Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the hands of an experienced rheumatologist and in adherence to the contraindications named in the article, anticytokines such asTNF-alpha blockers or interleukin-1 antagonists are regarded as relatively reliable, are well tolerated and in many cases, are very effective. Especially when used in combination with methotrexate, they demonstratively lower the disease activity score and significantly slow the radiographic progression.Thus, anticytokines are currently the most effective therapy for RA. An additional advantage compared to conventional DMARD is the rapid onset of action (usually within two to four weeks).TNF-alpha blockers are also presently employed in numerous other chronic inflammatory diseases. The efficacy of anticytokines in psoriasis and psoriatic arthritis, ankylosing spondylitis, juvenile arthritis and Crohn's disease has been proven.
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PMID:[Treatment of rheumatoid arthritis (RA) with anticytokines]. 1762 99

To find the susceptible genes of ankylosing spondylitis in Chinese population, we select 11 SNPs on gene HLA gene family that has strong linkage of ankylosing spondylitis in 6p21.3. By case-control study in 79 AS patients and 132 healthy subjects, the distribution of TNF-alpha-850 genotype TT is higher in AS group than that in normal control group (P=0.027); Mutational allele T has a significant statistically difference between AS group and normal control group (P=0.002). By linkage disequilibrium study, there are 5 SNPs present the linkage disequilibrium and the region is 15 kb, including gene LTA, TNF-alpha, LST1 and NCR3; In the haplotypes of the 5 SNPs , the distribution of haplotype TCTTC has statistical difference between AS group and normal control group (chi2=7.406, P=0.0065), the haplotype contains mutational allele T of TNF-alpha-850. The result hints that there may be susceptible sites of AS in this 15 kb region, which may be TNF-alpha-850 C-->T mutation or other sites that around the TNF-alpha-850.
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PMID:[Mapping study of ankylosing spondylitis on HLA region in Jilin population of China]. 1764 45

Renal amyloidosis is a complication of ankylosing spondylitis. A possible pathogenetic role is due to TNF-alpha, with a direct action on glomerular receptors TNFR2 and renal injury, secondary to deposition of amyloid fibrils. The most frequent clinical manifestation is proteinuria or nephrotic syndrome. Etanercept, a soluble receptor of TNF-alpha, binds this circulant cytokine with a progressive improvement of renal function and reduction of deposits of amyloid. Transient leukopenia, observed during ankylosing spondylitis, should not be considered a controindication to the use of Etanercept, but it requires a constant monitoring. The benefit observed in our patient can represent an indication to the use of Etanercept for the management of amyloidosis.
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PMID:[Response to anti-TNF-alpha treatment for secondary renal amyloidosis in a patient with ankylosing spondylitis]. 1789 85

Crohn's disease (CD) and ulcerative colitis (UC), both should be considered as systemic diseases as they are associated with clinical manifestations involving the organs outside the alimentary tract. In a genetically susceptible host with inflammatory bowel disease (IBD), complex interaction of bacterial or other local factors in the colon with antigen presenting cells may trigger an immune reaction to a shared antigen in the involved organs. These extraintestinal manifestations (EIM) are observed in up to 20-40% of the patients with IBD. Patients with CD are more susceptible to EIMs than patients with UC. Joints, eyes, skin and biliary tract are the most commonly involved organ systems. Some manifestations such as uveitis, episcleritis may precede the onset bowel disease and some may occur in conjunction with or subsequent to the diagnosis of active bowel disease. Although many EIMs tend to follow the clinical course of IBD and respond to the treatment of underlying bowel disease, some EIMs such as primary sclerosing cholangitis and ankylosing spondylitis tend to follow a course independent of the bowel disease activity. Biological agents, particularly anti-TNFa based therapies now assume an important role in the treatment of EIMs. Early recognition and treatment of EIMs are crucial in preventing major morbidity.
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PMID:Pathogenesis and clinical approach to extraintestinal manifestations of inflammatory bowel disease. 1791 86

TNF-alpha is a crucial pro-inflammatory and immunoregulatory cytokine that is central to the pathogenesis of various inflammatory and autoimmune conditions. A number of controlled trials have shown effectiveness for TNF-alpha inhibitors in several diseases, in particular rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and Crohn's disease. These agents may also be useful in additional autoimmune conditions. The introduction of TNF-alpha inhibitors has revolutionized the therapeutic approach and treatment paradigms especially for patients with rheumatoid arthritis. Despite extensive investigation, the full profile of their mechanisms of action remain incompletely understood. Optimal use of these agents requires consideration of their possible adverse effects. In addition to the presently available TNF-alpha blockers, other agents targeting this key mediator are under study. Recent advances and future directions in anti-TNF-alpha therapy are discussed in this paper.
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PMID:Tumor necrosis factor as a therapeutic target of rheumatologic disease. 1802 4

