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Abstract

L-Carnitine, an amino acid derivative critical for fatty acid metabolism, exhibits anti-inflammatory, antioxidant, and cytoprotective properties, with emerging applications in dermatology. This review explores its therapeutic potential, both topically and systemically, and its role as a biomarker in various skin disorders. A systematic search of Medline, EMBASE, and PubMed (1946-January 2025) was conducted, focusing on L-carnitine and dermatologic conditions, excluding acetyltransferases, acyltransferases, breast, and genetic metabolic diseases. From 420 articles, 59 were included after screening in Covidence. Data on study design, sample size, carnitine type, and outcomes were extracted and validated by two authors. Topically, L-carnitine (1%-5%) reduces acne lesions, sebum production, post-inflammatory hyperpigmentation, and cellulite, particularly when combined with agents like licochalcone-A or salicylic acid. Systemic L-carnitine mitigates inflammation, oxidative stress, and treatment-related side effects (eg, from corticosteroids, isotretinoin, vismodegib) while improving skin elasticity, microcirculation, wound healing, and fibrosis in conditions like Raynaud’s disease, venous leg ulcers, and sclerotic disorders. As a biomarker, altered carnitine levels and metabolites reflect disease mechanisms in genodermatoses (eg, restrictive dermopathy, recessive dystrophic epidermolysis bullosa), inflammatory dermatoses, and melanoma, aiding diagnosis and monitoring. L-Carnitine shows promise as a therapeutic and diagnostic tool in dermatology, with benefits in acne, sebum control, post-inflammatory hyperpigmentation, cellulite, inflammation, and tissue repair. Its biomarker potential enhances disease insights and personalized care. Further dermatology-specific trials are needed to optimize dosing, formulations, and long-term safety, particularly regarding trimethylamine-N-oxide-related cardiovascular risks.

Keywords

L-carnitine dermatology acne sebum biomarker inflammatory dermatoses amino acid carnitine acetyl-L-carnitine wound healing

Introduction

Carnitine, an amino acid derivative synthesized from L-methionine and L-lysine, exists primarily in its active form, L-carnitine, along with several other bioactive derivatives including propionyl-L-carnitine (PLC) and acetyl-L-carnitine (ALC).¹ L-carnitine is crucial for transporting long-chain fatty acids into mitochondria for β-oxidation and energy production.² Acylcarnitines, formed through conjugation of L-carnitine and fatty acids, contribute to the cellular carnitine pool and support mitochondrial function.¹

Beyond its metabolic function, L-carnitine exhibits anti-inflammatory, antioxidant, and cytoprotective effects, with emerging relevance in cardiovascular diseases, cancer and neuroprotection.³ ALC, in particular, enhances mitochondrial efficiency, supports cholinergic transmission and protects neural tissue.⁴

This review examines carnitine's growing relevance in dermatology, both as a therapeutic agent, used topically and systemically, and as a potential biomarker in various skin disorders and conditions (Table 1).

Table 1.

Clinical Applications and Biomarker Relevance of Carnitine in Dermatology.

Category	Indication	Role of carnitine	Key outcomes	Ref.
Topical use	Acne vulgaris	Adjunctive topical therapy	Reduced inflammatory and non-inflammatory lesions; decreased C. acnes; improved tolerability and maintenance of acne therapies; enhanced outcomes with procedural treatments	5-12
	Seborrhea / oily skin	Sebum-regulating agent	Significant reduction in sebum production and improved skin barrier parameters	5,6,13-15
	PIH and post-procedure care	Adjunct to energy-based treatments	Reduction or trend toward improvement in PIH; improved post-procedure recovery	9,16
	Cellulite / localized fat	Cosmetic topical therapy	Variable objective reductions in circumference; consistent subjective improvements in firmness and skin appearance	17-19
Systemic use	Inflammatory and autoimmune dermatoses	Anti-inflammatory and metabolic adjunct	Reduced inflammatory markers, oxidative stress, dyslipidemia, muscle wasting, and corticosteroid-related adverse effects	20-27
	Treatment-related adverse effects	Supportive therapy	Improved isotretinoin-associated myalgias and vismodegib-related muscle spasms; potential mitigation of radiation-induced skin inflammation	28-30
	Skin aging, elasticity, and repair	Nutraceutical and regenerative support	Improved skin elasticity, microcirculation, wound healing, and tissue remodeling; anti-fibrotic effects	31-38
Biomarker use	Select genodermatoses and hereditary conditions	Diagnostic/ prognostic biomarker	Altered carnitine or acylcarnitine profiles associated with disease severity, cardiomyopathy risk, and diagnostic differentiation	39-44
	Inflammatory dermatoses (AD, psoriasis)	Disease phenotype and severity biomarker	Dysregulated carnitine metabolism reflecting mitochondrial dysfunction and inflammatory activity	45-51
	Fibrotic, pruritic, infectious, and sebaceous disorders	Metabolic and inflammatory biomarker	Distinct carnitine profiles associated with fibrosis, chronic pruritus, infection, and acne risk	52-59
	Melanoma and psychodermatologic disease	Stage-specific and systemic biomarker	Altered carnitine pathways associated with melanoma progression and depression severity	4,60-66

Abbreviations: AD, atopic dermatitis; ALC, acetyl-L-carnitine; IPL, intense pulsed light; LC, L-carnitine; PIH, post-inflammatory hyperpigmentation.

Methods

The following bibliographic databases were searched individually on January 11, 2025: Medline (1946 to January 10, 2025), and EMBASE (1974 to 2025 January 09) via Ovid; PubMed (1946-2025) directly through the US National Library of Medicine. Systematic searches were completed using a combination of subject headings, such as Medical Subject Headings (MeSH), wherever they were available in the database and keywords. The search strategy consists of two main concepts: (1) carnitine and (2) dermatology, including skin diseases. Articles focused on the acetyltransferases or acyltransferases were excluded, and so were articles discussing breast diseases and metabolic diseases. No limits for publication date were used, but the search was restricted to the English language, those pertaining to human studies, and those with abstracts. The titles and abstracts were first screened for relevance in Covidence, and then the full-text was screened to ensure eligibility. Data was extracted from the papers at the full-text assessment. A total of 420 articles were found and after screening and reviewing the articles, 59 were included for data extraction. Two authors (EC, MS) independently evaluated the validity of the qualifying studies by evaluating their titles, abstracts and findings. This review excluded animal studies, books, conference abstracts, non-systematic reviews, and grey literature. The following information was extracted and checked by the two authors: first author’s name, nation, year of publication, type of study, study sample size, specific carnitine molecule, and other data were retrieved for further analysis.

Topical Use of L-Carnitine in Dermatology

Numerous studies evaluated the topical use of L-carnitine in dermatology, focusing on acne, sebum reduction, post-inflammatory hyperpigmentation (PIH) and cellulite management. The researchers employed various L-carnitine concentrations (1-5%), often in combination with other active ingredients. Most were randomized controlled trials (RCT), except for one multicenter observational study.⁵ Table 2 summarizes the studies reviewed.

Table 2.

Summary of Studies with Carnitine as Topical Therapy.

