Decompensated Patients Research Articles

Whole blood thrombin generation shows a significant hypocoagulable state in patients with decompensated cirrhosis

BackgroundPatients with cirrhosis have a normal to increased thrombin generation (TG) capacity in platelet-poor plasma (PPP). By reflecting the contribution of all circulating blood cells, whole blood (WB) TG may allow a more physiological assessment of coagulation. ObjectivesWe compared WB-TG vs PPP-TG in patients with cirrhosis. MethodsAssessment of coagulation included routine tests, factor VIII, natural anticoagulants, PPP-TG, and WB-TG. TG assays were performed with and without thrombomodulin. Twenty-five healthy subjects were included as controls. ResultsWe included 108 patients (Child-Pugh A/B/C, 44/24/40). Compared with controls, patients had significantly lower platelet count, longer international normalized ratio, higher FVIII, and lower levels of protein C/S and antithrombin. Regarding thrombomodulin-modified TG assays, in compensated cirrhosis, both PPP-TG and WB-TG indicated an increased TG capacity, as reflected by an endogenous thrombin potential (ETP) significantly higher than controls. In contrast, in decompensated cirrhosis, PPP-TG indicated a hypercoagulable state with increased ETP, higher peak height, and shorter time-to-peak than controls, whereas WB-TG revealed a progressive impairment of TG kinetics and total capacity, ultimately resulting in a profound hypocoagulable state in patients with Child-Pugh C cirrhosis (ie, significant prolongation of lag time and time-to-peak with reduction of both ETP and peak height). In decompensated patients, bacterial infections and severity of anemia were associated with a further reduction of both ETP and peak height. ConclusionCompensated cirrhosis is associated with an increased TG capacity. In decompensated cirrhosis, contrary to PPP-TG, which indicates hypercoagulability, WB-TG shows a significant hypocoagulable state. The clinical value of these findings deserves further investigation.

Interobserver agreement and prognostic value of image-based scoring systems in patients with primary sclerosing cholangitis.

Primary sclerosing cholangitis (PSC) is a cholestatic liver disease that progresses to cirrhosis and liver failure. The Anali and Amsterdam scores are based upon imaging features on MRI and ERCP, respectively. We aimed to compare the interobserver variability and performances of these scores. Patients with PSC with at least 1 MRCP were included. Images were independently scored by 2 experts. Agreement and prognostic performance with a primary end point of hepatic decompensation was assessed. Fifty-nine patients were included (67.8% male, 86.4% IBD). Interobserver agreement for the Anali and Amsterdam scores were moderate (k = 0.49; 95% CI 0.35-0.64 and k = 0.43; 95% CI 0.30-0.56, respectively). Among the Anali components, dysmorphy (caudate/right lobe ratio > 0.9) had fair agreement (k = 0.37; 95% CI 0.14-0.60) and portal hypertension (k = 0.64, 95% CI 0.32-0.89) and intrahepatic dilation (k = 0.70; 95% CI 0.53-0.87) had substantial agreement. The Amsterdam extrahepatic and intrahepatic scores had fair agreement (k = 0.38; 95% CI 0.23-0.52) and moderate agreement (k = 0.50; 95% CI 0.34-0.67), respectively. Anali score (HR 5.90, 95% CI 1.64-21.21), total bilirubin (HR = 3.23; 95% Cl 1.06-9.91), and age (HR = 1.05; 95% CI 1.00-1.11) were independent predictors of hepatic decompensation. Mayo risk score and Anali score had good discriminative ability with c-statistics of 0.78 (CI 0.59-0.96) and 0.76 (CI 0.56-0.91). Anali score remained an independent predictor after adjusting for Mayo risk score. Anali score adds additional predictive value for hepatic decompensation in patients with PSC.

