dermatoheliosis (photoaging, skin aging)
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Introduction
Polymorphic response of epidermal cells, dermal connective tissue & vascular system to prolonged &/or excessive exposure to ultraviolet radiation.
Etiology
- ultraviolet B (290-320 nm) is most potent offender
- ultraviolet A (320-400 nm) can induce the same pathology
Epidemiology
- whites
- most often in individuals > 40 years of age
- higher incidence in males
- people living in high altitudes & low latitudes
- individuals with outside occupation
- individuals with inability to tan
Pathology
- dermatopathology general
- severity depends upon the duration & intensity of sun exposure & facultative melanin pigmentation beginning with 1st exposures early in life
- increased fragility of skin
- decreased elasticity of skin
- epidermis
- acanthosis of the epidermis
- increased horny layer
- flattening of the dermal-epidermal junction
- atypia of keratinocytes
- dermis
- loss of small vessels in the papillary dermis
- elastosis
- an increase in fibroblasts
- decrease in collagen
- decreased synthesis (specifically procollagen 1)
- increased collagenase activity
- increase in elastin
- molecular
- cyclo-oxygenase 2 (COX2) may play a role[7]
- COX2 is elevated in aged skin & photoaged skin
- COX2 is higher in photoaged skin than normal aged skin
- COX2 correlates with the degree of solar elastosis in photoaging[7]
- cyclo-oxygenase 2 (COX2) may play a role[7]
Genetics
- variations in MC1R influence severity of photoaging[2]
- SNP in STXBP5L gene & haplotype linkage with another SNP that increases expression of FBXO40 is associated with less photoaging of facial skin[4]
Clinical manifestations
- patient appears wrinkled, looks older than chronologic age
- irregular diffuse pigmentation 'bronzing'
- actinic keratosis
- solar lentigo & ephelides (development of freckles)[10]
- telangiectasias, solar purpura, easy bruising
- venous lakes
- yellow dermal papules & plaques
- loss of skin elasticity
- pebbly texture of skin (elastosis)
- comedones (especially periorbital)
- distribution: sun-exposed areas
Complications
Differential diagnosis
Management
- dermatoheliosis is generally progressive & irreversible
- may continue even after sun-exposure is restricted
- spontaneous reversal has been observed
- Pharmacologic agents
- topical tretinoin
- topical 5-fluorouracil may cause disappearance of actinic keratosis
- methyl aminolevulinate (MAL) plus red light[2]
- MAL is incubated for 3 hours under occlusion before an 8-minute red-light irradiation
- treatments 3 weeks apart
- associated with considerable pain
- strictly avoid bright light for 1 or 2 days
- prevention
- sunscreen
- daily use of sunscreen can slow skin aging associated with middle age[5]
- protective clothing
- sunscreen
More general terms
More specific terms
References
- ↑ Color Atlas & Synopsis of Clinical Dermatology, Common & Serious Diseases, 3rd ed, Fitzpatrick et al, McGraw Hill, NY, 1997, pg 232-35
- ↑ Jump up to: 2.0 2.1 2.2 Elfakir A et al. Functional MC1R-gene variants are associated with increased risk for severe photoaging in facial skin. J Invest Dermatol 2010 Apr; 130:1107. PMID: https://www.ncbi.nlm.nih.gov/pubmed/19924138
- ↑ Sanclemente G et al. A prospective split-face double-blind randomized placebo- controlled trial to assess the efficacy of methyl aminolevulinate + red-light in patients with facial photodamage. J Eur Acad Dermatol Venereol 2011 Jan; 25:49 PMID: https://www.ncbi.nlm.nih.gov/pubmed/20456545
- ↑ Jump up to: 4.0 4.1 Le Clerc S et al. A genome-wide association study in Caucasian women points out a putative role of the STXBP5L gene in facial photoaging. J Invest Dermatol 2013 Apr; 133:929. PMID: https://www.ncbi.nlm.nih.gov/pubmed/23223146
- ↑ Jump up to: 5.0 5.1 Hughes MCB et al Sunscreen and Prevention of Skin Aging: A Randomized Trial. Ann Intern Med. 2013;158(11):781-790 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/23732711 <Internet> http://annals.org/article.aspx?articleid=1691733
- ↑ Medical Knowledge Self Assessment Program (MKSAP) 16, 17. American College of Physicians, Philadelphia 2012, 2015.
- ↑ Jump up to: 7.0 7.1 7.2 Habib MA et al. Comparative immunohistochemical assessment of cutaneous cyclooxygenase-2 enzyme expression in chronological aging and photoaging. Photodermatol Photoimmunol Photomed 2014 Feb; 30:43 PMID: https://www.ncbi.nlm.nih.gov/pubmed/24393208
- ↑ Geriatric Review Syllabus, 8th edition (GRS8) Durso SC and Sullivan GN (eds) American Geriatrics Society, 2013
- ↑ Jump up to: 9.0 9.1 9.2 9.3 Helfrich YR et al. Clinical, histologic, and molecular analysis of differences between erythematotelangiectatic rosacea and telangiectatic photoaging. JAMA Dermatol 2015 Mar 23; [e-pub]. PMID: https://www.ncbi.nlm.nih.gov/pubmed/25798811
Wilkin JK. Erythematotelangiectatic rosacea and telangiectatic photoaging: Same, separate, and/or sequential? JAMA Dermatol 2015 Mar 23 PMID: https://www.ncbi.nlm.nih.gov/pubmed/25798736 - ↑ Jump up to: 10.0 10.1 Praetorius C, Sturm RA, Steingrimsson E Sun-induced freckling: ephelides and solar lentigines Pigment Cell Melanoma Res. 2014 May;27(3):339-50 PMID: https://www.ncbi.nlm.nih.gov/pubmed/24517859 Review.
- ↑ Sunlight, Ultraviolet Radiation, and the Skin http://consensus.nih.gov/cons/074/074_intro.htm