DM DISEASE-A-MONTH疾病月刊
DM DISEASE-A-MONTH(英文缩写 DM-DIS MON),ISSN 0011-5029,eISSN 1557-8194,中文译名:疾病月刊 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.477 | Q2 |
| 2022 | 4.000 | Q2 |
| 2023 | 3.800 | Q1 |
| 2024 | 4.300 | Q1 |
| 2025 | 5.700 | Q1 |
DM DISEASE-A-MONTH 最新收录文献
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1. Foreword for common electrolyte disorders for the internist.
1. 内科医生常见电解质紊乱的前言PMID:日期:2026-08-25该文献暂无摘要。
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2. Common electrolyte disorders for the internist.
2. 内科医生常见的电解质紊乱PMID:日期:2026-08-22[中文摘要] 电解质、酸碱及矿物质代谢紊乱是内科患者最常见且具有重要临床意义的问题之一。其发生反映了肾脏、骨骼、内分泌系统及细胞离子转运等受调控的稳态机制出现紊乱。低钠血症、高钠血症、低钾血症、高钾血症、代谢性酸中毒、代谢性碱中毒以及钙磷代谢异常等紊乱若未及时识别和恰当治疗，则与显著的发病率和死亡率相关。准确诊断需要深入理解潜在的病理生理机制、评估容量状态、解读实验室检查结果，并识别相关的肾脏、内分泌、药物及全身性因素。本综述阐述了调控电解质和酸碱稳态的生理机制，并讨论了内科医师常见的电解质紊乱的临床表现、诊断评估及循证管理。我们着重强调鉴别病因并应用实用的诊断流程来指导治疗决策。此外，本综述重点介绍了甲状旁腺激素、维生素D及成纤维细胞生长因子23对钙磷的相互关联调控及其在肾脏疾病和其他疾病中的相关性。通过将基础生理学与当前临床实践指南相结合，本综述为内科医师提供了一个实用框架，以自信地解决其所面临的电解质问题。
[英文摘要] Electrolyte, acid-base, and mineral metabolism disorders are among the most common and clinically significant problems experienced in internal medicine patients. Their development reflects disturbances in regulated homeostatic mechanisms involving the kidneys, bones, endocrine systems, and cellular ion transport. Disorders such as hyponatremia, hypernatremia, hypokalemia, hyperkalemia, metabolic acidosis, metabolic alkalosis, and abnormalities of calcium and phosphorus metabolism are associated with substantial morbidity and mortality when not promptly recognized and appropriately treated. Accurate diagnosis requires a deep understanding of the underlying pathophysiology, assessment of volume status, interpretation of laboratory findings, and identification of contributing kidney, endocrine, medications, and systemic factors. This review describes the physiological mechanisms governing electrolyte and acid-base homeostasis and discusses the clinical presentation, diagnostic evaluation, and evidence-based management of common electrolyte disorders encountered by Internists. We place emphasis on distinguishing etiologies and applying practical diagnostic algorithms to guide treatment decisions. In addition, the review highlights the interconnected regulation of calcium and phosphorus by parathyroid hormone, vitamin D, and fibroblast growth factor 23 and its relevance in kidney disease and other disorders. By integrating foundational physiology with current clinical practice guidelines, this review provides internists with a practical framework to solve electrolyte issues they face with confidence.
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3. Pathobiology-guided diagnostic advances, biomarker discovery, and emerging therapeutic strategies in progressive multiple sclerosis.
