Aim. To evaluate the level of serum I-FABP (Fatty-Acid-Binding Protein a protein that binds fatty acids) and fecal zonulin as markers of the permeability of the mucous membrane of the small intestine in celiac patients. Materials and methods. A total of 151 celiac patients (25 men and 126 women) were examined. The median age was 42 years. Group I included 58 patients with newly diagnosed celiac disease; in group 2 38 patients, knowingly or unknowingly violating the gluten-free diet; group 3 consisted of 55 patients strictly observing gluten-free diet. The control group consisted of 20 healthy volunteers: 4 men and 16 women. All patients underwent esophagogastroduodenoscopy by biopsy of the mucous membrane of the small intestine and assessment of duodenobioptates according to Marsh. In the blood serum, the level of antibodies to tissue transglutaminase IgA and IgG was determined by the enzyme-linked immunosorbent assay using kits manufactured by Orgentec Diagnostics GmbH (Germany), the concentration of I-FABP in blood serum was determined using Hycult Biotech kits (Netherlands). The content of zonulin in feces was investigated by enzyme-linked immunosorbent assay using kits from Immundiagnostik AG (Germany). Statistical analysis was performed using the Statistica 13.3 software (StatSoft Inc., USA). Results. There was a significant increase in the level of antibodies to tissue transglutaminase IgA [120.0 (41.1200)] IU/ml and IgG [31.4 (5.578.9)] IU/ml in patients of group 1 compared with group 2 [IgA 9.1 (2.987.6)] and IgG [3.8 (2.219.7)] IU/ml and group 3 [IgA 1.6 (1.03.2)] and IgG [2.2 (1.152.53)] (p0.01). The level of I-FABP in blood serum in patients of group 1 averaged 2045 pg/ml, in patients in group 2 1406 pg/ml, in patients in group 3 1000 pg/ml. All patients showed a significant increase in the mean I-FABP values compared to controls (1, 2 and control p0.01, 3 and control p=0.016). In patients with Marsh grade III AC atrophy, the I-FABP level depended on the degree of damage to the mucosa and significantly differed from the control: March IIIA (median: 1310 pg/ml, interquartile range: 12121461 pg/ml), March IIIB (median: 2090 pg/ml, interquartile range: 18122322 pg/ml) as well as Marsh IIIC (median: 2058 pg/ml, interquartile range 18582678 pg/ml). The concentration of zonulin in feces in patients of group 1 averaged 111.6 pg/mg, in patients of group 2 90.5 pg/mg. In patients of group 3 50 IU/ml. The concentration of zonulin in feces increased as the degree of mucosa atrophy increased (r=0.585, p0.01). However, despite the fact that both of these markers may indicate impaired permeability, each of them indicates damage to a certain level of the intestinal barrier, which is not always associated with the degree of mucosa atrophy. Conclusion. Determination of serum I-FABP and fecal zonulin levels in celiac patients allows for the assessment of intestinal permeability and can serve as non-invasive markers for monitoring ongoing structural changes in the mucosa without the need for endoscopy.

