JCSM rapid communications最新文献

{"title":"Why Do Cancer Patients Die?","authors":"Timon Rausch, Thorsten Cramer","doi":"10.1002/rco2.113","DOIUrl":"https://doi.org/10.1002/rco2.113","url":null,"abstract":"<p>Cancer is a significant contributor to mortality on a global scale. But what actually causes a cancer patient to die? Here, we summarize the elegant review “Why do cancer patients die?” from Boire and colleagues [<span>1</span>], highlighting severe acute events, systemic factors, and their underlying causes in this context.</p><p>Cancer metastasis is often cited as the primary cause of cancer-related mortality [<span>2</span>]. However, this term is over simplistic, not completely precise and not largely supported by published literature. While it is true that patients with metastatic cancer are more likely to die than those with locally confined disease, cancer is intriguingly complex and results in a variety of symptoms, including acute single events or patient deterioration through systemic (organ) dysfunction. To effectively mitigate the destructive impact of cancer, it is essential to gain a deeper understanding of the physiological responses involved and identify more precisely the various cancer-related causalities.</p><p>Most advanced cancers can be considered as a chronic and systemic disease. However, it is likely that up to half of the cancer-induced deaths are functionally related to severe events such as vascular coagulation and cardiac failure, obstruction of vital organs, bacterial infection, or paraneoplastic syndromes. For instance, patients with cancer have an elevated risk of thromboembolic events, which may lead acutely to fatal strokes or pulmonary emboli and chronically to coronary heart disease and, subsequently, heart failure. Furthermore, congestive heart failure may also occur due to excessive loss of cardiac muscle, a phenomenon associated with and often caused by cancer cachexia. In addition, growing tumours can impair vital organ function. This can particularly be observed in primary brain cancers, where uncontrolled growth increases intracranial pressure, which can ultimately cause irreversible brain damage. A similar phenomenon can be observed in the lung, where pulmonary metastases can reduce gas exchange, resulting in severe respiratory distress. Because cancer patients often have compromised immune systems, both from the disease itself and from cancer therapy, they are at an increased risk for bacterial, viral, or fungal infections that can cause life-threatening complications. Moreover, paraneoplastic syndromes can irreversibly damage critical organs as a consequence of tissue dysfunction in the surrounding area of the tumour. For example, an inappropriate production of pro-inflammatory cytokines, hormones, or antibodies can result in severe adverse effects, potentially leading to critical organ damage and ultimately, death. Despite the principle objective of cancer treatments to target tumour cells, almost every therapeutic agent has unwanted adverse effects, including acute neutropenia (potentially leading to bacterial sepsis) or platelet depletion, which can also be life-threatening in some cases.</p><p>N","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"80-81"},"PeriodicalIF":0.0,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.113","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Gene-Therapy Responsive Blood Biomarkers in mdx Mouse Model","authors":"Camilla Johansson, Jessica F. Boehler, Kristy J. Brown, Zaïda Koeks, Esther J. Schrama, Nienke van de Velde, Jan J. G. M. Verschuuren, Erik H. Niks, Pietro Spitali, Cristina Al-Khalili Szigyarto","doi":"10.1002/rco2.112","DOIUrl":"https://doi.org/10.1002/rco2.112","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Identifying serum biomarkers that reflect the restoration of dystrophin in skeletal muscle is important for evaluating the effect of dystrophin-restoring therapies in preclinical and clinical trials. Many potential blood biomarkers have been identified in Duchenne muscular dystrophy (DMD) patients, which change with disease progression or respond to pharmacological treatment. In this study, it was suggested that a panel of such blood biomarker candidates could be used to monitor dystrophin rescue in <i>mdx</i> mice treated with microdystrophin based therapies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Plasma samples from <i>mdx</i> mice treated with the microdystrophin therapy SGT-001 were analysed with an antibody suspension bead array consisting of 87 antibodies. The array targets 83 unique proteins previously identified as biomarker candidates for DMD. Each sample was assayed at two different plasma dilutions to cover a broader concentration range. Protein concentrations estimated as Median fluorescent intensities (MFI) were correlated to dystrophin expression in muscle tissue, as measured by immunohistochemistry and Western blot. Thirteen of the targets were selected and analysed in a DMD and Becker muscular dystrophy (BMD) longitudinal natural history cohort using a suspension bead array.