Marianne S. Oliveira, Rafaela C.E. Santo, Jordana M.S. Silva, Paulo V.G. Alabarse, Claiton V. Brenol, Steve P. Young, Ricardo M. Xavier
Background
Rheumatoid arthritis (RA) is an autoimmune disease that affects the joints, leading to chronic synovial inflammation and local tissue destruction. Extra-articular manifestations may also occur, such as changes in body composition. Skeletal muscle wasting is often observed in patients with RA, but methods for assessing loss of muscle mass are expensive and not widely available. Metabolomic analysis has shown great potential for identifying changes in the metabolite profile of patients with autoimmune diseases. In this setting, urine metabolomic profiling in patients with RA may be a useful tool to identify skeletal muscle wasting.
Methods
Patients aged 40–70 years with RA have been recruited according to the 2010 ACR/EULAR classification criteria. Further, the Disease Activity Score in 28 joints using the C-reactive protein level (DAS28-CRP) determined the disease activity. The muscle mass was measured by Dual X-ray absorptiometry (DXA) to generate the appendicular lean mass index (ALMI) by summing the lean mass measurements for both arms and legs and dividing them by height squared (kg/height2). Finally, urine metabolomic analysis by 1H nuclear magnetic resonance (1H-NMR) spectroscopy was performed and the metabolomics data set analysed using the BAYESIL and MetaboAnalyst software packages. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) were applied to the 1H-NMR data, followed by Spearman's correlation analysis. The combined receiver operating characteristic curve (ROC) was calculated, as well as the logistic regression analyses to establish a diagnostic model. The significance level at P < 0.05 was set for all analyses.
Results
The total set of subjects investigated included 90 patients with RA. Most patients were women (86.7%), with a mean age of 56.5 ± 7.3 years old and a median DAS28-CRP of 3.0 (IQR 1.0–3.0). Fifteen metabolites were identified in the urine samples with high variable importance in projection (VIP scores) by MetaboAnalyst. Of these, dimethylglycine (r = 0.205; P = 0.053), oxoisovalerate (r = −0.203; P = 0.055), and isobutyric acid (r = −0.249; P = 0.018) were significantly correlated with ALMI. Based on the low muscle mass (ALMI ≤6.0 kg/m2 for women and ≤8.1 kg/m2 for men) a diagnostic model have been established with dimethylglycine (area under the curve [AUC] = 0.65), oxoisovalerate (AUC = 0.49), and isobutyric acid (AUC = 0.83) with significant sensit
{"title":"Urinary metabolomic biomarker candidates for skeletal muscle wasting in patients with rheumatoid arthritis","authors":"Marianne S. Oliveira, Rafaela C.E. Santo, Jordana M.S. Silva, Paulo V.G. Alabarse, Claiton V. Brenol, Steve P. Young, Ricardo M. Xavier","doi":"10.1002/jcsm.13240","DOIUrl":"https://doi.org/10.1002/jcsm.13240","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Rheumatoid arthritis (RA) is an autoimmune disease that affects the joints, leading to chronic synovial inflammation and local tissue destruction. Extra-articular manifestations may also occur, such as changes in body composition. Skeletal muscle wasting is often observed in patients with RA, but methods for assessing loss of muscle mass are expensive and not widely available. Metabolomic analysis has shown great potential for identifying changes in the metabolite profile of patients with autoimmune diseases. In this setting, urine metabolomic profiling in patients with RA may be a useful tool to identify skeletal muscle wasting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Patients aged 40–70 years with RA have been recruited according to the 2010 ACR/EULAR classification criteria. Further, the Disease Activity Score in 28 joints using the C-reactive protein level (DAS28-CRP) determined the disease activity. The muscle mass was measured by Dual X-ray absorptiometry (DXA) to generate the appendicular lean mass index (ALMI) by summing the lean mass measurements for both arms and legs and dividing them by height squared (kg/height<sup>2</sup>). Finally, urine metabolomic analysis by <sup>1</sup>H nuclear magnetic resonance (<sup>1</sup>H-NMR) spectroscopy was performed and the metabolomics data set analysed using the BAYESIL and MetaboAnalyst software packages. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) were applied to the <sup>1</sup>H-NMR data, followed by Spearman's correlation analysis. The combined receiver operating characteristic curve (ROC) was calculated, as well as the logistic regression analyses to establish a diagnostic model. The significance level at <i>P</i> < 0.05 was set for all analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The total set of subjects investigated included 90 patients with RA. Most patients were women (86.7%), with a mean age of 56.5 ± 7.3 years old and a median DAS28-CRP of 3.0 (IQR 1.0–3.0). Fifteen metabolites were identified in the urine samples with high variable importance in projection (VIP scores) by MetaboAnalyst. Of these, dimethylglycine (<i>r</i> = 0.205; <i>P</i> = 0.053), oxoisovalerate (<i>r</i> = −0.203; <i>P</i> = 0.055), and isobutyric acid (<i>r</i> = −0.249; <i>P</i> = 0.018) were significantly correlated with ALMI. Based on the low muscle mass (ALMI ≤6.0 kg/m<sup>2</sup> for women and ≤8.1 kg/m<sup>2</sup> for men) a diagnostic model have been established with dimethylglycine (area under the curve [AUC] = 0.65), oxoisovalerate (AUC = 0.49), and isobutyric acid (AUC = 0.83) with significant sensit","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1657-1669"},"PeriodicalIF":8.9,"publicationDate":"2023-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5730451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yuan-Li Chen, Yi-Cheng Ma, Jie Tang, Dan Zhang, Qiu Zhao, Jian-Jun Liu, Hong-Shu Tang, Jin-Yu Zhang, Guang-Hui He, Chi-Hui Zhong, Yu-Tong Wu, Heng-Ruo Wen, Lan-Qing Ma, Cheng-Gang Zou
Background
Although the adiponectin signalling exerts exercise-mimicking effects, whether this pathway contributes to the anti-ageing benefits of physical exercise has not been established yet.
Methods
Swim exercise training and wheel running were used to measure lifespan in the nematode Caenorhabditis elegans and skeletal muscle quality in mice, respectively. Muscle weight, muscle fibre cross-sectional area (CSA) and myonuclei number were used to evaluate muscle mass. RNA sequencing (RNA-Seq) analysis of skeletal muscle in exercised mice was used to study the underlying mechanisms. Western blot and immunofluorescence were performed to explore autophagy- and senescence-related markers.
Results
The C. elegans adiponectin receptor PAQR-1/AdipoR1, but not PAQR-2/AdipoR2, was activated (3.55-fold and 3.48-fold increases in p-AMPK on Days 1 and 6, respectively, P < 0.001), which was involved in lifespan extension in exercised worms. Exercise training increased skeletal muscle mass index (1.29-fold, P < 0.01), muscle weight (1.75-fold, P < 0.001), myonuclei number (1.33-fold, P < 0.05), muscle fibre CSA (1.39-fold, P < 0.05) and capillary abundance (2.19-fold, P < 0.001 for capillary density; 1.58-fold, P < 0.01 for capillary number) in aged mice. Physical exercise reduced protein (2.94-fold, P < 0.001) and mRNA levels (1.70-fold, P < 0.001) of p16INK4a, a marker for cellular senescence, in skeletal muscle of aged mice. These beneficial effects of exercise on skeletal muscle of mice were dependent on AdipoR1. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis for differentially expressed genes in skeletal muscle between exercised mice with and without AdipoR1 knockdown by RNA-Seq analysis revealed that several KEGG pathways, such as ‘AMPK signalling pathway’ (P < 0.001), ‘FOXO signalling pathway’ (P < 0.001) and ‘autophagy’ (P < 0.001) were overrepresented. Knockdown of FoxO3a inhibited exercise-mediated beneficial effects on skeletal muscle quality of mice by inhibiting autophagy/mitophagy (3.81-fold reduction in LC3-II protein, P < 0.001; 1.53-fold reduction in BNIP3 protein, P < 0.05). Knockdown of daf-16, the FoxO homologue in C. elegans, reduced autophagy (2.77-fold and 2.06-fold reduction in GFP::LGG-1 puncta in seam cells and the intestine, respectively, P < 0.05) and blocked lifespan extension by exercise in worms.
