Patients with chronic glucocorticoid treatment develop changes in muscle glycogen metabolism.
High dose glucocorticoid may induce a significant myopathy with loss of thick myofilament from muscle, particularly if administered in conjunction with depolarizing drugs. Remarkably, the effect of chronic low dose glucocorticoid in muscle is vastly different, although it may induce changes in muscle glycogen metabolism as evidenced in animal experimental trials. However, there is no clear confirmation that these changes could develop similarly in patients. We evaluate clinical, functional, histological and metabolic muscle changes during chronic low-dose glucocorticoid treatment in 11 asthmatic patients. Remarkably, these patients did not develop clinical symptoms of myopathy nor significant muscle weakness or morphological changes in muscle histology. However, glycogen concentration and the activity of the main regulatory enzymes 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 degradation process have been suggested. These changes were not related with malnutrition. There was not correlation between histological and biochemical changes. We conclude that chronic treatment with glucocorticoid causes clear changes in glycogen metabolism in the skeletal muscle, resulting in glycogen muscle storage. The significance of these biochemical changes is unknown, but it can be well an associated phenomenon with glucocorticoid treatment.
Fernandez-Sola
J
J
Department of Medicine, Hospital Clinic, University of Barcelona, Spain.
Cusso
R
R
Picado
C
C
Vernet
M
M
Grau
J M
JM
Urbano-Marquez
A
A
D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000032:analysis; D001219:Aspartate Aminotransferases / Q000032:analysis; D001249:Asthma / Q000188:drug therapy; D003402:Creatine Kinase / Q000032:analysis; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D005634:Fructose-Bisphosphate Aldolase / Q000032:analysis; D006003:Glycogen / Q000378:metabolism*; D006006:Glycogen Synthase / Q000032:analysis; D006801:Humans; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000032:analysis; D009132:Muscles / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D006005:Phosphorylases / Q000032:analysis; D011241:Prednisone / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology*
D007527:Isoenzymes; D009124:Muscle Proteins; D006003:Glycogen; D007770:L-Lactate Dehydrogenase; D006005:Phosphorylases; D006006:Glycogen Synthase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase; D005634:Fructose-Bisphosphate Aldolase; D011241:Prednisone