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• W2051249215 abstract "This is in response to the article by Miyake et al. [[1]Miyake Y. Iwasaki Y. Terada R. Takagi S. Okamaoto R. Ikeda H. et al.Persistent normalization of serum alanine aminotransferase levels improves the prognosis of type 1 autoimmune hepatitis.J Hepatol. 2005; 43: 951-957Abstract Full Text Full Text PDF PubMed Scopus (79) Google Scholar]. They have corroborated our findings by observing that normalization of transaminases during follow up improves prognosis in type 1 AIH. In our study we observed that patients who were in biochemical remission but still had abnormal transaminases (>ULN but <2ULN) in at least 50% of the out patient visits (i.e. abnormal transaminase index >2) had a 90% probability of developing cirrhosis, which in turn was an independent predictor of poor outcome [[2]Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar]. In contrast those with persistently normal transaminases had a 40% probability of developing cirrhosis/relapse. The current AASLD practice guidelines on management of AIH define relapse as transaminases >3ULN and remission as absence of symptoms and transaminases <2ULN [[3]Czaja A.J. Freese D.K. American Association for the Study of Liver Disease.Hepatology. 2002; 36: 479-497Crossref PubMed Scopus (545) Google Scholar]. While presence of transaminases >3ULN is invariably associated with appearance of interface hepatitis histologically [[3]Czaja A.J. Freese D.K. American Association for the Study of Liver Disease.Hepatology. 2002; 36: 479-497Crossref PubMed Scopus (545) Google Scholar], in the latter group the correlation is less clear. In fact Kallai et al. observed that 50% of patients with transaminases <2ULN had moderate-significant piecemeal necrosis on biopsy [[4]Kallai L. Hahn A. Roeder V. Zupanic V. Correlation between histological findings and serum transaminase values in chronic diseases of the liver.Acta Med Scand. 1964; 175: 49-56Crossref PubMed Scopus (48) Google Scholar]. Therefore, should remission in type 1 AIH be redefined as normalization of transaminases?We would also request clarification of certain data presented by Miyake et al. Firstly, of their total cohort only 7 (8%) had cirrhosis (stage F4 disease) at presentation. In contrast we and others have reported that approximately 30% have cirrhosis at onset [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 5Roberts S.K. Therneau T. Czaja A.J. Prognosis of histological cirrhosis in type 1 autoimmune hepatitis.Gastroenterology. 1996; 110: 847-848Abstract Full Text Full Text PDF Scopus (265) Google Scholar]. Secondly, of the 11 with a poor outcome, two had cirrhosis at presentation. Did the remaining nine develop cirrhosis during follow up? Of the 73 without a poor outcome, what proportion eventually developed cirrhosis during follow-up? It is well recognized that 30–40% of patients with type 1 AIH develop cirrhosis during follow up despite therapy [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 5Roberts S.K. Therneau T. Czaja A.J. Prognosis of histological cirrhosis in type 1 autoimmune hepatitis.Gastroenterology. 1996; 110: 847-848Abstract Full Text Full Text PDF Scopus (265) Google Scholar]. We have further shown that it is this cohort that has a poorer outcome and not those who have cirrhosis at presentation (develop cirrhosis complications/liver failure, need transplant or die 43% vs. 15%). The latter in fact have a similar prevalence of adverse events compared to those without cirrhosis at presentation or follow up (15% vs. 5%) [[2]Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar]. Thirdly, in Miyake et al.'s study of the 10 that stopped immunosuppressants, only 3(30%) relapsed. This relapse rate is lower that that previously published (75–87%) [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 6Hegarty J.E. Nouri-Aria K.T. Portmann B. Eddleston A.L.W.F. Williams R. Relapse following treatment withdrawal in patients with autoimmune chronic active hepatitis.Hepatology. 1983; 3: 685-689Crossref PubMed Scopus (153) Google Scholar]. In addition, of the 67 patients in whom prednisolone was continued 41 (61%) either relapsed or had an exacerbation. It is unclear if these 61% had a spontaneous relapse despite being on maintenance immunosuppression (which would be most unusual) or upon attempted dose reduction. Finally, what was the definition of remission in the study?Therefore in summary, we are in total agreement with Miyake et al. that achievement of normal transminases should be the goal of therapy in patients with type 1 AIH. However, some of their data is not consistent with previously published studies. Could the authors please confirm if this is because of ethnic differences in the natural history of AIH or if it is due to other factors? This is in response to the article by Miyake et al. [[1]Miyake Y. Iwasaki Y. Terada R. Takagi S. Okamaoto R. Ikeda H. et al.Persistent normalization of serum alanine aminotransferase levels improves the prognosis of type 1 autoimmune hepatitis.J Hepatol. 