Alimentary Pharmacology & Therapeutics最新文献

英文中文

Long-Term Use of Fenofibrate as Second-Line Therapy in Primary Biliary Cholangitis: A Retrospective Study 长期使用非诺贝特作为二线治疗原发性胆道胆管炎：一项回顾性研究

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-18 DOI: 10.1111/apt.70574

Mariko Maxwell, Yanhong Deng, Bonnie Chen, Marina G. Silveira, James L. Boyer, David N. Assis

Nearly 40% of patients with primary biliary cholangitis (PBC) have an incomplete response to first-line ursodeoxycholic acid (UDCA) therapy. Fenofibrate, a peroxisome proliferator-activated receptor alpha (PPAR-α) agonist, is an effective second-line treatment for PBC. Compared to the recently FDA-approved PPAR agonists, fenofibrate may provide a more cost-effective and accessible alternative. However, longitudinal data on fenofibrate use in PBC are lacking. Here, we review our experience using fenofibrate in PBC and its long-term effects on cholestatic biomarkers, prognostic scores, and fibrosis indices.

近40%的原发性胆管炎（PBC）患者对一线熊去氧胆酸（UDCA）治疗有不完全反应。非诺贝特是一种过氧化物酶体增殖激活受体α (PPAR-α)激动剂，是一种有效的PBC二线治疗药物。与最近fda批准的PPAR激动剂相比，非诺贝特可能是一种更具成本效益和可及性的替代药物。然而，非诺贝特在PBC中使用的纵向数据缺乏。在这里，我们回顾了我们在PBC中使用非诺贝特的经验及其对胆汁淤积生物标志物、预后评分和纤维化指标的长期影响。

引用次数: 0

Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis 信：氨基酸失衡是肝硬化患者死亡的一个独立因素

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-18 DOI: 10.1111/apt.70561

Zhanbo Qu

I read with great interest the study by Utakata et al. [1], which identified amino acid imbalance, specifically decreased branched-chain amino acids (BCAAs) and increased tyrosine levels, as independent prognostic factors for mortality in patients with liver cirrhosis. While the study provides valuable insights into metabolic derangements in liver disease, I have two major concerns regarding the validity of the independence of these factors and the interpretation of the results.

First, the study raises a critical concern regarding unmeasured confounding by sarcopenia. BCAAs are primarily metabolised in skeletal muscle, and low serum BCAA levels are inextricably linked to sarcopenia [2]. Sarcopenia itself is a well-established, potent predictor of mortality in cirrhosis. Although the authors adjusted for Body Mass Index (BMI) in their multivariable analysis, BMI is notoriously unreliable for assessing muscle mass in cirrhotic patients due to fluid retention. Notably, 35.1% of the study cohort had ascites, which artificially elevates body weight and masks muscle depletion [3]. Without adjusting for skeletal muscle mass (e.g., using the Skeletal Muscle Index via CT), it remains unclear whether low BCAA levels are truly an ‘independent’ driver of mortality or merely a biochemical surrogate for sarcopenia.

Second, the reporting of hazard ratios (HR) in multivariable analysis obscures the clinical relevance of the findings. In table 3, the HRs for BCAA and Tyrosine are reported as 1.00 (95% CI 1.00–1.00) and 1.01 (1.00–1.01), respectively. While statistically significant (p < 0.05), presenting HRs per 1 μmol/L change yields values that are mathematically indistinguishable from the null effect. This ‘unit bias’ makes it impossible for clinicians to gauge the magnitude of the risk. To demonstrate that the statistical significance translates into a meaningful clinical effect size rather than an artefact of sample size, I urge the authors to report standardised HRs (e.g., per 1 standard deviation change or per 100 μmol/L decrement).

I believe that clarifying the relationship between BCAA, muscle mass, and mortality, along with providing standardised effect sizes, is essential to validate the clinical utility of amino acid profiling in cirrhosis.

