Enteropathy https://greenmedinfo.com/taxonomy/term/20998/all en Ameliorating role of hydrogen-rich water against NSAID-induced enteropathy. https://greenmedinfo.com/article/ameliorating-role-hydrogen-rich-water-against-nsaid-induced-enteropathy PMID:  Dig Dis Sci. 2023 May ;68(5):1824-1834. Epub 2022 Dec 7. PMID: 36478314 Abstract Title:  Ameliorating Role of Hydrogen-Rich Water Against NSAID-Induced Enteropathy via Reduction of ROS and Production of Short-Chain Fatty Acids. Abstract:  BACKGROUND: Nonsteroidal anti-inflammatory drug (NSAID)-induced enteropathy, the mechanism of which is involved in oxidative stress, can be lethal due to hemorrhage. Thus, we aimed to investigate the effect of hydrogen-rich water (HRW), in terms of oxidative stress, on intestinal mucosal damage as well as changes in the gut microbiome and the short-chain fatty acids (SCFAs) content in feces.METHODS: Hydrogen-rich water was orally administered for 5 days to investigate the effectiveness of indomethacin-induced enteropathy in mice. Small intestinal damage and luminal reactive oxygen species (ROS) were evaluated to investigate the ameliorating effects of hydrogen. Then, components of the gut microbiome were analyzed; fecal microbiota transplantation (FMT) was performed using the cecal contents obtained from mice drinking HRW. The cecal contents were analyzed for the SCFAs content. Finally, cells from the macrophage cell line RAW264 were co-cultured with the supernatants of cecal contents.RESULTS: Hydrogen-rich water significantly ameliorated IND-induced enteropathy histologically and reduced the expression of IND-induced inflammatory cytokines. Microscopic evaluation revealed that luminal ROS was significantly reduced and that HRW did not change the gut microbiota; however, FMT from HRW-treated animals ameliorated IND-induced enteropathy. The SCFA content in the cecal contents of HRW-treated animals was significantly higher than that in control animals. The supernatant had significantly increased interleukin-10 expression in RAW264 cells in vitro.CONCLUSION: Hydrogen-rich water ameliorated NSAID-induced enteropathy, not only via direct antioxidant effects but also via anti-inflammatory effects by increasing luminal SCFAs. These results suggest that hydrogen may have therapeutic potential in small intestinal inflammatory diseases. <p><a href="https://greenmedinfo.com/article/ameliorating-role-hydrogen-rich-water-against-nsaid-induced-enteropathy" target="_blank">read more</a></p> https://greenmedinfo.com/article/ameliorating-role-hydrogen-rich-water-against-nsaid-induced-enteropathy#comments Enteropathy Hydrogen Water Oxidative Stress Anti-Inflammatory Agents Antioxidants Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Human Study Tue, 06 Feb 2024 04:06:18 +0000 greenmedinfo 287846 at https://greenmedinfo.com Amelioration of radiation enteropathy by dietary supplementation with reduced coenzyme Q10. https://greenmedinfo.com/article/amelioration-radiation-enteropathy-dietary-supplementation-reduced-coenzyme-q1 PMID:  Adv Radiat Oncol. 2019 Apr-Jun;4(2):237-245. Epub 2019 Jan 31. PMID: 31011668 Abstract Title:  Amelioration of Radiation Enteropathy by Dietary Supplementation With Reduced Coenzyme Q10. Abstract:  Purpose: Effective methods to ameliorate radiation enteropathy have not been developed. To address this issue, we investigated the reduced form of coenzyme Q10 (rCoQ10) as a potential radioprotector in a mouse model.Methods and Materials: rCoQ10 was added to a standard laboratory mouse diet at a final concentration of 1.0% 9 days before irradiation and 30 days thereafter or dissolved in corn oil and administered transorally. Accumulated amounts of coenzyme Q10 (CoQ10) or coenzyme Q9 in the intestine were measured by high-performance liquid chromatography. Reactive oxygen species (ROS), apoptosis, and morphologic changes in the intestine were assessed by