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Rivista di Angiologia

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899

Periodicità: Bimestrale

ISSN 0392-9590

Online ISSN 1827-1839


International Angiology 2002 Giugno;21(2):158-64


Decreasing plasma endothelin-1 and unchanged plasma neopterin during folate supplementation in hyperhomocysteinemia

Gottsäter A., Forsblad J., Mattiasson I., Lindgärde F.

Depart­ment of Vas­cu­lar Dis­ease, Uni­ver­sity of Lund, Uni­ver­sity Hos­pi­tal MAS, Malmö, Swe­den

Back­ground. Hyper­hom­o­cys­tei­ne­mia is a risk fac­tor for ath­ero­scler­o­sis and ­venous throm­bo­sis, prob­ably exert­ing its ­effects ­through endo­the­lial func­tion. Homo­cys­teine lev­els are low­ered by ­folate sup­ple­men­ta­tion, and such treat­ment ­improves endo­the­lial func­tion. How­ev­er, wheth­er ­folate sup­ple­men­ta­tion decreas­es vas­cu­lar risk and ­improves sur­vi­val is ­unknown. The aim of this study was to eval­u­ate endo­the­lial func­tion and mono­nu­cle­ar leu­ko­cyte inflam­ma­to­ry activ­ity dur­ing homo­cys­teine low­er­ing in ­patients with hyper­hom­o­cys­tei­ne­mia and vas­cu­lar dis­ease.
Meth­ods. Endo­the­lial func­tion ­assessed as plas­ma (p-)endo­the­lin(ET)-1 and intra­plate­let cGMP and cAMP, and mono­nu­cle­ar leu­ko­cyte inflam­ma­to­ry activ­ity, ­assessed as p-neop­te­rin were stud­ied dur­ing homo­cys­teine low­er­ing in 50 ­patients with hyper­hom­o­cys­tei­ne­mia and vas­cu­lar dis­ease, ran­dom­ized to ­folate sup­ple­men­ta­tion or no treat­ment for 3 ­months.
­Results. P-homo­cys­teine ­decreased dur­ing the 3 ­months not only in ­patients on ­folate sup­ple­men­ta­tion (from 27 [21-52] to 14 [8-41] µmol/l; p<0.001), but also in the untreat­ed group (from 23 [20-35] to 19 [4-31] µmol/l; p<0.001). P-ET-1 ­decreased dur­ing ­folate sup­ple­men­ta­tion (from 5.7 [2.7-11.6] to 4.1 [1.8-9.0] pg/ml; p<0.01), but was ­unchanged in the untreat­ed group 4.1 [2.0-9.5] pg/ml and 4.5 [2.7-7.1] pg/ml). P-neop­te­rin was ­unchanged in ­patients on ­folate sup­ple­men­ta­tion (9.7 [5.1-54.4] and 7.6 [5.7-73.0] nmol/l), but ­increased in the untreat­ed group (from 8.2 [4.7-19.5] to 8.6 [4.6-24.6] nmol/l; p<0.05). Intra­plate­let cGMP ­decrea-sed in ­patients on ­folate sup­ple­men­ta­tion (from 0.86 [0.21-2.00] plate­lets to 0.56 [0.17-1.42] pmol/109 plate­lets; p<0.05), but was ­unchanged in the untreat­ed group. No sig­nif­i­cant dif­fer­enc­es con­cern­ing intra­plate­let cAMP ­occurred in ­either group.
Con­clu­sions. ­Folate sup­ple­men­ta­tion in hyper­hom­o­cys­tei­ne­mia is asso­ciat­ed with decreas­ing lev­els of both ET-1 and intra­plate­let cGMP, and the ­absence of an ­increase in the lev­els of the inflam­ma­to­ry medi­a­tor neop­te­rin.

lingua: Inglese


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