Materiały źródłowe

• #1 Peptic Ulcer Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK534792/

  Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. Peptic ulcer disease (PUD) has various causes; however, Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology. H. pylorus is a gram-negative bacillus that is found within the gastric epithelial cells. This bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori infection is more prevalent among those with lower socioeconomic status and is commonly acquired during childhood. The organism has a wide spectrum of virulence factors, allowing it to adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria, leading to gastric ulceration. The peptic ulcer disease (PUD) mechanism results from an imbalance between gastric mucosal protective and destructive factors. With peptic ulcers, there is usually a defect in the mucosa that extends to the muscularis mucosa. Once the protective superficial mucosal layer is damaged, the inner layers are susceptible to acidity. Further, the ability of the mucosal cells to secrete bicarbonate is compromised. H. pylori is known to colonize the gastric mucosa and cause inflammation. H. pylori also impair the secretion of bicarbonate, promoting the development of acidity and gastric metaplasia.

• #1 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  The gram-negative spirochete H pylori was first linked to gastritis in 1983. Since then, further study of H pylori has revealed that it is a major part of the triad, which includes acid and pepsin, that contributes to primary peptic ulcer disease. The unique microbiologic characteristics of this organism, such as urease production, allows it to alkalinize its microenvironment and survive for years in the hostile acidic environment of the stomach, where it causes mucosal inflammation and, in some individuals, worsens the severity of peptic ulcer disease. […] When H pylori colonizes the gastric mucosa, inflammation usually results. The causal association between H pylori gastritis and duodenal ulceration is now well established in the adult and pediatric literature. In patients infected with H pylori, high levels of gastrin and pepsinogen and reduced levels of somatostatin have been measured. In infected patients, exposure of the duodenum to acid is increased. Virulence factors produced by H pylori, including urease, catalase, vacuolating cytotoxin, and lipopolysaccharide, are well described.

• #1 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Most patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has also proven to be caused by H pylori because its eradication reverses the defect. The combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion lowers the pH in the duodenum, which promotes the development of gastric metaplasia (ie, the presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of gastric metaplasia induces duodenitis and enhances the susceptibility to acid injury, thereby predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly significant predictor of subsequent development of duodenal ulcers in one study that followed 181 patients with endoscopy-negative, nonulcer dyspepsia.

• #1 Peptic ulcer disease – Wikipedia

  https://en.wikipedia.org/wiki/Peptic_ulcer_disease

  Common causes include infection with Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). […] Helicobacter pylori is one of the major causative factors of peptic ulcer disease. It secretes urease to create an alkaline environment, which is suitable for its survival. It expresses blood group antigen-binding adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as CagA and PicB, which cause stomach mucosal inflammation. […] Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can increase the risk of peptic ulcer disease by four times compared to non-users. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (COX-1), which is essential for the production of these prostaglandins.

• #1 Peptic Ulcer Disease (PUD) – Gastric Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.4.6.

  All NSAIDs, including acetylsalicylic acid (ASA) (even at the low doses used for cardiovascular indications), damage the gastrointestinal (GI) mucosa, primarily by reducing the production of prostaglandins as a result of inhibition of cyclooxygenase-1 (COX-1), and are associated with ulcer generation. The extent to which NSAIDs damage the mucosa depends on the type of NSAID, but all increase the risk of peptic ulceration; moreover, they inhibit platelet activity and, to a various degree, increase the risk of bleeding from those ulcers. The risk of serious upper GI events (including bleeding) is doubled with selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) or diclofenac and quadrupled with naproxen or ibuprofen. […] Risk factors for mucosal damage by NSAIDs include history of peptic ulcers or bleeding ulcers, H pylori infection, age 60 years, concomitant administration of several NSAIDs, treatment with high-dose NSAIDs, and NSAIDs combined with glucocorticoids. The risk seems increased by smoking, male sex, and presence of chronic medical conditions.

• #1 Peptic ulcer disease – Wikipedia

  https://en.wikipedia.org/wiki/Peptic_ulcer_disease

  Physiological (not psychological) stress due to serious health problems, such as those requiring treatment in an intensive care unit, is well described as a cause of peptic ulcers, which are also known as stress ulcers. […] Other causes of peptic ulcer disease include gastric ischaemia, drugs, metabolic disturbances, cytomegalovirus (CMV), upper abdominal radiotherapy, Crohn’s disease, and vasculitis.

