Sarcopenia diagnosed using masseter muscle area predictive of early mortality following severe traumatic brain injury.
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ABSTRACT:
SUBMITTER: Uhlich R
PROVIDER: S-EPMC6199947 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundElderly patients with glioblastoma (GBM) have a worse prognosis than do younger patients. The present study aimed to identify the patient, treatment, and imaging features, including measures of sarcopenia, associated with worse survival and 90-day postoperative mortality for elderly patients with GBM.MethodsA single-center retrospective study was conducted of patients aged ≥79 years at surgery who had undergone biopsy or resection of a World Health Organization grade IV GBM at the initial diagnosis. Imaging features of sarcopenia were collected, including the masseter and temporalis muscle diameters. Multivariate analyses were performed to identify factors associated with survival and 30-day complications.ResultsThe cohort included 110 patients with a mean age of 82.8 years at surgery and a median preoperative Karnofsky performance scale score of 80. The majority of patients underwent a surgical resection (66.4%) while a minority underwent biopsy (33.6%). Adjuvant chemo- and/or radiation therapy were used in 72.5% of the cohort. On multivariate analysis, age (hazard ratio [HR], 7.97; 95% confidence interval [CI], 1.63-36.3), adjuvant therapy (RT or TMZ vs. none: HR, 0.12; 95% CI, 0.05-0.3; RT plus TMZ vs. none: HR, 0.05; 95% CI, 0.02-0.14), surgical resection (HR, 0.46; 95% CI, 0.24-0.9), multifocality (HR, 2.7; 95% CI, 1.14-6.4), and masseter diameter (HR, 0.12; 95% CI, 0.02-0.78) were associated with survival. Masseter diameter was the only factor associated with 90-day mortality after surgical resection (P = 0.044).ConclusionsGBM patients over the age of 79 have acceptable outcomes after resection, followed by adjuvant chemotherapy and RT. In addition to the treatment factors that predicted for survival, a decreased masseter diameter on preoperative imaging, a marker of sarcopenia, was associated with shorter overall survival and 90-day mortality after surgical resection.
| S-EPMC9284942 | biostudies-literature
Project description:ImportanceOlder adults are disproportionately affected by trauma and accounted for 47% of trauma fatalities in 2016. In many populations and disease processes, described risk factors for poor clinical outcomes include sarcopenia and brain atrophy, but these remain to be fully characterized in older trauma patients. Sarcopenia and brain atrophy may be opportunistically evaluated via head computed tomography, which is often performed during the initial trauma evaluation.ObjectiveTo investigate the association of masseter sarcopenia and brain atrophy with 1-year mortality among trauma patients older than 65 years by using opportunistic computed tomography imaging.Design, setting, and participantsThis retrospective cohort study was conducted in a level 1 trauma center from January 1, 2011, to December 31, 2014, with a 1-year follow-up to assess mortality. Washington state residents 65 years or older who were admitted to the trauma intensive care unit with a head Abbreviated Injury Scale score of less than 3 were eligible. Patients with incomplete data and death within 1 day of admission were excluded. Data analysis was completed from June 2017 to October 2018.ExposuresMasseter muscle cross-sectional area and brain atrophy index were measured using a standard clinical Picture Archiving and Communication System application to assess for sarcopenia and brain atrophy, respectively.Main outcomes and measuresPrimary outcome was 1-year mortality. Secondary outcomes were discharge disposition and 30-day mortality.ResultsThe study cohort included 327 patients; 72 (22.0%) had sarcopenia only, 71 (21.7%) had brain atrophy only, 92 (28.1%) had both, and 92 (28.1%) had neither. The mean (SD) age was 77.8 (8.6) years, and 159 patients (48.6%) were women. After adjustment for age, comorbidity, complications, and injury characteristics, masseter sarcopenia and brain atrophy were both independently and cumulatively associated with mortality (masseter muscle cross-sectional area per SD less than the mean: hazard ratio, 2.0 [95% CI, 1.2-3.1]; P = .005; brain atrophy index per SD greater than the mean: hazard ratio, 2.0 [95% CI, 1.1-3.5]; P = .02).Conclusions and relevanceMasseter muscle sarcopenia and brain atrophy were independently and cumulatively associated with 1-year mortality in older trauma patients after adjustment for other clinical factors. These radiologic indicators are easily measured opportunistically through standard imaging software. The results can potentially guide conversations regarding prognosis and interventions with patients and their families.
