Archive for June, 2006

TNFalpha antagonist therapy in ankylosing spondylitis and psoriatic arthritis: recommendations of the French Society for Rheumatology.

Friday, June 30th, 2006

Related ArticlesTNFalpha antagonist therapy in ankylosing spondylitis and psoriatic arthritis: recommendations of the French Society for Rheumatology.

Joint Bone Spine. 2006 Jun 30;

Authors: Pham T, Guillemin F, Claudepierre P, Luc M, Miceli-Richard C, Fautrel B, de Bandt M, Breban M, Goupille P, Maillefert JF, Masson C, Saraux A, Schaeverbeke T, Wendling D, Mariette X, Combe B,

OBJECTIVES: To develop recommendations for TNFalpha antagonist therapy in patients with spondyloarthropathies. METHODS: The Delphi consensus procedure was used to select questions, to which evidence-based answers were sought in the literature. Expert opinion was used when needed to estimate the risks and benefits of TNFalpha antagonists. TNFalpha antagonists exert potent antiinflammatory effects but fail to provide a definitive cure. RESULTS: Recommendations were developed for patients with ankylosing spondylitis (AS) or psoriatic arthritis (PsA). The following criteria for TNFalpha antagonist therapy were selected: definitive diagnosis of AS or PsA, active disease for at least 4 consecutive weeks documented during two physician visits, overall physician’s assessment of disease activity>/=4/10 and BASDAI>/=4/10 in axial disease or at least three tender and swollen joints in peripheral disease, failure to respond adequately to at least three nonsteroidal antiinflammatory drugs given in optimal dosages for at least 3 months in axial disease or at least one disease-modifying antirheumatic drug (methotrexate, leflunomide, sulfasalazine) for at least 4 months, with local glucocorticoid injections if appropriate, in peripheral disease. Effectiveness and safety should be evaluated by a rheumatologist. The frequency of monitoring depends on the drug. Lack of effectiveness should be defined as inadequate improvement after 6-12 weeks, with a less than two-point decrease in the BASDAI in axial disease or a less than 30% decrease in the tender and swollen joint counts in peripheral disease. CONCLUSION: These clinical practice recommendations should help rheumatologists in their everyday decisions regarding the use of TNFalpha antagonist therapy in patients with AS or PsA.

PMID: 16843030 [PubMed - as supplied by publisher]

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AA amyloidosis in psoriatic arthritis.

Thursday, June 29th, 2006

Related ArticlesAA amyloidosis in psoriatic arthritis.

Ir J Med Sci. 2006 Apr-Jun;175(2):81-2

Authors: Ryan JG, Dorman AM, O’Connell PG

BACKGROUND: Amyloidosis is an extremely rare complication of psoriatic arthritis (PsA) and is associated with a poor prognosis. We report a case of amyloidosis secondary to severe PsA in a young patient and the course of his disease over a 13-year period of aggressive immunosuppression. METHODS: Diagnosis of renal amyloidosis was made on biopsy: multi-agent immunosuppressive therapy was continued with stabilisation of renal function. RESULTS: Marked deterioration in renal function subsequently occurred following a reduction in cyclosporin A (CyA) dose and repeat biopsy confirmed worsening amyloidosis. CONCLUSION: This case report emphasises the need for aggressive control of the inflammatory response in secondary amyloidosis.

PMID: 16872037 [PubMed - in process]

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Targeting cytosolic phospholipase A2 by arachidonyl trifluoromethyl ketone prevents chronic inflammation in mice.

Monday, June 26th, 2006

Related ArticlesTargeting cytosolic phospholipase A2 by arachidonyl trifluoromethyl ketone prevents chronic inflammation in mice.

