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Rheumatology 2001; 40: 243-246
© 2001 British Society for Rheumatology

Editorial

Psoriatic arthritis—emerging concepts

S. Patel, D. Veale, O. FitzGerald and N. J. McHugh

Royal National Hospital for Rheumatic Diseases, Upper Borough Walls, Bath, UK

The association between psoriasis and arthritis was initially made in the mid-19th century [1]. However, it was not until the 1960s that psoriatic arthritis (PsA) was distinguished clinically from rheumatoid arthritis (RA) [2–4]. There has been a relative lack of research into PsA, especially when compared with other forms of inflammatory joint disease. In an effort to establish more collaborative research within the UK and further afield, one of the authors (DV) organized the first international symposium on PsA in Leeds in 1996. Three further annual symposia have followed, two in Leeds and the latest in Bath (June 1999). The meetings have attracted growing interest and support and have underlined the opportunities for using PsA as a paradigm for studying pathological mechanisms occurring at separate sites in the same individual. Certain lines of investigation and developments touched upon at the last meeting warrant further discussion.

There are still fundamental difficulties in establishing a precise definition for PsA, as we are hampered by the lack of specific diagnostic tests. For example, does the patient with psoriasis, rheumatoid factor and a polyarthritis have RA and psoriasis, or PsA? Some of the newer imaging modalities may provide the answer but at present doubt remains. The subgroups described by Moll and Wright [5] remain clinically useful, but there is no agreed classification system for multicentre epidemiological studies and clinical trials. However, as a result of ongoing consultation generated by the PsA symposia and led by Dr Deborah Symmons (Manchester), some degree of agreement appears to have been achieved. Results of several questionnaires have produced points of common ground. It is agreed (at least by those attending the symposia, admittedly a self-selected group) that PsA exists as a distinct disease entity, but that not all patients with psoriasis and inflammatory arthritis have PsA. The absence of current psoriasis does not exclude a diagnosis of PsA, and certain other features are characteristic but not essential for the diagnosis (e.g. fingernail dystrophy, seronegativity for rheumatoid factor, distal interphalangeal joint involvement, oligoarthritis, asymmetry and dactylitis). It is intended that further consensus will be reached with a study to include sample cases, highlighting some of the current difficulties, and to assess whether current opinions are valid.

There are few data available regarding the incidence and prevalence of PsA in the population. However, recent work in the primary care setting has found an adjusted prevalence of 1.7 and 0.3% for psoriasis and PsA respectively [6]. Studies of early arthritis clinic data suggest that patients presenting with PsA are older than those with non-psoriatic seronegative arthritis (L. Stafford, personal communication).

Several studies have suggested a genetic basis for psoriasis. The prevalence of psoriasis in the general population is approximately 1.5%, but the sibling occurrence risk has been calculated at about 8%. Twin studies have shown increased concordance between monozygotic compared with dizygotic twins (65–72 vs 15–30%) [7, 8]. Strong linkage to chromosomes 6p (50% of all psoriatics in the UK), 17q, 4q and lq has been found in different ethnic groups [9–12]. The strongest allelic association has been with HLA-Cw0602 on a haplotype including HLA-B5701 and B1302. However, implication of HLA-Cw0602 in the disease pathogenesis has not been established. A possible explanation is that HLA-Cw0602 may be a marker for non-HLA genes in the MHC for psoriasis.

The MHC S gene (corneodesmosin) is located 160 kilobases telomeric of HLA-C and is expressed specifically during keratinocyte differentiation as a component of the corneodesmosomes [13, 14]. These are involved in the integrity of epithelial sheets and desquamation, and therefore the S gene is a strong functional candidate for psoriasis and/or PsA in this region. Recent work has linked psoriasis to the S (+1243) variant [15] then to allele 5 (+619, +1240, +1243) of the S/corneodesmosin gene [16, 17]. An association analysis between the S gene allele 5 and HLA-Cw06 in patients with guttate psoriasis and healthy matched controls has been undertaken [18]. The results showed that HLA-Cw06 positivity conferred a higher relative risk of guttate psoriasis [odds ratio, (OR) 19.2] than the presence of the S gene allele 5 (OR 6.2). A further analysis stratified patients according to their Cw06 status, to assess any effect independent of the S gene allele 5. The S gene haplotype exhibited a weak effect either in the presence (OR 2.7) or in the absence (OR 3.6) of Cw06. These findings suggest that both the HLA-C region and the S gene have a role in the development of guttate psoriasis, independently of each other. The proposed mechanism is that substitutions at positions +619, +1240 and +1243 may cause amino acid changes sufficient to interfere with the process of cleavage of the corneodesmosin during keratinocyte differentiation, which may contribute to the impairment of desquamation seen in psoriasis. Alternatively, the substitutions, rather than being causative themselves, are markers for true disease-associated polymorphisms.

