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Becker's nevus


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First documented in 1948 by US dermatologist Samuel William Becker (1894-1964), Becker's nevus (also naevus; pl. nevi or naevi) is a skin disorder predominantly affecting males. The nevus first appears as an irregular pigmentation (melanosis or hyperpigmentation) on the torso or upper arm, and gradually enlarges irregularly, becoming thickened and often hairy (hypertrichosis). It is also known as Becker nevus, Becker's pigmented hairy nevus, Becker pigmented hairy nevus, Becker melanosis and pigmented hairy epidermal nevus.

Clinical Information

Medical knowledge and documentation of this disorder is inextensive, likely due to a combination of factors including recent discovery, low prevalence, and the more or less aesthetic nature of the effects of the disease. Thus the pathophysiology of Becker's nevus remains unclear. While it is generally considered an acquired rather than congenital disorder, there exists at least one case report documenting what researchers claim is a congenital Becker's nevus with genetic association: a 16-month-old boy with a hyperpigmented lesion on his right shoulder whose father has a similar lesion on his right shoulder.

The apparently most extensive study to date (a 1981 survey of nearly 20,000 young Frenchmen ) served to disprove many commonly-held beliefs about the disease. In the French study, 100 subjects were found to have Becker's nevi, revealing a prevalence of 0.52%. Nevi appeared in one half the subjects before the age of 10, and between ages 10 and 20 in the rest. In one quarter of cases exposure sun appears to have played a role, a number apparently lower than that expected by researchers. Also surprising to researchers was the low incidence (32%) of Becker's nevi above the nipples, for it had generally been believed that the upper chest and shoulder area was the predominant site of occurrence. Pigmentation was light brown in 75% of cases, and average size of the nevus was 125cm².


A 1991 report documented the cases of nine patients with both Becker's nevus and malignant melanoma. Of the nine melanomas, five were in the same body area as the Becker's nevus, with only one occurring within the nevus itself. As this was apparently the first documented co-occurence of the two diseases, there is so far no evidence of higher malignancy rates in Becker's nevi versus normal skin. Nonetheless, as with any abnormal skin growth, the nevus should be monitored regularly and any sudden changes in appearance brought to the attention of one's doctor or nurse specialist.


As Becker's nevus is considered a benign lesion, treatment is generally not necessary except for cosmetic purposes. Shaving or trimming can be effective in removing unwanted hair, while laser hair removal may offer a longer-lasting solution. Different types of laser treatments may also be effective in elimination or reduction of hyperpigmentation, though the results of laser treatments for both hair and pigment reduction appear to be highly variable.


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Hyperpigmentation: a review of common treatment options
From Journal of Drugs in Dermatology, 11/1/04 by Kimberly A. Cayce


Hyperpigmentation disorders are common and include a multitude of forms. They are typically divided into three large categories: dermal, epidermal, or mixed, depending on the site of abnormality. The location of the increased melanin affects treatment options, but therapy within a group is often similar. This paper discusses the treatment modalities, including topical and surgical approaches, available for the different types of hyperpigmentation.



Hyperpigmentation is a darkening of the skin, which typically results from increased melanin. This may occur in the epidermis, dermis, or both (Figures 1 and 2). Either increased melanin production by existing melanocytes (melanotic hyperpigmentation) or proliferation of active melanocytes (melanocytic hyperpigmentation) is responsible.


Clinically, the lesions may appear as localized, circumscribed spots or in a more diffuse pattern. With diffuse involvement, the lesions may be scattered discrete macules, reticulated macules, or ill-defined. Epidermal involvement appears as brown discoloration, dermal as blue-gray, and mixed epidermal and dermal as brown-gray. Although these disorders can affect any site, certain diseases have a predilection for specific anatomic locations. For example, melasma generally involves the face, acral melanosis affects the hands, and tinea versicolor targets the trunk.

The topic of hyperpigmentation encompasses too many disorders to go into any great detail within this review article. However, many of the same therapies are used among all of the various hyperpigmentation disorders. This paper focuses on these treatment options.


Hyperpigmentation disorders of the skin are common. Although they typically affect all races, some forms, such as melasma and postinflammatory hyperpigmentation, are more prevalent in darker-complexioned individuals. A survey conducted by Halder et al revealed that, of 2,000 black patients seeking dermatologic care in a private-practice setting, pigmentary problems other than vitiligo were cited as the third most common skin disorder (1). On the other hand, solar lentigines are more common in those with Fitzpatrick skin types I-III. In fact, 90% of white adults older than 60 years of age possess these "age" spots (2). Age at the time of onset varies between specific disorders and ranges from as early as birth (i.e., Nevus of Ota) up until late adulthood (i.e., solar lentigines). Prevalence between the sexes also varies. Melasma is much more common in women, whereas Becker's nevus occurs five times more frequently in males.

