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Background: Functional dyspepsia (FD) is a common disorder characterized by chronic or recurrent upper abdominal pain or discomfort without any structural abnormalities in the gastrointestinal tract. FD is categorized into two subgroups based on symptoms: postprandial distress syndrome (PDS) and epigastric pain syndrome. Summary: The pathophysiology of FD involves several mechanisms. Delayed gastric emptying is observed in approximately 30% of FD patients but does not correlate with symptom patterns or severity. Impaired gastric accommodation is important in the pathophysiology, particularly for PDS. Visceral hypersensitivity, characterized by heightened sensitivity to normal activities, contributes to the perception of discomfort or pain in FD. Alterations to the duodenal mucosa, including impaired mucosal barrier function and low-grade inflammation, are also implicated in the pathogenesis of FD. Microbial dysbiosis and psychological factors such as stress can further exacerbate symptoms. Treatment options include dietary modifications, establishing a physician-patient relationship, acid suppressants, prokinetics, neuromodulators, and behavioral therapies. Dietary recommendations include eating smaller, more frequent meals, and avoiding trigger foods. Acid suppressants are used as the first-line treatment. Prokinetics and neuromodulators aim to improve gastric motility and central pain processing, respectively. Behavioral therapies, including cognitive behavioral therapy and hypnotherapy, have shown benefits for refractory FD. Severe and refractory cases may require combination therapies or experimental treatments. Key Messages: FD is a disorder of gut-brain interaction involving diverse pathophysiological mechanisms. Individualized treatment based on symptoms and responses to interventions is crucial. Further research is needed to improve the understanding of FD and advance the development of effective therapies.

Microinflammation is a non-traditional risk factor for the development of cardiovascular diseases in patients on hemodialysis. It occurs in 30-50% of these patients, and its main causes are: uremic toxins, oxidative stress, metabolic acidosis, vitamin D deficiency, overhydration, altered intestinal microbiome, impaired intestinal epithelial barrier integrity, increased translocation of endotoxin from the intestinal lumen into the systemic circulation, occult infection of the vascular approach for hemodialysis, periodontal disease, bioincompatibility of the hemodialysis membrane and the presence of endotoxin in the hemodialysis solution. The main clinical consequences of microinflammation are: accelerated atherosclerosis, malnutrition, anemia, resistance to the action of erythropoietin, hemoglobin variability and dialysis-related amyloidosis. Postdilution online hemodiafiltration, extended and adsorptive hemodialysis prevent the development of microinflammation. Optimal control of microinflammation prevents the development of cardiovascular diseases, improves the quality of life and the outcome of patients who are treated with regular hemodialysis.

Microinflammation is a non-traditional risk factor for the development of cardiovascular diseases in patients on hemodialysis. It occurs in 30–50% of these patients, and its main causes are: uremic toxins, oxidative stress, metabolic acidosis, vitamin D deficiency, overhydration, altered intestinal microbiome, impaired intestinal epithelial barrier integrity, increased translocation of endotoxin from the intestinal lumen into the systemic circulation, occult infection of the vascular approach for hemodialysis, periodontal disease, bioincompatibility of the hemodialysis membrane and the presence of endotoxin in the hemodialysis solution. The main clinical consequences of microinflammation are: accelerated atherosclerosis, malnutrition, anemia, resistance to the action of erythropoietin, hemoglobin variability and dialysis-related amyloidosis. Postdilution online hemodiafiltration, extended and adsorptive hemodialysis prevent the development of microinflammation. Optimal control of microinflammation prevents the development of cardiovascular diseases, improves the quality of life and the outcome of patients who are treated with regular hemodialysis.

Over almost 30 years since functional dyspepsia (FD) was defined, researchers have endeavored to elucidate the pathophysiology of functional gastrointestinal disorders. Now a consensus is emerging that the gastric symptoms of FD are caused mainly by gastric motility abnormalities and gastric hypersensitivity. The involvement of other causative factors including acid, Helicobacter pylori, psychological factors, and diet has been debated, but how they are involved in the manifestation of dyspeptic symptoms remains unclear. We believe that most of those factors cause FD symptoms by inducing gastric motility abnormalities and gastric hypersensitivity via the duodenum. Here, we discuss 2 possible reasons why patients with FD experience chronic upper abdominal symptoms: (1) the possibility that the contents of the duodenum of patients with FD differ from those of healthy persons and the different contents stimulate the duodenum, and (2) the possibility that the duodenum of patients with FD is more sensitive to noxious stimuli because of low-grade inflammation and increased mucosal permeability.