| S-EPMC6506900 | biostudies-literature
Project description:BackgroundChronic pain in masticatory muscles is a major medical problem. Although mechanisms underlying persistent pain in masticatory muscles are not fully understood, sensitization of nociceptive primary afferents following muscle inflammation or injury contributes to muscle hyperalgesia. It is well known that craniofacial muscle injury or inflammation induces regulation of multiple genes in trigeminal ganglia, which is associated with muscle hyperalgesia. However, overall transcriptional profiles within trigeminal ganglia following masseter inflammation have not yet been determined. In the present study, we performed RNA sequencing assay in rat trigeminal ganglia to identify transcriptome profiles of genes relevant to hyperalgesia following inflammation of the rat masseter muscle.ResultsMasseter inflammation differentially regulated >3500 genes in trigeminal ganglia. Predominant biological pathways were predicted to be related with activation of resident non-neuronal cells within trigeminal ganglia or recruitment of immune cells. To focus our analysis on the genes more relevant to nociceptors, we selected genes implicated in pain mechanisms, genes enriched in small- to medium-sized sensory neurons, and genes enriched in TRPV1-lineage nociceptors. Among the 2320 candidate genes, 622 genes showed differential expression following masseter inflammation. When the analysis was limited to these candidate genes, pathways related with G protein-coupled signaling and synaptic plasticity were predicted to be enriched. Inspection of individual gene expression changes confirmed the transcriptional changes of multiple nociceptor genes associated with masseter hyperalgesia (e.g., Trpv1, Trpa1, P2rx3, Tac1, and Bdnf) and also suggested a number of novel probable contributors (e.g., Piezo2, Tmem100, and Hdac9).ConclusionThese findings should further advance our understanding of peripheral mechanisms involved in persistent craniofacial muscle pain conditions and provide a rational basis for identifying novel genes or sets of genes that can be potentially targeted for treating such conditions.
| S-EPMC5066585 | biostudies-literature
Project description:OBJECTIVES:To examine the impact of early myocardial workload on in-hospital mortality following isolated severe traumatic brain injury. DESIGN:Retrospective cohort study. SETTING:Data from the National Trauma Databank, a multicenter trauma registry operated by the American College of Surgeons, from 2007 to 2014. PATIENTS:Adult patients with isolated severe traumatic brain injury (defined as admission Glasgow Coma Scale < 8 and head Abbreviated Injury Score ? 4). INTERVENTIONS:Admission rate-pressure product, categorized into five levels based on published low, normal, and submaximal human thresholds: less than 5,000; 5,000-9,999; 10,000-14,999; 15,000-19,999; and greater than 20,000. MEASUREMENTS AND MAIN RESULTS:Data from 26,412 patients were analyzed. Most patients had a normal rate-pressure product (43%), 35% had elevated rate-pressure product, and 22% had depressed rate-pressure product at hospital admission. Compared with the normal rate-pressure product group, in-hospital mortality was 22 percentage points higher in the lowest rate-pressure product group (cumulative mortality, 50.2%; 95% CI, 43.6-56.9%) and 11 percentage points higher in the highest rate-pressure product group (cumulative mortality, 39.2%; 95% CI, 37.4-40.9%). The lowest rate-pressure product group was associated with a 50% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.50; 95% CI, 1.31-1.76%; p < 0.0001), and the highest rate-pressure product group was associated with a 25% increased risk of mortality, compared with the normal rate-pressure product group (adjusted relative risk, 1.25; 95% CI, 1.18-1.92%; p < 0.0001). This relationship was blunted with increasing age. Among patients with normotension, those with depressed and elevated rate-pressure products experienced increased mortality. CONCLUSIONS:Adults with severe traumatic brain injury experience heterogeneous myocardial workload profiles that have a "U-shaped" relationship with mortality, even in the presence of a normal blood pressure. Our findings are novel and suggest that cardiac performance is important following severe traumatic brain injury.
