You are in: eMedicine Specialties > Dermatology > BENIGN NEOPLASMS Sebaceous HyperplasiaArticle Last Updated: Feb 27, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Daniel Hogan, MD, Chief of Dermatology, Professor, Departments of Internal Medicine and Pediatrics, Louisiana State University Medical Center Daniel Hogan is a member of the following medical societies: American Academy of Dermatology Coauthor(s): R Walker Jones, BS, Louisiana State University Health Sciences Center; Stephen H Mason, MD, Assistant Professor of Dermatology, Department of Internal Medicine, University of Kansas Medical Center Editors: David P Fivenson, MD, Director, Wound Care Service, Department of Dermatology, Henry Ford Health System; Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA; Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center Author and Editor Disclosure Synonyms and related keywords: senile sebaceous adenoma, senile sebaceous hyperplasia, SH INTRODUCTIONSection 2 of 11
  BackgroundSebaceous hyperplasia is a common, benign condition of sebaceous glands in adults of middle age or older. Lesions can be single or multiple and manifest as yellowish, soft, small papules on the face (particularly nose, cheeks, and forehead). Sebaceous hyperplasia occasionally also occurs on the chest, areola, mouth, and vulva. Rarely reported variants have included a giant form, a linear or zosteriform arrangement, a diffuse form, and a familial form. Juxtaclavicular beaded lines are an additional variant characterized by closely placed papules arranged in parallel rows. Lesions of sebaceous hyperplasia are benign, with no known potential for malignant transformation, but may be associated with nonmelanoma skin cancer in transplantation patients. PathophysiologySebaceous glands are found throughout the skin except on the palms and soles. They exist as a component of the pilosebaceous unit or, less frequently, open directly to the epithelial surface in areas of modified skin, including the lips and buccal mucosa (as Fordyce spots), glans penis or clitoris (as Tyson glands), areolae (as Montgomery glands), and eyelids (as meibomian glands). The largest sebaceous glands and the greatest number of sebaceous glands are found on the face, chest, back, and the upper outer arms. These holocrine glands are composed of acini attached to a common excretory duct. The life cycle of the sebocytes, the cells that form the sebaceous gland, begins at the periphery of the gland in the highly mitotic basal cell layer; as the sebocytes differentiate and mature, they accumulate increasing amounts of lipid and migrate toward the central excretory duct. The mature sebocytes complete their life cycle as they reach the central duct and release their lipid content as sebum by disintegrating. The turnover time of the sebocytes as they migrate from the basal layer of the gland to the central duct is approximately 1 month. Sebaceous glands are highly androgen sensitive, and, although the number of sebaceous glands remains approximately the same throughout life, their activity and size vary according to age and circulating hormone levels. The sebaceous glands, as well as the sweat glands, account for the vast majority of androgen metabolism in the skin. The enzymes found in the sebocytes that are involved in androgen metabolism include 5-alpha-reductase type I, 3-beta-hydroxysteroid dehydrogenase, and 17-beta-hydroxysteroid dehydrogenase type II. These enzymes metabolize the relatively weak circulating androgens, such as dehydroepiandrosterone-sulfate, into the more potent androgens, such as dihydrotestosterone; these potent androgens, in turn, bind to receptors within the sebocytes, resulting in an increase in the size and metabolic rate of the sebaceous gland. Studies have shown that the activity of 5-alpha-reductase is higher in the scalp and facial skin than in other areas, so that testosterone and dihydrotestosterone stimulate more sebaceous gland proliferation in these areas. Estrogens have been found to decrease sebaceous gland secretion. In the perinatal period, the sebaceous glands are initially large and are likely responsible for the production of vernix caseosa often seen in newborns; the activity and size of the sebaceous glands regress shortly after birth, due to withdrawal of maternal hormones, and remain small throughout infancy and childhood. At puberty, sebaceous glands enlarge and become increasingly active due to increased production of androgens, and they reach their maximum by the third decade of life. As androgen levels decrease with advancing age, the sebocyte turnover begins to slow down. This decrease in cellular turnover results in crowding of primitive sebocytes within the sebaceous gland, causing a benign hamartomatous enlargement of the sebaceous gland, or sebaceous hyperplasia. This is particularly apparent in the areas where sebaceous glands are concentrated, such as the face. Although the hyperplastic glands are often inflated up to 10 times their normal size, they secrete very little sebum. In contrast to normal sebocytes that are engorged with lipid, the hyperplastic sebaceous glands contain small undifferentiated sebocytes with large nuclei and scant cytoplasmic lipid. Sebaceous hyperplasia has also been linked to long-term immunosuppression in posttransplantation patients taking cyclosporin A. Although the mechanism for this reaction is poorly understood, this adverse effect is thought to be specific for the highly lipophilic cyclosporin A; other immunosuppressants have not been associated with an increased prevalence of sebaceous hyperplasia. Although more commonly found in the older population, premature or familial cases have been reported in which younger individuals are affected with multiple lesions, suggesting a genetic predisposition. In these cases of premature familial sebaceous