{"title":"Physical exercise attenuates age-related muscle atrophy and exhibits anti-ageing effects via the adiponectin receptor 1 signalling","authors":"Yuan-Li Chen, Yi-Cheng Ma, Jie Tang, Dan Zhang, Qiu Zhao, Jian-Jun Liu, Hong-Shu Tang, Jin-Yu Zhang, Guang-Hui He, Chi-Hui Zhong, Yu-Tong Wu, Heng-Ruo Wen, Lan-Qing Ma, Cheng-Gang Zou","doi":"10.1002/jcsm.13257","DOIUrl":"https://doi.org/10.1002/jcsm.13257","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Although the adiponectin signalling exerts exercise-mimicking effects, whether this pathway contributes to the anti-ageing benefits of physical exercise has not been established yet.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Swim exercise training and wheel running were used to measure lifespan in the nematode <i>Caenorhabditis elegans</i> and skeletal muscle quality in mice, respectively. Muscle weight, muscle fibre cross-sectional area (CSA) and myonuclei number were used to evaluate muscle mass. RNA sequencing (RNA-Seq) analysis of skeletal muscle in exercised mice was used to study the underlying mechanisms. Western blot and immunofluorescence were performed to explore autophagy- and senescence-related markers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The <i>C. elegans</i> adiponectin receptor PAQR-1/AdipoR1, but not PAQR-2/AdipoR2, was activated (3.55-fold and 3.48-fold increases in p-AMPK on Days 1 and 6, respectively, <i>P</i> < 0.001), which was involved in lifespan extension in exercised worms. Exercise training increased skeletal muscle mass index (1.29-fold, <i>P</i> < 0.01), muscle weight (1.75-fold, <i>P</i> < 0.001), myonuclei number (1.33-fold, <i>P</i> < 0.05), muscle fibre CSA (1.39-fold, <i>P</i> < 0.05) and capillary abundance (2.19-fold, <i>P</i> < 0.001 for capillary density; 1.58-fold, <i>P</i> < 0.01 for capillary number) in aged mice. Physical exercise reduced protein (2.94-fold, <i>P</i> < 0.001) and mRNA levels (1.70-fold, <i>P</i> < 0.001) of p16<sup>INK4a</sup>, a marker for cellular senescence, in skeletal muscle of aged mice. These beneficial effects of exercise on skeletal muscle of mice were dependent on AdipoR1. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis for differentially expressed genes in skeletal muscle between exercised mice with and without AdipoR1 knockdown by RNA-Seq analysis revealed that several KEGG pathways, such as ‘AMPK signalling pathway’ (<i>P</i> < 0.001), ‘FOXO signalling pathway’ (<i>P</i> < 0.001) and ‘autophagy’ (<i>P</i> < 0.001) were overrepresented. Knockdown of <i>FoxO3a</i> inhibited exercise-mediated beneficial effects on skeletal muscle quality of mice by inhibiting autophagy/mitophagy (3.81-fold reduction in LC3-II protein, <i>P</i> < 0.001; 1.53-fold reduction in BNIP3 protein, <i>P</i> < 0.05). Knockdown of <i>daf-16</i>, the FoxO homologue in <i>C. elegans</i>, reduced autophagy (2.77-fold and 2.06-fold reduction in GFP::LGG-1 puncta in seam cells and the intestine, respectively, <i>P</i> < 0.05) and blocked lifespan extension by exercise in worms.</p>\u0000 </section>\u0000 ","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1789-1801"},"PeriodicalIF":8.9,"publicationDate":"2023-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13257","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5840442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Masatsugu Okamura, Masaaki Konishi, Javed Butler, Kamyar Kalantar-Zadeh, Stephan von Haehling, Stefan D. Anker
Cachexia, in the form of unintentional weight loss >5% in 12 months or less, and secondary sarcopenia in the form of muscle wasting are serious conditions that affect clinical outcomes. A chronic disease state such as chronic kidney disease (CKD) often contributes to these wasting disorders. The purpose of this review is to summarize the prevalence of cachexia and sarcopenia, their relationship with kidney function, and indicators for evaluating kidney function in patients with CKD. It is estimated that approximately half of all persons with CKD will develop cachexia with an estimated annual mortality rate of 20%, but few studies have been conducted on cachexia in CKD. Hence, the true prevalence of cachexia in CKD and its effects on kidney function and patient outcomes remain unclear. Some studies have highlighted the concept of protein-energy wasting (PEW) which usually include sarcopenia and cachexia. Several studies have examined kidney function and CKD progression in patients with sarcopenia. Most studies use serum creatinine levels to estimate kidney function. However, creatinine may be influenced by muscle mass, and creatinine-based glomerular filtration rate may overestimate kidney function in patients with reduced muscle mass or muscle wasting. Cystatin C, which is least affected by muscle mass, has been used in some studies, and creatinine-to-cystatin-C ratio has emerged as an important prognostic marker. A previous study incorporating 428 320 participants reported that participants with CKD and sarcopenia had a 33% higher hazard of mortality compared with those without (7% to 66%, P = 0.011), and that those with sarcopenia were twice as likely to develop end-stage kidney disease (hazard ratio: 1.98; 1.45 to 2.70, P < 0.001). Future studies on cachexia and sarcopenia in patients with CKD are needed to report rigorously defined cachexia concerning kidney function. Moreover, in studies on sarcopenia with CKD, it is desirable to accumulate studies using cystatin C to accurately estimate kidney function.
