Creative Touch Permanent Makeup and Aesthetics

Topical steroid withdrawal (TSW) is a drug-related dermatosis that develops following the cessation – or sometimes the continued use – of medium- to high-potency topical corticosteroids (TCS) after prolonged application, characterised by burning, erythema, and barrier dysfunction that typically exceeds the original condition being treated. Also referred to as topical corticosteroid withdrawal, red skin syndrome, or topical steroid addiction syndrome, TSW is a condition that sits at an important junction in both clinical and aesthetic practice: it is increasingly formally recognised – NIH researchers proposed diagnostic criteria in 2025 – yet remains underdiagnosed, frequently misattributed to worsening eczema, and deeply distressing for the clients who experience it. ^[9] In aesthetics practice, clients presenting with TSW require a specifically adapted approach: standard interventions indicated for atopic dermatitis are not straightforwardly transferable, and the condition’s relationship with barrier biology, neurogenic inflammation, and immune dysregulation makes it one of the most mechanistically complex presentations a practitioner will encounter.

Topical corticosteroids have been a first-line treatment for atopic dermatitis and other inflammatory skin conditions for over six decades. Used appropriately – at the correct potency, for defined durations, with planned withdrawal – they are effective and safe. The problem arises with prolonged use, particularly of mid- to high-potency formulations on sensitive sites: the face, flexures, and genitals. In these contexts, a pattern of tachyphylaxis develops – the clinical effect of a given dose diminishes over time, requiring escalating potency or frequency to achieve the same suppression – followed, on cessation, by a rebound response that is frequently more severe than the original condition. This is TSW: not simply a return of the underlying disease, but a physiologically distinct withdrawal state driven by mechanisms that are now increasingly well characterised.

Recognition and the Diagnostic Landscape

TSW has historically occupied contested ground. Patient advocacy communities – particularly the International Topical Steroid Addiction Network (ITSAN) and the UK’s Scratch That – have documented and publicised the condition extensively for over a decade, whilst parts of the medical establishment have been slower to formalise it, citing the difficulty of distinguishing TSW from severe rebound eczema and the absence of agreed diagnostic criteria. ^[10] That picture has shifted materially. EuroGuiDerm guidelines now reference corticosteroid addiction syndrome as an adverse effect of prolonged TCS use; the American Academy of Dermatology updated guidelines acknowledge TSW; and in June 2025, NIH researchers published proposed formal diagnostic criteria – a development that marks the transition of TSW from a contested patient-reported phenomenon to a condition with clinical formalisation underway. ^[9]

The honest framing for this entity is that TSW is real, increasingly recognised, and mechanistically grounded – and that the gap between patient experience and medical acknowledgement has narrowed significantly in the last three years, though diagnostic standardisation is still in progress. ^[10] Clients presenting with TSW symptoms deserve to have the condition named and taken seriously, not reflexively reattributed to their underlying eczema.

Mechanisms: Why TSW Happens

Two converging mechanisms are currently the best-supported explanations for TSW, and they operate at different levels of the skin’s biology.

Nitric oxide rebound vasodilation. Topical corticosteroids exert a vasoconstrictive effect on superficial dermal blood vessels – the blanching response used in vasoconstriction assays to assess TCS potency. With prolonged use, the vasculature adapts: nitric oxide synthase (NOS) activity in the vessel wall is upregulated as a counter-regulatory response to sustained vasoconstriction. On cessation of TCS, the vasoconstrictive signal is removed but the compensatory NOS upregulation persists – producing a rebound vasodilation, the intense erythema, heat, and flushing that characterises the early TSW presentation. ^[7] This is most pronounced on the face and genitals, where the vasculature is most superficial and TCS absorption highest – explaining the characteristic distribution of TSW.

