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Continuing Medical Education
PMID: 17656934

Pharmacological interventions for psoriatic arthritis: Present and future

KK Raja Babu
 Dermatology, Gandhi Hospital & Gandhi Medical College, Hyderabad, India

Correspondence Address:
K K Raja Babu
A - 62, Road No. 12, Film Nagar, Jubilee Hills, Hyderabad - 500 033
How to cite this article:
Raja Babu K K. Pharmacological interventions for psoriatic arthritis: Present and future. Indian J Dermatol Venereol Leprol 2002;68:187-197
Copyright: (C)2002 Indian Journal of Dermatology, Venereology, and Leprology


Psoriatic arthritis is a common, chronic inflammatory arthritis that affects 5-7% of patients with psoriasis. Psoriatic arthritis is often treated in the same manner and with the same drugs as rheumatoid arthritis is. Currently much attention is being focused on the role of agents that inhibit the activity of pro-inflammatory cytokines, such as tumor necrosis factor a, which are believed to play a key role in joint destruction. The objective of this article is to review these newer developments besides taking a fresh look at the existing methods of therapy of this potentially disabling disorder.
Keywords: Psoriatic arthritis, Drug interventions, Newer developments in treatment, Cytokine blockers

′Psoriasis is an antidote for dermatologists ′ego′ - Paul Bechet (1936)

Psoriasis and psoriatic arthritis are common disorders. The association between psoriasis and arthritis was known for a long time (perhaps since biblical times) but, it was only in the 1960s and 1970s that a (some what) clear distinction was made between psoriatic arthritis and rheumatoid arthritis and psoriatic arthritis began to attract the attention of clinicians and researchers in its own right.

Nevertheless, psoriatic arthritis until recently remained a poorly studied subject despite the fact that the disease could well be a paradigm of cytokine-induced cutaneous and joint inflammation.

There have been major advances in our understanding of the pathomechanisms of rheumatological diseases in recent years leading to the emergence of several newer and highly specific therapeutic options and some of these fortunately have found an application in the treatment of psoriatic arthritis as well. The early results of their use have been encouraging. A few of these have already been approved for use and many are sitting on the therapeutic horizon waiting to be tested and cleared. There also have been advances in our understanding of the complex molecular genetics that determine the psoriatic phenotype, and gene therapy and pharmacogenomics are no longer utopian.

This review will attempt to critically evaluate some of these newer, especially pharmacological, developments besides taking a fresh and closer look at the existing methods of management of this intriguing disease within a disease.

Drug interventions in psoriatic arthritis

Psoriatic arthritis (PsA) is a potentially disabling disorder and it is only in recent years that the morbidity that can sometimes be associated with the disease has begun to be appreciated. There are still many grey areas in our understanding of the etiology and pathogenesis of PsA but there is a general agreement among researchers that most joint damage occurs in the early months and years of the disease and the rate of disease progression slows over time.[1],[2] Importantly, damage that occurs early in the disease may not manifest as functional impairment until later on.[3] Many believe that early pharmacological intervention may prevent joint damage but there is no concrete evidence that the presently available treatments have the ability to prevent disease progression to any significant degree.[4] Indeed, very few controlled and blinded studies exist making authoritative pronouncements difficult if not impossible.[5]

By and large, the treatment of PsA depends on the extent and severity of joint inflammation. Patient education, and physical and occupational therapy should precede any pharmacological intervention [Table - 1]. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be sufficient for patients with mild joint symptoms. More severe disease is likely to require treatment with diseasemodifying antirheurriatic drugs (DMARDs) like methotrexate, sulfasalazine, gold, or antimalarial drugs or with drugs like corticosteroids, cyclosporine or azathioprine.[3] Much attention is currently focused on agents that inhibit the activity of proinflammatory cytokines and there by disease progression. Drugs like etanercept, and infliximab fall under this category [Table - 2].

