Candida-Associated Gastric Ulcer Revisited

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Sasaki K ◽  
Keyword(s):  
Gastric Ulcer ◽  
Gastric Mucosa ◽  
Antineoplastic Agents ◽  
Cellular Damage ◽  
Healthy Individuals ◽  
Negative Patient ◽  
Systemic Corticosteroids ◽  
Typical Finding ◽  
History Of ◽  
H Pylori

Candida-associated gastric ulcer occurs not only in debilitated but healthy individuals. Though had been reported to demonstrate nothing but nonspecific endoscopic features, it occasionally exhibits a typical finding I designated a candidarium. The natural history of the disease had not been clarified and the recurrence had not been described. However, I demonstrated that the ulcer not only occurs but also recurs in a different site with a different shape in a non-diabetic, H. pylori-negative patient, who has not taken NSAIDs, antibiotics, antineoplastic agents, or systemic corticosteroids, advocating that, contrary to the prevailing opinion, Candida is no innocuous bystander but an etiologic perpetrator. It has recently been shown to secrete a cytolytic PFT, candidalysin, into a pocket in the epithelium after penetrating into it to activate MAPK/MKP1/ c-Fos pathway, triggering release of damage as well as immune cytokines in OPC and VVC. While candidalysin, exerting an effect even on the adjacent oropharyngeal cells, directly injures the tissue with damage cytokines, immune counterparts activate PMNs to eventually terminate inflammation. Though the epithelial response to the fungus is different from organ to organ, it invades into and induces necrotic cellular damage to the IECs through the toxin to translocate: the action of candidalysin is proven not only on the squamous but on the columnar epithelium. Since, by analogy with intestinal candidiasis, it is never difficult to speculate that the PFT inflicts such damage to the gastric mucosa, a theoretically strong possibility has come up that Candida-associated gastric ulcer is actually Candida-induced.

scholarly journals Tissue transglutaminase activity in human gastric mucosa according to Helicobacter pylori infection

2018 ◽  
Vol 243 (15-16) ◽  
pp. 1161-1164
Author(s):  
Maria Pina Dore ◽  
Giovanni Mario Pes ◽  
Alessandra Errigo ◽  
Alessandra Manca ◽  
Giuseppe Realdi
Keyword(s):  
Helicobacter Pylori ◽  
Animal Models ◽  
Gastric Mucosa ◽  
Natural History ◽  
Tissue Transglutaminase ◽  
Helicobacter Pylori Infection ◽  
Human Gastric Mucosa ◽  
Antral Mucosa ◽  
History Of ◽  
H Pylori

Tissue transglutaminase (t-TG) is a multifunctional protein involved in the healing of gastric erosions and ulcers in animal models. The aim of this study was to measure gastric t-TG activity in patients with dyspepsia according to Helicobacter pylori infection and cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) subtype status. Patients undergoing upper endoscopy not taking any medications were enrolled. Tissue-TG activity was determined in homogenates of antral specimens using a radiometric assay and was expressed in pmol/mg. The cagA and vacA genotypes were determined by PCR amplification using gene-specific oligoprimers. Data from 46 patients were available (17 of them were positive for H. pylori). Antral t-TG activity was significantly increased in H. pylori positive patients compared to H. pylori negative patients (6437 ± 3691 vs. 3773 ± 1530 pmol/mg; P = 0.001) according to Mann–Whitney U test. Patients with H. pylori negative gastritis had higher t-TG activity than patients with normal gastric mucosa. The specimens infected with cagA positive strains (72%) displayed greater t-TG activity than cagA negative samples (7358 ± 4318 vs. 4895 ± 1062 pmol/mg; P = 0.237). Similarly, t-TG activity was higher in H. pylori vacA s1/m1 strains vs. vacA s1/m2 (7429 vs. 5045 pmol/mg; P = 0.744), and vacA s1/m1 vs. s2/m2 (7429 vs. 4489 pmol/mg; P = 0.651) but the results were not significant. No differences were found between histology, endoscopy features and t-TG activity. These results show that t-TG activity is significantly greater in gastritis associated with H. pylori infection, suggesting that this enzyme is induced by inflammation and may have an important role in the natural history of human gastritis. Impact statement Tissue transglutaminase (t-TG) is unique among TG enzymes because of its additional role in several physiological and pathological activities, including inflammation, fibrosis, and wound healing. The presence of t-TG has previously been described in the intestine of human and animal models, yet studies on t-TG activity in human gastric mucosa are missing. Helicobacter pylori infection is the major cause of gastritis and peptic ulcers. For the first time, our results show that t-TG activity was significantly higher in antral specimens of patients with chronic active gastritis associated with H. pylori infection compared to H. pylori negative chronic gastritis and normal antral mucosa. These findings suggest that t-TG has a role in the natural history of human gastritis, which requires further investigation but may be an avenue for new therapeutic options.

