1Moscow Clinical Research-and-Practical Center, Moscow Healthcare Department, Moscow; 2A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow; 3Children’s Health Research Center, Ministry of Health of Russia, Moscow; 4I.I. Mechnikov North-Western State Medical University, Ministry of Health of Russia, Saint Petersburg; 5M.F. Vladimirsky Moscow Regional Research Clinical Institute, Moscow; 6Russian Medical Academy of Postgraduate Education, Ministry of Health of Russia, Moscow; 7Novosibirsk State Medical University, Ministry of Health of Russia, Novosibirsk; 8Russian Children’s Clinical Hospital, Moscow; 9Department of Pediatrics, Russian Medical Academy of Postgraduate Education, Ministry of Health of Russia, Moscow; 10I.P. Pavlov First Saint Petersburg State Medical University, Ministry of Health of Russia, Saint Petersburg; 11Acad. Yu.E. Veltishchev Research Clinical Institute of Pediatrics, N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia, Moscow; 12Clinic Four, Department of Pediatrics, I.P. Pavlov First Saint Petersburg State Medical University, Ministry of Health of Russia, Saint Petersburg; 13Childhood Diseases Department Two, N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia, Moscow; 14Research Laboratory of Surgical Gastroenterology and Endoscopy, N.I. Pirogov Russian National Research Medical University, Ministry of Health of Russia, Moscow; 15Department of Endoscopic Surgery, City Clinical Hospital Thirty-One, Moscow Healthcare Department, Moscow; 16A.N. Ryzhikh State Research Center of Coloproctology, Ministry of Health of Russia, Moscow; 17Department of Intermediate-Level Therapy, Tver State Medical University, Ministry of Health of Russia, Tver; 18Laboratory of Medical Genetics, Diagnostic Center of Medical Genetics, Saint Petersburg; 19HLA Typing Laboratory, Blood Transfusion Station, Moscow Healthcare Department, Moscow; 20S.P. Botkin City Clinical Hospital, Moscow Healthcare Department, Moscow; 21Department of Nervous System Diseases, I.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia, Moscow; 22Department of Endocrinology and Diabetology, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow; 23Acad. V.I. Kulakov Research Center of Obstetrics, Gynecology, and Perinatology, Ministry of Health of Russia, Moscow; 24Department of Therapy, Kazan State Medical Academy, Ministry of Health of Russia, Kazan; 25Department of Intermediate-Level Therapy with Course of Occupational Diseases, Faculty of General Medicine, Omsk State Medical University, Ministry of Health of Russia, Omsk; 26Dmitry Rogachev Federal Research Clinical Center of Pediatric Hematology, Oncology, and Immunology, Ministry of Health of Russia, Moscow The paper presents the All-Russian consensus on the diagnosis and treatment of celiac disease in children and adults, which has been elaborated by leading experts, such as gastroenterologists and pediatricians of Russia on the basis of the existing Russian and international guidelines. The consensus approved at the 42nd Annual Scientific Session of the Central Research Institute of Gastroenterology on Principles of Evidence-Based Medicine into Clinical Practice (March 2—3, 2016). The consensus is intended for practitioners engaged in the management and treatment of patients with celiac disease. Evidence for the main provisions of the consensus was sought in electronic databases. In making recommendations, the main source was the publications included in the Cochrane Library, EMBASE, MEDLINE, and PubMed. The search depth was 10 years. Recommendations in the preliminary version were reviewed by independent experts. Voting was done by the Delphic polling system.

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 define the frequency of adverse events and loss of the response in patients with ulcerative colitis (UC) and Crohns disease (CD), treated with original medicine infliximab (IFX) Remicaide and its biosimilars. Materials and methods. We included 154 patients with IBD: 78 UC patients (50.6%) и 76 CD patients (49.4%), treated with original medicine IFX Remicade and its biosimilars. In our study we did not include patients, who previously underwent induction treatment with IFX and its biosimilar. Results. Among 78 UC patients, IFX was cancelled in 25 (32.0%) patients and they were switched to the other anti-TNF inhibitor or medicine with the another mechanism of action; in patients group, treated with biosimilar 16 (20.5%) and 9 (11.5%) patients, who were interchanged biosimilar and/or original IFX. Among 76 CD patients IFX was cancelled in 20 (26.3%) patients: 11 (14.5%) patients in group, treated with similar trade name biosimilar, 8 (10.5%) patients, who were interchanged biosimilar and/or original IFX and 1 patient (1,3%), receiving original IFX. We found no difference in the secondary loss of response and adverse events in patients with CD and UC, switched from original IFX to biosimilar (p=0.6257 and p=0.6635, correspondingly). The frequency of the secondary loss of response or adverse events in patients with UC and CD, switched from original IFX to IFX biosimilar, was similar (p0.05). Conclusion. Approximately 30% of IBD patients, receiving IFX biosimilar, will be switched to the other anti-TNF therapy or medicine with the another mechanism of action because of secondary loss of response or adverse events.