• #1 Peptic Ulcer Disease | Veterans Affairs Canada

  https://www.veterans.gc.ca/en/mental-and-physical-health/mental-health-and-wellness/compensation-illness-or-injury/disability-benefits/entitlement-eligibility-guidelines/az-index/peptic-ulcer-disease

  H. pylori is associated with a greatly increased risk of duodenal and gastric ulceration. It is important to Note, however, that while the infection is extremely common throughout the world and that approximately 50% of adults in developed countries are colonized by the age of 60 years, not all of these persons will develop or have had peptic ulcer disease. […] Zollinger-Ellison syndrome (gastronomas) can produce peptic ulcer disease through hypersecretion of gastric acid within the upper gastrointestinal tract, thereby disturbing the delicate acid-pepsin balance. If peptic ulcer disease is caused by Zollinger-Ellison syndrome, entitlement should be sought for Zollinger-Ellison syndrome.

• #1 GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression | Nature Communications

  https://www.nature.com/articles/s41467-021-21280-7

  Genetic factors are recognized to contribute to peptic ulcer disease (PUD) and other gastrointestinal diseases, such as gastro-oesophageal reflux disease (GORD), irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). […] PUD is a complex disorder, for which Helicobacter (H.) pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs) are the main risk factors. The development of infection-relevant PUD is recognized to be a multistep process, with contributions from both H. pylori infection and subsequent inflammation and damage of mucosa. Eradicating H. pylori is effective for infection-relevant PUD treatment. […] Here, we identify eight independent and significant single nucleotide polymorphisms (SNPs) for PUD and the results highlight the role of host genetic susceptibility to infection, acid secretion, and gastric motility.

• #1 GWAS of peptic ulcer disease implicates Helicobacter pylori infection, other gastrointestinal disorders and depression | Nature Communications

  https://www.nature.com/articles/s41467-021-21280-7

  GWAS of PUD identified eight independent associated loci and 6 of 8 have potential links to H. pylori infection, highlighting the role of host genetic susceptibility. […] This finding deserves further investigation of the association between blood group and peptic ulcer. Of the six previously unreported PUD-associated SNPs, it is notable that rs681343 is statistically significant in both UKB discovery and GERA replication GWAS. This SNP is located in the FUT2 gene which has been implicated in susceptibility to H. pylori infection in humans and mice gastric tissue. […] The results highlight the role of host genetic variability to bacterial infection.

• #1 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer. […] Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.

• #1 Peptic ulcer pathophysiology – PubMed

  https://pubmed.ncbi.nlm.nih.gov/2072787/

  Despite extensive research, the etiology of peptic ulcer disease remains unclear. Given the multiple processes that control acid and pepsin secretion and defense and repair of the gastroduodenal mucosa, it is likely that the cause of ulceration differs between individuals. Acid and pepsin appear to be necessary but not sufficient ingredients in the ulcerative process. It is clear that the majority of gastric ulcers and a substantial number of duodenal ulcers do not have increased gastric acid secretion. […] Recent research has focused more on protection and repair of the stomach and duodenum. NSAIDs cause a significant number of gastric and duodenal ulcers; this is probably due to inhibition of prostaglandin production with loss of its protective effects. In the absence of NSAIDs and gastrinoma, it appears that most gastric ulcers and all duodenal ulcers occur in the setting of H. pylori infection. Evidence is mounting in support of H. pylori as a necessary ingredient in the ulcerative process, similar to acid and pepsin. It is not known whether the bacteria or the accompanying inflammation is the more important factor in the pathophysiology. Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity. These facts suggest the following process: increased peptic activity coupled with decreased duodenal buffering capacity may lead to increased mucosal injury and result in gastric metaplasia. In the presence of antral H. pylori, the gastric metaplasia can become colonized and inflamed. The inflammation or the infection itself then disrupts the process of mucosal defense or regeneration resulting in ulceration. A cycle of further injury and increased inflammation with loss of the framework for regeneration may then cause a chronic ulcer. Gastric ulcer often occurs with decreased acid-peptic activity, suggesting that mucosal defensive impairments are more important. The combination of inflammation, protective deficiencies, and moderate amounts of acid and pepsin may be enough to induce ulceration. Many questions remain in understanding the pathophysiology of peptic ulcer disease. The physiology and pathophysiology of mucosal regeneration and the mechanisms by which H. pylori and inflammation disrupt normal gastroduodenal function will be fruitful areas of future investigation.

• #1 Painting a Complete Picture of the Pathogenesis of Peptic Ulcers

  https://www.mentalhealthjournal.org/articles/painting-a-complete-picture-of-the-pathogenesis-of-peptic-ulcers.html

  Peptic ulcers, including duodenal and gastric ulcers, were currently considered an infectious disease caused by Helicobacter pylori. However, this etiology cannot explain the major characteristics and observations/phenomena of the disease. […] Peptic ulcers were identified as a psychosomatic disease triggered by psychological stress, whereas Helicobacter pylori plays a secondary role in the late phase of peptic ulceration. […] The early phase is a long-term abstract psychopathological process, starting from early life when the impacts of multiple psychosomatic factors are transformed into hyperplasia and hypertrophy of gastrin and parietal cells and/or negative life-views via superposition mechanism. […] These pre-existing abnormalities potentiate the individuals response to current psychological stress in the intermediate phase, resulting in hypersecretion of gastric acid and/or pre-ulcer lesions.