我饶有兴趣地阅读了Utakata等人的研究，发现氨基酸失衡，特别是支链氨基酸（BCAAs）减少和酪氨酸水平升高是肝硬化患者死亡的独立预后因素。虽然这项研究为肝脏疾病中的代谢紊乱提供了有价值的见解，但我对这些因素的独立性的有效性和对结果的解释有两个主要的担忧。首先，该研究提出了一个关于肌肉减少症的未测量混淆的关键问题。支链氨基酸主要在骨骼肌中代谢，低血清支链氨基酸水平与肌肉减少症有着不可分割的联系。肌少症本身是一个公认的肝硬化死亡率的有效预测指标。尽管作者在他们的多变量分析中调整了身体质量指数（BMI），但BMI在评估肝硬化患者由于液体潴留的肌肉质量方面是出了名的不可靠。值得注意的是，35.1%的研究队列有腹水，这人为地增加了体重，掩盖了肌肉消耗。如果不调整骨骼肌质量（例如，通过CT使用骨骼肌指数），目前尚不清楚低BCAA水平是否真的是死亡率的“独立”驱动因素，还是仅仅是肌肉减少症的生化替代品。其次，多变量分析中危险比（HR）的报告模糊了研究结果的临床相关性。在表3中，BCAA和酪氨酸的hr分别为1.00 （95% CI 1.00 - 1.00）和1.01 （95% CI 1.00 - 1.01）。虽然具有统计学意义（p < 0.05），但每1 μmol/L的hr变化产生的值在数学上与零效应无法区分。这种“单位偏差”使得临床医生无法评估风险的大小。为了证明统计显著性转化为有意义的临床效应大小，而不是样本量的人为影响，我敦促作者报告标准化的hr（例如，每1个标准差变化或每100 μmol/L减少）。我认为，澄清BCAA、肌肉质量和死亡率之间的关系，以及提供标准化的效应量，对于验证氨基酸谱分析在肝硬化中的临床应用至关重要。

{"title":"Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis","authors":"Zhanbo Qu","doi":"10.1111/apt.70561","DOIUrl":"https://doi.org/10.1111/apt.70561","url":null,"abstract":"<p>I read with great interest the study by Utakata et al. [<span>1</span>], which identified amino acid imbalance, specifically decreased branched-chain amino acids (BCAAs) and increased tyrosine levels, as independent prognostic factors for mortality in patients with liver cirrhosis. While the study provides valuable insights into metabolic derangements in liver disease, I have two major concerns regarding the validity of the independence of these factors and the interpretation of the results.</p>\u0000<p>First, the study raises a critical concern regarding unmeasured confounding by sarcopenia. BCAAs are primarily metabolised in skeletal muscle, and low serum BCAA levels are inextricably linked to sarcopenia [<span>2</span>]. Sarcopenia itself is a well-established, potent predictor of mortality in cirrhosis. Although the authors adjusted for Body Mass Index (BMI) in their multivariable analysis, BMI is notoriously unreliable for assessing muscle mass in cirrhotic patients due to fluid retention. Notably, 35.1% of the study cohort had ascites, which artificially elevates body weight and masks muscle depletion [<span>3</span>]. Without adjusting for skeletal muscle mass (e.g., using the Skeletal Muscle Index via CT), it remains unclear whether low BCAA levels are truly an ‘independent’ driver of mortality or merely a biochemical surrogate for sarcopenia.</p>\u0000<p>Second, the reporting of hazard ratios (HR) in multivariable analysis obscures the clinical relevance of the findings. In table 3, the HRs for BCAA and Tyrosine are reported as 1.00 (95% CI 1.00–1.00) and 1.01 (1.00–1.01), respectively. While statistically significant (<i>p</i> < 0.05), presenting HRs per 1 μmol/L change yields values that are mathematically indistinguishable from the null effect. This ‘unit bias’ makes it impossible for clinicians to gauge the magnitude of the risk. To demonstrate that the statistical significance translates into a meaningful clinical effect size rather than an artefact of sample size, I urge the authors to report standardised HRs (e.g., per 1 standard deviation change or per 100 μmol/L decrement).</p>\u0000<p>I believe that clarifying the relationship between BCAA, muscle mass, and mortality, along with providing standardised effect sizes, is essential to validate the clinical utility of amino acid profiling in cirrhosis.</p>","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"105 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146210072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis. Authors' reply 信：氨基酸失衡是肝硬化患者死亡的一个独立因素。作者的回复

