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

Anti-tumor necrosis factor (anti-TNF-alpha) are a group of new drugs able to inhibit the action of this cytokine. Although systemic side effects have been well described, cutaneous adverse reactions have not yet been clearly elucidated. The authors report a case of a 29-year-old man affected by Crohn disease and ankylosing spondylitis who developed psoriatic lesions after IV infusion of infliximab 5 mg/Kg. The patient underwent cyclosporine treatment after interruption of biological therapy, and had complete resolution of cutaneous lesions. The reason for this phenomenon is not clear, Obviously more studies are necessary to define more clearly this paradoxical reaction. In addition, dermatologists must be informed about this potential cutaneous adverse event.
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PMID:A case of infliximab-induced psoriasis. 1909 47

Vitiligo is a depigmenting skin disorder resulting from the loss of melanocytes in the epidermis. Although the exact aetiology of vitiligo has not yet been established, the abnormal immune responses have been frequently observed in vitiligo patients. Moreover, some vitiligo patients show higher lesion levels of tumor necrosis factor (TNF)-alpha. TNF-alpha is an important pleiotropic cytokine that exerts potent pro-inflammatory effects. There is growing evidence that TNF-alpha plays an important role in the pathomechanism process of some autoimmunity diseases, including ankylosing spondylitis (AS). Treated with anti-TNF agents infliximab, with the improvement of AS, a patient's vitiligo lesions also faded out. Therefore, we hypothesized that TNF-alpha play an important role in vitiligo. On the one hand, TNF-alpha destroys melanocytes through induction of various apoptotic pathways. On the other hand, TNF-alpha inhibits melanocyte stem cells differentiation. Anti-TNF therapy may be an effective treatment for vitiligo.
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PMID:Use of anti-tumor necrosis factor agents: a possible therapy for vitiligo. 1920 Nov 1

Specific antagonists of tumour necrosis factor (TNF-alpha) have rapidly gained popularity for the treatment of rheumatoid arthritis and ankylosing spondylitis (AS). Reported side effects from these agents include drug-induced autoimmune disorders. The monoclonal antibody against TNF-alpha, infliximab, has been associated with induction of systemic lupus erythematosus (SLE) in only one patient with AS in the literature. However, there have been no published reports of drug induced lupus-like syndrome (LLS) with positive anti-histone antibodies. We describe a 59-year-old woman with a 12-year history of refractory axial AS who developed signs and symptoms of LLS during treatment with infliximb with positive antinuclear and anti-histone antibodies. On diagnosis of LLS, infliximab was discontinued and the LLS-related symptoms promptly resolved.
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PMID:Drug-induced lupus-like syndrome in ankylosing spondylitis treated with infliximab. 1921 Aug 83

Systemic inflammatory disorders like rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are characterized by extensive dysregulation of bone metabolism recognized as focal articular bone erosions, juxta-articular and systemic bone loss. The complex interactions between bone cells, osteoprotegerin/RANKL pathway and a variety of inflammatory mediators are involved in the pathogenesis of focal and systemic osteopenia. Treatments with TNF-alpha blockers inhibit inflammation-induced bone resorption and might prevent structural bone damage in RA. In some studies with anti-TNF agents, an increase in BMD has been documented in spondyloarthropathies and in RA. The B-cell depleting antibody rituximab and the T-cell costimulation blocker abatacept are emerging as other effective treatment options in RA. Studies with anti- RANKL antibody Denosumab in RA demonstrate, that treatment targeting RANKL prevents development of erosions but not inflammation. This article reviews recent scientific literature regarding the effects of modern targeted therapies on bone turnover, bone mass and focal damage of joints.
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PMID:[Effects of biologic antirheumatic treatments on bone metabolism in rheumatoid arthritis and ankylosing spondylitis]. 1939 55

The pathogenesis of ankylosing spondylitis (AS) still remains an enigma. Although some studies have indicated the importance of T-cells and proinflammatory cytokines in the pathogenesis of the AS, it is still unknown whether co-stimulatory molecule CD154 participates in the pathogenesis of AS and how its level changes during the anti-TNF-alpha treatment of AS. This study is performed to evaluate the expression of CD154 in peripheral blood T-lymphocytes of patients with AS and observe the change of CD154 in etanercept-treated AS patient. We collected the peripheral blood and clinical data from 66 AS, 30 rheumatoid arthritis (RA) patients, and 30 healthy controls. Thirty-nine active AS patients were enrolled in a randomized double-blind placebo-controlled trial. We followed up 37 cases that fulfilled the ASAS20 response criteria after they finished etanercept treatment till week 48. The percentage of CD3+CD154+ in peripheral blood lymphocytes was evaluated by flow cytometry. We found that CD154 expression in AS patients was significantly higher than that in healthy volunteers and RA patients (both P < 0.001). The expressions of CD154 in AS patients at active stage or with peripheral joint involvement were significantly higher than those at stable stage or with axial involvement alone (P = 0.005 and 0.044, respectively). The expression of CD154 decreased in AS patients treated with etanercept compared with patients treated with placebo at week 6 (P < 0.001). Compared with healthy volunteers, the expression of CD154 in 16 AS patients who relapsed after finishing etanercept treatment was elevated again (P = 0.012). These findings show that co-stimulatory molecule CD154 is overexpressed on T-lymphocytes in peripheral blood of AS patients and can be down-regulated by etanercept treatment, which suggest that CD154 might be involved in the inflammatory evolvement of AS and might be a potential biomarker to monitor AS disease activity and the effect of etanercept treatment.
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PMID:Abnormal high-expression of CD154 on T lymphocytes of ankylosing spondylitis patients is down-regulated by etanercept treatment. 1946 23

