# Case Report: Efgartigimod demonstrates significant clinical efficacy in double seropositive myasthenia gravis: a case report of a rare variant and analysis of pathomechanisms

**Authors:** Xiaohui Huang, Yue Wan, Yu Chen, Keqi Lei

PMC · DOI: 10.3389/fimmu.2025.1610738 · 2025-10-13

## TL;DR

A 68-year-old woman with a rare form of myasthenia gravis showed significant improvement after treatment with efgartigimod, a promising new therapy for this condition.

## Contribution

This is the first documented case of efgartigimod's efficacy in treating double seropositive myasthenia gravis.

## Key findings

- The patient showed complete resolution of symptoms after efgartigimod treatment.
- Sustained clinical remission was maintained for 6 months post-treatment.
- Efgartigimod may offer a viable treatment option when conventional therapies fail.

## Abstract

Double Seropositive Myasthenia Gravis (DSP-MG), a rare variant of Myasthenia Gravis (MG), is defined by the simultaneous presence of both anti-acetylcholine receptor (AChR) antibodies and anti-muscle-specific tyrosine kinase (MuSK) antibodies in the serum of affected individuals. Currently, no standardized therapeutic protocol exists for DSP-MG due to its scarcity and clinical heterogeneity. Herein, we report a case of a 68-year-old female patient with DSP-MG who showed significant clinical improvement during an acute exacerbation after treatment with the FcRn antagonist efgartigimod, following the failure of conventional therapy. After a cycle of efgartigimod treatment, complete resolution of myasthenic symptoms was observed. During the 6-month follow-up, with sustained clinical remission and attainment of Minimal Manifestation Status (MMS). This case represents the first documented use of efgartigimod in a DSP-MG patient, providing preliminary clinical evidence for its potential efficacy in this rare and poorly understood subtype. Our findings contribute to the limited literature on DSP-MG and suggest that FcRn inhibition may offer a viable treatment option where conventional therapies fail. Efgartigimod may represent a potential therapeutic agent for DSP-MG.

## Linked entities

- **Diseases:** Myasthenia Gravis (MONDO:0009688)

## Full-text entities

- **Genes:** MUSK (muscle associated receptor tyrosine kinase) [NCBI Gene 4593] {aka CMS9, FADS}, FCGRT (Fc gamma receptor and transporter) [NCBI Gene 2217] {aka FCRN, FcgammaRn, alpha-chain}
- **Diseases:** myasthenic symptoms (MESH:D020294), DSP-MG (MESH:D009157), Seropositive (MESH:D006679)
- **Chemicals:** Efgartigimod (MESH:C000718373)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12554679/full.md

---
Source: https://tomesphere.com/paper/PMC12554679