1995
DOI: 10.1161/01.str.26.5.795
|View full text |Cite
|
Sign up to set email alerts
|

Plasma Homocysteine in the Acute and Convalescent Phases After Stroke

Abstract: The post-acute-phase increase in plasma homocysteine may explain why higher values were obtained for stroke patients than for control subjects in previous studies. Possible reasons for the variation in plasma homocysteine concentrations over time are (1) an acute-phase reduction secondary to a decrease in plasma albumin and (2) an increase in plasma homocysteine during the convalescent phase due to modified vitamin intake and/or lifestyle. The timing of plasma homocysteine measurements relative to stroke onset… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

9
120
2
2

Year Published

1995
1995
2017
2017

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 193 publications
(133 citation statements)
references
References 31 publications
9
120
2
2
Order By: Relevance
“…However, in vivo studies are contradictory (Dudman et al 1993a;Mansoor et al 1995;Young et al 1997). Homocysteine readily undergoes auto-oxidation in plasma (Velury & Howell, 1988;Stamler et al 1993;Andersson et al 1995) forming reactive oxygen species such as H 2 O 2 and superoxide, which may themselves cause oxidation of LDL (Heinecke et al 1987), and other products such as cysteinehomocysteine mixed disulfides, and homocysteine thiolactone. It has been proposed that homocysteine thiolactone reacts with LDL to form LDL-homocysteine thiolactone aggregates, which may then be taken up by macrophages and subsequently incorporated into foam cells in early atherosclerotic plaques (Naruszewicz et al 1994;Jakubowski, 1997;Ferguson et al 1999).…”
Section: Atherosclerotic Mechanismsmentioning
confidence: 99%
“…However, in vivo studies are contradictory (Dudman et al 1993a;Mansoor et al 1995;Young et al 1997). Homocysteine readily undergoes auto-oxidation in plasma (Velury & Howell, 1988;Stamler et al 1993;Andersson et al 1995) forming reactive oxygen species such as H 2 O 2 and superoxide, which may themselves cause oxidation of LDL (Heinecke et al 1987), and other products such as cysteinehomocysteine mixed disulfides, and homocysteine thiolactone. It has been proposed that homocysteine thiolactone reacts with LDL to form LDL-homocysteine thiolactone aggregates, which may then be taken up by macrophages and subsequently incorporated into foam cells in early atherosclerotic plaques (Naruszewicz et al 1994;Jakubowski, 1997;Ferguson et al 1999).…”
Section: Atherosclerotic Mechanismsmentioning
confidence: 99%
“…1,2 However, this finding could reflect an effect rather than the cause, because homocysteine concentrations may increase after the onset of acute stroke. 3 Thus, to reduce this bias, data from prospective studies are desirable. However, the findings from prospective studies have been inconsistent.…”
mentioning
confidence: 99%
“…High levels of homocysteine are correlated with significant increase risk of CAD, MI [80], peripheral occlusive disease (deep vein thrombosis) [81,82], and intermittent claudication [83]. According to Nygard et al [84], a serum homocysteine level of 12% greater than the upper limit of normal is associated with a threefold increased risk of acute MI.…”
Section: Figure 3c Schematic Illustration Of the Links Between Deficmentioning
confidence: 99%