Review articleInflammation and sarcopenia: A systematic review and meta-analysis
Introduction
Inflammation is an adaptive response of the immune system triggered by a homeostatic imbalance, to restore functionality. Whereas the acute inflammatory process induced by infection or tissue injury is clear, considerably less is known about the deleterious effects of chronic low-grade inflammation. The oxidative stress-induced redox imbalance and the sustained upregulation of pro inflammatory mediators are believed to act as the patho-physiological basis underpinning inflammatory disorders including cardiovascular diseases, cancer, diabetes, dementia and also sarcopenia [1].
According to the recent definitions of several working groups, sarcopenia is described as a syndrome characterized by a loss of muscle mass and strength with functional impairment and adverse outcomes [2], [3]. The age related muscle loss coincides with a micro and macro architecture disorganization of the entire muscle mass. For instance, the conversion of type II (fast) fibers to type I (slow) fibers and subsequent lipid infiltration, which translate into impairment of muscle power and a greatly increased risk of falls [4]. Several studies have shown that sarcopenic individuals are either three times more likely to fall or have an higher risk of death relative to non sarcopenic individuals [5], [6]. Moreover, sarcopenia itself is associated with disability and hospitalization [7].
A substantial body of literature has demonstrated that inflammatory cytokines activate many of the molecular pathways involved in skeletal muscle wasting leading to an imbalance between protein synthesis and catabolism [8], [9]. High levels of inflammatory cytokines have been demonstrated to be negatively related to muscle strength and mass [10], [11]. However, the research considering whether their serum cytokine levels could represent a biological marker of sarcopenia is equivocal [12].
Therefore, we conducted a systematic review and meta-analysis of observational studies exploring the association between serum inflammatory parameters and sarcopenia. We hypothesized that participants with sarcopenia have higher inflammatory parameters levels than normal controls.
Section snippets
Methods
This systematic review was conducted following the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) criteria for the quality assessment of included studies [13] and the indications of Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) statement. [14]
Results
The search identified 1370 potentially eligible studies, of which 354 duplicates were excluded due to duplication. After excluding 978 papers through title and abstract review, 38 full text articles were examined. Altogether, 19 studies were included in the qualitative synthesis [11], [19], [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [33], [34], [35], [36] and 17 in meta-analysis [20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30], [31], [32], [33]
Discussion
In this meta-analysis, involving 3072 people with sarcopenia and 8177 controls, we found evidence suggesting a significantly elevated inflammatory marker profile in people with sarcopenia. To the best of our knowledge, this is the first meta-analysis to investigate the possible relationship between sarcopenia and inflammation. Specifically, patients with sarcopenia experienced significantly higher levels of CRP, whilst no significant differences emerged for IL6 and TNF-α compared to controls.
Contributors
GB was responsible for producing the initial draft of the manuscript.
CT was responsible for data extraction and for producing the initial draft of the manuscript.
SC was responsible for data extraction.
MS was responsible for screening the papers and quality assessment.
CL was responsible for screening the papers.
BS was responsible for statistical analysis.
EM was responsible for quality assessment and revision of the manuscript.
GS was responsible for producing the initial draft of the manuscript.
Conflict of interest
The authors declare that they have no conflict of interest.
Funding
No funding was received for this review.
Provenance and peer review
This article has undergone peer review.
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