Strategies for the Prevention and Management of Nevi (Moles)

Release Date: June 1, 2013

Expiration Date: June 30, 2015

FACULTY:

Evangelina Berrios-Colon,
PharmD, MPH, BCPS, CACP

Associate Professor, Department
of Pharmacy & Health Outcomes
Touro College of Pharmacy
New York, New York
Clinical Pharmacy Educator, Ambulatory Care
The Brooklyn Hospital Center
Brooklyn, New York

Julie Anne Billedo, PharmD
PGY-2 Ambulatory Care Pharmacy Resident
The Brooklyn Hospital Center
Brooklyn, New York

FACULTY DISCLOSURE STATEMENTS:

The authors have no actual or potential conflicts of interest in relation to this activity.

Postgraduate Healthcare Education, LLC does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors may express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.

ACCREDITATION STATEMENT:

Pharmacy acpe
Postgraduate Healthcare Education, LLC is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
UAN: 0430-0000-13-014-H01-P
Credits: 2.0 hours (0.20 ceu)
Type of Activity: Knowledge

FEE INFORMATION:

Payment of $6.50 required for exam to be graded.

TARGET AUDIENCE:

This accredited activity is targeted to pharmacists. Estimated time to complete this activity is 120 minutes.

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DISCLAIMER:

Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients’ conditions and possible contraindications or dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities.

GOAL:

To educate pharmacists on how to distinguish between abnormal and common nevi (moles) in patients and to understand potential strategies to decrease nevi appearance.

OBJECTIVES:

After completing this activity, the participant should be able to:

  1. Discuss the epidemiology and clinical presentation of nevomelanocytic nevi (moles).
  2. Recognize the types of nevi and how to differentiate from melanoma.
  3. Identify options in the removal and treatment of moles.
  4. Describe preventive measures to decrease new nevi and slow progression of existing nevi.


ABSTRACT: The management of the appearance of new nevi (moles) and of the abnormal alteration of present nevi on the skin is of great importance in reducing the risk of melanoma. The number of nevi has been correlated with the risk of development of melanoma. The American Academy of Dermatology recommends regular self-examination of moles, decreased exposure to direct sunlight, and frequent use of sunscreen as ways to decrease risk. Community pharmacists play a vital role in the prevention of nevi by recommending appropriate sunscreens and advising patients on skin examination, with referral as necessary.

The skin is the body's largest and most accessible organ, with its chief function being protection. The two main layers of the skin are the epidermis and the dermis. Keratinocytes, or skin cells, are organized into four layers that further subdivide the epidermis (in order of inner to outermost layer): stratum basale (basal layer), stratum spinosum (spinous layer), stratum granulosum (granular layer), and stratum corneum (cornified layer). Melanocytes, dendritic cells located in the stratum basale, are dispersed among the keratinocytes. Melanocytes produce melanin, a brownish-black pigment, and transfer melanin to neighboring keratinocytes. The distribution of melanin to the stratum corneum provides a protective layer, especially against ultraviolet rays of the sun. For additional protection, increased synthesis of melanin and the proliferation of keratinocytes occur in response to ultraviolet radiation.1,2

As with any body organ, diseases of the skin can occur. When physically examining the skin for lesions, differentiating between normal and abnormal appearance and between insignificant and significant findings can be challenging. Important terminology in describing lesions includes macule, papule, and nodule. A macule is a flat, colored lesion that is typically <2 cm in diameter. A papule is a raised, solid lesion that is typically <0.5 cm in diameter. A nodule is similar to a papule, except larger with a typical diameter of 0.5 to 5 cm.3

Nevomelanocytic nevi (NMN), or melanocytic nevi, commonly referred to as moles, are benign proliferations of nevus cells that are usually regularly shaped and uniform in color. Nevus cells are variant forms of melanocytes that lack dendrites and cluster within the skin layers. NMN can be acquired or congenital. Acquired NMN can be further classified as typical (common) or atypical.3-5

EPIDEMIOLOGY AND ETIOLOGY

The majority of acquired NMN develop after infancy, peak in early adulthood (the second and third decades of life), and appear to occur equally between males and females. Over time, most nevi regress after the sixth decade of life. Acquired NMN are predominant in Caucasians and lighter-skinned individuals. They occur less commonly in blacks and those with darker skin and are rare in people with red hair and freckles. Ultraviolet (UV) radiation (i.e., sun exposure) is a major factor in the development of nevi found on exposed areas. Genetics also appears to play a role in the development of nevi, as similar patterns of appearance may occur within families. However, the exact mechanism of nevus development is unknown.4,5

