scholarly journals The effectiveness and safety of switching therapy with an original drug to biosimilars in treatment of inflammatory bowel diseases

2022 ◽  
pp. 35-41
Author(s):  
E. S. Peda ◽  
T. L. Alexandrov ◽  
T. A. Baranova ◽  
S. S. Belous ◽  
I. A. Tishaeva ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Research Centre ◽  
Unknown Etiology ◽  
Cost Of Treatment ◽  
Immune Mediated ◽  
Tnf Α ◽  
Switching Therapy ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
The Cost

Introduction. Inflammatory bowel diseases are a group of chronic, immune-mediated diseases of unknown etiology. Etiotropic therapy of IBD does not exist, all drugs used to treat IBD have a pathogenetic effect. In the treatment of IBD biologic therapy is used. The most previously registered group of biologics are anti-TNF-α. But, after the expiration of the relevant patents, biosimilars appeared on the market (analogs, comparable in quality to the already approved reference product).Materials and methods. A retrospective study was conducted on the basis of the Ryzhikh Natianal Medical Research Centre for Coloproctology of the Ministry of Health of the Russia, which included 46 patients who switched from therapy with the original infliximab or adalimumab to biosimilar therapy.Discussion. This study showed that when switching therapy with the original drugs infliximab and adalimumab to biosimilars, the effectiveness of therapy does not significantly decrease with the use of biosimilars Infliximab BIOCAD and Dalibra. However, a statistically significant decrease in efficacy was revealed when switching from therapy with the original Infliximab to Flammegis. Considering that the use of biosimilars can reduce the cost of treatment and reduce the burden on the health budget, it is necessary to continue this study in order to obtain longer-term results.

scholarly journals The Role of Enterobacteriaceae in Gut Microbiota Dysbiosis in Inflammatory Bowel Diseases

2021 ◽  
Vol 9 (4) ◽  
pp. 697
Author(s):  
Valerio Baldelli ◽  
Franco Scaldaferri ◽  
Lorenza Putignani ◽  
Federica Del Chierico
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Inflammatory Diseases ◽  
Species Level ◽  
Unknown Etiology ◽  
Gut Dysbiosis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Symbiotic Microbiota ◽  
Gut Microbiota Dysbiosis

Inflammatory bowel diseases (IBDs) are a group of chronic gastrointestinal inflammatory diseases with unknown etiology. There is a combination of well documented factors in their pathogenesis, including intestinal microbiota dysbiosis. The symbiotic microbiota plays important functions in the host, and the loss of beneficial microbes could favor the expansion of microbial pathobionts. In particular, the bloom of potentially harmful Proteobacteria, especially Enterobacteriaceae, has been described as enhancing the inflammatory response, as observed in IBDs. Herein, we seek to investigate the contribution of Enterobacteriaceae to IBD pathogenesis whilst considering the continuous expansion of the literature and data. Despite the mechanism of their expansion still remaining unclear, their expansion could be correlated with the increase in nitrate and oxygen levels in the inflamed gut and with the bile acid dysmetabolism described in IBD patients. Furthermore, in several Enterobacteriaceae studies conducted at a species level, it has been suggested that some adherent-invasive Escherichia coli (AIEC) play an important role in IBD pathogenesis. Overall, this review highlights the pivotal role played by Enterobacteriaceae in gut dysbiosis associated with IBD pathogenesis and progression.

scholarly journals Procoagulatory State in Inflammatory Bowel Diseases Is Promoted by Impaired Intestinal Barrier Function

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Luca Pastorelli ◽  
Elena Dozio ◽  
Laura Francesca Pisani ◽  
Massimo Boscolo-Anzoletti ◽  
Elena Vianello ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Intestinal Barrier ◽  
Systemic Circulation ◽  
Intestinal Barrier Function ◽  
Inflammatory Conditions ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Molecular Patterns ◽  
D Dimer