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ten proteins were found to be significantly elevated in untreated <i>mdx</i> mice compared with C57 wild-type mice and to correlate with dystrophin expression (Spearman's correlation, FDR < 0.05) upon gene transfer in <i>mdx</i> mice. Translatability of these biomarkers from animal models to patients was evaluated by exploring abundance trajectories over time in both DMD and BMD patients and association with dystrophin expression in BMD patients. Consistent with the observations in mouse, six of these biomarker candidates were more abundant in DMD patients compared with controls, and six were also differentially abundant between BMD and DMD patients. Among them, serum titin was shown to be associated with dystrophin expression in BMD patients, having a steeper decline over time in patients with low dystrophin expression in tibialis anterior compared with patients with high expression. Myosine light chain 3 had a steeper decline with time in DMD patients compared with BMD patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The 10 biomarker candidates identified in mouse plasma are related to muscle contraction, glycolysis, microtubule formation and protein de","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"187-198"},"PeriodicalIF":0.0,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Natural History Study of Hindlimb Physiology and Histopathology in a Heterozygous OPMD Mouse Model","authors":"Jorge Miguel Amaya,&nbsp;Sofie van Zanen-Gerhardt,&nbsp;Ernst Suidgeest,&nbsp;Jessica C. de Greef,&nbsp;Louise van der Weerd,&nbsp;Donnie Cameron,&nbsp;Christina J. J. Coenen de Roo,&nbsp;Maaike van Putten,&nbsp;Vered Raz","doi":"10.1002/rco2.101","DOIUrl":"https://doi.org/10.1002/rco2.101","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset autosomal dominant myopathy. OPMD is caused by a short alanine expansion in the gene encoding for poly(A) binding protein nuclear 1 (PABPN1) forming insoluble nuclear aggregates. OPMD patients are predominantly heterozygous, and the knock-in <i>Pabpn1</i>^+/A17 mouse, which expresses one copy of the expanded <i>Pabpn1</i> gene under the PABPN1 promoter genetically, mimics OPMD. Insights into the A17/+ mouse model are necessary to evaluate its preclinical value and test therapeutics for OPMD. Here, we performed a natural disease history study for the A17/+ model.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We combined muscle force measurements of the <i>tibialis anterior</i> with magnetic resonance imaging (MRI) measurements of the calf muscles made in 4-, 8- and 12-month-old wild-type and A17/+ mice. These measures were complemented by muscle histopathology staining and image quantification to detect PABPN1 aggregates and to assess muscle wasting. Statistical significance between genotypes over the three time points was assessed using ANOVA or Student's <i>t</i> test.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PABPN1 nuclear aggregates were found in the 12-month-old A17/+ mice at similar quantities of ~2% across hindlimb muscles. We did not observe changes in muscle strength of the <i>tibialis anterior</i> in A17/+ mice. MRI analyses of hindlimb muscles revealed no metabolic difference, no fatty infiltration and limited muscle atrophy between A17/+ and +/+ mice. The <i>plantaris</i> muscle in A17/+ showed 30% atrophy at 12 months of age, which was corroborated by a 30% myofiber shift in the myosin heavy chain −2A to −2B ratio. Histopathologic staining did not reveal muscle wasting in the hindlimb muscles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Despite the presence of PABPN1 insoluble aggregates in hindlimb muscles, muscle involvement in the 12-month-old A17/+ mice was limited. Our results query the usefulness of A17/+ hindlimb muscles for preclinical studies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"107-116"},"PeriodicalIF":0.0,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials”","authors":"","doi":"10.1002/rco2.110","DOIUrl":"https://doi.org/10.1002/rco2.110","url":null,"abstract":"<p>\u0000 <span>Fairman, C. M.