• #1 Painting a Complete Picture of the Pathogenesis of Peptic Ulcers

  https://www.mentalhealthjournal.org/articles/painting-a-complete-picture-of-the-pathogenesis-of-peptic-ulcers.html

  The late phase is a corrosion process caused by gastric acid, Helicobacter pylori, and/or NSAIDs, resulting in duodenal and/or gastric ulcers. […] This complete picture highlights the importance of past life experience in peptic ulcers and visualizes the non-causal roles of gastric acid, Helicobacter pylori, and NSAIDs. […] The theory based on this new etiology was designated as Theory of Nodes, which addresses all the major characteristics, observations/phenomena, controversies, and mysteries of peptic ulcers in a series of 6 articles. […] In Theory of Nodes, these reversals are due to the profound changes in social environments during the 20th century. […] The hyperplasia and hypertrophy and/or negative life-view potentiate the individuals response to immediate psychological stress, resulting in duodenal and gastric ulcerations, respectively.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  Peptic ulcers were identified as a psychosomatic disease triggered by psychological stress, where Helicobacter pylori plays a secondary role in only the late phase of the disease. […] The psychological stress triggers the release of aberrant neurotransmitters in the central nervous system, which in turn cause the transmission of pathogenic nerve impulses to the stomach, resulting in a pre-ulcer lesion in the gastric wall and eventually, gastric ulcer. […] The morphology of gastric ulcer is the key characteristic to understanding many other characteristics of the disease, as well as the roles of gastric acid, H. pylori, and NSAIDs. […] The most probable mechanism of gastric ulcers induced in animal models is that the manipulation in the CNS causes pathogenic nerve impulses transmitted to the stomach, leading to gastric ulcers.

• #1 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  The degree to which individuals suffer negative impacts from life events determines the properties of submucous nodes, such as the size, location, duration, relapse and multiplicity. […] Gastric ulcers are not penetrating lesions beginning in the mucosa and extending into the wall of the stomach, but are primed by the necrotic tissues (nodes) pre-existing within the gastric wall, which make the mucosa highly susceptible to the local aggressive factors. […] The impacts of the pathogenic nerve impulses are relieved at the ulcerated location once the distal ends of the nerve cells necrotize. As a result, gastric ulcers may heal up automatically via the regeneration of local tissues without treatment.

• #1

  https://link.springer.com/article/10.1163/156856002321544765

  The mechanism of peptic ulcer recurrence is still unclear. Since ulcerogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs and stress can increase expression of inflammatory cytokines in gastric mucosa, gastric mucosal inflammation may play key roles in ulcer recurrence. […] In a rat model of ulcer recurrence which we developed, inflammatory cytokines such as interleukin (IL)-1 are key mediators of ulcer recurrence. In this model, IL-1 increases expression of adhesion molecules on both leukocytes and endothelial cells, and cytokines, leading to neutrophil infiltration into scarred mucosa. Gastric acid also plays important roles in recurrence of gastric ulcer in this model. Acid regulates inflammatory processes, including expression of adhesion molecules and inflammatory cytokines during ulcer recurrence. […] This review focuses on recent advances in understanding of the mechanisms underlying development of gastric ulcer recurrence.

• #1 Stomach Ulcer Diet: Foods to Eat and Foods to Avoid

  https://www.verywellhealth.com/what-can-i-eat-if-i-have-a-peptic-ulcer-1742154

  The bacterium Helicobacter pylori (H. pylori) is a common cause of stomach ulcers that requires treatment with antibiotics. Peptic ulcers can also be caused by long-term use of certain medications, including nonsteroidal anti-inflammatory drugs (NSAIDs). […] An ulcer diet is designed to relieve peptic ulcer symptoms, prevent flares, and prevent more ulcers from developing. […] Dietary changes alone may not be enough to heal your ulcer, and you may require additional treatment from a healthcare provider. […] An ulcer diet adds foods with antibacterial effects and compounds that boost healing. It also limits excess acid production, which can aggravate an ulcer. These foods can include polyphenols that help to heal stomach lining ulcers faster, while others have antibacterial effects and help kill H. pylori. […] An ulcer is treated with medicines to reduce stomach acid. Further treatment depends on the cause of the ulcer, such as antibiotics to treat H. pylori infection. Your healthcare provider may also recommend proton pump inhibitors (PPIs) to help reduce stomach acid and promote healing.

