Chronic eczematous eruptions of aging: a clinical practice review

Introduction

The clinical expression, differential diagnosis, and optimal treatment of chronic eczematous skin disorders vary according to age of skin disease onset. Chronic eczematous dermatoses that present initially in the geriatric age group have been among the least well understood and studied. Such aging-onset dermatoses can carry substantial morbidity through sleep disruption and impaired daily function, underscoring the need for a pragmatic diagnostic framework tailored to later-life onset (1-3). Chronic eczematous eruption of aging (CEEA) has previously been used within a singular context (4). Here, we would like to introduce the clinical concept of chronic eczematous eruptions of aging (CEEsA) as a group designation for the various eczematous skin disorders that present later in life to focus more attention and needed research in this area.

Incomplete standardization of terms is not merely semantic. It can confuse patients and clinicians and complicate case identification and interpretation in the electronic health record, driving diagnostic delays, mismanagement, and increasing utilization (5-8). By defining CEEsA and integrating epidemiologic, drug-exposure, and targeted-therapy evidence into a practical diagnostic and treatment algorithm, this review reframes a common but underrecognized eruption in older adults. The approach enables rapid exclusion of mimickers, prompts antihypertensive medication review, and prioritizes low‑risk biologics over broad immunosuppression, with goal of shortening diagnostic delays, improving itch-related quality of life, reducing polypharmacy-related harm, and lowering healthcare costs.

The ambiguous nomenclature of eczematous skin diseases

The nomenclature of eczematous skin disorders displaying spongiotic dermatitis on skin biopsy is often confusing to non-dermatologist clinicians. Furthermore, international consensus regarding the nomenclature of spongiotic dermatoses remains elusive among dermatologists and allergists. An example is the differential usage of the designations “atopic dermatitis” and “atopic eczema” for the same clinical/pathologic/etiologic dermatologic entity (6). As will be discussed later, we will use the designation atopic dermatitis (AD) as we prefer not to use the morphologic designation, eczema, in a nominal sense for reasons discussed below.

To understand the causes and optimal management of eczematous skin disorders, one must first understand the traditional morphologic nomenclature used in this area.

Itchy rashes are one of the most common reasons why older people seek dermatologic care (9). The lay public and non-dermatology clinicians often refer broadly to red, scaly, pruritic rashes as eczema. However, a high percentage of such rashes are found by dermatologists to be clinical manifestations of various types of eczematous dermatitis (“dermatitis” simply meaning inflamed skin).

The unqualified clinical designation, eczema, is used widely in clinical medicine and the medical literature without a universally agreed upon definition. The word “eczema” is derived from the Greek word meaning “to boil over”. This was a reference to the vesicular, moist, crusted appearance of the skin in certain itchy red rashes. It is now known that those rashes share a common pattern of immune-mediated inflammation on skin biopsy—spongiotic dermatitis.

Thus, the designation eczema had its historical roots in the clinical appearance of endogenous and exogenous pruritic inflammatory skin conditions rather than signifying a specific dermatologic diagnosis. As such, we agree with other North American clinicians that the unqualified term eczema should not be used in modern medicine as a noun to identify any specific dermatologic disorder (8). However, we feel that the qualifying designation eczematous (as in eczematous dermatitis) does have value in referring to inflammatory skin conditions that share common morphologic skin changes and display spongiotic dermatitis on biopsy. However, as noted above, diagnostic subtypes of eczematous dermatitis such as “AD” continue to be referred to as “atopic eczema” by international clinicians.

Interestingly, the root designation eczema refers only to the clinical appearance of the acute temporal phase of eczematous dermatitis (Figure 1). The primary acute, exudative, wet, and crusted (“boiling-out”) phase of eczematous dermatitis is soon replaced by the subacute phase of eczematous dermatitis. In subacute eczematous dermatitis, the acute eczematous skin changes have evolved into an ill-defined red scaly rash appearance (Figure 2). In chronic eczematous dermatitis skin conditions, the subacute phase of eczematous dermatitis has been replaced by the thickened, scaly, pruritic skin (Figure 3). An alternative clinical designation for chronic eczematous dermatitis is lichen simplex chronicus.