恶病质(在12个月或更短时间内意外体重减轻5%)和继发性肌肉减少症(肌肉萎缩)是影响临床结果的严重疾病。慢性疾病状态，如慢性肾脏疾病(CKD)往往有助于这些消耗紊乱。本文综述了CKD患者恶病质和肌肉减少症的患病率、与肾功能的关系以及评估肾功能的指标。据估计，大约一半的CKD患者会出现恶病质，估计年死亡率为20%，但关于CKD中恶病质的研究很少。因此，CKD中恶病质的真实患病率及其对肾功能和患者预后的影响尚不清楚。一些研究强调了蛋白质-能量消耗(PEW)的概念，通常包括肌肉减少症和恶病质。一些研究已经检查了肌少症患者的肾功能和CKD进展。大多数研究使用血清肌酐水平来评估肾功能。然而，肌酐可能受到肌肉质量的影响，肌酐为基础的肾小球滤过率可能高估了肌肉质量减少或肌肉萎缩患者的肾功能。胱抑素C受肌肉质量影响最小，已在一些研究中使用，肌酐与胱抑素C比值已成为重要的预后指标。先前一项纳入428320名参与者的研究报告称，CKD和肌肉减少症患者的死亡率比无CKD和肌肉减少症患者高33%(7%至66%，P = 0.011)，而肌肉减少症患者发生终末期肾病的可能性是无CKD和肌肉减少症患者的两倍(风险比:1.98;1.45 - 2.70, P <0.001)。未来关于CKD患者恶病质和肌肉减少症的研究需要报道严格定义的与肾功能相关的恶病质。此外，在CKD骨骼肌减少症的研究中，利用胱抑素C来准确评估肾功能的研究是值得积累的。
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Markus S. Anker, Alessia Lena, Eric J. Roeland, Jan Porthun, Sebastian Schmitz, Sara Hadzibegovic, Philipp Sikorski, Ursula Wilkenshoff, Ann-Kathrin Fr?hlich, Luisa Valentina Ramer, Matthias Rose, Jan Eucker, Tienush Rassaf, Matthias Totzeck, Lorenz H. Lehmann, Stephan von Haehling, Andrew J.S. Coats, Tim Friede, Javed Butler, Stefan D. Anker, Hanno Riess, Ulf Landmesser, Lars Bullinger, Ulrich Keller, Johann Ahn
Background
Maintaining the ability to perform self-care is a critical goal in patients with cancer. We assessed whether the patient-reported ability to walk 4 m and wash oneself predict survival in patients with pre-terminal cancer.
Methods
We performed a prospective observational study on 169 consecutive hospitalized patients with cancer (52% female, 64 ± 12 years) and an estimated 1–12 months prognosis at an academic, inpatient palliative care unit. Patients answered functional questions for ‘today’, ‘last week’, and ‘last month’, performed patient-reported outcomes (PROs), and physical function assessments.
Results
Ninety-two (54%) patients reported the ability to independently walk 4 m and 100 (59%) to wash ‘today’. The median number of days patients reported the ability to walk 4 m and wash were 6 (IQR 0–7) and 7 (0–7) days (‘last week’); and 27 (5–30) and 26 (10–30) days (‘last month’). In the last week, 32% of patients were unable to walk 4 m on every day and 10% could walk on 1–3 days; 30% were unable to wash on every day and 10% could wash on 1–3 days. In the last months, 14% of patients were unable to walk 4 m on every day and 10% could only walk on 1–10 days; 12% were unable to wash on every day and 11% could wash on 1–10 days. In patients who could walk ‘today’ average 4 m gait speed was 0.78 ± 0.28 m/s. Patients who reported impaired walking and washing experienced more symptoms (dyspnoea, exertion, and oedema) and decreased physical function (higher Eastern Cooperative Oncology Group Performance Status, and lower Karnofsky Performance Status and hand-grip strength [unable vs. able to walk ‘today’: 205 ± 87 vs. 252 ± 78 Newton, P = 0.001; unable vs. able to wash ‘today’: 204 ± 86 vs. 250 ± 80 Newton, P = 0.001]). During the 27 months of observation, 152 (90%) patients died (median survival 46 days). In multivariable Cox proportional hazards regression analyses, all tested parameters were independent predictors of survival: walking 4 m ‘today’ (HR 0.63, P = 0.015), ‘last week’ (per 1 day: HR 0.93, P = 0.011), ‘last month’ (per 1 day: HR 0.98, P = 0.012), 4 m gait speed (per 1 m/s: HR 0.45, P = 0.002), and washing ‘today’ (HR 0.67, P = 0.024), ‘last week (per 1 day HR 0.94, p=0.019), and ‘last month’ (per 1 day HR 0.99, P = 0.040). Patients unable to walk and wash experienced the shortest survival and most reduced functional status.
Conclusions
背景:维持自我护理的能力是癌症患者的一个重要目标。我们评估了患者报告的行走4米和自己洗澡的能力是否能预测晚期癌症患者的生存。方法:我们对169例连续住院的癌症患者(52%为女性，64±12岁)进行了前瞻性观察研究，这些患者在学术住院姑息治疗单位估计预后为1-12个月。患者回答了“今天”、“上周”和“上个月”的功能问题，进行了患者报告的结果(PROs)和身体功能评估。结果92例(54%)患者报告能够独立行走4米，100例(59%)患者报告能够“今天”洗澡。患者报告行走4米和洗涤能力的中位数天数为6 (IQR 0-7)和7(0-7)天(“上周”);27天(5-30天)和26天(10-30天)(上个月)。在最后一周，32%的患者无法每天步行4米，10%的患者在1-3天内可以步行;30%的人不能每天洗，10%的人可以1-3天洗一次。在过去的几个月里，14%的患者无法每天行走400米，10%的患者只能在1-10天内行走;12%的人不能每天洗，11%的人可以在1-10天内洗。在“今天”能够行走的患者中，平均4米步速为0.78±0.28米/秒。报告行走和洗涤功能受损的患者出现更多症状(呼吸困难、用力和水肿)和身体功能下降(东部肿瘤合作组表现状态较高，Karnofsky表现状态和握力较低[“今天”不能行走vs.能够行走:205±87 vs. 252±78牛顿，P = 0.001;“今天”不能洗vs.能够洗:204±86 vs. 250±80牛顿，P = 0.001])。在27个月的观察中，152例(90%)患者死亡(中位生存期46天)。在多变量Cox比例风险回归分析,所有测试参数是生存的独立预测指标:步行4 m '今天' (HR 0.63, P = 0.015),“上周”(每1天:人力资源0.93,P = 0.011),“上个月”(每1天:人力资源0.98,P = 0.012), 4 m步态速度(每1 m / s:人力资源0.45,P = 0.002),和洗涤‘今天’(HR 0.67, P = 0.024),“上周(每1天人力资源0.94,P = 0.019),和“上个月”(每1天人力资源0.99,P = 0.040)。不能行走和洗涤的患者生存时间最短，功能状态下降最多。结论:在晚期癌症患者中，自我报告的4米行走能力和洗涤能力是生存的独立预测指标，并与功能状态下降有关。
{"title":"Patient-reported ability to walk 4 m and to wash: New clinical endpoints and predictors of survival in patients with pre-terminal cancer","authors":"Markus S. Anker, Alessia Lena, Eric J. Roeland, Jan Porthun, Sebastian Schmitz, Sara Hadzibegovic, Philipp Sikorski, Ursula Wilkenshoff, Ann-Kathrin Fr?hlich, Luisa Valentina Ramer, Matthias Rose, Jan Eucker, Tienush Rassaf, Matthias Totzeck, Lorenz H. Lehmann, Stephan von Haehling, Andrew J.S. Coats, Tim Friede, Javed Butler, Stefan D. Anker, Hanno Riess, Ulf Landmesser, Lars Bullinger, Ulrich Keller, Johann Ahn","doi":"10.1002/jcsm.13247","DOIUrl":"https://doi.org/10.1002/jcsm.13247","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Maintaining the ability to perform self-care is a critical goal in patients with cancer. We assessed whether the patient-reported ability to walk 4 m and wash oneself predict survival in patients with pre-terminal cancer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We performed a prospective observational study on 169 consecutive hospitalized patients with cancer (52% female, 64 ± 12 years) and an estimated 1–12 months prognosis at an academic, inpatient palliative care unit. Patients answered functional questions for ‘today’, ‘last week’, and ‘last month’, performed patient-reported outcomes (PROs), and physical function assessments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ninety-two (54%) patients reported the ability to independently walk 4 m and 100 (59%) to wash ‘today’. The median number of days patients reported the ability to walk 4 m and wash were 6 (IQR 0–7) and 7 (0–7) days (‘last week’); and 27 (5–30) and 26 (10–30) days (‘last month’). In the last week, 32% of patients were unable to walk 4 m on every day and 10% could walk on 1–3 days; 30% were unable to wash on every day and 10% could wash on 1–3 days. In the last months, 14% of patients were unable to walk 4 m on every day and 10% could only walk on 1–10 days; 12% were unable to wash on every day and 11% could wash on 1–10 days. In patients who could walk ‘today’ average 4 m gait speed was 0.78 ± 0.28 m/s. Patients who reported impaired walking and washing experienced more symptoms (dyspnoea, exertion, and oedema) and decreased physical function (higher Eastern Cooperative Oncology Group Performance Status, and lower Karnofsky Performance Status and hand-grip strength [unable vs. able to walk ‘today’: 205 ± 87 vs. 252 ± 78 Newton, <i>P</i> = 0.001; unable vs. able to wash ‘today’: 204 ± 86 vs. 250 ± 80 Newton, <i>P</i> = 0.001]). During the 27 months of observation, 152 (90%) patients died (median survival 46 days). In multivariable Cox proportional hazards regression analyses, all tested parameters were independent predictors of survival: walking 4 m ‘today’ (HR 0.63, <i>P</i> = 0.015), ‘last week’ (per 1 day: HR 0.93, <i>P</i> = 0.011), ‘last month’ (per 1 day: HR 0.98, <i>P</i> = 0.012), 4 m gait speed (per 1 m/s: HR 0.45, <i>P</i> = 0.002), and washing ‘today’ (HR 0.67, <i>P</i> = 0.024), ‘last week (per 1 day HR 0.94, p=0.019), and ‘last month’ (per 1 day HR 0.99, <i>P</i> = 0.040). Patients unable to walk and wash experienced the shortest survival and most reduced functional status.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 ","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1670-1681"},"PeriodicalIF":8.9,"publicationDate":"2023-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13247","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5807879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicholas A. Bradley, Amy Walter, Ross Dolan, Alasdair Wilson, Tamim Siddiqui, Campbell S.D. Roxburgh, Donald C. McMillan, Graeme J.K. Guthrie
Background
Endovascular aneurysm repair (EVAR) is the most common mode of repair of abdominal aortic aneurysms (AAA) in the UK. EVAR ranges from standard infrarenal repair to complex fenestrated and branched EVAR (F/B-EVAR). Sarcopenia is defined by lower muscle mass and function, which is associated with inferior perioperative outcomes. Computed tomography-derived body composition analysis offers prognostic value in patients with cancer. Several authors have evaluated the role of body composition analysis in predicting outcomes in patients undergoing EVAR; however, the evidence base is limited by heterogeneous methodology.
Methods
Six hundred seventy-four consecutive patients (58 (8.6%) female, mean (SD) age 74.4 (6.8) years) undergoing EVAR and F/B-EVAR at three large tertiary centres were retrospectively recruited. Subcutaneous and visceral fat indices (SFI and VFI), psoas and skeletal muscle indices, and skeletal muscle density were measured at the L3 vertebral level from pre-operative computed tomographies. The maximally selected rank statistic technique was used to define optimal thresholds to predict mortality.
Results
There were 191 deaths during the median follow-up period of 60.0 months. Mean (95% CI) survival in the low SMI versus high SMI subgroups was 62.6 (58.5–66.7) versus 82.0 (78.7–85.3) months (P < 0.001). Mean (95% CI) survival in the low SFI versus high SFI subgroups was 56.4 (48.2–64.7) versus 77.1 (74.2–80.1) months (P < 0.001). One-year mortality in the low SMI versus high SMI subgroups was 10% versus 3% (P < 0.001). Low SMI was associated with increased odds of one-year mortality (OR 3.19, 95% CI 1.60–6.34, P < 0.001). Five-year mortality in the low SMI versus high SMI subgroups was 55% versus 28% (P < 0.001). Low SMI was associated with increased odds of five-year mortality (OR 1.54, 95% CI 1.11–2.14, P < 0.01). On multivariate analysis of all patients, low SFI (HR 1.90, 95% CI 1.30–2.76, P < 0.001) and low SMI (HR 1.88, 95% CI 1.34–2.63, P < 0.001) were associated with poorer survival. On multivariate analysis of asymptomatic AAA patients, low SFI (HR 1.54, 95% CI 1.01–2.35, P < 0.05) and low SMI (HR 1.71, 95% CI 1.20–2.42, P < 0.01) were associated with poorer survival.
Conclusions
Low SMI and SFI are associated with poorer long-term survival following EVAR and F/B-EVAR. The relation
在英国，血管内动脉瘤修复(EVAR)是腹主动脉瘤(AAA)最常见的修复方式。EVAR的范围从标准的肾下修复到复杂的开窗和分支EVAR (F/B-EVAR)。肌肉减少症的定义是肌肉质量和功能降低，这与围手术期预后较差有关。计算机断层扫描衍生的身体成分分析为癌症患者的预后提供了价值。几位作者评估了体成分分析在预测EVAR患者预后中的作用;然而，证据基础受到异质性方法的限制。方法回顾性招募674例连续患者，其中58例(8.6%)为女性，平均(SD)年龄74.4(6.8)岁，在三个大型三级中心接受EVAR和F/B-EVAR。术前计算机断层扫描在L3椎体水平测量皮下和内脏脂肪指数(SFI和VFI)、腰肌和骨骼肌指数以及骨骼肌密度。采用最大选择秩统计技术确定预测死亡率的最佳阈值。结果中位随访60.0个月，死亡191例。低重度精神障碍亚组和高重度精神障碍亚组的平均(95% CI)生存期分别为62.6(58.5-66.7)和82.0(78.7-85.3)个月(P <0.001)。低SFI亚组和高SFI亚组的平均(95% CI)生存期分别为56.4(48.2-64.7)和77.1(74.2-80.1)个月(P <0.001)。低重度精神障碍亚组和高重度精神障碍亚组的1年死亡率分别为10%和3% (P <0.001)。低SMI与一年死亡率增加相关(OR 3.19, 95% CI 1.60-6.34, P <0.001)。低重度精神障碍亚组和高重度精神障碍亚组的5年死亡率分别为55%和28% (P <0.001)。低SMI与5年死亡率增加相关(OR 1.54, 95% CI 1.11-2.14, P <0.01)。在所有患者的多变量分析中，低SFI (HR 1.90, 95% CI 1.30-2.76, P <0.001)和低SMI (HR 1.88, 95% CI 1.34-2.63, P <0.001)与较差的生存率相关。无症状AAA患者的多因素分析，低SFI (HR 1.54, 95% CI 1.01-2.35, P <0.05)和低SMI (HR 1.71, 95% CI 1.20-2.42, P <0.01)与较差的生存率相关。结论:低SMI和SFI与EVAR和F/B-EVAR后较差的长期生存相关。体成分与预后的关系需要进一步评估，并需要对AAA患者提出的阈值进行外部验证。
{"title":"Evaluation of the prognostic value of computed tomography-derived body composition in patients undergoing endovascular aneurysm repair","authors":"Nicholas A. Bradley, Amy Walter, Ross Dolan, Alasdair Wilson, Tamim Siddiqui, Campbell S.D. Roxburgh, Donald C. McMillan, Graeme J.K. Guthrie","doi":"10.1002/jcsm.13262","DOIUrl":"https://doi.org/10.1002/jcsm.13262","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Endovascular aneurysm repair (EVAR) is the most common mode of repair of abdominal aortic aneurysms (AAA) in the UK. EVAR ranges from standard infrarenal repair to complex fenestrated and branched EVAR (F/B-EVAR). Sarcopenia is defined by lower muscle mass and function, which is associated with inferior perioperative outcomes. Computed tomography-derived body composition analysis offers prognostic value in patients with cancer. Several authors have evaluated the role of body composition analysis in predicting outcomes in patients undergoing EVAR; however, the evidence base is limited by heterogeneous methodology.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Six hundred seventy-four consecutive patients (58 (8.6%) female, mean (SD) age 74.4 (6.8) years) undergoing EVAR and F/B-EVAR at three large tertiary centres were retrospectively recruited. Subcutaneous and visceral fat indices (SFI and VFI), psoas and skeletal muscle indices, and skeletal muscle density were measured at the L3 vertebral level from pre-operative computed tomographies. The maximally selected rank statistic technique was used to define optimal thresholds to predict mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>There were 191 deaths during the median follow-up period of 60.0 months. Mean (95% CI) survival in the low SMI versus high SMI subgroups was 62.6 (58.5–66.7) versus 82.0 (78.7–85.3) months (<i>P</i> < 0.001). Mean (95% CI) survival in the low SFI versus high SFI subgroups was 56.4 (48.2–64.7) versus 77.1 (74.2–80.1) months (<i>P</i> < 0.001). One-year mortality in the low SMI versus high SMI subgroups was 10% versus 3% (<i>P</i> < 0.001). Low SMI was associated with increased odds of one-year mortality (OR 3.19, 95% CI 1.60–6.34, <i>P</i> < 0.001). Five-year mortality in the low SMI versus high SMI subgroups was 55% versus 28% (<i>P</i> < 0.001). Low SMI was associated with increased odds of five-year mortality (OR 1.54, 95% CI 1.11–2.14, <i>P</i> < 0.01). On multivariate analysis of all patients, low SFI (HR 1.90, 95% CI 1.30–2.76, <i>P</i> < 0.001) and low SMI (HR 1.88, 95% CI 1.34–2.63, <i>P</i> < 0.001) were associated with poorer survival. On multivariate analysis of asymptomatic AAA patients, low SFI (HR 1.54, 95% CI 1.01–2.35, <i>P</i> < 0.05) and low SMI (HR 1.71, 95% CI 1.20–2.42, <i>P</i> < 0.01) were associated with poorer survival.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Low SMI and SFI are associated with poorer long-term survival following EVAR and F/B-EVAR. The relation","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1836-1847"},"PeriodicalIF":8.9,"publicationDate":"2023-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5688973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sanne C.C. Vincenten, Karlien Mul, Dani?l van As, Julia J. Jansen, Linda Heskamp, Arend Heerschap, Baziel G.M. van Engelen, Nicol C. Voermans
Background
It is unclear how changes in quantitative muscle magnetic resonance imaging (MRI) relate to changes in clinical outcome in facioscapulohumeral muscular dystrophy (FSHD), although this information is crucial for optimal use of MRI as imaging biomarker in trials. We therefore assessed muscle MRI and clinical outcome measures in a large longitudinal prospective cohort study.
Methods
All patients were assessed by MRI at baseline and at 5-year follow-up, employing 2pt-Dixon and turbo inversion recovery magnitude (TIRM) sequences, after which fat fraction and TIRM positivity of 19 leg muscles were determined bilaterally. The MRI compound score (CoS) was defined as the mean fat fraction of all muscles weighted for cross-sectional area. Clinical outcome measures included the Ricci-score, FSHD clinical score (FSHD-CS), MRC sumscore (MRC-SS), and motor-function-measure (MFM).
Results
We included 105 FSHD patients [mean age 54 ± 14 years, median Ricci-score 7 (range 0–10)]. The median change over 5 years' time in the MRI-CoS was 2.0% (range −4.6 to +12.1; P < 0.001). The median change over 5 years' time in clinical outcome measures was small in all measures, with z-scores ranging from 5.0 to 7.2 (P < 0.001). The change in MRI-CoS correlated with change in FSHD-CS and Ricci-score (ρ = 0.25, respectively; ρ = 0.23, P < 0.05). The largest median increase in MRI-CoS was seen in baseline subgroups with an MRI-CoS 20–40% (6.1%), with ≥2 TIRM positive muscles (3.5%) or with an FSHD-CS 5–10 (3.1%).
Conclusions
This 5-year study showed significant changes in MRI and clinical outcome measures and a significant correlation between changes in MRI-CoS and changes in clinical outcome measures. In addition, we identified subgroups of patients that are most prone to radiological disease progression. This knowledge further establishes quantitative MRI parameters as prognostic biomarkers in FSHD and as efficacy biomarkers in upcoming clinical trials.
{"title":"Five-year follow-up study on quantitative muscle magnetic resonance imaging in facioscapulohumeral muscular dystrophy: The link to clinical outcome","authors":"Sanne C.C. Vincenten, Karlien Mul, Dani?l van As, Julia J. Jansen, Linda Heskamp, Arend Heerschap, Baziel G.M. van Engelen, Nicol C. Voermans","doi":"10.1002/jcsm.13250","DOIUrl":"https://doi.org/10.1002/jcsm.13250","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>It is unclear how changes in quantitative muscle magnetic resonance imaging (MRI) relate to changes in clinical outcome in facioscapulohumeral muscular dystrophy (FSHD), although this information is crucial for optimal use of MRI as imaging biomarker in trials. We therefore assessed muscle MRI and clinical outcome measures in a large longitudinal prospective cohort study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>All patients were assessed by MRI at baseline and at 5-year follow-up, employing 2pt-Dixon and turbo inversion recovery magnitude (TIRM) sequences, after which fat fraction and TIRM positivity of 19 leg muscles were determined bilaterally. The MRI compound score (CoS) was defined as the mean fat fraction of all muscles weighted for cross-sectional area. Clinical outcome measures included the Ricci-score, FSHD clinical score (FSHD-CS), MRC sumscore (MRC-SS), and motor-function-measure (MFM).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We included 105 FSHD patients [mean age 54 ± 14 years, median Ricci-score 7 (range 0–10)]. The median change over 5 years' time in the MRI-CoS was 2.0% (range −4.6 to +12.1; <i>P</i> < 0.001). The median change over 5 years' time in clinical outcome measures was small in all measures, with <i>z</i>-scores ranging from 5.0 to 7.2 (<i>P</i> < 0.001). The change in MRI-CoS correlated with change in FSHD-CS and Ricci-score (ρ = 0.25, respectively; ρ = 0.23, <i>P</i> < 0.05). The largest median increase in MRI-CoS was seen in baseline subgroups with an MRI-CoS 20–40% (6.1%), with ≥2 TIRM positive muscles (3.5%) or with an FSHD-CS 5–10 (3.1%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This 5-year study showed significant changes in MRI and clinical outcome measures and a significant correlation between changes in MRI-CoS and changes in clinical outcome measures. In addition, we identified subgroups of patients that are most prone to radiological disease progression. This knowledge further establishes quantitative MRI parameters as prognostic biomarkers in FSHD and as efficacy biomarkers in upcoming clinical trials.</p>\u0000 </section>\u0000 </div>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1695-1706"},"PeriodicalIF":8.9,"publicationDate":"2023-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13250","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5768401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Binh Duong Thai, Jürgen M. Bauer, Annette Eidam, Jane Durga, Stefan Grund, Thomas Mross, Petra Benzinger
Background
Anorexia of aging is characterized by an age-associated reduction of appetite, whose aetiology in most cases is multifactorial and which often triggers malnutrition. The Simplified Nutritional Appetite Questionnaire (SNAQ) is an established screening tool. This study aimed to investigate reliability, validity, and feasibility of its telephone administration (T-SNAQ) in German community-dwelling older adults.
