WASHINGTON — and conveys the skin’s vulnerability to serious medical complications, said Adam Friedman, MD, at the ElderDerm conference on dermatology in the older patient.
Key features of dermatoporosis include atrophic skin, solar purpura, white pseudoscars, easily acquired skin lacerations and tears, bruises, and delayed healing. “We’re going to see more of this, and it will more and more be a chief complaint of patients,” said Dr. Friedman, professor and chair of dermatology at George Washington University (GWU) in Washington, and co-chair of the meeting. GWU hosted the conference, describing it as a first-of-its-kind meeting dedicated to improving dermatologic care for older adults.
Dr. Adam Friedman
Dermatoporosis was described in the literature in 2007 by dermatologists at the University of Geneva in Switzerland. “It is not only a cosmetic problem,” Dr. Friedman said. “This is a medical problem ... which can absolutely lead to comorbidities [such as deep dissecting hematomas] that are a huge strain on the healthcare system.”
Dermatologists can meet the moment with holistic, creative combination treatment and counseling approaches aimed at improving the mechanical strength of skin and preventing potential complications in older patients, Dr. Friedman said at the meeting.
He described the case of a 76-year-old woman who presented with dermatoporosis on her arms involving pronounced skin atrophy, solar purpura, and a small covered laceration. “This was a patient who was both devastated by the appearance” and impacted by the pain and burden of dressing frequent wounds, said Dr. Friedman, who is also the director of the Residency Program, of Translational Research, and of Supportive Oncodermatology, all within the Department of Dermatology at GWU.
With 11 months of topical treatment that included daily application of calcipotriene 0.05% ointment and nightly application of tazarotene 0.045% lotion and oral supplementation with 1000-mg vitamin C twice daily and 1000-mg citrus bioflavonoid complex daily, as well as no changes to the medications she took for various comorbidities, the solar purpura improved significantly and “we made a huge difference in the integrity of her skin,” he said.
Dr. Friedman also described this case in a recently published article in the Journal of Drugs in Dermatology titled “What’s Old Is New: An Emerging Focus on Dermatoporosis”.
Likely Pathophysiology
Advancing age and chronic ultraviolet (UV) radiation exposure are the chief drivers of dermatoporosis. In addition to UVA and UVB light, other secondary drivers include genetic susceptibility, topical and systematic corticosteroid use, and anticoagulant treatment.
Its pathogenesis is not well described in the literature but is easy to envision, Dr. Friedman said. For one, both advancing age and exposure to UV light lead to a reduction in hygroscopic glycosaminoglycans, including hyaluronate (HA), and the impact of this diminishment is believed to go “beyond [the loss of] buoyancy,” he noted. Researchers have “been showing these are not just water-loving molecules, they also have some biologic properties” relating to keratinocyte production and epidermal turnover that appear to be intricately linked to the pathogenesis of dermatoporosis.
HAs have been shown to interact with the cell surface receptor CD44 to stimulate keratinocyte proliferation, and low levels of CD44 have been reported in skin with dermatoporosis compared with a younger control population. (A newly characterized organelle, the hyaluronosome, serves as an HA factory and contains CD44 and heparin-binding epidermal growth factor, Dr. Friedman noted. Inadequate functioning may be involved in skin atrophy.)
Advancing age also brings an increase in matrix metalloproteinases (MMPs)–1, –2, and –3, which are “the demolition workers of the skin,” and downregulation of a tissue inhibitor of MMPs, he said.
Adding insult to injury, dermis-penetrating UVA also activates MMPs, “obliterating collagen and elastin.” UVB generates DNA photoproducts, including oxidative stress and damaging skin cell DNA. “That UV light induces breakdown [of the skin] through different mechanisms and inhibits buildup is a simple concept I think our patients can understand,” Dr. Friedman said.