Background/Objectives:Pacing treatment of bradyarrhythmias is both to reduce symptoms and to prevent syncope and sudden cardiac death. The aim of our study was to analyze left bundle branch area pacing (LBBAP) in the prevention of new-onset AF and the improvement of echocardiographic parameters in patients with mildly reduced left ventricular ejection fraction (LVEF) compared to patients with bradyarrhythmias but preserved LVEF who underwent mid-septal right ventricular pacing. Methods: This research was structured as a retrospective observational cohort study that included 186 patients with LBBAP and 186 patients with RVP, enrolled for 3 years until March 2024 with a follow-up time of 1 year. The primary endpoint of our study was new-onset atrial fibrillation after pacemaker implantation. The secondary endpoint was the improvement of echocardiographic parameters. Results: We observed in the LBBAP group a mean QRS complex duration of 108.7 ± 8.83 ms (after pacemaker implantation), compared to a much longer duration in the RVP group (143.8 ± 9.851 ms, p = <0.0001). At 1 year of follow-up, 22 (11.82%) patients in the RVP group were diagnosed with new-onset atrial fibrillation, compared to 6 (3.22%) patients out of 186 included in the LBBAP group (p = 0.0017). Regarding LVEF, at follow-up, RVP patients had a decrease in LVEF compared to those in the LBBAP group who had an improved LVEF (54.54 ± 3.77%, p < 0.0001). Conclusions: LBBAP both prevents the onset of atrial fibrillation and improves echocardiographic parameters, especially left ventricular ejection fraction, thus contributing to significantly reducing the risk of developing/worsening advanced heart failure through pacing-induced cardiomyopathy.

(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.

Colorectal cancer (CRC) is a major public health problem worldwide, currently ranking third in cancer incidence and second in mortality. Multiple genes and environmental factors have been involved in the complex and multifactorial process of CRC carcinogenesis. VDR is an intracellular hormone receptor expressed in both normal epithelial and cancer colon cells at various levels. Several VDR gene polymorphisms, including FokI and BsmI, have been evaluated for their possible association with CRC susceptibility. The aim of our study was to investigate these two SNPs for the first time in Romanian CRC patients. FokI (rs228570 C>T) and BsmI (rs1544410 A>G) were genotyped by real-time polymerase chain reaction (RT-PCR) in 384-well plates using specific TaqMan predesigned probes on a ViiA™ 7 RT-PCR System. A total of 441 subjects (166 CRC patients and 275 healthy controls) were included. No statistically significant difference was observed between CRC patients and controls when we compared the wild-type genotype with heterozygous and mutant genotypes for both FokI (OR 0.85, 95% CI: 0.56–1.28; OR 0.95, 95% CI: 0.51–1.79, respectively) and BsmI (OR 0.97, 95% CI: 0.63–1.49; OR 1.10, 95% CI: 0.65–1.87, respectively) or in the dominant and recessive models. Also, we compared allele frequencies, and no correlation was found. Moreover, the association between these SNPs and the tumor site, TNM stage, and histological type was examined separately, and there was no statistically significant difference. In conclusion, our study did not show any association between FokI and BsmI SNPs and CRC susceptibility in a Romanian population. Further studies including a larger number of samples are needed to improve our knowledge regarding the influence of VDR polymorphism on CRC susceptibility.

The advent of highly active antiretroviral therapy (HAART) in 1996 has markedly enhanced the life expectancy of people living with HIV (PLWH), largely due to the effectiveness of reverse transcriptase inhibitors (RTIs). These drugs target the reverse transcriptase enzyme, crucial for the HIV virus to convert its RNA into DNA within host cells, effectively disrupting the viral replication process. This action reduces the patient's viral load, helping preserve immune function and prevent progression to AIDS. Consequently, the predominant causes of mortality among individuals living with HIV have transitioned from opportunistic infections and AIDS-related cancers to liver disease and cardiovascular complications. Liver damage in PLWH could arise from multiple sources including co-infections, chronic substance use, and notably, antiretroviral therapy itself, which can be hepatotoxic. This review highlights the risks of hepatic damage associated with nucleoside and non-nucleoside RTIs and underscores the variability in hepatotoxicity risks among different drugs. It emphasizes the necessity for regular monitoring of liver health in PLWH and adjusting antiretroviral regimens to minimize liver fibrosis risk. This risk is particularly pronounced in patients who associate the infection with hepatitis B or C virus, where the potential for hepatotoxicity significantly increases.

The study aimed to determine liver fibrosis in human immunodeficiency virus (HIV) positive individuals using transient elastography (FibroScan®), Fibrosis-4 (FIB-4) score, and aspartate aminotransferase (AST) to Platelet Ratio Index (APRI) in the HIV Department from Infectious Diseases Hospital “Victor Babeș” Craiova, Romania. Of the analyzed HIV-positive subjects (n = 161), 93 (57.76%) had HIV mono-infection, and 68 (42.24%) had Hepatitis B Virus (HBV) co-infection. The prevalence of advanced liver fibrosis was higher (F2: 11.76% and F3: 13.24%, F4: 4.41%) in the HIV-HBV co-infected group compared to the HIV mono-infected group. The univariate and multivariate analysis identified HBV co-infection (OR = 5.73) male sex (OR = 5.34), serum aspartate amino-transferase levels (Pearson’s rho = 0.273), low platelet count (Pearson’s rho = −0.149) and erythrocyte sedimentation rate (OR = 1.030) as risk factors for the presence of liver fibrosis. Body mass index (OR = 1.08), serum lipid levels (OR = 0.96), viral load at diagnosis (OR = 1.00005), and low CD4+ cell count (OR = 0.977) were also correlated with liver fibrosis. The FIB-4 and APRI scores were strongly correlated with each other. In conclusion, HBV co-infection seems to be a determinant factor for liver fibrosis development in people living with HIV, together with other risk factors.