</span>, <span>Lønbro, S.</span>, <span>Cardaci, T. D.</span>, <span>VanderVeen, B. N.</span>, <span>Nilsen, T. S.</span>, and <span>Murphy, A. E.</span> (<span>2022</span>) <span>Muscle wasting in cancer: opportunities and challenges for exercise in clinical cancer trials</span>. <i>JCSM Communications</i>, <span>5</span>: <span>52</span>–<span>67</span>, https://doi.org/10.1002/rco2.56.</p><p>The Ethics statement section for this article was missing. The below ethics statement has been added to the article:</p><p><b>Ethics Statement</b></p><p>The authors have nothing to report.</p><p>We apologize for this error.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"186"},"PeriodicalIF":0.0,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exocrine Pancreatic Insufficiency in Heart Failure: Clinical Features and Association With Cardiac Cachexia","authors":"Marlene A. T. Vijver,&nbsp;Olivier C. Dams,&nbsp;Thomas M. Gorter,&nbsp;Charlotte L. van Veldhuisen,&nbsp;Robert C. Verdonk,&nbsp;Dirk J. van Veldhuisen","doi":"10.1002/rco2.102","DOIUrl":"https://doi.org/10.1002/rco2.102","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Cardiac cachexia is a complex syndrome, and the underlying mechanisms are not completely understood. Exocrine pancreatic insufficiency (EPI) causes malabsorption, malnutrition and sarcopenia; and might contribute to cardiac cachexia. The prevalence of EPI and its clinical profile in patients with heart failure (HF) remain unknown. The objective of this study is to prospectively examine the prevalence and clinical characteristics of EPI in a wide spectrum of patients with HF and to relate these findings to malnutrition and cardiac cachexia.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Exocrine pancreatic function was examined in patients with HF using faecal elastase 1 (FE-1) measurements. A FE-1 level of ≤206 μg/g (&lt;200 ± 3%) supported the diagnosis of EPI. All patients were well characterized (including echocardiography and biomarkers); in 36 patients, invasive hemodynamics were measured. Cardiac cachexia was defined as non-edematous weight loss &gt;5% in at least six months. Malnutrition was assessed by the Simplified Nutritional Appetite Questionnaire (SNAQ). Comparisons were made between patients with and without EPI.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We enrolled 60 consecutive patients; mean age was 60 ± 10 years, 25 (42%) were women, mean left ventricular ejection fraction (LVEF) was 29 ± 14% and median N-terminal pro-B-type natriuretic peptide (NT-proBNP) was 3926 [2126–6645] pg/mL. Six patients (10%) had EPI. They had a lower body weight (61.7 versus 83.0 kg; &lt;i&gt;p&lt;/i&gt; = 0.003) and lower BMI (22.3 ± 3.3 versus 26.9 ± 4.5 kg/m&lt;sup&gt;2&lt;/sup&gt;, &lt;i&gt;p&lt;/i&gt; = 0.02), but functional class, LVEF and NT-proBNP were similar (&lt;i&gt;p&lt;/i&gt; = 0.53, &lt;i&gt;p&lt;/i&gt; = 0.78 and &lt;i&gt;p&lt;/i&gt; = 0.97, respectively). Patients with EPI had a higher SNAQ-score, indicating (more symptoms of) malnutrition (1 [0–3] versus 3 [2–4], &lt;i&gt;p&lt;/i&gt; = 0.045). Cardiac cachexia was present in three (50%) of the patients with EPI (versus 26% in patients without EPI, &lt;i&gt;p&lt;/i&gt; = 0.35). Patients with EPI exhibited lower serum lipase than patients without EPI (23 [14–25] U/L versus 39 [26–71] U/L, &lt;i&gt;p&lt;/i&gt; = 0.003). The aetiology of HF was different between groups (&lt;i&gt;p&lt;/i&gt; = 0.016); patients with congenital heart disease appeared to be more often affected by EPI (&lt;i&gt;p&lt;/i&gt; = 0.07).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;EPI is present in a significant proportion of patients with HF but is not associated with conventional HF parameters. Patients with HF and EPI are characterized by lower body weight and BMI, malnutrition and lower plasma","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"117-128"},"PeriodicalIF":0.0,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143186807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review of the Impact of Vegetarian Diets on Muscle Mass and Muscle Strength in Community-Dwelling, Healthy Adults","authors":"Linda Smillie,&nbsp;Michelle Minehan,&nbsp;Catherine R. Knight-Agarwal,&nbsp;Chris Oliver,&nbsp;Murray Turner","doi":"10.1002/rco2.109","DOIUrl":"https://doi.org/10.1002/rco2.109","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Loss of muscle mass and muscle strength are key characteristics of age-related muscle decline. Dietary protein is a key nutrient that supports optimal muscle health. However, there is a strong argument to reduce intake of animal protein for health and environmental reasons. The effects of vegetarian diets on determinants of muscle health are not clear. This systematic review aimed to investigate the impact of vegetarian diets on muscle mass and muscle strength.