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Objectives The pathogenesis and therapy of hypertrophic scar have not yet been established. Our aim was to investigate the antiproliferative and antisecretory effects of lapachol, isolated from the stem bark of Avicennia rumphiana Hall. f., on hypertrophic scar fibroblasts. Methods The effects of lapachol on hypertrophic scar fibroblast proliferation were measured using the MTT assay, cell-cycle analyses and lactate dehydrogenase assays. The type I collagen α-chain (COL1A1), interleukin-6 (IL-6) and plasminogen activator inhibitor-1 (PAI-1) mRNA and/or protein levels of hypertrophic scar-fibroblasts were quantitated by real-time PCR and ELISA. Key findings Lapachol at 25 and 50 µm significantly inhibited the in vitro proliferation of hypertrophic scar fibroblasts, but not fibroblasts from non-lesional skin sites. In addition, lapachol had no apparent effect on cell cycle and lactate dehydrogenase activity in conditioned medium from lapachol-treated hypertrophic scar fibroblasts was nearly equal to that in medium from vehicle-treated cells. Lapachol treatment also inhibited COL1A1 and PAI-1 mRNA levels in hypertrophic scar fibroblasts, but did not affect IL-6 mRNA levels. The protein levels of IL-6 and PAI-1 in conditioned medium from hypertrophic scar fibroblasts treated with 50 µm lapachol were lower than those from vehicle-treated hypertrophic scar fibroblasts. Conclusions Lapachol decreased the proliferation rate of hypertrophic scar fibroblasts. As IL-6 and PAI-1 secretion was also lowered in lapachol-treated hypertrophic scar fibroblasts, our findings suggested that lapachol may have suppressed extracellular matrix hyperplasia in wound healing and possibly alleviated the formation of hypertrophic scar.

A patient with psoriasis vulgaris developed multiple purpura on the extremities and hemorrhage at the oral mucosa and gingiva with marked thrombocytopenia. This thrombocytopenia was possibly induced by a retinoid agent, etretinate, from the clinical course and data. The total amount of etretinate administered was 2,410 mg over 191 days (41.9 mg/kg body weight, average 15.3 mg/day). A platelet transfusion partially restored the platelet count and the purpura and gingival hemorrhage disappeared approximately 10 days after the cessation of etretinate. However, the platelet count remains at 60-80 x 10 3 /mm 3 after two and a half years without etretinate therapy. Although there are only a few case reports of etretinate-induced thrombocytopenia, we should pay more attention to the peripheral platelet count during etretinate therapy.

Background Most paraneoplastic pemphigus (PNP) cases reported to date have been associated with lymphoproliferative neoplasms. Patients with PNP have autoantibodies against the plakin family (eg, envoplakin and periplakin). Antibodies against desmoglein 3 (Dsg3) and Dsg1, antigens for classic types of pemphigus, have also been reported to play an important role in the initial stage of PNP. Observations We describe a patient with PNP associated with follicular dendritic cell sarcoma. Antibodies to envoplakin and periplakin were detected. When only mucosal lesions were observed at the early stage, the antibody to Dsg3 but not to Dsg1 was detected by enzyme-linked immunosorbent assay. After skin lesions appeared, antibodies to Dsg1 and Dsg3 were detected. These titers were elevated, with exacerbation of skin lesions. Although the patient received corticosteroid therapy, double-filtration plasmapheresis, and intravenous human immunoglobulin therapy after surgical resection of follicular dendritic cell sarcoma, she died of fungal infective lung embolisms. A direct immunofluorescence study of autopsy samples showed IgG deposition in the epidermis of the skin and oral mucosal membrane, but not in the lungs and kidneys and follicular dendritic cell sarcoma of the para-aortic area. Conclusion In this patient with PNP and follicular dendritic cell sarcoma, there was an association between the clinical phenotype and the anti-Dsg antibody profile, as seen in pemphigus vulgaris.

Microscopic polyangiitis (MPA) is a systemic vasculitis histologically characterized by small-vessel involvement. Antineutrophil cytoplasmic antibodies (especially anti-myeloperoxidase antibodies) (MPO-ANCA) are often positive in serum. Although the skin is affected in 20-70% of patients, the precise description has been limited. This retrospective study analyzed clinical manifestations in patients of MPA with skin eruptions. Ten patients with skin eruptions diagnosed as MPA according to Chapel Hill consensus criteria consisted of 6 men and 4 women aged from 38 to 80 years (62.1 +/- 13.3). Clinical manifestations, laboratory data, and histological findings were examined. Purpura and petechiae in 6 patients, livedo in 2 patients, and erythema in 7 patients, especially erythema on the hands and\or fingers in 4 patients, were observed. Histological findings from the eruptions in 7 patients showed perivascular lymphocyte infiltration in the upper dermis in 4 patients, and infiltration of lymphocytes and a few neutrophils around small arteries in the middle to deep dermis in 2 patients and diffuse infiltration of histiocytes and lymphocytes in the middle dermis in 1 patient. Cutaneous involvements in MPA showed a wide spectrum of clinical and histological findings.

An antifungal drug, itraconazole (ITZ) is effective for chromomycosis patients, but the distribution of ITZ and its metabolite, hydroxy-intraconazole (OH-ITZ) is unclear in pathological tissues. This study investigated how much ITZ and OH-ITZ accumulated in the lesional tissues of chromomycosis and non-lesional skin after oral treatment with ITZ. We determined the concentrations of ITZ and OH-ITZ in the lesional tissues of chromomycosis by Foncecaea pedrosoi and non-lesional skin after oral treatment with a total dose of 2.3g of ITZ. ITZ concentration was significantly higher in pathological skin than non-pathological skin. The ITZ concentration in the lesional tissues was higher in the central site than in the marginal site. No difference was seen in the OH-ITZ concentrations among three skin parts, the center and the margin in lesional skin, and non-lesional skin adjacent to the lesion. This study showed higher concentrations of ITZ in pathological tissues than in non-pathological tissues.

Background: A patient with allergic contact dermatitis caused by hexavalent chromium plating on a cellular phone has already been reported. Objectives: This study described the clinical characteristics and results of patch tests in 8 patients with contact dermatitis possibly caused by handling a cellular phone. Patients: The 8 patients were 4 males and 4 females aged from 14 to 54 years. They each noticed skin eruptions after 9–25 days of using a cellular phone. All patients had erythema, and 7 had papules on the hemilateral auricle or in the preauricular region. Three of 8 patients had a history of metal allergy. Chromate, aluminium and acrylnitrile-butadiene-styrene copolymer were used as plating on the cellular phones used by these patients. Methods: Closed patch tests and photopatch tests were performed using metal standard antigens. Results: The patch test was positive for 0.5, 0.1 and 0.05% potassium dichromate in all 8 patients. The photopatch test showed the same results. One patient was positive for 2% cobalt chloride and one for 5% nickel sulfate. Conclusion: It is important to consider the possibility of contact dermatitis due to a cellular phone, possibly caused by chromate, when the patients have erythema and papules on the hemilateral auricle or in the preauricular region.