Search Results (11)

(1) Background: Patients admitted for gastrointestinal bleeding (GIB) who are diagnosed with COVID-19 at presentation may face significant therapeutic challenges. The delicate balance between the use of anticoagulant and anti-inflammatory therapy to address COVID-19 and hemostasis targets can, in turn, lead to delays in COVID-19 treatment until bleeding is controlled. The published systematic reviews and meta-analyses that were reviewed included patients with both GIB and COVID-19 regardless of GIB presence at admission, and a separate analysis of patients admitted for GIB and tested for COVID-19 infection during hospitalization was not performed. (2) Methods: PubMed, Web of Science, and Scopus databases were used to access articles published from 1 December 2019 to 20 December 2024. Retrospective studies involving human subjects with GIB and COVID-19 were included in the final analysis. The exclusion criteria were as follows: pediatric population studies; the absence of a GIB control group; reviews, conference abstracts, expert opinions, and letters. The risk of bias in the included studies was assessed using the rank correlation test and Begg’s and Egger’s regression tests. We estimated the outcomes using the pooled odds ratio (OR) and the 95% confidence interval (95% CI). (3) Results: Seven studies, which included 3291 patients admitted for GIB who tested positive for COVID-19 infection, were included in our systematic review; four studies with a control group of patients with GIB but without COVID-19 infection were included in our meta-analysis. The odds of mortality among COVID-19-infected patients admitted for GIB were 3.80. There was heterogeneity regarding the site of GIB (some studies included all forms of GIB, others included only UGIB) and the study period (most studies included only patients from the first pandemic wave, and only one study reported cases from the first 2 years of the pandemic, including the delta pandemic wave). (4) Conclusions: COVID-19 infection in patients admitted for GIB was associated with a higher overall mortality rate. Full article

(1) Background: Atrial fibrillation (A Fib) is a common arrhythmia that affects millions of people worldwide and is characterized by irregular and often rapid heartbeats that can cause stroke. The aim of our study was to assess the importance of predictors for the occurrence of atrial fibrillation in patients with cardiac pacemakers and to analyze their impact on these patients, especially the impact of hepatic impairment. (2) Methods: This study is an observational, retrospective study, including 182 patients who were implanted with a dual-chamber pacemaker (DDD), with no known history of A Fib. (3) Results: We identified as predictors for the occurrence of atrial fibrillation in patients with cardiac pacemakers, DDD with rate response mode, NYHA class III of heart failure, as well as the presence of hepatic impairment (HI). Analysis of echocardiographic parameters of the left atrium revealed a larger left atrial volume as well as a larger left atrial area compared to patients who had a much smaller area at baseline and who did not experience any atrial fibrillation at follow-up. The fact that there were no statistically significant differences between the two groups of patients in terms of left atrial ejection fraction at baseline was very interesting. Patients in the A Fib group had a higher percentage of atrial pacing at the 9-month follow-up (86.23 ± 22.19%) compared to patients in the group without A Fib (44.92 ± 29.99%, p < 0.0001) and had a 9-month follow-up rate of A Fib of 25.806% vs. 2.247% in those with a low percentage of atrial pacing (p < 0.0001). The percentage of ventricular pacing at the 9-month follow-up, the observations were almost similar. (4) Conclusions: The importance of pacemakers in detecting subclinical episodes of atrial fibrillation remains crucial for the prevention of embolic events in these patients. Hepatic impairment may be a risk factor for the occurrence of atrial fibrillation in patients with pacemakers, but it can also create significant problems in stroke prevention. Full article

