Conceptos Categóricos

DISFUNÇAO ENDOTELIAL E MICROALBUMINURIA EM DIABETES MELLITUS TIPO 1

DISFUNÇAO ENDOTELIAL E MICROALBUMINURIA EM DIABETES MELLITUS TIPO 1

(especial para SIIC © Derechos reservados)
A estreita correlação entre aumento da excreção de albumina, mesmo em fase inicial (microalbuminúria) e disfunção endotelial fortalece a importância da microalbuminúria como marcador precoce de aterotrombose, também em pacientes jovens e com curta duração de doença.
Autor:
Ana marice Ladeia
Columnista Experto de SIIC
Artículos publicados por Ana marice Ladeia
Coautor
Luís Adan* 
Professor Adjunto, Universidade Federal da Bahia, Bahia, Brasil*
Recepción del artículo
1 de Noviembre, 2006
Aprobación
23 de Febrero, 2007
Primera edición
9 de Abril, 2007

Resumen
A importância do endotélio no corpo humano está relacionado à sua extensão e suas múltiplas funções biológicas. A disfunção endotelial é a manifestação mais precoce da patologia vascular, decorrendo do desequilíbrio entre os fatores de relaxamento e os de contração, entre mediadores anti e pró-coagulantes ou de fatores de promoção e inibição do crescimento de células musculares lisas. Fatores de risco como dislipidemia, tabagismo e diabetes desencadeiam o processo aterosclerótico inicialmente pela simples ativação endotelial, posteriormente pela sua disfunção. Estudos têm sido desenvolvidos visando a compreender o papel da hiperglicemia e da duração do diabetes na patogênese da disfunção endotelial. Microalbuminúria é um marcador precoce de nefropatia em diabetes, cuja associação com disfunção endotelial em diabetes tipo 1 tem sido demonstrada em vários estudos. Mecanismos que expliquem essa associação sido sugeridos; entre eles, inflamação sub-clínica, aumento da pressão glomerular ou enfraquecimento da sua membrana basal e lesão do glicocálice endotelial. O melhor entendimento desses mecanismos poderá abrir perspectivas terapêuticas que visem a minimizar, ou interromper a agressão vascular na sua fase mais precoce e assim prevenir o aparecimento de complicações vasculares. Nesta revisão são discutidas evidências relacionadas ao papel da disfunção endotelial como marcador precoce de complicações vasculares em diabetes tipo 1.

Palabras clave
disfunção endotelial, microalbuminúria, diabetes tipo 1, aterosclerose, crianças


Artículo completo

(castellano)
Extensión:  +/-5.15 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
The importance of the endothelium to the human body is related to its extent and multiple biological functions. Endothelial dysfunction is the earliest manifestation of vascular pathology, resulting from imbalance between relaxation and contraction, and anti- and pro-coagulant mediators or factors that promote and inhibit the growth of smooth muscle cells. Risk factors such as, dyslipidemia, smoking and diabetes lead to the onset of the aterosclerotic process, initially simply by endothelial activation and later by its dysfunction. Studies have been designed with the aim of understanding the role of hyperglycemia and the duration of diabetes in the pathogenesis of endothelial dysfunction. Microalbuminuria is an early marker of nephropathy in diabetes, whose association with endothelial dysfunction in Type 1 diabetes has been shown in various studies. Mechanisms that explain this association have been suggested. Among them we can mention: sub-clinical inflammation, increase in glomerular pressure or weakening of its basal membrane and lesion of the endothelial glycocalyx. Better understanding of these mechanisms may bring about therapeutic perspectives that aim to minimize, or interrupt vascular aggression in its earliest stage, and thus prevent the appearance of vascular complications. In this review, the evidences related to the role of endothelial dysfunction as early marker of vascular complications in Type 1 diabetes are discussed.

Key words
endothelial dysfunction, microalbuminuria, type 1 diabetes tmellitus, atherosclerosis, children


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Cardiología
Relacionadas: Diagnóstico por Laboratorio, Medicina Interna, Nefrología y Medio Interno



