eMedicine Specialties > Dermatology > Malignant Neoplasms

Keratoacanthoma

Tsu-Yi Chuang, MD, MPH, Clinical Professor, Department of Dermatology, University of Southern California; Staff Dermatologist, Desert Specialty Group, Inc
Ryan Brashear, MD, Staff Physician, Department of Dermatology, Indiana University School of Medicine

Updated: Mar 11, 2009

Introduction

Background

Keratoacanthoma (KA) is a relatively common low-grade malignancy that originates in the pilosebaceous glands and closely and pathologically resembles squamous cell carcinoma (SCC). In fact, strong arguments support classifying keratoacanthoma as a variant of invasive SCC.¹ Keratoacanthoma is characterized by rapid growth over a few weeks to months, followed by spontaneous resolution over 4-6 months in most cases. Keratoacanthoma reportedly progresses, although rarely, to invasive or metastatic carcinoma; therefore, aggressive surgical treatment often is advocated. Whether these cases were SCC or keratoacanthoma, the reports highlight the difficulty of distinctly classifying individual cases.²

Pathophysiology

Both sunlight and chemical carcinogens have been implicated as pathologic factors in growth of the tumor. Trauma, human papilloma virus, genetic factors, and immunocompromised status also have been implicated as etiologic factors.

Frequency

United States

The sole published study in a white US population took place in Hawaii and estimated the incidence at 104 cases per 100,000. This study reported keratoacanthoma incidence equal to SCC and challenged the commonly reported incidence ratio of keratoacanthoma to SCC of 1:3. Peak incidence occurs in the seventh decade or beyond. Keratoacanthoma is uncommon in darker-skinned patients.^3,4,5,6

International

Based on the Hawaiian data, the incidence of keratoacanthoma in ethnic Japanese, Filipino, and Hawaiian populations has been estimated to be 22, 7, and 6 per 100,000, respectively, approximately one fifth to one sixteenth of the incidence rate found in American whites. In other studies, the ratio of keratoacanthoma to SCC has ranged from 1:0.6 to 1:5 in different geographic locations.^3,4,5,6

Mortality/Morbidity

Keratoacanthoma is believed to have a good prognosis; however, it has been reclassified as SCC-KA type to reflect the difficulty in histologic differentiation, as well as the uncommon but potentially aggressive nature of keratoacanthoma. Keratoacanthoma infrequently presents as multiple tumors and may enlarge (5-15 cm), become aggressive locally, or rarely, metastasize.^7,8

Race

Keratoacanthoma is less common in darker-skinned individuals.

Sex

Male-to-female ratio is 2:1.

Age

Keratoacanthoma has been reported in all age groups, but incidence increases with age. Keratoacanthoma is rare in persons younger than 20 years.

Clinical

History

Keratoacanthoma typically grows rapidly, attaining 1-2 cm within weeks, followed by a slow involution period lasting up to 1 year and leaving a residual scar if not excised preemptively. Since expedient therapy almost always is instituted, the true natural course of the tumor cannot be confirmed with certainty.

Physical

Pertinent physical findings are limited to the skin. Lesions typically are solitary and begin as firm, roundish, skin-colored or reddish papules that rapidly progress to dome-shaped nodules with a smooth shiny surface and a central crateriform ulceration or keratin plug that may project like a horn. Most keratoacanthomas occur on sun-exposed areas. The face, neck, and dorsum of the upper extremities are common sites. Truncal lesions are rare. Lesions usually are skin-colored to pinkish-red. Unaffected skin retains its normal appearance.

Keratoacanthoma (squamous cell carcinoma-keratoacanthoma or SCC-KA type) on inner canthus.

Keratoacanthoma of the left forehead.

Close-up view of the keratoacanthoma lesion seen in Media File 2.

Keratoacanthoma lesion (squamous cell carcinoma-keratoacanthoma or SCC-KA type).