Author (year)	Study type	Study’s aim	Patients	Population/disease	Intervention	Duration	Results	Level of evidence^a
Angelova-Fischer et al (2013)⁶	A double-blind, randomized, vehicle-controlled trial	Assess the efficacy of a skin care formulation containing LC-LCC-12DND for mild to moderately severe AV	60 enrolled, 51 completed	Patients 14-40 years-old with mild to moderately severe papulopustular AV	-Active: LC-LCC-12DND in an oil-in-water emulsion, applied twice daily for 8 weeks-Comparator: Vehicle (placebo)-1-week standardization phase before study	Outcomes measured at baseline, 4 and 8 weeks	-Reduction in papules and pustules (P < .05), total lesions (-6.9%)-Reduced sebum by 18.6% (P < 0.01)-C. acnes reduced by 49.4% in the active group vs 3.2% in vehicle group-Improvement in DLQI	1b
Chularojanamontri et al (2016)⁷	RCT	Compare tolerability and efficacy of a moisturizer containing LC-LCC-12DND with a placebo when used alongside adapalene gel for mild to moderate AV	120 (53 males, 67 females)	Asian patients > 18 years old with mild to moderate AV	-Active: Adapalene gel 0.1% + LC-LCC-12DND moisturizer applied twice daily-Comparator: Adapalene gel 0.1% + placebo moisturizer	8 weeks	Active group: Reduction in inflammatory (P = .003) and total acne lesions (P = .028); lower skin irritation (P = .048); improved skin hydration and reduced TEWL; higher percentage of “clear” or “almost clear” patients (17.9% active group vs 15% placebo vs 12.8% adapalene alone)	1b
Dall'Oglio et al (2019)⁵	Multicenter prospective observational clinical study	Assess efficacy and tolerability of a cosmetic regimen with L-carnitine, LicA, Salicylic acid (SA), and Hydroxy-Complex 10% for mild AV	91 (71 females, 20 males)	Adult patients (mean age 21.5 ± 3.8 years) with mild AV	-Morning: Fluid containing LicA, SA, and LC-Night: Cream with LicA and Hydroxy-Complex 10%	8 weeks	Reduction in GAGS score at 4 weeks (P < 0.001); 41% and 45% reduction in comedones and papules at 4 weeks; 64% and 71% reduction in comedones and papules at 8 weeks; sebum reduction of 52% at 8 weeks; excellent tolerability in 90% of patients	3b
Detudom et al (2023)¹⁵	RCT	Evaluate the efficacy of anti-sebum moisturizers containing LC, EGCG, and their combination for seborrhea treatment	90	Adults 18-40 years old with oily or combination skin, experiencing frequent oiliness and facial comedones	-2% LC cream-5% EGCG cream-Combination of 2% LC + 5% EGCG-All formulations in a base of dimethicone and glycerin-Applied twice daily for 4 weeks-Comparator: Different formulations tested against each other	Applied twice daily for 4 weeks	-Sebum reduction in all groups (P < 0.01)-LC group: 34.84% reduction in sebum-EGCG group: 41.36% reduction in sebum-Combination group: 43.45% reduction in sebum; significantly greater anti-sebum efficacy than LC alone (P = .009)-All groups showed improvement in skin hydration, TEWL, and subjective perception of oiliness	1b
Escalante et al (2019)¹⁹	RCT	Investigate the effectiveness of a lotion containing aminophylline, caffeine, yohimbe, LC, and gotu kola in reducing thigh fat mass, thigh circumference, and skinfold thickness when combined with a low-intensity exercise program and restricted calorie intake	7	Healthy, sedentary women aged 18-54 who exercised <60 minutes per week	-Active: Lipoxyderm™ lotion containing aminophylline, caffeine, yohimbe, LC, and gotu kola applied twice daily to one thigh-Comparator: Placebo lotion applied to the other thigh-Additional intervention: Hypocaloric diet and 150 minutes of walking per week	28 days	-Active lotion: greater reductions in thigh circumference (1.2 cm vs 0.8 cm), skinfold thickness (3.7 mm vs 2.0 mm), and fat mass (100.0 g vs 57.3 g) compared to placebo-Active treatment showed 33.3% more reduction in thigh circumference, 45.9% more in skinfold thickness, and 42.7% more in fat mass than placebo	2b
How et al (2023)¹²	RCT	Assess efficacy and tolerability of a sunscreen containing LC and LicA as an adjunct to adapalene for acne and post-acne pigmentation	56	Malaysian patients >18 years old with mild-to-moderate AV	-Active: Adapalene gel 0.1% + LC and LicA sunscreen applied every 4 hours during the daytime-Comparator: Adapalene gel 0.1% + niacinamide-containing sunscreen	4 weeks (with 2-week adapalene run-in period)	-Improvement in acne and post-acne hyperpigmentation in both groups-LicA/LC-containing sunscreen group reported better skin tolerability (less dryness, burning, and stinging) compared to comparator-More patients in the LicA/LC group reported excellent improvement at Week 4-No significant differences in overall efficacy between the two groups, but LicA/LC group had better tolerability	1b
Jeon et al (2024)¹¹	Individual cohort study	Exfoliation of skin through Mandelic acid_Carnitine ion-pairing complex (M_C complex)	64 (33 + 31)	Healthy females, 20-68 years old, with blackheads, whiteheads, pore volume, depth, density, and skin texture concerns	-Topical 1% M_C complex applied twice daily for 2 weeks.-The active formulation included LC, Mandelic acid, deionized water, potassium hydroxide, and hydrochloric acid for pH adjustment.	2 weeks	Improvements:25.75% reduction in blackhead area; 36.10% reduction in whitehead area;23.68% reduction in pore-affected areas; 83.04% decrease in dead skin cells; skin texture and pore characteristics improved after 1 week (6.47% improvement).	2b
Kulthanan et al (2020)⁸	RCT	To evaluate the efficacy and safety of a moisturizer containing LC-LCC-12DND and SA in preventing acne relapse in the maintenance phase of mild-moderate acne.	110 patients in the induction phase, with 50 in the maintenance phase.	Patients with mild to moderate AV, > 18 years.	-Induction Phase (8 weeks):110 patients with mild-moderate AV treated with adapalene 0.1%/benzoyl peroxide 2.5% gel once daily. Oral doxycycline was added for moderate cases.-Maintenance Phase (12 weeks):50 patients applied a moisturizer with active ingredients (LC-LCC-12DND, SA) or a placebo moisturizer twice daily for 12 weeks.	12 weeks	Treatment group showed a 56% maintenance rate for mean total lesion count, significantly higher than the placebo group (36%, P = .021); significant improvement in acne lesion counts, with higher patient and physician satisfaction, and better skin tolerability compared to placebo.	1b
Kwon et al (2023)¹⁰	RCT	To examine the anti-acne activity of a SA-based ionic pair with L-carnitine (IP-BHA) and its combination with magnolol, focusing on exfoliation, lipogenesis, bacterial growth, and inflammation	8 subjects for the anti-acne activity portion; 20 volunteers for the survey portion	19–38 years old (average 25.09 ± 5.93 years old) with acne classified as Investigator’s Global Assessment grades 2–3 and Investigator’s Static Global Assessment grade 1 or higher	-Topical emulsion containing 5% IP-BHA and 0.02% magnolol, applied twice daily for 4 weeks.-Compared to vehicle.	4 weeks	IP-BHA and magnolol improved acne (reduction in papules and pustules), enhanced erythema recovery (81.9%), and increased antibacterial activity against C. acnes (MIC improved 62.5 times for IP-BHA and 2.5 times for magnolol when used together).The treatment also improved sebum secretion, inflammation, and skin calming, with participants reporting high satisfaction (3.7–4.0/5) in reducing acne lesions, blackheads, and inflammation.	1b
Nasrollahi et al (2016)¹⁷	Randomized, double-blind, placebo-controlled, right-left comparison clinical trial	To assess the safety and efficacy of a topical anti-cellulite cream in the treatment of mild to moderate cellulite on the thighs and buttocks	12	12 healthy women, aged 22–58, with mild to moderate cellulite on thighs and buttocks	Active treatment: Twice-daily anti-cellulite cream containing 5% LC, Coenzyme A, 1% caffeine, 1.5% ginger root extract, 2.5% Bodyfit (mixture of glycerin, water, coco-glucoside, caprylyl glycol, alcohol, glaucine) vs placebo cream.	8 weeks	-The active cream did not show significant objective improvements (eg, thigh circumference, fat thickness, dermis thickness).-However, 90% of participants reported satisfaction based on Visual Analog Scale.-Subjective improvement in skin appearance and firmness noted.	1b
Peirano et al (2012)¹⁴	RCT	To investigate the effect of topically applied LC in reducing sebum production in oily skin	21	21 female volunteers (aged 22–56) with oily skin	Topical formulation containing 2% LC, applied twice daily for 3 weeks, compared to vehicle control.	3 weeks	Reduction in sebum secretion rate after 3 weeks of treatment with LC (P = .0027).	1b
Puaratanaarunkon et al. (2022)¹⁶	Randomized, Double-Blinded, Split-Face Study	To compare the efficacy of a sunscreen with an anti-inflammatory agent (sunscreen A) in reducing PIH after picosecond laser, compared to a regular sunscreen (sunscreen B).	60	Acne and atrophic acne scars, skin phototypes III and IV. The mean age of 28.56 ± 6.17 years (19–46 years). The majority was female (N=42, 71.2%). Most of the subjects had skin phototype III (N=33, 55.9%)	-Sunscreen A: Contains LicA, LC, octocrylene, and avobenzone.-Sunscreen B: Same ultraviolet filters, without anti-inflammatory agents.-Applied on opposite sides of the face after a single picosecond laser session.-Twice daily application.	6 weeks	-No significant difference in PIH reduction. But there was a trend towards lower pigmentation in sunscreen A.-Sunscreen A showed reduction in inflammatory acne lesions at weeks 2 (P = .017), 4 (P < 0.001), and 6 (P < 0.001); reduced porphyrins at weeks 1 (P = .022) and 6 (P = .029); higher patient satisfaction for sunscreen A (P < 0.05).	1b
Roure et al (2011)¹⁸	RCT	To evaluate the efficacy of a topical cosmetic slimming product for improving cellulite appearance, skin firmness, and hydration	78	Women aged 18-60 years with visible signs of cellulite (grades 2 or 3)	-Twice-daily anti-cellulite cream containing tetrahydroxypropyl ethylenediamine, caffeine, carnitine, forskolin, and retinol.-Compared with placebo (basic gel).	12 weeks	-Significant reduction in circumference of abdomen, hips, waist after 4 weeks; continued improvement through 12 weeks.-79% of participants showed improvements in skin condition compared to 56% in placebo group.	1b
Wanitphakdeedecha et al (2020)⁹	RCT	Effectiveness of PDT with IPL combined with a cream containing LC-LCC-12DND compared to PDT alone in treating AV.	29	Mild to severe facial AV	PDT with IPL (4 sessions, 2-week intervals) combined with a cream containing LC-LCC-12DND (active formulation) vs vehicle cream.Applied twice daily for 10 weeks.	10 weeks	-PDT with the active formulation led to faster and greater reductions in inflammatory and non-inflammatory acne lesions (34.5% of patients experiencing more than 25% improvement at 2 weeks after the second treatment compared to 17.2% in the vehicle group), reduced melanin index, and improved PIH.	1b
Wongtada et al (2022)¹³	An open-label explorative study.	To explore the lipid-modifying effect of a moisturizer containing LicA, 1,2-decanediol, L-carnitine, and salicylic acid (LDCS) in seborrhea, both with and without AV, and assess SSL.	20	Seborrhea participants (10 with AV, 10 without) aged 18–40 years	The intervention involved applying the LDCS moisturizer twice daily for 8 weeks.For AV participants, the treatment was combined with benzoyl peroxide 2.5% gel and adapalene 0.1%/benzoyl peroxide 2.5% gel.	8 weeks	-AV Group: Reduction in SSL from baseline (167.0 μg/cm²) to 120.0 μg/cm² at week 2 (P = .0124), continuing to week 8.-Non-AV Group: Reduction in SSL from baseline (158.0 μg/cm²) to 105.6 μg/cm² at week 6 (P = .0098).-Overall reductions in squalene, cholesterol, and fatty acids.	2b

Abbreviations: AV, acne vulgaris; DLQI, Dermatology Life Quality Index; EGCG, epigallocatechin gallate; GAGS, Global Acne Grading System; IP-BHA, SA-based ionic pair with L-carnitine; IPL, Intense Pulse Light; LC, L-carnitine; LC-LCC-12DND, L-carnitine, licochalcone-A, and 1,2-decanediol; LDCS, Licochalcone-A, 1,2-decanediol, L-carnitine, and salicylic acid; LicA - Licochalcone-A; M_C Complex, Mandelic acid Carnitine ion-pairing complex; MIC, minimal inhibitory concentration; PDT, photodynamic therapy; PIH, Post-inflammatory hyperpigmentation; RCT, Randomized controlled trial; SA, salicylic acid; SSL, skin surface lipid; TEWL, transepidermal water loss.