3. 病理生物学引导的 diagnostic advances、生物标志物发现以及进展型多发性硬化症中的新兴治疗策略PMID:日期:2026-08-21[中文摘要] 进展型多发性硬化（PMS）是多发性硬化的一种严重且致残的形式，其特征为神经功能损害的逐渐累积以及对常规疾病修饰治疗的应答有限。与复发型多发性硬化不同，进展型多发性硬化的驱动因素不仅包括外周免疫失调，还包括中枢神经系统内持续存在的神经炎症、小胶质细胞活化、线粒体功能障碍以及进行性神经变性。这些复杂且相互重叠的致病机制导致不可逆的轴突丢失，并为治疗干预带来了重大挑战。尽管近年来免疫调节治疗的进展改善了部分患者的结局，但目前可用的疗法在延缓疾病进展方面仅能提供有限的获益。因此，识别新的分子通路和治疗靶点已成为开发更有效的进展型多发性硬化治疗策略的主要焦点。在理解疾病进展的细胞和分子基础方面取得的快速进展，促进了对创新治疗方法的探索，包括靶向免疫治疗、神经保护剂、促进髓鞘再生的策略以及新兴的细胞干预疗法。在本综述中，我们总结了进展型多发性硬化治疗领域的最新进展，重点介绍了近期获批的治疗药物以及处于临床研究中的有前景的药物。特别强调了这些疗法的潜在作用机制及其在改变疾病进展、恢复神经功能以及支持为PMS患者制定个体化治疗策略方面的潜力。
[英文摘要] Progressive multiple sclerosis (PMS) represents a severe and disabling form of MS characterized by a gradual accumulation of neurological impairment and limited responsiveness to conventional disease-modifying therapies. Unlike the relapsing forms of the disease, progressive MS is driven not only by peripheral immune dysregulation but also by persistent neuroinflammation, microglial activation, mitochondrial dysfunction, and progressive neurodegeneration within the central nervous system. These complex and overlapping pathogenic mechanisms contribute to irreversible axonal loss and pose significant challenges for therapeutic intervention. Although recent advances in immunomodulatory treatments have improved outcomes for some patients, currently available therapies provide only limited benefits in slowing disease progression. Consequently, the identification of novel molecular pathways and therapeutic targets has become a major focus in the development of more effective strategies for progressive MS. Rapid progress in understanding the cellular and molecular basis of disease progression has facilitated the exploration of innovative therapeutic approaches, including targeted immunotherapies, neuroprotective agents, remyelination-promoting strategies, and emerging cell-based interventions. Here, in this review, we summarize current advances in the therapeutic landscape of progressive MS, highlighting recently approved treatments as well as promising agents under clinical investigation. Particular emphasis is placed on the underlying mechanisms of action of these therapies and their potential to modify disease progression, restore neural function, and support the development of personalized treatment strategies for patients with PMS.
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4. Foreword for pathobiology-guided diagnostic advances, biomarker discovery, and emerging therapeutic strategies in progressive multiple sclerosis.
4. 病理生物学引导的诊断进展、生物标志物发现及进展型多发性硬化新兴治疗策略前言PMID:日期:2026-08-15该文献暂无摘要。
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5. Foreword for genetic determinants of pregnancy loss: Mechanisms, diagnostic advances, and clinical implications.
5. 妊娠丢失的遗传决定因素：机制、诊断进展与临床意义PMID:日期:2026-07-15该文献暂无摘要。
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6. Genetic determinants of pregnancy loss: Mechanisms, diagnostic advances, and clinical implications.
6. 妊娠丢失的遗传决定因素：机制、诊断进展及临床意义PMID:日期:2026-07-14[中文摘要] 妊娠丢失影响高达15%的临床确认妊娠，构成重大的临床与情感负担。虽然染色体异常占早期流产的大多数，但许多既往不明原因的病例涉及单基因、线粒体、表观遗传、免疫遗传及父源因素。基因组技术的进步提高了对散发性和复发性妊娠丢失中致病性变异的检出能力。旨在综合当前关于妊娠丢失遗传决定因素的证据，涵盖染色体、单基因、线粒体、表观遗传、免疫及血栓形成倾向相关通路，并评估基因组诊断如何指导临床管理与生殖咨询。本叙述性综述整合了关于染色体异常、拷贝数变异、母源效应基因、父源遗传贡献、线粒体功能障碍、表观遗传失调、免疫介导机制及遗传性血栓形成倾向的研究数据。来自下一代测序、染色体微阵列、全外显子组测序及胚胎植入前遗传学检测的证据突出了诊断检出率与临床相关性。染色体异常，包括非整倍体及致病性拷贝数变异，仍是早期妊娠丢失的主要原因。母源效应基因突变、纤毛发生与形态发生缺陷、线粒体变异、印记紊乱及父源因素（如精子DNA碎片化）亦参与植入失败、胚胎停育及复发性丢失。免疫遗传及血栓形成倾向相关变异影响胎盘发育及晚期结局。基因组平台（CMA、WES、NGS、PGT）提高了诊断检出率并改善咨询，尤其对于复发性丢失。妊娠丢失源于染色体异常之外的一系列遗传机制。整合基因组、免疫及环境评估可提高诊断精确性，支持风险分层，并指导针对性管理。现代遗传学检测应作为妊娠丢失综合评估的一部分。妊娠丢失的遗传因素涵盖染色体异常、单基因疾病、线粒体变异、表观遗传紊乱、免疫失调及血栓形成倾向。基因组检测的进步提高了诊断精确性，并支持对受累患者进行个体化生殖咨询。