Causes

The definitive cause of keratoacanthoma remains unclear; however, several potentiating factors should be considered. Epidemiologic data of keratoacanthoma is notably similar to SCC and Bowen disease (SCC in situ) concerning age, sex, and the anatomic site of lesions. These data strongly support a common etiology among keratoacanthoma, SCC, and Bowen disease. Epidemiologic data support sunlight as an important etiologic factor.

Industrial workers exposed to pitch and tar have been well established as having a higher incidence of keratoacanthoma, as well as SCC.⁹ Additionally, a 2006 study suggested a strong association between cigarette smoking and the development of keratoacanthoma.¹⁰

Trauma, human papilloma virus (specifically types 9, 11, 13, 16, 18, 24, 25, 33, 37, and 57),^11,12 genetic factors, and immunocompromised status also have been implicated as etiologic factors. See Human Papillomavirus.

Finally, research has identified that up to one third of keratoacanthomas harbor chromosomal aberrations. Recurrent aberrations include gains on 8q, 1p, and 9q with deletions on 3p, 9p, 19p, and 19q. One other report identified a 46,XY,t(2;8)(p13;p23) chromosomal aberration.^13,14

Differential Diagnoses

Other Problems to Be Considered

• Eruptive keratoacanthoma of Grzybowski: This is a generalized distribution of multiple keratoacanthomas that typically do not involute.
• Multiple Ferguson-Smith keratoacanthoma: This is a rare autosomal dominant self-healing type of keratoacanthoma, with lesions arising in early adulthood.
• Internal malignancy
• Muir-Torre syndrome: Keratoacanthoma may be a component of Muir-Torre syndrome, which is a cancer-associated genodermatosis with multiple sebaceous neoplasms (adenomas, epitheliomas, carcinomas), keratoacanthomas, and gastrointestinal malignancies (most commonly colon), although other carcinomas have been reported (genitourinary, pulmonary, endometrial). When Muir-Torre syndrome is diagnosed, an age-appropriate cancer screening workup is indicated. An approximately equal number of internal malignancies are diagnosed before and after the cutaneous neoplasm. These internal malignancies tend to be low grade, but early diagnosis is important. Colonoscopy, rather than flexible sigmoidoscopy, is recommended, since the colon cancer frequently is found in the right ascending colon, proximal to the hepatic flexure.
• Sporotrichosis¹⁵

Workup

Procedures

One component of establishing the diagnosis is tissue examination for histopathology. Shave biopsy results from a keratoacanthoma are indistinguishable from invasive SCC; therefore, excisional or deep incisional biopsy of the lesion is preferred.

Histologic Findings

Keratoacanthomas are composed of singularly well-differentiated squamous epithelium that show only a mild degree of pleomorphism and likely form masses of keratin that constitute the central core of keratoacanthoma.

Pseudocarcinomatous infiltration in keratoacanthoma typically presents a smooth, regular, well-demarcated front that does not extend beyond the level of the sweat glands.

The term SCC-KA type has been introduced for otherwise classic keratoacanthomas that reveal a peripheral zone formed by squamous cells with atypical mitotic figures, hyperchromatic nuclei, and loss of polarity to some degree. These marginal cells also may penetrate into surrounding tissue in a more aggressive pattern.

Treatment

Medical Care

Treatment of keratoacanthoma is primarily surgical. Reserve medical treatment for exceptional cases where surgical intervention is either not feasible or desirable. For example, medical intervention may be appropriate in patients with multiple lesions, in lesions not amenable to surgery because of size or location, and in patients with comorbidities that dissuade surgical procedure.

Systemic retinoids, such as isotretinoin, are a consideration for patients with lesions too numerous for surgical intervention.

Intralesional methotrexate (MTX), 5-fluorouracil, bleomycin, and steroids have been used with success in patients who are either poor surgical candidates or have lesions not amenable to surgery because of size or location.^8,16 A 2007 review of the use of intralesional injection of MTX on 38 patients, including 18 of the researchers' patients, showed a 92% clinical "resolution" rate; however, patients needed an average of 2.1 injections to achieve it. Only 13% (5 patients) obtained histological confirmation.¹⁷ Both topical imiquimod and 5-fluorouracil have been used with anecdotal success.¹⁸

Note much of the literature concerning medical intervention for keratoacanthoma is limited to case reports and of unproved efficacy. Be cautious when making the decision to pursue medical in lieu of surgical intervention and perform appropriate follow-up.