Each study’s design was determined by the authors and was classified according to the 2009 Oxford Centre for Evidence-Based Medicine Levels of Evidence. (Oxford Centre for Evidence-Based Medicine: Levels of Evidence (March 2009) - Centre for Evidence-Based Medicine (CEBM), University of Oxford https://www.cebm.ox.ac.uk/resources/levels-of-evidence/oxford-centre-for-evidence-based-medicine-levels-of-evidence-march-2009. Accessed: 2025-08-04).

Acne Treatment

Topical L-carnitine reduced acne lesion counts, particularly when combined with other active ingredients. A 2013 trial of 51 patients demonstrated that a formulation with L-carnitine, licochalcone-A, and 1,2-decanediol (LC-LCC-12DND) reduced inflammatory acne lesions compared to a vehicle control.⁶ A 2016 study found that combining LC-LCC-12DND with adapalene enhanced lesion reduction, with greater decreases in both inflammatory and total acne lesions.⁷ In a multicenter study, a regimen incorporating LC-LCC-12DND and salicylic acid (SA) led to over 60% reduction in comedones and papules by week 8, suggesting efficacy against both non-inflammatory and inflammatory lesions.⁵ The use of LC-LCC-12DND containing moisturizer was also shown to maintain the benefits from active acne treatment better than placebo in an RCT of 50 patients.⁸ Finally, Wanitphakdeedecha et al⁹ evaluated the combination of Intense Pulsed Light (IPL) therapy with an LC-LCC-12DND containing cream, reporting more rapid and substantial lesion reductions, indicating enhanced benefit when paired with procedural treatments.

A small RCT testing a SA-L-carnitine ionic pair with magnolol showed significant reductions in inflammatory lesions, along with antibacterial, anti-inflammatory, and exfoliating properties, demonstrating greater potency against Cutibacterium acnes than clindamycin.¹⁰ Jeon et al¹¹ studied a mandelic acid-L-carnitine complex and found improvements in comedones, skin texture and pore appearance. However, an RCT by How et al¹² compared a sunscreen with L-carnitine and licochalcone-A to a niacinamide-based formulation as adjuncts to adapalene and found no significant difference in lesion reduction, though there was better tolerability of the adapalene in former group. This suggests that the efficacy of L-carnitine may vary depending on the comparator used.

In summary, the findings support topical L-carnitine’s potential role in acne management, particularly when combined with other active ingredients. While some findings vary, the overall evidence supports its role in reducing both inflammatory and non-inflammatory lesions and enhancing standard treatment regimens.

Sebum Reduction

Topical L-carnitine has been shown to reduce sebum production, a key factor in acne and seborrhea. A 2013 double-blind, randomized, vehicle-controlled trial reported decreased sebum levels after 8 weeks of treatment with a formulation containing LC-LCC-12DND in individuals with mild to moderate acne.⁶ Similarly, a 2022 open-label study observed reduced sebum following 8 weeks of treatment with a moisturizer containing LC-LCC-12DND and salicylic acid.¹³ Dall'Oglio et al⁵ also noted reduced sebum in users of a combination of L-carnitine and licochalcone A. In another vehicle-controlled trial, a 2% L-carnitine formulation significantly lowered sebum secretion within 2 weeks.¹⁴ Detudom et al¹⁵ further demonstrated a 34.84% sebum reduction after 4 weeks using L-carnitine with epigallocatechin gallate.

These findings support topical L-carnitine as an effective agent for sebum control, with potential applications in managing acne, seborrhea, and related disorders.

Post-Inflammatory Hyperpigmentation

Topical L-carnitine shows potential in managing PIH, though findings are mixed. Wanitphakdeedecha et al⁹ reported a significant PIH reduction at 1 month (P = .015) using IPL photodynamic therapy (endogenous photosensitizers) combined with a topical L-carnitine formulation. In contrast, Puaratanaarunkon et al¹⁶ observed only a trend towards reduced PIH with a L-carnitine-based sunscreen following picosecond laser treatment. These results suggest topical L-carnitine may aid PIH, particularly when used alongside IPL therapy.

Cellulite and Fat Reduction

Several studies have explored topical L-carnitine for cellulite and fat reduction. Nasrollahi et al¹⁷ reported subjective improvements in skin firmness with 5% L-carnitine cream, though no objective changes were noted. Roure et al¹⁸ found that a formulation with L-carnitine, caffeine, and forskolin led to significant reductions in body circumference and improved skin tone after 12 weeks. Escalante et al¹⁹ observed reductions in thigh circumference, skinfold thickness, and fat mass after 28 days of topical L-carnitine use, particularly when combined with diet and exercise. These findings suggest that topical L-carnitine may improve skin appearance and support fat reduction, though results vary with treatment protocols.

Section Summary

Topical L-carnitine is beneficial in dermatology, especially in acne treatment, sebum reduction, PIH management, and cellulite/fat reduction. Many studies have demonstrated its efficacy, often in combination with other active ingredients such as licochalcone-A. Since many studies were funded by Beiersdorf, the manufacturer of L-carnitine-based products, there could be a degree of bias. Only one study by Peirano et al¹⁴ evaluated L-carnitine as a single ingredient, emphasizing the need for further research to fully ascertain its effects.

Future studies should focus on determining the optimal concentrations and vehicle formulations for L-carnitine, as well as investigating its mechanisms of action. The current evidence supports its role in enhancing acne treatment, reducing PIH, controlling sebum production, and improving skin appearance in cellulite and fat reduction.

Oral or Systemic Carnitine in Dermatology

Several studies assessed oral L-carnitine in dermatology. Although most were RCTs, some were systematic reviews and case reports. L-carnitine, along with derivatives like ALC and PLC, was primarily used alone but occasionally combined with other supplements. The studies focused on L-carnitine’s effects on inflammatory and autoimmune skin diseases including acne, skin aging, wound healing, and metabolic dysregulation. The therapeutic potential of L-carnitine may stem from its ability to reduce inflammation, oxidative stress, and metabolic dysfunction in chronic inflammatory skin diseases^20,21, ²² Table 3 summarizes the studies reviewed.

Table 3.

Summary of Studies with Carnitine as Systemic Therapy.

