In-hospital use of antibiotics in internal medicine: A cross-sectional study before, during and after the COVID-19 pandemic in a COVID-19-free ward.

BACKGROUND: Coronavirus Disease-19 (COVID-19) pandemic impacted the use of antibiotics in hospitalized patients. However, most data on antibiotic therapy (AT) were recorded in COVID-19 settings. This study analyzed the appropriateness of AT in the real-world scenario of a COVID-19-free internal medicine ward before, during, and after the pandemic. METHODS: Clinical information of hospitalized patients was collected, and data related to AT prescription were analyzed. The appropriateness of AT was independently assessed by two specialists in internal medicine and infectious disease, combining evidence-based guidelines with a validated tool. RESULTS: Records of 1249 patients were analyzed: AT was prescribed in 229 (55.2 %) patients before, 134 (53.2 %) patients during, and 315 (54.1 %) patients after COVID-19 pandemic. Compared to the pre-pandemic period, there was a decrease in monotherapy with 3rd and 4th generation cephalosporins and fluoroquinolones, and an increase in ß-lactams + ß-lactamase inhibitors and antibiotic combinations. Furthermore, AT was longer and more expensive during the pandemic, with duration and cost remaining higher after its end. The inappropriateness of AT increased during and after COVID-19 pandemic. Compared to the pre-pandemic period, inappropriate AT was longer and more expensive than appropriate AT. The COVID-19 pandemic had a significant impact on changes related to AT type and antibiotic classes. CONCLUSIONS: The COVID-19 pandemic increased the inappropriateness of AT in a COVID-19-free internal medicine ward. Most modifications persist despite the end of pandemic, potentially leading to negative effects on in-hospital antimicrobial resistance. There is an urgent need to re-establish antimicrobial stewardship policies to address the longer-term global threat of antimicrobial resistance.

An Amino Acid Mixture to Counteract Skeletal Muscle Atrophy: Impact on Mitochondrial Bioenergetics.

Skeletal muscle atrophy (SMA) is caused by a rise in muscle breakdown and a decline in protein synthesis, with a consequent loss of mass and function. This study characterized the effect of an amino acid mixture (AA) in models of SMA, focusing on mitochondria. C57/Bl6 mice underwent immobilization of one hindlimb (I) or cardiotoxin-induced muscle injury (C) and were compared with controls (CTRL). Mice were then administered AA in drinking water for 10 days and compared to a placebo group. With respect to CTRL, I and C reduced running time and distance, along with grip strength; however, the reduction was prevented by AA. Tibialis anterior (TA) muscles were used for histology and mitochondria isolation. I and C resulted in TA atrophy, characterized by a reduction in both wet weight and TA/body weight ratio and smaller myofibers than those of CTRL. Interestingly, these alterations were lightly observed in mice treated with AA. The mitochondrial yield from the TA of I and C mice was lower than that of CTRL but not in AA-treated mice. AA also preserved mitochondrial bioenergetics in TA muscle from I and C mice. To conclude, this study demonstrates that AA prevents loss of muscle mass and function in SMA by protecting mitochondria.

Prognostic Nutritional Index and Instant Nutritional Assessement Are Associated with Clinical Outcomes in a Geriatric Cohort of Acutely Inpatients.

BACKGROUND: Among elderly inpatients, malnutrition is one of the most important predictive factors affecting length of stay (LOS), mortality, and risk of re-hospitalization. METHODS: We conducted an observational, retrospective study on a cohort of 2206 acutely inpatients. Serum albumin and lymphocytes were evaluated. Instant Nutritional Assessment (INA) and the Prognostic Nutritional Index (PNI) were calculated to predict in-hospital mortality, LOS, and risk of rehospitalization. RESULTS: An inverse relationship between LOS, serum albumin, and PNI were found. Deceased patients had lower albumin levels, lower PNI values, and third- and fourth-degree INA scores. An accurate predictor of mortality was PNI (AUC = 0.785) after ROC curve analysis; both lower PNI values (HR = 3.56) and third- and fourth-degree INA scores (HR = 3.12) could be independent risk factors for mortality during hospitalization after Cox regression analysis. Moreover, among 309 subjects with a lower PNI value or third- and fourth-class INA, hospitalization was re-hospitalization. CONCLUSIONS: PNI and INA are two simple and quick-to-calculate tools that can help in classifying the condition of hospitalized elderly patients also based on their nutritional status, or in assessing their mortality risk. A poor nutritional status at the time of discharge may represent an important risk factor for rehospitalization in the following thirty days. This study confirms the importance of evaluating nutritional status at the time of hospitalization, especially in older patients. This study also confirms the importance for adequate training of doctors and nurses regarding the importance of maintaining a good nutritional status as an integral part of the therapeutic process of hospitalization in acute departments.

