[Prostaglandins and collagen metabolism in chronic liver diseases]

Pg E, F2 alpha and F1 alpha, protein-bound plasmic oxyproline (PBPO) as well as 24-h oxyprolinuria (OPU) were measured in 119 patients suffering from various forms of chronic hepatic diseases. Composition of cellular infiltrates in histological specimens was assessed quantitatively for chronic hepatitis patients. Hepatic levels of Pg E, OPU and PBPO were elevated in all the patients, whereas PgF2 alpha and 6-keto-PgF1 alpha values were similar to controls. There were relationships between PBPO and OPU, PgE and 6-keto-PgF1 alpha. Unlike patients with active hepatitis and hepatic cirrhosis, those with chronic persistent hepatitis demonstrated a direct correlation between cellular infiltrate fibroblasts and PgE, PgF2 alpha; between PgF2 alpha and Kupffer's cells content. Inverse relationship occurred between PgE and free hepatic macrophages. In response to prostenon (PGE2) moderate PBPO decline went in line with elevation of cAMP/cGMP. A significant increase of PBPO during introduction of ensaprost-F (PgF2 alpha) did not result in changes in cyclic nucleotides. Prostenon treatment decreased PBPO under no shifts in OPU. A regulatory role of PgE is suggested in collagen metabolism stabilization. Prostenon is proposed for therapeutic use to inhibit sclerotic processes in liver impairment.