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Relevant bibliographies by topics / Chronic inflammatory

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Academic literature on the topic 'Chronic inflammatory'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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Journal articles on the topic "Chronic inflammatory"

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Elia, Domenico. "Chronic Inflammatory Arthritis: Ankylosing Spondylitis." Spinal Diseases and Research 1, no. 1 (2018): 01–03. http://dx.doi.org/10.31579/jsdr.2018/004.

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singh, Jagroop. "Inflammatory Markers in Chronic Kidney Disease." Journal of Virology and Vaccination 1, no. 1 (2023): 01–05. http://dx.doi.org/10.58489/2836-6387/004.

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Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting. Material and methods; This study was conducted on CKD patients attending OPD & IPD of Civil Hospital tarn taran. The participants having age more than 18 years & less than 60 years. We assessed 120 individuals out of 60 are normal healthy individuals comprising the control groups & rest 60 is of CKD cases. Serum CRP (mg/dl) concentration was measured by Latex agglutination test & ESR (mm/hour) was measured by Wintrobe’s method. Serum Creatinine (mg/dl), Urea (mg/dl) & Uric acid (mg/dl) concentration was measured by Modified Jaffe’s method, Urease & Uricase method respectively. Results: - In the present study, serum CRP & ESR was increased in CKD patients. The mean serum CRP levels of CKD patients & controls were 33.55 ± 22.8 & 2.07 ± 6121 respectively (p< 0.001), highly significant result was observed. Mean level of serum ESR (40.25 ± 14.93) of cases shows statistical significant differences as compared with the mean of serum ESR of controls (13.50 ± 3.421). Conclusion: - CRP & ESR are the markers used to evaluate kidney disease, however, each of these has its own limitation. The use of these inflammatory biomarkers may better assess overall patients’ risk & be able to stage patients more appropriately.

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Millichap, J. Gordon. "Chronic Inflammatory Polyneuropathy." Pediatric Neurology Briefs 21, no. 2 (2007): 14. http://dx.doi.org/10.15844/pedneurbriefs-21-2-6.

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Millichap, J. Gordon. "Chronic Inflammatory Neuropathies." Pediatric Neurology Briefs 10, no. 8 (1996): 57. http://dx.doi.org/10.15844/pedneurbriefs-10-8-1.

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Millichap, J. Gordon. "Chronic Inflammatory Polyradiculoneuropathy." Pediatric Neurology Briefs 11, no. 12 (1997): 92. http://dx.doi.org/10.15844/pedneurbriefs-11-12-6.

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Harbuz, Michael S. "Chronic inflammatory stress." Best Practice & Research Clinical Endocrinology & Metabolism 13, no. 4 (1999): 555–65. http://dx.doi.org/10.1053/beem.1999.0043.

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Seksik, Philippe. "Chronic inflammatory proctitis." Hépato-Gastro & Oncologie Digestive 31, no. 5 (2024): 506–8. http://dx.doi.org/10.1684/hpg.2024.2768.

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Rathore, Hemlata, Brijesh Rathore, and Seema Singh. "RHEUMATOID ARTHRITIS: A CHRONIC INFLAMMATORY DISEASE AND ITS PATHOPHYSIOLOGY." Era's Journal of Medical Research 6, no. 1 (2019): 88–92. http://dx.doi.org/10.24041/ejmr2019.113.

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Patel, Vikas, Rutvik Patel, Pratap V Lakum, and M. J Sonagara. "Sensory Motor Chronic Inflammatory Demyelinating Polyneuropathy in Upper Limbs." International Journal of Science and Research (IJSR) 11, no. 10 (2022): 673–74. http://dx.doi.org/10.21275/mr221013142831.

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Groß, V., T. Andus, H. G. Leser, M. Roth, and J. Schölmerich. "Inflammatory mediators in chronic inflammatory bowel diseases." Klinische Wochenschrift 69, no. 21-23 (1991): 981–87. http://dx.doi.org/10.1007/bf01645143.

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Dissertations / Theses on the topic "Chronic inflammatory"

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Cauli, Alberto. "The inflammatory milieu in chronic arthritis." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322233.