Association between Controlling Nutritional Status (CONUT) Score and Body Composition, Inflammation and Frailty in Hospitalized Elderly Patients.

The Controlling Nutritional Status (CONUT) score has demonstrated its ability to identify patients with poor nutritional status and predict various clinical outcomes. Our objective was to assess the association between the CONUT score, inflammatory status, and body composition, as well as its ability to identify patients at risk of frailty in hospitalized elderly patients. METHODS: a total of 361 patients were retrospectively recruited and divided into three groups based on the CONUT score. RESULTS: patients with a score ≥5 exhibited significantly higher levels of inflammatory markers, such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Neutrophil/Lymphocytes ratio (NLR), main platelet volume (MPV), and ferritin, compared to those with a lower score. Furthermore, these patients showed unfavorable changes in body composition, including a lower percentage of skeletal muscle mass (MM) and fat-free mass (FFM) and a higher percentage of fatty mass (FM). A positive correlation was found between the CONUT score and inflammatory markers, Geriatric Depression Scale Short Form (GDS-SF), and FM. Conversely, the Mini Nutritional Assessment (MNA), Mini-Mental Status Examination, activity daily living (ADL), instrumental activity daily living (IADL), Barthel index, FFM, and MM showed a negative correlation. Frailty was highly prevalent among patients with a higher CONUT score. The receiver operating characteristic (ROC) curve demonstrated high accuracy in identifying frail patients (sensitivity). CONCLUSIONS: a high CONUT score is associated with a pro-inflammatory status as well as with unfavorable body composition. Additionally, it is a good tool to identify frailty among hospitalized elderly patients.

Controlling Nutritional Status Score as a Predictor for Chronic Obstructive Pulmonary Disease Exacerbation Risk in Elderly Patients.

The Controlling Nutritional Status (CONUT) score is a simple screening tool able to assess poor nutritional status as well as to predict clinical adverse outcomes in different clinical settings. No data are available in older patients with chronic obstructive pulmonary disease (COPD). This study aimed to investigate the CONUT score as a predictor of frequent exacerbations. We retrospectively enrolled 222 patients aged 65 years or older, classified in two groups according to the number of exacerbations (or hospitalizations because AECOPD) during the previous year. The two groups were further divided according to low (<5) or high (≥5) CONUT scores. A total of 67.2% of frequent exacerbators had a high CONUT score. These patients exhibited a significantly higher CAT score, lower FEV1 percentage value, and higher prevalence of severe GOLD stages compared to those with low CONUT. Multivariate analysis showed that a CONUT score ≥ 5 was the best independent predictor (OR 20.740, p < 0.001) of the occurrence of ≥2 exacerbations (or 1 hospitalization) during the previous year. The CONUT score seemed to have a high prognostic value for frequent exacerbations for COPD in older patients. The predictive role of different CONUT score cut-off values needs to be validated in larger COPD populations in future multi-center, prospective clinical studies.

Sarcopenia Is Associated with Changes in Circulating Markers of Antioxidant/Oxidant Balance and Innate Immune Response.

(1) Background: The involvement of redox balance alterations and innate immunity is suggested to play a key role in the pathogenesis of sarcopenia. This investigation aimed to define and relate modifications in circulating markers of redox homeostasis and the innate immune response in human sarcopenia. (2) Methods: A total of 32 subjects aged >65 years old and affected by sarcopenia according to the second "European Working Group on sarcopenia in older people" guidelines were compared with 40 non-sarcopenic age-matched controls. To assess systemic redox homeostasis, reduced (GSH) and oxidized (GSSG) blood glutathione and plasma malondialdehyde (MDA)- and 4-hydroxy-2,3-nonenal (HNE)-protein adducts were measured. Immune cells and circulating interleukins were determined to compare the innate immune response between both groups. (3) Results: Impaired redox balance in sarcopenic patients, characterized by a high blood GSSG/GSH ratio and plasma MDA/HNE-protein adducts, was sustained by reduced antioxidants in peripheral blood mononuclear cells. Furthermore, sarcopenic patients showed higher neutrophil-to-lymphocyte ratios and interleukin (IL)-4, IL-6, IL-10, and tumor necrosis factor (TNF) with respect to non-sarcopenic patients. Linear regression analysis resulted in a strong association between redox balance and immune response markers in the sarcopenic group. (4) Conclusions: These results support the interplay between redox homeostasis alteration and disruption of the innate immune response in the pathogenesis of sarcopenia.

