ASSOCIATION BETWEEN DEFICIENCY OF FREE PROTEIN-S AND ANTICARDIOLIPIN ANTIBODIES IN PATIENTS LESS-THAN-OR-EQUAL-TO-65 YEARS OF AGE WITH ACUTE ISCHEMIC STROKE AND TIA
M. Vrethem et al., ASSOCIATION BETWEEN DEFICIENCY OF FREE PROTEIN-S AND ANTICARDIOLIPIN ANTIBODIES IN PATIENTS LESS-THAN-OR-EQUAL-TO-65 YEARS OF AGE WITH ACUTE ISCHEMIC STROKE AND TIA, European journal of neurology, 5(5), 1998, pp. 491-497
A possible association between anticardiolipin antibodies (ACA), which
are a marker for increased risk of cerebral ischemia, and deficiency
of free Protein S, a naturally occurring anticoagulant, has been suspe
cted in some studies of ischemic stroke, particularly in young adults.
In order to investigate this further, we prospectively studied all st
roke patients less than or equal to 65 years of age admitted to our st
roke unit during 1991-1992. A total of 66 patients with acute ischemic
stroke or transient ischemic attacks (TIA) (embolic/thrombotic infarc
tion n = 30, embolic infarction n = 13, thrombotic infarction n = 10,
and TIA n = 13) were analysed for ACA, protein C and S, free protein S
and antithrombin III (AT III). Traditional risk factors were scrutini
zed in each patient. Eight patients had some previously undetected der
angement of the coagulation process; five had elevated ACA levels, fou
r had low, free Protein S levels, and three had low AT III levels. Non
e of the patients showed any decrease in total protein C or S levels.
A striking association between the presence of ACA and free protein S
deficiency was noted. All patients with free protein S deficiency had
concomitant elevated ACA levels. Sixteen patients had had a previous e
pisode of ischemic stroke/TIA or mycocardial infarction, two of them h
ad lowered AT III levels. Thirty-four patients had one or more elevate
d infectious parameters but with no clear correlation to derangement o
f the coagulation factors. We conclude that a probable association bet
ween ACA and free protein S deficiency exist in ischemic stroke patien
ts, and that it may have a pathogenetic importance. (C) 1998 Lippincot
t Williams & Wilkins.