• #1 Painting a Complete Picture of the Pathogenesis of Peptic Ulcers

  https://www.mentalhealthjournal.org/articles/painting-a-complete-picture-of-the-pathogenesis-of-peptic-ulcers.html

  Theory of Nodes dictates that Psychosomatic Theory is indispensable to understand the early phase of peptic ulcers. […] The complete picture elucidates that 4 factors can predict which individual will have peptic ulcers, and proposed mind adjustment and creating harmonious environments for a complete cure of the disease without relapse.

• #2 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer. […] Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.

• #2 H. Pylori & Peptic Ulcer – Wake Gastroenterology

  https://wakegastro.com/patient-info/patient-education/h-pylori-peptic-ulcer/

  A peptic ulcer is a sore on the lining of the stomach or duodenum, which is the beginning of the small intestine. Peptic ulcers are common: One in 10 Americans develops an ulcer at some time in his or her life. One cause of peptic ulcer is bacterial infection, but some ulcers are caused by long-term use of nonsteroidal anti-inflammatory agents (NSAIDs), like aspirin and ibuprofen. […] Researchers believe that H. pylori is responsible for the majority of peptic ulcers, as well as chronic gastritis (inflammation of the stomach lining) and potentially gastric cancer. […] The H. pylori bacteria weakens the protective mucous coating of the stomach and duodenum, thus allowing acid to get through to the sensitive lining beneath. Both the acid and the bacteria irritate the lining and cause a sore, or ulcer.

• #2 Peptic ulcer disease – Wikipedia

  https://en.wikipedia.org/wiki/Peptic_ulcer_disease

  Common causes include infection with Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). […] Helicobacter pylori is one of the major causative factors of peptic ulcer disease. It secretes urease to create an alkaline environment, which is suitable for its survival. It expresses blood group antigen-binding adhesin (BabA) and outer inflammatory protein adhesin (OipA), which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as CagA and PicB, which cause stomach mucosal inflammation. […] Taking nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin can increase the risk of peptic ulcer disease by four times compared to non-users. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (COX-1), which is essential for the production of these prostaglandins.

• #2 An Overview on Peptic Ulcer Disease, Diagnosis and Management Approach – Pharmacophore

  https://pharmacophorejournal.com/article/an-overview-on-peptic-ulcer-disease-diagnosis-and-management-approach

  The exact mechanism of how the H.pylori causes peptic or gastric ulcers is not clearly understood, but it is associated with hypochlorhydria and hyperchlorhydria in addition to the location of the infection. […] It is well established that the Gastrin hormone is predominantly increased and the led to increasing histaminic receptor activity in the enterochromaffin-like cells, and the outcome is increasing acid secretion. This is also modulated by somatostatin releasing cell destruction, so there is a loss of inhibition and increase in activation in antral H.pylori infection, and this will lead to an increase the level of gastric acidity and increase the level of HCL -hyperchlorhydria- the outcome will be a peptic ulcer. […] When we discuss the effect of NSAIDs and Aspirin on the gastric ulcer, it will be linked directly with COX1 cyclooxygenase1- inhibition that leads to a sharp decrease in the level of prostaglandin, which protects the mucosal layer by increasing the mucus secretion from the mucosal cells, bicarbonate and by also increasing the mucosal layer blood supply. […] As a result, when NSAIDs stop the prostaglandin pathway and decrease its protective effect on the mucosal layer the stomach acidity will start its harmful effect on the gastric layers.

• #2 An Overview of History, Pathogenesis and Treatment of Perforated

  https://www.amhsr.org/articles/an-overview-of-history-pathogenesis-and-treatment-of-perforated-peptic-ulcer-disease-with-evaluation-of-prognostic-scoring-in-adul.html

  Production of alkaline ammonia by bacteria on the surface epithelium and in the glands of the antrum inhibits D cells in the glands from sensing the true level of acidity leading to inappropriate release of somatostatin and hypergastrinemia. […] Urease catalyzes production of ammonia, when in large concentrations lead to formation of toxic complexes such as ammonium chloride which along with bacterial phospholipases A and C impair the phospholipidrich layer in the mucosa that maintains mucosal hydration and integrity of the gastric epithelial barrier. […] Metaplasia is an essential prerequisite for H. pylori colonization of duodenal epithelium, because colonization is specific and exclusive to gastric epithelial cells. After colonization of islands of duodenal gastric metaplasia, the inflamed duodenal mucosa becomes more susceptible to peptic acid attack and ulceration.