Controlling Nutritional Status (CONUT) Score as a Predictive Marker in Hospitalized Frail Elderly Patients.

The Controlling Nutritional Status (CONUT) score is a simple screening tool able to detect altered nutritional status as well as to predict clinical adverse outcomes in specific populations. No data are available in frail patients. This study aims to investigate the predictive role of the CONUT score on mortality and length of stay (LOS) in frail patients admitted to an Internal Medicine Department. We consecutively enrolled 246 patients aged 65 years or older, divided into two groups based on frailty status. The two groups were further divided according to low (<5) or high (≥5) CONUT score. Length of stay (LOS) was higher in frail patients than not-frail patients, as well as in the frail group with high CONUT scores compared to the frail group with low CONUT scores. Multiple linear regression showed an increase of 2.1 days for each additional point to the CONUT score. In-hospital mortality was higher in frail compared to not-frail patients, but it did not differ between frail patients with high CONUT scores and frail patients with low CONUT scores. An analysis of the survival curve for 30-day mortality showed a higher mortality rate for frail/high-CONUT-score patients as compared to the not-frail/low-CONUT-score group. The CONUT score shows high prognostic value for higher LOS-but not mortality-in the clinical setting of internal medicine departments for old frail patients.

Alteration of circulating redox balance in coronavirus disease-19-induced acute respiratory distress syndrome.

BACKGROUND: Mechanisms underpinning ARDS induced by COVID-19 are mostly immune-mediated, but need to be completely clarified. This study aimed to investigate redox balance in COVID-19 patients with ARDS, trying to recognize possible differences from typical ARDS related to the pathophysiology of severe disease. METHODS: Patients affected by ARDS and positive for the SARS-CoV-2 virus (N = 40, COVID-19) were compared to ARDS patients negative to the molecular test (N = 42, No COVID-19). Circulating markers of redox balance were measured in serum and erythrocytes, and related to markers of inflammation and coagulability. RESULTS: No differences in serum markers of oxidative damage were found between both groups, but a reduction in total antioxidant status and serum ceruloplasmin level was observed in COVID-19 rather than No COVID-19 patients. Redox balance alterations were described in erythrocytes from COVID-19 with respect to No COVID-19 group, characterized by increased lipofuscin and malondialdehyde concentration, and reduced glutathione S-transferase and glutathione reductase activity. These markers were associated with circulating indexes of respiratory disease severity (Horowitz index and alveolar-to-arterial oxygen gradient), inflammation (interleukin-6 and interleukin-10), and hypercoagulability (D-dimer) in COVID-19 patients with ARDS. CONCLUSIONS: ARDS caused by COVID-19 is sustained by impairment of redox balance, particularly in erythrocytes. This alteration is associated with the pro-inflammatory and pro-coagulant status which characterizes severe COVID-19.

Hepatic Mitochondria-Gut Microbiota Interactions in Metabolism-Associated Fatty Liver Disease.

The prevalence of metabolism-associated fatty liver disease (MAFLD) represents an urgent pandemic, complicated by a higher risk of morbidity and mortality as well as an increased socio-economic burden. There is growing evidence proving the impact of gut microbiota modifications on the development and progression of MAFLD through changes in metabolic pathways, modulation of the immune response, and activation of pro-inflammatory signals. Concurrently, metabolites produced by gut microbiota consisting of short chain fatty acids and bile acids contribute to the regulation of hepatic homeostasis by interacting with mitochondria. Evolving research indicates that innovative therapeutic targets for MAFLD may focus on gut microbiota-mitochondria interplay to regulate hepatic homeostasis. Recent investigations have explored the potential of new treatment strategies, such as prebiotics, probiotics, and metabolites, to change the composition of gut microbiota and simultaneously exert a positive impact on mitochondrial function to improve MAFLD. This review summarizes the significance of mitochondria and reports modifications in the composition of gut microbiota and its metabolites in MAFLD in order to illustrate the fascinating interplay between liver mitochondria and intestinal microbiota, discussing the potential effects of innovative treatments to modulate gut microbiota.

