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Current Gastroenterology Reports Dec 2011Helicobacter pylori infects half of the world's population and plays a causal role in ulcer disease and gastric cancer. This pathogenic neutralophile uniquely colonizes... (Review)
Review
Helicobacter pylori infects half of the world's population and plays a causal role in ulcer disease and gastric cancer. This pathogenic neutralophile uniquely colonizes the acidic gastric milieu through the process of acid acclimation. Acid acclimation is the ability of the organism to maintain periplasmic pH near neutrality in an acidic environment to prevent a fall in cytoplasmic pH in order to maintain viability and growth in acid. Recently, due to an increase in antibiotic resistance, the rate of H. pylori eradication has fallen below 80% generating renewed interest in novel eradication regimens and targets. In this article, we review the gastric biology of H. pylori and acid acclimation, various detection procedures, antibiotic resistance and the role that gastric acidity plays in the susceptibility of the organism to antibiotics currently in use and propose several novel drug targets that would promote eradication in the absence of antibiotics.
Topics: Animals; Anti-Bacterial Agents; Bacterial Proteins; Drug Discovery; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Membrane Transport Proteins; Proton Pump Inhibitors; Stomach Diseases; Urease
PubMed: 21993716
DOI: 10.1007/s11894-011-0226-4 -
Gut Jun 1983
Topics: Bile Reflux; Duodenal Diseases; Gastric Emptying; Gastritis; Humans; Stomach Diseases; Stomach Ulcer
PubMed: 6852630
DOI: 10.1136/gut.24.6.507 -
Orphanet Journal of Rare Diseases Jan 2012Gastric lactobezoar, a pathological conglomeration of milk and mucus in the stomach of milk-fed infants often causing gastric outlet obstruction, is a rarely reported... (Review)
Review
Gastric lactobezoar, a pathological conglomeration of milk and mucus in the stomach of milk-fed infants often causing gastric outlet obstruction, is a rarely reported disorder (96 cases since its first description in 1959). While most patients were described 1975-1985 only 26 children have been published since 1986. Clinically, gastric lactobezoars frequently manifest as acute abdomen with abdominal distension (61.0% of 96 patients), vomiting (54.2%), diarrhea (21.9%), and/or a palpable abdominal mass (19.8%). Respiratory (23.0%) and cardiocirculatory (16.7%) symptoms are not uncommon. The pathogenesis of lactobezoar formation is multifactorial: exogenous influences such as high casein content (54.2%), medium chain triglycerides (54.2%) or enhanced caloric density (65.6%) of infant milk as well as endogenous factors including immature gastrointestinal functions (66.0%), dehydration (27.5%) and many other mechanisms have been suggested. Diagnosis is easy if the potential presence of a gastric lactobezoar is thought of, and is based on a history of inappropriate milk feeding, signs of acute abdomen and characteristic features of diagnostic imaging. Previously, plain and/or air-, clear fluid- or opaque contrast medium radiography techniques were used to demonstrate a mass free-floating in the lumen of the stomach. This feature differentiates a gastric lactobezoar from intussusception or an abdominal neoplasm. Currently, abdominal ultrasound, showing highly echogenic intrabezoaric air trapping, is the diagnostic method of choice. However, identifying a gastric lactobezoar requires an investigator experienced in gastrointestinal problems of infancy as can be appreciated from the results of our review which show that in not even a single patient gastric lactobezoar was initially considered as a possible differential diagnosis. Furthermore, in over 30% of plain radiographs reported, diagnosis was initially missed although a lactobezoar was clearly demonstrable on repeat evaluation of the same X-ray films. Enhanced diagnostic sensitivity would be most rewarding since management consisting of cessation of oral feedings combined with administration of intravenous fluids and gastric lavage is easy and resolves over 85% of gastric lactobezoars. In conclusion, gastric lactobezoar is a disorder of unknown prevalence and is nowadays very rarely published, possibly because of inadequate diagnostic sensitivity and/or not yet identified but beneficial modifications of patient management.
