[A study on the fatty acid composition of the plasma lipoprotein in patients with fractures]

Although the etiology of post-traumatic fat embolization still remains obscure, various concepts as to the pathophysiology of the syndrome have emerged in recent years. Extensive studies have indicated that trauma and surgical stress cause remarkable alterations in lipid metabolism. In the following study designed to characterize this situation more fully, the author has analyzed the changes of fatty acid composition of triacylglycerol, phospholipid and cholesterol ester in the circulating plasma lipoprotein of the patient with fractures.

Ten patients who sustained one or more fractures without chest injury between age 9 and 79 years and seven healthy human subjects as control were selected for study. Blood samples were withdrawn into EDTA-treated syringes from patients after overnight fast at intervals of 2, 3, 4, 5 and 14 days after injury. Lipoprotein fractions (very low density lipoprotein: VLDL, low density lipoprotein: LDL, high density lipoprotein: HDL, and very high density lipoprotein: VHDL) were prepared by the method of ultracentrifugation. Lipids were extracted from the lipoprotein fractions according to the procedure of Folch. Lipids separation and purification were carried out by one-dimension thin-layer chromatography. The purified lipids were methylated with BF3-methanol complex and the fatty acid composition of each lipid fraction was analyzed by gas-liquid chromatography.

In the blood samples of normal subjects and patients, myristic, palmitic, palmitoleic, stearic, oleic and linoleic acids (C14: 0, C16: 0, C16: 1, C18: 0, C18: 1 and C18: 2) were the principal fatty acids and these fatty acids were all altered after injury except C14: 0 and C18: 2. The distribution of fatty acids in VLDL-TL was especially altered from the 3rd to 5th hospital day. Stearic acid derived from VLDL-PL was decreased and C18: 1 derived from VLDL-TG was increased. Of the ten patients there were greater changes in those with the femoral fracture. In LDL-TL, the distribution of fatty acids was also altered, and C18:1 derived from LDL-TG was increased. In fatty acid composition of HDL-TL, C16: 0 derived from HDL-PL and C18: 1 derived from HDL-TG were increased and C18: 0 derived from HDL-PL was decreased. In fatty acid composition of VHDL-TL, C16: 1 derived from VHDL-TG was increased.