Literature on Psoriatic Arthritis

Juvenile psoriatic arthritis carrying familial Mediterranean fever gene mutations in a 14-year-old Turkish girl.

J Dermatol. 2007 May;34(5):344-8

Authors: Yeniay BS, Karaca NE, Yuksel SE, Midyat L, Kutukculer N

Juvenile psoriatic arthritis (JPsA) is characterized by asymmetric arthritis of big and small joints, enthesitis, dactylitis, psoriatic skin lesions and nail pitting. Investigators agree that JPsA is a relatively common chronic arthropathy of childhood that differs clinically, serologically, and genetically from both juvenile idiopathic arthritis and juvenile ankylosing spondylitis. Familial Mediterranean fever (FMF) is a multisystemic autosomal recessive disease occasionally accompanied by sacroiliitis. This is characterized by recurrent self-limited attacks of fever and accompanying abdominal, chest and arthricular pain. We present a 14-year-old Turkish girl with JPsA and carrying FMF gene mutations. In this patient, JPsA was diagnosed according to her physical, laboratory and skin biopsy findings and a treatment with methotrexate and sulfasalazine was started. As an inadequate clinical and laboratory response was obtained after the first month of therapy, the patient was investigated for FMF, and was diagnosed by molecular analyses of related gene (E148Q heterozygous/V726A homozygous mutation) besides clinical findings. After 2 weeks of the colchicine treatment, symptoms of the patient regressed and acute phase reactants decreased. To our knowledge, this is the first case presenting with psoriatic arthritis and FMF gene mutations together and responds to colchicine, methotrexate and sulfasalazine dramatically in clinical and laboratory findings. This case has been presented to remind that cases with psoriatic arthritis may also carry mutations in the MEFV gene.

PMID: 17408446 [PubMed - in process]

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Two years of experience with etanercept in recalcitrant psoriasis.

Br J Dermatol. 2007 Apr 4;

Authors: Ahmad K, Rogers S

Background The safety and efficacy of etanercept have been demonstrated in patients with rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. Placebo-controlled trials have indicated the efficacy of etanercept in moderate to severe psoriasis. Objectives To observe the efficacy and safety profile of etanercept in patients with severe psoriasis resistant to other systemic agents over a 2-year period. Methods In this retrospective study, 49 patients were treated with etanercept between March 2004 and March 2006. All patients were screened for tuberculosis with tuberculin test and a chest X-ray. Thirty-nine patients started on etanercept 25 mg twice weekly (BIW) and 10 started at 50 mg BIW when judged to be clinically indicated. In 19 of those on 25 mg BIW, the dose was increased to 50 mg BIW because of poor response and psoriasis flaring. Response to treatment was assessed by Psoriasis Area and Severity Index (PASI) and static Physician Global Assessment (PGA). Patients were reviewed at 8-week intervals, when clinical response and adverse effects were noted. Results Forty-four patients (90%) had chronic plaque psoriasis, two (4%) were suberythrodermic, one (2%) had palmoplantar pustular psoriasis and two (4%) had acrodermatitis continua of Hallopeau. At least 75% reduction in PASI was achieved in 47% of patients at week 24 and 66% at week 48. At week 24, 44% had a PGA score of excellent, and at week 48, 58% scored excellent. In 12 who cleared, etanercept was stopped. Ten of these relapsed and etanercept was recommenced, while two remained in remission (mean 12.5 weeks). One patient developed extrapulmonary tuberculosis. Conclusions Etanercept was effective in severe psoriasis recalcitrant to other systemic medication. The drug was well tolerated. Development of tuberculosis in one patient underlines the need for rigorous tuberculosis screening.

PMID: 17408393 [PubMed - as supplied by publisher]

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Elevated triglyceride and cholesterol levels after intravenous antitumour necrosis factor-alpha therapy in a patient with psoriatic arthritis and psoriasis vulgaris.

Br J Dermatol. 2007 Apr 4;

Authors: Antoniou C, Dessinioti C, Katsambas A, Stratigos AJ

PMID: 17408391 [PubMed - as supplied by publisher]

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Developing a magnetic resonance imaging scoring system for peripheral psoriatic arthritis.

J Rheumatol. 2007 Apr;34(4):859-61

Authors: McQueen F, Lassere M, Bird P, Haavardsholm EA, Peterfy C, Conaghan PG, Ejbjerg B, Genant H, O’connor P, Emery P, Ostergaard M

We describe the first steps in developing an OMERACT magnetic resonance imaging (MRI) scoring system for peripheral psoriatic arthritis (PsA). A preexisting MRI dataset (finger joints) from 10 patients with PsA was scored by 4 readers for bone erosion, bone edema, synovitis, tendinopathy, and extracapsular features of inflammation (including enthesitis) according to specified criteria. Scoring reliability between readers was moderate to high for bone edema and erosion, but lower for soft tissue inflammation. Measures to improve reliability for future exercises will include reviewing definitions of pathological features and prior reader calibration.

PMID: 17407240 [PubMed - in process]

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The OMERACT Magnetic Resonance Imaging Inflammatory Arthritis Group - Advances and Priorities.

J Rheumatol. 2007 Apr;34(4):852-3

Authors: Ostergaard M, McQueen F, Bird P, Peterfy C, Haavardsholm E, Ejbjerg B, Lassere M, O’connor P, Emery P, Edmonds J, Genant H, Conaghan PG

This article updates the work and research priorities of the OMERACT working group on magnetic resonance imaging (MRI) in inflammatory arthritis, as presented to the OMERACT 8 meeting in Malta in May 2006. This work focused on testing the reliability of dedicated extremity MRI in rheumatoid arthritis and on the initial steps in the development of an MRI score for peripheral psoriatic arthritis.