Another group has concentrated on studying MICA/ MICB proteins, which are membrane proteins very similar in structure to the MHC class I molecule [19]. The MICA-A9 allele is associated with PsA independent of HLA-Cw0602, and may be a possible candidate gene for PsA, independent of any HLA association. Other work has suggested that a composite genotype of interleukin 1 (IL-1) (especially ILIB+3954 and IL-1RN+2018) is associated with early onset psoriasis (A. Cox, personal communication).

The pathophysiology of psoriasis and PsA remains unclear, although there is much evidence to suggest a T-cell-mediated process. Psoriatic plaques show early T-cell infiltration [20], de novo cases of psoriasis occurring after bone marrow transplantation have been described [21], and anti-T-cell therapy [e.g. cyclosporin and interleukin-2 (IL-2)] is beneficial [22]. In psoriasis, the T-cell infiltrate is of the TH1 subtype. The secretion of interferon-{gamma} by such cells is likely to be critical in the light of its known proinflammatory effects and its ability to induced keratinocyte proliferation [23, 24]. Professor R. Winchester (New York), in collaboration with the Dublin group, presented recent findings in relation to T-cell clonality of psoriatic synovium. In PsA, synovial fluid analysis of the T-cell receptor repertoire shows unique oligoclonal expansions of both CD4- and CD8-positive T cells compared with peripheral blood, most likely reflecting a localized antigen-driven response [25]. Interestingly, treatment with methotrexate appears to reduce the polyclonal T-cell infiltrate but has less effect on resident oligoclonal expansions [26].

The clinical presentation of PsA and factors that may help to differentiate it from other inflammatory arthritides are also areas of interest. Stafford et al. (unpublished) reported on data from an early arthritis clinic, looking at cases of seronegative arthritis. Their results show a significant positive correlation between inflammatory markers (erythrocyte sedimentation rate and C-reactive protein) and the tender and swollen joint count scores in PsA, but not in other types of seronegative arthritis. They found a 10% rate of HLA B27 positivity amongst PsA patients compared with 35% of the non-PsA cases. Fiocco et al. [27] have examined the macroscopic vascular patterns of knee synovitis at arthroscopy in recent-onset vs long-lasting refractory knee synovitis. Vascular patterns similar to those found in nailfold capillaries in patients with psoriasis and psoriatic arthritis [5] were identified at the synovial level, suggesting specific microvascular abnormalities in psoriasis and its related arthritis. Their findings confirm those of Reece et al. [28], which suggest that different synovial vascular patterns occur in the two diseases; this may help in diagnosing the cause of recent-onset knee joint synovitis. Fraser et al. [29] have studied synovial membrane vascularity, endothelial cell apoptosis and angiogenesis (using matrix metalloproteinase-9) at knee arthroscopy in early PsA and RA, as well as in osteoarthritis [24]. Their results showed differential expression of synovial angiogenic and vascular apoptotic factors in PsA and RA, angiogenesis being seen in PsA with up-regulation of vascular endothelial growth factor and transforming growth factor ß (TGF-ß), whereas apoptosis was more prominent in RA.

The development of highly sensitive fat-suppression magnetic resonance imaging (MRI) may well be the most promising advance in helping to further our understanding of PsA and our ability to diagnose it. This technique is able to demonstrate bone pathology in advance of plain X-rays. MRI studies in PsA-associated hand synovitis have suggested either a capsular- or synovial-based pathology [30]. The recent application of fat-suppression MRI to knee joint swelling in PsA has increased our understanding of these capsular-based changes [31]. Knee pathology in PsA is strongly associated with enthesitis, which is shown as diffuse bone oedema or soft tissue and capsular swelling adjacent to the enthesis. The bone oedema is quite characteristic of spondyloarthritis but not RA. However, soft tissue and capsular changes adjacent to an enthesis are sometimes seen in RA, where they may be secondary to the non-specific extension of the inflammatory process from the joint cavity. Several clinical manifestations of PsA do not involve synovitis, and have therefore been difficult to explain using the current classification criteria, e.g. arthritis mutilans, the SAPHO syndrome and spondylodiscitis. Fat-suppression MRI has shown that all of these variations, as well as more classical distal interphalangeal disease, oligo-/monoarthritis, and also sacroiliitis, have the enthesis as their primary site of pathology. MRI is not foolproof, as enthesitis may be masked by synovitis or soft tissue changes, and the changes described above are not universal. This work may provide an accurate way of classifying PsA (based upon the primary site of pathology), as well as a greater understanding of the pathogenesis of the disease [32]. The results of longitudinal MRI studies are awaited with interest.

