The Journal of Japan Atherosclerosis Society
Online ISSN : 2185-8284
Print ISSN : 0386-2682
ISSN-L : 0386-2682
Serum Lecithin: Cholesterol Acyltransferase Rate in Cerebrovascular Diseases
Kei SATOHShigeru TAKAMATSUKazuho HENMIShigeru SAKUTASeitoku MIZUNOHirofumi METOKIMutsu TAKAMATSU
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1980 Volume 7 Issue 4 Pages 777-783

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Abstract

Serum lecithin: cholesterol acyltransferase (LCAT) rate was determined by the method of Nagasaki & Akanuma in 72 patients with cerebrovascular diseases and 147 controls. Liver function tests were within normal limits in all of these subjects.
The average values of non-obese healthy men and women, who had no abnormalities in physical findings, blood pressure, ECG, urinalysis, etc., were 107±38.0nmol/ml/hr and 82±39.9nmol/ml/hr, respectively. The value of female subjects was significantly higher than that of male. There was no significant change by age.
In male and female patients with cerebral infarction, average serum LCAT rates were 93±32.6nmol/ml/hr and 118±49.9nmol/ml/hr, respectively. The value of female patients was significantly higher than that. of age-matched healthy control. Among male patients with cerebral infarction, the cases with angiographically demonstrated obstruction of internal carotid or middle cerebral arteries showed significantly lower value as compared with those without such findings and healthy subjects. There was no such difference in the values of female patients.
The average values of male and female patients with cerebral hemorrhage were 99±31.8nmol/ml/hr and 129±35.6nmol/ml/hr, respectively. Again the value of female patients was significantly higher than that of control. No significant difference was observed between two types of disease.
In male subjects, LCAT rate correlated positively with α1-lipoprotein level which was lower in patients as compared with normal control. These results may suggest that the mechanisms involved in the activation of LCAT in vivo is defective in patients and such mechanisms posess the more decisive role in the pathogenesis of cerebrovascular diseases than the amount of this enzyme per se. The low LCAT level, in conjunction with defective activation, may possibly bring about the more pronounced atherosclerotic lesions especially in major cerebral arteries.
In female, there was no relation between LCAT rate and α1-lipoprotein level. In view of no significant difference in α1-lipoprotein level between patients and controls, our results may suggest the complexity of lipid metabolism in woman.

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