IntroductionThe objective of the study was to evaluate the prevalence of Clostridium difficile-associated diarrhoea (CDAD) among hospitalised patients with antibiotic-associated diarrhoea (AAD) in general and by specific types of medical care and hospital units.MethodsA prospective, cross-sectional, non-interventional, multicentre study. The main inclusion criteria were: patient age ≥ 18 years, hospital stay of at least 48 h, current antibiotic therapy or antibiotic therapy within the previous 30 days, loose stools (Bristol stool types 5–7 and stool frequency ≥ 3 within ≤ 24 consecutive hours or exceeding normal for the patient) and signed informed consent form. The stool sample was taken to the local (study site) microbiology laboratory for detection of glutamate dehydrogenase (GDH) and toxins A/B using enzyme immunoassay (EIA) stool test.ResultsFrom April 2016 to April 2017, a total of 1245 patients from 12 large hospitals were enrolled in the study. Data on 81 patients were excluded from the analysis for different reasons. Data on 1164 patients (45.2% males and 54.8% females) with a mean age of 54.9 years (range 18–95 years) were analysed. Length of hospitalisation was 2–188 days (median, 8 days). The EIA stool test showed CDAD-positive results in 21.7% (253/1164) patients. The patients were from surgery units (546/1164), internal medicine units (510/1164) and intensive care units (108/1164). The prevalence of CDAD among patients from surgery, internal medicine and intensive care units was 26.2, 17.8 and 17.6%, respectively. Oncology, gastroenterology, septic surgery, oncohaematology and general medical hospital units accounted for more than 75% of all patients included; the prevalence of CDAD by those hospital units was 11.3, 15.0, 39.2, 17.6, and 27.2%, respectively. The proportion of GDH-positive and toxin A/B-negative patients by the rapid stool test result was 16.8% (196/1164). The prevalence of CDAD varied widely between the hospitals (from 0 to 44.3%).ConclusionsThe prevalence of CDAD among hospitalised patients with AAD in this study was 21.7% (95% confidence interval: 14.8 and 28.7%). The percentage of CDAD varied widely between hospitals and by specific types of medical care and hospital units.

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Слизистая оболочка (СО) желудочно-кишечного тракта (ЖКТ) постоянно подвергается воздействию экзо-генных и эндогенных агрессивных субстанций, которые посредством различных механизмов способны вызывать ее повреждение. При этом в каждом биотопе пищевари-тельного тракта содержаться как общие, так и присущие только этому отделу факторы агрессии. Желудок является наиболее повреждаемым органом пищеварительной си-стемы, и в то же время обладает самыми мощными цито-протективными механизмами, противостоящими факто-рам агрессии [1,2]. Факторы агрессии присутствуют по-стоянно или поступают в желудок перорально и гемато-генным путем, а также продуцируются непосредственно в слизистой оболочке желудка (СОЖ) при различных пато- АннотацияРебамипид является цитопротективным препаратом, который стимулирует продукцию эндогенных простагландинов в сли-зистой оболочке желудка, тонкой кишке и ускоряет заживление эрозивно-язвенных повреждений, вызванных инфекцией Helicobacter pylori и приемом нестероидных противовоспалительных препаратов (НПВП). Основные свойства ребами-пида включают стимуляцию простагландинов и синтеза гликопротеинов слизи, ингибирование реактивных форм кисло-рода, воспалительных цитокинов и хемокинов и ингибирование активации нейтрофилов. В статье отражена способность ребамипида повышать эффективность терапии инфекции, вызванной H. pylori, уменьшать воспаление, в том числе после ее эрадикации, ускорять заживление язв и предотвращать прогрессирование пренеопластических повреждений. Rebamipide is a cytoprotесtive drug that stimulates the generation of endogenous prostaglandins in the gastric and small intestinal mucosa and accelerates the healing of erosions and ulcers caused by Helicobacter pylori infection and NSAID administration. The major properties of rebamipide include stimulation of prostaglandins and synthesis of muсus glycoproteins, inhibition of reactive oxygen species, inflammatory cytokines, and chemokines, and suppression of neutrophil activation. This paper shows the ability of rebamipide to enhance the efficiency of therapy for Helicobacter pylori-induced infection, to reduce inflammation, including that after infection eradication, to accelerate ulcer healing, and to prevent the progression of preneoplastic lesions.

Currently, biliary sludge (BS) is considered as a pathological process associated with an increase in the lithogenicity of bile and according to the modern classification of gallstone disease referred to the prestone stage of the disease. In the mechanism of BS formation, the main role belongs to four factors: glut of bile with cholesterol, formation of crystallization nucleus, dysfunction of the gallbladder (contraction, absorption, secretion), violation of the enterohepatic circulation of bile acids. Clinical manifestations in BS are most often associated with concomitant functional disorders of the biliary tract and chronic bacterial duodenitis with duodenal hypertension. The main directions in the treatment of BS are reduced to the restoration of the normal rheological properties of bile, the normalization of the motor function of the biliary system and the duodenum, the correction of the intestinal microbiome. The article discusses effective treatment regimens for BS depending on its morphological features and clinical course with the use of ursodeoxycholic acid or hofitol. The mechanism of Chophytol action (Mayoly Spindler, France) at BS is presented. The additional use of Meteospasmyl in the presence of intestinal antiseptic indications contributes to the rapid resolution of clinical manifestations in this pathology.