PRE-ECLAMPSIA: UM MODELO <I>IN VIVO</I> DE PERDA DE PROTECÇAO PELAS HDL





PRE-ECLAMPSIA: UM MODELO IN VIVO DE PERDA DE PROTECÇAO PELAS HDL

(especial para SIIC © Derechos reservados)
Os nossos resultados indicam que mulheres pré-eclâmpticas apresentando níveis baixos de HDL poderão perder protecção mediante o envolvimento dos sistemas inflamatório e hemostático
belo9.jpg Autor:
Belo, Luis
Columnista Experto de SIIC

Institución:
Facultad de Farmacia Universidad do Porto Porto, Portugal


Artículos publicados por Belo, Luis
Coautores
Alice Santos-Silva. Irene Rebelo*  Muriel Caslake**  Gordon Lowe***  Ann Rumley**  Luís Pereira-Leite****  Alexandre Quintanilha***** 
Professoras Auxiliares Faculdade de Farmácia e Instituto de Biologia Molecular e Celular da Universidade do Porto*
PhD Royal Infirmary, University of Glasgow**
MD, FRCP Royal Infirmary, University of Glasgow***
Professor Catedrático Faculdade de Medicina da Universidade do Porto, Hospital de S. João****
Professor Catedrático Instituto de Ciências Biomédicas Abel Salazar e Instituto de Biologia Molecular e Celular da Universidade do Porto*****
Recepción del artículo
27 de Mayo, 2004
Aprobación
15 de Septiembre, 2004
Primera edición
5 de Noviembre, 2004
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
A gravidez humana está associada a hiperlipidémia fisiológica marcada (com um perfil tipo "aterogénico") que é normalmente bem tolerada pela mãe; entre outras modificações, o aumento na concentração de lipoproteínas de alta densidade (HDL) durante a gravidez normal poderá ajudar a conferir protecção à mãe. Contudo, em gravidezes de elevado risco, como na pré-eclampsia (PE), o controlo da hiperlipidémia poderá não funcionar correctamente. A PE é uma alteração hipertensiva característica da gravidez humana, potencialmente perigosa para a mãe e para o feto. Embora os mecanismos exactos que desencadeiam esta síndrome permaneçam por esclarecer, a dislipidémia e a activação de leucócitos poderão contribuir para o desenvolvimento de stresse oxidativo e disfunção vascular observados na PE. Uma situação frequentemente observada na PE é o nível reduzido de HDL e verificámos existir uma correlação inversa e significativa entre os níveis de apolipoproteína (apo) A-I, o maior constituinte proteico das HDL, e marcadores de activação do neutrófilo (lactoferrina e elástase) assim como com o D-dímero (um produto de degradação da fibrina). Os nossos resultados indicam que mulheres pré-eclâmpticas apresentando níveis baixos de HDL poderão perder protecção mediante o envolvimento dos sistemas inflamatório e hemostático.

Palabras clave
HDL, inflamação, coagulação, gravidez normal, pré-eclampsia


Artículo completo

(castellano)
Extensión:  +/-5.87 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
Human pregnancy is associated with pronounced physiological hyperlipidaemia (with an "atherogenic-like" profile) that is usually well tolerated by the mother; among other changes, the increase in the concentration of high-density lipoprotein (HDL) particles during normal pregnancy may help to confer protection to the mother. However, in complicated pregnancies, such as pre-eclampsia (PE), the control of hyperlipidaemia may be disturbed. PE is a typical hypertensive disorder of human pregnancy, being potentially dangerous for both the mother and the fetus. Although the exact mechanisms leading to this syndrome remain to be clarified, dyslipidaemia and activated leukocytes may contribute to oxidative stress and vascular dysfunction observed in PE. One of the features often observed in PE is the reduced HDL level, and we found a significant inverse correlation between the concentrations of apolipoprotein (apo) A-I, the major protein constituent of HDL, and markers of neutrophil activation (lactoferrin and elastase) as well as with fibrin D-dimer. We believe that pre-eclamptic women presenting low levels of HDL may lose protection involving the inflammatory and haemostatic systems.