Figure 1 A clinical example of the less frequently seen intense, vesiculobullous, “boiling-out” phase of acute eczematous dermatitis resulting from poison ivy-induced allergic contact dermatitis (A), alongside the more commonly seen, less-intense phase of poison ivy-induced allergic contact dermatitis (B). Previously published photos reproduced here with permission from website moderator www.poison-ivy.org.

Figure 2 A clinical example of subacute eczematous dermatitis in an aging male of unknown cause, possibly representing a case of aging-onset atopic dermatitis. A version of the clinical image in this figure was published in our earlier work and is reprinted here with permission of the publisher, the American Medical Association.

Figure 3 A clinical example of chronic eczematous dermatitis. When present unabated over long periods of time, subacute eczematous dermatitis can evolve into chronic eczematous dermatitis. This is in part due to a patient’s persistent scratching and rubbing resulting from the extreme pruritus caused by spongiotic dermatitis inflammation. This clinical pattern of chronic eczematous dermatitis can be referred to as nummular eczematous dermatitis or lichen simplex chronicus depending on the clinical context. This image is published with the patient/participant’s consent.

It should be noted that all eczematous spongiotic skin conditions share ill-defined borders. And, all three temporal phases of eczematous dermatitis are distinctively very pruritic. The intense pruritus can disturb sleep and significantly alter quality-of-life.

Patients typically present to a clinician during the subacute or chronic phase of their eczematous skin problem rather than during the initial wet, boiling-out, crusting acute phase. Patients frequently initiate self-treatment with over-the-counter topical agents prior to seeking professional evaluation. Some chemicals in such self-treatments can produce a superimposed allergic contact dermatitis (similar to poison ivy) that can greatly complicate the clinical situation. Upon realizing that such treatments are not going to work, individuals then seek professional help.

Chronic eczematous eruptions of aging

In the past, the various eczematous skin disorders that appear initially in aging individuals have been referred to in the literature under various confusing designations. Those include immunologic eruption of aging, eruption of immunosenescence, AD in the elderly, eczema in the elderly, and adult-onset eczema (10). Until recently there has been no effort to systematize this nomenclature.

In 2007, a group of French investigators reported that chronic eczematous eruptions of the elderly can be induced by a hypersensitivity response to chronic exposure to calcium channel blocker drugs (11). This observation was in agreement with our clinical experience in caring for senior individuals having chronic, extremely-pruritic, upper-body, non-flexural, therapeutically-refractory eczematous eruptions. In a follow-up study, we were able to confirm that chronic calcium channel blocker therapy can produce a reversible, drug-induced eczematous eruption in aging individuals (1). In addition, our study found that long-term treatment with thiazide diuretics can also trigger a drug-induced eczematous eruption in aging individuals.

The various other designations used in referring to individuals in the latter phase of life are felt by some to be pejorative and ageist. Examples include: elderly, older, senile, senior, and old, among others (12). As such, we felt that the designation CEEsA might serve as a more acceptable and productive designation for the various clinical forms of eczematous dermatitis that present in the aging phase of life (Table 1). In this review, we summarize the published literature on individual CEEsA entities and highlight areas in gerontologic dermatology that require further study.

It has been our clinical experience that in some patients with aging-onset eczematous dermatitis no specific underlying cause can be identified. Others have reported that in 25% to 47% of their CEEsA study populations, no identifiable cause could be identified (13,14). We have previously used the designation idiopathic chronic eczematous eruption of aging (idiopathic CEEA) for one such patient who had an extremely good clinical response to dupilumab therapy (4). However, one could argue that such patients could also be categorized as having the intrinsic form of aging-onset AD. Our group has previously presented a proposed criteria set for the diagnosis of idiopathic CEEA (4).

Drug-induced CEEsA

In the authors’ experience, drug-induced CEEA is one of the more common entities under the CEEsA umbrella. We will outline the typical clinical presentation and management of a drug-induced CEEA patient seen in our clinics.

It is not uncommon for aging individuals (arbitrarily defined here as those 60 years of age and older) to present to their clinicians for an extremely itchy red rash of several months’ duration predominately involving the skin of their arms and trunk, but typically sparing their face. Upon questioning, patients often say that the rash first appeared on the extensor aspects of their forearms.

The physical exam reveals a patchy ill-defined subacute or chronic eczematous dermatitis as previously described. Such patients have typically self-treated with one or more over-the-counter treatments without lasting benefit (e.g., topical antibiotics, topical corticosteroids, topical anti-itch preparations).

