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The G191R variant in the PRSS2 gene does not play a role in protection against tropical calcific pancreatitis
  1. S Mahurkar1,2,
  2. S Bhaskar1,
  3. D N Reddy2,
  4. G V Rao2,
  5. S P Singh3,
  6. V Thomas4,
  7. G R Chandak1
  1. 1
    Genome Research Group, Centre for Cellular and Molecular Biology (CSIR), Hyderabad. Andhra Pradesh, India
  2. 2
    Asian Institute of Gastroenterology, Punjagutta, Hyderabad, Andhra Pradesh, India
  3. 3
    Department of Gastroenterology, SCB Medical College, Cuttack, Orissa, India
  4. 4
    Department of Gastroenterology, Calicut Medical College, Calicut, Kerala, India
  1. Dr G R Chandak, Genome Research Group, Centre for Cellular and Molecular Biology (CSIR), Uppal Road, Hyderabad, Andhra Pradesh, 500 007 India; chandakgrc{at}ccmb.res.in

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Recently, the G191R variant in anionic trypsinogen (coded by PRSS2) was reported to be strongly associated with chronic pancreatitis (CP) (odds ratio (OR) = 0.37, p = 1.1×10−8) in European patients with CP1 and subsequently replicated in Hungarian and Japanese patients with CP.2 3 We and others have earlier shown that CP in tropical countries such as India and Bangladesh, especially tropical calcific pancreatitis (TCP), has a variable genetic basis compared to that in Europeans and rather than cationic trypsinogen (coded by PRSS1) mutations,3 4 variants in SPINK1 encoding the pancreatic secretory trypsin inhibitor or cathepsin B (CTSB) or chymotrypsin C predict susceptibility to TCP.37 We, therefore, investigated using a case–control approach whether G191R PRSS2 variant also confers protection against TCP.

We analysed the G191R variant in the PRSS2 gene by direct sequencing in 700 patients with CP including 500 patients with TCP, 155 patients having idiopathic chronic pancreatitis (ICP) and 45 with alcoholic pancreatitis (see supplementary material). On initial screening of 299 patients with TCP and 277 control subjects, the minor allele frequency (MAF) of the G191R variant was significantly lower compared to Europeans1 and was similar in both the groups (0.3%). Genotyping and pooled analysis of additional patients with CP and normal subjects showed comparable frequency of …

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