scholarly journals AMBIVALENCE OF CHRONIC INFLAMMATION IN THE MUSCULOUS STOMACH

2020 ◽  
Vol 10 (2) ◽  
pp. 104-111
Author(s):  
O. V. Shtygasheva ◽  
E. S. Ageeva
Keyword(s):  
Gastric Cancer ◽  
Peptic Ulcer ◽  
Gastric Ulcer ◽  
Gastric Mucosa ◽  
Chronic Inflammation ◽  
Morphological Changes ◽  
Reference Points ◽  
Gastric Epithelium ◽  
H Pylori ◽  
Cag A

For peptic ulcer disease, the etiological role of H. pylori infection has been proven, 60-90% of gastric cancer cases are associated with H. pylori. The bacterium is recognized as a first-order carcinogen. An association has been established between the successful elimination of H. pylori and a reduced risk of gastric cancer and relapse of peptic ulcer. In the pathogenesis of chronic inflammation in the gastric mucosa associated with H. pylori, there are reference points that determine the further path of development of the pathology. If peptic ulcer is not a consequence of the direct damaging effect of NSAIDs, it is associated with the development of gastritis. In gastric ulcer, gastritis is found in both the antrum and the fundus of the stomach Atrophy of the glands begins in the antrum, then its foci are found in the fundus on the front and back walls. Gradu- ally they increase in size, merge with each other, the acid secreting zone decreases, and the border between the fundus and pyloric glands shifts in the proximal direction. With atrophic fundus gastritis, the likelihood of developing high ulcers and stomach cancer increases. Significant increase in apoptosis processes with relative rigidity of proliferation leads to the formation of ulcer, and carcinogenesis is due to excessive proliferation and accumulation of cell mutations. One of the subjects of damage is Cag A H. pylori protein, which implements remodeling of the gastric epithelial barrier. Among its effects are modulation and impaired proliferation of gastric epithelium, leading to morphological changes. The aggressive action of Cag A protein enhances toxic doses of alcohol and smoking, supporting inflammation and causing damage to the gastric mucosa. Despite the common etiology and pathogenesis of gastric ulcer and gastric cancer, the relationship with the de- velopment of atrophic pangastritis and the similarity of convention risk factors determines that the key point in the manifestation of gastric cancer is a genetic predisposition in the form of gene polymorphism causing severe atrophy as a result of chronic inflammation.

scholarly journals Detection of CagA, VacA, IceA1 and IceA2 virulent genes in Helicobacter pylori isolated from gastric ulcer patients

2018 ◽  
Vol 42 (4) ◽  
pp. 155-162
Author(s):  
Lijuan Fan ◽  
Ran Li ◽  
Hongyun Li ◽  
Jian Zhang ◽  
Lingyun Wang
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Virulence Genes ◽  
East Asian ◽  
Virulence Gene ◽  
Gastric Biopsy ◽  
History Of ◽  
Male Patients ◽  
Polymerase Chain ◽  
H Pylori

Abstract Background Virulence factors of Helicobacter pylori including cagA, vacA, iceA and their association with clinical manifestation varied widely with different subpopulations. The objective of the study was to determine the prevalence of cagA, iceA1, iceA2, vacA, vacA s1/s2, vacA m1/m2, Western type cagA and East Asian type cagA virulence genes in H. pylori isolated from gastric ulcer patients and evaluate the association of these genes with gender, age, smoking and alcohol consumption. Methods Gastric biopsy samples from 172 patients were collected. H. pylori virulence genes, cagA, vacA, iceA1, iceA2, vacA s1/s2, vacA m1/m2, Western type cagA and East Asian type cagA were detected using polymerase chain reaction (PCR). Results Of the gastric biopsy samples collected, 48.3% of samples grew H. pylori. The vacA (68.7%) was the predominant virulence gene detected and associated with male patients and patients within the age group of 31–40 years. The cagA was the second most common gene detected and significantly associated with alcoholic patients. Conclusions H. pylori infection rate was 48.3% and was associated with patients who were smokers or had a history of smoking. The majority of our isolates were positive for any one of the virulence genes tested indicating that these isolates were highly virulent in nature.