Inflammatory and immune mediated disorders are risk factors for arterial and venous thromboembolism. Inflammatory bowel diseases (IBD) confer an even greater risk of thromboembolic events than other inflammatory conditions. It has been shown that IBD patients display defective intestinal barrier functions. Thus, pathogen-associated molecular patterns (PAMPs) coming from the intestinal bacterial burden might reach systemic circulation and activate innate immunity receptors on endothelial cells and platelets, promoting a procoagulative state. Aim of the study was to test this hypothesis, correlating the presence of circulating PAMPs with the activation of innate immune system and the activation of the coagulatory cascade in IBD patients. Specifically, we studied lipopolysaccharide (LPS), Toll-like receptor (TLR) 2, TLR4, and markers of activated coagulation (i.e., D-Dimer and prothrombin fragmentF1+2) in the serum and plasma of IBD patients. We found that LPS levels are increased in IBD and correlate with TLR4 concentrations; although a mild correlation between LPS and CRP levels was detected, clinical disease activity does not appear to influence circulating LPS. Instead, serum LPS correlates with both D-Dimer andF1+2measurements. Taken together, our data support the role of an impairment of intestinal barrier in triggering the activation of the coagulatory cascade in IBD.

scholarly journals Innate Immunity Modulation by the IL-33/ST2 System in Intestinal Mucosa

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Marina García-Miguel ◽  
M. Julieta González ◽  
Rodrigo Quera ◽  
Marcela A. Hermoso
Keyword(s):  
Ulcerative Colitis ◽  
Innate Immunity ◽  
Intestinal Mucosa ◽  
Inflammatory Bowel Diseases ◽  
The Body ◽  
Unknown Etiology ◽  
Adequate Food ◽  
Bowel Diseases ◽  
Surface Contact Area ◽  
Inflammatory Bowel

Innate immunity prevents pathogens from entering and spreading within the body. This function is especially important in the gastrointestinal tract and skin, as these organs have a large surface contact area with the outside environment. In the intestine, luminal commensal bacteria are necessary for adequate food digestion and play a crucial role in tolerance to benign antigens. Immune system damage can create an intestinal inflammatory response, leading to chronic disease including inflammatory bowel diseases (IBD). Ulcerative colitis (UC) is an IBD of unknown etiology with increasing worldwide prevalence. In the intestinal mucosa of UC patients, there is an imbalance in the IL-33/ST2 axis, an important modulator of the innate immune response. This paper reviews the role of the IL-33/ST2 system in innate immunity of the intestinal mucosa and its importance in inflammatory bowel diseases, especially ulcerative colitis.

Anti-TNF-α agents and serum lipids in inflammatory bowel diseases

2016 ◽  
Vol 40 (4) ◽  
pp. e46-e47
Author(s):  
Çağdaş Kalkan ◽  
Fatih Karakaya ◽  
Murat Törüner ◽  
Hülya Çetinkaya ◽  
Irfan Soykan
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Serum Lipids ◽  
Tnf Α ◽  
Bowel Diseases ◽  
Inflammatory Bowel

scholarly journals Growth and Puberty in Children with Inflammatory Bowel Diseases

Biomedicines ◽  
2020 ◽  
Vol 8 (11) ◽  
pp. 458
Author(s):  
Flavia Amaro ◽  
Francesco Chiarelli
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Gastrointestinal Symptoms ◽  
Growth Failure ◽  
Active Phase ◽  
Underlying Mechanism ◽  
Delayed Puberty ◽  
Unknown Etiology ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Altered Immune Response

Inflammatory bowel diseases (IBD) are gastrointestinal tract pathologies of unknown etiology; they have an alternating trend, with active and silent phases. IBD are classified in two main forms: ulcerative colitis (UC) and Crohn’s disease (CD). Both have chronic and recurrent course, gastrointestinal symptoms, and extraintestinal manifestations. The altered immune response role seems to be important both in UC and CD. In the majority of cases, CD begins with abdominal pain, diarrhea, decrease in appetite, and weight loss; there can be also perianal fistulas, rhagades, and perianal recurrent abscesses. In addition, retarded growth and delayed puberty can precede the development of the disease or can even be predominant at onset. Growth retardation is found in 40% of IBD patients, but the underlying mechanism of this and other extra-intestinal manifestations are partially known: the main hypotheses are represented by malnutrition and inflammatory response during the active phase of the disease. The increased level of pro-inflammatory cytokines can influence growth, but also the onset of puberty and its progression. In addition, it could be essential to clarify the role and the possible effects of all the currently used treatments concerning growth failure and delayed puberty.

scholarly journals History of Inflammatory Bowel Diseases

2019 ◽  
Vol 8 (11) ◽  
pp. 1970 ◽  
Author(s):  
Giovanni Clemente Actis ◽  
Rinaldo Pellicano ◽  
Sharmila Fagoonee ◽  
Davide Giuseppe Ribaldone
Keyword(s):  
20Th Century ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Tuberculosis ◽  
Unknown Etiology ◽  
Biological Drugs ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Novel Strategy ◽  
Definition Of ◽  
Therapeutic Research

