Sebaceous Hyperplasia



Sebaceous 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,[1] areola,[2] mouth,[3] scrotum,[4] foreskin,[5] shaft of penis,[6] and vulva.[7, 8, 9] Rarely reported variants have included a giant form,[10] 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.[11] Lesions of sebaceous hyperplasia are benign, with no known potential for malignant transformation, but may be associated with nonmelanoma skin cancer in transplantation patients.[12, 13, 14]

Some authorities consider rhinophyma to represent a special form of sebaceous hyperplasia.

Typical facial papules appear in middle age, are larger than lesions on the areola or mouth, and display a central dell that corresponds to a central follicular infundibular ostium.


Sebaceous 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 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.[15, 16, 17]



Sebaceous hyperplasia is a common skin finding in aging adults, reported to occur in approximately 1% of the healthy US 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.[18, 19, 20]


The difference in prevalence between men and women is unknown.


Sebaceous hyperplasia is common in newborns.[21] Of 1000 consecutive neonates examined in an Iranian prospective cohort study, 43.7% had sebaceous hyperplasia.[22]

Typical facial papules begin to appear in middle age (usually fifth or sixth decade) and continue to appear into later life.



Sebaceous 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.[23] Sebaceous hyperplasia alone does not signify a predisposition to cancer or represent a sign of Muir-Torre syndrome.

One 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.[13] 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.


Patients may be concerned for cosmetic reasons or may be worried about possible malignancy. Lesions are usually described as asymptomatic, soft, discrete, and yellow, with a surface that ranges from smooth to slightly verrucous. Patients may report one or multiple lesions at various locations on the face. Lesions may become red and irritated and bleed after scratching, shaving, or other trauma.


Sebaceous hyperplasia is often found incidentally upon examination. The classic appearance of facial sebaceous hyperplasia on physical examination reveals whitish-yellow or skin-colored papules that are soft and vary in size from 2-9 mm. These papules have a central umbilication from which a very small globule of sebum can sometimes be expressed. Some papules may be associated with characteristics similar to basal cell carcinoma, such as telangiectasia.

Dermoscopy may be useful as a noninvasive tool to aid in the clinical diagnosis and in distinguishing between nodular basal cell carcinoma and sebaceous hyperplasia, reducing unnecessary surgery.[24, 25, 26, 27]


Facial papular sebaceous 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.

A decrease in circulating androgen results in a change in the rate sebocytes migrate from their points of differentiation into the sebaceous unit. Sebocytes in hyperplastic glands are actually smaller than the average sebocytes in normal glands; the nuclei are larger and less accumulation of cytoplasmic lipid occurs. The gland is enlarged, with a widened sebaceous duct and an increased number of basal cells.

Laboratory Studies

No laboratory studies are necessary. Biopsy is occasionally indicated to exclude basal cell carcinoma.

Histologic Findings

These lesions reveal discrete, enlarged glands. Within each gland, mature sebaceous lobules or acini surround and connect to a dilated central sebaceous duct. The lobules have one or more basal cell layers at their periphery, with undifferentiated sebocytes that contain large nuclei and scant cytoplasmic lipid, in contrast to normal sebocytes, which are engorged with lipid.

View Image

Normal sebaceous gland histology. Courtesy of Cooper Heard, MD.

View Image

Histology of sebaceous hyperplasia; enlarged sebaceous gland with multiple lobules grouped around a central dilated sebaceous duct. Courtesy of Cooper....

Medical Care

Sebaceous hyperplasia is completely benign and does not require treatment; however, lesions can be cosmetically unfavorable and sometimes bothersome when irritated. Treatments are mostly mechanical. Lesions tend to recur unless the entire unit is destroyed or excised. Risk of permanent scarring must be considered when treating benign lesions.

A biopsy may be necessary if concern exists that the lesion is a basal cell carcinoma.

Therapeutic options include photodynamic therapy (with combined use of 5-aminolevulinic acid and visible light),[28, 29] cryotherapy (liquid nitrogen), cauterization or electrodesiccation,[30] topical chemical treatments (eg, with bichloracetic acid or trichloroacetic acid),[31] laser treatment (eg, with argon, carbon dioxide, or pulsed-dye laser),[32, 33] shave excision, and excision. Complications of these nonspecific destructive therapies include atrophic scarring or transient dyspigmentation.

Oral isotretinoin has proven effective in clearing some lesions after 2-6 weeks of treatment, but lesions often recur upon discontinuation of therapy; maintenance doses of oral isotretinoin in the range of 10-40 mg every other day or 0.05% isotretinoin gel (not marketed in the United States) is rarely indicated as a suppressive treatment for widespread disfiguring sebaceous hyperplasia.[16, 34] Oral isotretinoin should be prescribed by a physician who is experienced in oral retinoid therapy and only for patients without contraindications and fully compliant with all restrictions on this medication. Other topical retinoids are considered less effective in treating this condition.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Isotretinoin (Amnesteem, Claravis, Myorisan, Sotret)

Clinical Context:  Isotretinoin is a synthetic 13-cis isomer of naturally occurring tretinoin (trans -retinoic acid). Both agents are structurally related to vitamin A.

It decreases sebaceous gland size and sebum production and may inhibit sebaceous gland differentiation and abnormal keratinization. Isotretinoin is used initially for severe cystic/scarring acne. Because of its action in reducing sebaceous gland size, it is used in sebaceous hyperplasia in lower doses than in acne.

The optimal dose and duration used to treat sebaceous hyperplasia not established. Clearance has been achieved within 2 weeks in some patients. Others may take longer. Recurrence within 1 month after stopping is common.

A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

Class Summary

Isotretinoin has been used for sebaceous hyperplasia because of its ability to temporarily shrink sebaceous glands. Lesions return after discontinuation of therapy. Consider only for the most severe disfiguring cases in men or women who cannot become pregnant. Should only be prescribed by dermatologic experts in oral retinoid therapy.


Irritation or bleeding may occur if lesions are in an area prone to trauma (eg, friction by a comb or brush).


Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Disclosure: Nothing to disclose.


Stephen H Mason, MD,

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD, Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Arash Taheri, MD, Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.


R Walker Jones, MD Harris M Blackman, MD, LLC

R Walker Jones, MD is a member of the following medical societies: American Chemical Society, American Medical Association, American Medical Student Association/Foundation, and Louisiana State Medical Society

Disclosure: Nothing to disclose.


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Normal sebaceous gland histology. Courtesy of Cooper Heard, MD.

Histology of sebaceous hyperplasia; enlarged sebaceous gland with multiple lobules grouped around a central dilated sebaceous duct. Courtesy of Cooper Heard, MD.

Normal sebaceous gland histology. Courtesy of Cooper Heard, MD.

Histology of sebaceous hyperplasia; enlarged sebaceous gland with multiple lobules grouped around a central dilated sebaceous duct. Courtesy of Cooper Heard, MD.