Global leadership initiative on malnutrition-defined malnutrition coexisting with visceral adiposity predicted worse long-term all-cause mortality among inpatients with decompensated cirrhosis
Global leadership initiative on malnutrition-defined malnutrition coexisting with visceral adiposity predicted worse long-term all-cause mortality among inpatients with decompensated cirrhosis"
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ABSTRACT BACKGROUND/OBJECTIVES Malnutrition coexisting with abdominal adipose tissue accumulation bring a double burden on prognosis. More recently, the Global Leadership Initiative on
Malnutrition (GLIM) has reached a novel consensus concerning the diagnostic criteria, that is, a two-step modality combining nutritional risk screening and subsequent phenotypic/etiologic
parameters for comprehensive evaluation in hopes of harmonizing the malnutrition diagnosis. We aimed to elucidate their synergistic impact among inpatients with decompensated cirrhosis
concerning long-term mortality. SUBJECTS/METHODS Malnutrition, visceral obesity, and visceral adiposity were defined by the Global Leadership Initiative on Malnutrition (GLIM), visceral fat
area (VFA), and visceral to subcutaneous adipose tissue area ratio (VSR) on computed tomography, respectively. Accordingly, the patients were categorized into different groups given their
nutritional status and visceral obesity/adiposity. Multivariate Cox regression was performed to identify independent risk factors associated with 1-year all-cause mortality. Kaplan–Meier
curves with log-rank tests were compared among distinct groups. RESULTS Totally, 295 patients were recruited. GLIM, VFA, and VSR identified 131 (44.4%), 158 (53.6%), and 59 (20%) patients
with malnutrition, visceral obesity and visceral adiposity, respectively. Malnutrition coexisted with visceral obesity in 55 (MO group) relative to visceral adiposity in 40 patients (MA
group). Multivariate Cox analysis showed that MA (hazard ratio: 2.48; 95% confidence interval: 1.06, 5.79; _P_ = 0.036) was independently associated with dire outcome rather than MO.
Moreover, patients with cirrhosis in the MA group had the worst survival status when compared with other groups (log-rank test: _P_ < 0.001). CONCLUSIONS The current study indicated that
coexisting GLIM-defined malnutrition and VSR-defined visceral adiposity were in relation to worse long-term mortality among inpatients. It is imperative to delicately manage nutritional
status and provide personalized treatment in this vulnerable subgroup for achieving better prognosis. SIMILAR CONTENT BEING VIEWED BY OTHERS DIFFERENCES IN NUTRITIONAL RISK ASSESSMENT
BETWEEN NRS2002, RFH-NPT AND LDUST IN CIRRHOTIC PATIENTS Article Open access 27 February 2023 GERIATRIC NUTRITIONAL RISK INDEX AND NEWLY DEVELOPED SCORING SYSTEM AS PROGNOSIS PREDICTION FOR
UNRESECTABLE HEPATOCELLULAR CARCINOMA PATIENTS TREATED WITH LENVATINIB Article Open access 02 January 2025 ASSOCIATION OF MYOSTEATOSIS WITH SHORT-TERM OUTCOMES IN PATIENTS WITH
ACUTE-ON-CHRONIC LIVER FAILURE Article Open access 13 June 2024 INTRODUCTION The onset of cirrhosis is always insidious, and it can progress to more advanced stages like hepatocellular
carcinoma and acute decompensation. The latter is manifested with variceal hemorrhage, ascites, and hepatic encephalopathy (HE), accounting for approximately 2.4% of the global deaths in
2019 [1]. It has been suggested that the etiologies of cirrhosis are ever-changing, probably due to improved therapy against chronic viral hepatitis, healthcare policy refinement, and life
style modification. Of note, global alcohol consumption is estimated to continuously grow, and the burden of non-alcoholic fatty liver disease (NAFLD)-associated cirrhosis tends to rise
steadily in alignment with the epidemics of type 2 diabetes mellitus (T2DM) and obesity. Moreover, another entity designated as metabolic-associated fatty liver disease (MAFLD) is
anticipated to apparently influence the etiologies of cirrhosis. MAFLD implicates hepatic steatosis with factors in relation to metabolic dysfunction, T2DM or obesity without the need to
