ABSTRACT
We evaluate the value of oral contrast-enhanced gastric ultrasonography (OCUS) by comparing it with conventional gastroscopy in diagnosing and staging benign peptic ulcer. From July 2018 to December 2020, 44 patients with gastroscopy-confirmed benign peptic ulcers (a total of 45 ulcers were detected), who also received OCUS, were retrospectively reviewed. Each patient's ultrasound images were compared with gastroscopy and pathology findings. The characteristics of ultrasonic images of different stages of ulcer were analysed. A total of 43 ulcers were detected by OCUS in 44 patients with benign peptic ulcers. There were no false positive results among the OCUS exams, but two ulcers were misdiagnosed. OCUS for benign peptic ulcer staging also shows acceptable clinical practice results. OCUS is useful for detecting and staging benign peptic ulcer, and may be considered an alternative method for conventional gastroscopy. OCUS is especially useful in the follow-up of BPU treatment, but futher study is needed to improve the diagnostic accuracy of benign and malignant ulcers.
Subject(s)
Contrast Media , Peptic Ulcer , Ultrasonography , Humans , Male , Female , Ultrasonography/methods , Middle Aged , Peptic Ulcer/diagnostic imaging , Peptic Ulcer/pathology , Aged , Adult , Retrospective Studies , Gastroscopy/methods , Stomach/diagnostic imaging , Stomach/pathology , Aged, 80 and over , Stomach Ulcer/diagnostic imaging , Stomach Ulcer/pathologyABSTRACT
Outer inflammatory protein A (OipA), which is encoded by the oipA gene, can induce interleukin-8 secretion in gastric epithelial cells. The functional status of the oipA gene is regulated by the slipped-strand mispairing mechanism based on the CT dinucleotide repeat number in the 5' region. This study aimed to investigate the oipA functional status ("on/off") of Helicobacter pylori (H. pylori) and its association with gastroduodenal diseases in southwestern Vietnam. The cross-sectional study was conducted on 173H. pylori isolates from 173 patients with gastroduodenal diseases. Sanger sequencing was used to determine the functional status of oipA. Multivariable logistic regression analysis was performed to identify the association between oipA status and gastroduodenal diseases. The oipA "on" status accounted for 96% of H. pylori isolates. Twenty-five CT repeat patterns of the oipA 5' signal region were observed, five of which were novel CT repeat patterns. The oipA "on" status was found in 100%, 97.8%, and 86.8% of H. pylori isolates from patients with peptic ulcer, precancerous lesions, and chronic gastritis, respectively (p < 0.01). The oipA "on" status was related to gastric precancerous lesions versus chronic gastritis (adjusted OR = 7.39, 95% CI: 1.35-40.59, p = 0.021) and peptic ulcers versus chronic gastritis (adjusted OR = 12.79, 95% CI: 1.19-1760.32, p = 0.033). Our data show a high prevalence of the oipA "on" status, which was associated with precancerous gastric lesions and peptic ulcers. Moreover, genetic diversity in the number and pattern of CT dinucleotide repeat of oipA among Vietnamese H. pylori strains was identified.
Subject(s)
Gastritis , Helicobacter Infections , Helicobacter pylori , Peptic Ulcer , Humans , Bacterial Outer Membrane Proteins/genetics , Helicobacter pylori/genetics , Helicobacter pylori/metabolism , Cross-Sectional Studies , Vietnam/epidemiology , Peptic Ulcer/pathology , Genetic Variation , Helicobacter Infections/epidemiology , Helicobacter Infections/pathology , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Antigens, Bacterial/geneticsABSTRACT
The prevalence of Helicobacter pylori (H. pylori) infection has exceeded 50% worldwide, and it is considered a high-risk factor for chronic gastritis, peptic ulcer, gastric adenocarcinoma, gastroesophageal reflux disease and functional dyspepsia. H. pylori drug resistance is a common problem worldwide. In recent years, the relationship between H. pylori infection and gastrointestinal microecology has received much attention. H. pylori infection changes the structure and composition of gastrointestinal microflora by regulating the gastrointestinal microecological environment, local pH value, cytokines and antimicrobial peptides, and immune response and then plays a crucial role in the occurrence and development of digestive system tumors, liver metabolism and extragastrointestinal diseases. The quadruple strategy of H. pylori eradication can also aggravate gastrointestinal microflora disorder. However, probiotics can reduce intestinal flora changes and imbalances through different mechanisms, thus enhancing the efficacy of H. pylori eradication therapy and reducing adverse reactions caused by eradication therapy. Therefore, this paper reviews the relationship between H. pylori infection and gastrointestinal microecology and its clinical application, providing a basis for clinical treatment.
