Managing Skin Side Effects Associated With Oncology Treatments: Asian Perspective on Use of Dermocosmetics

ABSTRACT

Skin adverse events (AEs) frequently accompany all types of anticancer treatments. The type and course of these skin AEs with different cancer treatments have been described and may be considered to generally have a similar pattern in differing world regions. However, some populations, including Asian populations, may have presentations that vary somewhat based on skin sensitivity and other factors. Education of both healthcare professionals and patients about how to identify, prevent, and manage these skin AEs is imperative in this era when not only is cancer on the rise but also there are longer life expectancies due to new, improved treatment approaches. Maintaining a good quality of life is a key target in oncology management, and skin AEs can have a profound effect on patient comfort, patient self‐image, and psychological ability to cope. Today, proactive skincare regimens, including dermocosmetics, can be put in place to minimize potential for AEs. If skin AEs occur, dermocosmetics may be employed alone or to augment the effects of medical treatments. Optimally, cancer patients should be managed by a multidisciplinary team with knowledge of skin and treatment‐related AEs. This publication discusses how recent international guidance on best‐practices use of dermocosmetics can be adapted to the North Asia region (China, Hong Kong, Japan, Republic of Korea, and Taiwan).

Skin adverse events (AEs) frequently accompany all types of anticancer treatments. This publication discusses how recent international guidance on best‐practices use of dermocosmetics can be adapted to the North Asia region (China, Hong Kong, Japan, Republic of Korea, and Taiwan).

1. Introduction

There is a wide and rapidly expanding variety of systemic anticancer treatments, including conventional chemotherapy, targeted therapies, immunotherapy, and hormonal therapies. All types of anticancer treatments are associated with adverse events (AEs), including a large proportion of skin AEs [1, 2, 3]. Examples include those associated with epidermal growth factor receptor inhibitors (EGFR‐I), which encompass acneiform rash, xerosis (sometimes with pruritus), paronychia, fissures, and trichomegaly [2, 4]. A recent study of Chinese patients (n = 266) treated with the tyrosinase kinase inhibitor fruquintinib showed that hand‐foot skin reaction (HFSR) was the second most common treatment‐related AE, occurring in 49.3% of patients [5]. Further, a relatively high proportion (10.5%) of those patients had AEs that were serious (grade 3 or higher) [5]. Currently, the majority of cancer patients (up to 93%) develop skin AEs associated with their cancer treatment and a large proportion experience treatment interruption (as exemplified by the finding that up to 76% of doctors treating patients with EGFR‐I have to decrease the dose of EGFR‐I, most of the time temporarily, and 32% discontinue treatment) [2, 6]. More recently, it was reported that over 50% of cancer patients experience an interruption in therapy secondary to dermatologic adverse events [7].

Not only have a variety of new drugs entered the market, but the number of patients also treated for cancer has risen at an average of 5% over the past 5 years, with more marked increases in some areas of Asia [1]. Siegel et al. reported that in 2022, the global number of newly diagnosed cancer cases was 19.6 million, and 24.1% of those were in Chinese patients and 7.1% were in Indian patients [8].

While the majority of cancer patients are not referred to a dermatologist, multidisciplinary collaboration, including dermatologists and oncologists, has been shown to improve outcomes. Thompson et al. assessed the effect of dermatologic consultation on survival with checkpoint inhibitor‐associated AEs [9]. They found that patients referred to dermatologists were more likely to receive treatment for a skin AE (odds ratio 6.08, p<0.001), had longer progression‐free survival (p<0.001), and overall survival (p = 0.007) compared to patients who did not have a dermatologist referral [9]. More recently, Barrios et al. retrospectively analyzed all cancer patients at their institution for 6 months [10]. They reported a high likelihood of positive outcomes of skin AEs in patients being managed with targeted therapy as well as a reduction in recurrence of skin AEs [10]. Conversely, Yang et al. found that a delay or lack of identification of skin AEs was likely to lead to medication discontinuation [11].

