Increased levels of inflammation in cancer patients and survivors can make them more prone to muscle wasting and sarcopenia. Diet can be an appropriate treatment for alleviating patient complications. Therefore, this study was performed to determine the association between sarcopenia and its components with the dietary inflammatory index (DII) among breast cancer survivors.

A total of 223 female breast cancer survivors were included in this research at the Cancer Prevention Research Center of Seyyed Al-Shohada Hospital and the Iranian Cancer Control Charity Institute (MACSA). Forty-three items of dietary inflammatory index (DII) were extracted from the Food Frequency Questionnaire. Sarcopenia detection was performed according to the Asian criteria. The linear and binary logistic regression was used to assess the association between sarcopenia and its components with DII.

Participants in the highest DII quartile had significantly elevated risk of impaired hand grip strength and calf circumference in both crude and adjusted models. Moreover, individuals consuming a more pro-inflammatory diet displayed a greater risk of abnormal appendicular skeletal muscle index in the crude model. After controlling for potential confounders, participants in the top quartile of DII had a 2.992-fold greater risk of possible sarcopenia than those in the bottom quartile (P value = 0.035). In addition, a decreasing linear trend was observed between higher DII score and 0.059 and 0.349- units lower in appendicular skeletal muscle mass index and hand grip strength variables in the crude Model (P-value < 0.05).

Diets with more pro-inflammatory features might be associated with increased risk of possible sarcopenia, as well as its components especially muscle mass and strength in women recovering from breast cancer.

This study investigates the impact of neoadjuvant therapy (NT) on body composition and its correlation with long-term survival and other clinical outcomes in patients with advanced gastric cancer. We utilized Computed Tomography (CT) scans to measure body composition before and after NT, including Subcutaneous Adipose Tissue Index (SATI), Visceral Adipose Tissue Index (VATI), Skeletal Muscle Index (SMI), and Muscle Density (MA). We then analyzed the decrease in body composition in relation to tumor regression, inflammatory markers, nutritional scores, and long-term survival. Our findings reveal a negative correlation between the decrease in SATI and VATI after NT, and both tumor regression and nutritional score. Notably, patients who experienced a significant loss in SATI or VATI post-NT had shorter Recurrence-Free Survival (RFS) and Overall Survival (OS). Additionally, significant loss in SATI and VATI emerged as an independent risk factor for both RFS and OS. In conclusion, our study convincingly demonstrates that in patients with advanced gastric cancer, SATI and VATI decreases after NT and is negatively associated with tumor regression and nutritional score. A significant loss in SATI and VATI is a risk factor for shorter RFS and OS, thereby underscoring the importance of maintaining body composition during NT.

We aimed to identify the impact of muscle mass on locally advanced oesophageal cancer (LAEC) in elderly patients receiving neoadjuvant chemoradiation therapy (NACRT).

We reviewed the medical records of 345 patients diagnosed with LAEC who underwent NACRT and surgery. Physical variables, including height, weight, skeletal muscle mass, and laboratory values, were obtained before and after NACRT. Body mass index (BMI, kg/m2), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and prognostic nutritional index (PNI) were calculated as height/(weight)2, ANC/ALC, platelet count/ALC, and (10 × albumin + 0.05 × ALC), respectively. The cutoff for low muscle mass was 43.0 cm2/m2 for BMI below 25 kg/m2 and 53.0 cm2/m2 for BMI 25 kg/m2 or higher. The skeletal muscle index (SMI) was defined as skeletal muscle area/(height)2 (cm2/m2). The ΔSMI (%/50 days) was defined as (SMI after NACRT - SMI before NACRT)/interval (days) × 50 (days) to compare changes over the same period. The excessive muscle loss (EML) group was defined as patients with ΔSMI ≤-10% following NACRT. An elderly patient was defined as aged ≥65 years. The primary outcome measure was overall survival (OS).