Surgical Care

• The primary therapy for keratoacanthoma is surgical excision of the tumor.
  • Excise tumors with adequate margins (3-5 mm) and histopathologic evaluation to exclude invasive SCC.
  • Partial shave biopsy usually inadequately distinguishes between keratoacanthoma and invasive SCC.
  • In some patients, smaller lesions may be treated with deep excisional shave and curettage or other destructive techniques.
  • Since the biological behavior of an individual keratoacanthoma cannot be predicted, many consider surgical treatment of keratoacanthoma to be equivalent to treatment for SCC.
  • Mohs micrographic surgery may be indicated for large or recurrent keratoacanthomas or keratoacanthomas located in anatomic areas with cosmetic or functional considerations.
• Keratoacanthomas are radiosensitive and respond well to low doses of radiation (<10 Gy).
• Radiation therapy may be useful in selected patients with large tumors in whom resection will result in cosmetic deformity or for tumors that have recurred following attempted excisional surgery.
• Radiation therapy is less appealing in younger patients in whom radiation damage worsens with time.
• Radiation therapy is an important alternative treatment for selected patients who understand the risks and benefits, who are not good surgical candidates, or who lack access to Mohs surgery.
• Both laser therapy and cryotherapy have been used successfully in small keratoacanthomas, in keratoacanthomas found in difficult to treat locations, and as an adjunct to surgical removal.

Consultations

Dermatologist: Consult to exclude invasive SCC.

Medication

Although primary consideration of treatment is surgical, in patients with clear-cut and multiple keratoacanthomas, a number of medical alternatives have been used with success.

Antineoplastic agents

Useful in patients with large or multiple tumors or tumors that are inoperable because of anatomic location or the patient's poor medical status. Agents (eg, topical 5-fluorouracil, intralesional MTX, interferon alfa-2a,¹⁹ and bleomycin) also have been used with some success in treating keratoacanthomas. When small amounts of medication are administered, the interactions and precautions listed below are less restrictive than when systemic doses are administered. As a rule, if after 4 wk the lesion has not responded fully to medical therapy, surgical removal is indicated.

Methotrexate (Folex, Rheumatrex)

Antimetabolite that inhibits DNA synthesis and cell reproduction in malignant cells. May suppress immune system. Satisfactory response seen within 3-6 wk following administration.
Marked response noticed after 2 injections (1 study).

Dosing

Adult

0.4-1.5 mL of 12.5 mg/mL injected intralesionally q2wk

Pediatric

Not established

Interactions

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral MTX; charcoal lowers MTX levels; coadministration with other potentially hepatotoxic medications (eg, retinoids) may increase hepatotoxicity of MTX; folic acid or its derivatives contained in some vitamins may decrease response to MTX; coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase MTX plasma levels; may decrease phenytoin serum levels; probenecid, salicylates, procarbazine, and sulfonamides, including TMP-SMZ, may increase effects and toxicity of MTX; may increase plasma levels of thiopurines

Contraindications

Documented hypersensitivity; alcoholism; hepatic insufficiency; immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency; pregnancy or breastfeeding

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Excreted mainly via kidney; monitor CBC counts monthly, and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); MTX has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant drop in blood counts; aspirin, NSAIDs, or low dose steroids may be administered concomitantly with MTX (possibility of increased toxicity with NSAIDs including salicylates has not been tested); may cause mucositis or cutaneous ulceration

Fluorouracil (Efudex, Adrucil, Fluoroplex)

Fluorinated pyrimidine antimetabolite that inhibits thymidylate synthase (TS) and also interferes with RNA synthesis and function. Has some effect on DNA. Useful in symptom palliation for patients with progressive disease.