Differential Diagnosis

Most of the hyperpigmentation disorders can be distinguished clinically. A list of the more common hyperpigmentation disorders is listed in Table 1. This table divides the conditions into epidermal (superficial) and dermal (deep) pigment disorders, and further classifies them as melanotic or melanocytic. Most of the epidermal and dermal pigment disorders are due to increased melanin production with normal melanocyte numbers (melanotic hyperpigmentation); however, other pigment disorders, such as lentigines, Mongolian spots, and Nevus of Ota, may result from increased melanocyte numbers (melanocytic hyperpigmentation).


Dermal hyperpigmentation

Dermal hyperpigmentation is recalcitrant to many therapeutic interventions. Cover-up with opaque cosmetics remains essentially the only option for aesthetically displeasing discolorations such as dermal melasma. An exception to this was reported in a pilot study of pulsed CO2 laser followed by Q-switched alexandrite laser in the treatment of dermal melasma that showed promising results (3). Nevus of Ota has effectively been treated with the selective photothermolysis with the Q-switched ruby laser as well. On the other hand, multiple therapies are available in the management of epidermal hyperpigmentation.

Epidermal Hyperpigmentation

Topical therapies

Topical agents commonly utilized in the treatment of hyperpigmentation disorders include phenols (i.e., hydroquinone, mequinol), retinoids (i.e., tretinoin), alpha-hydroxy acids (i.e., glycolic acid), salicylic acid, and azelaic acid. Hydroquinone works by inhibiting the tyrosinase enzyme, thereby preventing the conversion of dopa to melanin. Although a useful depigmenting agent, hydroquinone requires a prolonged treatment course before any significant improvement in the hyperpigmentation (up to 6 months). Most dermatologists recommend 4% hydroquinone, which is prescription strength, but infrequently higher strengths can be compounded. Some authors suggest continuation of low-dose, over-the-counter 2% hydroquinone for melasma maintenance therapy after an initial treatment period (4). Irritant and allergic contact dermatitis, nail discoloration, and postinflammatory hyper- or hypopigmentation are potential side effects (5). Ochronosis (a permanent, reticulated, ripple-like, sooty pigmentation), although uncommon, can occur, particularly after prolonged use of high concentration hydroquinone (6).

Though slow to work (24 weeks or more), tretinoin 0.1% cream can improve melasma and other hyperpigmentary disorders (7-9). Reduction of pigmentation results from the retinoid-induced dispersion of keratinocyte pigment granules, interference with pigment transfer, and acceleration of epidermal turnover (10). Other strengths and formulations (0.05% cream, 0.01% and 0.05% emollient cream) have also been used. Adverse effects include erythema, peeling, and possible postinflammatory hyperpigmentation (6).

Azelaic acid may also be helpful, particularly during pregnancy as it is pregnancy category B. This chemical inhibits DNA synthesis in melanocytes and has a modest antityrosinase effect (2). Comparisons of azelaic acid to 2% hydroquinone revealed superiority with azelaic acid, but no significant difference from 4% hydroquinone (11,12). Pruritus, mild transient erythema, scaling, and burning may occur (13).

Other topical medications have been applied to hyperpigmentation disorders. Attempts with kojic acid demonstrated no more efficacy than other therapies, but more irritation. In one study, premarin cream, a topical conjugated estrogen, improved the appearance of photodamaged skin including the appearance of lentigines (14).

Combination therapy offers the best results. The mixture of tretinoin 0.1%, hydroquinone 5%, and dexamethasone 0.1% (Kligman's formula) yield better results than any of the medications alone, and several adaptations of this regimen have confirmed this finding (10,15,16). A recent trial comparing a triple combination of tretinoin 0.05%, hydroquinone 4%, and fluocinolone acetonide 0.01% in 641 melasma patients demonstrated better results with the triple therapy than any of the dual combinations of the above agents (17). Contrary to monotherapy, clinically significant improvement with the triple therapy was noted as early as 4 weeks with maximum results at 8 weeks (17). Local irritation, which is generally mild, is the most common adverse event. Although the medication is typically only used for 2 to 3 months at a time, this triple therapy has proven safe even with 6 and 12 months of use (18). The addition of tretinoin to topical steroids increases the epidermal skin thickness (19), which may help explain the maintained safety of this drug.

