It has been described as bacterial infections (BIs) due to multidrug-resistant bacteria (MRB) in cirrhosis with acute decompensation (AD), with a potentially poor prognosis. This study aimed to determine the frequency of BIs due to MRB in a tertiary centre and its association with mortality. This is a prospective cohort study. Cirrhotics with AD were enrolled. At admission, polymorphonuclear leukocytes (PMN) count was performed in ascites patients. Blood, urine and fluids cultures were collected in patients with encephalopathy, ascites, digestive bleeding or because of IBs suspicion. Sample cultures were repeated during hospitalization when necessary. BIs diagnosis was established based on international consensus. Association among data versus BIs diagnosis was assessed through respective hypothesis testing. Data association with mortality was verified through univariate/multivariate logistic regression: Odds Ratio (OR), 95% confidence interval (CI). 327 males, median age of 56. Child-Pugh A, B and C were estimated in 22, 197, and 214 cases, respectively, median MELD of 16. BIs were diagnosed in 212/433 (49%) inpatients: 128/212 community-acquired (CA) infections, 22/212 healthcare-associated (HCA) infections and 62 nosocomial infections. The most frequent BIs were spontaneous bacterial peritonitis in 69/212 cases, followed by 59/212 respiratory tract infections and 29/212 urinary tract infections. Bacterial isolation was obtained in 108/212 BIs: 35/108 (32.4%) were MRB. MRB was more frequent in cases with HCA (53%) and nosocomial (41%) infections compared with CA (22%) infections; (P=.0279). Mortality was 17.6% in patients without BIs, 28.8% in non-isolation BIs, 24.7% in non-MRB BIs and 51.4% in BIs due to MRB (P<.001). Multivariate analysis showed that mortality was significantly associated with Child-Pugh C, acute kidney injury, but mainly with MRB BIs (OR 4.41; 95% CI 1.94-10.2; P<.001). MRB frequency was 32.4% among BIs with bacterial isolation. It represents an independent predictor for inpatient mortality.
Metabolic dysfunction-associated fatty liver disease (MAFLD) is a new nomenclature recently proposed by a panel of international experts so that the entity is defined based on positive criteria and linked to pathogenesis, replacing the traditional non-alcoholic fatty liver disease (NAFLD), a definition based on exclusion criteria. NAFLD/MAFLD is currently the most common form of chronic liver disease worldwide and is a growing risk factor for development of hepatocellular carcinoma (HCC). It is estimated than 25% of the global population have NAFLD and is projected to increase in the next years. Major Scientific Societies agree that surveillance for HCC should be indicated in patients with NAFLD/ MAFLD and cirrhosis but differ in non-cirrhotic patients (including those with advanced fibrosis). Several studies have shown that the annual incidence rate of HCC in NAFLD-cirrhosis is greater than 1%, thus surveillance for HCC is cost-effective. Risk factors that increase HCC incidence in these patients are male gender, older age, presence of diabetes and any degree of alcohol consumption. In non-cirrhotic patients, the incidence of HCC is much lower and variable, being a great challenge to stratify the risk of HCC in this group. Furthermore, large epidemiological studies based on the general population have shown that diabetes and obesity significantly increase risk of HCC. Some genetic variants may also play a role modifying the HCC occurrence among patients with NAFLD. The purpose of this review is to discuss the epidemiology, clinical and genetic risk factors that may influence the risk of HCC in NAFLD/MAFLD patients and propose screening strategy to translate into better patient care.
Metabolic dysfunction-associated steatotic liver disease (MASLD) patients have a higher incidence of cardiovascular events (CVE) compared to controls. Aim The aim of this study is to analyze association between liver fibrosis with CVE, incident diabetes, and cirrhosis complications. Methods Historic cohort of biopsy-proven MASLD patients, divided into two groups: F0–F2 vs F3–F4 fibrosis. Baseline data included metabolic traits and liver function tests. Patients were contacted and scheduled for laboratory analysis and elastography. Endpoints were (a) CVE, defined as any of acute myocardial infarction, coronary stenting, ischemic cardiopathy, and stroke; (b) incident diabetes; (c) cirrhosis complications. Baseline data were collected at the time of liver biopsy, while follow-up data were recovered through personal interview or medical records. A stepwise logistic regression determined predictive variables for each endpoint. Results Study population included 220 patients with median age 53 years, and 145 were women; baseline fibrosis was F0–F2 in 165 patients and F3–F4 in 55 patients; median follow-up was 9.9 years. A higher percentage of F3–F4 patients had CVE (29.4%) than F0–F2 ones (13.1%) (hazard ratio 2.42; 95% CI: 1.26–4.6; P = 0.008). Incident diabetes occurred in 53.3% of F3–F4 and 20.2% of F0–F2 cohort (hazard ratio 3.04; 95% CI: 1.99–4.86; P < 0.001); cirrhosis complications occurred in 9/55 F3–F4 patients and in 1/165 F0–F2 ones (hazard ratio 26.3; 95% CI: 3.3–208.3; P = 0.002). Multivariate analysis confirmed liver fibrosis as an independent predictor of incident diabetes and cirrhosis complications. CVE were associated with baseline diabetes and aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio. Conclusion In a cohort of 220 MASLD patients followed for 9.9 years, baseline F3–F4 was associated with incident diabetes and cirrhosis complications. AST/ALT ratio and diabetes were associated with CVE.
