Literature on Psoriatic Arthritis

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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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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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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Related ArticlesProlactin and growth hormone responses to hypoglycemia in patients with systemic sclerosis and psoriatic arthritis.

Ann N Y Acad Sci. 2006 Jun;1069:145-8

Authors: Rovensky J, Raffayova H, Imrich R, Radikova Z, Penesova A, Macho L, Lukac J, Matucci-Cerinic M, Vigas M

This study compared prolactin (PRL) and growth hormone (GH) responses to hypoglycemia in premenopausal females with systemic sclerosis (SSc) and psoriatic arthritis (PsA) with those in matched healthy controls. No differences were found in glucose and GH responses to hypoglycemia in both groups of patients compared to controls. SSc patients had lower PRL response (P

PMID: 16855141 [PubMed - in process]

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Related ArticlesConcepts and epidemiology of spondyloarthritis.

Best Pract Res Clin Rheumatol. 2006 Jun;20(3):401-17

Authors: Sieper J, Rudwaleit M, Khan MA, Braun J

The term ’spondyloarthritides’ (SpA) comprises ankylosing spondylitis (AS), reactive arthritis, arthritis/spondylitis with inflammatory bowel disease, and arthritis/spondylitis with psoriasis. The main links between these diseases are an association with HLA-B27 and a similar clinical picture. Patients normally present with chronic low back pain or asymmetrical arthritis, predominantly of the lower limbs, and an overlap of these symptoms often occurs. AS is regarded as the most severe subtype. Recent attention has focused on earlier diagnosis of AS among patients with chronic low back, and this is becoming more important as effective therapies for early treatment have become available. AS is a disease of young people, normally starting in the third decade of life. The incidence and prevalence rates of AS, and of SpA as a whole, are strongly dependent and are directly correlated to the prevalence of HLA-B27 in a given population. Incidence rates of 0.5-8.2/100 000 population and prevalence rates of 0.2-1.2% have been described for AS, and about double these figures have been reported for SpA.

PMID: 16777573 [PubMed - indexed for MEDLINE]

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Related ArticlesEfficacy and safety of infliximab for the treatment of psoriatic arthritis.

Nat Clin Pract Rheumatol. 2006 Jun;2(6):300-1

Authors: Ritchlin C

PMID: 16932707 [PubMed - in process]

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Related ArticlesProlactin and growth hormone responses to hypoglycemia in patients with systemic sclerosis and psoriatic arthritis.

Ann N Y Acad Sci. 2006 Jun;1069:145-8

Authors: Rovensky J, Raffayova H, Imrich R, Radikova Z, Penesova A, Macho L, Lukac J, Matucci-Cerinic M, Vigas M

This study compared prolactin (PRL) and growth hormone (GH) responses to hypoglycemia in premenopausal females with systemic sclerosis (SSc) and psoriatic arthritis (PsA) with those in matched healthy controls. No differences were found in glucose and GH responses to hypoglycemia in both groups of patients compared to controls. SSc patients had lower PRL response (P

PMID: 16855141 [PubMed - indexed for MEDLINE]

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Granulocyte and monocyte adsorption apheresis (GCAP) for refractory skin diseases caused by activated neutrophils and psoriatic arthritis: evidence that GCAP removes Mac-1-expressing neutrophils.

Ther Apher Dial. 2006 Jun;10(3):247-56

Authors: Kanekura T, Hiraishi K, Kawahara K, Maruyama I, Kanzaki T

In the present study, we have shown that granulocyte and monocyte adsorption apheresis (GCAP), an extracorporeal apheresis instrument whose column contains cellulose acetate (CA) beads, is useful for skin diseases attributable to activated granulocytes and psoriatic arthritis (PsA). We assessed the clinical effectiveness of GCAP and investigated the mechanisms underlying the adsorption of pathogenic granulocytes. The effect of GCAP was assessed in 14 patients with neutrophilic dermatoses and 16 with PsA. The mechanisms by which the instrument adsorbs activated granulocytes were investigated using an in vitro mini-column system that mimics the GCAP. Skin lesions and arthropathy improved in 22 of 29 patients (75.9%) and 14 of 18 (77.8%), respectively. Mac-1 (CD11b/CD18) expression on the peripheral neutrophils, increased compared with normal subjects, was reduced by GCAP. In the mini-column system, CA beads adsorbed 50% neutrophils; and adsorption was inhibited significantly by treating plasma with EDTA and blood cells with antihuman CD11b monoclonal antibody. GCAP was useful for treating neutrophilic dermatoses and PsA. GCAP adsorbs Mac-1-expressing neutrophils to the CA beads by the binding of complement component (iC3b) on CA beads and CD11b expressed on activated neutrophils.

PMID: 16817789 [PubMed - in process]

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[Psoriasis and psoriatic arthritis]

Rev Med Liege. 2006 May-Jun;61(5-6):334-40

Authors: Henno A, Rausin A, Malaise M, de la Brassinne M

Psoriasis is a frequent multifactorial chronic skin disease that can lead to a decreased quality of life. Some patients also present arthritis. Those two complex inflammatory diseases share some of their characteristics, but several clinical manifestations can be distinguished in each of them. In addition to classical medications (constituted of topical treatments, methotrexate, ciclosporin and retinoids for cutaneous psoriasis and non steroidal anti-inflammatory drugs or methotrexate for psoriatic arthritis), they are the target of a new generation of therapies: the biologics.

PMID: 16910258 [PubMed - in process]

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Related ArticlesJuvenile psoriatic arthritis and acquired sensorineural hearing loss in a teenager: is there an association?

Clin Exp Rheumatol. 2006 May-Jun;24(3):344-6

Authors: Giani T, Simonini G, Lunardi C, Puccetti A, De Martino M, Falcini F

Autoimmune inner ear disease is a cause of sensorineural hearing loss, first described in 1979 by McCabe. The occurrence during rheumatic diseases is already documented in adults, but to our knowledge, this evidence is still lacking in children. A 13-yr-old girl affected by juvenile psoriatic arthritis, treated with etanercept, developed a bilateral and asymmetric sensorineural deafness. The patient significantly improved after steroid administration. Once ruled out the principal causes of sensorineural hearing loss, we also considered the hypothesis of an anti-TNF side effect. However, the clinical presentation, the efficacy on steroid treatment and the presence of inner ear auto-antibodies prompt us to consider autoimmune-SNHL as the most plausible diagnosis. The young age of our patient seems to suggest a genetic susceptibility to autoimmunity and supports the concept of associated autoimmune diseases.

PMID: 16870107 [PubMed - in process]

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