Subject(s)
Dyspepsia , Gastritis , Helicobacter Infections , Helicobacter pylori , Peptic Ulcer , Dyspepsia/epidemiology , Helicobacter Infections/drug therapy , Humans , Peptic Ulcer/drug therapy , Peptic Ulcer/epidemiology , Peptic Ulcer/pathologyABSTRACT
BACKGROUND: The present study investigated the prevalence of Helicobacter pylori infection in peptic ulcer patients referred to the endoscopy departments in Khorramabad hospitals during 2013- 2016. METHODS: The early pool of the study included all patients who had been referred to the endoscopy department and whose endoscopic and pathology reports were available and complete. After recording endoscopic reports, 1224 peptic ulcer (gastric or duodenal ulcer) cases, in which biopsy assays were performed to examine the type of ulcer and the presence of Helicobacter pylori bacteria, were selected. Pathology reports were collected by referring to the pathology departments. The information in the pathology report, including demographic information, was included in a pre-designed questionnaire to match the endoscopic reports, the location of the pathology sample, and other details, including the presence or absence of Helicobacter pylori bacteria. Finally, the data were analyzed using SPSS, version 21. RESULTS: For all the 1224 patients studied, the mean age was 15.5 ± 17.5 years old. A total of 664 (54.2%) cases had gastric ulcers, 445 (36.4%) cases had duodenal ulcers, and 115 (9.4%) had both gastric and duodenal ulcers. Among gastric ulcer patients, 512 (65.7%) had a gastric ulcer in the antrum area, and 74.3% (579 patients) of the gastric ulcers were clean base type. CONCLUSION: The prevalence of infection was statistically significant in terms of the type, location, and number of peptic ulcers, including both gastric ulcer and duodenal ulcer.
Subject(s)
Duodenal Ulcer , Helicobacter Infections , Helicobacter pylori , Peptic Ulcer , Stomach Ulcer , Adolescent , Adult , Duodenal Ulcer/epidemiology , Endoscopy, Gastrointestinal , Helicobacter Infections/epidemiology , Hospitals, Urban , Humans , Iran/epidemiology , Peptic Ulcer/epidemiology , Peptic Ulcer/microbiology , Peptic Ulcer/pathology , Stomach Ulcer/epidemiology , Stomach Ulcer/microbiology , Young AdultSubject(s)
Liver Diseases/diagnostic imaging , Liver Diseases/etiology , Peptic Ulcer/complications , Peptic Ulcer/diagnostic imaging , Abdominal Pain/etiology , Adult , Endoscopy, Gastrointestinal , Hematemesis/etiology , Humans , Male , Melena/etiology , Peptic Ulcer/pathology , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Low-dose aspirin can cause gastric and duodenal ulceration, hereafter called peptic ulcer disease (PUD). Predisposition is thought to be related to clinical and genetic factors; our aim was to identify genetic risk factors associated with aspirin-induced PUD. METHODS: Patients (n=1478) were recruited from 15 UK hospitals. Cases (n=505) were defined as patients with endoscopically confirmed PUD within 2 weeks of using aspirin and non-aspirin Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). They were compared to two control groups: patients with endoscopically confirmed PUD without any history of NSAID use within 3 months of diagnosis (n=495), and patients with no PUD on endoscopy (n=478). A genome-wide association study (GWAS) of aspirin-induced cases (n=247) was compared to 476 controls. The results were validated by replication in another 84 cases and 162 controls. FINDINGS: The GWAS identified one variant, rs12678747 (p=1·65×10-7) located in the last intron of EYA1 on chromosome 8. The association was replicated in another sample of 84 PUD patients receiving aspirin (p=0·002). Meta-analysis of discovery and replication cohort data for rs12678747, yielded a genome-wide significant association (p=3·12×10-11; OR=2·03; 95% CI 1·65-2·50). Expression of EYA1 was lower at the gastric ulcer edge when compared with the antrum. INTERPRETATION: Genetic variation in an intron of the EYA1 gene increases the risk of endoscopically confirmed aspirin-induced PUD. Reduced EYA1 expression in the upper gastrointestinal epithelium may modulate risk, but the functional basis of this association will need mechanistic evaluation. FUNDING: Department of Health Chair in Pharmacogenetics, MRC Centre for Drug Safety Science and the Barts Cardiovascular NIHR Biomedical Research Centre, British Heart Foundation (BHF).
