[E.coli bacterial suspension in the treatment of hemorrhoids]. / Vozmozhnosti ispol'zovaniya preparatov suspenzii kul'tury bakterii E.coli v lechenii gemorroya v svete sovremennykh kontseptsii.

Hemorrhoidal disease is the most common proctologic disease and the search for new treatment methods, as well as an in-depth understanding of the mechanisms underlying effects of well-known agents on disease pathogenesis still remain relevant. There have been long recognized the effects of the E.coli bacterial culture suspension (BCS) as a therapeutic means eliciting decreased exudation during inflammation, wound healing, tissue regeneration, and stimulated immunity. Here, based on recent findings related to innate and adaptive immune cells, we set out to present mechanisms accounting for some effects coupled to commensal bacteria, particularly inactivated E.coli BCS, which are important for understanding pathogenesis-related action of drug Posterisan and Posterisan forte, and outline their broad application in therapy of hemorrhoids. Based on the analysis, it was concluded that such effects are mediated via multi-pronged and complementary interactions between diverse human receptors expressed in the anorectal region cells and microbial components: NOD ligands, metabolites, enzymes, heat shock proteins and nucleic acids, which lead to production of pro-inflammatory cytokines by anodermal colonocytes, innate and adaptive immune cells, neurons in the submucosal plexus covered by transitional zone epithelium, and hemorrhoid plexus endothelium. Based on current concepts, it may be plausible that E.coli BCS-derived biologically active components contained in drug Posterisan are capable of exerting both positive local and systemic effects, which extend our understanding and substantiate its use in hemorrhoidal disease. The effectiveness of using Posterisan and Posterisan forte is corroborated by their indications in real-life clinical practice, both as a conservative therapy as well as after surgical interventions.

Identification of anti-endothelial cell antibodies in patients with chronic anal fissure.

BACKGROUND: Recent studies demonstrate that chronic anal fissure can be the consequence of a local ischemic process. Thus hypothesizing that at the perianal level the interaction of immune component with endothelium could constitute a mechanism determining ischemia and hypertonia, the presence or absence of circulating anti-endothelial cell antibodies (AECAs) was determined in the serum of patients with anal fissure. METHODS: The study was carried out on 30 patients: 10 with posterior chronic anal fissure (group 1), 10 with grades III and IV hemorrhoids (group 2), and 10 without previous or active anorectal disease, or both (group 3). An indirect immunofluorescence assay on sections of rat kidney tissue was used to identify AECA in the peripheral blood. RESULTS: The assay result was positive for AECAs in 12 patients, all with anorectal disease when compared to the control group (P = .001). The basal anal tone was higher in the AECA-positive patients than in the AECA-negative patients (P = .001). CONCLUSIONS: Only the patients with anal fissure or hemorrhoids were AECA positive. All healthy controls tested negative for AECA. Although the number of subjects studied is small, the presence of auto-antibodies directed against the endothelial cells in the serum of these patients supports the hypothesis that the endothelium is involved in the anal disease.

Solid phase competitive luminescence immunoassay for immunoglobulin A in faeces: development and clinical validation.

We describe a new simple solid-phase competitive luminescence immunoassay (LIA) for the determination of immunoglobulin A (IgA) in faeces. The assay utilizes an anti-alpha-chain IgA antibody which is coated to polystyrene beads and acridinium ester-labelled human IgA as tracer and, therefore, measures both monomeric and polymeric IgA. Dilution recovery of an internal standard was 96, 100 and 103%. Interassay and intra-assay coefficients of variation (C.V.) ranged from 4.5 to 12.9%. The upper limit of normal of faecal IgA in 122 healthy controls was found to be 300 mg/l IgA (mean 73 mg/l, specificity of 99.2%). Patients with inactive Crohn's disease (Crohn's disease activity index (CDAI < 150, n = 14) had faecal IgA values up to 3317 mg/l (mean 1073 mg/l; P < 0.0001). In the active group (CDAI > 150, n = 26) faecal IgA values ranged from 49 to 4094 mg/l (mean 1253 mg/l; P < 0.0001). Patients with ulcerative colitis were divided into a group with active disease (n = 18) and a remission group (n = 16) with values up to 1843 mg/l faecal IgA (man 486 mg/l; P < 0.0032) and up to 602 mg/l faecal IgA (mean 176 mg/l; P < 0.4833), respectively. We also studied patients with non-inflammatory diseases of the gut with this assay. This LIA has proved to be a reliable method for the determination of elevated faecal IgA concentrations and for the detection of pathological findings in the gastrointestinal tract, especially in Crohn's disease.