Purpose: To identify the clinical and radiologic findings in patients with diaphragm-like strictures in the small bowel.
Patients And Methods: We reviewed the histories, radiologic findings, and pathologic findings in two men and two women, all in their sixties, with a history of long-term nonsteroidal antiinflammatory drug (NSAID) or aspirin (ASA) usage and one or more radiologically demonstrated diaphragm-like strictures in the small bowel.
Results: Two patients had long histories of NSAID usage, and two of ASA usage. One NSAID user had a long segment of jejunal involvement, and the other three had short segments of duodenal involvement. The ASA users presented with symptoms of esophageal disease, the small bowel lesions were unexpected, and ASA usage was not initially elicited. In one NSAID user and one ASA user, broader strictures with humps rather than diaphragms were also seen producing a lifesaver-like or bagel-like configuration.
Conclusions: Multiple diaphragm-like strictures can occur in NSAID injury and are pathognomonic except in the rare patient with ulcerative enteritis complicating celiac disease. Single or few diaphragm-like strictures can occur in NSAID injury and peptic ulceration. ASA should be considered an NSAID with regard to small-bowel toxicity. A careful medication history is required when an unexplained small bowel abnormality is seen radiologically, and a dedicated small bowel examination is required when NSAID injury is suspected.
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http://dx.doi.org/10.1007/s002619900282 | DOI Listing |
Cell Mol Gastroenterol Hepatol
January 2025
Department of Medicine, University of Western Ontario, London, Ontario N6A 5W9, Canada; Verspeeten Family Cancer Centre, London Health Sciences Centre, London, Ontario, Canada. Electronic address:
Background And Aims: Loss of the tumor suppressor gene Apc in Lgr5+ intestinal stem cells results in aberrant Wnt signaling and colonic tumorigenesis. In the setting of injury, however, we and others have also shown that non-stem cells can also give rise to colonic tumors. The mechanism by which inflammation leads to cellular plasticity and cancer, however, remains largely unknown.
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December 2024
Immunology Research Lab & BK21-Four Educational Research Group for Age-Associated Disorder Control Technology, Department of Biological Science, Chosun University, Gwangju 61452, Republic of Korea.
Neuroinflammation is a complex and dynamic response of the central nervous system (CNS) to injury, infection, and disease. While acute neuroinflammation plays a protective role by facilitating pathogen clearance and tissue repair, chronic and dysregulated inflammation contributes significantly to the progression of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Multiple Sclerosis. This review explores the cellular and molecular mechanisms underlying neuroinflammation, focusing on the roles of microglia, astrocytes, and peripheral immune cells.
View Article and Find Full Text PDFMol Med
January 2025
Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Gangnamdae-ro 540, Seoul, 135-896, Republic of Korea.
Background: Inflammation is a critical protective response in the body, essential for combating infections and healing injuries. However, chronic inflammation can be harmful and significantly contribute to the development and progression of chronic diseases, with macrophage-mediated responses being central to these processes. This study presents "SBR-Pel," a new therapeutic blend of Shinbaro tab (SBR), a traditional herbal formula, and pelubiprofen (Pel), a non-steroidal anti-inflammatory drug, and investigated their combined anti-inflammatory effects to create a treatment that both improves efficacy and reduces side effects.
View Article and Find Full Text PDFFP Essent
January 2025
Family medicine residency program at Rutgers University/Robert Wood Johnson University Hospital Somerset, Somerville, NJ.
Int J Cardiol
January 2025
Cardiology and Cardiothoracic Department, University Hospital "Santa Maria della Misericordia" (ASUFC) Udine, Italy.
Background: Patients with pericarditis may show elevation of C-reactive protein (CRP) and pericardial effusion at presentation. There are limited data on the prognostic implications of this inflammatory phenotype.
Objectives: Aim of the present study is to evaluate the outcome of the inflammatory phenotype in a cohort of patients with acute pericarditis.
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