Aim. To evaluate the possibility of using serum markers of atrophy (pepsinogens – PG I and II) to form high-risk groups for gastric cancer (Operative Link for Gastritis Assessment – OLGA stage III–IV) depending on the etiology of gastritis. Materials and methods. A total of 237 (56 men and 181 women) patients were examined. All patients underwent a 13C-urea breath test, a blood test for GastroPanel (PG I, PG II, gastrin-17, antibodies to Helicobacter pylori immunoglobulin G), a blood test for antibodies to gastric parietal cells. All patients underwent esophagogastroduodenoscopy with a biopsy of the gastric mucosa from 5 standard points according to the Sydney system and a histomorphological study according to the OLGA system, as well as a biopsy to detect H. pylori infection using the polymerase chain reaction. The patients were divided into 3 groups depending on the etiology of gastritis: Group 1 included 55 patients with chronic gastritis, autoimmune gastritis and associated with H. pylori gastritis (AIG+HP+); Group 2 – 47 patients with AIG and negative tests for H. pylori infection (AIG+HP-); Group 3 – 135 patients with chronic gastritis associated with H. pylori and negative markers of AIG (AIG-HP+). Results. The analysis showed that in patients with AIG (group 2), the most reliable serological markers of atrophy predicted severe atrophy (OLGA stage III–IV): when the ratio PG I/PG II was ≤ 3, it was detected in 70.21% of cases, and when PG I decreased to ≤ 30 μg/L, it was found in 68.08%. In group 1, stages III–IV according to OLGA were diagnosed in 20% of cases with PG I/PG II indicators ≤ 3; and in 18.18% with a decrease in PG I ≤ 30 μg/L. When analyzing the diagnostic accuracy of GastroPanel biomarkers in identifying severe atrophy (OLGA stages III–IV) in the total sample of patients (all 3 groups), it was possible to achieve cut-off indicators as close as possible to the reference values while maintaining a relatively high sensitivity and specificity – 75.81% and 81.50% for PG I ≤ 30 μg/L and 85.48% and 64.50% for PG I/PG II ≤ 3, respectively. The optimal cut-off in the study population for the PG I indicator was 22.5 μg/L (sensitivity – 72.58%, specificity – 88.00%), and for the PG I/PG II ratio ≤ 2 (sensitivity – 80.65%, specificity – 78.50%). Conclusion. Serum pepsinogens can be used in the Moscow population as a non-invasive marker of gastric mucosa atrophy for the formation of high-risk patient groups for gastric cancer requiring endoscopic examination.

Objective. This review provides an in-depth analysis of the current landscape in assessing pancreatic fibrosis. Key points. Pancreatic fibrosis is a common feature in various diseases, including inflammatory and neoplastic conditions, exacerbating their progression. Timely identification of fibrotic changes in pancreatic tissue plays a crucial role in halting or slowing down the advancement of glandular damage. Evaluation methods for fibrosis encompass both invasive and non-invasive approaches. Histological assessment remains the most dependable method for gauging the extent of pancreatic fibrosis. Among the numerous scales for the morphological assessment of pancreatic fibrosis, the system proposed by G. Kloppel, B. Maillet, which evaluates peri- and intralobular fibrosis along with an integrative index, currently stands out as the most applicable for research purposes. In the pursuit of novel non-invasive diagnostic methods for pancreatic tissue fibrosis, researchers are actively developing laboratory biomarkers such as matrix metalloproteinases and specific blood cytokines, as well as instrumental techniques like ultrasound, computed tomography, and magnetic resonance imaging. Conclusion. Each method possesses unique capabilities and limitations associated with the patient’s condition, the prevalence of the fibrotic process, and the presence of comorbidities. The most effective approach involves the integrated use of data obtained from an objective assessment of pancreatic tissue fibrosis. Notably, there is a current lack of standardized scales for the reproducibility of laboratory, instrumental and histological systems in assessing pancreatic fibrosis.