| S-EPMC5953788 | biostudies-literature
Project description:Background: Ultrasound is emerging as an effective method for measuring muscle mass in elderly people. It has been applied in numerous studies to obtain measurement of lower limbs. The study aims to explore the relationship between sarcopenia and ultrasound measurements of biceps brachii. Methods: Participants (n=179) aged over 60 years were enrolled from the first affiliated hospital of Zhejiang University. The muscle thickness (MT), cross-sectional area (CSA) and fat thickness (FT) of these participants were recorded. Spearman test and partial correlation test was used to determine the correlation between indicators. Mann-Whitney U test was performed to compare ultrasonic parameters between sarcopenia group and non-sarcopenia group. The binary logistic regression analysis was employed to detect the potential indicators and prediction equation of sarcopenia. Receiver operating characteristic (ROC) curve analysis was performed for the accuracy of equation. Results: The prevalence of sarcopenia were 16.3% and 10.8% respectively in men and women. CSA was significantly lower in sarcopenia group than non-sarcopenia group in women (P<0.05). CSA was positively correlated with skeletal muscle mass index (SMI) and grip strength (men: r=0.460, 0.433; women: r=0.267, 0.392). After controlling of age and BMI, these correlations disappeared. Binary logistic regression analysis showed that age (OR=1.149, 95%CI: 1.060-1.246; P=0.001) and CSA (OR=0.465, 95%CI: 0.225-0.963; P=0.039) was significant indicators associated with sarcopenia. Area Under Curve was 0.822 (95%CI: 0.725-0.919, P<0.001) for the prediction equation composed of age, gender and CSA for sarcopenia. Conclusion: CSA of the biceps brachii measured with ultrasound is an important indicator associated with sarcopenia.
| S-EPMC7646111 | biostudies-literature
Project description:Measurements of skeletal muscle cross-sectional area (SMA) at the level of the third lumbar (L3) vertebra derived from clinical computed tomography (CT) scans are commonly used in assessments of sarcopenia, the loss of skeletal muscle mass and function associated with aging. As SMA is correlated with height and Body Mass Index (BMI), body size adjustment is necessary to fairly assess sarcopenic low muscle mass in individuals of different height and BMI. The skeletal muscle index, a widely used measure, adjusts for height as [Formula: see text] but uses no BMI adjustment. There is no agreed upon standard for body size adjustment. We extracted L3 SMA using non-contrast-enhanced CT scans from healthy adults, split into 'Under-40' and 'Over-40' cohorts. Sex-specific allometric analysis showed that height to the power of one was the optimal integer coefficient for height adjusted SMA in both males and females. We computed two height-adjusted measures [Formula: see text] and [Formula: see text], comparing their Pearson correlations versus age, height, weight, and BMI separately by sex and cohort. Finally, in the 'Under-40' cohort, we used linear regression to convert each height-adjusted measure into a z-score ([Formula: see text], [Formula: see text]) adjusted for BMI. [Formula: see text] was less correlated with height in both males and females ([Formula: see text], [Formula: see text] and [Formula: see text], [Formula: see text]) than [Formula: see text] ([Formula: see text] and [Formula: see text], [Formula: see text]). [Formula: see text] was uncorrelated with BMI and weight, and minimally correlated with height in males and females ([Formula: see text], [Formula: see text] and [Formula: see text], [Formula: see text]). The final [Formula: see text] equation was: [Formula: see text], where [Formula: see text], [Formula: see text], [Formula: see text], and sex = 1 if male, 0 if female. We propose [Formula: see text] for optimal height adjustment and the [Formula: see text] score for optimal height and BMI adjustment. By minimizing correlations with height and BMI, the [Formula: see text] score produces unbiased assessments of relative L3 skeletal muscle area across the full range of body sizes.