Methods
This cross-sectional single-centre study recruited participants from April 2021 to September 2021. First, the SNAQ was translated into German according to an established methodology. After translation, reliability, construct validity, and feasibility of the T-SNAQ were analysed. A convenience sample of community-dwelling older adults aged ≥70 years was recruited. The following measurements were applied to all participants: T-SNAQ, Mini Nutritional Assessment – Short Form (MNA-SF), six-item Katz index of independence in activities of daily living (ADL), eight-item Lawton instrumental activities of daily living (IADL), telephone Montreal Cognitive Assessment (T-MoCA); FRAIL scale, Geriatric Depression Scale (GDS-15) and Charlson co-morbidity index as well as daily caloric and protein intake.
Results
One hundred twenty participants (59.2% female) with a mean age of 78.0 ± 5.8 years were included in the present study. The percentage of participants identified with poor appetite based on T-SNAQ was 20.8% (n = 25). T-SNAQ showed a good internal reliability with a Cronbach's alpha coefficient of 0.64 and a good test–retest reliability [intraclass coefficient of 0.95 (P < 0.05)]. Regarding construct validity, T-SNAQ was significantly positively correlated with MNA-SF (r = 0.213), T-MoCA (r = 0.225), daily energy (r = 0.222) and protein intake (r = 0.252) (P < 0.05). It also demonstrated a significant negative association with GDS-15 (r = −0.361), FRAIL scale (r = −0.203) and Charlson co-morbidity index (r = −0.272). Regarding applicability, the mean time for T-SNAQ was 95 s and completion rate was 100%.
Conclusions
The T-SNAQ is a feasible screening instrument for anorexia of aging in community-dwelling older adults via telephone interviews.
{"title":"Validation of a telephone-based administration of the simplified nutritional appetite questionnaire","authors":"Binh Duong Thai, Jürgen M. Bauer, Annette Eidam, Jane Durga, Stefan Grund, Thomas Mross, Petra Benzinger","doi":"10.1002/jcsm.13264","DOIUrl":"https://doi.org/10.1002/jcsm.13264","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Anorexia of aging is characterized by an age-associated reduction of appetite, whose aetiology in most cases is multifactorial and which often triggers malnutrition. The Simplified Nutritional Appetite Questionnaire (SNAQ) is an established screening tool. This study aimed to investigate reliability, validity, and feasibility of its telephone administration (T-SNAQ) in German community-dwelling older adults.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This cross-sectional single-centre study recruited participants from April 2021 to September 2021. First, the SNAQ was translated into German according to an established methodology. After translation, reliability, construct validity, and feasibility of the T-SNAQ were analysed. A convenience sample of community-dwelling older adults aged ≥70 years was recruited. The following measurements were applied to all participants: T-SNAQ, Mini Nutritional Assessment – Short Form (MNA-SF), six-item Katz index of independence in activities of daily living (ADL), eight-item Lawton instrumental activities of daily living (IADL), telephone Montreal Cognitive Assessment (T-MoCA); FRAIL scale, Geriatric Depression Scale (GDS-15) and Charlson co-morbidity index as well as daily caloric and protein intake.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>One hundred twenty participants (59.2% female) with a mean age of 78.0 ± 5.8 years were included in the present study. The percentage of participants identified with poor appetite based on T-SNAQ was 20.8% (<i>n</i> = 25). T-SNAQ showed a good internal reliability with a Cronbach's alpha coefficient of 0.64 and a good test–retest reliability [intraclass coefficient of 0.95 (<i>P</i> < 0.05)]. Regarding construct validity, T-SNAQ was significantly positively correlated with MNA-SF (<i>r</i> = 0.213), T-MoCA (<i>r</i> = 0.225), daily energy (<i>r</i> = 0.222) and protein intake (<i>r</i> = 0.252) (<i>P</i> < 0.05). It also demonstrated a significant negative association with GDS-15 (<i>r</i> = −0.361), FRAIL scale (<i>r</i> = −0.203) and Charlson co-morbidity index (<i>r</i> = −0.272). Regarding applicability, the mean time for T-SNAQ was 95 s and completion rate was 100%.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The T-SNAQ is a feasible screening instrument for anorexia of aging in community-dwelling older adults via telephone interviews.</p>\u0000 </section>\u0000 </div>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1848-1854"},"PeriodicalIF":8.9,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5753608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nicole Kiss, Carla M. Prado, Robin M. Daly, Linda Denehy, Lara Edbrooke, Brenton J. Baguley, Steve F. Fraser, Abbas Khosravi, Gavin Abbott
Background
Low muscle mass (MM) is a common component of cancer-related malnutrition and sarcopenia, conditions that are all independently associated with an increased risk of mortality. This study aimed to (1) compare the prevalence of low MM, malnutrition, and sarcopenia and their association with survival in adults with cancer from the UK Biobank and (2) explore the influence of different allometric scaling (height [m2] or body mass index [BMI]) on low MM estimates.
Methods
Participants in the UK Biobank with a cancer diagnosis within 2 years of the baseline assessment were identified. Low MM was estimated by appendicular lean soft tissue (ALST) from bioelectrical impedance analysis derived fat-free mass. Malnutrition was determined using the Global Leadership in Malnutrition criteria. Sarcopenia was defined using the European Working Group on Sarcopenia in Older People criteria (version 2). All-cause mortality was determined from linked national mortality records. Cox-proportional hazards models were fitted to estimate the effect of low MM, malnutrition, and sarcopenia on all-cause mortality.
Results
In total, 4122 adults with cancer (59.8 ± 7.1 years; 49.2% male) were included. Prevalence of low MM (8.0% vs. 1.7%), malnutrition (11.2% vs. 6.2%), and sarcopenia (1.4% vs. 0.2%) was higher when MM was adjusted using ALST/BMI compared with ALST/height2, respectively. Low MM using ALST/BMI identified more cases in participants with obesity (low MM 56.3% vs. 0%; malnutrition 50% vs. 18.5%; sarcopenia 50% vs. 0%). During a median 11.2 (interquartile range: 10.2, 12.0) years of follow up, 901 (21.7%) of the 4122 participants died, and of these, 744 (82.6%) deaths were cancer-specific All conditions were associated with a higher hazard of mortality using either method of MM adjustment: low MM (ALST/height2: HR 1.9 [95% CI 1.3, 2.8], P = 0.001; ALST/BMI: HR 1.3 [95% CI 1.1, 1.7], P = 0.005; malnutrition (ALST/height2: HR 2.5 [95% CI 1.1, 1.7], P = 0.005; ALST/BMI: HR 1.3 [95% CI 1.1, 1.7], P = 0.005; sarcopenia (ALST/height2: HR 2.9 [95% CI 1.3, 6.5], P = 0.013; ALST/BMI: HR 1.6 [95% CI 1.0, 2.4], P = 0.037).
