Peter R U
Capio Blausteinklinik, Gefäß- und Hautzentrum, Erhard-Grözinger-Str. 102, 89134, Blaustein/Ulm, Deutschland,
Hautarzt. 2013 Dec;64(12):894-903. doi: 10.1007/s00105-013-2625-y.
Accidental exposure of the human skin to single doses of ionizing radiation greater than 3 Gy results in a distinct clinical picture, which is characterized by a transient and faint erythema after a few hours, then followed by severe erythema, blistering and necrosis. Depending on severity of damage, the latter generally occurs 10-30 days after exposure, but in severe cases may appear within 48 hrs. Between three and 24 months after exposure, epidermal atrophy combined with progressive dermal and subcutaneous fibrosis is the predominant clinical feature. Even years and decades after exposure, atrophy of epidermis, sweat and sebaceous glands; telangiectases; and dermal and subcutaneous fibrosis may be found and even continue to progress. For this distinct pattern of deterministic effects following cutaneous accidental radiation exposure the term "cutaneous radiation syndrome (CRS)" was coined in 1993 and has been accepted by all international authorities including IAEA and WHO since 2000. In contrast to the classical concept that inhibition of epidermal stem cell proliferation accounts for the clinical symptomatology, research of the last three decades has demonstrated the additional crucial role of inflammatory processes in the etiology of both acute and chronic sequelae of the CRS. Therefore, therapeutic approaches should include topical and systemic anti-inflammatory measures at the earliest conceivable point, and should be maintained throughout the acute and subacute stages, as this reduces the need for surgical intervention, once necrosis has occurred. If surgical intervention is planned, it should be executed with a conservative approach; no safety margins are needed. Antifibrotic measures in the chronic stage should address the chronic inflammatory nature of this process, in which over-expression TGF beta-1 may be a target for therapeutic intervention. Life-long follow-up often is required for management of delayed effects and for early detection of secondary malignancies, which must be searched for especially in the borderline areas between clinically symptomatic and asymptomatic skin.
人体皮肤意外暴露于单剂量大于3 Gy的电离辐射会导致一种独特的临床表现,其特征是数小时后出现短暂而轻微的红斑,随后是严重红斑、水疱和坏死。根据损伤的严重程度,后者通常在暴露后10 - 30天出现,但在严重情况下可能在48小时内出现。暴露后三至二十四个月,表皮萎缩合并进行性真皮和皮下纤维化是主要临床特征。即使在暴露数年甚至数十年后,仍可发现表皮、汗腺和皮脂腺萎缩;毛细血管扩张;以及真皮和皮下纤维化,甚至这些情况可能会继续发展。针对皮肤意外辐射暴露后这种独特的确定性效应模式,1993年创造了“皮肤辐射综合征(CRS)”这一术语,自2000年以来已被包括国际原子能机构和世界卫生组织在内的所有国际权威机构所接受。与表皮干细胞增殖受抑制导致临床症状的经典概念不同,过去三十年的研究表明炎症过程在CRS急性和慢性后遗症的病因中也起着关键作用。因此,治疗方法应尽早包括局部和全身抗炎措施,并应在整个急性和亚急性阶段持续进行,因为这可以减少坏死发生后手术干预的必要性。如果计划进行手术干预,应采用保守方法;无需安全边界。慢性期的抗纤维化措施应针对该过程的慢性炎症性质,其中转化生长因子β - 1的过度表达可能是治疗干预的靶点。对于迟发效应的管理和继发性恶性肿瘤的早期检测通常需要终身随访,尤其必须在有临床症状和无症状皮肤的交界区域寻找继发性恶性肿瘤。