immunohistochemistry after administration of 13 Gy of x-ray to the mouse abdomen. Body weight and survival were monitored for 30 days after irradiation. Cytotoxicity using 3 human cancer cell lines and the tumor growth-inhibiting effect in a xenograft were investigated to determine whether rCoQ10 interferes with radiation-specific cytotoxic effects on tumor growth.Results: CoQ10 was greatly accumulated in all sections of the intestine after both massive transoral dosing and dietary administration, whereas coenzyme Q9 was not. Administration of rCoQ10 suppressed ROS production and inhibited apoptosis in the crypts, resulting in preservation of villi structures after irradiation. Notably, 92% of mice fed the rCoQ10-supplemented diet were healthy and alive 30 days after irradiation, whereas 50% of control mice died ( <p><a href="https://greenmedinfo.com/article/amelioration-radiation-enteropathy-dietary-supplementation-reduced-coenzyme-q1" target="_blank">read more</a></p> https://greenmedinfo.com/article/amelioration-radiation-enteropathy-dietary-supplementation-reduced-coenzyme-q1#comments Coenzyme Q10 Enteropathy Radiation Induced Illness Anti-Apoptotic Radioprotective Animal Study Fri, 16 Aug 2019 18:50:13 +0000 greenmedinfo 193941 at https://greenmedinfo.com Caution: Retinoic Acid and IL-15 promote breakdown of gluten tolerance and the development of enteropathy https://greenmedinfo.com/article/caution-retinoic-acid-and-il-15-promote-breakdown-gluten-tolerance-and-develop PMID:  Expert Rev Gastroenterol Hepatol. 2011 Jun ;5(3):315-7. PMID: 21651349 Abstract Title:  IL-15 modulates the effect of retinoic acid, promoting inflammation rather than oral tolerance to dietary antigens. Abstract:  The physiological immune response in the intestine against dietary proteins and commensal flora is characterized by regulatory mechanisms (tolerance) that prevent harmful consequences. Intestinal dendritic cells (DCs) have a central role in the development of immunosuppressive regulatory T cells owing to their ability to produce TGF-β and retinoic acid (RA). However, the article under evaluation shows an unexpected effect of RA - that of promoting a proinflammatory phenotype in intestinal DCs involved in the generation of inflammatory immune responses to dietary antigens. By using a double transgenic murine model that resembles human celiac disease, it was demonstrated that RA synergizes with IL-15 in promoting the breakdown of gluten tolerance and the development of enteropathy. The tissue microenvironment modulates DC function, and immune therapies that are based on RA aiming to restore oral tolerance should be used with caution because the presence of IL-15 (and/or other proinflammatory cytokines) may have undesirable effects. https://greenmedinfo.com/article/caution-retinoic-acid-and-il-15-promote-breakdown-gluten-tolerance-and-develop#comments Celiac Disease Enteropathy Inflammation Vitamin A Immunosuppressive Celiac Disease Enteropathy IL-15 Retinoic Acid Transgenic Animal Study Sun, 01 Apr 2012 01:13:43 +0000 greenmedinfo 73795 at https://greenmedinfo.com Could This Popular Pain-Killer Be Causing Celiac Disease? https://greenmedinfo.com/blog/could-popular-pain-killer-be-causing-celiac-disease <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2014<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="Could This Popular Pain-Killer Be Causing Celiac Disease? " src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/Sayer Ji/images/celiac_disease_NSAID.jpg" style="width: 692px; height: 564px;" /></p> <p>A new study published in the <em>American Journal of Physiology</em> reveals that a popular NSAID drug known as indomethacin may be triggering celiac disease in those who eat gluten-containing foods such as wheat.