• #2 Peptic ulcer disease and non-steroidal anti-inflammatory drugs – Australian Prescriber

  https://australianprescriber.tg.org.au/articles/peptic-ulcer-disease-and-non-steroidal-anti-inflammatory-drugs.html

  Non-steroidal anti-inflammatory drugs including low-dose aspirin are some of the most commonly used medicines. They are associated with gastrointestinal mucosal injury. […] A peptic ulcer is a defect in the upper gastrointestinal mucosa that extends through the muscularis mucosa into deeper layers of the gut wall. There are two major risk factors for peptic ulcer disease Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). […] Peptic ulcer disease is a well-recognised complication of NSAID use. Inhibition of COX-1 in the gastrointestinal tract leads to a reduction of prostaglandin secretion and its cytoprotective effects in gastric mucosa. This therefore increases the susceptibility to mucosal injury. […] Chronic use of NSAIDs including low-dose aspirin is associated with gastrointestinal mucosal injury. However, major adverse events are relatively infrequent. Patients with multiple risk factors such as a previous history of peptic ulcer disease, increasing age, co-prescription of corticosteroids and anticoagulants, and high-dose and long-term use of NSAIDs are at the highest risk of major gastrointestinal toxicity. […] Before prescribing an NSAID, prophylactic proton pump inhibitor therapy needs to be offered to patients with a past history of peptic ulcer disease and those on dual antiplatelet therapy or anticoagulant therapy.

• #2 Overview of Peptic Ulcer Disease

  https://www.uspharmacist.com/article/overview-of-peptic-ulcer-disease

  Peptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers, with common etiologies of Helicobacter pylori infection, NSAID use, and stress-related mucosal damage. […] The disease process of PUD is multifactorial based on etiology and risk factors. Ulcers may occur with hypersecretion of hydrochloric acid and pepsin, causing an imbalance between gastric luminal factors and degradation in the defensive function of the gastric mucosal barrier. […] H pylori contributes to mucosal injury by multiple mechanisms. […] Ulcers induced by nonselective NSAIDs can occur due to a topical irritation of the gastric epithelial cells and reduced protective prostaglandin synthesis. […] Due to their pharmacologic properties, many acidic NSAIDs cause alterations in the hydrophobic mucosal gel layer. […] As a result of COX-1 inhibition, adverse effects such as ulcers or GI bleeds may occur.

• #2 Peptic Ulcer Disease | Calgary Guide

  https://calgaryguide.ucalgary.ca/peptic-ulcer-disease/peptic-ulcer-disease-1/

  Peptic Ulcer Disease: Pathogenesis and clinical findings H. pylori (gram negative rod bacteria) Toxin release Inflammatory response Inhibition of H+ detection in gastric antrum H+ over-secretion NSAID use (including ASA +/- other anti- platelet agents) Ischemia ZollingerEllison Syndrome ( acid secretion due to gastrin secreting tumor) Stress (in ICU setting) Crohns disease Cancer (adenocarcinoma, SCC, lymphoma) Mucosal Injurious Substances: Acid: Gastrin, Histamine, ACh promote acid secretion in parietal cell Toxins: drugs (for instance, NSAIDs) directly toxic to gastric epithelial cells, drugs that reduce platelet adhesion/plug […] COX-1 inhibition Decreased prostaglandins H+ production, gastric mucous production Toxicity to Gastric epithelial cells […] Mechanism not well understood

• #2 Pathology of Peptic Ulcer | PPT

  https://www.slideshare.net/slideshow/pathology-of-peptic-ulcer/70439152

  STEROIDS INDUCED ULCER Steroids acts on cell membrane (phospholipid) Inhibit phospholipase Inhibits arachidonic acid no prostaglandins and damaging of mucosal lining […] ULCER DUE TO GENETIC DEFECT Rare genetics occurs some time having blood group O positive the size of parietal cell is increase Increase cell demand as HCL secretions increase Cause destruction of mucosal lining leading towards ulcer […] ZES(Zollinger-Ellison Syndrome) In this syndrome tumor of goblet cell occurs Abnormal mucus secretions(gastrin acts on parietal cells) Increase secretions of gastric juice Mucosal lining damage

• #2 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Causes-Peptic-Ulcers.aspx

  In other words, there is a lack of balance between the protective and ulcerogenic factors. […] Ulcer-producing factors are: The attack by gastric acid and pepsin, Local inflammation, Gastric metaplasia, Colonization by Helicobacter pylori, Bile salts with their mucus-dispersing effects, Drugs such as salicylates which reduce prostaglandin secretion, Other irritants such as alcohol. […] A common factor in peptic ulcer causation is the presence of the infectious agent Helicobacter pylori. […] This bacterium causes an inflammatory reaction locally, involving the release of neutrophil-derived lysosomal enzymes, leukotrienes and reactive oxygen species, all of which lower the level of local mucosal defense. […] The pro-inflammatory cytokines interfere with normal repair, and this allows the ulcer to linger and establish itself.

