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Nail lesions in psoriatic arthritis: recovery with sulfasalazine treatment
  1. J C Gerster1,
  2. D Hohl2
  1. 1Service de Rhumatologie, Médecine Physique et Réhabilitation, Centre Hospitalier, Universitaire Vaudois (CHUV), 1011 Lausanne, Switzerland; Jean-Charles.Gerster{at}
  2. 2Service Universitaire de Dermatologie, CHUV, 1011 Lausanne, Switzerland

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Treatment with sulfasalazine has been reported to be effective in psoriatic arthritis (PsA).1–,3 However, the role of sulfasalazine in cutaneous lesions has been surrounded by controversies. As far as we know its possible beneficial effect on nail lesions has not been reported.


A 25 year old man had presented with nail lesions considered to be psoriatic since 1996. During the same period he started to have pain in both knee joints. Since 1998 he had also had pain in the distal interphalangeal (DIP) joints. At the end of the same year the patient consulted a rheumatologist. On clinical examination, both knee joints were swollen and a Baker's cyst was present at the right side. The 4th and 5th DIP joints of both hands were red, painful, and slightly swollen. Nail deformities were present in both hands (fig 1A) and feet. Psoriatic lesions of the auditory canals and intergluteal fold were seen, prompting the diagnosis of psoriasis partime inversa.

Figure 1

Left index finger (A) before, (B) after six months' treatment with sulfasalazine. The nail deformities in both hands are no longer present.

Synovial fluid from the right knee joint contained 17.8×109 leucocytes/l (86% polymorphonuclear); no crystals were seen. The erythrocyte sedimentation rate was 33 mm/1st h. Rheumatoid factor was negative, as were cultures of nail specimens for fungi.

Radiographs of the hands and feet were normal. There were slight erosions of the sacroiliac joints and of the symphysis pubis.

The patient was treated with non-steroidal anti-inflammatory drugs (NSAIDs) and on several occasions with local injections of corticosteroids into the knee joints. For the psoriatic nails he took acitretine (Neotigason) at a daily dose of 20 mg, for 12 months, but the nail lesions did not improve. In view of the persisting arthritis, the patient has been treated since January 2000 with sulfasalazine (the dose being progressively increased from 0.5 g daily to 2 g daily), in addition to NSAIDs. Three months later, the nail lesions started to recede and they disappeared progressively (fig 1B); the improvement has persisted until now. Concomitantly, there was a marked improvement of the arthritis.


Nail disease is significantly associated with PsA.4 It is particularly common in cases with DIP joint involvement and tends to indicate more severe PsA.5 In view of the close chronological relationship between the administration of sulfasalazine and the improvement of the nail lesions, it can be considered that sulfasalazine played a beneficial part in the pathological condition of our patient. Dermatological assessment of patients treated with sulfasalazine for PsA has been reported in two series; according to the report published in the series of Gupta et al, patients treated with sulfasalazine for PsA showed signs of cutaneous improvement compared with those receiving placebo.1 The series of Farr et al reports improved cutaneous lesions in as few as 3/15 patients treated with sulfasalazine and 1/15 patients receiving placebo.2 However, we could not find any indication of the evolution of possible simultaneous psoriatic nail lesions.

Treatment of PsA with cyclosporin or etanercept is effective for both joint and skin lesions of psoriasis6,7; again no data about the outcome of psoriatic nail lesions were provided in these clinical studies. Our case report might be the occasion to draw the attention of rheumatologists to the possible beneficial effects of basic treatment such as sulfasalazine not only for PsA but also for treating psoriatic nails.