</p><p><a href="https://greenmedinfo.com/blog/could-popular-pain-killer-be-causing-celiac-disease" target="_blank">read more</a></p> https://greenmedinfo.com/blog/could-popular-pain-killer-be-causing-celiac-disease#comments Anti-gliadin Antibodies: Elevated Celiac Disease Celiac Disease: Early Onset Celiac Disease: Prevention Celiac Disease: Psychosocial Implications Celiac Disease: Recovery Celiac Disease: Refractory Enteropathy Food Allergies: Wheat Gastrointestinal Inflammation Gluten Enteropathy Gluten Sensitivity Intestinal Permeability Leaky Gut Syndrome Non-Celiac Gluten Sensitivity (NCGS) anti-inflammatory Aspirin Dark Side of Wheat Glyphosate Glyphosate formulations Ibuprofen Indomethacin Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Roundup (herbicide) NSAID Alternatives NSAIDs Sun, 29 Jun 2014 00:52:50 +0000 Sayer Ji 113061 at https://greenmedinfo.com Gliadin triggered insulinitis in type 1 diabetes associated with celiac disease https://greenmedinfo.com/article/gliadin-triggered-insulinitis-type-1-diabetes-associated-celiac-disease PMID:  J Immunol. 2011 Oct 15 ;187(8):4338-46. Epub 2011 Sep 12. PMID: 21911598 Abstract Title:  Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese diabetic-DQ8 mice. Abstract:  Celiac disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit Abs against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to have a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but not insulitis. Administration of anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25(+)Foxp3(+) T cells and led to severe insulitis, but did not exacerbate mucosal dysfunction. CD4(+) T cells isolated from pancreatic lymph nodes of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubation with gliadin but not with BSA. CD4(+) T cells isolated from nonsensitized controls did not response to gliadin or BSA. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice. However, insulitis development required gliadin-sensitization and partial systemic depletion of CD25(+)Foxp3(+) T cells. This humanized murine model provides a mechanistic link to explain how the mucosal intolerance to a dietary protein can lead to insulitis in the presence of partial regulatory T cell deficiency. https://greenmedinfo.com/article/gliadin-triggered-insulinitis-type-1-diabetes-associated-celiac-disease#comments Celiac Disease Diabetes Mellitus: Type 1 Enteropathy Insulinitis Gliadin Animal Study Fri, 04 May 2012 17:11:18 +0000 greenmedinfo 75286 at https://greenmedinfo.com Gluten-sensitive enteropathy has been observed in a cynomolgus monkey. https://greenmedinfo.com/article/gluten-sensitive-enteropathy-has-been-observed-cynomolgus-monkey PMID:  Lab Anim Sci. 1988 Oct ;38(5):592-4. PMID: 3193752 Abstract Title:  Gluten-sensitive enteropathy in a cynomolgus monkey. Abstract:  A malabsorption syndrome was observed in a cynomolgus macaque. Clinical signs included weight loss despite increased appetite, and diarrhea, characterized by an increased volume of soft, tan, malodorous feces. Clinicopathologic findings included hypoalbuminemia, generalized dilation of bowel loops with a prolonged transit time, steatorrhea and markedly diminished absorption of D-xylose. Biopsies of the duodenum and jejunum had total villous atrophy, crypt hyperplasia and a plasmacytic-lymphocytic infiltrate of the lamina propria. The monkey&#039;s diet was changed to a semi-synthetic diet containing no grain products. Subsequently, stool characteristics, body weight and intestinal villous morphology returned to normal. This response to removal of grain products from the diet suggests a syndrome similar to gluten-sensitivity enteropathy in human beings. https://greenmedinfo.com/article/gluten-sensitive-enteropathy-has-been-observed-cynomolgus-monkey#comments Enteropathy Gluten Animal Study Fri, 23 Mar 2012 18:27:07 +0000 greenmedinfo 73575 at https://greenmedinfo.com Intravenous nutrition given to at-risk premature infants may result in zinc deficiency and consequent adverse health effects. https://greenmedinfo.com/article/intravenous-nutrition-given-risk-premature-infants-may-result-zinc-deficiency- PMID:  Pediatr Dermatol. 