Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0003864 (arthritis)
69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biologics have advanced the therapy of adult and pediatric arthritis. They have been linked to rare serious adverse outcomes, but the actual risk of these events is controversial in adults, and largely unknown in pediatrics. Because of the paucity of safety and efficacy data in children, pediatric rheumatologists often rely on the adult literature. Herein, we reviewed the adult and pediatric literature on five classes of medicines: Tumor necrosis factor (TNF) inhibitors, anakinra, rituximab, abatacept, and tocilizumab. For efficacy, we reviewed randomized controlled studies in adults, but did include lesser qualities of evidence for pediatrics. For safety, we utilized prospective and retrospective studies, rarely including reports from other inflammatory conditions. The review included studies on rheumatoid arthritis and spondyloarthritis, as well as juvenile idiopathic arthritis. Overall, we found that the TNF inhibitors have generally been found safe and effective in adult and pediatric use, although risks of infections and other adverse events are discussed. Anakinra, rituximab, abatacept, and tocilizumab have also shown positive results in adult trials, but there is minimal pediatric data published with the exception of small studies involving the subgroup of children with systemic onset juvenile idiopathic arthritis, in whom anakinra and tocilizumab may be effective therapies.
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PMID:Biological therapies for the treatment of juvenile idiopathic arthritis: Lessons from the adult and pediatric experiences. 1970 57

The interleukin 1 family is composed by the interleukin 1 (IL-1) and its natural occurring inhibitor, the interleukin 1 receptor antagonist (IL-1Ra). The role of both molecules in rheumatoid arthritis has been widely established, and in this sense new molecules blocking IL-1 actions are under investigation. Anakinra is the recombinant form of IL-1Ra, and has proven to be well tolerated and indicated in the treatment of rheumatoid arthritis. Nevertheless, other molecules such as mAb anti-IL-1 and IL-1 Trap are being developed. Moreover, the recent relation of IL-1 in the inflammasome and pathways of innate immunity has lead to new indications of anti-IL-1 molecules, especially in the autoinflammatory syndromes as well as in other inflammatory diseases. Herein we have performed a review of the literature, limited to English language journals (PUBMED search: combination of descriptors IL-1 and anakinra, systemic juvenile idiopathic arthritis, adult's onset Still's disease, autoinflammatory syndromes, gout, pseudogout, ankylosing spondylitis, and systemic lupus erythematosus from January 1985-December 2008) emphasizing the possible new indications. Although sufficient data is not yet available to fully assess the efficacy and safety of anti-IL-1 molecules in patients with inflammatory disorders other than rheumatoid arthritis, new data is promising.
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PMID:Anti-IL-1 molecules: new comers and new indications. 2004 71

Tumour necrosis factor alpha (TNFalpha) has been identified in the pathogenesis of synovitis and joint destruction in rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). Therefore selected targeting of pathogenic elements of disease is possible (Chu et al., 1991). TNFalpha is a pro-inflammatory cytokine (mediator) and the over-expression of mediators is considered to be responsible for the damage to articular cartilage in bones. Elevated levels of TNFalpha, correlating with disease activity, have been measured in the serum and synovial fluid of patients with rheumatic diseases and are therefore an ideal target for therapy (Mangge et al., 1995; Cope et al., 1992). The National Institute for Clinical Excellence (NICE) approved the use of two therapies; entanercept (Enbrel) and infliximab (Remicade) for use in patients with active RA in 2002 (NICE, 2002). Other biologic treatments including adalimumab (D2E7) and anakinra (Kineret) will also be available for use in the future. This paper explores the development of a service to provide these therapies to patients.
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PMID:Developing a service for biologic therapies: a personal experience. 2021 62

Anakinra is a specific receptor antagonist of interleukin-1 that differs from naturally occurring interleukin-1 receptor antagonist by the presence of a methionine group. It is administered by daily subcutaneous injection. Anakinra improves the clinical signs and symptoms of rheumatoid arthritis, slows radiographic progression and improves patient physical function. The most common adverse event is an injection site reaction. Anakinra has been associated with an increased incidence of serious infections and has an increased standardized incidence ratio for lymphoma. It has not been found to be associated with the development of opportunistic infections, worsening of congestive heart failure or the development of demyelinating disease. It appears to be effective in treating adult Stills disease, systemic-onset juvenile idiopathic arthritis and chronic infantile neurological cutaneous and articular syndrome (also known as neonatal-onset multisystem inflammatory disease syndrome).
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PMID:Anakinra in the treatment of rheumatic disease. 2047 5

