The Efficacy of Complementary and Alternative Medicines in Medical Dermatology: A Comprehensive Review

J Clin Aesthet Dermatol. 2025;18(2):E61–E79.

by Promise Ufomadu, BSA; Bartley Joseph Gill, MD, PhD; Ida Orengo, MD; Theodore Rosen, MD; and Ikue ShImizu, MD

Mr. Ufomadu and Drs. Gill, Orengo, Rosen, and Shmizu are with the School of Medicine at Baylor College of Medicine in Houston, Texas. Dr. Gill is also with the Department of Dermatology at Baylor College of Medicine in Houston, Texas, and Memorial Hermann Health Systems in Houston, Texas. Drs. Orengo, Rosen, and Shimizu are also with the Department of Dermatology at Baylor College of Medicine in Houston, Texas.

FUNDING: No funding was provided for this article.

DISCLOSURES: The authors declare no conflicts of interest relevant to the content of this article.

ABSTRACT: Background: In recent years, there has been a widespread patient use of complementary and alternative medicines (CAMs) for dermatological application, despite few RCT-level studies on these supplements. This creates a barrier for dermatologists and others in counseling patients who may be using or might be tempted to use these CAM agents. This review investigates various CAM modalities used by patients for medical dermatology, exploring their efficacy and toxicity profiles. Methods: A comprehensive review was performed on the effectiveness of several CAMs utilized in medical dermatology by patients. A literature search was conducted using PubMed, Embase, Google Scholar, Web of Science, and Cochrane. Results: Most CAM modalities had statistically insignificant results, and for agents that had significant results in efficacy, these studies were questionable with flawed designs and methodologies. Conclusion: These CAM supplements have promising potential in dermatologic use and are deserving of further investigation in well-crafted RCT-level studies. A more practical focus in future studies should involve a comparison of CAM agents to conventional therapies either alone or in an integrative fashion. This would accurately represent how these agents will be used clinically by actual patients and will be more helpful to clinicians. In the meantime, dermatologists should be aware of bias in published studies demonstrating the effectiveness of certain CAM modalities, and their corresponding toxicity. By doing so, physicians act as a valuable resource to patients who would like to explore various CAM products, better guiding patient interactions and treatment with improved patient outcomes.

Keywords: Complementary and alternative medicines, integrative dermatology, papulosquamous diseases, atopic dermatitis, acne

Introduction

The National Center for Complementary and Alternative Medicine (NCCAM) defines CAM as practices and products outside conventional medicine, with “Integrative Medicine” combining CAM and conventional therapies having demonstrated efficacy.^1,2 National surveys show 30 to 50 percent of adults use some CAM agents, with higher usage among women, the elderly, non-whites, immigrants, and lower/higher income groups.³ CAM usage is even greater (35–69%) among patients with dermatologic conditions such as atopic dermatitis or psoriasis, most commonly homeopathy, special diets, and herbs.⁴ Additionally, a National Health Interview Survey found that 85 percent of patients reporting skin problems use CAM products.⁵

Despite high patient usage, physicians of almost all disciplines lack CAM training, reporting unfamiliarity with efficacy and side effects.^6,7 While skeptical of efficacy, most physicians desire more CAM knowledge to counsel patients meaningfully.^7,8 Limited dermatologist data suggests similar attitudes. Nonetheless, greater CAM familiarity is quite important considering higher CAM usage among dermatological patients.^9,10 Awareness of effective CAMs allows counseling on integrative plans and watching for drug interactions and adverse effects. High dermatology CAM usage could also suggest unmet patient needs, so comprehensive CAM knowledge could improve physician-patient interactions.⁴

This review explores CAM therapies across dermatologic conditions with elucidated mechanisms, focusing on those with randomized, controlled trials (RCTs). The Jadad Scale, Table 1, will assess evidence quality to guide practitioners on potential CAM efficacy.¹¹ Adverse effects are also outlined for physician awareness of risks from unsupervised CAM use.

Atopic Dermatitis 

Traditional chinese medicine. Traditional Chinese herbal medicine (TCM), typically an extract of 10 herbs, was reported effective for atopic dermatitis (AD) in early 1990s RCTs.¹² In RCTs from Sheehan et al,¹³ children followed by adults participated in cross-over, four-week oral administrations of either TCM or placebo plants, and TCM improved skin damage and erythema compared to the placebo group;¹⁴ however, subsequent students had high withdrawal rates (only 40% of pediatric and 50% of adult patients continuing treatment) potentially due to lack of response.^15,16 

Proposed TCM mechanisms for AD in non-human studies include inhibitory effects on both mononuclear and mast cells,^17,18 modulating effects on dendritic cells/Langerhans cells,^19,20 and reducing IgE complexes with CD23+ cells.^21,22 However, actual use in human-RCTs, such as Fung et al,²³ found no improvement with the TCM product Zemaphyte®. Though some studies found significant results with TCM therapy, most studies have found mixed or limited benefits for TCM use in AD management.^24–29 

Serious adverse effects like hypersensitivity, organ toxicities, and contamination with heavy metals, steroids, or NSAIDs have been reported with TCM use.^12,30–33 Jadad scoring (Average 3.5) is complicated by herb heterogeneity, preparation variation, and use of differing subjective outcomes across studies. While most were well-designed RCTs suggesting evidence for improving visual AD severity, the quality is affected by small sizes, varied outcome measures, and potential subjectivity caveats.

Dietary: Fatty acids and probiotics.Alterations in fatty acid metabolism in AD patients may lead to deficiencies in anti-inflammatory metabolites like prostaglandin E1 and 15-hydroxy-eicosatrienoic acid.³⁴ RCTs examining supplementation with γ-linolenic acid (GLA) sources like borage, primrose, black currant seed, and fish oils (n-3 fatty acids) showed modest improvements in total area affected and pruritus with low incidence of adverse effects.^35–37 Unfortunately, such improvements were not statistically significant.

Probiotics, such as Lactobacillus, have been studied for managing AD in infants, children, and adolescents.^37–48 RCTs giving Lactobacilli alone or in combination to pregnant mothers and infants showed significantly reduced AD incidence (RR: 0.51);⁴¹ (OR: 0.51) for non-IgE-associated AD;⁴² (RR: 0.32) for breastfed infants.⁴³ Kalliomaki et al⁴⁴ follow-up studies demonstrated that positive benefits persisted up to age 7.⁴⁵ Proposed mechanisms include increased breast milk TGF-β2.⁴³ However, other RCTs utilizing probiotics have shown either mixed results or no effect at all.^46–48

These RCTs were generally well-designed (Jadad of 5), with low risk of bias, but some of the equally well-designed and executed trials showed no improvement in AD incidence. For treatment of previous diagnosed pediatric AD, RCTs, such as Boyle et al,⁴⁹ showed slight but non-significant symptom improvements with 6 to 12 week probiotic treatment; this is quite modest compared to current conventional therapy. Thus, while probiotics show some potential as a preventative intervention, their role as AD treatment has limited supportive evidence. Additional research is needed on specific strains of probiotics, dosing, and treatment duration for both preventative and therapeutic applications.

Other botanicals and non-botanical CAM modalities. Other botanicals studied for AD include St. John’s Wort (Hypericum perforatum) due to known anti-inflammatory and anti-bacterial effects. A small RCT (n=18) showed topical St. John’s Wort improved SCORAD scores versus vehicle placebo but lacked inter-group analysis.⁵⁰ Camomile cream demonstrated mild superiority over placebo.⁵¹ Licorice (Glycyrrhiza glabra) gel at 1 to 2 percent reduced subjective itch, edema, and erythema scores versus placebo in a reported RCT lacking report of precise methodological details (Jadad of 4).⁵² Arnica, Calendula, tea tree oil, and witch hazel propose anti-inflammatory mechanisms but lack RCT-quality evidence.⁵³ Some of these agents have been reported to cause allergic dermatitis from sesquiterpenes or GI toxicity with ingestion.^{12, 34, 54}

Non-botanical CAMs include homeopathy, mind-body interventions, and energy medicine (acupuncture and bio-resonance). There have unsurprisingly been a few reproducible RCT-level studies that have shown a positive effect of homeopathy in AD.^34,55 Mind-body RCTs showing efficacy had major design flaws.⁵⁶ More structured parent-adolescent educational mind-body programs demonstrated some efficacy.^56,57 Massage therapy reduced anxiety and AD symptoms in one study but lacked proper control group matching and blinding.^34,58 Acupuncture has proposed protocols but limited RCT evidence,^59–61 and bio-resonance has been promoted in case reports but lacks well-designed RCTs showing efficacy.⁶² Overall, most botanicals and non-botanical CAM therapies lack rigorous RCT support for AD treatment despite proposed anti-inflammatory mechanisms. More high-quality research is needed.

Papulosquamous Diseases: Psoriasis

Vitamins, minerals and other botanicals. CAM usage is prevalent (43–69%) among patients with psoriasis.⁶³ Limited RCTs exist for vitamins and mineral supplements studied in psoriasis. Well-designed RCTs found no benefit of zinc,^64,65 selenium,⁶⁶ vitamin D3,^67,68 or both vitamin B12 and avocado cream⁶⁹ on improving psoriasis. Some of these studies had questionable study designs, lack of blinding, manufacturer funding, and small sample sizes.⁶⁶ 

For botanicals, one RCT found 0.5% aloe vera cream improved undefined subjective endpoints versus placebo but lacked inter- and intra-group statistics.⁷⁰ Another well-designed left/right trial showed no significant topical aloe vera benefit for psoriasis.⁷¹ Neem supplementation significantly reduced psoriatic symptoms when compared to topical tar and salicylic acid therapy.⁷² The commercial 10% Mahonia aquifolium (berberine) product, Relieva, significantly decreased psoriatic symptoms with minor side effects (pruritus and burning) in a large RCT study.⁷³ While suggesting some efficacy, botanicals have only limited RCTs to support clinical use. Nonetheless, what trials do exist are generally of good quality (Jadad range of 3–5).

