Heat-induced inhibition of erythrocyte sedimentation (HIES) was examined in 158 cases. HIES is significantly lower in patients with a liver cell damage isolated or due to metastases of a neoplastic process in comparison to that in patients suffering from inflammation or malign tumor not involving the liver. Generally, HIES depends upon the concentration of lysophosphatidyl choline (lysolecithin) which is set free in plasma by lecithin-cholesterol-acyltransferase (LCAT) during incubation. In patients with lever cell damage, LCAT is diminished. HIES is being influenced by several factors: Lysophosphatidyl choline is bound to albumin, and this prevents its reaction on the erythrocyte surface. Lysophospholipase reduces the concentration of lysophosphatidyl choline in the plasma by splitting off its fatty acid in the alpha-position. Specific serum proteins, the so-called agglomerines, which are responsible for the acceleration of erythrocyte sedimentation, are counteracting the HIES. The concentration of albumin and agglomerines in plasma and the activity of lysophospholipase are subject to physiologically and pathologically caused deviations. Thereby, HIES is being influenced individually at varying degrees. This makes it difficult to estimate the LCAT activity which represents the principal cause of HIES. As a consequence, HIES seems not to be suitable for clinical diagnostics.

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