Subject(s)
Aspirin/adverse effects , Intracellular Signaling Peptides and Proteins/genetics , Nuclear Proteins/genetics , Peptic Ulcer/genetics , Polymorphism, Single Nucleotide , Protein Tyrosine Phosphatases/genetics , Aged , Aged, 80 and over , Case-Control Studies , Down-Regulation , Endoscopy, Gastrointestinal , Female , Genetic Predisposition to Disease , Genome-Wide Association Study , Humans , Introns , Male , Middle Aged , Peptic Ulcer/chemically induced , Peptic Ulcer/pathology , United KingdomABSTRACT
INTRODUCTION: currently, the non-steroid anti-inflammatory drugs constitute a veritable object of auto medication throughout the world. The goal of this study was to evaluate the endoscopic and clinical aspects of gastro-duodenal ulcer secondary to taking of non-steroid anti-inflammatory of various sources. METHODS: this was a cross-sectional study which was conducted between July 2016 and December 2017. All adult patients admitted to hospital for clinical symptoms suggestive of gastroduodenal involvement after taking anti-inflammatory drugs and having undergone upper digestive endoscopy were included in this study. Data analysis was done with Epi-info version 7 Software. RESULTS: a total of 114 patients were included, the mean age was 47.18±26 years with a male predominance (64.9%). Among the patients, only 1.75% had taken a non-steroid anti-inflammatory (NSAIDs) from pharmacy. The NSAIDs used were of different types: diclofenac, aceclofenac, aspirin and non-selective NSAIDs. For each drug used, more than half were derived from the streets. Clinically we noted: the dyspepsia (38.58%), hemorrhages (11.40%), the ulcerous syndrome (77.19%), haematemesis (19.29%), haematemesis associated with melena (37.71%), and the rectorrhagia in 6.14 of cases. The specific endoscopic lesions were bulbar ulcer (45.61%), gastric ulcers (20.17%), antral ulcerations (5.26%) and acute gastritis (9.64%), esophagitis (7.89%), esophageal varices (6.14%), and uncomplicated hiatal hernia in 7.01% of cases. CONCLUSION: the serious gastroduodenal lesions observed in this study and due to use of NSAIDs are mainly attributable to unauthorized molecules due to safety concerns. It would be necessary to conduct sensitization days at the community level and in each health facility.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Duodenal Ulcer/diagnosis , Endoscopy, Gastrointestinal , Stomach Ulcer/diagnosis , Adolescent , Adult , Aged , Aged, 80 and over , Anti-Inflammatory Agents, Non-Steroidal/administration & dosage , Cross-Sectional Studies , Duodenal Ulcer/chemically induced , Duodenal Ulcer/pathology , Female , Humans , Male , Middle Aged , Peptic Ulcer/chemically induced , Peptic Ulcer/diagnosis , Peptic Ulcer/pathology , Stomach Ulcer/chemically induced , Stomach Ulcer/pathology , Young AdultABSTRACT
Peptic ulcer disease (PUD) is a common condition that is induced by acid and pepsin causing lesions in the mucosa of the duodenum and stomach. The pathogenesis of PUD is a many-sided scenario, which involves an imbalance between protective factors, such as prostaglandins, blood flow, and cell renewal, and aggressive ones, like alcohol abuse, smoking, Helicobacter pylori colonisation, and the use of non-steroidal anti-inflammatory drugs. The standard oral treatment is well established; however, several problems can decrease the success of this therapy, such as drug degradation in the gastric environment, low oral bioavailability, and lack of vectorisation to the target site. In this way, the use of strategies to improve the effectiveness of these conventional drugs becomes interesting. Currently, the use of drug delivery systems is being explored as an option to improve the drug therapy limitations, such as antimicrobial resistance, low bioavailability, molecule degradation in an acid environment, and low concentration of the drug at the site of action. This article provides a review of oral drug delivery systems looking for improving the treatment of PUD.