During a median follow-up of 32.8 months (range, 2.0-176.2), 192 patients died, with a median OS of 50.2 months. Elderly patients did not show inferior OS (young vs. elderly, 57.7% vs. 54.0% at 3 years, P = 0.247). 71.0% and 87.2% of all patients had low muscle mass before and after NACRT, respectively, which was not associated with OS (P = 0.270 and P = 0.509, respectively). Inflammatory (NLR and PLR) and nutritional index (PNI) values or their changes did not correlate with OS. However, the EML group had worse OS (41.6% vs. 63.2% at 3 years, P < 0.0001). In the multivariate analysis, EML was also a significant prognostic factor for OS. In the subgroup analysis by age, EML was a strong prognostic factor for OS in the elderly group. The 3-year OS was 36.8% in the EML group and 64.9% in the non-EML group (P < 0.0001) in elderly patients, and 47.4% and 62.1% (P = 0.063) in the young patients. In multivariate analysis of each subgroup, EML remained prognostic only in the elderly group (P = 0.008).

EML may be strongly associated with a deteriorated OS in elderly patients undergoing NACRT, followed by surgery for LAEC. The strategies for decreasing muscle loss in these patients should be investigated.

Sarcopenia, marked by a reduction in skeletal muscle mass and function, is a condition that can manifest in elderly patients with cancer and has been recognized as a possible adverse factor affecting the survival of individuals diagnosed with malignant tumors. This systematic review and meta-analysis aimed to examine the prevalence of sarcopenia in individuals with cholangiocarcinoma while concurrently investigating the potential correlations between the presence of sarcopenia and various critical factors, including survival outcomes and postoperative complications.

A comprehensive search was conducted across multiple databases, including EMBASE, PubMed, Web of Science, Cochrane Library, and CNKI, employing keywords such as sarcopenia, cholangiocarcinoma, and prognosis. This research explored the prognostic value of sarcopenia on the survival of cholangiocarcinoma. The findings of this meta-analysis were presented using forest plots and a summarized effects model. The Newcastle-Ottawa Scale (NOS) was employed to evaluate the quality of the studies included in the analysis.

A total of 33 articles from five databases were in in the quantitative analysis. A comprehensive meta-analysis revealed that the overall prevalence of sarcopenia among individuals diagnosed with cholangiocarcinoma was43%. Moreover, the analysis revealed a significant and noteworthy correlation between sarcopenia and key clinical parameters such as overall survival (OS), Recurrence-Free Survival (RFS), and Disease-Free Survival (DFS) in patients with cholangiocarcinoma. Subgroup analysis revealed that, when categorized by various ethnicities, diagnostic techniques, and tumor locations, sarcopenia consistently retained its status as a negative predictive factor. Furthermore, sarcopenia has emerged as a risk factor for postoperative complications. All included studies had an NOS score greater than 5, indicating a high quality of evidence.

The results suggest that sarcopenia is significantly related to survival outcomes and postoperative complications in cholangiocarcinoma. Appropriate diagnosis and treatment of sarcopenia should be implemented to improve the prognosis of individuals with cholangiocarcinoma.

https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023479866, identifier CRD42023479866.

The development and progression of gastric cancer (GC) are closely linked to the nutritional status of patients. Although immunotherapy has been demonstrated to be clinically effective, the relationships of sarcopenia and myosteatosis with the use of immune checkpoint inhibitors (ICIs) in patients with gastric cancer remain to be characterized.

To assess the effects of sarcopenia and myosteatosis on the clinical outcomes of patients with GC undergoing treatment with an ICI.

We performed a retrospective study of patients who were undergoing immunotherapy for GC. For the evaluation of sarcopenia, the optimal cut-off value for the skeletal muscle index was established using receiver operating characteristic analysis of data obtained from pre-treatment computed tomography images at the L3 vertebral level. Myosteatosis was defined using the mean skeletal muscle density (SMD), with a threshold value of < 41 Hounsfield units (HU) for patients with a body mass index (BMI) < 25 kg/m² and < 33 HU for those with a BMI ≥ 25 kg/m². The log-rank test was used to compare progression-free survival (PFS) and overall survival (OS), and a Cox proportional hazard model was used to identify prognostic factors. Nomograms were developed to predict the PFS and OS of patients on the basis of the results of multivariate analyses.

