Complications Of Liver Disease Research Articles

Kidney function after liver transplantation: the contrasting roles of inflammation and tubular repair

Kidney injury is a significant complication in end-stage liver disease (ESLD), leading to increased morbidity and mortality. While liver transplant alone (LTA) can promote kidney recovery (KR), non-recovery associates with adverse outcomes, but the underlying pathophysiology is still unclear. We studied 10 LTA recipients with or without kidney failure (KF) and measured serum levels of OPN and TIMP-1 (previously identified predictors of KR), 92 proinflammatory proteins (Olink), and urinary cell populations. Our findings revealed elevated OPN and TIMP-1 levels in KF patients, strongly correlated with tubular epithelial cells in urine. Proteomic analysis showed distinct profiles in KF, non-KF, and healthy donors, indicating an ongoing proinflammatory signature in KF. Cytokines correlated with OPN and TIMP-1 levels. We propose that high pre-LTA OPN and TIMP-1 levels are crucial for tubular regeneration and normalize with kidney recovery. Insufficient pre-LTA OPN levels may lead to persistent kidney failure. Our present data also newly indicate that kidney failure post-LTA is an active condition, in which tubular cells are persistently shed in the urine. The strict association between systemic inflammation and tubular cell loss suggests a pathogenic link that could offer therapeutic opportunities to promote kidney recovery.

Disorder of Glucose Metabolism and Therapy: Implications on the Natural History of Advanced Chronic Liver Disease

Introduction: Hepatogenous diabetes (HD) is a disorder of glucose metabolism (DGM) that develops as a complication of advanced chronic liver disease (ACLD) with an estimated prevalence of 20–70%. It appears to be associated with a larger number of decompensations, but its impact on the natural history of the disease is unclear. The treatment of DGM is hampered by the fact that some therapeutic agents are associated with a risk of complications in ACLD. The aim of this work was to study DGM in a population of patients with ACLD: prevalence, liver disease decompensation episodes, mortality analysis and study of the impact of antidiabetic therapies in patients with ACLD who developed DGM. Materials and Methods: A cohort of consecutive patients with ACLD without previous DGM, who attended a Hepatology clinic in the period of January to June 2015 was selected. Follow-up was carried out for 5 years. Data on age, gender, date of diagnosis and etiology of ACLD, Child-Pugh and MELD-Na classifications at enrollment, development of DGM, and antidiabetic therapy were collected. Logistic regression models for hospitalizations due to decompensated ACLD, ascites, hepatic encephalopathy (HE), upper gastrointestinal bleeding (UGB), hepatocellular carcinoma (HCC), portal vein thrombosis (PVT), infectious complications, acute-on-chronic liver failure (ACLF), and death were built. A survival analysis for patients with and without DGM was also performed. Treatment effectiveness for patients with DGM was assessed. Results: Initially, 221 patients were included, 154 (69.7%) of whom developed DGM after the diagnosis of ACLD. DGM patients presented a significantly higher number of hospitalizations. Odds ratio (OR) for death was not significantly related with DGM. At 5 years of follow-up, 68.9% of patients with DGM were alive, against 81.8% without DGM (p = 0.087). From the 154 patients who were diagnosed with DGM, 42.9% were not receiving pharmacological treatment for DGM. Treated patients were prescribed with either biguanides (34.8%), a SGLT2 inhibitor (8.6%), or insulin (7.7%). Only 1 patient was treated with a GLP-1 analogue. A tendency of OR favoring treatment was observed for biguanides and SGLT2 inhibitors in all outcomes except ascites. In the univariable analysis, the use of biguanides was associated with lower risk of death (OR: 0.84 [95% CI: 0.73–0.96]) and HE (OR: 0.85 [95% CI: 0.73–0.98]). Conclusion: DGM occurs with high prevalence in patients with ACLD and it seems to be related to more hospitalizations, which highlights the importance of its early identification and appropriate therapeutic approach. In the absence of contraindications, biguanides should be considered for treatment of patients with ACLD and DGM as they appear to be associated with a tendency to better outcomes and may present some advantage in terms of survival.