2005; 43: 951-957Abstract Full Text Full Text PDF PubMed Scopus (79) Google Scholar]. They have corroborated our findings by observing that normalization of transaminases during follow up improves prognosis in type 1 AIH. In our study we observed that patients who were in biochemical remission but still had abnormal transaminases (>ULN but <2ULN) in at least 50% of the out patient visits (i.e. abnormal transaminase index >2) had a 90% probability of developing cirrhosis, which in turn was an independent predictor of poor outcome [[2]Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar]. In contrast those with persistently normal transaminases had a 40% probability of developing cirrhosis/relapse. The current AASLD practice guidelines on management of AIH define relapse as transaminases >3ULN and remission as absence of symptoms and transaminases <2ULN [[3]Czaja A.J. Freese D.K. American Association for the Study of Liver Disease.Hepatology. 2002; 36: 479-497Crossref PubMed Scopus (545) Google Scholar]. While presence of transaminases >3ULN is invariably associated with appearance of interface hepatitis histologically [[3]Czaja A.J. Freese D.K. American Association for the Study of Liver Disease.Hepatology. 2002; 36: 479-497Crossref PubMed Scopus (545) Google Scholar], in the latter group the correlation is less clear. In fact Kallai et al. observed that 50% of patients with transaminases <2ULN had moderate-significant piecemeal necrosis on biopsy [[4]Kallai L. Hahn A. Roeder V. Zupanic V. Correlation between histological findings and serum transaminase values in chronic diseases of the liver.Acta Med Scand. 1964; 175: 49-56Crossref PubMed Scopus (48) Google Scholar]. Therefore, should remission in type 1 AIH be redefined as normalization of transaminases? We would also request clarification of certain data presented by Miyake et al. Firstly, of their total cohort only 7 (8%) had cirrhosis (stage F4 disease) at presentation. In contrast we and others have reported that approximately 30% have cirrhosis at onset [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 5Roberts S.K. Therneau T. Czaja A.J. Prognosis of histological cirrhosis in type 1 autoimmune hepatitis.Gastroenterology. 1996; 110: 847-848Abstract Full Text Full Text PDF Scopus (265) Google Scholar]. Secondly, of the 11 with a poor outcome, two had cirrhosis at presentation. Did the remaining nine develop cirrhosis during follow up? Of the 73 without a poor outcome, what proportion eventually developed cirrhosis during follow-up? It is well recognized that 30–40% of patients with type 1 AIH develop cirrhosis during follow up despite therapy [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 5Roberts S.K. Therneau T. Czaja A.J. Prognosis of histological cirrhosis in type 1 autoimmune hepatitis.Gastroenterology. 1996; 110: 847-848Abstract Full Text Full Text PDF Scopus (265) Google Scholar]. We have further shown that it is this cohort that has a poorer outcome and not those who have cirrhosis at presentation (develop cirrhosis complications/liver failure, need transplant or die 43% vs. 15%). The latter in fact have a similar prevalence of adverse events compared to those without cirrhosis at presentation or follow up (15% vs. 5%) [[2]Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar]. Thirdly, in Miyake et al.'s study of the 10 that stopped immunosuppressants, only 3(30%) relapsed. This relapse rate is lower that that previously published (75–87%) [2Verma S. Gunuwan B. Mendler H. Govindrajan S. Redeker A. Factors predicting relapse and poor outcome in type I autoimmune hepatitis: role of cirrhosis development, patterns of transaminases during remission and plasma cell activity in the liver biopsy.Am J Gastroenterol. 2004; 99: 1510-1516Crossref PubMed Scopus (147) Google Scholar, 6Hegarty J.E. Nouri-Aria K.T. Portmann B. Eddleston A.L.W.F. Williams R. Relapse following treatment withdrawal in patients with autoimmune chronic active hepatitis.Hepatology. 1983; 3: 685-689Crossref PubMed Scopus (153) Google Scholar]. In addition, of the 67 patients in whom prednisolone was continued 41 (61%) either relapsed or had an exacerbation. It is unclear if these 61% had a spontaneous relapse despite being on maintenance immunosuppression (which would be most unusual) or upon attempted dose reduction. Finally, what was the definition of remission in the study? Therefore in summary, we are in total agreement with Miyake et al. that achievement of normal transminases should be the goal of therapy in patients with type 1 AIH. However, some of their data is not consistent with previously published studies. Could the authors please confirm if this is because of ethnic differences in the natural history of AIH or if it is due to other factors?" @default.
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• W2051249215 title "In type 1 autoimmune hepatitis (AIH), should remission be redefined as normalization of transaminases?" @default.
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