The assessment of treatment in PsA has been very difficult. Dr Gustavo Citera (Buenos Aires) provided an excellent review of treatment strategies at the Bath meeting. There have been very few trials, which have often been too small and too short in duration. Different inclusion/exclusion criteria and outcome measures have been used. As a result of these factors, patients have often been distributed into inappropriate clinical subtypes. Sulphasalazine has been shown to be effective in the short term, with dose-related reversible side-effects (usually gastrointestinal) [33]. However, no long-term or radiological follow-up data are available. Methotrexate has been shown to be effective in the treatment of both skin and joint disease [34]. The main limitation is of hepatotoxicity, but liver biopsy does not appear necessary at the doses used by rheumatologists. Cyclosporin A works via suppression of T-cell activation, and treats both skin and joint disease [35]. Doses between 2.5 and 5 mg/kg/day have been effective. The main limitation has been renal toxicity, which has meant that is not the first-choice drug. Cyclosporin has been compared to methotrexate, both being equally effective, but there is a greater rate of withdrawal due to side-effects with cyclosporin [36]. Tacrolimus also suppresses T-cell activation, and down-regulates IL-8, TNF and IL-1. It may be used systemically or topically, but again has a high incidence of renal side-effects. Biological agents have been used in very small numbers of trials, but may represent the best hope for the future. Interferon-{gamma} has given a short-term improvement only (first 3 months). IL-2 receptor antagonists (DAB 389 IL-2) gave an improvement in 41% of patients, but there was a 25% dropout rate due to side- effects [37]. A TNF-{alpha} antagonist (etanercept) has shown early promise in the treatment of both psoriasis and psoriatic arthritis [38]. IL-10, a type 2 cytokine, has multiple effects: inhibition of interferon-{gamma} production and the down-regulation of IL-1, IL-6, IL-8 and tumour necrosis factor-{alpha}. Cutaneous levels of IL-10 mRNA are low in psoriasis and are increased by anti-psoriatic therapy. Phase II studies are ongoing with IL-10, particularly in RA. Corticosteroids may have some effect in the short term but long-term benefit has not been shown. In conclusion, there are very few trials that have effectively addressed the treatment of PsA.

Good outcome studies in PsA are needed for several reasons: to establish the natural history of the disease more accurately; to plan care and allocate resources more efficiently; to provide better patient education; and to assess the efficacy of therapy. Gladman's group in Toronto has made a substantial contribution to this area [39, 40]. Many different outcome measures have been used, including various joint/enthesopathy scores, modified radiological and functional indices, quality of life indices and mortality rates. However, the heterogeneity of PsA has led to multiple definitions of the disease and subsequent differences between studies.

Paediatric studies have shown that PsA accounts for 8–20% of childhood arthritis [41]. Wright [2] found that 5% of adult PsA patients developed the disease in childhood. At onset, 50% of paediatric cases are monoarticular and 25% pauciarticular. Follow-up showed that 10% developed a severe destructive arthropathy, 13% remained mono/pauciarticular, and the remainder became polyarticular.

There have been relatively few adult outcome studies, particularly when compared with other inflammatory arthritides. There are some common findings: <5% of cases have a benign course; peripheral joint disease tends to progress [42], whilst spinal disease does less so; and poor outcome is associated with polyarthritis, elevated inflammatory markers at presentation, and possibly genetic factors [40]. Mortality data show an increased death rate from all causes in PsA, particularly linked to increased levels of medication [43, 44].

PsA is an important and potentially disabling condition. There remains much work to be done in all aspects of the disease, from explaining the most fundamental pathological mechanisms to finding the optimum treatment. Recent developments in cellular pathology and genetics coupled with imaging techniques to locate early sites of pathology will provide useful leads for further research. More than anything else, the symposia have highlighted what a fertile area PsA is for investigators and the need for future meetings bringing together all those interested in studying such an intriguing condition.

The authors gratefully acknowledge all those who presented findings at the Fourth International Psoriatic Arthritis Symposium (Bath, 22–23 June 1999), including Dr Rachid Tazi-Ahnini, Dr Jonathan Barker, Dr Gustavo Citera, Dr Angela Cox, Dr Ugo Fiocco, Dr Alexander Fraser, Dr Sharon Jones, Dr David Kane, Dr Lesley Kay, Dr Carlos Lopez-Larrea, Dr Dennis McGonagle, Dr Leanne Stafford, Dr Deborah Symmons and Professor Robert Winchester.

Notes

Correspondence to: N. J. McHugh. Back

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