The Schilling test is performed by administering 58Co-labeled cobalamin orally and collecting urine for 24 h, and it is dependent on normal renal and bladder function. Urinary excretion of cobalamin will reflect cobalamin absorption provided that intrahepatic binding sites for cobalamin are fully occupied. To ensure saturation of hepatic cobalamin binding sites so that all absorbed radiolabeled cobalamin will be excreted in urine, 1 mg of cobalamin is administered intramuscularly 1 h after ingestion of the radiolabeled cobalamin. The Schilling test may be abnormal (usually defined as <10% excretion in 24 h) in pernicious anemia, chronic pancreatitis, blind loop syndrome, and ileal disease (Table e37-1). Therefore, whenever an abnormal Schilling test is found, 58Co-labeled cobalamin should be administered on another occasion bound to intrinsic factor, with pancreatic enzymes, or after a 5-day course of antibiotics (often tetracycline). A variation of the Schilling test can detect failure to split cobalamin from food proteins. The labeled cobalamin is cooked together with a scrambled egg and administered orally. People with achlorydria will excrete <10% of the labeled cobalamin in the urine. In addition to establishing the etiology for cobalamin deficiency, the Schilling test can be used to help delineate the pathologic process responsible for steatorrhea by assessing ileal, pancreatic, and small-intestinal luminal function. Unfortunately, the Schilling test is performed infrequently because of the unavailability of human intrinsic factor.