Volume 136 · Issue 22 · 2023

Over the past few years, the human virome and its complex interactions with microbial communities and the immune system have gained recognition as a crucial factor in human health. Individuals with compromised immune function encounter distinctive challenges due to their heightened vulnerability to a diverse range of infectious diseases. This review aims to comprehensively explore and analyze the growing evidence regarding the role of the virome in immunocompromised disease status. By surveying the latest literature, we present a detailed overview of virome alterations observed in various immunodeficiency conditions. We then delve into the influence and mechanisms of these virome changes on the pathogenesis of specific diseases in immunocompromised individuals. Furthermore, this review explores the clinical relevance of virome studies in the context of immunodeficiency, highlighting the potential diagnostic and therapeutic gains from a better understanding of virome contributions to disease manifestations.

Although antiretroviral therapy (ART) can reduce the viral load in the plasma to undetectable levels in human immunodeficiency virus (HIV)-infected individuals, ART alone cannot completely eliminate HIV due to its integration into the host cell genome to form viral reservoirs. To achieve a functional cure for HIV infection, numerous preclinical and clinical studies are underway to develop innovative immunotherapies to eliminate HIV reservoirs in the absence of ART. Early studies have tested adoptive T-cell therapies in HIV-infected individuals, but their effectiveness was limited. In recent years, with the technological progress and great success of chimeric antigen receptor (CAR) therapy in the treatment of hematological malignancies, CAR therapy has gradually shown its advantages in the field of HIV infection. Many studies have identified a variety of HIV-specific CAR structures and types of cytolytic effector cells. Therefore, CAR therapy may be beneficial for enhancing HIV immunity, achieving HIV control, and eliminating HIV reservoirs, gradually becoming a promising strategy for achieving a functional HIV cure. In this review, we provide an overview of the design of anti-HIV CAR proteins, the cell types of anti-HIV CAR (including CAR T cells, CAR natural killer cells, and CAR-encoding hematopoietic stem/progenitor cells), the clinical application of CAR therapy in HIV infection, and the prospects and challenges in anti-HIV CAR therapy for maintaining viral suppression and eliminating HIV reservoirs.

Atrial fibrillation (AF), the most common sustained arrhythmia, is associated with a range of symptoms, including palpitations, cognitive impairment, systemic embolism, and increased mortality. It places a significant burden on healthcare systems worldwide. Despite decades of research, the precise mechanisms underlying AF remain elusive. Current understanding suggests that factors like stretch-induced fibrosis, epicardial adipose tissue (EAT), chronic inflammation, autonomic nervous system (ANS) imbalances, and genetic mutations all play significant roles in its development. In recent years, the advent of wearable devices has revolutionized AF diagnosis, enabling timely detection and monitoring. However, balancing early diagnosis with efficient resource utilization presents new challenges for healthcare providers. AF management primarily focuses on stroke prevention and symptom alleviation. Patients at high risk of thromboembolism require anticoagulation therapy, and emerging pipeline drugs, particularly factor XI inhibitors, hold promise for achieving effective anticoagulation with reduced bleeding risks. The scope of indications for catheter ablation in AF has expanded significantly. Pulsed field ablation, as a novel energy source, shows potential for improving success rates while ensuring safety. This review integrates existing knowledge and ongoing research on AF pathophysiology and clinical management, with emphasis on diagnostic devices, next-generation anticoagulants, drugs targeting underlying mechanisms, and interventional therapies. It offers a comprehensive mosaic of AF, providing insights into its complexities.

Dual regimen dolutegravir (DTG) plus lamivudine (3TC) has demonstrated non-inferior efficacy compared to DTG-based three-drug regimens (3DRs), yet directly comparative data regarding the efficacy and safety of DTG + 3TC and bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) for therapy-naïve people with human immunodeficiency virus (HIV)-1 (PWH) are still limited. We aimed to assess the antiviral potency and safety profiles of DTG + 3TC vs. B/F/TAF based on antiretroviral therapy (ART)-naïve PWH in China.

This retrospective multicenter study enrolled PWH initiating ART with DTG + 3TC or B/F/TAF from 2020 to 2022 in Guangdong and Guangxi. We analyzed response rates based on target not detected (TND) status using intention-to-treat (ITT) analysis. Subgroups were formed based on baseline viral load (VL) (<100,000 vs. ≥100,000 copies/mL) and CD4⁺ cell count (<200 vs. ≥200 cell/µL). Median time to TND VL was assessed by Kaplan–Meier method. We also measured changes from baseline in CD4⁺ cell counts, CD4/CD8 ratio, lipid parameters, weight, creatinine (Cr), estimated glomerular filtration rate (eGFR), and drug-related adverse effects (DRAEs).

