Background: In esophagus whether antiplatelet drugs, such as low-dose aspirin (LDA) and clopidogrel, induce mucosal injury by pH changes or by acid reflux is unclear. We designed to clarify which mechanism was responsible.
Methods: In study 1, 80 patients taking LDA and 80 age- and sex-matched subjects who underwent endoscopy for dyspeptic symptoms or for a health check-up were evaluated the endoscopic incidence of esophageal mucosal injury and severity. In study 2, 35 healthy subjects were treated with LDA 100 mg (regimen A), and then 20 randomly selected subjects were dosed clopidogrel 75 mg (regimen C), LDA/clopidogrel (regimen AC), or LDA/clopidogrel/rabeprazole 10 mg for 7 days. Subjects underwent endoscopy and 24-hour pH measurements on day 7.
Results: In study 1, the prevalence of esophageal injury in LDA patients was 40.0%, significantly higher than in non-LDA subjects (25.0%, p = 0.042). In study 2, significant increases in incidence of injury were observed with regimens A (45.8%) and AC (50.0%), but not with C (20.0%), on day 7. Among subjects in whom pH was >5.0 and <4.0 for less than 40% of time, none developed esophageal injury.
Conclusions: LDA caused esophageal injury in half of patients and volunteers. Acid-inhibitory drugs effectively prevented the development of LDA-induced, not clopidogrel, esophageal injury.
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http://dx.doi.org/10.1159/000350438 | DOI Listing |
Gut Microbes
December 2025
State Key Laboratory of Bioreactor Engineering, East China University of Science and Technology, Shanghai, China.
IgA nephropathy (IgAN) is related to the balance of gut microbiota. However, it is unclear whether changes in the gut microbiota can cause IgAN or attenuate its progression. This study employed IgAN and human microbiota-associated (HMA)-IgAN models to investigate the impact of IgAN on gut microbiota alteration and the mechanisms by which gut microbiota might trigger IgAN.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Department of Molecular Biology & Genetics, Krishna Institute of Allied Sciences, Krishna Vishwa Vidyapeeth "Deemed to be University", Taluka-Karad, Dist- Satara, Pin-415 539, (Maharashtra) India.
Background: In this study we explored the association of polymorphisms of glutathione s transferase gene including GSTM1, GSTT1 and GSTP1 with adverse acute normal tissue reactions resulted from radiotherapy in HNC patients. We assessed the association of GSTM1 and GSTT1 null genotypes and Ile105Val of exon-5 and Ala114Val of exon-6 of GSTP1 gene polymorphisms with the risk of acute skin toxicity reactions after therapeutic radiotherapy in HNC patients.
Methods: Four hundred HNC patients administered with Intensity modulated radiation therapy were enrolled in this study for the evaluation of radiotherapy associated toxicity reactions.
World Neurosurg
January 2025
Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China. Electronic address:
Objective: To investigate the risk factors and their diagnostic efficacy for postoperative intestinal mucosal barrier dysfunction (IBD) following severe traumatic brain injury (sTBI).
Methods: There were 140 patients with sTBI enrolled in this study. Univariate and multivariate logistic regression analyses were conducted to assess the relationship between the clinical data and postoperative IBD in sTBI patients and determine the independent risk factors.
Introduction: Acute esophageal necrosis (AEN) is a rare and lethal condition that may progress to sepsis and perforations. Most related literature comes from case reports; however, a few small reviews have been published. We conducted a large systematic review of AEN using PubMed, MEDLINE, and Embase to organize data into one consolidated manuscript, find potential prognosticators of illness, and determine possible treatment guidelines for AEN.
View Article and Find Full Text PDFMol Immunol
January 2025
Department of Gastroenterology and Hepatology, Nantong Third People's Hospital, Affiliated Nantong Hospital 3 of Nantong University, Nantong, Jiangsu Province 226006, China. Electronic address:
Background: The intestinal mucosa of ulcerative colitis patients expresses high levels of interleukin 34, and mice lacking IL-34 have more severe DSS-induced experimental colitis. There are no studies on the effects of directly upregulating intestinal IL-34 on experimental colitis in mice.
Methods: The bacteria EcN/CSF-1 and EcN/IL-34, which express CSF-1 and IL-34, respectively, were genetically engineered from Escherichia coli Nissle 1917 (EcN).
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