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Current Pharmaceutical Design 2021Rheumatic diseases are a kind of chronic inflammatory and autoimmune disease affecting the connection or supporting structures of the human body, such as the most common... (Review)
Review
Rheumatic diseases are a kind of chronic inflammatory and autoimmune disease affecting the connection or supporting structures of the human body, such as the most common diseases Ankylosing spondylitis (AS), gout and Systemic lupus erythematosus (SLE). Although the precise etiology and pathogenesis of the different types of rheumatic diseases remain mostly unknown, it is now commonly believed that these diseases are attributed to some complex interactions between genetics and environmental factors, especially the gut microbiome. Altered microbiome showed clinical improvement in disease symptoms and partially restored to normality after prescribing disease-modifying antirheumatic drugs (DMARDs) or other treatment strategies. Recent advances in next-generation sequencing-based microbial profiling technology, especially metagenomics, have identified alteration of the composition and function of the gut microbiota in patients. Clinical and experimental data suggest that dysbiosis may play a pivotal role in the pathogenesis of these diseases. In this paper, we provide a brief review of the advances in the microbial profiling technology and up-to-date resources for accurate taxonomic assignment of metagenomic reads, which is a key step for metagenomics studies. In addition, we review the altered gut microbiota signatures that have been reported so far across various studies, upon which diagnostics classification models can be constructed, and the drug-induced regulation of the host microbiota can be used to control disease progression and symptoms.
Topics: Antirheumatic Agents; Dysbiosis; Humans; Metagenomics; Microbiota; Technology
PubMed: 33308114
DOI: 10.2174/1381612826666201211114609 -
Therapeutische Umschau. Revue... Aug 2022Secondary Immunodeficiency in Rheumatology For the treatment of autoimmune and autoinflammatory diseases an immunosuppressive therapy with conventional, small molecule...
Secondary Immunodeficiency in Rheumatology For the treatment of autoimmune and autoinflammatory diseases an immunosuppressive therapy with conventional, small molecule or biological disease modifying anti-rheumatic drugs (DMARDS) plays a key role. This may lead to secondary immunodeficiency with an increased risk for infections, which we discuss in the present article. The risk for reactivation of chronic hepatitis B increases particularly with glucocorticoid dosages of ≥ 20mg/d for longer than four weeks, with B-cell-depleting therapies, followed by anti-TNF-α-inhibitors. The latter also represent a risk for the reactivation of latent tuberculosis. High doses of glucocorticosteroids for prolonged periods increase the risk for pneumonia with Pneumocystis jirovecii, especially if combined with other DMARDs. An elevated risk for Herpes zoster exists for B-cell depletion, TNF-α-inhibition and for JAK blockade. Severe immunosuppression (B-cell depletion, cyclophosphamide, mycophenolate mofetil, JAK inhibitors, prednisone ≥ 20mg/d or combination therapy) increase the risk for severe COVID-19 infections.
Topics: Antirheumatic Agents; COVID-19; Humans; Rheumatology; Tumor Necrosis Factor Inhibitors; Tumor Necrosis Factor-alpha
PubMed: 35903826
DOI: 10.1024/0040-5930/a001363 -
Rheumatic Diseases Clinics of North... Nov 2019The treat-to-target principle of controlling inflammatory disease activity by means of disease-modifying antirheumatic drugs or immunosuppressive drugs also pertains to... (Review)
Review
The treat-to-target principle of controlling inflammatory disease activity by means of disease-modifying antirheumatic drugs or immunosuppressive drugs also pertains to systemic lupus erythematosus (SLE). However, in SLE, intensifying immunosuppression with higher-dose glucocorticoids may worsen outcomes. Therefore, all current recommendations favor better disease control while limiting daily glucocorticoid doses to a maximum of 5 or 7.5 mg of prednisolone daily. Hydroxychloroquine and other prophylactic measures are added, and antiphospholipid syndrome is treated with anticoagulation and not with immunosuppression, which makes the approach of treat to target slightly more complex, mirroring the complexity of the disease.
