LA RIVASTIGMINA SERIA ADECUADA PARA EL TRATAMIENTO DE LA DEMENCIA VASCULAR

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La rivastigmina es un inhibidor de la colinesterasa que, debido a sus características químicas y farmacológicas, sería adecuado para el tratamiento de los pacientes con demencia vascular.
moretti9.jpg Autor:
Rita Moretti
Columnista Experto de SIIC

Institución:
Dipartimento di Medicina Clinica e Neurologia, Università degli Studi di Trieste


Artículos publicados por Rita Moretti
Coautores
Paola Torre* Rodolfo M Antonello* Nadia Koscica* Gilberto Pizzolato* 
MD, Dipartimento di Medicina Clinica e Neurologia, Università degli Studi di Trieste, Trieste, Italia*
Recepción del artículo
3 de Agosto, 2006
Aprobación
8 de Agosto, 2006
Primera edición
20 de Noviembre, 2006
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La demencia vascular representa el segundo tipo más frecuente de demencia. La clasificación de la demencia vascular sigue tres procesos clínico patológicos generales: demencia multiinfarto, demencia por infarto único ubicado en una zona estratégica y demencia subcortical. Actualmente no existen tratamientos estandarizados establecidos para los trastornos cognitivos de causa vascular. La disminución de la actividad de la acetilcolinesterasa es una estrategia habitualmente utilizada tanto para el tratamiento de los pacientes que presentan enfermedad de Alzheimer como para aquellos con trastornos cognitivos de causa vascular. En consecuencia, es posible que los inhibidores de la colinesterasa sean una opción conveniente. La presente revisión se llevó a cabo con el propósito de evaluar la eficacia de la rivastigmina para el tratamiento de los individuos que presentan trastornos cognitivos de origen vascular. De acuerdo con los datos provenientes de diferentes estudios, la rivastigmina sería útil para tratar pacientes con deterioro cognitivo de origen vascular. No obstante, esta conclusión se efectuó sobre la base de estudios en los cuales se incluyó un número reducido de pacientes, se buscó comparar la rivastigmina con agentes diferentes del placebo o se extrapolaron datos a partir de estudios de gran magnitud efectuados con pacientes que presentaban enfermedad de Alzheimer y factores de riesgo vasculares de relevancia poco clara. Desde ese punto de vista, se puede concluir que es necesario realizar estudios de gran tamaño, controlados con placebo a doble ciego y adecuadamente aleatorizados antes de poder alcanzar conclusiones sólidas. La metodología empleada en dichos estudios debería responder a las características biológicas y clínicas particulares del deterioro cognitivo vascular y sus subtipos.

Palabras clave
demencia vascular, enfermedad vascular, rivastigmina


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Abstract
Vascular dementia represents the second most common type of dementia. The classification of vascular dementia broadly follows three clinico-pathological processes: multi-infarct dementia, single strategic infarct dementia and subcortical dementia. Currently, no established standard treatment for vascular cognitive impairment exists. Reductions in acetylcholine and acetyltransferase activity are common to both Alzheimer's disease and vascular cognitive impairment raising the possibility that cholinesterase inhibitors may also be beneficial for the latter. This review has been conducted to assess the efficacy of rivastigmine in the treatment of people with vascular cognitive impairment. From existing trial data there is some evidence of benefit of rivastigmine in vascular cognitive impairment. However, this conclusion is based on studies which had small numbers of patients, which sought to compare rivastigmine to treatments other than placebo or which used data extrapolated post hoc from large studies involving patients with Alzheimer's disease and vascular risk factors of unclear significance. From these perspectives, one can conclude that large placebo-controlled, double blind and adequately randomised trials are needed before firm conclusions can and should be drawn. The methodology of such trials should acknowledge the biological and clinical features unique to vascular cognitive impairment and its subtypes.

