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Association of tumour necrosis factor promoter haplotype with chronic pancreatitis

¹ Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
² Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan
³ Department of Radiology, National Taiwan University Hospital, Taipei, Taiwan
⁴ Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan

Correspondence to:
Correspondence to:
Dr J-M Wong
Department of Internal Medicine, National Taiwan University Hospital, No 7 Chung Shan South Rd, Taipei, Taiwan; jmwong@ha.mc.ntu.edu.tw

Keywords: chronic pancreatitis; haplotype; tumour necrosis factor promoter; polymorphism

The first 150 words of the full text of this article appear below.

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)-, a prototype proinflammatory cytokine, has been implicated as an important pathogenic mediator in a variety of inflammatory diseases. Several biallelic polymorphisms have been described within the TNF- promoter region upstream of the transcriptional start site.⁶ In the past, limited and conflicting data on . . . [Full text of this article]

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