Body composition analyses from computed tomography (CT) scans have been used to assess cachexia in cancer patients. We investigated body composition indices, tissue change and treatment outcome in patients with resectable gastric adenocarcinoma.
A cohort analysis of all patients treated with curative intent for gastric adenocarcinoma in two Scandinavian university hospitals from 2008–2011 was performed (n=137). Body composition analyses were performed on CT images taken for routine diagnostics and staging. Both preoperative single scans and repeat CT examinations were analyzed.
Perioperative chemotherapy was given to 58 (42.3%) patients. Forty patients (29.2%) suffered severe postoperative complications and 70 (51.1%) patients died within three years. There was a significant reduction in patients' lean tissue during neoadjuvant chemotherapy (p=0.001). There was no association between skeletal muscle tissue index and postoperative complications. Poorer survival was observed in patients with preoperative skeletal muscle tissue index within the lowermost quartile, independent of tumor characteristics and neoadjuvant treatment (HR=1.91, 95% CI 1.11–3.28, p=0.019).
Patients lost lean tissue during neoadjuvant treatment for gastric adenocarcinoma. Low preoperative skeletal muscle index was not associated with postoperative complications, but strongly associated with poorer survival.
Chronic kidney disease (CKD) is a silent clinical condition associated with adverse comorbidity and high cardiovascular disease (CVD) risk. An inverse relationship with body mass index (BMI) and mortality has been demonstrated in hemodialysis patients. However, it is unclear if this risk-factor paradox is evident in non-dialysis CKD patients. The aims of this study were to explore the relationship between, nutritional status, markers of inflammation, autonomic and cardiac function with BMI. Longitudinal follow-up explored the relationship between BMI and all-cause mortality.
211-consecutive CKD patients referred for dobutamine stress echocardiography to detect or exclude myocardial ischemia were recruited. BMI, albumin, C-reactive protein (CRP) and haemoglobin (Hb) were recorded as markers of nutritional and inflammatory status. Left ventricular ejection fraction (LVEF) and heart rate variability (HRV) as an indicator of cardiac function was recorded. All subjects were followed prospectively until November 2014 and study end-point was all-cause mortality.
BMI was inversely associated with CKD status. After covariate adjustment, this association remained. During a mean follow-up period of 3.3±0.9 years there were 35 deaths (17%). BMI was inversely associated with all-cause mortality (HR 0.81, 95% CI 0.71–0.9). Other important independent predictors of mortality were heart rate variability (HR 0.98, 95% CI 0.97–0.99), myocardial ischemia (HR 1.37, 95% CI 1.17–1.81), and albumin (HR 0.86, 95% CI 0.81–0.92).
The presence of a BMI paradox exists in non-dialysis CKD patients. This risk-factor paradox was an independent predictor of all-cause mortality and may have significant clinical implications relevant to screening, assessment and treatment and requires further study.
Chemotherapy can reduce muscle mass in cancer patients but the potential of exercise to ameliorate this is understudied, particularly at the myocellular level. The primary purpose was to investigate changes in lean body mass (LBM) and secondly single fibre cross-sectional area (CSA) in cancer patients during chemotherapy and in combination with 10 weeks of exercise.
In a single-arm trial, patients adhered to chemotherapy for at least 4 weeks (control period) before 10 weeks of exercise adjunct to chemotherapy (exercise period). LBM (Dual Energy X-ray Absorptiometry) and single fibre CSA (muscle biopsies) were assessed at baseline, pre- and post-exercise. Muscle strength, functional performance and aerobic capacity were also assessed.
Ten patients were included, however only six patients completed the protocol. LBM changed over time (p=0.013), but no significant changes were observed between specific time points. Numerically, LBM decreased by 0.3 kg (p=0.41, 95% CI: -1.1;0.5) from 41.3–41.0kg, during the control period and increased by 0.7 kg (p=0.16, 95% CI: -0.6;2.0) from 40.4–41.1 kg during exercise. Muscle fibre CSA did not change significantly over time (p=0.13), but decreased numerically in the control period by 703 μm2 (p=0.20, 95% CI: -1877; 470) and increased by 846 μm2 (trend, p=0.08, 95% CI: -162; 1854) following exercise. Muscle strength and functional performance were unchanged during the control period but improved post-exercise.
Despite non-significant changes in muscle mass (due to small sample size), this study adds novel information on LBM and myocellular changes in cancer patients during chemotherapy and concurrent exercise.
Sarcopenia is a syndrome characterized by progressive loss of skeletal muscle which can be detected by computed tomography (CT) by estimating total psoas muscle cross-sectional area (CSA). Relying on total psoas CSA alone takes into account abnormal muscle and intramuscular fat, both of which may be increased in sarcopenic obesity. We developed a novel CT-method to identify the proportion of normal to abnormal psoas muscle at the third lumbar (L3) level. The primary objective of our pilot study was to measure inter-observer agreement between measuring total psoas CSA and proportion of normal and abnormal psoas muscle using a novel CT-method. We hypothesized total psoas CSA and proportion of normal and abnormal psoas muscle would be reliably quantifiable.
CT abdomen images were obtained for 20 adults. Two radiologists independently identified and traced the L3 psoas muscle circumference to estimate CSA. Hounsfield units were applied to the tracing to identify proportion of normal muscle, abnormal muscle, and fat. Inter-observer agreement was assessed using Pearson's correlation coefficient.
