RESUMO
We describe a patient with probable dementia with Lewy bodies (DLB) whose Parkinsonism worsened after administration of rivastigmine within the therapeutic dose range. Some extrapyramidal signs (EPS) then reversed to pre-treatment level after rivastigmine dose reduction. We draw attention to the need of EPS monitoring during titration of cholinesterase inhibitors in patients with DLB. This is the first report to our knowledge of iatrogenic worsening of Parkinsonism which was successfully managed by dose reduction.
Assuntos
Acetilcolina/metabolismo , Inibidores da Colinesterase/administração & dosagem , Transtornos Parkinsonianos/tratamento farmacológico , Fenilcarbamatos/administração & dosagem , Idoso , Inibidores da Colinesterase/efeitos adversos , Progressão da Doença , Humanos , Doença por Corpos de Lewy/complicações , Masculino , Transtornos Parkinsonianos/etiologia , Fenilcarbamatos/efeitos adversos , Rivastigmina , Fatores de TempoRESUMO
Description of a case of probable dementia with Lewy bodies featuring parkinsonism, dementia and supranuclear gaze palsy. This is the first patient to our knowledge affected with vertical gaze palsy receiving clinical diagnosis of DLB when alive and to be treated with cholinesterase inhibitors.
Assuntos
Doença por Corpos de Lewy/patologia , Paralisia Supranuclear Progressiva/patologia , Idoso , Diagnóstico Diferencial , Lobo Frontal/diagnóstico por imagem , Humanos , Doença por Corpos de Lewy/complicações , Doença por Corpos de Lewy/diagnóstico por imagem , Masculino , Testes Neuropsicológicos , Tomografia por Emissão de Pósitrons/métodos , Escalas de Graduação Psiquiátrica , Paralisia Supranuclear Progressiva/complicações , Paralisia Supranuclear Progressiva/diagnóstico por imagemRESUMO
Two human neuroblastoma cell lines, LAN-5 and GI-CA-N, have been analyzed for their capability to adhere to different extracellular matrix (ECM) components. The GI-CA-N cells adhered to all the tested substrates: laminin (LN), type I and type IV collagen (Coll I, Coll IV), vitronectin (VN), and fibronectin (FN). Conversely LAN-5 cells weakly attached to FN and VN, whilst adhesion on LN and Coll I and IV was strong and induced a rapid elongation of cell processes. By means of RT-PCR and immunoprecipitation we showed that the integrin pattern of these two lines was different and could explain their diversity in adhesion capability. Both cell lines express a large amount of the beta 1 integrin subunit, associated with different alpha chains, probably responsible for their adhesion to some ECM proteins. After treatment of LAN-5 cells with biological differentiating agents, such as gamma-interferon, alone or in combination with tumour necrosis factor-alpha (TNF-alpha), or retinoic acid, the levels of alpha 1 beta 1, alpha 2 beta 1, and alpha 3 beta 1 integrin expression were enhanced, while the amount of alpha v remained constant. In contrast, treatment of LAN-5 cells with TNF-alpha, that did not induce any maturation, or starvation in 2% foetal calf serum, that inhibited cell proliferation without affecting neural differentiation, did not induce any change in the integrin assessment. Messenger-RNAs for the two alpha 6 isoforms, A and B, were present in both cell lines. However, in LAN-5 cells, the protein product was neither detectable nor inducible by differentiation. Our results confirm the specific modulation of the alpha 1 beta 1 integrin expression in human neuronal development, and show, for the first time, the involvement of alpha 2 beta 1 and alpha 3 beta 1 heterodimers in this maturational process.