Non-alcoholic fatty liver disease (NAFLD) is the main cause of chronic liver disease globally. NAFLD is a complex pathology, considered to be the hepatic expression of metabolic syndrome (MetS). It is supposed to become the main indication for liver transplantation in the coming years and is estimated to affect 57.5–74.0% of obese people, 22.5% of children and 52.8% of obese children, with 50% of individuals with type 2 diabetes being diagnosed with NAFLD. Recent research has proved that an increase in adipose tissue insulin resistance index is an important marker of liver injury in patients with NAFLD. Despite being the main underlying cause of incidental liver damage and a growing worldwide health problem, NAFLD is mostly under-appreciated. Currently, NAFLD is considered a multifactorial disease, with various factors contributing to its pathogenesis, associated with insulin resistance and diabetes mellitus, but also with cardiovascular, kidney and endocrine disorders (polycystic ovary syndrome, hypothyroidism, growth hormone deficiency). Hepatitis B and hepatitis C, sleep apnea, inflammatory bowel diseases, cystic fibrosis, viral infections, autoimmune liver diseases and malnutrition are some other conditions in which NAFLD can be found. The aim of this review is to emphasize that, from the clinician’s perspective, NAFLD is an actual and valuable key diagnosis factor for multiple conditions; thus, efforts need to be made in order to increase recognition of the disease and its consequences. Although there is no global consensus, physicians should consider screening people who are at risk of NAFLD. A large dissemination of current concepts on NAFLD and an extensive collaboration between physicians, such as gastroenterologists, internists, cardiologists, diabetologists, nutritionists and endocrinologists, is equally needed to ensure we have the knowledge and resources to address this public health challenge. Full article

Irritable bowel syndrome (IBS) is a common digestive disorder with a significant impact on both individuals and society in terms of quality of life and healthcare costs. A growing body of research has identified various communication pathways between the microbiota and the brain in relation to motility disorders, with the gut–brain axis being key to the pathogenesis of IBS. Multiple factors contribute to the pathogenetic pathways in IBS, including immune mechanisms, psychosocial factors, increased oxidative stress and pro-inflammatory cytokine release, as well as genetic and hormonal factors. Increased permeability of the normal intestinal barrier allows bacterial products to access the lamina propria, providing a mechanism for perpetuating chronic inflammation and characteristic symptoms. The microbiota influences inflammatory processes in IBS by altering the balance between pro-inflammatory factors and host defence. Probiotics modulate the pathophysiological mechanisms involved in IBS by influencing the composition of the microbiota and improving intestinal motility disorders, visceral hypersensitivity, immune function of the intestinal epithelium, metabolic processes in the intestinal lumen, dysfunction of the microbiota-GBA, and are recognised as effective and safe in IBS therapy. Our study aimed to provide a comprehensive overview of the relationship between the gut–brain axis, microbiota, and IBS, based on current information. Full article

Hematological abnormalities are frequently linked to chronic liver disease of any etiology. About 75% of patients with advanced chronic liver disease experience anemia. The causes of anemia are complex and multifactorial, particularly in cirrhotic patients. Acute and long-term blood loss from the upper gastrointestinal tract, malnutrition, an enlarged spleen brought on by portal hypertension, hemolysis, and coagulation issues are the main causes of anemia. Alcohol, a common cause of chronic liver disease, determines anemia through direct toxicity on the bone marrow, with the suppression of hematopoiesis, through vitamin B6, B12, and folate deficiency due to low intake and malabsorption. In patients with chronic hepatitis C virus infection, antiviral drugs such as pegylated interferon and ribavirin can also cause significant anemia. The use of interferon has been linked to bone marrow toxicity, and hemolytic anemia brought on by ribavirin is a well-known dose-dependent side effect. Within six months of the infection with hepatitis B, hepatitis C, and Epstein–Barr viruses, aplastic anemia associated with hepatitis is seen. This anemia is characterized by pancytopenia brought on by hypocellular bone marrow. Esophageal varices, portal hypertensive gastropathy, and gastric antral vascular ectasia can all cause acute and chronic blood loss. These conditions can progress to iron deficiency anemia, microcytic anemia, and hypochromic anemia. Another common hematologic abnormality in liver cirrhosis is macrocytosis, with multifactorial causes. Vitamin B12 and folate deficiency are frequent in liver cirrhosis, especially of alcoholic etiology, due to increased intestinal permeability, dysbiosis, and malnutrition. Many chronic liver diseases, like viral and autoimmune hepatitis, have a chronic inflammatory substrate. Proinflammatory cytokines, including tumor necrosis factor and interleukin 1, 6, and 10, are the main factors that diminish iron availability in progenitor erythrocytes and subsequent erythropoiesis, leading to the development of chronic inflammatory, normochromic, normocytic anemia. Full article