Posttreatment liver function, but not baseline liver function stratifies patient survival after direct-acting antiviral treatment in decompensated cirrhosis with hepatitis C virus

BackgroundThe prognosis of cirrhosis is clearly stratified by liver function. Although direct-acting antiviral (DAA) has recently been used to eliminate hepatitis C virus (HCV), it is not clear whether liver function stratifies the prognosis of decompensated cirrhotic patients treated with DAA.MethodsA total of 206 HCV-associated decompensated cirrhotic patients who started DAA from February 2019 to December 2021 at 31 Japanese hospitals were prospectively registered.ResultsThe median age was 68, and the proportions of patients with Child–Pugh class A (CP-A), CP-B and CP-C were 10% (20/206), 76% (156/206) and 15% (30/206), respectively. Twenty-six patients died, and two patients underwent liver transplantation (LT); the 2- and 3-year LT-free survival rates were 90.0% and 83.2%, respectively. We examined factors associated with LT-free survival using 2 models including either CP class (Model 1) or MELD score (Model 2). In multivariate Cox proportional hazard analysis, CP class at 12 weeks after the end of treatment (EOT) in Model 1 and MELD score at 12 weeks after the EOT in Model 2 were significant factors, while baseline CP class or MELD score was not. Two-year LT-free survival rates were 100%, 91.6% and 60.4% for patients with CP-A, CP-B and CP-C at 12 weeks after the EOT and 95.2% and 69.6% for patients with MELD < 15 and MELD ≥ 15 at 12 weeks after the EOT, respectively.ConclusionsThe prognosis of decompensated cirrhotic patients receiving DAA was stratified by liver function at 12 weeks after the EOT, not by baseline liver function.

Serum lipid profiling in decompensated patients with Hepatitis B virus -related cirrhosis

Serum lipid profiling in decompensated patients with Hepatitis B virus -related cirrhosis

Noninvasive assessment of hepatic decompensation.

Noninvasive tests (NITs) are used in all aspects of liver disease management. Their most prominent break-through since the millennium has been in advancing early detection of liver fibrosis, but their use is not limited to this. In contrast to the symptom-driven assessment of decompensation in patients with cirrhosis, NITs provide not only opportunities for earlier diagnoses but also accurate prognostication, targeted treatment decisions, and a means of monitoring disease. NITs can inform disease management and decision-making based on validated cutoffs and standardized interpretations as a valuable supplement to clinical acumen. The Baveno VI and VII consensus meetings resulted in tangible improvements to pathways of care for patients with compensated and decompensated advanced chronic liver disease, including the combination of platelet count and transient elastography to diagnose clinically significant portal hypertension. Furthermore, circulating NITs will play increasingly important roles in assessing the response to interventions against ascites, variceal bleeding, HE, acute kidney injury, and infections. However, due to NITs' wide availability, there is a risk of inaccurate use, leading to a waste of resources and flawed decisions. In this review, we describe the uses and pitfalls of NITs for hepatic decompensation, from risk stratification in primary care to treatment decisions in outpatient clinics, as well as for the in-hospital management of patients with acute-on-chronic liver failure. We summarize which NITs to use when, for what indications, and how to maximize the potential of NITs for improved patient management.

Albumin infusion reduces ascite occurrence in Child-Pugh B patients treated by Atezolizumab-Bevacizumab for advanced HCC.

Long-term albumin infusions have been associated with improved outcomes in decompensated cirrhotic patients. This study aimed to evaluate the impact of albumin infusion on the prognosis of Child-Pugh B patients undergoing treatment with AtezoBev for advanced hepatocellular carcinoma (HCC). We conducted a retrospective multicentric study that included all Child-Pugh B cirrhotic patients treated with AtezoBev since 2020. We examined the effects of albumin infusion (40g every 3 weeks) on overall survival (OS) and the occurrence of cirrhosis-related complications. Time-to-event data were analyzed using Kaplan-Meier with the log-rank test and Cox models. Forty-seven HCC patients with a Child-Pugh B score who received AtezoBev were included, of whom 26% also received albumin infusions every 3 weeks. The two groups were similar in terms of liver function and HCC parameters. The median OS was 4.4 and 5.8 months (p=0.42) for patients who did or did not receive albumin, respectively. The occurrence of hepatic encephalopathy and variceal bleeding was similar between the two groups. However, albumin infusions were associated with a significantly lower rate of ascites expansion/development (13% versus 57%, p=0.005). Cox analysis revealed that a history of ascites (HR=3.82 [95% CI: 1.73-8.48]) was independently associated with a higher risk of ascites expansion/development, whereas albumin infusions were protective (HR=0.07 [95% CI: 0.01-0.54]). Albumin infusion did not improve overall survival in Child-Pugh B HCC patients treated with AtezoBev, but it significantly reduced the expansion/development of ascites.

