Adjuvant alternative treatment with chemical peeling and subsequent iontophoresis for postinflammatory hyperpigmentation, erosion with inflamed red papules and non-inflamed atrophic scars in acne vulgaris.

The standard management of acne vulgaris in Japan includes a combination of topical treatment with benzoyl peroxide (BPO) and BPO/clindamycin (CLDM), topical adapalene and systemic antimicrobials. However, the treatment of therapy-resistant complications such as postinflammatory hyperpigmentation (PIH), erosions with inflamed red papules and atrophic scars has not been established. We performed chemical peeling with glycolic acid and iontophoresis with ascorbyl 2-phosphate 6-palmitate and DL-α-tocopherol phosphate for the treatment of PIH, erosions with inflamed red papules and non-inflamed atrophic scars in 31 patients with acne vulgaris (mild to severe severity), and evaluated the efficacy and safety of these interventions. In most of cases, there was remarkable improvement in PIH and erosions with inflamed red papules after treatment. There was also some improvement in non-inflamed atrophic scars without erythema. Mild redness and irritation was observed in four cases as adverse reactions. Early initial treatment of PIH and erosions with red papules by chemical peeling and iontophoresis is an effective and safe method to prevent the formation of atrophic scars in patients with acne vulgaris.

SLIT improves cedar pollinosis by restoring IL-10 production from Tr1 and Monocytes∼IL-10 productivity is critical for becoming allergic∼.

BACKGROUND: Allergen-specific immunotherapy (SIT) is currently used for several allergic disorders and IL-10-producing regulatory T cells (Tr1) induced by SIT suppress allergic reactions. We investigated the relation between IL-10 production and acquiring allergy. METHODS: A prospective study was undertaken to evaluate the effect of SIT on IL-10 production in T cells and other cell fractions in children with pollinosis. In addition, blood samples were collected from non-allergic healthy controls and patients with pollinosis to compare the levels of IL-10 production. PBMC were cultured with pollen peptides or control allergens, and the IL-10 production from monocyte and CD4 T cell was analyzed. RESULTS: Monocytes and CD4 T cells from SIT group of patients produced high levels of IL-10, suggesting that the induction of IL-10 is essential for inducing T cell tolerance. IL-10 production from monocytes and T cells was significantly increased in non-allergic controls compared to patients with pollinosis. This high IL-10 production was observed even when PBMC were stimulated with antigens other than pollen peptides. CONCLUSIONS: IL-10 is critical for induction of specific T cell tolerance, and increased production of IL-10 by monocytes and T cells during inflammatory responses or after SIT may influence effector cells in allergy. Present data implicates that the low productivity of IL-10 by monocytes and T cells is closely related with sensitivity to multiple allergens, and resistance to allergic diseases. Augmentation of constitutive IL-10 production from immune system is a potential therapeutic approach for allergic disorders.