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Enteroviruses
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Karen Straube-West, Burk Jubelt
Most enteroviral infections are inapparent (subclinical) [13]. Occasionally gastrointestinal infection may result in nausea, vomiting, abdominal discomfort, and loose stools. If viremia occurs, systemic manifestations may be seen. The most common (>50%) systemic illness of enteroviral infection is nonspecific febrile illness. The fever is manifested at 38.5°C–40°C and lasts an average of 3 days. Occasionally there is a biphasic pattern with fever for 1 day followed by 2–3 days of normal temperature, then fever again for 2–4 more days. Other symptoms that might present are malaise, myalgia, headache, sore throat, and mild conjunctivitis. Generally, after these symptoms clear the patient makes a complete and uneventful recovery. Because up to 50% of enteroviral infections are asymptomatic or cause only a mild febrile illness it is believed that many cases go undiagnosed or unreported. A seroepidemiological study conducted in New York found that 26% of the adult population had been exposed to an enterovirus [17] supporting the hypothesis that enteroviral infections are far more common than the reported number of cases would suggest.
Specific Effect of Infection and Malnutrition on Intestinal Longitudinal Smooth Muscle Response in Yersinia Enterocolitica Enteritis in the Rabbit
Published in William J. Snape, Stephen M. Collins, Effects of Immune Cells and Inflammation on Smooth Muscle and Enteric Nerves, 2020
Gastrointestinal infection is a common condition, the clinical manifestations of which may include abdominal cramping, emesis, and diarrhea. These signs and symptoms may reflect associated alterations of gastrointestinal smooth muscle contractility, or patterns of intestinal motor activity. However, specific abnormalities of contractility or motility patterns and the mechanism of their induction remain to be clarified.
Diarrhea in Short Bowel Syndrome
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
Badr Al-Bawardy, Vandana Nehra
The approach to diarrhea in SBS starts with an evaluation of the potential etiology excluding readily correctable causes not directly related to the altered bowel anatomy. This includes a careful review of the medication list and discontinuing possible offending medications. In addition, underlying gastrointestinal infection, particularly C. difficile, should be evaluated. The presence of active underlying bowel disease such as Crohn’s disease, radiation enteritis, celiac disease, or microscopic colitis should be investigated and treated when present. Partial or intermittent small bowel obstruction, especially in ostomy patients, can result in diarrhea and should be investigated with radiographic and/or endoscopic imaging. Once this initial evaluation is completed, when diarrhea persists, the management should focus on the altered bowel anatomy and the variety of mechanisms potentially contributing to the diarrhea as described previously. This includes incorporating dietary and fluid modifications based on the remaining bowel anatomy, treating gastric acid hypersecretion, judicious use of antimotility agents, treating SIBO when identified, and, occasionally, considering a trial of pancreatic enzymes if there is concern of mismatch of nutrient and enzyme mixing (Figure 5.1).
Ophthalmoplegia associated with anti-GQ1b antibodies: case report and review
Published in Orbit, 2023
Camille Yvon, Dominic Nee, Dennis Chan, Raman Malhotra
It is thought that the conditions hold a common immune-mediated etiology, where macrophages, T cells and serum antibodies are activated against gangliosides following a viral or bacterial infection (e.g. Campylobacter jejuni, Cytomegalovirus, Epstein–Barr virus, Haemophilus influenzae, Human Immunodeficiency Virus and possibly COVID-19).1,3–5 Animal model studies have demonstrated that molecular mimicry plays a key role.6 A lipooligosaccharide found in certain bacterial membranes (such as Campylobacter jejuni) is structurally close to gangliosides in the peripheral nerves.7 A natural immune response to the initial infection can hence induce a cross-reaction on host nerves, and result in anti-GQ1b antibody syndrome. Approximately two-thirds of patients describe preceding symptoms of upper respiratory tract or gastrointestinal infection.8 What predisposes patients to certain clinical phenotypes, however, remains unclear.
Randomized double-blinded controlled trial on the effect of synbiotic supplementation on IL-17/IL-23 pathway and disease activity in patients with axial spondyloarthritis
Published in Immunopharmacology and Immunotoxicology, 2023
Masoud Ahangari Maleki, Aida Malek Mahdavi, Mohammad Sadegh Soltani-Zangbar, Mehdi Yousefi, Alireza Khabbazi
This double-blind randomized placebo-controlled trial was carried out between December 2020 and November 2021 in the outpatient rheumatology clinic of Tabriz University of Medical Sciences (TUOMS). Inclusion criteria were: (i) axSpA diagnosis based on the Assessment of Spondylo Arthritis international Society (ASAS) criteria [26], (ii) age range between 20 and 60 years and (iii) fixed treatment regimen in the past three months. Exclusion criteria were: (i) consuming nutritional supplements or antioxidants one month before the study, (ii) pregnancy and breast-feeding, (iii) history of other autoimmune diseases, (iv) diabetes mellitus, (v) inflammatory bowel disease and current gastrointestinal infection and (vi) renal or hepatic failure. The sample size of 24 cases for each group was calculated taking into account the previous research information and assuming a 95% confidence level and 80% power [23]. The Ethics Committee of TUOMS approved the study protocol (ethics code: IR.TBZMED.REC.1398.591). In addition, the study was registered by the Iranian Registry of Clinical Trials (registration number: IRCT20190917044794N1). Participants were become aware regarding study and signed written informed consents. This study was performed in accordance with the Declaration of Helsinki and good clinical practice.
Intestinal inflammatory profile shows increase in a diversity of biomarkers in irritable bowel syndrome
Published in Scandinavian Journal of Gastroenterology, 2020
Leif Kyrre Berg, Rasmus Goll, Erik Fagerli, Judith Krey Ludviksen, Hilde Fure, Odd Sverre Moen, Sveinung W. Sørbye, Tom Eirik Mollnes, Jon Florholmen
One of the first reports suggesting IBS as a low-grade mucosal inflammatory disease was by Collins [8], but this hypothesis is still controversial [9]. Two features support this hypothesis: IBS is frequently seen both after a gastrointestinal infection [10] and in inflammatory bowel disease in remission [11]. However, the documentation of visceral hypersensitivity as a neuroimmune dysregulation in IBS is poor. At the level of mucosal immune cells, several reports describing increased number of T lymphocytes [12–14], mast cells [15,16] and degranulated mast cells [14,17]. Somewhat contradictory, decreased levels of T cells and mast cells have been reported [18] in post infectious and classical IBS. Moreover, various results have been reported for cytokines and chemokines at mucosal level: increased transcript levels of IL-1β [19] has been reported, decreased transcript levels were observed for IL-10 [20,21] and for the chemokines IL-8, CXCL-9 and MCP1 [22], an imbalance between TH1 and TH2 cytokines was observed [23], whereas no changes were observed for the proinflammatory TNF alpha, IL-6 and IL-beta [22]. Finally, in contrast to these reports, no significant differences between classical, non-postinfectious IBS and healthy control were found neither at the mucosal levels of immune cells nor at transcript levels [24,25]. Taken together, there are contradictory reports concerning the type of immune dysregulation involved if IBS can be explained as a low-grade inflammatory bowel disease.