世界胃肠病理生理学杂志(电子版)(英文版)最新文献

Background: Over 150000 new diagnoses of colorectal cancer (CRC) are diagnosed yearly, and 1 in 5 patients have distant metastases on diagnosis. Previous estimates approximate that brain metastases (BM) occur in 0.6% to 3.2% of patients with CRC.

Aim: To describe the updated literature about the incidence and risk factors of BM in CRC as well as their treatment with surgery, chemotherapy, and radiation.

Methods: We systematically searched the literature published between January 1, 2010 and April 1, 2025 in PubMed, Cochrane, Scopus, and EMBASE. All studies about BM from CRC were included. Studies only containing information about the treatment of primary CRC or primary brain tumors were not included. Articles were categorized and described as incidence, surgery, chemotherapy, or radiation to provide an overview of the state of research on BM from CRC.

Results: Our primary search resulted in 1648 articles that were eventually screened to 147. These articles were analyzed to provide the state of current literature on incidence and risk factors of BM from CRC as well as how these metastases are treated with chemotherapy, radiation, and surgery.

Conclusion: Prognosis is influenced by tumor burden, performance status, and emerging molecular markers. Stereotactic radiotherapy and surgical resection provide favorable outcomes for select patients, whereas chemotherapy and immunotherapy remain areas of limited evidence. Continued research is needed to identify high-risk patients and optimize multidisciplinary treatment approaches.

Once considered a concern solely for the gut, gluten is now recognized as an important factor in the pathogenesis of metabolic dysfunction-associated steatotic liver disease. Studies estimate that 18%-40% of individuals with gluten-related diseases have elevated liver enzyme levels, with 9% of patients with unexplained hypertransaminasemia ultimately diagnosed with gluten sensitivity. Hepatic manifestations of gluten sensitivity range from mild transaminase elevations to autoimmune liver diseases, metabolic dysfunction-associated steatotic liver disease, and even cirrhosis. Up to 50% of untreated cases of gluten-induced liver dysfunction show significant hepatic injury, which can lead to liver failure in severe cases. The pathophysiology is multifaceted and involves increased intestinal permeability, immune dysregulation, and shared genetic risk factors. A gluten-free diet leads to normalized liver enzymes in 75%-90% of cases within 1 year. Long-term gluten-free diet adherence has been paradoxically linked to higher body mass index, insulin resistance and increased hepatic steatosis risk, which raise concerns about its metabolic impact. Our review dissects the gluten-liver axis, emphasizing a need for early recognition, targeted screening, and personalized dietary interventions. Ultimately, given the increasing global burden of metabolic and autoimmune liver diseases, understanding gluten's role is essential for optimizing liver health and preventing progressive hepatic injury.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease with a continually rising global prevalence and significant mortality rates. Emerging evidence suggests a strong association between MASLD and mental health disorders such as depression and anxiety. In addition to the shared risk factors such as obesity, type 2 diabetes and insulin resistance which contribute to this relationship through mechanisms involving systemic inflammation and oxidative stress; other pathophysiological mechanisms such as dysregulation of hypothalamic-pituitary-adrenal axis, neurotransmitter imbalances and gut dysbiosis have also been proposed to play a significant role. The current paper aims to review the pathophysiological mechanisms underlying the association between MASLD and mood disorders such as depression and anxiety. We note a bidirectional relationship between these two disorders, and the dual burden of both these disease processes can be alleviated by early detection and encouraging a more proactive and holistic approach through diet and lifestyle changes. This review summarizes the existing literature on association between MASLD and depression.

Background: Colorectal cancer remains as one of the most common cancers that are diagnosed and remains as a significant contributor to morbidity and mortality. Despite advances in techniques, improving access to diagnostic modalities and increasing awareness, it often presents at a later stage and can recur despite treatment. Recurrence can be variable and can occur years after treatment. Liver is the most common location for metastasis to occur followed by lungs. However, atypical sites of metastasis can occur although unusual and colorectal cancer can spread to the spleen, hilum of the liver, adrenals, bone, skeletal muscles, skin, prostate, brain, parotid gland, thyroid gland and even the cardiac muscle. It is crucial to recognize the metachronous nature of the metastasis and to only present at a single site as within this lies the rarity of the case. The mass itself mimicked a cholangiocarcinoma or a Klatskin's tumor initially and only through pathology was the diagnosis established. We present an unusual case of recurrent colorectal cancer that occurred several years post treatment and presented as an isolated metastasis to the hilum of the liver leading to biliary obstruction without any other identifiable lesions including in the colon itself.

Case summary: A 68-year-old male with history of colon cancer presented with obstructive jaundice to the hospital. After evaluation with imaging studies was diagnosed with mass at the hilum of the liver that was leading to obstruction. With percutaneous biopsies obtained by interventional radiology, the diagnosis of metastatic adenocarcinoma originating from the colon was established. He was deemed not to be a surgical candidate and is currently pursuing chemotherapy.

