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The impact of low HER2 expression on clinicopathological features and clinical outcomes in patients with metastatic gastric cancer 低HER2表达对转移性胃癌患者临床病理特征及临床转归的影响
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102646
Murad Guliyev , Shamkhal Safarov , Murat Günaltılı , Mehmet Cem Fidan , Emir Çerme , Gülin Alkan Şen , Ahmet Emin Öztürk , Nuray Kepil , Özkan Alan , Nebi Serkan Demirci

Background

Metastatic gastric cancer (GC) is an extremely fatal malignant disease. Human epidermal growth factor receptor 2 (HER2) is an important therapeutic target in patients with HER2 overexpression or gene amplification. However, the prognostic value of HER2-low expression is still controversial. This study aims to investigate the effect of HER2 expression levels on clinicopathological characteristics and clinical outcomes in patients with metastatic GC.

Methods

The study included patients who had diagnosed de novo or recurrent metastatic GC from January 2011 to January 2023. We classified the patients into three categories based on their HER2 expression level: negative, low, and positive.

Results

The current study included 191 patients, with 99 (51.8 %) classified as HER2-negative, 42 (22.2 %) as HER2-low, and 50 (26.2 %) as HER2-positive. There were significant differences in the primary origin of gastroesophageal junction (25.3 %, 23.8 %, and 44 %), signet ring cell carcinoma (54.8 %, 44.4 %, and 16 %), mucinous cell carcinoma (40.9 %, 27.8 %, and 12 %), intestinal type histology (17.9 %, 50 %, and 48.9 %), high carcinoembryonic antigen level (34.5 %, 46.2 %, and 56.5 %), >2 metastatic sites (25.3 %, 45.2 %, and 42 %), liver metastasis (33.3 %, 42.9 %, and 66 %), peritoneal metastasis (44.4 %, 28.6 %, and 20 %), and distant lymph node metastasis (53.5 %, 83.3 %, and 58 %) among the HER2-negative, HER2-low, and HER2-positive groups, respectively. The HER2-low group had similar median overall survival (OS) compared to the HER2-negative group (14.8 vs. 14.5 months, p = 0.868), however, significantly shorter median OS than the HER2-positive group (14.8 vs. 18.6 months, p = 0.024).

Conclusions

Our findings demonstrated that patients with HER2-low metastatic GC had different clinical and pathological features. The poorer survival rates of the HER2-low group compared to the HER2-positive group might be due to the lack of effective targeted treatments for HER2-low disease. Further research is warranted to develop specific therapeutic strategies for this subgroup.
背景:转移性胃癌是一种极其致命的恶性疾病。人表皮生长因子受体2 (HER2)是HER2过表达或基因扩增患者的重要治疗靶点。然而,her2低表达的预后价值仍存在争议。本研究旨在探讨HER2表达水平对转移性胃癌患者临床病理特征及临床转归的影响。方法:研究纳入2011年1月至2023年1月诊断为新生或复发转移性胃癌的患者。我们根据HER2表达水平将患者分为三种类型:阴性、低水平和阳性。结果:目前的研究包括191例患者,其中99例(51.8%)为her2阴性,42例(22.2%)为her2低,50例(26.2%)为her2阳性。在胃食管交界处(25.3%、23.8%和44%)、印戒细胞癌(54.8%、44.4%和16%)、黏液细胞癌(40.9%、27.8%和12%)、肠型组织学(17.9%、50%和48.9%)、高癌胚抗原水平(34.5%、46.2%和56.5%)、bbb2转移部位(25.3%、45.2%和42%)、肝转移(33.3%、42.9%和66%)、腹膜转移(44.4%、28.6%和20%)、her2阴性组、her2低组和her2阳性组远处淋巴结转移率分别为53.5%、83.3%和58%。与her2阴性组相比,her2低组的中位总生存期(OS)相似(14.8个月vs 14.5个月,p = 0.868),但中位OS明显短于her2阳性组(14.8个月vs 18.6个月,p = 0.024)。结论:我们的研究结果表明,her2低转移性胃癌患者具有不同的临床和病理特征。与her2阳性组相比,her2低组的生存率较低可能是由于缺乏针对her2低疾病的有效靶向治疗。需要进一步的研究来制定针对这一亚群的具体治疗策略。
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引用次数: 0
Cap pressure characterization and band ligation for a tiny duodenal angioectasia with acute feeding vessel bleeding mimicking a Dieulafoy lesion 帽压特征和带结扎治疗伴有急性喂养血管出血的微小十二指肠血管扩张,模拟十二指肠溃疡病变。
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102643
Vincent Zimmer
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引用次数: 0
Specific association and independent predictive value of HBV RNA in the disease progression of hepatitis B with low-level viremia HBV RNA在乙型肝炎伴低水平病毒血症的疾病进展中的特异性关联和独立预测价值
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102648
Liang Xu , Bin Yin , Dandan Chen , Xia Xiong , Yongfeng Yang , Xuping Wu