Research Progress of Chinese Medicine in the Regulation of Liver Fibrosis-Related Signaling Pathways.

Liver fibrosis is a common complication of chronic liver disease, significantly affecting patients' quality of life and potentially leading to cirrhosis and hepatocellular carcinoma. Despite advancements in modern medicine, the treatment of liver fibrosis remains limited and challenging. Thus, identifying new therapeutic strategies is of great clinical importance. Signaling pathways related to liver fibrosis play a crucial regulatory role in immune response and inflammation. Aberrant activation of specific pathways, such as the NF-[Formula: see text]B signaling pathway, results in the overexpression of genes associated with liver inflammation and fibrosis, thereby promoting the progression of liver fibrosis. Chinese medicine offers unique potential advantages as a therapeutic approach. Recent studies have increasingly demonstrated that certain Chinese medicines can effectively treat liver fibrosis by regulating relevant signaling pathways. The active ingredients in these medicines can inhibit hepatic inflammatory responses and fibrotic processes by interfering with these pathways, thus reducing the severity of liver fibrosis. This paper aims to investigate the mechanisms of Chinese medicine in treating liver fibrosis and its modulation of related signaling pathways. Additionally, it discusses the prospects of the clinical application of these treatments and provides valuable references for further research and clinical practice.

Nutrition in pediatric end-stage liver disease.

The aim of this review is to outline recent studies relating to nutritional status and outcomes in pediatric end-stage liver disease. Pediatric patients with chronic and end-stage liver disease are at high risk of malnutrition. Given additional growth demands in children and the inherent complications of chronic liver disease, achieving adequate nutrition in these patients remains a challenge. In addition, while guidelines on nutrition in chronic liver disease exist, global approaches and definitions of malnutrition vary. Recent literature has focused on sarcopenia and nutrition-related transplant outcomes, with some studies exploring nutritional assessment and management. Pediatric studies however continue to lag adult research, with limited prospective and interventional studies. Optimizing nutrition in pediatric end-stage liver disease remains a challenge, however understanding of the mechanisms and clinical manifestations of malnutrition in this population is improving. Despite these efforts, high quality studies to determine optimal nutrition strategies and interventions are lacking behind adult evidence and should be the focus of future research.

Role of oral hypoglycaemic drugs in preventing complication in non-alcoholic fatty liver disease with type 2 diabetes mellitus.

To determine the prevalence of non-alcoholic fatty liver disease, and the effect of oral hypoglycaemic drugs and lifestyle modifications in reducing fatty liver changes and liver enzymes in these patients. The comparative, observational study was conducted at the Department of Pharmacology, Sohail University, Karachi, from October 2022 to October 2023, and comprised patients of either gender having elevated liver enzymes and ultrasound finding of fatty liver changes along with raised glycated haemoglobin, transaminases, total cholesterol and triglycerides. The participants were prescribed oral hypoglycaemic agents by endocrinologists. Those given empaglifazolin + metformin were in group A, empaglifazolin + linglaptin in group B, sitaglaptin + metformin in group C, metformin alone in group D and sitaglaptin alone in group E. Lifestyle modifications were advised in all the treatment groups, while control group F was only advised lifestyle modifications. The intervention lasted 3 months. Investigations included B-mode ultrasound liver, liver enzymes and glycated haemoglobin, which were done at baseline and after the intervention. Data was analysed using SPSS 25. Of 200 patients, 40 were males and 160 were females in ratio of 1:4. The overall mean age was 48±16 years. There were 154(77%) patients who had non-alcoholic fatty liver disease with type 2 diabetes mellitus, while 46(23%) had only fatty liver changes. There were 50(25%) patients in group A, 30(15%) in group B, 30(15%) in group C, 40(20%) in group D, 10(5%) in group E and 40(20%) in group F. Post-intervention improvement was noted in 48(24%) patients, with 20(41.7%) of them being in group A. The prevalence of non-alcoholic fatty liver disease with type 2 diabetes was high. Combination of empagliflozin + metformin along with lifestyle modifications was highly effective in reducing fatty changes and the level of liver enzymes.

Infections and liver cirrhosis

End-stage liver disease is alife-threatening clinical syndrome combined with a state of immune dysfunction. In this constellation patients are prone to bacterial, fungal and viral infections associated with markedly increased morbidity and mortality rates. Bacterial infections are the most prevalent kind of infection in patients with end-stage liver disease accounting for nearly 30%. The evolving rates of multidrug resistant organisms present enormous challenges in treatment strategies. Therefore, the urgent needs for prevention, early detection strategies and widespread treatment options are anecessity to handle the rising incidence of infection complications in end-stage liver disease.

Metabolic syndrome: a stealthy complication in alcoholic liver disease

Metabolic syndrome: a stealthy complication in alcoholic liver disease

Hepatitis co-infection in paediatric HIV: progressing treatment and prevention.

To analyse the main evidence and recommendations for the management of hepatitis co-infection in children living with HIV. We analysed available data pertaining to the natural history of liver disease and treatment of co-infected children. Viral hepatitis co-infection in people living with HIV (PLHIV) is a global problem owing to the shared routes of transmission, particularly in areas of high endemicity for the three viruses. Viral hepatitis co-infection can accelerate liver disease progression and increase morbidity and mortality, even in patients on suppressive antiretroviral treatment (ART). Viral hepatitis should be routinely screened in PLHIV and, once diagnosed with viral hepatitis, PLHIV should be closely monitored for liver disease progression and complications. Children living with HIV-HBV co-infection should be treated with ART containing agents which are active against both viruses. Children living with HIV-HCV co-infection should receive directly acting antivirals (DAA) to eradicate HCV infection. Prevention measures to reduce vertical and horizontal transmission of HBV and HCV (anti-HBV vaccination and immunoglobulins, anti-HBV treatment in pregnancy, anti-HCV DAAs in people of childbearing age, avoiding blood contact, sexual barrier precautions) should be adopted and encouraged, particularly in high endemicity countries.

Pulmonary complications of advanced chronic liver diseases: an updated review

Pulmonary complications of advanced chronic liver diseases: an updated review

Systolic and diastolic impairment in cirrhotic cardiomyopathy: insights from a cross-sectional study

BackgroundCirrhotic cardiomyopathy, an intricate and multifaceted complication of end-stage liver disease, manifests as systolic and diastolic dysfunction in patients without previously diagnosed cardiac disease. Our study aims to investigate the prevalence of systolic and diastolic function in patients with cirrhotic cardiomyopathy in our region.MethodsWe conducted a cross-sectional study on 68 patients with established cirrhosis, and no overt cardiac manifestations, who consequently underwent 2D echocardiography to quantify systolic and diastolic dysfunction, as defined by the 2019 Cirrhotic Cardiomyopathy Consortium. The severity of cirrhosis was determined using various validated scoring systems.ResultsA total of 19 out of 68 (28%) had systolic dysfunction, while 6/68 (9%) had evidence of diastolic dysfunction. Overall prevalence of cirrhotic cardiomyopathy was 23/68 (34%), and the presence of hepatitis C was strongly associated with systolic dysfunction with p-value of 0.007. However, it was not significantly associated with diastolic dysfunction, p-value = 0.59. Logistic regression analysis did not show any significant association between cardiac dysfunction and the severity of liver cirrhosis, as assessed by Child–Pugh, MELD, ALBI, PALBI, portal hypertension, and FIB-4 score (R2 = 3.66, F (13, 39) = 1.33, p = 0.234).ConclusionOur study reveals a remarkable prevalence of cirrhotic cardiomyopathy, which despite being a frequently occurring phenomenon often goes unrecognized. Lack of correlation with the severity of liver cirrhosis, based on currently available scoring system, suggests either a still poorly understood pathological mechanism or requires the development of a new validated reliable scoring system through multi-center longitudinal studies.