Redox-Dependent Modulation of Human Liver Progenitor Cell Line Fate.

Redox homeostasis is determinant in the modulation of quiescence/self-renewal/differentiation of stem cell lines. The aim of this study consisted of defining the impact of redox modifications on cell fate in a human hepatic progenitor line. To achieve this, the HepaRG cell line, which shows oval ductular bipotent characteristics, was used. The impact of redox status on the balance between self-renewal and differentiation of HepaRG cells was investigated using different methodological approaches. A bioinformatic analysis initially proved that the trans-differentiation of HepaRG toward bipotent progenitors is associated with changes in redox metabolism. We then exposed confluent HepaRG (intermediate differentiation phase) to oxidized (H2O2) or reduced (N-acetylcysteine) extracellular environments, observing that oxidation promotes the acquisition of a mature HepaRG phenotype, while a reduced culture medium stimulates de-differentiation. These results were finally confirmed through pharmacological modulation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2), a principal modulator of the antioxidant response, in confluent HepaRG. NRF2 inhibition led to intracellular pro-oxidative status and HepaRG differentiation, while its activation was associated with low levels of reactive species and de-differentiation. In conclusion, this study shows that both intra- and extracellular redox balance are crucial in the determination of HepaRG fate. The impact of redox status in the differentiation potential of HepaRG cells is significant on the utilization of this cell line in pre-clinical studies.

Muscle Delivery of Mitochondria-Targeted Drugs for the Treatment of Sarcopenia: Rationale and Perspectives.

An impairment in mitochondrial homeostasis plays a crucial role in the process of aging and contributes to the incidence of age-related diseases, including sarcopenia, which is defined as an age-dependent loss of muscle mass and strength. Mitochondrial dysfunction exerts a negative impact on several cellular activities, including bioenergetics, metabolism, and apoptosis. In sarcopenia, mitochondria homeostasis is disrupted because of reduced oxidative phosphorylation and ATP generation, the enhanced production of reactive species, and impaired antioxidant defense. This review re-establishes the most recent evidence on mitochondrial defects that are thought to be relevant in the pathogenesis of sarcopenia and that may represent promising therapeutic targets for its prevention/treatment. Furthermore, we describe mechanisms of action and translational potential of promising mitochondria-targeted drug delivery systems, including molecules able to boost the metabolism and bioenergetics, counteract apoptosis, antioxidants to scavenge reactive species and decrease oxidative stress, and target mitophagy. Even though these mitochondria-delivered strategies demonstrate to be promising in preclinical models, their use needs to be promoted for clinical studies. Therefore, there is a compelling demand to further understand the mechanisms modulating mitochondrial homeostasis, to characterize powerful compounds that target muscle mitochondria to prevent sarcopenia in aged people.

Impact of sodium glucose cotransporter-2 inhibitors on liver steatosis/fibrosis/inflammation and redox balance in non-alcoholic fatty liver disease.

BACKGROUND: Sodium glucose cotransporter-2 inhibitors (SGLT2-I) are the most recently approved drugs for type 2 diabetes (T2D). Recent clinical trials of these compounds reported beneficial cardiovascular (CV) and renal outcomes. A major cause of vascular dysfunction and CV disease in diabetes is hyperglycemia associated with inflammation and oxidative stress. Pre-clinical studies demonstrated that SGLT2-I reduce glucotoxicity and promote anti-inflammatory effects by lowering oxidative stress. AIM: To investigate the effects of SGLT2-I on markers of oxidative stress, inflammation, liver steatosis, and fibrosis in patients of T2D with non-alcoholic fatty liver disease (NAFLD). METHODS: We referred fifty-two consecutive outpatients treated with metformin monotherapy and exhibiting poor glycemic control to our centre. We introduced the outpatients to an SGLT2-I (dapagliflozin, empagliflozin, or canagliflozin; n = 26) or a different hypoglycemic drug [other glucose-lowering drugs (OTHER), n = 26]. We evaluated circulating interleukins and serum hydroxynonenal (HNE)- or malondialdehyde (MDA)-protein adducts, fatty liver index (FLI), NAFLD fibrosis score, aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, AST-to-platelet-ratio index (APRI), and fibrosis-4 on the day before (T0) and following treatment for six months (T1). We also performed transient elastography at T0 and T1. RESULTS: Add-on therapy resulted in improved glycemic control and reduced fasting blood glucose in both groups. Of note, following treatment for six months, a reduction of FLI and APRI, as well as of the FibroScan result, was reported in patients treated with SGLT2-I, but not in the OTHER group; furthermore, in the SGLT2-I group, we reported lower circulating levels of interleukin (IL)-1ß, IL-6, tumor necrosis factor, vascular endothelial growth factor, and monocyte chemoattractant protein-1, and higher levels of IL-4 and IL-10. We did not observe any modification in circulating interleukins in the OTHER group. Finally, serum HNE- and MDA-protein adducts decreased significantly in SGLT2-I rather than OTHER patients and correlated with liver steatosis and fibrosis scores. CONCLUSION: The present data indicate that treatment with SGLT2-I in patients with T2D and NAFLD is associated with improvement of liver steatosis and fibrosis markers and circulating pro-inflammatory and redox status, more than optimizing glycemic control.