Background and objective(s)

HBV RNA serve as a downstream transcriptional product of cccDNA within the liver. This study is the first to investigate the diagnostic significance of serum HBV RNA in HBV low-level viremia (LLV) patients, elucidating the interrelationships among serum HBV RNA, HBV DNA, and HBsAg.

Methods

A cohort of 514 HBV LLV patients was collected from The Second Hospital of Nanjing and divided into four groups: asymptomatic HBV carriers (ASC), chronic hepatitis B (CHB), liver cirrhosis (LC), and hepatocellular carcinoma (HCC). All were tested and analyzed for HBV RNA, HBV DNA, HBsAg, HBeAg, and liver function.

Results

serum pathological indicators showed statistically significant differences included RNA, DNA, HBsAg, HBeAg-positive, TBIL, DBIL, IBIL, TP, ALB, ALT, AST, ALP, GGT (P < 0.001), and HBeAg-negative (P = 0.019). Both HBV RNA and HBV DNA were positively correlated with HBsAg (r = 0.405, P < 0.001; r = 0.198, P < 0.001). The correlation between HBV RNA and HBsAg was stronger than that between HBV DNA and HBsAg, and this difference became more pronounced after stratifying patients based on disease progression stages. This was also the case in different HBeAg states. We further conducted multivariate logistic regression analysis, and the results showed that RNA had strong statistical significance in the ASC and CHB groups (P < 0.001).

Conclusions

Monitoring HBV RNA levels holds certain value in assessing antiviral therapy efficacy and predicting disease progression stages and clinical outcomes in HBV LLV patients.
背景和目的:HBV RNA在肝脏内作为cccDNA的下游转录产物。本研究首次探讨了血清HBV RNA在HBV低水平病毒血症(LLV)患者中的诊断意义,阐明了血清HBV RNA、HBV DNA和HBsAg之间的相互关系。方法:收集南京第二医院514例HBV LLV患者,将其分为无症状HBV携带者(ASC)、慢性乙型肝炎(CHB)、肝硬化(LC)和肝细胞癌(HCC) 4组。所有患者均进行了HBV RNA、HBV DNA、HBsAg、HBeAg和肝功能的检测和分析。结果:血清病理指标RNA、DNA、HBsAg、hbeag阳性、TBIL、DBIL、IBIL、TP、ALB、ALT、AST、ALP、GGT、hbeag阴性差异有统计学意义(P = 0.019)。HBV RNA、HBV DNA与HBsAg均呈正相关(r = 0.405,P < 0.001;r = 0.198,P < 0.001)。HBV RNA和HBsAg之间的相关性强于HBV DNA和HBsAg之间的相关性,并且在根据疾病进展阶段对患者进行分层后,这种差异变得更加明显。这在不同的HBeAg州也是如此。我们进一步进行多因素logistic回归分析,结果显示RNA在ASC组和CHB组具有较强的统计学意义(P < 0.001)。结论:监测HBV RNA水平对评估HBV LLV患者抗病毒治疗效果、预测疾病进展阶段及临床结局具有一定价值。
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引用次数: 0
Nonalcoholic fatty liver disease and hepatocellular carcinoma 非酒精性脂肪性肝病和肝细胞癌。
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102651
Kuan-Fu Liao , Shih-Wei Lai
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引用次数: 0
Interleukin-22 ameliorates alcohol-associated liver fibrosis via Nrf2-ARE signaling: mechanistic insights and clinical correlations 白细胞介素-22通过Nrf2-ARE信号改善酒精相关肝纤维化:机制见解和临床相关性
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102617
Xiaojuan Xu , Heping Zhao , Jie Zhang , Hongyou Yan , Xing Liu , Junyan Huo , Lijuan Huo