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Cexus, Olivier. "Immunological mechanisms controlling chronic inflammatory diseases." Thesis, University of Southampton, 2009. https://eprints.soton.ac.uk/67634/.

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Autoimmune diseases (AID) are chronic inflammatory diseases (CID) mediated by selfreactive T and B cells and are generally the results of the breakdown of T cell tolerance to self-antigen and failure of peripheral regulatory mechanisms. In this thesis I studied different mechanisms controlling the development of CIDs. I investigated the initial events involved in the activation of self-reactive CD4+ T cells which mediate the destruction of the thyroid in a mouse model of spontaneous thyroiditis. TAZ10 transgenic mice express a human T cell receptor (TCR) specific for a cryptic epitope of thyroid peroxidise (TPO) generated upon endogenous processing by thyroid epithelial cells (TEC), and a naturally occurring antagonistic epitope presented by dendritic cells (DC) upon exogenous processing of TPO. I have characterized the function of myeloid derived suppressor cells (MDSCs) in TAZ10 mice. MDSCs accumulate in lymphoid and non-lymphoid organs of TAZ10 mice during acute phases of inflammation and their number decrease as inflammation is fading. Despite their strong inhibitory function on T cell function and proliferation, MDSCs fail to prevent the activation of self-reactive T cells. I showed that the manipulation of MDSCs generated DCs that efficiently promoted the activation of T cells from TAZ10 mice. By contrast, peripheral T cells from patients with rheumatoid arthritis (RA) and lupus had a high proliferative activity compared to controls. Further analysis revealed that RA patients had reduced amounts of inhibitory MDSCs in peripheral blood. I showed that in TAZ10 mice TEC upregulate MHC class II molecules and present the cryptic epitope to TAZ10 T cells inducing their activation. I have demonstrated that DCs are responsible for the spreading of the TPO cryptic epitope from the thyroid to draining lymphnodes (DLN) resulting in the strong activation of transgenic T cells from TAZ10 mice. By adoptive transfer experiments, I showed that the activation of naive TAZ10 T cells occurs within days both in the thyroid and draining lymph-nodes (DLN) and resulted in the destruction of the thyroid. Altogether, this work shows for the first time that in a model devoid of any environmental insults, the normal turnover of TEC is sufficient to induce the activation of self-reactive T cells and the development of AID. In this thesis, I have highlighted the potential role of tissue transglutaminse 2 (TG2) in the treatment of CIDs. TG2 contributes to the pathogenesis of celiac disease and I have showed that TG2 activity promotes inflammation in patients with cystic fibrosis (CF). Mutation of the cystic fibrosis transmembrane regulator gene (CFTR) in CF patients is associated with increased TG2 expression and activity. In CF, TG2 promoted the crosslinking of the antiinflammatory peroxisome proliferator-activated receptor (PPAR) into perinuclear agresomes. The functional sequestration of PPAR was leading to increased inflammation. The finding of this function of TG2 in CF was relevant in TAZ10 mice as in-vivo inhibition of TG2 downregulated common markers of inflammation.

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Hood, Vivienne Claire. "Neurogenic influences on chronic inflammatory joint disease." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252151.

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Roberts, Helen Michelle. "Neutrophil function in chronic inflammatory disease states." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/7018/.

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Inflammation is a central component of the immune response. In its acute form it aids the transition from disease to health via the activation of numerous immune cells, enabling them to reach the site of infection/injury and orchestrate themselves to combat pathogens, facilitating resolution and repair to restore the host to health. However, chronic inflammation is deleterious to the host and differs from the “classical” acute inflammatory process in that the inflammation is not necessarily so readily obvious and is not self-limiting; rather, the immune system is in a constant state of low-grade activation and when challenged by pathogenic or sterile injury the response is heightened, resulting in prolonged tissue damage and a failure of efficient resolution mechanisms. Neutrophils are important mediators of acquired innate immune responses but may also contribute to the pathogenesis of chronic inflammatory diseases. Neutrophils are heavily involved in antimicrobial defence; their primary role is the localisation and elimination of pathogenic microorganisms. This, combined with their relatively short lifespan, has resulted in a traditional view of them as limited “kamikaze” cells. However, as detailed here, neutrophils have been shown to act with complexity and sophistication, orchestrating the immune/inflammatory response but also inadvertently contributing to tissue damage in different disease states. This thesis includes the study of neutrophil function in acute inflammatory episodes such as gingivitis and more chronic long-term health conditions such as obesity, chronic periodontitis and Papillon-Lefèvre Syndrome. The findings outlined here support the role of neutrophils as important contributors to both acute and chronic disease, showing these cells to be far more sophisticated than previously regarded.