Nonsteroidal anti-inflammatory drugs

NSAIDs may not alter the natural course of arthritis or prevent joint destruction but may provide symptomatic control of early joint disease or enthesopathy. Notwithstanding the fact that there are hardly any placebo-controlled trials on the possible benefits of NSAID use in PsA, many rheumatologists recommend use of NSAIDs as a first step in the management of early joint inflammation.[5],[6],[7] Different groups of NSAIDs with different chemical structures and safety profiles exist but without any significant difference in their anti-inflammatory efficacies [Table - 3].[8] The choice of a NSAID is primarily based on its cost, duration of action, side-effect profile and patient preference. Analgesic effects of NSAIDs are prompt but reduction in inflammation may take 1-2 weeks.[9] But it is important that a right dose is chosen to achieve optimal benefits. For example, in a 4-week, double-dummy, randomized control study, nimuselide 200 mg and 400 mg/day were found to be superior to nimuselide 100mg/day.[10]

All currently available NSAIDs have analgesic and antipyretic effects and several of them also have significant anti-inflammatory properties. NSAIDs have the ability to block the activity of cyclooxygenease (COX) enzymes that are responsible for the initial metabolism of arachinodonic acid into prostaglandins, prosrtacyclines and thromboxanes. Much of the anti-inflammatory benefits of NSAIDS stem from their capability to inhibit prostaglandin synthesis.[8] Two types of COX enzymes exist: COX 1 and COX 2. Importantly, COX 2 is specifically induced in response to inflammatory stimuli and is therefore the predominant enzyme seen at inflammatory sites. All nonselective or conventional NSAIDs, except paracetamol suppress both the enzymes. Selective COX 2 inhibitors are presently available. Some NSAIDs also inhibit expression of activity of certain cell adhesion molecules like ICAM1, VCAM-1 and leucocyte integrins.[8] Inhibition of neutrophil activation and aggregation and superoxide anion production are the other effects of NSAIDs.[5] In one subset of rheumatoid arthritis patients NSAIDs were shown to reduce laboratory correlates of acute phase reactants like ESR and C-reactive protein besides causing a reduction in the number of circulating activated T and B lymphocytes.[11]

Use of NSAIDs in a chronic inflammatory disease like PsA is beset with problems and require careful monitoring of their use. At least 60% of patients taking NSAIDs for 6 months or longer report one gastrointestinal complaint or another, most notably dyspepsia. All conventional NSAIDs have the potential to induce gastric mucosal damage leading to gastric erosions, ulcerations and bleeding.[5] Patients at an increased risk of developing gastrointestinal toxicity include the elderly, smokers, alcohol abusers and patients with previous peptic ulcer disease or those who require high doses of NSAIDs for their disease control, or those who are on glucocorticosteroids or anticoagulants. COX 1 and not COX 2 is continually expressed in the stomach and duodenum. Thus selective COX 2 inhibitors have the advantage of causing significantly less gastrointestinal mucosal damage and are particularly useful for patients at risk of gastrointestinal toxicity.[8],[12]

NSAIDs have little effect on renal function in normal individuals. However, patients of advanced age, renal or renovascular disease, diabetes mellitus, ischaemic heart disease, congestive heart failure, diuretic usage, hepatic insufficiency or SLE are at risk of developing nephrotoxicity from NSAID use.[13] In these clinical settings most of the apparent toxicity from NSAID use results from suppression of the much needed renal prostaglandin synthesis. Recent evidence suggests that selective COX 2 inhibitors also have the propensity to cause such effects as the COX 2 enzyme is expressed in the kidney.[8]

Cutaneous reactions from NSAID use are well known. These include photosensitivity, morbiliform rashes, fixed drug eruptions, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, erythroderma, purpura, and petechiae.[5] Flares of existing psoriasis including occurrence of generalized pustular psoriasis can occasionally follow use of indomethacin, diclofenac, ibuprofen or meclophenamates.[14],[15],[16],[17] owever, there is no definitive evidence that NSAIDS have any direct disease-worsening effects on psoriasis.[18]

Disease-modifying antirheumatic drugs

All patients whose disease remains active despite adequate treatment (at least for 3 months) with NSAIDs are candidates for DMARD therapy. DMARDs [Table - 4] have the potential to reduce or prevent joint damage and preserve joint integrity and function although this is not universal. All DMARDs are slow acting with a delay of 1-6 months before a clinical response is evident making it necessary to continue NSAID use,[12] unless such use is contraindicated. Many factors influence the choice of a DMARD for an individual patient. Convenience of administration, need for active monitoring, and frequency and severity of side effects are important considerations.


