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 ◽  
...  

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.

2018 ◽  
Vol 243 (15-16) ◽  
pp. 1161-1164
Author(s):  
Maria Pina Dore ◽  
Giovanni Mario Pes ◽  
Alessandra Errigo ◽  
Alessandra Manca ◽  
Giuseppe Realdi

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.


1996 ◽  
Vol 5 (2) ◽  
pp. 79-94 ◽  
Author(s):  
I. M. Garrelds ◽  
C. de Graaf-in't Veld ◽  
R. Gerth van Wijk ◽  
F. J. Zijlstra

The history of allergic disease goes back to 1819, when Bostock described his own ‘periodical affection of the eyes and chest’, which he called ‘summer catarrh’. Since they thought it was produced by the effluvium of new hay, this condition was also called hay fever. Later, in 1873, Blackley established that pollen played an important role in the causation of hay fever. Nowadays, the definition of allergy is ‘An untoward physiologic event mediated by a variety of different immunologic reactions’. In this review, the term allergy will be restricted to the IgE-dependent reactions. The most important clinical manifestations of IgE-dependent reactions are allergic conjunctivitis, allergic rhinitis, allergic asthma and atopic dermatitis. However, this review will be restricted to allergic rhinitis. The histopathological features of allergic inflammation involve an increase in blood flow and vascular permeability, leading to plasma exudation and the formation of oedema. In addition, a cascade of events occurs which involves a variety of inflammatory cells. These inflammatory cells migrate under the influence of chemotactic agents to the site of injury and induce the process of repair. Several types of inflammatory cells have been implicated in the pathogenesis of allergic rhinitis. After specific or nonspecific stimuli, inflammatory mediators are generated from cells normally found in the nose, such as mast cells, antigen-presenting cells and epithelial cells (primary effector cells) and from cells recruited into the nose, such as basophils, eosinophils, lymphocytes, platelets and neutrophils (secondary effector cells). This review describes the identification of each of the inflammatory cells and their mediators which play a role in the perennial allergic processes in the nose of rhinitis patients.


2017 ◽  
Vol 29 (7) ◽  
pp. 723-725
Author(s):  
Kuan Lai ◽  
Nicolas Pinto-Sander ◽  
Daniel Richardson ◽  
Shanshan Wei ◽  
Kang Zeng

Awareness of the spectrum of clinical manifestations of syphilis, especially uncommon changes, is essential for diagnosis and effective management of patients. A 48-year-old Han businessman presented to the ear, nose and throat surgeons with an eight-week history of epigastric pain, a four-week history of a widespread non-itchy rash including the scrotal skin and a one-week history of tinnitus and dizziness. On examination, he was afebrile with widespread lymphadenopathy and a maculopapular rash affecting his trunk and scrotum. His abdomen was soft but tender in the epigastrium. The Treponema pallidum particle agglutination assay result was positive, and the rapid plasma reagin was 1:2. Gastroscopy showed ulcers in the gastric antrum and pylorus. Histopathological examination of gastric mucosa lesions showed a large amount of lymphoplasmacytic infiltrate detected in the lamina propria of the gastric mucosa. The T. pallidum Liferiver real time polymerase chain reaction kit assay performed on specimens from skin lesions and gastric mucosal tissue were positive. The patient was treated with intravenous sodium penicillin followed by intramuscular benzathine penicillin. On the fourth day of the treatment, the rash, epigastric pain and lymphadenopathy subsided. Two weeks after treatment, the tinnitus alleviated and vertigo disappeared.