This article presents the management of skin‐associated AEs in Northern Asia, based on literature review and a consensus meeting of physicians (both dermatologists and oncologists) with an expertise in this area from five regions: China, Hong Kong, Japan, Republic of Korea, and Taiwan. Individual countries have published guidelines for specific AEs, but to our knowledge, there has not yet been a consensus publication intended to highlight how management of skin AEs may be similar and different in this area of the world. There is increasing awareness that skincare regimens, including dermocosmetics, can offer benefit in this setting, both as a preventative strategy and to directly manage some skin problems (alone or as adjunct to medical therapies). It is also increasingly important for healthcare professionals to be aware of the psychological effects of skin problems and to educate cancer patients in methods of caring for their skin that can minimize the toxicities of anticancer therapies and maximize quality of life (QOL). In many cases, gentle cleansing, proper moisturizing, and skin barrier repair utilizing products that are alcohol free, ceramide, and lipid containing, and formulated for sensitive skin should be standard of care in the field of oncology.

2. Understanding Skin AEs in Oncology

Generally, in cancer therapy, the primary goal is to achieve optimal dosing of the anticancer treatment while keeping treatment interruptions to a minimum. However, a very high proportion (up to 93%) of cancer patients experience some form of treatment‐related AEs [2, 12, 13]. Further, most (85%) are not referred to a dermatologist.

It is important to be aware of the expected timing/onset of AEs (which is quite variable); AEs with EGFR‐I and the FRESCO (Fruquintinib Efficacy and Safety in 3+ Line Colorectal Cancer Patients) study are presented as examples. With EGFR‐I, papulopustular eruptions may occur in the early phase of treatment (starting from initiation of treatment and peaking at week 4 with a gradual taper afterward), xeroderma starting at week 2 and gradually increasing in likelihood over the course of treatment, paronychia starting around week 5 and increasing in likelihood, and hair abnormalities starting at approximately week 8 of treatment [2, 4]. The phase 3 FRESCO trial of AEs associated with fruquintinib in Chinese patients with metastatic colorectal cancer reported that hypertension, HFSR, and proteinuria can all start any time after the first treatment cycle; hypertension was shown to occur in approximately 50% of patients at a likelihood that remains stable throughout treatment cycles, HFSR starting at 30% and rising to over 50% by the sixth cycle of treatment, and proteinuria starting at approximately 30% and decreasing in likelihood with repeated treatment cycles [5]. Thus, timing of the appearance of skin AEs can be variable and prevention/management strategies should be adapted to this awareness.

Table 1 presents information about specific skin AEs, which are also illustrated in the cases below [14].

TABLE 1.

Approaches to management of specific skin AEs.