In summary, vitamins and mineral supplements lack therapeutic evidence for psoriasis treatment, while some botanicals like neem and berberine show promising potential. 

Fish oil (omega-3 fatty acids). Fish oil supplements, containing omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are commonly used as complementary psoriasis treatment. Proposed mechanisms involve inhibiting inflammatory arachidonic acid metabolites.⁶³ Multiple RCTs examined fish oil with or without concomitant therapy, with mixed findings. Some studies have shown benefits, such as reduced itching, erythema, and scaling with 10 capsules of daily fish oil⁷⁴ and modest symptom reductions with an oily fish diet⁷⁵ or EPA supplementation to etretinate.⁷⁶ Few RCTs also found decreased psoriasis severity scores with intravenous omega-3 fatty acids, but have had methodological limitations.^77,78

Other well-designed RCTs such as Gupta et al,⁷⁹ found significant reduction in disease severity when comparing fish oil to olive oil controls;however, there were no significant improvements with fish oil use when compared to betamethasone controls,⁸⁰ or purified omega-6 (corn oil) fatty acids.⁸¹ A left/right comparison trial showed benefits only on plaque scale and thickness but not itching and erythema, with the latter being important and relevant clinical endpoints.⁸²

Despite some studies with significant positive results, the overall evidence quality for fatty acids in psoriasis management is limited (average Jadad 3.6) due to issues like lack of blinding, high supplement burden, and lack of comparison to conventional treatments. 

Climatotherapy/balneotherapy.Climatotherapy (exposure to Dead Sea-like conditions) and balneotherapy have been studied as complementary psoriasis treatments. Dawe et al⁸³ performed a left/right comparison study with 12-week treatments of combined dead sea salt soaks and narrow-band UVB therapy compared to the phototherapy alone. Study findings showed mixed results; however, large well-designed multicenter RCTs showed significant improvement in achieving a 50 percent reduction of psoriasis severity score (PASI 50) both with low (5–10%) or high (25%) concentration saline baths complementing phototherapy over phototherapy-only.^84,85 Another study found phototherapy-complementary saline treatment significantly reduced disease severity score outcomes when compared to groups treated with tap water or psoralen-containing bath add-ons.⁸⁶

Alas, a host of other studies have not demonstrated as much success with climatotherapy: 30% dead sea salt lotion was ineffective;⁸⁷ saline baths provided no added benefit to phototherapy;⁸⁸ saline water and tap water baths had equivalent findings;⁸⁹ dead sea salt and common salt baths showed no significant difference between treatment groups.^90,91

Adverse effects like erythema, burning and pruritus occurred, increasing dropout rates. Lack of patient blinding to salinity introduces potential placebo effects. Despite mixed results, the large high-quality RCTs, such as Brockow et al,^84,85 suggest benefit for saline balneotherapy complementing phototherapy; however, an average Jadad of 3 was given due to lack of proper blinding with the added caution that such therapy may produce irritation.

Mind/body, meditation, and stress relaxation. Psychological stress has been implicated as an exacerbating factor in psoriatic flare-ups. Several studies have examined stress alleviation techniques as complementary treatments for psoriasis, with ambiguous findings. A small pilot RCT (n=18) found a significant but modest improvement with daily home meditation for scalp psoriasis.⁹² Kabat-Zinn et al⁹³ studied stress relaxation audio tapes during phototherapy, concluding improved treatment outcomes, but with inconsistent and unblinded endpoint scoring. Zachariae et al⁹⁴ used psychotherapy and relaxation tapes, finding a modest positive effect, but no significant difference in severity index scores or correlation between disease activity measures and stress levels. A similar RCT comparing relaxation techniques with and without biofeedback found improved patient-reported scores but no difference in blinded physician assessments.⁹⁵ Tausk et al⁹⁶ used hypnosis with and without suggestion, finding no difference in disease severity score change between hypnosis types, and also lacked an untreated control group. 

While these mind-body interventions show potential beneficial effects and no reported negative adverse effects, the overall quality of evidence for their effectiveness as complementary psoriasis therapy is minimal, primarily due to improper blinding, risk of bias, and mixed or insignificant results (average Jadad score of 3).

Contact Dermatitis

While a substantial proportion of allergic contact dermatitis patients report use of a CAM agent for treatment, upwards of 40 percent in one survey,⁹⁷ relatively few have been tested in clinical studies. One notable CAM modality that has been studied, however, is jewelweed (Impatiens biflora), first studied in a report from the 1950s where investigators found it comparable to conventional therapy in the treatment of poison ivy contact dermatitis.⁵⁴ Abrams Motz et al⁹⁸ claimed to confirm this efficacy in a non-blinded study when they observed that jewelweed mashes resulted in a decreased rash score following poison ivy skin exposure. However, the control used, water-only, did not account for any potentially beneficial non-pharmacologic properties of the mash, and outcomes were selectively emphasized as most results were on balance negative with no effect found using a purified jewelweed extract (vs. mash), no relationship was found between concentration of active ingredient, lawsone, and clinical response, and no added benefit was found between groups exposed to jewelweed-containing soaps compared to regular dish soap. These on-balance negative findings seem to be confirmed in two other studies. Long et al⁹⁹ performed a small but well-designed left-right RCT that compared the treatment of rashes derived from urushiol patches (combined poison ivy and poison oak) with jewelweed extract or water-only control and found no difference in blinded rash scores over 9 days. This confirmed negative result from an earlier observational study.¹⁰⁰ Therefore, there seems to be inconsistency between study outcomes, and a possible risk of bias in the positive study [Abrams], even though the average quality of the evidence (i.e. Jadad score) was a 4. 

Acne

Acne vulgaris. Given the high prevalence of acne, numerous CAM modalities have been suggested as potential treatments, but only a few have been studied through randomized controlled trials.¹⁰¹ Tea tree oil (TTO) has shown anti-microbial and anti-inflammatory effects, with one industry-sponsored study finding significant improvement with 5% topical TTO gel over placebo.¹⁰² These significant findings were consistent in another RCT;¹⁰³ however, another study (n=124) reported greater effectiveness of 5% benzoyl peroxide compared to TTO gel, though accompanied with increased dryness, and lack of proper blinding due to TTO’s distinct odor.¹⁰⁴ An average Jadad score of 3.7 was assigned to these studies.

RCTs on fruit-derived alpha-hydroxy acids (AHAs) like gluconolactone, glycolic acid, and azelaic acid demonstrated mixed results compared to conventional treatments (i.e. benzoyl peroxide and tretinoin), with concerns on study design and adverse effect assessment (average Jadad score of 4)^105–108 Needless to say, many practitioners employ glycolic acid peels to help with both active acne and post-inflammatory hyperpigmentation. A study on topical basil oil reported implausibly rapid improvement but lacked blinding details, and omitted key statistics.^109,110 RCTs on Japanese Kampo drugs and 2% green tea extract had major flaws like absent endpoint assessment and lack of controls.^111,112 However, a better-crafted study on green tea extract showed no significant results.¹¹³ Other agents with limited RCT-level evidence include pyridoxine, vitamin A, Indian Ayurvedic herbs, Nigerian toto, and shark liver extract, but their efficacy cannot be reliably evaluated due to insufficient RCT-quality evidence.

Acne rosacea. Given the frustration with conventional acne rosacea therapies and the potentially high cost associated with prescription medications, patients may turn to CAM treatments. Niacinamide (vitamin B3) has anti-inflammatory and sebum-reducing properties, along with the potential for improving keratin synthesis and keratinocyte differentiation.^114–116 An open-label study on a niacinamide-zinc product showed promise but lacked proper match controls.^114,117 Studies on zinc alone have demonstrated conflicting results, showing efficacy in Sharquie et al¹¹⁸ and no significant improvement in Bamform et al.¹¹⁹ Licorice (Glycyrrhiza) extracts demonstrated anti-inflammatory effects in vitro, but human trials to date have lacked controls and investigator/patient blinding.^120–122 Feverfew has anti-inflammatory and anti-oxidant activity but hasn’t been studied in published RCTs for rosacea.^123,124 Colloidal oatmeal has anti-oxidant and anti-inflammatory properties in-vitro and animal studies but no RCT-level human studies.^125,126 Green tea and coffeeberry (used for antioxidant polyphenols), aloe vera (for anti-pruritic effect), chamomile, turmeric, and mushroom extracts may be tried as alternative therapies but lack rosacea-specific clinical human studies.¹²⁷ A recent RCT examined tea tree oil (TTO) with permethrin, showing positive improvements, but the TTO-specific contribution could not be adequately assessed.¹²⁸ Despite the limited high-quality CAM studies for acne rosacea, the average Jadad score was 4.3, indicating reasonable study design and quality.