Other patients who initially saw their primary health care providers for their rash were often given a prescription-strength topical corticosteroid or a combination of topical corticosteroid and antifungal drugs that did not help. Some patients might have seen other clinicians who treated them with non-steroidal topical treatments including pimecrolimus and/or tacrolimus that also did not provide significant relief.

Patients having extreme pruritus might have been given short-term, burst-and-taper oral or intramuscular corticosteroid therapy. While patients do get temporary relief, the pruritic skin changes characteristically return after such systemic corticosteroid therapy has been withdrawn. Such patients are then referred to a community-based or academic dermatologist.

When a lesional skin biopsy is obtained for histopathology, the dermatopathologist reports the presence of spongiotic dermatitis +/− an eosinophilic infiltrate or eosinophilic spongiosis. Occasionally, the skin biopsy can show both a spongiotic and interface dermatitis.

Such patients often have a history of hypertension and are typically on one or more antihypertensive medications such as thiazide diuretics, calcium channel blockers, angiotensive converting enzyme (ACE) inhibitors, and beta blockers. In this setting, patients and their healthcare providers typically do not think that their antihypertensive medications could be causing their skin problem since the patients have been taking those medications for months or years previously without difficulty. When the concept of immunosenescence is explained, they are more accepting.

Immunosenescence is the concept that aging causes a decline in the function and efficiency of the normal immune system (15). It is known that older individuals have higher rates of autoimmune disorders and allergic conditions including drug allergies. While the exact mechanisms are not known, it is thought that the aging process causes a relative decline in the immune tolerance side of the immune response. Thus, while foreign antigens such as drug molecules might be tolerated by a younger immune system, a less tolerant aging immune system could result in drug allergy (16).

Our research group initially became interested in drug-induced CEEA. Joly and coworkers used the designation chronic eczematous eruptions of the elderly in a 2007 report suggesting that such gerontologic rashes were associated with chronic exposure to calcium channel blocker drugs (11). Subsequent work from our group supported this clinical association and extended it by reporting a significantly positive association with hydrochlorothiazide (1,2). As aging individuals are frequently taking multiple drug classes simultaneously, our group attempted to identify a biomarker for specific drug classes that might be inducing a drug-induced CEEA in the setting of polypharmacy. Unfortunately, like the efforts of many prior investigators, our efforts in this area proved unhelpful (2).

In a recent large study of antihypertensive medications in older adults with eczematous dermatitis, the association of calcium channel blockers and thiazide diuretics with eczematous drug eruptions in aging individuals was confirmed (17). In this study cohort of 1,561,358 older adults {mean [SD] age, 67 [9] years; 54% female}, the prevalence of eczematous dermatitis during a median follow-up duration of 6 years was 6.7%. Incidence was higher among those participants receiving antihypertensive drugs compared to those who did not (12 vs. 9 per 1,000 person-years). Participants who received any antihypertensive drugs had a 29% increased hazard rate via adjusted Cox proportional hazards models of any eczematous dermatitis [hazard ratio (HR), 1.29; 95% confidence interval (CI): 1.26–1.31], “with the strongest associations seen for diuretics (HR, 1.21; 95% CI: 1.19–1.24) and calcium channel blockers (HR, 1.16; 95% CI: 1.14–1.18).

When drug-induced CEEA is suspected, we work with the patient’s other health care providers to have the suspected triggering drugs stopped for a period of at least 6 weeks but no later than 12 weeks. If the patient’s eczematous skin changes have not significantly improved or resolved by then, the suspected triggering drugs can be restarted. At that point, other aging-onset eczematous disorders should be considered (see Table 1).

It is our feeling that drug-induced CEEA is a very important clinical issue, as a simple change in triggering medication classes can completely resolve the clinical process and avoid the risks and costs of systemic immunomodulatory therapy. However, there is a caveat. When the triggering drug class cannot be safely withdrawn, as in the case of cancer treatment, treating the symptoms of the drug-induced CEEA would be appropriate. If the pruritus is severe or disabling, one could consider treatment with dupilumab and/or nemolizumab.

Some have questioned the clinical benefit of withdrawing or substituting a drug that is triggering a chronic eczematous drug eruption in aging individuals. In one study, the question of clinical utility versus possible harms of drug cessation was addressed (18).

