View clinical trials related to Hepatic Encephalopathy.
Filter by:This is a multi-center, nested cohort study intended to investigate the prevalence, risk factors, and outcomes of complications in patients with acutely decompensated cirrhosis, especially focused on Cytomegalovirus (CMV) reactivation, bacterial infections, hepatic encephalopathy, and Hepatorenal syndrome. Patients diagnosed with acutely decompensated cirrhosis were enrolled. Upon enrollment, detailed baseline data were collected and samples were harvested. Complications were assessed during hospitalization. Post-discharge follow-up was conducted through telephonic interviews at Day 30 and Day 90.
This interventional study aims to evaluate the safety and efficacy of oral capsule fecal microbiota transplantation (FMT) for treating hepatic encephalopathy refractory to conventional rifaximin and lactulose therapy in patients with liver cirrhosis. Patients diagnosed with hepatic encephalopathy refractory to rifaximin and lactulose therapy will be randomized into three groups. While continuing conventional therapy, the first group receives FMT via colonoscopy and oral capsule administration, the second group receives only oral capsule administration, and the third group serves as a control, receiving only conventional therapy. The aims of the study are: To evaluate the efficacy and safety of FMT by oral capsules in cirrhotic patients with hepatic encephalopathy refractory to standard therapy. To evaluate changes in the gut microbiota composition and in the intestinal and systemic inflammatory condition occurring after FMT and if they can be associated with clinical improvement. To evaluate metabolic modifications occurring after FMT and if they can be associated with clinical improvement.
Hepatic encephalopathy is a brain dysfunction caused by liver insufficiency and/or porto-systemic shunt. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma. According to the symptoms, it is classified as covert HE (CHE) and overt HE (OHE). CHE can progress to OHE and is associated with reduced driving ability, increased risk of accidents and hospitalization and weakened health-related quality of life, resulting in poor prognosis and socio-economic status. However, due to the absence of readily identifiable clinical symptoms and signs, CHE is often neglected in clinical practice. Presently, the diagnosis of CHE depends on psychometric and neurophysiological tests, including the psychometric hepatic encephalopathy score (PHES), critical flicker frequency (CFF) test, continuous reaction time (CRT) test, inhibitory control test, the SCAN test, and electroencephalography. Among them, PHES is most widely used and recommended by several guidelines. However, it is difficult to screen CHE among all cirrhotic patients in the clinic using PHES because of the time required and a dependence on trained experts. Moving beans from one container to another with tweezers involves dexterity, agility and coordination.The hypothesis was that the utility of the Clamping Bean Test (CBT) will enable early screening patients with CHE.
Earlier protein restriction was advocated in the treatment of HE but later this concept was refuted and increase protein intake was advocated in patients with HE. Diet in patients during an episode HE is also not known. It is advisable based on many case reports or case series that vegetable-based diet during the episode of HE is better than animal-based diet as it reduces ammonia level and other false neurotransmitters in brain and helps in early recovery of, HE . However, diet in patients who had recovered from an episode of, HE is not known and what type of protein (vegetarian or non-vegetarian) should be taken to prevent another episode of HE has never been evaluated. In India majority of the patients are vegetarian and patients with cirrhosis are malnourished and lack protein in their diet as per our previous published study
Acute liver failure in cirrhotic patients is associated with a one-month mortality of 48%. Encephalopathy, largely related to hyperammonemia, is a frequent complication of liver failure and is a poor prognostic marker. Lactulose decreases ammonia by acidification of the colon, replacement of urease-producing bacteria and creation of a laxative effect. Thus, the administration of lactulose in patients with severe hepatic encephalopathy reduces mortality by more than 40%. In intensive care patients, lactulose is often administered rectally. The use of simple rectal tubes is associated with frequent leakage of lactulose as well as faecal discharge and therefore risks of infection and skin lesions. Balloon rectal tubes with a drug delivery valve have recently been developed and used in this indication. The aim of this study is therefore to describe the use of these balloon rectal tubes to administer Lactulose in severe hepatic encephalopathy. This suggests that ammonia reduction in these patients may prolong survival time. No studies have described the administration of Lactulose via the rectal route with a balloon tube. The descriptive methodology is therefore appropriate. This is a preliminary study allowing data collection to establish the methodology for a subsequent clinical trial.