Comprar este artículo
Extensión: 5.15 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Enviar correspondencia a:
Ana Marice Ladeia, Escola Bahiana de Medicina e Saúde Pública, 41810-570, Rua Altino Seberto de Barros 241 sala 506 - Itaigara, Salvador, Brasil
Bibliografía del artículo
1. Rubanyl GM. The role of endothelium in cardiovascular homeostasis and diseases. J Cardiovasc Pharmacol 1993; 22(Suppl 4):S1-14.
2. Kawashima S. The two faces of endothelial nitric synthase in the pathophysiology of atherosclerosis. Endothelium 2003; 11:99-107.
3. Janssen-Heininger YM, Poynter ME, Baeuerle PA. Recent advances towards understanding redox mechanisms in the activation of nuclear factor kappaB. Free Radic Biol Med 2000; 28(9):1317-27.
4. Brownlee M. Biochemistry and molecular cell biology of diabetic complication. Nature 2001; 414:813-820.
5. Giuliano D, Marfella R, Coppola L et al. Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia. Circulation 1997; 95(7):1783-90.
6. The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329:977-86.
7. Unidet Kingdom Prospective Diabetes study (UKPDS). Relative efficacy of randomly allocated diet, sulphonylurea, insulin or metformin in patients with newly diagnosed non-insulin dependent diabetes followed for three years. BMJ 1995; 329:83-88.
8. Schalkwijk CG, Stehouwer CD.Vascular complications in diabetes mellitus: the role of endothelial dysfunction. Clin Sci 2005; 109(2):143-59.
9. Dogra G, Rich L, Stanton K, Watts GF. Endothelium-dependent and independent vasodilation studies at normoglycaemia in type 1 diabetes mellitus with and without microalbuminuria. Diabetologia 2001; 44:593-601.
10. Lekakis J, Papamichel C, Anastasiou H, et al. Endothelial dysfunction of conduit arteries in insulin-dependent diabetes mellitus without microalbuminuria. Cardiovasc Res 1997; 34(1):164-8.
11. Ladeia AM, Ladeia-Frota C, Pinho L, Stefanelli E, Adan L. Endothelial dysfunction is correlated with microalbuminuria in children with short-duration type 1 diabetes. Diabetes Care 2005; 28(8):2048-50.
12. Rosen P, Ballausen T, Stockklauser K, Honack C. Influence of glucose and diabetes on the endothelial NO-synthase. Diabetologia 1995; 38:A48.
13. Cosentino F, Hishikawa K, Katusic ZS, Lüscher TF. High glucose increases nitric oxide synthase expression and superoxide anion generation in human aortic endothelial cells. Circulation 1997; 96:25-28.
14.Hink U, Li H, Mollnau H, Oelze M, Matheis E, Hartmann M, et al. Mechanisms underlying endothelial dysfunction in diabetes mellitus. Circ Res 2001; 88:14-22.
15. Järvisalo M, Raitakari M, Toikka J, Putto-Laurila A, Rontu R, Laine S, et al. Endothelial dysfunction and increased arterial intima-media thickness in children with type diabetes. Circulation 2004; 109(14):1750-1755.
16. Singh TP, Groehn H, Kazmers A. Vascular function and carotid intimal-medial thickness in children with insulin-dependent diabetes mellitus. J Am Coll Cardiol 2003; 41(4):661-5.
17. Brands MW, Sharyn MF. Acute endothelium-mediated vasodilation is not impaired at the onset of diabetes. Hypertension 1998; 32:541-547.
18. Pickup JC, Mattock MB, Chusney GD, Burt D. NIDDM as a disease of innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X. Diabetologia 1997; 40:1286-1292.
19. Pradhan AD, Manson MB, Rifai N, Buring Je, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001; 286:327-334.
20. Ladeia, AM, Stefanelli E, Ladeia-Frota C, Moreira A, Hiltner A, Adan L. Association between elevated serum C-reactive protein and triglyceride levels in young subjects with type 1 diabetes. Diabetes Care 2006; 29(2):424-6.
21. Jarvisalo MJ, Harmoinen A, Hakanen M, Paakkunainen U, Viikari J, Hartiala J, Lehtimaki T, Simell O, Raitakari O: Elevated serum C-reactive protein levels and early changes in healthy children. Arterioscler Thromb Vasc Biol 2002; 22:1323-1328.
22. Verrroti A, Greco R, Basciani F, Morgese G, Chiarelli F. Von Willebrand factor and its propeptide in children with diabetes. Relation between endothelial dysfunction and microalbuminuria. Pedriatric Research 2003; 53(3):382-6.
23. Stehouwer CDA, Donker AJM. Urinary albumin excretion and cardiovascular disease risk diabetes mellitus: is endothelial dysfunction the missing link. J Nefrol 1993; 6:72-93.
24. Shestakova MV, Jarek-Martynova IR, Ivanishina NS et al. Role of endothelial dysfunction in the development of cardiorenal syndrome in patients with type 1 diabetes mellitus.Diabetes Res Clin Pract 2005 Jun; 68(Suppl1):S65-72.
25. Nieuwdorp M, Mooij HL, Kroon J et al. Endothelial glycocalyx damage coincides with microalbuminuria in type 1 diabetes. Diabetes 2006; 55(4):1127-32.
26. Davi G, Chiarelli F, Santilli F et al. Enhanced lipid peroxidation and platelet activation in the early phase of type 1 diabetes mellitus: role of interleukin-6 and disease duration. Circulation 2003; 107(25):3199-203.
27. Targher G, Bertolini L, Zoppini G, Zenari L, Falezza G. Increased plasma markers of inflammation and endothelial dysfunction and their association with microvascular complications in Type 1 diabetic patients without clinically manifest macroangiopathy. Diabet Med 2005; 22(8):999-1004.
28. Dogra GK, Watts GF, Chan DC, Stanton K. Statin therapy improves brachial artery vasodilator function in patients with Type 1 diabetes and microalbuminuria. Diabet Med 2005; 22(3):239-42.

 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
ua31618