Mechanism of Severe Acute Pancreatitis: Focusing on Development and Progression.
10.15279/kpba.2015.20.3.115
- Author:
Jae Hyuk DO
1
Author Information
1. Division of Gastroenterology, Department of Internal Medicine, Chung-Ang University School of Medicine, Seoul, Korea. jhdo@cau.ac.kr
- Publication Type:Review
- Keywords:
Severe acute pancreatitis;
Pathogenesis;
Organ failure;
Pancreatic infection
- MeSH:
Acinar Cells;
Apoptosis;
Cell Death;
Chemokines;
Cytokines;
Inflammation;
Leukocytes;
Mortality;
Pancreatitis*;
Transcription Factors;
Up-Regulation
- From:Korean Journal of Pancreas and Biliary Tract
2015;20(3):115-123
- CountryRepublic of Korea
- Language:English
-
Abstract:
Acute pancreatitis (AP) is an inflammatory disorder and the severity range from mild to severe form. The mortality of severe form of AP is still high despite of tremendous improvement of diagnostic modalities and therapeutic options. Although pathogenesis of AP is still not fully understood, autodigestion theory is regarded as an initial common pathophysiologic mechanism of AP for about 2 centuries. However, it is obscure which mechanisms are involving the disease severity. Upregulation of adhesion molecules, leukocytes, proinflammatory cytokines and chemokines are also concerned local injury, systemic exacerbation of inflammation and ultimately organ failure. In addition, transcription factor Nuclear factor-kappa B is also influence the severity through upregulate the proinflammatory genes. The patterns of acinar cell death are closely correlated with disease severity of AP. The degree of acinar cell apoptosis is reversed correlated whereas necrotic cell death is proportionate to severity.