Key words
vascular dementia, vascular disease, rivastigmine


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Especialidades
Principal: Salud Mental
Relacionadas: Farmacología, Geriatría, Medicina Familiar, Medicina Farmacéutica, Medicina Interna, Neurología



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Rita Moretti, Dipartimento di Medicina Clinica e Neurologia, Università degli Studi di Trieste, Ospedale di Cattinara 34149, Trieste, Italia
Bibliografía del artículo
1. Chui HC. Dementia. A review emphasizing clinico-pathologic correlation and brain-behaviour relationships. Arch Neurol 1989; 46(7):806-814.
2. Skoog I, Nilsson L, Palmertz B et al. A population-based study of dementia in 85-year olds. N Engl J Medicine 1993; 328:153-158.
3. Meyer JS, Rauch GM, Crawford K et al. Risk factors accelerating cerebral degenerative changes cognitive decline and dementia. Int J Geriatr Psychiatry 1999; 14:1050-1061.
4. Meyer JS, Rauch G, Rauch RA, Haque A. Risk factors for cerebral hypoperfusion, mild cognitive impairment, and dementia. Neurobiology of Aging 2000; 21:161-169.
5. Wetterling T, Kanitz RD, Borgis KJ. The ICD-10 criteria for vascular dementia. Dementia 1994; 5:185-188.
6. Chui H. Dementia associated with subcortical ischemic vascular disease. American Academy (AAN), Philadelphia, 2001; 2FC.005:89-107.
7. Pantoni L, Rossi R, Inzitari D et al. Efficacy and safety of nimodipine in subcortical vascular dementia: a subgroup analysis of the Scandinavian Multi-Infarct Dementia Trial. J Neurol Sci 2000; 175:124-34.
8. European Pentoxifylline Multi-Infarct Dementia (EPMID) Study Group. European pentoxifylline multi-infarct dementia. Eur Neurol 1996; 36:315-21.
9. Marcusson J, Rother M, Kittner B et al. A 12-month, placebo-controlled trial of propentofylline (HWA 285) in patients with dementia according to DSM III-R. Dement Geriatr Cogn Disord 1997; 8:320-328.
10. Vasquez J, Purve MJ. The cholinergic pathway to cerebral blood vessels. I. Morphological studies. Pflugers Arch 1979; 379:157-163.
11. Vanhoute PM. Endothelium and control of vascular function. State of the art. Hypertension 1989; 13:658-667.
12. Saito H, Togashi H, Yoshiaka M et al. Animal models of vascular dementia with emphasis on stroke-prone spontaneously hypertensive rats. Clin Exp Pharmacol Physiol 1995; 22:S257-9.
13. Togashi H, Matsumoto M, Yoshioka M et al. Neurochemical profiles in cerebrospinal fluid of stroke-prone spontaneously hypertensive rats. Behav Lett 1994; 166:117-20.
14. Kimura S, Saito H, Minami M et al. Pathogenesis of vascular dementia in stroke-prone spontaneously hypertensive rats. Toxicology 2000; 153:167-87.
15. Togashi H, Kimura S, Matsumoto M et al. Cholinergic changes in the hippocampus of stroke-prone spontaneously hypertensive rats. Stroke 1996; 27:520-526.
16. Scremin OU, Li MG, Scremin AM, Jenden DJ. Cholinesterase inhibition improves blood flow in the ischemic cerebral cortex. Brain Res Bull 1997; 42:59-70.
17. Gottfries CG, Blennow K, Karlsson I, Wallin A. The neurochemistry of vascular dementia. Dementia 1994; 5:163-7.
18. Wallin A, Blennow K, Gottfries CG. Neurochemical abnormalities in vascular dementia. Dementia 1989; 1:120-30.
19. Tohgi H, Abe T, Kimura M et al. Cerebrospinal fluid acetylcholine and choline in vascular dementia of Binswanger and multiple small infarct types as compared with Alzheimer type dementia. J Neurol Transm 1996; 103:1211-20.