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-18 DOI: 10.1111/apt.70588

Yuki Utakata, Takao Miwa, Shinji Unome, Naoya Masuda, Mikita Oi, Masashi Aiba, Kenji Imai, Koji Takai, Makoto Shiraki, Naoki Katsumura, Masahito Shimizu

<p>We thank the author for the careful reading of our study and for the thoughtful comments regarding the assessment of amino acid imbalance in patients with cirrhosis [<span>1, 2</span>]. We appreciate the opportunity to clarify the robustness and clinical relevance of our findings, particularly in the independence of amino acid imbalance and sarcopenia.</p><p>First, regarding the concern about the potential influence of sarcopenia, we agree that skeletal muscle mass is an important determinant of amino acid imbalance and prognosis in patients with cirrhosis and that body mass index may inadequately reflect muscle status in the presence of fluid retention [<span>3</span>]. In response, we conducted additional multivariable Cox regression analyses adjusting for the skeletal muscle mass index (SMI) using the CT image at the third lumbar vertebra level [<span>4</span>].</p><p>After exclusion of patients with missing SMI data, the analysis was conducted in 416 patients (Table 1). In multivariable models, SMI itself was not independently associated with mortality in either model. Importantly, amino acid measures remained significantly associated with mortality even after adjustment for SMI. Specifically, a lower branched-chain amino acid to tyrosine ratio (BTR) was associated with increased mortality risk (hazard ratio [HR], 0.82; 95% confidence interval [CI], 0.71–0.95; <i>p</i> = 0.007), while lower branched-chain amino acid (BCAA) levels (HR per 50 μmol/L increase, 0.87; 95% CI, 0.78–0.98; <i>p</i> = 0.016) and higher tyrosine levels (HR per 50 μmol/L increase, 1.48; 95% CI, 1.12–1.95; <i>p</i> = 0.005) were also associated with mortality in models including SMI.</p><div><header><span>TABLE 1. </span>Multivariable model assessing the impact of amino acid imbalance and skeletal muscle mass on mortality.</header><div tabindex="0"><table><thead><tr><th>Characteristic</th><th>HR (95% CI)</th><th><i>p</i>*</th><th>HR (95% CI)</th><th><i>p</i>*</th></tr></thead><tbody><tr><td>Age</td><td>1.03 (1.01–1.05)</td><td>0.001</td><td>1.03 (1.01–1.05)</td><td>0.001</td></tr><tr><td>Male sex</td><td>2.41 (1.51–3.84)</td><td>< 0.001</td><td>2.49 (1.56–3.96)</td><td>< 0.001</td></tr><tr><td>Aetiology of cirrhosis</td><td></td><td></td><td></td><td></td></tr><tr><td style="padding-left:2em;">Viral<sup>a</sup></td><td>1.00</td><td></td><td>1.00</td><td></td></tr><tr><td style="padding-left:2em;">ALD</td><td>1.52 (0.95–2.42)</td><td>0.080</td><td>1.53 (0.96–2.44)</td><td>0.076</td></tr><tr><td style="padding-left:2em;">MASLD</td><td>0.80 (0.24–2.67)</td><td>0.715</td><td>0.83 (0.25–2.79)</td><td>0.766</td></tr><tr><td style="padding-left:2em;">Others</td><td>2.26 (1.35–3.78)</td><td>0.002</td><td>2.36 (1.40–3.96)</td><td>0.001</td></tr><tr><td>Child–Pugh score</td><td>1.33 (1.20–1.48)</td><td>< 0.001</td><td>1.30 (1.17–1.45)</td><td>< 0.001</td></tr><tr><td>Sodium (meq/L)</td>

