David G. Cogan Laboratory of Ophthalmic Pathology, Massachusetts Eye and Ear/Harvard Medical School, Boston, Massachusetts.
Department of Ophthalmic Pathology, Wills Eye Hospital, Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania.
Ophthalmic Plast Reconstr Surg. 2020 Jan/Feb;36(1):e6-e12. doi: 10.1097/IOP.0000000000001497.
The purpose of this study is to codify the microscopic diagnostic criteria for ocular adnexal brow and caruncular sebaceous gland hyperplasias (pseudoadenomatoid) that distinguish it from an adenoma. Clinical records and photographs were critically reviewed and microscopic slides were stained with hematoxylin and eosin and immunochemically stained for adipophilin, androgen receptor, p16, p53, a spectrum of cytokeratins, Ki-67 and mismatch repair nuclear protein expression for MLH1, MSH2, PMS2, and MSH6. The patients and their close relatives had no history of cancer. Cytokeratin 7 and especially cytokeratin 17 highlighted the presence of ducts in the hyperplastic lesion, which are not present in adenomas. p16 and p53 were negative and Ki-67 immunostaining demonstrated similar low proliferation indices for normal and hyperplastic glands. The mismatch repair nuclear protein expressions were preserved in both lesions. Histopathologic misdiagnosis of adenomatoid sebaceous gland hyperplasia as an adenoma can lead to the impression of an association with the Muir-Torre syndrome. Cytokeratins 7 and 17 immunostaining can be helpful in highlighting compressed ducts that in exuberant sebaceous gland hyperplasias may lead to a diagnosis of an adenoma (in which ducts are absent). Negative immunostaining for p16 rules out a possible etiologic role of human papillomavirus in hyperplasias and the negative p53 staining indicates the lesions are not truly neoplastic. The preservation of mismatch repair nuclear protein expression rules out the likelihood of the Muir-Torre syndrome. The current cases convincingly establish that sebaceous hyperplasia is not associated with the Muir-Torre syndrome by both clinical findings and immunohistochemical testing.Two yellow lesions, from the brow and caruncle, were examined microscopically and immunohistochemically to establish the diagnosis of sebaceous gland hyperplasia and to rule out the Muir-Torre syndrome.
本研究旨在编纂眼附属器眉毛和眦部皮脂腺增生（假性腺瘤样）的微观诊断标准，将其与腺瘤区分开来。仔细回顾了临床记录和照片，并对显微镜载玻片进行了苏木精和伊红染色，以及免疫化学染色，用于检测脂肪细胞素、雄激素受体、p16、p53、一系列细胞角蛋白、Ki-67 和错配修复核蛋白表达，用于 MLH1、MSH2、PMS2 和 MSH6。患者及其近亲没有癌症病史。细胞角蛋白 7 尤其是细胞角蛋白 17 突出了增生病变中存在导管，而腺瘤中不存在导管。p16 和 p53 均为阴性，Ki-67 免疫染色显示正常和增生腺体的增殖指数相似。两种病变的错配修复核蛋白表达均保存。如果将腺瘤样皮脂腺增生误诊为腺瘤，可能会误认为与 Muir-Torre 综合征有关。细胞角蛋白 7 和 17 的免疫染色有助于突出增生的皮脂腺中受压的导管，这些导管可能导致腺瘤的诊断（其中导管不存在）。p16 的免疫染色阴性排除了人乳头瘤病毒在增生中的可能病因作用，而 p53 染色阴性表明病变不是真正的肿瘤。错配修复核蛋白表达的保存排除了 Muir-Torre 综合征的可能性。目前的病例通过临床发现和免疫组织化学检测令人信服地证实，皮脂腺增生与 Muir-Torre 综合征无关。两个黄色病变，分别来自眉毛和眦部，进行了显微镜和免疫组织化学检查，以确立皮脂腺增生的诊断，并排除 Muir-Torre 综合征。