Author (year)	Study type	Study’s aim	Patients	Population/disease	Intervention	Duration	Results	Level of Evidence^a
Biagiotti et al (2001)³⁷	RCT	To determine if oral ALC is useful in treating acute and early chronic Peyronie's disease, and compare it with tamoxifen.	48	48 patients (15 acute phase, 33 early chronic phase); mean age 53 (range 24-72); all males with Peronei’s disease.	-Group 1: Tamoxifen 20 mg twice daily for 3 months.-Group 2: ALC 1 g twice daily for 3 months.-No placebo.	3 months	-ALC better than tamoxifen in reducing erectile pain, penile curvature, and disease progression (8% progression in ALC vs 54% in tamoxifen group).-Both treatments reduced plaque size.-Tamoxifen caused more side effects (6 patients), including skin rashes, loss of libido, and epigastric pain. ALC had no side effects.	2b
Cannon et al (2018)²⁹	RCT	To evaluate the effect of LC on vismodegib-associated muscle spasms in patients with BCC.	12 (8 evaluable)	Adults with BCC, on vismodegib (150 mg daily), with muscle spasms after starting treatment	LC (495 mg orally twice daily) for 4 weeks followed by a 4-week washout period and cross-over to placebo for 4 weeks	4 weeks	-LC reduced muscle spasm frequency by 48%, whereas placebo increased it by 54% (P = .02).-LC also reduced the median number of body locations affected by spasms by 1 (P = .04).	1b
Czajka et al (2018)³¹	RCT	To investigate the effects of daily supplementation with hydrolyzed fish collagen, vitamins, antioxidants, and other active ingredients on skin elasticity and joint health	120	Adults (ages 21-70), mainly Caucasian, 70% women, Fitzpatrick skin types (mostly type III)	-Once daily of either active ingredients or placebo.-Gold Collagen Active: hydrolyzed fish collagen, hyaluronic acid, glucosamine, LC, chondroitin sulfate, vitamins, minerals, black pepper extract, maca extract.-Comparator: placebo (water with natural preservatives and flavorings).	90 days	-The treatment group had significant improvement in skin elasticity (+40%, P < 0.0001), joint pain reduction (−43%), increased joint mobility (+39%).-Histological improvements in skin architecture, no adverse effects reported	1b
Famularo et al (1993)²⁴	RCT	To investigate the immunomodulatory properties of LC and its effects on immune cell function and lipid metabolism	23	23 hospitalized individuals (15 males, 8 females, mean age 75.5 ± 8 years) with cardiovascular diseases (eg, cardiomyopathy, atrioventricular block, atrial fibrillation, ventricular fibrillation, sick sinus syndrome)	-Intervention: LC (3 g per day, IV for 7 days) vs placebo;-Ex vivo intervention: LC (1 g/hr) + Intralipid (20%) for 6 hours in healthy volunteers.-Other ingredients: Intralipid (fat emulsion) used in combination with LC in some experiments.-The study also compared the immune response (mixed lymphocyte reaction, skin reactivity to recall antigens) before and after treatment.	7 days	-LC reduced lipid levels (lipemia, cholesterolemia, triglyceridemia) and enhanced immune responsiveness (increased skin reactivity to recall antigens and improved mixed lymphocyte reaction).-In healthy volunteers, LC reversed the immunosuppressive effects of Intralipid.-Some patients showed no effect on lipid levels or immune response.-Adverse effects: None reported.	2b
Farahzadi et al (2016)³²	Experimental study	To evaluate the effect of LC on telomerase gene expression and telomere length in aged adipose-derived human mesenchymal stem cells	6 participants (women, aged 45–58)	Six healthy women, aged 45–58, undergoing liposuction surgery, from Iran	0.1, 0.2, and 0.4 mM LC treatments, 48-hour incubation; control group with no treatment	48 hours	-Significant increase in hTERT gene expression and telomere length with 0.2 mM LC (P < 0.0001).	4b
Fietta et al (2007)³⁸	Case report	To report on the successful treatment of a 15-year-old boy with psoriatic onycho-pachydermo-periostitis (POPP) using LC	1	15-year-old boy with POPP, a rare subset of psoriatic arthritis	LC (2 g/day orally)	9 months	-Treatment led to reduction in pain, discomfort, swelling, and soft tissue thickening.-Symptoms recurred after discontinuation of treatment but improved when LC was restarted.	4
Fukami et al (2013)³⁶	RCT, Single-Center	To assess the effects of oral LC on skin AGEs in HD patients with carnitine deficiency	102 (51 in LC group, 51 in control)	Mean age 67.5 ± 12.7 years, patients with carnitine deficiency undergoing HD	LC 900 mg/day, orally, for 6 months, compared to a control group	6 months	LC increased carnitine levels and decreased skin AGE (P = .036 for total carnitine, P = .016 for free carnitine).	2b
Gasser et al (1997)³³	Non-randomized experimental study (pilot study)	To evaluate the effects of LC on capillary blood cell velocity and cold-induced blood flow in Raynaud’s disease	12	Females, mean age 41.5 ± 14.5 years; without signs of organic or laboratory disorders.	LC 3g/day (1g three times per day)	20 days	Cold-induced blood flow stop duration was significantly (P < .05) decreased and capillary blood cell velocity significantly (P < .05) increased after local cooling.	4
Georgala et al (1999)²⁸	RCT	To evaluate whether LC supplementation could treat muscular symptoms (myalgia, stiffness) associated with isotretinoin therapy in cystic acne patients.	230	121 females, 109 males, mean age 20.8 ± 1.5 years, patients with cystic acne on isotretinoin therapy	LC 100 mg/day for 45 days, compared to placebo	45 days	-LC ameliorated muscular symptoms within 5-6 days and normalized liver enzyme and carnitine levels, and improved liver and muscle enzymes.-Placebo group continued to complain of myalgias.	2b
Jamilian et al (2019)²¹	RDBPCT	To evaluate the effect of LC and chromium co-supplementation on mental health, hormonal, inflammatory, genetic, and oxidative stress parameters in women with PCOS.	54	Women aged 18–40 years, with PCOS (diagnosed by Rotterdam criteria).	Intervention: 1000 mg/day of LC + 200 mg/day of chromium picolinate for 12 weeks.Placebo group received a matching placebo.	12 weeks	Therapy improved mental health (Beck Depression Inventory, General Health Questionnaire, Depression Anxiety Stress Scale), lowered testosterone, reduced hirsutism, decreased high sensitivity-CRP, reduced MDA, increased Total Antioxidant Capacity.	1b
Khan et al (2011)³⁰	Review	To review the role of LC in managing radiation toxicity and radiotherapy side effects		Cancer patients undergoing radiotherapy with side effects like fatigue, nausea, hair loss, anemia, and more	LC (oral/systemic) was explored for its potential protective effects against radiation-induced damage. The review also mentions ALC and acylcarnitines		-LC reduced radiation-induced damage in various organs, improved oxidative stress markers, and enhanced tissue function.-Benefits included protection against testicular, brain, kidney, and cochlear damage.	4
Mohammadi et al (2018)²²	RDBPCT	To determine the effect of LC on oxidative stress biomarkers, antioxidant capacity, and lipid profile in patients with PV	52	30-65 years old, diagnosed with PV, on corticosteroid therapy	LC 2g/day (1g before breakfast and dinner) vs placebo.	8 weeks	LC reduced triglycerides, TC, LDL-C, VLDL-C, and oxidative stress index, and increased Total Antioxidant Capacity and serum carnitine.	2b
Noormohammadi et al (2023)²⁵	RDBPCT	To investigate whether LC supplementation can reduce or counteract the muscle-wasting effects of glucocorticoid therapy in PV patients.	44	PV patients aged 30-65 years, undergoing corticosteroid therapy.	-LC tartrate 2g per day (1g before breakfast and dinner).-Placebo group received a placebo for the same duration.	8 weeks	-LC group had increase in serum IGF-1 and decrease in creatine kinase and myostatin levels; preserved Myogenin levels compared to placebo.	1b
Pirmadah et al (2020)²³	Systematic review and meta-analysis of RCT	To assess the effect of LC supplementation on serum liver enzymes (ALT, AST, GGT) in adults.	1161 participants	Mixed population (patients with liver diseases, hemodialysis patients, hypothyroidism, cystic acne, obesity, myocardial infarction, healthy participants)	-Oral LC supplementation (500-4000 mg/day).-Comparators included placebo, no treatment, and active drugs.	2-48 weeks	-Significant reductions in ALT (MD = −8.65 IU/L, AST (MD = −8.52 IU/L), GGT (MD = −8.80 IU/L) levels.-Higher doses (≥2000 mg/day) and longer durations (>12 weeks) were more effective.	1a
Pola et al (1991)³⁵	Non-randomized experimental study	To evaluate the effectiveness of PLC in treating refractory arterial and venous cutaneous ulcers in vasculopathic patients	18	Patients (aged 47–82) with chronic, drug-resistant arterial (7), venous (8), and mixed (3) cutaneous ulcers of the lower extremities	PLC, administered either:- Orally: 1500 mg/day for 30 days- IV: 5000 mg/day for 10 days, then oral 3000 mg/day for 20 days	30 days total (either fully oral, or IV for 10 days followed by oral for 20 days)	-Out of 19 ulcers: 6 (31.8%) completely healed, 7 (36.8%) good response, 2 (10.5%) fair, 2 (10.5%) modest, 2 (10.5%) failed-Venous ulcers: 55% healed completely, rest reduced >50%-Arteriopathics: increase in distal arterial blood flow (P = .001 for total flow velocity)-Some cases showed avoidance of amputation or major surgery	4
Rastgoo et al (2023)²⁰	Systematic Review and Meta-Analysis	To investigate the effects of LC on inflammatory and oxidative stress markers, liver enzymes (ALT, AST, ALP), and overall liver function in patients with chronic conditions.	3,255 (from 48 RCTs)	Adults with various health conditions, including end-stage kidney disease, non-alcoholic fatty liver disease, and other chronic inflammatory conditions.	-LC supplementation (varied doses) vs placebo or control groups.-Optimal dose identified: ~2 g/day.-Optimal duration for liver enzyme improvement: 50 weeks.	50 weeks	-Inflammatory and Oxidative Stress Markers:↓ CRP (P < 001), IL-6 (P = .001), TNF-α (P = .002), MDA (P = .001)-↑ Total Antioxidant Capacity, (P = .029), nitric oxide, GSH≥2 g/day was most effective for TNF-α reduction>12 weeks of supplementation showed stronger anti-inflammatory effects-Liver Function:↓ ALT, AST (P < .001), ALP-Optimal duration for ALT/AST reduction = 50 weeks-Subgroup Findings:More pronounced benefits in patients with type 2 diabetes or BMI ≥25-Trials lasting ≥12 weeks showed stronger anti-inflammatory effects	1a
Signorelli et al (2001)³⁴	RCT	To compare the therapeutic benefits of PLC with pentoxifylline in treating chronic critical limb ischemia.	188	Patients with peripheral arterial disease, specifically chronic critical limb ischemia.	PLC (1.2 g/day) or pentoxifylline (1.2 g/day) administered intravenously for 2 weeks with calcium heparin (25,000 U/day) for thromboembolism prophylaxis in both groups.	2 weeks	PLC group showed significantly better results: 78% increase in pain-free walking distance vs 30% with pentoxifylline (P < 0.001); 83% reduction in pain vs 46% (P < 0.001); 48% reduction in ulcer size vs 25% (P < 0.001).	1b
Sepandar et al (2020)²⁶	RDBPCT	To assess LC supplementation on serum omentin-1, visfatin, SFRP5, and glycemic indices in PV patients on corticosteroid treatment	52	30-65 years old with PV on corticosteroid therapy	LC 2g daily for 8 weeks vs placebo;	8 weeks	-LC significantly decreased visfatin (p = .05) and increased omentin-1 (P < 0.01) and SFRP5 (P < 0.006);-No significant changes in glycemic indices.	2b
Yaghubi et al (2019)²⁷	RDBPCT	To evaluate the protective effects of LC in PV patients on corticosteroid treatment, regarding cardiovascular and bone turnover markers	48 (24 in LC group, 24 in placebo group)	Age 30-65, women and men PV patients treated with corticosteroids	2 g/day LC or placebo for 8 weeks (1 g before breakfast and 1 g before dinner).	8 weeks.	-LC group showed decrease in BMP4 (P = .003) and ostepontin (P = .03 after adjustment);-Cystatin C did not change significantly in L-carnitine group (P = P = .27) but decreased in placebo (P = .001).	1b

Abbreviations: AGEs, advanced glycation end products; ALC, acetyl-L-carnitine; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BCC, Basal Cell Carcinoma; BMI, body mass index; BMP4, bone morphogenic protein 4; BMP4, bone morphogenic protein 4; CRP, C-reactive protein; GGT, gamma-glutamyl transferase; HD, hemodialysis; HDL-C, high density lipoprotein C; hTERT, human telomerase reverse transcriptase; IGF-1, insulin-like growth factor – 1; IL-, interleukin-; IV, intravenous; LDL-C, low density lipoprotein Cholesterol; MD, mean differences; MDA, malondialdehyde; PCOS, polycystic ovarian syndrome; PLC, propionyl L-carnitine; POPP, psoriatic onycho-pachydermo-periostitis; PV, pemphigus vulgaris; RCT, randomized controlled trial; RDBPCT, Randomized, double-blind, placebo-controlled trial; ROS, Reactive oxygen species; SFRP5, secreted frizzled-related protein-5; TC, total cholesterol; TNF-α, tumor necrosis factor alpha; VLDL-C, very low density lipoprotein Cholesterol.