PMID: 17407237 [PubMed - in process]

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Immune-mediated inflammatory diseases (IMIDs) and biologic therapy: a medical revolution.

Postgrad Med J. 2007 Apr;83(978):251-60

Authors: Kuek A, Hazleman BL, Ostör AJ

Targeted biologic therapies have revolutionised treatment of immune-mediated inflammatory diseases (IMIDs) due to their efficacy, speed of onset and tolerability. The discovery that clinically unrelated conditions, such as rheumatoid arthritis and Crohn’s disease, share similar immune dysregulation has led to a shift in the management of IMIDs from one of organ-based symptom relief to mechanism-based treatment. The fact that anticytokine therapy has been effective in treating multiple orphan inflammatory conditions confirms the IMID paradigm. In this review we examine the biologic agents currently licensed for use in the US and Europe: infliximab, etanercept, adalimumab, rituximab, abatacept, anakinra, alefacept and efalizumab. We also discuss the rationale behind the management of IMIDs using rheumatoid arthritis, Crohn’s disease, psoriasis and psoriatic arthritis as examples. For the medical profession, IMID represents a breakthrough in the way pathology is classified. In this burgeoning era of biologic therapy the prospect of complete disease remission is conceivable.

PMID: 17403952 [PubMed - in process]

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Primer: establishing a clinical trial unit-regulations and infrastructure.

Nat Clin Pract Rheumatol. 2007 Apr;3(4):234-9

Authors: Fleischmann R

The performance of clinical trials can be very rewarding for the practicing or academic clinical rheumatologist. There are at least 50 new compounds-small molecules and biologics-in development for rheumatic diseases such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus, ankylosing spondylitis, psoriatic arthritis, scleroderma, gout and fibromyalgia. Clinical trials are important to try to determine the appropriate use of these compounds, as well as to answer questions about their safety. To carry out clinical trials effectively, the physician-investigator must be aware of, and adhere to, the regulatory requirements. The purpose of this article is to review these requirements in depth, as well as to discuss the infrastructure required to establish a successful clinical trial unit.

PMID: 17396109 [PubMed - in process]

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Drug Insight: different mechanisms of action of tumor necrosis factor antagonists-passive-aggressive behavior?

Nat Clin Pract Rheumatol. 2007 Apr;3(4):227-33

Authors: Rigby WF

Antagonists of tumor necrosis factor (TNF) have revolutionized the treatment of selected inflammatory diseases. In rheumatology, this has been most notable for ankylosing spondylitis, psoriatic arthritis and rheumatoid arthritis. Despite their specificity for TNF, these agents, which include the soluble p75 receptor etanercept and the anti-TNF antibodies adalimumab and infliximab, have demonstrated differential clinical efficacy in studies of rheumatoid arthritis; patients who do not respond to one antagonist often respond to another. Therapeutic disparity of these agents is also seen in specific diseases, most notably Crohn’s disease. Differences in pharmacodynamics, pharmacokinetics and mechanisms of action, as well as disease heterogeneity, have been proposed to account for these effects. Reverse signaling by transmembrane TNF in response to anti-TNF antibodies, but not soluble receptor, might also influence the therapeutic response.

PMID: 17396108 [PubMed - in process]

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Mechanism of action, pharmacokinetics, and drug interactions of etanercept in dermatology.

J Cutan Med Surg. 2007 Apr;11 Suppl 1:S3-S13

Authors: Papp KA, Keystone EC, Shear NH

Etanercept, a dimeric soluble form of the p75 tumor necrosis factor (TNF) receptor, has been shown to be efficacious for the treatment of psoriatic arthritis and moderate to severe chronic plaque psoriasis, as well as rheumatoid arthritis, juvenile rheumatoid arthritis, and ankylosing spondylitis. In this article, we review the mechanism of action, pharmacokinetics, and drug interactions of etanercept. Differences between etanercept and other anti-TNF antagonists with respect to membrane binding, the effect on T lymphocytes, the effect on the blood-brain barrier, adverse event profiles, and disease efficacy are also discussed.

PMID: 17394851 [PubMed - in process]

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Efficacy of etanercept in the management of plaque psoriasis and psoriatic arthritis.

J Cutan Med Surg. 2007 Apr;11 Suppl 1:S14-22

Authors: Poulin Y, Gupta AK, Amiss JD

Etanercept is a fully human dimeric fusion protein that reversibly binds tumor necrosis factor alpha. The first approved indication for etanercept was for the treatment of rheumatoid arthritis. It has also been shown to be highly efficacious in numerous large-scale trials for the treatment of plaque psoriasis; this indication was approved in Canada, the United States, and Europe. The recommended dosing of etanercept for plaque psoriasis is 50 mg twice weekly for 12 weeks, followed by a maintenance dose of 50 mg per week. Etanercept given at 50 mg twice weekly for 12 weeks significantly improved plaque psoriasis, as assessed by the Psoriasis Area and Severity Index (PASI), in which 75% reduction in PASI scores (PASI 75) has been the gold standard for judging effective therapy. Dosing given for 12 weeks produced PASI 75 rates of 47 to 49% in the phase 3 clinical trials. Longer treatment periods at this dosage have been investigated, from 24 to 48 weeks, with PASI 75 increasing to 63%. The importance of quality of life for psoriasis patients has been the focus of recent trials, and etanercept has been shown significant improvement in quality of life measures. Interim results from a phase 3b study suggest that etanercept may help reduce the burden of health care resources use by psoriatics. Etanercept has also shown efficacy in nail psoriasis. Case reports indicate that etanercept may be useful in psoriatic erythroderma, pustular psoriasis, guttate psoriasis, and palmopustular psoriasis. Etanercept is an effective biologic agent currently approved for the management of plaque psoriasis and psoriatic arthritis.

PMID: 17394849 [PubMed - in process]

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