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Red blood cell aggregation and primary hyperlipoproteinemia
A Vayá1, M Martínez, R Carmena
1Dept. of Clinical Pathology, Hospital La Fe, Valencia, Spain.
Thrombosis Research
|October 15, 1993
Summary
Erythrocyte aggregation (EA) increases in patients with primary hyperlipoproteinemia (PHLP). Factors like fibrinogen, apolipoproteins, and erythrocyte membrane changes contribute to this heightened EA, impacting cardiovascular health.
Area of Science:
- Hematology
- Cardiovascular Medicine
- Biochemistry
Background:
- Primary hyperlipoproteinemia (PHLP) encompasses conditions like familial hypercholesterolemia (FH), familial combined hyperlipemia (FCHL), and primary hypertriglyceridemia (PHTG).
- Erythrocyte aggregation (EA) is a rheological parameter potentially affected by lipid disorders.
Purpose of the Study:
- To investigate erythrocyte aggregation levels in patients with PHLP compared to a control group.
- To identify correlations between EA and various hematological and biochemical parameters in PHLP patients.
Main Methods:
- Erythrocyte aggregation was measured using a Myrenne aggregometer at stasis (EAMo) and low shear (EAM1).
- Blood samples from 102 PHLP patients (FH, FCHL, PHTG) and healthy controls were analyzed.
- Measurements included fibrinogen, lipids, apolipoproteins, glucose, HbA1c, and erythrocyte membrane lipids (cholesterol, phospholipids).
Main Results:
- All PHLP patient groups exhibited increased EAMo and EAM1 compared to controls.
- Elevated fibrinogen was observed in FH and FCHL patients.
- Increased erythrocyte membrane cholesterol was noted primarily in FH and FCHL.
- EA correlated with fibrinogen, apolipoproteins, and in FH, with membrane cholesterol/phospholipid ratio.
- A significant correlation between EA and HbA1c was found in FCHL patients.
Conclusions:
- Erythrocyte aggregation is elevated in patients with primary hyperlipoproteinemia.
- Fibrinogen, apolipoproteins, and erythrocyte membrane alterations likely contribute to increased EA in PHLP.
- These findings suggest potential mechanisms influencing blood flow and cardiovascular risk in lipid disorders.