Does the effective diminution of nonenzymatic glycation by D-lysine really highlight its potential use in vivo?

vere shock, encephalopathy, pyrexia, watery or bloody diarrhea, and disseminated intravascular coagulation, with a failure to identify a causative infective organism. The marked increase in CK (maximum activity, 4201 U/L; reference interval 24-195 U/L) was largely of skeletal muscle origin (CK-MB <1%). We decreased the potential of adenylate kinase to falsely enhance the measured CK activity by using an assay procedure incorporating, per liter, 5 mmol of adenosine monophosphate and 10 tmol of diadenosine 5’-pentaphosphate, components shown (5) to inhibit 75% of CK activity in serum that originates from liver and over 97% of the activity of the muscle and erythrocyte isoenzymes. Thus it is difficult to attribute the massive increase in CK activity to interference from this source. This, coupled with the rapid return of CK, AST, and LDH activities to normal values (see Figure 1) without residual liver damage either by clinical or biochemical means, suggests that the increased AST described in this condition is largely derived from damage to skeletal muscle rather than liver. We therefore consider it important to measure CK in cases of sudden onset coagulopathy without an obvious cause and not merely to assume that increased transaminase activity results exclusively from liver damage. Measurement of CK may also prove valuable in differentiating HSES from similar conditions such as Reye’s syndrome, in which increases in AST and ALT are not accompanied by an increased CK activity.