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Pimecrolimus is an ascomycin derivative and belongs to the family of calcineurin inhibitors. Its mechanism of action is the blockage of T-cell activation. In contrast with topical steroids, pimecrolimus is not thought to induce skin atrophy with prolonged use.8 Our patient was successfully managed with topical 0.1% pimecrolimus and adequate sun protection. He remains free of recurrence over a period of 24 months of follow-up. Although topical 0.1% pimecrolimus has been successfully used for the treatment of mucosal lichen planus,9 its use in the management of actinic lichen planus has not been investigated so far. We postulate that topical 0.1% pimecrolimus could be useful in the treatment of ALP. K Ezzedine,* T Simonart, P Vereecken, M Heenen
Department of Dermatology, Hpital Erasme, Universit Libre de Bruxelles, Brussels, B-1070 Belgium *Correspondence: K Ezzedine. E-mail: ezzedinekhaled@hotmail.com

References
1 Macfarlane AW. A case of actinic lichen planus. Clin Exp Dermatol 1989; 14: 6568. 2 Salman SM, Kibbi AG, Zaynoun S. Actinic lichen planus. A clinicopathologic study of 16 patients. J Am Acad Dermatol 1989; 20: 226231. 3 Kilaimy M. Lichen planus subtropicus. Arch Dermatol 1976; 112: 12511253. 4 Simonart T, Heenen M. Inflammatory verrucous epidermal naevus presenting as a psoriasiform plaque. Dermatology 2007; 215: 167168. 5 Bolognia JL, Orlow SJ, Glick SA. Lines of Blaschko. J Am Acad Dermatol 1994; 31: 157190. 6 Lipsker D, Cribier B, Girard-Lemaire F, Flori E, Grosshans E. Genetic mosaicism in an acquired inflammatory dermatosis following the lines of Blaschko. Arch Dermatol 2000; 136: 805807. 7 Martin S. Clarification of lichen planus actinicus. Arch Dermatol 1977; 113: 1615. 8 Queille-Roussel C, Paul C, Duteil L et al. The new topical ascomycin derivative SDZ ASM 981 does not induce skin atrophy when applied to normal skin for 4 weeks: a randomized, double-blind controlled study. Br J Dermatol 2001; 144: 507513. 9 Wollina U. The role of topical calcineurin inhibitors for skin diseases other than atopic dermatitis. Am J Clin Dermatol 2007; 8: 157173. DOI: 10.1111/j.1468-3083.2008.02903.x
LETTERS Letters the Editor Letters to TO THE XXX to the EditorEDITOR

Figure 1 (a) Clinical aspect characterized by pinhead sized hyperpigmented papules in a linear arrangement following a Blaschkos line. (b) Skin biopsy showing thinning of the epidermis, orthokeratosis, focal basal liquefaction, a sparse perivascular inammatory inltrate, and pigmentary incontinence with a bandlike lymphohistiocytic inltrate in the upper dermis.

Multiple basal cell carcinomas arising on a thermal-burn scar. Successful treatment with photodynamic therapy
Editor Burn scars are considered risk factors for skin cancer. Although squamous cell carcinoma (SCC) is the most frequent type of tumour developed on scars, other malignancies such as basal cell carcinoma (BCC)1 sarcoma and melanoma have also been described.

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Figure 1 Multiple supercial BCCs scattered on the scar of a thermal burn.