• #2 Peptic Ulcer Disease Different Pathogenesis of Duodenal and Gastric Ulcer | Koncoro | The Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy

  https://www.ina-jghe.com/index.php/jghe/article/view/501

  Peptic ulcer disease as a manifestation of this infection is still remain a health burden. […] Understanding the physiology of gastric acid secretion and its alteration by H. pylori induced inflammation will aid physician in differentiating peptic ulcer disease based on its location. […] Recognition of symptoms and its pathogenesis may lead physician to understand the fate of each condition in the future. […] This article reviews concept of peptic ulcer pathogenesis according to ulcer etiology.

• #2 Painting a Complete Picture of the Pathogenesis of Peptic Ulcers

  https://www.mentalhealthjournal.org/articles/painting-a-complete-picture-of-the-pathogenesis-of-peptic-ulcers.html

  Peptic ulcers, including duodenal and gastric ulcers, were currently considered an infectious disease caused by Helicobacter pylori. However, this etiology cannot explain the major characteristics and observations/phenomena of the disease. […] Peptic ulcers were identified as a psychosomatic disease triggered by psychological stress, whereas Helicobacter pylori plays a secondary role in the late phase of peptic ulceration. […] The early phase is a long-term abstract psychopathological process, starting from early life when the impacts of multiple psychosomatic factors are transformed into hyperplasia and hypertrophy of gastrin and parietal cells and/or negative life-views via superposition mechanism. […] These pre-existing abnormalities potentiate the individuals response to current psychological stress in the intermediate phase, resulting in hypersecretion of gastric acid and/or pre-ulcer lesions.

• #2 A Novel Psychopathological Model Explains the Pathogenesis of Gastric Ulcers

  https://www.mentalhealthjournal.org/articles/a-novel-psychopathological-model-explains-the-pathogenesis-of-gastric-ulcers.html

  The degree to which individuals suffer negative impacts from life events determines the properties of submucous nodes, such as the size, location, duration, relapse and multiplicity. […] Gastric ulcers are not penetrating lesions beginning in the mucosa and extending into the wall of the stomach, but are primed by the necrotic tissues (nodes) pre-existing within the gastric wall, which make the mucosa highly susceptible to the local aggressive factors. […] The impacts of the pathogenic nerve impulses are relieved at the ulcerated location once the distal ends of the nerve cells necrotize. As a result, gastric ulcers may heal up automatically via the regeneration of local tissues without treatment.

• #2 Gastritis and Peptic Ulcer Disease | Nutrition Guide for Clinicians

  https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342027/all/Gastritis_and_Peptic_Ulcer_Disease

  Upper gastrointestinal endoscopy is the most accurate diagnostic test for gastritis and peptic ulcer disease. […] Patients should avoid agents known to exacerbate the symptoms of gastritis or PUD. These include tobacco, alcohol, NSAIDs, aspirin, and steroids. […] It is important to treat H. pylori infection, if present. Eradication of H. pylori infection decreases the annual ulcer recurrence risk from over 50% to less than 10% and reduces the likelihood of complications such as bleeding. […] Ulcer disease tends to be more severe in the absence of H. pylori infection. […] Exercise has been hypothesized to influence the risk for ulcer disease or gastritis through reductions in basal or meal-stimulated acid secretion. […] Probiotics (e.g., Lactobacillus casei) interfere with H. pylori adhesion to epithelial cells, attenuate H. pylori-induced gastritis, and inhibit growth of H. pylori in humans, in addition to reducing the side effects of eradication treatment.

• #2 Gastrointestinal Disorders | Special Issue : Peptic Ulcer Disease: From Pathophysiology to Novel Therapeutic Approaches

  https://www.mdpi.com/journal/gastrointestdisord/special_issues/pud

  The simultaneous presence of H. pylori infection in patients treated with drugs harmful to the gastric and duodenal mucosa increases their ulcer potential and the risk of peptic ulcer bleeding. […] The idea of the current Special Issue of Gastrointestinal Disorders is to offer the possibility of collecting high-quality publications and to provide an interdisciplinary approach by submitting original papers and updated reviews on various aspects of the pathogenesis of acute erosions, mucosal bleedings, and chronic peptic ulcers, including the effect of H. pylori, NSAID with or without novel anticoagulant therapies, clinical and experimental studies on protective action of classic antiulcer drugs, and novel therapeutics such as prodrugs releasing gaseous molecules or nutraceutical agents. […] Furthermore, the identification of physiological molecules, therapeutic targets, and new methods of treatment PUD in humans and different peptic ulcer animal models is awaited.

• #3 Peptic Ulcer Disease (PUD) – Gastric Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.4.6.

