Cynthia St. Hilaire, Ph.D., Shira G. Ziegler, B.A., Thomas C. Markello, M.D., Ph.D., Alfredo Brusco, Ph.D., Catherine Groden, M.S., Fred Gill, M.D., Hannah Carlson-Donohoe, B.A., Robert J. Lederman, M.D., Marcus Y. Chen, M.D., Dan Yang, M.D., Ph.D., Michael P. Siegenthaler, M.D., Carlo Arduino, M.D., Cecilia Mancini, M.Sc., Bernard Freudenthal, M.D., Horia C. Stanescu, M.D., Anselm A. Zdebik, M.D., Ph.D., R. Krishna Chaganti, M.D., Robert L. Nussbaum, M.D., Robert Kleta, M.D., Ph.D., William A. Gahl, M.D., Ph.D., and Manfred Boehm, M.D.: NT5E Mutations and Arterial Calcifications.However, we cannot rule out a detrimental aftereffect of rosuvastatin. Aspartate aminotransferase amounts were higher in the rosuvastatin group, and adverse occasions of elevated aspartate aminotransferase amounts were more often reported in this group. Some patients with elevated aspartate aminotransferase levels got concomitant elevations in creatine kinase and alanine aminotransferase levels, findings that suggest that the source of aspartate aminotransferase was skeletal muscle or liver, respectively. There were no significant between-group variations in the number of patients with degrees of alanine aminotransferase or creatine kinase above protocol-specified thresholds. Moreover, although levels of creatine kinase and alanine aminotransferase through the study period were considerably higher in the rosuvastatin group than in the placebo group, the differences between the groups were small and the clinical significance of these biochemical alterations is usually unclear.