Alopecia

Alopecia areata. A few RCTs have been performed assessing CAM agents in the treatment of alopecia areata. Hay et al¹²⁹ studied a seven-month aromatherapy treatment with a combination of essential oils from thyme, rosemary, lavender, and cedarwood in a carrier with jojoba and grapeseed oil compared to a carrier oil-only control. The treatment group showed significant improvement in the primary outcome (subjective disease severity judging of photographs by two blinded physicians) and in the secondary outcome of affected area reduction (measured by tracings). It is unclear, however, if groups were well-randomized before the trial; no data is provided on baseline disease severity or area affected. Furthermore, primary outcome measures were intra-group with limited information provided as to how scores were “improved” and secondary outcomes of area affected were only measured in a small fraction of study participants with no explanation offered. Two other studies have been performed assessing topical treatment with onion and garlic for alopecia areata due to purported therapeutic effects of their constituent sulfur amino acid allicin.^130,131 While both studies report effectiveness, both suffer fatal design and methodological flaws. The onion study does not assess baseline randomization, does not describe the determination of “response” endpoint or its blinding, and critically, does not perform an intention-to-treat analysis to account for the substantial drop-out rate (~50%) in the treatment group.¹³⁰ The garlic study reports significantly better baseline data on patch sizes, terminal hair number, and total hair number in the treatment group, but does not address this randomization problem and proceeds with inter-group comparisons after three months of treatment.¹³¹ Several other CAM modalities have shown promise as alopecia areata therapies in isolated case reports or in small patient series, including hypnotherapy, massage and relaxation therapy, energy healing therapies (magnetic stimulation, acupuncture), and other biologics (vitamin A, TCM), but these have yet to be examined in an RCT-level study to properly analyze efficacy.^132,133

Androgenic alopecia. A few CAMs have also been examined in RCTs for effectiveness in androgenic alopecia. Kessels et al¹³⁴ examined a commercial product called Dabao composed of multiple different Chinese herbal extracts including saffron, Mulberry, sesame, ginger, and peppers. The authors conclude a modest, but statistically significant improvement of the product lotion over placebo in blinded hair counts and cosmetic evaluation by subjective panel evaluation. However, while the study was well-randomized and blinded, the statistics used to assess differences were inappropriate (one-sided t-test) and unclear (somehow analyzed the difference between inter-group means). Further, it is difficult to parse out the exact medicinal and mechanistic effect of a product containing dozens of botanicals. Takahashi et al¹³⁵ tested a topical application of the apple-derived procyanidin B-2 in a small study (n=29) due to purported polyphenol-related antioxidant effects.¹³⁵ This investigator group concluded strong effectiveness based upon improvements in total hair number per 0.25cm² area, increased ratio of large hairs, and subjective disease improvement. However, there was no change in one of their primary outcomes, overall hair diameter, and methodology on the areas from which hair counts were derived were not described. Furthermore, overall design was in doubt as there was no description of placebo-matching to ensure blinding and no baseline comparisons made between groups in the outcomes measured, a critical oversight as most changes were evaluated in an intra-group fashion. 

Many other CAMs have been tested in vitro, in animal studies, and in non-RCT level human studies for potential application in androgenic alopecia. Topical application of raspberry ketones derived from red raspberries (Rubus idaeus) may activate sensory neurons to promote insulin-like growth factor-I release and showed promising results in hair regrowth in mice and non-placebo-matched humans.¹³⁶ Several other botanical agents, mostly postulated to act through 5α-reductase inhibition-related mechanisms, have shown positive effects in animal studies including botanicals green tea-derived EGCG,¹³⁷ red ginseng (Panax ginseng C),¹³⁸ Cuscuta reflexa,¹³⁹ a polyherbal mixture of E. officinalis, C. asiatica and aloe vera,¹⁴⁰ and other herbal systems including traditional Thai herbal plants¹⁴¹ and Indian Ayurvedic herbs.¹⁴² Finally, Nioxin, a popular commercial system of shampoos, conditioners, and other topical products with multiple constituents including botanicals (tea extracts, peppermint oil, many others), vitamins, and amino acids is purported to help with a variety of causes of thinning hair.¹⁴³ However, no scientific studies (in vitro, animal, or human) solely investigating this agent have been published, assessing its efficacy in improving thinning hair or in treating any other form of alopecia.

Pigmentation Disorders: Melasma

Azelaic acid. Azelaic acid, a dicarboxylic acid, acts in melasma by competitive inhibition of tyrosinase, inhibiting melanocyte proliferation and decreasing reactive oxygen species formation.¹⁴⁴ Two RCTs tested a 20% topical formulation, with one study comparing it to a vehicle-only control¹⁴⁵ and the other combining it with glycolic acid and comparing it to 4% hydroquinone (with glycolic acid lotion vehicle).¹⁴⁶ While these studies reported efficacy, they lacked proper randomization, baseline comparisons, and assessor blinding descriptions, resulting in an average Jadad score of 3. Baliña et al¹⁴⁷(n=329) found no significant differences between 20% azelaic acid and 4% hydroquinone but higher local irritation in the azelaic acid group, while Sivayathorn (n=340) reported significantly greater improvements with azelaic acid compared to 2% hydroquinone.¹⁴⁸ However, both studies had serious methodological flaws, including lack of randomization and blinding descriptions, no intention-to-treat analysis, and potential conflicts of interest. Other RCTs on this agent reported mixed findings.^149,150 Overall, there were also opportunities for serious risk of bias issues, (average Jadad of 3.2). It is worth noting that the risk of application site irritation is greater with azelaic acid compared to conventional treatments, despite at-best equivalent efficacy.

Kojic acid. Kojic acid is a compound derived from Aspergilline oryzae and is postulated to act in melasma by inhibiting tyrosinase, and chelating copper at its active site.¹⁵¹ Lim et al¹⁵² compared a 2% kojic acid gel with 2% hydroquinone in a left-right study with both treatments used in combination with 10% glycolic acid, assessing subjective disease clearance percentage and overall effectiveness. The authors conclude that kojic acid is effective with higher 50 percent clearance at 12 weeks than hydroquinone and better or equivalent patient-reported overall effectiveness, but they offered no description of how outcomes were tabulated, do not indicate that assessment was blinded, and offered no statistics to properly compare the treatments. Thus, this study has diminished weight in determining kojic acid efficacy; the study only rates a Jadad score of 2. Garcia et al¹⁵³ performed a similar left-right comparison with the same treatment groups, concluding equivalent efficacy based on similar overall reductions in pigment. The methodology for measuring this outcome was not described, no statistics were provided, and there is no indication that the study was blinded. Greater irritation side effects were described in the kojic acid group but not elaborated upon. Even a recent study by Al-Dhalimi et al¹⁵⁴ which explored combination therapy of kojic acid and Yttrium Aluminum Garnet Laser vs. kojic acid alone found using only kojic acid as treatment to have less statistically improved clinical outcomes compared to the combination therapy.  As a result, we give these studies an overall average quality of evidence of 2 per the Jadad scale, for risk of bias and note that the serious methodological problems with these studies make the kojic acid treatment especially difficult to recommend without more rigorous study.

Vitamin C (ascorbic acid). Vitamin C is also thought to inhibit tyrosinase, interacting with copper at the active site to decrease activity; it may also potentially act by reducing dopaquinone through inhibition of dihydrochinindol-2-carboxyl acid oxidation.^151,155 A few studies have examined its utility as an alternative or complementary treatment for melasma. One small left-right comparison study from Espinal-Perez et al¹⁵⁶ examined 16-week topical application of a 5% L-ascorbic acid formulation compared to a 4% hydroquinone emulsion and measured colorimetry and subjective patient-reported lightening. Patients reported significantly greater “very good” and “excellent” responses on the hydroquinone side with colorimetric results favoring hydroquinone, but that difference was not significant. The authors conclude that vitamin C may play a role in melasma therapy despite poorer results as it featured fewer irritation side effects. The actual significance of these results is questionable. However, as blinding for colometry assessment was not described and the methodology for patient-reported treatment efficacy was not explained. Soliman et al¹⁵⁷ compared a group receiving 5% ascorbic acid treatment with 20% TCA peels to a group receiving the peels alone and concluded that complementary Vitamin C helped improve and maintain treatment results based on a greater and more sustained intra-group decrease in melasma area and severity index (MASI) score. There was, however, no difference in the other measured study outcome (patient-reported global assessment), and the implications of the MASI outcome are uncertain given study methodology problems; there was no matched complementary placebo gel used in the control group and no indication that score evaluation was done by blinded assessors. Finally, in a left-right study, Huh et al¹⁵⁸ examined application of a more readily ionizing Vitamin C preparation compared to water using an iontophoresis machine with authors claiming efficacy based on a statistically significant intragroup decrease in colorimeter-measured luminance in a representative spot on the treatment side compared to control.¹⁵⁸ However, blinded participants rated the treatment and control responses as equally efficacious. While the study was described as double-blind, investigator blinding was not detailed and calorimetry measurement methodology poorly described with the possibility of variability in the measurement of treatment spots, reference comparison spots or both causing this mis-match between investigator- and patient-reported outcomes. Overall, when factoring in the risk of bias, flawed randomization, and design, the average Jadad score for the quality of the evidence of the aforementioned articles is a 2.7. 