Type of AE	Type of treatment	Proactive (prevention/step 0)	Reactive (management in case of AE)
Xerosis/pruritus	Targeted therapy (EGFR inhibitors, MEK inhibitors, FGFR inhibitors, BRAF inhibitors, PI3K inhibitors) Cytotoxic chemotherapy Radiation therapy Immune checkpoint inhibitors	Initiate at same time as cancer treatment Gentle cleanser close to skin pH with lipid replenishing ingredient Moisturizers, including moisturizers able to maintain diverse skin microbiome (emollient “plus”), with key ingredients such as shea butter, niacinamide, and/or ceramides Apply moisturizer to face, hands, feet, neck, and back daily plus reapply as needed	Gentle cleanser close to skin pH with lipid replenishing ingredient Emollients “plus” balm, able to rebalance microbiome Preferred formulas: moisturizing ointment and balms Urea 3–10% in case of severe xerosis, avoid in red/irritated areas and with radiation dermatitis Hydrating lip balms, preferably with sunscreen Fissures may occur
			If eczematous eruption: TCS/TCI once‐twice per day (maximum of 4 weeks for TCS) might be needed if pruritus uncontrolled by DC Antihistamines GABA agonist Doxepin/aprepitant/antidepressants TENS or acupuncture
Maculopapular rash a	Targeted therapy (BRAF inhibitors) Conventional chemotherapy Antimetabolites (5‐FU etc.) Alkylating agents (cyclophosphamide, cisplatin) Mitotic inhibitors (taxanes, vinca alkaloids) Immunotherapy (immune checkpoint inhibitors, anti‐Nectin 4)	Emollients “plus” balm, able to rebalance microbiome, with key ingredients such as shea butter, niacinamide, and/or ceramides Moisturizing lotion with key ingredients such as shea butter, niacinamide, ceramides Sunscreen with UV‐broad spectrum UVA/UVB filters to prevent possible PIH in darker phototypes	Continue Step 0 Camphor‐menthol‐hydrocortisone lotion/cream
			TCS (once‐twice per day for a maximum of 4 weeks) Oral antihistamines Oral corticosteroids for grade 3 toxicities Oncologist may suspend or alter treatment at grade 3; resume after 2 weeks if rash has faded to 0–1 Grade 4, admit to hospital
Acneiform rash	Targeted therapy (EGFR inhibitors including tyrosine kinase inhibitors, MEK inhibitors, mTOR inhibitors) Multikinase inhibitors Other anticancer treatments	Gentle cleanser with pH ∼5 Use light weight moisturizers (individualize to patient's preference) Sunscreen with UV‐broad spectrum (UVA/UVB) on all sun‐exposed areas. Patients with darker phototypes are at higher risk for PIH	Continue Step 0 Moisturizing cream and balms Barrier repair cream on face such as soothing balm, able to rebalance microbiome Acne dermocosmetics with niacinamide Sunscreen with UV‐broad spectrum (UVA/UVB) on all sun‐exposed areas. Patients with darker phototypes are at higher risk for PIH
		Oral doxycycline b (100 mg BID) or minocycline when using EGFR and MEK inhibitors	Be cautious using topical retinoids, BPO, and AzA Minocycline/doxycycline Topical corticosteroids after checking there is no local superinfection Systemic steroids c If not enough, oncologist may suspend or alter treatment
Photosensitivity	BRAF inhibitors EGFR inhibitors Multikinase inhibitors Vandetanib Chemotherapy (fluorouracil, dacarbazine, methotrexate, paclitaxel, vinblastine) Radiation therapy	Education for all patients due to higher innate risk for PIH in Asian populations Gentle cleanser with pH ∼5 Sun avoidance: especially direct sun at mid‐day a Sun protection when outside with UV‐broad spectrum UVB/UVA SPF 50 or greater sunscreens and strong UVA protection, especially with targeted therapy; clothing, sunglasses, and hats; patients with darker phototypes are at higher risk for PIH Avoid sun exposure/UV light exposure/indoor tanning Reapply sunscreen q2h Educate patient that sun can penetrate glass windows and in cloudy weather (home, car, workplace)	Continue Step 0 Cool colloidal oatmeal baths may help Soothing emollients Aloe vera
			NSAIDs, other painkillers Topical corticosteroids
Skin/nail pigmentation changes	Conventional chemotherapy Antimetabolites (5‐FU etc.) Alkylating agents (cyclophosamide, cisplatin) Mitotic inhibitors (taxanes, vinca alkaloids) Cytotoxic (bleomycin) EGFR/HER inhibitors Capecitabine Multikinase, checkpoint inhibitors MEK/BRAF/VEGFR inhibitors	Gentle cleanser with pH ∼5 Sun avoidance: especially direct sun at mid‐day a Sun protection when outside with UV‐broad spectrum UVB/UVA SPF 50 or greater sunscreens and strong UVA protection, especially with targeted therapy; clothing, sunglasses, and hats; Asian patients are at higher risk for PIH Reapply sunscreen q2h Opaque nail lacquers Avoid heat, humidity	Continue Step 0 Dermocosmetics containing niacinamide Nail laquer to strengthen nails and protect against UV Paronychia is the most prominent problem