Non-invasive prediction of fibrosis in non-alcoholic fatty liver diseaseJournal of HepatologyVol. 55Issue 2PreviewNon-alcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease worldwide. It includes a wide spectrum of liver diseases, ranging from pure steatosis to nonalcoholic steatohepatitis (NASH), and eventually to liver cirrhosis with its complications. Full-Text PDF Open Access We would like to address the concerns presented by Dr. Dogru et al. in their letter to the Editor. The first issue commented on pertains to one of the six variables included in the formula of the NAFLD fibrosis score: impaired fasting glucose/diabetes. For that variable, we took the same definition from the original paper by Angulo et al. [[1]Angulo P. Hui J.M. Marchesini G. Bugianesi E. George J. Farrell G.C. et al.The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD.Hepatology. 2007; 45: 846-854Crossref PubMed Scopus (2048) Google Scholar]. Diabetes was defined as a fasting glucose level ⩾126 mg/dl or a patient who was already under treatment with anti-diabetic drugs; and impaired fasting glucose, as a fasting glucose level ⩾110 mg/dl. We did not perform any glucose tolerance test in our patients. As stated in our paper [[3]Ruffillo G. Fassio E. Alvarez E. Landeira G. Longo C. Domínguez N. et al.Comparison of NAFLD fibrosis score and BARD score in predicting fibrosis in nonalcoholic fatty liver disease.J Hepatol. 2011; 54: 160-163Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar], we just retrospectively analyzed data of consecutive patients with biopsy proven NAFLD that had been prospectively collected. One advantage of both, the NAFLD fibrosis score and the BARD score [[2]Harrison S.A. Oliver D. Arnold H.L. Gogia S. Neuschwander-Tetri B.A. Development and validation of a simple NAFLD clinical scoring system for identifying patients without advanced disease.Gut. 2008; 57: 1441-1447Crossref PubMed Scopus (585) Google Scholar], is that they include 6 and 3, respectively, easily available variables. Being a group that is especially interested in research on NAFLD, we had all of these variables available in our database. In fact, at present if we wanted to repeat the analysis of comparison between both scoring systems, data on 182 biopsy proven NAFLD patients would be available (instead of 138 in our published paper). The second concern raises the point about the lack of information on medications that patients could be receiving. We agree that some drugs may influence the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and we do not have the complete information about medications taken by our patients. Some of them were receiving antihypertensive drugs such as enalapril, or antihyperlipidemic drugs such as statins. However, the pattern of liver enzymes in our NAFLD patients conformed to those commonly found; with a mild to moderate elevation and an ALT predominance. Median ALT was 69 IU/L, interquartile range 50–96.5 IU/L and, in only 4 out of 138 patients (2.9%), levels above 200 IU/L (that is, five times above upper limit of normal) were found (maximal value, 294). AST/ALT ratios in these 4 patients were 0.61, 0.52, 0.78 and 0.55, similar to the whole group of patients. Thus, we might suggest that most of the patients were not showing a drug-induced liver injury able to modify AST or ALT levels. The AST/ALT ratio is a very important variable, strongly associated with the presence of advanced fibrosis in the univariate analysis (with higher odds ratio than other variables) and therefore, is included in both scoring systems, the NAFLD fibrosis score and the BARD score. Furthermore, in the BARD score, an AST/ALT ratio ⩾0.8 sums 2 points while the other two variables, presence of diabetes or body mass index ⩾28, sum only 1 point. However, the information on the list of medications taken by the patients is also lacking in the two original studies [1Angulo P. Hui J.M. Marchesini G. Bugianesi E. George J. Farrell G.C. et al.The NAFLD fibrosis score: a noninvasive system that identifies liver fibrosis in patients with NAFLD.Hepatology. 2007; 45: 846-854Crossref PubMed Scopus (2048) Google Scholar, 2Harrison S.A. Oliver D. Arnold H.L. Gogia S. Neuschwander-Tetri B.A. Development and validation of a simple NAFLD clinical scoring system for identifying patients without advanced disease.Gut. 2008; 57: 1441-1447Crossref PubMed Scopus (585) Google Scholar]. The authors declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript.