Search Results (395)

Background: Splenic artery embolization (SAE) is commonly used in cirrhosis to manage hypersplenism and cytopenia. However, its longer-term clinical impact beyond hematologic parameters remains insufficiently characterized. Aim: To characterize longitudinal inpatient trajectories, clinical patterns, and follow-up features after SAE in patients with cirrhosis treated at a tertiary referral center in Kazakhstan. Methods: This retrospective single-center study included 149 patients with cirrhosis who underwent SAE. Clinical, laboratory, and imaging data were collected across sequential inpatient episodes. Outcomes included longitudinal patterns of hospitalization, laboratory trends, and baseline factors associated with a favorable clinical course. Subsequent hospitalization was defined as any inpatient episode following the index SAE admission, regardless of whether it was planned or unplanned. Results: During follow-up, 59.1% of patients had a second inpatient episode, with progressively fewer patients contributing to later observations. Liver disease severity remained largely stable, with no significant changes in Child–Pugh distribution. Portal hypertension manifestations, including varices and splenomegaly, remained highly prevalent, while recurrent variceal bleeding was relatively uncommon. Laboratory parameters demonstrated modest changes without sustained statistically significant improvement, and the number of recorded inpatient episodes decreased across sequential follow-up. Relatively stable documented follow-up trajectories were more frequently observed in patients with preserved liver function (Child–Pugh A), absence of ascites, and higher albumin levels. The most common causes of subsequent hospitalization were ascites and hepatic decompensation (38.9%) and varices without bleeding (26.2%), while documented major procedure-related complications were infrequent. Conclusions: In this retrospective single-center cohort, predominantly coil-based proximal or selective SAE demonstrated an acceptable documented major complication profile in selected patients with cirrhosis and portal hypertension. Because no untreated control group was available, the findings should be interpreted as descriptive real-world longitudinal data rather than causal evidence of reduced hospitalization burden. Full article

Background. This rat study reveals a new point: the considerable impact of unilateral adrenalectomy, severe vascular and multiorgan failure, occlusion/occlusion-like syndrome, and the stable gastric pentadecapeptide BPC 157 therapy. Based on the recent Fourier transform infrared (FTIR) spectroscopy vascular disturbance studies, particularly those after unilateral adrenalectomy in rats, the noted cytoprotective vascular recovery effect of the BPC 157 therapy may be useful. Methods. In rats, unilateral adrenalectomy (at 15 min, 5 h, 24 h) leads to integrated gross and morphological changes, vascular alterations, oxidative stress parameters, molecular markers and occlusion/occlusion-like syndrome and BPC 157 as useful therapy (/kg ig) (10 µg, 10 ng). Results. Peripherally and centrally, counteraction includes the lesions (adrenal, brain, heart, lung, liver, kidney, gastrointestinal tract), organ hemorrhage, and thrombosis. Attenuated/eliminated were arrhythmias, intracranial (superior sagittal sinus), portal, caval hypertension, and aortic hypotension. Significant resolution occurred via activation of collateral pathways, the azygos vein (direct blood flow delivery), and the recovered peduncle of the inferior suprarenal artery and superior suprarenal vein. Virchow’s triad circumstances were reversed. Occlusion/occlusion-like syndrome was counteracted as a whole. Also, BPC 157 counteracted adrenal lesions (lipid depletion, congestion). There were higher cortisol values, but still very low, and a shift toward the left of the adrenal compensatory weight increase. For the indicative conclusion along with previous studies, mechanistically, BPC 157 therapy exhibits the NO-system modulation/oxidative stress balance, increases NO-level, counteracts oxidative stress (malondialdehyde (MDA)), upregulates NOS1–3, and VEGF-A expression. Conclusions. These effects of BPC 157 therapy and its easy applicability deserve further consideration. Full article