rule out alternative reasons for chronic liver diseases [2, 3]. Therefore, the burden of MAFLD-associated cirrhosis is speculated to increase over time, alluding a pivotal role of obesity as
the pathogenic or precipitating factor among this vulnerable population. Regarding obesity, a dilemma exists since there is a lack of universally accepted and well-built diagnostic
criterion. For instance, the validity and reliability of body mass index (BMI), a typical metric assessing obesity, have been considerably curtailed in the context of cirrhosis, given that
proportional patients may experience various magnitudes of fluid retention [4]. Another inherent flaw of BMI is its inability to differentiate distinct adipose tissue compartments, that is,
subcutaneous, visceral, intramuscular, and intermuscular adiposity. It is highlighted that visceral fat area (VFA) and associated indices have been linked to the risk of inferior outcomes in
contrast to BMI [5]. Intriguingly, the accumulation of visceral adipose tissue defined by increased VFA refers to a novel terminology “visceral obesity”, serving as a more reliable
indicator of obesity [6, 7]. We previously clarified a synergically negative impact of muscle wasting and VFA-defined obesity on prognosis among hospitalized patients with cirrhosis [8]. On
the other hand, another term “visceral adiposity” indicative of high visceral to subcutaneous adipose tissue area ratio (VSR) has also been applied in the existing literature [9,10,11].
Malnutrition is another nutritional extremity in relative to obesity, whose prevalence is around 5% to 92% among patients with cirrhosis according to different assessing toolkits [12].
Despite there are no unanimous diagnostic criteria for malnutrition, the close connection between undernourished status and a wide range of poor outcomes has been validated in patients with
advanced liver diseases. Notably, the presence of cirrhosis-related malnutrition is linked to worse survival conditions, dysregulated body composition, decreased health-related quality of
life as well as increased likelihood of complications [13,14,15,16]. In hopes of standardizing and harmonizing the malnutrition diagnosis, a novel consensus on the criteria, known as the
Global Leadership Initiative on Malnutrition (GLIM), has been launched and endorsed in 2018 [17]. This recommendation argues a two-step modality covering initial nutritional risk screening
by any validated tools along with subsequent phenotypic/etiologic parameters for comprehensive evaluation [18]. The confirmatory malnutrition diagnosis relies on at least one phenotypic plus
one etiologic criterion, whose effectiveness, performance, and validity have been corroborated in versatile clinical scenarios [19,20,21]. In addition, the World Health Organization (WHO)
has addressed a phenomenon pertaining to “a double burden of malnutrition” where obesity, undernutrition in addition to diet-related non-communicable diseases concurrently occur,
representing a real, growing, and challenging health concern globally [22]. In this regard, some researchers have investigated the predictive value of nutritional status in combination with
BMI-defined obesity [23,24,25]. However, there is a paucity of data utilizing VFA-defined visceral obesity as a more reliable surrogate, and current evidence review retrieves only one
article in the context of patients with rectal malignancies [26]. Furthermore, the utility of VSR-defined visceral adiposity and its combined effect with malnutrition on prognosis is still
elusive. In this study, we hypothesized that malnutrition coexisting with visceral obesity or visceral adiposity may exhibit incremental risk of deaths among hospitalized patients with
cirrhosis. SUBJECTS AND METHODS STUDY POPULATION This study enrolled hospitalized patients with cirrhosis on account of acute decompensation to the Department of Gastroenterology and
Hepatology, Tianjin Medical University General Hospital (TJMUGH) from 2018 to 2021. Acute decompensation was defined by the presence of at least one of the following complications:
gastroesophageal variceal hemorrhage (GEV) on endoscopic examination [27], ascites (fluids in the abdominal cavity) classified by the international Ascites Club [28], HE categories in terms
of the West Haven Criteria in addition to severe jaundice suggestive of serum total bilirubin ≥51 µmol/L [29, 30]. Inclusion criteria: (1) age ≥18 years; (2) confirmatory cirrhosis in terms
of laboratory, radiologic, endoscopic, elastographic, or histopathologic data and (3) informed consent to participate. Exclusion criteria: (1) presence of acute-on-chronic liver failure
(ACLF) upon index admission; (2) without computed tomography (CT) images 3 months prior to hospitalization; (3) liver malignancies or other extrahepatic cancers and (4) refusal to regular
follow-up. ACLF definition conformed to the guideline established by the Asian Pacific Association for the Study of the Liver, including coagulation abnormalities (prothrombin
time-international normalized ratio [PT-INR] ≥1.5) and jaundice (total bilirubin ≥85 µmol/L) alongside HE and/or ascites within 4 weeks in the patients experiencing chronic liver disease or
cirrhosis [31]. Totally, 295 inpatients were left for final analysis (see flow chart in Fig. S1). This study was carried out according to the Declaration of Helsinki and approved by the
TJMUGH ethics committee. Written informed consent was provided. CLINICAL AND BIOCHEMICAL DATA Clinical and biochemical data were obtained as follows: age, sex, cirrhosis etiologies,
hemoglobulin, white blood cell counts (WBC), platelet, total bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, sodium, low-density lipoprotein
cholesterol (LDL-C), albumin, PT-INR, comorbidities (hypertension, coronary heart diseases (CHD) and T2DM). Some indicators/scoring systems concerning inflammation and liver disease severity
were calculated as neutrophil-to-lymphocyte ratio (NLR), Child-Turcotte-Pugh score/class and model for end-stage liver disease-sodium (MELD-Na) score. In current study, proportional
patients with cirrhosis had ascites, thus the dry weight was retrieved by subtracting 15%, 10%, and 5% for bulky, moderate, and mild ascites, respectively, and additional 5% for peripheral
edema [32]. The primary outcome of current study was 1-year all-cause mortality. Outcome data were collected through self-report from patients or their relatives (i.e., survival on telephone
follow-up/clinic consultation) and validated through review of city-wide electronic medical records (i.e., date of death and death reasons). The patients were censored if they remained
alive at one year and the last follow-up date was December 2022. COMPUTED TOMOGRAPHY-DEMARCATED PARAMETERS The study population underwent abdominal CT scans for a variety of indications
including disease severity stratification, disease progression monitoring along with malignancy transformation surveillance. All images were derived from a spectral CT scanner (Discovery 750
HD 64-row, GE corporation, U.S.), and then, analyzed and read by two independent observers (G.Y.G. and W.T.Y.). The final results were validated by a senior radiologist with sufficient
expertise (H.H.W.). The body composition compartments regarding skeletal muscle and various adipose tissue were determined in terms of tissue-specific Hounsfield Unit (HU) at the third
lumbar vertebra level (L3) by using an open-source project based on R2010a Matlab (Mathworks, Natick, U.S.). The specific CT thresholds of skeletal muscle, subcutaneous adipose tissue, and
visceral adipose tissue were −29 ~ 150 HU, −190 ~ −30 HU, and −150 ~ −50 HU, respectively. The skeletal muscle index (SMI) was calculated by dividing the L3 muscle area by height in square
(m2). The diagnosis of visceral obesity was defined by VFA > 100 cm2 for both sexes [33]. Moreover, visceral adiposity was determined according to our previous report, that is, VSR >
1.47 for males and VSR > 1.29 for females [34]. MALNUTRITION SCREENING AND ASSESSMENT The diagnosis of malnutrition was established conforming to the 2-step manner GLIM criteria. The
first step indicated a Royal Free Hospital‐Nutritional Prioritizing Tool (RFH-NPT) ≥ 1 to identify the subjects at malnutrition risk. Regarding RFH-NPT, this analytic metric has been
