Dissertations / Theses on the topic 'ARTHRITIS DRUG'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'ARTHRITIS DRUG.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
Allen, Rosamund Elizabeth. "Liposomes as drug delivery systems." Thesis, University of Essex, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.352982.
Full textWebster, Amy Philomena. "Epigenetics of response to biologic drug therapy in rheumatoid arthritis." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/epigenetics-of-response-to-biologic-drug-therapy-in-rheumatoid-arthritis(d1518a5c-ef1c-4d8f-b210-8a2342139a45).html.
Full textVugler, Alexander David. "Predicting anti-arthritic drug effects in collagen-induced arthritis using short-term mechanistic models of collagen II immunity." Thesis, Open University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.494617.
Full textGregg, Catherine Nicola. "Structure-activity studies in non-steroidal anti-inflammatory drugs." Thesis, Liverpool John Moores University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238686.
Full textSpeirs, A. "Gold chemistry and its use in the treatment of rheumatoid arthritis." Thesis, University of Strathclyde, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371977.
Full textMina, James. "Hyaluronic acid based polymer drug conjugates for the treatment of rheumatoid arthritis." Thesis, University of the West of Scotland, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.739391.
Full textKou, Eric Yao-Chung. "Child resistant drug packaging and arthritis can older consumers access their medications? /." Diss., Connect to online resource - MSU authorized users, 2006.
Find full textDunagan, Fiona M. "Non-steroidal anti-inflammatory drugs : pharmacokinetics and clinical response in rheumatoid arthritis." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236497.
Full textSingh, Jennifer. "Polymer-drug conjugates based on hyaluronic acid for the treatment of rheumatoid arthritis." Thesis, University of the West of Scotland, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415937.
Full textWalker, K. A. "An investigation into the mechanisms responsible for altered drug disposition in adjuvant-induced arthritis." Thesis, University of Aberdeen, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372625.
Full textPeltomaa, Ritva. "Outcome of early rheumatoid arthritis : with special reference to early institution of drug treatment." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/peltomaa2/.
Full textBarrie, Nicola. "ENDOCANNABINOID-BASED NANOPARTICLES TARGETED TO THE SYNOVIUM FOR THE TREATMENT OF ARTHRITIS." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/21185.
Full textNama, Nelisa Petronella Vuyo. "Potentiometric and spectrophotometric investigation of copper diclofenac as an anti inflammatory drug for the treatment of Rheumatoid Arthritis." Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/6349.
Full textCopper and Diclofenac (DCL) separately, are used to alleviate inflammation associated with RA. It has been postulated that their combination would have a synergistic effect i.e., their combination would be more effective than when administered independently. Cu(II)-DCL system is studied potentiometrically in order to evaluate this hypothesis.
Baecklund, Eva. "Associations Between Rheumatoid Arthritis and Malignant Lymphomas." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5928.
Full textAust, Julia Katharina. "Einfluss von Polymorphismen der Methylentetrahydrofolat Reduktase sowie des Multi-Drug-Resistance Proteins auf die Therapie der Rheumatoiden Arthritis mit Methotrexat." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-130248.
Full textKrasnitski, Raisa [Verfasser]. "Calprotectin bei DMARD (Disease Modifying Anti-Rheumatic Drug)-naiver früher rheumatoider Arthritis als Aktivitäts- und Verlaufsmarker unter Therapie / Raisa Krasnitski." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1228861064/34.
Full textHe, Bing. "Toward precision medicine: a combination of leflunomide and ligustrazine attenuates progressive bone erosion in rheumatoid arthritis patients with high baseline serum c-reactive protein level." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/316.
Full textSmith, Christine. "Efficacy and Safety of Pharmacological and Non-Pharmacological Interventions in Juvenile Idiopathic Arthritis: A Series of Systematic Reviews and Network Meta-Analyses." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35744.
Full textKnight-Schrijver, Vincent. "Towards systems pharmacology models of druggable targets and disease mechanisms." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289731.
Full textTettey-Amlalo, Ralph Nii Okai. "In vitro release of ketoprofen from proprietary and extemporaneously manufactured gels." Thesis, Rhodes University, 2005. http://eprints.ru.ac.za/295/.
Full textRafei, Moutih. "Fusokine design as novel therapeutic strategy for immunosuppression." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115882.