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Yan, Wei Xing. "Target antigen in chronic inflammatory demyelinating polyradiculoneuropathy." Thesis, The University of Sydney, 2001. https://hdl.handle.net/2123/27718.

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The primary purposes of this study were to investigate humoral factors in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), to determine pathogenicity of the factors found, and to detect possible target antigens in CIDP. Sera from 22 CIDP patients of whom 12 responded to plasma exchange therapy and 10 needed other therapy, were tested by means of enzyme-linked immunosorbent assay, immunofluorescence and Western blot techniques. Anti-whole myelin, anti-myelin glycoproteins (e.g. P0, P2, PMP22 and myelin associated glycoprotein), anti-myelin glycolipids (e.g. GMl, GM2, Gle, GDla, Gle, Gal-C and Gal-S) antibodies and complement reactivity were detected. Using systemic administration after opening the blood-nerve barrier (BNB) and intraneural injection, Lewis rats were assessed electrophysiologically, morphologically and clinically before and after administrated CIDP serum. Methods of antibody purification and protein sequencing were also applied. The results revealed that one or more antibodies to whole peripheral nerve myelin, myelin glycolipids (GMl, Gle, Qle, GM2 and Gal-S) and myelin glycoproteins (P0) and complement (C3) reactivity were found in 16 (73%) of 22 CIDP sera. Six had anti—P0 IgG antibody, four of which had antimyelin IgG antibody and C3 reactivity. Five had anti-myelin IgM antibody, of which four were directed against gangliosides and two showed C3 reactivity. Five had anti-ganglioside antibody, of which two showed C3 reactivity. One had C3 reactivity alone. Five had neither anti-PO, anti-myelin or anti— ganglioside antibody, nor C3 reactivity. No sera had detectable antibodies to myelin associated glycoprotein, PMP22, P2, GDla or Gal-C. Pathogenicity to peripheral nerve was demonstrated in four of six sera which contained IgG anti-P0 antibody and C3 reactivity. Conduction block and demyelination were induced by intraneural injection of these four sera and their IgG, and by systemic transfer when the BNB had been opened by activated T cells. The specificity of the antigen-antibody reaction was displayed by the binding of F(ab)2 to the P0 protein. Loss of pathogenicity was showed following absorption by P0 but not by P2. Protein sequencing showed that the target antigen is a 30kDa peripheral nervous system myelin protein, the P0 protein.

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Thornton, Catherine Clare. "Mechanisms of vascular protection in chronic inflammatory disease." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/26595.