我们感谢作者仔细阅读了我们的研究，并就肝硬化患者氨基酸失衡的评估提出了周到的意见[1,2]。我们很高兴有机会澄清我们研究结果的稳健性和临床相关性，特别是氨基酸失衡和肌肉减少症的独立性。首先，关于肌肉减少症的潜在影响，我们同意骨骼肌质量是肝硬化患者氨基酸失衡和预后的重要决定因素，并且体重指数可能不能充分反映存在液体潴留bbb的肌肉状态。作为回应，我们使用第三腰椎水平[4]的CT图像进行了额外的多变量Cox回归分析，调整了骨骼肌质量指数（SMI）。排除SMI数据缺失的患者后，对416例患者进行分析（表1）。在多变量模型中，SMI本身与两种模型中的死亡率都没有独立关联。重要的是，即使在调整SMI后，氨基酸测量仍然与死亡率显著相关。具体而言，较低的支链氨基酸与酪氨酸之比（BTR）与死亡风险增加相关（风险比[HR]为0.82,95%可信区间[CI]为0.71-0.95,p = 0.007），而较低的支链氨基酸（BCAA）水平（每50 μmol/L增加的HR为0.87,95% CI为0.78-0.98,p = 0.016）和较高的酪氨酸水平（每50 μmol/L增加的HR为1.48,95% CI为1.12-1.95,p = 0.005）也与包括SMI在内的模型的死亡率相关。表1。多变量模型评估氨基酸失衡和骨骼肌质量对死亡率的影响。CharacteristicHR (95% CI) p *人力资源(95% CI) p * Age1.03(1.01 - -1.05) 0.0011.03男性sex2.41 (1.01 - -1.05) 0.001 (1.51 - -3.84) & lt; 0.0012.49 (1.56 - -3.96) & lt; 0.001病因学cirrhosisVirala1.001.00ALD1.52 (0.95 - -2.42) 0.0801.53 masld0.80 0.076 (0.96 - -2.44) (0.24 - -2.67) 0.7150.83 others2.26 0.766(0.25 - -2.79)(1.35 - -3.78) 0.0022.36(1.40 - -3.96) 0.001儿童score1.33 (1.20 - -1.48) & lt; 0.0011.30 & lt(1.17 - -1.45), 0.001(0.97毫克当量/ L)钠(0.92 - -1.03)0.3440.97氨(0.91 - -1.03)0.252(1.00μg / dL) 0.6321.00 (1.00 - -1.01)（1.00 - 1.01）0.676BTR0.82 (0.71-0.95)0.007BCAA (μmol/L)0.87(0.78-0.98)0.016酪氨酸（μmol/L）1.48 (1.12-1.95)0.005SMI (cm2/m2)1.00(0.98-1.02)0.6030.99(0.97-1.02)0.615缩写：ALD，酒精相关性肝病；支链氨基酸（BCAA）；BTR：支链氨基酸与酪氨酸的比值；CI，置信区间；HR：风险比；MASLD，代谢功能障碍相关的脂肪变性肝病；SMI，骨骼肌质量指数。参考组*采用Cox比例风险模型进行多变量分析。这些发现表明，BCAA、酪氨酸和BTR与预后的关系不能完全用骨骼肌量减少来解释，也不是简单的肌少症的生化替代品。这些发现表明，氨基酸失衡可能反映了与预后相关的代谢过程，而骨骼肌损失不能完全解释这一过程。其次，为了增强临床相关性，我们进行了额外的分析，根据50 μmol/L的增加，重新测量血清BCAA和酪氨酸浓度。在调整年龄、性别、体重指数、肝硬化病因、Child-Pugh评分、血清钠和氨水平后，血清BCAA（每50 μmol/L升高的HR， 0.89; 95% CI, 0.80-0.98; p = 0.019）和酪氨酸浓度（每50 μmol/L升高的HR， 1.49; 95% CI, 1.16-1.93; p = 0.002）与死亡率独立相关。这些重新调整的估计值表明，观察到的关联不仅具有统计学意义，而且具有临床意义的效应量。总之，我们感谢作者们深思熟虑的评论，这些评论使我们能够进一步阐明肝硬化患者中氨基酸失衡、骨骼肌质量和死亡率之间的关系。我们的进一步分析表明，除了肌肉质量的差异外，BCAA、酪氨酸和BTR仍与死亡率相关。总之，这些发现表明氨基酸失衡在评估肝硬化患者预后时提供了额外的价值。