recommended by the International Society for Hepatic Encephalopathy and Nitrogen Metabolism [35, 36]. One study showed that the RFH-NPT independently predicted clinical deterioration and
transplant-free survival in patients with chronic liver disease [37]. Another investigation implicated that the RFH-NPT was one of the most accurate screening tools in detecting malnutrition
in cirrhosis, whilst other six tools exhibited insufficient performance [38]. Taken account of this recommendation which has been further confirmed by us and others, thus we selected the
RFH-NRT in current study for stratifying nutritional status in cirrhosis [37, 39]. Next, malnutrition was determined when one of the three phenotypic criteria was fulfilled since patients
with decompensated cirrhosis were inclined to dramatical disease burden meeting the etiologic criterion [40]. In detail, non-volitional weight loss was defined by >5% or >10% weight
loss within or over 6 months; low BMI value was defined as <18.5 kg/m2 or <20 kg/m2 among subjects with age <70 years or ≥70 years; decreased muscle mass was in agreement with our
previously outcome-based SMI thresholds to evaluate sarcopenia [34]. STATISTICAL ANALYSIS The study population was categorized into four groups in terms of their visceral obesity and
nutritional status: well-nourished non-visceral obesity group (WN), well-nourished visceral obesity group (WO), malnourished non-visceral obesity group (MN) and malnourished visceral obesity
group (MO). Furthermore, another four groups by applying VSR were constructed as follows: well-nourished non-visceral adiposity group (WNa), well-nourished visceral adiposity group (WA),
malnourished non-visceral adiposity group (MNa) and malnourished visceral adiposity group (MA) group. The descriptive data were presented as median (interquartile range) for continuous
variables and simple frequencies (proportions, %) for categorical variables. Multiple comparisons among continuous data were conducted by applying Kruskal–Wallis test with Dunn’s post hoc
test. The Fisher’s exact test or Chi-squared test was used for comparisons regarding categorical data. Univariate and Multivariate Cox proportional hazard models were used to assess risk
factors associated with 1-year all-cause mortality among inpatients. The entry criterion was _P_ < 0.05 in the univariate model. We included MELD-Na, NLR, the presence of ascites, albumin
and stratified groups by GLIM-defined malnutrition and CT-demarcated visceral obesity/adiposity, but excluded WBC, creatinine, CTP score, alcoholic etiology, total bilirubin, PT-INR and BMI
to avoid collinearity with the aforementioned variables. The selection of MELD-Na relied on its advantageous over the CTP score, in particular, on the basis of objective variables rather
than subjective assessment of clinical manifestations (i.e., HE and ascites) [41]. The Kaplan–Meier curves concerning 1‐year all‐cause mortality were performed to demonstrate survival status
and compared with log-rank test. Statistical significance was suggestive of a 2-sided _P_ < 0.05. SPSS 23.0 (IBM) and MedCalc 20.0.3 (MedCalc) were used. RESULTS Totally, 295 inpatients
with cirrhosis were recruited, and the sex predominance was female (51.5%). The median CTP and MELD-Na score were 8 and 7.6 points, respectively. Cirrhosis-associated complications comprised
ascites in 176 patients (59.7%), HE in 21 patients (7.1%) and infection in 38 patients (12.9%). Regarding comorbidities, the presence of hypertension, CHD, and T2DM was observed in 86, 22,
and 66 patients, respectively. Nutritional risk screening with the RFH-NPT identified 202 (68.5%) subjects. Following diagnostic criteria, 131 (44.4%) and 158 (53.6%) patients were
identified as exhibiting malnutrition and visceral obesity, respectively. Regarding sex discrepancies, 53.1% of males and 36.2% of females were identified as malnourished, while 61.5% of
males and 46.1% of females as visceral obesity. In this regard, the numbers of patients in WN, WO, MN, and MO groups were 61 (20.7%), 103 (34.9%), 76 (25.8%), and 55 (18.6%), respectively.