Adult-onset Still's disease (AOSD) is a systemic inflammatory disorder, characterized by spiking fever, skin rash, and arthritis. First-line treatment consists of corticosteroids. Methotrexate is commonly used in resistant cases or as a steroid-sparing drug. The availability of biologic drugs in the rheumatic diseases, such as anti-TNFs and IL-1ra, has allowed to treat very refractory cases of AOSD and provided new clues for the pathophysiology. However, anakinra and anti-TNFs may also fail or may be contraindicated in AOSD, and other treatment strategies are then necessary. Given that T cell activation may be a relevant part of the AOSD pathophysiology, abatacept, CTLA4IgFc, was administered in a 57-year-old man with AOSD failing traditional DMARDs and to anti-IL-1 and anti-TNF therapies, with a good outcome.
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PMID:Efficacy of abatacept in a refractory case of adult-onset Still's disease. 2048 52

Only limited data have been published about the therapeutic use of anakinra in patients with psoriatic arthritis. We undertook this study to evaluate the efficacy and safety of anakinra in patients with active psoriatic arthritis. In a prospective open-label single-center study, 20 patients were treated with 100 mg anakinra everyday either alone or in combination with ongoing methotrexate over 6 months. Safety and efficacy was evaluated using Psoriasis Arthritis Response Criteria (PsARC), Disease Activity Score (DAS) 28, American College of Rheumatology (ACR), European League Against Rheumatism (EULAR), Psoriasis Area and Severity Index Score, Dactylitis Score and Health Assessment Questionnaire (HAQ), and the C-reactive protein, and erythrocyte sedimentation rate. Of the 20 patients enrolled, six completed 24 weeks, 18 completed 12 weeks, and 19 completed 4 weeks of treatment. Early-treatment termination was mainly due to inefficacy (13 patients) and only one drop-out occurred because of an unrelated adverse event. Six patients fulfilled continuously the PsARC until week 24. A moderate EULAR response was achieved by four patients and a good EULAR response by three patients in week 24. Five patients reached ACR 20, four patients ACR 50, and two patients ACR 70 in week 24. HAQ improved slightly throughout the study (n = 19, mean (SD); baseline, 1.127 (0.671); week 24, 1.055 (0.812)) just as DAS 28 (n = 16; baseline, 4.7(1.5); week 24, 4.0(2.0)). Only nine patients showed skin manifestations affecting >3% of their body surface area which improved in two, worsened in four, stabilized in two patients, and newly evolved in one patient. Adverse events were mainly mild (95%). Fifteen (75%) patients showed injection site reactions. No serious infections occurred. Anakinra was well tolerated with no occurrence of serious drug-associated adverse events and lead to improvement of signs and symptoms in nine out of 19 patients, therefore providing a potential therapeutic option in patients with active psoriatic arthritis.
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PMID:An open-label pilot study of the efficacy and safety of anakinra in patients with psoriatic arthritis refractory to or intolerant of methotrexate (MTX). 2053 37

Interleukin (IL)-1 plays an important role not only in the mediation of inflammation but also in the destruction of cartilage and bone. Together with TNF-alpha it is one of the most important cytokines in the pathogenesis of rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). The first IL-1 antagonist to be approved for RA was Anakinra, an IL-1 receptor antagonist. Anakinra appears to be less effective for RA than TNF blockers. Hence, Anakinra is rarely used for the treatment of RA, but more for the treatment of IL-1-mediated diseases such as autoinflammatory syndromes, adult-onset Still's disease and systemic onset JIA. Two newer IL-1 antagonists have recently been approved for the treatment of CAPS (cryopyrin-associated periodic syndromes): Canakinumab, a fully human IL-1beta antibody, and rilonacept, a fusion protein consisting of the ligand-binding domain of the IL-1 receptor and the IL-1-receptor accessory protein, bound to human IgG1. For RA, there is only one proof-of-concept study to date with canakinumab. There are no prospective data for the treatment of patients with RA who did not respond to or tolerate TNF antagonists; in a retrospective analysis, only 8% of anti-TNF pretreated patients achieved an ACR 20 response.
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PMID:[IL-1 antagonists]. 2070 89