Others have had success in melasma treatment with just the combination of lower concentration hydroquinone 2% and tretinoin 0.5% (4). Lentigines have been successfully managed with the combination of mequinol (a phenolic compound) and tretinoin, the first combination therapy approved for the treatment of solar lentigines. The presence of two different mechanisms of action on the inhibition of the pigmentary process appears to account for the synergy of these two compounds. Fleischer et al found this compound to be more effective for solar lentigines then either agent alone (20). Local irritation is the most common side effect. One study of melasma patients demonstrated a more rapid response (3 months vs. 10 months) with the addition of chemical peels to a tretinoin/hydroquinone regimen (21).

Superficial and medium-depth peels with trichloracetic acid (TCA), glycolic acid, salicylic acid, and tretinoin benefit some individuals. One clinical trial examining the effects of TCA peels noted success with 40% complete regression and 50% partial regression of lentigines (22). Following pretreatment with topical tretinoin and localized 20% TCA, a peel consisting of 50% salicylic acid, methyl salicylate, and croton oil proved efficacious in the treatment of solar lentigines, even after one application (23). Another trial looking at the effects of the addition of glycolic acid peels to a topical regimen of 2% hydroquinone, 10% glycolic acid, and 0.05% tretinoin cream for postinflammatory hyperpigmentation in black patients showed improved results with the peels with minimal adverse effects (24). Benefits of tretinoin peels have also been observed in certain hyperpigmentation disorders, including that of photodamaged skin. In addition, a more rapid response occurs than that observed with topical retinoid creams (25). The addition of glycolic acid peels to a modified Kligman's formula displayed more rapid and greater improvement than the topical regimen alone in melasma patients (26). However, peels must be used with caution in darker pigmented persons because of the greater risk of postinflammatory hyperpigmentation. The association of hypo- and hyperpigmentation, scarring, and keloid formation decreases the utilization of deep peels, especially in dark-complexioned patients (27). Other potential side effects of the chemical peels include atrophy, bacterial and viral infections, milia, telangiectasias, and pore enlargement (28).


Dermabrasion is one technique used in the management of hyperpigmentation disorders, but again the increased risk of postinflammatory hyperpigmentation in dark-skinned individuals makes this option less desirable. For many decades, cryosurgery has been employed as a means to treat lentigines. Selective destruction of melanocytes, which are most susceptible to cold, explains the success of cryosurgery. A study looking at cryosurgery compared to local dermabrasion for the treatment of solar lentigo on the back of the hands found comparable results between the two therapies, but less temporary side effects and a faster healing time were noted with dermabrasion (29). However, another clinical trial evaluating liquid nitrogen versus both argon and CO2 lasers demonstrated superiority of the liquid nitrogen (30). Cryosurgery can lead to permanent hypopigmentation. Proper technique, in which one freezes the lesion intermittently for 10 seconds, producing a 1-to-2 millimeter halo around the spot (31), minimizes this risk. Additional possible side effects include erythema, hyperpigmentation, atrophy, and pain.

Therapy with various lasers including erbium yttrium-aluminum-garnet (Er:YAG), Q-switched ruby, dye (510 nm), CO2, argon, and neodymium (Nd:YAG) lasers have been attempted. Thermal injury damages the epidermis and removes the pigmented lesions. To localize tissue destruction to the target lesions and minimize side effects such as textural changes or scarring, lasers such as the frequency-doubled Q-switched Nd:YAG and Q-switched ruby lasers are used. These lasers emit wavelengths that are absorbed more specifically by the targeted tissue and also use shorter pulse durations (specific photothermolysis) (32,33). Melasma is resistant to most lasers. The Er:YAG laser revealed some improvement in melasma, but significant postinflammatory hyperpigmentation requiring 6 months of treatment resulted (34). Goldberg (35) and McBurney (36) demonstrated encouraging responses with the Q-switched ruby laser and the argon laser, but these results were short-lived. In contrast to that of melasma, many of the lasers are successful in the management of solar lentigines, even after a single treatment. The frequency-doubled Q-switched Nd:YAG laser demonstrated better results after one treatment of facial lentigines when compared to 35% trichloracetic acid (37). Another study revealed that the Q-switched ruby laser removed lentigines more effectively and with less irritation than did glycolic acid peels (33). Although decreased pigmentation of solar lentigines with CO2 lasers has been shown (38), the effects are not as impressive as those with cryosurgery and more adverse events may ensue from the nonselective thermal damage. Intense pulsed light (IPL) appears promising as an effective means to treat lentigines with minimal side effects (39,40). Complications of the lasers include atrophy, hypertrophic scarring, and hypo- and hyperpigmentation (6). Because of the melanocyte-destructive nature of techniques, such as cryosurgery (41) and pigmented lesion dye lasers (42), their adverse effects are more likely to be permanent.