Key words
HDL, inflammation, coagulation, normal pregnancy, pre-eclampsia


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

Especialidades
Principal: Obstetricia y Ginecología
Relacionadas: Bioquímica, Endocrinología y Metabolismo, Medicina Interna, Medicina Reproductiva



Comprar este artículo
Extensión: 5.87 páginas impresas en papel A4

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



Enviar correspondencia a:
Belo, Luis
Patrocinio y reconocimiento:
Agradecimentos: Os autores desejam agradecer a Laura Pereira, Maria Ondina, Dorothy Bedford e Grace Stewart pelo apoio técnico e à Universidade do Porto bem como à Fundação para a Ciência e a Tecnologia (FCT-Portugal) pelo apoio financeiro (PRAXIS XXI/BD/16061/98).
Bibliografía del artículo
  1. Piechota W, Staszewski A. Reference ranges of lipids and apolipoproteins in pregnancy. Eur J Obstet Gynecol Reprod Biol 1992;45:27-35.
  2. Desoye G, Schweditsch MO, Pfeiffer KP, et al. Correlation of hormones with lipid and lipoprotein levels during normal pregnancy and postpartum. J Clin Endocrinol Metab 1987;64:704-712.
  3. Alvarez JJ, Montelongo A, Iglesias A, et al. Longitudinal study on lipoprotein profile, high density lipoprotein subclass, and postheparin lipases during gestation in women. J Lipid Res 1996;37:299-308.
  4. Potter JM, Nestel PJ. The hyperlipidemia of pregnancy in normal and complicated pregnancies. Am J Obstet Gynecol 1979;133:165-170.
  5. Ordovas JM, Pocovi M, Grande F. Plasma lipids and cholesterol esterification rate during pregnancy. Obstet Gynecol 1984;63:20-25.
  6. Tikkanen MJ. Sex hormones. In: Betteridge DJ, Illingworth DR, Shepherd J, eds. Lipoproteins in health and disease. London: Arnold, 1999: 967-984.
  7. Sattar N, Greer IA, Louden J, et al. Lipoprotein subfraction changes in normal pregnancy: threshold effect of plasma triglyceride on appearance of small, dense low density lipoprotein. J Clin Endocrinol Metab 1997;82:2483-2491.
  8. Iglesias A, Montelongo A, Herrera E, et al. Changes in cholesteryl ester transfer protein activity during normal gestation and postpartum. Clin Biochem 1994;27:63-68.
  9. Winkler K, Wetzka B, Hoffmann MM, et al. Low density lipoprotein (LDL) subfractions during pregnancy: accumulation of buoyant LDL with advancing gestation. J Clin Endocrinol Metab 2000;85:4543-4550.
  10. Hubel CA, Shakir Y, Gallaher MJ, et al. Low-density lipoprotein particle size decreases during normal pregnancy in association with triglyceride increases. J Soc Gynecol Investig 1998;5:244-250.
  11. Belo L, Caslake M, Gaffney D, et al. Changes in LDL size and HDL concentration in normal and preeclamptic pregnancies. Atherosclerosis 2002;162:425-432.
  12. Pocovi M, Ordovas JM, Grande-Covian F. Plasma lipids and apolipoproteins A and B in human pregnancy. Rev Esp Fisiol 1984;40:183-190.
  13. Silliman K, Shore V, Forte TM. Hypertriglyceridemia during late pregnancy is associated with the formation of small dense low-density lipoproteins and the presence of large buoyant high-density lipoproteins. Metabolism 1994;43:1035-1041.
  14. NHBPEP Working Group. National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 1990;163:1691-1712.
  15. Sibai BM. Hypertension. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: normal and problem pregnancies. 4th ed. Philadelphia: Churchill Livingstone, 2002: 945-1004.
  16. Roberts JM, Pearson G, Cutler J, et al. Summary of the NHLBI Working Group on Research on Hypertension During Pregnancy. Hypertension 2003;41:437-445.
