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Perianal Comedones



Comedones represent pilosebaceous ductal hyperkeratinization that begins at the junction of the isthmus and the infundibulum .

 Within the duct, the proliferation of keratinocytes blocks sebaceous secretion with ensuing accumulation of abnormal levels of sebaceous lipids [1, 3]. The etiology of comedone formation is not concretely established but formation mechanisms include hyperproliferation and abnormal desquamation of ductal keratinocytes .

The transformation from a normal pilosebaceous duct into a comedone occurs when the sebaceous gland progenitor cells or leucine-rich repeats and immunoglobulin-like domain 1 cells  differentiate into epithelial type cells due to comedogenic factors . Multiple contributing factors to comedone formation have been identified including abnormal levels of lipids such as linoleate and squalene, androgenic factors, the proinflammatory cytokine interleukin-1? , vitamin A deficiency, and possibly bacteria . The oxidation of lipids and squalene is specifically associated with comedone formation as the oxidized sebaceous materials instigate the release of IL-1? and keratin hyperproliferation. In regard to squalene, its oxidation may be precipitated by cigarette smoke . Comedones can also arise with use of ingredients seen in skin care products such as cocoa butter and esters like isopropyl myristate and isopropyl isostearate that have varying levels of comedogenicity. Leptin, which regulates sebum lipogenesis, has also been identified as a contributor to the comedogenic process. Leptin is mTORC1 pathway dependent, and when mTORC1 is overactivated and upregulated, sebum production and proinflammatory sebum lipids increase . Thus, comedone formation is multifactorial. We describe a case of a 57-year-old female with focal, perianal open comedones with no associated illness. To the best of our knowledge, there has only been three reports of perianal comedones to date.

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