Inflammatory bowel diseases (IBD) are characterized by chronic inflammation of the intestinal mucosa and unknown etiology. In this review, we identified three main eras in the IBD history. Between the 19th and the 20th century, the primary task had been the definition of the diagnostic criteria in order to differentiate the new entity from intestinal tuberculosis. In the 20th century, an intense and prolific therapeutic research prevailed, culminating in the introduction of biological drugs in the clinical setting. Since the beginning of the 21st century, traditional definition criteria have been challenged by holistic criteria in an effort to seek a still unattained cure. Centuries of worldwide efforts on IBD etiology and therapy search have culminated in this novel strategy.

scholarly journals Evidence for a Potential Role of Metallothioneins in Inflammatory Bowel Diseases

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
Anouk Waeytens ◽  
Martine De Vos ◽  
Debby Laukens
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Potential Role ◽  
Current Knowledge ◽  
Zinc Homeostasis ◽  
Central Position ◽  
Small Proteins ◽  
Immune Mediated ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel diseases (IBDs) are a group of chronic, relapsing, immune-mediated disorders of the intestine, including Crohn's disease and ulcerative colitis. Recent studies underscore the importance of the damaged epithelial barrier and the dysregulated innate immune system in their pathogenesis. Metallothioneins (MTs) are a family of small proteins with a high and conserved cysteine content that are rapidly upregulated in response to an inflammatory stimulus. Herein, we review the current knowledge regarding the expression and potential role of MTs in IBD. MTs exert a central position in zinc homeostasis, modulate the activation of the transcription factor nuclear factor (NF)-B, and serve as antioxidants. In addition, MTs could be involved in IBD through their antiapoptotic effects or through specific immunomodulating extracellular effects. Reports on MT expression in IBD are contradictory but clearly demonstrate a deviant MT expression supporting the idea that these aberrations in IBD require further clarification.

Evaluation of metabolites levels in feces of patients with inflammatory bowel diseases

2020 ◽  
Vol 66 (3) ◽  
pp. 233-240
Author(s):  
E.S. Zhgun ◽  
Y.V. Kislun ◽  
T.N. Kalachniuk ◽  
V.A. Veselovsky ◽  
A.S. Urban ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Microflora ◽  
Fecal Microbiota ◽  
Unknown Etiology ◽  
Published Data ◽  
Resonance Spectroscopy ◽  
Healthy Donors ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel diseases (IBD), which include ulcerative colitis (UC) and Crohn's disease (CD), are chronic intestinal inflammatory disorders with an unknown etiology. They are characterized by chronic recurrent inflammation of the intestinal mucosa and lead to a significant decrease in the quality of life and death of patients. IBD are associated with suppression of normal intestinal microflora, including a decrease in bacteria, producers of short chain fatty acids (SCFAs), exhibiting anti-inflammatory and protective properties. Among the various methods of intestinal microflora correction, fecal microbiota transplantation (FMT), which engrafts the fecal microbiota from a healthy donor into a patient recipient, is of a particular interest. As a result, a positive therapeutic effect is observed, accompanied by the restoration of the normal intestinal microflora of the patient. A significant drawback of the method is the lack of standardization. Metabolites produced by intestinal microflora, namely SCFAs, allow objective assessment of the functional state of the intestinal microbiota and, consequently, the success of the FMT procedure. Using gas chromatography and nuclear magnetic resonance spectroscopy techniques, we have analyzed concentrations and molar ratios of SCFAs in fecal samples of 60 healthy donors. Results were in good accord when comparing two methods as well as with published data. Analysis of SCFAs in feces of patients with UC (19 patients) and CD (17 patients) revealed a general decrease in the concentration of fatty acids in the experimental groups with significant fluctuations in the values in experimental groups compared to control group of healthy donors. On the limited group of IBD patients (6 patients with UC and 5 patients with CD) concentration of SCFAs before and within 30 days of observation after FMT was determined. It was shown that FMT had a significant impact on the SCFAs levels within 1 month term; tendency to reach characteristics of healthy donors is unambiguously traced for both diseases.