Other botanicals. RCTs have been performed using a few other topical botanical CAM agents to assess efficacy in melasma therapy. Licorice extract has been evaluated due to reported effects inhibiting the rate-limiting step of tyrosinase activity and other purported anti-inflammatory mechanisms.¹⁵¹ One small left-right comparison study by Amer et al¹⁵⁹ tested a cream with 2% liquiritin, the active ingredient in licorice, compared to a vehicle control with authors concluding efficacy after four weeks based on an ill-defined pigmentation scale. This study contained no essential methodological information in the methods with no information provided on blinding, baseline scores, placebo matching, or outcome measurements, lending little credibility to its results. Costa et al¹⁶⁰ examined a 60-day application of a commercial combination product of licorice, emblica (Phyllanthus emblica), and belides (Bellis perennis) compared to 2% hydroquinone cream and measured subjective clinical response and photograph-derived UV spot count and score (size and tone). Authors found statistically significant intra-group improvement over the study course in all measures, no inter-group differences between any measure at study endpoint, and fewer adverse events (mild erythema, burning), concluding that the combination product is an effective alternative to hydroquinone. The study featured appropriate inter-group comparisons and mostly well-detailed methodology, but suffered from a few limitations; it was only single-blind (patients knew group assignment), the description of a key outcome of UV spot score was poorly described and no intention-to-treat analysis was performed despite some dropouts. Furthermore, while authors claim no conflict of interest, the study funding was provided by the product manufacturer.

Other agents with potential application for melasma include arbutin, derived from berry plants with potential mechanism on tyrosinase inhibition and melanosome maturation, and soy, with its constituent soybean trypsin inhibitor acting on the protease-activated receptor-2 pathway important in keratinocyte malanosome phagocytosis.¹⁵¹ While in vitro studies suggest a role for these agents in hyperpigmentation, limited clinical studies have been performed in patients with solar lentigines and melasma,¹⁶¹ with no properly designed and blinded RCT-level studies performed on patients with melasma.

Cutaneous Side Effects of Dermatologic and Non-dermatologic CAM

Practicing dermatologists should be aware of potential dermatologic side effects that may result from patients using CAM therapies to treat both their dermatologic and non-dermatologic conditions. Unfortunately, many of the above studies and other CAM studies on other non-dermatologic conditions fail to do a complete accounting of adverse events occurring during trials, and even if adverse events are recorded, the study size is often so small that some low-frequency events may be missed. However, myriad case reports have been published on dermatologic diseases resulting from CAM use which will be briefly discussed here and summarized in Table 9.^31,162

Contact dermatitis and exacerbation of other dermatides. Inclusion of various metals in CAM preparations may lead to hypersensitivity reactions and both systemic and local contact dermatitis. Nickel, for instance, is found in many homeopathic remedies in addition to both Nigerian and Chinese herbal preparations in sufficient amounts to cause systemic or local contact dermatitis.¹⁶³ Allergic contact dermatitis can result from metals contained in acupuncture needles, with a patient presenting in one case report with papulovesicular dermatitis resulting from zinc exposure at acupuncture sites following treatment for dizziness.¹⁶⁴ Other non-metal CAM sensitizers have been implicated in contact dermatitis. For example, several case reports exist of occupational contact dermatitis resulting from exposure to essential oils and fragrances derived from CAM agents and used in aromatherapy settings (masseuse, reflexologist.), typically resulting in multiple different sensitizations.^165,166 Mercury contained in a homeopathic coughing remedy caused Baboon Syndrome in a pediatric patient in another case report,¹⁶⁷ and mercury contamination in TCM or Indian Ayurvedic medicines can have dermatologic effects including dryness, ulceration, erythroderma and hyperkeratotic palmar eczema.¹⁶² Notable botanical CAM modalities reported to cause allergic contact dermatitis include echinacea used as an immune stimulant,¹⁶⁸ chamomile and curcumin/turmeric used for general anti-inflammatory purposes,^169–171 TCM and other Chinese herbal preparations,¹⁷² TTO used for a variety of applications.^31,173,174 Some reports describe exacerbations of previously diagnosed disorders with CAM therapy. For example, reports documenting atopic dermatitis exacerbation with homeopathic therapies containing metals or other substances³¹ and an erythrodermic psoriasis flare-up in a patient with chronic plaque psoriasis resulting from high concentration dead sea salt exposure.¹⁷⁵ As such, CAM treatments should be considered as potential triggers of dermatitis flare-ups.

Stevens-Johnson’s Syndrome. A few case reports describe cases of Stevens-Johnson’s Syndrome (SJS) thought to result from CAM exposure. One patient suffered SJS with diffuse bullae and erosions over her entire body with erythema, swelling, fever, and liver dysfunction following consumption of a commercial “health drink” containing Ophiopogonis tuber, an herb used in TCM for a variety of maladies.¹⁷⁶ Another case report described erosions and blistering over mucus membranes throughout the body following consumption of a multi-component herbal tablet taken as a general health tonic with recurrence upon re-exposure.¹⁷⁵ Both patients recovered with discontinuation of CAM treatment and systemic steroid therapy.

Photosensitivity. Potential photosensitivity may be a risk for a few CAM therapies. Psoralens contained in some aromatherapy preparations may lead to photosensitivity and burns. A case report detailed a patient who suffered 70 percent partial thickness burns after sunbed exposure preceded by a bath with bergamot oil (constituent 5-methoxypsoralen).¹⁷⁷ Another report describes extensive rash and blister formation resulting from sun exposure following application of juice from kaffir limes (Citrus hystrix) as an insect bite treatment.¹⁷⁸ Psoralens are found in many members of the citrus family (Rutaceae) as well as members of the carrot/parsley, fig, and legume/pea families (Umbelliferae, Moraceae and Leguminosae, respectively), and phytophototoxicity should be a noted risk with use of CAM therapies containing these agents.¹⁷⁸ Finally, several reports have documented the photosensitivity risk of St. John’s Wort (Hypericum perforatum) used for depression and other psychological and non-psychological diseases. Cases document pigment changes, itching, erythema, and neuropathy (made evident by stinging pain) in sun-exposed areas following ingestion of St. John’s Wort, likely caused by photoactivity of its constituent hypericins.^162,179

Bruising, lesion formation, cupping injuries. Many of the more physically oriented CAM therapies can result in traumatic skin injuries, bruising, and lesion formation. Coin rubbing, a Chinese and Vietnamese practice of firmly rubbing spoons or worn coins over lubricated skin to treat a variety of maladies, results in parallel bands of petechial bruising on patient skin.¹⁸⁰ There is also the possibility of systemic intoxication effects from absorption of toxic constituents like camphor in the lubricant.¹⁸¹ Cupping is another Asian therapy used to treat a wide variety of conditions including pain disorders, cervical spondylosis, herpes zoster, and acne; this involves the application of suction to the skin with a cup, leaving circular patches of petechiae and ecchymosis.¹⁸² The technique sometimes involves burning cotton to create a vacuum or incision of the skin (“wet cupping”). Complications have been reported with cupping, mostly attributed to improper or overzealous application of the technique and include crusting bullae formation,¹⁸³ panniculitis,¹⁸⁴ and even second-degree burns,¹⁸⁵ but it is generally considered a safe procedure. Finally, several reports describe a variety of adverse dermatologic presentations resulting from acupuncture therapy including blue nevus-like macules diagnosed as localized argyria, waxy orange-brown papules indicative of lymphocytoma cutis, amongst others, all at acupuncture sites and attributed to the procedure.³¹

Other diseases, relevance to peri-operative period and steroid contamination. Other dermatologic conditions of note resulting from CAM include alopecia with associated polyneuropathy from thallium contained in a Chinese herbal remedy¹⁸⁶ and erythema nodosum resulting from oral echinacea supplements.³¹ A few reports have been published concerning Sweet’s syndrome resulting from CAM exposure in patients. A leukemia patient with progressing necrotic lesions on the face and legs and fever was ultimately diagnosed with Sweet’s syndrome attributed to the use of a cream with 1.5% arnica, a much higher than homeopathic dose.¹⁸⁷ A separate report describes Sweet’s syndrome as likely resulting from extensive exposure to jalapeno peppers and their constituent capsaicin,¹⁸⁸ a CAM modality used primarily for neuropathic pain (Table 2). 

Finally, as already mentioned, contamination of some topical and oral TCM agents with corticosteroids may be widespread. Analyses have reported the percentage of TCM agents contaminated with steroids to be as high as ~25 percent with steroid concentrations as high as 1500mg/g (mean 456mg/g).^32,189 This presents obvious potential for interference with treatment for many dermatologic disorders and may necessitate adjustments of the current treatment regimen. 

Conclusion

The use of CAM agents has become widespread in dermatology. Driven by positive anecdotal evidence and promising in-vitro or animal findings, investigators have aimed to transition these CAM agents from folk medicine to scientific medicine through placebo-controlled, double-blind human RCTs. However, this effort has not been widely successful, as most studies concluding CAM benefit suffer from major methodological problems that impact the credibility of their claims. As documented throughout this revie, CAM studies often suffer from: poor or no blinding, subjective outcomes, inadequate randomization, and selective reporting of positive outcomes while ignoring negative or null findings. Despite these reservations, some study results and plethora of in-vitro and animal evidence suggest that many CAM agents deserve further investigation via well-crafted RCTs. Moving forward, a more useful focus would be comparing CAM treatments to common or effective conventional therapies, either alone or in an integrative approach, as this would accurately mimic how patients typically use these agents. In the meantime, given the prevalence of CAM use, practicing dermatologists should be aware of purported or demonstrated efficacy from available studies and be vigilant for adverse effects of popular CAM agents.

