Reumatologia clinica · 2025
Cognitive dysfunction in systemic lupus erythematosus: Insights from a two-year longitudinal study in a Brazilian cohort.
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Scoto Dias Eduarda, Tercziany Vanzin José Henrique, Augusto Borba Eduardo, Freitas Dos Santos Mahara, Dos Santos Thiago Alberto F G, Skare Thelma, Nisihara Renato
Аннотация
OBJECTIVES: The objective of this study was to examine cognitive dysfunction in a Brazilian sample of SLE patients for two years.
METHODS: A sample of 50 individuals with SLE was assessed at baseline for epidemiological and treatment data, disease activity by SLEDAI 2K (SLE disease activity 2000), cumulative damage by SLICC/ACR DI (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index), depression by CES-D (Center for Epidemiological Studies-Depression) and cognitive function through MoCA (Montreal Cognitive Assessment). The same assessment was repeated after two years.
RESULTS: The prevalence of cognitive impairment at baseline was 68%. The baseline cognitive assessment showed impairment in visuospatial/executive function (p=0.002), naming (p=0.04), attention (p<0.0001) and delayed recall (p<0.0001). The median MoCA results did not change in two years (p=0.45), but 6 individuals (12%) that had normal cognitive function at baseline developed mild cognitive impairment and two (4%) that had mild cognitive impairment, improved. When considering the MoCA domains the only significant difference was improvement in abstraction (p=0.001). No correlations between MoCA delta (difference between second and first value) and delta SLEDAI, delta SLICC and delta CES-D were found (all with p>0.05). Also, no associations were found with used treatment or autoantibodies profile.
CONCLUSIONS: Cognitive dysfunction in SLE is dynamic and may require periodic re-assessments. Changes in cognition were not associated with disease activity, depression or cumulative damage in this sample.
METHODS: A sample of 50 individuals with SLE was assessed at baseline for epidemiological and treatment data, disease activity by SLEDAI 2K (SLE disease activity 2000), cumulative damage by SLICC/ACR DI (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index), depression by CES-D (Center for Epidemiological Studies-Depression) and cognitive function through MoCA (Montreal Cognitive Assessment). The same assessment was repeated after two years.
RESULTS: The prevalence of cognitive impairment at baseline was 68%. The baseline cognitive assessment showed impairment in visuospatial/executive function (p=0.002), naming (p=0.04), attention (p<0.0001) and delayed recall (p<0.0001). The median MoCA results did not change in two years (p=0.45), but 6 individuals (12%) that had normal cognitive function at baseline developed mild cognitive impairment and two (4%) that had mild cognitive impairment, improved. When considering the MoCA domains the only significant difference was improvement in abstraction (p=0.001). No correlations between MoCA delta (difference between second and first value) and delta SLEDAI, delta SLICC and delta CES-D were found (all with p>0.05). Also, no associations were found with used treatment or autoantibodies profile.
CONCLUSIONS: Cognitive dysfunction in SLE is dynamic and may require periodic re-assessments. Changes in cognition were not associated with disease activity, depression or cumulative damage in this sample.