Malnutrition in Hospitalized Old Patients: Screening and Diagnosis, Clinical Outcomes, and Management.

Malnutrition in hospitalized patients heavily affects several clinical outcomes. The prevalence of malnutrition increases with age, comorbidities, and intensity of care in up to 90% of old populations. However, malnutrition frequently remains underdiagnosed and undertreated in the hospital. Thus, an accurate screening to identify patients at risk of malnutrition or malnourishment is determinant to elaborate a personal nutritional intervention. Several definitions of malnutrition were proposed in the last years, affecting the real frequency of nutritional disorders and the timing of intervention. Diagnosis of malnutrition needs a complete nutritional assessment, which is often challenging to perform during a hospital stay. For this purpose, various screening tools were proposed, allowing patients to be stratified according to the risk of malnutrition. The present review aims to summarize the actual evidence in terms of diagnosis, association with clinical outcomes, and management of malnutrition in a hospital setting.

Redox Homeostasis and Immune Alterations in Coronavirus Disease-19.

The global Coronavirus Disease 2019 (COVID-19) pandemic is characterized by a wide variety of clinical features, from no or moderate symptoms to severe illness. COVID-19 is caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that first affects the respiratory tract. Other than being limited to lungs, SARS-CoV-2 may lead to a multisystem disease that can even be durable (long COVID). The clinical spectrum of COVID-19 depends on variability in the immune regulation. Indeed, disease progression is consequent to failure in the immune regulation, characterized by an intensification of the pro-inflammatory response. Disturbance of systemic and organ-related redox balance may be a further mechanism underlying variability in COVID-19 severity. Other than being determinant for SARS-CoV-2 entry and fusion to the host cell, reactive species and redox signaling are deeply involved in the immune response. This review sums up the present knowledge on the role of redox balance in the regulation of susceptibility to SARS-CoV-2 infection and related immune response, debating the effectiveness of antioxidant compounds in the management of COVID-19.

Impact of senescence on the transdifferentiation process of human hepatic progenitor-like cells.

BACKGROUND: Senescence is characterized by a decline in hepatocyte function, with impairment of metabolism and regenerative capacity. Several models that duplicate liver functions in vitro are essential tools for studying drug metabolism, liver diseases, and organ regeneration. The human HepaRG cell line represents an effective model for the study of liver metabolism and hepatic progenitors. However, the impact of senescence on HepaRG cells is not yet known. AIM: To characterize the effects of senescence on the transdifferentiation capacity and mitochondrial metabolism of human HepaRG cells. METHODS: We compared the transdifferentiation capacity of cells over 10 (passage 10 [P10]) vs P20. Aging was evaluated by senescence-associated (SA) beta-galactosidase activity and the comet assay. HepaRG transdifferentiation was analyzed by confocal microscopy and flow cytometry (expression of cluster of differentiation 49a [CD49a], CD49f, CD184, epithelial cell adhesion molecule [EpCAM], and cytokeratin 19 [CK19]), quantitative PCR analysis (expression of albumin, cytochrome P450 3A4 [CYP3A4], γ-glutamyl transpeptidase [γ-GT], and carcinoembryonic antigen [CEA]), and functional analyses (albumin secretion, CYP3A4, and γ-GT). Mitochondrial respiration and the ATP and nicotinamide adenine dinucleotide (NAD+)/NAD with hydrogen (NADH) content were also measured. RESULTS: SA ß-galactosidase staining was higher in P20 than P10 HepaRG cells; in parallel, the comet assay showed consistent DNA damage in P20 HepaRG cells. With respect to P10, P20 HepaRG cells exhibited a reduction of CD49a, CD49f, CD184, EpCAM, and CK19 after the induction of transdifferentiation. Furthermore, lower gene expression of albumin, CYP3A4, and γ-GT, as well as reduced albumin secretion capacity, CYP3A4, and γ-GT activity were reported in transdifferentiated P20 compared to P10 cells. By contrast, the gene expression level of CEA was not reduced by transdifferentiation in P20 cells. Of note, both cellular and mitochondrial oxygen consumption was lower in P20 than in P10 transdifferentiated cells. Finally, both ATP and NAD+/NADH were depleted in P20 cells with respect to P10 cells. CONCLUSION: SA mitochondrial dysfunction may limit the transdifferentiation potential of HepaRG cells, with consequent impairment of metabolic and regenerative properties, which may alter applications in basic studies.