References 

1. Fan KW. National center for complementary and alternative medicine website. J Med Libr Assoc. 2005;93(3):410–412. 
2. Tindle HA, Davis RB, Phillips RS, et al. Trends in use of complementary and alternative medicine by US adults: 1997–2002. Altern Ther Health Med. 2005;11(1):42–49.
3. Wootton JC, Sparber A. Surveys of complementary and alternative medicine: part I. General trends and demographic groups. J Altern Complement Med. 2001;7(2):195–208.
4. Ernst E. The usage of complementary therapies by dermatological patients: a systematic review. Br J Dermatol. 2000;142(5):857–861.
5. Fuhrmann T, Smith N, Tausk F. Use of complementary and alternative medicine among adults with skin disease: updated results from a national survey. J Am Acad Dermatol. 2010;63(6):1000–1005.
6. Milden SP, Stokols D: Physicians’ attitudes and practices regarding complementary and alternative medicine. Behav Med. 2004;30(2):73–82. 
7. Wahner-Roedler DL, Vincent A, Elkin PL, et al. Physicians’ attitudes toward complementary and alternative medicine and their knowledge of specific therapies: a survey at an academic medical center. Evid Based Complement Alternat Med. 2006;3(4):495–501.
8. Godin G, Beaulieu D, Touchette JS, et al. Intention to encourage complementary and alternative medicine among general practitioners and medical students. Behav Med. 2007;33(2):67–77.
9. Renzi C, Mastroeni S, Paradisi M, et al. Complementary and alternative medicine: knowledge and attitudes among dermatologists. Acta Derm Venereol. 2009;89(6):642–644.
10. Renzi C, Mastroeni S, Paradisi M, et al. Complementary and alternative medicine: knowledge and attitudes among dermatologists. Acta Derm Venereol. 2009;89(6):642–644.
11. Jadad AR, Moore RA, Carroll D, et al. Assessing the quality of reports of randomized clinical trials: is blinding necessary? Control Clin Trials. 1996;17(1):1–12.
12. Artik S, Ruzicka T. Complementary therapy for atopic eczema and other allergic skin diseases. Dermatol Ther. 2003;16(2):150–163.
13. Sheehan MP, Atherton DJ. A controlled trial of traditional Chinese medicinal plants in widespread non-exudative atopic eczema. Br J Dermatol. 1992;126(2):179–184.
14. Sheehan MP, Rustin MH, Atherton DJ, et al. Efficacy of traditional Chinese herbal therapy in adult atopic dermatitis. Lancet. 1992;4;340(8810):13–17. Erratum in: Lancet. 1992;18;340(8812):188. Harris DJ [corrected to Harris DW]. 
15. Sheehan MP, Atherton DJ. One-year follow up of children treated with Chinese medicinal herbs for atopic eczema. Br J Dermatol. 1994;130(4):488–493. 
16. Sheehan MP, Stevens H, Ostlere LS, et al. Follow-up of adult patients with atopic eczema treated with Chinese herbal therapy for 1 year. Clin Exp Dermatol. 1995;20(2):136–140.
17. Leung TF, Wong KY, Wong CK, et al. In vitro and clinical immunomodulatory effects of a novel pentaherbs concoction for atopic dermatitis. Br J Dermatol. 2008;158(6):1216–1223.
18. Chan BC, Hon KL, Leung PC, et al. Traditional Chinese medicine for atopic eczema: pentaherbs formula suppresses inflammatory mediators release from mast cells. J Ethnopharmacol. 2008;30;120(1):85–91.
19. Novak N, Haberstok J, Kraft S, et al. Standardized extracts from Chinese herbs induce IL-10 production in human monocyte-derived dendritic cells and alter their differentiation in vitro. J Allergy Clin Immunol. 2001;108(4):588–593.
20. Xu XJ, Banerjee P, Rustin MH, et al. Modulation by Chinese herbal therapy of immune mechanisms in the skin of patients with atopic eczema. Br J Dermatol. 1997;136(1):54–59.
21. Latchman Y, Banerjee P, Poulter LW, et al. Association of immunological changes with clinical efficacy in atopic eczema patients treated with traditional Chinese herbal therapy (Zemaphyte). Int Arch Allergy Immunol. 1996;109(3):243–249.
22. Latchman Y, Bungy GA, Atherton DJ, et al. Efficacy of traditional Chinese herbal therapy in vitro. A model system for atopic eczema: inhibition of CD23 expression on blood monocytes. Br J Dermatol. 1995;132(4):592–598.
23. Fung AY, Look PC, Chong LY, et al. A controlled trial of traditional Chinese herbal medicine in Chinese patients with recalcitrant atopic dermatitis. Int J Dermatol. 1999;38(5):387–392.
24. Hon KL, Leung TF, Ng PC, et al. Efficacy and tolerability of a Chinese herbal medicine concoction for treatment of atopic dermatitis: a randomized, double-blind, placebo-controlled study. Br J Dermatol. 2007;157(2):357–363.
25. Shapira MY, Raphaelovich Y, Gilad L, et al. Treatment of atopic dermatitis with herbal combination of Eleutherococcus, Achillea millefolium, and Lamium album has no advantage over placebo: a double blind, placebo-controlled, randomized trial. J Am Acad Dermatol. 2005;52(4):691–693.
26. Ma T, Chai Y, Li S, et al. Efficacy and safety of Qinzhuliangxue decoction for treating atopic eczema: a randomized controlled trial. Ann Palliat Med. 2020;9(3):870–882.
27. Ahn JH, Yun Y, Kim MH, et al. Exploring the efficacy and safety of topical Jaungo application in patients with atopic dermatitis: A pilot randomized, double-blind, placebo-controlled study. Complement Ther Med. 2018;40:22–28.
28. Liu J, Mo X, Wu D, et al. Efficacy of a Chinese herbal medicine for the treatment of atopic dermatitis: a randomised controlled study. Complement Ther Med. 2015;23(5):644–651.
29. Cheng HM, Chiang LC, Jan YM, et al. The efficacy and safety of a Chinese herbal product (Xiao-Feng-San) for the treatment of refractory atopic dermatitis: a randomized, double-blind, placebo-controlled trial. Int Arch Allergy Immunol. 2011;155(2):141–148.
30. Espinoza EO, Mann MJ, Bleasdell B. Arsenic and mercury in traditional Chinese herbal balls. N Engl J Med. 1995;21;333(12):803–804. 
31. Mevorah B, Orion E, Matz H, et al. Cutaneous side effects of alternative therapy. Dermatol Ther. 2003;16(2):141–149.
32. Keane FM, Munn SE, du Vivier AW, et al. Analysis of Chinese herbal creams prescribed for dermatological conditions. BMJ. 1999;27;318(7183):563–564.
33. Hughes JR, Higgins EM, Pembroke AC. Oral dexamethasone masquerading as a Chinese herbal remedy. Br J Dermatol. 1994;130(2):261.
34. Boneberger S, Rupec RA, Ruzicka T. Complementary therapy for atopic dermatitis and other allergic skin diseases: facts and controversies. Clin Dermatol. 2010;28(1):57–61.
35. van Gool CJ, Zeegers MP, Thijs C. Oral essential fatty acid supplementation in atopic dermatitis-a meta-analysis of placebo-controlled trials. Br J Dermatol. 2004;150(4):728–740.
36. Komulainen M, Saros L, Vahlberg T, et al. Maternal fish oil and/or probiotics intervention: allergic diseases in children up to two years old. Pediatr Allergy Immunol. 2023;34(8):e14004.
37. Palmer DJ, Sullivan T, Gold MS, et al. Effect of n-3 long chain polyunsaturated fatty acid supplementation in pregnancy on infants’ allergies in first year of life: randomised controlled trial. BMJ. 2012;30;344:e184.
38. Feíto-Rodríguez M, Ramírez-Boscà A, Vidal-Asensi S, et al. Randomized double-blind placebo-controlled clinical trial to evaluate the effect of a mixture of probiotic strains on symptom severity and use of corticosteroids in children and adolescents with atopic dermatitis. Clin Exp Dermatol. 2023;27;48(5):495–503.
39. Michelotti A, Cestone E, De Ponti I, et al. Efficacy of a probiotic supplement in patients with atopic dermatitis: a randomized, double-blind, placebo-controlled clinical trial. Eur J Dermatol. 2021;1;31(2):225–232.
40. Prakoeswa CRS, Bonita L, Karim A, et al. Beneficial effect of Lactobacillus plantarum IS-10506 supplementation in adults with atopic dermatitis: a randomized controlled trial. J Dermatolog Treat. 2022;33(3):1491–1498.
41. Kalliomäki M, Salminen S, Arvilommi H, et al. Probiotics in primary prevention of atopic disease: a randomised placebo-controlled trial. Lancet. 2001;7;357(9262):1076–1079.
42. Dotterud CK, Storrø O, Johnsen R, et al. Probiotics in pregnant women to prevent allergic disease: a randomized, double-blind trial. Br J Dermatol. 2010 Sep;163(3):616–623.
43. Rautava S. Probiotics during pregnancy and breast-feeding might confer immunomodulatory protection against atopic disease in the infant. J Allergy Clin Immunol. 2002;109(1):119–121. 
44. Kalliomaki M, Salminen S, Poussa T, et al. Probiotics and prevention of atopic disease: 4-year follow-up of a randomised placebo-controlled trial. Lancet. 2003;31;361(9372):1869–1871.
