Syndrome of acquired factor X deficiency and systemic amyloidosis; in vivo studies of the metabolic fate of factor X.
To determine the metabolic fate of factor X in primary amyloidosis associated with factor X deficiency, we examined the pathways of its catabolism in a man with this syndrome. Intravenous infusion of human or bovine 131I-labeled factor X established a triphasic plasma clearance pattern for factor X. About 85 per cent of the factor X disappeared, with a disappearance half-time of less than 30 seconds. A second and third phase showed a T1/2 of 90 minutes and nine hours respectively. 131I-labeles factor X in plasma did not appear to be rapidly modified or degraded. Relatively minor quantities of 131I were cleared into the urine. We observed a diffuse distribution of radioactivity over the body surface, with a concentration in the hepatic and splenic regions. These studies demonstrate than factor X deficiency associated with systemic amyloidosis is due to binding of factor X to body tissue, probably within the circulatory system.
D000686:Amyloidosis / Q000097:blood / Q000150:complications* / Q000378:metabolism; D000818:Animals; D001780:Blood Coagulation Tests; D001808:Blood Vessels / Q000378:metabolism; D002417:Cattle; D005170:Factor X / Q000008:administration & dosage / Q000378:metabolism* / Q000627:therapeutic use / Q000652:urine; D005171:Factor X Deficiency / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D006801:Humans; D007020:Hypoprothrombinemias / Q000150:complications*; D007457:Iodine Radioisotopes; D008297:Male; D008875:Middle Aged; D011817:Rabbits; D013577:Syndrome; D013997:Time Factors
D007457:Iodine Radioisotopes; D005170:Factor X