Adalimumab prevents barrier dysfunction and antagonizes distinct effects of TNF-α on tight junction proteins and signaling pathways in intestinal epithelial cells

2013 ◽  
Vol 304 (11) ◽  
pp. G970-G979 ◽  
Author(s):  
Andreas Fischer ◽  
Markus Gluth ◽  
Ulrich-Frank Pape ◽  
Bertram Wiedenmann ◽  
Franz Theuring ◽  
...  
Keyword(s):  
Tight Junction ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Barrier ◽  
Model Systems ◽  
Tight Junction Proteins ◽  
Barrier Dysfunction ◽  
Tnf Α ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Junction Proteins

Intestinal barrier dysfunction is pivotal in the etiology of inflammatory bowel diseases. Combined clinical and endoscopic remission (“mucosal healing”) in patients who received anti-TNF-α therapies suggests restitution of the intestinal barrier, but the mechanisms involved are largely unknown. We therefore investigated the impact of the anti-TNF-α antibody adalimumab on barrier function in two in vitro models. Combined stimulation of Caco-2 and T-84 cells with interferon-γ and TNF-α resulted in a significant decrease of transepithelial electrical resistance (TEER) within 6 h that was prevented by adalimumab in concentrations down to 100 ng/ml. Adalimumab furthermore antagonized the appearance of irregular membrane undulations and prevented internalization of tight junction proteins upon cytokine exposure. In addition, TNF-α induced a downregulation of claudin-1, claudin-2, claudin-4, and occludin as well as activation of phosphatidylinositol 3-kinase signaling in T-84 but not Caco-2 cells, which was reversed by adalimumab. At the signaling level, adalimumab prevented increased phosphorylation of myosin light chain as well as activation of p38 MAPK and NF-κB accompanying the decline in TEER in both model systems. Pharmacological inhibition of NF-κB signaling partially prevented the TNF-α-induced TEER loss, whereas inhibition of p38 worsened barrier dysfunction in Caco-2 but not T-84 cells. Taken together, these data demonstrate that adalimumab prevents barrier dysfunction induced by TNF-α both functionally and structurally as well as at the level of signal transduction. Barrier protection might therefore constitute a novel mechanism how anti-TNF-α therapy contributes to epithelial restitution and tissue repair in inflammatory bowel diseases.

scholarly journals Immunotherapeutic Effects of β-D Mannuronic Acid on IL-4, GATA3, IL-17 and RORC Gene Expression in the PBMC of Patients with Inflammatory Bowel Diseases

2018 ◽  
Author(s):  
Hussaini Alhassan Mohammed ◽  
Ali Akbar Saboor-Yaraghi ◽  
Homayoun Vahedi ◽  
Ghordratollah Panahi ◽  
Gholamreza Hemmasi ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Immunological Response ◽  
Quantitative Real Time Pcr ◽  
Mannuronic Acid ◽  
Immune Mediated ◽  
Genes Expression ◽  
Bowel Diseases ◽  
Research Findings ◽  
Inflammatory Bowel ◽  
Normal Controls

Inflammatory bowel diseases (IBD) are chronic relapsing immune-mediated disorders that result from an aberrant immunological response. IBD comprises of Crohn's disease (CD) and ulcerative colitis (UC). The precise aetiology of IBD has not been fully understood, however, recent studies support the hypothesis that patients with IBD have a dysregulated immune response to endogenous bacteria in the gastrointestinal tract (GIT). The increasing number of hospitalisation coupled with the high economic burden faced by IBD patients, calls for more concerted research efforts, to design a potent and credible treatment option for these strata of patients. This research was designed to test the efficacy and potency of β-D Mannuronic acid (M2000) in the treatment of IBD. Ten ml of blood was aseptically collected from 24 IBD patients and 24 normal controls. PBMC was isolated and stimulated with 1 µg/mL of LPS and incubated for 4 hours. The cells were later treated with 10 µg/mL or 50 µg/mL of Mannuronic acid and incubated for 24 hours at 370C under 5% CO2 and 100% humidity. After the incubation, RNA was extracted from the cells, cDNA was synthesised, and the expression of the gene was evaluated using quantitative real-time PCR. The result indicated a significant down-regulation of RORC and IL-17 genes expression, while the expression of IL-4 and GATA3 genes were significantly up-regulated. These research findings have shown that M2000 a biocompatible agent, that has an immunotherapeutic, immunomodulatory and immunosuppressive effects on the PBMC of IBD patients.

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