Subject(s)
Anti-Ulcer Agents/administration & dosage , Drug Delivery Systems , Peptic Ulcer/drug therapy , Administration, Oral , Animals , Anti-Ulcer Agents/pharmacokinetics , Biological Availability , Gastric Mucosa/pathology , Humans , Peptic Ulcer/etiology , Peptic Ulcer/pathology , Protective Factors , Risk FactorsABSTRACT
Infection with Helicobacter pylori (H. pylori) is of great distress because of its vital role in the pathogenesis of chronic gastritis, peptic ulcers, and in the multi-step carcinogenic process of gastric cancer. The increasing antibiotic resistance pattern of H. pylori worldwide has prompted the World Health Organization to put this organism in the priority pathogens list. To study the disease biology, evaluation of drugs, treatment outcome and to come up with probable vaccination strategies, competent animal models that reproduce the signature of human infection are essential. Initial reports about animal colonization with H. pylori have shown significant heterogeneity, to such an extent that Barry Marshall, Nobel laureate for the discovery of H. pylori , infected himself with the bacterium to show its involvement in acute gastric illness. A paradigm-shift discovery of the H. pylori mouse-adapted strain SS1 has opened the avenues of research regarding the organism and its pathogenicity. Although the mouse model of H. pylori infection is being utilized all over the world, there are certain issues that need awareness and specific information to achieve successful, consistent colonization with symptoms resembling human. This chapter details an established and reliable protocol for the development of a competent mouse model for H. pylori infection leading to various gastro-intestinal diseases.
Subject(s)
Gastric Mucosa/pathology , Helicobacter Infections/pathology , Helicobacter pylori/pathogenicity , Animals , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/therapeutic use , Disease Management , Disease Models, Animal , Gastric Mucosa/microbiology , Gastritis/microbiology , Gastritis/pathology , Helicobacter Infections/drug therapy , Helicobacter pylori/classification , Helicobacter pylori/drug effects , Humans , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Peptic Ulcer/microbiology , Peptic Ulcer/pathology , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathologyABSTRACT
Peptic ulcer refers to the inflammatory response and necrotic lesions of the mucosa under the action of various pathogenic factors, which goes deeply into the mucosal muscle layer and often occurs to the gastrointestinal mucosa related to gastric acid secretion, among which the stomach and duodenum are the most common. The clinical manifestations include slow onset, prolonged course and weekly upper abdominal pain. Nitric oxide (NO) is an intracellular and intercellular signaling molecule that plays an important role in many physiological and pathological processes. Studies have found that a small amount of NO produced in vivo plays a role in many physiological homeostasis, such as regulating blood pressure, platelet aggregation, nitrogenization of hemoglobin, and regulating proliferation and differentiation of stem cells. However, under the action of some cytokines and oxidative stress, intracellular NO synthase will catalyze the synthesis of large amounts of NO and participate in the inflammatory response, causing beneficial or harmful effect on the body. Numerous basic studies have focused on the relationship between NO and peptic ulcer. The purpose of this review is to summarize the role of NO in peptic ulcer and its possible mechanism.
Subject(s)
Nitric Oxide/metabolism , Peptic Ulcer/metabolism , Animals , Humans , Peptic Ulcer/pathologyABSTRACT
Upper gastrointestinal bleeding (UGIB) is common in liver cirrhosis. Although esophageal and gastric varices (EGV) is the main bleeding source, there were still a proportion of patients with peptic ulcer bleeding. Thus, this study aimed to analyze the characteristic of variceal bleeding and peptic ulcer bleeding in liver cirrhosis. Cirrhotic patients with confirmed UGIB by urgent endoscopy from July 2012 to June 2018 were enrolled, and classified into peptic ulcer bleeding group (n = 248) and variceal bleeding group (n = 402). Clinical and endoscopic characteristics, therapeutic efficacy and prognosis were evaluated, and independent risk factors for 42-day morality were determined. The mean age and gender ratio of peptic ulcer bleeding group were higher than those in variceal bleeding group (55.58 ± 11.37 vs. 52.87 ± 11.57, P < 0.01; 4.51:1 vs. 2.87:1, P = 0.023). Variceal bleeding group most commonly presented as red blood emesis and coffee grounds (67.16%), while peptic ulcer group primarily manifested as melena (62.10%). Hepatocellular carcinoma was more prevalent in peptic ulcer group (141 vs. 119, P < 0.01). Albumin level in variceal bleeding group was lower higher (P < 0.01), but serum bilirubin, creatinine and prothrombin time were significantly higher (all P < 0.01). Success rate of endoscopic hemostasis for variceal bleeding and peptic ulcer bleeding was 89.05% and 94.35% (P = 0.021). Univariate and multivariate analysis identified prothrombin time (P = 0.041, OR [95% CI] 0.884 [0.786-0.995]), MELD score (P = 0.000, OR [95% CI] 1.153 [1.073-1.240]), emergency intervention (P = 0.002, OR [95% CI] 8.656 [2.219-33.764]), hepatic encephalopathy before bleeding (P = 0.003, OR [95% CI] 8.119 [2.084-31.637]) and hepatic renal syndrome before bleeding (P = 0.029, OR [95% CI] 3.877 [1.152-13.045]) as the independent predictors for 42-day mortality. Peptic ulcer bleeding should be distinguished from variceal bleeding by clinical and endoscopic characteristics.
