Obesity and Liver Decompensation

Ahn, Joseph; Sundaram, Vinay

doi:10.1002/cld.807

Cited by 10 publications

(11 citation statements)

References 15 publications

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“…Meanwhile, this study observed that MAFLD patients with positive HBsAg increased the risk of death [28]. Furthermore, it was demonstrated that metabolic disorders were risk factors for adverse outcomes among cirrhosis patients [17,18,29,30]. Taken together, we speculate that MAFLD in patients with hepatitis B cirrhosis is still a powerful factor in predicting death.…”

Section: Discussionmentioning

confidence: 83%

“…Berzigotti et al . found that the proportion of patients with compensated cirrhosis who experienced clinical decompensation increased with increasing baseline BMI, which was independent of portal pressure and liver function [18]. Obesity and insulin resistance might also have negative effects on portal hypertension, raising the risk of clinical decompensation in turn [38].…”

Section: Discussionmentioning

confidence: 99%

“…It was acknowledged that NAFLD was a liver component of a series of diseases related to metabolic dysfunction and could progress to liver fibrosis, cirrhosis and portal hypertension, which significantly increased liver-related mortality and the risk of complications such as ascites, hepatic encephalopathy, variceal bleeding [14][15][16]. Simultaneously, some components of metabolic syndrome (diabetes, obesity, dyslipidemia) also predicted lower survival rates, worse liver function and more decompensation events in patients with liver cirrhosis [17][18][19]; however, the impact of MAFLD on the long-term clinical outcome of cirrhotic patients is yet unknown.…”

Section: Introductionmentioning

confidence: 99%

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The impact of concomitant metabolic dysfunction-associated fatty liver disease on adverse outcomes in patients with hepatitis B cirrhosis: a propensity score matching study

Wang

Wei

et al. 2023

European Journal of Gastroenterology &Amp; Hepatology

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Background and aims In cirrhotic patients, the clinical relevance of metabolic dysfunction-associated fatty liver disease (MAFLD) is unclear. We aimed to research the relationship between MAFLD and adverse clinical outcomes in patients with hepatitis B cirrhosis. Methods A total of 439 patients with hepatitis B cirrhosis were enrolled. Abdominal MRI and computed tomography were used to calculate liver fat content in order to evaluate steatosis. The Kaplan–Meier method was implemented to generate survival curves. The independent risk factors for prognosis were identified by multiple Cox regression. Propensity score matching (PSM) was used to reduce the influence of confounding factors. This study explored the relevance between MAFLD and mortality, first decompensation and further decompensation. Results In our study, most patients were decompensated cirrhosis (n = 332, 75.6%) and the ratio of decompensated cirrhosis patients in non-MAFLD to MAFLD group was 199 : 133. Compared to the non-MAFLD group, patients with MAFLD had worse liver function which mainly reflected that there were more Child–Pugh C patients and higher model for end-stage liver disease score in the MAFLD group. A total of 207 adverse clinical events occurred in the total cohort during a median follow-up of 47 months, including 45 deaths, 28 hepatocellular carcinoma, 23 first decompensation and 111 further decompensation. Cox multivariate analysis showed that MAFLD was an independent risk factor for death [hazard ratio (HR) 1.931; 95% confidence interval (CI) 1.019–3.660; P = 0.044 HR 2.645; 95% CI, 1.145–6.115; P = 0.023] and further decompensation (HR 1.859; 95% CI, 1.261–2.741; P = 0.002 HR 1.953; 95% CI, 1.195–3.192; P = 0.008) before and after PSM. In decompensated group with MAFLD, diabetes had a more significant effect on adverse prognosis than overweight or obesity and other metabolic risk factors. Conclusion In patients with hepatitis B cirrhosis, concomitant MAFLD can predict a higher risk of further decompensation and death among decompensated individuals. According to patients among MAFLD, diabetes may be a major factor in the occurrence of adverse clinical events.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The impact of concomitant metabolic dysfunction-associated fatty liver disease on adverse outcomes in patients with hepatitis B cirrhosis: a propensity score matching study

Wang

Wei

et al. 2023

European Journal of Gastroenterology &Amp; Hepatology

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“…16 This is reflected in our study, where one-third of patients with cirrhosis and ascites had underlying NAFLD. Given the changing etiology of cirrhosis and prevalence of obesity in patients with end-stage liver disease, 17 the safety of a "blind" (i.e., conventional anatomic) paracentesis comes into question. POCUS theoretically has the ability to find areas on the abdominal wall where adipose tissue is not a significant barrier to the procedure, as well as to search for optimal fluid pockets that may have been redistributed due to increased intraabdominal pressures.…”

Section: Discussionmentioning

confidence: 99%

Does Point-of-Care Ultrasound Change the Needle Insertion Location During Routine Bedside Paracentesis?