Topics: Antirheumatic Agents; Disease Management; Humans; Lupus Erythematosus, Systemic; Patient Acuity; Patient Care Planning; Remission Induction; Symptom Flare Up
PubMed: 31564295
DOI: 10.1016/j.rdc.2019.07.004 -
British Journal of Clinical Pharmacology Oct 2019Methotrexate at low doses (5-25 mg/week) is first-line therapy for rheumatoid arthritis. However, there is inter- and intrapatient variability in response, with... (Review)
Review
Methotrexate at low doses (5-25 mg/week) is first-line therapy for rheumatoid arthritis. However, there is inter- and intrapatient variability in response, with contribution of variability in concentrations of active polyglutamate metabolites, associated with clinical efficacy and toxicity. Prescribing remains heterogeneous across population groups, disease states and regimens. This review examines current knowledge of dose-response of oral methotrexate in the setting of rheumatoid arthritis, and how this could help inform dosage regimens.
Topics: Administration, Oral; Antirheumatic Agents; Arthritis, Rheumatoid; Dose-Response Relationship, Drug; Humans; Methotrexate; Polyglutamic Acid; Practice Patterns, Physicians'
PubMed: 31276602
DOI: 10.1111/bcp.14057 -
Rheumatology (Oxford, England) Mar 2024Biologic and targeted synthetic DMARDs (b/tsDMARDs) have revolutionized the management of multiple rheumatic inflammatory conditions. Among these, polyarticular JIA... (Review)
Review
Biologic and targeted synthetic DMARDs (b/tsDMARDs) have revolutionized the management of multiple rheumatic inflammatory conditions. Among these, polyarticular JIA (pJIA) and RA display similarities in terms of disease pathophysiology and response pattern to b/tsDMARDs. Indeed, the therapeutic efficacy of novel targeted drugs is variable among individual patients, in both RA and pJIA. The mechanisms and determinants of this heterogeneous response are diverse and complex, such that the development of true 'precision'-medicine strategies has proven highly challenging. In this review, we will discuss pathophysiological, patient-specific, drug-specific and environmental factors contributing to individual therapeutic response in pJIA in comparison with what is known in RA. Although some biomarkers have been identified that stratify with respect to the likelihood of either therapeutic response or non-response, few have proved useful in clinical practice so far, likely due to the complexity of treatment-response mechanisms. Consequently, we propose a pragmatic, patient-centred and clinically based approach, i.e. personalized instead of biomarker-based precision medicine in JIA.
Topics: Adult; Humans; Arthritis; Precision Medicine; Inflammation; Antirheumatic Agents
PubMed: 37725352
DOI: 10.1093/rheumatology/kead490 -
Transplantation and Cellular Therapy Jul 2023
Topics: Interleukin 1 Receptor Antagonist Protein; Antirheumatic Agents
PubMed: 37400190
DOI: 10.1016/j.jtct.2023.06.004 -
The Journal of Rheumatology Nov 2023
Topics: Humans; Arthritis, Rheumatoid; Antirheumatic Agents
PubMed: 37263650
DOI: 10.3899/jrheum.2022-1253 -
RMD Open Mar 2021We summarised four pivotal Randomised Controlled Trials (RCTs) with antirheumatic drugs on the secondary prevention of cardiovascular events. The favourable effects of... (Review)
Review
We summarised four pivotal Randomised Controlled Trials (RCTs) with antirheumatic drugs on the secondary prevention of cardiovascular events. The favourable effects of canakinumab and colchicine confirm (low-grade) inflammation as an independent risk factor for cardiovascular events. While colchicine might be the first drug in the clinic, we expect that this is only the first in a future series of anti-inflammatory drugs used in secondary prevention of cardiovascular events.
Topics: Anti-Inflammatory Agents; Antirheumatic Agents; Cardiovascular Diseases; Colchicine; Humans; Inflammation
PubMed: 33727219
DOI: 10.1136/rmdopen-2020-001560 -
La Revue Du Praticien May 2024
Topics: Humans; Arthritis, Rheumatoid; Antirheumatic Agents
PubMed: 38833243
DOI: No ID Found -
Annals of Internal Medicine Sep 2023
Topics: Humans; Glucocorticoids; Arthritis, Rheumatoid; Antirheumatic Agents
PubMed: 37579309
DOI: 10.7326/M23-1991