Chemical leukoderma induced by dimethyl sulfate

Abstract Chemical leukoderma occurs due to the toxic effect of a variety of chemical agents. Mechanisms include either destruction or inhibition of melanocytes. We report two male patients (36 and 51 years old) who presented with multiple hypopigmented macules and patches on the neck, wrist, and legs after exposure to dimethyl sulfate in a chemical industry. Physical examination revealed irregular depigmentation macules with sharp edges and clear hyperpigmentation around the lesions. History of repeated exposure to a chemical agent can help the clinical diagnosis of chemical leukoderma. This diagnosis is very important for prognosis and therapeutic management of the disease.

Update on treatment of photodermatosis.

Photodermatoses are a group of skin conditions associated with an abnormal reaction to ultraviolet (UV) radiation. There are several of the photosensitive rashes which mainly affect the UV exposed areas of the skin. It can be classified into four groups: immunology mediated photodermatoses, chemical and drug induced photosensitivity, photoaggravated dermatoses, and genetic disorders. A systematic approach including history, physical examination, phototesting, photopatch testing, and laboratory tests are important in diagnosis of a photodermatosis patient. In order to optimally treat a disease of photodermatoses, we need to consider which treatment offers the most appropriate result in each disease, such as sunscreens, systemic medication, topical medication, phototherapy, and others. For all groups of photodermatoses, photoprotection is one of the essential parts of management. Photoprotection, which includes sunscreening and wearing photoprotective clothing, a wide brimmed hat, and sunglasses, is important. There are also promising emerging photoprotective agents.

Photodynamic therapy inhibit Fibroblast Growth Factor-10 induced keratinocyte differentiation and proliferation through ROS in Fibroblast Growth Factor Receptor-2b pathway.

5-aminolevulinic acid-photodynamic therapy (ALA-PDT) is known to be effective in several skin diseases such as acne, actinic keratoses, condyloma acuminata. However, some detailed mechanisms of ALA-PDT to treat these skin diseases still remain elusive. In this study, we aimed to investigate mechanism of ALA-PDT in in-vitro and in-vivo models. For in vitro, we use human keratinocyte cell line (HaCaT) cells. CCK-8 was used to detect cell proliferation activity, immunofluorescence and western blotting method to detect the content of keratin (K)1, K6, K16, protein kinase C (PKC), fibroblast growth factor receptor-2b (FGFR2b) protein, ELISA and RT-PCR to detect expression of interleukin (IL) 1α in the cell supernatant, and detect reactive oxygen species (ROS). For in vivo, we use 20 rabbits to induce hyperkeratosis acne model in their ear. Dermatoscope was used to see follicle hyperkeratosis and skin biopsy to analyze histology and immunohistochemical of PKC, FGFR2b, K1, K6 and K16. Results from this study suggest that ROS stimulated by ALA-PDT lead to inhibition of FGFR2b pathway in PKC downstream to cause reduction of IL1α expression, and eventually, keratinocytes differentiation and proliferation. Our data thus reveal a treatment mechanism of ALA-PDT underlying hyperkeratosis related dermatoses.

MiR-23a-depressed autophagy is a participant in PUVA- and UVB-induced premature senescence.

Autophagy is a cellular catabolic mechanism that is activated in response to stress conditions, including ultraviolet (UV) irradiation, starvation, and misfolded protein accumulation. Abnormalities in autophagy are associated with several pathologies, including aging and cancer. Furthermore, recent studies have demonstrated that microRNAs (miRNAs) are potent modulators of the autophagy pathway. As a result, the current study aims to elucidate the role of the autophagy-related miRNA miR-23ain the process of photoaging. Experiments demonstrated that the antagomir-mediated inactivation of miR-23a resulted in the stimulation of PUVA- and UVB-depressed autophagy flux and protected human fibroblasts from premature senescence. Furthermore, AMBRA1 was identified as a miR-23a target. AMBRA1 cellular levels increased following the introduction of miR-23a antagomirs. And a bioinformatics analysis revealed that the AMBRA1 3' UTR contains functional miR-23a responsive sequences. Finally, it was also demonstrated that both AMBRA1 overexpression and Rapamycin treatment were both able to rescue fibroblasts from PUVA and UVB irradiation-induced autophagy inhibition, but that these effects could also be mitigated by miR-23a overexpression. Therefore, this study concludes that miR-23a-regulated autophagy is a novel and important regulator of ultraviolet-induced premature senescence and AMBRA1 is a rate-limiting miRNA target in this pathway.

Chemical leukoderma induced by dimethyl sulfate.

Chemical leukoderma occurs due to the toxic effect of a variety of chemical agents. Mechanisms include either destruction or inhibition of melanocytes. We report two male patients (36 and 51 years old) who presented with multiple hypopigmented macules and patches on the neck, wrist, and legs after exposure to dimethyl sulfate in a chemical industry. Physical examination revealed irregular depigmentation macules with sharp edges and clear hyperpigmentation around the lesions. History of repeated exposure to a chemical agent can help the clinical diagnosis of chemical leukoderma. This diagnosis is very important for prognosis and therapeutic management of the disease.

Generalized lentiginosis in an 11 year old boy.

Generalized lentiginosis refers to generalized lentigines without systemic abnormalities, characterized by multiple brown or black macules owing to increased proliferation of melanocytes. There are also lentiginosis syndromes associated with systemic abnormalities such as Peutz-Jeghers syndrome, Leopard syndrome, and Carney complex. Generalized lentiginosis can be diagnosis by patient's history, physical and laboratory examination, and histopathology. We report an 11-year-old boy who presented with multiple dark brown macules, varying in size, but less than 0.5 cm, with no abnormalities of other systemic organs.

Effective treatments of atrophic acne scars.

Atrophic scarring is often an unfortunate and permanent complication of acne vulgaris. It has high prevalence, significant impact on quality of life, and therapeutic challenge for dermatologists. The treatment of atrophic acne scars varies depending on the types of acne scars and the limitations of the treatment modalities in their ability to improve scars. Therefore, many options are available for the treatment of acne scarring, including chemical peeling, dermabrasion, laser treatment, punch techniques, fat transplantation, other tissue augmenting agents, needling, subcision, and combined therapy. Various modalities have been used to treat scars, but limited efficacy and problematic side effects have restricted their application. In order to optimally treat a patient's scar, we need to consider which treatment offers the most satisfactory result. There are also promising procedures in the future, such as stem cell therapy. In this article, the authors review the different treatment options of atrophic acne scars. This may be useful for selecting the best therapeutic strategy, whether it be single or combined therapy, in the treatment of atrophic acne scars while reducing or avoiding the side effects and complications.