Adalimumab is a fully human IgG1 monoclonal antibody that specifically binds to tumor necrosis factor (TNF)-alpha, and is administered by subcutaneous injection. The mechanism of action is based on both the neutralization of TNF-alpha bioactivity and the induction of apoptosis of TNF-expressing mononuclear cells. The drug is approved for the treatment of rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis (PsA), and recently also for the treatment of Crohn's disease. The effectiveness of adalimumab in psoriasis was previously suggested by the subset analysis of patients enrolled in PsA trials who were affected by concomitant psoriasis, and recently confirmed by a phase II trial and the preliminary results from phase III trials in moderate to severe psoriasis. These results demonstrate that adalimumab is effective in improving psoriasis and quality of life, with sustained effects over >/= 1-year treatment period. The safety data from psoriasis studies were similar to those of previous studies in other diseases. The risk of adverse events did not appear to increase with continuous long-term exposure to adalimumab.
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PMID:Drug focus: adalimumab in the treatment of moderate to severe psoriasis. 1970 19

Ankylosing spondylitis is a chronic inflammatory condition which preferentially affects the axial skeleton, often beginning in the sacroiliac joints. The etiology of the pathologic lesions of this condition including enthesitis, erosive articular changes, osteitis, and fibrous ankylosis, as well as changes which occur in the eye, gastrointestinal tract, cardiovascular system, and lungs is unknown; however, there is a strong association with HLA-B27, which indicates altered immunity. One of the major mediators of the immune response is TNF-alpha, which functions as a pleiotrophic soluble messenger primarily from macrophages. TNF-alpha is principally involved with activation of both normal and transformed cells, including endothelium, synoviocytes, osteoclasts, chondrocytes, and fibroblasts. The cornerstone of medical management of ankylosing spondylitis includes intensive physical therapy and nonsteroidal anti-inflammatories for symptomatic relief. However, it is becoming increasingly recognized that TNF-alpha blockade has an important role in the reduction of spine and joint inflammation. This review discusses the data that supports use of etanercept in the treatment of ankylosing spondylitis.
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PMID:Treatment of ankylosing spondylitis: focus on etanercept. 1970 47

Sexual dysfunction is a common problem among patients with ankylosing spondylitis (AS). This study was an open-label study without placebo to assess sexual dysfunction in male patients with AS, and to determine whether sexual function might improve with the use of tumor necrosis factor (TNF)-alpha blockers. Twenty-two males with AS (age, 29-48 years) were treated for 3 months with TNF-alpha blockers. Before and after treatment, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) was measured, and all patients completed the International Index of Erectile Function (IIEF) questionnaire, a self-administered measure of sexual dysfunction with five domains: erectile function (EF), intercourse satisfaction (IS), orgasmic function (OF), sexual desire (SD) and overall satisfaction (OS). There were significant improvements in BASDAI after treatment with TNF-alpha blockers (P<0.001). Anti-TNF-alpha treated patients showed significant improvements in four out of the five IIEF domains (EF, P<0.001; IS, P<0.001; SD, P=0.006; OS, P=0.033). Among patients with erectile dysfunction, there were significant improvements in three IIEF domains (EF, P=0.006; IS, P=0.007; SD, P=0.018). Only IS domain of IIEF showed a significant correlation with BASDAI (partial correlation coefficient = -0.484, P=0.026). This study showed that anti-TNF-alpha therapy may improve sexual dysfunction in male AS patients, in addition to reducing disease activity.
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PMID:The effect of anti-tumor necrosis factor agents on sexual dysfunction in male patients with ankylosing spondylitis: a pilot study. 1975 42

The treatment of the two most frequent inflammatory rheumatic diseases rheumatoid arthritis (RA) and ankylosing spondylitis (AS) has some similarities but in total more differences. Thus, therapy with non-steroidal anti-inflammatory agents (NSAIDs), conventional disease modifying anti-rheumatic drugs (DMARDs) and biologic agents has a different role in the management and different efficacy in AS and RA. This implies signs and symptoms, function, and structural damage. This is in part due to the different pathogenesis: (i) while the synovium is an important target in RA it is rather the bone in AS and (ii) while the pathology in RA is rather osteodestructive to cartilage and bone presenting with erosions, it is predominantly osteoproliferative in AS as indicated by syndesmophytes and ankylosis. Biologic agents targeting tumor necrosis factor (TNF-alpha) work clinically well in both diseases but, while they clearly inhibit structural damage in RA, they do not seem to have much influence on new bone formation in AS. DMARDs are efficacious in RA but less so in AS. NSAIDs are efficacious in both RA and AS, but they are considered first line of therapy in AS while they are rather adjunctive agents in RA. In AS, NSAIDs, potentially especially coxibs, may even prevent new bone formation due to their inhibitory effect on cyclooxygenase-2.
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PMID:Treatment of rheumatoid arthritis and ankylosing spondylitis. 1982 62

There are clear differences in the clinical picture and in the pathogenesis between rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Biologic agents targeting TNF-alpha are efficacious in both diseases, with some tendency to work even better in spondyloarthritides (SpA) on a clinical basis. However, anti-TNF therapy was shown to inhibit radiographic progression in RA but not in AS. This is probably due to the outstanding difference in pathogenesis: while in RA osteodestructive lesions such as erosions predominate, AS patients will rather develop osteoproliferative changes such as syndesmophytes. There is some evidence that anti-TNF agents may show longterm efficacy and acceptable safety profiles over 5-10 years. There are some differences between the agents.Whether the recent developments of targeted therapies in RA with agents such as rituximab, abatacept and tocilizumab will also work for AS is unknown at present.
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PMID:Biologics in the treatment of rheumatoid arthritis and ankylosing spondylitis. 1982 66


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