A Comparative Analysis of Norepinephrine with Midodrine/Octreotide in Patients with Hepatorenal Syndrome-acute Kidney Injury

Background Hepatorenal Syndrome (HRS) is a severe complication of end-stage liver disease characterized by functional renal impairment. This study aimed to assess the efficacy of norepinephrine compared to midodrine/octreotide in managing patients diagnosed with hepatorenal syndrome type 1. Materials and Methods In this double-blind Randomized Clinical Trial, 50 patients with hepatorenal syndrome type 1 were randomly assigned to the norepinephrine and midodrine/octreotide groups. The norepinephrine group received an initial dose of 1 mg/h (up to a maximum of 4 mg/h) along with daily intravenous injections of 20% albumin (20-40 grams per day) throughout the study period. The control group received midodrine (maximum dose of 15 mg three times a day), octreotide (maximum dose of 200 micrograms intravenously three times a day), and 20 to 40 mg of 20% albumin daily. The primary efficacy measure was the percentage of patients achieving a complete response, defined by the restoration of serum creatinine levels to within 0.3 mg/dl of the baseline by the end of treatment. Results There was no significant difference in the rate of complete response between the norepinephrine group (7/25, 28%) and the midodrine/octreotide group (3/25, 12%) (p=0.15). The mortality rate was 10 (40%) in the norepinephrine group and 12 (48%) in the midodrine/octreotide group. Although the mortality rate was higher in the midodrine/octreotide group (12/25, 48%) compared to the norepinephrine group (10/25, 40%), this difference was not statistically significant (p=0.77). Conclusion The study findings suggest that the norepinephrine treatment regimen can be as effective as or more effective than the midodrine/octreotide regimen in treating hepatorenal syndrome in cirrhotic patients. Therefore, these two treatment regimens can be used interchangeably. Clinical Trial Registration Number IRCT20230228057568N1

Ascites with a Chance of Flooding: A Rare Complication of Cirrhosis

Flood Syndrome, characterized by ruptured umbilical hernias with ascitic fluid leakage in decompensated liver cirrhosis, presents a rare but potentially fatal complication of cirrhotic liver disease. We present a case study of a patient with decompensated cirrhosis who underwent multiple medical encounters before the severity of his condition, characterized by ascitic fluid leakage, was recognized. Flood Syndrome was ultimately identified on admission to the hospital, prompting multidisciplinary interventions and discussions, including antibiotics, surgical consultation, and optimization for hernia repair. Due to the patient’s complexity of his medical condition and surgical risks, a transjugular intrahepatic portosystemic shunt (TIPS) was performed to alleviate ascites before a planned umbilical hernia repair. This case underscores the importance of early recognition of umbilical hernias in cirrhotic patients and highlights the complexity of management decisions, balancing surgical risks with medical optimization to improve outcomes. Further research is warranted to refine treatment strategies and enhance patient care in Flood Syndrome cases.

Chronic Edema Management of the Lower Extremities.

Peripheral edema is a prevalent condition affecting patients dealing with an assortment of health conditions, such as congestive heart failure (CHF), liver disease, venous insufficiency, and postoperative surgical complications. Edema can present in a variety of ways, ranging from mild localized symptoms to severely debilitating forms that impact patients' daily lives. Despite the vast number of publications addressing the underlying causes of peripheral edema, there seems to be an absence of literature that presents the effectiveness and compliance of current management techniques. This paper aims to condense the current literature on the effectiveness and compliance of current edema management approaches across various common etiologies, with the intentionof identifying alternative therapies that could enhance the quality of care for patients with chronic lower extremity edema. Several promising new therapies such as exogenous calf muscle stimulation, leg raise exercises, high-dose albumin injections, and device-based negative pressure lymph drainage (NPLD), deviate from the currentestablished standard of care. This scoping review revealed diverse treatment methods tailored to the specific underlying etiology of edema. The use of diuretics and vasodilators has shown benefits in treating CHF-induced edema but failed to alleviate and prevent the recurrence of edema in hospitalized and recently discharged patients. Albumin injections have emerged as a potential alternative treatment for edema due to liver disease, addressing hypoalbuminemia symptoms caused by liver failure. Patients with vascular causes of edema are efficaciously treated conservatively with compression stockings, although patient adherence remains a hurdle. For postoperative edema, device-based NPLD appears promising, with potential benefits over elastic bandage wraps and kinesiology taping.