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A systematic literature search of the CINAHL, Medline, Scopus and Web of Science Core Collection databases, as well as the Cochrane Central Register of Controlled Trials, was conducted according to PRISMA guidelines. Studies reporting the effects of vegetarian diets on muscle mass and strength were analysed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of three interventions and 11 observational studied were eligible to be included (<i>n</i> = 14) in this review. Five of the 12 studies that reported muscle mass found no difference in muscle mass between participants consuming an omnivorous versus vegetarian diet. One observational study reported higher muscle mass for vegetarians. Of the studies that reported muscle strength (<i>n</i> = 5), three reported no difference between participants consuming an omnivorous and vegetarian diet.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Half of the included studies reported no difference in muscle mass or strength between vegetarians and omnivores. Further high-quality studies are needed to better understand the relationship between vegetarian diets and determinants of muscle health.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"173-185"},"PeriodicalIF":0.0,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143186545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Dietary Nitrate Supplementation on Physical Performance and Muscle Strength in Older People—A Systematic Review","authors":"Rebecca Renji,&nbsp;Sian M. Robinson,&nbsp;Miles D. Witham","doi":"10.1002/rco2.105","DOIUrl":"https://doi.org/10.1002/rco2.105","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Sarcopenia, the loss of muscle strength and mass with age, is a major cause of morbidity for older people. Dietary nitrate supplementation has been proposed as an intervention to improve skeletal muscle function via action as nitric oxide (NO) donors. However, the effect of nitrate supplementation on physical performance and muscle strength in older people is unclear. We aimed to systematically review evidence on whether dietary nitrate supplementation improves markers of muscle strength, muscle mass and physical performance in older people.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a systematic review of randomised controlled trials according to a prespecified protocol by two reviewers. We included interventional studies using dietary nitrate supplementation, mean participant age of &gt;60 years, with or without muscle weakness. Outcomes of interest were physical performance, muscle strength and muscle mass. Risk of bias was assessed using a modified version of the Cochrane Risk of Bias tool. Results were grouped by intervention and outcome measures and were described by narrative synthesis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Twenty-eight studies were included, with a size range of 8–72 participants. Intervention duration ranged from a single dose to 12 weeks. Seven studies were in healthy older people. Most studies had a high or unclear risk of bias; three had a low risk of bias. One-hundred-two outcomes were reported; 67 were related to physical performance, and 35 were related to muscle strength. No included study measured muscle mass. Thirty-three outcomes showed significant improvement, two showed significant worsening and 67 showed no statistically significant difference. Meta-analysis was not possible due to data heterogeneity. Subgroup analyses for different doses of nitrate (above or below 10 mmol nitrate per day), duration of treatment or specific commonly measured outcomes did not indicate any subgroup more likely to show positive results. The proportion of positive outcomes was similar in studies using beetroot extract, nitrate alone or exercise as a co-intervention.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Current evidence is insufficient to decide if dietary nitrate supplementation improves skeletal muscle function in older people. Future studies should be longer, larger and target older people with sarcopenia or frailty.