Sunlight exacerbates most hyperpigmentary disorders. Therefore, daily use of sunscreens (SPF at least 15 with both UVA and UVB protection) and avoidance of UV radiation is recommended. When possible, treatment of the underlying process is key. Inciting compounds, such as psoralen-containing vegetables, fruits, plants, cosmetics, and coal tars, should be avoided if photocontact dermatitis is suspected. Patients with primary inflammatory conditions, such as acne and atopic dermatitis, need early intervention to keep the inflammation under tight control, decreasing the risk of post-inflammatory hyperpigmentation. Table 2 summarizes the treatment options for both dermal and epidermal hyperpigmentation disorders.

Funding Source: The Center for Dermatology Research is funded by a grant from Galderma Laboratories, L.P.


1. Halder RM, et al. Incidence of common dermatoses in a predominantly black dermatologic practice. Cutis 1983; 32:388, 390.

2. Ortonne JP, et al. Hypomelanoses and Hypermelanoses. In: Freedberg IM, et al., editors. Fitzpatrick's Dermatology in General Medicine. New York: McGraw-Hill Medical Publishing Division; 2003; 836-81.

3. Nouri K, et al. Combination treatment of melasma with pulsed CO2 laser followed by Q-switched alexandrite laser: a pilot study. Dermatol Surg 1999; 25:494-7.

4. Pathak MA, Fitzpatrick TB, Kraus EW. Usefulness of retinoic acid in the treatment of melasma. J Am Acad Dermatol. 1986; 15:894-9.

5. Grimes PE. Vitiligo. An overview of therapeutic approaches. Dermatol Clin. 1993; 11:325-38.

6. Grimes PE. Melasma. Etiologic and therapeutic considerations. Arch Dermatol. 1995; 131:1453-7.

7. Griffiths CE, et al. Topical tretinoin (retinoic acid) improves melasma. A vehicle-controlled, clinical trial. Br J Dermatol. 1993; 129:415-21.

8. Tadaki T, et al. The effect of topical tretinoin on the photodamaged skin of the Japanese. Tohoku J Exp Med. 1993; 169:131-9.

9. Kimbrough-Green CK, et al. Topical retinoic acid (tretinoin) for melasma in black patients. A vehicle-controlled clinical trial. Arch Dermatol. 1994; 130:727-33.

10. Kligman AM, Willis I. A new formula for depigmenting human skin. Arch Dermatol. 1975; 111:40-8.

11. Verallo-Rowell VM, et al. Double-blind comparison of azelaic acid and hydroquinone in the treatment of melasma. Acta Derm Venereol. Suppl (Stockh) 1989; 143:58-61.

12. Balina LM, Graupe K. The treatment of melasma. 20% azelaic acid versus 4% hydroquinone cream. Int J Dermatol. 1991; 30:893-5.

13. Fitton A, Goa KL. Azelaic acid. A review of its pharmacological properties and therapeutic efficacy in acne and hyperpigmentary skin disorders. Drugs. 1991; 41:780-98.

14. Creidi P, et al. Effect of a conjugated oestrogen (Premarin) cream on ageing facial skin. A comparative study with a placebo cream. Maturitas. 1994; 19:211-23.

15. Gano SE, Garcia RL. Topical tretinoin, hydroquinone, and betamethasone valerate in the therapy of melasma. Cutis. 1979; 23:239-41.

16. Kang WH, Chun SC, Lee S. Intermittent therapy for melasma in Asian patients with combined topical agents (retinoic acid, hydroquinone and hydrocortisone): clinical and histological studies. J Dermatol. 1998; 25:587-96.

17. Taylor SC, et al. Efficacy and safety of a new triple-combination agent for the treatment of facial melasma. Cutis. 2003; 72:67-72.

18. Torok HM, et al. Tri-Luma: a safe and efficacious 12 months treatment for melasma. Cutis. 2003. Ref Type: In Press

19. McMichael AJ, et al. Concurrent application of tretinoin (retinoic acid) partially protects against corticosteroid-induced epidermal atrophy. Br J Dermatol. 1996; 135:60-4.