Furthermore, the number of NMN is related to the risk of melanoma. Multiple nevi are associated with an increased risk of melanoma, but the nevi themselves are not necessarily precancerous. Since nevi tend to regress with age, a growing lesion in an older adult is associated with a greater chance of being a melanoma. The risk of melanoma is further increased with atypical nevi and a family history of melanoma. The annual risk of a nevus developing into a melanoma is approximately 1 in 200,000.4

CLINICAL PRESENTATION

Acquired NMN are mainly dispersed randomly and are located on sun-exposed areas, such as the face, trunk, extremities, and scalp. Persons with darker skin tones tend to have more nevi on the lighter parts of their body, such as the palms, soles, and nail beds. Typical NMN are uniformly pigmented, round or oval shaped, regularly outlined, and sharply bordered. They range from macules to papules and nodules, which can be firm or soft. Macular nevi are usually darker in pigment compared to papular or nodular nevi. Nevi surfaces may reveal hairs that are coarser, longer, and darker than those found on the surrounding skin. Lesions of palms and soles are usually hairless. Nevi of the nails may be dark or light brown in color, extending from the nail matrix to the distal edge of the nail plate.4

Acquired NMN are 1 cm or less in diameter. If greater in size, the nevus is typically congenital, atypical, or a melanoma. The nevi are asymptomatic but may be associated with itchiness when growing. If a nevus persistently itches or is tender, careful monitoring or even excision should be considered, as that may be an early indication of malignancy.5

A nevus encircled by a ring of depigmentation, or leukoderma, is referred to as a halo nevus. This presentation typically indicates regression. The central nevus may persist, eventually disappear over months to years, and/or reappear. The halo can vary in size, usually ranging from 0.5 to 5 cm in radius around the central nevus. It can be seen with both acquired and congenital NMN as well as with melanomas.4-5

A lesion can recur, referred to as a recurrent melanocytic nevus, if a benign NMN was incompletely removed. This scenario is also called pseudomelanoma and is common after destructive procedures that are merely superficial, such as dermabrasion or shave biopsy. Recurrent melanocytic nevi confine to the original site of the lesion that was excised but may be irregular.4

TYPES OF LESIONS

Typical acquired NMN are further categorized by the location of their clusters, relating to their evolution— junctional, compound, or dermal. Nevus cells of junctional nevi nest in the dermal-epidermal junction. Junctional nevi are macules or are minimally elevated and are highly pigmented. The ability to produce melanin is greatest at the junctional stage. Nevus cells of compound nevi nest in both the epidermal and dermal areas. Compound nevi are papules or small nodules and are pigmented. Junctional and compound nevi are typically seen in childhood and young adulthood. Nevus cells of dermal nevi nest in the dermis, and this is the last stage of NMN. Dermal nevi are papules or nodules and are minimally pigmented.4,5

Dysplastic, or atypical, melanocytic nevi (DN) are irregularly pigmented and shaped lesions, which can present as solitary or multiple lesions. They are recognized as precursor lesions of malignant melanoma and are highly associated with familial melanoma. The most common type of malignant melanoma is superficial spreading melanoma (SSM). SSM has color variegation and irregular borders (TABLE 1).4,6 Examples of an NMN, DN, and SSM are shown in FIGURE 1 for comparison.


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fig1

Other types of acquired lesions that are rarely malignant include blue nevus, nevus spilus, and spitz nevus. A blue nevus is a firm papule or nodule that is dark blue to grayish-black in color with regular borders. These nevi differ from other nevi in that they are proliferations of melanin-producing dermal melanocytes, which are not nevus cells. A nevus spilus is a melanocytic lesion varying in size from only a few centimeters to >15 cm. It consists of a macule, typically slightly pigmented to light brown in color, with disseminated small macules or papules, typically darker in color. A spitz nevus is a small, hairless, dome-shaped nodule, <1 cm in diameter. These nevi are uniform in color, ranging from pink or tan to brown or black. Spitz nevi usually grow rapidly, within months, and can occur at any age. They typically occur on the head and neck.5