Pulmonary arterial hypertension (PAH) is a progressive, fatal disease of the pulmonary vasculature characterized by obliterative remodeling of small pulmonary arteries, leading to sustained elevation of pulmonary vascular resistance, right ventricular failure, and premature death. The diagnostic gold standard remains right heart catheterization, requiring a mean pulmonary artery pressure greater than 20 mmHg at rest, a pulmonary arterial wedge pressure of 15 mmHg or below, and a pulmonary vascular resistance exceeding 2 Wood units. PAH is an autosomal dominant disorder with markedly incomplete penetrance of approximately 20–30%, indicating that germline mutations alone are insufficient to cause disease. Disease manifestation requires additional “second hits”, including chronic hypoxia, systemic inflammation, hemodynamic stress, hormonal influences, and common genetic modifiers such as single-nucleotide polymorphisms (SNPs). This genetic and environmental complexity underpins the broad clinical heterogeneity observed across PAH subtypes, which include idiopathic PAH, heritable PAH, and disease associated with connective tissue disorders, HIV infection, portal hypertension, congenital heart disease, schistosomiasis, and drug or toxin exposure. This review provides a comprehensive and critical appraisal of the molecular-genetic architecture of PAH. Thirty genes have now been implicated in disease pathogenesis, spanning seven functional categories: receptors of the TGF-β/BMP signaling family (BMPR2, ACVRL1, ENG, BMPR1B); circulating BMP ligands (GDF2, BMP10); transcription factors (TBX4, SOX17, KLF4, FOXF1, SMAD1, SMAD4, SMAD9); membrane and polyamine transporters (ATP13A3, AQP1); potassium channel regulators (KCNA5, KCNK3, ABCC8); metabolic and mitochondrial genes (EIF2AK4, NFU1, GGCX); signaling receptors and structural proteins (NOTCH3, KDR, CAV1, PLEKHH2); vasoactive and extracellular matrix regulators (KLK1, CBLN2, CD248); and epigenetic regulators (TET2, TOPBP1). Among these, BMPR2 is the dominant contributor, accounting for 53–86% of heritable PAH and 14–35% of idiopathic cases. The remaining genes each account for fewer than 5% of cases individually, collectively reflecting a broad landscape of rare and ultra-rare genetic contributions. For each gene, we critically evaluate the strength of genetic evidence, pathogenic mechanisms, degree of mechanistic resolution, and clinical relevance. We further discuss the contribution of emerging technologies, including whole-genome sequencing, single-cell and spatial transcriptomics, multi-omics integration, iPSC-derived vascular models, and artificial intelligence, to expanding the PAH genetic architecture beyond single-gene discovery. A key theme across this landscape is convergence: despite mechanistic diversity at the gene level, most PAH-associated variants ultimately impair endothelial quiescence, promote smooth muscle proliferation, and drive apoptosis resistance through disruption of BMP signaling amplitude, transcriptional stability, ion channel homeostasis, metabolic integrity, or epigenetic regulation. This convergence supports both a unified therapeutic rationale and a precision medicine framework for genotype-stratified intervention in PAH. Full article

Pembrolizumab is standard adjuvant therapy for high-risk clear cell renal cell carcinoma, but serositis is an uncommon immune-related adverse event that may mimic recurrence or infection. We report a 55-year-old man who achieved no evidence of disease after nephrectomy and metastasectomy and developed anasarca, large bilateral pleural effusions, mild ascites, peripheral eosinophilia, and a small pericardial effusion after six cycles of adjuvant pembrolizumab. Pleural fluid was exudative and contained 20% eosinophils. Cytology showed inflammatory cells without evidence of malignancy; bacterial, mycobacterial, and fungal studies were negative; and mildly elevated adenosine deaminase did not support tuberculosis. Cardiac function and natriuretic peptides were preserved. Pembrolizumab was discontinued, thoracentesis and corticosteroids were administered, and symptoms, eosinophilia, renal function, and albumin improved rapidly. Follow-up through March 2026 showed no oncologic progression, although some residual pleural and abdominal fluid persisted alongside imaging findings suggestive of portal-hypertension physiology, which may have contributed to residual fluid but did not explain the eosinophilic pleural syndrome. In a targeted literature review, effusion eosinophil data were infrequently reported. This case highlights a likely underrecognized eosinophilic pleural-fluid phenotype within pembrolizumab-associated polyserositis and supports routine differential cell counts in drained serosal fluid when immune-related serositis is suspected. Full article