The systemic inflammatory response index (SIRI), a novel inflammation maker, has proven to be associated with prognostic outcomes in various diseases. However, few studies have been conducted assessing how SIRI may influence outcomes of patients on peritoneal dialysis (PD). Herein, we assessed the predictive value of SIRI on mortality all-cause mortality, including cardiovascular disease (CVD) in PD patients. A total of 646 PD patients were enrolled in this study. PD patients received regular PD treatments at the Zhujiang Hospital from 1 January 2011 to 31 December 2018. SIRI values could be computed as follows: neutrophil count × monocyte count/lymphocyte count. Patients were divided into two groups according to the median level of SIRI. Cox regression analysis and Kaplan-Meier methods were applied to analyze the relationship between SIRI and mortality outcomes in PD patients. During the median 31-month follow-up period, 97 (15.0%) PD patients died from all-causes, and 47 (49.0%) died of CVD. Kaplan-Meier analyses revealed that a high SIRI corresponded to the high mortality of all-cause deaths, including CVD (both p < 0.001) in patients on PD. After adjusting for potential confounders, the higher SIRI level was significantly associated with an increased all-cause mortality (HR: 2.007, 95% CI: 1.304-3.088, p = 0.002) and cardiovascular mortality (HR: 2.847, 95% CI: 1.445-5.608, p = 0.002). SIRI was a promising predictor of mortality in PD patients, with a higher SIRI corresponding to increased risk of mortality.

This review examines the impact of obesity on the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and focuses on novel mechanisms for HFpEF prevention using a glucagon-like peptide-1 receptor agonism (GLP-1 RA). Obesity can lead to HFpEF through various mechanisms, including low-grade systemic inflammation, adipocyte dysfunction, accumulation of visceral adipose tissue, and increased pericardial/epicardial adipose tissue (contributing to an increase in myocardial fat content and interstitial fibrosis). Glucagon-like peptide 1 (GLP-1) is an incretin hormone that is released from the enteroendocrine L-cells in the gut. GLP-1 reduces blood glucose levels by stimulating insulin synthesis, suppressing islet α-cell function, and promoting the proliferation and differentiation of β-cells. GLP-1 regulates gastric emptying and appetite, and GLP-1 RA is currently indicated for treating type 2 diabetes (T2D), obesity, and metabolic syndrome (MS). Recent evidence indicates that GLP-1 RA may play a significant role in preventing HFpEF in patients with obesity, MS, or obese T2D. This effect may be due to activating cardioprotective mechanisms (the endogenous counter-regulatory renin angiotensin system and the AMPK/mTOR pathway) and by inhibiting deleterious remodeling mechanisms (the PKA/RhoA/ROCK pathway, aldosterone levels, and microinflammation). However, there is still a need for further research to validate the impact of these mechanisms on humans.

Androgenetic alopecia (AGA) is characterized by microinflammation and abnormal immune responses, particularly in the upper segment of hair follicles (HFs). However, the precise patterns of immune dysregulation remain unclear, partly due to limitations in current analysis techniques to preserve tissue architecture. The infundibulum, a major part of the upper segment of HFs, is associated with significant clusters of immune cells. In this study, we investigated immune cells around the infundibulum, referred to as peri-infundibular immune infiltration (PII). We employed spatial transcriptome profiling, a high-throughput analysis technology, to investigate the immunological disruptions within the PII region. Our comprehensive analysis included an evaluation of overall immune infiltrates, gene set enrichment analysis (GSEA), cellular deconvolution, differential expression analysis, over-representation analysis, protein-protein interaction (PPI) networks, and upstream regulator analysis to identify cell types and molecular dysregulation in immune cells. Our results demonstrated significant differences in immune signatures between the PII of AGA patients (PII-A) and the PII of control donors (PII-C). Specifically, PII-A exhibited an enrichment of CD4+ helper T cells, distinct immune response patterns, and a bias toward a T helper (Th) 2 response. Immunohistochemistry revealed disruptions in T cell subpopulations, with more CD4+ T cells displaying an elevated Th2 response and a reduced Th1-cytotoxic response compared to PII-C. These findings reveal the unique immune landscapes of PII-A and PII-C, suggesting potential for the development of innovative treatment approaches.