45. Kalliomaki M, Salminen S, Poussa T, et al. Probiotics during the first 7 years of life: A cumulative risk reduction of eczema in a randomized, placebo-controlled trial. J Allergy Clin Immunol. 2007;119(4):1019–1021.
46. Niers L, Martín R, Rijkers G, et al. The effects of selected probiotic strains on the development of eczema (the PandA study). Allergy. 2009;64(9):1349–1358.
47. Boyle RJ, Ismail IH, Kivivuori S, et al. Lactobacillus GG treatment during pregnancy for the prevention of eczema: a randomized controlled trial. Allergy. 2011;66(4):509–516.
48. Kopp MV, Hennemuth I, Heinzmann A, et al. Randomized, double-blind, placebo-controlled trial of probiotics for primary prevention: no clinical effects of Lactobacillus GG supplementation. Pediatrics. 2008;121(4):e850–856.
49. Boyle RJ, Bath-Hextall FJ, Leonardi-Bee J, et al. Probiotics for the treatment of eczema: a systematic review. Clin Exp Allergy. 2009;39(8):1117–1127.
50. Schempp CM, Windeck T, Hezel S, et al. Topical treatment of atopic dermatitis with St. John’s wort cream–a randomized, placebo controlled, double blind half-side comparison. Phytomedicine. 2003;10 Suppl 4:31–37.
51. Patzelt-Wenczler R, Ponce-Poschl E. Proof of efficacy of Kamillosan(R) cream in atopic eczema. Eur J Med Res. 2000;19;5(4):171–175.
52. Saeedi M, Morteza-Semnani K, Ghoreishi MR. The treatment of atopic dermatitis with licorice gel. J Dermatolog Treat. 2003;14(3):153–157.
53. Brown DJ, Dattner AM. Phytotherapeutic approaches to common dermatologic conditions. Arch Dermatol. 1998;134(11):1401–1404.
54. Bedi MK, Shenefelt PD. Herbal therapy in dermatology. Arch Dermatol. 2002;138(2):232–242.
55. Smolle J. Homeopathy in dermatology. Dermatol Ther. 2003;16(2):93–97.
56. Chida Y, Steptoe A, Hirakawa N, et al. The effects of psychological intervention on atopic dermatitis. A systematic review and meta-analysis. Int Arch Allergy Immunol. 2007;144(1):1–9.
57. Staab D, Diepgen TL, Fartasch M, et al. Age related, structured educational programmes for the management of atopic dermatitis in children and adolescents: multicentre, randomised controlled trial. BMJ. 2006;22;332(7547):933–938. 
58. Schachner L, Field T, Hernandez-Reif M, et al. Atopic dermatitis symptoms decreased in children following massage therapy. Pediatr Dermatol. 1998;15(5):390–395.
59. Rotter G, Ahnert MW, Geue AV, et al. Acupuncture and osteopathic medicine for atopic dermatitis: a three-armed, randomized controlled explorative clinical trial. Clin Exp Dermatol. 2022;47(12):2166–2175.
60. Park JG, Lee H, Yeom M, et al. Effect of acupuncture treatment in patients with mild to moderate atopic dermatitis: a randomized, participant- and assessor-blind sham-controlled trial. BMC Complement Med Ther. 2021;29;21(1):132. 
61. Kang S, Kim YK, Yeom M, et al. Acupuncture improves symptoms in patients with mild-to-moderate atopic dermatitis: a randomized, sham-controlled preliminary trial. Complement Ther Med. 2018;41:90–98. 
62. Schöni MH, Nikolaizik WH, Schöni-Affolter F. Efficacy trial of bioresonance in children with atopic dermatitis. Int Arch Allergy Immunol. 1997;112(3):238–246.
63. Smith N, Weymann A, Tausk FA, et al. Complementary and alternative medicine for psoriasis: a qualitative review of the clinical trial literature. J Am Acad Dermatol. 2009;61(5):841–856.
64. Burrows N, Turnbull A, Punchard N, et al. A trial of oral zinc supplementation in psoriasis. Cutis. 1994;54(2):117–188.
65. Yu C, Yu N, Jiang X, et al. Efficacy and safety of supramolecular active zinc in the treatment of scalp psoriasis: a multicentre, randomized, observed-blind, parallel-group, placebo- and active-controlled noninferiority trial. Clin Exp Dermatol. 2023;19;48(10):1138–1144.
66. Serwin AB, Mysliwiec H, Hukalowicz K, et al. Soluble tumor necrosis factor-α receptor type 1 during selenium supplementation in psoriasis patients. Nutrition. 2003;19(10):847–850.
67. Siddiqui MA, Al-Khawajah MM. Vitamin D3 and psoriasis: a randomized double-blind placebo-controlled study. J Dermatol Treat. 1990;1(5):243–245. 
68. Jenssen M, Furberg AS, Jorde R, et al. Effect of vitamin d supplementation on psoriasis severity in patients with lower-range serum 25-hydroxyvitamin d levels: a randomized clinical trial. JAMA Dermatol. 2023; 1;159(5):518–525. Erratum in: JAMA Dermatol. 2 Oct 2024.
69. Stucker M, Memmel U, Hoffmann M, et al. Vitamin B12 cream containing avocado oil in the therapy of plaque psoriasis. Dermatology. 2001;203(2):141–147. 
70. Syed TA, Ahmad SA, Holt AH, et al. Management of psoriasis with aloe vera extract in a hydrophilic cream: a placebo-controlled, double-blind study. Trop Med Int Health. 1996;1(4):505–509.
71. Paulsen E, Korsholm L, Brandrup F. A double-blind, placebo-controlled study of a commercial Aloe vera gel in the treatment of slight to moderate psoriasis vulgaris. J Eur Acad Dermatol Venereol. 2005;19(3):326–331.
72. Pandey SS, Jha AK, Kaur V. Aqueous extract of neem leaves in treatment of psoriasis vulgaris. Indian J Dermatol Venereol Leprol. 1994;60:63–67. 
73. Bernstein S, Donsky H, Gulliver W, et al. Treatment of mild to moderate psoriasis with Reliéva, a Mahonia aquifolium extract–a double-blind, placebo-controlled study. Am J Ther. 2006;13(2):121–126. 
74. Bittiner S, Cartwright I, Tucker W. A double-blind, randomised, placebo-controlled trial of fish oil in psoriasis. Lancet. 1988;20;1(8582):378–380. 
75. Collier P, Ursell A, Zaremba K. Effect of regular consumption of oily fish compared with white fish on chronic plaque psoriasis. Eur J Clin Nutr. 1993;47(4):251–254. 
76. Danno K, Sugie N: Combination therapy with low-dose etretinate and eicosapentaenoic acid for psoriasis vulgaris. J Dermatol. 1998;25(11):703–705. 
77. Grimminger F, Mayser P, Papavassilis C, et al. A double-blind, randomized, placebo-controlled trial of n-3 fatty acid based lipid infusion in acute, extended guttate psoriasis. Clin Investig. 1993;71(8):634–643.
78. Mayser P, Mrowietz U, Arenberger P, et al. Omega-3 fatty acid-based lipid infusion in patients with chronic plaque psoriasis: results of a double-blind, randomized, placebo-controlled, multicenter trial. J Am Acad Dermatol. 1998;38(4):539–547.
79. Gupta A, Ellis C, Tellner D. Double-blind, placebo-controlled study to evaluate the efficacy of fish oil and low-dose UVB in the treatment of psoriasis. Br J Dermatol. 1989;120(6):801–807.
80. Gupta A, Ellis C, Goldfarb M, et al. The role of fish oil in psoriasis. A randomized, double-blind, placebo-controlled study to evaluate the effect of fish oil and topical corticosteroid therapy in psoriasis. Int J Dermatol. 1990;29(8):591–595.
81. Soyland E, Funk J, Rajka G, et al. Effect of dietary supplementation with very-long-chain n-3 fatty acids in patients with psoriasis. N Engl J Med. 1993;24;328(25):1812–1816.
82. Escobar SO, Achenbach R, Iannantuono R, et al. Topical fish oil in psoriasis–a controlled and blind study. Clin Exp Dermatol. 1992;17(3):159–162.
83. Dawe RS, Yule S, Cameron H, et al. A randomized controlled comparison of the efficacy of Dead Sea salt balneophototherapy vs. narrowband ultraviolet B monotherapy for chronic plaque psoriasis. Br J Dermatol. 2005;153(3):613–619.
84. Brockow T, Schiener R, Franke A, et al. A pragmatic randomized controlled trial on the effectiveness of low concentrated saline spa water baths followed by ultraviolet B (UVB) compared to UVB only in moderate to severe psoriasis. J Eur Acad Dermatol Venereol. 2007;21(8):1027–1037.
85. Brockow T, Schiener R, Franke A, et al. A pragmatic randomized controlled trial on the effectiveness of highly concentrated saline spa water baths followed by UVB compared to UVB only in moderate to severe psoriasis. J Altern Complement Med. 2007;13(7):725–732.
86. Schiener R, Brockow T, Franke A, et al. Bath PUVA and saltwater baths followed by UV-B phototherapy as treatments for psoriasis. Arch Dermatol. 2007;143(5):586–596.
87. Cheesbrough MJ. Treatment of psoriasis with 30% Dead Sea salt lotion. J Dermatol Treat. 1992;3(4):201–203. 
88. Leaute-Labreze C, Saillour F, Chene G, et al. Saline spa water or combined water and UV-B for psoriasis vs conventional UV-B. Arch Dermatol. 2001;137(8):1035–1039.