Because antimalarials are effective in rheumatoid arthritis, by analogy it is assumed that they are also effective in PsA. ′True′ efficacy studies are however lacking.[5] In one retrospective study 30 patients of PsA treated with hydroxychloroquine (HCQ) 200-400 mg/day and 2 patients with chloroquine (CQ) 250 mg/day along with different NSAIDS for periods ranging from 4-6 years did well without any need for other drugs.[5] In one series, 32 patients were treated with HCQ 200400mg/daily along with high dose aspirin and another 18 received HCQ alone. 60% achieved remission, improvement or stabilization of their disease.[19] In another report, none of the 20 patients of PsA treated with CQ improved and furthermore had to discontinue treatment because of cutaneous toxicity.[20]

Indeed, cutaneous toxicity, especially (psoriatic) disease flares, is the main deterrent for use of anrtimalarials in PsA.[21] The mechanism of antimalarial-induced psoriasis flares is not known. An in vitro study suggests that antimalarials cause inhibition of tranglutaminase activity, leading to epidermal proliferation.[22] 42% of subjects treated with CQ and primaquine for malaria experienced some degree of worsening of their psoriasis.[23] Many studies have reported of patients treated with quinacrine or CQ developing cutaneous reactions that included psoriasis flares and erythroderma. Of 32 patients of PsA treated with HCQ, only 3 demonstrated a possible flare of their psoriasis.[5] A review of 50 patients of PsA treated with HCQ showed no exacerbation of skin lesions.[24] 32 PsA patients treated with CQ 250 mg/daily also did not demonstrate any worsening of their psoriasis.[25] However, the general consensus is that both quinacrine (no longer made) and CQ should probably be avoided in patients of PsA, and cautious use of HCQ may be appropriate, but before any strong recommendation for its use can be made, further studies are necessary.[5]

Other cutaneous complications of antimalarial use are: a blue-grey pigmentation of the face, hard palate, neck, lower extremities or forearms; pruritus, exfoliative dermatitis, photosensitivity, alopecia and lichenoid eruptions. Gastrointestinal side effects are common. Ocular toxicity is one of the feared complications of antimalarial use in rheumatological disorders. Both CQ and HCQ have a tendency to get deposited in the melanin-containing tissues of the iris, choroid and retinal pigment epithelium. Reversible corneal deposition of antimalarial salts is common.[26] There appears to be a direct relationship between ocular toxicity and daily doses of antimalarial drugs. A daily dose of 4 mg/kg or less of CQ and 6 mg/kg or less of HCQ are likely to be safe.[27] Neurological and musculoskeletal symptoms and hematological toxicity are the other adverse effects of antimalarial use.

Both anti-inflammatory and immunosuppressive effects seem to be responsible for the putative benefits of antimalarials in rheumatological conditions. Lysosomal stabilization, inhibition of prostaglandin and other cytokine production, suppression of monocyte chemotaxis, inhibition of neutrophil activity and direct actions on cellular DNA and RNA are some of the effects attributed to antimalarials.[26]

Gold compounds

It was 56 years ago that the use of parenteral gold in the treatment of PsA was reported for the first time.[28] There have been subsequently, several reports of use of both parenteral (gold sodium thiomalate, 25-50 mg i.m. every 2-4 weeks) and oral gold (auranofin 3-6mg/day) in the treatment of PsA. In many of these studies, the efficacy at best was modest and toxicity was the limiting factor.[29],[30],[31] However, 51 of 45 patients of PsA treated with auranofin in a 12 month prospective open study demonstrated disease improvement or remission. The rate of withdrawal because of side effects was low.[32] In a double-blind placebo-controlled study, it was shown that auranofin treatment was statistically superior to placebo treatment.[33] But in a comparative study of methotrexate (MTX) and intramuscular gold, it was found that the likelihood of a clinical response was 8.9 times greater with MTX than with gold and patients were 5 times more likely to discontinue therapy with i.m. gold than with MTX.[34] Interestingly auranofin therapy was found to clear both skin lesions and arthritis besides causing an increase in CD4 count in a HIV positive patient with disabling psoriatic arthritis.[35]