The baseline clinical and biochemical features can be found in Table 1. There were significant differences concerning sex, age, CTP score, MELD-Na score, NLR, total bilirubin, albumin,
creatinine, sodium, WBC, SMI, BMI, the presence of hypertension, ascites, infection and cirrhosis etiologies. However, no significant differences were observed regarding PT-INR, ALT, AST,
LDL-C, platelet, hemoglobin, CHD, T2DM, GEV and HE. Notably, patients in the MO group were inclined to be male (_P_ < 0.001), and had highest CTP score (_P_ < 0.001), MELD-Na score
(_P_ < 0.001), highest levels of total bilirubin (_P_ = 0.047), NLR (_P_ < 0.001), creatinine (_P_ = 0.003), WBC (_P_ < 0.001), lowest levels of albumin (_P_ = 0.001), sodium (_P_
< 0.001), BMI (_P_ < 0.001), and experienced most prevalent hypertension (_P_ < 0.001), ascites (_P_ < 0.001), and infection (_P_ = 0.015). During the follow-up period, a total
of 50 deaths has been recorded, and the reasons can be attributed to organ failure in 28, infection in 11, HE in 4, massive bleeding in 3, cardiovascular disease in 2 and cerebrovascular
disease in 2 subjects. The survival rates in the WN, WO, MN, and MO groups were 94.3%, 90.3%, 73.7%, and 70.9%, respectively. Figure 1a illustrated the Kaplan–Meier curves in terms of
nutritional and visceral obesity status among patients hospitalized for acute decompensation (log-rank test: _P_ = 0.0001). In the univariate Cox regression analysis, MO was associated with
461% higher risk of death compared with MN (Table S1). However, in the multivariate Cox regression analysis, HE, GEV, MELD-Na, and albumin were independently associated with 1-year all-cause
mortality, while MO dropping out of the model (Table 2). Intriguingly, emerging evidence has highlighted that the distribution of adipose tissues rather than their volumes represented a
closer relationship with disease severity [11, 42]. Therefore, we further performed in-depth investigation by using VSR to identify individuals with concurrent malnutrition and visceral
adiposity in the same cohort. As a result, a total of 294 were left for final analysis (one patient were excluded due to inaccessible subcutaneous adiposity tissue area). Accordingly, the
baseline features of another four groups designated as WNa (145, 49.2%), WA (19, 6.4%), MNa (90, 30.5%), and MA (40, 13.6%) were demonstrated in Table 3. Patients in the MA group were prone
to be male (_P_ < 0.001), and had highest CTP score (_P_ < 0.001), MELD-Na score (_P_ < 0.001), highest levels of NLR (_P_ = 0.003), total bilirubin (_P_ < 0.001), creatinine
(_P_ = 0.002), WBC (_P_ = 0.020), lowest levels of albumin (_P_ = 0.001), sodium (_P_ < 0.001), SMI (_P_ < 0.001), BMI (_P_ < 0.001), and experienced most prevalent ascites (_P_
< 0.001) and infection (_P_ = 0.031). Figure 1b also demonstrated the Kaplan–Meier curves in terms of nutritional and visceral adiposity status (log-rank test: _P_ < 0.001). The
survival rates in the WNa, WA, MNa, and MA groups were 91.0%, 94.7%, 77.8%, and 62.5%, respectively. In the univariate Cox regression analysis, MA was associated with 450% higher risk of
death compared with WNa (Table S2). Moreover, in the multivariate Cox regression analysis (Table 4), MA was independently associated with 1-year all-cause mortality (hazard ratio: 2.48, 95%
confidence interval: 1.06, 5.79, _P_ = 0.036). DISCUSSION In this study, we elaborate on the predictive value of coexisting malnutrition and excessive accumulation of abdominal adipose
tissue on long-term prognosis among inpatients with decompensated cirrhosis. Our preliminary results implicated that VSR-defined visceral adiposity rather than VFA-defined visceral obesity
was independently associated with 1-year all-cause mortality in the context of cirrhosis. Moreover, patients with cirrhosis in the MA group exhibited the worst survival status compared with
those in other three groups. Taken together, it is imperative to delicately manage the nutritional status and provide personalized treatment for this vulnerable subgroup with the purpose of
improving prognosis. The prevalence of malnutrition among cirrhosis is of great variation due to heterogenous target populations and mixed screening/assessing tools which give rise to
challenges surrounding comparisons between different studies. To offset aforesaid barriers, the GLIM criteria have been advocated to harmonize diagnosis across multiple healthcare settings,
pathophysiological entities and geographic areas [17]. More recently, the relationship between GLIM-defined malnutrition and a variety of dire health consequences has been verified in the