Full textAlong those lines, we also found that mesenchymal stromal cells (MSCs) lead to the paracrine conversion of CCL2 to an antagonist form capable of specifically inhibiting plasma cells and activated Th17 cells. This mechanistic insight informed the design of a second class of suppression fusokine. Namely, the fusing of antagonist CCL2 to GMCSF - aka GMME1. We tested its potential use in autoimmune diseases such as EAE and rheumatoid arthritis (RA). We demonstrated that GMME1 leads to asymmetrical signalling and inhibition of plasma cells as well as Th17 EAE/RA-reactive CD4 T-cells. The net outcome of these pharmacological effects is the selective depletion of CCR2-reactive T-cells as demonstrated both in vitro and in vivo.
Overall, our data support the use of our fusion proteins as part of a powerful and specific immunosuppressive strategy either as directly injectable protein biopharmaceuticals or through the ex vivo generation of autologous Bregs in the case of GIFT15.
Mendes, Mariana Trivilin. "Efeito de drogas sintéticas inibidoras do fator de necrose tumoral alfa na artrite reumatoide em ratos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-28102017-113448/.
Full textRheumatoid arthritis (RA) is an autoimmune, inflammatory, chronic and systemic disease with unknown etiology that can be experimentally induced in animals by administration of collagen and adjuvant (CIA). Biological drugs against tumor necrosis factor (TNF)- α are therapeutic indications currently consolidated for the most severe cases of RA. The limitations for the use of this class of drugs have been the high cost and the difficulty to manufacture a generic or similar ones with equivalent composition, quality and performance under the same dosage and route of administration. The present study evaluated the hypothesis that synthetic drugs that inhibit the production of TNF-α and/or related factors would have potential to become efficient complementary or alternative therapies for this disease. For this purpose, male rats submitted to the CIA model were chronically treated with pentoxifylline (PTX), rolipram (ROL), thalidomide (TAL) and rupatadine (RUP). The treatment with prednisolone (PRED) was also performed to evaluate its influence on the possible antiarthritic action of PTX, ROL, TAL and RUP, in order to mimic its immunosuppressive effect when acutely (AG) administered prior to biological drugs, as well as due to its known anti-inflammatory effect when administered chronically (CR) to treat RA. The development of RA and the efficacy of these drugs on RA were evaluated, by selective and sequential ways, through the detection of erythema and cyanosis, as well as measurements of edema, body mass, hemogram, plasma TNF-α, rheumatoid factor (FR) and anti-nuclear antibody (ANA) in serum, interleukin (IL)-1β and IL-6 in serum and synovial fluid, basic aminopeptidase activity (APB) in soluble fraction (FS) from synovial tissue (TS) and from peripheral blood mononuclear cells (PBMCs), bone densitometry and histological analysis. The hepatotoxicity of these drugs was evaluated by measurements of alanine-transaminase (ALT) and aspartate-transaminase (AST). RA was characterized by increased TNF-α in plasma and IL-1β and IL-6 in synovial fluid, histological alterations in the tibio-tarsal joint, as well as edema, cyanosis, erythema, decreased lymphocyte number and increased APB activity in TS and decreased APB activity in PBMCs. RA produced increased ALT and AST. As expected, the chronic treatment with PRED promoted an antiedematogenic effect. The cocktail (MIX of PTX+ROL+RUP+TAL) also presented antiedematogenic effect. Concomitant administration of acute or chronic PRED with MIX did not produce synergism or potentiation of the antiedematogenic effect due to the single administration of MIX or chronic PRED. In addition to MIX, ROL and TAL were also antiedematogenic. MIX, ROL and TAL ameliorated plasma TNF-α and APB in FS from TS without hepatotoxicity, as reflected by ALT and AST levels. TAL recovered ALT and AST, but it did not affect the hemogram. Since PTX and RUP did not present antiedematogenic effects, ROL and TAL were hypothesized as probable responsible for the antiarthritic activity of MIX. Thus, the treatments with ROL, TAL and ROL+TAL were selected for evaluation of bone histology and measurements of differential parameters between healthy control and arthritic animals. This evaluation showed that the treatment of RA with ROL or TAL alone did not alter IL-6 levels, but recovered IL-1β in the synovial fluid. Both these effects were not different from those of the concomitant treatment with ROL+TAL, except that this combination also decreases the body mass. TAL stands out for its hepatoprotective effect in RA animals. Considering the known effects of RUP, PTX, TAL and ROL it can be hypothesized that antiarthritic action of TAL and ROL is due to the inhibition of TNF-α synthesis as consequence of its inhibition in its main cellular sources by PDE4. Data from this prospective study provide additional subsidies that stimulate further and more comprehensive clinical trials on the antiarthritic effects of ROL and TAL. In conclusion, the treatment with TAL alone emerges as an economical, simple and effective therapeutical alternative for RA, while the combination of ROL+TAL can be a viable option for RA sufferers with overweight or obesity
Mohajane, Mamohale. "Dipeptides as potential anti-flammatory drugs for rheumatoid arthritis." Master's thesis, University of Cape Town, 2013. http://hdl.handle.net/11427/6340.
