RESUMO
An 81-year-old woman presented with blurred vision in the left eye. Best corrected visual acuity was 20/100. Ophthalmologic examination in the left eye revealed tilted disc syndrome with exudative change at the margin of inferior staphyloma. The exudative change persisted despite monthly intravitreal ranibizumab injections for 5 months. Subsequently, two intravitreal aflibercept injections 1 month apart were substituted for the ranibizumab injections, resulting in successful resolution of the exudative change.
Assuntos
Inibidores da Angiogênese/uso terapêutico , Anticorpos Monoclonais Humanizados/uso terapêutico , Anormalidades do Olho/tratamento farmacológico , Disco Óptico/anormalidades , Receptores de Fatores de Crescimento do Endotélio Vascular/uso terapêutico , Proteínas Recombinantes de Fusão/uso terapêutico , Doenças Retinianas/tratamento farmacológico , Líquido Sub-Retiniano/efeitos dos fármacos , Idoso de 80 Anos ou mais , Corantes , Substituição de Medicamentos , Membrana Epirretiniana/diagnóstico , Membrana Epirretiniana/tratamento farmacológico , Anormalidades do Olho/diagnóstico , Feminino , Angiofluoresceinografia , Humanos , Verde de Indocianina , Injeções Intravítreas , Edema Macular/diagnóstico , Edema Macular/tratamento farmacológico , Ranibizumab , Descolamento Retiniano/diagnóstico , Descolamento Retiniano/tratamento farmacológico , Doenças Retinianas/diagnóstico , Epitélio Pigmentado da Retina/efeitos dos fármacos , Epitélio Pigmentado da Retina/patologia , Tomografia de Coerência Óptica , Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidoresRESUMO
We review the utility of serum anticholinergic activity (SAA) as a peripheral marker of anticholinergic activity (AA) in the central nervous system (CAA). We hypothesize that the compensatory mechanisms of the cholinergic system do not contribute to SAA if their system is intact and that if central cholinergic system deteriorates alone in conditions such as Alzheimer's disease or Lewy body dementia, CAA and SAA are caused by way of hyperactivity of inflammatory system and SAA is a marker of the anticholinergic burden in CNS. Taking into account the diurnal variations in the plasma levels of corticosteroids, which are thought to affect SAA, it should be measured at noon or just afterward.
Assuntos
Acetilcolina/sangue , Doença de Alzheimer/sangue , Sistema Nervoso Central/metabolismo , Biomarcadores/sangue , HumanosRESUMO
We report the case of a 74-year-old woman who presented with amnesia and positive serum anticholinergic activity (SAA), which disappeared after treatment with the cholinesterase inhibitor donepezil for 1 year. Her only other regular medications were topical glaucoma preparations. We suggest that mental stress, mild cognitive impairment and Alzheimer's disease pathology combined to generate SAA in this patient. We also consider that SAA may have subsequently become negative because of upregulation of acetylcholine production by donepezil, and because the patient's other medications and physical condition (including glaucoma) remained unchanged during the 1-year period.
Assuntos
Amnésia/tratamento farmacológico , Inibidores da Colinesterase/uso terapêutico , Disfunção Cognitiva/tratamento farmacológico , Indanos/uso terapêutico , Nootrópicos/uso terapêutico , Piperidinas/uso terapêutico , Idoso , Amnésia/diagnóstico , Disfunção Cognitiva/diagnóstico , Donepezila , Feminino , HumanosRESUMO
We previously speculated that anticholinergic activity (AA) endogenously appeared in Alzheimer's disease (AD) and accelerated AD pathology. In this article we introduce manuscripts supporting the endogenous appearance of AA in AD and the acceleration of AD pathology. We speculate that acethylcholine (ACh) not only is related to cognitive functions but also regulates the inflammatory system. Therefore in AD, in which the ACh system is down-regulated, the hyperactivity of the inflammatory system may be caused and among cyctokines, substances having anticholinergic properties may appear. We also refer to a case in which serum anticholinergic activity (SAA) disappeared with the prescription of memantine (an antidementia agent that has the property of the N-methyl-D-aspartate (NMDA) receptor blocker) and speculate that because the hyperactivity of the inflammatory system occurs by way of the hyperactivity of NMDA receptor, memantine could abolish the AA.