2010 Jul-Aug;27(4):380-3. PMID: 20653858 Abstract Title:  Symptomatic acquired zinc deficiency in at-risk premature infants: high dose preventive supplementation is necessary. Abstract:  Zinc is a cofactor for several enzymes involved in many metabolisms. Zinc deficiency induces various disorders such as acrodermatitis enteropathica, either inherited or acquired. We report three cases of premature infants (24-31 wks gestational age) with low birthweight (650 to 940 g) and enteropathy, two of whom presented with necrotizing enterocolitis. All infants were fed by total parenteral nutrition. At a chronological age ranging from 73 to 80 days, all infants developed a periorificial dermatitis. Before the onset of the first signs, they had received zinc supplementation ranging from 146% to 195% of the recommended dose (400 microg/kg/day). Increased zinc supplementation over a course of 6-18 days induced a complete resolution of symptoms in all cases. No abnormality in the neurologic examination and no recurrence were observed at the end of the zinc treatment. Low birthweight premature infants with enteropathy on total parenteral nutrition are at risk of developing zinc deficiency. The usual recommended zinc supplementation is probably insufficient for those infants. A delay in the diagnosis of zinc deficiency may lead to severe complications. https://greenmedinfo.com/article/intravenous-nutrition-given-risk-premature-infants-may-result-zinc-deficiency-#comments Enteropathy Necrotising enterocolitis Premature Birth Zinc Zinc Deficiency Human Study Thu, 09 Dec 2010 17:35:41 +0000 greenmedinfo 59430 at https://greenmedinfo.com Oregano and onion controls proliferative enteropathy in weaning pigs. https://greenmedinfo.com/article/oregano-and-onion-controls-proliferative-enteropathy-weaning-pigs PMID:  Pol J Vet Sci. 2009;12(3):407-14. PMID: 19886265 Abstract Title:  Effect of Origanum vulgaris and Allium sativum extracts for the control of proliferative enteropathy in weaning pigs. Abstract:  The aim of the present trial was to investigate the efficacy of Virbamix PE (Virbac SA, France) an appetite enhancer and feed flavouring material containing plant extracts of Origanum vulgaris and Allium sativum, added to the feed at one single dose in the control of proliferative enteropathy (PE) in weaning pigs, in comparison to reference treatment with tiamulin (Tiamutine 6.5 Premix/Ceva Animal Health) group and a negative control group. The trial was conducted on a farm with a previous history of ileitis outbreaks. At weaning day (25 +/- 3 days old / day 0 of the trial) a total of 288 (144 male + 144 female) piglets were selected and allocated into three experimental groups, each group comprising of four pens with 24 piglets in each pen. Group 1 (T1 group) served as negative control group (unmedicated), group T2 received medication in feed at the dose of 1 kg Virbamix PE per tonne of feed and T3 group received 32 ppm of tiamulin. Treatments lasted for six weeks (up to the age of 67 +/- 3 days), and no other antibacterial or growth promoter was added to the feed or drinking water in the same period. Administration of Virbamix PE was found to be effective for the control of PE, as shown by the reduction of prevalence of Lawsonia intracellularis in the intestine at the end of the treatment period, as determined by PCR method comparatively with the T1 group, while no significant difference was found between T2 and T3 groups. The diarrhoea score (DS) was significantly higher (P0.05). Treatment of piglets with Virbamix PE and Tiamutine 6.5 Premix resulted in significantly higher body weight and average daily gain (ADG) than in T1 group for the total treatment period (P https://greenmedinfo.com/article/oregano-and-onion-controls-proliferative-enteropathy-weaning-pigs#comments Enteropathy Garlic Oregano Plant Extracts Animal Study Sat, 13 Feb 2010 00:31:30 +0000 greenmedinfo 51156 at https://greenmedinfo.com Potassium chloride is associated with enteropathy. https://greenmedinfo.com/article/potassium-chloride-associated-enteropathy PMID:  Schweiz Med Wochenschr. 