ReviewCurrent gastroenterology reports2008
Patterns of gastrointestinal disease associated with mutations of CFTR.
Review in Current gastroenterology reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 20 citations in OpenAlex.
- Animal models of biliary injury and altered bile acid metabolism.Biochimica et biophysica acta. Molecular basis of disease · 2018Review
- Article
- Increased levels of anti-glycan antibodies in patients with cystic fibrosis.European journal of medical research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review focuses on the pathobiology of the gastrointestinal and hepatic manifestations of cystic fibrosis (CF) disease in relation to their genetic basis in mutations of the CF transmembrane conductance regulator (CFTR) gene. It reviews the nature of the CFTR protein, a categorization of the types of gene mutations underlying CF's various manifestations, and the ways in which absent or reduced CFTR produces various functional abnormalities in the different organs affected by CF. Subsequently, the particular organ-related clinical manifestations of CF directly associated with loss of CFTR function are addressed. Thereafter, the review discusses some of the complexities of the genotype-phenotype relationships related to milder mutations or complex genetic disorders in which CFTR abnormalities interact with other genetic and environmental factors, and the potential diagnostic roles of sweat testing or other electrophysiologic testing. This discussion examines secondary gastrointestinal manifestations of CF and the particular cases of diseases that may be related to abnormalities of CFTR.
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.