Clinical and immunological markers of transformation of an acute demyelinating episode to a chronic demyelinating disease

An acute demyelinating episode (ADE) is the acute onset of clinical symptoms characteristic of multiple sclerosis (MS) or other demyelinating diseases (DD). Patients with ADE may experience either a monophasic course of the disease, relapses, or transformation to MS (up to 33 per cent). To date, there are no criteria for predicting the transformation of ADE to MS in adults; therefore, identifying prognostic factors for the development of MS in such patients is of significant diagnostic importance.

Objective: to identify the clinical and immunological markers of the transformation of ADE into a chronic demyelinating process (MS).

Material and methods. The study was conducted from 2023 to 2026. The main group comprised 29 patients: 22 diagnosed with acute disseminated encephalomyelitis (ADEM) and 7 with acute transverse myelitis (ATM); the control group comprised 29 individuals. All patients were followed up for 24 months. The laboratory component of the study, which involved measuring the levels of interleukin-1b (IL-1b), IL-2, IL-6, tumour necrosis factor-a, glial fibrillary acidic protein and C-reactive protein in the patients’ serum, was carried out in the neuroimmunology laboratory of the Institute of Clinical Neurology at the Federal Center for Brain and Neurotechnologies.

Results. During the follow-up period, 8 out of 29 patients were diagnosed with MS following ADE according to the 2017 McDonald criteria. The overall rate of transformation from ADE to MS was 28 per cent. Patients in whom ADE progressed to MS were more likely to have the following characteristics: no recent infection (p=0.002), sensory disturbances at disease onset (p=0.021), type 2 oligoclonal bands (OCB) pattern (p<0.001) and lesions in the brainstem on magnetic resonance imaging (p=0.024). Serum IL-6 concentrations in patients with ADE transforming to MS were higher than in patients without transformation to MS during the acute phase and at 3–6 months; however, the differences were not statistically significant (p₁=0.366; p₂=0.471). As a result of the multivariate logistic regression analysis, the best combination of predictors for the transformation of ADE to MS included: 1) absence of a pre-existing infection (OR 14.31; 95% CI 1.04–196.3; p=0.046), 2) OCB synthesis type 2 (OR 0.05; 95% CI 0.003–0.832; p=0.037).

Conclusion. The results of this study show that certain clinical characteristics (absence of a preceding infection, specific abnormalities at disease onset), laboratory parameters (type 2 OCB synthesis) and neuroimaging findings (foci of demyelination in the brainstem) may help to distinguish patients with a monophasic course of ADE at the early stage of the disease from those who will go on to develop MS.

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