Introduction

Non-alcoholic fatty liver disease (NAFLD) can progress to fibrosis and cirrhosis. The evaluation of fibrosis in chronic liver disease using non-invasive methods is a current topic. Standard methods are liver stiffness measurement and serum biomarkers. Splenic elasticity measurement is a recent and interesting non-invasive approach that arouses the interest of the latest studies to evaluate fibrosis severity in NAFLD.
The aim of this study is to identify patients with NAFLD and advanced liver fibrosis, by establishing correlations between splenic and liver elasticity and fibrosis serum biomarkers.

Aims & Methods

This is a prospective study conducted in the hepato-gastroenterology department including all patients followed for hepatic steatosis during the period from July 2022 to January 2023. Patients with a family or personal history of chronic liver disease, and women with acute steatohepatitis in pregnancy or cholestasis in pregnancy were excluded. Measurement of hepatic and splenic stiffness and the degree of hepatic steatosis was done using liver elastrography (Fibroscan®) and Transient elastography with controlled attenuation parameter (CAP), respectively. NAFLD fibrosis (NFS) and Fibrosis-4 scores were calculated. Data were entered and processed using SPSS software version 22.0.

Results

We included 44 patients, divided into 28 women and 16 men (Sex-ratio F/M = 1.75), with a mean age of 61.4 years [32 to 84 years]. Three patients were smokers and four were alcoholics. Hypertension was found in 56.8%, 54.5% were diabetics and 52.3% were dyslipidemics. The mean BMI was 29.6 kg/m²±4.15 kg/m². Obesity was found in 45.5%, 36.4% were overweight and 18.2% of patients were normal weight. Hepatic steatosis was discovered following pain in the right hypochondrium in 79.5% of the cases and in front of a cytolysis in the remaining cases. All patients had diffuse steatosis without portal hypertension or degeneration signs on ultrasound.
Biological results showed cytolysis in seven patients. No patient had cholestasis. All patients had preserved liver function: normal prothrombin level and albumin. Hyperglycemia and lipid disturbance were observed in 43.2% and 36.4% of cases respectively.
Fibrosis was assessed by FIB4 score with a mean value of 1.11± 0.78; NFS score with a mean value of -1.16±1.18 and liver stiffness ranging from 2.4Kpa to 28.4Kpa (mean value 6.67Kpa). The degree of fibrosis judged by Fibroscan results was F0-F1 in 31 cases, F2 in 5 cases, F3 in 5 cases and F4 in 3 cases. Advanced fibrosis was correlated with NFS score (p=0.016), FIB-4 (p=0.001); but not associated with CAP value (p=0.51).
The mean splenic elasticity was 27.57 Kpa (ranging from 8.3 to 75 Kpa). It was significantly associated with liver elasticity (p=0.012) with an AUROC of 0.784. A threshold of 17.4 Kpa was predictive of advanced fibrosis with a specificity of 85.7% and a sensitivity of 73.5% (CI [0.029-0.404]). Similarly, splenic elasticity was correlated with CAP value (p=0.013). No association was identified with NFS and FIB4 scores.

Conclusion

Measurement of splenic elasticity is a simple and reliable non-invasive tool, comparable to liver elasticity, for the prediction of liver fibrosis during NAFLD.

Disclosure

no conflict of interest

Introduction

Transjugular intrahepatic portosystemic shunt (TIPS) is a well-established interventional treatment for complications of portal hypertension. Post-TIPS transient or persistent acute bilirubin elevation (ABE) is common, possibly due to impairment of portal perfusion. The outcomes of patients with ABE is not clear.

Aims & Methods

This study investigates the incidence, clinical outcomes, and prognostic factors associated with ABE in cirrhotic patients undergoing TIPS. Between January 2009 and November 2022, 1,287 patients (882 men, 405 women; mean age, 52 years) were included in this retrospective analysis. ABE was defined as a total serum bilirubin level exceeding 85.5 μmol/L (5 mg/dL) within one week after TIPS. Statistical analyses included the Kaplan-Meier method, log-rank test, multivariate Cox regression, and stepwise regression.

Results

Post-TIPS ABE occurred in 67 patients (5.2%). Patients with ABE had significantly higher baseline Child-Pugh scores (8.39 ± 1.62 vs. 7.41 ± 1.54, P < 0.001) and MELD scores (13.98 ± 4.13 vs. 10.72 ± 2.99, P < 0.001). Refractory ascites as the TIPS indication was more frequent in the ABE group (17.91% vs. 7.21%, P = 0.001). ABE was associated with a significantly higher incidence of hepatic encephalopathy (HE): 62.7% vs. 38.3% at 1 year and 80.6% vs. 62.8% at 5 years (P = 0.042). During follow-up, 441 patients died, with causes including liver failure (n = 129), gastrointestinal bleeding (n = 100), sepsis (n = 16), multi-organ dysfunction (MOD) (n = 41), hepatocellular carcinoma (HCC) (n = 43), and other or unknown causes (n = 112). Survival rates were significantly lower in the ABE group: 1-year (52.2% vs. 85.2%), 3-year (34.3% vs. 68.3%), and 5-year (25.4% vs. 46.6%) (P < 0.001). Multivariate analysis identified ABE (hazard ratio [HR]: 2.09; 95% confidence interval [CI]: 1.41–3.10; P < 0.001), age (HR: 1.05; 95% CI: 1.04–1.06; P < 0.001), albumin level (HR: 0.95; 95% CI: 0.94–0.97; P < 0.001), pre-TIPS grade 4 HE (HR: 1.93; 95% CI: 1.19–3.14; P = 0.008), presence of HCC (HR: 1.81; 95% CI: 1.24–2.65; P = 0.002), baseline MELD score (HR: 1.09; 95% CI: 1.04–1.14; P < 0.001), and change in MELD score (HR: 1.08; 95% CI: 1.06–1.11; P < 0.001) as independent predictors of post-TIPS mortality.