[英文摘要] Pregnancy loss affects up to 15% of clinically recognized pregnancies, posing a major clinical and emotional burden. While chromosomal abnormalities account for most early miscarriages, many previously unexplained cases involve monogenic, mitochondrial, epigenetic, immunogenetic, and paternal factors. Advances in genomic technologies have improved detection of pathogenic variants in both sporadic and recurrent pregnancy loss. To synthesize current evidence on genetic determinants of pregnancy loss across chromosomal, monogenic, mitochondrial, epigenetic, immunologic, and thrombophilia-related pathways, and evaluate how genomic diagnostics inform management and reproductive counseling. This narrative review integrates data from studies on chromosomal abnormalities, copy-number variants, maternal-effect genes, paternal genetic contributions, mitochondrial dysfunction, epigenetic dysregulation, immune-mediated mechanisms, and inherited thrombophilias. Evidence from next-generation sequencing, chromosomal microarray, whole-exome sequencing, and preimplantation genetic testing highlights diagnostic yield and clinical relevance. Chromosomal abnormalities, including aneuploidy and pathogenic copy-number variants, remain the predominant cause of early pregnancy loss. Mutations in maternal-effect genes, ciliogenesis and morphogenesis defects, mitochondrial variants, imprinting disturbances, and paternal factors, such as sperm DNA fragmentation, also contribute to implantation failure, embryonic arrest, and recurrent loss. Immunogenetic and thrombophilia-associated variants affect placental development and late outcomes. Genomic platforms (CMA, WES, NGS, PGT) increase diagnostic detection and improve counseling, especially for recurrent loss. Pregnancy loss arises from a spectrum of genetic mechanisms beyond chromosomal abnormalities. Integrating genomic, immunologic, and environmental assessment improves diagnostic precision, supports risk stratification, and informs targeted management. Modern genetic testing should be part of comprehensive evaluation for pregnancy loss. Genetic contributors to pregnancy loss span chromosomal abnormalities, single-gene disorders, mitochondrial variants, epigenetic disturbances, immune dysregulation, and thrombophilia. Advances in genomic testing improve diagnostic precision and support individualized reproductive counseling for affected patients.
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8. Disturbances due to cold.
8. 因寒冷引起的困扰PMID:日期:2026-07-02[中文摘要] 低体温症的经典定义是核心体温降至95.0°F（35.0°C）以下。大多数报道的低温症病例是由于暴露于低环境温度所致（意外性低温症）。低温症的其他病因包括脓毒症、严重甲状腺功能减退症（黏液性水肿昏迷）、急性脊髓损伤、糖尿病酮症酸中毒、多系统创伤以及长时间心脏骤停。冻伤、冻疮和战壕足均有特定的治疗方法以防止肢体丧失。过去十年间，这些治疗选择已取得显著进展，本期将对此进行详细阐述。
[英文摘要] Hypothermia is classically defined as a reduction in the body's core temperature below 95.0°F (35.0 °C). Most reported cases of hypothermia are due to environmental exposure to low ambient temperatures (accidental hypothermia). Other causes of hypothermia include sepsis, severe hypothyroidism (myxedema coma), acute spinal cord injury, diabetic ketoacidosis, multisystem trauma, and prolonged cardiac arrest. Frostbite, chillblain and trench foot all have specific therapies to prevent limb loss. There have been significant advances in these therapeutic options over the past decade which are detailed in this issue.
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9. GLP-1 agonist and neuroprotection in Stroke and Parkinson's disease: A systematic review.