et al. 2021

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BACKGROUND: Paracentesis is a bedside procedure to obtain ascitic fluid from the peritoneum. Point-of-care ultrasound (POCUS) improves the safety of some medical procedures. However, the evidence supporting its utility in paracentesis is limited. OBJECTIVE: We aimed to assess if POCUS would yield a user-preferred site for needle insertion compared to conventional landmarking, defined as a ≥ 5 cm change in location. DESIGN: This was a prospective non-randomized trial comparing a POCUS-guided site to the conventional anatomic site in the same patient. PARTICIPANTS: Adult patients at Kingston Health Sciences Centre undergoing paracentesis were included. INTERVENTIONS: Physicians landmarked using conventional technique and compared this to a POCUS-guided site. The paracentesis was performed at whatever site was deemed optimal, if safe to do so. MAIN MEASURES: Data collected included the distance from the two sites, depth of fluid pockets, and anatomic considerations. KEY RESULTS: Forty-five procedures were performed among 30 patients and by 24 physicians, who were primarily in their PGY 1 and 2 years of training (33% and 31% respectively). Patients' ascites was mostly due to cirrhosis (84%) predominantly due to alcohol (47%) and NAFLD (34%). Users preferred the POCUSguided site which resulted in a change in needle insertion ≥ 5 cm from the conventional anatomic site in 69% of cases. The average depth of fluid was greater at the POCUS site vs. the anatomic site (5.4±2.8 cm vs. 3.0±2.5 cm, p < 0.005). POCUS deflected the needle insertion site superiorly and laterally to the anatomic site. The POCUS site was chosen (1) to avoid adjacent organs, (2) to optimize the fluid pocket, and (3) due to abdominal wall considerations, such as pannus. Six cases landmarked anatomically were aborted when POCUS revealed inadequate ascites. CONCLUSIONS: POCUS changes the needle insertion site from the conventional anatomic site for most procedures, due to optimizing the fluid pocket and safety concerns, and helped avoid cases where an unsafe volume of ascites was present.

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“… 4 , 5 Obesity can play a role in nonalcoholic steatohepatitis, leading to liver decompensation, HCC, and death. 6 , 7 Yet, both alcohol drinking and obesity are common. The risk of cirrhosis and HCC in people with heavy alcohol intake and obesity also varies considerably, contributing to the difficulty of developing a clinically useful risk stratification strategy.…”

Section: Introductionmentioning

confidence: 99%

Synergistic Associations of PNPLA3 I148M Variant, Alcohol Intake, and Obesity With Risk of Cirrhosis, Hepatocellular Carcinoma, and Mortality

et al. 2022

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ImportanceAlcohol drinking and obesity are associated with an increased risk of cirrhosis and hepatocellular carcinoma (HCC), but the risk is not uniform among people with these risk factors. Genetic variants, such as I148M in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene, may play an important role in modulating cirrhosis and HCC risk.ObjectiveTo investigate the joint associations of the PNPLA3 I148M variant, alcohol intake, and obesity with the risk of cirrhosis, HCC, and liver disease–related mortality.Design, Setting, and ParticipantsThis prospective cohort study analyzed 414 209 participants enrolled in the UK Biobank study from March 2006 to December 2010. Participants had no previous diagnosis of cirrhosis and HCC and were followed up through March 2021.ExposuresSelf-reported alcohol intake (nonexcessive vs excessive), obesity (body mass index ≥30 [calculated as weight in kilograms divided by height in meters squared]), and PNPLA3 I148M variant status (noncarrier, heterozygous carrier, or homozygous carrier) from initial assessment.Main Outcomes and MeasuresThe primary outcomes were incident cirrhosis and HCC cases and liver disease–related death ascertained from inpatient hospitalization records and death registry. The risks were calculated by Cox proportional hazards regression models.ResultsA total of 414 209 participants (mean [SD] age, 56.3 [8.09] years; 218 567 women [52.8%]; 389 452 White race and ethnicity [94.0%]) were included. Of these participants, 2398 participants (0.6%) developed cirrhosis (5.07 [95% CI, 4.87-5.28] cases per 100 person-years), 323 (0.1%) developed HCC (0.68 [95% CI, 0.61-0.76] cases per 100 person-years), and 878 (0.2%) died from a liver disease–related cause (1.76 [95% CI, 1.64-1.88] cases per 100 person-years) during a median follow-up of 10.9 years. Synergistic interactions between the PNPLA3 I148M variant, obesity, and alcohol intake were associated with the risk of cirrhosis, HCC, and liver disease–related mortality. The risk of cirrhosis increased supramultiplicatively (adjusted hazard ratio [aHR], 17.52; 95% CI, 12.84-23.90) in individuals with obesity, with excessive drinking, and who were homozygous carriers compared with those with no obesity, with nonexcessive drinking, and who were noncarriers. Supramultiplicative associations between the 3 factors and risks of HCC were found in individuals with 3 risk factors (aHR, 30.13; 95% CI, 16.51-54.98) and liver disease–related mortality (aHR, 21.82; 95% CI, 13.78-34.56). The PNPLA3 I148M variant status significantly differentiated the risk of cirrhosis, HCC, and liver disease–related mortality in persons with excessive drinking and obesity.Conclusions and RelevanceThis study found synergistic associations of the PNPLA3 I148M variant, excessive alcohol intake, and obesity with increased risk of cirrhosis, HCC, and liver disease–related death in the general population. The PNPLA3 I148M variant status may help refine the risk stratification for liver disease in persons with excessive drinking and obesity who may need early preventive measures.

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Obesity and Liver Decompensation

Abstract: http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/video/14-1-reading-ahn a video presentation of this article http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/video/14-1-interview-ahn the interview with the author

Cited by 10 publications

References 15 publications

The impact of concomitant metabolic dysfunction-associated fatty liver disease on adverse outcomes in patients with hepatitis B cirrhosis: a propensity score matching study

The impact of concomitant metabolic dysfunction-associated fatty liver disease on adverse outcomes in patients with hepatitis B cirrhosis: a propensity score matching study

Does Point-of-Care Ultrasound Change the Needle Insertion Location During Routine Bedside Paracentesis?

Synergistic Associations of PNPLA3 I148M Variant, Alcohol Intake, and Obesity With Risk of Cirrhosis, Hepatocellular Carcinoma, and Mortality

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