In this study, drug cessation trials were performed in 40 of the study cohort of 89 CEEsA participants. The suspected candidate drug classes that were withdrawn were statins, calcium channel blockers, angiotensin-converting enzyme inhibitors, salicylates, thiazides, proton pump inhibitors, angiotensin receptor blockers, and beta-blockers. Based on the results of this study, the authors concluded that the clinical benefits of candidate drug cessation did not justify the risks of worsening the study subjects’ underlying medical conditions. Unfortunately, there were several aspects of this study that could challenge the authors’ conclusions.

As previously discussed, only calcium channel blockers and thiazide diuretics have been shown to have a statistically significant causal association with CEEsA (1). The study in question included six other candidate drug classes, potentially leading to inappropriate cessation of necessary therapy and worse outcomes.

In addition, the timeframes of observation for clinical improvement following drug cessation were quite variable. In approximately 35% of the drug cessation studies, the observation period was either unknown or less than 1 month. It has been our experience that improvement and clearance require an observation period of at least 6 to 8 weeks, with potentially up to 12 weeks for complete resolution. We agree with the authors that further studies are needed in this area.

Adult-onset AD

AD encompasses a broad clinical domain of medicine. A PubMed search in March 2025 identified over 41,000 publications on AD (search terms: “atopic dermatitis OR atopic eczema”), reflecting the extensive literature on this condition. Historically, AD was viewed primarily as a pediatric disorder, but it is now recognized that disease onset can occur during adulthood and even in older age.

Adult-onset AD is a relatively new concept, and its recognition has been accompanied by a surge in publications—possibly driven in part by the advent of effective targeted therapies such as dupilumab (approved in 2017 for moderate-to-severe AD in adults). Previously, any AD flares in adults were often assumed to be recurrences of childhood-onset disease; however, it is now well-established that some patients experience their first onset of AD in adulthood or even late in life. Because many studies on “adult-onset” AD do not distinguish between mid-adulthood and later-life onset, some insights into aging-onset AD must be extrapolated from broader adult cohorts.

Adult-onset AD is generally defined by initial disease onset after approximately 18 years of age. Epidemiological data indicate that this subtype represents a significant subset of the AD population. Recent studies report that roughly 26% of adults with AD experienced symptom onset during adulthood, with some cohorts suggesting adult-onset rates as high as 54% (19-21). Overall, AD affects an estimated 7–10% of adults in the United States, and 2–17% of adults internationally, depending on the population studied and diagnostic criteria applied (20,22). The recognition that a substantial proportion of AD cases begin in adulthood challenges the traditional paradigm of AD as chiefly a pediatric condition.

Clinically, adult-onset AD often presents with patterns that differ from those of childhood-onset disease. It tends to involve the head, neck, and hands as predominant sites, with relatively less classic flexural involvement (19,20,22). Adult-onset cases may also follow a more chronic, treatment-refractory course compared to early-onset AD (19,22,23). Moreover, lesions in adult-onset AD can be morphologically atypical—often nummular, prurigo-like, or lichenoid in appearance—which complicates clinical recognition and may lead to initial misdiagnoses (19,22). This variability in presentation underscores the need for heightened clinical awareness and possibly refined diagnostic criteria tailored to adult-onset disease (22,23).

Currently, there are no diagnostic criteria specifically validated for adult-onset AD, so diagnosis relies heavily on clinical judgment and the exclusion of other etiologies (21,24). Historically, the Hanifin and Rajka (H-R) criteria have served as a diagnostic gold standard for AD across all ages; however, the H-R criteria were developed with pediatric patients in mind and emphasize early onset and flexural dermatitis—features that are less applicable to adult-onset cases (19,24). Similarly, the United Kingdom Working Party criteria weight early-onset and flexural manifestations, potentially reducing their sensitivity in adult presentations (21,24). As a result, clinicians must carefully exclude other eczematous conditions that can mimic AD in adults, such as allergic contact dermatitis, chronic actinic dermatitis, cutaneous T-cell lymphoma, or psoriasis (21,24). Patch testing is often recommended in cases of adolescent- or adult-onset AD to identify occult contact allergens that might either masquerade as AD or coexist with it (21,24). Skin biopsy can provide supportive evidence (e.g., spongiosis with acanthosis and eosinophilic infiltration), but these histopathologic features are non-specific and overlap with other dermatitis types (21,24). Thus, a thorough clinical history, focused physical examination, and judicious use of patch testing, biopsy, and laboratory studies remain essential for accurate diagnosis of adult-onset AD.

