ReviewWorld journal of gastrointestinal pathophysiology2014
Genetics of acute and chronic pancreatitis: An update.
Review in World journal of gastrointestinal pathophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 55 citations in OpenAlex.
- Development and validation of dynamic clinical subphenotypes in acute pancreatitis patients using vital sign trajectories in intensive care units: a multinational cohort study.Signal transduction and targeted therapy · 2025Article
- Genetic Variability in theInternational journal of molecular sciences · 2024Article
- Surgical management of acute pancreatitis: Historical perspectives, challenges, and current management approaches.World journal of gastrointestinal surgery · 2023Review
- An investigation of codon usage pattern analysis in pancreatitis associated genes.BMC genomic data · 2022Article
- Pancreas Divisum Increases the Risk of Recurrent Acute Pancreatitis in Patients with rs12338 Polymorphism in the Cathepsin B Gene.Digestive diseases and sciences · 2021Article
- Transgenic Expression of PRSS1Gastroenterology · 2020Article
- Observational longitudinal multicentre investigation of acute pancreatitis (GOULASH PLUS): follow-up of the GOULASH study, protocol.BMJ open · 2019Observational
- SPINK-1 Polymorphism as a Pancreatitis Risk Factor.Cureus · 2019Article
- Glycemic Outcomes of Islet Autotransplantation.Current diabetes reports · 2018Review
- Progression of recurrent acute to chronic pancreatitis: More questions than answers!Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2018Article
- Review
- Pancreatic Aquaporin-7: A Novel Target for Anti-diabetic Drugs?Frontiers in chemistry · 2018Review
- Pancreatitis after human papillomavirus vaccination: a matter of molecular mimicry.Immunologic research · 2017Article
- CTRC gene polymorphism (p.G60=; c.180 C > T) in acute pancreatitis.BMC gastroenterology · 2017Article
- Genophenotypic Analysis of Pediatric Patients With Acute Recurrent and Chronic Pancreatitis.Pancreas · 2016Article
- Calcium signalling in salivary gland physiology and dysfunction.The Journal of physiology · 2016Review
- Clinical Genetic Testing in Gastroenterology.Clinical and translational gastroenterology · 2016Review
- Epithelial Anion Transport as Modulator of Chemokine Signaling.Mediators of inflammation · 2016Review
- Hereditary pancreatitis: current perspectives.Clinical and experimental gastroenterology · 2016Review
- Lipase gene fusion: a new route to chronic pancreatitis.Oncotarget · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progress made in identifying the genetic susceptibility underlying acute and chronic pancreatitis has benefitted the clinicians in understanding the pathogenesis of the disease in a better way. The identification of mutations in cationic trypsinogen gene (PRSS1 gene; functional gain mutations) and serine protease inhibitor kazal type 1 (SPINK1 gene; functional loss mutations) and other potential susceptibility factors in genes that play an important role in the pancreatic secretory functions or response to inflammation during pancreatic injury has changed the current concepts and understanding of a complex multifactorial disease like pancreatitis. An individual's susceptibility to the disease is governed by genetic factors in combination with environmental factors. Candidate gene and genetic linkage studies have identified polymorphisms in cationic trypsinogen (PRSS1), SPINK1, cystic fibrosis trans-membrane conductance regulator (CFTR), Chymotrypsinogen C (CTRC), Cathepsin B (CTSB) and calcium sensing receptor (CASR). Individuals with polymorphisms in the mentioned genes and other as yet identified genes are at an enhanced risk for the disease. Recently, polymorphisms in genes other than those involved in "intra-pancreatic trypsin regulatory mechanism" namely Claudin-2 (CLDN2) and Carboxypeptidase A1 (CPA1) gene have also been identified for their association with pancreatitis. With ever growing number of studies trying to identify the genetic susceptibility in the form of single nucleotide polymorphisms, this review is an attempt to compile the available information on the topic.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.