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.

Introduction

Liver elastography is one of the basic diagnostic tools in hepatology practice. The most widely used and most studied tool in the world is transient elastography (Fibroscan), however, this system is unevenly available in Slovakia. Shear-wave elastography is a more accessible method because it is built into standard ultrasound systems. However, the problem of shear-wave elastography remains the interpretation of its results, since the threshold values for significant fibrosis (SF) and advanced fibrosis (AF) are unique for each system.

Aims & Methods

To compare the results of transient elastography (TE) and point shear-wave elastography (pSWE) in a cohort of patients examined simultaneously with both systems and to determine the clinical benefit of pSWE in practice.
We examined all indicated patients over a 15-month period using both TE and pSWE (Hitachi Arietta V70). We recorded liver stiffness values in kPa, and baseline demographic and laboratory parameters. We used TE as the gold standard, with a threshold of >10 kPa for SF and >15 kPa for AF. We evaluated the accuracy of pSWE in predicting the detection of SF and AF. We used three models: the first one containing only pSWE values, and two logit models using pSWE together with common demographic and laboratory parameters. We identified the area under the curve (AUROC) and threshold values for each model and evaluated the probability of SF and AF according to these values.

Results

We examined 500 patients with a median age of 60 (IQR 48-69), male/female 214/286, with a SF rate of 30.8% and AF of 18.4%. The stiffness values according to TE and pSWE showed a highly significant correlation (rho=0.593, P<0.001). We found the accuracy of pSWE alone in predicting SF (AUROC=0.812), and AF (AUROC=0.839) with threshold values of SF>6.34 and AF>8.45 kPa. For values of pSWE<6.34, 6.34-8.45, and >8.45 kPa, the probability of SF was 11.1, 40.9, and 65.4% and AF was 5.0, 14.77, and 48.9%. We created two probability models (for P, range 0 to 1): ASTEL1 (N=369) that included pSWE, GGT, and platelets (AUROC SF=0.856, AUROC AF=0.908), and ASTEL2 (N=467) using pSWE, age, sex, AST/ALT, GGT (AUROC SF=0.857, AUROC AF=0.901). We set a threshold of P<0.33 to exclude SF and P>0.66 to confirm AF. At P<0.33, P=0.33-0.66, and P>0.66, SF was present in 15.6, 62, and 94.2% (ASTEL1) and 13.92, 50.7, and 86.8% (ASTEL2). At P<0.33, P=0.33-0.66 and P>0.66, AF was present in 5.6, 30, and 79.7% (ASTEL1) and in 4.4, 28, 73.68% (ASTEL2).

Conclusion

pSWE alone has an excellent negative predictive value (<6.34 kPa, 88.9-95%) in the diagnosis of SF and AF. Higher accuracy of positive prediction of SF (86.8-94.2%) and AF (73.7-79.7%) can be achieved by using one of two probability models (for P>0.66) combining SWE values with common demographic and laboratory parameters.

Clinical Case Summary

Introduction: Rituximab, a monoclonal anti-CD20 antibody, is widely used for treating hematologic malignancies and autoimmune disorders due to its B-cell depleting action. While gastrointestinal side effects like diarrhea are seen in up to 15% of patients, these are typically mild and self-limiting. Severe colitis is a rare but increasingly recognized complication.
Case Description: A 76-year-old diabetic male with a history of ACS (post-PTCA in 2021) presented with 2 months history of generalized abdominal pain, watery diarrhea (6–7 episodes/day), and weight loss. He had a history of follicular lymphoma diagnosed 4 years prior, treated with 6 cycles of CHOP-R followed by rituximab maintenance (375 mg/m² every 3 months). Symptoms began after the 6th maintenance dose.Physical exam revealed mild pallor;abdomen was soft, nontender. Labs showed normocytic anemia and mild neutrophilic leukocytosis. Stool tests were negative for common pathogens, including C. difficile. The patient was planned for a Colonoscopy, which revealed ulcers over the ileocecal valve and rectal erosions. Biopsies showed mixed inflammatory infiltrates, cryptitis, crypt abscesses, and crypt rupture, consistent with severe active ileocolitis. AFB culture and GeneXpert were negative for tuberculosis.The patient was started on oral mesalamine (500 mg TID) along with Rifaximin(400mg) BD for 2 weeks, showing marked clinical improvement.
Discussion: Rituximab-induced colitis is rare and poorly understood. It may result from disruption of mucosal immunoregulation due to B-cell depletion, leading to T-cell-mediated inflammation. Histology may resemble patterns seen in GVHD or autoimmune enteropathy. Most cases resolve with supportive care and discontinuation of the drug; however, some, like this case, may require treatment in the form of 5ASA, or steroids.There is no previous data on the use of rifaximin in such cases. Differentiating drug-induced IBD from primary IBD remains a diagnostic challenge.

References

There is limited evidence in the literature establishing a definitive association between rituximab therapy and the onset of colitis. However, emerging hypotheses suggest that rituximab-induced depletion of peripheral CD19+ B cells and colonic CD20+ lymphoid aggregates may disrupt mucosal immune homeostasis, thereby contributing to structural alterations in the intestinal architecture and promoting inflammation.
The role of the gut microbiota in the pathogenesis and persistence of mucosal inflammation in inflammatory bowel disease (IBD) provides a rationale for the therapeutic use of antibiotics in selected cases. While systemic antibiotics such as ciprofloxacin and metronidazole have demonstrated clinical efficacy in IBD management, their utility may be limited in drug-induced colitis due to the potential for systemic adverse effects.
In contrast, rifaximin, a non-systemic, presents a favorable safety profile and has shown promise as a therapeutic option in both idiopathic and drug-induced enterocolitis. Its targeted antimicrobial activity within the gastrointestinal tract, combined with minimal systemic exposure, renders it an attractive alternative. However, further prospective, randomized studies are warranted to substantiate its efficacy and long-term safety in this context.