Identifying patients at risk for myasthenic crisis with hemogram and inflammation-related laboratory parameters - a pilot study

Front Neurol. 2024 Feb 26:15:1297997. doi: 10.3389/fneur.2024.1297997. eCollection 2024.

Abstract

Background: Myasthenia gravis (MG) is a rare autoimmune disease characterized by fatigable weakness of the voluntary muscles and can exacerbate to life-threatening myasthenic crisis (MC), requiring intensive care treatment. Routine laboratory parameters are a cost-effective and widely available method for estimating the clinical outcomes of several diseases, but so far, such parameters have not been established to detect disease progression in MG.

Methods: We conducted a retrospective analysis of selected laboratory parameters related to inflammation and hemogram for MG patients with MC compared to MG patients without MC. To identify potential risk factors for MC, we applied time-varying Cox regression for time to MC and, as a sensitivity analysis, generalized estimating equations logistic regression for the occurrence of MC at the next patient visit.

Results: 15 of the 58 examined MG patients suffered at least one MC. There was no notable difference in the occurrence of MC by antibody status or sex. Both regression models showed that higher counts of basophils (per 0.01 unit increase: HR = 1.32, 95% CI = 1.02-1.70), neutrophils (per 1 unit increase: HR = 1.40, 95% CI = 1.14-1.72), potentially leukocytes (per 1 unit increase: HR = 1.15, 95% CI = 0.99-1.34), and platelets (per 100 units increase: HR = 1.54, 95% CI = 0.99-2.38) may indicate increased risk for a myasthenic crisis.

Conclusion: This pilot study provides proof of the concept that increased counts of basophils, neutrophils, leukocytes, and platelets may be associated with a higher risk of developing MC in patients with MG.

Keywords: hemogram; inflammation; laboratory parameters; myasthenia; myasthenia gravis; myasthenic crisis; risk prediction.

Grants and funding

The author(s) declare financial support was received for the publication of this article. This study did not receive dedicated funding. PM is Einstein Junior Fellow, and AB is Einstein Visiting Fellow, both funded by the Einstein Foundation Berlin. PM acknowledges funding support by the Einstein Foundation Berlin (EJF-2020-602; EVF-BUA-2022-694), PM and AB acknowledge joint funding by the Einstein Foundation Berlin (EVF-2021–619), and the Leducq Foundation for Cardiovascular and Neurovascular Research (Consortium International pour la Recherche Circadienne sur l’AVC). The authors acknowledge financial support for open access publication from the Open Access Publication Fund of Charité - Universitätsmedizin Berlin. The funding organizations did not play any role in the design of the study, preparation, review, approval of the manuscript, or decision to submit the manuscript for publication.