Clinically significant portal hypertension (CSPH) is a key driver of decompensation events and complications in patients with liver cirrhosis. The manifestation of hepatic decompensation is, in turn, associated with a drastic deterioration in prognosis in this vulnerable population. Therefore, a timely identification of patients at risk as well as an optimal drug treatment are key elements in the therapeutic management of patients with cirrhosis to improve survival. While invasive measurements represent the gold standard for assessing portal hypertension, significant progress has been made in recent years in developing non-invasive methods for evaluating CSPH, including the NICER and the ANTICIPATE model. These models, combining variables such as liver and spleen stiffness in combination with biomarkers such as platelet count for risk prediction, reliably identify patients with CSPH who are at risk for hepatic decompensation. In addition to advances in diagnostics, new evidence has emerged regarding optimal drug management strategies. Non-selective beta blockers are an important treatment option, even though a certain proportion of patients respond inadequately. Therefore, updated strategies are needed to identify these non-responders and improve treatment effectiveness. This review article provides a comprehensive overview of modern diagnostic approaches for CSPH, describes current management strategies including updated approaches, and provides an outlook on emerging potential treatment options. Full article

Schistosomiasis (bilharzia) is a parasitic infection caused by trematodes of the Schistosoma genus and remains a significant health burden in endemic regions. Granulomatous host responses to deposited Schistosoma eggs in small veins and tissues result in progressive changes and characteristic imaging findings. This diagnostic radiological review synthesizes the published literature and highlights key and robust imaging findings that facilitate the diagnosis of Schistosoma mansoni and Schistosoma haematobium, with emphasis on modality-specific patterns and disease staging. Schistosoma mansoni primarily affects the liver, causing periportal fibrosis visible as “pipe-stem” echogenic thickening upon ultrasonography, which may progress to portal hypertension and chronic liver disease. Liver cirrhosis is the end-stage disease manifested as an irregular liver contour with surface nodularity and lobar redistribution as right lobe atrophy with left and/or caudate lobe hypertrophy. Schistosoma haematobium predominantly affects the genitourinary system, causing urinary bladder wall thickening and calcification. Early disease, within three months of infection, may present with fine calcification, firstly in the bladder base and then extending to the whole bladder and even to the ureters. Calcification appears as a line or two parallel lines on radiography and as a circle in axial computed tomography (CT) images, which is pathognomonic for early-stage Schistosomiasis. In contrast studies, including conventional urography and CT urography, Schistosoma eggs appear as bubble-like filling defects in the ureter, kidney, and bladder, manifested as ureteritis, pyelitis, and cystitis cystica. Late stages appear as coarse calcification, fibrosis, strictures, and reduced bladder capacity and are associated with an increased risk of bladder squamous cell carcinoma. Moreover, Schistosomiasis calcification can present in genital organs, especially in the seminal vesicles; in the prostate in males; and in the vulva, cervix, and perineum in females. Ultimately, Schistosoma mansoni and haematobium eggs can reach the spinal cord, leading to acute myelopathy with paraparesis, urinary retention, or paraplegia. Recognition of characteristic imaging patterns of Schistosomiasis is essential for early diagnosis, accurate staging, and prevention of long-term complications. Full article

Background: Coronavirus disease 2019 (COVID-19), caused by the SARS-CoV-2 virus, had profound primary effects on global health and secondary effects through widespread disruption of healthcare systems, limiting access to elective medical services essential for the management of chronic diseases such as liver cirrhosis. Elective hospitalizations play a key role in disease monitoring, prevention of complications, and therapeutic optimization. This study aimed to evaluate the impact of the pandemic on the clinical profile, disease severity, and outcomes of patients electively admitted with liver cirrhosis across three periods: pre-pandemic, pandemic, and post-pandemic. Methods: This retrospective, single-center cohort study included 248 adult patients electively admitted with a primary diagnosis of liver cirrhosis between February 2018 and February 2024. Patients were stratified according to admission period. Data on demographics, clinical presentation, etiology, decompensation markers, severity scores (Child–Pugh, Baveno), procedures, and hospitalization outcomes were analyzed. Results: A total of 248 patients were included, with a significant reduction in elective admissions during the pandemic (23.0% vs. 46.4% pre-pandemic), followed by partial recovery post-pandemic (30.6%) (p = 0.031). A higher proportion of urban patients was observed during the pandemic (70.2%, p = 0.004). Disease severity increased during the pandemic, with a higher prevalence of Child–Pugh C (17.5%) and Baveno stage 6 (10.5%), whereas post-pandemic data showed improvement (Child–Pugh C: 6.57%; no Baveno stage 6; p = 0.004). Ascites (47.4%) and paracentesis (21.1%) peaked post-pandemic (p = 0.012; p = 0.003). Endoscopic activity decreased during the pandemic (22.8%, p = 0.017), while interventional procedures were more frequent (8.8%, p = 0.045). Transfusion requirements (17.5%, p = 0.001) and hospitalization costs (€467.08, p = 0.01) were highest during the pandemic, while no deaths were recorded post-pandemic. In-hospital mortality was observed in 1.7% of patients during the pre-pandemic period and increased to 3.5% during the pandemic period, while no deaths were recorded post-pandemic. Conclusions: The COVID-19 pandemic significantly altered elective cirrhosis care, leading to reduced admissions, increased disease severity, and higher resource utilization. Although partial recovery was observed post-pandemic, persistent evidence of delayed decompensation underscores the importance of maintaining continuity in elective hepatology services. Full article

