Barnhill R L, Hurwitz S, Duray P H, Arons M S
Department of Dermatology, Yale University School of Medicine, New Haven, Conn.
Plast Reconstr Surg. 1988 Feb;81(2):280-9. doi: 10.1097/00006534-198802000-00027.
The recognition of atypical or dysplastic nevomelanocytic nevi potentially provides clinicians with another means of identifying individuals at increased risk for cutaneous malignant melanoma. However, a great deal of controversy still surrounds these lesions, their significance, and the clinical and histologic criteria needed for their diagnosis at present. In general, dysplastic nevi tend to be asymmetrical and larger (greater than 5 mm) than ordinary acquired nevi, have a macular component, irregular and ill-defined borders, and haphazard (variegate) coloration. A clinical diagnosis of dysplastic nevi must be confirmed by histopathology, since not all clinically atypical nevi are dysplastic. While precise histopathologic criteria for dysplastic nevi are lacking, most authorities agree that an abnormal nevomelanocytic proliferative pattern as manifested by increased numbers of basilar melanocytes and/or abnormal junctional nevomelanocytic nesting in the setting of lentiginous epidermal hyperplasia, variable degrees of nevomelanocytic nuclear atypia, and a lymphocytic host response are consistent with a histologic diagnosis of dysplastic nevi. Current data for individuals with dysplastic nevi and a family history of cutaneous malignant melanoma (at least two family members with cutaneous malignant melanoma) indicate a relative risk for cutaneous malignant melanoma about 148 times that of the general population. In comparison, cutaneous malignant melanoma risk seems lower for individuals with familial dysplastic nevi (but without familial cutaneous malignant melanoma) and "sporadic" dysplastic nevi. With respect to progression to melanoma, probably the vast majority of dysplastic nevi remain stable or possibly regress. Management of individuals with histologically confirmed dysplastic nevi involves periodic skin examinations. Regional overview and life-size photography are helpful in following these patients. Patients should also be instructed in the examination of their own skin. While a definite relationship between sun exposure and dysplastic nevi remains unproved, the use of sunscreens and avoidance of unnecessary sun exposure are advised. Examination of family members for atypical melanocytic lesions is also recommended.
非典型或发育异常的痣黑素细胞痣的识别，可能为临床医生提供了另一种识别皮肤恶性黑色素瘤风险增加个体的方法。然而，围绕这些病变、它们的意义以及目前诊断所需的临床和组织学标准，仍然存在大量争议。一般来说，发育异常的痣往往不对称，比普通后天性痣更大（大于5毫米），有斑疹成分，边界不规则且不清晰，颜色斑驳。发育异常痣的临床诊断必须通过组织病理学确认，因为并非所有临床非典型痣都是发育异常的。虽然缺乏发育异常痣的确切组织病理学标准，但大多数权威人士一致认为，在雀斑样表皮增生的背景下，基底黑素细胞数量增加和/或交界性痣黑素细胞巢异常所表现出的异常痣黑素细胞增殖模式、不同程度的痣黑素细胞核异型性以及淋巴细胞宿主反应，与发育异常痣的组织学诊断一致。目前针对有发育异常痣且有皮肤恶性黑色素瘤家族史（至少两名家庭成员患有皮肤恶性黑色素瘤）的个体的数据表明，其患皮肤恶性黑色素瘤的相对风险约为普通人群的148倍。相比之下，有家族性发育异常痣（但无家族性皮肤恶性黑色素瘤）和“散发性”发育异常痣的个体，患皮肤恶性黑色素瘤的风险似乎较低。关于进展为黑色素瘤，可能绝大多数发育异常痣保持稳定或可能消退。对组织学确诊为发育异常痣的个体的管理包括定期皮肤检查。区域概述和真人大小的摄影有助于跟踪这些患者。还应指导患者自行检查皮肤。虽然阳光暴露与发育异常痣之间的确切关系尚未得到证实，但建议使用防晒霜并避免不必要的阳光暴露。也建议对家庭成员进行非典型黑素细胞病变的检查。