Keratinocyte cortisol suppression. A parallel mechanism operates at the keratinocyte level. Keratinocytes are not simply passive targets of topical corticosteroids – they synthesise their own glucocorticoids locally, producing cortisol through an intracrine pathway involving 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Prolonged exogenous TCS application suppresses this local cortisol synthesis: the keratinocyte downregulates its own steroidogenic capacity in the presence of sustained exogenous supply. On TCS cessation, the keratinocyte’s intrinsic cortisol production capacity remains suppressed – leaving the epidermis without the local anti-inflammatory and barrier-regulating cortisol signal it would normally generate, independent of the systemic HPA axis. ^[12] This contributes to the prolonged barrier dysfunction, inflammatory hypersensitivity, and impaired recovery that outlast the initial vasodilatory rebound – and explains why TSW can persist for months to years rather than resolving quickly once the vasodilation settles.

Barrier disruption as perpetuating mechanism. Superimposed on both is the direct effect of prolonged TCS use on the skin barrier itself. High-potency TCS suppress ceramide synthesis, reduce filaggrin expression, and thin the epidermis through reduced keratinocyte proliferation – effects that persist beyond cessation and leave the TSW skin with a compromised stratum corneum that is both highly susceptible to TEWL and hypersensitive to topical products, including emollients that would normally be well tolerated. This emollient intolerance – widely reported in TSW patients and listed in the DermNet clinical features – is one of the most practically challenging aspects of TSW management and one that conventional eczema management frameworks, which emphasise aggressive emollient use, do not adequately address. ^[2]

Clinical Presentation

TSW presents with a characteristic symptom cluster that distinguishes it, in most cases, from a simple return of underlying atopic dermatitis – though the distinction can be genuinely difficult in practice, particularly in the early phase.

The cardinal features are burning skin (rather than itch as the primary sensation), erythema extending beyond the original eczema distribution, and a timeline that worsens in the days to weeks following TCS cessation rather than simply returning to the pre-treatment baseline. ^[7] Burning pain and erythema are the two most consistent features across all patients; their co-presence following TCS cessation in a patient with a history of prolonged high-potency TCS use is the primary diagnostic pointer.

Two subtypes have been identified: erythematoedematous TSW, characterised by redness, swelling, and burning – more common in patients with underlying atopic dermatitis; and papulopustular TSW, characterised by papules, pustules, and erythema – more common following TCS use for cosmetic or acneiform indications, and typically without the burning or stinging of the erythematoedematous form. ^[3]

Pathognomonic signs documented in the clinical literature include: ^[2] * Elephant wrinkles – thickened, reduced-elasticity skin with characteristic wrinkling, typically on extensor surfaces * Red sleeve sign – erythema covering the limbs but sparing the palms and soles * Headlight sign – facial erythema sparing the nose and perioral skin * Serous ooze and desquamation – exudate and widespread shedding during the acute phase

Systemic symptoms are not uncommon in moderate to severe TSW, and their presence is important for distinguishing TSW from localised eczema flare. Fatigue, sleep disturbance, mood disturbance and depression, shivering, lymphadenopathy, and weight loss have all been reported – with fatigue documented in 79% of adults and lymphadenopathy in 57% in one large patient cohort. ^{[6] [3]} In severe or prolonged cases, hypoadrenalism – suppression of the systemic HPA axis through prolonged high-potency TCS use – can contribute to weakness, low blood pressure, and systemic symptoms that sit beyond the skin entirely. ^[5]

In more pigmented skin tones, the characteristic erythema may present as darkened or grey-brown discolouration rather than red, and the condition has historically been under-recognised in darker skin types as a consequence. Fitzpatrick type-aware assessment is important in TSW recognition across the full client population.

The TSW Timeline

Recovery from TSW is genuinely protracted, and honest communication about this timeline is one of the most clinically important things a practitioner can offer. The literature consistently describes a recovery arc measured in months to years rather than weeks. ^[2]

The broad phases, while individual in their timing, follow a recognisable pattern:

Acute phase (weeks 1–12): The most intense period – peak erythema, burning, oozing, and desquamation. Emollient intolerance is often at its most pronounced. Systemic symptoms, if present, tend to peak here. Skin feels hypersensitive to almost everything, including water temperature, clothing, and airflow.