			Topical corticosteroids Hydroquinone for hyperpigmentation (limited to 6 months of use max)
Inflammatory hand and foot syndrome	Conventional chemotherapy Liposomal doxorubicin Mitotic inhibitors (taxanes) Capecitabine (5‐FU)	Moisturizer with urea 10% d For doxorubicin and taxane infusions—cooling gloves/socks during infusions including 15 min before and 30 min after e	Continue Step 0 Moisturizing cream and balms Monitor for change in severity
		Optional Oral steroids for doxorubicin HFS, celecoxib for capecitabine f	TCS (once‐twice per day for a maximum of 4 weeks) including under occlusion Oral dexamethasone For capecitabine, on/off regimens can help reduce HFS Oncologists may reduce, interrupt, or discontinue treatment at higher grades
Hyperkeratotic HF reactions	Targeted therapy: RAS‐BRAF‐MEK‐ERK inhibitors, multikinase inhibitors	Gentle cleanser with pH ∼5 Moisturizer with urea (2−3 times per day) g Remove hyperkeratosis before the start of treatment (pedicure) Soft/padded footwear, avoid walking barefoot, avoid high heels	Continue Step 0 Topical urea‐based 10–40% emollient (2−3 times per day on hyperkeratotic areas) Refer to podiatrist if feasible Cautious pedicure without removing cuticle Avoid weight‐bearing exercise
		Clobetasol h	Lidocaine patches/cream (as needed for pain) Painkillers, NSAIDs Potent topical corticosteroids Oncologist may reduce, interrupt, or discontinue treatment at higher grades
Acute radiation dermatitis	Radiation therapy, enhanced by concomitant radiation therapy with chemotherapy or targeted therapy (especially 5‐fluorouracil and EGFR‐I) but not necessarily by checkpoint inhibitors	Cleanser with pH ∼5 Daily moisturizer a but not to be applied within 2 h before radiation therapy Sun protection when outside with UV‐broad spectrum UVB/UVA SPF 50 or greater sunscreens and strong UVA protection, especially with targeted therapy; clothing, sunglasses, and hats; Asian patients at higher risk for PIH Avoidance of skin irritants Sterile transparent film dressing from Day 1 through 1 week post‐radiation therapy (applied continuously)	Gentle skin care Zinc oxide for low infectious risk dermatitis (nonimmunosuppressed patients) Silvadene if risk of superinfection or refractory to OTC topicals Drying solution TID as drying/healing agent Lidocaine gel for pain Wound hydrogel pads for inflammatory reactions in regions that can support the pad without adhesive (such as inframammary fold) Medicated powder for initial moist desquamation also provides antifungal activity
		Mid‐potency TCS (betamethasone/mometasone, betamethasone is superior) once daily from Day 1 and throughout course	Mid‐potency TCS Monitor for secondary infection (culture and use oral antibiotic as needed) Antibiotics in case of superinfection Oncologist may interrupt treatment in case of grade 3 ulceration
Chronic radiation dermatitis	Radiation therapy, enhanced by concomitant radiation therapy with chemotherapy or targeted therapy (especially 5‐fluorouracil and EGFR‐I) but not necessarily by checkpoint inhibitors	Proper radiation therapy techniques Gentle cleanser with pH ∼5 Moisturizer Sun protection	Gentle skin care Educate patient about risk of late development of skin cancers in treated areas Thermal water Use dermocosmetic containing niacinamide for PIH
			Pentoxifylline 400 mg TID to prevent radiation‐induced fibrosis (in later part of radiation therapy or following development of fibrosis; use for at least 6 months as long as it is still improving the condition) Vitamin E (use with caution in patients taking anticoagulant or antiplatelet therapy)
Alopecia from chemotherapy	Conventional chemotherapy (alkylating agents, antimetabolites, mitotic inhibitors)	Scalp cooling for cytotoxic‐infused chemotherapy i Gentle shampoo Moisturizing cream	Ensure proper nutrition, use scarves, wigs, and synthetic hair fiber Scalp cooling (low evidence, use if patient wishes)
			Topical bimatoprost can be considered with eyelash loss
Alopecia from hormonal and targeted therapy	Aromatase inhibitors Kinase inhibitors: FGF, BRAF, CDK inhibitors Sonic hedgehog inhibitors Multikinase inhibitors	Gentle shampoo Moisturizing cream	Oral vitamins
			Topical 5% and oral minoxidil PRP for patients who cannot tolerate minoxidil Spironolactone
Hypertrichosis and trichomegaly	EGFR inhibitors	None	Hypertrichosis: cosmetic techniques, laser, epilation, threading Trichomegaly: eyelash clipping, referral to ophthalmologist

