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)

It has recently been reported that tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) plays various roles in such autoimmune diseases as diabetes, multiple sclerosis (MS), and systemic lupus erythematosus (SLE). However, it has still remained unclear whether there is a close relationship between TRAIL and ankylosing spondylitis (AS). In this study, we investigated the association between the expression of TRAIL and AS. The specific messenger ribonucleic acid (mRNA) levels of TRAIL in peripheral blood mononuclear cells (PBMCs), serum sTRAIL, and TNF-alpha concentrations from 60 AS patients, 20 rheumatoid arthritis (RA) patients, and 30 healthy controls were determined by real-time fluorescent quantitative polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). The results indicated that the expression levels of TRAIL mRNA, and serum sTRAIL were significantly elevated in AS patients, compared with RA patients and healthy controls, and there was a close association between TRAIL mRNA and sTRAIL levels. However, there was no significant difference between human leukocyte antigen (HLA)-B27-positive and -negative AS patients. In HLA-B27-positive patients, TRAIL mRNA and sTRAIL closely correlated with serum TNF-alpha and C-reactive protein (CRP), but did not correlate in HLA-B27-negative patients. In conclusion, upregulated expression of TRAIL might be somewhat specific for evaluation of AS.
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PMID:Preliminary clinical measurement of the expression of TNF-related apoptosis inducing ligand in patients with ankylosing spondylitis. 1834 11

Psoriasis and psoriatic arthritis are debilitating inflammatory immunemediated diseases which are chronic in nature and often require lifelong attention. Traditional therapies used to combat these diseases lack sufficient long-term efficacy and are associated with a number of toxicities. Failing to adequately satisfy both patients and physicians, traditional therapies have proven insufficient and have left few options. Etanercept is a tumor necrosis factor (TNF) antagonist that reduces elevated TNF levels by competitively binding to both TNF-alpha and TNF-beta and inhibiting the proinflammatory cascade. Providing a valuable treatment option alone, etanercept can also be effectively administered in conjunction with traditional treatments. Etanercept is self administered by subcutaneous (SC) injection, making treatment less of a burden for patients by eliminating the need for frequent office visits and laboratory testing. Etanercept is approved in the US for the treatment of psoriasis, psoriatic arthritis, rheumatoid arthritis, juvenile rheumatoid arthritis, and ankylosing spondylitis.
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PMID:Use of etanercept in the treatment of psoriasis and psoriatic arthritis. 1847 78

Diagnosis of ankylosing spondylitis (AS) is still delayed for several years in some patients. The correct diagnosis of early disease has always been a challenge, which has become even more important as with the introduction of TNF-alpha inhibitors, very effective new treatments have become available. For diagnosis of AS imaging methods such as conventional radiography and computer tomography are well established. Functional imaging modalities including magnetic resonance imaging and contrast-enhanced colour Doppler ultrasound provide additional information on the presence of active inflammatory changes in the sacroiliac joints and may help to diagnose AS before radiographic changes become visible. Magnetic resonance imaging and sonography also identifiy other non-sacroiliac axial manifestations of AS and peripheral involvement such as enthesitis and synovitis of peripheral joints.
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PMID:[Imaging techniques for early diagnosis of ankylosing spondylitis]. 1850 Apr 69

New pathogenetic insights have identified the key role of TNF-alpha in inflammatory rheumatic diseases and have revolutionized the therapy of spondyloarthritides. TNF-alpha-antagonists specifically inhibit the pro-inflammatory effects of TNF-alpha. Clinical studies with infliximab (Remicade), Etanercept (Enbrel) or Adalimumab (Humira) in ankylosing spondylitis or related diseases demonstrate superior efficacy to conventional drugs like non-steroidal antirheumatic drugs or traditional disease modifying antirheumatic drugs.
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PMID:[Biologics in the early treatment of ankylosing spondylitis and related forms of spondyloarthritis]. 1850 Apr 71

Anti-TNF-alpha agents have been tried in cases of refractory sarcoidosis, giving favourable results. Thus, the occurrence of a granulomatous disease in a patient receiving such drug seems paradoxical. We describe 2 patients with inflammatory rheumatic disease, the first with ankylosing spondylitis, the second with rheumatoid arthritis, under anti-TNF-alpha treatment (infliximab and etanercept respectively) who developed non-caseating granulomas of the lungs and lymph nodes consistent with the diagnosis of sarcoidosis. Limited and various similar cases have been reported. It is generally considered that these granulomatous diseases are related to the anti-TNF-alpha agent.
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PMID:Sarcoidosis occuring during anti-TNF-alpha treatment for inflammatory rheumatic diseases: report of two cases. 2014 30

Adalimumab is the first fully human anti-tumor necrosis factor (TNF-alpha) monoclonal antibody and it binds to both soluble and cell-bound TNF-alpha, modulating biological responses linked to this cytokine. Different trials have probed the efficacy of adalimumab even after one week, and accumulated experience in rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis and Crohn's disease shows adalimumab as a safe drug sharing a similar adverse effects profile with the other anti-TNF-alpha molecules. Specific features of adalimumab are revised.
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PMID:[What is special about adalimumab?]. 1868 Jun 88

We describe a patient presenting with acute hepatitis while receiving infliximab for ankylosing spondylitis. A slight increase in serum aminotransferases was first observed in this patient after 4 infusions of infliximab. The treatment was stopped after the 6th infusion when laboratory work-up revealed a 10-fold increase in serum levels of aminotransferases. A liver biopsy showed interportovenular bridging necrosis with macrophage accumulation consistent with the diagnosis of acute toxic hepatitis. After infliximab discontinuation, hepatic abnormalities resolved and the patient was treated with etanercept for more than 2 years without recurrence of hepatitis. This case underlines the lack of hepatic cross-toxicity between infliximab and etanercept making possible the continuation of anti-TNF-alpha therapy with etanercept in patients who have presented infliximab-related hepatic dysfunction.
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PMID:Infliximab-induced hepatitis: absence of cross-toxicity with etanercept. 1869 25