scholarly journals Prevalence of Helicobacter pylori infection in patients with gastric ulcer perforation admitted in a tertiary care centre

2019 ◽  
Vol 6 (3) ◽  
pp. 898
Author(s):  
Muhammed Rashim P. ◽  
S. Vineed
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Tertiary Care ◽  
Gastric Ulcers ◽  
Care Centre ◽  
Tertiary Care Centre ◽  
Ulcer Perforation ◽  
History Of ◽  
Perforation Peritonitis ◽  
H Pylori

Background: Gastric ulcers are one of the most prevalent gastro intestinal diseases. Perforation of gastric ulcer is most common and dreaded complication of a gastric ulcer. Causes of gastric ulcer include Helicobacter Pylori, the NSAID, smoking and alcohol. Helicobacter Pylori infection is a curable cause of gastric ulcer. As prevalence of H. pylori differ in populations, prevalence of H. pylori in our population need to be assessed for determining treatment strategy for gastric ulcer.Methods: Cross sectional study conducted in patients operated for perforation peritonitis and diagnosed to have gastric ulcer perforation in a tertiary care centre. Full thickness biopsy was taken from gastric ulcer perforation edge during the surgery for perforation peritonitis. The biopsy was stained with Giemsa stain and looked for the presence of H. pylori.Results: Helicobacter pylori prevalence was 48.8% in our study. 8 females (out of 16) and 51 males (out of 105) had H. pylori positivity. 43 had history of smoking. Among them 20 were diagnosed to be having H. pylori positive. 26 persons had history of pan chewing. Among pan chewers 17 were H. pylori positive. Among 50 patients with history of alcoholism, 24 got H. pylori positivity. Among 40 patients with history of NSAIDs, 14 were positive for H. pylori.Conclusions: Prevalence of Helicobacter pylori in gastric ulcer perforation in present study is 48.8%. Helicobacter Pylori eradication should be added in treatment protocols for perforated gastric ulcers.

scholarly journals Disappearance of Helicobacter without Antibiotics in 12 Patients with Gastritis

1997 ◽  
Vol 11 (2) ◽  
pp. 167-172 ◽  
Author(s):  
Hugh James Freeman
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Natural History ◽  
Gastric Biopsy ◽  
Endoscopic Procedures ◽  
History Of ◽  
Gastric Biopsies ◽  
H Pylori ◽  
Upper Gastrointestinal

Detection ofHelicobacter pyloriin endoscopic gastric biopsies has been associated with a variety of diseases, including ulcers and gastritis. Although the natural history ofH pyloriin the gastric mucosa is unknown, antibiotic regimens have been used for eradication. Gastric biopsies from 6050 endoscopic procedures done by a single gastroenterologist from 1981 to 1994 were evaluated. Of these, 2860 from April 1, 1991 to September 30, 1994 had silver-stained biopsies to facilitateH pyloridetection, and at least two upper endoscopic procedures were done with gastric biopsies in 188 patients. Twelve of the 188 patients with an initially positiveH pylorigastric biopsy becameH pylori-negative without antibiotic treatment forH pylorior other infection; 10 received omeprazole and two received no drug treatment. In two of the 12 patients recurrentH pyloriin the gastric mucosa was also documented. These findings indicate thatH pylorimay disappear and reappear in the gastric mucosa with no specific antibiotic eradication regimen, although omeprazole may eradicateH pyloriin vivo in some patients. The natural history ofH pyloriin gastric biopsies is poorly understood. Improved understanding, especially regarding the pathogenesis of upper gastrointestinal ulcerative and inflammatory disease processes, is essential before recommendations for specific antibiotic eradication regimens can be made.