Conclusion

AEB is not rare in cirrhotic patients undergoing TIPS and is associated with an increased risk of HE and mortality. Risk factors for post-TIPS mortality include AB, older age, higher and fluctuating MELD scores, concurrent HCC, severe pre-TIPS HE, and lower albumin levels. Early identification, close monitoring, and prompt management of complications are essential to improving clinical outcomes and reducing the risk of liver failure after TIPS.

Introduction

Chronic liver disease remains one of the most common causes for hospital admission and is associated with high morbidity and mortality rates. Timely and adequate management within the first 24 hours is crucial for improving clinical outcomes in cases of decompensated cirrhosis. This study aimed to evaluate the impact of implementing a care bundle checklist during the first 24 hours of hospital admission on management and outcomes of decompensated cirrhosis.

Aims & Methods

We developed an adapted care bundle (based on the BSG/BASL care bundle, AASLD quality measures proposal, Baveno VII consensus, and EASL guidelines) and compared two patient groups from two Portuguese hospital centers: Group-A (retrospective, pre-care bundle implementation) and Group-B (prospective, post-care bundle implementation).

Results

A total of 224 patients (Group-A: 148; Group-B: 76) were included. More than one decompensation was observed in 118 patients (52.7%), and 69 patients (30.8%) were experiencing their index hospitalization for liver decompensation. Regarding etiology, alcoholic liver disease was the most common (n=200; 89.3%). The groups were similar in terms of gender, age, length of hospital stay, and Child-Pugh and MELD-Na scores at admission. The most common decompensations were gastrointestinal bleeding (n=91; 40.6%), ascites (n=75; 33.5%), and hepatic encephalopathy (n=72; 32.1%). Group B was more likely to present with multiple decompensations at admission and exhibited significantly higher rates of acute kidney injury, hepatocellular carcinoma, acute-on-chronic liver failure, and portal vein thrombosis (p<0.05). Following care bundle implementation, we found significant improvements in patient care. At admission, patients were significantly more likely to undergo urine and blood cultures, chest X-ray, and abdominal ultrasound (p<0.05), receive diagnostic paracentesis (p<0.05), and have an accurate alcohol history documented (p=0.04). During admission, Group-B was significantly more likely to be prescribed lactulose for encephalopathy prophylaxis, vasopressor therapy for gastrointestinal bleeding, and venous thromboembolism prophylaxis, as well as undergo nutritional assessment (p<0.05). While in-hospital mortality rates were similar (4.7% vs. 5.3%; p=1), 6-week mortality rates (8.8% vs. 3.9%; p=0.01) and 3-month readmission rates (31.1% vs. 15.8%; p=0.02) were significantly lower in the post-intervention cohort.

Conclusion

The implementation of a standardized care bundle was associated with higher rates of appropriate investigation and treatment within the first 24 hours of hospital admission and improved patient outcomes, reducing 6-week mortality and 3-month readmission rates.

Clinical Case Summary

Case report: We report a case of a 51-year-old patient who initially presented in 2014 with thrombocytopenia, and splenomegaly. Liver parameters were within the normal range. Comprehensive diagnostic evaluations, including CT scans and liver biopsy, excluded cirrhosis, vascular occlusions, bypass circuits and other potential etiologies such as toxic, autoimmune, or infectious causes. Additional investigations, including bone marrow and spleen puncture as well as genetic tests did not reveal any hematological or neoplastic diseases.
At the age of 66, the patient suffered an episode of variceal hemorrhage due to grade IV oesophageal varices. Subsequently, after referral to our clinic in March 2020, a transjugular portosystemic shunt (TIPSS) was placed for persistent grade III varices (Figure 1), reducing the varices to grade I (2024). Despite successful management of varices, the patient developed mild hepatic encephalopathy, managed with lactulose and rifaximin.
Biopsy revealed nodular regenerative hyperplasia (Figure 2). We diagnosed idiopathic non-cirrhotic portal hypertension (INCPH), an infrequent yet significant clinical entity characterized by intrahepatic portal hypertension without cirrhosis or other liver diseases. Management challenges included the patient's intolerance to non-selective beta-blockers due to sinus bradycardia and ongoing low-grade hepatic encephalopathy, which precluded further TIPSS modification. Future management may include splenic vein embolization should varices recur.
Conclusion: The diagnosis of INCPH necessitates evident portal hypertension, no cirrhosis or advanced fibrosis, and no hepatic or portal vein thrombosis on imaging. Due to limited data, management typically mirrors that of cirrhosis-induced portal hypertension. This case highlights the diagnostic and management challenges of INCPH, stressing the importance of comprehensive assessments to rule out other causes and customize treatment for complications.