Background: Acute portal vein thrombosis (aPVT) is a severe complication of the splanchnic venous system, often associated with portal hypertension, intestinal ischemia, and hepatic dysfunction. Anticoagulation is the first-line therapy but is frequently insufficient in advanced Yerdel grade III–IV cases, where recanalization rates remain low. Endovascular interventions have emerged as alternative therapeutic strategies in selected patients. Methods: We present three cases of patients with Yerdel grade III–IV aPVT who underwent endovascular management. The techniques included: (1) transhepatic aspiration thrombectomy combined with intra-thrombus thrombolysis using alteplase (Actilyse); (2) combined aspiration thrombectomy, intra-thrombus thrombolysis with alteplase, portal vein stenting, and transjugular intrahepatic portosystemic shunt (TIPS) creation; and (3) transsplenic aspiration thrombectomy followed by angioplasty, stent placement, and TIPS creation in a post-liver transplant patient. Results: All procedures were technically successful, achieving complete or near-complete recanalization of the portal venous system. Restoration of patency in the extrahepatic portal circulation was confirmed, and portal pressures were reduced in the TIPS-assisted case. No major periprocedural complications occurred. Clinical outcomes included preservation of transplant candidacy and graft salvage. Conclusions: Endovascular therapy may be an option in selected patients with acute portal vein thrombosis. Careful patient selection and an individualized technical approach are essential. Full article

Background: Portal hypertension is a major cause of esophagogastric variceal bleeding in children. Endoscopic therapy is widely used for acute hemostasis; however, it primarily controls the bleeding episode rather than the underlying portal hypertensive physiology, and definitive management often requires surgical portal decompression. Evidence regarding the outcomes of a staged endoscopic–surgical management strategy in pediatric patients remains limited. This study aimed to evaluate the clinical outcomes of children with portal hypertensive bleeding managed with endoscopic hemostasis as a bridging therapy followed by definitive portal decompression surgery. Methods: We conducted a retrospective consecutive cohort study including 12 children presenting with portal hypertension-related variceal bleeding at our tertiary pediatric center between January 2021 and December 2024. All patients underwent endoscopic hemostasis, followed by evaluation for portal decompression surgery when anatomically feasible. Clinical outcomes including hemostasis success, rebleeding, shunt patency, and survival were analyzed. An age-stratified exploratory analysis was performed to examine the association with early dysfunction after Rex shunt reconstruction. Results: Endoscopic hemostasis was successfully achieved in all patients, with no early rebleeding prior to surgery. Ten patients underwent portal decompression surgery within 7 days (Rex shunt, n = 8; splenorenal shunt, n = 2). During a median follow-up of 18 months, early Rex shunt dysfunction (<3 months) was observed in 2 of 8 patients (25%), both of whom were younger than 3 years, whereas no dysfunction was observed in older children. Given the small sample size, this observation should be interpreted descriptively. Rebleeding and mortality occurred exclusively in association with shunt dysfunction. Conclusions: A staged endoscopic–surgical strategy appears feasible for stabilizing children with acute portal hypertensive bleeding and enabling timely definitive portal decompression. In this small cohort (n = 12), an age-related signal in early Rex shunt dysfunction was observed in very young children; however, this finding should be interpreted cautiously and requires further validation in larger studies. Full article