scholarly journals Modern approaches to pharmacotherapy of chronic gastritis

2021 ◽  
pp. 40-47
Author(s):  
V. V. Skvortsov ◽  
L. V. Zaklyakova ◽  
B. N. Levitan ◽  
M. Yu. Bolgova ◽  
I. K. Zaklyakov ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Clinical Manifestations ◽  
Acid Reflux ◽  
Histological Features ◽  
Acute Gastritis ◽  
Modern Classification ◽  
History Of ◽  
Mycobacterium Avium Intracellulare ◽  
H Pylori ◽  
Definition Of

The definition of gastritis is based on the histological features of the gastric mucosa. This is not the erythema observed during gastroscopy, and there are no specific clinical manifestations or symptoms that determine it. The modern classification of gastritis is based on time (acute and chronic), histological features, anatomical distribution and the main pathological mechanisms. Acute gastritis will develop into chronic if left untreated. Helicobacter pylori (H. pylori) is the most common cause of gastritis worldwide. However, from 60 to 70% H. pylori-negative subjects with functional dyspepsia or non-erosive gastroesophageal reflux were also found to have gastritis. H. pylori-negative gastritis is considered when a person meets all four of these criteria: negative triple staining of biopsies of the gastric mucosa, no history of treatment of H. pylori. In these patients, the cause of gastritis may be associated with tobacco smoking, alcohol consumption and / or the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids. Other causes of gastritis include autoimmune gastritis associated with antibodies of serum anti-parietal and anti-internal factor; organisms other than H. pylori, such as Mycobacterium avium intracellulare, Herpes simplex and Cytomegalovirus; gastritis caused by acid reflux; Rare causes of gastritis include collagen gastritis, sarcoidosis, eosinophilic gastritis and lymphocytic gastritis. The clinical picture, laboratory studies, gastroscopy, as well as histological and microbiological examination of tissue biopsies are important for the diagnosis of gastritis and its causes. Treatment of gastritis caused by H. pylori leads to the rapid disappearance of polymorphic-nuclear infiltration and a decrease in chronic inflammatory infiltrate with gradual normalization of the mucous membrane. Other types of gastritis should be treated based on their etiology.

scholarly journals Higher Proportions of a Healthy Gastric Mucosa in Healthy Japanese Adults with Later Birth Year: Analysis of 41,957 Participants

2021 ◽  
Author(s):  
Yoko SAITO ◽  
Shogo KIKUCHI
Keyword(s):  
Gastric Mucosa ◽  
Individual Risk ◽  
Negative Results ◽  
Healthy Mucosa ◽  
Japanese Adults ◽  
History Of ◽  
H Pylori ◽  
The Individual ◽  
Antibody Levels ◽  
Upper Gastrointestinal

Abstract Purpose: In Japan, most gastric cancers are associated with gastric mucosal atrophy caused by chronic infection with Helicobacter pylori (H. pylori). To recognize the condition of the gastric mucosa and to determe the infection status of H. pylori are important for predicting the individual risk of gastric cancer. The present study aimed to determine the proportion of Japanese adults with a healthy gastric mucosa (without H. pylori infection) among 12 birth-year groups encompassing 1935 to 1990.Methods: The gastric mucosa was classified as healthy or having gastritis based on routine double-contrast upper gastrointestinal barium X-ray radiopgraphy examination (UGI-XR). The participants were 41,957 healthy Japanese adults. Serum or urine H. pylori antibody levels were also assessed.Results: In total, 25,424 participants had a healthy mucosa without a history of H. pylori eradication. The proportions of participants with a healthy mucosa by birth year were 19.8% (57/288), 27.1% (306/1,128), 32.4% (569/1,756), 37.6% (1,808/4,811), 49.2% (3,207/6,522), 60.1% (3,966/6,550), 71.2% (5,224/7,342), 77.2% (5,114/6,624), 80.6% (3,342/4,149), 85.0% (1,404/1,652), 85.3% (302/354), and 94.7% (125/132) in 1935, 1940, 1945, 1950, 1955, 1960, 1965, 1970, 1975, 1980, 1985, and after 1990, respectively (p for trend < 0.01). All participants with a healthy mucosa showed negative results in H. pylori antibody tests.Conclusion: The proportion of participants with a normal gastric mucosa increased linearly with birth years. Prevalence of a morphologically healthy gastric mucosa may have been increasing, in parallel with prevalence of H. pylori infection has been decreasing.