Conclusions
In adults with cancer, malnutrition was more common than low MM or sarcopenia, although all conditions were associated with a higher mortality risk, regardless of the method of adjusting for MM. In co
背景:低肌肉质量(MM)是癌症相关营养不良和肌肉减少症的常见组成部分，这些疾病都与死亡风险增加独立相关。本研究旨在(1)比较来自英国生物银行(UK Biobank)的成人癌症患者中低MM、营养不良和肌肉减少症的患病率及其与生存率的关系;(2)探索不同异速测量尺度(身高[m2]或体重指数[BMI])对低MM估计的影响。方法在基线评估后2年内被诊断为癌症的英国生物银行参与者被确定。通过生物电阻抗分析得出无脂质量，通过阑尾瘦软组织(ALST)估计低MM。营养不良是根据全球营养不良领导标准确定的。肌少症的定义采用欧洲老年人肌少症工作组标准(版本2)。全因死亡率根据相关的国家死亡率记录确定。拟合cox比例风险模型来估计低MM、营养不良和肌肉减少症对全因死亡率的影响。结果共4122例成人肿瘤患者(59.8±7.1岁;49.2%为男性)。当分别使用ALST/BMI与ALST/身高2调整MM时，低MM(8.0%对1.7%)、营养不良(11.2%对6.2%)和肌肉减少症(1.4%对0.2%)的患病率更高。低MM使用ALST/BMI识别出更多的肥胖病例(低MM 56.3%对0%;营养不良50% vs. 18.5%;肌肉减少50% vs. 0%)。在中位随访11.2年(四分位数间距:10.2,12.0)期间，4122名参与者中有901人(21.7%)死亡，其中744人(82.6%)死亡是癌症特异性死亡。使用MM调整的任何一种方法，所有疾病都与较高的死亡风险相关:低MM (ALST/height2: HR 1.9 [95% CI 1.3, 2.8]， P = 0.001;Alst / bmi: hr 1.3 [95% ci 1.1, 1.7]， p = 0.005;营养不良(ALST/ high2: HR 2.5 [95% CI 1.1, 1.7]， P = 0.005;Alst / bmi: hr 1.3 [95% ci 1.1, 1.7]， p = 0.005;肌肉减少症(ALST/height2: HR 2.9 [95% CI 1.3, 6.5]， P = 0.013;Alst / bmi: hr 1.6 [95% ci 1.0, 2.4]， p = 0.037]。结论:在成年癌症患者中，营养不良比低MM或肌肉减少症更常见，尽管所有情况都与更高的死亡风险相关，无论MM调整方法如何。相反，与身高调整相比，BMI调整低MM发现了更多的低MM、营养不良和肌肉减少症的病例，并且在肥胖的参与者中，这表明它是首选的调整。
{"title":"Low muscle mass, malnutrition, sarcopenia, and associations with survival in adults with cancer in the UK Biobank cohort","authors":"Nicole Kiss, Carla M. Prado, Robin M. Daly, Linda Denehy, Lara Edbrooke, Brenton J. Baguley, Steve F. Fraser, Abbas Khosravi, Gavin Abbott","doi":"10.1002/jcsm.13256","DOIUrl":"https://doi.org/10.1002/jcsm.13256","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Low muscle mass (MM) is a common component of cancer-related malnutrition and sarcopenia, conditions that are all independently associated with an increased risk of mortality. This study aimed to (1) compare the prevalence of low MM, malnutrition, and sarcopenia and their association with survival in adults with cancer from the UK Biobank and (2) explore the influence of different allometric scaling (height [m<sup>2</sup>] or body mass index [BMI]) on low MM estimates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Participants in the UK Biobank with a cancer diagnosis within 2 years of the baseline assessment were identified. Low MM was estimated by appendicular lean soft tissue (ALST) from bioelectrical impedance analysis derived fat-free mass. Malnutrition was determined using the Global Leadership in Malnutrition criteria. Sarcopenia was defined using the European Working Group on Sarcopenia in Older People criteria (version 2). All-cause mortality was determined from linked national mortality records. Cox-proportional hazards models were fitted to estimate the effect of low MM, malnutrition, and sarcopenia on all-cause mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In total, 4122 adults with cancer (59.8 ± 7.1 years; 49.2% male) were included. Prevalence of low MM (8.0% vs. 1.7%), malnutrition (11.2% vs. 6.2%), and sarcopenia (1.4% vs. 0.2%) was higher when MM was adjusted using ALST/BMI compared with ALST/height<sup>2</sup>, respectively. Low MM using ALST/BMI identified more cases in participants with obesity (low MM 56.3% vs. 0%; malnutrition 50% vs. 18.5%; sarcopenia 50% vs. 0%). During a median 11.2 (interquartile range: 10.2, 12.0) years of follow up, 901 (21.7%) of the 4122 participants died, and of these, 744 (82.6%) deaths were cancer-specific All conditions were associated with a higher hazard of mortality using either method of MM adjustment: low MM (ALST/height<sup>2</sup>: HR 1.9 [95% CI 1.3, 2.8], <i>P</i> = 0.001; ALST/BMI: HR 1.3 [95% CI 1.1, 1.7], <i>P</i> = 0.005; malnutrition (ALST/height<sup>2</sup>: HR 2.5 [95% CI 1.1, 1.7], <i>P</i> = 0.005; ALST/BMI: HR 1.3 [95% CI 1.1, 1.7], <i>P</i> = 0.005; sarcopenia (ALST/height<sup>2</sup>: HR 2.9 [95% CI 1.3, 6.5], <i>P</i> = 0.013; ALST/BMI: HR 1.6 [95% CI 1.0, 2.4], <i>P</i> = 0.037).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In adults with cancer, malnutrition was more common than low MM or sarcopenia, although all conditions were associated with a higher mortality risk, regardless of the method of adjusting for MM. In co","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1775-1788"},"PeriodicalIF":8.9,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5777908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chao Xia, Yonghui Wang, Tianyuan Jiang, Yan Hu, Yang Chen, Xinrun Ma, Xuemei Zhang, Yanhong Gao
Background
It has been observed that Slo1 knockout mice have reduced motor function, and people with certain Slo1 mutations have movement problems, but there is no answer whether the movement disorder is caused by the loss of Slo1 in the nervous system, or skeletal muscle, or both. Here, to ascertain in which tissues Slo1 functions to regulate motor function and offer deeper insight in treating related movement disorder, we generated skeletal muscle-specific Slo1 knockout mice, studied the functional changes in Slo1-deficient skeletal muscle and explored the underlying mechanism.
Methods
We used skeletal muscle-specific Slo1 knockout mice (Myf5-Cre; Slo1flox/flox mice, called CKO) as in vivo models to examine the role of Slo1 in muscle growth and muscle regeneration. The forelimb grip strength test was used to assess skeletal muscle function and treadmill exhaustion test was used to test whole-body endurance. Mouse primary myoblasts derived from CKO (myoblast/CKO) mice were used to extend the findings to in vitro effects on myoblast differentiation and fusion. Quantitative real-time PCR, western blot and immunofluorescence approaches were used to analyse Slo1 expression during myoblast differentiation and muscle regeneration. To investigate the involvement of genes in the regulation of muscle dysfunction induced by Slo1 deletion, RNA-seq analysis was performed in primary myoblasts. Immunoprecipitation and mass spectrometry were used to identify the protein interacting with Slo1. A dual-luciferase reporter assay was used to identify whether Slo1 deletion affects NFAT activity.
