Academic literature on the topic 'Gastric mucosal erosion'

1. An increasing body of data suggests that the anti-haemostatic as well as the ulcerogenic actions of aspirin and other non-steroidal anti-inflammatory drugs may be operative when patients present with haematemesis and melaena. 2. We therefore developed methods to allow separate evaluation of the erosive and anti-haemostatic actions of aspirin in the human gastric mucosa. Volunteer subjects took 300 mg of aspirin daily in the morning or 600 mg of aspirin four times a day for 5 days under blinded randomized conditions. Changes in spontaneous gastric microbleeding, endoscopic signs of injury, spontaneous bleeding per gastric erosion, biopsy-induced bleeding and eicosanoids were studied. 3. Both doses of aspirin significantly inhibited gastric mucosal synthesis of prostaglandin E2 and reduced the serum thromboxane concentration. Erosions developed and regressed rapidly; compared with baseline 300 mg of aspirin daily in the morning caused substantial numbers of gastric erosions to develop (mean 5.3, 95% confidence limits 2.7–10.2) but this was significantly less than that caused by 600 mg of aspirin four times a day (10.9, 7.2–16.5, P < 0.05). The presence of erosions was associated with enhanced spontaneous bleeding, but only during aspirin administration. 4. Aspirin significantly increased bleeding induced by mucosal biopsy and was associated with significant enhancements in the rate of bleeding per gastric erosion. Bleeding rate per erosion but not biopsy-induced bleeding showed a significant dose-related increase with 600 mg of aspirin four times a day. Enteric coating reduced endoscopic signs of injury, but did not affect the impaired haemostasis caused by aspirin. 5. We conclude that aspirin can be shown to have both erosive and anti-haemostatic effects in the human stomach. Each can be evaluated separately in our model system. Both are potential therapeutic targets for the prevention of major upper-gastrointestinal bleeding caused by aspirin and probably other non-steroidal antiinflammatory drugs.

Patients with gastric mucosal erosions are predisposed to chronic gastritis, ulcer or even cancer. The repair of mucosal erosions involves several events including proliferation of gastric epithelial stem cells. The aim of this study was to investigate the effects of the probiotic mixture of De Simone Formulation on gastric epithelial stem cell lineages in mouse models of gastric mucosal erosions. Gastric erosions were induced by a single oral gavage of 80% ethanol containing 15 mg/mL acetylsalicylic acid (5 mL/kg) following a daily dose of probiotic mixture (5 mg/day/mouse) for 10 days. In another protocol, erosions were induced by a daily gavage of acetylsalicylic acid (400 mg/kg/day/mouse) for 5 days before or after daily administration of probiotic mixture for 5 days. Control mice received water gavage for 10 days. All mice were injected with bromodeoxyuridine two hours before sacrifice to label S-phase cells. The stomachs of all mice were processed for histological examination, lectin binding, and immunohistochemical analysis. The results reveal that mice that received probiotics before or after the induction of erosion showed a decrease in erosion index with an increase in gastric epithelial stem/progenitor cell proliferation and enhanced production of mucus, trefoil factors, and ghrelin by mucous and enteroendocrine cell lineages. These mice also showed restoration of the amount of H+,K+-ATPase and pepsinogen involved in the production of the harsh acidic environment by parietal and chief cell lineages. In conclusion, this study demonstrates the beneficial effects of probiotics against gastric mucosal erosion and highlights the involvement and modulation of proliferative stem cells and their multiple glandular epithelial cell lineages.

This study investigates the protective effects of GamiHyangsa-Yukgunja (GHY, a popular herbal medicine formula) on indomethacin-induced gastric mucosal lesions and morphological change in rats. Subcutaneous injection of indomethacin (25 mg/kg) produced the following gastric morphological alterations; mucosa hermorrhagic infarct, mucosa cell necrosis, leukocyte infiltration, mucosa hemorrhagic erosion, and gastric pit disappearance. Tissue damages were accompanied by increased oxidative stress, lipid peroxidation, and decreases in superoxide dismutase (SOD), and catalase (CAT) activities, and glutathione (GSH) concentrations. Our results show that pretreatment of the rats with orally administered GHY extract (3.3 ml/kg/day) significantly reduced gastric lesion formation and caused the amelioration of several pathological changes in the above-mentioned gastric mucosal lesions. Concomuitantly, GHY-pretreatment increased gastric mucosal SOD and CAT activities and GSH concentrations. We therefore propose that GHY exerts a prophylactic effect on the indomethacin-induced gastric mucosal lesions by enhancing antioxidant defense systems.