S1345 Clinical Outcomes of Antibiotic Use Before Paracentesis in Hospitalized Decompensated Cirrhosis Patients: A Retrospective Study

S1345 Clinical Outcomes of Antibiotic Use Before Paracentesis in Hospitalized Decompensated Cirrhosis Patients: A Retrospective Study

CLINICAL PRESENTATION AND OUTCOME IN HOSPITALIZED PATIENT WITH DECOMPENSATED CIRRHOSIS OF LIVER IN A TERTIARY CARE CENTRE OF NEPAL

Background: Decompensated liver cirrhosis is a progressive and potentially life-threatening condition characterized by the loss of liver function and the development of severe complications. This study aimed to assess the clinical presentation and outcomes among admitted decompensated liver cirrhosis patients. Methods: This hospital-based descriptive, cross-sectional study included 127 decompensated cirrhotic patients of college of medical sciences, Bharatpur, Nepal. Data were collected between August 2022 and April 2023. The data analysis was done using statistical package for the social sciences version 20. Statistical analysis was performed using descriptive statistics. Results: Abdominal distension, jaundice and hematemesis/melena were present in 43%, 23.6% and 15% of patients respectively. Common complications amongst the study population were upper GI bleeding (15 %), hepatic encephalopathy (12.6%), and hepatorenal syndrome (11%). Inpatient mortality was 12.6%, of which most common complication related to mortality was hepatorenal syndrome 43.7%. Presence of shock, severe sepsis, severe anemia, hyponatremia (&lt;130 mEq/L) were also common in mortality. Conclusions: Abdominal distension, jaundice and hematemesis/melena were the common presentation amongst the hospitalized decompensated cirrhotic patients. Hepatorenal syndrome, shock and severe sepsis complicating decompensated cirrhosis of liver were common in mortality.

The majority of pediatric Fontan patients have excellent post-transplant survival

ObjectiveMany pediatric Fontan patients require heart transplant, but this cohort is understudied given the difficulty in identifying these patients in national registries. We sought to characterize survival post-transplant in a large cohort of pediatric patients undergoing the Fontan. MethodsThe United Network for Organ Sharing and Pediatric Health Information System were used to identify Fontan heart transplant recipients aged less than 18 years (n = 241) between 2005 and 2022. Decompensation was defined as the presence of extracorporeal membrane oxygenation, ventilation, hepatic/renal dysfunction, paralytics, or total parenteral nutrition at transplant. ResultsMedian age at transplant was 9 (interquartile range, 5-12) years. Median waitlist time was 107 (37-229) days. Median volume across 32 center was 8 (3-11) cases. Approximately half (n = 107, 45%) of recipients had 1A/1 initial listing status. Sixty-four patients (28%) were functionally impaired at transplant, 10 patients (4%) were ventilated, and 18 patients (8%) had ventricular assist device support. Fifty-nine patients (25%) had hepatic dysfunction, and 15 patients (6%) had renal dysfunction. Twenty-one patients (9%) were dependent on total parenteral nutrition. Median postoperative stay was 24 (14-46) days, and in-hospital mortality was 7%. Kaplan–Meier analysis showed 1- and 5-year survivals of 89% (95% CI, 85-94) and 74% (95% CI, 81-86), respectively. Kaplan–Meier of Fontan patients without decompensation (n = 154) at transplant demonstrated 1- and 5-year survivals of 93% (95% CI, 88-97) and 88% (95% CI, 82-94), respectively. In-hospital mortality was higher in decompensated patients (11% vs 4%, P = .023). Multivariable analysis showed that decompensation predicted worse post-transplant survival (hazard ratio, 2.47; 95% CI, 1.16-5.22; P = .018), whereas older age at transplant predicted superior post-transplant survival (hazard ratio, 0.89/year; 95% CI, 0.80-0.98; P = .019). ConclusionsPediatric Fontan post-transplant outcomes are promising, although early mortality remains high. For nondecompensated pediatric patients at transplant without end-organ disease (>63% of cohort), early mortality is circumvented and post-transplant survival is excellent and similar to all pediatric transplantation.

