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Association of tumour necrosis factor α promoter haplotype with chronic pancreatitis
  1. M-C Chang1,
  2. Y-T Chang1,
  3. Y-W Tien2,
  4. P-C Liang3,
  5. S-C Wei4,
  6. J-M Wong4
  1. 1Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  2. 2Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan
  3. 3Department of Radiology, National Taiwan University Hospital, Taipei, Taiwan
  4. 4Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  1. Correspondence to:
    Dr J-M Wong
    Department of Internal Medicine, National Taiwan University Hospital, No 7 Chung Shan South Rd, Taipei, Taiwan; jmwong{at}ha.mc.ntu.edu.tw

http://dx.doi.org/10.1136/gut.2006.103085

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    Genetic risk factors are attributed an important role in the pathogenesis of chronic pancreatitis.1 The genetic basis of chronic pancreatitis is complex. The cationic trypsinogen gene,2 serine protease inhibitor Kazal type 1 (SPINK1),3 and cystic fibrosis transmembrane conductance regulator4 genes have been most extensively studied in chronic pancreatitis. However, the frequency of hereditary pancreatitis, which may be related to the trypsinogen gene and SPINK1 in Orientals, is regarded as relatively low and hardly explains the genetic susceptibility of chronic pancreatitis in Chinese.5 Chronic pancreatitis is a progressive chronic inflammatory disease characterised by irreversible destruction of exocrine pancreatic tissue and extensive fibrosis. Tumour necrosis factor (TNF)-α, a prototype proinflammatory cytokine, has been implicated as an important pathogenic mediator in a variety of inflammatory diseases. …

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    • Conflict of interest: None declared.