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Antibiotic-induced diarrhea (AID), also known as antibiotic-induced intestinal flora imbalance, is a frequent complication of antibiotic therapy, which occurs shortly or up to 8 weeks after the start of drug therapy and is reported in 5-30% of cases [1]. Antibiotics cause significant disruption of the normal composition and functional attributes of the gut microbiome [2]. The damage to this ecosystem, especially by reducing its diversity of microorganisms, can occur in the long term [3]. AID developed with a higher prevalence in women in the age category 61-70 years, on the background of viral Pneumonia (48.9% of cases) caused by the SARS-CoV-2 virus, independent of the number of antibiotics previously administered. Diarrhea and abdominal pain are the most common manifestations appreciated in the clinical picture, in contrast fever is less common. Aim of our study was to evaluate the epidemiological and clinical aspects of antibiotic-induced diarrhea. [ABSTRACT FROM AUTHOR]

Aim: To determine the effect of Saccharomyces boulardii CNCM I-745 (S. boulardii) plus sequential therapy on Helicobacter pylori (H. pylori) eradication rate. Methods: This open-label prospective study randomized (1:1) patients with confirmed H. pylori infection to standard sequential therapy of twice-daily (bid) omeprazole 20 mg plus amoxicillin 1 g for 5 days, followed by bid omeprazole 20 mg, clarithromycin 500 mg and metronidazole 500 mg for the next 5 days (control group), or sequential therapy plus bid S. boulardii 250 mg (experimental group). Adverse events (AEs) were recorded throughout the study, and the H. pylori eradication rate was determined 4 weeks after treatment. Results: The study was conducted from May 2013 to May 2016 and included 199 patients (51.3% male; mean age 44.6 ± 13.6 years). The H. pylori eradication rate was higher in the experimental group than the control group (86.0% vs. 74.7%; P = 0.02). Compared with the control group, patients in the experimental group experienced a significantly lower overall incidence of AEs (17.0% vs. 55.7%; p < 0.001) and the incidence of antibiotic-associated diarrhea (2.0% vs. 46.4%; P = 0.02). The experimental group showed improved treatment compliance over the 10-day study period compared with the control group (95.0% vs. 91.2%, P < 0.001). Conclusion: Addition of S. boulardii to sequential therapy improved H. pylori eradication rate and reduced the incidence of treatment-associated AEs in Moroccan patients with H. pylori infection. [ABSTRACT FROM AUTHOR]

Establishing causal links between bacterial metabolites and human intestinal disease is a significant challenge. This study reveals the molecular basis of antibiotic-associated hemorrhagic colitis (AAHC) caused by intestinal resident Klebsiella oxytoca. Colitogenic strains produce the nonribosomal peptides tilivalline and tilimycin. Here, we verify that these enterotoxins are present in the human intestine during active colitis and determine their concentrations in a murine disease model. Although both toxins share a pyrrolobenzodiazepine structure, they have distinct molecular targets. Tilimycin acts as a genotoxin. Its interaction with DNA activates damage repair mechanisms in cultured cells and causes DNA strand breakage and an increased lesion burden in cecal enterocytes of colonized mice. In contrast, tilivalline binds tubulin and stabilizes microtubules leading to mitotic arrest. To our knowledge, this activity is unique for microbiota-derived metabolites of the human intestine. The capacity of both toxins to induce apoptosis in intestinal epithelial cells--a hallmark feature of AAHC--by independent modes of action, strengthens our proposal that these metabolites act collectively in the pathogenicity of colitis. [ABSTRACT FROM AUTHOR]

Frequently and protractedly ill children constitute a special for pediatricians group of patients. Acute respiratory infections with severe and frequently relapsing course badly affect children’s health and contribute to the decrease of the functional activity of the immune system. Risk factors of the high prevalence of acute respiratory infections are changes in the immune responses at the background of unfavorable ante- and perinatal conditions, numerous contacts with potential causative agents at the beginning of attendance of infant schools, widespread intra- and inter-family contacts as well as susceptibility to Th2 immune response (allergy) and prolonged course of inflammatory process. Etiotropic treatment of acute respiratory infections often includes antibacterial drugs, which, however, have negative effects on intestinal microflora, such as dyspeptic syndrome and antibiotic-induced diarrhea. Intestinal dysbiosis affects homeostasis, leads to significant changes in functional activity of various organs and systems. That is why correction and prophylaxis of intestinal dysbacteriosis is very important in pediatric practice. In this article the main data on epidemiology, pathogenesis, forms, clinical manifestation, diagnostics and treatment of antibiotic-induced diarrhea in children.

Abstract: Drug secretion into bile is typically considered a safe route of clearance. However, biliary delivery of some drugs or their reactive metabolites to the intestinal tract evokes adverse consequences due to direct toxic actions or indirect disruption of intestinal homeostasis. Biliary concentration of the chemotherapy agent 5-fluorodeoxyuridine (FUDR) and other compounds is associated with bile duct damage while enterohepatic cycling of antibiotics contributes to the disruptions of gut flora that produce diarrhea. The goal of this review is to describe key evidence that biliary delivery is an important factor in the intestinal injury caused by representative drugs. Emphasis will be given to 3 widely used drugs whose reactive metabolites are plausible causes of small intestinal injury, namely the nonsteroidal anti-inflammatory drug (NSAID) diclofenac, the immunosuppressant mycophenolic acid (MPA), and the chemotherapy agent irinotecan. Capsule endoscopy and other sensitive diagnostic techniques have documented a previously unappreciated, high prevalence of small intestinal injury among NSAID users. Clinical use of MPA and irinotecan is frequently associated such severe intestinal injury that dosage must be reduced. Observations from clinical and experimental studies have defined key events in the pathogenesis of these drugs, including roles for multidrug resistance-associated protein 2 (MRP2) and other transporters in biliary secretion and adduction of enterocyte proteins by reactive acyl glucuronide metabolites as a likely mechanism for intestinal injury. New strategies for minimizing the adverse intestinal consequences of irinotecan chemotherapy illustrate how basic information about key events in the biliary secretion of drugs and the nature of their proximate toxicants can lead to safer protocols for drugs. [Copyright &y& Elsevier]