Note: Sun avoidance can depend on the region and individual patient variables.

Abbreviations: AE, adverse event; BID, twice daily; BRAF, BRAF gene; CDK, cyclin‐dependent kinase; DC, discontinuation; EGFR, epidermal growth factor receptor gene; ERK, extracellular signal‐regulated kinase; 5‐FU, 5 fluorouracil; FGF, fibroblast growth factor; FGFR, FGF receptor; GABA, gamma aminobutyric acid; HER, human epidermal growth factor receptor; HFS, hand foot syndrome; HFSR, hand‐foot skin reaction; MEK, mitogen‐activated protein kinase; mTOR, mechanistic target of rapamycin; NSAIDS, nonsteroidal anti‐inflammatory drugs; OTC, over the counter; PI3K, phosphoinositide 3‐kinase; PRP, platelet‐rich plasma; q2h, every 2 h; RAS, renin angiotensin system inhibitor; SPF, sun protection factor; TCI, topical calcineurin inhibitor; TCS, topical corticosteroids; TENS, transcutaneous electrical nerve stimulation; TID, three times daily; UV, ultraviolet; VEGFR, vascular epithelial growth factor.

^a Warning—Check that rash is not a cutaneous toxicity that would necessitate drug interruption, viral infection, or relapse of previous skin condition. Avoid oral steroids for maculopapular rash >grade 3 without a dermatology consultation.

^b Can cause photosensitivity.

^c In extreme cases, which occur rarely in clinical practice.

^d With doxorubicin and antimetabolites; may use higher percentage depending on patient response.

^e When using doxorubicin and taxanes, Bun et al. Support Care Cancer 2018.

^f When using capecitabine in colorectal patients.

^g May use higher percentage depending on patient response.

^h With multikinase inhibitor regorafenib.

ⁱ Contraindications: hematologic cancers and cancers of head/neck, those receiving platinum‐based therapy due to cold sensitivity.

Source: Adapted from Dreno et al. [14].

2.1. Cases: Asian Patients

2.1.1. Case 1. Skin AEs in Patient With History of Dermatologic Disease

The patient (male, 65 years of age) was diagnosed with lung cancer in September 2023 and treated with paclitaxel, carboplatin, and nivolumab. The patient had a 10‐year history of dermatitis and eczema. He experienced worsening pruritus and a forearm rash after the first treatment. Lung surgery was performed in December, and the same medical anticancer treatment was repeated twice after surgery. Pruritus continued to worsen with the development of diffuse papulonodular erythema with desquamation over the whole body.

Treatment with topical propionate cream twice a day, and oral olopatadine hydrochloride 5 mg twice a day was initiated. The pruritus resolved rapidly and the visual analog score (VAS) decreased from 7 at initiation to 3 after 14 days of the treatment.

2.1.2. Case 2. Vitiligo of Hands Associated With Immunotherapy

A 70‐year‐old male was referred to the dermatology service for multiple hypopigmented macules widespread on for the whole body since the past several weeks. The patient had been diagnosed with esophageal cancer in 2016 and experienced relapses after surgery and chemotherapy. Treatment with PD‐1 combined with capecitabine was initiated in August 2019. In February 2020, the patient had multiple hypopigmented macules and patches which affected approximately 7% of his body surface area, including his hands, as shown in Figure 1. The patient received topical treatment with halometasone cream (a high‐potency topical corticosteroid) and pimecrolimus cream (a calcineurin inhibitor). After 1 month, the progression of the vitiligo lesions was successfully controlled and some of the lesions were repigmented.