We studied 115 patients who were undergoing ICI therapy for GC, of whom 27.4% had sarcopenia and 29.8% had myosteatosis. Patients with sarcopenia or myosteatosis had significantly shorter PFS and OS than those without these conditions. Furthermore, both sarcopenia and myosteatosis were found to be independent predictors of PFS and OS in patients with GC administering an ICI. The prediction models created for PFS and OS were associated with C-indexes of 0.758 and 0.781, respectively.

The presence of sarcopenia or myosteatosis is a reliable predictor of the clinical outcomes of patients with GC who are undergoing treatment with an ICI.

Gastric cancer (GC) is the fifth most common cancer and the third leading cause of cancer death worldwide, which seriously endangers human health. A number of studies have shown that sarcopenia occurs more frequently in patients with gastric cancer than in the general population and can significantly affect the disease status and survival of patients, which is of great significance in predicting the prognosis of gastric cancer. Patients with gastric cancer may suffer sarcopenia no matter before or after surgery, and the pathogenesis is complex. Abnormal nutrient metabolism and reduced exercise are the leading causes. In addition, surgical treatment and chemotherapy for gastric cancer might participate in the physiological and pathological mechanism of sarcopenia. Generally speaking, exercise and nutritional therapy are the main prevention and treatment methods for sarcopenia. But more prospective evidence is needed to establish reasonable interventions, and other drug treatments are in their infancy. For the diagnostic criteria of sarcopenia, the cut-off values of the skeletal muscle mass index obtained from CT images vary widely and need to be standardized and unified. We also need to explore simple predictors to facilitate sarcopenia risk assessment. More research is needed to formulate more appropriate treatments for gastric cancer patients with sarcopenia.

In patients with cancer, sarcopenia is associated with treatment related complications, treatment cessation, poor quality of life and reduced overall survival. Despite this, there is limited knowledge about changes in skeletal muscle mass during chemotherapy. The aim of this systematic review and meta-analysis was to investigate the change of skeletal muscle mass and sarcopenia during chemotherapy treatment among patients with lung cancer.

A systematic literature search was conducted in three databases, PubMed, EMBASE and Web of Science. Observational studies with patients with lung cancer were eligible for inclusion if skeletal muscle mass was measured before and after receiving chemotherapy treatment.

Ten cohort studies with a total of 867 participants met the inclusion criteria. During 5.2 ± 2.9 months of chemotherapy treatment, patients with lung cancer experienced a significant loss of skeletal muscle mass with a standardized mean difference (SMD) of: -0.25 (95% CI -0.47 to -0.03). The pretreatment prevalence of sarcopenia varied across studies from 35% to 74%. Only one study reported prevalence of sarcopenia both before and after chemotherapy treatment with an increase from 35% to 59%.

The present data demonstrate a marked loss of skeletal muscle mass in patients with lung cancer undergoing chemotherapy treatment, as well as a high prevalence of sarcopenia. As sarcopenia is associated with poor clinical outcomes, it seems important to include and use assessments of skeletal muscle mass in clinical practice to identify patients in need for interventions. Moreover, interventional studies to hinder development of sarcopenia are needed.

Loss of muscle mass is associated with negative clinical outcome in breast cancer (BC) patients. Therefore, the aim of the study is to evaluate if there is pectoralis muscle area (PMA) depletion, reflecting loss of muscle mass, in breast cancer patients of reproductive age (≤ 45 years) undergoing neoadjuvant chemotherapy (NAC) and to correlate PMA with clinical and histopathological data.