The effect of rifaximin and lactulose treatments to chronic hepatic encephalopathy rats: An [18F]PBR146 in-vivo neuroinflammation imaging study.

Hepatic encephalopathy (HE) is a severe neuropsychiatric complication of liver diseases characterized by neuroinflammation. The efficacies of nonabsorbable rifaximin (RIF) and lactulose (LAC) have been well documented in the treatment of HE. [18F]PBR146 is a translocator protein (TSPO) radiotracer used for in vivo neuroinflammation imaging. This study investigated anti-neuroinflammation effect of RIF or/and LAC in chronic HE rats by [18F]PBR146 micro-PET/CT. Bile duct ligation (BDL) operation induced chronic HE models, and this study included Sham+normal saline (NS), BDL+NS, BDL+RIF, BDL+LAC, and BDL+RIF+LAC groups. Behavioral assessment was performed to analyze the motor function, and fecal samples were collected after successfully established the chronic HE model (more than 28 days post-surgery). In addition, fecal samples collection and micro-PET/CT scans were performed sequentially. And we also collected the blood plasma, liver, intestinal, and brain samples after sacrificing the rats for further biochemical and pathological analyses. The RIF- and/or LAC-treated BDL rats showed similar behavioral results with Sham+NS group, while the treatment could not reverse the biliary obstruction resulting in sustained liver injury. The RIF or/and LAC treatments can inhibit IFN-γ and IL-10 productions. The global brain uptake values of [18F]PBR146 in BDL+NS group was significantly higher than other groups (p<.0001). The brain regions analysis showed that the basal ganglia, hippocampus, and cingulate cortex had radiotracer uptake differences among groups (all p<.05), which were consistent with the brain immunohistochemistry results. Sham+NS group was mainly enriched in Christensenella, Coprobacillus, and Pseudoflavonifractor. BDL+NS group was mainly enriched in Barnesiella, Alloprevotella, Enterococcus, and Enterorhabdus. BDL+RIF+LAC group was enriched in Parabacteroides, Bacteroides, Allobaculum, Bifidobacterium, and Parasutterella. RIF or/and LAC had anti-neuroinflammation in BDL-induced chronic HE rats with gut microbiota alterations. The [18F]PBR146 could be used for monitoring RIF or/and LAC treatment efficacy of chronic HE rats.

Глифлозины как средства коррекции неврологических осложнений неалкогольной жировой болезни печени. Часть 1

Глифлозины как средства коррекции неврологических осложнений неалкогольной жировой болезни печени. Часть 1

Acute Kidney Injury in Patients with Chronic Liver Disease: A Review

Introduction: Acute kidney injury (AKI) is a frequent complication of chronic liver disease (CLD) contributing to high morbidity and mortality worldwide. While liver transplantation (LT) has shown favorable outcomes, early identification and management of AKI is imperative for survival. This review aims to highlight the epidemiology, pathophysiology, management, and prognosis of AKI in CLD. Methods: An extensive literature search was performed using PubMed, Medline, and Google Scholar to identify literature related to epidemiology, burden, clinical presentations, prognosis, and management of AKI in CLD. Results: The identified studies highlighted a wide range of prevalence of AKI in hospitalized patients with CLD. The etiology and pathophysiology are multifactorial and include prerenal AKI, acute tubular injury, sepsis, gastrointestinal bleeding, bacterial translocation from the gut, and hepatorenal syndrome (HRS). AKI is associated with a higher risk of morbidity and mortality and progression to chronic kidney disease following LT. Management of AKI in CLD varies based on the underlying etiology. While vasoconstrictors like terlipressin have shown great potential in the treatment of HRS-AKI and is widely used in Europe and United States, LT remains the definitive therapy of choice. In most cases, kidney replacement therapy serves as a bridge to liver transplant. Conclusion: AKI is a serious complication of CLD and early identification is essential. Diagnosis and management, particularly HRS is challenging and requires a high index of suspicion. More research is required to identify novel therapies to improve outcomes of AKI in patients with CLD.