Compensated liver cirrhosis: Natural course and disease-modifying strategies.

Compensated liver cirrhosis (CLC) is defined as cirrhosis with one or more decompensating events, such as ascites, variceal haemorrhage, or hepatic encephalopathy. Patients with CLC are largely asymptomatic with preserved hepatic function. The transition from CLC to decompensated cirrhosis occurs as a result of a complex interaction between multiple predisposing and precipitating factors. The first decompensation event in CLC patients is considered a significant turning point in the progression of cirrhosis, as it signals a drastic decline in median survival rates from 10-12 years to only 1-2 years. Furthermore, early cirrhosis has the potential to regress as liver fibrosis is a dynamic condition. With the advent of effective non-invasive tools for detecting hepatic fibrosis, more and more patients with CLC are currently being recognised. This offers clinicians a unique opportunity to properly manage such patients in order to achieve cirrhosis regression or, at the very least, prevent its progression. There are numerous emerging approaches for preventing or delaying decompensation in CLC patients. A growing body of evidence indicates that treating the underlying cause can lead to cirrhosis regression, and the use of non-selective beta-blockers can prevent decompensation by lowering portal hypertension. Additionally, addressing various cofactors (such as obesity, diabetes, dyslipidaemia, and alcoholism) and precipitating factors (such as infection, viral hepatitis, and hepatotoxic drugs) that have a detrimental impact on the natural course of cirrhosis may benefit patients with CLC. However, high-quality data must be generated through well-designed and adequately powered randomised clinical trials to validate these disease-modifying techniques for CLC patients. This article discussed the natural history of CLC, risk factors for its progression, and therapeutic approaches that could alter the trajectory of CLC evolution and improve outcomes.

Serum liver fibrosis markers predict hepatic decompensation in compensated cirrhosis

Background and aimThe literature is sparse on the association between serum liver fibrosis markers and the development of hepatic decompensation in patients with compensated cirrhosis. We aimed to assessed whether the serum liver fibrosis markers are predictive of the occurrence of hepatic decompensation.MethodsWe ascertained 688 cirrhotic patients with varying etiologies, between December 2015 to December 2019. Serum hyaluronic acid (HA), laminin (LN), collagen IV (CIV), and N-terminal propeptide of type III collagen (PIIINP) levels were measured at enrollment. All subjects were followed for at least 6 months for occurrence of hepatic decompensation. Cox proportional hazard regression models were used to estimate the hazard ratios (HRs) of hepatic decompensation during follow-up.ResultsDuring a median follow-up of 22.0 (13.0–32.0) months, decompensation occurred in 69 (10.0%) patients. Multivariate analysis indicated that higher LN (HR: 1.008, 95% confidence interval [CI]: 1.002–1.014, P = 0.011) and CIV (HR: 1.004, 95% CI: 1.001–1.007, P = 0.003) levels were independently associated with hepatic decompensation. Furthermore, patients in the tertile 2 and tertile 3 groups for CIV levels had HRs of 4.787 (1.419, 16.152) (P = 0.012) and 5.153 (1.508, 17.604) (P = 0.009), respectively, for occurrence of decompensation event compared with those in the tertile 1 group.ConclusionSerum liver fibrosis markers, particularly in CIV, appeared to be reliable biomarkers of disease progression and liver decompensation in patients with compensated cirrhosis with varying etiologies.

