1458 Correspondence

asked to complete a brief questionnaire regarding their preferences and to explain the reasons for their choice. Psoriasis Area Severity Index (PASI) and Dermatology Life Quality Index (DLQI) were completed for all patients. Of the whole group, 54/99 (55%) expressed a preference for bath PUVA. Among female patients, 31/51 (61%) preferred bath PUVA. Among male patients, 23/48 (48%) preferred bath PUVA. Thus, 61% of women, 13% more [95% confidence limits 7%, 32%] than the 48% of men, favoured bath PUVA, P = 010). The mean DLQI for male patients who preferred bath PUVA was 68 vs. 10 for those who preferred systemic PUVA and this difference was statistically significant (P = 0047). For female patients, DLQI score was the same for both modes of PUVA. Additionally, PASI score did not influence patients’ preferences in either sex. Stated reasons for female patients’ preferences for bath PUVA were as follows: 55% did not like taking tablets; 19% did not like the prospect of possible side-effects of systemic therapy; 13% considered bath PUVA to be more convenient; 6% did not like wearing protective glasses with systemic PUVA; only 3% preferred bath PUVA due to the lower frequency of treatment (once every 5 days in our unit, compared with twice weekly for systemic PUVA). Stated reasons for male patients were as follows: 48% did not like taking tablets; 22% considered bath PUVA more convenient; 17% preferred the idea of bath PUVA due to absence of side-effects from systemic medication; 9% stated that they disliked wearing sunglasses after treatment; 4% preferred bath PUVA due to their previous good experience with this modality. In the group of female patients who preferred systemic PUVA, 50% stated that they preferred the shorter course duration compared with bath PUVA (e.g. treatment given twice weekly takes 8–12 weeks, whereas treatment given every 5 days takes 12–16 weeks); 35% considered systemic PUVA as more convenient as it avoids the need for a bath; 5% preferred systemic due to their previous experience. In the group of male patients who preferred systemic PUVA, 60% considered it more convenient; 20% selected this modality due to the shorter course duration; 12% believed that systemic PUVA was more effective (despite the fact that they had been informed that there was no evidence to support this view); 4% preferred systemic PUVA due to their previous experience. We assessed the influence of previous experience on patient’s preferences. Seventeen of the 99 patients had previously received PUVA (12 bath, 4 systemic and 1 both): 9/12 (75%) who had previously received bath PUVA preferred bath PUVA; 4/4(100%) who had previously received systemic PUVA preferred the same treatment. The one patient who had both modes of PUVA preferred bath PUVA. There was no influence of comorbidities on patient preferences. The results of this questionnaire demonstrate several findings. Firstly, female patients with psoriasis preferred bath PUVA to systemic PUVA while there was no preference either way amongst male patients. Secondly, higher DLQI British Journal of Dermatology (2015) 172, pp1436–1461

scores in male patients may influence their preference toward systemic PUVA. Thirdly, previous experience with PUVA may influence patient preferences and this issue could be explored in subsequent studies. Finally, there is no influence of PASI score or comorbidities on patient preference for mode of PUVA in either sex. We recommend the inclusion of patients in the decision-making process when prescribing PUVA, for units that offer both bath and systemic PUVA. 1

Department of Dermatology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan 2 Department of Dermatology, University Hospital of Wales, Cardiff, U.K. 3 Academic Dermatology Unit, St Woolos Hospital, Newport, U.K. 4 Cardiff University, Cardiff, U.K. Correspondence: Alexander V. Anstey. E-mail: [email protected]

D. ALSHIYAB1 M.F. CHIN2 C. EDWARDS3 A . V . A N S T E Y 3,4

References 1 Wan J, Abuabara K, Andra B et al. Dermatologist preferences for first-line therapy of moderate to severe psoriasis in healthy adult patients. J Am Acad Dermatol 2010; 66:376–86. 2 Man I, Kwok YK, Dawe RS et al. The time course of topical PUVA erythema following 15- and 5-minute methoxsalen immersion. Arch Dermatol 2003; 139:331–4.

Supporting Information Additional Supporting Information may be found in the online version of this article at the publisher’s website: Data S1. Patient information sheet S1. Funding sources: none. Conflicts of interest: none declared.

Arthritis possibly induced and exacerbated by a tumour necrosis factor antagonist in a patient with psoriasis vulgaris DOI: 10.1111/bjd.13587 DEAR EDITOR, We report a case in which tumour necrosis factor (TNF) inhibitor treatment possibly induced new-onset arthritis. A 71-year-old Japanese man with psoriasis vulgaris had been treated with etretinate. In July 2013, treatment with biweekly 40-mg injections of adalimumab was started. At that time, the patient’s Psoriasis Area and Severity Index (PASI) score was 111; on physical examination, he had no history of © 2014 British Association of Dermatologists

Correspondence 1459

Fig 1. Clinical image of the both hands. Note the prominently swollen left third finger.