Full textIncludes bibliographical references.
The H⁺ and Cu²⁺ equilibria of four glycine peptides (glycyl-glycine, glycyl-L-leucine, glycyl-L-phenylalanine and glycyl-L-histidine) and four sarcosine peptides (sarcosylglycine, sarcosyl-L-leucine, sarcosyl-L-phenylalanine and sarcosyl-L-histidine) have been studied using glass electrode potentiometry and isothermal titration calorimetry at 25 °C and an ionic strength 0.15 M (NaCl). The terminal amine of the sarcosine peptides is more basic than the glycine analogues. The methyl group on the terminal amine (for sarcosine peptides) does not affect the stability constants of the ML species, significantly. Log K for ML species for all the Cu(II)/peptides complexes ranged between 5.79 and 6.54, except for glycyl-L-histidine that showed log KML = 9.16. Heat accompanying the formation of ML for all the species ranged between -5.1 kcal mol⁻¹ and-6.6 kcal mol⁻¹, except for glycyl-L-histidine that showed ΔHML = -3.6 kcal.mol⁻¹. Structures for the different species in solution were postulated based on nuclear magnetic resonance and ultraviolet-visible spectrophotometry data. Molecular mechanics was used to investigate the possible structures. The minimum energy of the trans form of most the complexes was less than the cis form of the complexes.
Bondeson, Jan. "Effects of disease-modifying antirheumatic drugs on macrophage signal transduction and the induction of proinflammatory cytokines." Lund : Section of Molecular Pathogenesis, Dept. of Cell and Molecular Biology, Lund University, 1996. http://books.google.com/books?id=dgxsAAAAMAAJ.
Full textBeverly, Bart J. "Mechanism of action of aurothioalkyl antiarthritic drugs : role of myeloproxidase /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487330761219101.
Full textAird, Sheelagh Ann. "The pharmacokinetics of D-penicillamine in normal and adjuvant arthritic rats." Thesis, University of Bath, 1987. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376332.
Full textCoste, Emmanuel. "Development of small molecules as anti-inflammatory and anti-resorptive drugs." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/9941.
Full textMohamed, Ahmed A. "Redox studies on the anti-rheumatoid arthritis gold drugs : Auranofin and Solganol /." Fogler Library, University of Maine, 2000. http://www.library.umaine.edu/theses/pdf/MohamedAA2000.pdf.
Full textFrean, Stephen Philip. "Effects of anti-arthritic drugs on equine articular tissue metabolism." Thesis, Royal Veterinary College (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263731.
Full textGarrett, Neil Edward. "Substance P and experimental joint inflammation." Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244679.
Full textMulhearn, Ben. "Identifying immune biomarkers to predict treatment response to biologic drugs in rheumatoid arthritis." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/identifying-immune-biomarkers-to-predict-treatment-response-to-biologic-drugs-in-rheumatoid-arthritis(c311fc8c-4239-444a-9912-ddd4fde5f7fa).html.
Full textTsumbu, Evariste Umba. "Evaluation of tissue permeability of novel copper based anti-arthritic drugs." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/12361.
Full textRinaudo-Gaujous, Mélanie. "Etude de marqueurs biologiques prédictifs de la perte de réponse aux anti-TNF." Thesis, Saint-Etienne, 2015. http://www.theses.fr/2015STET016T/document.