The genetics of portal hypertension: Recent developments and the road ahead.

Portal hypertension (PH), defined as a pathological increase in the portal vein pressure, has different aetiologies and causes. Intrahepatic PH is mostly secondary to the presence of underlying liver disease leading to cirrhosis, characterized by parenchymal changes with deregulated accumulation of extracellular matrix and vascular abnormalities; liver sinusoidal endothelial cells and hepatic stellate cells are key players in PH progression, able to influence each other. However, PH may also develop independently of parenchymal damage, as occur in portosinusoidal vascular disorder (PSVD), a group of clinical and histological entities characterized by portal vasculature dysfunctions. In this particular group of disorders, the pathophysiology of PH is still poorly understood. In the last years, several genetic studies, based on genome-wide association studies or whole-exome sequencing analysis, have highlighted the importance of genetic heritability in PH pathogenesis, both in cirrhotic and non-cirrhotic cases. The common PNPLA3 p.I148M variant, one of the main determinants of the susceptibility to steatotic liver disease, has also been associated with decompensation in patients with PH. Genetic variations at loci influencing coagulation, mainly the ABO locus, may directly contribute to the pathogenesis of PH. Rare genetic variants have been associated with familiar cases of progressive PSVD. In this review, we summarize the recent knowledges on genetic variants predisposing to PH development, contributing to better understand the role of genetic factors in PH pathogenesis.

Predictors of clinical trajectories of patients with acutely decompensated cirrhosis. An external validation of the PREDICT study.

The PREDICT study recently showed that acutely decompensated (AD) patients with cirrhosis can present three different clinical phenotypes in the 90 days after admission: (1) pre-ACLF, developing acute-on-chronic liver failure (ACLF); (2) unstable decompensated cirrhosis (UDC), being re-admitted for AD without ACLF and (3) stable decompensated cirrhosis (SDC), not presenting readmission or ACLF. This study aimed to externally validate the existence of these three distinct trajectories and to identify predictors for the occurrence of each trajectory. Baseline data, 3-month ACLF and readmission incidence and 1-year survival were analysed in a prospective cohort of patients admitted for AD. A multinomial multivariable model was used to evaluate the association between baseline features and clinical trajectories. Of the 311 patients enrolled, 55% met the criteria for SDC, 18% for UDC and 27% for pre-ACLF, presenting a significantly different 1-year mortality: pre-ACLF 65%, UDC 46%, SDC 21% (p < .001). The presence of hepatic encephalopathy (HE) was associated with UDC (p = .043), while the absence of ascites to SDC (p = .017). Among laboratory parameters, an increase in MELD-Na (p = .001) and C-reactive protein (p = .009) and a decrease in haemoglobin (p = .004) and albumin (p = .008) levels were associated with pre-ACLF. The present study confirms that AD patients have three different clinical trajectories with different mortality rates. Besides the severity of cirrhosis, the association with C-reactive protein supports the predominant role of systemic inflammation in ACLF pathophysiology. Finally, HE is associated with the UDC phenotype highlighting the need for better management of this complication after discharge.

THE TREATMENT OF HEPATORENAL SYNDROME WITH TERLIPRESSIN: CONTINUOUS INTRAVENOUS INFUSION VS INTRAVENOUS BOLUSES A RANDOMISED CONTROLLED STUDY ON SYNDROME