EXAMINING AND DIAGNOSING SKIN LESIONS

Diagnoses of lesions are made by physical examination and monitoring using the ABCDE rule. The ABCDEs of examining lesions are: Asymmetry, Border, Color, Diameter, and Enlargement (TABLE 2).4,6 Besides SSM, the other common clinicopathologic melanoma subtypes are lentigo maligna and acral lentiginous. All three display distinct features: asymmetry, with half of the lesion varying from the other half; irregular circumferential border; uneven coloration and tone with varying shades in different areas of the lesion; and a diameter typically >6 mm.6


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Dermoscopy, also referred to as epiluminescence microscopy, can be used to further examine skin lesions via a magnified and unobstructed view. If malignancy of a lesion is still suspected and additional testing is warranted, the lesion can be excised for histopathology. Fluorescence in situ hybridization or comparative genomic hybridization analysis is used to further distinguish lesions, from being benign to having metastatic tendency.4,5

TREATMENT OF MOLES

NMN are usually found to be benign and not harmful. If NMN are left untreated, moles may lighten over time and thus not necessitate treatment. Nontreatment of NMN has the advantage of no additional acquired risk of adverse treatment effects. Treatment of NMN depends on lesion size, lesion location, patient age, and the risk for nevi to become malignant.7 If treatment is chosen, there are various options. The two main reasons for treatment are to decrease the risk of cutaneous melanocytic melanoma and to improve aesthetic appearance.

Excision is recommended as the first-line treatment for nevi in cases where treatment benefits outweigh risk.8 Excision is always recommended in patients presenting with giant congenital melanocytic nevi (GMN) due to the increased risk of malignant transformation. These lesions are removed whenever possible. Removal procedures may be classified as full-or partial-thickness removal. Full-thickness removal eliminates more nevus cells than partial-thickness procedures, in addition to removing the whole dermis and epidermis. It is still unclear whether full-thickness removal will ultimately lead to less risk or to cases of malignancy.9

There has been high patient satisfaction reported with excision procedures. NMN removal involving nevi <20 cm in size and on the head or neck have been associated with positive patient reports and high rates of satisfaction.10 Repigmentation or new larger nevi are a possibility after excision procedures. Depending on the depth of the excisions, scarring, disfiguration, and loss of joint motion are possibilities. Upon excision, suspicious nevi may be sent for histopathologic examination. Other types of treatment for NMN, as discussed below, do not remove as many NMN cells as surgical excision.

Destructive Therapies

Various nonexcision-based treatments, known as destructive therapies, are available for NMN. Dermabrasion, chemical peels, cryotherapy, and lasers have all been used to treat NMN. The use of destructive therapy had been considered as a second-line or alternative option in NMN. Overall, destructive therapies should be avoided because they do not allow for the removal of excised tissue, which would be used for histopathologic assessment. Redness and peeling are common with destructive therapies. Mild soaps should be used for cleansing the affected areas. If crusting occurs, antibacterial ointments should be used to prevent infection.11

Dermabrasion: Dermabrasion reduces up to 20% of the initial mole color in nearly all patients, as long as it is used early in life. It does not remove as many nevi cells as excision.8 Hypertrophic scarring is possible after dermabrasion. A retrospective review in congenital melanocytic nevi showed no serious long-term complications of dermabrasion.8 Postdermabrasion, the skin may grow back a pinkish or red color. Patients who undergo dermabrasion have an increased risk of sunburn because of skin peeling. Sunscreen use should be encouraged during this time.12

Chemical Peels: Chemical peels are one of the oldest treatments for NMN. The depth of a peel is dependent upon the type of chemical used, the number of coats applied, and the amount of time the chemical is left on the skin. For superficial or mild peels, alpha-hydroxy acid and lipo-hydroxy acids are used on the epidermis. For medium-depth peels, trichloroacetic acid at <50% concentration is used, which causes epidermal to papillary dermal peel and regeneration. Deep peels with trichloroacetic acid at concentrations >50% or phenol-based formulations are used to reach deeper into the reticular dermis to induce dermal regeneration.13

Currently, not many patients are treated with these peels; thus, data are lacking. Complications associated with chemical peels include infection, recurrence of pigmentation, and scarring.10

Cryotherapy: Cryotherapy is the use of carbonic acid snow on the skin to remove malformations. It has been used for NMN; however, there are limited data available, with no recent data supporting its use. It was first reported as an option to remove skin lesions in 1907 without much reproducible data since then.14 Blister formation, bleeding, and pain at the freezing site are common adverse reactions associated with cryotherapy.