Dosing

Adult

0.1 mL of 5% sol injected intralesionally qd into keratoacanthoma base and at 4 peripheral quadrants for 2 wk (1 study) or 0.1-0.3 mL (of 50 mg/mL sol) injected circumferentially and 0.1-0.2 mL (of 50 mg/mL sol) injected sublesionally qwk for 3 wk (second study)

Pediatric

Administer as in adults

Interactions

Increased risk of bleeding with anticoagulants, NSAIDs, platelet inhibitors, thrombolytic agents; enhanced bone marrow toxicity with other immunosuppressive agents; may increase risk of infection by live vaccine; cimetidine may increase toxicity; thiazide diuretics may increase myelosuppressive effects of antineoplastic agents; increased risk of phenytoin toxicity exists with concomitant use; therapeutic efficacy may be enhanced by leucovorin coadministration; addition of cyclophosphamide, MTX, and fluorouracil to tamoxifen may increase risk of thromboembolic events in postmenopausal women being treated for breast cancer

Contraindications

Documented hypersensitivity; poor nutritional state, bone marrow suppression, pregnancy, severe renal function impairment, hepatic function impairment, chicken pox or herpes zoster, potentially serious infections; dihydropyrimidine dehydrogenase enzyme deficiency (topical route)

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Carcinogenic, mutagenic; monitor mouth for ulceration; monitor CBC counts; monitor for GI ulceration and bleeding; inflammatory reactions may occur with occlusive dressings; porous gauze dressing may be applied for cosmetic reasons without increase in reaction; caution in metastases involving bone marrow; caution if previous high-dose pelvic irradiation administered or previous treatment with alkylating agents; caution in renal or hepatic impairment; use proper procedures for handling and disposal of chemotherapy

Bleomycin (Blenoxane)

Glycopeptide antibiotic that inhibits DNA synthesis.
Concentration usually is 1 mg/mL and diluted further with local anesthetic.

Dosing

Adult

0.2-0.4 mg as single intralesional injection (case reports) or 0.2 mg qwk for 4 wk (other reports)

Pediatric

Not established

Interactions

May decrease plasma levels of digoxin and phenytoin; cisplatin may increase toxicity of bleomycin; increases risk of infection with live vaccine

Contraindications

Documented hypersensitivity; significant renal function impairment; compromised pulmonary function; pregnancy or breastfeeding

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal impairment; possibly secreted in breast milk; may cause mutagenesis and pulmonary toxicity (10%); idiosyncratic reactions similar to anaphylaxis (1%) may occur; monitor for adverse effects during and after treatment; vaso-occlusive phenomenon with distal necrosis of digit; permanent damage to nail matrix may occur; pain with injection, local urticaria, tissue necrosis, and Raynaud phenomenon may occur; bleomycin can cause decrease in platelets, hemorrhagic cystitis, and thrombotic microangiopathy; caution in coronary artery disease, myocardial infarction, arterial thrombosis, and cerebrovascular accidents; flagellate pigmentation (a typical form of localized skin hyperpigmentation) occurs in 8-38% of patients

Retinoids

Efficacious in treatment of keratoacanthomas with good cosmetic outcome.²⁰ Decrease sebaceous gland size and sebum production. May inhibit sebaceous gland differentiation and abnormal keratinization.

Isotretinoin (Accutane)

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.
FDA–mandated registry now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information, see iPLEDGE. Registry aims to further decrease risks of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

Dosing

Adult

20 mg PO qd; can increase to 80 mg PO qd if tolerated and lab results allow

Pediatric

Not recommended

Interactions

Toxicity may occur with vitamin A coadministration or excessive alcohol intake; pseudotumor cerebri or papilledema may occur when coadministered with tetracyclines; may reduce plasma levels of carbamazepine

Contraindications

Documented hypersensitivity; pregnancy; significant liver disease

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC counts, blood sugar in patients with diabetes, triglycerides, hepatic function, and pregnancy in women of childbearing age; adverse effects include teratogenicity, hepatotoxicity, hypertriglyceridemia, hyperostosis, pseudotumor cerebri; may decrease night vision; may be associated with development of hepatitis; occasional exaggerated healing response of acne lesions (excessive granulation with crusting) may occur; patients with diabetes may experience problems in controlling blood sugar; avoid exposure to UV light or sunlight until tolerance achieved

Follow-up

Further Outpatient Care

• Patients who develop nonmelanoma skin cancer, such as keratoacanthoma, SCC, Bowen disease, or basal cell carcinoma, are at high risk for developing subsequent nonmelanoma skin cancer. Education, periodic follow-up examinations, and early detection and treatment of actinic keratosis and skin cancer are important in these patients.