Background & Aims

Alcohol-associated liver fibrosis (ALF) is a key, potentially reversible stage leading to alcohol-associated liver cirrhosis, but effective treatments are lacking. This study explored whether interleukin (IL)-22, a hepatocyte survival factor, plays an anti-fibrotic role in ALF by modulating the Nrf2-ARE antioxidant pathway.

Methods

IL-22 and Nrf2-ARE inhibitor, ML385, were administered to rat hepatic stellate cells (HSCs) exposed to acetaldehyde. Cell proliferation, cell cycle distribution, and Nrf2-ARE activation were investigated. An ALF mouse model was used to evaluate the effects of IL-22 and ML385 on liver function, fibrosis, and Nrf2-ARE pathway activation. The expression of IL-22 and Nrf2-ARE pathway in ALF/cirrhosis patients was also examined, along with correlations to liver function and liver fibrosis degree.

Results

In vitro, IL-22 upregulated the Nrf2-ARE pathway, and inhibited acetaldehyde-induced HSC proliferation and activation. In ALF mice, IL-22 promoted Nrf2-ARE pathway activation, reduced oxidative stress levels and serum transaminases, and ameliorated fibrosis. The ALF patients showed increased expression of IL-22, IL-22R1, and Nrf2-ARE pathway, positively correlating with the Child-Pugh score and fibrosis severity, suggesting a compensatory response.

Conclusions

IL-22 alleviates ALF by activating the Nrf2 antioxidant stress pathway, and may offer a promising therapeutic option for ALF/cirrhosis patients.
背景与目的:酒精相关性肝纤维化(ALF)是导致酒精相关性肝硬化的关键、潜在可逆阶段,但缺乏有效的治疗方法。本研究探讨肝细胞生存因子白细胞介素(IL)-22是否通过调节Nrf2-ARE抗氧化途径在ALF中发挥抗纤维化作用。方法:将IL-22和Nrf2-ARE抑制剂ML385给予暴露于乙醛的大鼠肝星状细胞(hsc)。研究细胞增殖、细胞周期分布和Nrf2-ARE活化情况。采用ALF小鼠模型评价IL-22和ML385对肝功能、纤维化和Nrf2-ARE通路激活的影响。同时检测IL-22和Nrf2-ARE通路在ALF/肝硬化患者中的表达,以及与肝功能和肝纤维化程度的相关性。结果:IL-22在体外可上调Nrf2-ARE通路,抑制乙醛诱导的HSC增殖和活化。在ALF小鼠中,IL-22促进Nrf2-ARE通路激活,降低氧化应激水平和血清转氨酶,改善纤维化。ALF患者IL-22、IL-22R1、Nrf2-ARE通路表达升高,与Child-Pugh评分和纤维化严重程度呈正相关,提示存在代偿反应。结论:IL-22通过激活Nrf2抗氧化应激途径缓解ALF,可能为ALF/肝硬化患者提供一个有希望的治疗选择。
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引用次数: 0
Involvement of oxidative stress, lipid dysmetabolism and gut microbiol dysbiosis in oxaliplatin-induced fatty liver disease: evidence from a tree shrew model 氧化应激、脂质代谢紊乱和肠道微生物失调在奥沙利铂诱导的脂肪肝疾病中的参与:来自树鼩模型的证据
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102645
Yulei Lu , Fei Yi , Wende Chen , Xinglong Tan , Kezhi Li , Chun Yang , Youzhi Lin

Background

Oxaliplatin is cornerstone treatment for colorectal cancer, yet a significant proportion of patients develop drug-induced fatty liver disease (DILI). How it induces such liver injury is poorly understood and whether the gut microbiome is involved remains unknown.

