Topical steroid rebound phenomena (TSRP), commonly known as topical steroid withdrawal (TSW), red burning skin syndrome or steroid dermatitis, has been reported in people who apply topical steroids for 2 weeks or longer and then discontinue use. Symptoms affect the skin and include redness, a burning sensation, and itchiness, which may then be followed by peeling.

This condition generally requires the daily application of a topical steroid for more than 2 weeks but sometimes can occur with even less steroid use. It appears to be a specific adverse effect of topical corticosteroid use. People with atopic dermatitis are most at risk.

Treatment involves discontinuing the use of topical steroids, either gradually or suddenly. Counselling and cold compresses may also help. Thousands of people congregate in online communities to support one another throughout the healing process, and cases have been reported in both adults and children. It was first described in 1979.

Before discontinuation, steroid dermatitis is characterised by spreading dermatitis and worsening skin inflammation, which requires a stronger topical steroid to get the same result as the first prescription. This cycle is known as steroid addiction syndrome. When topical steroid medication is stopped, the skin experiences redness, burning, itchiness, scabs, hot skin, swelling, stinging, hives, or oozing. This is known as topical steroid withdrawal. After the withdrawal period is over, the atopic dermatitis can cease or is less severe than it was before. Topical steroid withdrawal has also been reported in the male scrotum area. Other symptoms include nerve pain, insomnia, excessive sweating, anxiety, depression, fatigue, eye problems, and frequent infections.^{[citation needed]}

The duration of acute topical corticosteroid withdrawal is variable; the skin can take months to years to return to its original condition. The duration of steroid use may influence the recovery factor time, with the patients who used steroids for the longest reporting the slowest recovery.

To experience this withdrawal, it generally requires the misuse or application of a topical steroid daily for 2 to 4 months, depending on the potency of the topical corticosteroid. In some cases, this has been reported after as little as 2 weeks of use.

Historically, it was believed that cortisol was only produced by the adrenal glands, but research has shown that keratinocytes in human skin also produce cortisol. Prolonged topical steroid (TS) application changes the glucocorticoid receptor (GR) expression pattern on the surface of lymphocytes; a patient experiencing resistance to a TS has a low ratio of GR-α to GR-β. In addition, the erythema characteristic of ‘red skin syndrome’ is due to a release of stored endothelial nitric oxide (NO) and subsequent vasodilation of dermal vessels.

A 2025 pilot study by Shobnam et al. (n=16) reported that topical steroid withdrawal is associated with overexpression of mitochondrial complex I, leading to elevated NAD+ and the conversion of tryptophan into kynurenine metabolites; the authors also reported symptom improvement in an open-label series treated with mitochondrial complex I inhibitors. The findings have been the subject of academic correspondence in the United Kingdom. Brown and Burleigh argued in the Journal of Investigative Dermatology that the small sample size and underpowered analyses meant the proposed molecular and cellular mechanisms remained unexplained and warranted further research. In reply, Shobnam et al. agreed that larger studies are needed and that the diagnostic criteria lacked specificity, while maintaining that the work nonetheless provided initial mechanistic insights. A separate letter by Tan, Dawe and Affleck in Clinical and Experimental Dermatology raised concerns that recruitment through topical steroid withdrawal advocacy organisations introduced collider bias. In a 2026 narrative review in Frontiers in Medicine, Myles and Ratley defended the study design while acknowledging that biomarkers obtainable in standard clinical laboratories have not yet been identified and that the proposed mechanisms require validation in larger cohorts.