field of hepatology [14, 15, 43, 44]. In current study, malnourished patients accounted for more than two-fifths of participants enrolled (44.4%), which highlighted the clinical importance
to evaluate nutritional conditions, taking into account cirrhosis as a predisposing state to nutrients imbalance (excess or deficiency) [45]. Another issue warranted further in-depth
exploration is the combined effect of malnutrition and abdominal adipose tissue accumulation. Actually, the overlap between malnutrition and obesity/adiposity appears to be underestimated in
clinical practice, therefore, limited data has clarified their synergistic impact [26]. This is similar to another unique phenotype, known as sarcopenic obesity in the circumstance of fat
mass masking underpinning muscle depletion [46]. Malnutrition may serve as both a cause and a consequence of obesity, indicative of an abnormal pathophysiological state triggered by
inadequate, unbalanced, or excessive macronutrients/micronutrients assimilation [47, 48]. In this obesity background, malnutrition can result from a wider availability of cheap
nutrient-deficiency foods, responsible for a positive energy balance and micronutrients deficiency. In addition, massive adipose tissue can sequester vitamins instigating subsequently their
decreased concentrations in the circulation. For instance, vitamin D deficiency has been linked to the risk of abdominal obesity in adults [49]. Neito et al. reported that blood levels of
vitamin D, zinc, and other micronutrients were decreased in patients with decompensated cirrhosis [50]. In this regard, we herein found that there was 18.6% and 13.6% of patients categorized
into the MO and MA group, respectively. Of note, the proportions of MO or MA are likely to grow since cirrhosis attributable to NAFLD continues to increase, raising intensive attention and
specific concern to this subgroup [1]. The synergic impact of abdominal adipose tissue accumulation and malnutrition in cirrhosis is multifactorial and complicated. Referring to survival
status analysis, Kaplan–Meier curves showed that the survival rate was lowest in the group experiencing concomitant malnutrition and obesity/adiposity regardless of categories in terms of
VFA or VSR. However, MA remained its independently predictive role for long-term mortality while MO dropped out of the multivariate Cox regression model. Actually, emerging evidence has
proved that the distribution of abdominal adipose tissue exhibits more intimate correlation with underlying disease severity. For instance, one study recruiting patients with cirrhosis
undergoing liver transplantation revealed that higher VSR was an independent predictor of histologic VAT inflammation, and the authors verified the effectiveness of CT-quantified VSR as a
prognostic marker for dire outcomes [42]. Moreover, fat deposit in visceral sites may lead to insulin resistance and persistent chronic inflammation [51, 52]. The existing literature has
clarified that both inflammatory milieu and insulin resistance are predisposing factors with contributory role to the progression of malnutrition and visceral adiposity [47, 53].
Collectively, the coexistence of malnutrition and visceral adiposity may pinpoint a more aggressively dysmetabolic imbalance in the context of cirrhosis. The worse prognosis of patients in
the MA group means more delicate management as well as personalized treatment should be provided. Some academic institutional consensus have recommended a reduced caloric intake of 20–25
kcal/kg/day but increased protein intake up to 2.5 g/kg in patients with cirrhosis and obesity [54, 55]. This hypocaloric diet may be accompanied with weight loss, but other concerns
regarding decreases in lean mass and bone mineral density can not be underestimated [56]. Notably, significant weight loss can give rise to ascites, potentially HE and sarcopenia in
decompensated cirrhosis, thus tailored strategy to ensure a slow weight loss and sufficient protein intake is of utmost importance [57]. A cluster of pragmatic actions for patients with
cirrhosis and visceral adiposity has been proposed: empowerment of patients, prescription of nutritional support and exercise (aerobic and resistance training) even for decompensated
subjects by adapting to their health conditions [58]. This study has several limitations. First, the applicability of VSR to determine visceral obesity is controversial. This metric would be
equivalent in subject with large or small amounts of visceral adipose tissue and subcutaneous adipose tissue at the same time, resulting in misclassification of patients [59]. Second, we
assumed that all patients with cirrhosis at decompensating stage met the etiologic criterion pertinent to disease burden which may overestimate the prevalence of malnutrition. Last, the