  Peptic ulcer disease (PUD) is a recurring formation of gastric and/or duodenal peptic ulcers. A peptic ulcer is a demarcated mucosal defect extending through the muscularis mucosa with associated inflammatory infiltrates and coagulative necrosis. Peptic ulcers are most frequently located in the duodenal bulb or stomach or less commonly in the lower part of the esophagus or duodenal loop. […] H pylori infection is responsible for 50% of duodenal and gastric ulcers. H pylori is able to survive in the gastric environment thanks to the production of urease, which degrades urea, thus releasing ammonia that neutralizes gastric acid and creates a less acidic microenvironment within the gastric mucus layer. Initially H pylori causes acute gastritis in the prepyloric region, which after several weeks progresses to chronic gastritis; H pylori also induces hypergastrinemia, leading to an increased secretion of hydrochloric acid, which plays an important role in the pathogenesis of duodenal ulcers.

• #3 Peptic ulcer disease – Wikipedia

  https://en.wikipedia.org/wiki/Peptic_ulcer_disease

  Physiological (not psychological) stress due to serious health problems, such as those requiring treatment in an intensive care unit, is well described as a cause of peptic ulcers, which are also known as stress ulcers. […] Other causes of peptic ulcer disease include gastric ischaemia, drugs, metabolic disturbances, cytomegalovirus (CMV), upper abdominal radiotherapy, Crohn’s disease, and vasculitis.

• #3 Management of H. pylori Induced Peptic ulcer – A Phytotherapeutic Approach – Journal of Pure and Applied Microbiology

  https://microbiologyjournal.org/management-of-h-pylori-induced-peptic-ulcer-a-phytotherapeutic-approach/

  A peptic ulcer is a chronic infectious disease that creates erosion on the epithelial lining of the stomach. […] H. pylori has been the main focus of study for gastrointestinal tract diseases for a long. It is a Gram-negative, microaerophilic organism that is associated with a variety of diseases like chronic gastritis, peptic ulcer, non-cardio gastric adenocarcinoma, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. […] Duodenal ulcers and 70% of gastric ulcers are due to H. pylori infection. […] The most common cause of peptic ulcer is infection with H. pylori. It is a gram-negative, spiral-shaped bacteria having flagella that help in motility. The root of transmission is by fecal-oral route or through oral-oral route. […] The important virulence factor that H. pylori possess includes lipopolysaccharide which helps in adhering the cells, so it can attach itself to the gastric cells of the stomach by secreting adhesion molecule which is recognized by glycan structure that is expressed on the surface of gastric epithelial cells and the surface of mucus layer lining.

• #3 Peptic Ulcer Disease (PUD) – Gastric Diseases – Gastrointestinal Diseases – Gastroenterology – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.4.6.

  All NSAIDs, including acetylsalicylic acid (ASA) (even at the low doses used for cardiovascular indications), damage the gastrointestinal (GI) mucosa, primarily by reducing the production of prostaglandins as a result of inhibition of cyclooxygenase-1 (COX-1), and are associated with ulcer generation. The extent to which NSAIDs damage the mucosa depends on the type of NSAID, but all increase the risk of peptic ulceration; moreover, they inhibit platelet activity and, to a various degree, increase the risk of bleeding from those ulcers. The risk of serious upper GI events (including bleeding) is doubled with selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) or diclofenac and quadrupled with naproxen or ibuprofen. […] Risk factors for mucosal damage by NSAIDs include history of peptic ulcers or bleeding ulcers, H pylori infection, age 60 years, concomitant administration of several NSAIDs, treatment with high-dose NSAIDs, and NSAIDs combined with glucocorticoids. The risk seems increased by smoking, male sex, and presence of chronic medical conditions.

• #3 Gastritis and Peptic Ulcer Disease | Nutrition Guide for Clinicians

  https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342027/all/Gastritis_and_Peptic_Ulcer_Disease

  Nonsteroidal anti-inflammatory drugs (NSAIDs) suppress prostaglandin formation in the mucosa, which is normally a part of the protective mechanism of the mucosal barrier. NSAIDs and aspirin are major causes of PUD. […] Tobacco use. Nicotine increases acid secretion and reduces mucosal blood flow in the stomach and duodenum. […] Alcohol can cause gastritis by stimulating acid secretion and damaging the mucosal barrier. […] Prophylaxis for gastritis and ulcers may be administered in hospitalized patients, especially those on mechanical ventilation or those undergoing major surgery. […] Extreme psychological stress, especially that associated with traumatic events. […] The diagnosis is suspected when a patient presents with signs and symptoms suggestive of peptic ulcer disease or gastritis and especially in the setting of NSAID use and/or H. pylori infection.

