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Moleculaire mechanismen van spierzwakte tijdens kritieke ziekte en effect van nutritie

Tijdschriftbijdrage - Tijdschriftartikel

Muscle weakness is a severe complication of critical illness prolonging the patient's dependency on intensive care, hampering rehabilitation and associated with an increased risk of death. Muscle weakness can arise from a neurogenic and/or myogenic disturbance. This review focuses on the alterations at muscle level during critical illness. Especially the problem of loss of muscle mass has been highlighted in the literature, whereas no or much less attention has been paid to the actual quality of the remaining muscle. Muscle atrophy during critical illness reflects an imbalance between a decreased synthesis and an increased breakdown of myofibrillary proteins. Several proteolytic systems are strongly activated, including the ubiquitin-proteasome system, the calpains, and the lysosomal proteases. Also excessive autophagy has initially been implicated in the aggravation of muscle loss. However, a phenotype of deficient autophagy has recently been documented, which could compromise muscle quality during critical illness. Whereas it has long been presumed that inadequate feeding of the patients plays a crucial role in muscle cachexia of critically ill patients, several nutritional interventions were unable to prevent considerable muscle loss. Hence, this condition has been labeled the "feeding-resistant wasting syndrome". Recent studies point to the potential interference of hyperglycemia as a catabolic factor, but also highlight that the suppression by feeding of autophagy as a cellular quality control mechanism may exert adverse consequences for the quality of the muscle.
Tijdschrift: Tijdschrift voor Geneeskunde
ISSN: 0371-683X
Issue: 3
Volume: 69
Pagina's: 131 - 140
Jaar van publicatie:2013