Worldwide, the leading cause of chronic liver disease is represented by nonalcoholic fatty liver disease (NAFLD) which has now become a global epidemic of the 21st century, affecting 1 in 4 adults, and which appears to be associated with the steadily increasing rates of metabolic syndrome and its components (obesity, type 2 diabetes mellitus (T2DM), and dyslipidemia). NAFLD has been reported to be associated with extrahepatic manifestations such as cardiovascular disease, T2DM, chronic kidney disease, extrahepatic malignancies (e.g., colorectal cancer), endocrine diseases (e.g., hypothyroidism, polycystic ovarian syndrome, psoriasis, and osteoporosis), obstructive sleep apnea, and iron overload. The prevalence of NAFLD is very high, affecting 25–30% of the world population and encloses two steps: (1) nonalcoholic fatty liver (NAFL), which includes steatosis only, and (2) nonalcoholic steatohepatitis (NASH) defined by the presence of steatosis and inflammation with hepatocyte ballooning, with or without fibrosis which can progress to liver fibrosis, hepatocellular carcinoma, and liver transplantation. Current data define a more complex relationship between NAFLD and T2DM than was previously believed, underlining a bidirectional and mutual association between the two entities. This review aims to summarize the current literature regarding the incidence of T2DM among patients with NAFLD and also the prevalence of NAFLD in T2DM patients, highlighting the recent key studies. Clinicians should screen, diagnose, and treat T2DM in patients with NAFLD in order to avoid short- and long-term complications.

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most frequent cause of liver disease worldwide, comprising a plethora of conditions, ranging from steatosis to end‐stage liver disease. Cardiovascular disease (CVD) has been associated with NAFLD and CVD‐related events represent the main cause of death in patients with NAFLD, surpassing liver‐related mortality. This association is not surprising as NAFLD has been considered a part of the metabolic syndrome and has been related to numerous CVD risk factors, namely, insulin resistance, abdominal obesity, dyslipidemia, hyperuricemia, chronic kidney disease, and type 2 diabetes. Moreover, both NAFLD and CVD present similar pathophysiological mechanisms, such as increased visceral adiposity, altered lipid metabolism, increased oxidative stress, and systemic inflammation that could explain their association. Whether NAFLD increases the risk for CVD or these diagnostic entities represent distinct manifestations of the metabolic syndrome has not yet been clarified. This review focuses on the relation between NAFLD and the spectrum of CVD, considering the pathophysiological mechanisms, risk factors, current evidence, and future directions.

Background/Objectives: Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset neurodevelopmental disorder, characterized by difficulty maintaining attention, impulsivity, and hyperactivity. While the cause of this disorder is still unclear, recent studies have stated that heredity is important in the development of ADHD. This is linked to a few comorbidities, including depression, criminal behavior, and anxiety. Although genetic factors influence ADHD symptoms, there are also non-genetic factors, one of which is oxidative stress (OS), which plays a role in the pathogenesis and symptoms of ADHD. This review aims to explore the role of OS in ADHD and its connection to antioxidant enzyme levels, as well as the gut–brain axis (GBA), focusing on diet and its influence on ADHD symptoms, particularly in adults with comorbid conditions. Methods: The literature search included the main available databases (e.g., Science Direct, PubMed, and Google Scholar). Articles in the English language were taken into consideration and our screening was conducted based on several words such as “ADHD”, “oxidative stress”, “diet”, “gut–brain axis”, and “gut microbiota.” The review focused on studies examining the link between oxidative stress and ADHD, the role of the gut–brain axis, and the potential impact of dietary interventions. Results: Oxidative stress plays a critical role in the development and manifestation of ADHD symptoms. Studies have shown that individuals with ADHD exhibit reduced levels of key antioxidant enzymes, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), as well as a diminished total antioxidant status (TOS) compared to healthy controls. Additionally, there is evidence of a close bidirectional interaction between the nervous system and gut microbiota, mediated by the gut–brain axis. This relationship suggests that dietary interventions targeting gut health may influence ADHD symptoms and related comorbidities. Conclusions: Oxidative stress and the gut–brain axis are key factors in the pathogenesis of ADHD, particularly in adults with comorbid conditions. A better understanding of these mechanisms could lead to more targeted treatments, including dietary interventions, to mitigate ADHD symptoms. Further research is required to explore the therapeutic potential of modulating oxidative stress and gut microbiota in the management of ADHD.