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Premature cardiovascular disease (CVD) complicates chronic systemic inflammatory disease, and is initiated by endothelial dysfunction. Despite an ever-improving array of medications to treat these diseases, how to prevent CVD is not known. Studying the actions of endogenous mediators of endothelial cytoprotection and of disease-modifying drugs might establish how best to protect patients with systemic inflammatory diseases from atherosclerosis, if specific beneficial effects on vascular endothelium could be demonstrated. High flow laminar shear stress (LSS) and vascular endothelial growth factor (VEGF) are two well known endogenous drivers of endothelial cytoprotection. Both can induce expression of protective genes but it is not known how confluent endothelial cells (EC) respond to VEGF when conditioned with LSS. Methotrexate (MTX) is the most widely prescribed treatment for rheumatoid arthritis and clinical data suggests that it reduces CV mortality. Known mechanisms of action of MTX result in intracellular accumulation of activators of AMP-activated protein kinase (AMPK). AMPK regulates cytoprotective genes in EC and its activation is associated with diverse desirable effects. I hypothesised that EC conditioned with LSS would be primed to respond to VEGF, resulting in a synergistic induction of cytoprotective genes. Secondly I investigated whether MTX exerts beneficial protective effects on vascular endothelium via activation of AMPK, which enhance endothelial resistance to injury. Studies of human umbilical vein EC (HUVEC) exposed to LSS showed that responses to VEGF are not enhanced in these conditions. However, MTX phosphorylated AMPKαThr172 and induced expression of several cytoprotective genes, notably manganese superoxide dismutase (MnSOD). The addition of folic acid did not alter this; and it was also preserved when HUVEC were pre-treated with TNFα to mimic dysfunctional endothelium. siRNA depletion of AMPK attenuated MTX-mediated MnSOD induction. MTX treatment led to AMPK-dependent phosphorylation of the transcription factor CREBSer133. siRNA depletion of CREB also reduced MnSOD induction by MTX, and chromatin immunoprecipitation demonstrated binding of CREB to the MnSOD promoter in MTX-treated samples. Moreover, MTX protected HUVEC against apoptosis induced by glucose deprivation, demonstrating the functional importance of this pathway. Finally, treatment of the murine (BXSB x NZW)F1 SLE model of inflammatory vasculopathy with MTX improved the intramyocardial arterial vasculopathy and reduced end-organ damage, increased aortic MnSOD and phosphorylated AMPKαThr172, and reduced ICAM-1 expression. I have shown that MTX activates an AMPK-CREB pathway in vascular endothelium leading to enhanced expression of cytoprotective genes and protection against apoptosis in vitro and inflammatory vascular injury in vivo. This novel mechanism may explain its observed benefits in reducing CVD in chronic systemic inflammation.

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Raunio, T. (Taina). "Gene polymorphism and systemic inflammatory response in chronic periodontitis." Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514292361.

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Abstract In this study, associations between periodontitis expression, serum levels of inflammatory markers and genetic factors were investigated. The periodontal status of 56 subjects with chronic periodontitis, 28 control subjects and 80 subjects with type I diabetes mellitus (DM) was examined. In addition, a reference group (n=178) with genetic but not with periodontal health data was included. The single nucleotide polymorphisms of CD14 -260, IL-6 -174, TNF-α -308, IL-10 -1082, IL-1A -889, IL-1B +3954, and TLR4 +896 were determined using PCR with RFLP or allele-specific primers, and comparisons of the genotype frequencies were made between the study groups and reference subjects. The serum concentrations of IL-6 and sCD14 were assayed using ELISA. The distributions of all the studied genotypes were similar in the periodontitis and the reference subjects. However, in the periodontitis group, the carriage of the T-containing genotype of the CD14 -260 and the GG genotype of the IL-6 -174 associated significantly with the extent of periodontitis, indicating that genetic factors play a role in the pathogenesis of the disease. Both the extent of periodontal infection and the IL-6 -174 genotype were significant determinants for the serum IL-6 level, subjects carrying the GG genotype having significantly higher serum IL-6 levels than those carrying the CC/CG genotype. The serum level of sCD14 was significantly higher in subjects carrying the T-containing than the CC genotype of the CD14 -260 in the control group but not in the periodontitis group, suggesting that severe periodontal infection overshadows the influence of the genotype on serum sCD14 level. Overall, the serum studies indicated that periodontal infection is associated with a low-grade systemic inflammatory response. Type 1 DM subjects carrying the GG genotype of the IL-6 -174 had a higher extent of periodontitis when compared with those carrying the CG/CC genotype. Our results also suggest that the IL-6 -174 genotype is a more significant determinant of the extent of periodontitis in type 1 DM than glycemic control.

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Saha, Shironjit K. "Inflammatory profiles in chronic obstructive pulmonary disease and asthma." Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/8206.

