[Detection and distriburion of slow pre-betalipoprotein in agar gel electrophoresis of total serum in 204 cases of mixed hyperlipidemia].

The demonstration in certain sera by electrophoresis an Agar gel, according to Noble's technique, of a further band of intermediate pre-betalipoprotein, between the betalipoproteins and the usual rapid pre-betalipoproteins, led to the designation of this fraction under the name of slow pre-betalipoprotein or pre-beta-lipoprotein. To the rare studies so far published on this subject, we bring here our contribution in the form of a routine analysis of the variations, and not only the presence, but also the relative concentration of the slow pre-beta-lipoproteins with regard to the rapid prebetalipoproteins. On the fasting serum, after 12 hours fasting, comparative studies of normal control subjects (104 cases) of essential hypercholesterolemia, with or without tendinous xanthomas, corresponding to type IIa (110 cases), mixed hyperlipidemia of type II + IV or III, on paper electrophoresis, corresponds usually to type IIb (204 cases) and, finally, massive endogenous hypertriglyceridemia, corresponding to type IV (95 cases). These indicate clearly the elective concentration of the band of slow pre-betalipoproteins persisting after 12 hours fasting in cases of mixed hyperlipidemia (73% of cases), whilst it is rare in the other groups (no more than 5% of cases). A more complete study of 204 cases of mixed hyperlipidemia showed that the high frequency of slow pre-betalipoproteins is situated in a fairly narrow range of relatively moderate hypertriglyceridemia, between the lower limit of 1.50 and the upper limit of 6 to 7 g/l: the maximum frequency and intensity is situated within the area of 2.50 to 4 g/l. The cases who have already had cardiovascular accidents are more often found to have this band than the cases without complications in a fairly similar age group. However, longitudinal studies, both midterm in relation to therapeutic correction, and short term throughout the day or between the 8th and 12th hour of fasting, have clearly revealed the potential labile nature of this fraction, and show the pathological nature of its sometimes massive persistence beyond the 8th hour and even beyond the 12th hour of fasting. This is a sign of pathological blocking of its transformation rather than of a constitutional lipoprotein abnormality.