Of the 20 patients, 13 were male and six were obese. Mean age was 66 years. Correlation coefficient was excellent for total psoas CSA (r=0.93, p-value<0.00001) and proportion of normal psoas muscle (r=0.94, p-value<0.0001). Correlation was excellent between BMI and abnormal muscle (r=0.67, p-value=0.001). Correlation was poor between total psoas CSA and body mass index (BMI) (r=0.369, p-value=0.108) and negative between proportion of normal muscle and BMI (r= -0.50, p-value=0.025).
Our study findings demonstrate that total psoas CSA and proportion of normal and abnormal psoas can be reliably quantified. Our CT-method may be superior to total psoas CSA in identifying sarcopenic obesity, the results of which can be used to explore clinical outcomes.
Low alanine transaminase (ALT) has been shown to serve as a marker for sarcopenia and frailty in both healthy populations and in patients with chronic illness. Its yield in cancer patients in general and in particular in lung-cancer patients was not assessed.
Lung cancer patients presenting to an outpatient thoracic oncology clinic in a tertiary hospital were included. ALT plasma levels as well as other potential prognostic factors were collected retrospectively. Associations of those factors with survival were examined by univariate and multivariate analyses.
203 patients were eligible for analysis, of which 149 (73.4%) were diagnosed to have advanced disease. During median follow-up period of 15.4 months, 79 (38.9%) died. The mean ALT level of activity was 17.53±7.8 IU/L. The following parameters were found to be associated with increased risk of mortality: histologic type, male gender, advanced disease and low performance status upon diagnosis. Low ALT levels were not found to be associated with increased risk of mortality.
Low ALT activity levels, associated with sarcopenia, frailty and shortened survival in other patients' populations might not be predictive for shortened survival in lung cancer patients.
Myostatin, a member of the transforming growth factor beta (TGF-β) superfamily that is highly expressed in skeletal muscle, was first described in 1997. It has been known that loss of myostatin function induces an increase in muscle mass in mice, cow, dogs and humans. Therefore, myostatin and its receptor have emerged as a therapeutic target for loss of skeletal muscle such as sarcopenia and cachexia, as well as muscular dystrophies. At the molecular level, myostatin binds to and activates the activin receptor IIB (ActRIIB)/Alk 4/5 complex. Therapeutic approaches therefore are being taken both pre-clinically and clinically to inhibit the myostatin signaling pathway. Several myostatin inhibitors, including myostatin antibodies, anti-myostatin peptibody, activin A antibody, soluble (decoy) forms of ActRIIB (ActR II B-Fc), anti-myostatin adnectin, ActR II B antibody have been tested in the last decade. The aim of this review is to present the current knowledge of several myostatin inhibitors as a therapeutic approach for patients with loss of skeletal muscle.
This article details the principles of ethical authorship and publishing in the Journal of Cachexia, Sarcopenia and Muscle Clinical Reports (JCSM Clinical Reports). At the time of submission to JCSM Clinical Reports, the corresponding author, on behalf of all co-authors, needs to certify adherence to these principles. The principles are obtained below:
The patient above all else. Because it is the patient and the clinics that truely drive physician scientists and that are the heart of a clinical journal. The apt title given to JCSM Clinical Reports hence indicates a clear dedication to cachexia, sarcopenia and body composition in the clinical setting. As the legitimate daughter of the Journal of Cachexia, Sarcopenia and Muscle (JCSM), JCSM Clinical Reports focuses on the physiological and pathophysiological changes of body composition during the lifespan and in response to different illnesses from all fields of the life sciences.
Ever since its first appearance in September 2010, our mother JCSM has cultivated to offer a reliable resource to all professionals who are interested in research related to cachexia, sarcopenia and muscle or who are involved in the clinical care of affected patients. Within only few years and following the strict ethical guidelines for authorship and publishing in JCSM [1], JCSM's authors and editorial board have not only reached an inaugural impact factor of 7.413 for 2013, but have further increased the impact factor 7.883 by 2015. JCSM's noteworthy success story not only underlines the community's interest in this research field, but also JCSM's tremendous and substantiated relevance to the field [2].
As part of the editorial group responsible for this project, we first of all want to pay special tribute to our mother journal JCSM, to whom we owe our name and spirit. Second, JCSM Clinical Reports is grateful to stand in the tradition of novel ideas, cutting-edge research and quality publishing as incorporated by our senior consulting editors Stefan D. Anker (Germany) and Andrew Coats (Australia).
“There are only two lasting bequests we can hope to give our children. One of these is roots, the other, wings” the German poet Johann Wolfgang von Goethe has been quoted. Hence, the mission of this crown princess is clear: first, do not forget where you come from, and second, strive for the stars. Within the family of Cachexia, Sarcopenia and Muscle, JCSM Clinical Reports hopes to not only help in clinical decision making, but in serving as a source of clinical information and case reports as well. Much like our sibling and other contemporary publications JCSM Clinical Reports will be 2.0 Journal: online, peer-reviewed and international. We embrace a full open-access culture, meaning immediate and free availability to read, download and share [3]. We see JCSM Clinical Reports amongst other peer and rival Journals from General & Internal Medicine, Nutrition & Dietetics as well as Geriatrics & Gerontology (Table 1) and aim to close the gap of unmet clinical needs and applications.
JCSM Clinical Reports wants to reach out to a growing community of researchers and clinicians, serving authors for whom a specialized readership is a
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