Esteatohepatitis alcohólica y no alcohólica: ¿quiénes son los pacientes y qué podemos hacer por ellos?

Gallego‐Durán, Rocío; Ampuero, Javier; Funuyet, Jorge; Romero‐Gómez, Manuel

doi:10.1016/j.gastrohep.2013.06.005

Cited by 8 publications

(2 citation statements)

References 64 publications

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“…The explanation for a smaller nuclear area observed in the alcohol groups could be that the direct damage to cellular DNA is among the dangers of alcohol consumption [27]. Moderate physical activity can help reduce the hepatic oxidative stress through modulation of reactive oxygen species, increase the synthesis of antioxidant enzymes, up-regulation of protective systems against gene mutation and thermal shock, and increase growth 0.331 SC = sedentary control (no alcohol), EC = exercise control (no alcohol), EA = exercise alcohol, SA = sedentary alcohol.…”

Section: Morphometry Of Hepatocyte Nucleusmentioning

confidence: 98%

Liver Histology after Chronic Use of Alcohol and Exercise Training in Rats

Lucca¹,

Pereira²,

Righi³

et al. 2018

JPP

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Abstract:Objectives: To investigate the effects of physical training on the liver morphology and morphometry after chronic use of alcohol in rats. Methods: Twenty-four Wistar rats were housed in cages with controlled environment and randomly divided into four groups according to treatment received. In the initial treatment, alcohol was administered to SA (sedentary alcohol) and EA (exercise alcohol) groups. After four weeks, physical training program was held on a treadmill with EA and EC (exercise control) groups. Area, perimeter, maximum and minimum diameter and form factor of nucleus and cytoplasm of hepatocytes were analyzed. Key findings: Micro-vesicular fatty degeneration, predominantly pericentrolobular, of mild to moderate intensity, was found especially in animals treated with alcohol. EC group showed nucleus area greater than the nucleus area of EA and SA groups. The form factor was lower in the EC group than in the EA group. EA group showed maximum cytoplasm diameter is smaller than in SC (sedentary control) group. Conclusions: Physical training for two weeks was not enough to suppress histopathologic changes in the liver caused by chronic use of alcohol in rats. Chronic use of alcohol seems to have minimized the beneficial effect of physical training in the nucleus area of hepatocytes.

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Section: Morphometry Of Hepatocyte Nucleusmentioning

confidence: 98%

Liver Histology after Chronic Use of Alcohol and Exercise Training in Rats

Lucca¹,

Pereira²,

Righi³

et al. 2018

JPP

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“…Alcohol consumption is an additive factor that potentially interacts synergistically with those metabolic risk factors commonly present in MASLD (i.e., obesity, diabetes mellitus, hypertension). 20 21 If we assume that this holds true for all MASLD patients, then we must accept that an important bias is present in the available evidence regarding the natural history of MASLD as well as in therapeutic trials that do not account accurately for alcohol consumption as a variable. Thus, every effort to avoid this bias must be made in prospective studies involving subjects with steatotic liver disease.…”

Section: Alcohol Consumption In Patients With Steatotic Liver Diseasementioning

confidence: 99%

Is There a Safe Alcohol Consumption Limit for the General Population and in Patients with Liver Disease?

Romero-Gómez,

Arab,

Oliveira

et al. 2024

Semin Liver Dis

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Excessive alcohol consumption represents an important burden for health systems worldwide and is a major cause of liver- and cancer-related deaths. Alcohol consumption is mostly assessed by self-report that often underestimates the amount of drinking. While alcohol use disorders identification test - version C is the most widely used test for alcohol use screening, in patients with liver disease the use of alcohol biomarker could help an objective assessment. The amount of alcohol that leads to significant liver disease depends on gender, genetic background, and coexistence of comorbidities (i.e., metabolic syndrome factors). All patients with alcohol-associated liver disease are recommended to follow complete abstinence and they should be treated within multidisciplinary teams. Abstinence slows down and even reverses the progression of liver fibrosis and can help recompensate patients with complicated cirrhosis. Whether there is a safe amount of alcohol in the general population is a matter of intense debate. Large epidemiological studies showed that the safe amount of alcohol to avoid overall health-related risks is lower than expected even in the general population. Even one drink per day can increase cancer-related death. In patients with any kind of chronic liver disease, especially in those with metabolic-associated steatotic liver disease, no alcohol intake is recommended. This review article discusses the current evidence supporting the deleterious effects of small-to-moderate amounts of alcohol in the general population and in patients with underlying chronic liver disease.

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