25 research outputs found
Drug-associated gastropathy: diagnostic criteria
Drugs are widely used to treat different diseases in modern medicine, but they are often associated with adverse events. Those located in the gastrointestinal tract are common and often mild, but they can be serious or life-threatening and determine the continuation of treatment. The stomach is often affected not only by drugs taken orally but also by those administered parenterally. Here, we review the mechanisms of damage, risk factors and specific endoscopic, histopathological and clinical features of those drugs more often involved in gastric damage, namely NSAIDs, aspirin, anticoagulants, glucocorticosteroids, anticancer drugs, oral iron preparations and proton pump inhibitors. NSAID- and aspirin-associated forms of gastric damage are widely studied and have specific features, although they are often hidden by the coexistence of Helicobacter pylori infection. However, the damaging effect of anticoagulants and corticosteroids or oral iron therapy on the gastric mucosa is controversial. At the same time, the increased use of new antineoplastic drugs, such as checkpoint inhibitors, has opened up a new area of gastrointestinal damage that will be seen more frequently in the near future. We conclude that there is a need to expand and understand drug-induced gastrointestinal damage to prevent and recognize drug-associated gastropathy in a timely manner
Evaluation of the CDX2 protein distribution in the gastric mucosa in chronic gastritis by a semi-quantitative index and its reproducibility
The purpose of the study was to assess the reproducibility of the semi-quantitative CDX2 index calculation in chronic atrophic gastritis stages I-IV.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ β ΠΎΡΠ΅Π½ΠΊΠ° Π²ΠΎΡΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠΌΠΎΡΡΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΈΠΊΠΈ ΡΠ°ΡΡΠ΅ΡΠ° ΠΏΠΎΠ»ΡΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ ΠΈΠ½Π΄Π΅ΠΊΡΠ° CDX2 ΠΏΡΠΈ I-IV ΡΡΠ°Π΄ΠΈΡΡ
Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π°ΡΡΠΎΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π³Π°ΡΡΡΠΈΡΠ°
PDCD4 and CDX-2 as immunohistochemical markers of gastric mucosa atrophy in chronic gastritis
The aim of the work is to evaluate the possibility of using immunohistochemical markers PDCD4 and CDX-2 to diagnose atrophy of the gastric mucosa in chronic gastritis and increase the informative value of biopsy examination.Π¦Π΅Π»Ρ ΡΠ°Π±ΠΎΡΡ β ΠΎΡΠ΅Π½ΠΊΠ° Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ² PDCD4 ΠΈ CDX-2 Π΄Π»Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π°ΡΡΠΎΡΠΈΠΈ ΡΠ»ΠΈΠ·ΠΈΡΡΠΎΠΉ ΠΎΠ±ΠΎΠ»ΠΎΡΠΊΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ° ΠΏΡΠΈ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΌ Π³Π°ΡΡΡΠΈΡΠ΅, ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΡ ΠΈΠ½ΡΠΎΡΠΌΠ°ΡΠΈΠ²Π½ΠΎΡΡΠΈ Π±ΠΈΠΎΠΏΡΠΈΠΉΠ½ΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ
Consensus as a method for evaluating the reproducibility of gastric intraepithelial neoplasia/dysplasia: possibility of using in the process of continuing professional education of pathologists
The reproducibility of the Modified Vienna classification of gastrointestinal neoplasia on the gastric mucosal biopsies was evaluated by using the kappa statistic. The work of a group of pathologists-experts was organized in the remote access mode with a demonstration of 26 cases (98 microphotographs) and an evaluation of the diagnostic category of gastric intraepithelial neoplasia/dysplasia. Different levels of agreement between the opinions of the participating experts have been established in depending on the diagnostic difficulty level. The kappa level ranged from 0.2 (poor agreement) to 0.66 (good agreement) and was depending from the chosen method of correction of the result. , This circumstance contributed to the formation of opinion that the diagnoses indefinite neoplasia/dysplasia-low and high grade neoplasia/dysplasia were the most difficult decisions. Possible reasons which reduce the level of consistency of pathologists are discussed.ΠΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ ΠΊΠ°ΠΏΠΏΠ°-ΡΡΠ°ΡΠΈΡΡΠΈΠΊΠΈ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½Π° ΠΎΡΠ΅Π½ΠΊΠ° Π²ΠΎΡΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠΌΠΎΡΡΠΈ ΠΠΎΠ΄ΠΈΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΠΠ΅Π½ΡΠΊΠΎΠΉ ΠΊΠ»Π°ΡΡΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΉ ΠΏΠΈΡΠ΅Π²Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΡΠ°ΠΊΡΠ° Π½Π° ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π΅ Π±ΠΈΠΎΠΏΡΠΈΠΉ ΡΠ»ΠΈΠ·ΠΈΡΡΠΎΠΉ ΠΎΠ±ΠΎΠ»ΠΎΡΠΊΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. Π Π΄ΠΈΡΡΠ°Π½ΡΠΈΠΎΠ½Π½ΠΎΠΌ ΡΠ΅ΠΆΠΈΠΌΠ΅ ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΎΠ²Π°Π½Π° ΡΠ°Π±ΠΎΡΠ° Π³ΡΡΠΏΠΏΡ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΎΠ°Π½Π°ΡΠΎΠΌΠΎΠ²-ΡΠΊΡΠΏΠ΅ΡΡΠΎΠ² Ρ Π΄Π΅ΠΌΠΎΠ½ΡΡΡΠ°ΡΠΈΠ΅ΠΉ 26 Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΠΉ (98 ΡΠΎΡΠΎΠ³ΡΠ°ΡΠΈΠΉ) Ρ ΠΎΡΠ΅Π½ΠΊΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΅Π³ΠΎΡΠΈΠΈ ΠΈΠ½ΡΡΠ°ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΠΈ/Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΡΠ»ΠΈΠ·ΠΈΡΡΠΎΠΉ ΠΎΠ±ΠΎΠ»ΠΎΡΠΊΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°. Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Ρ ΡΠ°Π·Π»ΠΈΡΠ½ΡΠ΅ ΡΡΠΎΠ²Π½ΠΈ ΡΠΎΠ²ΠΏΠ°Π΄Π΅Π½ΠΈΡ ΠΌΠ½Π΅Π½ΠΈΡ ΡΡΠ°ΡΡΠ²ΠΎΠ²Π°Π²ΡΠΈΡ
ΡΠΊΡΠΏΠ΅ΡΡΠΎΠ² Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΡΠ»ΠΎΠΆΠ½ΠΎΡΡΠΈ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ Π·Π°Π΄Π°ΡΠΈ. Π£ΡΠΎΠ²Π΅Π½Ρ ΠΊΠ°ΠΏΠΏΠ° ΠΊΠΎΠ»Π΅Π±Π°Π»ΡΡ ΠΎΡ 0,2 (ΠΏΠ»ΠΎΡ
ΠΎΠ΅ ΡΠΎΠ³Π»Π°ΡΠΈΠ΅) Π΄ΠΎ 0,66 (Ρ
ΠΎΡΠΎΡΠ΅Π΅ ΡΠΎΠ³Π»Π°ΡΠΈΠ΅) Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ Π²ΡΠ±ΡΠ°Π½Π½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Π° ΠΊΠΎΡΡΠ΅ΠΊΡΠΈΠΈ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΠ°, ΡΡΠΎ ΡΠΏΠΎΡΠΎΠ±ΡΡΠ²ΠΎΠ²Π°Π»ΠΎ ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΌΠ½Π΅Π½ΠΈΡ ΠΎ Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ ΡΠ»ΠΎΠΆΠ½ΡΡ
Ρ ΡΠΎΡΠΊΠΈ Π·ΡΠ΅Π½ΠΈΡ ΡΠΎΠ³Π»Π°ΡΠΎΠ²Π°Π½Π½ΠΎΠ³ΠΎ ΠΌΠ½Π΅Π½ΠΈΡ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΊΠ°ΡΠ΅Π³ΠΎΡΠΈΡΡ
, Π½Π°Ρ
ΠΎΠ΄ΡΡΠΈΡ
ΡΡ Π² ΡΡΠ΄Ρ Π½Π΅ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π½Π°Ρ Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΡ/ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΡ β Π½Π΅ΠΎΠΏΠ»Π°Π·ΠΈΡ/Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΡ Π½ΠΈΠ·ΠΊΠΎΠΉ ΠΈ Π²ΡΡΠΎΠΊΠΎΠΉ ΡΡΠ΅ΠΏΠ΅Π½ΠΈ. ΠΎΠ±ΡΡΠΆΠ΄Π°ΡΡΡΡ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΡΠ΅ ΠΏΡΠΈΡΠΈΠ½Ρ, ΡΠ½ΠΈΠΆΠ°ΡΡΠΈΠ΅ ΡΡΠΎΠ²Π΅Π½Ρ ΡΠΎΠ³Π»Π°ΡΠΎΠ²Π°Π½Π½ΠΎΡΡΠΈ ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΎΠ°Π½Π°ΡΠΎΠΌΠΎΠ²-ΡΠΊΡΠΏΠ΅ΡΡΠΎΠ²
Neuroendocrine Tumour as a Diagnostic and Prognostic Criterion for Autoimmune Gastritis
Aim. To describe modern approaches to the diagnosis and treatment of neuroendocrine gastric tumours associatedΒ with chronic autoimmune gastritis on the example of a clinical case.General provisions. Patient H., born in 1948, suffered from a dyspepsia syndrome, the presence of chronic exhelicobacter gastritis and neuroendocrine tumour of unclear histogenesis in the upper third of the stomach body.Β The patient also suffered from systemic lupus erythematosus with skin lesions (discoid rash, palmar and plantar capillaries) and joint lesions (migrating polyarthritis). A general clinical examination revealed mild chronic iron deficiencyΒ anemia and increased neuron-specific enolase (NSE). An EGDS examination using expert-class equipment with theΒ NBI function of close focus identified subepithelial formations of the stomach body. The histological results showedΒ a morphological pattern consistent with a highly differentiated neuroendocrine tumour (G1), type 1, associated withΒ chronic autoimmune gastritis.Conclusion. The autoimmune genesis of the chronic inflammation of the gastric mucosa may serve as a backgroundΒ for the development of neuroendocrine tumours of the stomach, which determines the management tactics in suchΒ conditions