Full textThe use of anti-TNF agents has greatly improved the management of chronic inflammatory diseases such as rheumatoid arthritis (RA), or chronic inflammatory bowel disease (IBD). However, about a quarter of patients will not respond to treatment or will present a secondary loss of response. Predictive biomarkers of response are needed to reduce side effects and unnecessary costs by targeting patients that could be improved by anti-TNF. This research work was initially focused on the importance of immunogenicity of these treatments. Anti-drug antibodies (ADAs) were well associated with low levels of anti-TNF with clinical consequences in terms of loss of clinical response and absence of mucosal healing in IBD. Clinical thresholds for drug and ADAs have been defined and correspond to 4.9 μg/ml for infliximab and 200 ng/ml for ADAS. These results obtained by ELISA correlate well with functional tests done in parallel, and confirm the value of this technique for screening. The ADAs were decreased with concomitant immunosuppressive therapy. Then, the persistence of chronic infection as evidenced by anti-bacterial antibody was evaluated as a predictive marker for response to anti-TNF. No statistically significant results could be raised on these first data, for antibodies against the intestinal flora in IBD or against the oral microbiota in RA. Only high levels of MMP-3 at the initiation of infliximab in RA patients predicted a good clinical response according to the EULAR criteria
Hatch, Lashley. "Statistical Information Included in Labeling for Disease-Modifying Anti-Rheumatic Drugs for Rheumatoid Arthritis." The University of Arizona, 2012. http://hdl.handle.net/10150/623641.
Full textSpecific Aims: To evaluate the presence of statistical information from clinical studies in official product labeling specific for disease-modifying anti-rheumatic drugs (DMARDs) used in the treatment of rheumatoid arthritis. Methods: Data were abstracted from official product labeling DMARDs with FDA approval for treatment of rheumatoid arthritis. Each document was examined for the presence of statement regarding a priori type 1 error rate, p-values, and measures of variance. Medications were classified as either biologic or non-biologic. Main Results: A total of 14 DMARDs, 7 biologics (50%) and 7 non-biologics (50%), were found to be FDA approved for the treatment of rheumatoid arthritis. Primary outcomes consisted of American College of Rheumatology (ACR) response rates, radiographic changes, and health assessment questionnaire score (HAQ). Any measure of variance and the presence of a p-value were both found in six (43%) of the drug labels. Inclusion of p- values was found to be significantly greater in biologics compared to non-biologics for both ACR and radiographic results. Inclusion of variance was found to be significantly greater in biologics compared to non-biologics for radiographic changes only. No package inserts contained statements regarding the a priori type I error rate. Conclusions: Measures of variance are not frequently included in product labeling for either biologic or non-biologic DMARDs. However, inclusion of variance and p-values for ACR response rates and radiographic changes were more likely to be reported for biologics therapies as compared to non-biologics. A statement regarding Type 1 error rates were absent from labels regardless of outcome assessed.
Hatch, Lashley, and Daniel C. Malone. "Statistical Information Included in Labeling for Disease-Modifying Anti-Rheumatic Drugs for Rheumatoid Arthritis." The University of Arizona, 2012. http://hdl.handle.net/10150/614497.
Full textSpecific Aims: To evaluate the presence of statistical information from clinical studies in official product labeling specific for disease-modifying anti-rheumatic drugs (DMARDs) used in the treatment of rheumatoid arthritis. Methods: Data were abstracted from official product labeling DMARDs with FDA approval for treatment of rheumatoid arthritis. Each document was examined for the presence of statement regarding a priori type 1 error rate, p-values, and measures of variance. Medications were classified as either biologic or non-biologic. Main Results: A total of 14 DMARDs, 7 biologics (50%) and 7 non-biologics (50%), were found to be FDA approved for the treatment of rheumatoid arthritis. Primary outcomes consisted of American College of Rheumatology (ACR) response rates, radiographic changes, and health assessment questionnaire score (HAQ). Any measure of variance and the presence of a p-value were both found in six (43%) of the drug labels. Inclusion of p-values was found to be significantly greater in biologics compared to non-biologics for both ACR and radiographic results. Inclusion of variance was found to be significantly greater in biologics compared to non-biologics for radiographic changes only. No package inserts contained statements regarding the a priori type I error rate. Conclusions: Measures of variance are not frequently included in product labeling for either biologic or non-biologic DMARDs. However, inclusion of variance and p-values for ACR response rates and radiographic changes were more likely to be reported for biologics therapies as compared to non-biologics. A statement regarding Type 1 error rates were absent from labels regardless of outcome assessed.