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"143-156"},"PeriodicalIF":0.0,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143186415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Food Aversion, Systemic Inflammation and Intramuscular Adipose Tissue are Mortality Predictors in Advanced Lung Cancer Patients","authors":"Willian das Neves,&nbsp;Ana Paula de Souza Borges,&nbsp;Vinicius Jardim Carvalho,&nbsp;André Fujita,&nbsp;Gilberto de Castro Jr","doi":"10.1002/rco2.106","DOIUrl":"https://doi.org/10.1002/rco2.106","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer cachexia, systemic inflammation and muscle wasting are associated with poor survival in non–small cell lung cancer (NSCLC) patients (pts). We hypothesized whether neutrophil-to-lymphocyte ratio (NLR) and intramuscular adipose tissue/skeletal muscle index (IMAT/SMI) would predict prognosis in metastatic NSCLC (mNSCLC). In addition, we verified the role of a cancer cachexia questionnaire (EORTC-QLQ-CAX24) in the survival prediction.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analysed a prospective cohort of 128 treatment-naive mNSCLC pts (April 2017 to May 2020). We evaluated QoL using the EORTC-QLQ-C30 and EORTC-QLQ-CAX24 scales. We used the baseline NLR as a surrogate of systemic inflammation. We did evaluate IMAT/SMI using baseline plain computed tomography imaging. Cox multivariate regression, including age, sex, ECOG-PS and histology as covariates, was performed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Elevated NLR (hazard ratio [HR] 1.26, 95% confidence interval [CI]: 1.01–1.59, <i>p</i> = 0.038), IMAT/SMI ratio (HR 1.37, 95% CI: 1.03–1.84, <i>p</i> = 0.032) and high CAX24 scores for food aversion (HR 1.52, 95% CI: 1.13–2.03, <i>p</i> = 0.006) were associated with worse prognosis in mNSCLC. Indeed, higher ECOG-PS (Spearman rho = 0.208, <i>p</i> = 0.027), CAX24 scores for food aversion (Spearman rho = 0.197, <i>p</i> = 0.036), loss of control (Spearman rho = 0.212, <i>p</i> = 0.024) and eating and weight loss worry domains (Spearman rho = 0.219, <i>p</i> = 0.020) were associated with elevated NLR levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Elevated NLR, IMAT/SMI ratio and CAX24 score for food aversion are independently associated with worse survival in mNSCLC. These data underscored the importance of cachexia features as negative prognostic factors in mNSCLC and revealed the EORTC-QLQ-CAX24 questionnaire as a new tool for helping clinical decision-making.</p>\u0000 \u0000 <p><b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT03960034 and NCT04306094</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"157-163"},"PeriodicalIF":0.0,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143186312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detection of Sarcopenia in Community-Dwelling Older Adults Using the SARC-F Questionnaire: Findings From the Southampton Longitudinal Study of Ageing (SaLSA)","authors":"Harnish P. Patel,&nbsp;Evie Boswell,&nbsp;Faidra Laskou,&nbsp;Leo D. Westbury,&nbsp;Gregorio Bevilacqua,&nbsp;Ilse Bloom,&nbsp;Cyrus Cooper,&nbsp;Pritti Aggarwal,&nbsp;Elaine M. Dennison","doi":"10.1002/rco2.108","DOIUrl":"https://doi.org/10.1002/rco2.108","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Sarcopenia is associated with substantial morbidity and mortality. The SARC-F self-rated questionnaire is a simple tool that can be rapidly implemented by clinicians to identify individuals with probable sarcopenia who may require further in-depth assessment. A score ≥ 4 is predictive of sarcopenia and poorer outcomes. We sought to identify the prevalence and demographic correlates of probable sarcopenia in a newly formed cohort of community-dwelling older adults.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cross-sectional analysis of 480 participants (219 men and 261 women) identified from primary care in whom a questionnaire ascertaining demographic, lifestyle factors, comorbidities, nutrition risk and SARC-F score was completed between 2021 and 2022. Participant characteristics in relation to probable sarcopenia were examined using sex-stratified logistic regression. Age was included as a covariate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The median (lower quartile, upper quartile) age was 79.8 (76.9, 83.5) years. 