Eur J Pharmacol. 2006 Jun 13;539(3):195-204

Authors: Malaviya R, Ansell J, Hall L, Fahmy M, Argentieri RL, Olini GC, Pereira DW, Sur R, Cavender D

Cytosolic phospholipase A(2) (cPLA(2)) plays a pivotal role in inflammation by catalyzing the release of arachidonic acid, a substrate for lipoxygenase and cyclooxygenase enzymes, from membrane phospholipids. In the present study we examined the role of cPLA(2) in inflammatory responses through the use of a specific inhibitor of the enzyme, cPLA(2), arachidonyl trifluoromethyl ketone (AACOCF3). Interestingly, we observed that AACOCF3 is an inhibitor of chronic but not acute inflammatory responses. Specifically, AACOCF3 inhibited phorbol 12-myristate 13-acetate (PMA)-induced chronic ear edema in mice. Additionally, oral treatment of ovalbumin-sensitized/ovalbumin-challenged BALB/c mice with 20 mg/kg AACOCF3 prevented the development of airway hyper-responsiveness in a model of asthma. Furthermore, AACOCF3 decreased cellular recruitment in the airway lumen and airway inflammation after the ovalbumin challenge. Taken together, these results suggest that a potent and specific chemical inhibitor of cPLA(2) may be useful for the treatment of chronic inflammatory diseases including rheumatoid arthritis, inflammatory bowel disease, psoriasis, and asthma.

PMID: 16712837 [PubMed - indexed for MEDLINE]

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PPAR-gamma Gene Polymorphisms and Psoriatic Arthritis.

Sunday, June 25th, 2006
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PPAR-gamma Gene Polymorphisms and Psoriatic Arthritis.

J Rheumatol. 2006 Jun 15;

Authors: Butt C, Gladman D, Rahman P

OBJECTIVE: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation has been shown to play a role in suppressing angiogenesis and inflammation, both important pathological features of psoriatic arthritis (PsA). Given the potential physiological role for PPAR-gamma in PsA, we examined known coding polymorphisms in the PPAR-gamma gene in a Caucasian population. METHODS: PsA was diagnosed as an inflammatory arthritis in patients with psoriasis, in the absence of other etiologies for inflammatory arthritis. Control subjects were ascertained from the same population and were all Caucasian. DNA samples were genotyped for 4 PPAR-gamma variants by time-of-flight mass spectrometry using the Sequenom platform. All 4 single-nucleotide polymorphisms (SNP) were previously-reported coding variations, 3 of which caused an amino acid change: Pro12Ala (rs1801282), Pro40Ala (rs1805192), and Pro115Gln (rs1800571); the fourth SNP, C161T (rs3856806), was synonymous. All primers were designed using Sequenom SpectroDesigner software, and scanned using a mass spectrometry workstation. RESULTS: Of the 4 SNP examined, Pro40Ala and Pro115Gln were found to be nonpolymorphic in our population. Minor allele frequency for patients with PsA and controls for Pro12Ala (G) were 9.0% vs 13.8% (p = 0.017) and for C161T (T) 10.7% vs 12.0% (p = 0.56), respectively. All genotypes satisfied Hardy-Weinberg equilibrium. CONCLUSION: An association between PsA and a known coding SNP of the PPAR-gamma gene was observed in our Caucasian population. Further studies are now warranted for validation of our findings in an independent cohort.

PMID: 16783862 [PubMed - as supplied by publisher]

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Estimating the cost and health status consequences of treatment with TNF antagonists in patients with psoriatic arthritis.

Sunday, June 25th, 2006
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Estimating the cost and health status consequences of treatment with TNF antagonists in patients with psoriatic arthritis.