Subject(s)
Esophageal and Gastric Varices/physiopathology , Gastrointestinal Hemorrhage/complications , Liver Cirrhosis/complications , Peptic Ulcer/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Female , Follow-Up Studies , Humans , Male , Middle Aged , Peptic Ulcer/etiology , Prognosis , Retrospective Studies , Risk Factors , Young AdultABSTRACT
Peptic ulcers are caused by the interaction between bacterial and host factors. This study demonstrates enhanced expression of caspase-4 in peptic ulcer patient biopsies, indicating that pyroptosis and noncanonical inflammasome activity may be processes involved in peptic ulcer disease. We show that primary murine macrophages infected with Helicobacter pylori upregulate caspase-11 (the ortholog of human caspase-4), activate caspase-1, and secrete IL-1ß. We demonstrate that misoprostol (a stable PGE1 analogue) decreased IL-1ß secretion and delayed lethality in vivo in a murine peritonitis model. PGE2 was shown to inhibit caspase-11-driven pyroptosis and IL-1ß secretion in macrophages. Overall, we provide evidence for a pathological role of caspase-4/11 in peptic ulcer disease and propose that targeting caspase-4 or inhibiting pyroptosis may have therapeutic potential in the management of peptic ulcers.
Subject(s)
Caspases, Initiator/metabolism , Helicobacter Infections/metabolism , Helicobacter pylori/pathogenicity , Interleukin-1beta/metabolism , Peptic Ulcer/metabolism , Animals , Caspases, Initiator/drug effects , Helicobacter Infections/complications , Helicobacter Infections/microbiology , Humans , Inflammasomes/metabolism , Macrophages/drug effects , Macrophages/metabolism , Mice , Misoprostol/pharmacology , Peptic Ulcer/pathology , Pyroptosis/drug effectsABSTRACT
Helicobacter pylori, present in the stomach lining, is a Gramnegative bacterium that causes various gastrointestinal diseases, including gastritis and peptic ulcers. Propolis is a natural resinous substance collected from a variety of plants, and contains several natural bioactive substances. The aim of this study was to investigate the anti-inflammatory and antioxidative effects of Korean propolis on H. pylori-induced damage in the human adenocarcinoma gastric cell line. The propolis used in this study was obtained from the Korea Beekeeping Association in South Korea. The expression of pro-inflammatory interleukins (ILs), such as IL-8, IL-12, IL-1ß, tumor necrosis factor alpha, cyclooxygenase-2, and inducible nitric oxide synthase, which was increased after H. pylori infection, significantly decreased in a dose-dependent manner upon pretreatment with Korean propolis, because of the suppression of mitogen-activated protein kinases and nuclear factor kB pathway. The anti-oxidative activity of propolis was assessed using the 2,2-diphenyl-1-picrylhydrazyl hydrate free radical assay. Korean propolis showed significant anti-oxidative effects via reactive oxygen species scavenging. In addition, pretreatment with Korean propolis upregulated the expression of anti-oxidant enzymes through Nrf2 signaling activation. These findings indicate that the use of Korean propolis, which has anti-inflammatory and anti-oxidative effects, can be promising for the prevention of H. pylori-induced gastric damage.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Antioxidants/pharmacology , Gastritis/pathology , Helicobacter Infections/pathology , Peptic Ulcer/pathology , Propolis/pharmacology , Cell Line, Tumor , Cytokines/metabolism , Gastritis/drug therapy , Gastritis/microbiology , Helicobacter pylori/pathogenicity , Humans , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism , Oxidative Stress/drug effects , Peptic Ulcer/drug therapy , Peptic Ulcer/microbiology , Republic of Korea , Signal Transduction/drug effectsABSTRACT
BACKGROUND: The ability to compare findings across surgical research is important. Inadequate description of participants, interventions or outcomes could lead to bias and inaccurate assessment of findings. The aim of this study was to assess consistency of description of participants using studies comparing laparoscopic and open repair of peptic ulcer as an example. METHODS: This systematic review is reported in line with the PRISMA checklist. Searches of MEDLINE and Embase databases were performed to identify studies comparing laparoscopic and open repair of perforated peptic ulcer in adults, published in the English language. Manuscripts were dual-screened for eligibility. Full texts were retrieved and dual-screened for inclusion. Data extracted from studies included descriptors of participants in studies from tables and text. Descriptors were categorized into conceptual domains by the research team, and coverage of each domain by study was tabulated. RESULTS: Searches identified 2018 studies. After screening, 37 full texts were retrieved and 23 studies were included in the final synthesis. A total of 76 unique descriptors were identified. These were classified into demographics (11 descriptors), vital signs (9 descriptors), disease-specific characteristics (10 descriptors), presentation and pathway factors (4 descriptors), risk factors (8 descriptors), laboratory tests (14 descriptors) and baseline health (28 descriptors). The number of descriptors in a single study ranged from three to 31. All studies reported at least one demographic descriptor. Laboratory tests was the least frequently described domain. CONCLUSION: Study participants are described inconsistently in studies of a single example surgical condition.