Each study’s design was determined by the authors and was classified according to the 2009 Oxford Centre for Evidence-Based Medicine Levels of Evidence. (Oxford Centre for Evidence-Based Medicine: Levels of Evidence (March 2009) - Centre for Evidence-Based Medicine (CEBM), University of Oxford. https://www.cebm.ox.ac.uk/resources/levels-of-evidence/oxford-centre-for-evidence-based-medicine-levels-of-evidence-march-2009. Accessed: 2025-08-04).

Anti-inflammatory and Immunomodulatory Effects

Although not originally studied within dermatology, several investigations into oral L-carnitine have yielded findings with clear relevance to dermatologic care. A systematic review and meta-analysis (SR-MA) of 48 RCTs, demonstrated that L-carnitine supplementation significantly reduced inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).²⁰ Importantly, these studies also reported improvements in liver enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), particularly in trials of ≥ 12 weeks duration. Similarly, another SR-MA found notable reductions in ALT, AST and gamma-glutamyl transferase (GGT) with higher L-carnitine doses (≥2 g/day), reinforcing its hepatoprotective properties.²³ These findings are especially pertinent in dermatology, where systemic therapies such as isotretinoin and methotrexate pose risks of hepatotoxicity, suggesting L-carnitine may offer a supportive role in liver function monitoring or adjunctive care.

Further, Famularo et al²⁴ demonstrated immunomodulatory effects of L-carnitine in cardiovascular patients, showing improved lymphocyte responsiveness and increased skin reactivity to recall antigens, findings potentially applicable to dermatologic conditions with altered immune reactivity such as allergic contact dermatitis. In another study, Jamilian et al²¹ found that L-carnitine combined with chromium improved inflammatory and hormonal parameters in women with polycystic ovary syndrome (PCOS), including reductions in high-sensitivity CRP and testosterone levels. This is particularly relevant given the high prevalence of acne and hidradenitis suppurativa in PCOS patients, conditions influenced by both inflammation and androgen levels.

Together, these studies support L-carnitine’s systemic anti-inflammatory, hormonal, and hepatic benefits, all of which are highly relevant in dermatology. Whether used to support patients on hepatotoxic medications, modulate immune reactivity in eczematous conditions, or aid in managing hormonally driven dermatoses, L-carnitine represents a promising adjunctive therapeutic avenue deserving further exploration in dermatologic populations.

Alleviating Treatment-Related Side Effects

L-carnitine can alleviate treatment-related adverse effects in patients undergoing dermatology therapies including corticosteroids, isotretinoin, vismodegib, and radiation. In patients with pemphigus vulgaris (PV) treated with oral corticosteroids, a randomized double-blind, placebo-controlled trial (RDBPCT) demonstrated that 2g of L-carnitine daily for 8 weeks improved muscle biomarkers [increased serum insulin-like growth factor 1 (IGF-1)] and reduced myostatin and creatine kinase levels, key indicators of reduced muscle atrophy.²⁵ This indicates the potential role of L-carnitine in preventing muscle wasting, a common side effect of long-term corticosteroid use. Another RDBPCT of 52 patients showed that oral L-carnitine improved insulin sensitivity and reduced inflammation in PV patients treated with corticosteroids.²⁶ Mohammadi et al²² demonstrated reductions in lipid markers [triglycerides, low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C)] and oxidative stress, in a similar population of PV patients, suggesting L-carnitine's potential in managing dyslipidemia and oxidative damage, common concerns in PV patients receiving corticosteroid therapy. Beyond metabolic effects, Yaghubi et al²⁷ found that L-carnitine reduced bone turnover biomarkers [bone morphogenic protein 4 (BMP4) and osteopontin] in PV patients treated with corticosteroids, indicating its potential to ameliorate bone and cardiovascular risks associated with corticosteroid use. These studies suggest L-carnitine may serve as a useful addition to reduce muscle wasting, metabolic disturbances, bone loss and oxidative stress in patients undergoing corticosteroid therapy.

In patients treated with isotretinoin for severe acne, Georgala et al²⁸ administered 100mg of L-carnitine daily for 45 days and found relief from muscle pain and stiffness, enabling continued isotretinoin treatment without dose reduction. In addition, Cannon et al²⁹ demonstrated that L-carnitine reduced muscle spasms by 48% in patients with basal cell carcinoma undergoing vismodegib therapy. Khan et al³⁰ suggested that L-carnitine could help mitigate radiation-induced skin damage (erythema and inflammation), although more studies are needed for dermatologic confirmation.

These findings highlight L-carnitine as an adjunct in alleviating various side effects associated with dermatologic treatments including corticosteroids, isotretinoin, vismodegib, and radiation therapy. Its ability to address muscle wasting, metabolic disturbances, and oxidative stress suggests it as a useful therapy for improving patient outcomes in dermatologic care.

Elasticity and Aging

Systemic L-carnitine has been shown to improve skin elasticity and combat aging. Czajka et al³¹ found that a nutraceutical containing L-carnitine, hydrolyzed fish collagen, vitamins, and antioxidants improved skin elasticity by 40% over 90 days (P < 0.0001), suggesting a significant role in collagen synthesis and skin rejuvenation, although the specific attribution of the effect to L-carnitine can not be proven. Additionally, Farahzadi et al³² showed L-carnitine’s ability to increase telomerase gene expression and telomere length in human mesenchymal stem cells, suggesting a potential role in skin rejuvenation at the cellular and stem cell level. These findings indicate that L-carnitine could be an important ingredient in anti-aging formulations for collagen synthesis and promotion of cellular regeneration.

Microcirculation, Wound Healing and Anti-Fibrotic Effects

L-carnitine’s systemic administration has demonstrated potential benefits in dermatology-related contexts by improving microcirculation, enhancing wound healing, and exerting anti-fibrotic effects across various clinical settings. Several studies have highlighted L-carnitine’s role in improving vascular function and microcirculation, which may be relevant in dermatologic conditions associated with impaired blood flow. For example, Gasser et al³³ evaluated patients with primary Raynaud’s disease and found that a 20-day course of oral L-carnitine (3 g/day) significantly increased capillary blood cell velocity and reduced the cold-induced blood flow stop duration, indicating enhanced microcirculatory function. Similarly, Signorelli et al³⁴ demonstrated that PLC improved pain-free walking distance and reduced ulcer size in patients with chronic critical limb ischemia, suggesting benefits in circulation and wound healing. In a study of 18 patients with chronic, drug-resistant arterial and venous lower leg ulcers, Pola et al³⁵ used oral or intravenous PLC for 30 days resulting in complete healing in 32% of the ulcers and significant improvement in another 37%, with a marked increase in distal arterial blood flow among arteriopathic patients. These findings are particularly notable given that patients had previously failed to respond to standard therapies.

Beyond its effects on circulation, L-carnitine has shown potential in tissue regeneration and anti-fibrotic activity. Fukami et al³⁶ reported that L-carnitine supplementation reduced advanced glycation end products (AGEs) in hemodialysis patients, improving skin elasticity and supporting tissue regeneration. Biagiotti et al³⁷ found ALC to be more effective than tamoxifen in improving tissue remodeling in patients with Peyronie’s disease, showcasing its potential in addressing fibrosis, which may have implications in sclerotic skin disorders. Additionally, Fietta et al³⁸ reported reduced pain, swelling, and tissue thickening in a patient with psoriatic onycho-pachydermo-periostitis following L-carnitine treatment, further supporting its role in tissue repair.

Collectively, these findings suggest that oral L-carnitine may offer supportive therapeutic roles in dermatology by improving microcirculation, promoting wound healing, and modulating fibrotic processes, warranting further exploration in targeted dermatologic conditions.

Section Summary

Systemic L-carnitine shows promise as an adjunctive therapy in dermatology, with demonstrated benefits including anti-inflammatory and immunomodulatory effects, mitigation of treatment-related side effects, improved skin elasticity, enhanced microcirculation, and wound healing, as well as anti-fibrotic activity. While existing studies suggest meaningful clinical potential, many are limited by small sample sizes and variation in dosage and formulations. Future well-designed RCTs are needed to define optimal use in dermatologic care. Nonetheless, L-carnitine represents a versatile systemic agent that aligns with dermatology’s broader goals of reducing inflammation, minimizing treatment toxicity and supporting overall skin health.

Use of Carnitine as a Biomarker for Dermatologic Disease or Disease-State

Given its central role in fatty acid metabolism and mitochondrial function, carnitine has emerged as a promising biomarker across a range of dermatologic and systemic conditions. Alterations in carnitine levels and derivatives reflect underlying metabolic, inflammatory, or fibrotic processes, offering diagnostic and prognostic insights. This section examines how shifts in carnitine metabolism, whether through depletion, accumulation, or altered ratios, can inform on disease presence, subtype, or progression in both hereditary and acquired dermatologic disorders. Table 4 summarizes the studies reviewed.

Table 4.

Summary of Studies with Carnitine as Biomarker.