Laser Treatments: Laser treatments, which directly target pigmented cells, have also been used to treat NMN. Laser lights with a specific wavelength and pulse are used to destroy nevi. The laser does not penetrate into deeper tissue, which may lead to nevi recurrence. Some pigment-specific lasers are ruby, alexandrite, and neodymium-doped yttrium aluminum garnet. They target pigmented cells with minimal effect to surrounding areas. There are only theoretical data available supporting laser use, without much safety or efficacy reports.15 Scarring is the most common adverse effect associated with laser treatment. There are some in vitro data suggesting an increased risk of melanoma after laser nevi treatment.16

Overall, treatment effectiveness for NMN is not well established. Literature reviews, including evidence-graded recommendations, are available to treat congenital melanocytic nevi (TABLES 3 and 4).10 Some congenital nevi treatment data have been applied to noncongenital nevi. The risk of malignant melanoma is greatly reduced by nevi excision, which is known to remove the greatest number of nevi. Cosmetic outcomes have been evaluated through trials; however, study design and data are limited, making it difficult to apply to practice.


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PREVENTION

Decreased use of sunscreen, use of tanning salons, and increased exposure to the sun during peak times (from 10 am to 2 pm) may all increase the number of nevi. Decreasing sun exposure and tanning salon use and increasing sunscreen use will minimize the development of nevi, especially in patients at high risk.17 Patients at high risk for melanoma are fair-skinned with blue or green eyes. A family history of melanoma, previous exposure to tanning beds, or a history of blistering burns prior to adolescence would all place patients at high risk for nevi and subsequently melanoma. Patients should consider avoiding outdoor activities, wearing protective clothing, and applying a sunscreen with a high sun protection factor (SPF 15 or above) during high noon to avoid the most dangerous UVA and UVB rays. Reapplication of sunscreen when swimming or sweating is vital, especially in children.

An observational study was performed on data from a sun protection trial in 1,623 children in Perth, Australia.18 The study intervention encouraged children to stay indoors in the middle of the day during summer, to wear protective clothing while outdoors, and to use sunscreen. The primary study outcome was to evaluate if these interventions decreased the amount of nevi measured. The researchers measured the number of nevi on children's backs 6 years after the initial intervention, when the children were 12 years old. Children whose backs were covered <70% of the time while outdoors had 1.53 (95% CI, 1.34-1.75) times more nevi than children whose backs were always covered.18 Using sunscreen on the back when it was uncovered was not associated with the number of nevi (P = .59). Children who stayed indoors in the middle of the day and wore clothing while outdoors had fewer nevi.18

This study demonstrates the importance of preventing sun exposure in children in order to decrease nevi and the risk of melanoma.18 Sunscreen use should be encouraged as a preventive measure during primary care and pharmacy visits to all patients, especially children.

Sunscreens

Sunscreens are used to protect from sun damage. Sunscreens may be classified as physical or chemical (TABLE 5).19,20


tbl5

They are effective in preventing UVA and/or UVB rays from being absorbed into the skin. Chemical sunscreens absorb UV radiation, and physical sunscreens scatter the sun's rays and reduce absorption into the skin. Some of the active ingredients found in physical blocking sunscreens are zinc oxide and titanium dioxide. These ingredients are thick and could be messy. Using sunscreens with appropriate spectrum coverage will decrease exposure to the sun's harmful rays, in turn decreasing new or changing nevi appearance.19

Sunscreens have various SPFs. The SPF determines how long a sunscreen is effective on the skin. SPF is only a measure of UVB protection. Choosing an appropriate SPF requires patients to identify how long it usually takes for them to burn. If they burn after 10 minutes without any sun protection, a sunscreen with an SPF of 30 will protect them for 300 minutes or 5 hours (10 minutes multiplied by the SPF of 30). In the aforementioned example, the person should technically reapply sun protection after 5 hours or after swimming or sweating; however, according to the American Academy of Dermatology (AAD), reapplication would be optimal every 2 hours to ensure maximal protection. Sunscreens should be applied 15 minutes before sun exposure in order to allow a protective film to develop.19

