世界胃肠病理生理学杂志(电子版)(英文版)最新文献

Background: The rising global prevalence of gastroesophageal reflux disease (GERD) has been closely linked to lifestyle changes driven by globalization. GERD imposes a substantial public health burden, affecting quality of life and leading to potential complications. Early intervention through lifestyle modification can prevent disease onset; however, there is a lack of effective risk prediction models that emphasize primary prevention.

Aim: To develop and validate a GERD Risk Scoring System (GRSS) aimed at identifying high-risk individuals and promoting primary prevention strategies.

Methods: A 45-item questionnaire encompassing major lifestyle and demographic risk factors was developed and validated. It was administered to healthy controls and GERD patients. Two regression models-one using continuous variables and another using categorized variables-were used to develop a computational prediction equation and a clinically applicable scoring scale. An independent validation cohort of 355 participants was used to assess model performance in terms of discrimination (C-index), calibration, sensitivity, specificity, internal consistency (Cronbach's alpha), and test-retest reliability (intraclass correlation coefficient, Bland-Altman analysis).

Results: Significant associations were observed between GERD and key lifestyle factors. The derived GRSS equation and scoring scale demonstrated strong discriminative ability, with high sensitivity and specificity. The scoring system exhibited excellent internal consistency (Cronbach's alpha) and strong test-retest reliability. The C-index indicated excellent predictive accuracy in both derivation and validation cohorts.

Conclusion: GRSS offers a novel and validated approach to GERD risk prediction, combining a robust equation for digital applications and a practical scale for clinical use. Its ability to accurately identify at-risk individuals supports a paradigm shift toward primary prevention, underscoring its significance in addressing the growing burden of GERD at the population level.

Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease characterized by damage and loss of the epithelial lining of small intrahepatic bile ducts, leading to ductopenia and cholestasis. In advanced stages, this process results in cirrhosis and liver failure. The disease belongs to cholangiopathies. The review addressed historical questions concerning: The history of the first mention of this disease; how its nomenclature was formed; when specific serological tests were discovered and their importance in the diagnosis of PBC; the history of ursodeoxycholic and other bile acids for the treatment of PBC; and the significance of modern data on impaired bicarbonate production by cholangiocytes in the pathogenesis of PBC.

Pancreatic neuroendocrine tumors (pNETs) are rare, presenting significant challenges in timely diagnosis and subsequent treatment. The clinical and pathobiological behavior of these tumors varies significantly, making follow-up and therapeutic approaches challenging for clinicians. Although the majority of these neoplasms are hormonally inactive, some can be associated with endocrine dysfunction. Very rarely, a nonfunctional tumor can later become hormonally active, further complicating prognostication and management. Depending on the character of the disease, clinical picture and prognosis, different treatment modalities are instituted with varying effectivities. We recently came across a unique case of nonfunctioning malignant pNET at an advanced stage, metastatic disease upon diagnosis, managed medically with somatostatin analog therapy (Octreotide) and targeted therapy (Everolimus) with stable disease for 40 months that subsequently turned out to become functional (insulinoma). With the aid of this unique case, we update the current clinical, diagnostic and therapeutic approach to pNETs in this evidence-based review.

Anastomotic stricture (AS) remains a significant complication following rectal anastomosis, with an incidence ranging from 5% to 30% depending on surgical technique, patient factors, and postoperative management. This review aims to elucidate the pathophysiology of AS, exploring the underlying mechanisms that contribute to its development, including ischemia, inflammation, fibrosis, and impaired healing. Key risk factors such as low anterior resection, preoperative radiotherapy, and anastomotic leakage are critically analyzed based on recent clinical and experimental evidence. The article synthesizes current insights into the molecular and cellular processes, such as excessive collagen deposition and myofibroblast activation, that drive stricture formation. Furthermore, preventive strategies, including optimized surgical techniques (e.g., tension-free anastomosis), enhanced perioperative care, and emerging therapeutic interventions (e.g., anti-fibrotic agents), are discussed with an emphasis on translating research into clinical practice. By integrating findings from preclinical studies, clinical trials, and meta-analyses, this review highlights gaps in current knowledge and proposes future directions for research, such as the role of personalized medicine and novel biomaterials in reducing AS incidence. This comprehensive analysis underscores the need for a multidisciplinary approach to mitigate this challenging postoperative complication.

