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 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. References 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-lesionsof-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.
Cherry angiomas are also known as Campbell de Morgan spots, cherry hemangiomas, and senile angiomas. These lesions are the most common benign vascular tumors affecting primarily older, paleskinned individuals.1,2 Cherry angiomas are well-demarcated, blanchable, bright red, domeshaped papules and pinpoint macules most commonly found on the trunk and arms measuring several millimeters in diameter.1 The number and size of lesions increase with age with prevalence increasing from approximately 5% in adolescents to approximately 75% in adults aged >75 years.1,2 Diagnosis is based on patient history and clinical presentation. Lesions do not require treatment although several cosmetic therapies exist. The etiology and pathogenesis of cherry angiomas are poorly understood.1,2 For a time it was even unclear if these lesions should be classified as vascular tumors or vascular malformations. Recent studies have shown the cytoplasmic expression of Wilms tumor protein 1, a marker of endothelial plasticity, in cherry angioma tumor cells.3 This evidence thus classifies cherry angiomas as vascular tumors given the proliferative nature of the contained endothelial cells. Other studies have attempted to discover somatic mutations associated with cherry angiomas. One such study found that mutations in genes GNAQ and GNA11 were found to be present in 50% of cherry angioma samples taken (n=10); these are the same mutations present in port wine stains and Sturge-Weber syndrome.4 Of note, pathogenesis of cherry angiomas may be associated with malignancy as sudden appearance is often associated with systemic internal malignancy.3
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