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lysolecithin/proteinúria
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Corneal opacification and lecithin-cholesterol acyltransferase (LCAT) deficiency: a case report.
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Bilateral corneal opacities are the first clinical sign of a familial lecithin-cholesterol acyltransferase (LCAT) deficiency and can be found in early childhood. Familial LCAT deficiency includes the following typical clinical findings: corneal opacification, proteinuria, anemia, turbid or milky
Familial plasma lecithin: cholesterol acyltransferase deficiency.
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A WOMAN WITH FAMILIAL PLASMA LECITHIN: cholesterol acyltransferase (L.C.A.T.) deficiency showed, like the other reported cases, obvious corneal opacity, proteinuria, and moderate anaemia with a slight haemolytic component. In the plasma the concentrations of free cholesterol, triglycerides, and
Plasma lipids and acyltransferase activities in experimental nephrotic syndrome.
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Lecithin:cholesterol acyltransferase (LCAT) and lysolecithin acyltransferase (LAT) are two activities carried out by the same plasma enzyme, but require different apoprotein activators. The LCAT reaction takes place primarily on high density lipoproteins (HDL) and is activated by serum albumin,
Classical LCAT deficiency resulting from a novel homozygous dinucleotide deletion in exon 4 of the human lecithin: cholesterol acyltransferase gene causing a frameshift and stop codon at residue 144.
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Lecithin: cholesterolacyltransferase (LCAT) transacylates the fatty acid at the sn-2 position of lecithin to the 3beta-OH group of cholesterol forming lysolecithin and the majority of cholesteryl ester found in plasma. LCAT participates in the reverse cholesterol transport pathway in man where it
Familial LCAT deficiency and fish-eye disease.
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Familial LCAT deficiency is due to deficiency of plasma lecithin-cholesterol acyltransferase. The plasma is rich in free cholesterol and lecithin while cholesterol ester and lysolecithin levels are reduced. Analysis of the abnormal lipoproteins has helped our understanding of plasma lipid and
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