Esophageal Mucosal Resistance in Reflux Esophagitis: What We Have Learned So Far and What Remains to Be Learned
Gastroesophageal reflux disease (GERD) has the highest prevalence among diseases of the digestive system and is characterized by a significant decrease in patientsβ quality of life, comparable to arterial hypertension and coronary heart disease. One in every ten cases of reflux esophagitis leads to the formation of Barrettβs esophagus, which is associated with a high risk of esophagus adenocarcinoma. The key factors determining the progression of the disease are the frequency and duration of the reflux of the stomachβs contents. As a result, refluxate, which includes hydrochloric acid, pepsin, and, in the case of concomitant duodeno-gastric reflux, bile acids and lysolecithin, is thrown into the overlying sections of the digestive tract. At the same time, in addition to aggression factors, it is necessary to take into account the state of resistance in the esophageal mucosa to the effects of aggressive refluxate molecules. This review was prepared using systematized data on the protective properties of the esophageal mucosa and modern methods to assess the mucosal barrier in reflux esophagitis. Lesions of the epithelial barrier structure in the esophagus are recognized as the main pathogenetic factor in the development of reflux esophagitis and are a potentially significant therapeutic target in the treatment of GERD and Barrettβs esophagus. This article presents the characteristics of the esophageal mucosal barrier and the protective mechanisms of the esophagusβs mucous membrane in conditions of gastroesophageal reflux. Diagnostic approaches for assessing the course of reflux esophagitis are described for both histological criteria and the possibility of a comprehensive assessment of the state of mucins, tight-junction proteins, and the proliferative activity of the mucosa, including under the conditions of ongoing therapy
Diagnostic Principles for Chronic Gastritis Associated with Duodenogastric Reflux
This article systematizes available data from the literature on biliary gastritis (BG) in order to increase the awareness of specialists about the latest possibilities for diagnosing the disease. BG occurs as a result of pathological duodenogastric reflux. In patients with a preserved duodenogastric junction, the dominant factor is represented by motor disorders of the upper digestive tract (primary biliary gastritis), while in patients recovering from surgical interventions it is represented by structural changes (secondary biliary gastritis). Progressive BG can lead to atrophy of the gastric mucosa, intestinal metaplasia, epithelial dysplasia, and eventually to gastric cancer. Diagnostic methods for BG are carried out to identify risk factors, exclude alarm symptoms and identify persistent motor disorders and pathological reflux (24 h pH-impedancemetry, hepatobiliary scintigraphy, 24 h monitoring of bilirubin content in the reflux using a Bilitec 2000 photometer), as well as to diagnose gastritis itself (esophagogastroduodenoscopy, morphological gastrobiopsy examination). The diagnosis of BG should be based on a multidisciplinary approach that combines a thorough analysis of a patientβs complaints, an anamnesis of the disease, and the results of endoscopic and histological research methods