scholarly journals Serum Pepsinogens and Their Comparison with Endoscopic and Histologic Results for Gastric Mucosa in Relatives of Gastric Cancer Patients

Doctor Ru ◽  
2020 ◽  
Vol 19 (7) ◽  
pp. 41-48
Author(s):  
O.V. Karpenko ◽  
◽  
N.P. Mitkovskaya ◽  
◽  
Keyword(s):  
Gastric Cancer ◽  
Family History ◽  
Gastric Mucosa ◽  
Test Group ◽  
Study Objective ◽  
Keywords Screening ◽  
Study Results ◽  
History Of ◽  
H Pylori ◽  
Gastric Cancer Patients

Study Objective: to study the possibility of using serological markers pepsinogen 1 (PG-1), pepsinogen 2 (PG-2) and their ratio in pre-cancer screening in genetic heredity of gastric cancer (GC), in relatives of GC patients. Materials and Methods. The study included 114 relatives of GC patients (study group) and 117 patients without family history of GC who were examined for dyspepsia (controls). All subjects underwent clinical examination, questionnaire survey and esophagogastroduodenoscopy with biopsy to assess the gastric mucosa status in accordance with the modified Sydney System, OLGA and OLGIM systems, and had Helicobacter pylori infection assessed. PG-1, PG-2 and their ratio were measured in blood serum. Pepsinogen test (PT) results were used to distribute the subjects (226 individuals, 5 were excluded) into three groups: negative PT (nPT) (PG-1 > 70 ng/mL and PG-1/2 > 3.0); controversal PT (cPT) (PG-1 ≤ 70 ng/mLor PG-1/2 ≤ 3.0); positive PT (pPT) (PG-1 ≤ 70 ng/mL and PG-1/2 ≤ 3.0). Study Results. Relatives of GC patients vs. controls had more frequent atrophy of any location (49.1 vs. 23.9%, p = 0.000), antral gastratrophia (43.9% vs. 23.1%, p = 0.000). Metaplasia (any location) in relatives of GC patients was also more common vs. controls (22.8% vs. 12.8%; p = 0.047). Incidence of H. pylori in test group was 57.9%, in controls it was 53.9%. In relatives of GC patients, atrophy had earlier onset (45.9 vs. 54.7 years old in controls; p < 0.001). Analysis of PT results revealed the association between pPT and overweight (85.2% vs. 57.7% in cPT and 55.2% in nPT; p = 0.024), age (37.3 years in pPT vs. 39.1 years in cPT and 49 years in nPT; p = 0.002), and family history of GC (66.7% vs. 51.3% in cPT and 44.6% in nPT; p = 0.043). Also, PT results depended on any atrophy (nPT — 28.9%, cPT — 41.0%, pPT — 62.9%; p = 0.001), particularly on antral atrophy (nPT — 28.1%, cPT — 37.2%, pPT — 51.9%; p = 0.015). Gastritis stages I–IV as per OLGA were found in 28.9% of nPT subjects, in 41.0% of cPT subjects, and 63.0% in pPT subjects. When gastritis metaplasia severity as per OLGIM was assessed, we found significant increase in the number of I-II stage cases in cPT (19.2%) and pPT (37.0%) groups vs. nPT group (9.1%) (p = 0.003). Multivariate analysis demonstrated the following atrophy risk factors (serological PT results): family history of gastric cancer (RR = 1.6; 95% CI: 1.0–2.8; p = 0.037), overweight (BMI > 25 kg/m2) (RR = 2.1; 95% CI: 1.3–3.7; p = 0.003), marked gastric inflammation (stage 2–3) (RR = 1.8; 95% CI: 1.1–3.0; p = 0.018), and metaplasia (of any location) (RR = 2.3; 95% CI: 1.2–4.5; p = 0.008). Conclusion. A non-invasive assessment of gastric mucosa changes using H. pylori antibody and blood PG-1 tests is a promising method. However, serological PTs should be studied across various populations and regions. Keywords: screening, family history, gastric cancer, chronic gastratrophia, metaplasia, pepsinogen.

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