1977 Aug 27;107(34):1195-8. PMID: 918579 Abstract Title:  [4 cases of potassium enteropathy]. Abstract:  The oral use of enteric-coated potassium chloride (and apparently of its slow-release form too) to compensate potassium loss during thiazide diuretic treatment may engender ischemic enteropathy. This iatrogenic condition is linked to the vaso-active properties of KCl, which act on blood vessels often damaged by hypertension or chronic heart failure. Four observations are presented involving stenosing ulceration or perforation of the small bowel following oral KCl treatment. The main clinical, pathological and therapeutic aspects are discussed. https://greenmedinfo.com/article/potassium-chloride-associated-enteropathy#comments Enteropathy Potassium Chloride Human Study Fri, 19 Feb 2010 02:55:11 +0000 greenmedinfo 51783 at https://greenmedinfo.com Quercetin could protect against pantoprazole sodium induced enteropathic damage in a dose dependent manner. https://greenmedinfo.com/article/quercetin-could-protect-against-pantoprazole-sodium-induced-enteropathic-damag PMID:  Exp Toxicol Pathol. 2016 Oct 22. Epub 2016 Aug 22. PMID: 27780667 Abstract Title:  Co-administration of quercetin with pantoprazole sodium prevents NSAID-induced severe gastroenteropathic damage efficiently: Evidence from a preclinical study in rats. Abstract:  Management of Nonsteroidal anti-inflammatory drug (NSAID)-induced gastroenteropathy has emerged as a major medical and socioeconomic problem mainly because the highly efficacious gastroprotective drugs i.e. proton pump inhibitors (PPIs) like pantoprazole sodium (PTZ), worsen the NSAID-induced enteropathic damage and lack of approved therapeutic strategies/interventions to prevent this damage. Hence, the primary objective of the current study was to assess whether we can protect the GI mucosa against gastroenteropathic damage caused by diclofenac sodium (DIC) in rats by co-administration of PTZ and quercetin (QCT). Rats were treated twice daily with QCT (35, 50 and 100mgkg(-1) peroral) and/or PTZ (4mgkg(-1)) or vehicle for a total of 10 days. In some experiments, DIC (9mgkg(-1)) was administered orally twice daily for the final 5days of PTZ/QCT+PTZ/vehicle administration. Rats in all the groups were fasted after the last dose on 9th day, but, water was provided ad libitum. 12h after the last dose on 10th day, rats were euthanized and their GI tracts were assessed for haemorrhagic damage, lipid peroxidation, intestinal permeability and GI luminal pH alterations along with haematological and biochemical estimations. The experimental evidences suggested that co-administration of QCT with PTZ significantly attenuated the exacerbation of NSAID-induced enteropathic damage in a dose dependent manner. The combination of PTZ 4mgkg(-1) and QCT at the doses of 50 or 100mgkg(-1) was found to effective in preventing the DIC-induced gastroenteropathy. The present report focuses on the gastroenteroprotective ability of QCT and the mechanisms may be related to its ability to prevent GI blood loss, the lipid peroxidation, intestinal permeability alteration and alteration in GI luminal pH. <p><a href="https://greenmedinfo.com/article/quercetin-could-protect-against-pantoprazole-sodium-induced-enteropathic-damag" target="_blank">read more</a></p> https://greenmedinfo.com/article/quercetin-could-protect-against-pantoprazole-sodium-induced-enteropathic-damag#comments Enteropathy Quercetin Gastroprotective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Dose Response Animal Study Wed, 02 Nov 2016 21:18:31 +0000 greenmedinfo 138753 at https://greenmedinfo.com