医学
纤维化
病理
炎症
免疫组织化学
皮肤病科
内科学
作者
peipei Pan,J. Liao,C. Hong
标识
DOI:10.1016/j.jid.2023.03.1357
摘要
Radiation dermatitis is a common cutaneous side effect after radiotherapy. It also occurred in some patients receiving fluoroscopy-guided interventions such as percutaneous coronary intervention. The pathophysiology of radiation dermatitis is complex, but may be associated with vasculopathy, chronic inflammation and fibrosis. The mTOR signal is important to regulate the development of vasculopathy, chronic inflammation, and fibrosis; however, its role in in radiation dermatitis is not well understood. This study aims to investigate the role of mTOR in radiation dermatitis. A retrospective study was carried out at the Kaohsiung Veterans General Hospital, a tertiary medical hospital in Southern Taiwan. Patients with diagnosis of radiation dermatitis between 2011 and 2022, with available pathological specimens were included. Clinical parameters were collected. Expression of S6K1 protein, a downstream substrate of mTOR pathway, was measured by immunohistochemistry in skin tissue. We also analyzed the clinical findings and pathological features. The results showed that mean age of the 9 (M:F=9:0) patients was 62.1-year-old. The characteristic histopathology features include bizarre fibroblasts (100%), fibrosis/sclerosis (100%), telangiectasia (89%), and loss of cutaneous appendages (100%). Marked decreased or loss CD34+ stromal cells were recorded in 6 cases (67%). S6K1 protein showed intranuclear enhancement in the epidermal keratinocytes, grading as intense (67%), moderate (22%) and mild (11%). The overall S6K1 expression is stronger in radiation dermatitis than that in normal skin control and inflammatory skin control (atopic dermatitis). S6K1 expression appears to be associated with the size of the clinical ulcer, although statistical significance was not reached. This pilot study demonstrates that mTOR signaling pathway may be involved in the pathophysiology of radiation dermatitis although more case numbers are warranted to validate it.
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