{"title":"Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis. Authors' reply","authors":"Yuki Utakata, Takao Miwa, Shinji Unome, Naoya Masuda, Mikita Oi, Masashi Aiba, Kenji Imai, Koji Takai, Makoto Shiraki, Naoki Katsumura, Masahito Shimizu","doi":"10.1111/apt.70588","DOIUrl":"https://doi.org/10.1111/apt.70588","url":null,"abstract":"<p>We thank the author for the careful reading of our study and for the thoughtful comments regarding the assessment of amino acid imbalance in patients with cirrhosis [<span>1, 2</span>]. We appreciate the opportunity to clarify the robustness and clinical relevance of our findings, particularly in the independence of amino acid imbalance and sarcopenia.</p>\u0000<p>First, regarding the concern about the potential influence of sarcopenia, we agree that skeletal muscle mass is an important determinant of amino acid imbalance and prognosis in patients with cirrhosis and that body mass index may inadequately reflect muscle status in the presence of fluid retention [<span>3</span>]. In response, we conducted additional multivariable Cox regression analyses adjusting for the skeletal muscle mass index (SMI) using the CT image at the third lumbar vertebra level [<span>4</span>].</p>\u0000<p>After exclusion of patients with missing SMI data, the analysis was conducted in 416 patients (Table 1). In multivariable models, SMI itself was not independently associated with mortality in either model. Importantly, amino acid measures remained significantly associated with mortality even after adjustment for SMI. Specifically, a lower branched-chain amino acid to tyrosine ratio (BTR) was associated with increased mortality risk (hazard ratio [HR], 0.82; 95% confidence interval [CI], 0.71–0.95; <i>p</i> = 0.007), while lower branched-chain amino acid (BCAA) levels (HR per 50 μmol/L increase, 0.87; 95% CI, 0.78–0.98; <i>p</i> = 0.016) and higher tyrosine levels (HR per 50 μmol/L increase, 1.48; 95% CI, 1.12–1.95; <i>p</i> = 0.005) were also associated with mortality in models including SMI.</p>\u0000<div>\u0000<header><span>TABLE 1. </span>Multivariable model assessing the impact of amino acid imbalance and skeletal muscle mass on mortality.</header>\u0000<div tabindex=\"0\">\u0000<table>\u0000<thead>\u0000<tr>\u0000<th>Characteristic</th>\u0000<th>HR (95% CI)</th>\u0000<th>\u0000<i>p</i>\u0000*\u0000</th>\u0000<th>HR (95% CI)</th>\u0000<th>\u0000<i>p</i>\u0000*\u0000</th>\u0000</tr>\u0000</thead>\u0000<tbody>\u0000<tr>\u0000<td>Age</td>\u0000<td>1.03 (1.01–1.05)</td>\u0000<td>0.001</td>\u0000<td>1.03 (1.01–1.05)</td>\u0000<td>0.001</td>\u0000</tr>\u0000<tr>\u0000<td>Male sex</td>\u0000<td>2.41 (1.51–3.84)</td>\u0000<td>< 0.001</td>\u0000<td>2.49 (1.56–3.96)</td>\u0000<td>< 0.001</td>\u0000</tr>\u0000<tr>\u0000<td>Aetiology of cirrhosis</td>\u0000<td></td>\u0000<td></td>\u0000<td></td>\u0000<td></td>\u0000</tr>\u0000<tr>\u0000<td style=\"padding-left:2em;\">Viral<sup>a</sup></td>\u0000<td>1.00</td>\u0000<td></td>\u0000<td>1.00</td>\u0000<td></td>\u0000</tr>\u0000<tr>\u0000<td style=\"padding-left:2em;\">ALD</td>\u0000<td>1.52 (0.95–2.42)</td>\u0000<td>0.080</td>\u0000<td>1.53 (0.96–2.44)</td>\u0000<td>0.076</td>\u0000</tr>\u0000<tr>\u0000<td style=\"padding-left:2em;\">MASLD</td>\u0000<td>0.80 (0.24–2.67)</td>\u0000<td>0.715</td>\u0000<td>0.83 (0.25–2.79)</td>\u0000<td>0.766</td>\u0000</tr>\u0000<tr>\u0000<td style=\"padding-left:2em;\">Others</td>\u0000<td>2.26 (1.35–3.78)</td>\u0000<td>0.002</td>\u0000<td>2.36 (1.40–3.96)</td>\u0000<td>0.001</td>\u0000</tr>\u0000<tr>\u0000<td>Child–Pugh score</td>\u0000<td>1.33 (1.20–1.48)</td>\u0000<td>< 0.001</td>\u0000<td>1.30 (1.17–1.45)</td>\u0000<td>< 0.001</td>\u0000</tr>\u0000<tr>\u0000<td>Sodium (meq/L)</td>\u0000","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"52 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146210071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Letter: The Unresolved Issue of NSBB Confounding in Statin Research for Cirrhosis 信：肝硬化他汀类药物研究中未解决的NSBB混淆问题

