Risk Of Non-alcoholic Liver Disease Research Articles

Liver Lesions in Estuarine Dolphins in the Indian River Lagoon, Florida: Does Microcystin Play a Role?

Microcystin (MC), a hepatotoxin produced by cyanobacteria, was introduced into the Indian River Lagoon (IRL), Florida, in 2005 through freshwater outflows. Since then, MC has been detected in humans, domestic animals, and wildlife in the lagoon. Potential public health effects associated with MC exposure along the IRL include an increased risk of non-alcoholic liver disease among area residents. Yet, there are limited studies characterizing liver disease, as well as the potential role of MC, in humans and animals in this region. Thus, histopathology reports (n = 133) were reviewed in the stranded common bottlenose dolphin (Tursiops truncatus truncatus) (n = 156, 2005-2024) to describe liver lesions in this important IRL sentinel. Liver and fecal samples (n = 161) from stranded individuals were screened for MC via an enzyme immunoassay (ELISA). These samples were then confirmed via the 2-methyl-3-methoxy-4-phenylbutyric acid technique (MMPB) to evaluate whether liver histopathologic lesions were linked to MC exposure. Minimally invasive MC screening methods were also assessed using respiratory swabs and vapor. Inflammation (24%, n = 32), fibrosis (23%, n = 31), lipidosis/vacuolation (11%, n = 15), and necrosis (11%, n = 14) were the most common liver anomalies observed. These non-specific lesions have been reported to be associated with MC exposure in numerous species in the peer-reviewed literature. Ten bottlenose dolphins tested positive for the toxin via ELISA, including two individuals with hepatic lipidosis, but none were confirmed by MMPB. Thus, this study did not provide evidence for MC-induced liver disease in IRL bottlenose dolphins. Other causes should be considered for the lesions observed (e.g., heavy metals, metabolic disease, and endoparasites). Respiratory swabs require further validation as a pre-mortem MC screening tool in free-ranging wildlife.

Helicobacter pylori and non-alcoholic fatty liver disease.

Helicobacter pylori is the most prevalent infection worldwide, while non-alcoholic fatty liver disease emerged as the most frequent liver disease. The common occurrence can be either by chance or due to certain pathogenetic factors. Epidemiologic studies revealed that the risk of non-alcoholic liver disease is increased in patients infected with Helicobacter pylori. DNA fragments of Helicobacter pylori were rarely identified in human samples of liver carcinoma and fatty liver. Helicobacter pylori could influence the development of non-alcoholic fatty liver either by hormonal (ghrelin? gastrin? insulin?), or by effect of pro-inflammatory cytokines (interleukin 1 and 8, tumor necrosis factor ɑ, interferon ɣ) and by changes of gut microbiome as well. Probiotic supplementation could improve some clinical parameters of non-alcoholic fatty liver disease and eradication rates of Helicobacter pylori. Regimens used for eradication can be safely administered, although non-alcoholic fatty liver increases the risk of drug-induced liver damage. Controlled studies of the effect of eradication on the development and progression of non-alcoholic fatty liver are warranted.

Obese boys at increased risk for nonalcoholic liver disease: evaluation of 16 390 overweight or obese children and adolescents

Comorbidities of childhood obesity challenge health-care systems in Europe. Further, there is a lack of population-specific prevalence data and diagnostic strategies available, especially for obesity-related disturbances of liver function. Therefore, the prevalence of elevated liver enzymes and their relationship to biological parameters were studied in a large pediatric obesity cohort. In 111 specialized pediatric obesity centers in Germany, Austria and Switzerland, 16,390 children and adolescents (age 12.4±2.6 years, 58% boys) were categorized as overweight (body mass index (BMI) >90th percentile) and obese (>97th percentile) and studied for related comorbidities, especially nonalcoholic fatty liver disease (NAFLD; as defined by aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) >50 U l(-1)). Data were collected using a standardized software program (APV) for longitudinal multicenter documentation. Pseudonymized data were transmitted for central statistical analysis. In this pediatric cohort, 16% of the study population was overweight, 46% obese and 35% extremely obese (>99.5th percentile extreme obesity (Xob)). NAFLD was present in 11% of the study population, but predominantly in boys (boys vs girls; 14.4:7.4%; P<0.001), in Xob (obese vs Xob; 9.5:17.0%; P<0.001) and in older age (< 12 vs ≥12 years; 8:12%; P<0.001; adjusted for BMI). ALT >50 U l(-1) was significantly associated with fasting insulin and BMI-SDS. In multiple logistic regression models, Xob and male gender were strongly associated with NAFLD (odds ratio Xob vs normal weight=3.2; boys vs girls OR=2.3). In a large cohort of overweight and obese European children and adolescents, markers of nonalcoholic liver disease, especially ALT, are frequent and predicted by Xob and male gender. The results underline the epidemiological dimension of this obesity-related morbidity even in childhood. Therefore, at least ALT is recommended as a screening parameter in basic care.