Helicobacter pylori (H. pylori) infection is one of the most prevalent bacterial infections affecting mankind. About half of the world's population is infected with it. It causes several upper gastrointestinal diseases, including gastric cancer (GC). It has been identified as a major risk factor for GC. GC is one of the most common cancers affecting humans and the third leading cause of cancer-related deaths worldwide. H. pylori infection causes an inflammatory response that progresses through a series of intermediary stages of precancerous lesions (gastritis, atrophy, intestinal metaplasia, and dysplasia) to the final development of GC. Among infected individuals, approximately 10% develop severe gastric lesions such as peptic ulcer disease, 1%-3% progress to GC, and 0.1% develop mucosa-associated lymphoid tissue followed by the development of lymphoma. The bacterium has many virulence factors, including cytotoxin-associated gene A, vacuolating cytotoxin A, and the different outer membrane proteins that cause cancer by different mechanisms. These virulence factors activate cell signaling pathways such as PI3-kinase/Akt, JAK/STAT, Ras, Raf, and ERK signaling that control cell proliferation. Uncontrolled proliferation can lead to cancer. In addition, the repair of DNA damage may also be impaired by H. pylori infection. Reduced DNA repair in combination with increased DNA damage can result in carcinogenic mutations. The accurate identification of pathogenetic pathways is imperative for the development of targeted diagnostic markers and personalized treatments. This scoping review aims to update the readers on the role of H. pylori in the development of GC. It will focus on the molecular mechanisms underpinning gastric carcinogenesis in H. pylori infection. It will highlight the interaction between bacterial virulence factors and host cellular pathways, providing insights into potential therapeutic targets and preventive strategies.

Background: Autoimmune hepatitis (AIH) is typically treated with immunomodulators and steroids. However, some patients are refractory to these treatments, necessitating alternative approaches. Biological therapies have recently been explored for these difficult cases.

Aim: To assess the efficacy and safety of biologics in AIH, focusing on patients unresponsive to standard treatments and evaluating outcomes such as serological markers and histological remission.

Methods: A case-based systematic review was performed following the PRISMA protocol to evaluate the efficacy and safety of biological therapies in AIH. The primary focus was on serological improvement and histological remission. The secondary focus was on assessing therapy safety and additional outcomes. A standardized search command was applied to MEDLINE, EMBASE, and Cochrane Library databases to identify relevant studies. Inclusion criteria encompassed adult AIH patients treated with biologics. Data were analyzed based on demographics, prior treatments, and therapy-related outcomes. A narrative synthesis was employed to address biases and provide a comprehensive overview of the evidence.

Results: A total of 352 studies were reviewed, with 30 selected for detailed analysis. Key findings revealed that Belimumab led to a favourable response in five out of eight AIH patients across two studies. Rituximab demonstrated high efficacy, with 41 out of 45 patients showing significant improvement across six studies. Basiliximab was assessed in a single study, where the sole patient treated experienced a beneficial outcome. Additionally, a notable number of AIH cases were induced by anti-tumor necrosis factor (TNF) medications, including 16 cases associated with infliximab and four cases with adalimumab. All these cases showed improvement upon withdrawal of the biologic agent.

Conclusion: Belimumab and Rituximab show promise as effective alternatives for managing refractory AIH, demonstrating significant improvements in clinical outcomes and liver function. However, the variability in patient responses to different therapies highlights the need for personalized treatment strategies. The risk of AIH induced by anti-TNF therapies underscores the need for vigilant monitoring and prompt symptom recognition. These findings support the incorporation of biologic agents into AIH treatment protocols, particularly for patients who do not respond to conventional therapies.

This comprehensive review addresses the global health challenge of disparities in pancreas transplant access, particularly in low- and middle-income countries (LMICs) compared to high-income countries. Despite advancements in surgical techniques and immunosuppression for procedures like simultaneous pancreas-kidney, pancreas-after-kidney, and pancreas-transplant alone, LMICs face significant challenges, including limited infrastructure, financial constraints, and a shortage of skilled medical professionals. Donation after brain death remains constrained by sociocultural barriers. Region-specific analyses highlight progress in Latin America, Asia, Russia, and South Africa, showcasing the regional disparities in access and outcomes. Future prospects involve minimally invasive surgeries, telemedicine for enhanced post-operative care, international collaborations with organizations like the European Union of Medical Specialists, and robust funding networks to improve organ availability. In conclusion, the review underscores the importance of multifaceted strategies to address economic, sociocultural, and infrastructural barriers, aiming to improve accessibility, quality, and effectiveness of pancreas transplantation services in LMICs.

Microbiome is an endocrine organ that refers to both the complicated biological system of microbial species that colonize our bodies and their genomes and surroundings. Recent studies confirm the connection between the microbiome and eye diseases, which are involved in the pathogenesis of eye diseases, including age-related macular disorders, diabetic retinopathy, glaucoma, retinitis pigmentosa, dry eye, and uveitis. The aim of this review is to investigate the microbiome in relation to eye health. First, a brief introduction of the characteristics of the gut microorganisms terms of composition and work, the role of dysbiosis, the gut microbiome and the eye microbiome in the progression of eye illnesses are highlighted, then the relationship among the microbiome and the function of the immune system and eye diseases, the role of inflammation and aging and the immune system, It has been reviewed and finally, the control and treatment goals of microbiome and eye diseases, the role of food factors and supplements, biotherapy and antibiotics in relation to microbiome and eye health have been reviewed.