Factors Related to Nurses' Burnout during the First Wave of Coronavirus Disease-19 in a University Hospital in Italy.

Safety of healthcare workers in hospitals is a major concern during the COVID-19 pandemic. Being exposed for several working hours per day to infected patients, nurses dealing with COVID-19 face several issues that lead to physical/psychological breakdown. This study focused on burnout and its associated factors in nurses working in an Italian University Hospital during the first wave of COVID-19 pandemic. We designed a web-based cross-sectional study addressed to nurses working at the University Hospital in Foggia, Italy. The online questionnaire was organized in sections aimed at collecting demographic and occupational variables, including the Maslach Burnout Inventory (MBI) and the Oldenburg Burnout Inventory (OBI). Two hundred and ninety-three nurses agreed to participate. According to MBI, we reported moderate/high emotional exhaustion in 76.5%, depersonalization in 50.2%, and personal gratification in 54.6% of participants. COVID-19-related burnout measured by OBI resulted medium/high in 89.1% of participants. Among demographic and occupational factors, a multivariate regression analysis identified emotional support, consideration of leaving job, and workload as predictive of burnout in nurses. In conclusion, this study suggests that the improvement of employer and family support to nurses, as well as reduction of workload and job-related stress, would contribute to reducing burnout in nurses during COVID-19 pandemics.

Mitochondrial Impairment in Sarcopenia.

Sarcopenia is defined by the age-related loss of skeletal muscle quality, which relies on mitochondrial homeostasis. During aging, several mitochondrial features such as bioenergetics, dynamics, biogenesis, and selective autophagy (mitophagy) are altered and impinge on protein homeostasis, resulting in loss of muscle mass and function. Thus, mitochondrial dysfunction contributes significantly to the complex pathogenesis of sarcopenia, and mitochondria are indicated as potential targets to prevent and treat this age-related condition. After a concise presentation of the age-related modifications in skeletal muscle quality and mitochondrial homeostasis, the present review summarizes the most relevant findings related to mitochondrial alterations in sarcopenia.

Comparison of Three Nutritional Screening Tools with the New Glim Criteria for Malnutrition and Association with Sarcopenia in Hospitalized Older Patients.

The integrated assessment of nutritional status and presence of sarcopenia would help improve clinical outcomes of in-hospital aged patients. We compared three common nutritional screening tools with the new Global Leadership Initiative on Malnutrition (GLIM) diagnostic criteria among hospitalized older patients. To this, 152 older patients were assessed consecutively at hospital admission by the Malnutrition Universal Screening Tool (MUST), the Subjective Global Assessment (SGA), and the Nutritional Risk Screening 2002 (NRS-2002). A 46% prevalence of malnutrition was reported according to GLIM. Sensitivity was 64%, 96% and 47%, and specificity was 82%, 15% and 76% with the MUST, SGA, and NRS-2002, respectively. The concordance with GLIM criteria was 89%, 53% and 62% for the MUST, SGA, and NRS-2002, respectively. All the screening tools had a moderate value to diagnose malnutrition. Moreover, patients at high nutritional risk by MUST were more likely to present with sarcopenia than those at low risk (OR 2.5, CI 1.3-3.6). To conclude, MUST is better than SGA and NRS-2002 at detecting malnutrition in hospitalized older patients diagnosed by the new GLIM criteria. Furthermore, hospitalized older patients at high risk of malnutrition according to MUST are at high risk of presenting with sarcopenia. Nutritional status should be determined by MUST in older patients at hospital admission, followed by both GLIM and the European Working Group on Sarcopenia in Older People (EWGSOP2) assessment.