ANTECEDENTES: La capacidad de comparar los hallazgos en la investigación quirúrgica es importante. Una descripción inadecuada de los participantes, las intervenciones o los resultados podría conllevar sesgos y una evaluación incorrecta de los hallazgos. El objetivo de este estudio fue evaluar la consistencia en la descripción de los participantes utilizando los estudios comparativos de la cirugía laparoscópica con la cirugía abierta en el tratamiento de la úlcera péptica, como modelo. MÉTODOS: Esta revisión sistemática se presenta de acuerdo con la lista de verificación PRISMA. Se realizaron búsquedas en las bases de datos MEDLINE y EMBASE para identificar estudios, publicados en inglés, que compararan el tratamiento quirúrgico laparoscópico y abierto de la úlcera péptica perforada en adultos. Los artículos elegibles fueron sometidos a un doble cribaje para su selección. Se recuperaron los textos completos de los artículos y se evaluaron por partida doble para su inclusión. Los datos extraídos correspondían a los términos que describían las poblaciones de estudio en el texto y en las tablas de los artículos. Dichos términos descriptores fueron clasificados por el equipo de investigación en dominios conceptuales, registrándose la cobertura de cada dominio en cada estudio. RESULTADOS: Las búsquedas bibliográficas identificaron 2.018 estudios. Después de la selección, se recuperaron 37 artículos de texto completo y se incluyeron 23 estudios en la síntesis final. Se identificaron un total de 76 descriptores únicos. Dichos descriptores se clasificaron en demográficos (11 variables), signos vitales (9 variables), características específicas de la enfermedad (10 variables), factores de presentación y del proceso (4 variables), factores de riesgo (8 variables), pruebas de laboratorio (14 variables) y estado de salud basal (28 variables). El número de descriptores en un solo estudio varió de 3 a 31. Todos los estudios presentaron al menos un descriptor demográfico. Las pruebas de laboratorio fueron el dominio descrito con menor frecuencia. CONCLUSIÓN: Esta revisión demuestra que los participantes en los estudios se describen de manera inconsistente, tras haber tomado como modelo los estudios de una sola patología quirúrgica.
Subject(s)
Peptic Ulcer/surgery , Terminology as Topic , Humans , Laparoscopy , Peptic Ulcer/pathology , Randomized Controlled Trials as TopicABSTRACT
Peptic ulcer disease is common and can be diagnosed easily if the patient has an ulcer history or characteristic abdominal symptoms. On the other hand, it may take a long time for the patient to visit the hospital due to severe complications if the patient is old or insensitive to symptoms caused by peptic ulcers. In the present case, a 72-year-old female visited the hospital due to general weakness and inadequate oral intake, which started two weeks ago. Endoscopy and abdominal CT revealed huge gastric ulcer findings. Through a tissue examination by endoscopy, hepatic cells were identified, and the patient was diagnosed with peptic ulcer perforation to the liver and later received surgical treatment.