Objective. To investigate aspirin-related gastric and small-intestinal mucosal injury in elderly patients by magnetically controlled capsule endoscopy (MCCE). Methods. Patients taking enteric-coated aspirin attending the outpatient department of Beijing Anzhen Hospital, Capital Medical University, from September 2017 to July 2019 underwent MCCE to assess injury to the gastric and small-intestinal mucosa. The patients were divided into the elderly group (age≥60 years) and middle-aged group (45 years≤age<60 years), and their clinical data were evaluated. Results. Sixty-eight patients (34 per group) taking enteric-coated aspirin were recruited, and the elderly and middle-aged groups did not differ significantly in sex, history of smoking, history of alcohol consumption, body mass index, or accompanying diseases. In the elderly and middle-aged groups, the gastric Lanza scores were 2.0 (2.0, 3.0) and 2.0 (1.0, 3.0; P=0.192), the numbers of patients with small-intestinal mucosal injuries (at least one erosion and/or ulcer) were 30 (88.2%) and 15 (44.1%; P<0.001), the numbers of patients with more severe small-intestinal mucosal injuries (larger erosion and/or ulcer) were 11 (32.4%) and 3 (8.8%; P=0.033), the numbers of patients with ileal erosion were 22 (64.7%) and 8 (23.5%; P=0.001), and the durations of aspirin use were 30.0 (12.0, 120.0) and 10.5 (2.0–48.0) months (P=0.007), respectively. Conclusions. The rate of small-intestinal mucosal injury was significantly higher in elderly than in middle-aged patients taking enteric-coated aspirin, especially the rate of ileal erosion. MCCE enables the monitoring of aspirin-related gastric and small-intestinal mucosal injury in elderly patients, which can guide treatment decision making.

1. Differing amounts of human pepsins 1, 3 (pepsin A) and 5 (pepsin C or gastriscin) in aqueous HCl/NaCl at pH 1.3 were placed in Perspex rings on the exposed luminal surface of the perfused cat stomach to test for mucolytic and erosive activity in vivo, with the acid medium in control rings. 2. After incubation at 37°C for 60 or 120 min, the test and control solutions were replaced by the same volume of each test or control solution containing 18 mg of aspirin and incubated for a further 120 min. 3. The number of bleeding points or erosions was counted at 15 min intervals. None was observed with human pepsins 1, 3 and 5 or with pig pepsin A or in the control rings. 4. With aspirin, erosions developed in all ringed areas. Their rate of development with time for pepsin 1 and pig pepsin did not differ from controls. Significantly more erosions developed with human pepsins 3 (5 mg per ring, P < 0.001) and 5 (0.32 mg per ring, P < 0.05). 5. Human pepsins 3 and 5, applied at pH 1.3 to the mucosal surface of the perfused cat stomach, therefore cause erosions when administered with aspirin, but do not produce erosions when given alone. In man, pepsins secreted in increased amount or concentration may therefore be unlikely to cause significant mucosal erosion unless human gastric mucosa is less resistant to pepsins than cat mucosa. Pepsins may perhaps facilitate the action of a second factor, such as aspirin, or infection with Helicobacter pylori.

Pancreatic cancer with gastrointestinal tract metastasis is a fairly rare occurrence, and gastric metastasis in such cases has been seldom reported. We herein present a case of gastric involvement secondary to pancreatic cancer in a 74-year-old woman in whom the metastatic lesion only presented as mucosal erosion in the stomach. The patient had a 1-month history of progressive right upper quadrant pain before admission. Computed tomography and endoscopic examinations revealed a solid and hypo-enhancing mass in the head of the pancreas. The patient underwent conventional upper endoscopy before pancreatic biopsy, and mucosal erosion was observed in the gastric pylorus. We obtained gastric and pancreatic biopsies by gastroscopy and endoscopic ultrasound-guided fine needle aspiration, respectively. Pathologically, the biopsies taken from the area of gastric erosion showed poorly differentiated invasive adenocarcinoma that was morphologically consistent with the pancreatic specimens. Moreover, the gastric section showed tumor thrombi within the vessels. Hence, the suspected diagnosis was unresectable pancreatic cancer with gastric metastasis. The patient immediately underwent two courses of chemotherapy, but her condition rapidly deteriorated and she died 2 months later.

