Cárdenas A, Ginès P. Management of patients with cirrhosis awaiting liver transplantation

GI Unit, Institut Clinic de Malalties Digestives i Metaboliques, Hospital Clinic,and University of Barcelona, Institut d’Investigacions Biomédiques August Pi-Sunyer (IDIBAPS), Ciber de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain.
Gut (Impact Factor: 14.66). 03/2011; 60(3):412-21. DOI: 10.1136/gut.2009.179937
Source: PubMed


The demand for OLT continues to be on the rise with patients spending a long time on the waiting list; this not only increases the risk of developing further decompensation but also mortality. The complications discussed above may not only lead to removal from the waiting list in some cases but also a poorer outcome following transplantation. Therefore the appropriate prevention, recognition and treatment of the above-mentioned complications of cirrhosis will have a positive impact on the outcome before and after liver transplantation.

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Available from: Andres Cardenas, Jan 08, 2014
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    • "The probability of mortality as 50% or more has been reported for patients with serum sodium concentrations below 120 mmol/L independently of underlying disease [2] [3] [4]. Second, adverse outcomes, including mortality, are higher in hyponatremic patients with a wide range of underlying diseases [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]. "
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    ABSTRACT: Background Hyponatraemia increases morbidity and mortality, but the extent to which this condition influences mortality independently of other contributing factors is unclear. Materials and methods All hyponatremic patients admitted to the internal medicine department during a six month period were included. Medical records were reviewed and patients' demographics, underlying disease, cause of hyponatremia and in-hospital deaths were noted. Control group consisted of patients with normonatremia admitted to the same department during the same period matched 1:1 by sex, age and underlying disease. Difference in in-hospital mortality rate between the study and control groups was tested by chi-square test. Baseline demographics, underlying diseases, cause of hyponatremia and state of hyponatremia correction as possible risk factors for mortality were tested in a multivariate analysis. Results The baseline cohort of all admitted patients consisted of 2171 patients. Hyponatraemia was found in 278 (13%) patients (160 females and 118 males). The three most common causes of hyponatremia included gastrointestinal loss (52 patients), decreased oral intake (47 patients), and dilution hyponatremia (45 patients). The in-hospital mortality rate in the hyponatremic group was significantly higher compared with the control group (22% vs 7%, respectively; OR 3.75, 95% CI 2.17–6.48, p < 0.0001). In a multivariate analysis age above 65 years, dilution hyponatremia, decreased oral intake as etiologic factors of hyponatremia, and unsuccessful hyponatremia correction were independent factors associated with increased mortality. Conclusion Hyponatraemia represents independent factor associated with in-hospital mortality. Age above 65 years, failure to correct hyponatremia and some specific etiologic factors of hyponatremia are related to increased mortality.
    European Journal of Internal Medicine 04/2014; 25(8). DOI:10.1016/j.ejim.2014.02.002 · 2.89 Impact Factor
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    • "When hepatic decompensation has occurred, the morbidity increases rapidly. After the first manifestation of ascites the one year mortality increases up to 40% [1], [2]. The patients' prognosis further deteriorates upon occurrence of spontaneous bacterial peritonitis or hepatorenal syndrome. "
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    ABSTRACT: Liver cirrhosis is associated with high morbidity and mortality. MicroRNAs (miRs) circulating in the blood are an emerging new class of biomarkers. In particular, the serum level of the liver-specific miR-122 might be a clinically useful new parameter in patients with acute or chronic liver disease. Here we investigated if the serum level of miR-122 might be a prognostic parameter in patients with liver cirrhosis. 107 patients with liver cirrhosis in the test cohort and 143 patients in the validation cohort were prospectively enrolled into the present study. RNA was extracted from the sera obtained at the time of study enrollment and the level of miR-122 was assessed. Serum miR-122 levels were assessed by quantitative reverse-transcription PCR (RT-PCR) and were compared to overall survival time and to different complications of liver cirrhosis. Serum miR-122 levels were reduced in patients with hepatic decompensation in comparison to patients with compensated liver disease. Patients with ascites, spontaneous bacterial peritonitis and hepatorenal syndrome had significantly lower miR-122 levels than patients without these complications. Multivariate Cox regression analysis revealed that the miR-122 serum levels were associated with survival independently from the MELD score, sex and age. Serum miR-122 is a new independent marker for prediction of survival of patients with liver cirrhosis.
    PLoS ONE 09/2012; 7(9):e45652. DOI:10.1371/journal.pone.0045652 · 3.23 Impact Factor
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    • "This is reflected by the lack of a clear definition of the components of malnutrition, the largely descriptive but not mechanistic studies, and the consequent lack of clear therapeutic strategies [11]. Although, it is believed that liver transplantation is curative for cirrhosis, this therapeutic option does not exist for the majority of patients [12]. Therefore, nontransplant therapeutic options remain the primary management option with the need to focus on reduced muscle mass because of its clinical relevance. "
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    ABSTRACT: Cirrhosis is the consequence of progression of many forms of necro-inflammatory disorders of the liver with hepatic fibrosis, hepatocellular dysfunction, and vascular remodeling. Reversing the primary hepatic disorder, liver transplantation, and controlling the complications are the major management goals. Since the former options are not available to the majority of cirrhotics, treating complications remains the mainstay of therapy. Sarcopenia and/or cachexia is the most common complication and adversely affects survival, quality of life, development of other complications of cirrhosis, and outcome after liver transplantation. With the increase in number of cirrhotic patients with hepatitis C and nonalcoholic fatty liver disease, the number of patients waiting for a liver transplantation is likely to continue to increase above the currently estimated 72.3/100,000 population. One of the critical clinical questions is to determine if we can treat sarcopenia of cirrhosis without transplantation. No effective therapies exist to treat sarcopenia because the mechanism(s) of sarcopenia in cirrhosis is as yet unknown. The reasons for this include the predominantly descriptive studies to date and the advances in our understanding of skeletal muscle biology and molecular regulation of atrophy and hypertrophy not being translated into the clinical practice of hepatology. Satellite cell biology, muscle autophagy and apoptosis, and molecular signaling abnormalities in the skeletal muscle of cirrhotics are also not known. Aging of the cirrhotic and transplanted population, use of mTOR inhibitors, and the lack of definitive outcome measures to define sarcopenia and cachexia in this population add to the difficulty in increasing our understanding of hepatic sarcopenia/cachexia and developing treatment options. Recent data on the role of myostatin, AMP kinase, impaired mTOR signaling resulting in anabolic resistance in animal models, and the rapidly developing field of nutriceuticals as signaling molecules need to be evaluated in human cirrhotics. Finally, the benefits of exercise reported in other disease states with sarcopenia may not be safe in cirrhotics due to the risk of gastrointestinal variceal bleeding due to an increase in portal pressure. This article focuses on the problems facing both muscle biologists and hepatologists in developing a comprehensive approach to sarcopenia in cirrhosis.
    05/2012; 3(4). DOI:10.1007/s13539-012-0069-3
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