Roux, Ilanca. "Prescribing patterns of biologic immunomodulating medicine in the South African private health care sector / Ilanca Roux." Thesis, North-West University, 2010. http://hdl.handle.net/10394/4936.
Full textThesis (M.Pharm (Pharmacy Practice))--North-West University, Potchefstroom Campus, 2011.
Leblanc, Daren James. "Thiol complexes of gold(I), structure and chemistry of the gold based anti-arthritis drugs." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0018/NQ30153.pdf.
Full textLeBlanc, Daren James. "Thiol complexes of gold(I) : structure and chemistry of the gold based anti-arthritis drugs /." *McMaster only, 1996.
Find full textWarhurst, Jannette. "DRUMBEAT© for arthritis “ a shared purpose” rather than a “lonely struggle”." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2021. https://ro.ecu.edu.au/theses/2452.
Full textMhlambiso, Zizile. "Design of novel copper(II) based anti-inflammatory drugs for the elevation associated with Rheumatoid Arthritis." Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/9280.
Full textIt has been shown that copper complexes are able to alleviate inflammation associated with Rheumatoid Arthritis (RA). Serum copper levels are elevated in RA and it has been postulated that endogenous copper might have a protective function in chronic inflammatory conditions. In designing Cu(I1) anti-inflammatory drugs, one needs to know the stability constants of the ligand together with Cu(I1) and the competitive metal ions, Zn(I1) and Ca(I1) in blood plasma. For this purpose glass electrode potentiometry, infrared (lR) spectroscopy, nuclear magnetic resonance (NMR) spectroscopy, UV/Visible spectroscopy as well as blood plasma modelling were used to explore the coordination chemistry of a newly designed ligand, PCUL (Bis-(3- aminoethy-2-aminomethylpyridine )-oxahexacyclo-dodecane). PCUL protonation and formation constants with Cu(I1) and Zn(I1) were investigated by potentiometric analysis at 2SoC and 0.ISmol/dm3 Na + (CI) The potentiometric analysis showed that CU(I1) formed far more stable complexes at physiological pH with PCUL than the in vivo competitor Zn(I1). In this study the IR spectroscopic analysis was used to determine the Cu(I1)-PCUL complexation sequence. The IR spectra show that the central amines are coordinated to the metal ion first. The small frequency shift between pH 4.02 to 6.91 proves that the pyridyl nitrogen atoms are also coordinated to CU(I1).
Madeira, Jocelyn Marie. "Old drugs in a new light : investigating the gold Rheumatoid Arthritis medications as novel inhibitors of neuroinflammation." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43622.
Full textOmetto, Francesca. "Validation of the italian version of the 5-item compliance questionnaire for rheumatology (i-cqr5) and a cross-sectional study on treatment adherence in rheumatoid arthritis patients." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3421828.