FIGURE 1.

Vitiligo on hands of patient treated with immunotherapy for esophageal cancer.

2.1.3. Case 3. Drug‐Induced Bullous Polymorphous Erythema Associated With Immunotherapy

A 66‐year‐old male consulted a dermatologist for diffuse targetoid erythema and bulla of 2 weeks duration. The patient was diagnosed with nasopharyngeal cancer with cervical lymph node metastasis in December 2023. He accepted an immune‐chemotherapy treatment regimen, including sindilisumab, paclitaxel liposome, and cisplatin. After two treatment cycles, targetoid erythema and bulla appeared rapidly throughout the body along with fever, joint pain, and mucosal erosion (Figure 2). Laboratory examinations revealed ENA‐SSA positive (+), anti‐Dsg1, Dsg3, BP180, and BP230 antibodies negative (−). The skin histopathology revealed subepidermal blisters, epidermal degeneration and necrosis, liquification, and degeneration of basal cells. The diagnosis of generalized bullous erythema multiforme was made. The patient was treated with intravenous methylprednisolone (at an initial dose of 60 mg), intravenous immunoglobulin, and plasmapheresis, leading to a gradual improvement 10 days after hospitalization.

FIGURE 2.

Patient treated with immunochemotherapy who developed bullous polymorphous erythema multiforme.

2.1.4. Case 4. Radiation Dermatitis

A 69‐year‐old male patient was diagnosed with nasopharyngeal carcinoma (cT1N2M0). After two cycles of induction therapy (Taxel, nedaplatin, and sintilimab), he started radiotherapy (planned dose 69.96 Gy on nasopharyngeal region and cervical lymph nodes) concurrent with chemotherapy and EGFR inhibitor (nedaplatin + nitolizumab). He displayed symptoms of radiodermatitis grade 2 on week 4 (Figure 3). He was treated with gentle cleansing of the affected area and application of water‐in‐oil type hydrophilic moisturizers to maintain skin hydration. In addition, he was instructed to use topical steroids 1–2X/day as needed for 2 weeks after radiotherapy.

FIGURE 3.

A) Grade 2 radiodermatitis in 60‐year‐old male during treatment for nasopharyngeal carcinoma. (B) Progression to grade 4 radiodermatitis. (C) Patient after radiodermatitis lessened.

As the radiotherapy increased, the severity of his radiodermatitis increased to grade 4 on week 6. At that time, anticancer treatments, including chemoradiotherapy and EGFR inhibitor, were suspended, and antimicrobial agents were initiated. In addition, GM‐CSF‐solution‐soaked gauze was applied at 40 µg/cm² twice a day (BID) along with silicone film‐forming gel or silver ion dressings. The patient continued the radiotherapy after 1 week break and finished the radiotherapy at week 8. One month after that, his radiodermatitis lessened, and he was advised to avoid friction and infection, as well as to incorporate active and passive exercises to improve mobility and reduce contractures.

2.1.4.1 Discussion

Actively intervening in the early stages of cancer treatment is an important period for preventing and treating skin AEs. Consultation with a multidisciplinary team, along with education, is important to provide standardized prevention and treatment methods for skin side effects related to antitumor treatment to reduce the occurrence and severity of skin side effects and improve patients’ QOL and ability to adhere to treatment.

2.1.5. Case 5. Papulopustular Rash Associated With EGFR‐I Treatment

A male patient with sigmoid colon adenocarcinoma (RAS and BRAF wild type) and multiple liver metastases was treated with panitumumab plus FOLFIRI. At initiation of treatment, he was provided with education for general skin care, including principles of photoprotection and skin hygiene. He was also given pre‐emptive topical and systemic antibiotics for 1 week to be used as prophylaxis (note that a longer duration may be needed for severe cases and multiple courses are frequently necessary with ongoing targeted therapy). However, the patient had poor adherence and did not use antibiotics nor any skincare regimen. Seven days after the first cycle of panitumab, the patient presented to the oncology team with diffuse acneiform eruption with pustules (Figure 4). The patient came to the outpatient department and was re‐educated about the need for self‐care. The rash was resolved at 1 month post EGFR‐I treatment.

