Critical illness myopathy: what is happening?

Friedrich, Oliver (2006) Critical illness myopathy: what is happening?. Current Opinion in Clinical Nutrition and Metabolic Care, 9 4: 403-409. doi:10.1097/01.mco.0000232900.59168.a0


Author Friedrich, Oliver
Title Critical illness myopathy: what is happening?
Journal name Current Opinion in Clinical Nutrition and Metabolic Care   Check publisher's open access policy
ISSN 1363-1950
1473-6519
Publication date 2006-07
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1097/01.mco.0000232900.59168.a0
Volume 9
Issue 4
Start page 403
End page 409
Total pages 7
Editor John M. Kinney
Luc A. Cynober
Yvonne Carpentier
Place of publication Philadelphia, PA, U.S.A.
Publisher Lippincott-Raven Publishers
Language eng
Subject 1111 Nutrition and Dietetics
Formatted abstract
Purpose of review: The current review focuses on recent studies, both clinical and from basic sciences, which approach possible pathomechanisms of critical illness myopathy in order to better derive potential clinical strategies for a preventive or curative clinical setting. Trends and concepts of clinical diagnosis and handling will be evaluated and their implications for muscle physiology and nutritional/metabolic intervention discussed.
Recent findings: Conventional electrophysiology was combined with direct muscle stimulation to better differentiate critical illness myopathy from other neuromuscular disorders in critical illness. Muscle weakness was the result of impaired excitation–contraction-coupling at the level of the sarcolemma and the sarcoplasmic reticulum membrane. Critical illness may alter sodium and ryanodine receptor calcium-release channels. Also, increased muscle proteolysis contributes to weakness in critical illness myopathy. Myosin loss is due to the risk factors systemic inflammatory response syndrome/sepsis, steroids and neuromuscular blocking agents. Steroids can also induce necrosis and apoptosis in muscle. Inflammatory mediators aggravated muscle metabolic failure in critical illness myopathy. Ubiquitin–proteasome pathways, cyclooxygenase activation, altered glucose transporter expression, MyoD suppression, impaired respiratory chain enzymes, ATP depletion, glucose toxicity and insulin resistance can all contribute to the critical illness myopathy pathomechanism.
Summary: The search for pathomechanisms is an important task for both clinical and basic sciences. Targets for treatment or prevention of critical illness myopathy include systemic inflammatory response, increased proteolysis and reduced antioxidative capacitance in critically ill patients.
©2006 Lippincott Williams & Wilkins.

Keyword Pathomechanisms
Critical illness
ec-coupling
Myopathy
SIRS
Steroids
Ubiquitin
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Excellence in Research Australia (ERA) - Collection
School of Biomedical Sciences Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 28 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 33 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Wed, 07 Apr 2010, 09:34:48 EST by June Temby on behalf of Faculty of Science