Acute-on-chronic liver failure (ACLF) is a syndrome characterized by acute and severe decompensation of chronic liver disease (CLD) correlated with multiple organ failure, poor prognosis, and increased mortality. In 40–50% of ACLF cases, the trigger is not recognized; for many of these patients, bacterial translocation associated with systemic inflammation is thought to be the determining factor; in the other 50% of patients, sepsis, alcohol consumption, and reactivation of chronic viral hepatitis are the most frequently described trigger factors. Other conditions considered precipitating factors are less common, including acute alcoholic hepatitis, major surgery, TIPS insertion, or inadequate paracentesis without albumin substitution. Host response is likely the primary factor predicting ACLF severity and prognosis, the host immune response having a particular significance in this syndrome, together with the inflammatory cascade. The management of ACLF includes both the prevention of the precipitating factors that lead to acute liver decompensation and the support of vital functions, the prevention and management of complications, the estimation of prognosis, and the opportunity for liver transplantation. Full article

The outbreak of the coronavirus pandemic in March 2020 has caused unprecedented pressure on public health and healthcare. The spectrum of COVID-19 onset is large, from mild cases with minor symptoms to severe forms with multi-organ dysfunction and death. In COVID-19, multiple organ damage has been described, including lung damage, acute kidney injury, liver damage, stroke, cardiovascular and digestive tract disorders. The aspects of liver injury are different, sometimes presenting with only a slight increase in liver enzymes, but sometimes with severe liver injury, leading to acute liver failure requiring liver transplantation. In patients with chronic liver disease, especially liver cirrhosis, immune dysfunction can increase the risk of infection. Immune dysfunction has a multifactorial physiopathological mechanism, implying a complement system and macrophage activation, lymphocyte and neutrophil activity dysfunction, and intestinal dysbiosis. This review aims to evaluate the most relevant studies published in the last years related to the etiopathogenetic, biochemical, and histological aspects of liver injury in patients diagnosed with COVID-19. Liver damage is more evident in patients with underlying chronic liver disease, with a significantly higher risk of developing severe outcomes of COVID-19 and death. Systemic inflammation, coagulation disorders, endothelial damage, and immune dysfunction explain the pathogenic mechanisms involved in impaired liver function. Although various mechanisms of action of SARS-CoV-2 on the liver cell have been studied, the impact of the direct viral effect on hepatocytes is not yet established. Full article

Background: The association of chronic heart failure (CHF) and iron deficiency (ID) with or without anemia is frequently encountered in current medical practice and has a negative prognostic impact, worsening patients’ exercise capacity and increasing hospitalization costs. Moreover, anemia is common in patients with chronic kidney disease (CKD) and CHF, an association known as cardio-renal anemia syndrome (CRAS) possessing a significantly increased risk of death. Aim: This review aims to provide an illustrative survey on the impact of ID in CHF patients—based on physiopathological traits, clinical features, and the correlation between functional and absolute ID with CHF—and the benefit of iron supplementation in CHF. Method: We selected the most recent publications with important scientific content covering the association of CHF and ID with or without anemia. Discussions: An intricate physiopathological interplay is described in these patients—decrease in erythropoietin levels, activation of the renin-angiotensin-aldosterone system, systemic inflammation, and increases in hepcidin levels. These mechanisms amplify anemia, CHF, and CKD severity and worsen patients’ outcomes. Conclusions: Anemia is frequently encountered in CHF and represents a negative prognostic factor. Data from randomized controlled trials have underlined the administration of intravenous iron therapy (ferric carboxymaltose) as the only viable treatment option, with beneficial effects on quality of life and exercise capacity in patients with ID and systolic heart failure. Full article