Infliximab is a chimeric monoclonal antibody of the IgG1 class. Experience from its use has been accumulated in rheumatology and gastroenterology by the treatment of rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and inflammatory bowel disease, respectively. Because of its TNF-alpha binding capacity it has been approved for the treatment of moderate-to-severe plaque psoriasis. Moreover, it has also been evaluated in other inflammatory dermatoses as well as systemic diseases involving the skin such as severe atopic dermatitis, pityriasis rubra pilaris, pyoderma gangrenosum and cutaneous sarcoidosis. The possible future uses of infliximab in dermatology are being reviewed herein.
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PMID:Infliximab in dermatological treatment: beyond psoriasis. 1808 42

The pathophysiology and the treatment of diseases with clinical presentation so different as rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and psoriasis vulgaris have been revolutionized by the discovery of common pro-inflammatory effector mechanisms involving TNF-alpha and by the use of targeted therapies, the anti-TNF-alpha antibodies. In the past 10 years, our experience has helped several hundreds of patients who were treated with novel drugs, years before they became routinely available. In parallel tools of metrology were developped that can now be applied to the routine patient. Lastly, clinical research on these new drugs has also generated derived research works allowing the university hospital to satisfactorilly fullfil its specific missions.
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PMID:[Biological therapy of inflammatory diseases]. 1821 62

Adalimumab is a fully humanized recombinant anti-tumour-necrosis-factor (TNF-alpha) monoclonal antibody which has been approved for rheumatoid arthritis, active ankylosing spondylitis, psoriatic arthritis and Crohn's disease. We report a case of alopecia areata (AA) universalis occurring 6 months after administration of adalimumab monotherapy in a patient with a long-standing history of psoriatic arthritis and psoriasis. The diagnosis was confirmed by a scalp biopsy which showed a peribulbar infiltrate of both CD4+ and CD8+ T cells, CD1a+ dendritic cells as well as CD68+ and CD163+ macrophages. In addition, immunofluorescence staining for TNF-alpha was found in the mononuclear cell infiltrate. This case suggests a complex role of TNF-alpha in the induction of AA.
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PMID:Alopecia areata universalis elicited during treatment with adalimumab. 1823 Sep 80

Infliximab is a monoclonal antibody directed against TNF-alpha. It has been approved for use in rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriatic arthritis and plaque-type psoriasis. In case reports, positive effects on pustular variants of psoriasis have also been reported. However, paradoxically, manifestation of pustular psoriasis and plaque-type psoriasis has been reported in patients treated with TNF antagonists including infliximab for other indications. Here, we report on 5 patients with chronic plaque-type psoriasis who developed palmoplantar pustulosis during or after discontinuation of infliximab therapy. In two of the five cases, manifestation of palmoplantar pustulosis was not accompanied by worsening of plaque-type psoriasis. Possibly, site-specific factors or a differential contribution of immunological processes modulated by TNF inhibitors to palmoplantar pustulosis and plaque-type psoriasis may have played a role.
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PMID:Manifestation of palmoplantar pustulosis during or after infliximab therapy for plaque-type psoriasis: report on five cases. 1823 25

The concurrence of ankylosing spondylitis (AS) in a patient with mixed connective tissue disease (MCTD) is rarely described in the literature. Significant and sustained efficacy with tumor necrosis factor (TNF)-alpha blockers has been demonstrated in AS patients. However, evidence to date has revealed associated side effects, including antinuclear antibody induction and development of a lupus-like syndrome. Several authors have reported lupus-like manifestations in MCTD patients treated with TNF-alpha blockers used to control peripheral polyarthritis. In our case report, we demonstrate a good response to etanercept therapy for refractory sacroiliitis in a patient with coexisting AS and MCTD, without development of a lupus-like syndrome. This demonstrates that etanercept therapy may be an appropriate therapeutic agent for sacroiliitis in MCTD patients, as it is in AS alone.
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PMID:Successful etanercept therapy for refractory sacroiliitis in a patient with ankylosing spondylitis and mixed connective tissue disease. 1830 84


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