Cutaneous rashes including exacerbation of existing psoriasis, stomatitis, myelosuppression, thrombocytopenia, aplastic anemia and membranous nephropathy (manifest as proteinuria and hematuria) are some of the important side effects of gold therapy, warranting careful monitoring of its use. Systemic toxicity is less but patients taking oral gold compounds may develop severe and frequent diarrhoea. Although parenteral gold is more effective, oral gold is better tolerated.[36],[37],[38]

The mechanisms of action of gold compounds in PsA are not clear. Auranofin has been shown to inhibit interleukin-1 beta-induced prostaglandin E2 synthesis and COX-2 suppression.[39] Gold compounds do not seem to directly suppress neutrophil functions.[40]


Sulfasalazine (SSZ) or salazopyrin is a drug that is essentially used in the treatment of ulcerative colitis and regional enteritis. The drug is poorly absorbed after oral administration and is broken down by intestinal bacteria to 5-amino salicylate and sulfapyridine, the former responsible for antiinflammatory benefits and the later, for its toxicity.[41] SSZ and the recent olsalazine appear to be relatively safe and effective therapies for patients of PsA who have not adequately responded to NSAIDs and the benefits can appear as early as 1 month after starting therapy. Indeed, sulfasalazine is one of the few drugs that has a well demonstrated published efficacy in the management of PsA.[42] SSZ is given in starting doses of 500 mg t.i.d and the dose then can be gradually increased up to 4 G/day. The usefulness of SSZ in PsA has been established in several studies. A double-blind, placebo-controlled study of SSZ in 30 patients with PsA showed greater improvement in patients in the SSZ group than in those receiving placebo. SSZ treatment was discontinued in 26% of patients because of side effects.[43] A 1996 study of 221 patients of PsA, in which SSZ was compared with placebo, concluded that 2G of SSZ/day was well tolerated and was more effective than a placebo.[44] Some of the patients treated with SSZ for their PsA manifested improvement of their skin disease. A prospective, double-blind, placebocontrolled randomized study of 24 weeks duration of 120 patients from 9 centres showed that SSZ at 2 g/day was a safe and effective remedy for PsA, especially in the relief of pain.[45] In one report SSZ was found to improve even nail lesions of PsA.[46] Adverse effects of SSZ therapy include headache, gastrointestinal symptoms, cutaneous rashes, photosensitivity and rarely extrinsic allergic alveolitis and myelosuppression.[9],[47]


Perhaps the most widely used DMARD in PsA and rheumatoid arthritis is methotrexate (MTX). It is now more or less clear that much of the therapeutic benefits of MTX in psoriasis and PsA are the result of the drug′s anti-inflammatory and, to a lesser extent, of its antiproliferative actions.[48] Although few studies support any specific effect of MTX on T cell numbers or function, MTX does seem to exert both in vivo and in vitro clear inhibitory effects on neutrophils and on monocyte/macrophage series that are believed to play a central role in the pathogenesis of both rheumatoid arthritis and PsA. However, the direct inhibitory effects on the proliferation, especially of the immature differentiating monocytes and the induction of apoptosis in these and other inflammatory cells appear to represent the first step of MTX′s actions. The reported inhibition of monocyte/macrophage cytokines (IL1, IL6 and TNF alpha) and TH1 cytokines (IL2 and IFN gamma) and increase in the gene expression of antiinflammatory TH2 cytokines (IL4 and IL10) seem to contribute for the sustained anti-inflammatory benefits of the drug. A further action of MTX is its indirect inhibitory effect on cyclooxygenase and lipoxygenase enzymes and their products. These actions appear to be mediated through increased production of extracellular adenosine and its binding to A2a receptors and to a lesser extent to A3 receptors.[49]