Targeting 5-Hydroxytryptamine Receptor 1A in the Portal Vein to Decrease Portal Hypertension

Backgrounds & aimsPortal hypertension (PH) is one of the most frequent complications of chronic liver disease. The peripheral 5-Hydroxytryptamine (5-HT) level was increased in cirrhotic patients. We aimed to elucidate the function and mechanism of 5-HT receptor 1A (HTR1A) in portal vein (PV) on PH. MethodsPH models were induced by thioacetamide (TAA) injection, bile duct ligation (BDL) or partial portal vein ligation (PPVL). HTR1A expression was detected using real-time PCR, in situ hybridization and immunofluorescence staining. In situ intraportal infusion was employed to assess the effects of 5-HT, the HTR1A agonist 8-OH-DPAT, and the HTR1A antagonist WAY-100635 on portal pressure (PP). Htr1a knock-out (Htr1a-/-) rats and vascular smooth muscle cell (VSMC)-specific Htr1a knock-out (Htr1aΔVSMC) mice were utilized to confirm the regulatory role of HTR1A on PP. ResultsHTR1A expression was significantly increased in the hypertensive PV of PH model rats and cirrhotic patients. Additionally, 8-OH-DPAT increased but WAY-100635 decreased PP in rats, without affecting liver fibrosis and systemic hemodynamics. Furthermore, 5-HT or 8-OH-DPAT directly induced the contraction of isolated PVs. Genetic deletion of Htr1a in rats and VSMCs-specific Htr1a knock-out in mice prevented the development of PH. Moreover, 5-HT triggered the cAMP pathway-mediated PVSMCs contraction via HTR1A in PV. We also confirmed alverine as an HTR1A antagonist and demonstrated its capacity to decrease PP in TAA-, BDL-, and PPVL-induced portal hypertensive rats. ConclusionsOur findings reveal that 5-HT promotes PH by inducing the contraction of PV, and identify HTR1A as a promising therapeutic target for attenuating PH. As an HTR1A antagonist, alverine is expected to become a candidate for clinical PH treatment.

Hepatic myelopathy neurological complication of chronic liver disease: two case reports

BackgroundHepatic myelopathy is a very rare neurological complication of chronic liver disease. Patients habitually present with progressive pure motor spastic paraparesis. This neurological dysfunction is almost always due to cirrhosis and portocaval shunt, either surgical or spontaneous.Cases reportWe report two cases of a 57-year-old man and a 37-year-old woman with progressive spastic paraparesis linked to cirrhosis and portal hypertension. The two patients are of Tunisian origin (north Africa). Magnetic resonance imaging of the spinal cord of two patients was normal, while brain magnetic resonance imaging showed a T2 hypersignals of the pallidums. These signs, in favor of hepatic encephalopathy in the two patients with cirrhosis with isolated progressive spastic paraparesis without bladder or sensory disorders, help to retain the diagnosis of hepatic myelopathy.ConclusionHepatic myelopathy is a severe and debilitating neurological complication of chronic liver disease. The pathogenesis is misunderstood and seems to be multifactorial, including the selective neurotoxic role both of ammonia and other pathogenic neurotoxins. Usually a pathological brain magnetic resonance imaging showing a hepatic encephalopathy was documented, contrasting with a normal spinal cord magnetic resonance imaging that contributed to diagnosis of hepatic myelopathy. Conservative therapies such as ammonia-lowering measures, diet supplementation, antispastic drugs, and endovascular shunt occlusion show little benefit in improving disease symptoms. Liver transplantation performed at early stage can prevent disease progression and could probably allow for recovery.

Sarcopenia in cirrhosis: Unraveling the prevalence and relationships with liver disease severity and complications.