In 2012, the FDA updated sunscreen requirements and labeling for products sold in the United States. The FDA now requires manufacturers of sunscreen products to accurately report how they test and establish SPF values, with a requirement to accurately report the information on sunscreen labels.20 The required testing will determine which products could be classified as "broad spectrum." Broad spectrum means the product will protect from both UVA and UVB rays. UVA and UVB rays both cause sunburn, skin cancer, and skin aging; however, UVB has been associated with more burns. Historically, the focus was primarily on UVB rays since they were associated with causing more sunburn; however, now findings identify UVA rays as also contributing to an increased risk of skin cancer and damage. Patients should be advised to check sunscreen labels to ensure they clearly state "broad spectrum" on the front of the bottle.

Products that are not a minimum SPF value of 15 must carry a warning stating, "Skin Cancer/Skin Aging Alert."20 The FDA also now limits the allowable reported SPF on sunscreen to a maximum value of SPF 50+. In contrast to the FDA, the AAD has a more stringent minimum SPF requirement of SPF 30 or higher.21

Manufacturers must also adhere to specific language restrictions that prohibit the use of the words "sunblock," "waterproof," or "sweatproof," all of which may be misleading to the public.20 When making a claim that a product is water resistant, manufacturers may only specify two time periods: 40 or 80 minutes. Patients should be instructed to use enough sunscreen when covering all exposed areas, which generally means enough to fill a shot glass.

For those patients seeking insect repellent and sunscreen, the AAD recommends the use of two separate products rather than a combination.21 Patients should be instructed to first apply the sunscreen and then apply the repellent in order to increase absorption of the sunscreen. Finally, patients should reapply sunscreen at least every 2 hours.20

Self-Examination (Mole Check)
Patients must also know their skin and the pattern of their moles, birthmarks, and freckles. They should be advised to use a full-length and hand mirror to examine skin after showering or bathing (TABLE 6).22 Skin checks should be performed monthly, or even more frequently if instructed by a dermatologist. Patients may choose to utilize a "body mole map" found on the AAD's Web site (www.aad.org) to chart and track mole growth.22 If a mole begins to itch, bleed, or grow, then a patient should be instructed to make an appointment to see a dermatologist. A patient's general medical provider could also conduct mole checks at routine yearly follow-ups.


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PHARMACIST'S ROLE

Pharmacists can assist patients in the selection of makeup products like concealers, foundations, and blemish tints to cover up moles. These products may help to alleviate cosmetic concerns. Some nevi may also have hair growth, which may be permanently removed by a dermatologist.

Pharmacists can make important contributions to patients' self-care of the skin by recommending sunscreens and educating patients on the ABCDEs of melanoma screening. Pharmacists are also in the prime position to prompt patients to seek further evaluation for suspicious-looking moles and to make referrals. Assisting patients in the selection of sunscreens with the appropriate SPF is an important step in preventing nevi.

CONCLUSION

There is a direct relationship between sun exposure and nevi appearance. Exhibiting sun protective behaviors is an important part of decreasing new nevi development. Health care providers should regularly recommend the use of sunscreens with appropriate SPFs all year round. Nevi found on the skin should be checked regularly by both patients and primary care physicians in order to monitor for potential melanoma transformation. The selection of removal treatments in NMN is limited. Efficacy data are not robust and many times derived from anecdotal, noncontrolled trials. Excision is first-line therapy and removes the most tissue. Destructive therapies are alternatives to excision; however, strong supportive data are lacking.

