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1.
Acta Neurol Scand ; 144(2): 209-215, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-33961285

RESUMO

BACKGROUND: Nutritional visual defects are apparently uncommon nowadays in developed nations. Retinal change-related visual defects caused by hypovitaminoses may be underdiagnosed. AIM OF THE STUDY: To investigate the retinal structural and functional changes in a patient with multivitamin deficiency before and during vitamin supplementation. METHODS: A 51-year-old female had been on vegetarian diet as a child, and on restrict vegan diet during the last 2 years, developing severe bilateral deterioration of visual function and polyneuropathy. Blood test revealed low levels of vitamin A, B6 and D. The patient underwent examinations with optical coherence tomography (OCT), computerized visual field examination (VF), electroretinography (ERG), visual evoked potentials (VEP) and neurography before and after vitamin supplementation. RESULTS: Visual acuity (VA) was 20/1000 and VF examination showed central scotoma in both eyes. Color vision was significantly affected. Full-field ERG showed normal rod and cone function, but a clearly reduced central peak was registered in multifocal ERG (mf-ERG), indicating impaired fovea function. VEP showed delayed latency and low amplitude of P100 in both eyes. Neurography showed sensory polyneuropathy. OCT showed significant thinning of macular ganglion cell plus inner plexiform layer (GCIPL) with rapid progression. Retinal nerve fiber layer (RNFL) was preserved and normal, which is in contrast to neuroinflammatory conditions. After 2.5 years of multivitamin supplementation, the visual functions were improved. GCIPL thickness was stable without further deterioration. CONCLUSIONS: Multivitamin deficiency results in progressive thinning of GCIPL with severe visual deterioration. In contrast to neuroinflammation, RNFL is preserved and normal. Stabilized GCIPL during vitamin supplementation was associated with improved visual function. OCT provides a sensitive and objective measure for differential diagnosis, monitoring retinal change and response to therapy.


Assuntos
Suplementos Nutricionais , Transtornos da Visão/etiologia , Deficiência de Vitamina A/complicações , Deficiência de Vitaminas do Complexo B/complicações , Deficiência de Vitamina D/complicações , Dieta Vegana/efeitos adversos , Feminino , Humanos , Pessoa de Meia-Idade
2.
Acta Neurol Scand ; 142(5): 418-427, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32416627

RESUMO

BACKGROUND: Optical coherence tomography (OCT) could be complementary to magnetic resonance imaging (MRI) of the brain in monitoring course of multiple sclerosis (MS) and clinically isolated syndrome (CIS). Thinning of neurons in ganglion cell-inner plexiform layer (GCIPL) measured by OCT is assumed to be associated with brain atrophy. OBJECTIVES: To evaluate association of GCIPL with brain parameters detected by quantitative MRI (qMRI) and MR-spectroscopy (MRS) in early MS and CIS. METHODS: Seventeen newly diagnosed MS and 18 CIS patients were prospectively included. The patients were assessed at baseline as well as at 1 year follow-up by OCT, qMRI and MRS. Brain parenchymal and myelin volumes (BPV, MYV respectively) and the corresponding fractions (BPF, MYF) were measured with qMRI. Metabolites including myo-inositol (myo-Ins) were measured in the normal-appearing white matter (NAWM) using MRS. T-tests and ANOVA were used to analyze group differences, and linear regression models to evaluate association of GCIPL with BPV, MYV and myo-Ins after correlation analysis. RESULTS: Disease activity reflected by lesions on MRI and presence of CSF oligoclonal IgG bands were more prominent in MS compared to CIS. GCIPL, BPV, MYV, BPF and MYF were reduced, while concentration of myo-Ins was increased in MS compared to CIS. Follow-up showed consistency of thinner GCIPL in MS compared to CIS. GCIPL thinning correlated with reduced BPV and MYV (P < .05 for both), but with increased myo-Ins (P < .01). CONCLUSIONS: Significant GCIPL thinning occurs in early MS and is associated with enhanced brain inflammation and atrophy.


Assuntos
Doenças Desmielinizantes/patologia , Esclerose Múltipla/patologia , Retina/patologia , Tomografia de Coerência Óptica/métodos , Adolescente , Adulto , Atrofia/patologia , Doenças Desmielinizantes/diagnóstico por imagem , Progressão da Doença , Diagnóstico Precoce , Feminino , Humanos , Imageamento por Ressonância Magnética/métodos , Espectroscopia de Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Esclerose Múltipla/diagnóstico , Neuroimagem/métodos , Adulto Jovem
3.
J Clin Immunol ; 23(2): 100-6, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12757262

RESUMO

To detect a possible effect of dehydroepiandrosterone (DHEA) in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG), DHEA (0.5 mg/rat) was administrated intraperitoneally to Lewis rats every other day from day 4 postimmunization (p.i.) to day 35 p.i. with Torpedo acetylcholine receptor (AChR) and Freund's complete adjuvant. Rats treated with DHEA had a lower clinical score (mean clinic score, 2 versus 0.5 on day 37 p.i.) and a lower body weight loss (mean body weight, 169 versus 142 g on day 37 p.i.) compared with control EAMG rats. DHEA treatment decreased serum anti-AChR IgG and IgG2b antibody titers on days 7, 14, and 21 p.i. and inhibited the levels of anti-AChR IgG antibody secreting cells (60%), accompanied by decreased IL-4 (33%) and augmented TGF-beta1-positive cells (41%) among lymph node mononuclear cells. These results obtained from EAMG in Lewis rats further encourage us to study DHEA treatment in human MG.


Assuntos
Desidroepiandrosterona/farmacologia , Miastenia Gravis Autoimune Experimental/tratamento farmacológico , Acetilcolinesterase/imunologia , Animais , Autoanticorpos/sangue , Autoanticorpos/efeitos dos fármacos , Desidroepiandrosterona/uso terapêutico , Imunoglobulina G/sangue , Interleucina-4/análise , Leucócitos Mononucleares/química , Linfonodos/citologia , Miastenia Gravis Autoimune Experimental/imunologia , Ratos , Ratos Endogâmicos Lew , Fator de Crescimento Transformador beta/análise
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