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Historically, asthma and chronic obstructive pulmonary disease (COPD) represent polar ends of the spectrum of airways disease defined in part by distinctive profiles of airway inflammation; in practice, overlap can exist between asthma and COPD. This thesis examined the pattern of inflammatory cell infiltration and cytokine expression within the bronchus in COPD and asthma with further study of moderate-severe asthma. In addition using sputum, cytokine expression was further assessed in COPD and asthma and its relation to severity. Based on previous studies, this thesis examined the expression of specifically Interleukin (IL)-13 and Granulocyte Macrophage Colony Stimulating Factor (GMCSF). We demonstrated mast cell myositis in moderate and severe asthma which reflected increased disease symptoms. Preferential localization of inflammatory cells to airway smooth muscle (ASM) was absent in COPD. CD3+ T-cells infiltration of large airway glands was increased in COPD which may influence mucus hyper-secretion. We demonstrated IL-13 overexpression within the submucosa in moderate-severe asthma with specific increase in the ASM in severe disease. IL-13 expression was related to eosinophilic inflammation. In sputum, IL-13 protein was increased in mild and severe asthma reflecting IL-13 expression in ASM. There was a general absence of bronchus and sputum IL-13 in COPD. Sputum GMCSF was increased in moderate-severe asthma and mild-severe COPD. Parallel upregulation of GMCSF and associated receptor (GMCSFr) expression in the submucosa and ASM was present in severe asthma. GMCSF/GMCSFr expression did not exhibit preferential expression in the large airway of COPD. Our findings suggest inflammatory cell infiltration of the airway structures is present in asthma and COPD which may influence the phenotype. In addition IL-13 is important in severe asthma whilst GMCSF is expressed in asthma and COPD across a range of severity, but to a greater degree in severe asthma.

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Arsenescu, Violeta. "ROLE OF ARYL HYDROCARBON RECEPTOR IN CHRONIC INFLAMMATORY DISEASES." UKnowledge, 2009. http://uknowledge.uky.edu/gradschool_diss/772.

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Aryl Hydrocarbon Receptor (AhR) is a ligand-actviated receptor known as the dioxin receptor. Environmental pollutants called dioxin-like toxicants are found in food, cigarette smoke, automobile exhaust and air. Therefore, they could chronically amplify the pathology of numerous chronic inflammatory diseases. AhR is a well known target of these environmental chemicals that disrupt endocrine signaling. By the year 2020, the number of people older than 60 years is expected to top 1 billion. The burden of treating chronic disease is significant both in dollars spent and in lost productivity. The need to identify risk factors for chronic diseases must be evaluated along with diet and lifestyle factors that will promote healthy aging. The studies presented in this dissertation tested the hypothesis that habitual exposure to dioxin-like contaminants contributes to chronic inflammatory disease states through activation of AhR pathway. Due to their lipophilicity, dioxin like toxicants (like PCB 77) accumulated in mice' visceral adipose tissue and induced adipocytes maturation and ectopic fat deposition. Exposure to persistent organic pollutants, such as polychlorinated biphenyls (PCB 77) can cause endothelial cells activation and inflammation by inducing pro-inflammatory signaling pathways. In our studies, PCB 77 had cumulative effects in Angiotensin II - induced Abdominal Aortic Aneurysm (AAA) by exacerbating inflammation in and around the aortic wall. More, PCB 77 increased mortality in mice that developed AAA. In order to appreciate the AhR involvement in inflammation we used a mouse model of Inflammatory Bowel Disease(IBD). Mice that had a reduced Ahr Receptor expression developed a less severe colitis and had a decreased general inflammatory status. These data provide evidence that exposure to environmental toxicants could augment inflammation and contribute to the social burden of obesity and obesity related chronic inflammatory diseases.

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Bethune, Jörn [Verfasser]. "Network-Assisted Analysis of Chronic Inflammatory Diseases / Jörn Bethune." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/1118499875/34.

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Books on the topic "Chronic inflammatory"

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Persson, Carl G. A., Ralph Brattsand, Lauri A. Laitinen, and Per Venge, eds. Inflammatory Indices in Chronic Bronchitis. Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7488-5.

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A, Persson C. G., ed. Inflammatory indices in chronic bronchitis. Birkhäuser, 1990.

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Gupta, Subash Chandra, Sahdeo Prasad, and Bharat B. Aggarwal, eds. Anti-inflammatory Nutraceuticals and Chronic Diseases. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41334-1.

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T, Macdonald Thomas, and Walker-Smith J. A, eds. Chronic inflammatory bowel disease in childhood. Baillière Tindall, 1994.

