Case of Sweet's syndrome with extensive necrosis and ulcers accompanied by myelodysplastic syndrome.

A 43-year-old woman presented with a persistent high fever of 39 degrees C and edematous erythema accompanied by pustules on the face, trunk and extremities. Conjunctivitis and nodules were also observed in the right eye. On the basis of the clinical symptoms and histopathological findings. Sweet's syndrome was diagnosed. Eruptions quickly progressed to extensive necrosis and ulcers, mimicking clinical features of pyoderma gangrenosum. A bone marrow biopsy indicated myelodysplastic syndrome. Oral administration of 50 mg/day of prednisolone induced epithelialization of ulcers, with remaining scarring and pigmentation. Six months later, myelodysplastic syndrome had progressed to acute myelogenous leukemia.

Light-emitting diode phototherapy at 630 +/- 3 nm increases local levels of skin-homing T-cells in human subjects.

BACKGROUND AND AIMS: Red light phototherapy with laser sources has been used successfully for a number of indications. A new generation of quasimonochromatic 630 +/- 3 nm light-emitting diode (LED) systems has recently been yielding good results for the same indications, but no study has examined changes in visible red light irradiated skin at an immunological level. This study was thus designed to examine changes in skin-homing T-cell levels induced in normal human skin by visible red LED energy. SUBJECTS AND METHODS: Six adult male volunteers (35 approximately 48 years old) who satisfied all study criteria had the skin over the lateral aspect of the leg irradiated once per week for 8 weeks with a visible red (630 +/- 3 nm) LED-based system, with irradiance of 105 m/cm2, 15 minutes/session, and a radiant flux of 94 J/cm2. Skin biopsies were performed after the eighth treatment session, and cultures were prepared to assay the type and quantity of skin-homing T-cells using qualitative and quantitative polymerase chain reaction (PCR) techniques. Ultrastructural changes were also assessed with transmission electron microscopy. RESULTS: Transmission electron microscopy revealed mild fibroplastic changes in fibroblasts, with no acute inflammatory changes throughout the treatment session. Qualitative PCR showed the presence of both Th-1 and Th-2 T-cells, and quantitative PCR showed an increase in the numbers of both types of skin-homing T-cells, much more so for Th-2 than for Th-1. CONCLUSIONS: Visible red LED irradiation appears to activate the skin-homing immune system.

Human airway trypsin-like protease induces PAR-2-mediated IL-8 release in psoriasis vulgaris.

Human airway trypsin-like protease (HAT), a novel serine protease in the airways, enhances cell growth and IL-8 production. The expression and role of HAT in the skin however, is unknown. Immunofluorescence staining and reverse transcription (RT)-PCR were done to know HAT production in normal and psoriatic tissues and keratinocyte cell lines. Cell growth and/or IL-8 release analyses were made by bromo-deoxyuridine (BrdU) uptake and ELISA. Psoriatic epidermis showed more extensive immunofluorescence expression of HAT, and less extensive expression of protease-activated receptor (PAR)-2. RT-PCR demonstrated a higher HAT and a lesser PAR-2 mRNA expressions in psoriatic epidermis. Normal keratinocyte and epidermoid carcinoma cell lines expressed HAT and PAR-2 mRNA, and immortalized keratinocytes (HaCaT) expressed PAR-2, but not HAT mRNA. PAR-2 was detected along the keratinocyte surface in culture and became invisible upon HAT stimulation, suggesting a process of its internalization. HAT or PAR-2 activating peptide did not enhance BrdU uptake, but induced an IL-8 release. Treatment with HAT and IL-1beta synergistically increased the effect of IL-8 release. Inhibition of PAR-2 resulted in a decreased HAT-induced IL-8 release. Thus, HAT might promote PAR-2-mediated IL-8 production to accumulate inflammatory cells in the epidermal layer of psoriasis.