Abstract Atrial fibrillation (AF) is a prevalent cardiac arrhythmia, affecting millions worldwide and increasing in frequency with age. Despite progress in treatment and prevention, AF remains a significant contributor to stroke, heart failure, and overall cardiovascular morbidity. One particularly challenging type of AF, paroxysmal atrial fibrillation (PAF), is often asymptomatic, leading to delayed diagnosis and increasing the risk of severe complications like stroke. The advent of cardiac implantable electronic devices (CIEDs) has significantly improved the ability to detect subclinical AF or atrial high-rate episodes (AHRE), even in patients with no symptoms. These devices, particularly pacemakers, offer long-term, continuous monitoring of atrial rhythms, making them an invaluable tool for diagnosing AF early and assessing its burden in real time. This study focused on a cohort of patients from the Oltenia region who received dual-chamber pacemakers with no prior diagnosis of AF. The research aimed to monitor the incidence of AF in these patients over a follow-up period of 12 to 18 months and to identify potential clinical predictors for developing AF. A total of 91 patients were assessed in this study, all of whom received dual-chamber pacemakers by the pacing guidelines for conditions such as atrioventricular block and sick sinus syndrome. None of the patients had a history of AF at the time of implantation. Follow-up results indicated an incidence of AHRE in 13.19% of patients, with significant predictors including advanced age and the presence of hypertension. These findings align with the broader literature, which consistently associates both factors with an increased risk of AF. The study underscores the importance of continuous monitoring in pacemaker patients, particularly for detecting asymptomatic AF, which may necessitate specific therapeutic interventions. Although the study’s sample size was limited, its findings contribute valuable insights into managing AF in pacemaker patients, particularly regarding early detection and potential risk factors. Future research with larger cohorts is necessary to confirm and expand these results.

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.

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.

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.

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.

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.

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.

A high risk of developing insulin resistance (IR) and, eventually, type 2 diabetes mellitus (T2DM) is associated with chronic hepatitis C virus (HCV). Multiple mechanisms can account for the development of IR in chronic HCV patients, steatosis or fatty liver that can lead to metabolic syndrome, and the inflammatory process associated with the presence of HCV infection. In this article, we analyze the reported values of homoeostasis model assessment (HOMA-IR) before and after successful direct-acting agents (DAAs) treatment in the literature (23 studies) at certain intervals, respectively 12, 24, and 52 weeks depending on the presence of T2DM among patients. The meta-analysis showed improvement of IR in most cases except for three studies that presented a minimal increase in HOMA-IR value for the non-T2DM group at the 12- and 24-week check-ups possibly hinting at a prediabetes group. All other studies showed an important decrease in HOMA-IR post-DAA treatment specifically for the T2DM group. The most significant change in HOMA-IR values was noticed after 24 weeks in all categories. Our meta-analysis showed that clearance of HCV leads to improvement of IR, especially in the case of patients with T2DM.

Since COVID-19 was declared a pandemic by the World Health Organization, the scientific community has tried to protect the population from the infection and its effects through multiple lines of evidence. Patients at high risk of developing severe disease were advised to protect themselves and practice effective physical distancing. Phenotypes specific to this infection need to be reviewed to understand COVID-19 and its clinical manifestations. When the pandemic began, the scientific community was concerned with the unfavorable outcome of cases with pre-existing liver disease. There have been speculations about risk factors for severe diseases such as liver disease, age, gender, and association with obesity or diabetes.

Even with the availability of HIV self-testing kits in some areas12, testing remains a major challenge in environments with limited access to these kits. [...]increased efforts are needed to increase access and facilitate testing. From the anamnesis, we found that the patient was hospitalized in June 2016 at NHS Hospital in UK, where she was diagnosed and with HIV C3 category infection, pulmonary and meningeal tuberculosis, diffuse non-Hodgkin's lymphoma (NHL) with large cells and was initiated on specific treatment but the patient cannot provide details about its nature, and she also underwent brain surgery to remove NHL-derived tumors. WBC = 6.8 ·10л3/шшл3, LYM = 1.67 ·10л3/шшл3, LYM = 24.4%, MON = 0.5·10Л3/шшЛ3, MON = 7.3%, NEU = 4.57·10Л3/шшЛ3, NEU = 66.9%, EOS = 0.06·10Л3/шшЛ3, EOS = 0.9%, BAS = 0.03 ·10Л3/шшЛ3, BAS = 0.5%, RBC = 3.79 ·10Л6/шшЛ3, HGB = 13.6 g/dl, HCT = 42.3%, MCV = 111 ;_

Diabetes Mellitus (DM) and Chronic Hepatitis C Virus (HCV) have a strong interconnection in general practice. Recent studies have correlated insulin resistance risk with liver dysfunction. Haptoglobin is a biomarker that is modified in liver disease and is involved in metabolic diseases. Our study aims to investigate the changes in haptoglobin and bilirubin levels after direct -acting antiviral (DAA) treatment for viral hepatitis C in relation to diabetes status and hypertension in order to identify potential biomarkers for the prognosis of liver disease in diabetic patients after obtaining sustained virological response (SVR). Eighty patients (40 with Type 2-DM (T2DM) and 40 without T2DM) treated with DAAs for HCV infection that obtained SVR were monitored for biochemical markers before and 3 years after treatment. We report that HCV clearance improves not only the biomarkers of liver function but also TB and Hp, which are strongly connected with insulin resistance in T2DM, leading to better control of blood glucose levels, obesity, and lipid metabolism. These two biomarkers should be further investigated not only to understand better the physiopathological pathways by which they affect TD2M progression, but also how their levels might be raised in the pursuit of better control of diabetes, cardiovascular complications, and other diseases.

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.