EpistemisSkin atrophy
Specialty: Skin.
Why it occurs
- Prolonged and chronic use of high-potency topical or systemic corticosteroids (inhibition of the transcription of collagen types I and III genes and proliferation of keratinocytes)
- Intrinsic aging and chronic accumulated sun damage (dermatoheliosis with loss of dermal elastic fibers)
- Severe protein malnutrition or vitamin deficiencies (scurvy due to vitamin C deficiency)
- Peripheral tissue ischemia secondary to chronic arterial occlusive disease
- Genetic connective tissue syndromes (such as Ehlers-Danlos syndrome or progeria).
Initial workup
Clinical diagnosis through visualization of translucent skin with very evident vascular relief and loss of elasticity. Analytical measurement of basal cortisol levels or dexamethasone suppression test if iatrogenic or endogenous Cushing's syndrome is suspected. Skin biopsy if it is necessary to type structural collagen abnormalities.
red flags
Spontaneous formation of extensive skin tears due to minimal mechanical friction (skin tears), extreme delay in the healing of simple wounds, giant or recurrent spontaneous hematomas of acral location (severe Bateman's senile purpura) without demonstrable coagulopathy, or associated painful ischemic ulcers.
Standard management
- Tretinoin cream 0.025% or 0.05% — topical retinoid that stimulates the synthesis of dermal collagen by fibroblasts and partially reverses atrophy induced by corticosteroids or photoaging
- Protective barrier creams with neutral lipids and glycerin — epidermal hydration and cushioning
- Ascorbic acid/Vitamin C supplementation — indispensable cofactor for the hydroxylation of proline and lysine in collagen synthesis
- Avoid the continued use of powerful topical corticosteroids by replacing them with calcineurin inhibitors such as pimecrolimus.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Skin
- Listed causes
- 5
- Treatment options
- 4