Topics: Abdomen, Acute; Bezoars; Child, Preschool; Diagnosis, Differential; Female; Humans; Infant; Infant, Newborn; Male; Rare Diseases; Stomach Diseases
PubMed: 22216886
DOI: 10.1186/1750-1172-7-3 -
American Journal of Physiology.... Nov 2021Gastric peristalsis is critically dependent on an underlying electrical conduction system. Recent years have witnessed substantial progress in clarifying the operations... (Review)
Review
Gastric peristalsis is critically dependent on an underlying electrical conduction system. Recent years have witnessed substantial progress in clarifying the operations of this system, including its pacemaking units, its cellular architecture, and slow-wave propagation patterns. Advanced techniques have been developed for assessing its functions at high spatiotemporal resolutions. This review synthesizes and evaluates this progress, with a focus on human and translational physiology. A current conception of the initiation and conduction of slow-wave activity in the human stomach is provided first, followed by a detailed discussion of its organization at the cellular and tissue level. Particular emphasis is then given to how gastric electrical disorders may contribute to disease states. Gastric dysfunction continues to grow in their prevalence and impact, and while gastric dysrhythmia is established as a clear and pervasive feature in several major gastric disorders, its role in explaining pathophysiology and informing therapy is still emerging. New insights from high-resolution gastric mapping are evaluated, together with historical data from electrogastrography, and the physiological relevance of emerging biomarkers from body surface mapping such as retrograde propagating slow waves. Knowledge gaps requiring further physiological research are highlighted.
Topics: Animals; Biological Clocks; Cell Communication; Gastric Emptying; Gastroparesis; Humans; Interstitial Cells of Cajal; Membrane Potentials; Peristalsis; Stomach; Stomach Diseases
PubMed: 34549598
DOI: 10.1152/ajpgi.00065.2021 -
BioMed Research International 2022The microenvironment in the stomach is different from other digestive tracts, mainly because of the secretion of gastric acid and digestive enzymes, bile reflux, special... (Review)
Review
The microenvironment in the stomach is different from other digestive tracts, mainly because of the secretion of gastric acid and digestive enzymes, bile reflux, special mucus barrier, gastric peristalsis, and so on, which all contribute to the formation of antibacterial environment. Microecological disorders can lead to gastric immune disorders or lead to the decrease of dominant bacteria and the increase of the abundance and virulence of pathogenic microorganisms and then promote the occurrence of diseases. The body performs its immune function through innate and adaptive immunity and maintains microbial balance through the mechanism of immune homeostasis. Microecological imbalance can lead to the invasion of pathogenic microorganisms and damage mucosal barrier and immune system. The coexistence of gastric microorganisms (including viruses and fungi) may play a synergistic or antagonistic role in the pathogenesis of gastric diseases. Probiotics have the ability to compete with intestinal pathogens, increase the secretion of immunoglobulin A (IgA), stimulate the production of mucin, bacteriocin, and lactic acid, regulate the expression and secretion of cytokines, and regulate the growth of microbiota, which all have beneficial effects on the host microbial environment. At present, most studies focused on , ignoring other stomach microbes and the overall stomach microecology. So, in this article, we reviewed advances in human gastric microecology, the relationship between gastric microecology and immunity or gastric diseases, and the treatment of probiotics in gastric diseases, in order to explore new area for further study of gastric microorganisms and treatment of gastric diseases.
Topics: Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Probiotics; Stomach Diseases
PubMed: 35321071
DOI: 10.1155/2022/6263423 -
Biomedicine & Pharmacotherapy =... Dec 2021Portal hypertensive gastropathy (PHG) is a complication of cirrhotic or noncirrhotic portal hypertension. PHG is very important in the clinic because it can cause acute... (Review)
Review
Portal hypertensive gastropathy (PHG) is a complication of cirrhotic or noncirrhotic portal hypertension. PHG is very important in the clinic because it can cause acute or even massive blood loss, and its treatment efficacy and prognosis are poor. Currently, the incidence of PHG in patients with cirrhosis is 20-80%, but its pathogenesis is complicated and poorly understood. Studies have shown that portal hypertension can cause changes in gastric mucosal microcirculation hemodynamics, leading to changes in gastric mucosal histology and function and thereby weakening the mucosal defense barrier. However, no specific drug treatment plans are currently available. This article reviews the current literature to further our understanding of the mechanism underlying PHG and the relationship between PHG and the posterior mucosal defense barrier and to explore new therapeutic targets.
