# L-carnitine as a novel approach for pain and inflammation relief in rheumatoid arthritis

**Authors:** Abdallah A. Eldisouky, Sahar K. Hegazy, Salwa Elmorsy Abd Elghany

PMC · DOI: 10.1007/s10787-025-01956-y · Inflammopharmacology · 2025-10-02

## TL;DR

This study explores L-carnitine as a potential supplement to treat rheumatoid arthritis by reducing inflammation and improving symptoms.

## Contribution

The study introduces L-carnitine as a novel adjunct therapy for rheumatoid arthritis targeting inflammation pathways.

## Key findings

- L-carnitine improved morning stiffness, pain, and joint counts in rheumatoid arthritis patients.
- L-carnitine showed no significant effect on STAT3 or TGF-β1 levels.
- Combining L-carnitine with standard drugs may enhance clinical outcomes.

## Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation, largely mediated by pro-inflammatory cytokines. Considering the established involvement of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and transforming growth factor-beta1 (TGF-β1) in RA, this research aimed to assess efficacy and safety of L-carnitine as an adjunct therapy targeting these pathways. Forty-six patients with active RA were randomly divided into two equal groups. Group1 (control group) received disease-modifying antirheumatic drugs (DMARDs), including methotrexate, leflunomide, and hydroxychloroquine. Group2 (L-carnitine group) received, DMARDs plus L-carnitine 500 mg twice daily for 12 weeks. A clinical evaluation was conducted, which included tender joint count (TJC), swollen joint count (SJC), pain intensity quantified via the visual analogue scale (VAS), and morning stiffness duration. Additionally, the Disease Activity Score in 28 joints (DAS28) and functional capability as measured by a modified health assessment questionnaire (MHAQ) were assessed. Laboratory evaluation included C-reactive protein (CRP), STAT3, and TGF-β1 measurement. All evaluations were executed both at baseline and following a 12-week treatment period. After 12 weeks, the L-carnitine group showed significant improvement in morning stiffness, VAS, TJC, CRP, DAS28, and MHAQ compared to baseline. While no significant within-group changes were observed in STAT3, TGF-β1 in the L-carnitine group, STAT3 levels increased significantly in the control group compared to baseline. In conclusion, L-carnitine in combination with DMARDs may enhance clinical outcomes in RA by mitigating systemic inflammation. Nevertheless, its impact on STAT3 and TGF-β1 remains unclear and warrants further research.

## Linked entities

- **Proteins:** STAT3 (signal transducer and activator of transcription 3), TGFB1 (transforming growth factor beta 1)
- **Chemicals:** L-carnitine (PubChem CID 288), methotrexate (PubChem CID 4112), leflunomide (PubChem CID 3899), hydroxychloroquine (PubChem CID 3652)
- **Diseases:** rheumatoid arthritis (MONDO:0008383)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}
- **Diseases:** inflammation (MESH:D007249), pain (MESH:D010146), autoimmune disorder (MESH:D001327), tender (MESH:D063806), morning stiffness (MESH:D048968), RA (MESH:D001172)
- **Chemicals:** L-carnitine (MESH:D002331), methotrexate (MESH:D008727), leflunomide (MESH:D000077339), hydroxychloroquine (MESH:D006886)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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Source: https://tomesphere.com/paper/PMC12618341