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Michael D Levitt,1 Sophie M Hapak,2 David G Levitt3 1Medicine Service, Veterans Affairs Medical Center, Minneapolis, MN, 55417, USA; 2Department of Medicine, University of Minnesota, Minneapolis, MN, 55455, USA; 3Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, 55455, USACorrespondence: David G Levitt, Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN, 55455, USA, Email levit001@umn.eduAbstract: While serum alkaline phosphatase activity has become a routine clinical measurement, we have found that physiciansâ knowledge of the pathophysiology of this enzyme is almost solely limited to the concept that an elevated serum alkaline phosphatase suggests disease of liver or bone. For example, physicians at all levels of training had no understanding of such basic physiological information as the function of alkaline phosphatase in the liver or how this enzyme is eliminated from the serum. Based on a patient with an enormously elevated alkaline phosphatase, this report provides a review of existing clinically relevant information concerning the pathophysiology of alkaline phosphatase with emphasis on the mechanisms involved in the homeostasis of this enzyme. A novel aspect of this paper is the discussion of the previously neglected concept that defective enzyme elimination could play a major role in the pathogenesis of serum alkaline phosphatase elevations.Keywords: alkaline phosphatase catabolism, alkaline phosphatase isoforms, galactose receptor, galactomannan |