FIGURE 4.

Patient with acneiform eruption and pustules (A) days after first cycle of EGFR‐I treatment and (B) at 1‐month post‐treatment after utilization of skincare regimen.

2.1.6. Case 6. Hand and Foot Syndrome Associated With Capecitabine Therapy

A 50‐year‐old Chinese man was treated with capecitabine‐based chemotherapy after resection of colorectal carcinoma. He developed palmoplantar xerosis, scaling, and irritation a few weeks after chemotherapy, which was heavily disturbing his daily activities (Figure 5). Medical management for the patient included twice a day use of a moisturizer with 10–20% urea plus a gentle cleanser, along with education to avoid irritants to hands and feet (physical, chemical, etc.). He was also prescribed topical corticosteroids and a short course of oral prednisolone. A calcineurin inhibitor was instituted as maintenance and the patient was advised to use a hypoallergenic body cleanser.

FIGURE 5.

Hand foot syndrome associated with capecitabine therapy.

2.1.7. Case 7. Pustular Eruption Associated With Radiotherapy

A 20‐year‐old female with glioblastoma was treated with surgical excision of the tumor and postoperative radiotherapy. A few days after the initiation of radiotherapy, multiple pruritic erythematous pustules developed on the irradiated site and surrounding skin. Histology showed it was eosinophilic and polymorphic (Figure 6). Antihistamine and topical corticosteroids were prescribed, and the eruption was resolved after 2 weeks.

FIGURE 6.

Patient with glioblastoma who developed multiple pruritic erythematous pustules.

3. Role of Dermocosmetics in Managing Skin AEs

There is increasing evidence in the medical literature that the use of dermocosmetics as adjunct to systemic cancer treatments can improve outcomes by reducing skin AEs and improving QOL [12, 14, 15, 16]. It is thought that dermocosmetics have a variety of positive actions in skin, including reducing inflammation, phototoxicity, and autoimmune responses, as well as supporting skin barrier function. It is important to implement dermocosmetics with a proactive approach, since skin AEs can occur within days after the first treatment and it is challenging to identify patients at higher risk [14]. In a 2023 international consensus, Dreno et al. recommend the use of emollients on the body—especially upper and lower limbs (use a gentle moisturizer with urea if the patient has dry skin or a tendency to dry skin), incorporate a non‐alcohol‐based cleanser (neutral pH of approximately 5), use sunscreen as appropriate, avoid irritating and drying environmental factors, and consider clear nail gel or topical antiseptic for nail hygiene [14].

In 2010, Lacouture and colleagues conducted the 6‐week STEPP (Skin Toxicity Evaluation Protocol with Panitumumab) study to compare outcomes in patients randomized to a pre‐emptive skincare regimen and those who incorporated skincare in a reactive manner (after skin AEs had appeared) [17]. The pre‐emptive regimen consisted of moisturizer daily in the morning, sunscreen, a topical steroid at night‐time, and doxycycline 100 mg BID [17]. The incidence of grade 2 or higher skin AEs was 29% in the pre‐emptive group compared with 62% in the reactive group (a >50% lower occurrence of skin AEs for the pre‐emptive group) [17]. Further, not only was QOL less impaired in the patients in the pre‐emptive versus reactive groups, time to onset of skin AEs was delayed in the pre‐emptive group versus reactive [17]. In 2014, Wohlrab et al. conducted a cross‐over study involving the use of a niacinamide‐based emollient and showed significant improvements in VAS scoring of pruritus/dryness when emollients were included versus not included (p<0.05) [18]. This was also reflected in the symptoms/feeling subscale of Dermatology Life Quality Index, which was superior in the emollient group after week 4 [18]. Similarly, Luftner et al. utilized a 12‐product skincare kit in 147 patients in five countries and found that regular users of skincare were significantly less likely to have skin AEs at the start of chemotherapy (p = 0.029) [19]. In a 12‐week study, Ren et al. reported that 10% urea‐based cream used pre‐emptively was associated with a reduced incidence of HFSR as well as a delay in onset of HFSR when it did occur (compared with control group) [20]. Berger et al. had similar results with the use of a skincare kit at initiation of radiation therapy; skincare users had significantly less likelihood of skin reaction within first 10 days of treatment and a higher opinion of both treating physician and benefits of products [21, 22].

