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- W586264191 abstract "A study was made on clinical and biochemical features of sibling patients, a 13 year-old girl and a 15 year-old boy, with hyperchylomicronemia. They both were usually in good health and asymptomatic. Neither hepatosplenomegaly nor xanthomas were observed. Serum triglyceride concentrations were very high, 1094mg/dl and 1090mg/dl, but cholesterol levels were within normal range on a mild fat-restricted diet. The lipoprotein pattern on polyacrylamide gel disc electrophoresis revealed a high chylomicron peak in each patient but normal patterns were observed in other relatives.In our patients, analysis of apoprotein of triglyceride-rich lipoproteins demonstrated the lack of apo C-II which is an important activator for LPL. Although a marked reduction in LPL activity was observed by standard assay procedure of PHLA, the activity was completely recovered by addition of normal serum or purified apo C-II to the assay mixture. These results indicate that the patients are not really deficient in LPL but the cause of chylomicronemia is a deficiency in its activator.Their parents who had normal lipoprotein cencentrations were first cousins. The activating power of their sera upon guinea pig postheparin lipolytic activity were reduced approximately a half of the control values, suggesting that there was a reduction of apo C-II level in both parents. However the father had almost normal LPL activity in postheparin plasma, and the activity was not influenced by the addition of the normal serum.Our observations in thie study strongly suggest that familial apo C-II deficiency is transmitted as an autosomal recessive mode of inheritance and heterozytotes have no abnormalities of plasma lipid and lipoprotein concentrations in spite of the reduced plasma apo C-II levels." @default.
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- W586264191 date "1979-01-01" @default.
- W586264191 modified "2023-10-04" @default.
- W586264191 title "Familial Apolipoprotein C-II Deficiency" @default.
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- W586264191 doi "https://doi.org/10.5551/jat1973.7.3_529" @default.
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