Fig 2. T2-weighted magnetic resonance images of the left hand. Front and lateral images.

joint pain and no apparent signs of arthritis. A blood test revealed normal C-reactive protein (CRP; 007 mg dL 1) and erythrocyte sedimentation rate (ESR; 4 mm h 1) levels. Three months later, the patient’s PASI score decreased to 19, but he began to complain of joint pain in the left fifth metacarpophalangeal joint. Matrix metalloproteinase-3 (307 ng mL 1), ESR (10 mm h 1) and CRP (068 mg dL 1) levels were elevated. Antinuclear antibody and antidouble-stranded DNA antibody were negative. Owing to negative serological study, hepatitis C virus-related arthritis was ruled out. On consultation with rheumatologists, the joint symptoms were deemed compatible with psoriatic arthritis (PsA). These symptoms worsened, with a swollen left third finger (Fig. 1), despite the continuation of adalimumab, and magnetic resonance images suggested tenosynovitis compatible with psoriatic dactylitis (Fig. 2). Considering the onset and worsening of arthritis and dactylitis despite treatment, adalimumab was suspended in January 2014, and the patient was switched in March 2014 to ustekinumab along with methotrexate 6 mg weekly. Severe joint Ó 2015 British Association of Dermatologists

pain and finger swelling have improved gradually since the switch in treatment (4-month follow-up period). Induction of psoriatic skin lesions by TNF antagonists has been well described.1,2 These lesions are generally managed without discontinuation of anti-TNF therapy, although its mechanism of action is unknown. Some postulate that these paradoxical lesions are attributable to the unopposed production of interferon-a (IFN-a) by plasmacytoid dendritic cells.3 In contrast, reports on arthritis induced or exacerbated by these agents are rare. Among a total of 988 Spanish patients with psoriasis treated with biologics, new-onset PsA was observed in 58%, 055% and 045% of patients treated with efalizumab, infliximab and etanercept, respectively, while none of the patients on adalimumab developed arthritis.4 Three of 107 patients with rheumatoid arthritis receiving infliximab experienced exacerbation 3 months to 1 year after its initiation, and a dose increase resulted in deterioration.5 We cannot deny the possibility that our patient developed PsA 3 months after the initiation of the adalimumab by coincidence. However, considering the timing of the onset and aggravation despite the therapy, it is more likely that TNF antagonism induced new-onset arthritis, or at least exacerbated subclinical arthritis. Importantly, a patient with hepatitis who received IFN-a therapy developed polyarthritis with psoriatic skin lesions after the initiation of the therapy.6 Our case might help to ascertain the potential association of polyarthritis with psoriatic skin lesions in the context of an IFN-a signature. In our patient, skin lesions responded well to adalimumab, despite the fact that arthritis was possibly induced and exacerbated by adalimumab. Not all patients with PsA are responsive to anti-TNF treatment, and there is a discrepancy between response rates of skin lesions and arthritis symptoms to TNF inhibitors. In a clinical trial of adalimumab with patients with PsA, while 75% of patients achieved > 50% improvement in PASI (PASI50), only 39% achieved > 50% improvement in American College or Rheumatology 50 response criteria for arthritis at week 24.7 These observations might further indicate the need to understand the mechanisms of PsA in another context, including the recently disputed interleukin (IL)-17/IL-23 axis.8 In our case, arthritis was alleviated after switching to ustekinumab. Although the alleviation might have been due to the cessation of adalimumab, it is also conceivable that this ‘paradoxical’ arthritis showed good response to IL-23 blockade in the context of this IL-23/IL-17 axis. In our case, the enhanced IFN-a signature induced by TNF antagonism might have induced the onset of PsA, and its activity sustained through the IL-23/IL-17 axis, which was not directly affected by anti-TNF therapy but was alleviated by IL-12/IL-23 blockade. Despite the widespread use of adalimumab, arthritis possibly induced by this biologic is quite rare in psoriasis (none reported in the large Spanish study mentioned earlier),4 which raises two important issues. The first is racial difference. For example, adverse arthritis by efalizumab occurs more frequently in Taiwanese patients with psoriasis than in Spanish patients (286% vs. 58%);9 therefore, genetic factors may influence the onset of efalizumab-induced arthritis, as may be the case with adalimumab. The second is the involvement of British Journal of Dermatology (2015) 172, pp1436–1461