• #3 Journal of Gastroenterology | Best Scientific Journals

  https://scholars.direct/Articles/gastroenterology/jgr-7-056.php?jid=gastroenterology

  The immediate cause of peptic ulcer disease is disturbance in normal protective mucosal ‘barrier’ by acidpepsin, resulting in digestion of the mucosa. However, in contrast to duodenal ulcers, the patients of gastric ulcer have low-to-normal gastric acid secretions, though true achlorhydria in response to stimulants never occurs in benign gastric ulcer. Besides, 10-20% patients of gastric ulcer may have coexistent duodenal ulcer as well. Thus, the etiology of peptic ulcers possibly may not be explained on the basis of a single factor but is multifactorial. These factors are discussed below but the first two- H. Pylori gastritis and NSAIDs-induced injury are considered most important. […] Although the role of various etiologic factors just described is well known in ulcerogenesis, two most important factors in peptic ulcer are as under: Exposure of mucosa to gastric acid and pepsin secretion. Strong etiologic association with H. pylori infection. There are distinct differences in the pathogenetic mechanisms involved in duodenal and gastric ulcers as under.

• #3 A Differential Approach to Form and Site of Peptic Ulcer | Scientific Reports

  https://www.nature.com/articles/s41598-019-44893-x

  The vast majority of gastric ulcers is situated in the gastric antrum. […] Although both the form and site of human gastric ulcers have been documented in depth, Aschoffs postulate constitutes a timeless challenge to every formal theory of ulcer formation. […] It is therefore highly relevant to review the anatomy of the arterial network as the basis for the structural details of any limitation of arterial blood flow even in such a complex organ as the stomach. […] The differential haemodynamic model of the intestinal wall is capable of explaining form and site of gastric and duodenal ulcers in man. […] The morphology of gastric ulcer can be understood based upon the energy requirements of acid secretion and the limited arterial influx through a contracted muscle mantle in the given vascular supply of the gastric wall.

• #3 H. Pylori & Peptic Ulcer – Wake Gastroenterology

  https://wakegastro.com/patient-info/patient-education/h-pylori-peptic-ulcer/

  H. pylori is able to survive in stomach acid because it secretes enzymes that neutralize the acid. This mechanism allows H. pylori to make its way to the “safe” area – the protective mucous lining. Once there, the bacterium’s spiral shape helps it burrow through the lining. […] H. pylori peptic ulcers are treated with drugs that kill the bacteria, reduce stomach acid, and protect the stomach lining. Antibiotics are used to kill the bacteria. Two types of acid-suppressing drugs might be used: H2 blockers and proton pump inhibitors. […] H2 blockers work by blocking histamine, which stimulates acid secretion. They help reduce ulcer pain after a few weeks. Proton pump inhibitors suppress acid production by halting the mechanism that pumps the acid into the stomach. […] The majority of peptic ulcers are caused by the H. pylori bacterium. Many of the other cases are caused by NSAIDs (a class of pain-reliever). None are caused by spicy food or stress.

• #4 Peptic Ulcer Disease: Background, Anatomy, Pathophysiology

  https://emedicine.medscape.com/article/181753-overview

  Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer. […] Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.

• #4 Helicobacter pylori: A Contemporary Perspective on Pathogenesis, Diagnosis and Treatment Strategies

  https://www.mdpi.com/2076-2607/12/1/222

  The pathogenesis of H. pylori may be studied at three distinct stages: the attachment to and colonization of the gastric mucosa, triggering and evading the immune responses of the host, and finally, the establishment of the disease. […] H. pylori infections are often asymptomatic and usually acquired during childhood. However, around 30% of infected persons may show signs of gastrointestinal diseases, such as mild-to-severe cases of peptic ulcers, gastritis, and even gastric cancer and MALT lymphoma. […] The molecular mechanisms orchestrating H. pylori infections are sophisticated processes crucial for the bacterium’s successful establishment in the gastric mucosa. At the forefront of infection initiation is H. pylori’s adhesion and colonization strategies. […] Various virulence factors, including those involved in motility, adhesion, urease and cytotoxin production, are essential for the pathogenesis of this bacterium.

• #5 Gastroprotective Mechanisms | IntechOpen

  https://www.intechopen.com/chapters/79812

  The gastric epithelium is formed by a continuous layer of narrow junctions cells with secretory and digestive functions. The main cells that the infectious agent H. pylori tries to attach are the gastric epithelial cells. […] Some of the protective mechanisms of the gastric epithelium include cell barrier against the entry of toxic or pathogenic agents, stem cells that differentiate into gastric epithelial cells, and sensors located on the mucosal surface capable of detecting microbial antigens, leading to the induction of autonomic mechanisms that result in the effective killing of bacteria. […] Adequate gastric blood flow (GBF) is a protective factor for the gastric mucosa that has the primary role of maintaining its integrity. […] Gastric neurons act on gastric motility, interact with hormones, regulate HCl and bicarbonate secretion, and induce immune responses.

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