20. Sakurada T, Alufuzoff I, Winblad B, Nordberg A. Substance P like immunoreactivity, choline acetyltransferase activity and cholinergic muscarinic receptors in Alzheimer's disease and multi-infarct dementia. Brain Res 1990; 521(1-2):329-332.
21. Szilagy AK, Nemeth A, Martini E, Lendvai B, Venter V. Serum and CSF cholinesterase activity in various kind of dementia. Eur Arch Psychiatry Neurol Sci 1987; 236:309-311.
22. Grossberg GT Cholinesterase inhibitors for the treatment of Alzheimer's disease: getting on and staying on. Current Therapeutic Research 2003; 64(4):216-235.
23. Nordberg A, Svensson AL. Cholinesterase inhibitors in the treatment of Alzheimer's disease: A comparison of tolerability and pharmacology. Drug Sat 1998; 19:465-480.
24. Blackard WG .Ir, Sood GK, Crowe DR, Fallon MB. Tacrine. A cause of fatal hepatotoxicity? J Clin Gastroenterol 1998; 26:57-59.
25. Sifton OW, ed. Physicians' Desk Reference@. N.I: Medical Economics; 2002: 1792, 2342, 2665.
26. Svensson AL. Cholinesterase inhibitors in Alzheimer's disease: An experimental study on mechanisms for interaction with muscarinic and nicotinic receptors and neuroprotection [published doctoral dissertation]. Huddinge, Sweden: Division of Nicotine Research, Department of Clinical Neuroscience and Family Medicine, Karolinska Institute, Huddinge University Hospital; 1997: Publication no. 884, S-141 86.
27. Barnes CA, Meltzer J, Houston F, et al. Chronic treatment of old rats with donepezil or galantamine: Effects on memory, hippocampal plasticity and nicotinic receptors. Neuroscience 2000; 99:17-23.
28. Svensson A, Nordberg A. Interaction of tacrine, gaIantamine, NXX-066 and E2020 with neuronal alpha4beta2 nicotinic receptors expressed in fibroblast cells. In: Iqbal K, Winblad B, Nishimura T et al. eds. Alzheimer's Disease: Biology, Diagnosis, and Therapeutics. New York: Wiley; 1997:751-756.
29. Bryson HM, Benfield P. Donepezil. Drugs Aging 1997; 10:234-239; discussion 240-241.
30. Kasa P, Papp H, Kasa P JR, Torok L. Donepezil dose-dependently inhibits acetylcholinesterase activity in various areas and in the presynaptic cholinergic and the postsynaptic cholinoceptive enzyme-positive structures in the human and rat brain. Neuroscience 2000; 101:89-100.
31. Amici S, Lanari A, Romani R, et al. Cerebrospinal fluid acetylcholinesterase activity after long-term treatment with donepezil and rivastigmina. Mech Ageing Dev 2001; 122:2057-2062.
32. Davidsson P, Blennow K, Andreasen N, et al. Differential increase in cerebrospinal fluid-acetylcholinesterase after treatment with acetylcholinesterase inhibitors in patients with Alzheimer's disease. Behav Lett 2001; 300:157-160.
33. Parnetti L, Amici S, Lanari A, et al. Cerebrospinal fluid levels of biomarkers and activity of acetylcholinesterase (AchE) and butyryl cholinesterase in AD patients before and after treatment with different AchE inhibitors. Neurol Sci 2002; 23(Suppl 2):S95-S96.
34. Darreh-Shori T, Almkvist O, Guan ZZ, et al. Sustained cholinesterase inhibition in AD patients receiving rivastigmine for 12 months. Neurology 2002; 59:563-572.
35. Weinstock M. Selectivity of cholinesterase inhibition. CNS Drugs 1999; 12:307-323.
36. Samochocki M, Zerlin M, Jostock R, et al. Galantamine is an allosterically potentiating ligand of the human alpha4-beta2 nAChR. Acta Neurol Scand Suppl 2000; 176:68-73.
