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Health Benefits of Garlic (Allium sativum) in Gastrointestinal Disorders
Published in Megh R. Goyal, Preeti Birwal, Durgesh Nandini Chauhan, Herbs, Spices, and Medicinal Plants for Human Gastrointestinal Disorders, 2023
Yaw Duah Boakye, Daniel Obeng Mensah, Eugene Kusi Agyei, Richard Agyen, Doreen Kwankyewaa Adjei, Christian Agyare
Inflammatory bowel disease (IBD) refers to ulcerative colitis and Chron’s disease that involves inflammation of chronic nature of the GI tract. The development of targeted, monoclonal antibody-based therapies has greatly improved the treatment of IBD. Key interventions have been the use of tumor necrosis factor antagonists, but its utilization has been associated with side effects and their efficacy has been shown to decrease with time. The resort to nonconventional remedies, which includes nutraceuticals, has increased in recent times the with IBD.27
Crohn’s Disease
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Lohith Umapathi, Divya Manikandan, Govind Nandakumar
The association between anti-tumor necrosis factor (TNFα) agents and complications in patients with Crohn’s disease remains controversial. The pharmacokinetics of monoclonal antibodies, such as infliximab, permit persistent therapeutic concentrations for at least eight weeks post-infusion. Although it is controversial, we prefer to wait at least four weeks after the last dose was administered [5]. Urgent or emergent procedures can be performed while on infliximab.
Endotoxin Tolerance
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
F. Ulrich Schade, Regina Flach, Sascha Flohé, Matthias Majetschak, Ernst Kreuzfelder, Emilio Domínguez-Fernández, Jochen Börgermann, Martin Reuter, Udo Obertacke
The importance of cytokines, in particular tumor necrosis factor α, as a mediator of host defense and inflammatory responses is well documented (67). A key role has been attributed to TNF in models of shock induced by endotoxin and gram-negative bacteria (68,69). The finding that TNF formation in rabbits and rats pretreated with LPS was considerably blocked upon challenge with LPS, therefore, provided new insight in the mechanism of endotoxin tolerance (13,14,70). The assumption that mononuclear phagocytes have a central function in endotoxin tolerance was suggested by the finding that macrophages from tolerant rats in vitro were greatly impeded in their ability to produce TNF (70,71).
Systematic review of TNFα-induced paradoxical psoriasis: Treatment outcomes of switching to alternative biologic therapies in inflammatory bowel disease patients
Published in Journal of Dermatological Treatment, 2023
Rishab Revankar, Heli Patel, Mary Rojas, Samantha Walsh, Jean S. McGee
Introduction of biologic therapies has transformed the way we manage inflammation in the gut and the skin. Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal (GI) tract. Over the past several decades, anti-tumor necrosis factor (anti-TNFα), such as infliximab (IFX) and adalimumab (ADA), has been the mainstay biologic therapy for these patients. However, with increasing utilization of anti-TNFα agents, paradoxical inflammation of the skin, specifically paradoxical psoriasis (PXP), has been reported in IBD patients (1). For these patients, switching to a different class of biologic therapies has been shown to successfully treat PXP as well as control GI symptoms (2). Here, we performed a systematic review to evaluate the efficacies of different biologic therapies in treating PXP and controlling symptoms of IBD.
Circular RNA circ_0003420 mediates inflammation in sepsis-induced liver damage by downregulating neuronal PAS domain protein 4
Published in Immunopharmacology and Immunotoxicology, 2021
Huawei Xiong, Hao Wang, Qichun Yu
Sepsis is systemic inflammation that can result in circulatory dysfunction and/or organ dysfunction in severe clinical conditions [1]. This pathological state is presently considered a growing problem in the clinic and has a considerable incidence rate and mortality rate. The mortality rate of patients with severe sepsis is within the range of approximately 28–50% [2,3]. By definition, sepsis is severe systemic inflammation in response to infection [4]. If the inflammation is especially strong, then the liver system’s homeostasis is disrupted, leading to septic liver damage. In the case of sepsis, proinflammatory cytokines can lead to immune dysfunction and may injure multiple tissues or organs [5,6]. Tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β modulate an immune response in its early phase. In this process, they are mainly produced and released by cells involved in immunity via the regulation of transcription and post-translational events [7]. The inflammation cascade generates reactive oxygen species, which participate in organ damage and can be upregulated by the release of IL-6, IL-1β, and TNF-α [8]. The liver releases cytokines, acute-phase proteins, and coagulation factors and promotes the clearance of infectious factors and products, thus participating in the reaction to sepsis [9]. Nevertheless, it is not clear whether the possible molecular mechanisms of damage in the liver result from sepsis.
Efficacy and safety of adalimumab in Japanese patients with psoriatic arthritis and inadequate response to non-steroidal anti-inflammatory drugs (NSAIDs): A prospective, observational study
Published in Modern Rheumatology, 2020
Akimichi Morita, Ryuhei Okuyama, Norito Katoh, Chiharu Tateishi, Koji Masuda, Toshifumi Komori, Eisaku Ogawa, Takamitsu Makino, Emi Nishida, Shohei Nishimoto, Kenzo Muramoto, Daisuke Tsuruta, Hironobu Ihn
Tumor necrosis factor-α (TNF-α) is pivotal to the chronic inflammation and aberrant immune responses associated with rheumatoid arthritis (RA), psoriasis, and PsA, and is present in higher concentrations in the joints and skin of patients with PsA than those without [8,9]. In addition to the aforementioned genotypic differences, population differences exist with regard to an association between TNF-α gene polymorphisms and PsA; for example, an association was not found in Japanese studies but was observed, especially with regard to joint erosion in early PsA, in studies involving Caucasians [10]. Biologic agents that inhibit TNF-α (e.g. etanercept, infliximab, and adalimumab) are efficacious in the treatment of RA, psoriasis, and PsA either as monotherapy or in combination with methotrexate [1,2,11–16]. In a study in a clinic setting, methotrexate was associated with a significant increase in radiographic damage compared to TNF-α blockers in patients with erosive PsA [17]. Moreover, according to the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2015 treatment recommendations for PsA, TNF-α inhibitors are strongly recommended in patients with inadequate response to DMARDs or other biologics, regardless of clinical manifestation (peripheral PsA, axial PsA, enthesitis, dactylitis, psoriasis, and nail psoriasis) [18].