Objective: Hepatorenal syndrome (HRS) is a severe complication of cirrhosis, with terlipressin and albumin being the most common treatment. The study aimed to compare the effectiveness and safety of continuous intravenous infusion vs. intravenous boluses of terlipressin in treating type 1 h.&#x0D; Methods: A randomized controlled trial was conducted on cirrhosis patients with type 1 h. Patients were allocated to receive terlipressin via continuous infusion (TERLI-INF group) or intravenous boluses (TERLI-BOL group). Demographic, clinical, and laboratory data were collected, and treatment details were recorded. The primary endpoint was the frequency of drug-related adverse events. Secondary endpoints included therapy responsiveness and 90-day transplant-free survival.&#x0D; Results: Both groups exhibited similar baseline characteristics. While treatment length and cumulative albumin doses were comparable, TERLI-INF patients received lower terlipressin doses. Severe treatment-related adverse events differed between groups. Univariate analysis identified several baseline parameters significantly associated with response to terlipressin. The study supports continuous terlipressin infusion's superiority in treating type 1 h, with lower adverse event rates and improved patient response.&#x0D; Conclusion: The study concludes that continuous intravenous terlipressin infusion is safer and more effective in treating type 1 h in decompensated cirrhosis patients compared to intravenous boluses. Lower terlipressin dosages were effective in continuous infusion, indicating improved safety. The MELD score was an independent predictor of response, and therapy responsiveness was associated with improved 90 d survival.

MEFIB-Index and MAST-Score in the assessment of hepatic decompensation in metabolic dysfunction-associated steatosis liver disease-Individual participant data meta-analyses.

There are limited data regarding the longitudinal association between MEFIB-Index (MRE combined with FIB-4) versus MAST-Score (MRI-aspartate aminotransferase) and hepatic decompensation. To examine the longitudinal association between MEFIB-Index versus MAST-Score in predicting hepatic decompensation in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). This was a longitudinal, retrospective analysis of subjects from United States, Japan, and Turkey who underwent a baseline MRE and MRI-PDFF and were followed for hepatic decompensation. Cox-proportional hazard analyses were used to assess the association between MEFIB-Index versus MAST-Score with a composite primary outcome (hepatic decompensation) defined as ascites, hepatic encephalopathy, and varices needing treatment. This meta-analysis of individual participants (IPDMA) included 454 patients (58% women) with a mean (±SD) age of 56.0 (±13.5) years. The MEFIB-Index (MRE ≥3.3 kPa + FIB 4 ≥1.6) and MAST-Score (>0.242) were positive for 34% and 9% of the sample, respectively. At baseline, 23 patients met criteria for hepatic decompensation. Among 297 patients with available longitudinal data with a median (IQR) of 4.2 (5.0) years of follow-up, 25 incident cases met criteria for hepatic decompensation. A positive MEFIB-Index [HR = 49.22 (95% CI: 6.23-388.64, p < 0.001)] and a positive MAST-Score [HR = 3.86 (95% CI: 1.46-10.17, p < 0.001)] were statistically significant predictors of the incident hepatic decompensation. MEFIB-Index (c-statistic: 0.89, standard error (SE) = 0.02) was statistically superior to the MAST-Score (c-statistic: 0.81, SE = 0.03) (p < 0.0001) in predicting hepatic decompensation. A combination of MRI-based biomarker and blood tests, MEFIB-Index and MAST-Score can predict the risk of hepatic decompensation in patients with MASLD.

Impact of emergency department-based intensive care unit on outcomes of decompensating boarding emergency department patients.

Emergency department (ED) boarding, or remaining in the ED after admission before transfer to an inpatient bed, is prevalent. Boarding patients may decompensate before inpatient transfer, necessitating escalation to the intensive care unit (ICU). We evaluated the impact of an ED-ICU on decompensating boarding ED patients. This is a retrospective single-center observational study. We identified decompensated boarding ED patients necessitating critical care before departure from the ED from October 2012 to December 2021. An automated query and manual chart review extracted data. Three cohorts were defined: pre-ED-ICU implementation (Group 1), post-ED-ICU implementation with ED-ICU care (Group 2), and post-ED-ICU implementation with inpatient ICU admission without ED-ICU care (Group 3). Primary outcome was ICU length of stay (LOS). Secondary outcomes included hospital LOS, in-hospital mortality, and ICU admissions with ICU LOS<24hours. Between-groups comparisons used multiple regression analysis for continuous variables, χ2 tests and multivariable logistic regression analysis for binary variables, and follow-up contrasts for statistically significant omnibus tests. A total of 1123 visits met inclusion criteria: 225 in Group 1, 780 in Group 2, and 118 in Group 3. Mean ICU LOS was shorter for Group 2 than Group 1 or 3 (47.4vs 92.3vs 103.9hours, P<0.001). Mean hospital LOS was shorter for Group 2 than Group 1 or 3 (185.1vs 246.8vs 257.3hours, P<0.01). In-hospital mortality was similar between groups. The proportion of ICU LOS<24hours was lower for Group 2 than Group 1 or 3 (16.5vs 27.1vs 32.2%, P<0.01). For decompensating boarding ED patients, ED-ICU care was associated with decreased ICU and hospital LOS, similar mortality, and fewer short-stay ICU admissions, suggesting ED-ICU care is associated with downstream resource preservation.

