Our prospective study represents the largest multicenter sample of metastatic cancer patients collected in France, assessing low muscle mass prevalence was among 766 patients. Although EWGSOP guidelines [11, 12] recommend a holistic approach involving both muscle mass and strength assessments to diagnose sarcopenia, cut-offs for strength assessments have yet to be validated in large cohorts. So despite collecting hand-grip test measures in 666 patients – of which 205 (30.8%) presented with both myopenia and dynapenia – our study has concentrated on evaluating muscle mass. As previously reported with different cut-offs for SMI [25, 32], low muscle mass was found to be highly prevalent among these cancer patients (69.1%). These data demonstrate how commonly available CT imagery may be used to objectively measure the myopenic component of sarcopenia, thus facilitating diagnosis and subsequent treatment of this common condition in cancer patients.
We found that low muscle mass was significantly more prevalent in men than women. Multivariate analyses also confirmed a strong association between low muscle mass prevalence and gender, with females being at lower risk. A similar gender-based association has been previously reported in other cancer sarcopenia populations [3, 7, 27]. Low muscle mass prevalence was found to be highest in prostate cancer (94.4%) and lower in breast cancer patients (54.3%). Indeed, prostate cancer patients have multiple risk factors for muscle mass loss, such as advanced age, advanced cancer and testosterone deprivation. In our study, prostate cancer patients had a mean age of 70.6 ± 8.5 versus 60.4 ± 13.4 years in breast cancer patients. Among sex-neutral cancers in this study, sarcopenia was similarly prevalent in each sex. Multivariate analysis did not reveal any associations between cancer type and the presence of low muscle mass.
The choice of the cut-off may be another factor explaining the differences in low muscle mass prevalence by gender. In studies where notably different SMI cut-off values were used, no significant differences in sarcopenia prevalence by gender was identified, such as in a recent study by Cortellini et al. [10], where L3 SMI thresholds for low muscular mass were < 43 cm2/m2 for men with BMI ≤ 25, <53 cm2/m2 for men with BMI ≥ 25, and ≤ 41 cm2/m2 for women. A 2016 literature review reported a sarcopenia prevalence ranging from 5 to 89%, depending on the malignancy and methods used for sarcopenia diagnosis [29]. Elsewhere, a prevalence of 25–30% has been reported, equivalent to about 1 million cancer patients in Europe [36]. There could also be other confounding factors influencing the apparent differences in sarcopenia prevalence by gender, such as behavioral characteristics (smoking, alcoholism, food habits). Nevertheless, an analysis that accounts for confounding factors was beyond the scope of our study, which is not longitudinal and was intended to be descriptive.
Our study is the first to demonstrate a potential association between brain metastases and low muscle mass. Patients with cerebral metastases are often prescribed corticosteroids, resulting in greater fatigue, and they also are at risk of developing hemiplegia. Both factors may lead to an overall reduction in the patients’ physical activity, increasing the risk of low muscle mass.
We documented a cachexia prevalence of 45.4% in low muscle mass patients (Fig. 2), which is higher compared to Fearon’s [14] definitions of cachexia measurement that assessed only percentage weight loss and BMI. Thus, these differences vouch for the use of CT imagery to detect low muscle mass defined sarcopenia, promising a more reliable diagnosis of cachexia.
The most worrying result of our study is that despiteits high prevalence, practitioners were unable to recognize sarcopenia in nearly half of those patients with low muscle mass during the survey, even while completing nutritional status data. Low muscle mass was more poorly recognized in obese patients (Fig. 2). Our findings also demonstrate the general lack of nutritional and physical therapy support available to cancer patients in France. Sarcopenic patients have a higher risk of being bedridden for longer durations and having abnormal food intake. It is well known that suitable nutritional programs and physical exercise regimes are helpful countermeasures to prevent muscle wasting, and hence cachexia development [1, 4].
These observations are sadly not novel, as highlighted in the cross-sectional NutriCancer2012 study [16, 20] that evaluated malnutrition prevalence in over 2000 cancer patients in France. Malnutrition prevalence was around 40%, and it was often diagnosed belatedly. Approximately 10% of these patients lacked any type of nutritional management, and there was only 70% concordance between the patients’ true conditions and the physicians’ evaluations. The study explained that such a low recourse to nutritional management was due to a lack of knowledge on malnutrition diagnosis and nutritional treatments (64% of interviewed physicians) and the lack of a nutrition team in the hospital (56% of physicians)[28].
While we could describe the existing nutrition and physical activity trends in patients with and without low muscle mass as part of this study, a longitudinal study would be better suited to investigate the link between these factors, their development and progression.
Sarcopenic patients have been reported to be more likely to accumulate treatment-related events [6, 30, 34]. In our study, we found an effect of low muscle mass on increased delay in treatment administration due to treatment-related toxicities. However, no links could be established with dose reductions, treatment interruptions, and occurrence of grade 3 AEs. We suggest that our study design was such that it favored the selection of patients with low toxicity prevalence. This might also be explained by the relative heterogeneity in our sample with regards to ongoing treatment and cancer type (compared to other studies assessing sarcopenia and treatment toxicity [6, 30, 34]). However, the principal objective of this study was not to assess such toxicity, but to evaluate low muscle mass prevalence in a population of patients with metastatic cancers most frequently encountered in clinical settings.
We aimed to demonstrate the prevalence and impact of low muscle mass in a population of metastatic cancer patients in various healthcare settings in France. Measures taken to ensure data quality included the study’s multicentric design, large sample size, oncologist and radiologist training in data collection and collaboration with a coordinating center. However, some limitations were duly noted. This was a cross-sectional study that evaluated a patient’s low muscle mass status at a certain timepoint, using their medical records to obtain much of the historical data reported. Such a study design offers limited control over center-based variability in the level of completeness, methods of measuring and recording of past data. Additionally, a cross-sectional design is inadequate for obtaining data on the development and evolution of cancer related low muscle mass over the course of a person’s illness, the evaluation of contributing factors, and its eventual impact on patient outcomes. Future longitudinal prospective studies, with a reasonable follow-up durations, will be required to better understand this complex disorder.