Methods

A male tree shrew model of oxaliplatin-induced DILI was established by six intraperitoneal injections (7 mg/kg every two weeks). During the early and late phases of liver injury, liver tissue was analyzed in terms of histopathology, oxidative stress and transcriptional profiling, while feces were subjected to microbial profiling based on 16S rRNA sequencing.

Results

The model recapitulated key features of DILI, including severe hepatocyte steatosis and ballooning in the early phase after the final treatment, mild hepatic steatosis with sinusoidal dilatation in the late phase, and persistent hepatic oxidative stress during both phases. Transcriptional analysis of liver tissue identified 1503 differentially expressed genes (DEGs) between oxaliplatin-treated and control animals, of which 601 DEGs differed between treated animals in the early or late phases after the final treatment of DILI. Pathway enrichment revealed significant dysregulation in oxidative stress (e.g. NDUFA12, OSR1, MPO) and lipid metabolism (e.g., LDAH, ACACB, CH25H, LIPE) genes. Gut microbiota profiling showed an increase in the relative abundance of potentially harmful bacteria (e.g., Parabacteroides, Rikenella, Alistipes and Faecalitalea) and a concurrent decrease in the abundance of anti-oxidative bacteria (e.g., Lactococcus and Flavobacterium). Notably, abundance of several microbial genera in the gut correlated with liver expression of genes involved in oxidative stress and lipid metabolism as well as with levels of oxidative stress markers, and/or fat deposition in the liver.