To investigate the effects of TNF-alpha -308, -238 promoter polymorphisms on TNF-alpha transcription in B27 positive Chinese patients with ankylosing spondylitis (AS). The possible relationship between polymorphisms, MHC antigens, and quantitative TNF-alpha mRNA expression were evaluated. Single nucleotide polymorphisms (SNPS) of TNF-alpha -308 and -238 were performed by PCR-amplification refractory mutation system method (PCR-ARMS) in sixty-seven B27-positive AS patients and 60 HLA-B27 positive healthy controls in Chinese. Quantitative measurement of TNF-alpha mRNA in peripheral blood mononuclear cells was performed with real time RT-PCR. The polymorphisms were correlated to quantitative TNF-alpha mRNA, and MHC antigens (determined by SSP method) in AS patients. The prevalence rate of both -308G/A and -238G/A TNF-alpha promoter polymorphisms in patients were not significantly different from those in normal subjects. However, a significant high LPS-stimulated TNF-alpha mRNA expression was found in peripheral blood mononuclear cells from patients with promoter -308G/A polymorphism (TNF2) as compared to those in -308G/G genotype (TNF1). Furthermore, -308G/A polymorphism in patients was found to be tightly associated with distinct haplotypes of A33/B58/Cw10 [12 out of 14 -308G/A patients (85.7%) versus none in 53 -308G/G patients], independent of B27 antigen. HLA-A33-B58-Cw10 haplotypes associated TNF-alpha promoter -308G/A polymorphism might play an important role in disease pathogenesis of AS in Chinese population, partially related to a driving force of a higher TNF-alpha production. It confirms once again the importance and complexity of MHC related molecules in disease pathogenesis of AS.
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PMID:Higher LPS-stimulated TNF-alpha mRNA levels in peripheral blood mononuclear cells from Chinese ankylosing spondylitis patients with -308G/A polymorphism in promoter region of tumor necrosis factor: association with distinct A33/B58/Cw10 haplotypes. 1871 20

The objective is to report a case of atypical acute infectious mononucleosis in a juvenile ankylosing spondylitis patient who was treated with infliximab. A 20-year-old man was hospitalized for the evaluation of lymphadenopathy and systemic symptoms. His symptoms developed at the eighth week of the infliximab treatment and he required hospitalization. Lymph node biopsy was performed and he was diagnosed as atypical infectious mononucleosis (absence of fever, pharyngitis, lymphocytosis and negative atypical lymphocytosis on blood smear). Infections have become major concerns in patients treated with TNF-blocking agents. In theoretical base, it is not surprising as TNF-alpha has a crucial role in the body's defense against both bacterial and viral invasion. Blocking the action of TNF may also change the course of the disease and could lead to a delay in the diagnosis. TNF-alpha-blocking treatment may mask the typical symptoms of infectious mononucleosis and atypical cases should be included in the differential diagnosis of lymphadenopathy in patients receiving anti-TNF-alpha agents.
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PMID:Atypical infectious mononucleosis in a patient receiving tumor necrosis factor alpha inhibitory treatment. 1903 55

Biological therapies for immune based chronic inflammatory diseases, especially cytokine inhibitors such as TNF-alpha antagonists, have been acceptably well tolerated in clinical trials with patients suffering rheumatic, dermatologic and intestinal diseases in which they have been subsequently indicated. However, the pharmacovigilance studies and long-term follow-up have clarified several aspects on their safety in the everyday clinical use. The adverse effects associated with TNF-alpha inhibitors can generally be classified into those related to the target (or class) and those related to the agent. Target-related adverse events include those potentially attributable to the immunosuppression inherent in blocking a key cytokine, a phenomenon that could increase the susceptibility to infections and neoplasms. Specific inhibition of TNF-alpha could also facilitate hepatotoxicity, production of autoantibodies, development of demyelinizing diseases and it is also possibly associated to the worsening of congestive heart failure. The side effects related to the agent itself, such as allergic reactions and immunogenicity, are idiosyncratic phenomena of each molecule. Infliximab is an IgG1 class chimeric monoclonal antibody with extensive accumulated experience in the treatment of rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, intestinal inflammatory disease and, recently, moderate-to-severe plaque psoriasis. It is also being evaluated in other inflammatory dermatitis and systemic diseases with skin expression, such as severe atopic dermatitis, pityriasis rubra pilaris, pyoderma gangrenosum, cutaneous sarcoidosis, Adult Still's disease, inverted acne and refractory graft -versus- host disease. Predisposition of infliximab-treated individuals, as occurs with other anti-TNF-alpha agents, to cause an increase of conventional pyogenic infections (of the skin and soft tissues, respiratory tract, genitourinary tracts and bacteriemias) and an increase in granulomatous and opportunistic infections due to invasive or intracellular pathogens (such as Mycobacterium tuberculosis), has been well established and quantified in the last five years. We presently know that the initiation of screening strategies of latent infections (especially tuberculosis) in the host candidate to receive anti-TNF-alpha drugs, with their corresponding early treatment to avoid reactivations, and other prophylaxis, hygiene and vaccination measures have not only minimized these risks of suffering infections but also have practically reduced and equalized the different capacity to trigger infections belonging to each one of the biological agents individually.
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PMID:[Infectious risk]. 1908 Sep 87


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