Prognosis

• Prognosis is excellent following excisional surgery.
• Recurrent tumors may require more aggressive therapy.
• Follow patients with a history of keratoacanthoma for development of new primary skin cancers (SCC in particular).

Patient Education

• Educate patients about prevention (including sunscreen), sun-protection techniques, and skin self-examination.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose keratoacanthoma can result in substantial morbidity and, occasionally, mortality. Since both metastatic disease and local destruction have been reported with keratoacanthoma, accurate diagnosis is critical. Physicians diagnosing and/or treating keratoacanthoma are held legally responsible for actions (or actions not taken) that fall outside of the standard of care.
• Failure to treat keratoacanthoma appropriately may result in unacceptably high levels of recurrence and metastasis, or in other cases, may result in an unfavorable risk-to-benefit ratio. Since over or under treating keratoacanthoma can have untoward effects, physicians treating keratoacanthoma bear the liability for selecting and performing the appropriate level of treatment.
• Failure to educate patients about prevention, self-examination, and the nature of the tumor may result ultimately in an unacceptable level of morbidity and mortality. Since keratoacanthoma is a strong risk factor for future occurrences of nonmelanoma skin cancer and may be a marker for internal malignancy in the context of some syndromes, appropriate education and follow-up must be performed.

Special Concerns

• Be sure to rule out SCC.

Multimedia

Media file 1: Keratoacanthoma (squamous cell carcinoma-keratoacanthoma or SCC-KA type) on inner canthus.

Media file 2: Keratoacanthoma of the left forehead.

Media file 3: Close-up view of the keratoacanthoma lesion seen in Media File 2.

Media file 4: Keratoacanthoma lesion (squamous cell carcinoma-keratoacanthoma or SCC-KA type).

References

1. Manstein CH, Frauenhoffer CJ, Besden JE. Keratoacanthoma: is it a real entity?. Ann Plast Surg. May 1998;40(5):469-72. [Medline].

2. Schwartz RA. Keratoacanthoma. J Am Acad Dermatol. Jan 1994;30(1):1-19; quiz 20-2. [Medline].

3. Chuang TY, Reizner GT, Elpern DJ, Stone JL, Farmer ER. Keratoacanthoma in Kauai, Hawaii. The first documented incidence in a defined population. Arch Dermatol. Mar 1993;129(3):317-9. [Medline].

4. Chuang TY, Reizner GT, Elpern DJ, Stone JL, Farmer ER. Non-melanoma skin cancer and keratoacanthoma in Filipinos: an incidence report from Kauai, Hawaii. Int J Dermatol. Oct 1993;32(10):717-8. [Medline].

5. Reizner GT, Chuang TY, Elpern DJ, Stone JL, Farmer ER. Keratoacanthoma in Japanese Hawaiians in Kauai, Hawaii. Int J Dermatol. Dec 1995;34(12):851-3. [Medline].

6. Reizner GT, Chuang TY, Elpern DJ, Stone JL, Farmer ER. Basal cell carcinoma and keratoacanthoma in Hawaiians: an incidence report. J Am Acad Dermatol. Nov 1993;29(5 Pt 1):780-2. [Medline].

7. Frank TL, Maguire HC Jr, Greenbaum SS. Multiple painful keratoacanthomas. Int J Dermatol. Sep 1996;35(9):648-50. [Medline].

8. Sanders S, Busam KJ, Halpern AC, Nehal KS. Intralesional corticosteroid treatment of multiple eruptive keratoacanthomas: case report and review of a controversial therapy. Dermatol Surg. Oct 2002;28(10):954-8. [Medline].

