Real-World Data Regarding Long-Term Administration of Natalizumab Derived from a Neurology Department along with Literature Review.

BACKGROUND: Natalizumab is a humanized monoclonal antibody with high efficacy and an acceptable safety profile used in the treatment of patients with multiple sclerosis (MS). OBJECTIVE: Our aim was to report data regarding long-term administration of Natalizumab in patients with Relapsing-Remitting Multiple Sclerosis (RRMS) from our clinic. METHODS: A retrospective observational study was performed including RRMS patients who underwent treatment with ≥ 24 Natalizumab infusions. We analyzed EDSS values, the relapse rate and the rate and type of adverse events related to Natalizumab administration. RESULTS: 51 subjects were included with a predominance of women (62.74%), with an average age of 40.43±1.49 years, a mean disease duration of 9.86±0.7 years and mean number of Natalizumab infusions of 45.58±2.74. An increased number of patients (80.39%) were relapse-free and a mild reduction of the mean EDSS value following Natalizumab initiation in patients who had not been treated with other disease modifying therapies anteriorly was observed. Among the encountered adverse events such as increased liver transaminases (13.72%), local infections (7.84%) and dysmenorrhea in one patient were registered in this study. The rate of severe adverse events was 3.92 and no cases of Progressive Multifocal Leukoencephalopathy (PML) were registered. CONCLUSION: Natalizumab proves to be effective, has an adequate safety profile and can be administered with good tolerability for a rather extended period of time, provided that the patients are closely monitored.

Central pontine and extrapontine myelinolysis.

At the crossover of specialties, the osmotic demyelination syndromes are under-diagnosed clinical entities. Even if the knowledge and the management of these entities have evolved in the latest years, many issues are still unsolved. Initially described as diseases affecting alcoholics and malnourished and considered affecting solely the pons, it is now known that osmotic demyelination can produce extrapontine lesions (extrapontine myelinolysis). Rapid correction of sodium in hyponatremic patients is pathogenically involved in the genesis of central pontine and extrapontine myelinolysis. The aim of this review is to focus on the main characteristics of the disease, which can represent a challenge for the clinicians in respect to its recognition and treatment.

An immunological approach to cerebral ischemia (I). Immune cells and adhesion molecules.

Ischemic stoke is a major cause of death and an important source of disability in industrialized countries. Since there is no ideal treatment for cerebral ischemia, any approach aiming to limit the devastating consequences of the ischemic process is justified. Concerning immune responses, it has become clear in the latest years that actors of the immune system are involved in multiple and various neurobiological processes such as cerebral ischemia, neurodegeneration, neuroprotection and neuroregeneration. An immunological approach to cerebral ischemia can distinguish, besides the implication of inflammation in the developing of atherothrombosis thus leading to stroke, the clear involvement of immune cells and mediators in processes continuing the initial stage of ischemia, having consequences on recovery or lesion extent. Cerebral infarctions develop within minutes to hours of cessation of the cerebral blood flow, but may expand over subsequent days. There is increasing evidence that leukocytes, cytokines, cell adhesion molecules, and other immune mediators contribute to secondary infarction growth, but inflammatory cytokines are also involved in signaling pathways leading to neuroprotection related to ischemic pre-conditioning. The aim of this review is to show some aspects concerning the complex and diverse functions of immune modifications occurring in cerebral ischemia. This first part will focus on the involvement of immune cells, adhesion molecules and immunological transcription factors in the development of ischemic lesion.