Subject(s)
Liver/pathology , Peptic Ulcer Perforation/diagnosis , Peptic Ulcer/pathology , Abdomen/diagnostic imaging , Aged , Female , Gastroscopy , Humans , Peptic Ulcer/complications , Peptic Ulcer Perforation/etiology , Peptic Ulcer Perforation/therapy , Tomography, X-Ray ComputedABSTRACT
BACKGROUND: Perforation of a marginal peptic ulcer after pancreaticoduodenectomy (PD) can lead to severe conditions, although its clinical features have not been well reported. In this article, we present three cases of marginal peptic ulcer perforation after PD that we experienced in our institute and attempt to clarify its appropriate treatment and prevention. CASE PRESENTATION: Marginal ulcer perforation confirmed with computed tomography and/or surgical exploration occurred in 3 (1.8%) of 163 consecutive patients who underwent PD (including 160 patients who underwent a total or subtotal stomach-preserving procedure) at our institution. The three patients (one man and two women) had a median age of 77 (65-79) years. Two of these patients had a medical history of duodenal peptic ulcer. All three patients had biliary neoplasms. Two of the patients underwent subtotal stomach-preserving PD with antro-jejunal anastomosis, and the other patient underwent pylorus-preserving PD with duodenal jejunostomy. The perforation occurred with a sudden and severe onset of abdominal pain 34, 94, and 1204 days, respectively, after the PDs. At the time of the perforation, all of the patients had been withdrawn from postoperative prophylactic antipeptic ulcer agents, with the cessation periods ranging from 12 to 1008 days. In addition, all the patients were in fasting conditions for 1 to 13 days just before the perforation. Surgical treatment with direct suturing of the perforated ulcer was performed for two patients, while conservative therapy was performed for one patient. Their primary treatment courses were satisfactory. Chronic antisecretory agent therapy was prescribed for 562, 271, and 2370 days, respectively, from marginal ulcer perforation, and no ulcer recurrence was noted in any of the patients. CONCLUSIONS: Lack of antisecretory therapy and fasting were considered an essential cause of marginal peptic ulcer perforation after PD. In addition, unlike the native duodenum, the jejunal limb used for reconstruction to a preserved stomach may be at increased risk of ulceration. Chronic permanent administration of antisecretory agents and fasting avoidance are desirable for patients who have undergone stomach-preserving PD to prevent marginal ulcer perforation.
Subject(s)
Pancreaticoduodenectomy/methods , Peptic Ulcer Perforation/etiology , Peptic Ulcer/pathology , Aged , Anastomosis, Surgical/methods , Duodenal Ulcer/pathology , Female , Humans , Male , Postoperative PeriodABSTRACT
Helicobacter pylori is a Gram-negative bacterium that causes chronic atrophic gastritis and peptic ulcers and it has been associated with the development of gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT). One of the more remarkable characteristics of H. pylori is its ability to survive in the hostile environment of the stomach. H. pylori regulates the expression of specific sets of genes allowing it to survive high acidity levels and nutrient scarcity. In the present study, we determined the expression of virulence associated protein D (VapD) of H. pylori inside adenocarcinoma gastric (AGS) cells and in gastric biopsies. Using qRT-PCR, VapD expression was quantified in intracellular H. pylori-AGS cell cultures at different time points and in gastric mucosa biopsies from patients suffering from chronic atrophic gastritis, follicular gastritis, peptic ulcers, gastritis precancerous intestinal metaplasia and adenocarcinoma. Our results show that vapD of H. pylori presented high transcription levels inside AGS cells, which increased up to two-fold above basal values across all assays over time. Inside AGS cells, H. pylori acquired a coccoid form that is metabolically active in expressing VapD as a protection mechanism, thereby maintaining its permanence in a viable non-cultivable state. VapD of H. pylori was expressed in all gastric biopsies, however, higher expression levels (p = 0.029) were observed in gastric antrum biopsies from patients with follicular gastritis. The highest VapD expression levels were found in both antrum and corpus gastric biopsies from older patients (>57 years old). We observed that VapD in H. pylori is a protein that is only produced in response to interactions with eukaryotic cells. Our results suggest that VapD contributes to the persistence of H. pylori inside the gastric epithelial cells, protecting the microorganism from the intracellular environment, reducing its growth rate, enabling long-term infection and treatment resistance.