Hepatic encephalopathy is (HE) defined by the neurological and/or neuropsychological symptoms caused by an acute or chronic liver disease and/or a portosystemic shunt. Its pathophysiology is still debated, although the synergic role of hyperammonemia and inflammation is now admitted for years. Several additional mechanisms have been suspected, one of them being an altered permeability of the brain blood barrier (BBB). Nevertheless, many aspects remain poorly understood. The rise of "-omics" techniques, and especially metabolomics, allowed to identify more precisely the different metabolic pathways that are involved in the pathophysiology of HE. Using a high flow chemistry technique and multivariate data analysis, metabolomics is an accurate way to understand the pathophysiology and pathogenesis of multifactorial diseases such as HE. Several studies have been published in cirrhosis. It has been suggested that serum metabolites at admission, as well as thyroxine, can predict advanced HE in patients without brain failure. In a cohort including more than 600 patients, a higher microbially-derived metabolites, together with a lower thyroxine level, were associated with further development of brain failure. In another study from the same team, serum and urinary metabolites were significantly different in hospitalised patients who had developed poor outcome or not. Another study conducted in the CANONIC cohort as also found changes in metabolites of patients with cirrhosis and acute-on-chronic liver failure (ACLF), revealing mitochondrial dysfunction in peripheral organs that may contribute to organ failures. Last, our team previously analysed plasma and cerebrospinal fluid (CSF) samples of patients with cirrhosis and HE hospitalised in intensive care unit (ICU), showing alteration in ammonia and amino-acids metabolism, and also in energy metabolism. However, in the latest study, ALCF grading was not available. As many of these patients were in a severe condition, one could hypothesize that the metabolomic changes observed in these patients may have been confounded by an ACLF profile. Therefore, the objective of this study is to characterize the metabolomic fingerprints of HE in patients with cirrhosis, using 4 different groups of patients: patients with or without HE, with or without ALCF.
This study aims to investigate the influences behind patient choices regarding involvement, discontinuation, or re-engagement in hepatic encephalopathy clinical trials. Uncovering these factors is essential to enhance the relevance and efficacy of future research endeavors. In essence, this trial aims to deepen understanding of the factors influencing participation in hepatic encephalopathy clinical trials. Elevating participation rates could expedite the development of innovative treatments for this challenging condition.
Liver plays an important role in the metabolism of thyroid hormones, as it is the most important organ in the peripheral conversion of tetraiodothyronine (T4) to triiodothyronine (T3) by Type 1 deiodinase.
Vegetables are thought to be beneficial not only because of their high content of fiber, which promotes bacterial fermentation and decreases colonic transit time, decreasing ammonia absorption from the gut, but also because of their high BCAA content, low methionine and tryptophan contents, and the induction of gut microbiota which, in turn, increases fecal nitrogen excretion. Also the fact supporting the underlying rationale for the use of vegetable proteins is that dietary fiber contributes to the improvement of glycemic control in these patients. Smaller sample studies also support the idea that vegetable based protein diets have better effect on cognition in patients with HE; in these studies vegetable protein diet was compared to meat protein diet and patients with HE showed improvement in cognition on former diets. However, no positive effects were shown by Shaw or Chiarino. Similarly, another older single blind crossover study (n=10) showed that as compared to meat proteins, vegan diet has a better effect on mental status as determined on psychometric testing in patients with HE. As a result of the limited studies and small number of participants of the effect of vegetable proteins on HE, the purpose of this study is to investigate the effects of a vegetable versus mixed animal and vegetable protein diet on hepatic encephalopathy.
The aim of this study is to evaluate the efficacy of lactoferrin as an adjunct therapy in improving clinical symptoms and laboratory indices in individuals with hepatic encephalopathy.