PATIENTS WITH CHRONIC GLUCOCORTICOID TREATMENT DEVELOP CHANGES IN MUSCLE GLYCOGEN-METABOLISM

High dose glucocorticoid may induce a significant myopathy with loss o f thick myofilament from muscle, particularly if administered in conju nction with depolarizing drugs. Remarkably, the effect of chronic low dose glucocorticoid in muscle is vastly different, although it may ind uce changes in muscle glycogen metabolism as evidenced in animal exper imental trials. However, there is no clear confirmation that these cha nges could develop similarly in patients. We evaluate clinical, functi onal, histological and metabolic muscle changes during chronic low-dos e glucocorticoid treatment in 11 asthmatic patients. Remarkably, these patients did not develop clinical symptoms of myopathy nor significan t muscle weakness or morphological changes in muscle histology. Howeve r, glycogen concentration and the activity of the main regulatory enzy mes of glycogen metabolism, aldolase and creatine kinase were modified in comparison with controls. An increase in the synthesis and muscle cell deposition of glycogen and a decrease in the muscle glycogen degr adation process have been suggested. These changes were not related wi th malnutrition. There was not correlation between histological and bi ochemical changes. We conclude that chronic treatment with glucocortic oid causes clear changes in glycogen metabolism in the skeletal muscle , resulting in glycogen muscle storage. The significance of these bioc hemical changes is unknown, but it can be well an associated phenomeno n with glucocorticoid treatment.