2021 ◽  
Vol 19 (4) ◽  
Author(s):  
A.A. Avramenko

The aim of the work – to study the regularity of changes in the level of acidity, H.pylori infection and the clinical manifestation of heartburn in patients with chronic nonatrophic gastritis before and after treatment that did not include proton pump inhibitors.Material and methods. We have analyzed the results of a comprehensive examinationof 38 patients with chronic non-atrophic gastritis, suffering from heartburn, before andafter treatment that did not include proton pump inhibitors. Comprehensive examinationbefore treatment included a step-by-step pH-metry, esophagogastroduodenoscopy,double testing for Helicobacter pylori infection (urease test and microscopy of the stainedsmears-prints) using mucosal biopsy specimens from 4 topographic zones of the stomach;histological examination of the gastric mucosa, material for which was taken from thesame areas, and HELIC test. After the treatment, pH-meter control and HELIС test wereperformed.Results. When carrying out a comparative characteristic of the obtained data, ithasbeen found that the average level of acidity after the treatment increased from moderateminimal hypoacidity to pronounced absolute hyperacidity, while the average level ofcontamination of the gastric mucosa by H. pylori infection, tracked by the level of theHELIC test, decreased from 16.4 ± 0.12 mm to 2.3 ± 0.12 mm, and the "heartburn"symptom disappeared in 100% of cases.Conclusions. In the formation of the “heartburn”symptom in patients with chronicnon-atrophic gastritis, the leading factor is the level of ammonia produced by H. pyloriinfection.


1997 ◽  
Vol 11 (2) ◽  
pp. 167-172 ◽  
Author(s):  
Hugh James Freeman

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.


2021 ◽  
Author(s):  
Yoko SAITO ◽  
Shogo KIKUCHI

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.


Author(s):  
E. Shrayner ◽  
A. Havkin ◽  
N. Kokh ◽  
A. Klimova ◽  
G. Lifshits

The aim of the study was to examine an association of the rs602662 FUT2 genetic locus with the status of H. pylori infection and development of related diseases (chronic gastritis, gastric ulcer and 12 duodenal ulcer).Methods: The study included 91 patients, divided into two groups - "case" and "control". Criteria for the “case” group enrollment: diagnosis of gastric or duodenal ulcer, chronic non-atrophic gastritis; positive test for H. pylori.The “control” group included patients with episodic complaints of dyspepsia while undergoing a comprehensive examination, with negative test for H. pylori, as well as having no history of former therapy on H. pylori elimination.The study for the presence of the polymorphic locus rs602662 of the FUT2 gene was carried out by the standard TaqMan PCR method on a Real-Time CFX96 Touch amplifier. The follow-up period was 6 months.Results: The main group included 50 patients aged 21 to 50 years, the control group – 41 patients. Patients infected with H. pylori more often noticed symptoms of dyspepsia - in 36%, compared with the control group - 9.7%. A family history of associated diseases in the main group was significantly differed, χ2 = 4.97, p <0.05.To assess the contribution of the rs602662 locus genotype in FUT2 gene to the risk of clinically manifested H. pylori infection, the main group was divided into subgroups. In the distribution of alleles in these groups, significant differences were revealed. Allele "A" has a protective effect regarding the onset of clinical symptoms of dyspepsia. The odds ratio (OR) with the carriage of allele "A" (genotypes A / A and G / A versus G / G) to have clinical symptoms with a positive H. pylori status was 0.175 (CI = [0.049-0.625] chi2 = 7.79 p = 0.0053 ).Conclusion:1. No association of alleles and genotypes of the rs602662 locus of the FUT2 gene with the status of H. pylori infection was revealed.2. Carriage of allele "A" have a significant association with the absence of clinical symptoms in patients with a positive status of H. pylori infection, OR 0.175 (CI = [0.049-0.625] chi2 = 7.79 p = 0.0053).


Author(s):  
Sasaki K ◽  

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.


1997 ◽  
Vol 2 (2) ◽  
pp. 126-131 ◽  
Author(s):  
Stefan A Carter

Patients with critical limb ischemia are at risk of limb loss and have very high cardiovascular and total mortality rates, which are greater than can be accounted for by the usual risk factors for atherosclerosis. A definition of critical ischemia is necessary to determine the natural history of the disease and to assess and compare the efficacy of various forms of therapy. The definition needs to be based on hemodynamic criteria because clinical manifestations and outcomes are not reliable. The reasons for the difficulties in arriving at a generally acceptable definition are explored. Building on the previous work of others, modified hemodynamic definitions for critical and subcritical ischemia, which include measurements of pressures and of indices of microcirculation, are proposed.


Doctor Ru ◽  
2020 ◽  
Vol 19 (7) ◽  
pp. 41-48
Author(s):  
O.V. Karpenko ◽  
◽  
N.P. Mitkovskaya ◽  
◽  

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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