The epidemiology of adult-onset AD shows considerable variation across different populations. Higher prevalence rates have been reported in Western countries compared to some Asian populations, though these differences may reflect variability in study methodologies or diagnostic criteria as well as underlying environmental factors (19,25). Importantly, the incidence of new AD cases does not plateau after childhood but continues into adulthood and appears to increase again in later life. A distinct subset of patients experience late-onset AD, with initial disease onset after approximately age 50, and this older presentation is increasingly recognized as a meaningful clinical entity (21,23). In geriatric populations, features such as age-related xerosis, chronic pruritus, and other forms of eczematous dermatitis (e.g., asteatotic eczema) can overlap with or mask AD, creating diagnostic challenges (10). These observations highlight the importance of considering AD in the differential diagnosis of eczematous dermatitis even among older adults.

Gender differences observed in AD also appear to shift with age. While female predominance is typical in childhood-onset AD, the gender distribution in adult-onset disease is more balanced, and some studies even report a slight male predominance among patients with late-onset AD (23,26). Adult-onset AD additionally exhibits a distinct risk factor profile compared to childhood-onset disease. For example, a personal or family history of atopy (allergic rhinitis, asthma, or infantile eczema) is less common among adult-onset patients, whereas environmental and lifestyle factors have been implicated as triggers for disease onset in adulthood (21,22). Occupational exposure to irritants or allergens, as well as migration from a rural to an urban/industrialized environment, are examples of factors that might precipitate AD in predisposed adults (21,22). Together, these data demonstrate that adult-onset AD represents a significant and clinically distinct component of the broader AD spectrum. It warrants further investigation into its unique risk factors, triggering events, and natural history across the life course, as well as the development of age-tailored management strategies.

Aging-onset AD

Aging-onset AD is a recent and evolving clinical concept. As previously mentioned, adult-onset AD appears to increase with age. And population-based data demonstrate that the proportion of new AD cases occurring in adulthood is particularly high in older adults, with late-onset AD, specifically onset after age 50 years, representing a distinct clinical entity (2,11). And, some adult-onset AD studies even suggest a slight male predominance in older adults (11,27).

Like adult-onset AD, aging-onset AD tends to involve extensor surfaces more than flexural surfaces, whereas childhood- or adolescent-onset AD more often shows the opposite pattern. As such, chronic lichenified eczematous dermatitis of the antecubital and popliteal fossae is less common in aging-onset AD than in early-onset AD. Generalized upper body prurigo lesions are characteristically seen in aging-onset AD.

Facial skin is characteristically spared in aging-onset AD, further distinguishing it from early-life onset AD. This also distinguishes it from another chronic skin change that affects aging men, chronic actinic dermatitis. The face is characteristically affected in chronic actinic dermatitis.

Like earlier life-onset AD, aging-onset AD can present in both intrinsic and extrinsic forms. As such, the presence of elevated Immunoglobulin E (IgE) blood levels would favor extrinsic aging-onset AD over the other CEEsA entities (see Table 1).

As in early life-onset AD, aging-onset AD patients have been observed to have sensitivity to aeroallergens, especially dust mites. And, it has been suggested that erythroderma is more common in aging-onset AD compared to AD presenting earlier in life.

Other CEEsA

There are several other pruritic eczematous dermatoses that can present in a manner similar to drug-induced CEEA and aging-onset AD (see Table 1). These differential diagnostic entities should be ruled out before a diagnosis of aging-onset AD is made.

Management of CEEsA patients

The first step in the management of CEEsA should be to establish a specific diagnosis whenever possible. Only then can the optimal treatment strategies be formulated.

Our first step in evaluating a new patient with CEEA is to perform a total-body skin examination. If the history shows subacute or chronic eczematous skin changes on the lower legs and/or feet as well as the arms and trunk, we first consider tinea pedis or stasis dermatitis with an autoeczematization reaction. A history of the eczematous skin changes first appearing on their legs and/or feet would support one of these mimicking skin disorders.