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70558

Deliang Huang, Zhibin Zhu, Jun Chen

引用次数: 0

Letter on ‘Clinical Features of Portal Hypertension and Their Prognostic Implications in Patients With Autoimmune Hepatitis’: Authors' Reply 关于“自身免疫性肝炎患者门静脉高压的临床特征及其预后意义”的信函：作者的答复

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70518

Lukas Burghart, Thomas Reiberger, Albert Friedrich Stättermayer

引用次数: 0

Letter on “Inherited Genetic Risk of Liver Fibrosis in Lean Versus Nonlean Metabolic Dysfunction‐Associated Steatotic Liver Disease ( MASLD )” 关于“瘦肉与非瘦肉代谢功能障碍相关的脂肪变性肝病（MASLD）的肝纤维化遗传风险”的信函

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70555

Di Chang, Yimeng Zhou

引用次数: 0

Letter: The Unresolved Issue of NSBB Confounding in Statin Research for Cirrhosis—Authors' Reply 信：肝硬化他汀类药物研究中未解决的NSBB混淆问题-作者回复

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70563

Bernardo de Faria Moraes, Gustavo André Pedral Diniz Leite, Igor Boechat Silveira, Gabriel André Pedral Diniz Leite, Maria Luisa Motta Fonseca, Leonardo Corrêa Suffert, Luisa Medeiros Visentini, Luis Pedro Possapp Beis, Guilherme Grossi Lopes Cançado

引用次数: 0

Letter on ‘Inherited Genetic Risk of Liver Fibrosis in Lean Versus Nonlean Metabolic Dysfunction‐Associated Steatotic Liver Disease ( MASLD )’; Authors’ reply 关于“瘦肉与非瘦肉代谢功能障碍相关脂肪变性肝病（MASLD）的肝纤维化遗传风险”的信函；作者的回复

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70577

Kaleb Tesfai, Luis Antonio Díaz, Veeral Ajmera

引用次数: 0

Altered Pathogen Spectrum of Spontaneous Bacterial Peritonitis in Patients Treated With Proton Pump Inhibitors 质子泵抑制剂对自发性细菌性腹膜炎病原菌谱的影响

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70593

Philip Kitchen, Sarah L. Schütte, Tammo L. Tergast, Benjamin Maasoumy, Leonie Braun, Ulrich vor dem Esche, Georg Häcker, Marcus M. Mücke, Marlene Reincke, Michael Schultheiss, Robert Thimme, Siegbert Rieg, Dominik Bettinger, Lukas Sturm

Proton pump inhibitor (PPI) treatment leads to significant changes in the gut microbiota composition. We hypothesized that these alterations may transfer into distinct changes in the causative agents of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis.

质子泵抑制剂（PPI）治疗导致肠道菌群组成的显著变化。我们假设这些改变可能转化为肝硬化患者自发性细菌性腹膜炎（SBP）病原体的明显变化。

引用次数: 0

Editorial: Steroid‐Induced Diabetes in Autoimmune Hepatitis—A Call for Treatment Optimization 社论：自身免疫性肝炎中类固醇诱导的糖尿病-呼吁优化治疗

IF 7.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Alimentary Pharmacology & Therapeutics

Pub Date : 2026-02-17 DOI: 10.1111/apt.70549

Pranab M. Barman

引用次数: 0

首页上一页

下一页尾页

类型

全部化学•材料生命科学医学物理工程技术环境•农林材料科学地球科学法学管理学化学环境科学与生态学计算机科学教育学经济学农林科学人文科学生物学数学物理与天体物理心理学综合性期刊其他工业工程理学历史学农学文学信息工程

数据库

全部 ACS Publications Elsevier ieeexplore Springer The Royal Society of Chemistry Wiley

期刊

Alimentary Pharmacology & Therapeutics

全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.

﹀