About 30% of patients with cirrhosis have diabetes mellitus (DM). Nowadays, it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease. DM, which develops as a complication of cirrhosis, is known as "hepatogenous diabetes". Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease. An impaired response of the islet beta-cells of the pancreas and hepatic insulin resistance are also contributory factors. Non-alcoholic fatty liver disease, alcoholic cirrhosis, chronic hepatitis C (CHC) and hemochromatosis are more frequently associated with DM. Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis. DM in cirrhotic patients may be subclinical. Hepatogenous diabetes is clinically different from that of type 2 DM, since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis. DM increases the mortality of cirrhotic patients. Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs. This manuscript will review evidence that exists in relation to: type 2 DM alone or as part of the metabolic syndrome in the development of liver disease; factors involved in the genesis of hepatogenous diabetes; the impact of DM on the clinical outcome of liver disease; the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.

No abstract

No abstract

No abstract

Severe acute respiratory syndrome coronavirus 2 infection is the cause of coronavirus disease 2019 (COVID-19), which predominantly affects the respiratory system; it also causes systemic and multi-organic disease. Liver damage is among the main extrapulmonary manifestations. COVID-19-associated liver injury is defined as any liver damage occurring during the disease course and treatment of COVID-19 in patients with or without pre-existing liver disease, and occurs in approximately one in five patients. Abnormal liver test results have been associated with a more severe course of COVID-19 and other complications, including death. Mechanisms linking COVID-19 to liver injury are diverse. Particular consideration should be made for patients with pre-existing liver disease, such as metabolic dysfunction-associated fatty liver disease, chronic liver disease due to viral or autoimmune disease, liver transplant carriers, or cirrhosis, given the risk for more severe outcomes. This manuscript summarizes the current lines of evidence on COVID-19-associated liver injury regarding pathophysiology, clinical significance, and management in both patients with or without pre-existing liver disease, to facilitate clinicians’ access to updated information and patient care. Finally, we mention the ideas and recommendations to be considered for future research.

Objective: to determine the independent predictors of in-hospital death of Hispanic patients with nonvariceal upper gastrointestinal bleeding (NVUGB).Experimental design: prospective and observational trial. Patients: in a period between 2000 and 2009, all patients with NVUGB admitted to our hospital were studied. Demographical and clinical characteristics, endoscopic findings and laboratory tests were evaluated. χ² and Mann-Whitney U analyses were performed for comparisons, and binary logistic regression was employed to identify independent predictors of in-hospital mortality.Results: 1,067 patients were included, 65% male with a mean age of 58.8 years. Mean number of comorbidities per patient was 1.6 ± 0.76. The most frequent cause of bleeding were gastric and duodenal ulcers (55.4%); 278 patients (25.8%) received endoscopic treatment of which 69.1% had combined therapy. Rebleeding occurred in 36 patients (3.4%) of which 50% died. Inhospital mortality was 10.2%, of which only 3.1% was associated to bleeding. When comparing causes of death among patients with and without comorbidities, only hypovolemic shock was found significative (48.3 vs. 25%; p = 0.020). Binary logistic regression found that the number of comorbidities, Rockall scale serum albumin < 2.6 g/dL on admission; rebleeding and length of hospital stay were independent risk factors of in-hospital mortality.Conclusion: the number of comorbidities, the Rockall scale score, an albumin level < 2.6 g/dL, the presence of rebleeding and hospital stay were predictors of in-hospital mortality in patients with UNVGB. INTRODUCTIONNon-variceal upper gastrointestinal bleeding (NVUGB) is a critical condition in which a mortality of 5 to 10% has been reported in different series of patients. This variability may be explained in part by the different clinical and demographic characteristics of the studied population (1,2). Recent prospective studies have identified different predictors of mortality; it is worth noting that the use of proton pump inhibitors (PPIs) significantly reduces mortality in patients both with and without high risk stigmata of rebleeding. Moreover, the use of endoscopic treatment has been demonstrated to reduce mortality in greater proportion than drug treatment (3-6). However, it has been shown that the risk factors, complications and mortality rates described in controlled trials are lower than those reported in patients who received their attention on "day-today conditions" in a tertiary care community hospital (7), which illustrates more accurately the actual conditions of medical care.The main objective of our study is to describe the clinical characteristics, endoscopic findings, and treatment used, as well as risk factors of complications and in-hospital mortality in Hispanic patients with NVUGB on "day-to-day conditions". Predictors of in-hospital mortality in patients with non-variceal upper gastrointestinal bleedingJosé Alberto González-González, Genaro Vázquez-Elizondo, Diego García-Compeán, Juan Obed Gaytán-Torres, Ángel Ricardo ...

SAGT was associated with lower survival. SAGT, Child-Pugh B, and high Child-Pugh and MELD scores were independent negative predictors of survival.

No abstract