Patient satisfaction and outcomes of crisis resolution home treatment for the management of acute psychiatric crises: a study during the COVID-19 pandemic in Madrid.

Crisis Resolution Home Treatment (CRHT) seem to offer comparable results to the traditional hospitalization model, at a lower cost and offering greater flexibility and scope. However, in Madrid, its implementation in Mental Health did not occur until the midst of the COVID-19 pandemic. In this work we analysed the effectiveness of a mental health CRHT unit promoted during the COVID-19 pandemic, as well as the degree of satisfaction of patients and their families. 90 patients were treated by the CRHT unit in the period between October 2020 and June 2022. All patients met the inclusion criteria: (1) Acute psychopathological decompensation in patients suffering from psychotic disorders, major affective disorder, obsessive compulsive disorder, personality disorder and other severe mental disorders causing functional disability, according to ICD-10 diagnostic criteria; (2) Ages between 18-90 years old; (3) Living in the urban area of Vallecas, Madrid; and (4) Counting with sufficient social and family support. The effectiveness of the intervention was evaluated with the SF-36 health questionnaire, the caregiver burden with the Zarit questionnaire, and patient satisfaction with a survey specifically designed for this work. 55 (61.1%) patients completed the SF-36 at baseline and at the end of hospitalization. Statistically significant improvements were observed in the 8 dimensions of the SF-36 (p < 0.05). However, CRHT did not achieve a statistically significant decrease in caregiver burden. Regarding the satisfaction of the patients with the attention and care received, an average score of 47.72/50 was obtained. The Crisis Resolution Home Treatment intervention resulted in significant improvement in patients' quality of life with high satisfaction scores. However, it did not effectively reduce caregiver burden. Future research should focus on randomized controlled trials with long-term follow-up to assess the effectiveness of CRHT compared to traditional hospitalization and utilize specific assessment scales for different mental disorders.

Presurgical Decompensation in Patients Affected by Class III Dentoskeletal Malocclusion: A Comparison between Two Different Bracket Systems

The aim of this study was to analyse if bracket systems could affect the incisors’ decompensation in a group of patients affected by dentoskeletal Class III malocclusion and on the duration of presurgical orthodontics. A single-centre retrospective study was carried out on two groups of patients affected by dentoskeletal Class III and who underwent orthognathic surgery. Group 1, comprising 25 subjects (13 males, 12 females; mean age, 27.4 y.o.), was treated with interactive self-ligating brackets; group 2, comprising 10 subjects (5 males, 5 females; mean age, 27.2 y.o.), was treated with conventional twin brackets. Bracket prescription and archwire sequence were the same for both groups. Data were collected about age, upper incisors’ axis (UI^ANS-PNS), lower incisors’ axis (IMPA), and the total duration of presurgical orthodontics and were then compared between the two groups. The variation in the upper incisor axis and the duration of presurgical orthodontics was not significant between the groups, while the difference in the IMPA was small but significant. The use of a self-ligating bracket did not influence the decompensation of the upper incisors or the duration of presurgical orthodontics when compared with conventional ligating brackets. The difference in the IMPA was significantly different but clinically negligible.

Risk and predictors of hepatic decompensation in grey zone patients by the Baveno VII criteria: A competing risk analysis.