Atezolizumab–bevacizumab is established as first-line therapy for unresectable hepatocellular carcinoma (HCC) based on phase III randomized evidence. Although overall safety outcomes were acceptable in the registration trial, the risk of gastrointestinal (GI) and variceal bleeding remains a clinically relevant concern, particularly in patients with cirrhosis and portal hypertension. Differences between trial-based safety estimates and observational data necessitate a focused evaluation of hemorrhagic risk in this setting. Randomized trial data indicate low rates of high-grade bleeding under protocol-driven endoscopic screening and predefined eligibility criteria. In contrast, real-world cohorts report higher incidences of GI and variceal hemorrhage, especially among patients with prior bleeding, untreated or high-risk varices, reduced hepatic reserve, and extensive portal vein tumor thrombosis. Pooled analyses confirm an increased prevalence of bleeding with atezolizumab–bevacizumab compared with non-antiangiogenic systemic therapies, although event rates vary across studies due to differences in patient selection and bleeding definitions. Severe and fatal hemorrhage occurs in a minority of cases and is concentrated in clinically high-risk subgroups. Bleeding during atezolizumab–bevacizumab therapy is influenced by baseline portal hypertension severity, hepatic functional status, and tumor-related vascular involvement. Trial-derived safety data reflect outcomes under controlled conditions and may underestimate risk in broader populations. Structured baseline assessment, endoscopic evaluation, and risk-adapted portal hypertension management are integral to clinical implementation. Prospective studies incorporating standardized hemorrhage definitions and predefined risk stratification frameworks are required to refine patient selection and optimize safety in routine practice. Full article

Background/Objectives: The objective of this study was to map and synthesize the current evidence on hemostasis in chronic and acute liver disease within the framework of Patient Blood Management (PBM). Methods: Because research in this field is heterogeneous—spanning mechanistic studies, observational data, randomized controlled trials, guidelines, and expert reviews—a scoping review was selected to comprehensively map concepts. Findings were synthesized narratively to reflect the breadth and heterogeneity of available research. Results: Hemostasis in liver disease is characterized by a fragile state of rebalanced coagulation, where parallel reductions in pro- and anticoagulant factors coexist with variable fibrinolytic disturbances and thrombocytopenia. Conventional coagulation tests (CCTs) do not accurately reflect bleeding risk, whereas viscoelastic assays and thrombomodulin-modified thrombin generation testing provide a more physiologic assessment, though with limitations. Most bleeding events arise from portal hypertension rather than coagulopathy, and the routine prophylactic correction of abnormal results of CCTs is not supported by evidence. PBM-aligned strategies—such as restrictive transfusion, targeted fibrinogen replacement, and use of thrombopoietin receptor agonists (TPO-RAs)—reduce unnecessary blood product use. Thrombosis burden is increasingly recognized in this patient population. Anticoagulation is generally safe when individualized to liver function and clinical context, however significant variability persists in clinical practice, and high-quality data remain limited for advanced disease. Conclusions: Hemostasis in liver disease reflects a dynamic and unstable equilibrium rather than a simple bleeding tendency. Diagnostic and therapeutic strategies grounded in PBM principles improve safety by avoiding unnecessary transfusion and emphasize individualized care. Despite advances in understanding rebalanced hemostasis, major gaps remain in predicting thrombotic risk, standardizing advanced coagulation testing, and defining optimal management across disease stages. Full article

Endothelial dysfunction (ED) arises in multiple pathologies, and its severity correlates with disease progression. Common ED biomarkers could provide prognostic value for associated complications. This study aims to identify shared ED biomarkers and assess their prognostic significance. Endothelial cells in culture (human microvascular endothelial cells, HMEC-1) were exposed to sera from patients in five disease groups (n = 20 patients/group)—liver cirrhosis with portal hypertension, idiopathic pulmonary arterial hypertension, placental disorders such as intrauterine growth restriction, coronary artery disease with acute myocardial infarction, and chronic kidney disease—or matched controls, in the absence/presence of anti-inflammatory (apixaban) and antioxidant (EUK134) compounds. We explored changes in: VCAM-1, ICAM-1, eNOS, VWF, extracellular matrix thrombogenicity, and reactive oxygen species (ROS). In serum samples, proteomics and metabolomics analyses (including lipids, amino acids, and polar metabolites) were performed through an extraction protocol to identify common ED biomarkers. Expression of VCAM-1, ICAM-1, VWF, platelet adhesion, and ROS increased in most groups versus controls (p < 0.05). Both drugs decreased all biomarker levels except eNOS (n = 6 for in vitro experiments). For serum ED biomarkers, 18 metabolites and 24 proteins showed AUC-ROC and hit rates >77.5%, and six metabolites were associated with event-free survival. These diseases share ED driven by systemic inflammatory, oxidative, and metabolic stress, are partially reversible in vitro, and are linked to biomarkers associated with clinical outcomes. Overall, ED emerges as a modifiable pathological axis with potential prognostic value. Full article

