Ocular Adnexal Adenomatoid Sebaceous Gland Hyperplasia: A Clinical and Immunopathologic Analysis in Relation to the Muir-Torre Syndrome

Ocular Adnexal Adenomatoid Sebaceous Gland Hyperplasia: A Clinical and Immunopathologic Analysis in Relation to the Muir-Torre Syndrome: The purposeof 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.

Accepted for publication August 22, 2019.

Supported by Department of Ophthalmology Research Fund, Massachusetts Eye and Ear.

The authors have no conflicts of interest to disclose.

Address correspondence and reprint requests to Frederick A. Jakobiec, M.D., D.Sc., David G. Cogan Laboratory of Ophthalmic Pathology, Massachusetts Eye and Ear, 243 Charles Street, Suite 328, Boston, MA 02114. E-mail: Fred_Jakobiec@meei.harvard.edu

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