Background/Aims: Patients with cirrhosis hospitalized in the intensive care unit (ICU) have a high risk for acute-on-chronic liver failure (ACLF) and short-term mortality. A major factor in the pathogenesis of ACLF is systemic inflammation, the assessment of which includes the use of surrogate markers, such as neutrophil-to-lymphocyte ratio (NLR). This study aimed to assess the accuracy of NLR in predicting the outcome of patients with cirrhosis and ACLF hospitalized in the ICU. Materials and Methods: This was a retrospective observational study on patients with cirrhosis with acute decompensation hospitalized in the ICU of a Romanian tertiary care center. ACLF was defined according to the CANONIC criteria, and NLR was calculated by dividing the absolute neutrophil count by the absolute lymphocyte count. Results: A total of 70 patients were included, of whom 70% were men with a mean age of 62±6.2 years. ACLF was diagnosed in 58 (82.9%) patients who presented with higher in-hospital mortality rates than patients without ACLF (84.5% vs. 33.3%, p=0.001). The mean NLR value was 11.7±9.5, higher in non-survivors than in survivors (12.6±9.8 vs. 8.6±7.8, p=0.170). NLR had a poor accuracy in predicting the outcome in patients without ACLF (area under the curve [AUC]=0.611) but a better accuracy in patients with ACLF (AUC=0.776). Patients with cirrhosis and a high NLR had higher levels of bilirubin; higher Child-Turcotte-Pugh score; and higher incidence of ascites, coagulation, and circulatory failure, presenting a poor outcome. Receiver operating characteristic analysis showed a good accuracy for predicting mortality for the Child-Turcotte-Pugh score (AUC= 0.864) and NLR (AUC=0.732). Conclusion: NLR is a promising and cost-effective method for the prediction of a poor outcome in critically ill patients with cirrhosis hospitalized in the ICU and shows greater accuracy in those with ACLF.

Capsule endoscopy (CE) has been proven to be a sensitive and a safe tool for the examination of the small bowel. However, careful patient selection is required to avoid complications, primarily capsule retention. The aims of this study were to evaluate the rate of capsule retention in patients with suspected chronic small bowel obstruction and to analyze the role and the impact of subsequent surgical intervention. Fifteen patients referred for CE with a clinical picture suggestive of chronic small bowel obstruction and with negative imaging studies were retrospectively analyzed. Capsule retention occurred in three (20%) patients who developed symptoms of subacute obstruction and subsequently underwent surgery. Radiation enteritis, Crohn’s disease, and an ileal tumor were demonstrated as the causes of the capsule retention in these patients. Surgical removal of the retained capsule was performed and the underlying small bowel disease was treated. Capsule retention is a frequent complication of CE in patients with symptoms of chronic small bowel obstruction. Surgery, with the removal of the retained capsule, is proven to be beneficial in identifying the location of, and treating, the underlying disease in these patients.

Nonalcoholic fatty liver disease (NAFLD) has a rising prevalence worldwide. Its potential for evolution towards liver cirrhosis and hepatocellular carcinoma, as well as associations with extrahepatic manifestations, represents a double burden for patients and physicians alike. Recently, there has been increasing evidence of the association between NAFLD and a number of endocrinopathies, such as hypothyroidism, polycystic ovarian syndrome (PCOS), hypopituitarism, growth hormone deficiency (GHD), hypogonadism, and hypercortisolism. Definite correlations are supported by clear evidence so far, but further studies are needed in order to completely clarify the pathogenic mechanisms and, especially, to identify therapeutic implications. In this review, we present the main relationships between NAFLD and endocrinopathies, emphasizing the reciprocal causality, evolutive interconnections, and current clinical scenarios of presentations of which the clinicians should be aware.