Stabilisation phase (months 3–12): The acute intensity reduces but intermittent flares continue. The skin begins to cycle – periods of relative calm followed by flares that may last days to weeks. The distribution often begins to contract toward original eczema sites. Sleep and systemic symptoms typically improve. Some clients begin to tolerate a basic skincare routine again.

Recovery and remodelling phase (months 6–36+): Progressive reduction in flare frequency and severity. Barrier function gradually rebuilds. The timeline varies considerably with prior duration and potency of TCS use – clients with years of high-potency facial TCS use may experience a longer recovery arc than those with shorter-duration use of lower-potency preparations.

The variability in recovery duration is one of the most distressing aspects of TSW. Recovery is the trajectory for the majority of patients who cease TCS use, but the timeline is individual and cannot be predicted with precision.

Management of TSW

TSW management is an area where the evidence base is still developing and where the aesthetics practitioner’s role is supportive rather than primary. The fundamental intervention is cessation of TCS use – there is no management of TSW that involves continuing the causative agent. Beyond that, the approach is largely symptom management and barrier support, with emerging evidence for several targeted interventions.

Dupilumab. The most significant pharmacological development in TSW management is the emerging evidence for dupilumab – the IL-4Rα antagonist established for atopic dermatitis – as a bridge therapy during TSW. The rationale is mechanistically sound: dupilumab addresses the Th2-driven inflammatory component of the underlying AD that may be sustaining and amplifying the TSW response, without the vasoconstrictive and cortisol-suppressive effects of TCS. Case series and retrospective chart reviews suggest meaningful benefit in TSW patients, with reductions in erythema, itch, and flare frequency. ^[8] This is not yet RCT-level evidence, but the mechanistic rationale and accumulating clinical observation make it the most evidence-adjacent pharmacological option currently available. Clients on or being considered for dupilumab for TSW should be under the care of a dermatologist; this is not aesthetics-clinic territory to initiate.

Barrier support. Re-establishing the stratum corneum is a central management goal – but the emollient intolerance that characterises TSW means the standard AD approach of aggressive moisturisation cannot be directly applied. Many TSW patients find that thick emollients, fragranced products, and products containing common sensitisers provoke burning and flushing rather than relief. ^[2] The practical approach is to start minimal – unfragranced, low-ingredient formulations, introduced cautiously, at times when the skin is in a calmer phase rather than a flare. Ceramide-containing preparations, when tolerated, are the most mechanistically rational choice given the TCS-driven ceramide synthesis suppression that contributes to the barrier deficit.

Wet wrap therapy. Modified wet wrapping – using water-soaked layers over minimal emollient – provides cooling relief and transient TEWL reduction during the acute phase for some patients, without the need for TCS under the wraps as in conventional eczema protocols.

Lifestyle and systemic support. Sleep deprivation is both a consequence and an amplifier of TSW – impaired sleep reduces NK cell activity and barrier repair capacity simultaneously. Temperature regulation, breathable clothing, and reducing friction load on affected skin are practically important rather than cosmetically incidental during the acute phase.

What is not recommended: Reasserting TCS use to manage the withdrawal response – however tempting as short-term relief – resets the withdrawal cycle and prolongs recovery. Immunosuppressants such as ciclosporin and methotrexate are sometimes used in severe cases under dermatological supervision; these are outside aesthetics practice scope entirely. ^[8]

Cold Atmospheric Plasma in AD and TSW

This is where the distinction between what the evidence establishes and what the mechanistic rationale supports needs to be handled with particular care.

Cold Atmospheric Plasma for Atopic Dermatitis: The Evidence Base

Cold Atmospheric Plasma (CAP) has accumulated a meaningful evidence base for AD specifically – more than for most aesthetic applications – because AD’s three primary pathogenic drivers (immune dysregulation, barrier disruption, and Staphylococcus aureus colonisation) each map onto mechanisms that CAP is known to address.