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Jonathan, Barker, ed. Clinical diagnosis: Chronic inflammatory skin diseases. London, 1998.

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Chellappan, Dinesh Kumar, Kavita Pabreja, and Md Faiyazuddin, eds. Advanced Drug Delivery Strategies for Targeting Chronic Inflammatory Lung Diseases. Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-4392-7.

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Clements, David Graham. Bone density in inflammatory bowel disease and chronic active hepatitis. University of Birmingham, 1993., 1993.

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Gross, Gerhard, and Thomas Häupl. Stem cell-dependent therapies: Mesenchymal stem cells in chronic inflammatory disorders. De Gruyter, 2013.

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Burman, Angela Claire. The role of leukocyte - stromal interactions in chronic inflammatory joint disease. University of Birmingham, 2003.

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Research & Forecasts, Inc., ed. Arthritis and other chronic pain conditions: Problems associated with drug therapy. Research & Forecasts, 1985.

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Book chapters on the topic "Chronic inflammatory"

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Rossi, Armando, and Giorgio Rossi. "Chronic Inflammatory Diseases." In CT of the Peritoneum. Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56488-8_7.

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McCann, Liza, Michael W. Beresford, Gabriele Hahn, and Christian M. Hedrich. "Chronic Nonbacterial Osteomyelitis." In Auto-Inflammatory Syndromes. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-96929-9_17.

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Makide, Kumiko, Asuka Inoue, and Junken Aoki. "Lysophosphatidylserine as an Inflammatory Mediator." In Chronic Inflammation. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_38.

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Grisham, M. B., S. Aiko, and T. E. Zimmerman. "Nitric oxide and chronic colitis." In Inflammatory Bowel Disease. Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_12.

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Van den Bergh, P. Y. K., R. D. M. Hadden, Pierre Bouche, et al. "Chronic Inflammatory Demyelinating Polyradiculoneuropathy." In European Handbook of Neurological Management. Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328394.ch20.

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Kuwabara, Satoshi, and Sonoko Misawa. "Chronic Inflammatory Demyelinating Polyneuropathy." In Advances in Experimental Medicine and Biology. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9636-7_21.

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Khadilkar, Satish V., Rakhil S. Yadav, and Bhagyadhan A. Patel. "Chronic Inflammatory Demyelinating Polyradiculoneuropathy." In Neuromuscular Disorders. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5361-0_38.

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Hund, Ernst F., Hans-Peter Hartung, Allan H. Ropper, and Daniel F. Hanley. "Chronic Inflammatory Demyelinating Polyneuropathy." In Neurocritical Care. Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-87602-8_68.

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Benatar, Michael. "Chronic Inflammatory Demyelinating Polyradiculoneuropathy." In Neuromuscular Disease. Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-106-2_12.

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Suzuki, Miki, and Gérard Said. "Chronic Inflammatory Demyelinating Polyneuropathy." In Neuroimmune Diseases. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19515-1_25.

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Conference papers on the topic "Chronic inflammatory"

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Abla, Hedia Ben, Sonia Rekik, Samia Jammali, et al. "AB0299 COXITIS DURING CHRONIC INFLAMMATORY RHEUMATISM." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3829.

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Gapeshin, R. A., E. R. Barantsevich, D. I. Rudenko, and T. R. Stuchevskaya. "Timeframes for chronic inflammatory demyelinating polyneuropathy diagnosis." In Scientific achievements of the third millennium. LJournal, 2019. http://dx.doi.org/10.18411/scienceconf-05-2019-20.

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Borges, Isabella Sabião, João Victor Aguiar Moreira, Eustaquio Costa Damasceno Junior, et al. "Chronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.413.

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Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.

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Viana, Izabela Prado, Renata Borges de Lima, Ana Paula Rodrigues Oliveira, et al. "CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY IN A SLE PATIENT." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.2191.

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Hmimass M, Saber, Driss Azzouzi, Mohamed Borahma, et al. "P320 Metabolic steatopathy and chronic intestinal inflammatory disease." In BSG LIVE’24, 17-20 June 2024, ICC Birmingham. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2024. http://dx.doi.org/10.1136/gutjnl-2024-bsg.402.

