ArticleBMC gastroenterology2017
CTRC gene polymorphism (p.G60=; c.180 C > T) in acute pancreatitis.
Article in BMC gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Genetic Variability in theInternational journal of molecular sciences · 2024Article
- GGT1 is a SNP eQTL gene involved in STAT3 activation and associated with the development of Post-ERCP pancreatitis.Scientific reports · 2024Article
- CaMKII/proteasome/cytosolic calcium/cathepsin B axis was present in tryspin activation induced by nicardipine.Bioscience reports · 2019Article
- Genetic Polymorphisms: A Novel Perspective on Acute Pancreatitis.Gastroenterology research and practice · 2017Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of the study was to determine the relationship between the presence of p.G60 = polymorphism (c.180C > T; rs497078) CTRC and the incidence together with the clinical course of acute pancreatitis (AP).
methodsTwo hundred ninety-nine people suffering from AP and 417 healthy volunteers were subjected to the study. DNA was isolated from blood samples.
resultsCTRC p.G60 = polymorphism (c.180C > T) occurred more frequently in the AP group (p = 0.015). The CT and TT genotype was found in 27.8% of the AP patients and in 19.9% of the healthy subjects (p = 0.017). No significant correlation was found between having the CT and TT genotype and the severity of the AP clinical course. In 6 patients (2%) with the CT genotype, a SPINK1 gene mutation was found, while in the control group it was found in 3 patients (0.7%), (p > 0.05). All patients with the present SPINK1 mutation with the CT genotype had a moderate or a severe course of the disease (p = 0.0007).
conclusionsCTRC polymorphism Hetero p.G60=; c.180C > T increases the risk of an AP occurrence and together with the SPINK 1 mutation, may be responsible for a more severe course of the disease.
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