Evaluate the contribution of the isoforms of ALP from liver, bone, and bowel to total ALP; investigate elevations of ALP to determine the tissue of origin. Liver is the isoenzyme most frequently elevated when total ALP levels are elevated. Liver ALP increases in the blood early in liver disease before most other liver function tests show abnormalities. The wide group of conditions leading to increased liver ALP include acute hepatitis, cirrhosis, fatty liver, drug-induced liver disease, obstruction of biliary flow by carcinoma at the head of the pancreas, bile duct stricture, primary biliary cirrhosis, and metastatic carcinoma of the liver. Bone isoenzyme is elevated as a result of increased osteoblastic activity. This isoenzyme is normally elevated in growing children and adults over the age of 50. The highest total ALP values have been attributed to an increased bone isoenzyme level due to Paget disease or renal rickets. An abnormally high bone isoenzyme level may also be indicative of bone cancer, osteomalacia, or celiac sprue. A decreased bone ALP in children may be attributed to cretinism or to hypophosphatasia. Intestinal alkaline phosphatase is seen normally in the serum of subjects who have B or O blood types, especially after a fatty meal. Pathologically, the band may be present in perforation of the bowel, ulcerative disease of the intestine, and faintly in liver cirrhosis. Acute infarction of the intestine will cause a release of intestinal ALP from the mucosa. Large erosive or ulcerative lesions of the stomach, duodenum or other small intestinal areas, or colon may result in an elevation of the serum ALP level. The small intestinal lesions associated with malabsorption are associated with an elevation of the serum intestinal ALP level only if there is an erosive or ulcerative mucosal lesion.