Among the most widespread childhood infections, Helicobacter pylori (H. pylori) develops potentially life-threatening conditions in adults if not appropriately treated. Helicobacter pylori is a common human pathogen that was first described in the stomach many years ago. The discovery of H. pylori was crucial in gastroenterology; this bacterium is associated with chronic gastritis, peptic ulcers, gastric cancer, and lymphoid tissue lymphoma related to the gastric mucosa. Studies published so far estimate that approximately 10% of subjects infected with H. pylori develop a peptic ulcer, and 1–3% of subjects develop gastric cancer. The clinical manifestations are variable and characteristically depend on the individual factors of the host. Various methods of detection and diagnosis of H. pylori infection have been developed, each with advantages, disadvantages, and/or limitations. Available diagnostic tests are usually performed using invasive (endoscopy, biopsy, rapid urease test, cultures, and molecular tests) and noninvasive methods (urea breath test, stool antigen examination, and serological and molecular tests). Although there is extensive accessibility for diagnosing and treating H. pylori infection, the prevalence of antibiotic resistance is not negligible. Thus, numerous studies and meta-analyses are focused on a new orientation of gastroenterologists in diagnosing and treating H. pylori infections. A fascinating perspective hypothesis is the administration of probiotics to reduce H. pylori adhesion to gastric epithelial cells, preventing H. pylori colonization, especially in children, or reinfection with H. pylori in high-risk adult patients. Full article

COVID-19 pneumonia represents a maximum medical challenge due to the virus’s high contagiousness, morbidity, and mortality and the still limited possibilities of the health systems. The literature has primarily focused on the diagnosis, clinical-radiological aspects of COVID-19 pneumonia, and the most common possible differential diagnoses. Still, few studies have investigated the rare differential diagnoses of COVID-19 pneumonia or its overlap with other pre-existing lung pathologies. This article presents the main radiological features of COVID-19 pneumonia and the most common alternative diagnoses to establish the vital radiological criteria for a differential diagnosis between COVID-19 pneumonia and other lung pathologies with similar imaging appearance. The differential diagnosis of COVID-19 pneumonia is challenging because there may be standard radiologic features such as ground-glass opacities, crazy paving patterns, and consolidations. A multidisciplinary approach is crucial to define a correct final diagnosis, as an overlap of COVID-19 pneumonia with pre-existing lung diseases is often possible and suggests possible differential diagnoses. An optimal evaluation of HRTC can help limit the clinical evolution of the disease, promote therapy for patients and ensure an efficient allocation of human and economic resources. Full article

Background: Chronic pancreatitis (CP) has been described as a multifactorial, ongoing inflammatory condition of the pancreas of varying intensity that produces persistent pain, leading to exocrine and endocrine insufficiency and a decreased lifespan. Currently, there are three primary forms of chronic pancreatitis: chronic autoimmune pancreatitis (steroid-sensitive pancreatitis), chronic obstructive pancreatitis, and chronic calcific pancreatitis, the latter being closely related to excessive alcohol consumption for one or even two decades before the onset of symptoms. Case report: We present the case of a 29 year old man who required medical attention for a significant unintentional weight loss and a history of upper abdominal pain. Blood tests revealed substantial abnormalities, and the patient was admitted for further investigation. CT and MRI confirmed the presence of a pancreatic pseudocyst and extensive pancreatic parenchymal calcifications and revealed multiple hepatosplenic microabscesses of fungal etiology. Conclusions: Chronic calcifying pancreatitis is a complex clinical entity that can lead to secondary diabetes due to progressive destruction of the pancreatic parenchyma. Protein malnutrition, caused by malabsorption syndrome, immune cell dysfunction, and a high glucose environment caused by diabetes mellitus, may create a state of immunodeficiency, predisposing the patient to opportunistic infections. Full article