Author (year)	Study type	Study’s aim	Patients	Population/disease	Type of carnitine molecule	Results	Level of Evidence^a
Adachi et al (2012)⁵²	Cross-sectional, noninterventional	To examine whether carnitine deficiency is independently associated with increased tissue accumulation of AGEs in HD patients.	129 HD patients, 75 healthy controls	129 haemodialysis patients (75 male, 54 female; mean age 68.2) vs 75 healthy controls (mean age 65.4)	LC (serum)	-Serum carnitine was lower in HD patients (P < 0.001).-Skin AGEs were higher in HD patients compared to healthy controls (P < 0.001).-Carnitine levels were independently associated with AGEs levels (P = .024).	4b
Chen et al (2021)⁴⁵	Case-control study with experimental animal model	To investigate metabolic alterations in amino acids and carnitines in PSO and their potential role in pathogenesis and therapy	90 (45 PSO patients, 45 healthy controls)	Adults (age ≥18, women and men) with PSO	Palmitoylcarnitine, C6, C18:1, LC (plasma)	-PSO patients had elevated levels of BCAAs, C6, and C18:1-Palmitoylcarnitine was negatively correlated with PASI score.-Supplementation of LC in an animal model reduced epidermal thickening and Th17 cell infiltration, suggesting its therapeutic potential.	2b
Chiang et al (2008)³⁹	Case report	To report a case of restrictive dermopathy, a rare autosomal recessive genodermatosis, and investigate metabolic and post-mortem findings.	1	Male preterm infant, born at 31 weeks gestation, Taiwanese, diagnosed with restrictive dermopathy.	Free carnitine (urine and blood)	-The infant exhibited organic aciduria, low free carnitine levels (10.29 µM), and thymic hypoplasia.-At autopsy, severe dermal fibrosis and hyperkeratosis were found. The findings suggest restrictive dermopathy may be associated with metabolic disturbances, including a carnitine deficiency.	4c
Geamanu et al (2016)⁵³	Cross-sectional, Metabolomics study	To investigate the metabolomic profile of sarcoidosis patients using 1H NMR spectroscopy to identify altered serum metabolites.	37 (20 sarcoidosis patients, 17 healthy controls)	Adults, sarcoidosis patients, healthy controls matched by race, age, and body mass index.	LC (serum)	-Increased serum carnitine in sarcoidosis patients (P = .019), along with other metabolites like 3-Hydroxybutyrate and acetoacetate.-Altered metabolic pathways identified (eg, fatty acid β-oxidation, TCA cycle).	2b
Guo et al (2023)⁵⁵	Cohort Study, Metabolomic Profiling	To identify serum metabolic alterations in SSc patients, comparing before and after treatment, and investigate the potential biomarkers related to disease progression	326 human samples, 33 mouse samples	142 healthy controls, 127 untreated SSc patients, 57 treated SSc patients, Age and gender-matched	C6 (serum)	-SSc patients showed a unique metabolic profile with 375 elevated and 471 decreased metabolites.-C6 was positively correlated with the modified Rodnan skin score (P < 0.05).-Treatment partially restored metabolic alterations, with metabolites linked to clinical progression.	2b
Hu et al (2022)⁵⁶	Cohort study	To investigate keloid-related circulating metabolic signatures using metabolomic analysis	236 (118 keloid patients, 118 healthy volunteers)	Keloid patients and age- and sex-matched healthy volunteers.No history of metabolic syndrome, obesity, dyslipidemia, hypertension, diabetes, or other metabolic diseases.	Plasma palmitoylcarnitine, sphingosine, phosphocholine, and phenylalanylisoleucine (plasma)	elevated levels of palmitoylcarnitine and sphingosine, and lower levels of phosphocholine and phenylalanylisoleucine are strongly correlated with the early identification of keloids.	2b
Huang et al (2014)⁴⁹	Cohort study	To explore metabolic mechanisms and potential biomarkers of AD using metabolomics and eicosanoids analysis	42 AD patients (19 high IgE, 23 normal IgE), 23 healthy controls (first batch); 41 AD patients (19 high IgE, 22 normal IgE), 22 controls (second batch)	Children aged 3–36 months diagnosed with AD	Carnitines, various including C18:2 (serum)	-AD children with high IgE had increased serum carnitine levels. -Combination markers including C18:2 distinguished high IgE vs normal IgE phenotypes with high sensitivity and specificity (AUC 0.906).	2b
Ilves et al (2022)⁵¹	Cross-sectional study (metabolomic analysis)	To compare the metabolomic profiles of the lesional and non-lesional skin, and blood sera of patients with AD and PSO	15 AD, 20 PS (skin biopsies), 25 AD, 55 PSO (blood serum), 17 controls (skin biopsies), 63 controls (blood serum)	Adults with AD (ages 20-50, 4 men, 11 women), PSO (ages 20-75, 13 men, 7 women), healthy controls (ages 23-75, 10 men, 7 women), all Caucasians of Eastern European descent	Carnitine, ALC, C18:2, C18:1 (serum)	-Elevated ALC and C18:2 in PSO-lesional skin compared to AD-lesional skin; significant differences in metabolite concentrations (eg, P = .0043 for ADMA in PSO-lesional skin).-Serum carnitine was higher in PSO vs AD patients.	2b
Kanepa et al (2024)⁴²	Cohort Study	To explore disease-specific metabolite signatures in HAE patients and identify potential diagnostic biomarkers	45 (10 HAE patients, 15 IAE patients, 20 healthy controls)	Adults with HAE (types 1 and 2), IAE, and healthy controls	C5 (serum)	C5, cystine, and hydroxyproline were altered in HAE patients vs controls.	3b
Lee et al (2024)⁴⁷	Retrospective Cohort Study	To compare the metabolic profiles of PSO and PPP with HC using metabolomics analysis.	93 patients (73 PSO, 20 PPP)	Korean patients with PSO (mean age 42.0 ± 13.1, 22 females) and PPP (mean age 54.7 ± 9.5, 10 females), matched with HC s for age and gender.	PLC, ALC (plasma)	-Increased sarcosine, serotonin, PLC, proline, and others in PSO patients.-Decreased ALC in PSO.	2b
Li et al (2025)⁵⁹	Mendelian Randomization Study	The aim of the study was to investigate the causal relationship between blood metabolites and AV by conducting a metabolomic Mendelian randomization analysis. The goal was to identify potential biomarkers for acne and to explore the metabolic pathways involved in its development.	486	The study used a genome-wide association dataset (no specific demographic details on age, gender, or ethnicity provided)	Nonanoylcarnitine, Isobutyrylcarnitine, 1-stearoylglycerol, and others (metabolites from 486 metabolites screened in serum)	-Findings included a genetic correlation between nonanoylcarnitine and acne (rg = 2.0641, P = .0171), and significant inverse associations with acne for isobutyrylcarnitine (OR = 0.65, P = .0192) and 3-methoxytyrosine (OR = 0.58, P = P = .0073).-However, after Benjamini-Hochberg adjustment, none of the metabolites retained statistical significance for all metabolites.	1b
Liu et al (2019)⁵⁸	Case-Control Study (Untargeted Metabolomics)	To analyze serum metabolite profiles in syphilis patients and identify potential biomarkers for diagnosis	40 (20 syphilis patients, 20 healthy controls)	Mean age: 53.3 years; (13 males (65%), 7 females (35%) in syphilis group; 11 males (55%), 9 females (45%) in control group; Ethnicity: not specified; Condition: Syphilis	ALC (serum)	-ALC was significantly reduced (P = .04) whereas TMAO was 3.922 times higher (P = .013) in syphilis patients compared to controls.	4
Liu et al (2022)⁴	Systematic Review	To clarify the effects of acylcarnitines (ACs) in depressive patients and explore whether ACs might be biomarkers for depression and potential treatment options.		The review included data from multiple studies on depression, bipolar disorder, and other mental diseases.	Various acylcarnitines (ACs) and ALC (serum)	-Multiple studies indicated that AC levels are altered in depressive patients.-Supplementation with ALC appears beneficial in treatment, and certain ACs may be potential biomarkers for depression.	1a
Ma et al (2024)⁴⁸	Metabolomic analysis, case-control study	To investigate circulating blood metabolomic and cytokine profiles in AD compared to healthy controls.	20 AD patients, 24 healthy controls (metabolomics); 19 AD patients, 33 healthy controls (cytokine analysis); 18 overlapping AD patients in both analyses.	Adults (>18 years) diagnosed AD per Hanifin & Rajka criteria; moderate-to-severe pruritus (Numeric Rating Scale ≥5, Investigator’s Global Assessment ≥3).	ALC and LC (plasma)	-Both ALC and LC levels were decreased (>2-fold, P < .0001) in AD vs healthy controls.-Decreased metabolites were positively correlated with TARC and MCP-4 and negatively correlated with IL-1a and CCL20.	3b
Macpherson et al (2020)⁴⁴	Cohort Study	To investigate the association between the TMAO, gut microbiota dysbiosis, and systemic inflammation in CVID patients.	104 CVID patients, 30 healthy controls	Mean age of CVID patients: 51.2 ± 11.8 years; 65% females. CVID patients with autoimmune or inflammatory complications, compared to healthy controls.	TMAO, carnitine, choline, betaine (plasma)	-CVID patients had higher plasma TMAO vs healthy controls (5.0 vs 3.2 µmol/L, P = .022). TMAO levels correlated with TNF-α and IL-12 (P = .008, P = .012, respectively).-Increased Gammaproteobacteria abundance in CVID gut microbiota correlated with TMAO levels (P = .021).-No significant temporal changes in metabolites during 8-week follow-up.	2b
Manjunath et al (2024)⁵⁷	Cross-sectional study	To investigate changes in blood metabolites in CPUO patients and identify potential therapeutic targets.	22 (11 CPUO patients, 11 matched controls)	11 CPUO patients (chronic pruritus >6 weeks, matched by age, sex, and race)	DL-carnitine and ALC (plasma)	Compared to controls, CPUO patients had downregulation of 15 metabolites including creatinine, DL-carnitine, acetyl-L-carnitine), which were also significantly correlated with itch severity.	2b
Masutin et al (2022)⁴⁶	Systematic review, Cross-study comparison	To review and analyze metabolic changes in the skin caused by internal and external factors, focusing on skin diseases like PSO.		Studies included various factors like irradiation, xenobiotics, aging, and skin diseases (mainly PSO).	Carnitine derivatives, carnitine shuttle activity (plasma, serum, lesional skin cells),	-Oxidative stress and lipid metabolism (β-oxidation and carnitine shuttle activity) were elevated in psoriasis.-Elevated carnitine and acylcarnitine levels indicated upregulation of β-oxidation, with some studies showing impaired β-oxidation in response to xenobiotics.	1a
Nie et al (2021)⁶⁵	Case-Control Study	To determine if serum LC and ALC can be used as biomarkers for MDD	89 patients with MDD, 89 HC	Age 18-70, both genders, primarily Chinese ethnicity, MDD diagnosis	LC and ALC (serum)	-LC and ALC were significantly lower in the MDD group vs HC (P < 0.001 for both).-ALC negatively correlated with depression severity (P = .007).-Significant increase in LC and ALC in the effective (responsive) treatment group (P = .001 for LC, P = .047 for ALC), no significant change in the ineffective (non-responsive) group.	2b
Ottria et al (2020)⁵⁴	Cohort study	To investigate dysregulation of fatty acid and carnitine metabolism in SSc patients	27 SSc patients; 20 HC	Adults (age range, gender and ethnicity not specified) with SSc	LC, acylcarnitines (in plasma and dendritic cells)	Increased carnitine (P = .025) and Isovaleryl-carnitine (P = .03) and decreasedOctanoyl-carnitine (P = .04) and Palmitoyl-carnitine (P = .06; in the plasma of SSc patients.	2b:
Salera et al (2020)⁴¹	Review	To assess micronutrient deficiencies in RDEB with a focus on carnitine and selenium.	19-25 (for carnitine and selenium analysis)	RDEB patients (age and gender unspecified)	Free and total carnitine (plasma)	-Free carnitine was low in 61.5% of patients, while total carnitine was low in only 1 patient.-Carnitine supplementation prevents progression of DCM but does not reverse it.	4b
Shepelin et al (2016)⁶¹	High-throughput analysis (Bioinformatic/Statistical Modeling)	To identify molecular pathways linked with the transition from normal skin to primary and metastatic melanomas, with a focus on carnitine biosynthesis	478 (samples, not individual patients)	Samples from primary and metastatic melanoma, nevi, and normal skin.Ethnicity and gender not specified.	LC biosynthesis pathway (cells)	-LC biosynthesis as significantly upregulated in nevi and downregulated in melanomas.-Pathway activation was found to correlate with melanoma progression, with a balanced accuracy of ~0.93 in classification models.-Carnitine biosynthesis regulation appears associated with the hypoxic environment of melanomas, potentially.	4b
Sidwell et al (2000)⁴⁰	Cohort Study	To investigate the relationship between carnitine deficiency and DCM in children with severe RDEB	61 children with severe RDEB	Children with severe RDEB, both genders, affected by severe RDEB and DCM.	Free and total carnitine (serum)	Lower concentrations of free and total carnitine were significantly associated with DCM (P = .006).	3b
Yang et al (2024)⁵⁰	Mendelian Randomization Study	To investigate the causal relationships between immune cells, AD, and the mediating effects of plasma metabolites	22,474 AD cases, 774,187 controls	European cohorts; (age, gender, or ethnicity breakdown not provided)	Carnitine, plasma metabolite (glycerol-to-carnitine ratio) (plasma)	Glycerol-to-carnitine ratio positively regulated HLA-DR on CD14- CD16- cells in AD (ME = 0.00209; MP = 7.8%)	2b
Yu et al (2018)⁶⁰	Metabolomics Case Study	To investigate differential metabolite profiles between primary and metastatic melanoma cell lines and identify key metabolites related to melanoma progression	20 (8 primary cell samples, 12 metastatic cell samples)	Melanoma cell lines (WM226-4 and WM-115), derived from the same individual, representing primary and metastatic melanoma stages	Carnitine, acylcarnitines (PLC, palmitoylcarnitine), (cell culture medium)	Elevation in carnitine and acylcarnitines in metastatic cells, involved in the carnitine shuttle pathway; upregulation of fatty acid transport for ATP production in metastatic cells.Pathways linked to tumor survival.	4