Baveno VII was proposed for non-invasive identification of clinically significant portal hypertension. However, a substantial proportion of patients is classified in the grey zone (i.e., liver stiffness 15-24.9 kPa and/or platelet count <150 × 109 /L). To evaluate the risk and predictors of hepatic decompensation in patients in the grey zone, and to determine the prognostic role of spleen stiffness measurement. We included prospective cohorts (from Hong Kong, Korea and France) of patients who had undergone transient elastography examination for chronic liver disease. We estimated risk of hepatic decompensation using competing risk regression with hepatocellular carcinoma and non-liver-related death as competing events. We identified 2763 patients with compensated advanced chronic liver disease (cACLD). There were 1243 (44.9%) and 536 (19.4%) patients in the Baveno VII grey zone and high-risk groups, respectively. The cumulative incidence of decompensation at 5 years was significantly different among low-risk (0.6% [95% CI: 0.2%-1.3%]), grey zone 4.2% (95% CI: 3.1%-5.4%) and high-risk groups (11.4% [95% CI: 8.7%-14.6%]). By competing risk analysis, aetiology of liver disease (alcohol-related liver disease), albumin-bilirubin score and alkaline phosphatase level were independently associated with decompensation among patients in the grey zone. The combination of Baveno VII and spleen stiffness significantly reduced patients classified into grey zone (12.8% in cACLD patients), while maintaining high discrimination of decompensation in low- and high-risk groups. Patients in grey zone of Baveno VII criteria remain at high risk of hepatic decompensation. Clinical risk factors and spleen stiffness can further stratify the risk in such patients.

Validation of the albumin-bilirubin score for identifying decompensation risk in patients with compensated cirrhosis.

The albumin-bilirubin (ALBI) score is an index of liver function recently developed to assess prognosis in patients with hepatocellular carcinoma (HCC). It can detect small changes in liver dysfunction and has been successfully applied to the prediction of survival in patients with non-malignant liver diseases of various etiologies. To investigate the ALBI score for identifying decompensation risk at the 3-year follow-up in patients with compensated cirrhosis. One-hundred and twenty-three patients with compensated cirrhosis without HCC in King Chulalongkorn Memorial Hospital diagnosed by imaging were retrospectively enrolled from January 2016 to December 2020. A total of 113 patients (91.9%) had Child A cirrhosis with a median model for end-stage liver disease (MELD) score of less than 9. Baseline clinical and laboratory variables and decompensation events were collected. The ALBI score was calculated and validated to classify decompensation risk into low-, middle-, and high-risk groups using three ALBI grade ranges (ALBI grade 1: ≤ -2.60; grade 2: > -2.60 but ≤ -1.39; grade 3: > -1.39). Decompensation events were defined as ascites development, variceal bleeding, or grade 3 or 4 hepatic encephalopathy. Among 123 cirrhotic patients enrolled, 13.8% (n = 17) developed decompensating events at a median time of 25 [95% confidence interval (CI): 17-31] mo. Median baseline ALBI score in compensated cirrhosis was significantly lower than that of patients who developed decompensation events [-2.768 (-2.956 to -2.453) vs -2.007 (-2.533 to -1.537); P = 0.01]. Analysis of decompensation risk at 3 years showed that ALBI score had a time-dependent area under the curve (tAUC) of 0.86 (95%CI: 0.78-0.92), which was significantly better than that of ALBI-Fibrosis-4 (ALBI-FIB4) score (tAUC = 0.77), MELD score (tAUC = 0.66), Child-Pugh score (tAUC = 0.65), and FIB-4 score (tAUC = 0.48) (P < 0.05 for all). The 3-year cumulative incidence of decompensation was 3.1%, 22.6%, and 50% in the low-, middle-, and high-risk groups, respectively (P < 0.001). The odds ratio for decompensation in patients of the high-risk group was 23.33 (95%CI: 3.88-140.12, P = 0.001). The ALBI score accurately identifies decompensation risk at the 3-year follow-up in patients with compensated cirrhosis. Those cirrhotic patients with a high-risk grade of ALBI score showed a 23 times greater odds of decompensation.