PubMed · 6098117
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S Jablonska. 1984. Other modalities.. https://pubmed.ncbi.nlm.nih.gov/6098117/
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BACKGROUND: Conventional treatment for autoimmune hepatitis results in a significant percentage of failures and several, poorly tolerated, side-effects. Therapy for autoimmune cholangitis and giant cell hepatitis associated with autoimmune haemolysis is poorly documented. Ciclosporin is a promising treatment for all of these diseases. METHODS: We reviewed the records of 12 patients treated in our unit between 1987 and 2001. Eight had autoimmune hepatitis, two had autoimmune cholangitis and two had giant cell hepatitis. Indications for ciclosporin were treatment failure (four patients) and contraindications to/refusal of steroids (eight patients). Ciclosporin was administered in five untreated cases and in seven patients during relapse. The mean duration of ciclosporin administration was 35.6 months (8-89 months). The median follow-up was 6.5 years (1.5-15 years). RESULTS: All patients achieved complete remission in a median period of 4.5 weeks (2-12 weeks). No treatment withdrawal due to side-effects occurred. Three patients required a combination of ciclosporin with conventional treatment due to severe liver function impairment. Tolerance to ciclosporin was excellent. A 20% transient elevation of serum creatinine occurred in one case, gingival hypertrophy in two and moderate hypertrichosis in two. CONCLUSIONS: Ciclosporin may be considered as a safe treatment for all autoimmune liver diseases and as an effective alternative for front-line therapy.
The ubiquitin-proteasome pathway constitutes the major system for nuclear and extralysosomal cytosolic protein degradation in eukaryotic cells. A plethora of cell proteins implicated in the maintenance and regulation of essential cellular processes undergoes processing and functional modification by proteolytic degradation via the ubiquitin-proteasome pathway. Deregulations of the pathway have been shown to contribute to the pathogenesis of several human diseases, such as cancer, neurodegenerative, autoimmune, genetic and metabolic disorders, most of them exhibiting abnormal accumulation and altered composition of components of the pathway that is suitable for diagnostic proceedings. While the ubiquitin-proteasome pathway is currently exploited to develop novel therapeutic strategies, it is less regarded as a diagnostic area. Future research should lead to an improved understanding of the pathophysiology of the ubiquitin-proteasome pathway with the aim of allowing the development of subtle diagnostic strategies.