Topics: Animals; Antioxidants; Apoptosis; Endothelial Cells; Gastric Mucosa; Gastrointestinal Agents; Hemodynamics; Humans; Hypertension, Portal; Microcirculation; Oxidative Stress; Splanchnic Circulation; Stomach Diseases
PubMed: 34614465
DOI: 10.1016/j.biopha.2021.112258 -
Current Gene Therapy Jun 2008Gene therapy for gastric cancer and gastric ulcer is a rationalized strategy since various genes correlate with these diseases. Since gene expressions in non-target... (Review)
Review
Gene therapy for gastric cancer and gastric ulcer is a rationalized strategy since various genes correlate with these diseases. Since gene expressions in non-target tissues/cells cause side effects, a selective gene delivery system targeted to the stomach and/or cancer must be developed. The route of vector transfer (direct injection, systemic, intraperitoneal, gastric serosal surface and oral administration) is an important issue which can determine efficacy and safety. Strategies for cancer gene therapy can be categorized as suicide gene therapy, growth inhibition and apoptosis induction, immunotherapy, anti-angiogenesis, and others. Combination of the target gene with other genes and/or strategies such as chemotherapy and virotherapy is promising. Candidates for treatment of gastric ulcer are vascular endothelial growth factor, angiopoietin-1, serum response factor, and cationic host defense peptide cathelicidin. In this review, we discuss stomach- and cancer-targeted gene transfer methods and summarize gene therapy trials for gastric cancer and gastric ulcer.
Topics: Animals; Apoptosis; Genetic Therapy; Genetic Vectors; Humans; Immunotherapy; Mice; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer
PubMed: 18537593
DOI: 10.2174/156652308784746431 -
Journal of Diabetes and Its... Nov 2019Although slow gastric emptying (gastroparesis) is a well-known complication of chronic hyperglycemia in diabetes mellitus (DM), it recently has become clear that rapid... (Review)
Review
Although slow gastric emptying (gastroparesis) is a well-known complication of chronic hyperglycemia in diabetes mellitus (DM), it recently has become clear that rapid gastric emptying also is a frequent and important diabetic complication. In contrast, acute hyperglycemia causes slow gastric emptying, and acute hypoglycemia causes rapid gastric emptying. Rapid gastric emptying is frequent in T2DM; however, it may also occur in T1DM, particularly in the early stages of the disease, but may persist even into late stages. Recent studies suggest that usually, the stomach restricts the emptying of nutrients to 1-4 kcals/min. This restriction is due to the action of the gastric 'braking' hormones such as GLP-1, leptin, and amylin acting via the gastric inhibitory vagal motor circuit (GIVMC). Disruption of this braking system leads to rapid gastric emptying. Acute hyperglycemia also slows gastric emptying by stimulating the GIVMC, while acute hypoglycemia causes rapid gastric emptying by stimulating the gastric excitatory vagal motor circuit (GEVMC). In contrast, chronic hyperglycemia causes rapid gastric emptying by inducing oxidative stress in the stomach wall that disrupts inhibitory neuromuscular transmission and increases the contractility of the smooth muscle, while chronic hyperglycemia may also cause slow gastric emptying via severe inflammatory stress caused by proinflammatory macrophages and reduce contractility of the smooth muscle. There is a bidirectional relationship between blood glucose and gastric emptying. Thus, rapid gastric emptying may lead to a sizeable postprandial spike, and slow gastric emptying may blunt it. Postprandial hyperglycemia is involved in the development, progression, and complications of DM. Correction of fast gastric emptying involves agents that activate GIVMC and the use of gastric 'braking' hormones or their analogs. Recognition and treatment of rapid gastric emptying may contribute to better management of postprandial hyperglycemia and prevention of some diabetic complications.