37. Albuquerque EX, Alkondon M, Pereira EF, et al. Properties of neuronal nicotinic acetylcholine receptors: Pharmacological characterization and modulation of synaptic function. J Pharmacal Exp Ther 1997; 280:1117-1136.
38. Giacobini E. Selective inhibitors of butyrylcholinesterase: A valid alternative for therapy of Alzheimer's disease? Drugs Aging 2001; 18:891-898.
39. Perry EK, Perry RH, Blessed G, Tomlinson BE. Changes in brain cholinesterases in senile dementia of Alzheimer type. Neuropathol Appl Neurobiol 1978; 4:273-277.
40. Mesulam M, Guillozet A, Shaw P, Quinn B. Widely spread butyrylcholinesteras can hydrolyze acetylcholine in the normal and Alzheimer brain. Neurobiol Dis 2002; 9:88-93.
41. Arendt T, Bruckner MK, Lange M, Bigl V. Changes in acetylcholinesterase and butyrylcholinesterase in Alzheimer's disease resemble embryonic developmenta study of molecular forms. Neurochem Int 1992; 21:381-396.
42. Bullock R. Cholinesterase inhibitors and vascular dementia: another string to their bow? CNS Drugs 2004; 18(2):79-92.
43. Olsen CE, Poulsen HD, Lublin HK. Drug therapy of dementia in elderly patients. A review. Nord J Psychiatry 2005; 59(2):71-7.
44. Erkinjuntti T, Kurz A, Gauthier S, et al. Efficacy of galantamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: a randomised trial. Lancet 2002; 359:1283-1290.
45. Erkinjuntti, T. Treatment options. The latest evidence with galantamine (Reminyl(R)). J Neurol Sci, 2002. 203-204(C):125-30.
46. Erkinjuntti, T., Broad therapeutic benefits in patients with probable vascular dementia or Alzheimer's disease with cerebrovascular disease after treatment with galantamine. Eur J Neurol 2002; 9(5):545.
47. Wilkinson D, Doody R, Helme R, Taubman K, Mintzer J, Kertesz A, et al. Donepezil in vascular dementia: A randomized, placebo-controlled study. Neurology 2003; 61(4):479-86.
48. Black S, Roman GC, Geldmacher DS, Salloway S, Hecker J, Burns A, et al. Efficacy and tolerability of donepezil in vascular dementia: positive results of a 24-week, multicenter, international, randomized, placebo controlled clinical trial. Stroke 2003; 34(10):2323-30.
49. Mesulam MM, Guillozet A, Shaw P, Levey A, Duysen EG, Lockridge O. Preservation of cholinergic systems in AChE knockouts and the role of BuChE in acetylcholine hydrolysis. Society of Neuroscience Abstracts 2001; 27:2565.
50. Giacobini E, Spiegel R, Enz A, et al. Inhibition of acetyl- and butyryl-cholinesterase in the cerebrospinal fluid of patients with Alzheimer's disease by rivastigmine: Correlation with cognitive benefit. J Neural Transm 2002; 109:1053-1065.
51. Massoulie J, Bon S. The molecular forms of cholinesterase and acetylcholine in vertebrates. Annu Rev Neurosci 1982; 37:57-106.
52. Siek GC, Katz LS, Fishman EB, et al. Molecular forms of acetylcholinesterase in subcortical areas of normal and Alzheimer disease brain. Biol Psychiatry 1990; 27:573-580.
53. Poirier J. Evidence that the clinical effects of cholinesterase inhibitors are related to potency and targeting of action. Int J Clin Pract Suppl 2002; 6-19.
54. Inglis F. The tolerability and safety of cholinesterase inhibitors in the treatment of dementia. Int J Clin Pract Suppl 2002; 45-63.
55. Venneri A, Shanks MF, Sta¡ RT, Pestell SJ, Forbes KE, Gemmell HG, Murray AD. Cerebral blood flow and cognitive responses to rivastigmine treatment in Alzheimer's disease. NeuroReport 2002; 13:83-96.
56. Okamoto K, Tanaka M, Kondo S. treatmetn of vascular dementia. Ann NY Acad Sci 2002; 977:507-512.