A 55-year-old male, with no remarkable past medical history, referred the appearance of several lesions on his back, with occasional bleeding. He had suffered a severe thermal burn at the age of 5, when someone spilled boiling water on his back and right thigh. The burns healed by secondary intention, leaving a 25 30 cm burn scar on the upper right area of his back and a 7 10 cm scar on the lateral aspect of his right thigh. On clinical examination, more than twenty 1- to 2-cm scaly patches were observed. These were scattered on the patients back and right thigh, limited to the scar surface (Fig. 1). Histologic examination confirmed the diagnosis of multiple superficial BCCs. Because a surgical approach was found to be difficult due to the low elasticity of the scar tissue and the high number of lesions to be excised, treatment with photodynamic therapy (PDT) was chosen. After two cycles [two treatments using metilaminolevulinate (MAL) and red light, 1 week apart], complete clearance of the lesions was observed (Fig. 2). This was confirmed both using fluorescence diagnosis and histologically. Recently, two retrospective epidemiological studies have been published evaluating the risk of skin cancer on burn scars. No causal association has been found in any of them. However, the mean follow-up period in both studies might have been too short in order to evaluate the real incidence.2,3 BCC is the second most common burn scar tumour; it represents 12% of all tumours developed on burn scars. It has been shown that it has a shorter latency period (22 years) and occurs in older patients than SCC.4 Treves and Pack5 addressed that 0.03% of BCC originates in burn scars. The pathogenic mechanism, however, remains unclear. Mutations of p53 have been reported in carcinomas developed on burn

Figure 2 Disappearance of BCCs after PDT.

scars.6 It has been suggested that BCC occurs more easily in superficial burns in which the adnexa are spared. The basal cells present in these adnexal structures are necessary to regenerate the epidermis but also facilitate the development of BCC.5 Moreover, healing by secondary intention has also been considered a risk factor for malignant tumours on burn scars. Today, a reduction of incidence of such cases would be expected since the current standard of care requires early grafting.4 Nevertheless, development of BCC on skin graft secondary to thermal burn scar has also been reported.7 PDT was been shown to be effective in the treatment of nodular and superficial BCC.8 This case illustrates the effectiveness of PDT for treating BCC and represents a good alternative when a surgical approach is complex. In conclusion, to our knowledge, there are no previous reports of multiple BCCs arising on a thermal burn scar. Recently performed epidemiological studies could not confirm any increased risk of malignant tumours on burn injuries.2 Our patients light skin colour and intermittent intense sporadic sun exposure history could be involved in the development of the multiple BCC.

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However, the fact that the BCCs where only located on the burn scar surface suggest that the thermal burn played a key role in the appearance of these tumours. PDT seems to be an effective and safe therapy for BCCs arising on scars. L Bagazgoitia,* S Bea, JL Santiago, J Cuevas, Juarranz, P Jan
Dermatology Department, Hospital Ramn y Cajal, Madrid, Universidad de Alcal de Henares, Madrid, Spain, Pathology Department, Hospital Universitario de Guadalajara, Guadalajara, Spain, Biology Department, Universidad Autnoma de Madrid, Madrid, Spain *Correspondence: L Bagazgoitia. E-mail: lorea_b@yahoo.com

Table 1 Lipid prole of psoriatic and normal subjects Patients with psoriasis Triglyceride (mg/dL) 138.819 73.3576 Total cholesterol (mg/dL) LDL-C (mg/dL) VLDL-C (mg/dL) HDL-C (mg/dL) Control group P-value

87.234 34.1661 < 0.0001

193.032 42.6004 161.734 22.9728 < 0.0001 123.783 34.7339 27.763 14.6715 46.483 7.3588 90.933 25.2854 < 0.0001 17.446 6.8332 50.941 6.4912 < 0.0001 0.001

Table 2 Frequency of abnormal serum triglyceride, total cholesterol, LDL-C and HDL-C in psoriasis patients and control subjects Patients with psoriasis No (%) Triglyceride > 150 mg/dL Total cholesterol > 200 mg/dL LDL-C > 130 mg/dL HDL-C < 35 mg/dL 25/62 (40.32%) 24/63 (36.36%) 27/64 (42.18%) 5/64 (7.81%) Control group No (%) 1/64 (1.56%) 5/63 (7.93%) 3/60 (5%) 1/63 (1.58%) P-value