Conclusion

Our results suggest that our tree shrew model can faithfully replicate key characteristics of oxaliplatin-induced fatty liver disease, and that such disease involves oxidative stress and lipid dysmetabolism in the liver as well as dysbiosis of microbiota in the gut.
背景:奥沙利铂是结直肠癌的基础治疗药物,但仍有相当比例的患者发生药物性脂肪性肝病(DILI)。它是如何引起这种肝损伤的尚不清楚,肠道微生物群是否参与其中仍不清楚。方法:采用6次腹腔注射(7 mg/kg / 2周)建立奥沙利铂致DILI雄性树鼩模型。在肝损伤的早期和晚期,对肝组织进行组织病理学、氧化应激和转录谱分析,并对粪便进行基于16S rRNA测序的微生物谱分析。结果:该模型重现了DILI的主要特征,包括最终治疗后早期出现严重的肝细胞脂肪变性和肝球囊化,晚期出现轻度肝脂肪变性伴窦状动脉扩张,两期均出现持续的肝脏氧化应激。肝脏组织转录分析鉴定出奥沙利铂治疗动物和对照动物之间有1503个差异表达基因(DEGs),其中601个差异表达基因在DILI最终治疗后的早期或晚期存在差异。途径富集显示氧化应激(如NDUFA12、OSR1、MPO)和脂质代谢(如LDAH、ACACB、CH25H、LIPE)基因明显失调。肠道菌群分析显示,潜在有害细菌(如拟副杆菌、里氏菌、阿里士菌和粪菌)的相对丰度增加,同时抗氧化细菌(如乳球菌和黄杆菌)的丰度减少。值得注意的是,肠道中几种微生物属的丰度与肝脏中参与氧化应激和脂质代谢的基因表达以及氧化应激标志物的水平和/或肝脏中的脂肪沉积有关。结论:我们的研究结果表明,我们的树鼩模型可以忠实地复制奥沙利铂诱导的脂肪性肝病的关键特征,并且这种疾病涉及肝脏的氧化应激和脂质代谢紊乱以及肠道微生物群的失调。
{"title":"Involvement of oxidative stress, lipid dysmetabolism and gut microbiol dysbiosis in oxaliplatin-induced fatty liver disease: evidence from a tree shrew model","authors":"Yulei Lu ,&nbsp;Fei Yi ,&nbsp;Wende Chen ,&nbsp;Xinglong Tan ,&nbsp;Kezhi Li ,&nbsp;Chun Yang ,&nbsp;Youzhi Lin","doi":"10.1016/j.clinre.2025.102645","DOIUrl":"10.1016/j.clinre.2025.102645","url":null,"abstract":"<div><h3>Background</h3><div>Oxaliplatin is cornerstone treatment for colorectal cancer, yet a significant proportion of patients develop drug-induced fatty liver disease (DILI). How it induces such liver injury is poorly understood and whether the gut microbiome is involved remains unknown.</div></div><div><h3>Methods</h3><div>A male tree shrew model of oxaliplatin-induced DILI was established by six intraperitoneal injections (7 mg/kg every two weeks). During the early and late phases of liver injury, liver tissue was analyzed in terms of histopathology, oxidative stress and transcriptional profiling, while feces were subjected to microbial profiling based on 16S rRNA sequencing.</div></div><div><h3>Results</h3><div>The model recapitulated key features of DILI, including severe hepatocyte steatosis and ballooning in the early phase after the final treatment, mild hepatic steatosis with sinusoidal dilatation in the late phase, and persistent hepatic oxidative stress during both phases. Transcriptional analysis of liver tissue identified 1503 differentially expressed genes (DEGs) between oxaliplatin-treated and control animals, of which 601 DEGs differed between treated animals in the early or late phases after the final treatment of DILI. Pathway enrichment revealed significant dysregulation in oxidative stress (e.g. NDUFA12, OSR1, MPO) and lipid metabolism (e.g., LDAH, ACACB, CH25H, LIPE) genes. Gut microbiota profiling showed an increase in the relative abundance of potentially harmful bacteria (e.g., <em>Parabacteroides, Rikenella, Alistipes</em> and <em>Faecalitalea)</em> and a concurrent decrease in the abundance of anti-oxidative bacteria (e.g., <em>Lactococcus</em> and <em>Flavobacterium)</em>. Notably, abundance of several microbial genera in the gut correlated with liver expression of genes involved in oxidative stress and lipid metabolism as well as with levels of oxidative stress markers, and/or fat deposition in the liver.</div></div><div><h3>Conclusion</h3><div>Our results suggest that our tree shrew model can faithfully replicate key characteristics of oxaliplatin-induced fatty liver disease, and that such disease involves oxidative stress and lipid dysmetabolism in the liver as well as dysbiosis of microbiota in the gut.</div></div>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":"49 7","pages":"Article 102645"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A call for increased advocacy and universal resources to support effective nutritional interventions in the comprehensive management of patients with cirrhosis 呼吁加强宣传和普遍资源,以支持有效的营养干预在肝硬化患者的综合管理。
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102650
Cristal Brown
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引用次数: 0
Steatosis non-invasive tests accurately predict metabolic dysfunction-associated steatotic liver disease, while fibrosis non-invasive tests fall short: Validation in U.S. adult population 脂肪变性非侵入性试验准确预测代谢功能障碍相关的脂肪变性肝病,而纤维化非侵入性试验不足:在美国成年人中的验证
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-07-01 DOI: 10.1016/j.clinre.2025.102649
Ayesha Sualeheen , Sze-Yen Tan , Robin M. Daly , Ekavi Georgousopoulou , Gavin Abbott , Stuart K. Roberts , Jacob George , Elena S. George

Introduction

Metabolic dysfunction associated steatotic liver disease (MASLD) has replaced NAFLD as the diagnostic standard. This study aimed to validate non-invasive tests (NITs) for hepatic steatosis and fibrosis, originally used for NAFLD, in predicting MASLD and advanced fibrosis, respectively, compared to transient elastography (TE).