This monocentric study, approved by our institutional review board, enrolled a total of 52 consecutive patients (mean age 37 ± 4.96 years) with histologically proven primary breast cancer between January 2019 and September 2021, treated with NAC and in whom tumor response and PMA were assessed with breast MRI. Two radiologists calculated PMA before and after NAC independently and blindly on axial 3D FLASH pre-contrast T1-weighted images. Wilcoxon-Mann-Whitney U test compared median values and percentage changes of pectoralis muscle area at the beginning and at the end of NAC (158 ± 25.5 days). Multivariate regression analysis on ΔPMA (difference between PMA pre-NAC and PMA post-NAC) was done according to clinical and histopathological data. Inter-reader and intra-reader agreement was estimated with K statistics.

Pre-NAC PMA mean value was larger than post-NAC PMA mean value (9.6 ± 2.6 cm2 vs. 8.7 ± 2.2 cm2, p < 0.001, delta value 1.41). According to the RECIST criteria, no significant differences between complete and partial response were found. Multivariate regression analysis did not show any significant relationships between ΔPMA and age, time between MRI examinations, estrogen and progesterone receptor status, human epidermal growth factor receptor 2 status, Ki-67 expression, lymph node involvement, RECIST criteria, histological type, and different regimes of NAC. Inter-reader (k = 0.74) and intra-reader agreement (0.67 and 0.73) in PMA assessment was good.

PMA variation in BC young patients, directly estimated on breast MRI, could be a potential tool to monitor body composition during NAC with potential implications in improving outcome.

To evaluate the correlation between sarcopenia and inflammation- and nutrition-based markers in metastatic colorectal cancer (mCRC) patients.

Age, body mass index (BMI), neutrophil/lymphocyte ratio (NLR), modified Glasgow prognostic score (mGPS), prognostic nutrition index (PNI), cachexia index (CIn), skeletal muscle index (SMI), controlling nutritional status (CONUT) score, and geriatric nutritional risk index (GNRI) were evaluated in 185 patients. Ideal cut-off values for the GNRI score were determined with the ROC curve analysis, and the patients were divided into two groups as low and high GNRI. Sarcopenia was diagnosed using CT scanning, the gold standard method. Univariate and multivariate Cox proportional hazard analyses were done based on the above-listed parameters to assess the correlation between sarcopenia and changes in immuno-nutrition and inflammatory response. Kaplan-Meier analysis was also done to evaluate survival.

Univariate analysis of the 185 patients based on the EGWSOP 2018 threshold values showed correlation between the presence of sarcopenia and male gender, diagnosed colon cancer, history of metastasectomy, BMI < 24, high mGPS score, PNI score ≥ 45, high CONUT score, and low GNRI score (p < 0.05). In multivariate analysis, low GNRI (HR: 2.40; 95% CI: 1.03-5.544; p = 0.040), and high-CONUT scores (HR: 2.01; 95% CI: 1.06-3.73; p = 0.029) were identified as independent prognostic factors for the presence of sarcopenia.

GNRI and CONUT scores are elementary and practical predictors for sarcopenia, a condition which is associated with poor outcomes in mCRC patients.

Sarcopenia is almost constantly observed in patients with cirrhosis and hepatocellular carcinoma (HCC).

Chronic liver disease represents a unique pathophysiological scenario in which sarcopenia develops and all factors involved in the pathogenesis should be taken into account for an appropriate management of the disease. No properly designed intervention studies on this topic are available and, thus, no effective strategies have been developed for clinical practice. Apart from any targeted intervention, treatment, and optimization of liver disease is crucial.

In patients with cirrhosis and HCC, nutritional support to maintain and restore nutrition status, a targeted use of branched-chain amino acids and a guided physical exercise, should all be an integral part of the multidimensional assessment and tailored interventions.

