MG‑specific biomarkers validated in study

By Litha Mfiki

A multicenter study in the European Journal of Neurology identifies and validates serum inflammatory protein biomarkers that distinguish acetylcholine receptor (AChR)–positive myasthenia gravis (MG) from healthy controls, multiple sclerosis (MS), and chronic inflammatory demyelinating polyneuropathy (CIDP).

Findings from this study demonstrate clear disease-specific inflammatory patterns. The authors note “The identification of MG subgroup‑specific biomarkers and treatment‑associated protein changes provides new insights into disease pathogenesis and reveals potential targets for therapeutic monitoring.”

Amol Bhandage (Uppsala University, Sweden) and colleagues analyzed serum from 200 AChR–positive patients with MG, 192 matched controls, 93 patients with MS, and 51 patients with CIDP using a 92‑plex Olink inflammation panel. The MG cohort had a median age of 59  years, with subgroups categorized as early‑onset, late‑onset, and very late–onset MG.

The investigators identified 14 proteins significantly altered in MG versus controls, with AXIN1, STAMBP, ST1A1, CDCP1, and SIRT2 serving as MG‑specific biomarkers across all groups.

Principal component analyses revealed clear clustering patterns between groups, and several biomarkers demonstrated strong odds ratios in logistic models adjusted for age and sex. Notably, AXIN1, ST1A1, and STAMBP remained robust across all analytical approaches, underscoring their value as core disease‑specific markers.

The study also identified a 15‑protein signature associated with MG severity, with higher levels of FGF‑23, IL‑24, CXCL9, CDCP1, OPG, and CSF‑1 correlating with more severe disease compared with ocular or remission states. Many of these markers also showed significant associations with MG‑ADL and QMG scores.

Importantly, inflammatory profiles varied across subgroups: 28 proteins changed with age at onset, and 18 differed between patients who were immunosuppression‑naive and those who were immunosuppressed. Newer biologic therapies also reduced markers such as CD6 and TNFRSF9.

The author concluded that “These findings support the use of blood‑based biomarkers for monitoring and stratification in MG clinical trials and care.”

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