Methods

This cross-sectional study used the NHANES database (2017–2020). Adults aged ≥18 years with valid TE status and without other steatotic liver diseases were included. Hepatic steatosis NITs were compared against controlled attenuation parameter (CAP)- diagnosed MASLD and fibrosis NITS were compared against liver stiffness measurement (LSM)-diagnosed advanced fibrosis. The diagnostic accuracy was assessed using weighted ROC analysis.

Results

Among 5305 participants (49.1 % males), MASLD prevalence was 42.8 % (CAP-diagnosed) and advanced fibrosis was identified in 10.4 % (LSM-diagnosed) in those with MASLD. Steatosis NITs showed good diagnostic accuracy for predicting MASLD (AUROC 0.836 to 0.862), with fatty liver index having the maximum Youden index (0.55). Fibrosis NITs indicated poor to fair diagnostic accuracy for predicting advanced fibrosis (AUROC 0.564 to 0.691) but indicated high negative predicted value (89 %-94 %). In age categorized subgroup analysis, fibrosis NITs performed poorly in those aged ≤ 35 years and had low specificity to exclude fibrosis in those aged ≥65 years but performed comparably to the overall MASLD cohort in those aged 36–64 years.

Conclusion

In this population-based cohort of U.S. adults, all steatosis NITs demonstrated good diagnostic accuracy for MASLD. However, the fibrosis NITs showed limited diagnostic ability and were influenced by age, suggesting they should be used cautiously in general population.
代谢功能障碍相关脂肪变性肝病(MASLD)已取代NAFLD成为诊断标准。与瞬时弹性成像(TE)相比,本研究旨在验证肝脂肪变性和肝纤维化的无创试验(NITs)在预测MASLD和晚期纤维化方面的作用,NITs最初用于NAFLD。方法:本横断面研究使用NHANES数据库(2017-2020)。年龄≥18岁、有效TE状态且无其他脂肪变性肝脏疾病的成年人纳入研究。将肝脂肪变性NITs与控制衰减参数(CAP)诊断的MASLD进行比较,将纤维化NITs与肝刚度测量(LSM)诊断的晚期纤维化进行比较。采用加权ROC分析评估诊断准确性。结果:在5305名参与者中(49.1%男性),MASLD患病率为42.8% (cap诊断),在MASLD患者中,10.4% (lsm诊断)确诊为晚期纤维化。脂肪变性NITs对预测MASLD具有较好的诊断准确性(AUROC为0.836 ~ 0.862),其中脂肪肝指数约登指数最高(0.55)。纤维化NITs显示预测晚期纤维化的诊断准确性较差(AUROC为0.564 ~ 0.691),但显示较高的阴性预测值(89% ~ 94%)。在年龄分类亚组分析中,纤维化NITs在年龄≤35岁的人群中表现不佳,在年龄≥65岁的人群中排除纤维化的特异性较低,但在36-64岁的人群中与整体MASLD队列的表现相当。结论:在这个以人群为基础的美国成年人队列中,所有脂肪变性nit对MASLD的诊断都具有良好的准确性。然而,纤维化NITs的诊断能力有限,且受年龄的影响,提示在普通人群中应谨慎使用。
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引用次数: 0
Biopsy of a hepatic small vessel neoplasm: beware of bleeding 肝小血管肿瘤活检:小心出血。
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-06-22 DOI: 10.1016/j.clinre.2025.102644
Claire Michoud , Valérie Hervieu , Hélène Gimonet , Jérôme Dumortier
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引用次数: 0
Trends, disparities, and outcomes of drug-induced pancreatitis in the United States: A nationwide analysis (2016–2020) 美国药物性胰腺炎的趋势、差异和结果:一项全国性分析(2016-2020)。
IF 2.6 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY Pub Date : 2025-06-20 DOI: 10.1016/j.clinre.2025.102641
Guy Loic Nguefang Tchoukeu , Sarpong Boateng , Joel Gabin Konlack Mekontso , Yazan A Al-Ajlouni , Basile Njei

Background

Drug-induced pancreatitis (DIP) is an underreported etiology of acute pancreatitis. DIP risk and prevalence has increased over the years with polypharmacy. Data on affected patients in the U.S. remain limited. We aim to assess disparities and outcomes in DIP hospitalizations.