  17. Zeek PM, Assali NS. Vascular changes in the decidua associated with eclamptogenic toxemia of pregnancy. Am J Clin Pathol 1950;20:1099-1109.
  18. Roberts JM, Hubel CA. Is oxidative stress the link in the two-stage model of pre-eclampsia Lancet 1999;354:788-789.
  19. Roberts JM. Endothelial dysfunction in preeclampsia. Semin Reprod Endocrinol 1998;16:5-15.
  20. Myatt L, Miodovnik M. Prediction of preeclampsia. Semin Perinatol 1999;23:45-57.
  21. Hubel CA, McLaughlin MK, Evans RW, et al. Fasting serum triglycerides, free fatty acids, and malondialdehyde are increased in preeclampsia, are positively correlated, and decrease within 48 hours post partum. Am J Obstet Gynecol 1996;174:975-982.
  22. Hubel CA, Lyall F, Weissfeld L, et al. Small low-density lipoproteins and vascular cell adhesion molecule-1 are increased in association with hyperlipidemia in Preeclampsia. Metabolism 1998;47:1281-1288.
  23. Murai JT, Muzykanskiy E, Taylor RN. Maternal and fetal modulators of lipid metabolism correlate with the development of preeclampsia. Metabolism 1997;46:963-967.
  24. Rosing U, Samsioe G, Ölund A, et al. Serum levels of apolipoprotein A-I, A-II and HDL-cholesterol in second half of normal pregnancy and in pregnancy complicated by pre-eclampsia. Horm Metab Res 1989;21:376-382.
  25. Sattar N, Bendomir A, Berry C, et al. Lipoprotein subfraction concentrations in preeclampsia: pathogenic parallels to atherosclerosis. Obstet Gynecol 1997;89:403-408.
  26. Wakatsuki A, Ikenoue N, Okatani Y, et al. Lipoprotein particles in preeclampsia: susceptibility to oxidative modification. Obstet Gynecol 2000;96:55-59.
  27. Wetzka B, Winkler K, Kinner M, et al. Altered lipid metabolism in preeclampsia and HELLP syndrome: links to enhanced platelet reactivity and fetal growth. Semin Thromb Hemost 1999;25:455-462.
  28. Ware-Jauregui S, Sanchez SE, Zhang C, et al. Plasma lipid concentrations in pre-eclamptic and normotensive Peruvian women. Int J Gynaecol Obstet 1999;67:147-155.
  29. Winkler K, Wetzka B, Hoffmann MM, et al. Triglyceride-rich lipoproteins are associated with hypertension in preeclampsia. J Clin Endocrinol Metab 2003;88:1162-1166.
  30. Sattar N, Gaw A, Packard CJ, et al. Potential pathogenic roles of aberrant lipoprotein and fatty acid metabolism in pre-eclampsia. Br J Obstet Gynaecol 1996;103:614-620.
  31. Schjetlein R, Abdelnoor M, Haugen G, et al. Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia. Acta Obstet Gynecol Scand 1999;78:191-197.
  32. Barden A, Ritchie J, Walters B, et al. Study of plasma factors associated with neutrophil activation and lipid peroxidation in preeclampsia. Hypertension 2001;38:803-808.
  33. Belo L, Santos-Silva A, Caslake M, et al. Neutrophil activation and C-reactive protein concentration in preeclampsia. Hypertens Pregnancy 2003;22:129-141.
  34. Belo L, Santos-Silva A, Rumley A, et al. Elevated tissue plasminogen activator as a potential marker of endothelial dysfunction in pre-eclampsia: correlation with proteinuria. Br J Obstet Gynaecol 2002;109:1250-1255.
  35. Nofer JR, Kehrel B, Fobker M, et al. HDL and arteriosclerosis: beyond reverse cholesterol transport. Atherosclerosis 2002;161:1-16.
  36. Harlan JM. Leukocyte-endothelial interactions. Blood 1985;65:513-525.
  37. Rodgers GM. Hemostatic properties of normal and perturbed vascular cells. FASEB J 1988;2:116-123.
  38. van-Hinsbergh VWM. The endothelium: vascular control of haemostasis. Eur J Obstet Gynecol Reprod Biol 2001;95:198-201.

 
 
 
 
 
 
 
 
 
 
 
 
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