12.8% (28) of men and 23% (60) of women had probable sarcopenia. Older age was associated with probable sarcopenia in both sexes (odds ratio [95% CI]: men 1.10 [1.02, 1.19], <i>p</i> = 0.01; women 1.08 [1.02, 1.14], <i>p</i> = 0.01) as was higher malnutrition risk score (men: 1.30 [1.12, 1.51], <i>p</i> = 0.001; women: 1.32 [1.17, 1.50], <i>p</i> &lt; 0.001 per unit increase). Among men, being married or in a civil partnership or cohabiting was protective against probable sarcopenia (0.39 [0.17, 0.89], <i>p</i> = 0.03) as was reporting drinking any alcohol (0.34 [0.13, 0.92], <i>p</i> = 0.03), whereas in women generally similar relationships were seen though these were weaker. Higher BMI (1.14 (1.07, 1.22), <i>p</i> &lt; 0.001 per unit increase) and more comorbidities (1.61 [1.34, 1.94], <i>p</i> &lt; 0.001 per extra medical condition) were also associated with probable sarcopenia in women.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Probable sarcopenia (SARC-F score ≥ 4) was common in older adults living in their own homes. In addition to advancing age and malnutrition, socio-demographic factors were also important. Patients with a higher SARC-F and who are living with associated risk factors should be prioritised for further in-depth assessment for sarcopenia to allow the planning and implementation of interventions to mitigate potential adverse consequences.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"164-172"},"PeriodicalIF":0.0,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Resistance Training on Markers of Cachexia in Patients with Heart Failure: A Systematic Review and Meta-Analysis","authors":"Reina Hanania,&nbsp;Nephtali Marina,&nbsp;Brittany Cucchiaro,&nbsp;Adrian Slee","doi":"10.1002/rco2.104","DOIUrl":"https://doi.org/10.1002/rco2.104","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Cachexia is a metabolic syndrome characterised by muscle wasting that is highly prevalent in subjects with heart failure (HF) and negatively affects physical function, quality of life, morbidity and mortality. Resistance training has been recently incorporated into cardiac rehabilitation exercise programmes to increase muscle strength in patients with HF. This systematic review and meta-analysis aim to assess the effects of resistance training on markers of cachexia in patients with HF.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Four electronic databases (MEDLINE, Embase, CENTRAL and CINAHL) were searched to identify randomised controlled trials (RCTs) evaluating the effects of resistance training-only programmes on published criteria for cachexia assessment including muscle strength, body composition (e.g. lean mass/muscle mass) or biochemical markers of cachexia (e.g. inflammatory markers) in patients with HF. Studies were selected based on pre-specified inclusion and exclusion criteria, with a risk of bias assessment carried out. Meta-analyses of muscle strength outcomes were completed using RevMan 5.4.1.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Nine studies were included in this review. Pooled analysis of one repetition-maximum strength test of the lower [SMD 0.67 (95% Cl – 0.12, 1.22) &lt;i&gt;p&lt;/i&gt;-value = 0.02] and upper extremities [SMD 1.20 (95% Cl – 0.62, 1.79) &lt;i&gt;p&lt;/i&gt;-value &lt;0.0001] showed a significant increase in muscle strength associated with resistance training, which are both important indicators of physical function. Resistance training did not increase muscle strength during rapid movements measured via peak torque at 60, 90 or 180°/s. There were no significant results recorded for changes in body composition and biochemical markers of cachexia. There were inconsistent findings for the effect of resistance training on quality of life. No studies reported findings on measures of anorexia or fatigue.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The findings of this review reveal the potential benefits of resistance training in preserving and enhancing muscle strength in patients with HF who are at risk of cardiac cachexia. Despite inconclusive results on body composition and quality of life, the inclusion of resistance training in cardiac rehabilitation guidelines has the potential to address issues of muscle weakness and frailty. Specific resistance training protocol recommendations to prevent or treat the development of cachexia cannot be made without the publication of more robu","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 2","pages":"129-142"},"PeriodicalIF":0.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}