References
1 Roewert-Huber J, Lange-Asschenfeldt B, Stockfleth E, Kerl H. Epidemiology and aetiology of basal cell carcinoma. Br J Dermatol 2007; 157: 4751. 2 Mellemkjaer L, Holmich LR, Gridley G, Rabkin C, Olsen JH. Risks for skin and other cancers up to 25 years after burn injuries. Epidemiology 2006; 17: 668673. 3 Lindelof B, Krynitz B, Granath F, Ekbom A. Burn injuries and skin cancer: a population-based cohort study. Acta Derm Venereol 2008; 88: 2022. 4 Kowal-Vern A, Criswell BK. Burn scar neoplasms: a literature review and statistical analysis. Burns 2005; 31: 403413. 5 Treves N, Pack GT. Development of cancer in burn scars. Surg Gynecol Obstet 1930; 51: 749782. 6 Harland DL, Robinson WA, Franklin WA. Deletion of the p53 gene in a patient with aggressive burn scar carcinoma. J Trauma 1997; 42: 104107. 7 Martin JM, Monteagudo C, Alonso V et al. Basal cell carcinomas arising on a skin graft secondary to a thermal burn scar. Burns 2005; 31: 789791. 8 Braathen LR, Szeimies RM, Basset-Seguin N et al. Guidelines on the use of photodynamic therapy for nonmelanoma skin cancer: an international consensus. International Society for Photodynamic Therapy in Dermatology, 2005. J Am Acad Dermatol 2007; 56: 125143. DOI: 10.1111/j.1468-3083.2008.02904.x
LETTERS Letters the Editor Letters to TO THE XXX to the EditorEDITOR

< 0.0001 < 0.0001 < 0.0001 0.145

Lipid prole in patients with psoriasis in Zahedan, south-east Iran

Editor Psoriasis, which affects about 2% to 3% of the adult population,1 is characterized by marked increases in keratinocyte proliferation, abnormal pattern of keratinocyte differentiation, prominent alterations in dermal capillary vasculature and infiltration of T cells, monocytes/macrophages and neutrophils to dermal and epidermal. The aetiology of psoriasis is unknown, but genetic, metabolic and immune mechanisms have been proposed. Patients with psoriasis seem to have an increased morbidity and mortality from cardiovascular events. Abnormalities of plasma lipids and lipoproteins are likely to play an important role in the increased risk of atherosclerosis.2,3 There is still controversy about the lipid profile in psoriasis patients.4,5

The aim of the present study was to evaluate the lipid profile in psoriasis patients. This case-control study which consist of 65 psoriasis patients (38 males and 27 females; age; 771 years) and 64 control subjects (28 males and 36 females; age: 1378 years) was carried out from April 2006 to November 2007 in clinic of dermatology, Khatam-al-Anibia hospital, Zahedan, Iran. The age was not statistically differences between case and control. The project was approved by local ethical committee, and informed consent was taken from patients and normal subjects. The patients were assessed by medical history and physical examination, and psoriasis area and severity index (PASI) was calculated. Exclusion criteria were as follows: diabetes, obesity, family history of hyperlipidemia, renal and liver failure, hypothyroidism, taking systemic drugs especially lipids lowering agents in order to eliminate damaging factors on serum lipids level of the patients. Serum total cholesterol, triglycerides and HDL-C were assessed by enzymatic methods using commercially available kits. LDL-C was estimated by the Friedewald formula (LDL-C = total cholesterol-HDLC-triglycerides/5), and VLDL-C calculated by: triglycerides/5. We found that 25.3% of patients had positive family history of psoriasis. Serum triglyceride, total cholesterol, LDL-C and VLDL-C were significantly higher and HDL-C was significantly lower in psoriasis patients than control subjects (Table 1). The results showed that the frequency of abnormal serum level of triglyceride, total cholesterol and LDL-C were significantly higher in patients, while the frequency of abnormal HDL-C was not significant between the patients and control group (Table 2). There were no significant differences in lipid profile regarding severity of disease (data not shown).

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