89. Gambichler T, Rapp S, Senger E, et al. Balneophototherapy of psoriasis: highly concentrated salt water versus tap water–a randomized, one-blind, right/left comparative study. Photodermatol Photoimmunol Photomed. 2001;17(1):22–25.
90. Halevy S, Giryes H, Friger M, et al. Dead sea bath salt for the treatment of psoriasis vulgaris: a double-blind controlled study. J Eur Acad Dermatol Venereol. 1997;9(3):237–242. 
91. Beylot-Barry M, Mahé E, Rolland C, et al. Evaluation of the benefit of thermal spa therapy in plaque psoriasis: the PSOTHERMES randomized clinical trial. Int J Biometeorol. 2022;66(6):1247–1256.
92. Gaston L, Crombez J, Lassonde M, et al. Psychological stress and psoriasis: experimental and prospective correlational studies. Acta Derm Venereol Suppl (Stockh). 1991;156:37–43.
93. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med. 1998;60(5):625–632.
94. Zachariae R, Oster H, Bjerring P, et al. Effects of psychologic intervention on psoriasis: a preliminary report. J Am Acad Dermatol. 1996;34(6):1008–1015.
95. Keinan G, Segal A, Gal U, et al. Stress management for psoriasis patients: the effectiveness of biofeedback and relaxation techniques. Stress Med. 1995;11(1):235–241. 
96. Tausk F, Whitmore SE. A pilot study of hypnosis in the treatment of patients with psoriasis. Psychother Psychosom. 1999;68(4):221–225. 
97. Nicolaou N, Johnston GA. The use of complementary medicine by patients referred to a contact dermatitis clinic. Contact Dermatitis. 2004;51(1):30–33. 
98. Abrams Motz V, Bowers CP, Mull Young L, et al. The effectiveness of jewelweed, Impatiens capensis, the related cultivar I. balsamina and the component, lawsone in preventing post poison ivy exposure contact dermatitis. J Ethnopharmacol. 2012;30;143(1):314–318.
99. Long D, Ballentine N, Marks J. Treatment of poison ivy/oak allergic contact dermatitis with an extract of jewelweed. Am J Contact Dermat. 1997;8(3):150–153.
100. Guin J, Reynolds R. Jewelweed treatment of poison ivy dermatitis. Contact Dermatitis. 1980;6(4):287–288. 
101. Magin PJ, Adams J, Pond CD, et al. Topical and oral CAM in acne: a review of the empirical evidence and a consideration of its context. Complement Ther Med. 2006;14(1):62–76.
102. Enshaieh S, Jooya A, Siadat A, et al. The efficacy of 5% topical tea tree oil gel in mild to moderate acne vulgaris: a randomized, double-blind placebo-controlled study. Indian J Dermatol Venereol Leprol. 2007;73(1):22–25.
103. Lubtikulthum P, Kamanamool N, Udompataikul M. A comparative study on the effectiveness of herbal extracts vs 2.5% benzoyl peroxide in the treatment of mild to moderate acne vulgaris. J Cosmet Dermatol. 2019;18(6):1767–1775. 
104. Bassett I, Pannowitz D, Barnetson R. A comparative study of tea-tree oil versus benzoylperoxide in the treatment of acne. Med J Aust. 1990;15;153(8):455–458.
105. Hunt MJ, Barnetson RS. A comparative study of gluconolactone versus benzoyl peroxide in the treatment of acne. Australas J Dermatol. 1992;33(3):131–134.
106. Kim S, Moon S, Kim J, et al. Glycolic Acid versus Jessner’s solution: which is better for facial acne patients? Dermatol Surg. 1999;25(4):270–273.
107. Spellman MC, Pincus SH. Efficacy and safety of azelaic acid and glycolic acid combination therapy compared with tretinoin therapy for acne. Clin Ther. 1998;20(4):711–721.
108. Abels C, Kaszuba A, Michalak I, et al. A 10% glycolic acid containing oil-in-water emulsion improves mild acne: a randomized double-blind placebo-controlled trial. J Cosmet Dermatol. 2011;10(3):202–209.
109. Orafidiya L, Agbani E, Oyedele A. Preliminary clinical tests on topical preparations of Ocimum gratissimum Linn leaf essential oil for the treatment of acne vulgaris. Clin Drug Investig. 2002;22(5):313–319. 
110. Orafidiya L, Agbani E, Oyedele A, et al. The effect of aloe vera gel on the anti-acne properties of the essential oil of Ocimum gratissimum Linn leaf—a preliminary clinical investigation. Int J Aroma. 2004;14(1):15–21. 
111. Higaki S, Toyomoto T, Morohashi M. Seijo-bofu-to, Jumi-haidoku-to and Toki-shakuyaku-san suppress rashes and incidental symptoms in acne patients. Drugs Exp Clin Res. 2002;28(5):193–196.
112. Elsaie M, Abdelhamid M, Elsaaiee L. The efficacy of topical 2% green tea lotion in mild-to-moderate acne vulgaris. J Drugs Dermatol. 2009;8(4):358–364. 
113. Lu PH, Hsu CH. Does supplementation with green tea extract improve acne in post-adolescent women? A randomized, double-blind, and placebo-controlled clinical trial. Complement Ther Med. 2016;25:159–163. 
114. Niren NM. Pharmacologic doses of nicotinamide in the treatment of inflammatory skin conditions: a review. Cutis. 2006;77(1 Suppl):11–16.
115. Jacobson EL, Kim H, Kim M, et al. A topical lipophilic niacin derivative increases NAD, epidermal differentiation and barrier function in photodamaged skin. Exp Dermatol. 2007;16(6):490–499.
116. Surjana D, Halliday GM, Damian DL. Role of nicotinamide in DNA damage, mutagenesis, and DNA repair. J Nucleic Acids. 2010;2010:157591.
117. Niren NM, Torok HM. The Nicomide Improvement in Clinical Outcomes Study (NICOS): Results of an 8-week trial. Cutis. 2006;77(1 Suppl):17–28.
118. Sharquie KE, Najim RA, Al-Salman HN. Oral zinc sulfate in the treatment of rosacea: a double-blind, placebo-controlled study. Int J Dermatol. 2006;45(7):857–861.
119. Bamford JT, Gessert CE, Haller IV, et al. Randomized, double-blind trial of 220mg zinc sulfate twice daily in the treatment of rosacea. Int J Dermatol. 2012;51(4):459–462. 
120. Kolbe L, Immeyer J, Batzer J, et al. Anti-inflammatory efficacy of Licochalcone A: correlation of clinical potency and in vitro effects. Arch Dermatol Res. 2006;298(1):23–30.
121. Morteza-Semnani K, Saeedi M, Shahnavaz B. Comparison of antioxidant activity of extract from roots of licorice (Glycyrrhiza glabra L.) to commercial antioxidants in 2% hydroquinone cream. J Cosmet Sci. 2003;54(6):551–558.
122. Weber TM, Ceilley RI, Buerger A, et al. Skin tolerance, efficacy, and quality of life of patients with red facial skin using a skin care regimen containing Licochalcone A. J Cosmet Dermatol. 2006;5(3):227–232.
123. Martin K, Sur R, Liebel F, et al. Parthenolide-depleted Feverfew (Tanacetum parthenium) protects skin from UV irradiation and external aggression. Arch Dermatol Res. 2008;300(2):69–80.
124. Sur R, Martin K, Liebel F, et al. Anti-inflammatory activity of parthenolide-depleted Feverfew (Tanacetum parthenium). Inflammopharmacology. 2009;17(1):42–49.
125. Cerio R, Dohil M, Downie J, et al. Mechanism of action and clinical benefits of colloidal oatmeal for dermatologic practice. J Drugs Dermatol. 2010;9(9):1116–1120.
126. Lee-Manion AM, Price RK, Strain JJ, et al. In vitro antioxidant activity and antigenotoxic effects of avenanthramides and related compounds. J Agric Food Chem. 2009;25;57(22):10619–10624.
127. Emer J, Waldorf H, Berson D. Botanicals and anti-inflammatories: natural ingredients for rosacea. Semin Cutan Med Surg. 2011;30(3):148–155.
128. Ebneyamin E, Mansouri P, Rajabi M, et al. The efficacy and safety of permethrin 2.5% with tea tree oil gel on rosacea treatment: a double-blind, controlled clinical trial. J Cosmet Dermatol. 2020;19(6):1426–1431. 
129. Hay I, Jamieson M, Ormerod A. Randomized trial of aromatherapy: successful treatment for alopecia areata. Arch Dermatol. 1998;134(11):1349–1352.
130. Sharquie KE, Al-Obaidi HK. Onion juice (Allium cepa L.), a new topical treatment for alopecia areata. J Dermatol. 2002;29(6):343–346.
131. Hajheydari Z, Jamshidi M, Akbari J, et al. Combination of topical garlic gel and betamethasone valerate cream in the treatment of localized alopecia areata: a double-blind randomized controlled study. Indian J Dermatol Venereol Leprol. 2007;73(1):29–32.
132. Willemsen R, Vanderlinden J, Deconinck A, et al. Hypnotherapeutic management of alopecia areata. J Am Acad Dermatol. 2006;55(2):233–237.
133. Tkachenko E, Okhovat JP, Manjaly P, et al. Complementary and alternative medicine for alopecia areata: a systematic review. J Am Acad Dermatol. 2023;88(1):131–143.
134. Kessels AG, Cardynaals RL, Borger RL, et al. The effectiveness of the hair-restorer “Dabao” in males with alopecia androgenetica. A clinical experiment. J Clin Epidemiol. 1991;44(4–5):439–447.
135. Takahashi T, Kamimura A, Yokoo Y, et al. The first clinical trial of topical application of procyanidin B-2 to investigate its potential as a hair growing agent. Phytother Res. 2001;15(4):331–336.