9. Letzel S, Drexler H. Occupationally related tumors in tar refinery workers. J Am Acad Dermatol. Nov 1998;39(5 Pt 1):712-20. [Medline].

10. Miot HA, Miot LD, da Costa AL, Matsuo CY, Stolf HO, Marques ME. Association between solitary keratoacanthoma and cigarette smoking: a case-control study. Dermatol Online J. Feb 28 2006;12(2):2. [Medline].

11. Hsi ED, Svoboda-Newman SM, Stern RA, Nickoloff BJ, Frank TS. Detection of human papillomavirus DNA in keratoacanthomas by polymerase chain reaction. Am J Dermatopathol. Feb 1997;19(1):10-5. [Medline].

12. Lu S, Syrjanen SL, Havu VK, Syrjanen S. Known HPV types have no association with keratoacanthomas. Arch Dermatol Res. Mar 1996;288(3):129-32. [Medline].

13. Clausen OP, Beigi M, Bolund L, et al. Keratoacanthomas frequently show chromosomal aberrations as assessed by comparative genomic hybridization. J Invest Dermatol. Dec 2002;119(6):1367-72. [Medline].

14. Kim DK, Kim JY, Kim HT, Han KH, Shon DG. A specific chromosome aberration in a keratoacanthoma. Cancer Genet Cytogenet. Apr 1 2003;142(1):70-2. [Medline].

15. Meffert JJ. Cutaneous sporotrichosis presenting as a keratoacanthoma. Cutis. Jul 1998;62(1):37-9. [Medline].

16. Sayama S, Tagami H. Treatment of keratoacanthoma with intralesional bleomycin. Br J Dermatol. Oct 1983;109(4):449-52. [Medline].

17. Annest NM, VanBeek MJ, Arpey CJ, Whitaker DC. Intralesional methotrexate treatment for keratoacanthoma tumors: a retrospective study and review of the literature. J Am Acad Dermatol. Jun 2007;56(6):989-93. [Medline].

18. Dendorfer M, Oppel T, Wollenberg A, Prinz JC. Topical treatment with imiquimod may induce regression of facial keratoacanthoma. Eur J Dermatol. Jan-Feb 2003;13(1):80-2. [Medline].

19. Grob JJ, Suzini F, Richard MA, et al. Large keratoacanthomas treated with intralesional interferon alfa-2a. J Am Acad Dermatol. Aug 1993;29(2 Pt 1):237-41. [Medline].

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21. Fitzpatrick T, Eisen A, Wolff K, et al, eds. Keratoacanthoma. In: Dermatology in General Medicine. 1993. 4^th ed. New York, NY: McGraw-Hill; 848-855.

Keywords

keratoacanthoma, KA, squamous cell carcinoma, SCC, invasive SCC, invasive squamous cell carcinoma, squamous cell cancer, skin cancer, skin malignancy, pilosebaceous gland cancer, pilosebaceous glands

Contributor Information and Disclosures

Author

Tsu-Yi Chuang, MD, MPH, Clinical Professor, Department of Dermatology, University of Southern California; Staff Dermatologist, Desert Specialty Group, Inc
Tsu-Yi Chuang, MD, MPH is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, and International Society of Dermatology
Disclosure: Nothing to disclose.

Coauthor(s)

Ryan Brashear, MD, Staff Physician, Department of Dermatology, Indiana University School of Medicine
Ryan Brashear, MD is a member of the following medical societies: American Academy of Dermatology and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Susan M Swetter, MD, Director, Pigmented Lesion and Cutaneous Melanoma Clinic, Associate Professor, Department of Dermatology, Stanford University Medical Center, Veterans Affairs Palo Alto Health Care System
Susan M Swetter, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Clinical Oncology, Eastern Cooperative Oncology Group, Pacific Dermatologic Association, Society for Investigative Dermatology, Society for Melanoma Research, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

John G Albertini, MD, Consulting Staff, Dermatologic Surgery, The Skin Surgery Center
John G Albertini, MD is a member of the following medical societies: American Academy of Dermatology and American College of Mohs Micrographic Surgery and Cutaneous Oncology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

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