Treatment patterns and persistence on disease modifying therapies for multiple sclerosis and its associated factors.

BACKGROUND: Effective interventions for Multiple Sclerosis require timely treatment optimization which usually involves switching disease modifying therapies. The patterns of prescription and the reasons for changing treatment in people with MS, especially in low prevalence populations, are unknown. OBJECTIVES: To describe the persistence, reasons of DMT switches and prescription patterns in a cohort of Colombian people with MS. METHODS: We conducted a retrospective observational study including patients with confirmed MS with at least one visit at our centre. We estimated the overall incidence rate of medication changes and assessed the persistence on medication with Kaplan-Meier survival estimates for individual medications and according to efficacy and mode of administration. The factors associated with changing medications were assessed using adjusted Cox proportional-hazards models. The reasons for switching medication changes were described, and the prescription patterns were assessed using network analysis, with measures of centrality. RESULTS: Seven hundred one patients with MS were included. Mean age was 44.3 years, and 67.9% were female. Mean disease duration was 11.3 years and 84.5% had relapsing MS at onset, with median EDSS of 1.0. Treatment was started in 659 (94%) of the patients after a mean of 3 years after MS symptom onset. Among them, 39.5% maintained their initial DMT, 29.9% experienced a single DMT change, while 18.7% went through two, and 11.9% had three or more DMT changes until the final follow-up. The total number of treatment modifications reached 720, resulting in an incidence rate of 1.09 (95% confidence interval: 1.01-1.17) per patient per year The median time to change after the first DMT was 3.75 years, and was not different according to the mode of administration or efficacy classification. The main reasons for changing DMT were MS activity (relapses, 56.7%; MRI activity, 18.6%), followed by non-serious adverse events (15.3%) and disability (11.1%). Younger age at MS onset, care under our centre and insurer status were the main determinants of treatment change. Network analysis showed that interferons and fingolimod were the most influential DMTs. CONCLUSIONS: A majority of patients switch medications, mostly due to disease activity, and in association with age and insurer status.

Leucoencefalopatía multifocal progresiva / Progressive multifocal leukoencephalopathy

RESUMEN La leucoencefalopatía multifocal progresiva es una enfermedad desmielinizante secundaria a la infección por el virus de John Cunnigham, con baja incidencia a pesar de su alta seroprevalencia en la población general. Su principal factor de riesgo es la inmunosupresión, incluyendo la infección por el virus de la inmunodeficiencia humana (VIH), cánceres hematológicos, enfermedades inflamatorias crónicas y medicamentos inmunosupresores sistémicos. Después de la infección primaria, el virus queda latente y por mutaciones en su genoma adquiere la capacidad neuroinvasiva e infecta a los oligodendrocitos, a los que lleva a su destrucción, con el consecuente proceso desmielinizante, mientras se enfrenta a la inmunidad celular del huésped. El diagnóstico se basa en manifestaciones clínicas secundarias al compromiso encefálico, clásicamente supratentorial, así como la demostración de la presencia de genoma viral o anticuerpos en suero o líquido cefalorraquídeo y hallazgos imagenológicos e histopatológicos de lesiones en la sustancia blanca cerebral. El tratamiento, en general, consiste en la recuperación de la función inmune alterada, con reparos cuando esta se presenta en el contexto de un estado de reconstitución inmune. En este escrito se revisan los aspectos básico-clínicos más relevantes de esta enfermedad.

SUMMARY The progressive multifocal leukoencephalopathy is a demyelinating disease secondary to infection to John Cunningham Virus, it has a low incidence despite a high seroprevalence in the general population. The principal risk factor for its development is an immunosuppression, including Human Immunodeficiency Virus infection, hematologic neoplasms, chronic inflammatory diseases and systemic immunosuppressive drugs. After the primary infection, the virus stays in a latent state, acquiring a neuroinvasive capacity following a set of mutations in its genome. After infecting oligodendrocytes it takes them to destruction with the consequent demyelinating process whilst its fight to the host's cellular immune system. The diagnosis is based on a set of clinical findings secondary to encephalic compromise, classically supratentorial, in addition to a demonstration of viral genome or antibodies in serum or cerebrospinal fluid and the presence of diagnostic images and histopathologic findings on the cerebral white matter. Its treatment is based on the enhancement of the disturbed immune function, with the exception of immune reconstitution state where other strategies are applied. In this paper we will review the more relevant basic and clinical aspects of this disease.