Genetic Ancestry, Race, and Severity of Acutely Decompensated Cirrhosis in Latin America.

BACKGROUND & AIMS: Genetic ancestry or racial differences in health outcomes exist in diseases associated with systemic inflammation (eg, COVID-19). This study aimed to investigate the association of genetic ancestry and race with acute-on-chronic liver failure (ACLF), which is characterized by acute systemic inflammation, multi-organ failure, and high risk of short-term death. METHODS: This prospective cohort study analyzed a comprehensive set of data, including genetic ancestry and race among several others, in 1274 patients with acutely decompensated cirrhosis who were nonelectively admitted to 44 hospitals from 7 Latin American countries. RESULTS: Three hundred ninety-five patients (31.0%) had ACLF of any grade at enrollment. Patients with ACLF had a higher median percentage of Native American genetic ancestry and lower median percentage of European ancestry than patients without ACLF (22.6% vs 12.9% and 53.4% vs 59.6%, respectively). The median percentage of African genetic ancestry was low among patients with ACLF and among those without ACLF. In terms of race, a higher percentage of patients with ACLF than patients without ACLF were Native American and a lower percentage of patients with ACLF than patients without ACLF were European American or African American. In multivariable analyses that adjusted for differences in sociodemographic and clinical characteristics, the odds ratio for ACLF at enrollment was 1.08 (95% CI, 1.03-1.13) with Native American genetic ancestry and 2.57 (95% CI, 1.84-3.58) for Native American race vs European American race CONCLUSIONS: In a large cohort of Latin American patients with acutely decompensated cirrhosis, increasing percentages of Native American ancestry and Native American race were factors independently associated with ACLF at enrollment.

Factors associated with health-related quality of life in patients with cirrhosis: a systematic review.

BACKGROUND: Patients with cirrhosis have a poor health-related quality of life (HRQoL). Recognizing factors that affect HRQoL is key in delivering patient-centred care. AIM: To identify factors most commonly associated with a poor HRQoL in adults with cirrhosis in a systematic review of the literature. METHODS: Four databases (MEDLINE, EMBASE, CENTRAL and PsycINFO) were searched from inception to March 2020, using terms related to patient-reported outcomes plus cirrhosis. Studies that analysed an association between at least one factor and HRQoL in adult patients with cirrhosis were included. Abstract and full-text screening was performed by two reviewers. Data were collected on factors evaluated in each study and the significance of their association with HRQoL. RESULTS: A total of 10647 citations were reviewed, of which 109 met eligibility criteria. 76% of the studies used a generic instrument while only 45% used liver-specific instruments. Among identified factors, demographic factors and cirrhosis aetiology were not generally associated with poor HRQoL except for poor social support. Depression, poor sleep and muscle cramps affected HRQoL in all the studies that evaluated them. Among comorbidities, frailty, falls, malnutrition and cognitive impairment were also associated with poor HRQoL in the majority of studies. Among cirrhosis-specific decompensating events, only hepatic encephalopathy (HE) was consistently associated with impairment in HRQoL (75% of studies). CONCLUSION: Many factors impact poor HRQoL in patients with cirrhosis such as depression, muscle cramps, poor sleep, falls, frailty and malnutrition. Among cirrhosis decompensating events, HE was the complication most commonly associated with a poor HRQoL.

ß-Blocker therapy for cirrhotic cardiomyopathy: a randomized-controlled trial.

BACKGROUND: Cirrhotic cardiomyopathy is characterized by an attenuated contractile response to stress. Long-term exposure of ß-adrenergic receptors to persistently high levels of catecholamines has been implicated in its pathogenesis. We hypothesized that ß-blockade with metoprolol could reverse the changes in heart function and morphology in cirrhotic cardiomyopathy. PATIENTS AND METHODS: In this prospective randomized trial, we included 78 patients aged between 18 and 60 years with abnormal cardiac output response under dobutamine stress echocardiography, without primary cardiac disease or a history of alcohol intake. Patients were assigned randomly to receive metoprolol or placebo for 6 months. The primary endpoint was the improvement in cardiac output response to stress, measured by an increase in the left ventricle stroke volume more than 30%. RESULTS: Three (7.3%) patients in the metoprolol group and nine (24.3%) patients in the placebo group showed improved stroke volume (P=0.057). Diastolic dysfunction was found in two (4.8%) patients before and in five (15.6%) patients after therapy in the metoprolol group, and in 10 (27%) patients before and nine (31%) patients after therapy in the placebo group (P=0.67). After treatment, no echocardiography parameter of morphology was significantly different between metoprolol or placebo groups. No significant differences were observed in noradrenaline, plasma renin activity, and troponin levels between groups. Cirrhosis-related clinical events, including hospitalizations and mortality, were not significantly different between the two groups. Six months of therapy with ß-blocker did not ameliorate heart function and morphology in patients with cirrhotic cardiomyopathy.

Early predictors of acute kidney injury in patients with cirrhosis and bacterial infection: urinary neutrophil gelatinase-associated lipocalin and cardiac output as reliable tools.

BACKGROUND: Hemodynamic abnormalities and acute kidney injury (AKI) are often present in infected cirrhotic patients. Hence, an early diagnosis of AKI is necessary, which might require the validation of new predictors as the determinations of urinary neutrophil gelatinase-associated lipocalin (uNGAL) and cardiac output. METHODS: We evaluated 18 infected cirrhotic patients subdivided into two groups at admission (0 hours). In Group I, we collected urine samples at 0 hours, 6 hours, 24 hours, and 48 hours for uNGAL and fractional excretion of sodium determinations. In Group II, we measured cardiac output using echocardiography. RESULTS: The age of patients was 55.0±1.9 years, and 11 patients were males. The Model for End-Stage Liver Disease score was 21±1, whereas the Child-Pugh score was C in 11 patients and B in 7 patients. Both patients in Group I and Group II showed similar baseline characteristics. In Group I, we diagnosed AKI in 5 of 9 patients, and the mean time to this diagnosis by measuring serum creatinine was 5.4 days. Patients with AKI showed higher uNGAL levels than those without AKI from 6 hours to 48 hours. The best accuracy using the cutoff values of 68 ng uNGAL/mg creatinine was achieved at 48 hours when we distinguished patients with and without AKI in all cases. In Group II, we diagnosed AKI in 4 of 9 patients, and cardiac output was significantly higher in patients who developed AKI at 0 hours. CONCLUSION: Both uNGAL and cardiac output determinations allow the prediction of AKI in infected cirrhotic patients earlier than increments in serum creatinine.