Tranexamic acid versus kojic acid in facial post-inflammatory hyperpigmentation following acne: a narrative review

Sanjana R. Tummala; Swetha Donakonda; B. Uday Kumar

doi:10.18203/issn.2455-4529.IntJResDermatol20262352

Authors

Sanjana R. Tummala Department of Dermatology, MNR Medical College and Hospital, Sangareddy, Telangana, India
Swetha Donakonda Department of Dermatology, MNR Medical College and Hospital, Sangareddy, Telangana, India
B. Uday Kumar Department of Dermatology, MNR Medical College and Hospital, Sangareddy, Telangana, India

DOI:

https://doi.org/10.18203/issn.2455-4529.IntJResDermatol20262352

Keywords:

Tranexamic acid, Kojic acid, Post-inflammatory hyperpigmentation, Acne vulgaris, Facial hyperpigmentation, Skin of colour

Abstract

Facial post-inflammatory hyperpigmentation (PIH) following acne is a frequent and distressing sequela, especially in darker Fitzpatrick skin phototypes. Tranexamic acid (TXA) and kojic acid are increasingly used as non-hydroquinone depigmenting agents, but their comparative role in acne-induced PIH remains insufficiently defined. Objective of the study was to compare the mechanistic rationale, clinical evidence, safety profile, and practical role of TXA versus kojic acid in facial PIH after acne. A focused narrative review was performed using DOI-traceable studies and reviews on acne-induced PIH, TXA, kojic acid, and facial hyperpigmentation. Evidence from acne-specific PIH studies was prioritized, while melasma studies were used only as indirect supportive evidence because melasma and PIH differ in pathogenesis. Acne-induced PIH is driven by inflammation-mediated melanocyte stimulation, excess epidermal melanin, and, in some cases, dermal melanophages. TXA acts upstream by inhibiting plasminogen activation and reducing inflammatory and vascular mediators involved in melanogenesis. Clinical evidence for TXA in PIH includes systematic review data and a randomized trial showing topical 5% TXA to be comparable to 20% azelaic acid for acne-related PIH, with favourable early tolerability. Kojic acid acts mainly by copper chelation and tyrosinase inhibition. Its evidence in acne-PIH is more limited, with small preliminary data in post-acne hyperpigmentation and stronger indirect evidence from melasma studies, often in combination with hydroquinone, glycolic acid, or vitamin C. No robust direct head-to-head trial of TXA versus kojic acid for facial post-acne PIH was identified. Current evidence supports both agents as useful non-hydroquinone options. TXA may be preferable where inflammation, erythema, recurrence, or sensitive skin are prominent, while kojic acid may be useful for epidermal brown macular pigmentation in patients tolerating tyrosinase inhibitors. Direct comparative randomized trials are needed.

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