A 2021 prospective comparative pilot study of CAP in atopic dermatitis – the most clinically grounded human evidence available – found significant improvements in EASI score, SCORAD, modified ADAS, and pruritic VAS scores after three CAP sessions compared to controls, alongside a significant reduction in the proportion of S. aureus in skin microbiome sampling. ^[4] This is not a large RCT, but it is human clinical data with objective outcome measures – a meaningful step above the case series and in vitro data that characterises much of the CAP literature.

A 2023 review in the Karger journal International Archives of Allergy and Immunology specifically addressed CAP as a therapeutic strategy for AD, concluding it was both promising and safe, and identifying three mechanistic pathways through which it addresses AD pathogenesis: ^[1]

• Immune modulation – CAP suppresses Th2-associated cytokines including IL-4, IL-13, and IL-31 (the primary itch-driving cytokine in AD) through RONS-mediated signalling, shifting the inflammatory environment away from the Th2 polarisation that perpetuates AD
• Barrier repair – CAP reduces TEWL, upregulates tight junction proteins, and supports keratinocyte proliferation and differentiation, addressing the structural deficit at the core of AD pathogenesis
• Antimicrobial activity – CAP reduces S. aureus colonisation directly through RONS-mediated bactericidal activity; S. aureus is present on the skin of over 90% of AD patients and its superantigen activity amplifies Th2 inflammation, meaning microbial reduction has an anti-inflammatory effect beyond the direct killing

A January 2026 preclinical study comparing helium and argon CAP against topical corticosteroid control in a DNCB-induced AD mouse model found that both plasma types reduced IL-13, IL-31, and IL-12 – with reductions comparable to or exceeding the TCS control in some cytokine profiles. ^[11] This is preclinical, but the direct comparison with TCS as a reference standard is a significant framing: CAP is not being positioned as an adjunct but as a potential steroid-free alternative.

CAP for TSW Specifically: Mechanistic Rationale Without Established Evidence

For TSW specifically, there are no published clinical trials as of early 2026. The evidence base is currently practitioner-observed and mechanistically reasoned – and honesty about this distinction is both clinically necessary and a YMYL strength rather than a limitation.

The mechanistic case for CAP in TSW is, however, genuinely strong:

Barrier repair without steroids. The defining management challenge in TSW is supporting barrier recovery without returning to TCS. CAP’s documented ability to reduce TEWL and support keratinocyte differentiation addresses the same barrier deficit that TCS would conventionally treat – through a completely different mechanism that does not involve glucocorticoid receptor activation, vasoconstrictive adaptation, or keratinocyte steroidogenesis suppression. It is a steroid-free route to some of the outcomes that TCS was being used to achieve.

NF-κB suppression and SASP attenuation. CAP suppresses NF-κB-driven inflammation – the same mechanism relevant to the SASP discussion in the Cellular Senescence entity – reducing the pro-inflammatory cytokine environment in treated tissue without glucocorticoid signalling. For TSW skin, where the inflammatory response is dysregulated and TCS suppression is no longer available, a non-steroidal anti-inflammatory mechanism at the tissue level is directly relevant.

Th2 cytokine suppression. The established CAP effect on IL-4 and IL-13 – the same cytokines that drive filaggrin suppression and perpetuate the barrier-immune cycle in AD – addresses the immune component of TSW that dupilumab targets pharmacologically, at a tissue-localised level and without systemic exposure.

Antimicrobial activity. S. aureus colonisation, already elevated in AD, tends to worsen during TSW as the barrier collapses further. CAP’s bactericidal activity against S. aureus is one of its most consistently demonstrated effects – reducing the colonisation that amplifies inflammation without the antibiotic resistance concerns associated with prolonged topical antibiotic use.

The honest calibration: These are mechanistic arguments supported by CAP’s AD evidence, not by TSW-specific clinical trials. They provide a rational basis for carefully applied CAP in TSW clients – and they are the arguments a practitioner can make with intellectual honesty. Claims beyond this – that CAP is an established treatment for TSW – would overstate the current evidence and do a disservice to clients who deserve accurate information.

Any use of CAP in TSW is, at present, off‑label and should be framed as supportive, not as an established treatment.