes in the eye (most frequently into the cornea) and, exceptionally, in the central nervous system (meningitis and encephalitis). Considering the frequency of the HSV1 infection in the general population and the associated morbidity (approximately 15 % of people have relapsing cold sores, and 90,000 French people have an history of ocular herpes disease), many research projects are focused on the biologic patterns regulating the switch between viral latency and reactivation. In spite of the multitude of scientific publications, numerous points are still poorly understood. However, molecular biology allowed consequent progress. The putative roles of Latency Associated Transcripts (LAT), until recently considered as the only viral transcripts during viral latency, are now better identified. It is now obvious that LAT interact with other viral partners. The transcripts encoding ICP0, a viral protein which is known to have a key role in the reactivation process, could be involved in this phenomenon, since their properties are opposite to those of LAT. The couple LAT-ICP0 transcripts could thus represent the molecular aspect of the classic opposition between latency and reactivation of HSV1.

A targeted approach significantly increases the identification rate of patients with undiagnosed haemochromatosis.

OBJECTIVE: To determine the optimal means of identifying patients with undiagnosed haemochromatosis. DESIGN: Case-control study where cases are defined by the presence of specific clinical diagnoses or symptoms. SETTING: Primary care patients were recruited from three Oxfordshire practices and secondary care patients were recruited from those patients attending specialist clinics in Amiens University Hospital. SUBJECTS: A total of 569 patients recruited via hospital clinics and 60 primary care patients (recruited from 4022 consultations) presenting with the following haemochromatosis associated conditions, diabetes, arthralgia/chronic fatigue, osteoporosis or arthropathy were studied. The control group, a total of 991 healthy volunteers, were recruited through a Health Appraisal Centre. Patients and controls were included in the study if they or their family members had not previously been diagnosed with hereditary haemochromatosis. MAIN OUTCOME MEASURES: Serum ferritin concentration, transferrin saturation (Tsat) and presence of HFE mutations, C282Y and H63D. The check-up in controls consisted of a questionnaire, clinical examination, biochemical tests and screening for the presence of the C282Y and H63D mutations. RESULTS: Patient groups presenting with unstable diabetes or chronic fatigue and arthralgia together with a raised serum ferritin concentration showed an enrichment in the haemochromatosis-associated genotype HH/YY, odds ratio (OR) = 40.1, confidence interval (CI) = 8.0-202.1 and OR = 103, CI = 22.9-469.7, respectively. CONCLUSION: Patients presenting to hospital clinics with haemochromatosis associated conditions should be screened biochemically for iron overload. Only those with a serum ferritin >300 microg L-1 or Tsat >40% should subsequently go on to be genotyped for HFE mutations. The patients at greatest risk of having undiagnosed haemochromatosis are those presenting with unstable diabetes, or fatigue and/or arthralgia in the absence of any other explanation.