20. Fleischer AB, Jr., et al. The combination of 2% 4-hydroxyanisole (Mequinol) and 0.01% tretinoin is effective in improving the appearance of solar lentigines and related hyperpigmented lesions in two double-blind multicenter clinical studies. J Am Acad Dermatol. 2000; 42:459-67.

21. Lawrence N, Cox SE, Brody HJ. Treatment of melasma with Jessner's solution versus glycolic acid: a comparison of clinical efficacy and evaluation of the predictive ability of Wood's light examination. J Am Acad Dermatol. 1997; 36:589-93.

22. Cotellessa C, et al. The use of chemical peelings in the treatment of different cutaneous hyperpigmentations. Dermatol Surg. 1999; 25:450-4.

23. Swinehart JM. Salicylic acid ointment peeling of the hands and forearms. Effective nonsurgical removal of pigmented lesions and actinic damage. J Dermatol Surg Oncol. 1992; 18:495-8.

24. Burns RL, et al. Glycolic acid peels for postinflammatory hyperpigmentation in black patients. A comparative study. Dermatol Surg. 1997; 23:171-4.

25. Cuce LC, et al. Tretinoin peeling. Dermatol Surg. 2001; 27:12-4.

26. Sarkar R, et al. The combination of glycolic acid peels with a topical regimen in the treatment of melasma in dark-skinned patients: a comparative study. Dermatol Surg. 2002; 28:828-32.

27. Pandya AG, Guevara IL. Disorders of hyperpigmentation. Dermatol Clin. 2000; 18:91-8, ix.

28. Moy LS, Murad H, Moy RL. Glycolic acid peels for the treatment of wrinkles and photoaging. J Dermatol Surg Oncol. 1993; 19:243-6.

29. Hexsel DM, et al. Clinical comparative study between cryotherapy and local dermabrasion for the treatment of solar lentigo on the back of the hands. Dermatol Surg. 2000; 26:457-62.

30. Stern RS, et al. Laser therapy versus cryotherapy of lentigines: a comparative trial. J Am Acad Dermatol. 1994;30:985-7.

31. Graham GF, Cerveny KA, Jr, SanFilippo J. Cryosurgery. In: Fitzpatrick, editor. Dermatology in General Medicine. New York: McGraw Hill Medical Publishing; 2003: 2575-81.

32. Kilmer SL, et al. Treatment of epidermal pigmented lesions with the frequency-doubled Q-switched Nd:YAG laser. A controlled, single-impact, dose-response, multicenter trial. Arch Dermatol. 1994; 130:1515-9.

33. Kopera D, Hohenleutner U, Landthaler M. Q-switched ruby laser application is safe and effective for the management of actinic lentigo (topical glycolic acid is not). Acta Derm Venereol. 1996; 76:461-3.

34. Manaloto RM, Alster T. Erbium:YAG laser resurfacing for refractory melasma. Dermatol Surg. 1999; 25:121-3.

35. Goldberg DJ. Benign pigmented lesions of the skin. Treatment with the Q-switched ruby laser. J Dermatol Surg Oncol. 1993; 19:376-9.

36. McBurney EI. Clinical usefulness of the argon laser for the 1990s. J Dermatol Surg Oncol. 1993; 19:358-62.

37. Li YT, Yang KC. Comparison of the frequency-doubled Q-switched Nd:YAG laser and 35% trichloroacetic acid for the treatment of face lentigines. Dermatol Surg. 1999; 25:202-4.

38. Dover JS, et al. Low-fluence carbon dioxide laser irradiation of lentigines. Arch Dermatol 1988; 124:1219-24.

39. Kawada A, et al. Clinical improvement of solar lentigines and ephelides with an intense pulsed light source. Dermatol Surg. 2002; 28:504-8.

40. Moreno Arias GA, Ferrando J. Intense pulsed light for melanocytic lesions. Dermatol Surg. 2001; 27:397-400.

41. Gage AA, et al. Sensitivity of pigmented mucosa and skin to freezing injury. Cryobiology. 1979; 16:348-61.

42. Grekin RC, et al. 510-nm pigmented lesion dye laser. Its characteristics and clinical uses. J Dermatol Surg Oncol. 1993; 19:380-7.




Amy J. McMichael MD

Department of Dermatology

Wake Forest University School of Medicine

Medical Center Boulevard

Winston-Salem, NC 27157

Phone: (336) 716-2768

Fax: (336) 716-7732



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