Conclusion: A metastatic adenocarcinoma of the colon that presents as a hilar mass and mimics cholangiocarcinoma is very rare. The metachronous nature along with the isolated metastasis involving the hilum of the liver makes this case unique. Diagnosis can be challenging and needs a tissue specimen along with immunostaining to achieve an accurate diagnosis and provide appropriate treatment. Biliary decompression is performed either endoscopically or percutaneously and is part of the multidisciplinary approach involving medical and surgical oncology teams.

The gut microbiome, a complex ecosystem of trillions of microorganisms, plays a crucial role in immune system regulation and overall health. This review explores the intricate cross-talk between the gut microbiota and the host immune system, emphasizing how microbial communities shape immune cell differentiation, modulate inflammatory responses, and contribute to immune homeostasis. Key interactions between innate and adaptive immune cells - including macrophages, dendritic cells, natural killer cells, innate Lymphoid cells, T cells, and B cells - and gut microbiota-derived metabolites such as short-chain fatty acids are discussed. The role of commensal bacteria in neonatal immune system development, mucosal barrier integrity, and systemic immunity is highlighted, along with implications for autoimmune diseases, inflammatory conditions, and cancer immunotherapy. Recent advances in metagenomics, metabolomics, and single-cell sequencing have provided deeper insights into the microbiota-immune axis, opening new avenues for microbiome-based therapeutic strategies. Understanding these interactions paves the way for novel interventions targeting immune-mediated diseases and optimizing health through microbiome modulation.

Background: Esophageal cancer is a significant global health concern, characterized by high mortality rates and diverse histological types, primarily adenocarcinoma and squamous cell carcinoma.

Aim: To analyze trends in esophageal cancer using Surveillance, Epidemiology, and End Results (SEER) data, focusing on patient characteristics, stage at diagnosis, treatment modalities, and survival outcomes, to provide insights that may guide clinical practice and public health initiatives.

Methods: Age-adjusted incidence and mortality rates for esophageal cancer, 2004-2021, were obtained from SEER rate sessions using SEER*Stat version 8.4.4. Average percent changes (APC) over time in age-adjusted incidence and mortality rates relative to gender, race/ethnicity, and stage at diagnosis were assessed using Joinpoint's log-linear regression. Finally, Poisson regression was used to ascertain incidence and mortality rate ratios to ascertain associations between age, gender, race/ethnicity, and staging with incidence and mortality rates. All analyses were further stratified by gender to assess interactions between gender and the other demographic and clinical characteristics.

Results: Overall, the data reveals significant trends in both the incidence and mortality rates of esophageal cancer, with notable variations across gender, race, and stage at diagnosis. Age-adjusted incidence and mortality rates were higher in males compared to females (incidence: 4.1 per 100000 vs 0.9 per 100000, mortality: 3.4 per 100000 vs 0.7 per 100000), P < 0.001. Furthermore, the APC among males decreased more significantly over time [APC (95%CI): -1.14 (-1.52 to -0.78); P < 0.001]. Both non-Hispanic (NH) Blacks and NH Whites showed significant decreases in cancer incidence, with NH Blacks observing a 3.27% decline and NH Whites a 0.51% decline. Patients with distant staging had a 5% APC increase in mortality rates over time (P = 0.003). Additionally, mortality rates increased with age, and all minority groups showed declines in incidence and mortality compared to NH Whites. Cancer diagnosed at a distant stage had a mortality rate 4.16 times higher than in situ cases.

Conclusion: The analysis reveals clear disparities in both the incidence and mortality of esophageal cancer, with males, particularly NH Whites, experiencing significantly higher rates than females. Despite a general decline in incidence rates over time, the upward trend in mortality for certain subgroups warrants further investigation into potential contributing factors such as healthcare access, treatment efficacy, and underlying socio-economic disparities.

Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped, microaerophilic bacterium that infects over 43% of the global population, with higher prevalence in regions of low socioeconomic status and poor sanitation. It is transmitted mainly through oral-oral and fecal-oral routes and has evolved multiple mechanisms that allow colonization of the acidic gastric environment, including urease production, chemotaxis, and a variety of adhesins. The bacterium expresses several virulence factors that enhance its pathogenicity, such as cytotoxin-associated antigen A, vacuolating cytotoxin A, and the small regulatory RNA NikS, found to be essential for the fine-tuning of the bacterial virulence. Although many infected individuals remain asymptomatic, H. pylori infection is associated with multiple clinical outcomes, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma, all correlated to the host immune response and chronic inflammation. Diagnosis relies on both invasive and non-invasive methods, and growing antibiotic resistance poses a major challenge to treatment. New therapeutic strategies, such as tailored therapy, potassium-competitive acid blockers, and probiotics are under investigation. Vaccine development remains a key area of research, with several candidates currently in preclinical and clinical evaluation.

Background: Gastric motility is an essential gastrointestinal function. It can be influenced by age, gender, body composition, and metabolic status. However, published data on these associations remains limited.

Aim: To assess the relationship between gastric motility and adiposity, and metabolic indicators in a cohort of Sri Lankan office workers.

