Although the persistence of CSF OB suggests the lymphocytes were not eliminated from the CNS, the follow-up MRI studies showed no enhanced T1 brain lesions and a reduction in the T2 lesion load that correlated with the clinical stabilization of MS after AHSCT.
Multiple sclerosis (MS) is a disease supposedly of autoimmune origin, with reactivity directed against myelin antigens. From the neuropathological point of view, MS produces inflammation, demyelination and axonal and neuronal degeneration. Inflammatory phenomena are predominant in the initial phase of the disease, followed later by neurodegenerative processes. Over the last decade, early treatment, during the most inflammatory phase of the disease, has been considered the best strategy to treat MS. Accordingly, we decided to determine the periods of delay between the first symptoms and the time to the first medical visit, the time to referral to a specialised MS unit, the delay in undertaking clinical and paraclinical tests, the diagnostic criteria used and the overall delay in diagnosis and treatment. The median time from onset of first symptoms to the first visit to a physician was 19.2 months, which represented the greatest delay. The median time between this initial medical consultation and the confirmation of the diagnosis by a specialised MS unit was 5.7 months, and the overall time from symptom onset to diagnosis was 24.9 months (2.08 years). The median time between onset of the first symptoms and the decision to give the first treatment was 2 years. The most important delay was that from symptom onset to the first medical visit, with the other delays being less. Thus, it is during this initial period that greater effort is required in order to reduce the time to diagnosis, by increasing awareness of the problem of MS among the general population and primary care physicians.
The authors report the outcome of 14 patients with severe multiple sclerosis treated with autologous hematopoietic stem cell transplantation (AHSCT) after a median follow-up period of 3 years. The 3-year actuarial probability of progression-free survival was 85.7% and that of disease activity-free survival was 46.4%. On MRI, no T1-enhanced lesions were detected after AHSCT. The mean change in T2 lesion volume from baseline to the third year was -20.2% and that of the corpus callosum area was -12.7%; 50% of this reduction was seen during the first year.
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