Abbreviations: 1H NMR, 1H nuclear magnetic resonance; ABC, ATP binding cassette; AC, acylcarnitines; AD, atopic dermatitis; ADMA, asymmetric dimethylarginine; AGEs, advanced glycation end products; ATP, Adenosine Triphosphate; AUC, area under the curve; AV, acne vulgaris; BCAA, branched-chain amino acids; C5, Isovalerylcarnitine; C6, hexanoylcarnitine; C18:1, octadecenoylcarnitine; C18:2, Octadecadienylcarnitine,; CCL20, C-C Motif Chemokine Ligand 20 (LARC); CD, cluster of differentiation; CPUO, chronic pruritus of unknown origin; CVID, Common variable immunodeficiency; DCM, dilated cardiomyopathy; HAE, hereditary angioedema; HC, healthy controls; HD, hemodialysis; HLA-DR, Human Leukocyte Antigen – DR isotype; IAE, idiopathic angioedema; IgE, immunoglobulin E; IL-, interleukin- ; LC, L-carnitine; MCP-4, Monocyte Chemoattractant Protein-4 (CCL13); MDD, major depressive disorder; ME, mediation effect; MP, morphological parameters; OR, odds ratio; PASI, psoriasis area severity index; PPP, palmoplantar pustulosis; PSO, psoriasis vulgaris; RDEB, recessive dystrophic epidermolysis bullosa; ROC, Receiver Operating Characteristic; SSc, systemic sclerosis; TARC, Thymus and Activation-Regulated Chemokine (CCL17); Th17, T-helper 17; TMAO, Trimethylamine N-oxide; TNF-α, tumor necrosis factor alpha.

Carnitine as a Biomarker in Genodermatoses and Hereditary Conditions

Carnitine and its metabolites show promise as biomarkers in genetic and hereditary dermatoses, offering insights into disease mechanisms, progression, and therapeutic strategies.

Chiang et al³⁹ reported low free carnitine levels in a case of restrictive dermopathy, a rare autosomal recessive condition. Although this was based on a single case, this study points to the potential of carnitine as a potential biomarker in this rare disease. Early detection of carnitine deficiency could enable interventions like supplementation to improve outcomes.

In recessive dystrophic epidermolysis bullosa (RDEB), Sidwell et al⁴⁰ and Salera et al⁴¹ found significantly reduced carnitine levels, linking deficiency to dilated cardiomyopathy (DCM). While supplementation did not reverse established DCM, it prevented further deterioration, highlighting the importance of monitoring carnitine levels to mitigate cardiovascular risks in RDEB.

In hereditary angioedema (HAE), Kanepa et al⁴² and Wang et al⁴³ showed decreased isovalerylcarnitine (C5) levels, with a diagnostic ratio distinguishing HAE from idiopathic angioedema with high sensitivity and specificity. This suggests that carnitine metabolites, like C5, could be used as a biomarker for diagnosing rare and often misdiagnosed conditions like HAE.

Macpherson et al⁴⁴ found elevated trimethylamine-N-oxide (TMAO), a carnitine metabolite, in patients with Common Variable Immunodeficiency (CVID). TMAO levels correlated with inflammatory markers and gut microbiota, indicating its potential as biomarker for chronic inflammation in immune-mediated skin diseases.

These findings highlight carnitine and its metabolite as valuable biomarkers in genodermatoses and hereditary conditions, from restrictive dermopathy to RDEB, and HAE. Monitoring carnitine levels could enhance the management of these conditions, through further research is needed to confirm clinical utility.

Carnitine as Biomarker in Atopic Dermatitis and Psoriasis

Carnitine studies in atopic dermatitis (AD) and psoriasis (PSO) illustrate its potential as a biomarker in these chronic diseases. While altered carnitine metabolism is consistently shown, discrepancies exist in the direction and implications of these changes.

Both PSO and AD show altered carnitine metabolism. In PSO, systemic carnitine depletion correlates with disease severity, ⁴⁵, ⁴⁶ while increased lesional carnitine suggests increased β-oxidation in inflamed skin.⁴⁶ Lee et al⁴⁷ further refined the biomarker potential of carnitine-related metabolites by identifying elevated PLC and decreased ALC in PSO patients compared to healthy controls. In AD, systemic carnitine changes appear to vary by disease phenotype, indicating different metabolic adaptations. Ma et al⁴⁸ reported significant reductions in plasma L-carnitine and ALC levels in AD patients. Conversely, Huang et al⁴⁹ observed elevated serum carnitine levels in AD patients with high immunoglobulin E levels, suggesting possible mitochondrial dysfunction and impaired fatty acid β-oxidation. Additionally, Yang et al⁵⁰ found that the glycerol-to-carnitine ratio significantly influenced inflammatory responses. A metabolomic study by Ilves et al⁵¹ further highlighted differences in carnitine metabolism between PSO and AD. They found that serum carnitine levels were higher in PSO than in AD, and certain carnitine metabolites were more elevated in PSO-lesional skin compared to AD-lesional skin.

The evidence supports carnitine as a potential biomarker in PSO and AD, though its utility may depend on disease phenotype, systemic versus localized changes, and possibly environmental factors. Future research should integrate metabolomic and immunologic data to optimize its role in inflammatory skin diseases and guide personalized treatment strategies.

Carnitine as Biomarkers in in Other Chronic Dermatologic and Systemic Disorders

Carnitine’s role in skin pathology may extend beyond metabolic support to include potential utility as a biomarker of fibrosis and tissue remodeling. While a cross-sectional study of 129 hemodialysis patients by Adachi et al⁵² found that carnitine deficiency was associated with increased accumulation of AGEs - known contributors to skin damage, aging, and fibrosis - other studies suggest that elevated carnitine levels may also reflect fibrotic processes. For example, a metabolomics study of patients with sarcoidosis⁵³ and a separate cohort study in systemic sclerosis (SSc)⁵⁴ both reported increased carnitine and acylcarnitine species, suggesting impaired fatty acid oxidation and mitochondrial dysfunction. Moreover, hexanoyl-carnitine was positively correlated with skin fibrosis in SSc⁵⁵ while elevated palmitoylcarnitine levels were linked to inflammation and fibroblast proliferation in keloid patients.⁵⁶ Taken together, these findings indicate that both deficiency and dysregulation of carnitine metabolism may serve as markers of skin pathology, whether through accumulation of toxic metabolites like AGEs or through altered mitochondrial function associated with fibrosis and inflammation.