Somatostatin is a potent endocrine regulator and neurotransmitter, exerting predominantly inhibitory effects in different tissues of the body, via G-protein coupled receptors. Five such specific receptors have been identified, with different effects and tissue distribution. The multifaceted actions and effects of somatostatin make it useful as a potential therapeutical means in various pathologies; however, in clinical practice, somatostatin analogues, namely octreotide, lanreotide and pasireotide, are commonly used instead, due to their increased half-life and increased receptor selectivity, with pasireotide showing a more extensive receptor binding profile and high affinity for somatotastin receptor (SSTR) 5, which may prove effective in cases of resistance to first-generation analogues. Apart from their many uses in neoplastic pathologies, somatostatin analogues represent viable treatment choices in some ocular pathologies, congenital hyperinsulinism, gastrointestinal bleedings and portal hypertension, acute pancreatitis, and dumping syndrome. They have also been used in some cases, with varying degrees of success, in patients with post-surgical gastrointestinal and lymphatic fistulas, refractory chronic diarrhoea and polycystic kidney disease; many applications in paediatric patients have also been documented. The aim of this review is to present the applications of somatostatin and its analogues as alternative or second-line therapies, along with insights into their effectiveness and future potential. Full article

Background: Pregnancy in women with liver cirrhosis is considered a rare clinical condition due to the decreased fertility commonly associated with chronic liver disease. Hormonal disturbances, anovulation and impaired hepatic function contribute to the lower conception rates observed in this population. However, when pregnancy occurs, it is associated with a significantly increased risk of maternal and fetal complications. Maternal risks include hepatic decompensation, variceal bleeding, ascites, coagulopathy and a higher rate of hypertensive disorders during pregnancy and related complications. Fetal complications involve prematurity, intrauterine growth restriction, and increased perinatal mortality. Methods: We present the clinical case of a woman with idiopathic liver cirrhosis who experienced four consecutive pregnancies with different clinical courses and outcomes. Results: The case highlights the complexity of managing pregnancy in patients with chronic liver disease and underscores the importance of individualized clinical assessment and multidisciplinary management. This report also reviews current management strategies and discusses key considerations for optimizing care in pregnant women with liver cirrhosis. Conclusions: Advances in multidisciplinary care and improved management strategies have contributed to better pregnancy outcomes in recent years. Careful monitoring during pregnancy, appropriate management of portal hypertension, and coordinated care between obstetricians, hepatologists, and neonatologists are essential to minimizing potential complications, ensuring favorable maternal and fetal outcomes. Full article

The transjugular intrahepatic portosystemic shunt (TIPS) is a cornerstone intervention for complications of portal hypertension, including variceal bleeding and refractory ascites. As the population with cirrhosis ages, clinicians increasingly face the question of whether and how to perform TIPS safely in older adults. We reviewed observational cohorts, registry analyses, and systematic reviews/meta-analyses. Existing evidence does not support chronological age as an absolute contraindication; however, multiple studies suggest that advanced age is associated with higher rates of post-TIPS hepatic encephalopathy (HE), early mortality, and readmissions. These findings underscore the need to shift from a binary “eligible vs. ineligible” paradigm to a structured, actionable framework that addresses modifiable risks and anticipates age-related vulnerabilities. Recent clinical practice guidance emphasizes comprehensive pre-TIPS assessment and vigilant post-procedure care, with specific attention to HE risk factors (e.g., prior HE, hyponatremia, renal dysfunction, sarcopenia) and cardiopulmonary reserve. In this narrative review, we propose an elderly-focused clinical pathway built around a four-domain assessment (Liver–Brain–Body–Heart/Kidney) and a traffic-light risk tiering system to guide patient selection, procedural strategy, follow-up scheduling, and triggered management of HE, cardiac decompensation, and renal dysfunction. This pathway aims to preserve the benefits of portal decompression while reducing preventable complications and improving outcomes that are meaningful to older patients, including functional status and quality of life. This narrative review emphasizes that outcomes after TIPS in older adults are determined not by chronological age alone but by multidomain physiological reserve. The proposed pathway informs patient selection, procedural planning, and early post-discharge monitoring in older adults. Full article