relative small size of patients with malnutrition and visceral adiposity may underpower the comparison among different groups, although statistical significance already existed with this
sample size. In conclusion, this study elaborated on a synergically negative impact of coexisting malnutrition and VSR-defined visceral adiposity, that was a double burden, on long-term
mortality among hospital inpatients. It is imperative to delicately manage the nutritional status and provide personalized treatment in this vulnerable subgroup with the purpose of improving
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Surg. 2013;17:133–43. Article PubMed Google Scholar Download references ACKNOWLEDGEMENTS We thank Dr. HuanHuan Wu for her technical support in this study. AUTHOR INFORMATION Author notes
* These authors contributed equally: Han Wang, Tianming Zhao, Gaoyue Guo. AUTHORS AND AFFILIATIONS * Department of Health Management, Tianjin Hospital, No. 406 Jiefang South Road, Hexi
District, Tianjin, 300211, China Han Wang & Huanli Jiao * Department of Gastroenterology, Nanjing Drum Tower Hospital, Graduate School of Peking Union Medical College, Chinese Academy of
Medical Sciences & Peking Union Medical College, Nanjing, 210008, Jiangsu, China Tianming Zhao * Department of Gastroenterology and Hepatology, Tianjin Medical University General
Hospital, Anshan Road 154, Heping District, Tianjin, 300052, China Gaoyue Guo, Wanting Yang, Jie Yang, Yangyang Hui, Xiaoyu Wang, Xiaofei Fan & Chao Sun * Department of Gastroenterology
and Hepatology, China Aerospace Science & Industry Corporation 731 Hospital, No. 3 Zhen Gang Nan Li, Fengtai District, Beijing, 100074, China Xuqian Zhang * Department of Digestive
System, Baodi Clinical College of Tianjin Medical University, No. 8, Guangchuan Road, Baodi District, Tianjin, 301800, China Fang Yang * Department of Gastroenterology, Tianjin Medical
University General Hospital Airport Hospital, East Street 6, Tianjin Airport Economic Area, Tianjin, 300308, China Binxin Cui & Chao Sun Authors * Han Wang View author publications You
can also search for this author inPubMed Google Scholar * Tianming Zhao View author publications You can also search for this author inPubMed Google Scholar * Gaoyue Guo View author
publications You can also search for this author inPubMed Google Scholar * Wanting Yang View author publications You can also search for this author inPubMed Google Scholar * Xuqian Zhang
View author publications You can also search for this author inPubMed Google Scholar * Fang Yang View author publications You can also search for this author inPubMed Google Scholar * Jie
Yang View author publications You can also search for this author inPubMed Google Scholar * Yangyang Hui View author publications You can also search for this author inPubMed Google Scholar
* Xiaoyu Wang View author publications You can also search for this author inPubMed Google Scholar * Binxin Cui View author publications You can also search for this author inPubMed Google
Scholar * Xiaofei Fan View author publications You can also search for this author inPubMed Google Scholar * Huanli Jiao View author publications You can also search for this author inPubMed
Google Scholar * Chao Sun View author publications You can also search for this author inPubMed Google Scholar CONTRIBUTIONS Han Wang: Conceptualization, formal analysis. Tianming Zhao:
Investigation, methodology. Gaoyue Guo: Investigation, software. Wanting Yang: Investigation, software. Xuqian Zhang: Investigation. Fang Yang: Investigation. Jie Yang: Investigation.
Yangyang Hui: Investigation. Xiaoyu Wang: Investigation. Binxin Cui: Investigation. Xiaofei Fan: Investigation. Huanli Jiao: Supervision. Chao Sun: Conceptualization, roles/writing—original
draft; writing—review & editing. CORRESPONDING AUTHORS Correspondence to Huanli Jiao or Chao Sun. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no competing interests.
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Wang, H., Zhao, T., Guo, G. _et al._ Global Leadership Initiative on Malnutrition-defined malnutrition coexisting with visceral adiposity predicted worse long-term all-cause mortality among
inpatients with decompensated cirrhosis. _Nutr. Diabetes_ 14, 76 (2024). https://doi.org/10.1038/s41387-024-00336-9 Download citation * Received: 23 October 2023 * Revised: 05 September 2024
* Accepted: 16 September 2024 * Published: 27 September 2024 * DOI: https://doi.org/10.1038/s41387-024-00336-9 SHARE THIS ARTICLE Anyone you share the following link with will be able to
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