Rheumatology (Oxford). 2006 Jun 16;

Authors: Bansback NJ, Ara R, Barkham N, Brennan A, Fraser AD, Conway P, Reynolds A, Emery P

Objectives. Tumour necrosis factor (TNF) has been shown to improve the outcomes in patients with psoriatic arthritis (PsA). We estimate the long-term impact on health status of prescribing the TNF antagonist etanercept, and evaluate the cost-effectiveness in a health economic model. Methods. The relationship between disability (Health Assessment Questionnaire) and health state utility was explored to estimate the quality-adjusted life years (QALYs) gained from the TNF antagonist etanercept. A model was then used to compare sequences of treatments for PsA after failure of two conventional disease modifying anti-rheumatic drugs (DMARDs). One arm commences on etanercept therapy and this is compared with a strategy commencing with combination therapy of methotrexate and ciclosporin and another commencing with leflunomide. Individual patient data from Phase III etanercept trials is used to populate the model supported by published evidence from extensive literature searches. By incorporating a life table specific for a PsA population, and using a number of evidence- and expert opinion-based assumptions for disease progression, the model was extended beyond the trial duration to a 10-yr time horizon. Cost offsets were produced by avoiding surgery through delayed progression; drug and monitoring costs were also modelled. Results. Over the 10 yrs, modelled etanercept treatment gave 0.82 more QALYs when compared with combination therapy with methotrexate and ciclosporin, and 0.65 more QALYs in comparison with leflunomide. This equates to a central estimate for the cost per QALY of pound28 189 and pound28 189 for ciclosporin and leflunomide, respectively. Sensitivity analyses demonstrated this could vary by as much as +/-28%. Conclusions. With limited data currently available, the potential cost-effectiveness of etanercept in DMARD failures for adults with PsA appears encouraging. The result for other TNF antagonists will depend on how their relative efficacy and drug price compares with etanercept. A number of limitations are described and priorities for further research suggested.

PMID: 16782734 [PubMed - as supplied by publisher]

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Psoriatic arthritis: One or more diseases?

Sunday, June 25th, 2006
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Psoriatic arthritis: One or more diseases?

Best Pract Res Clin Rheumatol. 2006 Jun;20(3):435-50

Authors: Fitzgerald O, Dougados M

Psoriatic arthritis (PsA) is a common, debilitating auto-immune disease with diverse clinical features. In this paper, published evidence is examined, which addresses the issues that (a) PsA exists; and (b) PsA can or cannot be viewed as a distinct rheumatic disease from other spondyloarthritides. Evidence derived from epidemiological, clinical, genetic and immunohistological studies is included. Summarizing the evidence, it is clear that PsA does indeed exist, with the prevalence of rheumatic disease in patients with psoriasis (Ps) higher than would be expected. Certain clinical features also occur more commonly in PsA, although none can differentiate consistently from other arthropathies. Both genetic and immunohistological studies suggest that PsA, both oligo- and polyarticular disease, can be clearly separated from rheumatoid arthritis and that it belongs to the family of spondyloarthritides. The presence of Ps may confer a more severe clinical phenotype with poor radiological outcome. It may be that, with time, a specific genetic marker or diagnostic feature will emerge; additional, more detailed pathogenic studies are required. In the meanwhile, particularly with new treatments being evaluated, it is important to continue to develop specific classification or diagnostic criteria and to define both clinical and laboratory-based outcome measures.

PMID: 16777575 [PubMed - in process]

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Nail and Distal Interphalangeal Joint in Psoriatic Arthritis.

Sunday, June 25th, 2006
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Nail and Distal Interphalangeal Joint in Psoriatic Arthritis.

J Rheumatol. 2006 Jun 1;

Authors: Scarpa R, Soscia E, Peluso R, Atteno M, Manguso F, Del Puente A, Spanò A, Sirignano C, Oriente A, Di Minno MN, Iervolino S, Salvatore M

