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Autoimmune pancreatitis and complement activation system
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- MURAKI Takashi
- 信州大学医学部内科学第2教室
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- HAMANO Hideaki
- 信州大学医学部内科学第2教室
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- OCHI Yasuhide
- 信州大学医学部内科学第2教室
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- KOMATSU Kenichi
- 信州大学医学部内科学第2教室
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- KOMIYAMA Yuichi
- 信州大学医学部内科学第2教室
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- ARAKURA Norikazu
- 信州大学医学部内科学第2教室
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- Yoshizawa KANAME
- 信州大学医学部内科学第2教室
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- OTA Masao
- 信州大学医学部法医学教室
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- KAWA Shigeyuki
- 信州大学健康安全センター
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- KIYOSAWA Kendo
- 信州大学医学部内科学第2教室
Bibliographic Information
- Other Title
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- 自己免疫性膵炎における補体活性化機序の検討
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Description
Autoimmune pancreatitis is characterized by increased serum level of IgG4, but its pathogenesis has not been fully elucidated. Because this disease is occasionally associated with decreased levels of complements, we sought to clarify which complement activation system was operating in its active state.We measured serum levels of complements, mannose-binding lectin, and circulating immune complex in patients with autoimmune pancreatitis, patients with chronic pancreatitis, and healthy controls.We found high serum circulating immune complex values, which decreased significantly after corticosteroid therapy. In patients with autoimmune pancreatitis, elevated levels of circulating immune complex, as determined by C1q assay, were significantly associated with increased serum levels of IgG1 and decreased levels of C4, as well as with a tendency toward decreased levels of C3. There were no significant differences in the serum levels of mannose-binding lectin or in the frequency of a mutant allele of mannose-binding lectin between patients with autoimmune pancreatitis and those with chronic calcifying pancreatitis. Furthermore, corticosteroid therapy had no effect on the level of mannose-binding lectin.Autoimmune pancreatitis exhibits a high serum circulating immune complex values in its active state, which links to a complement activation system with a classic pathway rather than the mannose-binding lectin pathway or alternative pathways.
Journal
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- Suizo
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Suizo 21 (5), 454-455, 2006
Japan Pancreas Society