| S-EPMC7801425 | biostudies-literature
Project description:In skeletal muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac muscle. Despite extensive studies in cardiac muscle, the physiological roles of the β-AR subtypes in skeletal muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on masseter and cardiac muscles in mice. In cardiac muscle, chronic β1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In masseter muscle, however, chronic β1-AR stimulation did not induce muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic β2-AR stimulation in masseter muscle induced muscle hypertrophy without histological abnormalities, as in the case of cardiac muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the β1-AR pathway is deleterious and the β2-AR is protective in masseter muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal muscle wasting and weakness.
| S-EPMC6464212 | biostudies-literature
Project description:This series includes the global gene expression profile of the vastus lateralis muscle for 10 young (19-25 years old) and 12 older (70-80 years old) male subjects. Keywords: other
2004-08-15 | GSE1428 | GEO
Project description:Following injury to different tissues, macrophages can contribute to both regenerative and fibrotic healing. These seemingly contradictory roles of macrophages may be related to the markedly different phenotypes that macrophages can assume upon exposure to different stimuli. We hypothesized that fibrotic healing after traumatic muscle injury would be dominated by a pro-fibrotic M2a macrophage phenotype, with M1 activation limited to the very early stages of repair. We found that macrophages accumulated in lacerated mouse muscle for at least 21?days, accompanied by limited myofibre regeneration and persistent collagen deposition. However, muscle macrophages did not exhibit either of the canonical M1 or M2a phenotypes, but instead up-regulated both M1- and M2a-associated genes early after injury, followed by down-regulation of most markers examined. Particularly, IL-10 mRNA and protein were markedly elevated in macrophages from 3-day injured muscle. Additionally, though flow cytometry identified distinct subpopulations of macrophages based on high or low expression of TNF?, these subpopulations did not clearly correspond to M1 or M2a phenotypes. Importantly, cell therapy with exogenous M1 macrophages but not non-activated macrophages reduced fibrosis and enhanced muscle fibre regeneration in lacerated muscles. These data indicate that manipulation of macrophage function has potential to improve healing following traumatic injury.
| S-EPMC4019602 | biostudies-literature
Project description:Trauma is a leading cause of death worldwide and in South Africa. We aimed to quantify the in-hospital trauma mortality rate in Pietermaritzburg, South Africa.BackgroundThe in-hospital trauma mortality rate in South Africa remains unknown, and it is unclear whether deficits in hospital care are contributing to the high level of trauma-related mortality.MethodsAll patients hospitalized because of trauma at the Department of Surgery at Grey's Hospital, Pietermaritzburg Metropolitan Trauma Service, were prospectively entered in an electronic database starting in 2013 and the data were retrospectively analyzed. The trauma service adheres to Advanced Trauma Life Support and the doctors have attended basic and advanced courses in trauma care. The primary outcome was in-hospital mortality.ResultsOf 9795 trauma admissions, 412 (4.2%) patients died during hospital care between January 2013 and January 2019. Forty-six percent died after road traffic accidents, 19% after gunshot wounds, 13% after stab wounds, and 10% after assaults. Sixteen percent were classified as avoidable deaths due to inappropriate care and resource limitations. Fifty percent died because of traumatic brain injury and 80% of them were unavoidable.ConclusionsIn conclusion, the in-hospital trauma mortality rate at a South African trauma center using systematic trauma care is lower than that reported from other trauma centers in the world during the past 20 years. Nevertheless, 16% of death cases were assessed as avoidable if there had been better access to intensive care, dialysis, advanced respiratory care, blood for transfusion, and improvements in surgery and medical care.
| S-EPMC10405992 | biostudies-literature