Harvell Jeff D, Bastian Boris C, LeBoit Philip E
Department of Pathology, Stanford University Medical Center, Stanford, California, USA.
Am J Surg Pathol. 2002 May;26(5):654-61. doi: 10.1097/00000478-200205000-00012.
This report describes 22 Spitz nevi that seemed to have been clinically removed but persisted and clinically recurred at the biopsy site. These were evaluated in terms of histopathology, immunohistochemistry, and molecular pathology using comparative genomic hybridization (CGH) and fluorescent in situ hybridization. One of these 22 lesions was originally reported as an atypical melanocytic proliferation with some features of a Spitz nevus and was included in the study set at an early stage but was later recognized as melanoma after metastasis to regional lymph nodes 3 years after the local recurrence. We noted four histopathologic patterns in the recurrent lesions: 1) a predominantly intraepidermal pattern resembling "pseudomelanoma" as seen in recurrent "common" melanocytic nevi, 2) a compound, mostly nested pattern above or within a scar that was nearly identical to the originally biopsied Spitz nevus, 3) a nodular growth pattern that closely simulated invasive melanoma, and 4) a desmoplastic pattern resembling an intradermal desmoplastic Spitz nevus. Although the majority of recurrent lesions exhibited asymmetry and pagetoid spread, the dermal component usually had a low mitotic rate and retained architectural and cytologic maturation, which allowed distinction from invasive melanoma. Except for the metastasizing melanoma, the immunostaining pattern with S-100 and HMB-45 was identical to that previously reported for Spitz nevi. Ki67 revealed a very low proliferation rate in all cases, including the melanoma. CGH performed in 10 cases yielded results consistent with Spitz nevi in eight cases. The remaining two cases showed CGH profiles more typical of melanoma, and one of these was the above-referenced case of melanoma, proven by metastasis. Although ancillary molecular techniques such as CGH are of great help in distinguishing these from melanoma, until such techniques become widely available we advocate complete but conservative excision of any recurrent Spitz nevus.
本报告描述了22例临床看似已切除但仍持续存在且在活检部位出现临床复发的斯皮茨痣。采用比较基因组杂交（CGH）和荧光原位杂交技术，对这些病例进行了组织病理学、免疫组织化学及分子病理学评估。这22个病变中的1例最初报告为具有某些斯皮茨痣特征的非典型黑素细胞增生，在研究初期被纳入研究组，但在局部复发3年后区域淋巴结转移，后来被确诊为黑色素瘤。我们在复发病变中发现了四种组织病理学模式：1）主要为表皮内模式，类似于复发性“普通”黑素细胞痣中所见的“假黑色素瘤”；2）复合模式，大多为巢状，位于瘢痕上方或瘢痕内，与最初活检的斯皮茨痣几乎相同；3）结节状生长模式，酷似浸润性黑色素瘤；4）促纤维组织增生模式，类似于皮内促纤维组织增生性斯皮茨痣。尽管大多数复发病变表现出不对称性和派杰样扩散，但真皮成分通常有丝分裂率低，且保留结构和细胞学成熟度，这有助于与浸润性黑色素瘤相鉴别。除了发生转移的黑色素瘤外，S-100和HMB-45免疫染色模式与先前报道的斯皮茨痣相同。Ki67显示所有病例增殖率都很低，包括黑色素瘤。对10例进行的CGH检测结果显示，8例与斯皮茨痣一致。其余2例显示出更典型的黑色素瘤CGH图谱，其中1例是上述经转移证实的黑色素瘤病例。尽管诸如CGH等辅助分子技术在将这些病变与黑色素瘤鉴别方面有很大帮助，但在这些技术广泛应用之前，我们主张对任何复发性斯皮茨痣进行完整但保守的切除。
