원저 : 포도구균성 열상 피부 증후군 25예의 임상적 분석에 의한 재분류

저작시기 2004.01 |등록일 2004.10.29 파일확장자어도비 PDF (pdf) | 8페이지 | 가격 4,000원
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발행기관 : 대한피부과학회 수록지정보 : 대한피부과학회지 / 42권 / 4호 / 398 ~ 405 페이지
저자명 : 강정대 ( Kang Jeong Dae ) , 박석돈 ( Park Seog Don )

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Background: Dermatofibromas are common benign tumors which occur in the skin. They have been divided into "fibrous" lesions, composed entirely of almost entirely of fibroblasts and collagen, and "cellular" lesions composed to a significant degree of phagocytic cells with the appearance of histiocytes. A cellular variant characterized by increased cellularity, storiform arrangement, larger size, and location in the deep dermis, often with extension into the superficial subcutaneous tissue may be difficult to differentiate from dermatofibrosrcoma protuberans. There is an incessant controversy over the histogenesis of dermatofibromas, although many authors consider that these tumors derive from primitive mesenchymal cells. The recent development in immunohistochemical staining technology and ultrastructural study revealed various cellular proliferation in the lesion, including fibroblast, histiocyte and myofibroblast. Objective: Our purpose was to study by immunohistochemistry the defferences between fibrous and cellular dermatofibromas and to find the relationship between the myofibroblast and the histogenesis of dermatofibroma. Methods: We will select 36 cases of dermatofibromas which include 27 fibrous and 9 cellular types. We have studied the immunophenotype of 36 dermatofibromas using antibodies against vimentin, smooth muscle actin, desmin, CD34, factor XⅢa, CD68 and MMP 11. Results: All dermatofibromas were positive for vimentin, smooth muscle actin, and factor XⅢa, but negative for desmin and CD34. All cellular type were positive for CD68, but 24/27 of the fibrous type were positive for CD68. MMP 11 was positive in 6/9 of the cellular type and 25/27 of the fibrous type. The degree of staining for vimentin, factor XⅢa, CD68, and MMP 11 was not different in both types. But the degree of staining for smooth muscle actin in the fibrous type was higher than in the cellular type. Conclusion: The differences in the degree of staining for smooth muscle actin and the positivity for CD68 suggest the possibility of a different differentiation of dermatofibroma between cellular and fibrous types. The prominent vimentin and smooth muscle actin immunoreactivity and desmin non-reactivity may suggest that the myofibroblast may play a role, in part, for developing dermatofibromas. Further investigations with ultrastructural study using electron microscopy and double/triple immunohistochemical staining would be necessary. (Korean J Dermatol 2004;42(3):256~263)

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