Abstract
Autoimmune pancreatitis (AIP) is a peculiar form of pancreatitis that has been known for the last two decades. Sarles et al. [1] first reported pancreatitis associated with hypergammaglobulinemia in 1961. They suggested that autoimmunity was one of the etiologies of pancreatitis. The first case that led researchers to suggest a new concept of autoimmune pancreatitis (AIP) was treated with steroids by gastroenterologists (led by Professor Tadashi Takeuchi) in Tokyo Medical Women’s University, and the concept was proposed by Yoshida, a member of that group, in 1995 [2]. The characteristic histological feature of the AIP is lymphoplasmacytic sclerosing pancreatitis (LPSP) [3]. AIP has been increasingly seen over the last decade and is now considered a distinct entity [4, 5]. Based on histological and immunohistochemical examinations of various organs and extrapancreatic lesions of AIP patients, a new clinicopathological entity called “IgG4-related systemic disease” was proposed [4, 6]. AIP is now considered to be a pancreatic manifestation of IgG4-related disease [4, 5, 7].
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Acknowledgment
This study was partially supported by the Intractable Disease, supported by the Ministry of Health, Labour, and Welfare of Japan.
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Kamisawa, T., Takeuchi, T., Shiratori, K. (2015). Overview of Type 1 and Type 2 AIP. In: Kamisawa, T., Chung, J. (eds) Autoimmune Pancreatitis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-55086-7_1
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DOI: https://doi.org/10.1007/978-3-642-55086-7_1
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