Rhabdomyolysis: A review

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Rhabdomyolysis, a syndrome of skeletal muscle breakdown with leakage of muscle contents, is frequently accompanied by myoglobinuria, and if sufficiently severe, acute renal failure with potentially life-threatening metabolic derangements may ensue. A diverse spectrum of inherited and acquired disorders affecting muscle membranes, membrane ion channels, and muscle energy supply causes rhabdomyolysis. Common final pathophysiological mechanisms among these causes of rhabdomyolysis include an uncontrolled rise in free intracellular calcium and activation of calcium-dependent proteases, which lead to destruction of myofibrils and lysosomal digestion of muscle fiber contents. Recent advances in molecular genetics and muscle enzyme histochemistry may enable a specific metabolic diagnosis in many patients with idiopathic recurrent rhabdomyolysis. Copyright 2002 Wiley Periodicals, Inc.

Related collections

Most cited references 131

Record: found
Abstract: not found
Article: not found

The spectrum of rhabdomyolysis.

William Kaehny, Erin S Kelleher, Aaron Gabow (1982)

0 comments Cited 113 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Exercise intolerance due to mutations in the cytochrome b gene of mitochondrial DNA.

S. DiMauro, H. Reichmann, B Lach … (1999)

The mitochondrial myopathies typically affect many organ systems and are associated with mutations in mitochondrial DNA (mtDNA) that are maternally inherited. However, there is also a sporadic form of mitochondrial myopathy in which exercise intolerance is the predominant symptom. We studied the biochemical and molecular characteristics of this sporadic myopathy. We sequenced the mtDNA cytochrome b gene in blood and muscle specimens from five patients with severe exercise intolerance, lactic acidosis in the resting state (in four patients), and biochemical evidence of complex III deficiency. We compared the clinical and molecular features of these patients with those previously described in four other patients with mutations in the cytochrome b gene. We found a total of three different nonsense mutations (G15084A, G15168A, and G15723A), one missense mutation (G14846A), and a 24-bp deletion (from nucleotide 15498 to 15521) in the cytochrome b gene in the five patients. Each of these mutations impairs the enzymatic function of the cytochrome b protein. In these patients and those previously described, the clinical manifestations included progressive exercise intolerance, proximal limb weakness, and in some cases, attacks of myoglobinuria. There was no maternal inheritance and there were no mutations in tissues other than muscle. The absence of these findings suggests that the disorder is due to somatic mutations in myogenic stem cells after germ-layer differentiation. All the point mutations involved the substitution of adenine for guanine, but all were in different locations. The sporadic form of mitochondrial myopathy is associated with somatic mutations in the cytochrome b gene of mtDNA. This myopathy is one cause of the common and often elusive syndrome of exercise intolerance.

0 comments Cited 70 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Infectious etiologies of rhabdomyolysis: three case reports and review.

W. Scheld, U. Singh (1996)

Rhabdomyolysis can be precipitated by trauma, ischemia, metabolic defects, electrolyte abnormalities, drugs, and a wide variety of infectious diseases. At our institution, recent cases of rhabdomyolysis induced by influenza prompted us to review the infectious etiologies of this entity. In addition, a thorough literature search revealed numerous case reports but no general review on this subject. This study describes representative recent cases from our institution and details the wide variety of infections that can cause muscle damage. The pathophysiological mechanisms, muscle histology, and correlation with renal dysfunction are also discussed.