REFERENCES

  1. McCalmont TH. Chapter 8. Diseases of the skin. In: McCalmont TH, ed. Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed. New York, NY: McGraw-Hill; 2010. www.accesspharmacy.com/content. aspx?aID=5368751. Accessed March 9, 2013.
  2. Law RM, Law DT. Chapter 105. Dermatologic drug reactions and common skin conditions. In: Talbert RL, DiPiro JT, Matzke GR, et al, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. New York, NY: McGraw-Hill; 2011. www.accesspharmacy.com/content. aspx?aID=7998475. Accessed March 9, 2013.
  3. Lawley TJ, Yancey KB. Chapter 51. Approach to the patient with a skin disorder. In: Fauci AS, Kasper DL, Jameson JL, et al, eds. Harrison's Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy.com/content.aspx?aID=9098080. Accessed March 9, 2013.
  4. Grichnik JM, Rhodes AR, Sober AJ. Chapter 122. Benign neoplasias and hyperplasias of melanocytes. In: Goldsmith LA, Katz SI, Gilchrest BA, et al, eds. Fitzpatrick's Dermatology in General Medicine. 8th ed. New York, NY: McGraw-Hill; 2012. www.accessmedicine.com.lb-proxy13. touro.edu/content.aspx?aID=56061751. Accessed March 9, 2013.
  5. Suurmond D. Section 9. Benign neoplasms and hyperpla-sias. In: Suurmond D, ed. Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology. 6th ed. New York, NY: McGraw-Hill; 2009. www.accessmedicine.com.lb-proxy13.touro.edu/ content.aspx?aID=5202138. Accessed March 9, 2013.
  6. Lawley TJ, Swerlick RA. Chapter e16. Atlas of skin manifestations of internal disease. In: Fauci AS, Kasper DL, Jameson JL, et al, eds. Harrison's Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy.com/content.aspx?aID=9109168. Accessed March 9, 2013.
  7. Berg P, Lindelof B. Congenital nevocytic nevi: follow-up of a Swedish birth register sample regarding etiologic factors, discomfort, and removal rate. Pediatr Dermatol. 2002;19: 293-297.
  8. Rompel R, Moser M, Petres J. Dermabrasion of congenital nevocellular nevi: experience in 215 patients. Dermatology. 1997;194:261-267.
  9. Marghoob AA, Agero AL, Benvenuto-Andrade C, Dusza SW. Large congenital melanocytic nevi, risk of cutaneous melanoma, and prophylactic surgery. J Am AcadDermatol. 2006;54:868-870.
  10. Ibrahimi OA, Alikhan A, Eisen DB. Congenital melanocytic nevi: where are we now? Part II. Treatment options and approach to treatment. J Am Acad Dermatol. 2012;67:515.e1-515.e13.
  11. Anitha A. Prevention of complications in chemical peeling. J Cutan Aesthet Surg. 2010;3:186-188.
  12. Tanzi EL, Alster TS. Skin resurfacing: ablative lasers, chemical peels, and dermabrasion. In: Wolff K, Goldsmith L, Katz S, et al, eds. Fitzpatrick's Dermatology in General Medicine. Vol 2. 7th ed. New York, NY: McGraw-Hill Medical; 2008:2364-2371.
  13. Fischer T, Perosino E, Poli F, et al; Cosmetic Dermatology European Expert Group. Chemical peels in aesthetic dermatology: an update 2009. J Eur Acad Dermatol Venereol. 2010;24:281-292.
  14. Lortat-Jacobs L, Solente G. The use of carbon dioxide snow in the treatment of nevi and other lesions of the skin: a preliminary report. JAMA. 1907;49:1354-1356.
  15. Burd A. Laser treatment of congenital melanocytic nevi. Plast Reconstr Surg. 2004;113:2232-2233.
  16. Woodrow SL, Burrows NP. Malignant melanoma occurring at the periphery of a giant congenital naevus previously treated with laser therapy. Br J Dermatol. 2003;149:886-888.
  17. Ramirez R, Schneider J. Practical guide to sun protection. Surg Clin N Am. 2003;83:97-107.
  18. English DR, Miline E, Simpson J. Sun protection and the development of melanocytic nevi in children. Cancer Epidemiol Biomarkers Prev. 2005;14:2873-2876.
  19. Facts about sunscreen. American Melanoma Foundation. www.melanomafoundation.org/prevention/facts.htm. Accessed March 10, 2013.
  20. FDA sheds light on sunscreens. FDA. May 17, 2012. www.fda.gov/forconsumers/consumerupdates/ucm258416. htm. Accessed May 15, 2013.
  21. How to select a sunscreen. American Academy of Dermatology. www.aad.org/dermatology-a-to-z/health-and-beauty/general-skin-care/sun-protection/sunscreen-labels/ how-to-select-a-sunscreen. Accessed May 15, 2013.
  22. How to perform a self-exam. American Academy of Dermatology. www.aad.org/spot-skin-cancer/understanding-skin-cancer/how-do-i-check-my-skin/how-to-perform-a-self-exam. Accessed March 14, 2013.

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