Nutrient metabolism is regulated by several factors. Social determinants of health with or without genetics are the primary regulator of metabolism, and an unhealthy lifestyle affects all modulators and mediators, leading to the adaptation and finally to the exhaustion of cellular functions. Hepatic steatosis is defined by presence of fat in more than 5% of hepatocytes. In hepatocytes, fat is stored as triglycerides in lipid droplet. Hepatic steatosis results from a combination of multiple intracellular processes. In a healthy individual nutrient metabolism is regulated at several steps. It ranges from the selection of nutrients in a grocery store to the last step of consumption of ATP as an energy or as a building block of a cell as structural component. Several hormones, peptides, and genes have been described that participate in nutrient metabolism. Several enzymes participate in each nutrient metabolism as described above from ingestion to generation of ATP. As of now several publications have revealed very intricate regulation of nutrient metabolism, where most of the regulatory factors are tied to each other bidirectionally, making it difficult to comprehend chronological sequence of events. Insulin hormone is the primary regulator of all nutrients' metabolism both in prandial and fasting states. Insulin exerts its effects directly and indirectly on enzymes involved in the three main cellular function processes; metabolic, inflammation and repair, and cell growth and regeneration. Final regulators that control the enzymatic functions through stimulation or suppression of a cell are nuclear receptors in especially farnesoid X receptor and peroxisome proliferator-activated receptor/RXR ligands, adiponectin, leptin, and adiponutrin. Insulin hormone has direct effect on these final modulators. Whereas blood glucose level, serum lipids, incretin hormones, bile acids in conjunction with microbiota are intermediary modulators which are controlled by lifestyle. The purpose of this review is to overview the key players in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) that help us understand the disease natural course, risk stratification, role of lifestyle and pharmacotherapy in each individual patient with MASLD to achieve personalized care and target the practice of precision medicine. PubMed and Google Scholar databases were used to identify publication related to metabolism of carbohydrate and fat in states of health and disease states; MASLD, cardiovascular disease and cancer. More than 1000 publications including original research and review papers were reviewed.

Background: There exists a link between irritable bowel syndrome (IBS) and depression. Similarly, chronic depression is known to increase the risk of cancer in general. In this population-based analysis, we investigated the prevalence and the odds of colorectal cancer (CRC) in young-depressed patients with IBS.

Aim: To investigate the relationship between IBS and CRC in young, depressed patients using a nationally representative United States inpatient sample.

Methods: The 2019 National Inpatient Sample was used to identify young (18-44 years) patients admitted with comorbid depression in the presence vs absence of IBS using relevant International Classification of Diseases, Tenth Revision, Clinical Modification codes. Primary endpoint was the prevalence and odds of CRC in age matched (1:1) young-depressed cohort hospitalized with IBS (IBS+) vs without IBS (IBS-). Multivariable regression analysis was performed adjusting for potential confounders.

Results: Age-matched (1:1) young-depressed IBS+ (83.9% females, median age 36 years) and IBS- (65.8% females, median age 36 years) cohorts consisted of 14370 patients in each group. IBS+ cohort had higher rates of hypertension, uncomplicated diabetes, hyperlipidemia, obesity, peripheral vascular disease, chronic obstructive pulmonary disease, hypothyroidism, prior stroke, prior venous thromboembolism, anxiety, bipolar disorder, and borderline personality disorder (P < 0.005) vs the IBS- cohort. However, prior myocardial infarction, acquired immunodeficiency syndrome, dementia, smoking, alcohol abuse, and drug abuse (P < 0.005) are high in IBS- cohort. The rate of CRC was comparable in both cohorts [IBS+ n = 25 (0.17%) vs IBS- n = 35 (0.24%)]. Compared to the IBS- cohort, the odds ratio (OR) of developing CRC was not significantly higher [OR 0.71, 95% confidence interval (CI) 0.23-2.25)] in IBS+ cohort. Also, adjusting for baseline sociodemographic and hospital characteristics and relevant comorbidities, the OR was found to be non-significant (OR 0.89, 95%CI 0.21-3.83).

Conclusion: This nationwide propensity-matched analysis revealed comparable prevalence and risk of CRC in young-depressed patients with vs without IBS. Future large-scale prospective studies are needed to evaluate the long-term effects of depression and its treatment on CRC risk and outcomes in IBS patients.