Flat, Brown Macules on the Body


  • Slide

A 60-year-old man presents with brown macules on his face, arms, hands, and back. He reports that the spots first appeared after he moved to California 20 years ago, and he has been noticing new spots ever since. He denies pruritus or fading of the spots during winter. The patient previously worked as a lifeguard at a local beach. He does not have significant medical or family history. Examination reveals numerous 1-cm, well-defined, dark brown, evenly pigmented, flat macules over his face, arms, hands, and back.

Solar lentigines (SLs) are stable, hyperpigmented patches or macules that increase in number with age in sun-exposed areas.1,2 Also known as liver spots or aging spots, SLs occur due to proliferation of melanocytes and consequent accumulation of melanin.1 The main...

Submit your diagnosis to see full explanation.

Solar lentigines (SLs) are stable, hyperpigmented patches or macules that increase in number with age in sun-exposed areas.1,2 Also known as liver spots or aging spots, SLs occur due to proliferation of melanocytes and consequent accumulation of melanin.1 The main risk factors for developing these lesions include fair skin, chronic sun exposure, age, and diabetes.1-4 These lesions are diagnosed clinically, although histology, immunohistochemistry, and electron microscopy features have been described.1 Solar lentigines are confused most often with ephelides, as both types of lesions are used to describe sun-induced freckling; however, distinction can be made based upon size, seasonal pigmentation changes, and age at onset. While treatment is not necessary, several physical and topical therapies exist for cosmetic purposes.

The etiology and pathogenesis of SLs are largely associated with skin damage from chronic exposure to ultraviolet (UV) radiation.1-9 When exposed to UV light, keratinocytes release reactive oxygen species that can induce genetic and/or epigenetic changes within keratinocytes.1 Melanocytes serve to protect the skin by producing the pigment melanin, which absorbs these radicals.1-3 Melanocytes, arising from the neural crest, differentiate in the basal epidermis to create dendritic contacts with surrounding keratinocytes.1 Through these connections, melanocytes transfer melanin, which in turn pigments the skin. Intense and chronic UV exposure overpowers this physiologic system and genetic damage occurs, thus inducing formation of SLs.1,3 Specific gene mutations have been associated with the development of SLs, namely inactivating mutations in MC1R.3 Other associated genes include SLC45A2, GFR3, and PIK3CA.1 Additional studies have shown that malfunction of Notch 1-dependent keratinocytes leads to the hyperpigmentation seen in SLs.2

Several factors increase the risk of developing SLs, namely chronic sun exposure, increased age, and lighter skin tones.2,3,6 A recent study of white women determined additional risk factors to include frequent sunburns, chronic sun exposure, tanning, intake of oral contraceptives, and progesterone treatment.5 Interestingly, diabetes mellitus is an independent risk factor, possibly due to the effects of diminished glucose metabolism in skin.4 The presence of SLs and lentigine density have been associated with increased risk of melanoma.1,3,6

SLs vary from light yellow to dark brown in color, have well-defined borders, are measured in millimeters to centimeters, and are stable under varying amounts of sunlight.1,3 Lesions are most commonly found on the hands and other sun-exposed areas such as the face, trunk, and arms.1,2,4,8 Histologically, SLs appear with epidermal thickening and hyperplasia, a hyperpigmented basal layer, functionally active melanocytes, and extended epidermal ridges.1,2,6 Of note, melanocyte size and melanosome size and number are normal in SLs.1 Other distinctive features have been noted on immunohistochemistry and electron microscopy.1 Immunohistochemical studies have shown an increased number of melanocytes, increased tyrosine kinase receptor expression in melanocytes, increased melanoblasts in hair follicular infundibulum, and increased melanocyte stem cells in the bulge of hair follicles. Electron microscopy studies have shown microinvaginations into keratinocytes, a well-developed endoplasmic reticulum, increased mitochondria density, disorganized and disrupted dermal-epidermal junction, and a thin lamina densa.

The differential diagnosis for SLs includes ephelides, seborrheic keratoses, lentigo maligna, lentigo maligna melanoma (LMM), and psoralens and ultraviolet A (PUVA) lentigines.1,3 Patient history and physical examination findings are sufficient to narrow the diagnosis. Briefly, seborrheic keratoses are genetically predisposed and present with palpable lesions and horn cysts.3 Patients with lentigo maligna have macular lesions with irregular borders of varying size and pigmentation; LMM has a similar presentation except these lesions are palpable. Lastly, PUVA lentigines are induced by PUVA light therapy as opposed to the sun in SLs.