If the anatomic distribution of the patient’s eczematous skin changes was more suggestive of scabies, we would then perform a scabies prep and/or initiate a clinical trial of oral ivermectin. If the history and examination suggest allergic contact dermatitis, patch testing should be considered, particularly for allergens that may contact both arms and the trunk, such as disperse dyes in new sportswear.

Next, a lesional punch skin biopsy for hematoxylin and eosin (H&E) could address the possibility of cutaneous T-cell lymphoma. In addition, a peri-lesional biopsy specimen for direct immunofluorescence exam could address the possibility of non-bullous/prodromal bullous pemphigoid. Alternatively, blood tests for basement membrane zone autoantibodies could be ordered.

Once those mimicking eczematous skin conditions have been ruled out, we would then address the possibility of a drug-induced CEEA as previously described. Potentially reversible forms of CEEsA, such as drug-induced CEEA, should be excluded before traditional broad-spectrum immunosuppressants or newer targeted agents are used, in order to avoid unnecessary adverse effects and cost.

Using traditional broad-spectrum systemic immunosuppressive drugs (e.g., corticosteroids, methotrexate, azathioprine, cyclosporine, mycophenolate mofetil) in aging individuals can be challenging. Complications can include drug interactions due to polypharmacy, age-related decline in renal function, nonalcoholic fatty liver disease, and altered hepatic metabolism. As such, modern targeted therapy could possibly be a safer and perhaps even more effective treatment strategy.As previously mentioned, patients with drug-induced CEEA and aging-onset AD tend to be refractory to traditional topical and systemic immunomodulatory therapy. As such, there has been interest in the possibility of modern targeted immunomodulatory therapy being able to fill this need.The spongiotic pattern of skin inflammation that underlies eczematous skin disorders is known to be driven by Th2 helper cytokine overexpression. Interleukin (IL)-4 and IL-13 are two such key cytokines. Dupilumab was the first-in-class monoclonal antibody that blocked both IL-4 and IL-13 (28). After its federal drug administration (FDA) approval for moderate-to-severe adult AD in 2017, dupilumab has proved to be a highly beneficial medication for disabling adult-onset and childhood/juvenile-onset AD patients. And dupilumab has proven to be a relatively low risk drug in adults and children with respect to adverse effects.Thus, the question arose: could dupilumab be safe and effective in treating moderate-to-severe aging-onset AD? Pharmaceutical clinical trials of new drugs characteristically exclude aging individuals. As such, virtually all of the published experience on this question has been anecdotal.In 2018, treatment with dupilumab of an aging male with refractory idiopathic CEEA produced a rapid and dramatically good clinical response (4). In 2020, 15 consecutive aging-onset AD patients were treated with dupilumab. A rapid and highly effective clinical response was seen in all 15 patients without major adverse effects (29). Subsequently, 30 more aging-onset AD patients were described as having equally good clinical responses to dupilumab therapy (30,31). Tralokinumab, an IL-13 inhibitor, has also been reported to produce similarly favorable responses in individual cases of aging-onset AD (32). Likewise, a small-molecule Janus kinase (JAK) inhibitor, upadacitinib, has been reported to produce good clinical responses in small case series (33).

Conclusions

CEEsA represent a spectrum of eczematous dermatitis in aging adults that often pose diagnostic and therapeutic challenges. By recognizing CEEsA as a distinct category—which includes entities such as drug-induced eczematous dermatitis and aging-onset AD—clinicians can adopt a more systematic approach: excluding mimickers, identifying reversible causes, and utilizing newer targeted therapies when appropriate. Embracing the term CEEsA may reduce ambiguity in nomenclature and encourage further research into the unique pathophysiology and optimal management of eczematous dermatoses in the geriatric population.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://atm.amegroups.com/article/view/10.21037/atm-25-142/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-25-142/coif). R.D.S.’s research career has been supported by a Dermatology Foundation Fellowship, a National Institutes of Health (NIH) Clinical Investigator Award, an NIH Research Career Development Award and an NIH R01 Research Grant, “Mechanisms of Cutaneous Injury in Lupus Erythematosus” (AR19101). In addition, his research career was supported by funds from the John S. Strauss Endowed Chair in Dermatology at the University of Iowa Carver School of Medicine and the Fleischaker Endowed Chair in Dermatology at the University of Oklahoma School of Medicine. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.Written informed consent was taken from all the patients.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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