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Roc, Marta Valls, Meritxell Sallés Lizarzaburu, Sonia Mínguez Blasco, et al. "AB1108 COEXISTENCE OF SARCOIDOSIS AND CHRONIC INFLAMMATORY RHEUMATIC DISEASES." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.2834.

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Borker, P. V., B. Macatangay, A. Morris, and S. R. Patel. "Sleep Apnea and Inflammatory Markers in Chronic HIV Infection." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4688.

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Lavras Costallat, Lilian Tereza, Paulo Rogério Julio, Mateus De Miranda Moura Cortês, Juliana Zonzini Gaino, Marcondes Cavalcante França Junior, and Simone Appenzeller. "CHRONIC INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY ASSOCIATED WITH SYSTEMIC LUPUS ERYTHEMATOSUS." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17167.

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Wang, Weihua, Wei le, Gabriel Tsao, Do-Yean Cho, Peter H. Hwang, and D. Upadhyay. "The Regulation Of Inflammatory Cytokines In Chronic Airway Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4218.

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Stulberg, Eric, Michael Chamberlain, Yoji Hoshina, Piotr Tekiela, and Kyle Mahoney. "Microscopic Polyangiitis Mimicking Chronic Inflammatory Demyelinating Polyneuropathy (P13-8.013)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000204183.

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Reports on the topic "Chronic inflammatory"

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Shilova, L. N., and S. S. Spitsina. LIPID EXCHANGE DISORDERS IN PATIENTS WITH CHRONIC INFLAMMATORY JOINT DISEASES. DOI CODE, 2021. http://dx.doi.org/10.18411/wco-iof-esceo-2021-386.

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González Lara, Cristina, and Irene Cortés Pérez. EFFECTIVENESS OF IMMERSIVE VIRTUAL REALITY IN REDUCING PELVIC PAIN IN PATIENTS WITH ENDOMETRIOSIS:A SYSTEMATIC REVIEW. Fundación Avanza, 2025. https://doi.org/10.60096/fundacionavanza/1952025.

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Endometriosis (EM) is a chronic inflammatory disease characterized by the presence of endometrium-like tissue outside the uterus, often leading to severe symptoms. This systematic review aimed to evaluate the effectiveness of IVR interventions.

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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, et al. Physical activity, abdominal obesity and inflammatory response in the elderly: a systematic review and meta-analysis of randomized-controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.

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Review question / Objective: The purpose of this study was to explore the effects of physical activity (i.e., type of exercise, FITT criteria, control group, other interventions) on abdominal obesity and inflammatory response in elderly? The study method was a randomized controlled trial. Condition being studied: An increasing number of studies have demonstrated that chronic inflammation is closely associated with the initiation and progression of a broad range of age-related diseases, such as cardiovascular disease, cancer, diabetes, Alzheimer’s disease, and other neurodegenerative diseases and is an independent risk factor for mortality in healthy adults. Moreover, there is strong evidence that the development of age-related diseases is linked to low-grade elevation of circulating inflammatory mediators. Therefore, future interventional researches should focus on preserving overall homeostatic balance and controlling inflammatory status in the aging patient.

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ZARATE, NASHELY NICKOL CHAVEZ, NICOLL SARAÍ RIVERA LEDEZMA, CESAR ALONSO PONCE LOZANO, and Martin Andres Chavez Mendez. Clinical effectiveness of the infrared diode laser (810-980 nm) in conjunction with scaling and root planing in comparison with scaling and root planning alone (placebo) in the non-surgical treatment of periodontitis: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0037.

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Review question / Objective: What is the efficacy of the use of diode laser (810-980 nm) in association with scaling and root planing compared to scaling and root planing alone (placebo) in the non-surgical treatment of periodontitis? Condition being studied: Periodontitis is a chronic multifactorial inflammatory disease associated with a dysbiotic biofilm and characterized by progressive destruction of the tooth-supporting apparatus, which can lead to toothloss.

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Spitsina, S. S., L. N. Shilova, A. S. Trofimenko, et al. ASSESSMENT OF QUALITY OF LIFE IN PATIENTS WITH CHRONIC INFLAMMATORY DISEASES OF THE JOINTS ON BASIC THERAPY WITH METHOTREXATE. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-164-168.