Results
We found that the body weight and size of CKO mice were not significantly different from those of Slo1flox/flox mice (called WT). Deficiency of Slo1 in muscles leads to reduced endurance (~30% reduction, P < 0.05) and strength (~30% reduction, P < 0.001). Although there was no difference in the general morphology of the muscles, electron microscopy revealed a considerable reduction in the content of mitochondria in the soleus muscle (~40% reduction, P < 0.01). We found that Slo1 was expressed mainly on the cell membrane and showed higher expression in slow-twitch fibres. Slo1 protein expression is progressively reduced during muscle postnatal development and regeneration after injury, and the expression is strongly reduced during myoblast differentiation. Slo1 deletion impaired myoblast differentiation and slow-twitch fibre formation. Mechanistically, RNA-seq analysis showed that Slo1 influences the expression of g
{"title":"Slo1 deficiency impaired skeletal muscle regeneration and slow-twitch fibre formation","authors":"Chao Xia, Yonghui Wang, Tianyuan Jiang, Yan Hu, Yang Chen, Xinrun Ma, Xuemei Zhang, Yanhong Gao","doi":"10.1002/jcsm.13253","DOIUrl":"https://doi.org/10.1002/jcsm.13253","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>It has been observed that Slo1 knockout mice have reduced motor function, and people with certain Slo1 mutations have movement problems, but there is no answer whether the movement disorder is caused by the loss of Slo1 in the nervous system, or skeletal muscle, or both. Here, to ascertain in which tissues Slo1 functions to regulate motor function and offer deeper insight in treating related movement disorder, we generated skeletal muscle-specific Slo1 knockout mice, studied the functional changes in Slo1-deficient skeletal muscle and explored the underlying mechanism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We used skeletal muscle-specific Slo1 knockout mice (Myf5-Cre; Slo1<sup>flox/flox</sup> mice, called CKO) as in vivo models to examine the role of Slo1 in muscle growth and muscle regeneration. The forelimb grip strength test was used to assess skeletal muscle function and treadmill exhaustion test was used to test whole-body endurance. Mouse primary myoblasts derived from CKO (myoblast/CKO) mice were used to extend the findings to in vitro effects on myoblast differentiation and fusion. Quantitative real-time PCR, western blot and immunofluorescence approaches were used to analyse Slo1 expression during myoblast differentiation and muscle regeneration. To investigate the involvement of genes in the regulation of muscle dysfunction induced by Slo1 deletion, RNA-seq analysis was performed in primary myoblasts. Immunoprecipitation and mass spectrometry were used to identify the protein interacting with Slo1. A dual-luciferase reporter assay was used to identify whether Slo1 deletion affects NFAT activity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that the body weight and size of CKO mice were not significantly different from those of Slo1<sup>flox/flox</sup> mice (called WT). Deficiency of Slo1 in muscles leads to reduced endurance (~30% reduction, <i>P</i> < 0.05) and strength (~30% reduction, <i>P</i> < 0.001). Although there was no difference in the general morphology of the muscles, electron microscopy revealed a considerable reduction in the content of mitochondria in the soleus muscle (~40% reduction, <i>P</i> < 0.01). We found that Slo1 was expressed mainly on the cell membrane and showed higher expression in slow-twitch fibres. Slo1 protein expression is progressively reduced during muscle postnatal development and regeneration after injury, and the expression is strongly reduced during myoblast differentiation. Slo1 deletion impaired myoblast differentiation and slow-twitch fibre formation. Mechanistically, RNA-seq analysis showed that Slo1 influences the expression of g","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1737-1752"},"PeriodicalIF":8.9,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13253","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5777911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lisa Bagnall, Oliver Grundmann, Marilyn G. Teolis, Saun-Joo L. Yoon
Cancer cachexia is a severe multifactorial syndrome1 that affects up to 80% of patients with advanced cancer, causing death in 20–80% with no effective treatments.2, 3 It causes multi-organ alteration and loss of skeletal and cardiac (myocardium) muscle mass.4, 5 Cardiac muscle wasting may result from cardiac protein loss associated with increased oxygen consumption and energy expenditure, resulting in cardiac insufficiency.5 It is hypothesized that significant tissue inflammation and oxidative stress during cancer progression cause cardiac wasting-associated cardiomyopathy, such as a thinned ventricular wall, local tissue hypoxia and arrhythmias.6 This review provided available evidence of cancer-induced cardiac cachexia in human and non-human models by examining biomarkers and the contributing factors to the development and progression of cardiac cachexia. Investigation of the potential biomarkers affecting cardiac muscle wasting is essential for improving patient outcomes.
Our knowledge about the causes of cardiac cachexia in cancer remains limited and the possible mechanisms have only been explored in animal studies to date. A better understanding of the pathophysiology of cardiac cachexia may help to determine if targeted therapies can effectively block the upregulation of various genes and cytokines that initiate and facilitate cancer-induced cardiac cachexia. Understanding the distinct nature of cancer-related cardiac cachexia and what distinguishes it from other causes may also lead to finding targeted, effective treatments. Treating cardiac cachexia early and before clinical changes are noted may improve overall cardiac function and lead to better patient outcomes.
{"title":"Biomarkers and mechanisms associated with cancer-induced cardiac cachexia: A systematic review","authors":"Lisa Bagnall, Oliver Grundmann, Marilyn G. Teolis, Saun-Joo L. Yoon","doi":"10.1002/jcsm.13267","DOIUrl":"https://doi.org/10.1002/jcsm.13267","url":null,"abstract":"<p>Cancer cachexia is a severe multifactorial syndrome<span><sup>1</sup></span> that affects up to 80% of patients with advanced cancer, causing death in 20–80% with no effective treatments.<span><sup>2, 3</sup></span> It causes multi-organ alteration and loss of skeletal and cardiac (myocardium) muscle mass.<span><sup>4, 5</sup></span> Cardiac muscle wasting may result from cardiac protein loss associated with increased oxygen consumption and energy expenditure, resulting in cardiac insufficiency.<span><sup>5</sup></span> It is hypothesized that significant tissue inflammation and oxidative stress during cancer progression cause cardiac wasting-associated cardiomyopathy, such as a thinned ventricular wall, local tissue hypoxia and arrhythmias.<span><sup>6</sup></span> This review provided available evidence of cancer-induced cardiac cachexia in human and non-human models by examining biomarkers and the contributing factors to the development and progression of cardiac cachexia. Investigation of the potential biomarkers affecting cardiac muscle wasting is essential for improving patient outcomes.</p><p>Our knowledge about the causes of cardiac cachexia in cancer remains limited and the possible mechanisms have only been explored in animal studies to date. A better understanding of the pathophysiology of cardiac cachexia may help to determine if targeted therapies can effectively block the upregulation of various genes and cytokines that initiate and facilitate cancer-induced cardiac cachexia. Understanding the distinct nature of cancer-related cardiac cachexia and what distinguishes it from other causes may also lead to finding targeted, effective treatments. Treating cardiac cachexia early and before clinical changes are noted may improve overall cardiac function and lead to better patient outcomes.</p><p>The authors have no conflicts of interest.</p>","PeriodicalId":186,"journal":{"name":"Journal of Cachexia, Sarcopenia and Muscle","volume":"14 4","pages":"1900-1905"},"PeriodicalIF":8.9,"publicationDate":"2023-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.13267","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"5656013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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