Full textIntroduzione Il Compliance Questionnaire for Rheumatology (CQR5) a 5 domande permette l’identificazione dei pazienti che sono aderenti al trattamento anti-reumatico (high adherers, HA), ovvero pazienti che assumono ≥80% del trattamento correttamente, oppure poco aderenti (low adherers, LA). L’obiettivo dello studio era validare una versione italiana del CQR5 (I-CQR5) in pazienti con artrite reumatoide (AR). Inoltre è stata condotta una analisi trasversale per individuare i fattori associati ad elevata aderenza al trattamento. Metodi Sono stati arruolati pazienti con AR con una durata di malatti > 1 anno, in trattamento con ≥1 farmaco anti-reumatico biologico (bDMARD) o convenzionale (csDMARD) auto-somministrato, in grado di completare il questionario da soli e che avessero acconsentito alla partecipazione allo studio. L’adattamento cross-culturale in italiano di I-CQR5 ha seguito le linee guida stansardizzata. I-CQR5 è stato completato dai pazienti in una unica occasione. I dati sono stati analizzati con Partial Credit model Parametrisation (PCM) per valutare la validità strutturale e la reliability del I-CQR5. I pazienti che hanno acconsentito all’utilizzo dei loro dati clinici sono stati inclusi nell’analisi dei fattori associati all’aderenza al trattamento. I fattori analizzati erano: caratteristiche sociali e demografiche dei pazienti e informazioni cliniche e del trattamento. Tutti i fattori che hanno raggiunto una associazione con p<0.10 nell’analisi univariata sono stati inclusi nell’analisi di regressione multivariata. Modelli separati sono stati utilizzati per l’analisi nell’intera coorte di pazienti e nella coorte di pazienti in trattamento con soli csDMARD e nella coorte di pazienti trattati con bDMARDs. Risultati Di 604 pazienti con RA, 401 sono stati inclusi nell’analisi. Di questi 274 sono stati inclusi nell’analisi di validazione e 328 anche nello studio trasversale. L’età media dei pazienti era 57 anni (48-134), la maggior parte erano femmine (232, 82%) con durata mediana di malattia di 12 anni (7-19); 64.3% (193/300) erano trattati con bDMARDs e 54.6% (107/300) con csDMARD; 90.3% (270/299) presentavano una bassa attività di malattia o remissione. Le problematiche relative all’adattamento cross-culturale del CQR5 sono state discusse e risolte da una commissione di esperti. I-CQR5 è stato ben compreso dai pazienti. L’analisi dei fattori e la PCM hanno confermato la validità, l’unidimensionalità e la consistenza interna del I-CQR5. Gli HA erano 35.2% (109/310) dei pazienti: 40.2% (79/193) tra coloro trattati con bDMARDs e 22.4% (24/107) con soli csDMARDs. Il trattamento con bDMARD e l’impiego lavorativo sono rislutati indipendentemente associati con elevata aerenza al trattamento: OR 2.88 (1.36-6.1), p=0.006 e OR 2.36 (1.21-4.62), p=0.012 rispettivamente. Una età maggiore, un basso livello di educazione una dose maggiore giornaliera di corticosteroide e l’utilizzo di un csDMARD (in particolare idrossiclorochina e sulfasalazina) e la percezione di una maggiore attività di malattia da parte del paziente erano significativamente più frequenti tra i LA rispetto agli HA ma l’associazione non è stata confermata all’analisi multivariata. Nessun predittore di elevata aderenza al trattamento è emerso nel gruppo di pazienti trattati con soli csDMARDs. L’impiego lavorativo è risultato invece significativanente associato ad elevata aderenza al trattamento in pazienti trattati con bDMARDs: OR 2.89 (1.3-6.44), p=0.009. Conclusioni Solo un terzo di pazienti Italiani con AR sono risultati molto aderenti al trattamento misurando l’aderenza con I-CQR5. I maggiori determinanti di elevata aderenza al trattamento erano il trattamento con bDMARDs e l’impiego lavorativo aumentanto di circa 3 volte la probabilità di essere molto aderenti al trattamento.
Garrett, Ian Ross. "Studies of the effect of metal containing drugs on acute and chronic inflammation /." Title page, table of contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phg2386.pdf.
Full textMcCappin, Thomas Robertson. "The effects of adjuvant-induced arthritis and two models of renal failure on the hepatic uptake and pharmacokinetics of three drugs." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385477.
Full textKalkan, Almina. "Diffusion, implementation and consequences of new health technology : The cases of biological drugs for rheumatoid arthritis and the Swedish national guidelines." Doctoral thesis, Linköpings universitet, Avdelningen för hälso- och sjukvårdsanalys, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-113306.
Full textHo, Yee-wa Eva, and 何綺華. "Effects of Ganoderma lucidum on rheumatoid synovial fibroblasts." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29489933.
Full textYue, Xiaomeng. "Medication Patterns and Comparative Effectiveness Research of Biologic Disease-modifying Antirheumatic Drugs in Children Newly Diagnosed with Juvenile Idiopathic Arthritis using Electronic Medical Records." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1613751938659097.
Full textGrant, Donna. "Mutations in the hypoxanthine phosphoribosyltransferase (hprt) gene in T lymphocytes from arthritis patients and in human B lymphoid cell lines exposed to nitric oxide-donating drugs." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0001/MQ46576.pdf.