Background/Aims Bacterial translocation (BT) promotes microinflammation in predialysis patients with end-stage renal disease (ESRD). However, the change in BT has not been reported in ESRD patients undergoing regular hemodialysis treatment. The present study investigated whether hemodialysis promotes gut BT and microinflammation. Methods The blood, gut, and dialysate of hemodialysis patients were analyzed using bacterial 16S rDNA amplification and DNA pyrosequencing to determine the presence of bacteria and alteration in gut microbiomes. High-sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), and endotoxin were also determined. Plasma d -lactate was tested for gut permeability. Results Bacteria were present in the plasma of 12 out of 52 ESRD patients. The majority of the bacteria detected in the blood were also distributed in the gut of ESRD patients on the basis of the phylogenetics of the blood and gut microbial specimens in the patients. In patient, groups treated with and without hemodialysis, the plasma hs-CRP, IL-6, and endotoxin levels differed between the positive and negative plasma bacterial DNA. In patients who were positive in blood bacteria, the bacterial DNA concentration was positively correlated with plasma levels of CRP and IL-6. The ESRD patients who underwent hemodialysis had a different flora and showed slightly higher levels of hs-CRP, IL-6, and plasma endotoxin, compared with those in ESRD patients who did not undergo hemodialysis. Conclusion ESRD, rather than hemodialysis, primarily contributes to BT and microinflammation in ESRD patients. Hemodialysis may exaggerate microinflammation in ESRD patients to some extent.

Noninfectious risk factors in peritoneal dialysis (PD) are often overlooked, yet they significantly worsen patient outcomes. This review highlights nine key risk factors: advanced age and psychosocial vulnerability, malnutrition and sarcopenia, glucose and lipid metabolism disorders, hypoalbuminemia, chronic microinflammation, gut dysbiosis, kidney anemia, chronic kidney disease-mineral and bone disorder, and volume overload with elevated intra-abdominal pressure. These factors interact to increase the risks of death, decline of residual kidney function, peritoneal fibrosis and cardiovascular events. We outline practical, evidence-based protective strategies that integrate nutritional and physical rehabilitation, biocompatible dialysis regimens, individualized fluid and dialysis prescription, targeted pharmacotherapy, psychosocial support, and regular monitoring of integrated inflammatory and nutritional biomarkers. The goal is to help clinicians improve long-term outcomes and quality of life for PD patients.

Objective This pilot study aimed to preliminarily investigate the short‐term effects of a combination regimen of acarbose combined with standard glucose dialysate on residual renal function and microinflammatory status in patients newly initiated on peritoneal dialysis and to preliminarily analyze the mediating role of volume load and microinflammatory status in these outcomes. Method A randomized controlled design was employed, with 128 patients newly initiating peritoneal dialysis randomly assigned in a 1:1 ratio. Ultimately, 110 patients completed full follow‐up and were included in the analysis (55 patients in each of the experimental and control groups). The mean age of patients was approximately 54.5 years, with males accounting for 55.5%. At the conclusion of follow‐up, both groups comprised 55 patients each. The experimental group received treatment with “1.5% glucose solution during the day + 7.5% acarbose solution at night,” while the control group received standard glucose dialysate throughout the entire study period. The intervention period lasted 24 weeks. The primary outcome measure was residual renal Kt/V at 6 months (T2). Primary outcomes were compared using covariance analysis, and mediation effects were evaluated. The mediating roles of volume load (ΔECW/TBW) and microinflammation status (Δhs‐CRP) at 3 months postintervention (T1) were evaluated. Results After 6 months of intervention, patients in the experimental group demonstrated significantly higher residual kidney Kt/V at T2 compared to the control group (0.62 ± 0.14 vs. 0.54 ± 0.16, p = 0.012), and their estimated glomerular filtration rate (eGFR) was also significantly superior to that of the control group (p < 0.001). Concurrently, the experimental group demonstrated improved microinflammation status (hs‐CRP at T2: 3.70 vs. 5.70 mg/L, p < 0.001), with volume load controlled (ECW/TBW at T2: 0.394 vs. 0.402, p < 0.001), and nutritional status enhanced (serum albumin at T2: 38.80 vs. 35.80 g/L, p < 0.001). Mediation analysis indicated that treatment grouping significantly improved volume load and microinflammation status at T1 (pathway a significant, p < 0.01). However, neither of these factors significantly predicted residual renal function changes at T2 (pathway b not significant), and the indirect effect failed to reach statistical significance. Conclusion For patients initiating peritoneal dialysis, the 6‐month acarbose combination regimen demonstrated superior short‐term effects compared to the standard glucose regimen in delaying residual renal function decline, alleviating microinflammatory states, and improving volume load. The protective effects, however, may not primarily result from volume load improvement and microinflammatory reduction.