Freckles are colloquially used to describe both ephelides and SLs. Both lesions are characterized as benign spots induced by sun exposure most commonly seen in Asian and white populations; however, ephelides and SLs can be distinguished based on size and temporal pigmentation changes.1,5,6 Ephelides are small, 1- to 2-mm macules that appear around age 2 years, and these red- to light brown-colored spots increase in pigmentation with increased sun exposure. On the other hand, SLs are larger, darker, appear most commonly in sun-exposed areas, and do not present with seasonal variation. While SLs increase in number as patients age, ephelides peak during adolescence and regress with age.

SLs do not require treatment but are often treated for cosmetic reasons.7 Of note, as these lesions are induced by chronic sun exposure, all patients should be counseled about sun protection.3 If patients wish to pursue treatment, 2 broad methods exist: physical and topical treatments.7 Physical treatments include cryotherapy, laser treatments, intense pulsed lights, and chemical peeling.7,8 Of all the treatment options available, cryotherapy with liquid nitrogen is the preferred method.3,7 In patients with darker skin types III and IV, pulsed-dye laser was shown to be superior to cryotherapy for lightening SLs; this difference was not seen for patients with lighter skin tones.7 Combination of picosecond-switched lasers and biophotonic therapy has produced successful results.8 Compared with these physical therapies, topical therapies require extended treatment but are associated with fewer risks.7 The most common of these options include hydroquinone and tretinoin.7 Lastly, recent studies have also shown a modest whitening effect of lotions with L-ascorbate-2-phosphate trisodium salt.9

The 60-year-old patient mentioned in the case was diagnosed with solar lentigines. No treatment was administered since he did not want a cosmetic procedure. The patient was advised to apply sunscreen daily and wear protective gear to prevent further photodamage. He was also advised to return for evaluation if his lentigines changed in size or color.

Saira E. Alex, BS, is a medical student; McKenna E. Boyd, BS, is a medical student; and Christopher Rizk, MD, is a dermatology fellow at Baylor College of Medicine, in Houston, Texas.


  1. Praetorius C, Sturm RA, Steingrimsson E. Sun-induced freckling: ephelides and solar lentigines. Pigment Cell Melanoma Res. 2014;27(3):339-350.
  2. Barysch MJ, Braun RP, Kolm I, et al.  Keratinocytic malfunction as a trigger for the development of solar lentigines. Dermatopathology (Basel). 2019;6(1):1-11.  
  3. Goldstein BG, Goldstein AO. Overview of benign lesions of the skin. UpToDate. https://www.uptodate.com/contents/overview-of-benign-lesions-of-the-skin?search=solar%20lentigo%20treatment&source=search_result&selectedTitle=2~24&usage_type=default&display_rank=2#H1101421390. Updated February 19, 2019. Accessed March 19, 2019.  
  4. Moazzami B, Razavi N, Babaei M, Haghparast M, Bayani MA. The association between solar lentigines and type- 2 diabetes. Caspian J Intern Med. 2017;8(4):317-320.  
  5. Ezzedine K, Mauger E, Latreille J, et al. Freckles and solar lentigines have different risk factors in Caucasian women. J Eur Acad Dermatol Venereol. 2013;27(3):e345-e356.
  6. Bastiaens MT, Westendorp RG, Vermeer BJ, Bavinck JN. Ephelides are more related to pigmentary constitutional host factors than solar lentigines. Pigment Cell Res. 1999;12(5):316-322.
  7. Seirafi H, Fateh S, Farnaghi F, Ehsani AH, Noormahammadpour N. Efficacy and safety of long-pulse pulsed dye laser delivered with compression versus cryotherapy for treatment of solar lentigines. Indian J Dermatol. 2011;56(1):48-51.
  8. Scarcella G, Dethlefsen MW, Nielson MCE. Treatment of solar lentigines using a combination of picosecond laser and biophotonic treatment. Clin Case Rep. 2018;6(9):1868-1870.
  9. Ishikawa Y, Niwano T, Hirano S, Numano K, Takasima K, Imokawa G. Whitening effect of L-ascorbate-2-phosphate trisodium salt on solar lentigos.Arch Dermatol Res. 2019;311(3):183-191.
Next hm-slideshow in Dermatology Clinics