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Guede-Rojas, Francisco, Alexis Benavides-Villanueva, Sergio Salgado-González, Cristhian Mendoza, Gonzalo Arias-Álvarez, and Claudio Carvajal-Parodi. Effect of strength training on knee proprioception in patients with knee osteoarthritis. A systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.5.0102.

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Review question / Objective: To analyze the effect of strength training (ST) on knee proprioception in patients with knee osteoarthritis (KOA). Condition being studied: KOA is a chronic and degenerative joint disease characterized by articular cartilage loss, marginal bone hypertrophy, and inflammatory involvement of periarticular tissue of the knee. Symptoms of KOA are pain, stiffness, reduced range of motion, and muscle weakness, although proprioception may also be affected, contributing to the associated functional limitation.

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Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta та Alfredo J. Lucendo. Influence of HLA-DQA1*05 allele in the response to anti-TNFα drugs in inflammatory bowel diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.2.0076.

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Review question / Objective: Do patients with inflammatory bowel disease and treated with any anti-TNFα drug who had the HLA-DQA1*05 allele (in heterozygosis or homozygosis) have lower response or persistence to those drugs than patients without HLA-DQA1*05 allele? Condition being studied: Inflammatory bowel diseases (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition that may affect any part of the digestive tract (CD) or be limited to the colon (UC). While the specific aetiology of IBD remains unknown, it is believed to involve a complex impairment in the immunity of the gut mucosa due to a combination of several genetic and environmental factors, being the microbiota one of the latest that more attraction has received in recent years. Symptoms of IBD (such as abdominal pain, diarrhoea, fever, tiredness or rectal bleeding) may be either constant or alternate between periods of limited disease activity and flares with remarkable presence of symptoms. As IBD is associated with significant morbidity and disability, pharmacological treatment is required in most cases, especially in CD, aimed at reducing the inflammatory response and attenuating the activity of the immune system. In the moderate and severe forms of the disease, therapy is usually based on immunosuppressant and/or biological drugs. Among the latest, anti-TNFα drugs (infliximab or adalimumab) are normally chosen as the initial biological therapy.

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Chen, Haofeng, xinyue Huang, Yifang Bao, Chongbo Zhao, and Jie Lin. The diagnostic value of quantitative assessment of MR neurography in chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.5.0088.

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Czerwaty, Katarzyna, Karolina Dżaman, Krystyna Maria Sobczyk, and Katarzyna Irmina Sikrorska. The Overlap Syndrome of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.11.0077.

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Review question / Objective: To provide the essential findings in the field of overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea, including prevalence, possible predictors, association with clinical outcomes, and severity compared to both chronic obstructive pulmonary disease and obstructive sleep apnea patients. Condition being studied: OSA is characterized by complete cessation (apnea) or significant decrease (hy-popnea) in airflow during sleep and recurrent episodes of upper airway collapse cause it during sleep leading to nocturnal oxyhemoglobin desaturations and arousals from rest. The recurrent arousals which occur in OSA lead to neurocognitive consequences, daytime sleepiness, and reduced quality of life. Because of apneas and hypopneas, patients are experiencing hypoxemia and hypercapnia, which result in increasing levels of catecholamine, oxidative stress, and low-grade inflammation that lead to the appearance of cardio-metabolic consequences of OSA. COPD is a chronic inflammatory lung disease defined by persistent, usually pro-gressive AFL (airflow limitation). Changes in lung mechanics lead to the main clini-cal manifestations of dyspnea, cough, and chronic expectoration. Furthermore, patients with COPD often suffer from anxiety and depression also, the risk of OSA and insomnia is higher than those hospitalized for other reasons. Although COPD is twice as rare as asthma but is the cause of death eight times more often.

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Tang, Xiangqi, Xiaoqian Guo, Lisha Tang, and Qianyi Huang. Explore the correlation between IgG4 antibodies against (para)nodal proteins and prognosis of patients with chronic inflammatory demyelinating polyradiculoneuropathy via meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.6.0078.

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