Non‐alcoholic fatty liver disease: a review of epidemiology,risk factors,diagnosis and management

Due to the rising prevalence of obesity and type II diabetes mellitus, non‐alcoholic fatty liver disease is becoming the leading cause of chronic liver disease in the Western world. In some patients, simple steatosis can result in non‐alcoholic steatohepatitis which over time can lead to liver cirrhosis and its associated sequelae, including hepatocellular carcinoma. Early identification and management of patients at risk with intensive dietary and lifestyle modification are essential to prevent the development of advanced liver disease and its complications. In this review, we will discuss the epidemiology of non‐alcoholic fatty liver disease, pathogenesis, diagnosis, management and surveillance strategies to offset the morbidity and mortality of this disease, as well as liver and non‐liver‐related complications.     

Paediatric non‐alcoholic fatty liver disease: an overview

Non‐alcoholic fatty liver disease (NAFLD) is a progressive disease that encompasses a spectrum of liver diseases, ranging from simple steatosis to non‐alcoholic steatohepatitis (NASH). Data related to survival in children are scarce, but these data firmly associate NAFLD with higher risks of hepatic and non‐hepatic morbidities and mortalities compared with the general population. More recently, the association between NAFLD and cardiovascular disease among children has increasingly been recognized. Given that obesity is a major risk factor for the disease, paediatric NAFLD is becoming a global issue, paralleling the dramatic rise in obesity worldwide. NASH, which is more common in obese children, has the potential to advance to liver fibrosis and failure. It is unclear why certain patients undergo such transformation but this susceptibility is likely related to an interaction between a genetically susceptible host and the surrounding environment. Currently, treatment is largely conservative and includes lifestyle modification, attainable through healthy weight reduction via diet and exercise. In this review, current knowledge about NAFLD in children is summarized. This review aims to increase the awareness of the medical community about a hidden public health issue and to identify current gaps in the literature while providing directions for future research.     

Clinical usage of serum ferritin to assess liver fibrosis in patients with non‐alcoholic fatty liver disease: Proceed with caution

Serum ferritin was recently reported to have low diagnostic accuracy for the detection of advanced fibrosis in patients with non‐alcoholic fatty liver disease (NAFLD). To corroborate these findings, we investigated the diagnostic accuracy of serum ferritin levels for detecting liver fibrosis in NAFLD patients utilizing a large Japanese cohort database. A total 1201 biopsy‐proven NAFLD patients, seen between 2001 and 2013, were enrolled into the Japan Study Group of NAFLD. Analysis was performed on data from this cohort comparing between serum ferritin levels and hepatic histology. Serum ferritin increased with increasing histological grade of steatosis, lobular inflammation and ballooning. Multivariate analyses revealed that sex differences, steatotic grade and fibrotic stage were independently associated with serum ferritin levels (P < 0.0001, <0.0001, 0.0248, respectively). However, statistical analyses performed using serum ferritin levels demonstrated that the area under the receiver–operator curve for detecting fibrosis was not adequate for rigorous prediction. Several factors including sex differences, steatosis and fibrosis were found to correlate with serum ferritin levels. Therefore, serum ferritin may have low diagnostic accuracy for specifically detecting liver fibrosis in NAFLD patients due to the involvement of multiple hepatocellular processes.     

The lifestyle influence on alcoholic pancreatitis versus alcoholic liver disease: a case-control study

Objective: To evaluate the association of lifestyle with the development of alcoholic liver disease (ALD) or alcoholic pancreatitis (AlcP).

Methods: A case-control study was conducted on 80 patients attending a tertiary university hospital, subdivided into three groups: ALD (n?=?34), AlcP (n?=?21) and a control (CT) group (n?=?25) of alcohol abusers without clinical evidence of hepatic or pancreatic disease. Participants were interviewed regarding alcohol consumption, tobacco use and diet. A physical examination was concomitantly performed and we had access to their complementary investigation.

Results: We included 10 females and 70 males (mean age 57?±?10 years). The pure amount of alcohol consumed by the ALD group was significantly higher than the AlcP group, regarding both daily (grams/day) and lifetime (kilograms) consumptions (p?=?.018 and p?=?.009, respectively); no statistically significant differences were seen with the CT group. We found no differences regarding the beverage type or drinking outside meals. Smoking was very common in every study group, with higher consumptions and a significantly higher prevalence of ever smokers in the AlcP group, in comparison with ALD and CT patients (p?=?.033 and p?=?.036, respectively). There were significant differences in the patients’ eating habits before the onset of disease between groups (p?Conclusion: We found differences in lifestyle between ALD and AlcP, not considered sufficient to explain the subjects’ susceptibility to one disease or the other.     

Relationship of non‐alcoholic fatty liver disease to colorectal adenomatous polyps

Background and Aims: Metabolic syndrome and insulin resistance are associated with a higher risk of colon cancer. Non‐alcoholic fatty liver disease (NAFLD) is regarded as a manifestation of metabolic syndrome in the liver. This investigation was initiated to determine whether NAFLD has a relationship to colorectal adenomatous polyps. Methods: We examined the 2917 participants who underwent a routine colonoscopy at Kangbuk Samsung Hospital in 2007. We divided the 2917 subjects into the adenomatous polyp group (n = 556) and the normal group (n = 2361). Anthropometric measurements, biochemical tests for liver and metabolic function, and abdominal ultrasonographs were assessed. Results: The prevalence of NAFLD was 41.5% in the adenomatous polyp group and 30.2% in the control group. By multiple logistic regression analysis, NAFLD was found to be associated with an increased risk of colorectal adenomatous polyps (odds ratio, 1.28; 95% confidence interval, 1.03–1.60). An increased risk for NAFLD was more evident in patients with a greater number of adenomatous polyps. Conclusion: NAFLD was associated with colorectal adenomatous polyps. Further studies are needed to confirm whether NAFLD is a predictor for the development of colorectal adenomatous polyps and cancer.