Development of autoimmune hepatitis type 1 after pulsed methylprednisolone therapy for multiple sclerosis: A case report

Takahashi, Atsushi; Kanno, Yukiko; Takahashi, Yuta; Sakamoto, Natsumi; Monoe, Kyoko; Saito, Hironobu; Abe, Kazumichi; Yokokawa, Junko; Irisawa, Atsushi; Ohira, Hiromasa

doi:10.3748/wjg.14.5474

Cited by 28 publications

(24 citation statements)

References 19 publications

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“…The mechanisms and determinants underlying transient, reversible elevation of liver enzymes after IV-MP in this case remain obscure. Several cases with MS involving autoimmune hepatitis have been reported [4] . However, an association between liver injury and MS, including the coexistence of autoimmune hepatitis, is unlikely in our patient, as both anti-smooth-muscle antibody and antimitochondria antibody were negative and hepatopathy completely resolved.…”

Section: Discussionmentioning

confidence: 99%

Recurrent High-Dose Intravenous Methylprednisolone Succinate Pulse Therapy-Induced Hepatopathy in a Patient with Multiple Sclerosis

et al. 2011

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Objective: We describe recurrent and reversible hepatopathy in a girl with multiple sclerosis (MS) after glucocorticoid pulse therapy, to point out the possibility that glucocorticoid may harm the liver. Clinical Presentation and Intervention: An 11-year-old girl with MS, who was treated with high-dose methylprednisolone succinate pulse therapy, developed elevation of liver enzymes. The episodes of hepatopathy occurred 1–5 weeks after the therapy and disappeared within several weeks. The examination for antinuclear antibody and viruses which can cause hepatitis produced negative results. Conclusion: The present case emphasizes the possible effects of high-dose glucocorticoids in the induction of liver enzymes and the importance of follow-up liver tests after pulse therapy.

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Section: Discussionmentioning

confidence: 99%

Recurrent High-Dose Intravenous Methylprednisolone Succinate Pulse Therapy-Induced Hepatopathy in a Patient with Multiple Sclerosis

et al. 2011

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“…Other medications, such as recombinant a-interferon [61,62], antibodies to anti-cytotoxic T lymphocyte antigen 4 [63,64], and pulsed methylprednisolone [65], have immune-modulatory actions that can facilitate the emergence of a latent classical autoimmune hepatitis.…”

Section: Etiological Candidates For Drug-induced Autoimmunelike Hepatmentioning

confidence: 99%

Drug-Induced Autoimmune-Like Hepatitis

2011

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The clinical phenotype of classical autoimmune hepatitis can be mimicked by idiosyncratic drug-induced liver injury, and differentiation can be difficult. The goals of this review are to enumerate the major agents of drug-induced autoimmune-like hepatitis, describe the clinical findings and risk factors associated with it, detail the clinical tools by which to assess causality, discuss putative pathogenic mechanisms, and describe treatment and outcome. The frequency of drug-induced autoimmune-like hepatitis among patients with classical features of autoimmune hepatitis is 9%. Minocycline and nitrofurantoin are implicated in 90% of cases. Female predominance, acute onset, and absence of cirrhosis at presentation are important clinical manifestations. Genetic factors affecting phase I and phase II transformations of the drug, polymorphisms that protect against cellular oxidative stress, and human leukocyte antigens that modulate the immune response may be important pathogenic components. Clinical judgment is the mainstay of diagnosis as structured diagnostic methods for drug-induced liver injury are imperfect. The covalent binding of a reactive drug metabolite to a hepatocyte surface protein (commonly a phase I or phase II enzyme), formation of a neoantigen, activation of CD8 T lymphocytes with nonselective antigen receptors, and deficient immune regulatory mechanisms are the main bases for a transient loss of self-tolerance. Discontinuation of the offending drug is the essential treatment. Spontaneous improvement usually ensues within 1 month. Corticosteroid therapy is warranted for symptomatic severe disease, and it is almost invariably effective. Relapse after corticosteroid withdrawal probably does not occur, and its absence distinguishes drug-induced disease from classical autoimmune hepatitis.

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“…L'association à plusieurs maladies autoimmunes a été décrite, dominée par la polyarthrite rhumatoïde et la dysthyroïdie auto-immune [1]. L'association de la maladie à l'HAI est rare, rapportée uniquement sous forme de faits cliniques [2][3][4]. La prévalence de l'HAI semble, cependant, être dix fois supérieure chez les malades ayant une SEP par rapport à la population générale [5].…”

Section: Discussionunclassified

Bolus de méthylprednisolone révélant une hépatite auto-immune chez une patiente atteinte de sclérose en plaques

Màamouri

Ketari

Hariz

et al. 2009

J Afr Hepato Gastroenterol

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Development of autoimmune hepatitis type 1 after pulsed methylprednisolone therapy for multiple sclerosis: A case report

Cited by 28 publications

References 19 publications

Recurrent High-Dose Intravenous Methylprednisolone Succinate Pulse Therapy-Induced Hepatopathy in a Patient with Multiple Sclerosis

Recurrent High-Dose Intravenous Methylprednisolone Succinate Pulse Therapy-Induced Hepatopathy in a Patient with Multiple Sclerosis

Drug-Induced Autoimmune-Like Hepatitis

Bolus de méthylprednisolone révélant une hépatite auto-immune chez une patiente atteinte de sclérose en plaques

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