Methods: A cross-sectional study was conducted among 130 office workers (58.5% females) aged 20-50 years (mean 36.81, SD 8.85 years) of the University of Kelaniya, Sri Lanka. Gastric motility was assessed by real-time ultrasonography, using a previously validated method. Fasting antral area (FAA), postprandial antral areas at 1 minutes and 15 minutes (AA1, AA15), and antral contraction frequency (FAC) were measured, and gastric emptying rate (GER) and antral motility index were calculated. Anthropometric parameters were obtained using sensitive scales. Glycated hemoglobin, lipid profile, and liver enzyme levels were measured at an accredited laboratory.

Results: The mean body mass index (BMI) was 24.36 (SD 4.09) kg/m², and 39.2% were overweight or obese. Increased abdominal adiposity was detected in 29.2% and 40.8% had high waist-to-hip ratios. Prediabetes/diabetes were observed in 20.0%, hypercholesterolemia in 47.7%, hypertriglyceridemia in 14.7%, high low-density lipoproteins in 39.2%, and elevated aspartate transaminase and alanine transaminase in 5.4% and 21.5% respectively. FAA had a weak negative correlation with high-density lipoprotein level (r = -0.227, P = 0.009), and a positive correlation with waist circumference (r = 0.235, P = 0.007), and waist-to-hip ratio (r = 0.244, P = 0.005). GER and AA1 correlated weakly with triglyceride (GER: r = 0.174, P = 0.048; AA1: r = 0.194, P = 0.027) and VLDL levels (GER: r = 0.183, P = 0.038; AA1: r = 0.195, P = 0.026). In females, AA1 positively correlated with triglycerides (r = 0.333, P = 0.003), and VLDL levels (r = 0.337, P = 0.003), and AA15 with BMI (r = 0.284, P = 0.013) and hip circumference (r = 0.229, P = 0.047). FAC negatively correlated with BMI (r = -0.234, P = 0.042) and hip circumference (r = -0.247, P = 0.032).

Conclusion: Gastric motility parameters showed weak associations with metabolic indicators, particularly lipid profiles, and to a lesser extent, with adiposity indicators. The greater number of correlations observed in females suggests the possibility of sex-specific differences in these associations. These findings highlight potential relationships that require confirmation through longitudinal studies.

Pancreatitis is one of the largest contributors to increased healthcare costs. It is widely accepted that exposure of acinar cells to injurious agents leads to necrosis and pancreatic enzyme activation. Inappropriate activation of trypsinogen in the pancreas is related to infiltration of leukocytes recruited by chemokines, which directly leads to acinar cell damage, and indirectly to a strong systemic inflammatory response. Otherwise, chemokines exert pleiotropic effects by recruiting immune cells during inflammation, immune surveillance, and directing cells to target organs in homeostasis. Here, we give a brief introduction to the basic molecular and cellular sources of chemokines, and focus on their pleiotropic functions in acute pancreatitis, chronic pancreatitis, autoimmune pancreatitis, and pancreatic cancer. Understanding the interaction between these processes is helpful for devising therapeutic strategies for pancreatitis.

Background: Functional abdominal pain disorders (FAPDs) are common gut-brain interaction disorders with unclear pathophysiology. While impaired gastrointestinal motility is thought to play a key role, small intestinal dysmotility remains largely unexplored. Orocecal transit time (OCTT), an indirect indicator of small intestinal transit, offers an insight into its potential contribution to FAPD's pathophysiology.

Aim: To assess OCTT in children with FAPDs compared with healthy children using the lactulose breath hydrogen test.

Methods: Thirty-four children (44.1% males, age 5-12 years, mean 7.2 ± 2.4 years) with FAPDs attending North Colombo Teaching Hospital, Ragama, Sri Lanka, were included in the analysis. FAPDs were diagnosed using the Rome IV criteria. None had clinical or laboratory evidence of organic diseases. They were compared with 19 healthy controls (47.1% males, age 5-12 years, mean 7.8 ± 2.7 years) from the same geographical area. OCTT was calculated after an 8-hour fast using a previously validated technique. Breath hydrogen levels were measured at baseline and 15-minute intervals for 180 minutes post-lactulose ingestion (10 g in 10% solution). At each time point, 3 breath samples were collected and analyzed. OCTT was quantified as the time taken to achieve a sustained breath hydrogen increase > 10 parts per million above baseline. Symptoms were recorded using the Rome IV questionnaire, and symptom severity was graded on a 0-4 Likert scale.

Results: Patients with FAPDs had increased OCTT (median, 90 minutes; interquartile range, 75-120 minutes) compared to controls (median, 75 minutes; interquartile range, 60-75 minutes) (P = 0.0045, Mann-Whitney U-test). Children with functional dyspepsia had the longest mean OCTT (110.8 ± 26.7 minutes). There was no significant correlation between abdominal pain severity and OCTT (r = 0.18, P = 0.35, Spearman correlation coefficient). OCTT did not differ between those exposed to stressful events and those not exposed to such events (P > 0.05).

Conclusion: Children with FAPDs have longer OCTT than healthy controls. However, the lack of a significant correlation between OCTT and symptom severity suggests that delayed small intestinal transit alone is not a substantial contributor to FAPD pathophysiology.