9. GLP-1激动剂和中风和帕金森病的神经保护：系统综述PMID:日期:2026-06-12[中文摘要] 胰高血糖素样肽-1受体激动剂已被证实在代谢性疾病中具有神经保护作用，但其在神经退行性疾病（卒中和帕金森病）中的应用尚未得到充分研究。旨在从机制、干预特征和主要神经学结局方面评估GLP-1受体激动剂在实验性卒中和帕金森病模型中的神经保护作用。按照PRISMA指南进行了系统综述。检索了Cochrane CENTRAL、PubMed、Web of Science和Scopus四个数据库，共识别出1643条记录，最终纳入13项实验动物研究。采用SYRCLE工具提取数据并评估偏倚风险。共纳入2013至2026年间发表的13项实验研究，涉及卒中和帕金森病模型。MCAO模型是卒中研究中使用的主要模型，梗死体积显著减小，例如利拉鲁肽组为15.4%±1.3%，利格列汀组减小40%。神经功能缺损评分也得到改善（1.1±0.14；P<0.05），治疗组梗死面积亦缩小（从36.5%降至8.2%；P=0.001）。帕金森病研究表明，运动功能显著改善（P<0.001），多巴胺能神经元得到保护，α-突触核蛋白聚集减少。GLP-1激动剂降低了神经炎症（TNF-α、IL-1b、IL-6）、氧化应激（ROS、4-HNE）和凋亡（Bcl-2升高、Bax降低）标志物。治疗时长为24小时至20周不等，各药物的剂量亦存在差异。偏倚风险评估的总体质量为中等，其中四项研究因样本量小以及随机化和盲法报告不充分而具有高偏倚风险。GLP-1受体激动剂在卒中和帕金森病的临床前模型中具有强大的多靶点神经保护活性。为确保转化潜力并优化治疗策略，需要开展标准化研究和临床试验。
[英文摘要] Glucagon-like peptide-1 receptor agonists have been shown to have neuroprotective effects in metabolic diseases, but their application in neurodegenerative diseases (stroke and Parkinson's disease) has not been adequately studied. To assess the neuroprotective effects of GLP-1 receptor agonists in experimental stroke and Parkinson's disease models, in terms of mechanisms, properties of intervention, and major neurological outcomes. A systematic review was performed according to PRISMA. Four databases Cochrane CENTRAL, PubMed, Web of Science and Scopus were searched and 1643 records identified and 13 experimental animal studies were included. The SYRCLE tool was used to extract data and assess the risk of bias. 13 experimental studies published in 2013-2026 were included, which involved models of stroke and Parkinson disease. The MCAO models were the main models used in stroke studies, with a significant decrease in infarct volume, such as 15.4 % ± 1.3 % (liraglutide) and 40 % reduction with linagliptin. The score in neurological deficit was also found to improve (1.1 ± 0.14; P < 0.05) and the size of the infarct in treated groups had also reduced (36.5 % to 8.2 %; P = 0.001). The research on Parkinson disease showed that there was a notable improvement in motor functions (P < 0.001), preservation of dopaminergic neurons, and a decrease in the aggregation of α-synuclein. GLP-1 agonists decreased neuroinflammatory (TNF-α, IL-1b, IL-6), oxidative (ROS, 4-HNE), and apoptotic (increased Bcl-2, decreased Bax) markers. The treatment was between 24 h and 20 weeks, and the doses also differed among the agents. The overall quality of risk of bias assessment was moderate, with four studies having a high risk because of small sample size and inadequate reporting on the randomization and blinding. GLP-1 receptor agonists have powerful neuroprotective activity in preclinical models of stroke and Parkinson disease, which is multi-targeted. To ensure translational potential and to maximize therapeutic strategies, standardized studies and clinical trials are needed.
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10. GLP-1 receptor agonists for weight management and potential thromboembolic risk reduction in high risk population with cancer, diabetes, cardiovascular disease: A systematic review.
10. GLP-1受体激动剂用于癌症、糖尿病、心血管疾病高危人群的体重管理及潜在血栓栓塞风险降低：一项系统综述PMID:日期:2026-05-29Thromboembolic risk is increased in obesity and cardiometabolic disorders. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) also facilitate weight loss and cardiovascular benefits, yet their effects on thromboembolic events risk reduction in high-risk populations are not completely understood. The PRISMA 2020 guidelines were followed to search Scopus, PubMed, Cochrane Library and Web of Science (WoS). We identified 110 records, 8 of which were included in this review. Data extraction, risk of bias assessment and narrative synthesis were independently conducted. GLP-1RAs consistently demonstrated greater weight reduction compared with controls. Semaglutide trials reported up to 15.2 % weight loss versus 2.6 % in controls (p < 0.0001), while liraglutide showed approximately 5 % reduction versus no change. Cardiovascular outcome trials showed significant risk reduction, with hazard ratios of 0.80 (0.72-0.90) and 0.74 (0.58-0.95), indicating decreased major cardiovascular events. However, direct venous thromboembolism reporting was limited; one study showed fewer events (1 vs 3) without statistical significance. Safety profiles were acceptable, with slightly increased gallbladder events (2.8 % vs 2.3 %), rare pancreatitis, and no consistent cancer risk. Serious adverse events were similar or lower in intervention groups (33.4 % vs 36.4 %). GLP-1RAs yield substantial weight loss and cardiovascular risk reduction in a high-risk group. There is limited direct evidence about thromboembolism, but there is evidence that it may be beneficial. Their role in reducing thromboembolic risk needs to be confirmed in further large-scale studies.