Interestingly, while elevated carnitine levels have been associated with fibrotic and inflammatory skin conditions, a contrasting pattern emerges in disorders characterized by chronic irritation or microbial etiology. In chronic pruritus of unknown origin (CPUO), reduced levels of L-carnitine and ALC have been correlated with more severe pruritus, implicating mitochondrial dysfunction and impaired epidermal barrier repair.⁵⁷ Similarly, metabolomic profiling in syphilis patients has revealed diminished ALC, likely reflecting oxidative stress and compromised energy metabolism during systemic infection and cutaneous involvement.⁵⁸ In acne, a condition marked by sebaceous gland hyperactivity and immune dysregulation, a recent Mendelian randomization study identified elevated nonanoylcarnitine as a potential risk marker, while isobutyrylcarnitine may exert protective effects further supporting the role of lipid metabolism perturbations in disease pathogenesis.⁵⁹ These findings suggest that distinct carnitine profiles, whether elevated or depleted, may signify divergent pathological processes, with deficiencies aligning more closely with chronic itch, infectious dermatoses, and microbial inflammation.

Carnitine as Biomarker in Melanoma

Carnitine metabolism plays a significant role in melanoma progression, with two key studies, one by Yu et al⁶⁰ and another by Shepelin et al⁶¹ offering complementary insights into its potential as a biomarker. Yu et al⁶⁰ used metabolomics to compare primary and metastatic melanoma cell lines and found that carnitine and acylcarnitines were significantly upregulated in metastatic melanoma. These metabolites are key intermediates in the carnitine shuttle pathway, which transports fatty acids into mitochondria for β-oxidation and adenosine triphosphate (ATP) production, a process that becomes crucial when metastatic cells face glucose deprivation. Their findings suggest that enhanced carnitine shuttle activity supports metastatic survival and could serve as biomarker of advanced disease, as well as therapeutic target.

In contrast, Shepelin et al.⁶¹ performed a bioinformatics analysis and found that carnitine biosynthesis (distinct from shuttle activity), was upregulated in nevi but progressively downregulated in primary and metastatic melanoma. This suggests that endogenous carnitine production may be more active in early stages (nevi), but becomes suppressed as melanoma progresses, potentially reflecting a shift in how melanoma cells acquire and utilize metabolic substrates.

Rather than being contradictory, these studies highlight different aspects of carnitine metabolism across melanoma stages. Yu et al.⁶⁰ emphasized the importance of carnitine shuttle function in metastasis, while Shepelin et al.⁶¹ highlight the loss of carnitine biosynthesis early in tumor development. Together, they imply that carnitine-related pathways may have stage-specific diagnostic of therapeutic relevance – biosynthesis-related pathways for early detection, and shuttle-related metabolites for monitoring metastasis. Clinically, carnitine metabolism warrants further investigation as a potential biomarker system and therapeutic target in melanoma.

Carnitine as Biomarker of Depression

Although depression is not specifically a dermatologic condition, there is an intricate and well-documented relationship between psychiatric disorders and the skin. Many dermatologic diseases significantly impact patients’ quality of life, with an estimated one third of patients in dermatology clinics needing assessment for mental health symptoms.⁶² In turn, psychiatric medications may produce cutaneous side effects, and some dermatologic treatments can influence mental health status.^63,64 In this context, carnitine has drawn attention as a shared biomarker in both domains. A case-control study of 89 patients reported significantly lower serum levels of L-carnitine and ALC in individuals with Major Depressive Disorder (MDD), with ALC levels inversely correlating with depression severity.⁶⁵ Similarly, a 2022 systematic review found that depressed patients had reduced free carnitine and short-chain acylcarnitines, suggesting that impaired mitochondrial function and altered neurotransmitter regulation may contribute to mood instability.⁴ Moreover, a 2018 SR-MA concluded that ALC supplementation significantly decreases depressive symptoms compared with placebo.⁶⁶ These findings propose that carnitine metabolism may not only serve as a biomarker for depression but may also help explain overlapping metabolic dysfunction in dermatologic conditions with psychiatric comorbidities, such as psoriasis, acne, and chronic pruritus.

Section Summary

Current evidence supports the potential of carnitine and its derivatives as emerging biomarkers in dermatology. Altered carnitine metabolism provides insight into disease mechanisms, severity, and progression across genodermatoses, inflammatory, fibrotic, pruritic, neoplastic, and psychodermatologic conditions. While promising, variability in study design and metabolite profiling highlights the need for standardized, dermatology-focused research. Future studies should aim to validate these biomarkers in larger cohorts and explore their integration into personalized care.

Discussion

L-carnitine is emerging as a multifaceted agent in dermatology, with growing evidence supporting its therapeutic, adjunctive, and diagnostic potential across a wide range of skin diseases. Systemically, its has demonstrated anti-inflammatory, metabolic, and immunomodulatory effects. It also has a potential role in mitigating treatment-related adverse effects from agents like isotretinoin, and corticosteroids. Its roles in tissue repair, microcirculation, and fibrosis modulation further highlight its utility in wound healing and sclerotic skin disorders. Topically, L-carnitine demonstrates promise in acne management, sebum regulation, post-inflammatory hyperpigmentation, and cellulite, with favorable results across multiple studies, particularly when combined with other active agents.

Beyond its therapeutic applications, carnitine and its metabolites are increasingly recognized as potential biomarkers, offering insight into disease pathophysiology, severity, and subtype differentiation. Altered carnitine profiles have been observed in genodermatoses, inflammatory dermatoses, fibrotic conditions, and neoplastic disease such as melanoma, as well as in psychodermatologic overlaps, suggesting that carnitine metabolism may reflect systemic immune or metabolic dysfunction relevant to skin disease.

Importantly, most studies have not shown significant adverse effects associated with carnitine supplementation at standard doses. While some reviews list multiple side effects,^20,67 closer examination suggests these may not be directly attributable to carnitine itself. For instance, one study reported gastrointestinal symptoms in patients taking orlistat plus carnitine,⁶⁸ though orlistat alone is known to cause such effects. Other studies reported adverse event rates similar to placebo.^69,70 Taken together, the evidence supports a favorable safety profile for systemic carnitine.

While carnitine supplementation is generally safe, concerns remain regarding its association with cardiovascular disease (CVD) through increased production of trimethylamine-N-oxide (TMAO), a gut-derived metabolite of carnitine, choline, and phosphatidylcholine.⁷¹, ⁷² Although TMAO has been linked to atherosclerosis via macrophage activation,⁷¹ its direct role in CVD remains unclear. Several studies have found that elevated TMAO levels following carnitine supplementation do not consistently correlate with traditional cardiovascular risk markers,⁷³, ⁷⁴ suggesting that TMAO may serve more as a biomarker rather than a causative agent in CVD.⁷¹ Emerging evidence also indicates that probiotics, such as Lactobacillus rhamnosus GG, can lower TMAO levels by modulating gut microbiota,⁷² offering a potential strategy to mitigate risks. Given carnitine’s therapeutic benefits for skin conditions, further research into microbiome-targeted interventions may help optimize its safe and effective use in dermatology.

Conclusion

L-carnitine represents a multifaceted agent in dermatology, offering therapeutic, adjunctive, and diagnostic benefits across a wide range of skin diseases. Its systemic and topical effects, ranging from anti-inflammatory action to metabolic regulation and barrier repair, are supported by a growing body of evidence. Furthermore, its emerging role as a biomarker opens the door to personalized dermatologic care, with potential applications in diagnosis, disease monitoring, and stratified treatment approaches. Although questions remain regarding long-term safety and disease-specific dosing strategies, L-carnitine’s favorable tolerability profile and broad physiologic relevance position it as a valuable tool in the evolving landscape of integrative dermatology. Future research should focus on dermatology-specific clinical trials, biomarker validation, and mechanistic studies to fully define its place in routine dermatologic practice.

Supplemental Material

sj-docx-1-cms-10.1177_12034754261427402 – Supplemental material for L-Carnitine in Dermatology: A Systematic Review of Therapeutic Potential and Biomarker Applications

Supplemental material, sj-docx-1-cms-10.1177_12034754261427402 for L-Carnitine in Dermatology: A Systematic Review of Therapeutic Potential and Biomarker Applications by Eunice Y. Chow and Mariusz Sapijaszko in Journal of Cutaneous Medicine and Surgery

Supplemental Material

sj-docx-2-cms-10.1177_12034754261427402 – Supplemental material for L-Carnitine in Dermatology: A Systematic Review of Therapeutic Potential and Biomarker Applications

Supplemental material, sj-docx-2-cms-10.1177_12034754261427402 for L-Carnitine in Dermatology: A Systematic Review of Therapeutic Potential and Biomarker Applications by Eunice Y. Chow and Mariusz Sapijaszko in Journal of Cutaneous Medicine and Surgery

Footnotes

Author Contributions

Dr. Chow and Dr. Sapijaszko contributed equally to the conception of the review. Dr. Chow conducted the literature search, performed data extraction, prepared the tables, and drafted the manuscript. Dr. Sapijaszko contributed to data verification and critical revision of the manuscript. Both authors reviewed and approved the final version.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical Approval

There are no human participants in this article

Informed Consent Statement

Informed consent is not required.

ORCID iDs

Eunice Y. Chow

Mariusz Sapijaszko

Supplemental Material

Supplemental material for this article is available online.

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