hyperplasia, extensive sebaceous hyperplasia appears at puberty and tends to progress with age. FrequencyUnited StatesSebaceous hyperplasia is a common skin finding in aging adults, reported to occur in approximately 1% of the healthy population. However, the prevalence of sebaceous hyperplasia has been reported to be as high as 10-16% in patients receiving long-term immunosuppression with cyclosporin A. Mortality/MorbiditySebaceous hyperplasia has no direct association with malignant degeneration and is not a cause of morbidity, except perhaps related to cosmesis. Sebaceous hyperplasia has been reported in association with internal malignancy in the setting of Muir-Torre syndrome. Muir-Torre syndrome is a rare autosomal dominant disorder in which visceral malignancies, sebaceous neoplasms (eg, sebaceous adenoma, sebaceous carcinoma), and keratoacanthoma coincide. Colon cancer is the leading internal malignancy associated with Muir-Torre syndrome, followed by hematologic malignancies. Sebaceous hyperplasia alone does not signify a predisposition to cancer or represent a sign of Muir-Torre syndrome. One study has shown a higher prevalence of sebaceous hyperplasia in patients with a heart transplant on immunosuppressive drugs compared with sex-matched control patients. A second study found that 29.9% of patients with a renal transplant had sebaceous hyperplasia; 45.7% of these patients had a history of nonmelanoma skin cancer, compared with 7.3% of patients without sebaceous hyperplasia. This strong association of nonmelanoma skin cancer with sebaceous hyperplasia remained significant after correction of factors such as age, sex, skin type, and duration since the transplantation. SexThe difference in prevalence between men and women is unknown. AgeSebaceous hyperplasia lesions begin to appear in middle age (usually fifth or sixth decade) and continue to appear into later life. Most authors have dropped "senile" from the formerly used "senile sebaceous hyperplasia" because the occurrence of lesions in middle life is more common than in later life. Of 1000 consecutive neonates examined in an Iranian prospective cohort study, 43.7% had sebaceous hyperplasia. CLINICALSection 3 of 11
HistoryPatients may be concerned for cosmetic reasons or may be worried about possible malignancy.
PhysicalSebaceous hyperplasia is often found incidentally upon examination.
CausesSebaceous hyperplasia is thought to be caused by a decrease in the circulating levels of androgen associated with aging. Ultraviolet radiation and immunosuppression have been postulated as cofactors in causing sebaceous hyperplasia. Ultraviolet radiation is considered only a cofactor, because sebaceous hyperplasia occasionally occurs on areas of the body where sunlight is not a relevant issue, including the buccal mucosa, areolae, and vulva.
DIFFERENTIALSSection 4 of 11
Acrochordon Basal Cell Carcinoma Calcinosis Cutis Colloid Milium Cowden Disease (Multiple Hamartoma Syndrome) Fibrous Papule of the Face Follicular Infundibulum Tumor Folliculoma Granuloma Annulare Lichen Nitidus Lipoid Proteinosis Lupus Miliaris Disseminatus Faciei Milia Molluscum Contagiosum Muir-Torre Syndrome Multiple Endocrine Neoplasia Type 1 Sarcoidosis Sebaceous Adenoma Sebaceous Carcinoma Syringoma Trichilemmoma Trichoepithelioma Trichofolliculoma Xanthomas
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| Drug Name | Isotretinoin (Accutane) |
|---|---|
| Description | Oral agent that treats serious dermatologic conditions. Synthetic 13-cis isomer of naturally occurring tretinoin (trans-retinoic acid). Both agents are structurally related to vitamin A. Decreases sebaceous gland size and sebum production. May inhibit sebaceous gland differentiation and abnormal keratinization. Used initially for severe cystic/scarring acne. Because of its action in reducing sebaceous gland size, used in sebaceous hyperplasia in lower doses than in acne. Optimal dose and duration used to treat sebaceous hyperplasia not established. Clearance has been achieved within 2 wk in some patients. Others may take longer. Recurrence within 1 mo after stopping is common. |
| Adult Dose | 10-40 mg PO qd |
| Pediatric Dose | Not established |
| Contraindications | Absolute: Pregnancy or a woman who is likely to become pregnant or who intend to become pregnant; females who cannot use reliable contraception while undergoing treatment; noncompliance with contraception; breastfeeding; concurrent use of methotrexate (increased liver toxicity) or tetracyclines (pseudotumor cerebri); documented hypersensitivity Relative: Leukopenia; moderate-to-severe cholesterol or triglyceride Elevations; significant hepatic or renal dysfunction |
| Interactions | Toxicity may occur with vitamin A coadministration; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines; may reduce plasma levels of carbamazepine |
| Pregnancy | X - Contraindicated in pregnancy |
| Precautions | May decrease night vision; inflammatory bowel disease may occur; may be associated with development of hepatitis; occasional exaggerated healing response of acne lesions (excessive granulation with crusting) may occur; diabetes patients may experience problems in controlling their blood glucose; avoid exposure to UV light or sunlight until tolerance achieved; discontinue treatment if rectal bleeding, abdominal pain, or severe diarrhea occurs' should only be prescribed by physicians thoroughly familiar and experienced in its use |
| Media file 1: Normal sebaceous gland histology. Courtesy of Cooper Heard, MD. | |
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| Media file 2: Histology of sebaceous hyperplasia; enlarged sebaceous gland with multiple lobules grouped around a central dilated sebaceous duct. Courtesy of Cooper Heard, MD. | |
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Article Last Updated: Feb 27, 2007