Topics: Blood Glucose; Diabetes Complications; Diabetes Mellitus; Gastric Emptying; Gastroparesis; Humans; Hyperglycemia; Postprandial Period; Prognosis; Stomach Diseases
PubMed: 31439470
DOI: 10.1016/j.jdiacomp.2019.107414 -
Current Topics in Microbiology and... 2017The innate immune response is a critical hallmark of Helicobacter pylori infection. Epithelial and myeloid cells produce effectors, including the chemokine CXCL8,... (Review)
Review
The innate immune response is a critical hallmark of Helicobacter pylori infection. Epithelial and myeloid cells produce effectors, including the chemokine CXCL8, reactive oxygen species (ROS), and nitric oxide (NO), in response to bacterial components. Mechanistic and epidemiologic studies have emphasized that dysregulated and persistent release of these products leads to the development of chronic inflammation and to the molecular and cellular events related to carcinogenesis. Moreover, investigations in H. pylori-infected patients about polymorphisms of the genes encoding CXCL8 and inducible NO synthase, and epigenetic control of the ROS-producing enzyme spermine oxidase, have further proven that overproduction of these molecules impacts the severity of gastric diseases. Lastly, the critical effect of the crosstalk between the human host and the infecting bacterium in determining the severity of H. pylori-related diseases has been supported by phylogenetic analysis of the human population and their H. pylori isolates in geographic areas with varying clinical and pathologic outcomes of the infection.
Topics: Animals; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Stomach Diseases
PubMed: 28124148
DOI: 10.1007/978-3-319-50520-6_2 -
Acta Veterinaria Scandinavica Dec 2022Although left and right displacement of the abomasum and abomasal volvulus are well-known disorders of cattle, a comparative evaluation of the clinical, laboratory and...
BACKGROUND
Although left and right displacement of the abomasum and abomasal volvulus are well-known disorders of cattle, a comparative evaluation of the clinical, laboratory and ultrasonographic findings of these types of abomasal displacements has not been undertaken. Therefore, the objective of this study was to compare these conditions in a large population of cows. The medical records of 1982 dairy cows with left displaced abomasum (LDA, n = 1341), right displaced absomasum (RDA, n = 338) and abomasal volvulus (AV, n = 303) were searched for the results of clinical, laboratory and ultrasonographic evaluations.
RESULTS
The main clinical findings were an abnormal demeanour in 48.2% of the cows, reduced rumen motility in 89.7% and decreased intestinal motility in 61.1%. Ballottement and simultaneous auscultation and percussion and simultaneous auscultation were positive on the left side in 96.9% of the cows with LDA and on the right in 98.5% of the cows with RDA and in 99.3% of the cows with AV. Ultrasonography was useful for diagnosing LDA in 97.9% of the cows and RDA/AV in 90.2% of the cows. The laboratory findings characteristic of abomasal reflux syndrome varied in severity; 83% of the cows had hypokalaemia, 67% had increased rumen chloride concentration, 67% had an increased base excess and 50% had haemoconcentration. Based on the clinical signs, a definitive diagnosis was made in 75.0% of the cows with LDA and in 22.5% of the cows with RDA/AV. Ultrasonography was required for a definitive diagnosis in another 22.0% of the cows with LDA and in 53.0% of the cows with RDA/AV. Laparotomy or postmortem examination was required for reliable differentiation of RDA and AV.
CONCLUSIONS
LDA, RDA and AV differ with respect to the severity and the frequency of several abnormal clinical, laboratory and ultrasonographic findings as well as the methods required for a diagnosis.
Topics: Female; Cattle; Animals; Pregnancy; Intestinal Volvulus; Abomasum; Stomach Diseases; Rumen; Cattle Diseases
PubMed: 36539887
DOI: 10.1186/s13028-022-00656-9