Answer: A

Sebaceous hyperplasia (SH) is a common benign proliferation of sebaceous glands surrounding hair follicles. These glands are described as holocrine glands composed of acini, berry-like structures attached to a common excretory duct that aids in secreting sebum to help lubricate and protect the skin and hair.9-11 Sebaceous glands are present across the entire surface of the body except for the palms of the hands and soles of the feet and tend to be the most concentrated on the face and scalp. In conditions such as SH, the glands appear relatively normal but develop an increased number of acini and mature sebocytes.11

Sebaceous hyperplasia can be seen at any age but typically affects the face of middle-aged and older adults, occurring more commonly in men because of the high androgen sensitivity of the glands.10-13 The condition is seen in approximately 1% of the healthy population.11 Risk factors for the development of SH include ultraviolet radiation and immunosuppression. In one study, SH was reported in 15% to 30% of transplant patients taking cyclosporine.14 The condition is also more likely to occur in patients with certain genetic syndromes such as Muir-Torre syndrome (MTS), an autosomal-dominant phenotypic variant of hereditary nonpolyposis colorectal cancer characterized by sebaceous skin tumors and visceral malignancies.13 Despite its association with this syndrome, screening for MTS is unnecessary because of the high prevalence of SH in the general population.13

The etiology of SH includes decreased turnover of sebocytes and an age-related change in the hormonal environment.11 Sebocytes are the predominant cell forming sebaceous glands and turnover occurs monthly in younger ­individuals.12 However, with aging and reduced androgen levels, these cells migrate slower and begin accumulating within sebaceous glands.13,15 This results in the benign hamartomatous enlargements known as SH. Genetic changes are also an important consideration in the pathogenesis of SH. These changes include overexpression of the Smad7 gene and parathyroid hormone-related protein.15 In a study of 43 cases of SH, patients had activation of mutations in HRAS, KRAS, and EGFR genes in 60% of the lesions.16


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Clinically, SH appears as asymptomatic, soft, yellow papules varying in size from 2 mm to 9 mm.10,11 Lesions can be solitary or multiple, are often umbilicated, and typically increase in number with age. They are commonly found on the forehead, cheeks, and nose and may bleed with shaving or other trauma. When these lesions are associated with telangiectasias, they may be confused with nBCC on physical examination. Dermoscopy can be used to help differentiate SH from nBCC. The lesions have a “cumulus sign,” which is defined as an asymmetrical milky-white structure that ­surrounds the central umbilication.10 Another defining feature of SH is an aggregate of white-yellow nodules surrounded by nonarborizing, branching vessels that never cross the center.10,17 This pattern can be described by the term crown vessels and is specific to SH.17 On histopathology, SH presents as an enlarged gland with normal morphology.11 An important diagnostic clue is the presence of more than 3 sebaceous lobules surrounding a hair follicle.11

In addition to nBCC, it is important to include fibrous papules, sebaceous adenoma, milia, syringoma, xanthomas, and viral infections in the differential diagnosis of SH. Molluscum contagiosum should also be considered and presents as smooth, flesh-colored, 2 to 6 mm, umbilicated papules that are generally self-limited. Close inspection with a dermatoscope can help differentiate SH from these other lesions. A biopsy may also be necessary if there is high concern for BCC.

Once SH has been diagnosed, treatment is generally not needed unless the patient has cosmetic concerns. These lesions are particularly challenging to eradicate as the entire sebaceous unit needs to be removed to prevent relapse. Treatment options include cryotherapy, photodynamic and laser therapy, electrodesiccation, topical treatment with trichloroacetic acid, oral isotretinoin, and shave excisions. Unfortunately, the cosmetic results of these therapies vary between individuals and may be associated with scarring and changes in pigmentation.11 A literature review investigating treatment with laser therapy found that the 1450-nm diode laser produced approximately 75% clinical improvement and greater than 50% reduction in lesion size with limited adverse effects.18 Oral isotretinoin has also been found to be effective but is associated with high relapse rates after discontinuation.11

The patient in this case was diagnosed clinically with sebaceous hyperplasia and was reassured of the benign nature of the condition.

Sidra Deen and Briana Fernandez are medical students at Baylor College of Medicine in Houston, Texas; Tara Braun, MD, is a resident physician at Baylor College of Medicine.

References

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2. Cameron MC, Lee E, Hibler BP, et al. Basal cell carcinoma: epidemiology; pathophysiology; clinical and histological subtypes; and disease associations. J Am Acad Dermatol. 2019;80(2):303-317. doi:10.1016/j.jaad.2018.03.060

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5. McDaniel B, Badri T, Steele RB. Basal Cell Carcinoma. In: StatPearls. StatPearls Publishing; 2022. Accessed March 20, 2022. http://www.ncbi.nlm.nih.gov/books/NBK482439/

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7. Cameron MC, Lee E, Hibler BP, et al. Basal cell carcinoma: contemporary approaches to diagnosis, treatment, and prevention. J Am Acad Dermatol. 2019;80(2):321-339. doi:10.1016/j.jaad.2018.02.083

8. Wozniak-Rito A, Zalaudek I, Rudnicka L. Dermoscopy of basal cell carcinoma. Clin Exp Dermatol. 2018;43(3):241-247. doi:10.1111/ced.13387

9. Makrantonaki E, Ganceviciene R, Zouboulis C. An update on the role of the sebaceous gland in the pathogenesis of acne. Dermatoendocrinol. 2011;3(1):41-49. doi:10.4161/derm.3.1.13900

10. Hogan D, Mohammad S. Sebaceous hyperplasia. Expert Rev Dermat. 2011;6(1):91-97. doi:10.1586/edm.11.2

11. Farci F, Rapini RP. Sebaceous hyperplasia. In: StatPearls. StatPearls Publishing; 2022. Accessed March 12, 2022. http://www.ncbi.nlm.nih.gov/books/NBK562148/

12. Smith MA, Usatine RP. Sebaceous hyperplasia. In: Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley HS, eds. The Color Atlas and Synopsis of Family Medicine. 3rd ed. McGraw-Hill Education; 2019.

13. Eisen DB, Michael DJ. Sebaceous lesions and their associated syndromes: part I. J Am Acad Dermatol.  2009;61(4):549-560. doi:10.1016/j.jaad.2009.04.058

14. de Berker DA, Taylor AE, Quinn AG, Simpson NB. Sebaceous hyperplasia in organ transplant recipients: shared aspects of hyperplastic and dysplastic processes? J Am Acad Dermatol. 1996;35(5 Part 1):696-699. doi:10.1016/S0190-9622(96)90723-9

15.  Zouboulis CC, Boschnakow A. Chronological ageing and photoageing of the human sebaceous gland. Clin Exp Dermatol. 2001;26(7):600-607. doi:10.1046/j.1365-2230.2001.00894.x

16. Groesser L, Singer S, Peterhof E, et al. KRAS, HRAS and EGFR mutations in sporadic sebaceous gland hyperplasia. Acta Derm Venereol. 2016;96(6):737-741. doi:10.2340/00015555-2351

17. Zaballos P, Ara M, Puig S, Malvehy J. Dermoscopy of sebaceous hyperplasia. Arch Dermatol. 2005;141(6):808. doi:10.1001/archderm.141.6.808

18. Liu A, Taylor MB, Sotoodian B. Treatment of sebaceous hyperplasia by laser modalities: a review of the literature and presentation of our experience with Erbium-doped Yttrium Aluminium Garnet (Er:YAG). J Drugs Dermatol. 2020;19(5):547-552.