136. Harada N, Okajima K, Narimatsu N, et al. Effect of topical application of raspberry ketone on dermal production of insulin-like growth factor-I in mice and on hair growth and skin elasticity in humans. Growth Horm IGF Res. 2008;18(4):335–344.
137. Kwon OS, Han JH, Yoo HG, et al. Human hair growth enhancement in vitro by green tea epigallocatechin-3-gallate (EGCG). Phytomedicine. 2007;14(7–8):551–555. 
138. Murata K, Takeshita F, Samukawa K, et al. Effects of ginseng rhizome and ginsenoside Ro on testosterone 5α-reductase and hair re-growth in testosterone-treated mice. Phytother Res. 2012;26(1):48–53.
139. Pandit S, Chauhan NS, Dixit VK. Effect of Cuscuta reflexa Roxb on androgen-induced alopecia. J Cosmet Dermatol. 2008;7(3):199–204.
140. Jain R, Jain N, Singh N, et al. Development and evaluation of polyherbal ointment for hair growth activity. Int J Pharm Pharm Sci. 2011;3:180–182. 
141. Kumar N, Rungseevijitprapa W, Narkkhong NA, et al. 5α-reductase inhibition and hair growth promotion of some Thai plants traditionally used for hair treatment. J Ethnopharmacol. 2012;15;139(3):765–771.
142. Roy RK, Thakur M, Dixit VK: Hair growth promoting activity of Eclipta alba in male albino rats. Arch Dermatol Res. 2008;300(7):357–364.
143. Does Nioxin work? Hims blog. 12 Nov 2021. https://www.hims.com/blog/does-nioxin-work
144. Fitton A, Goa K. Azelaic acid. A review of its pharmacological properties and therapeutic efficacy in acne and hyperpigmentary skin disorders. Drugs. 1991;41(5):780–798.
145. Lowe NJ, Rizk D, Grimes P, et al. Azelaic acid 20% cream in the treatment of facial hyperpigmentation in darker-skinned patients. Clin Ther. 1998;20(5):945–959.
146. Kakita LS, Lowe NJ. Azelaic acid and glycolic acid combination therapy for facial hyperpigmentation in darker-skinned patients: a clinical comparison with hydroquinone. Clin Ther. 1998;20(5):960–970.
147. Baliña L, Graupe K. The treatment of melasma 20% azelaic acid versus 4% hydroquinone cream. Int J Dermatol. 1991;30(12):893–895.
148. Sivayathorn A, Verallo-Rowell V, Graupe K. 20% azelaic acid cream in the topical treatment of melasma: a double-blind comparison with 2% hydroquinone. Eur J Dermatol. 1995;5(8):680–684. 
149. Dayal S, Sahu P, Dua R. Combination of glycolic acid peel and topical 20% azelaic acid cream in melasma patients: efficacy and improvement in quality of life. J Cosmet Dermatol. 2017;16(1):35–42.
150. Farshi S. Comparative study of therapeutic effects of 20% azelaic acid and hydroquinone 4% cream in the treatment of melasma. J Cosmet Dermatol. 2011;10(4):282–287. 
151. Sheth VM, Pandya AG. Melasma: a comprehensive update: part II. J Am Acad Dermatol. 2011;65(4):699–714. 
152. Lim JT. Treatment of melasma using kojic acid in a gel containing hydroquinone and glycolic acid. Dermatol Surg. 1999;25(4):282–284. 
153. Garcia A, Fulton J. The combination of glycolic acid and hydroquinone or kojic acid for the treatment of melasma and related conditions. Dermatol Surg. 1996;22(5):443–447.
154. Al-Dhalimi MA, Yasser RH. Evaluation of the of the efficacy of fractional erbium-doped yttrium aluminum garnet laser-assisted drug delivery of kojic acid in the treatment of melasma; a split face, comparative clinical study. J Cosmet Laser Ther. 2021;19;23(3–4):65–71. 
155. Choi Y, Rho Y, Yoo K, et al. Effects of vitamin C vs. multivitamin on melanogenesis: comparative study in vitro and in vivo. Int J Dermatol. 2010;49(2):218–226.
156. Espinal-Perez LE, Moncada B, Castanedo-Cazares JP. A double-blind randomized trial of 5% ascorbic acid vs. 4% hydroquinone in melasma. Int J Dermatol. 2004;43(8):604–607.
157. Soliman MM, Ramadan SA, Bassiouny DA, et al. Combined trichloroacetic acid peel and topical ascorbic acid versus trichloroacetic acid peel alone in the treatment of melasma: a comparative study. J Cosmet Dermatol. 2007;6(2):89–94.
158. Huh C, Seo K, Park J, et al. A randomized, double-blind, placebo-controlled trial of vitamin C iontophoresis in melasma. Dermatology. 2003;206(4):316–320.
159. Amer M, Metwalli M. Topical liquiritin improves melasma. Int J Dermatol. 2000;39(4):299–301.
160. Costa A, Moisés TA, Cordero T, et al. Association of emblica, licorice and belides as an alternative to hydroquinone in the clinical treatment of melasma. An Bras Dermatol. 2010;85(5):613–620.
161. Morag M, Nawrot J, Siatkowski I, et al. A double-blind, placebo-controlled randomized trial of Serratulae quinquefoliae folium, a new source of β-arbutin, in selected skin hyperpigmentations. J Cosmet Dermatol. 2015;14(3):185–190.
162. Ernst E. Adverse effects of herbal drugs in dermatology. Br J Dermatol. 2000;143(5):923–929.
163. De Medeiros LM, Fransway AF, Taylor JS, et al. Complementary and alternative remedies: an additional source of potential systemic nickel exposure. Contact Dermatitis. 2008;58(2):97–100. 
164. Koizumi H, Tomoyori T, Kumakiri M, et al. Acupuncture needle dermatitis. Contact Dermatitis. 1989;21(5):352.
165. Trattner A, David M, Lazarov A. Occupational contact dermatitis due to essential oils. Contact Dermatitis. 2008;58(5):282–284.
166. Schaller M, Korting HC. Allergic airborne contact dermatitis from essential oils used in aromatherapy. Clin Exp Dermatol. 1995;20(2):143–145.
167. Audicana M, Bernedo N, Gonzalez I, et al. An unusual case of baboon syndrome due to mercury present in a homeopathic medicine. Contact Dermatitis. 2001;45(3):185.
168. Mullins R. Echinacea-associated anaphylaxis. Med J Aust. 1998;16;168(4):170–171.
169. Foti C, Nettis E, Panebianco R, et al. Contact urticaria from Matricaria chamomilla. Contact Dermatitis. 2000;42(6):360–361. 
170. Rodriguez-Serna M, Sanchez-Motilla J, Ramon R, et al. Allergic and systemic contact dermatitis from Matricaria chamomilla tea. Contact Dermatitis. 1998;39(4):192–193. 
171. Liddle M, Hull C, Liu C, et al. Contact urticaria from curcumin. Dermatitis. 2006;17(4):196–197. 
172. Leow YH. Contact dermatitis due to topical traditional Chinese medication. Clin Dermatol. 1997;15(4):601–605. 
173. Hausen B. Evaluation of the main contact allergens in oxidized tea tree oil. Dermatitis. 2004;15(4):213–214.
174. Crawford G, Sciacca J, James W. Tea tree oil: cutaneous effects of the extracted oil of Melaleuca alternifolia. Dermatitis. 2004;15(2):59–66.
175. Monk B. Severe cutaneous reactions to alternative remedies. Br Med J (Clin Res Ed). 1986;13;293(6548):665–666.
176. Mochitomi Y, Inoue A, Kawabara H, et al. Stevens-Johnson syndrome caused by a health drink (Eberu®) containing ophiopogonis tuber. J Dermatol. 1998;25(10):662–665.
177. Cocks H, Wilson D. Dangers of the intake of psoralens and subsequent UV exposure producing significant burns. Burns. 1998;24(1):82. 
178. Koh D, Ong CN. Phytophotodermatitis due to the application of citrus hystrix as a folk remedy. Br J Dermatol. 1999;140(4):737–738.
179. Bove G. Acute neuropathy after exposure to sun in a patient treated with St John’s wort. Lancet. 1998;3;352(9134):1121–1122.
180. Hulewicz BS. Coin-rubbing injuries. Am J Forensic Med Pathol. 1994;15(3):257–260.
181. Rampini SK, Schneemann M, Rentsch K, et al. Camphor intoxication after cao gío (coin rubbing). JAMA. 2002;3;288(1):45.
182. Yoo SS, Tausk F. Cupping: East meets west. Int J Dermatol. 2004;43(9):664–665.
183. Tuncez F, Bagci Y, Kurtipek GS, et al. Suction bullae as a complication of prolonged cupping. Clin Exp Dermatol. 2006;31(2):300–301.
184. Lee JS, Ahn SK, Lee SH. Factitial panniculitis induced by cupping and acupuncture. Cutis. 1995;55(4):217–218.
185. Kose A, Karabağli Y, Cetin C. An unusual cause of burns due to cupping: complication of a folk medicine remedy. Burns. 2006;32(1):126–127. 
186. Schaumburg H, Berger A. Alopecia and sensory polyneuropathy from thallium in a Chinese herbal medication. JAMA. 1992;23–30;268(24):3430–3431.
187. Delmonte S, Brusati C, Parodi A, et al. Leukemia-related Sweet’s syndrome elicited by pathergy to arnica. Dermatology. 1998;197(2):195–196.
188. Greer J, Rosen T, Tschen J. Sweet’s syndrome with an exogenous cause. Cutis. 1993;51(2):112–114. 
189. Huang W, Wen K, Hsiao M. Adulteration by synthetic therapeutic substances of traditional Chinese medicines in Taiwan. J Clin Pharmacol. 1997;37(4):344–350.