Accumulating evidence suggests that central thyrotropin-releasing hormone (TRH) administration induces gastric erosion 4 h after administration through the vagal nerves. However, early changes in the gastric mucosa during these 4 h have not been described. To assess early changes in the gastric mucosa after intracisternal injection of a stable TRH analog, pGlu-His-(3,3′-dimethyl)-ProNH2 (RX-77368), we measured the blood-to-lumen 51Cr-labeled EDTA clearance and examined the effects of vagotomy, atropine, omeprazole, and hydrochloric acid (HCl) on RX-77368-induced mucosal permeability. A cytoprotective dose of RX-77368 (1.5 ng) did not increase mucosal permeability. However, higher doses significantly increased mucosal permeability. Permeability peaked within 20 min and gradually returned to control levels in response to a 15-ng dose (submaximal dose). Increased mucosal permeability was not recovered after a 150-ng dose (ulcerogenic dose). This increase in permeability was inhibited by vagotomy or atropine. Intragastric perfusion with HCl did not change the RX-77368 (15 ng)-induced increase in permeability, but completely inhibited the recovery of permeability after the peak. Pretreatment with omeprazole did not change the RX-77368 (15 ng)-induced increase in permeability, but quickened the recovery of permeability after the peak. These data indicate that the RX-77368-induced increase in permeability is mediated via the vagal-cholinergic pathway and is not a secondary change in RX-77368-induced acid secretion. Inhibited recovery of permeability on exposure to an ulcerogenic RX-77368 dose or on exposure to HCl plus a submaximal dose of RX-77368 may be crucial for the induction of gastric mucosal lesions by central RX-77368 administration.

ABSTRACT Background: Studies with latest technologies such as endoscopy with magnification and chromoendoscopy showed that various endoscopic aspects are clearly related to infection by Helicobacter pylori (HP). The description of different patterns of erythema in gastric body under magnification of images revived interest in identifying these patterns by standard endoscopy. Aim: To validate the morphologic features of gastric mucosa related to H. pylori infection gastritis allowing predictability of their diagnosis as well as proper targeting biopsies. Methods: Prospective study of 339 consecutive patients with the standard videoendoscope image analysis were obtained, recorded and stored in a program database. These images were studied with respect to the presence or absence of H. pylori, diagnosed by rapid urease test and/or by histological analysis. Were studied: a) normal mucosa appearance; b) mucosal nodularity; c) diffuse nonspecific erythema or redness (with or without edema of folds and exudate) of antrum and body; d) mosaic pattern with focal area of hyperemia; e) erythema in streaks or bands (red streak); f) elevated (raised) erosion; g) flat erosions; h) fundic gland polyps. The main exclusion criteria were the use of drugs, HP pre-treatment and other entities that could affect results. Results: Applying the exclusion criteria, were included 170 of the 339 patients, of which 52 (30.58%) were positive for HP and 118 negative. On the positive findings, the most associated with infection were: nodularity in the antrum (26.92%); presence of raised erosion (15.38%) and mosaic mucosa in the body (21.15%). On the negative group the normal appearance of the mucosa was 66.94%; erythema in streaks or bands in 9.32%; flat erosions 11.86%; and fundic gland polyps 11.86%. Conclusion: Endoscopic findings are useful in the predictability of the result and in directing biopsies. The most representative form of HP related gastritis was the nodularity of the antral mucosa. The raised erosion and mucosa in mosaic in the body are suggestive but not specific to the infection. The other forms were not conclusive of the presence of HP.

Background/Aims: Endoscopic submucosal dissection (ESD) for gastric neoplasms is a widely performed procedure. Local recurrence is rare, but various post-ESD scars are encountered during follow-up endoscopy. Therefore, we investigated atypical scar patterns and evaluated the associated factors.Materials and Methods: Clinicopathologic and endoscopic reviews of gastric neoplasms treated with ESD from January 2009 to December 2015 were conducted. Atypical scar patterns were classified as irregular erythema, nodularity, or mucosal defect.Results: A total of 264 patients with 274 gastric neoplasms, including 201 adenomas and 73 early gastric cancers, were enrolled. The key endoscopic findings at the resection scar were defined on the basis of gross morphology as follows: irregular erythema, mucosal defect (erosion or ulcer), and nodularity. An irregular erythema scar pattern was associated with male sex, a nodularity scar pattern with smoking, and a mucosal defect scar pattern with infra-angle location (angle and antrum) and cancer. An irregular erythema with nodularity scar pattern was also associated with male sex. An irregular erythema with nodularity and mucosal defect scar pattern was associated with liver disease and chronic kidney disease.Conclusions: The atypical scar patterns after gastric ESD are associated with various clinicopathologic factors.