In cancer patients, chemotherapeutic medication induces aberrant ROS (reactive oxygen species) accumulation in skeletal muscles, resulting in myofiber degradation, muscle weakness, and even cachexia, which further leads to poor therapeutic outcomes. Acting as an antioxidant, taurine is extensively used to accelerate postexercise muscle recovery in athletes. The antioxidant effects of taurine have been shown in mature myotubes and myofibers but not yet in myoblasts, the myotube precursor. The proliferation and differentiation ability of myoblasts play a very important role in myofiber repair and regeneration, which is usually impaired during chemotherapeutics in cancer patients as well. Here, we explored the effects of taurine supplementation on C2C12 myoblasts exposed to cisplatin-induced ROS. We found that cisplatin treatment led to dramatically decreased cell viability; accumulated ROS level; down-regulated expressions of MyoD1 (myoblast determination protein 1), myogenin, and MHC (myosin heavy chain); and impaired myotube differentiation in myoblasts. Significantly, taurine supplementation protected myoblasts against cisplatin-induced cell viability decrease, promoted cellular ROS clearance, and, most importantly, preserved the expressions of MyoD1, myogenin, and MHC as well as myotube differentiation ability. We further conducted NMR-based metabolomic analysis to clarify the underlying molecular mechanisms. We identified 14 characteristic metabolites primarily responsible for the discrimination of metabolic profiles between cisplatin-treated cells and normal counterparts, including increased levels of BCAAs (branched-chain amino acids: leucine and isoleucine), alanine, glycine, threonine, glucose, ADP (adenosine diphosphate), phenylalanine, and PC (O-phosphocholine), and decreased levels of lysine, β-alanine, choline, GPC (sn-glycero-3-phosphocholine), and myo-inositol. Evidently, taurine supplementation partially reversed the changing trends of several metabolites (isoleucine, threonine, glycine, PC, β-alanine, lysine, and myo-inositol). Furthermore, taurine supplementation promoted the proliferation and myotube differentiation of myoblasts by alleviating cellular catabolism, facilitating GSH (reduced glutathione) biosynthesis, improving glucose utilization and TCA (tricarboxylic acid) cycle anaplerosis, and stabilizing cellular membranes. Our results demonstrated the protective effects of taurine on cisplatin-impaired myoblasts and elucidated the mechanistic rationale for the use of taurine to ameliorate muscle toxicity in clinical chemotherapy cancer patients.

Although the chemotherapy-induced sarcopenia has some explanatory presence in clinical practice, the mechanisms underlying this phenomenon have not been clearly distinguished in patients with cancer. Therefore, we aimed with this study to investigate the role of inflammation by examining the inflammatory markers in the physiopathology of adjuvant chemotherapy-induced sarcopenia in patients with gastrointestinal tract cancer.

To detect the presence of sarcopenia, patients' body composition measurements were assessed using the BIA, and their muscular strength was assessed with a handgrip dynamometer in both pre- and post-adjuvant chemotherapy. At the same time, we examined the baseline and post-adjuvant chemotherapy anthropometric measurements and inflammatory markers in serum (Hs-CRP, IL8, and TNF-α). Patients were divided in three groups. Group 1 consisted of patients who presented post-treatment sarcopenia although they did not have it prior to the treatment, group 2 included the patients who had no pre- or post-treatment sarcopenia, and group 3 was comprised of patients who presented pre-treatment sarcopenia. Each group included 30 patients.

A total of 90 patients were included in the study. Fifty-one of them were female patients. Median age was 60.5 (range 27-83). The patients consisted of cases with colorectal and gastric cancers. In group 1, Wilcoxon signed-rank test revealed a significant difference between scores of IL-8 (pg/mL), TNF-α (pg/mL) and Hs-CRP (mg/dL) given for the post-chemotherapy compared with the pre-chemotherapy ((Z 3.61, p < 0.001), (Z 3.254, p = 0.001), (Z 3.319, p = 0.001)). The post-chemotherapy median scores of IL-8 (pg/mL), TNF-α (pg/mL), and Hs-CRP were 76.31, 7.34, and 1.55, respectively, which remained on the levels of 12.25, 1.6, and 0.51 for the pre-chemotherapy. For group 2, a Wilcoxon signed-rank test indicated no significant difference between scores of the same markers given for the post-chemotherapy compared with the pre-chemotherapy. In all patients (including groups 1, 2, and 3), a comparison of the patients with pre-treatment sarcopenia (n = 30) and non-sarcopenic patients (n = 60) in terms of baseline IL-8, TNF-α, and Hs-CRP mean levels, IL-8 and Hs-CRP were found to be statistically different (146.02 (SD 311.96) vs. 47.24 (SD 66.3) (p = 0.009), 3.91 (SD 4.26) vs. 0.75 (SD 1.08) (p < 0.001), respectively).

