A possible link between superoxide dismutase activity and malondialdehyde level with the clinical manifestations of rosacea was investigated. We found differences in superoxide dismutase activities between mild rosacea (stages I and II) and severe involvement (stage III) groups, as well as between disease and control groups that were statistically significant (P < 0.05). In the mild involvement group (stages I and II), the superoxide dismutase activity was higher than in the control group (P < 0.05), while the malondialdehyde levels did not differ from the control. In the severe involvement group (stage III), the superoxide dismutase activity was lower than in the control group (P < 0.05), and this was coupled to a raised level of malondialdehyde (P < 0.05). These findings clearly show that in the mild involvement phase of rosacea patients, superoxide dismutase activity was stimulated to protect the skin against reactive oxygen species so that the malondialdehyde levels were maintained. In contrast, in more severe disease, due to a decrease in the capacity of the antioxidant defence system, the malondialdehyde levels were increased. These findings support the 'antioxidant system defect hypothesis' in rosacea patients.

Inflammation in Behcet's disease is thought to be mediated by cytokines derived from T-helper type 1 (Th1) lymphocytes. In this study, we tried to determine serum interleukin (IL)-18 and tumour necrosis factor (TNF)-alpha levels of patients with Behcet's disease. Twenty-seven patients with active Behcet's disease, and 20 healthy control subjects were included in this study. Differences between mean serum IL-18 and TNF-alpha level of patients with Behcet's disease were significantly increased when compared with the control group. A significant correlation was found between serum IL-18 and TNF-alpha levels of Behcet patients (rs = 0.627, P < 0.0001). IL-18 and TNF-alpha levels may be related to disease pathogenesis. Increased levels of IL-18 also support Th1 predominance in Behcet's disease.

Brooke-Spiegler syndrome (BSS, familial cylindromatosis or turban tumor syndrome) is an inherited disease characterized by neoplasms of the skin appendages such as cylindroma, trichoepithelioma, and spiradenoma. The disease has been mapped to 16q12-13, and mutations in the CYLD gene have been identified in families with this disorder. Of interest, multiple familial trichoepithelioma (MFT) has been described as a distinct disorder characterized by the familial occurrence of trichoepitheliomas. MFT has been mapped to 9p21; however, to date a candidate gene has not been identified. In this report, we describe a four-generation family with BSS presenting predominantly with trichoepitheliomas (resembling MFT phenotype). We identified a novel missense mutation in the CYLD gene, designated E474G, in the affected individuals of this family. Our findings exemplify clinical heterogeneity within BSS and extend the body of evidence that mutations in CYLD are implicated in this disease. Although not conclusive, these findings suggest that BSS and MFT may represent a single entity.

We studied the reliability of teledermatology diagnoses made using a Web-based system. Clinical photographs and information relating to 125 patients were placed on a Web server. Three dermatologists made the most likely diagnosis via a Web interface. The reference diagnosis was made in a face-to-face consultation with a fourth dermatologist; where appropriate it was confirmed histologically. The teledermatologists were correct in 57% of cases when viewing the images alone. Their diagnostic accuracy improved to 70% when additional clinical information was available. The rate of agreement between the teledermatologists ranged from 44% to 70% (kappa= 0.22-0.32). Seventy-seven per cent of the patients were correctly diagnosed by at least two dermatologists when clinical information was provided. A Web-based system appears to be reliable for teledermatology. A single well trained teledermatologist may give better results than a group of less well trained clinicians.

Case 1 A 9‐year‐old girl applied a temporary henna tattoo to her right arm and 1 week later repeated the same process. In the following 2 days, erythema and papulovesicular eruptions developed at the application site (Fig. 1). Patch tests were performed with the European Standard Series, specific hairdressing agents, and commercial and natural henna. The patient showed a 3+ reaction to both natural henna and ‘‘para‐phenylenediamine (PPD)’' 1% and a 3+ reaction to nickel sulfate 5% at 48, 72, and 96 h (Fig. 2). She was treated with topical steroid cream (beclomethasone dipropionate), applied twice daily. A slight postinflammatory hypopigmentation was observed at the time of the patch test. The hypopigmentation has gradually decreased in severity over time (Fig. 3). 1 Case 1: temporary henna tattoo reaction with papulovesicular eruptions 2 Case 1: patch test results. (A) 3+ reaction to nickel sulfate 5%; (B) 3+ reaction to para‐phenylenediamine (PPD) 1%; (C) 3+ reaction to natural henna 3 Case 1: postinflammatory hypopigmentation Case 2 An 11‐year‐old boy was admitted to our outpatient clinic with itchy, erythematous, papulovesicular eruptions on the left arm. These lesions appeared after application of a temporary henna tattoo with a ‘‘do‐it‐yourself’' kit to the left arm. Patch tests were performed with the European Standard Series and commercial tattoo products. The patient showed only a 1+ reaction to commercial henna. He was treated with topical steroid cream (beclomethasone dipropionate), and 2 weeks later his lesions had totally disappeared. Case 3 A 12‐year‐old girl applied a temporary henna tattoo to her left arm. Several hours later, erythema, edema, and itching developed. Patch tests were performed as for Case 2. The patient showed a 2+ reaction to commercial henna. Topical steroid cream (beclomethasone dipropionate) was effective, and 3 weeks later the lesions had healed with slight hypopigmentation. The postinflammatory hypopigmentation traced the tattoo design exactly, which was in the form of a fish (Fig. 4). On follow‐up, the hypopigmentation was not permanent. 4 Case 3: fish‐shaped postinflammatory hypopigmentation