Abstract Gastric erosions are superficial mucosal breaks. With the exception of bleeding, they are considered harmless, but their aetiology, histopathology and long-term course have remained unknown and even the evolution of gastritis in patients with gastric erosions is unclear. The present study aimed to solve clinical significance and pathology of gastric erosions in a long-term follow-up study. Initially, 117 patients and 117 controls were studied in 1974–1981, and a follow-up study was performed in 1996. We evaluated the presence of Helicobacter pylori and Herpes simplex virus (HSV) infections, use of NSAIDs and alcohol, smoking, and assessed features of gastric histopathology. For follow-up, 52 patients and 66 controls were available. In the follow-up visit, 39% patients still had gastric erosions while 11% of the controls had developed erosions (p = 0.001). In H. pylori-positive subjects, peptic ulcer or a scar was more common in patients (17%) than in controls (4%, p = 0.006), but otherwise no increased morbidity or mortality was seen. High antibody titres against HSV predicted the persistence of erosions (p = 0.000), but H. pylori infection, use of NSAIDs, alcohol or smoking were not associated. Initially, inflammation was more active in the region of erosions than elsewhere in the antral mucosa, and more active inflammation in the erosion was associated with HSV seropositivity, H. pylori infection and the recent use of NSAIDs. Initially, H. pylori-positive subjects with chronic or recurrent erosions had higher scores of neutrophils compared to those with non-chronic/non-recurrent erosions. In H. pylori-positive subjects, body gastritis was initially less active in the patient group. With time, antral gastritis worsened only in the patient group. In H. pylori-negative subjects, there was no evolution of gastritis. These results show that a significant proportion of gastric erosions are chronic/recurrent but mostly without serious complications. However, H. pylori-positive patients have a significant risk to develop a peptic ulcer. A significant proportion of chronic gastric erosions is related to HSV infection. Focally enhanced inflammation modified by HSV or NSAID may be important in the pathogenesis of gastric antral erosions. Active inflammation in the erosions seems to predict their chronicity/recurrency. Patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype
Tiivistelmä Eroosiot ovat mahalaukun pinnallisia limakalvovaurioita. Niitä pidetään vaarattomina lukuun ottamatta niihin liittyvää verenvuototaipumusta. Niiden etiologiaa, histopatologiaa ja taudinkulkua ei tunneta. Ei myöskään tiedetä eroosiopotilaiden mahan limakalvon tulehduksen kulkua. Tämän tutkimuksen tavoitteena oli selvittää mahalaukun eroosioiden kliininen merkitys ja patologia pitkäkestoisena seurantatutkimuksena. Alkujaan 117 potilasta ja 117 kontrollihenkilöä tutkittiin vuosina 1974–1981, ja seurantatutkimus tehtiin vuonna 1996. Selvitimme helikobakteerin ja Herpes simplex -viruksen (HSV) aiheuttamien infektioiden, tulehduskipulääkkeiden (NSAID) ja alkoholin käytön, sekä tupakoinnin esiintymistä. Lisäksi tutkimme histopatologisesti mahalaukun limakalvoa. Lopulta oli 52 potilaan ja 66 kontrollihenkilön aineisto käytettävissä. Seurantakäynnillä 39 prosentilla potilaista oli yhä mahalaukun eroosioita, kun taas kontrolliryhmästä vain 11 prosentilla oli kehittynyt eroosioita. Helikobakteeri -infektoituneilla maha- tai pohjukaissuolen haava/arpi oli yleisempää eroosioryhmässä (17 %) kuin kontrolleilla (4 %), mutta muuten ei esiintynyt lisääntynyttä sairastuvuutta tai kuolleisuutta. Tulehdus oli aktiivisempaa eroosioissa kuin viereisellä limakalvolla, ja tämä tulehdus liittyi korkeisiin HSV-vasta-ainetasoihin, helikobakteeri-infektioon ja NSAID:n käyttöön. Korkeat HSV-vasta-ainetasot ennustivat eroosioiden pysyvyyttä. Ensimmäisellä käynnillä aktiivinen tulehdus eroosioissa oli voimakkaampaa niillä helikobakteeri-infektoituneilla, joilla eroosiot olivat pysyviä kuin niillä, joilla eroosiot eivät uusineet. Helikobakteeri-infektoituneilla eroosiopotilailla mahalaukun runko-osan limakalvon tulehdus oli aluksi vähemmän aktiivista kuin vastaavilla kontrolliryhmän henkilöillä, mutta ajan myötä mahalaukun corpusosan limakalvon tulehdus voimistui vain eroosioryhmällä. Limakalvotulehdus ei edennyt helikobakteeri-infektoitumattomilla henkilöillä. Tulokset osoittavat, että merkittävä osa mahalaukun eroosioista on kroonisia/toistuvia, mutta enimmäkseen ilman vakavia komplikaatioita. Kuitenkin helikobakteeri-infektoituneilla eroosiopotilailla on merkittävä riski saada maha- tai pohjakaissuolen haava. HSV- infektio liittyy merkittävään osaan kroonisia mahalaukun eroosioita. Paikallisella tulehdusaktiivisuudella, jota HSV ja NSAID:n käyttö muokkaavat, saattaa olla tärkeä rooli eroosioiden synnyssä ja niiden kroonistumisessa. Eroosiopotilailla on samanlainen mahalaukun limakalvon tulehduksen jakauma kuin pohjakaissuolihaavaa sairastavilla