Full textOliveira, Silvia Coimbra de. "Itinerário terapêutico de pacientes com artrite reumatoide em uso de medicamentos modificadores do curso da doença biológicos." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/6/6135/tde-05012018-095623/.
Full textIntroduction Rheumatoid arthritis (RA) is a chronic degenerative autoimmune disease of high prevalence and with high morbidity and mortality, worldwide difficult to diagnose. Its prompt diagnosis and rapid onset with disease modifying drugs (DMARD) have a relevant impact on the patient\'s prognosis. For some patients, the synthetic DMARDs will not be effective so these patients should receive a biological DMARD - a high cost medication both to the patient and the health system. Objective - To explore the trajectories performed by patients with RA using biological DMARD in the search for care in the city of São Paulo. Methods - Qualitative research, with an exploratory character, with analytical-descriptive orientation, through semi-structured interviews with open questions, initiated after prior approval of the Committee on Ethics in Research and informed consent of the interviewees. The subjects are patients using biological DMARD to treat RA that were dispensed by SUS. The therapeutic itinerary tool (TI) was used to understand the path chosen by these patients in the search for health care. Results and Discussion Among those interviewees, the search for care occurred late, usually without the suspicion that there was a degenerative rheumatic disease. The first accessed professionals were the general practitioner or the orthopedist, who rarely ever investigated the reported symptoms with attention to direct the patient to the rheumatologist quickly. In the described TIs, the treatments are mostly composed only by the medicines, and without the participation of other professionals in the follow-up besides the rheumatologist. The patients interviewed reached the biological DMARDs after an attempt to control the disease with synthetic DMARD, as described in the Ministry of Health recommendations. There are several actors representing the private sector described in the TI\'s, who support and influence the patients in the choice of their care pathways, which should be better understood in future studies
Xie, Fenglong. "Assessing the Comparative Effect of Tocilizumab on Risk of Cardiovascular Disease among Rheumatoid Arthritis Patients Using Claims Data| A Direct Comparison among Biologic Disease-Modifying Antirheumatic Drugs." Thesis, The University of Alabama at Birmingham, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10750692.
Full textTocilizumab is a humanized monoclonal anti-body against the interleukin-6 receptor and is effective in the treatment of rheumatoid arthritis (RA). Multiple studies have observed unfavorable changes in the lipid profile of tocilizumab-treated RA patients. Few studies have compared the cardiovascular disease (CVD) risk associated with tocilizumab to other biologic disease-modifying antirheumatic drugs (bDMARDS). Due to limitations in existing studies, the real-world association of tocilizumab with CVD risk remains uncertain.
We conducted a retrospective cohort study using 2006–2015 Medicare and MarketScan claims data to assess the comparative effect of tocilizumab on CVD risk. Medicare claims data provide a unique opportunity to estimate disease burden and conduct comparative effectiveness studies with much larger sample sizes than cohorts, which require primary data collection. However, Medicare claims data lack information on cause of death. To address this limitation, we developed claims-based algorithms for identifying fatal CVD in Medicare claims data using The Reasons for Geographic and Racial Difference in Stroke (REGARDS) data linked to Medicare claims. CVD events iv and cause of death in the REGARDS study were adjudicated by two experts. Our algorithm can identify fatal CVD events with high sensitivity and specificity.
Our study confirmed that tocilizumab was not associated with increased or decreased CVD risk compared to etanercept: the hazard ratio for tocilizumab compared to etanercept was 0.91 (95%CI: 0.66, 1.25). However, unlike the clinical trial, which enrolled only high-risk patients, we extended this finding to “low CVD risk” RA patients. We also showed that tocilizumab was not associated with increased or decreased CVD risk compared to abatacept or rituximab. We further showed that tocilizumab was associated with reduced CVD risk when compared to a pooled TNFi group. This is most likely due to slightly increased CVD risk associated with infliximab.
We also conducted a retrospective cohort study using Medicare claims data to assess the effect of methotrexate on CVD risk among bDMARDS users and found that methotrexate was associated with an overall 27% (95%CI: 18–35%) reduction in CVD risk. The hazard ratio for tocilizumab concomitantly with methotrexate compared to tocilizumab only was 0.66 (95%CI: 0.40–1.09).