Low-dose MTX administration is now the standard practice of delivery of MTX in many rheumatological conditions, including PsA. Early studies have employed high-dose MTX (1 -3 mg/kg i.v.) to improve skin and joint symptoms but was associated with acute and severe side effects leading to discontinuity of use.[50] However, short term, high-dose weekly MTX (40mg/m2) induced complete and prolonged remission in a patient with severe psoriasis and arthritis.[51] But, low-dose MTX (10-25 mg/weekly, orally or i.m.) with relatively fewer side effects became popular among rheumatologists but produced only equivocal results in several controlled studies. One randomized, double-blind, placebo-controlled trial of MTX 7.5 to 15 mg/weekly demonstrated a statistical superiority to placebo only in physician assessment of arthritis activity and in improvement of skin lesions.[52] MTX(15 mg/weekly) was found to improve PsA within 3 months, with only small further improvement even with continued use up to 1 year.[53] A 24-month study of patients with PsA found no difference in radiographic joint damage scores between MTX-treated cases(5-20 mg/ week) and retrospectively matched historical controls.[54] A recent comprehensive review of randomized controlled studies avers that only highdose MTX demonstrated published efficacy for PsA and not low-dose MTX.[42] Whatever, patients tend to remain on therapy with MTX longer than they remain on any other DMARD at least because of the drug′s symptomatic usefulness.[34] Intraarticular MTX was shown to be a short term effective measure in one report.[55] Where necessary, NSAIDs like ketoprofen, flurobiprofen and piroxicam can be given safely along with MTX as these drugs have been found not to interfere MTX levels in the serum.[56]

Short term or long term side effects of MTX are well known. For proper guidelines of use of MTX, the readers′ attention is directed to an excellent review on this subject by Boffa and Chalmers.[51]


Although there are data supporting the therapeutic usefulness of cyclosporine A (CSA) in psoriasis, there are few controlled studies in PsA. 3 open studies using 3-6 mg/kg of CSA per day attested to the effectiveness of the drug in reducing disease activity by 50%.[58],[59],[60] A comparative study of CSA with sulfasalazine and symptomatic therapy revealed a statistically significant difference in favour of CSA in terms of mean change in pain score, and in general was more efficacious than the other two.[61] In an open 18-week study the lowest optimal maintenance dose of CSA in PsA was 3.26 mg/kg/day and improvement was noticeable after an average of 10 weeks of the drug′s use.[62] CSA is generally well tolerated and in the low doses in which it is used in PsA has very few adverse effects. However, physicians intent on using CSA should be familiar with the drug′s side effects and also the accepted guidelines of its use. A combination of CSA and MTX was used in a cohort of 19 patients with recalcitrant psoriasis 15 of whom had concomitant PsA. A good response to treatment was noticeable and the only side effect observed was transient impairment of renal function which normalized after reduction of CSA dose.[63]

The mechanism of usefulness of CSA in psoriasis and in PsA appears to be related to the drug′s inhibitory effects on T cells. CSA preferentially inhibits antigen-triggered signal transduction in T lymphocytes from its ability to suppress phosphatase calcineurin and the drug also blunts the expression of many lymphokines including IL 2 as well as expression of antiapoptotic proteins.[64]


Systemic corticosteroids are not generally recommended in psoriasis for fear of exacerbation of the disease on their withdrawal but they seem to have some role in the management of PsA. They can be used as a short term measure while awaiting a possible positive outcome with a DMARD.[5] Corticosteroids may occasionally be needed and in high doses (40 mg of prednisolone/day) to control hyperactive polyarthritis that is threatening to cause severe and irreversible joint damage.[18] However, very small doses (less than 7.5 mg of prednisolone/day) should be used for long-term treatment. Intravenous methyl prednisolone pulses have been used successfully in PsA without worsening of skin disease.[5] Intraarticular steroid injections may help an isolated episode of severe synovitis or enthesopathy.[65]

The anti-inflammatory and immunosuppressive effects of corticosteroids are well known.


