Experimental Koebner phenomenon in patients with psoriasis.

BACKGROUND: The Koebner phenomenon is defined as 'the development of psoriasis at sites of traumatized skin'. The 'all-or-none principle' means that, if psoriasis occurs in one area of injury, all injured areas develop psoriasis or vice versa. The aim is to demonstrate the concordance of patients with the all-or-none principle when a standard method of trauma is employed. METHODS: Sixty-two patients with psoriasis were enrolled in the study. Demographic data and disease characteristics were recorded. The medial aspects of both forearms, devoid of lesions, were pricked using two sets of five 30-gauge needles at an angle of 30 degrees , with 2-cm intervals. On days 14 and 28, the patients' forearms were checked for the presence of a typical psoriatic plaque of white scales on an erythematous papule. RESULTS: On day 28, 45 patients (72.5%) had a negative Koebner response in all prick sites whereas 1 patient (1.6%) had psoriatic papules in 10 out of 10 prick sites. The rest of the patients (n = 16, 25.8%) had between 1 and 9 papules in number. CONCLUSION: Using standard methods of trauma, it is possible to induce psoriasis lesions as a Koebner response but this response is not always in concordance with the all-or-none principle previously described.

Nicotine and biochanin A, but not cigarette smoke, induce anti-inflammatory effects on keratinocytes and endothelial cells in patients with Behçet's disease.

During periods of smoking, patients with Behçet's disease have less oral aphthae than in abstinence. To elucidate this observation, human keratinocytes and dermal microvascular endothelial cells (HMEC-1) were incubated with serum of 20 patients with Behçet's disease and 20 healthy controls for 4 hours. Maximum non-toxic concentrations were determined and the cells were further treated with 6 microM nicotine, 3.3% cigarette smoke extract (CES), 100 microM biochanin A, and 6.25/12.5 microM pyrrolidine dithiocarbamate alone and in combinations for 24 hours. Serum IL-8 levels of patients were significantly lower than those of controls. However, after 4 hours incubation with patients' sera, IL-8 release by both cell types was markedly increased when compared with the corresponding serum levels. The levels of IL-6 and vascular endothelial growth factor (VEGF) release were after 4 hours similar with the corresponding levels in serum. IL-1 was not detected. Nicotine significantly decreased IL-8 and -6 release by HMEC-1 maintained in both patients' and controls' sera, but only IL-6 release by keratinocytes maintained in patients' sera. VEGF release by both cells was markedly increased after nicotine treatment in either serum. CES significantly decreased IL-8 release and increased production of VEGF in keratinocytes maintained in patients' serum. The phytoestrogen biochanin A alone and in combination with nicotine further decreased the secretion of IL-8, -6, and VEGF in all experimental settings. Our data support a specific anti-inflammatory effect of nicotine on keratinocytes and endothelial cells maintained in the serum of patients with Behçet's disease. Moreover, biochanin A is likely to exhibit similar and even more profound results than nicotine.

Life-threatening disorders of mucous membranes.

Oral mucosa is one of the first barriers to the outside world which encounters various antigens, microorganisms and physical agents. Numerous oral pathologies challenge the dermatologists. Some may be the first sign of an underlying immunosuppression, while others are the inevitable serious outcomes of long-lasting mucosal disease. The differential diagnosis is crucial in terms of prompt and effective treatment.

Milia in regressing plaques of mycosis fungoides: provoked by topical nitrogen mustard or not?

OBJECTIVE: To report three cases of mycosis fungoides with milia formation in the regressing lesions. PATIENTS AND SETTING: Dermatology clinic of a university hospital (referral center). Three patients with mycosis fungoides with body surface involvement of 10% in one case (stage IIb) and exceeding 30% in two cases (stages IIb and III). All patients were treated with photochemotherapy and topical nitrogen mustard ointment in a concentration of 0.01%. After approximately 3 months multiple milia erupted on regressing plaques. RESULTS: The presence of milia was evident and was confirmed by histopathology. Regression of mycosis fungoides was noted in these plaques both clinically and in comparison with the pretreatment histologic appearance. Two of the patients showed a histological picture of follicular mucinosis. CONCLUSIONS: We do not know the significance of milia in mycosis fungoides (MF). However, we suggest that follicular rupture or a degenerative process might result in milia formation.

Stiff skin syndrome: a case report.

Stiff skin syndrome (SSS) is a disease similar to scleroderma with an unknown etiology. Stone-hard areas of skin are observed from birth or in early childhood. In this article we describe a 15-year-old girl with skin hardening and limitation of movement. We diagnosed the case as SSS, of which we have not encountered a similar report in the Turkish literature.

Familial atrophia maculosa varioliformis cutis.

Atrophia maculosa varioliformis cutis (AVMC) was first described by Heidingsfeld in 1918, as a rarely reported form of idiopathic macular atrophy on the cheek (1). It is characterized, clinically, by shallow, sharply demarcated depressions in various shapes. Extrahepatic biliary atresia (2) and pachydermodactyly (3) have been the only conditions associated with AMVC reported in the past 80 years. Although keratosis pilaris is a common skin disorder, it is related to other idiopathic atrophic conditions considered in the differential diagnosis of AMVC, namely keratosis pilaris atrophicans (4). However, the two associations may be coincidental. We observed a patient with keratosis pilaris, and her brother and an unrelated young man, whose findings led to a diagnosis of AMVC.