There is a generally recognized need for a morphological assessment of the individual risk of developing gastric cancer in a patient with chronic gastritis, according to the OLGA system (Operative Link for Gastritis Assessment). At the same time, the role of assessing the biopsy from the incisura angularis remains controversial. The aim of our study was to assess the value of incisura angularis biopsy in staging gastritis according to the OLGA system by examining the atrophic and inflammatory changes in the antrum, incisura angularis, and body. Materials and Methods: A total of 718 patients (576 women and 142 men) aged 20 to 84 years were examined. Most of the patients were in the age group of 50 to 70 years (54.6%). Depending on the detection of H. pylori and autoimmune gastritis markers, all patients were divided into three groups. The first group included 380 patients with H. pylori gastritis without signs of autoimmune gastritis. The second group consisted of 209 patients with autoimmune gastritis, in whom no infection was detected during the examination, and there were no indications of H. pylori eradication. The third group consisted of 129 patients with chronic gastritis of combined etiology (autoimmune and H. pylori). Endoscopy biopsies were taken according to the updated Sydney System. Histological assessments of the grade and the stage of gastritis were carried out according to the standard OLGA-based protocol. Then, the same assessments were evaluated without taking into account histological changes in the incisura angularis. Results: When assessing the severity of inflammatory changes in the gastric mucosa according to the OLGA system, grade II (72.3%) was most often detected in all groups of patients. A severe degree of activity of chronic gastritis was most often observed in the group of patients with H. pylori gastritis (6.1%). These indicators practically did not change if the assessment did not take the angulus biopsy into account. When assessing the severity of atrophy of the glands in the gastric mucosa in patients of the first group, mild stages of atrophy prevailed. Without taking into account the angulus biopsy, a decrease in the stage of atrophy was observed in 27 cases (7.11%), and in only 4 cases did stage IV change to stage III, while in 23 cases, discrepancies were noted only within groups with a mild stage of atrophy. There were no transitions from stage III to stage II. In the group of patients with autoimmune gastritis, pronounced stages of atrophy prevailed—in more than 77%. Without taking into account the angulus biopsy, a decrease in the stage of atrophy was observed in eight cases (3.83%), and in three (1.4%) patients, stage III was changed to stage II. In the group of patients with combined etiology (autoimmune + H. pylori), severe stages of atrophy also prevailed (70.5%). A decrease in the stage of atrophy without taking into account the angulus biopsy was only observed in three patients (2.32%), of which two cases concerned patients with mild stages of atrophy. Thus, in general, severe stages of atrophy of the gastric mucosa (stages III and IV according to the OLGA staging system) were detected in 313 patients (43.59%). If the assessment of the atrophy stage did not take into account changes in the angulus biopsy, then severe stages of atrophy (III and IV according to OLGA) were detected in 310 patients (43.17%). In total, changes in the assessment of the atrophy stage occurred in 38 patients (5.29%), and this was more often observed in patients with stages I and II of atrophy. Conclusions: Accounting for histological changes in the incisura angularis does not significantly affect the assessment of the grade and stage of chronic gastritis according to the OLGA system, regardless of the etiology of atrophic gastritis.

The aim of the article is to improve the differential diagnosis of specific and nonspecific inflammatory bowel diseases. In Russia, this scientific direction is associated with the name of G.F. Lang, who performed in 1901–1902 the study „On ulcerative inflammation of the large intestine caused by balantidiasis“. The etiology of specific colitis is associated with infection with parasites, bacteria and viruses that cause inflammation of the intestinal wall, diarrhea, often with an admixture of mucus, pus and blood. Specific colitis (SC) may be accompanied by fever, abdominal pain, and tenesmus. Bacterial colitis is commonly caused by Salmonella, Shigella, Escherichia coli, Clostridium difficile, Campylobacter jejuni, Yersinia enterocolitica, and Mycobacterium tuberculosis. Viral colitis is caused by rotavirus, adenovirus, cytomegalovirus, and norovirus. Parasitic colitis can be caused by Entamoeba histolytica and balantidia. In gay people, SC can cause sexually transmitted infections: Neisseria gonorrhoeae, Chlamydia trachomatis, and treponema pallidum, affecting the rectum. Stool microscopy, culture, and endoscopy are used to establish the diagnosis. Stool culture helps in the diagnosis of bacterial colitis in 50% of patients, and endoscopic studies reveal only nonspecific pathological changes. Differential diagnosis of SC should be carried out with immune-inflammatory bowel diseases (ulcerative colitis, Crohn's disease, undifferentiated colitis), radiation colitis and other iatrogenic bowel lesions. The principles of diagnosis and therapy of inflammatory bowel diseases associated with various etiological

Лекарственные поражения печени, индуцированные нестероидными противовоспалительными препаратами: лекция и клиническое наблюдение