pubmed-article:21323990 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21323990 | lifeskim:mentions | umls-concept:C0205147 | lld:lifeskim |
pubmed-article:21323990 | lifeskim:mentions | umls-concept:C0149521 | lld:lifeskim |
pubmed-article:21323990 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
pubmed-article:21323990 | lifeskim:mentions | umls-concept:C0003980 | lld:lifeskim |
pubmed-article:21323990 | lifeskim:mentions | umls-concept:C1527178 | lld:lifeskim |
pubmed-article:21323990 | pubmed:dateCreated | 2011-2-17 | lld:pubmed |
pubmed-article:21323990 | pubmed:abstractText | Chronic pancreatitis (CP) is a disease characterized by irreversible destruction and fibrosis of the parenchyma, leading to pancreatic exocrine insufficiency. In developed countries, the etiology for 60% to 70% of CP amongst male patients is alcohol and 25% are classified as idiopathic chronic pancreatitis (ICP). The genetic predisposition to CP could be an inappropriate activation of trypsinogen in the pancreas. Two common haplotypes, c.101A>G (p.N34S) and c.-215G>A, and four intronic alterations of the serine protease inhibitor Kazal type 1 (SPINK1) gene have been found to increase the risk for CP in the Asia Pacific region. Hence, SPINK1 is thought to be a candidate gene for pancreatitis. A loss-of-function alteration in chymotrypsinogen C (CTRC) gene has been shown to be associated with tropical calcific pancreatitis (TCP). Cathepsin B (CTSB) is also found to be associated with TCP. However mutations in cationic and anionic trypsinogen gene do not play an important role in causing CP in Asia Pacific region. | lld:pubmed |
pubmed-article:21323990 | pubmed:language | eng | lld:pubmed |
pubmed-article:21323990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21323990 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:21323990 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21323990 | pubmed:month | Mar | lld:pubmed |
pubmed-article:21323990 | pubmed:issn | 1440-1746 | lld:pubmed |
pubmed-article:21323990 | pubmed:author | pubmed-author:ReddyD... | lld:pubmed |
pubmed-article:21323990 | pubmed:author | pubmed-author:PrasadS... | lld:pubmed |
pubmed-article:21323990 | pubmed:copyrightInfo | © 2011 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd. | lld:pubmed |
pubmed-article:21323990 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21323990 | pubmed:volume | 26 Suppl 2 | lld:pubmed |
pubmed-article:21323990 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21323990 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21323990 | pubmed:pagination | 2-5 | lld:pubmed |
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pubmed-article:21323990 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21323990 | pubmed:articleTitle | Genetic basis of chronic pancreatitis in Asia Pacific region. | lld:pubmed |
pubmed-article:21323990 | pubmed:affiliation | Asian Healthcare Foundation, Asian Institute of Gastroenterology, Somajiguda, Hyderabad, Andhra Pradesh, India. aigindia@yahoo.co.in | lld:pubmed |
pubmed-article:21323990 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21323990 | pubmed:publicationType | Review | lld:pubmed |
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