1460 News and Notices

antidrug antibody. Given that anti-infliximab antibody is associated with decreased clinical response and increased adverse events,10 low immunogeneity of a fully human adalimumab antibody compared with a chimeric infliximab antibody may explain the low incidence of adverse arthritis following adalimumab treatment. In summary, we experienced a case in which adalimumab treatment possibly induced new-onset arthritis, which seemed to show a good response to ustekinumab. It might have interesting implications in the pathogenesis of PsA, and further accumulation of relevant cases is awaited. Department of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan Correspondence: Yoshihide Asano. E-mail: [email protected]

T. TAKAHASHI Y. ASANO S. SHIBATA K. NAKAMURA M. NAKAO R. SHIDA A. MITSUI M. ARAKI R. WATANABE H. FUJITA Y. TADA S. SATO

References 1 Cohen JD, Bournerias I, Buffard V et al. Psoriasis induced by tumor necrosis factor-alpha antagonist therapy: a case series. J Rheumatol 2007; 34:380–5.

2 de Gannes GC, Ghoreishi M, Pope J et al. Psoriasis and pustular dermatitis triggered by TNF-{alpha} inhibitors in patients with rheumatologic conditions. Arch Dermatol 2007; 143:223–31. 3 Collamer AN, Guerrero KT, Henning JS et al. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum 2008; 59:996–1001. 4 Sanchez-Regana M, Dilme E, Puig L et al. [Adverse reactions during biological therapy for psoriasis: results of a survey of the Spanish Psoriasis Group]. Actas Dermosifiliogr 2010; 101:156–63 (in Spanish). 5 Rozenbaum M, Boulman N, Slobodin G et al. Polyarthritis flare complicating rheumatoid arthritis infliximab therapy: a paradoxic adverse reaction. J Clin Rheumatol 2006; 12:269–71. 6 Makino Y, Tanaka H, Nakamura K et al. Arthritis in a patient with psoriasis after interferon-alpha therapy for chronic hepatitis C. J Rheumatol 1994; 21:1771–2. 7 Mease PJ, Gladman DD, Ritchlin CT et al. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2005; 52:3279–89. 8 Suzuki E, Mellins ED, Gershwin ME et al. The IL-23/IL-17 axis in psoriatic arthritis. Autoimmun Rev 2014; 13:496–502. 9 Tsai TF, Liu MT, Liao YH et al. Clinical effectiveness and safety experience with efalizumab in the treatment of patients with moderateto-severe plaque psoriasis in Taiwan: results of an open-label, singlearm pilot study. J Eur Acad Dermatol Venereol 2008; 22:345–52. 10 Vincent FB, Morand EF, Murphy K et al. Antidrug antibodies (ADAb) to tumour necrosis factor (TNF)-specific neutralising agents in chronic inflammatory diseases: a real issue, a clinical perspective. Ann Rheum Dis 2013; 72:165–78. Funding sources: none. Conflicts of interest: none.

News and Notices DOI: 10.1111/bjd.13847 95th Annual Meeting of the British Association of Dermatologists 7th–9th July 2015, Manchester The 95th Annual Meeting of the British Association of Dermatologists will be held at the Manchester Central, 7th–9th July 2015, organised by Prof Irene Leigh, BAD Academic Vice-President. Abstracts of papers and posters should be submitted for consideration by the Scientific Committee. Original communications will be allotted 15 min, which must include time for discussion. Online submission will be the only method of abstract submission available. Full instructions and the submission form can be accessed via the BAD website www.bad.org.uk/annualmeeting The closing date for the receipt of abstracts is Monday 12th January 2015 and the deadline will be adhered to strictly. Any British Journal of Dermatology (2015) 172, pp1436–1461

abstracts received after this date will not be considered. The deadline for abstract submissions to any of the special interest group meetings will be Monday 9th February 2015. Poster submissions on the following topics are strongly encouraged: audit, medical education, and service delivery. Conference & Event Services, British Association of Dermatologists, 4 Fitzroy Square, London, W1T 5HQ, UK or email [email protected] FRT - FONDATION RENE TOURAINE FELLOWSHIPS ANNOUNCEMENT 2015:  Fellowships 2015: one fellowship of 18000 € (for a long exchange period) and four fellowships of 4500 € each (for short exchange periods) are awarded to hospital-based clinical dermatologists and pre or post-doctoral research fellows for international exchanges between laboratories, one of which must be European. Eligibility and application forms can be downloaded at: http://www.fondation-r-touraine.org/Presentation-and-rules Ó 2015 British Association of Dermatologists

This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.

Arthritis possibly induced and exacerbated by a tumour necrosis factor antagonist in a patient with psoriasis vulgaris.

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