Occupational hand eczema is frequent in hospital workers, especially in nurses. A comprehensive understanding regarding hand eczema is essential for establishing proper prevention and treatment strategies. The purpose of this study was to identify the risk factors for hand eczema in hospital nursing staffs. A self-administered questionnaire study was performed on hospital nursing staffs at a single general hospital in Korea. In addition, 70 patients with hand eczema underwent patch testing. Five hundred and twenty-five of 700 invited nurses completed the study (response rate, 75.0%). The overall frequency of symptom-based hand eczema was 75.6%, and self-reported hand eczema was 31.0%. Risk factors for hand eczema were young age, history of atopic dermatitis, frequent hand washing (>20 times/day) and long duration of glove wearing (>5 min). Hand eczema was less frequent among frequent hand moisturizer users (>3-4 times/day). Positive patch test reactions were observed in 61.4%. Frequent allergens were nickel sulfate (35.7%), cobalt chloride (28.6%) and thiomersal (21.4%). Among various antibiotics, ciprofloxacin (11.4%), trimethoprim/sulfamethoxazole (11.4%) and gentamicin (7.1%) were revealed as common allergens, in order of frequency. Hand eczema is quite common among hospital nursing staffs. Proper preventive programs and educations are demanded.

.95-fold after IPL treatment and up to 2.85-fold after PDT. TGF-β1 mRNA and protein showed slight increases after both IPL treatment and PDT, of which the latter induced slightly larger increases. TNF-α mRNA and protein showed no induction or reduction after PDT. Conclusion: Increased expressions of IL-10 and TGF-β1 was observed after PDT. The induction of IL-10 may contribute to the anti-inflammatory effect, which explains the therapeutic benefit of PDT for inflammatory dermatoses, and that of TGF-β1 may be related to the therapeutic effect for psoriasis. The finding that IL-10 induction was more marked after IPL treatment than after PDT suggests that other mechanisms than IL-10 induction in keratinocytes after PDT may participate in the anti-inflammatory effect of PDT.

Recognition of apoptotic cells by macrophages is crucial for resolution of inflammation, immune tolerance, and tissue repair. Cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) and hepatocyte growth factor (HGF) play important roles in the tissue repair process. We investigated the characteristics of macrophage COX-2 and PGE2 expression mediated by apoptotic cells and then determined how macrophages exposed to apoptotic cells in vitro and in vivo orchestrate the interaction between COX-2/PGE2 and HGF signaling pathways. Exposure of RAW 264.7 cells and primary peritoneal macrophages to apoptotic cells resulted in induction of COX-2 and PGE2. The COX-2 inhibitor NS-398 suppressed apoptotic cell-induced PGE2 production. Both NS-398 and COX-2-siRNA, as well as the PGE2 receptor EP2 antagonist, blocked HGF expression in response to apoptotic cells. In addition, the HGF receptor antagonist suppressed increases in COX-2 and PGE2 induction. The in vivo relevance of the interaction between the COX-2/PGE2 and HGF pathways through a positive feedback loop was shown in cultured alveolar macrophages following in vivo exposure of bleomycin-stimulated lungs to apoptotic cells. Our results demonstrate that upregulation of the COX-2/PGE2 and HGF in macrophages following exposure to apoptotic cells represents a mechanism for mediating the anti-inflammatory and antifibrotic consequences of apoptotic cell recognition.

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Our study shows that the prevalence of items that release nickel or cobalt among jewellery and metal clothing items is high in Korea.