ReviewTranslational gastroenterology and hepatology2017
Deciphering the pathophysiology of irritable bowel syndrome and functional gastrointestinal disorders-an alternative model for pathogenesis: cytokine controlled transepithelial multi-feedback loop.
Review in Translational gastroenterology and hepatology, 2017. 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
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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, 7 citations in OpenAlex.
- Transcriptomic Module Discovery of Diarrhea-Predominant Irritable Bowel Syndrome: A Causal Network Inference Approach.International journal of molecular sciences · 2024Article
- Comparison of Laughter Yoga and Anti-Anxiety Medication on Anxiety and Gastrointestinal Symptoms of Patients with Irritable Bowel Syndrome.Middle East journal of digestive diseases · 2019Article
- Current insights into the innate immune system dysfunction in irritable bowel syndrome.Annals of gastroenterologyReview
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A working theoretical model for irritable bowel syndrome (IBS) and other functional gastrointestinal disorders (FGIDs) does not exist, hampered by the lack of any clear cut invention that address all symptom and signs of the disease. Reports of cessation of symptom and signs of both major types of IBS have been published using a non-systemic, topically active agent-high potency polymerized cross-linked sucralfate (HPPCLS). The unique clinical effect of this non-systemic agent restricted to the luminal surface of the gut provides opportunity to elaborate on an alternative working model for the pathogenesis of IBS and FGIDs. While the chemical determinants of HPPCLS and the mucosal lining contribute to the clinical effects, the sequence of events resides in the functional interplay among elements within the mucosa itself. The proposed model assumes that failure of a pre-existing genomic-controlled surveillance of the epithelium localized to the luminal surface triggers primary and secondary immune activation of inflammation intent on restoring epithelial homeostasis. Delayed restoration of homeostasis results in all the symptoms, signs and likely molecular events that characterize IBS and FGIDs.
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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.