Azathioprine, an immunosuppressive and anti-inflammatory agent, has proven its usefulness in PsA in a few studies. In an open study of 10 patients who received 2.5 mg/kg/day of the drug and followed for 4.5 to 67 months, 9 of the 10 showed excellent or good response. Leucopenia was encountered in 2 patients.[66] In a 12 month, double-blind, placebo-controlled crossover trial of 6 PsA patients given 3 mg/kg/day, a 50% reduction in mean active joint count with marked improvement was noticed in 4 of the 6 patients.[67]

Oral retinoids

Several open studies suggest that etretinate is an effective drug in PsA. In one study of 20 patients who were given etretinate 1 mg/kg/day and then followed for 2 years on maintenance therapy of 10-25 mg/kg/day, positive benefits were described in all patients, sometimes occurring as early as 4-6 weeks.[68] Similar benefits were reported in another open study of 40 paients of PsA using a mean of 50 mg of etretinate per day.[69] However a controlled trial (0.5 mg/kg/day for 24 weeks) demonstrated only a modest effect.[70] However, a dramatic response to etretinate was reported in a Chinese patient with PsA.[71] The concurrent use of etretinate and MTX did not produce any added benefit in one patient with prominent arthritis and erythrodermic psoriasis.[72] Mucocutaneous side effects were common in all studies. 5 of 9 patients of PsA treated with oral retinoids and PUVA responded favourably.[73],[74] PUVA by itself may be ineffective. While NSAIDs remain the first line of therapy in HIV-associated PsA, etretinate may be an useful drug because of the absence of significant immunosuppressive effects.[65]

In the body, etretinate is converted into acitretin which is its active metabolite. With the availability of acitretin, etretinate has been withdrawn from the market. Etretinate doses should be lowed by approximately 20-33% for appropriate acitretin dosing.[75] Bexarotene is a newly developed retinoid which is retinoic X receptor-specific and has a potential to be of use in PsA. Oral retinoids prevent the overexpression of ICAM-1 and ECAM-1 and correct HLA-DR abnbormalities. They also decrease the release of leukotrienes and HETE products and suppress the neutrophil and eosinophil chemotactic effects of the compounds.[76]

Other treatments

In a 16-week, placebo-controlled, double-blind crossover study of 15 patients, colchicine 0.5 mg t.i.d. was better than a placebo.[77] Significant decreases were reported in the visual analog scale and the ESR of 11 patients of PsA in a double-blind, 4 month crossover study using 750 mg of d-penicillamine per day.[78] Somatostatin, a growth hormone-inhibitor, alone or combined with gold salts was found to decrease joint symptoms significantly.[79],[80] Similar benefits occurred with use of bromocriptine, a pituitary prolactin suppressor.[81] A 6-month, open-label trial of oral vitamin D3, 2mg/kg/day given to 10 patients with active PsA led to 50% improvement in 4 patients.[82] Several studies have shown that extracorporeal photochemotherapy can ameliorate joint inflammation in patients of PsA who have been recalcitrant to or intolerant of standard therapy.[83],[84],[85] 28 patients of PsA and fibromyalgia reported improvement after they were treated with various modalities of balneotherapy at the Dead Sea area.[86]

