New research found that long-term corticosteroid use can silently damage the skin’s structure, causing it to thin prior to the appearance of visible changes.
The damage begins deep in the skin, where elastic fibers normally help maintain firmness and flexibility. Researchers described a condition called subclinical elastosis, in which these fibers become fragmented and disorganized. This weakens the skin’s ability to stretch and recover, making it more prone to bruises and injuries.
The researchers showed that corticosteroids interfered with fibroblasts—cells responsible for producing collagen and elastin. As fibroblast activity declined, the skin’s support framework deteriorated.
“Elastin metabolism is also significantly affected, leading to the accumulation of fragmented and nonfunctional elastic fibers, a condition referred to as subclinical elastosis,” said lead study author Alejandra Sataray-Rodriguez, of the University of Nevada Reno School of Medicine, and colleagues.
These changes can occur at a microscopic level prior to the emergence of any clinical signs of skin thinning.
Using high-resolution imaging tools—such as ultrasound, optical coherence tomography, and multiphoton microscopy—the researchers detected early elastin damage in the deeper layers of the skin. Ultrasound elastography, in particular, helped measure changes in skin stiffness. The researchers noted that softer skin may be an early sign of damage.
Electron microscopy confirmed that elastic fibers began to lose their structure within weeks of steroid use. Healthy, branching fibers became loose and tangled, further weakening the skin.
In a survey of over 6,500 glucocorticoid users, 80% reported weight gain, and skin thinning was among the most common complications. Fractures and cataracts were less frequent but clinically significant.
To address these effects, the study explored potential treatments. Antioxidants may reduce oxidative stress, while growth factors can stimulate fibroblast activity to restore collagen and elastin.
In animal studies, agents like tretinoin and rapamycin prevented steroid-induced thinning, pointing to possible future therapies for humans.
The researchers emphasized early detection and regular monitoring. Since subclinical changes can occur prior to symptom onset, imaging technologies may help clinicians intervene before the damage becomes permanent.
Understanding subclinical elastosis could guide long-term care planning among patients receiving steroids. Early intervention and combination therapies may allow continued treatment while minimizing skin-related side effects.
The authors declared no conflicts of interest.
Source: Dermis