Methods

Retrospective study including adults diagnosed with DIP using the National Inpatient Sample (NIS) database (2016–2020). The primary outcomes were inpatient mortality, and complications. Secondary outcomes included resource utilization metrics. Descriptive statistics, linear regression, and logistic regression were performed using SAS 9.4.

Results

5666 patients (mean age: 56.5 years; females 53.6 %) were included. Common comorbidities were hypertension (61.3 %), hyperlipidemia (42.3 %), and diabetes (22.9 %). The mortality rate was 1.5 %, with acute kidney injury (20.6 %), Sepsis (5.0 %), ileus (3.5 %) the common complications. The Mean LOS was 5.5 days, and the mean hospital charges were $60,811.20. Compared to White, Hispanics had significant odds of DIP admission (aOR: 1.11, 95 % CI: 1.01–1.21, p = 0.03) and increased risk of cardiac arrest (aOR 4.34, 95 % CI 1.17–15.35, p = 0.02). Black patients had significantly higher odds of severe DIP (aOR 1.26, 95 % CI 1.02–1.56, p = 0.03) and acute kidney injury (aOR 1.29, 95 % CI 1.04–1.61, p = 0.02), while Asian were more likely to develop sepsis (aOR 2.10, 95 % CI 1.07–3.83, p = 0.02), had higher hospital charges (+$42,008, p = 0.039) and longer LOS (+2.5 days, p < 0.01)..

Conclusion

There are significant racial disparities among patients and a substantial economic burden on healthcare systems. Multifaceted strategies and research into genetic and socioeconomic predispositions are needed to address DIP.
背景:药物性胰腺炎(DIP)是一种被低估的急性胰腺炎病因。多年来,多药联用增加了DIP的风险和患病率。美国受影响患者的数据仍然有限。我们的目的是评估DIP住院治疗的差异和结果。方法:采用2016-2020年国家住院患者样本(NIS)数据库对诊断为DIP的成年人进行回顾性研究。主要结局是住院死亡率和并发症。次要结果包括资源利用指标。采用SAS 9.4进行描述性统计、线性回归和逻辑回归。结果:5666例患者(平均年龄56.5岁;女性53.6%)。常见的合并症是高血压(61.3%)、高脂血症(42.3%)和糖尿病(22.9%)。死亡率为1.5%,常见并发症为急性肾损伤(20.6%)、脓毒症(5.0%)、肠梗阻(3.5%)。平均住院时间为5.5天,平均住院费用为60 811.20美元。与白人相比,西班牙裔患者有显著的DIP入院几率(aOR: 1.11, 95% CI: 1.01-1.21, p = 0.03)和增加的心脏骤停风险(aOR 4.34, 95% CI 1.17-15.35, p=0.02)。黑人患者发生严重DIP (aOR 1.26, 95% CI 1.02-1.56, p=0.03)和急性肾损伤(aOR 1.29, 95% CI 1.04-1.61, p=0.02)的几率明显更高,而亚洲人更容易发生败血症(aOR 2.10, 95% CI 1.07-3.83, p=0.02),住院费用更高(+ 42008美元,p=0.039),住院时间更长(+2.5天,p)。结论:患者之间存在显著的种族差异,给医疗保健系统带来了巨大的经济负担。要解决DIP问题,需要采取多方面的战略并对遗传和社会经济倾向进行研究。
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引用次数: 0
期刊
Clinics and research in hepatology and gastroenterology
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