Schnitzler syndrome is a rare disorder characterized clinically by chronic urticarial rash accompanied by fever, arthralgia or arthritis, bone pain and lymphoadenopathy and biochemically by monoclonal gammopathy and elevation of inflammatory indices. The disorder is very likely under-recognized and its origin remains obscure although it may be included among the immune mediated inflammatory diseases with features of autoinflammation and autoimmunity. We describe here two patients affected by Schnitzler syndrome, both refractory to corticosteroids and immunosuppressive therapy, successfully treated with the interleukin-1 receptor antagonist Anakinra. Unfortunately after two weeks, one patient experienced an important local adverse reaction to the biological drug. We decided to discontinue Anakinra with flare of the disease after 24 h. We therefore switched to Rituximab obtaining a complete remission in two months. We searched MEDLINE in order to analyze the frequency of the disease, its pathogenesis and outcome. The electronic search was conducted using the following key words "Schnitzler syndrome" and "Treatment of Schnitzler syndrome". All the selected papers, except the clinical reviews, described at least one case of Schnitzler syndrome. The review of the literature highlighted that Schnitzler syndrome remains an enigmatic disorder hard to categorize and to treat.
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PMID:Schnitzler syndrome, an autoimmune-autoinflammatory syndrome: report of two new cases and review of the literature. 2125 51

Dendrimers are highly branched "tree-like" polymers that have demonstrated therapeutic potential in drug delivery, medical imaging, and tissue engineering in recent years. In addition, we have shown that an azabisphosphonate (ABP)-capped dendrimer selectively targets monocytes and directs them toward anti-inflammatory activation. We explored this property to assess the therapeutic potential of dendrimer ABP in the treatment of an inflammatory disease, rheumatoid arthritis. Intravenous injections of dendrimer ABP inhibited the development of inflammatory arthritis in two animal models: IL-1ra(-/-) mice and mice undergoing K/BxN serum transfer. Suppression of disease was characterized by normal synovial membranes, reduced levels of inflammatory cytokines, and the absence of cartilage destruction and bone erosion. Dendrimer ABP also exhibited anti-osteoclastic activity on mouse and human cells, mediated by c-FMS (cellular-feline McDonough strain sarcoma virus oncogene homolog) inhibition. These preclinical demonstrations suggest the potential use of dendrimer ABP as a nanotherapeutic for rheumatoid arthritis.
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PMID:A phosphorus-based dendrimer targets inflammation and osteoclastogenesis in experimental arthritis. 2169 24

Postoperative or postinjury inflammation after knee surgery is a significant clinical challenge. Cytokines, particularly interleukin-1 (IL-1), released by inflammatory cells have been shown to have a role in cartilage homeostasis and tissue repair and fibrosis. Anakinra, an IL-1 receptor antagonist (IL-1ra), has shown promising results from its use in treating rheumatoid arthritis, juvenile inflammatory arthritis, and autoimmune inflammatory syndromes. We hypothesized that intra-articular anakinra injection may result in sustained improvements of persistent effusion of the knee joint refractory to other modalities. We retrospectively reviewed 6 patients (3 female, 3 male), ranging in age from 17 to 50 years, who underwent injection of intra-articular anakinra, 200 mg, between November 15, 2007, and April 29, 2010, for persistent effusions of the postoperative knee. All of the patients treated with intra-articular anakinra for persistent effusions failed conservative treatment with physical therapy, oral anti-inflammatory medication, and 4 of 6 patients failed prior corticosteroid injections. After intra-articular anakinra, 66% had improvement in knee arc of motion (15 to 30 degrees) and pain, and 5 of 6 (83%) had improvement in swelling. All of these patients were able to return to sports. We found intra-articular anakinra to be safe and effective in this small group of patients with persistent effusions. There were no adverse clinical reactions or infections. These findings provide support for further study of IL-1 inhibition in the management of postsurgical inflammation.
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PMID:Clinical benefits of intra-articular anakinra for persistent knee effusion. 2161 40


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