The present prospective observational study suggested an association of chemotherapy-induced sarcopenia with inflammatory markers Hs-CRP, IL8, and TNF-α. Inflammation may play a role in chemotherapy-induced sarcopenia in newly diagnosed non-metastatic patients.

Sarcopenia is being consistently recognized as a condition not only associated with the presence of a malignancy but also induced by the oncologic therapies. Due to its negative impact on tolerance to chemotherapy and final outcome in both medical and surgical cancer patients, sarcopenia should be always considered and prevented, and, if recognized, should be appropriately treated. A CT scan at the level of the third lumbar vertebra, using an appropriate software, is the more common and easily available way to diagnose sarcopenia. It is now acknowledged that mechanisms involved in iatrogenic sarcopenia are several and depending on the type of molecule included in the regimen of chemotherapy, different pharmacologic antidotes will be required in the future. However, progression of the disease and the associated malnutrition per se are able to progressively erode the muscle mass and since sarcopenia is the hallmark of cachexia, the therapeutic approach to chemotherapy-induced sarcopenia parallels that of cachexia. This approach mainly relies on those strategies which are able to increase the lean body mass and include the use of anabolic/anti-inflammatory agents, nutritional interventions, physical exercise and, even better, a combination of different therapies. There are some phase II studies and some small controlled randomized trials which have validated these treatments using single agents or combined multimodal approaches. While these approaches may require the cooperation of some specialists (nutritionists with a specific knowledge on pathophysiology of catabolic states, accredited exercise physiologists and physiotherapists), the oncologist too should directly enter these issues to coordinate the choice and priority of the treatments. Who better than the oncologist knows the natural history of the disease, its evolution, and the probability of tolerance and response to the oncologic therapy? Only the oncologist knows when it is essential to potentiate any effort to better achieve a control of the disease, using all the available armamentarium, and when the condition is too advanced and hence requires a more palliative than supporting care. The oncologist also knows when to expect a gastrointestinal toxicity (mucositis, nausea, vomiting, and diarrhea) and hence it is more convenient using a parenteral than an enteral nutritional intervention or, on the contrary, when patient is suitable for discharge from hospital and oral supplements should be promptly tested for compliance and then prescribed. When patients are at high risk for malnutrition or if, regardless of their nutritional status, they are candidate to aggressive and potentially toxic treatments, they should undergo a jointed evaluation by the oncologist and the nutritionist and physical therapist to assess together a combined approach. In conclusion, the treatment of both cancer- or chemotherapy-related sarcopenia represents a challenge for the modern oncologist who must be able to coordinate a new panel of specialists with the same skill necessary to decide the priority of different oncologic treatments within a complex multidisciplinary context.

Cancer is a catabolic inflammatory disease that causes patients to often experience weight loss, or even cachexia in severe cases. Undernourishment in patients with cancer impairs the quality of life and therapeutic response, further leading to poor prognosis. Active and frequent nutritional screening and assessment using valid tools are important for fast and appropriate nutritional intervention. Additionally, a suitable individualized nutritional intervention strategy should be established based on the nutritional assessment result. In general, nutritional intervention begins with nutritional counseling of patients diagnosed with cancer, and a well-planned nutritional counseling improves the treatment adherence and nutritional status. When planning nutritional supplementation for cancer patients, specific nutrients, including amino acids and fatty acids, should be considered. However, there has been no consistent result showing that any particular nutrient significantly improves the prognosis of cancer patients. Hence, continuous attention from clinical physicians is needed to plan nutritional improvement in patients with cancer.