57. Sharma T, Kumari V, Mitterschiffthaler M et al. Cognitive effects of rivastigmine in Alzheimer's disease: an fMRI study. Poster presented at the American College of Neuropsychopharmacology 40th Annual Meeting, Waikoloa, Hawaii, 9-13 December 2001.
58. Adler G, Brassen S. Short-term rivastigmine treatment reduces EEG slow-wave power in Alzheimer patients. Neuropsychobiology 2001; 43:273-6.
59. Nordberg A, Darreh-Shori T, Svensson A, Guan Z. Acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activities in CSF of mild AD patients following 12 months of rivastigmine treatment. J Neurol Sci 2001; 187(Suppl 1):P0144.
60. Giacobini E, Spiegel R, Enz A, Veroff AE, Cutler NR. Inhibition of acetyl- and butyryl-cholinesterase in the cerebrospinal fluid of patients with Alzheimer's disease by rivastigmine: correlation with cognitive benefit. J Neural Trans 2003; 143-7.
61. Vincent S, Lane R.Rivastigmine in vascular dementia. Int Psychogeriatr 2003; 15 Suppl 1:201-5.
62. Almkvist O, Darreh-Shori T, Spiegel R, Nordberg A. Improved cognition and plasma cholinesterase (ChE) inhibition in AD patients receiving rivastigmine for 1 year: differential effects across time. J Neurol Sci 2001; 187(Suppl 1):P0143.
63. Roman GC. Rivastigmine for subcortical vascular dementia. Expert Rev Neurother 2005 May; 5(3):309-313.
64. Moretti R, Torre P, Antonello RM, Cazzato G. Rivastigmine in subcortical vascular dementia: a comparison trial on efficacy and tolerability for 12 months follow up. Eur J Neurol 2001; 8:361-362.
65. Moretti R et al., Rivastigmine in subcortical vascular dementia. An open 22-month study. J Neurol Sci 2002; 203-204(C):141-6.
66. Moretti R, Torre P, Antonello RM, Cazzato G, Bava A. Rivastigmine in subcortical vvascular dementia: a randomized, controlled, open 12-mont study in 208 patients. Am J Alzh Dis Oth Demen 2003; 18(5):265-272.
67. Moretti R, Torre P, Antonello RM, Bava A, Cazzato G. Rivastigmine superior to aspirin plus nimodipine in subcortical vascular dementia: an open, 16-month comparative study. International Journal of Clinical Practice 2004; 58(4):346-353.
68. Moretti R, Torre P, Antonello RM, Cattaruzza T, Cazzato G. Delirium in vascular dementia: cholinesterase inhibition as a possibile therapy. A controlled, open 24-month study in 246 patients. American Journal of Alzheimer Disease and other Dementias 2004; 19(6):333-339.
69. Aupperle PM, Koumaras B, Chen M, Rabinowicz A, Mirski D. Long-term effects of rivastigmine treatment on neuropsychiatric and behavioral disturbances in nursing home residents with moderate to severe Alzheimer's disease : results of a 52 week open-Iabel study. Curr Med Research and Opinion 2004 20/10:1605-1612.
70. Finkel SI. Effects of rivastigmine on behavioral and psychological symptoms of dementia in Alzheimer's disease. Clin Therapeutics 2004; 26/7:980-989.
71. Moretti R, Torre P, Antonello RM, Cazzato G , Pizzolato G. Differences in response to rivastigmine in subcortical vascular dementia and multi-infarct dementia. J Neurol Neurosurg Psychiatry, 2006 in press.
72. Moretti R, Torre P, Antonello RM, Cazzato G. Therapy of vascular dementia: perspectives and milestones. Therapy, Future Drugs 2005; 2(4):649-658.
73. Craig D, Birks J. Rivastigmine for vascular cognitive impairment. Cochrane Database Syst Rev 2005; (2):CD004744.

 
 
 
 
 
 
 
 
 
 
 
 
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