The Phosphatides of Human Plasma. Ii. Abnormalities Encountered in the Nephrotic Syndrome*

Abnormalities of High Density Lipoproteins in Abetalipoproteinemia*

“…A similar but less striking reduction in the lecithin: sphingomyelin ratio is found in fetal cord whole plasma, LDL, and HDL (13,38). Changes equal to those in abetalipoproteinemia have been found in the whole plasma of patients with nephrotic syndrome by Nye and Waterhouse, but they were apparently confined to the low density lipoproteins (34). Since malabsorption is a prominent feature of abetalipoproteinemia, we have evaluated plasma phospholipid distribution in four patients with steatorrhea of another etiology.…”

“…Total HDL is absent in Tangier disease (29), absent or reduced in chronic biliary obstruction (30,31), and decreased in liver disease (32), in some patients with the nephrotic syndrome (30,33,34), and in certain hyperlipemias (30,35). In most of these conditions, however, there are accompanying changes in the very low density (D < 1.019) and low density (D 1.019 to 1.063) lipoproteins, with an apparent inverse relationship be-tween very low density and high density lipoprotein concentrations (36,37).…”

Quantitative Determination of Plasma Phospholipids in Pregnant and Non‐pregnant Women, with Special Reference to Lysolecithin

“…Low values for lysolecithin have been found only in serious liver disease (28) and some cases of myocardial infarction (2 1). The hyperlipemia of nephrosis usually shows high lysolecithin values (26). Other hyperlipemias have not been investigated.…”

Interaction Between Lysolecithin and Platelets and Its Relationship to Disease

“…Plasma LPC levels were elevated in the nephrotic syndrome, which is usually accompanied by HLP. 38 The acute-phase reaction occurring in myocardial infarction leads to a decrease in LCAT acti~ity'~ and in plasma LPC levels.4o Severe liver disease is also characterized by low LCAT activity and decreased LPC concentration in p l a~m a . '~ Therefore, the acutephase reaction and liver disease should be excluded when considering the low levels of plasma LPC reported in cardiovascular patient^.^.^ In considering plasma LPC levels it must be remembered that LPC is produced not only through the LCAT-mediated reaction but also by phospholipase action on plasma le~ithin.~' Also, plasma LPC levels represent the balance between its production and its removal, by cell or tissue uptake or by its metabolism to PC or glycerophosphor ylcholine.…”