OBJECTIVE: To study distal interphalangeal (DIP) joints in patients with psoriatic arthritis (PsA) with or without onychopathy, using magnetic resonance imaging (MRI). METHODS: Twenty-three patients with PsA (9/14 F/M, median age 47 yrs), 12 with onychopathy (2/10 F/M, median age 44 yrs) and 11 without (7/4 F/M, median age 52 yrs), and 10 control subjects (5/5 F/M, median age 43.2 yrs) were enrolled. MRI of nail and distal phalanx (DP) including examination of DIP joints was carried out. MRI was performed with a surface coil in a 1.5 T device. For each selected finger, both longitudinal and axial scans were performed. The involvement of nail, DP, and DIP joint was scored. RESULTS: Nail thickening with or without surface irregularity occurred in 95.7% of cases (100% with onychopathy and 90.9% without). MRI nail involvement was more frequent in patients with clinical evidence of onychopathy than in those without (p = 0.003). Similarly, 95.7% of patients showed MRI abnormalities of DP (100% with onychopathy and 90.9% without). MRI DP abnormalities were more marked in patients with clinical evidence of onychopathy than in those without (p = 0.009). Involvement of DIP joints was present in 34.8% of cases (58.3% with onychopathy and 9.1% without), and onychopathic patients showed marked MRI DIP joint involvement in 5 cases and mild in 2, while patients without onychopathy showed minimal changes in one case (p = 0.03). Considering the entire group of patients, MRI involvement of DIP joints was always associated with MRI DP changes, and in no case was it present alone. CONCLUSION: MRI nail involvement was present in almost all patients with PsA studied, even in those without clinically evident onychopathy. MRI involvement of DP always overlapped with nail involvement, since it was present in all psoriatic cases showing MRI nail involvement. In contrast, MRI DIP joint involvement was almost exclusively in a lower percentage of the patients with clinical nail involvement and was always associated with MRI DP changes. Our results suggest that DIP joint involvement is always secondary to nail and DP involvement.

PMID: 16758507 [PubMed - as supplied by publisher]

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PSORS2 Markers Are Not Associated with Psoriatic Arthritis in the Italian Population.

Sunday, June 25th, 2006
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PSORS2 Markers Are Not Associated with Psoriatic Arthritis in the Italian Population.

Hum Hered. 2006;61(2):120-2

Authors: Giardina E, Predazzi I, Sinibaldi C, Peconi C, Amerio P, Costanzo A, Paradisi A, Capizzi R, Paradisi M, Chimenti S, Taccari E, Novelli G

Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy characterized by the association of arthritis and psoriasis (Ps). The precise etiology of PsA is unknown, but epidemiological studies supported the existence of a genetic component for the disease. Here we report an association study on a large PsA Italian cohort for DNA variants recently reported as associated alleles at PSORS2 (17q25) in Ps cohorts from the US. We focused on discovering a possible involvement of PSORS2 associated SNPs in pathogenesis of PsA. We selected two SNPs (rs7420, rs734232) within the proximal peak and two SNPs (rs869190 and rs1561946) within distal peak of PSORS2. Our results ruled out PSORS2 alleles as susceptibility factors in arthritis psoriatic patients of Italian origin and suggested that previous linkage signal reported for chromosome 17q25 should be independent on the presence of PsA. Copyright (c) 2006 S. Karger AG, Basel.

PMID: 16733365 [PubMed - in process]

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Flare of psoriasis and psoriatic arthritis following treatment with granulocyte colony-stimulating factor.

Tuesday, June 20th, 2006
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Flare of psoriasis and psoriatic arthritis following treatment with granulocyte colony-stimulating factor.

Am J Med. 1996 Nov;101(5):567-8

Authors: Kavanaugh A

PMID: 8948284 [PubMed - indexed for MEDLINE]

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Psoriasis onset during infliximab treatment: description of two cases.

Tuesday, June 20th, 2006
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Psoriasis onset during infliximab treatment: description of two cases.

Rheumatol Int. 2006 Jun 1;

Authors: Volpe A, Caramaschi P, Carletto A, Pieropan S, Bambara LM, Biasi D

The authors describe two patients with no personal or family history of psoriasis who developed psoriatic lesions during infliximab treatment: a woman affected by seronegative rheumatoid arthritis and a man affected by ankylosing spondylitis.

PMID: 16738903 [PubMed - as supplied by publisher]

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