Sarcopenia in cirrhosis is associated with poor survival and adverse pre and post-transplant outcomes. The study aimed at determining the prevalence of sarcopenia and its association with the severity, complications and etiology of liver disease. As many as 416 cirrhotic patients who met the inclusion criteria underwent muscle strength testing using a dynamometer. As many as 109 probable sarcopenia patients underwent computed tomography (CT) scan to measure skeletal muscle index (SMI) at the L3 vertebral level and gait-speed testing. The gender-specific cut-offs used to define sarcopenia were an SMI of 36.54 cm2/m2 in males and 30.21 cm2/m2 in females. A gait speed ≤ 0.8m/s was taken as a cut-off to define severe sarcopenia in both genders. The mean age was 54.7 ± 9.51years and male:female ratio was 2.2:1.The mean body mass index (BMI) was 24.2 ± 1.34kg/m2. Alcohol and non-alcoholic steatohepatitis (NASH) were the two most common etiologies (45.9% and 31.2%). The proportion of patients belonging to Child-Pugh class A, B and C was 26.6%, 48.6% and 24.8%, respectively. Forty out of 109 (36.7%) patients had a model for end-stage liver disease (MELD) > 14. Ascites, upper gastrointestinal bleeding and hepatic encephalopathy (HE) were present in 59 (54.1%), 60 (55.0%) and 24 (22.0%) patients, respectively. The prevalence of probable sarcopenia, sarcopenia and severe sarcopenia was found to be 26.20%, 10.09% and 6.73%, respectively. Sarcopenia and severe sarcopenia were associated with Child-Pugh class (p < 0.001, p < 0.001), MELD (p = 0.007, 0.002), upper gastrointestinal bleed (p = 0.007, 0.004), ascites (p = 0.038, 0.025) and HE (0.001, < 0.001). The prevalence of sarcopenia and severe sarcopenia was found to be 10.09% and 6.73%, respectively. Sarcopenia and severe sarcopenia had a significant association with the severity and complications of cirrhosis. However, no association was observed with etiology of liver disease.

The impact of MELD exception points for hydrothorax on posttransplant mortality: a propensity score-matched analysis.

Hepatic hydrothorax is a challenging complication of end-stage liver disease, and.patients with this complication can receive model for end-stage liver disease (MELD) exception points if they meet specific criteria as defined by United Network for Organ Sharing (UNOS). This research aimed to analyze the effect of receiving MELD exception points for hepatic hydrothorax on posttransplant mortality, using a national transplant database. Patients >18 years in the UNOS database awaiting liver transplant between 2012 and 2023 were identified based on their petition for MELD exception points. Using a 1: 1 propensity score-matched analysis, 302 patients who received MELD exception points for hepatic hydrothorax were compared with 302 patients who did not receive MELD exception points.Demographic, clinical and laboratory values were compared. The primary outcome was posttransplant mortality. Multivariate logistic regression controlled for potential confounders. No significant difference was observed in mean age (58.20 vs 57.62 years), mean initial MELD score (16.93 vs 16.54), or mean Child-Pugh score (9.77 vs 9.74) in patients with hepatic hydrothorax receiving MELD exception points versus their matched cohort who did not recieve exception points. The proportion of males was slightly higher among patients who received MELD exception points (57.6% males vs 53.6% males). A majority of patients in both groups had Child-Pugh grade C (>56%). Patients receiving MELD exception points for hepatic hydrothorax had a statistically significant 44% decrease in the odds of posttransplant death compared to those who did not (OR 0.56; 95% CI 0.37-0.88; P = 0.01). Among the combined cohort, each year increase in age resulted in a 3.9% increase in mortality (OR 1.04; 95% CI 1.01-1.07; P = 0.005), and every one-unit increase in serum creatinine resulted in a 40% increase in mortality (OR 1.40; 95% CI 1.03-1.92; P = 0.03). Receiving MELD exception points for hepatic hydrothorax is associated with a significant reduction in the odds of posttransplant mortality. These findings underscore the importance of MELD exception points for hepatic hydrothorax among patients with decompensated cirrhosis, potentially improving patient prioritization for liver transplantation and influencing clinical decision-making.