Newer developments

A growing body of evidence supports the role of proinflammatory cytokines, such as tumour necrosis factor a, IL1, IL6, and IL8, in the pathophysiology of psoriasis and PsA.[87],[88] These data provide a basis for the use of cytokine blockers and other newer ′biological agents′ in the treatment of both the disorders.[89] TNF a neutralizers were the first such agents to reach clinical trials. TNF a inhibitors like etanercept and infliximab have shown significant clinical efficacy in rheumatoid arthritis and now are being examined for use in PsA. Etanercept is a human recombinant soluble p75 TNF a receptor linked to the Fc portion of IgG 1. Like the endogenous soluble receptor, etanercept binds tightly to TNF and to lymphotoxin a, rendering them biologically inactive. In a placebo-controlled, randomized double-blind clinical trial, 60 patients with PsA received either etanercept (25 mg subcutaneously twice weekly) or a placebo for 12 weeks. Patients receiving MTX, NSAIDS or low-dose prednisolone were allowed to continue them. All other DMARDs and topical medicines were discontinued. Patients treated with etanercept had significant improvement in disease activity compared with those on placebo at the end of the study period and the effect in many was swift. Skin lesions also improved in several patients. Etanercept was well tolerated and no patient discontinued treatment. 20% of the etanercepttreated patients experienced mild injection site reactions that resolved with continued use.[90] Additional studies of 9 severe, treatment- resistant patients with PsA and 12 patients with DMARDrefractory PsA also reached similar conclusions of etanercept′s clinical effectiveness.[91] A 47-yearold man with seven years of disabling psoriatic polyarticular arthritis responded dramatically to subcutaneous injections of 25 mg of etanercept given two times weekly.[92]A similar clinical outcome was obtained with etanercept in another report.[93] In one uncontrolled trial, etanercept when added to the treatment regimen (oral MTX, CSA, or acitretin, or topical calcipotriol) in six patients with severe recalcitrant psoriasis {three also with PsA} showed a marked improvement in disease activity.[94]

The most common side effect of etanercepttherapy remains injection site reactions that are characterized by erythema, and/or pruritus, pain and oedema. Their incidence ranges from 20-40% and their occurrence do not generally necessitate discontinuation of treatment.[95],[96] There are reports to suggest that etanercept can induce leucocytoclastic vasculitis, discoid lupus erythematosus and urticarial eruptions with prurigo. Some studies show that TNFa blockade may stimulate certain aspects of autoimmunity and 0.4% to 3% of patients develop antibodies to the drug at some point during their treatment course.[96]

Infliximab is a chimeric (mouse-human) monoclonal antibody that binds and neutralizes TNF It should be used in combination with MTX to avoid the induction of antibodies and the potential blunting of clinical response. The drug is given by intravenous infusion. In a small open label study of 6 patients with severe PsA resistant to MTX, infliximab (5 mg/kg once every 2weeks) was added to the MTX regimen and responses were evaluated after 6 weeks. At the end of the study period, swollen joint counts improved by 88% and tender joint counts by 86%. MRI evaluation revealed that inflammation was reduced.[97] Additional open label studies attest to the efficacy of infliximab in reducing articular symptoms and in improving the skin lesions.[98] A recent report has documented that infliximab is a well-tolerated and effective modality for both joint and skin involvement in psoriasis.[99] Further effectiveness of anti-TNFa antibody in the treatment of PsA was also demonstrated in more recent reports.[100]

Other TNF neutralizing agents, including a fully human monoclonal antibody to TNF, are in the early stages of development.[101] Inhibitors of TNF thus appear to have good potential for treating PsA. Whether these agents will be able to improve long-term outcomes, such as disability, is not known at present time. Whether other cytokine inhibitors, such as agents that neutralize IL1, will have similar effects is being investigated. Another promising agent is the cytokine, IL 10. IL 10 inhibits INF gamma production and down regulates IL 1, IL 6, IL 8 and TNF a. Phase II trials are on for rheumatoid arthritis and its role in PsA remains to be investigated.[102]

A large scale, multinational study is currently under way to test the efficacy of leflunomide in PsA. This drug acts at the level of pyrimidine synthesis and affects T cell proliferation and has been found to be effective in rheumatoid arthritis.[101] In one recent report, Ieflunomide (10mg daily) was shown to improve both skin and joint symptoms in a 56-year-old woman of PsA and generalized pustular psoriasis who was resistant to multiple treatments.[103]


Psoriatic arthritis is a serious and potentially disabling condition. We are still handicapped by the absence of a precise definition of the disease, although the development of highly sensitive fat-suppression magnetic resonance imaging can help us to diagnose the disorder with more precision. The treatment of psoriatic arthritis remains unsatisfying at present time and there is an urgent need for new therapies. Advent of TNF blockers is a singular advance in the therapy of psoriatic arthritis but the long term outcomes are still unknown. The synthesis of agents that interfere with specific steps in the immune pathogenesis of psoriasis is a heartening development currently and it is to be hoped that such agents will expand our options of treatment of this difficult and devastating disease in future.

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