Background: Albumin acts as a scavenger of reactive oxygen species and an inhibitor of inflammatory processes that underlie hepatic encephalopathy (HE). However, the role of albumin in hepatic encephalopathy is not well-established. The authors performed this meta-analysis to evaluate the efficacy and safety of albumin in the management of hepatic encephalopathy.
Methods: The authors carried out an extensive search across multiple databases, including MEDLINE (via PubMed), Embase, CENTRAL, and various trial registries, to identify randomized controlled trials (RCTs) evaluating the impact of albumin administration in HE. The authors used a random-effects model for analyses and presented dichotomous outcomes and continuous outcomes as relative risk and mean difference, along with corresponding 95% CIs, respectively. Heterogeneity was assessed using both the I index and χ test.
Results: Our meta-analysis included 4 RCTs involving 306 patients. Our primary outcomes, mortality, and persistence of HE were reported by all four studies. Albumin was found to significantly decrease mortality in patients with HE [risk ratio (RR) 0.52, 95% CI 0.32-0.83; =0%]. Persistence of HE was found to be comparable between the two groups (RR 0.83, 95% CI 0.68-1.00; =24%). There was no significant difference between the albumin and control groups regarding length of hospital stay (MD -1.55, 95% CI -3.5 to 0.14; =41%), adverse events (RR 1.00, 95% CI 0.87-1.16; =0%), and severe adverse events (RR 0.89, 95% CI 0.59-1.35).
Conclusion: Albumin administration in patients with hepatic encephalopathy decreases mortality but does not significantly impact the persistence of HE. Further high-quality, large-scale randomized controlled trials are needed to provide conclusive evidence.
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http://dx.doi.org/10.1097/MS9.0000000000002039 | DOI Listing |
Metab Brain Dis
January 2025
Brain Liver Pitié-Salpêtrière (BLIPS) Study Group, Centre de recherche Saint- Antoine, Maladies métaboliques, biliaires et fibro-inflammatoire du foie, Institute of Cardiometabolism and Nutrition (ICAN), INSERM UMR_S 938, Paris, France.
Near Infrared Spectroscopy (NIRS) is a non-invasive optical technique allowing a continuous measurement of brain's hemoglobin (Hb) saturation in oxygen (rSO2). It is a marker of cerebral insult and rSO2 < 50% is associated with increased neurological impairment. Cirrhotic patients with gastrointestinal bleeding (GIB) often develop hepatic encephalopathy (HE).
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January 2025
Department of Public Health, College of Public Health, China Medical University, No. 100, Sec. 1, Jingmao Rd., Beitun Dist., Taichung, 406040, Taiwan.
The role of pre-treatment HBV DNA levels on the prognosis of hepatitis B virus-related decompensated cirrhosis is unclear. This study investigated the effects of pre-treatment HBV DNA and other determinants on short-term and long-term survival of chronic hepatitis B (CHB) patients with decompensated cirrhosis. A total of 278 cirrhotic decompensated CHB patients treated with entecavir or tenofovir disoproxil fumarate were retrospectively enrolled.
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December 2024
Internal Medicine, Unidade Local de Saúde de São José, Lisbon, PRT.
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December 2024
LKS Faculty of Medicine, University of Hong Kong, Hong Kong 999077, China.
Background: Neurocognitive impairment, including minimal hepatic encephalopathy (MHE) and overt hepatic encephalopathy, is one of the most common complications of all types of primary liver diseases, such as hepatitis B, biliary cholangitis, and autoimmune hepatitis. The EncephalApp Stroop test is a smartphone application-based test that is time-saving for MHE screening. However, neurocognitive impairment is different between alcoholic cirrhosis patients and nonalcoholic cirrhosis patients, so the cutoff value for MHE diagnosis might be inflated.
View Article and Find Full Text PDFMymensingh Med J
January 2025
Dr Mousumi Saha, Assistant Professor, Fetomaternal Medicine Subspeciality (FCPS) Course Student, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh; E-mail:
Wilson's disease is an autosomal recessive disorder that affects copper transport due to deficiency of ceruloplasmin and causes deposition of copper mainly in the liver, brain and cornea. It causes hepatic and/or neuropsychiatric manifestations. This copper deposition causes cirrhosis of the liver, encephalopathy and liver failure.
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