There are several current regional guidelines for anticancer drug supportive management, including the ISKIMO, EADV Task Force, guidelines from Taiwan, China, and Japan, and a Korean guideline for management of radiation dermatitis. In 2023, a survey was conducted with Chinese cancer patients and oncologists that investigated the prevalence of cutaneous adverse reactions among cancer patients and its impact on their psychological and physical health. In 2024, a similar survey was conducted with dermatologists to deep dive on current clinical management patterns of oncology skin side effects in China. In addition, the international consensus published by Dreno et al. provides a stepped approach to skin AE management.

Japan has created a consensus management guidance for skin disorders induced by EGFR inhibitors by a panel, including dermatologists, oncologists, pharmacists, and nurses [23]. This group created a grading system to assess the severity of symptoms for xerosis, acneiform rash, paronychia, keratosis/fissure, and hand‐foot syndrome [23]. In addition, the group reached a consensus on the most appropriate treatments and skincare regimens [23]. They note that EGFR inhibitors cause skin symptoms in a specific sequence while targeting cancer cells [23]. They also underscore the importance of collaborative teams involving dermatologists, oncologists, pharmacists, and nurses in managing skin issues from cancer therapies [23]. It is important to develop and utilize treatment algorithms to guide the multidisciplinary team on recommended medical approaches and when a dermatologist referral is needed.

3.1. Management of Specific Skin AEs: North Asia Consensus Update

All oncology patients should be educated about what skincare routines they should follow during oncology treatment. The patient should be made aware of what may happen in the skin during and after each cancer treatment, know a basic routine (cleansers, moisturizers, sun protection), as well as avoiding hot water, manicures, and tight shoes (depending on the treatment). They should be informed about how to prevent and treat the most frequent skin AEs and when to seek medical help. Further, the entire oncology team should be educated about both the most frequent skin AEs, preventive measures, and when to encourage patients to seek dermatologic treatment. We recommend the utilization of mild cleansing and skin barrier supporting emollient use. These factors may be particularly important for Asian patients, who may have more sensitive skin and are at higher risk for post‐inflammatory hyperpigmentation (PIH). For patients with history of select skin diseases (multiple moles, previous skin cancer, psoriasis, atopic dermatitis, androgenetic alopecia/alopecia areata), referral to a dermatologist before initiation of anticancer treatment can often be helpful. As seen previously, patients treated with immunotherapy may develop or have worsening psoriasis, those with atopic dermatitis may need to exercise extra caution with skincare routine to prevent flares of disease and eczema, those with androgenetic alopecia may be refractory to scalp cooling or may have worsening of alopecia after chemotherapy or hormonal therapies.

4. Conclusions

In conclusion, skin AEs are a clinical challenge and increasingly important in the realm of cancer treatment. We recommend that patients and healthcare professionals be continuously educated about how skin AEs can manifest in the setting of anticancer treatment including novel treatments, and that we adopt a proactive integrative approach to preventing/minimizing the potential for skin AEs during treatment.

Funding

Funding for editorial support provided by Cosmetics Active International, La Roche Posay, a L'Oreal company.

Patient Consent

All patients provided consent for their images to be used in an educational publication.

Conflicts of Interest

Pan, Sun, Chu, Kawashima, Kim, Chun, Liang, and Chang have served as advisors to L'Oreal. Dreno has served as consultant/received honoraria from Bristol Meyers Squibb, Almirall, Galderma, La Roche Posay, Pierre Fabre, and Bioderma. Kerob is an employee of L'Oreal.

Data Availability Statement

The authors have nothing to report.