550

Correspondence

stimulates other sensory neurones.' SP can also increase inflammation through mediators released from macrophages and T cells. SP enhances the production of the keratinocyte-derived inflammatory mediators, interleukin i and granulocyte-macrophage colony-stimulating factor which are involved in the pathogenesis of psoriasis.* Capsaicin is derived from plants of the Solanaceae family and depletes SP through inducing degeneration of primary sensory neurones. We treated io patients with psoriasis vulgaris (seven men, three women; mean age 32 years) with topical capsaicin in an 8-week open trial. The patients had severe psoriasis with involvement of 15-30% of the total body surface area. The patients were instructed not to take any medication 4 weeks before the treatment and during the trial. The patients were provided with tubes of 0 025% capsaicin in a cream base (GenDerm Corp., Northbrook, IL, U.S.A.). The cream was applied to the psoriatic plaques on one side of the body, four times daily. Psoriatic lesions on the other side were treated with a petrolatum placebo. Evaluation was performed by the same physician before therapy, and then at weekly intervals. At each visit the itching, scaling and erythema were graded according to a four point scale (o, absent; i, trace; 2, mild; 3, moderate; 4, severe). The severity score was obtained by adding the scores. All of the patients completed the trial. At the end of the study, seven patients showed marked improvement with capsaicin as regards itching, scaling and erythema. In the non-responders, the itching disappeared. There was no significant change in the placebo-treated lesions. The patients tolerated the treatment well, and no side-effects were observed. The results of this preliminary study show that capsaicin therapy seems to be effective in the treatment of psoriasis, especially in relieving itching, by inhibiting the release of SP from cutaneous sensory neurones. Dermatology Unit, Memorial Ahmet Ors Hospital, 006510 Emek, Ankara, Turkey

N.KuRKguo6LU F.ALAYBEYI

REFERENCES

1 Naukkarinen A, Nickoloflf BJ, Farber EM. Quantification of cutaneous sensory nerves and their substance P content in psoriasis. J Invest Dermatol 1989; 92: 126-9. 2 Kurk^uoglu N, Qakar N. Substance P immunoreactivity in active edges of psoriatic plaques. Clin Exp Dermatol 1990, 15:000-000.

3 Toyry S, Fraki J, Tammi R. Mast cell density in psoriatic skin. The effect of PUVA and corticosteroid therapy. Arch Dermatol Res 1988; 280: 282-5. 4 Brown J, Perry P, Ansel J. Substance P induction of keratinocyte cytokines. J Invest Dermatol 1989; 92: 407.

Treatment of lichen planus with a short course of oral prednisolone SIR, A variety of systemic treatments have been suggested for lichen planus but corticosteroids remain the most widely used. There have been no clinical studies of the effectiveness of this therapy although a course of up to 6 weeks is recommended.' It is also stated that corticosteroid therapy does not affect the total duration of the disease.^ We therefore undertook a double-blind study of oral prednisolone in 38 patients with lichen planus. The short duration of the course of steroids allowed the dose not to be reduced gradually. The diagnosis of lichen planus was made on clinical grounds and contraindications to the study were a history of peptic ulceration, diabetes and previous treatment with corticosteroids. The patients were randomly allocated to either active or placebo therapy coded by the pharmacist. Active treatment consisted of prednisolone 30 mg daily for 10 days and placebo treatment consisted of a similar course of inactive tablets of identical appearance. Hydrocortisone-17-butyrate cream was given for topical treatment with instructions to use it twice daily. Patients were seen on the initial visit prior to entering the study, 6 weeks later then at intervals of 3 months until either the condition had cleared or 2 years had elapsed from the time of thefirstvisit. At each visit the observer recorded a score of severity of the lichen planus on a 10 cm linear analogue scale on which 0 represented 'much less severe' and 10 'very much worse'. A similar assessment was carried out by the patients themselves and there was a separate

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551

assessment of degree of itch also on a 10 cm visual analogue. The observer noted any change in the lichen planus according to the following scale: o, worse; i, no change; 2, better; 3, clearing; 4, cleared. The Wilcoxon rank sum test was used for statistical analyses. Twenty-eight of the 38 patients completed the study, 14 in the active group and 14 in the placebo group. The profile of both groups in terms of age, duration and severity of lichen planus was very similar. The time taken for lichen planus to clear was significantly different between the two groups (P = o 02). The median time in the prednisolone group was 18 weeks (range 4-61) and in the placebo group was 29 weeks (6-104). Three patients in the placebo group but none in the active group failed to clear within 2 years. At the 6-week visit the linear analogue scores of severity of rash by the patients were significantly different between active and placebo groups (P = ooi) (Table i). The improvement in the observers' linear analogue scores for severity from entry to 6 weeks (score at entry—score at 6 weeks) was significantly different between the two groups {P < o 05). The patients' linear analogue scores for itch at 6 weeks failed to show a significant difference, although the median value in the prednisolone group (22) was less than that in the placebo group (30). The observers' scores for change at 6 weeks were significantly different between active and placebo groups (P < o 05). At 6 weeks four patients in the prednisolone group were considered cleared and four improved compared with one patient that cleared and one with clearing in the placebo group. At 18 weeks 10 patients in the prednisolone group had cleared compared with seven on placebo. The side-effects were minimal. One patient experienced mild heartburn while on prednisolone but did not stop treatment and another patient experienced euphoria. There were no side-effects in the placebo group. Three of the 14 patients on prednisolone had a degree of rebound after an initial symptomatic improvement whilst one patient in the placebo group also described a dramatic improvement with a slight relapse after finishing the tablets. Two patients with very severe lichen planus improved on prednisolone, TABLE I. Severity of lichen planus, scored by patient at 6 weeks and improvement of lichen planus, scored by observer at 6 weeks (score at entry minus score at 6 weeks). Median values, range in parentheses Prednisolone

Placebo

Severity (patient) 1-3 (O-4-5-2) 4 9 (10-71) Improvement (observer) 25 (-0-5-74) 0-85 (-2-8-50)

P = ooi P

Treatment of lichen planus with a short course of oral prednisolone.

550 Correspondence stimulates other sensory neurones.' SP can also increase inflammation through mediators released from macrophages and T cells. SP...
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