To investigate the impact of bariatric surgery (BS) on the level of vitamins in obese patients. One hundred obese patients (78 women and 22 men) aged 19 to 61 years were examined. Controlled gastric banding (CGB) was carried out in 20 patients (mean body mass index (BMI), 41.3 ± 8.2 kg/m2); gastric sleeve resection (GSR) in 40 patients, and gastric shunting (GS) in 40 (the mean BMI in these groups were 41.1 ± 17.8 and 45.9 ± 6.2 kg/m2, respectively). A control group consisted of 10 apparently healthy individuals (BMI, 24.9 ± 3.2 kg/m2). An enzyme immunoassay was used to determine the serum concentrations of vitamins B1, B2, B5, B6, B9, B12, C, and D, niacin, biotin, and retinol-binding protein (RBP) before and 1 year after surgery. All the three groups showed a considerable decrease in the levels of vitamins C, B5, B6, and D, and RBP both prior to and following BS. More than 50% of the patients who had undergone GSR had also a lower baseline niacin level. A year after CGB, GSR, and GS, the number of patents with deficiency of these vitamins remained the same or increased. The majority of patients with the same level of vitamin B2, niacin, and folic acid (FA) were observed to have its decrease a year postsurgery. The concentration of the other test vitamins was also reduced a year after all operations; however, it remained within the normal range. GS had no substantial impact on the concentrations of FA, vitamins B2, B12, B1, and biotin. The lower serum vitamin levels were not accompanied by clinical symptoms in most patients following BS. In 80% of the patients with obesity, the levels of vitamins C, B6, and D were decreased to a variable degree. After BS, there was a rise in the number of patients with low serum vitamin C, D, B6, B5, niacin, FA, and RBP concentrations, at the same time the number of patients with FA deficiency increased by more than twice. BS did not significantly affect the metabolism of vitamins B1 B2 B12, and biotin.

Aim. To clinically evaluate the activity of glucoamylase, maltase, saccharase, and lactase in the small intestinal mucosa (SIM) of patients with celiac disease. Subjects and methods. Twenty-nine patents with celiac disease were examined. The disease was first detected in 8 patients; in the remaining patients, it had been diagnosed 6 months to 35 years before. The diagnosis was verified by histological examinations of duodenal biopsy specimens and by determination of immunoglobulin (Ig) A and G antibodies to tissue transglutaminase (atTG) and gliadin (AGA) by an enzyme-linked immunosorbent assay (ELISA). Carbohydrase activities were estimated in the duodenal biopsy specimens, by applying the method of A. Dahlquist. Results. In the control group, the activities of glucoamylase, maltase, saccharase, and lactase averaged 598.8+184.2, 825.3+239.3, 180.2-68.1, and 53.4+16.3 ng/glucose/mg tissue min, respectively. In the patients with celiac disease, the average activities of all the examined enteric enzymes were significantly below the normal value even they had been on a gluten-free diet (GFD) for 10 years or longer. Complete SIM structural recovery (Marsh stage 0) occurred in only 7 of 18 patients who had been on a strictly GFD. Serological (atTG and AGA) tests got also negative in all the 7 patients with completely recovered SIM. Six of the latter patients continued to have abdominal bloating and borborygmus, unstable stool with a propensity for diarrhea and weakness. Each was detected to have a lower activity of one or a few enzymes. The activity of all the carbohydrases reached its normal value in only 1 patient and she felt healthy, without perceiving any food intolerance. Conclusion. The activity of membrane enzymes may serve as a marker for the degree of SIM recovery in patients with celiac disease.

Background. Inflammatory bowel diseases (IBD) are characterized by chronic immune inflammation of the mucous membrane and/or the thickness of the intestinal wall, and are also accompanied by disorders of the blood clotting system and the development of a hypercoagulation state. Aim. To identify the frequency of thromboembolic complications (TEC) in IBD patients and to determine the influence of acquired and inherited hypercoagulation factors that contribute to the development of TEС. Materials and methods. The clinical status of 1,238 IBD patients who were treated in 2019 was evaluated. Of these, 748 patients with ulcerative colitis (UC) and 490 patients with Crohn's disease (CD). Among UC patients, there were 369 (49.3%) men and 379 (50.7%) women. In 10.1% of patients with UC, there were clinically significant feasibility studies. There were 227 (46.3%) men and 263 (53.7%) women among patients with CD; 7.3% of patients with CD had clinically significant feasibility studies. Results. In general 112 (9.0%) of 1,238 IBD patients had clinically significant feasibility studies. Among patients with UC (n=748), 76 (10.2%) showed clinically significant feasibility studies. Among patients with CD (n=490), 36 (7.3%) had a feasibility study. Of 112 IBD patients with clinically significant TEC, 45 (40.2%) had genetic polymorphisms that increase affinity for fibrinogen, increase platelet aggregation, and contribute to a decrease in the activity of folate cycle enzymes, including methylenetetrahydrofolate reductase, which may be manifested by a moderate increase in homocysteine levels. Of the 45 IBD patients with clinically significant TEC due to inherited factors, 30 (66.6%) patients had UC, 15 (33.7%) patients had CD (hazard ratio 1.038, 95% confidence interval 0.7461.444; 2=0.049; p=0.83921); 67 (59.8%) patients with IBD who had clinically significant TEC did not have genetic polymorphisms leading to hypercoagulation. Conclusion. Based on the analysis, we can conclude that such risk factors for the development of TEC as the status of a smoker, long bed rest, taking hormonal contraceptives, varicose veins of the lower extremities, high activity of the disease, glucocorticoids therapy, the extent of intestinal damage in patients with IBD, genetic factors, should be taken into account by gastroenterologists in the treatment of patients with UC and CD. The hereditary factor of hypercoagulation equally affects the development of TEC, both in patients with UC and CD.