Background: 20 to 30% of patients with GORD respond inadequately to conventional therapy. Most of these patients belong to the non-­‐erosive reflux disease group. Despite not having oesophagitis, in these patients oesophageal mucosal integrity appears to be impaired. Aims: To study the dynamic in vitro and in vivo properties of oesophageal mucosal integrity in patients with non-­‐erosive reflux disease, and to test the feasibility of a topical mucosal protectant therapy. Methods: In vitro studies of mucosal integrity were done on human oesophageal biopsies using Ussing chambers. Change in transepithelial electrical resistance (TER) on exposure to acidic solutions was measured. Integrity was assessed in vivo by measuring impedance change and subsequent recovery after oesophageal acid perfusion in symptomatic patients. Proximal and distal oesophageal mucosal integrity was assessed in vitro and in vivo. The effect of in vitro topical application of an alginate-­‐based solution on acid-­‐induced changes in mucosal integrity was tested. Results: In vitro exposure of biopsies to acidic and weakly acidic solutions caused a greater impairment of integrity in symptomatic patients than in controls. In vivo oesophageal acid perfusion causes a profound drop in distal oesophageal impedance that is slow to recover. Recovery is slower in patients with non-­‐erosive reClux disease than in patients with functional heartburn, and a low baseline impedance is associated with painful perception of acid. Proximal oesophageal sensitivity appears unrelated to impaired mucosal integrity, but rather to a distinct sensory afferent nerve distribution. Topical pre-­‐treatment with an alginate solution is able to prevent acid-­‐induced changes in integrity in vitro. Conclusion: Patients with non-­‐erosive reClux disease have a distinct mucosal vulnerability to acidic and weakly acidic solutions that may underlie persistent symptoms. A topical therapeutic approach may be a feasible add-­‐on strategy to treat GORD in the future.

The term ‘anisakiosis (anisakidosis)’ or ‘anisakiasis’ collectively defines human infections caused by larval anisakids belonging to the nematode family Anisakidae or Raphidascarididae. Anisakis simplex, Anisakis physeteris, and Pseudoteranova decipiens are the three major species causing human anisakiosis. Various kinds of marine fish and cephalopods serve as the second intermediate hosts and the infection source. Ingestion of viable anisakid larvae in the fillet or viscera of these hosts is the primary cause of infection. The parasite does not develop further in humans as they are an accidental host. Clinical anisakiosis develops after the penetration of anisakid larvae into the mucosal wall of the alimentary tract, most frequently the stomach and the small intestine. The affected sites undergo erosion, ulceration, swelling, inflammation, and granuloma formation around the worm. The patients may suffer from acute abdominal pain, indigestion, nausea, vomiting, and in some instances, allergic hypersensitive reactions. Symptoms in gastric anisakiosis often resemble those seen in peptic ulcer or gastric cancer, and symptoms in intestinal anisakiosis resemble those of appendicitis or peritonitis. Treatments include removal of larval worms using a gastroendoscopic clipper or surgical resection of the mucosal tissue surrounding the worm. No confirmed effective anthelmintic drug has been introduced, though albendazole and ivermectin have been tried in vivo and in vitro. Prevention of human anisakiosis can be achieved by careful examination of fish fillet followed by removal of the worms in the restaurant or household kitchen. Immediate freezing of fish and cephalopods just after catching them on fishing boats was reported helpful for prevention of anisakiosis. It is noteworthy that anisakiosis is often associated with strong allergic and hypersensitivity reactions, with symptoms ranging from isolated angioedema to urticaria and life threatening anaphylactic shock.