Subject(s)
Bacterial Proteins/genetics , Gastritis, Atrophic/etiology , Helicobacter pylori/genetics , Membrane Glycoproteins/genetics , Stomach/microbiology , Stomach/pathology , Adenocarcinoma/etiology , Adenocarcinoma/microbiology , Adenocarcinoma/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Biopsy , Coculture Techniques/methods , Female , Gastric Mucosa/microbiology , Gastric Mucosa/pathology , Gastritis, Atrophic/microbiology , Gastritis, Atrophic/pathology , Gastroscopy/methods , Helicobacter Infections/complications , Helicobacter Infections/pathology , Humans , Intestines/microbiology , Intestines/pathology , Male , Metaplasia/microbiology , Metaplasia/pathology , Middle Aged , Peptic Ulcer/metabolism , Peptic Ulcer/pathology , Precancerous Conditions/etiology , Precancerous Conditions/microbiology , Precancerous Conditions/pathology , Pyloric Antrum/microbiology , Pyloric Antrum/pathology , Stomach Neoplasms/etiology , Stomach Neoplasms/microbiology , Stomach Neoplasms/pathology , Virulence/genetics , Young AdultABSTRACT
Gastric cancer is one of the most common worldwide types of cancer. It is a multifactorial disease and both environmental and genetic factors play an important role in its etiology. Evaluation of the relative expression level of NFKB2 gene in two groups of patients: peptic ulcer and gastric cancer and its role in the pathomechanism of these diseases was the aim of this study. RNA was isolated from: 79 samples of peptic ulcer, 22 gastric cancer and 11 control tissue. The real-time PCR technique was used to study the expression of NFKB2 gene. The relative expression level of NFKB2 gene was a variable in all three studied groups. The relative NFKB2 gene expression depends on the type of a disease. Peptic ulcer cases showed the increased relative NFKB2 gene expression to control group (p = 0.0000). Cancer cases presented decreased relative NFKB2 gene expression to normal stomach tissue (p = 0.0183). There are statistically important differences in the investigated gene expression between peptic ulcer, where the expression level is higher comparing to gastric cancer and control tissue which confirmed that such an activation is connected with an inflammatory process. The relative expression level of NFKB2 is decreased in cancer cases as opposed to control tissue and peptic ulcer cases which could suggest that during carcinogenesis of gastric cancer inhibition of NF-kB pathway takes place which could be a promising factor for patients.
Subject(s)
Gene Expression , Genetic Predisposition to Disease , NF-kappa B p52 Subunit/genetics , Peptic Ulcer/etiology , Stomach Neoplasms/etiology , Adult , Aged , Female , Genetic Association Studies , Helicobacter Infections/complications , Helicobacter Infections/microbiology , Humans , Male , Middle Aged , Neoplasm Staging , Peptic Ulcer/pathology , RNA, Messenger , Stomach Neoplasms/pathology , Tumor BurdenABSTRACT
The immunopathologic responses play a major role in the development of H. pylori (HP)-related gastrointestinal diseases. IL-37 is an anti-inflammatory cytokine with potent suppressive effects on innate and adaptive immune responses. Here, we investigated the IL-37 levels and two single nucleotide polymorphisms (SNPs) including rs3811047 and rs2723176 in IL-37 gene in HP-infected peptic ulcer (PU) patients to identify any relationship. Three groups, including 100 HP-infected PU patients, 100 HP-infected asymptomatic (AS) subjects and 100 non-infected healthy control (NHC) subjects were enrolled to study. Serum IL-37 levels and the genotyping at rs3811047 and rs2723176 were determined using ELISA and SSP-PCR methods, respectively. Significantly higher IL-37 levels were observed in PU patients compared with AS and NHC groups (P < 0.0001). In both PU and AS groups, the CagA+ HP-infected participants displayed higher IL-37 levels compared with those infected with CagA- strains (P < 0.0001). There were significant differences between PU, AS and NHC groups regarding the distribution of genotypes and alleles at rs3811047 and rs2723176 SNPs. The genotype GG and allele G at IL-37 rs3811047 SNP, and the genotype CC and allele C at IL-37 rs2723176 SNP more frequently expressed in PU patients than total healthy subjects (AS + NHC groups) and were associated with an increased risk of PU development (genotype GG: RR = 3.08, P < 0.009; allele G: RR = 2.94, P < 0.01; genotype CC: RR = 5, P < 0.01; and allele C: RR = 5.0, P < 0.02, respectively). The PU patients with allele A at IL-37 rs2723176 SNP expressed higher amounts of IL-37 compared with patients carried allele C at the same position (P < 0.05). In AS carriers and NHC individuals, the IL-37 levels in subjects carried genotype AA or allele A at IL-37 rs2723176 SNP were higher than those carried genotype CC or allele C at the same location (P < 0.01 and P < 0.02 for AS group; P < 0.0001 and P < 0.001 for NHC subjects, respectively). The increased IL-37 levels may be considered as a valuable marker of PU development in HP-infected individuals. The SNPs rs3811047 and rs2723176 were associated with PU development. The CagA status of HP and IL-37 rs2723176 SNP may affect the IL-37 levels.