# Multimodal Approach for Recalcitrant Melasma Using Picosecond Laser and Topical JAK Inhibition: A Case Report

**Authors:** Hasan Ashkanani, Maryam AlZaabi, Abdulaziz AlRasheed, Wael AlDaraji

PMC · DOI: 10.1111/jocd.70783 · 2026-03-25

## TL;DR

A woman with long-lasting melasma achieved near-total clearance using a combination of laser treatment, topical JAK inhibition, and visible light protection.

## Contribution

A novel multimodal treatment approach for recalcitrant melasma combining picosecond laser and JAK inhibition is proposed and demonstrated.

## Key findings

- The patient achieved a 98.7% improvement in melasma severity after 11 months of treatment.
- No adverse events or relapse were observed, even after treatment cessation.
- The combination therapy suggests potential for durable remission in difficult-to-treat melasma cases.

## Abstract

Melasma is a chronic hyperpigmentation disorder with high relapse rates, particularly in Fitzpatrick skin types III–V. Increasing evidence implicates cytokine‐driven inflammation and visible light–induced melanogenesis as key contributors to disease persistence. These mechanisms support the rationale for exploring a multimodal therapeutic approach.

A woman in her early 30s with phototype IV presented with a 5‐year history of recalcitrant centrofacial melasma. Previous treatments—including hydroquinone, oral tranexamic acid, and superficial chemical peels—produced only transient and incomplete improvement. Baseline Melasma Severity Index (MSI) score was 7.9, consistent with moderate‐to‐severe disease.

Treatment consisted of low‐fluence picosecond 755 nm alexandrite laser, short‐term topical corticosteroid post‐procedure, initiation of topical tofacitinib 2% cream twice daily for 11 months, and continuous iron oxide–based visible light–blocking photoprotection. Laboratory monitoring during therapy remained normal.

At 11 months, the patient achieved near‐total clearance with an MSI reduction from 7.9 to 0.10 (98.7% improvement). No adverse events, post‐inflammatory hyperpigmentation, or relapse were observed, including 3 months after treatment cessation.

This case illustrates the potential clinical value of combining pigment‐targeted picosecond laser therapy with topical JAK inhibition and visible light–specific photoprotection for recalcitrant melasma. The durable remission achieved supports further investigation into anti‐inflammatory and photoreactive pathway modulation as adjunctive strategies in melasma management.

## Linked entities

- **Chemicals:** hydroquinone (PubChem CID 785), tranexamic acid (PubChem CID 5526), iron oxide (PubChem CID 123289)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, OPN3 (opsin 3) [NCBI Gene 23596] {aka ECPN, PPP1R116}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}
- **Diseases:** vitiligo (MESH:D014820), pigmentary disorders (MESH:C535508), III (MESH:C537189), hyperpigmentary disorder (MESH:D009358), PIH (MESH:D017495), Melasma (MESH:D008548), pigmentation (MESH:D010859), systemic (MESH:D015619), Inflammation (MESH:D007249), skin (MESH:D012871)
- **Chemicals:** creatinine (MESH:D003404), Heliocare 360 (-), tranexamic acid (MESH:D014148), hydroquinone (MESH:C031927), glycolic acid (MESH:C031149), alexandrite (MESH:C112654), hydrocortisone acetate (MESH:C021650), fusidic acid (MESH:D005672), ruxolitinib (MESH:C540383), iron oxide (MESH:C000499), melanin (MESH:D008543), tofacitinib (MESH:C479163), Fucicort (MESH:C524642)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC13019006/full.md

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Source: https://tomesphere.com/paper/PMC13019006