Alteration of cobalt absorption in portal cirrhosis and idiopathic hemochromatosis.

Abstract

Abstract Inorganic cobalt or iron tagged with Co 57 and Fe 59 , respectively, were given by mouth to selected patients, and the absorption and body retention of the dose were measured by the recovery of radioactivity in the urine and feces. In 5 patients with fatty infiltration of the liver and 7 with portal cirrhosis associated with normal iron stores, the average absorption of cobalt was similar to the absorption in 11 control subjects with normal iron stores. In contrast, cobalt absorption was increased in 6 patients with portal cirrhosis complicated by iron deficiency and in 6 control subjects with iron deficiency. It was also increased in 4 patients with portal cirrhosis associated with endogenous iron overload and in 4 with idiopathic hemochromatosis. A direct correlation was present between the absorption of iron and cobalt in both the control subjects and patients with liver disease. Unlike iron, cobalt was excreted in the urine, and the body retention of the test dose of cobalt was not increased in patients with enhanced absorption. The results indicate that cobalt absorption is increased in idiopathic hemochromatosis and portal cirrhosis complicated by either iron deficiency or endogenous iron overload. The increase in cobalt absorption in patients with liver disease appears to be secondary to a disturbance in iron metabolism.