We enrolled 280 participants, including 137 (48.9%) on DTG + 3TC and 143 (51.1%) on B/F/TAF. At week 48, 96.4% (132/137) on DTG+3TC and 100% (143/143) on B/F/TAF achieved TND (P = 0.064). At week 12, TND responses were higher with B/F/TAF (78.3% [112/143]) than DTG+3TC (30.7% [42/137]) (P <0.001). This trend held across subgroups. B/F/TAF achieved TND faster (12 weeks) than DTG+3TC (24 weeks) (P <0.001). No differences were seen in CD4⁺ cell count and CD4/CD8 ratio, except in the high-VL subgroup, where B/F/TAF showed better recovery. DRAEs were significantly lower with B/F/TAF (4.9% [7/143]) than with DTG + 3TC (13.1% [18/137]) (P = 0.016). Lipid parameters, body weight, and Cr increased in both groups over 48 weeks, with DTG+3TC showing a more favorable effect on triglycerides, high-density lipoprotein (HDL) cholesterol, and weight gain.

In this real-life study, B/F/TAF led to a faster viral decline and fewer DRAEs compared to DTG+3TC. No significant difference was observed in the TND rate at week 48, regardless of baseline VL and CD4⁺ cell count. CD4⁺ recovery was superior for B/F/TAF in participants with high VL. The DTG + 3TC regimen had less impact on metabolic changes than B/F/TAF.

Hepatitis B surface antigen (HBsAg) clearance is vital for a functional cure of hepatitis B virus (HBV) infection. However, the incidence and predictors of HBsAg seroclearance in patients co-infected with HBV and human immunodeficiency virus (HIV) remain largely unknown in Guangdong, China.

Between 2009 and 2019, patients co-infected with HBV/HIV undergoing antiretroviral therapy (ART) in Guangzhou Eighth People’s Hospital affiliated to Guangzhou Medical University were retrospectively reviewed with the endpoint on December 31, 2020. The incidence and risk factors for HBsAg seroclearance were evaluated using Kaplan–Meier and multivariate Cox regression analyses.

A total of 1550 HBV/HIV co-infected patients were included in the study, with the median age of 42 years and 86.0% (1333/1550) males. Further, 98.3% (1524/1550) received ART containing tenofovir disoproxil fumarate (TDF) plus lamivudine (3TC). HBV DNA was examined in 1283 cases at the last follow-up. Over the median 4.7 years of follow-up, 8.1% (126/1550) patients achieved HBsAg seroclearance, among whom 50.8% (64/126) obtained hepatitis B surface antibody, 28.1% (137/488) acquired hepatitis B e antigen seroconversion, and 95.9% (1231/1283) undetectable HBV DNA. Compared with patients who maintained HBsAg positive, cases achieving HBsAg seroclearance showed no differences in age, gender, CD4⁺ T cell count, alanine aminotransferase (ALT) level, or fibrosis status; however, they presented lower HBV DNA levels, lower HBsAg levels, and higher rates of HBV genotype B at the baseline. Multivariate analysis showed that baseline HBsAg <1500 cutoff index (COI) (adjusted hazard ratio [aHR], 2.74, 95% confidence interval [95% CI]: 1.48–5.09), ALT elevation >2 × upper limit of normal during the first six months after receiving ART (aHR, 2.96, 95% CI: 1.53–5.77), and HBV genotype B (aHR, 3.73, 95% CI: 1.46–9.59) were independent predictors for HBsAg seroclearance (all P <0.01).

Long-term TDF-containing ART has high anti-HBV efficacy including relatively high overall HBsAg seroclearance in HBV/HIV co-infected patients. Lower baseline HBsAg levels, HBV genotype B, and elevated ALT levels during the first six months of ART are potential predictors of HBsAg seroclearance.

Previous studies have examined the bulk transcriptome of peripheral blood immune cells in acquired immunodeficiency syndrome patients experiencing immunological non-responsiveness. This study aimed to investigate the characteristics of specific immune cell subtypes in acquired immunodeficiency syndrome patients who exhibit immunological non-responsiveness.

A single-cell transcriptome sequencing of peripheral blood mononuclear cells obtained from both immunological responders (IRs) (CD4⁺ T-cell count >500) and immunological non-responders (INRs) (CD4⁺ T-cell count <300) was conducted. The transcriptomic profiles were used to identify distinct cell subpopulations, marker genes, and differentially expressed genes aiming to uncover potential genetic factors associated with immunological non-responsiveness.

Among the cellular subpopulations analyzed, the ratios of monocytes, CD16⁺ monocytes, and exhausted B cells demonstrated the most substantial differences between INRs and IRs, with fold changes of 39.79, 11.08, and 2.71, respectively. In contrast, the CD4⁺ T cell ratio was significantly decreased (0.39-fold change) in INRs compared with that in IRs. Similarly, the ratios of natural killer cells and terminal effector CD8⁺ T cells were also lower (0.37-fold and 0.27-fold, respectively) in the INRs group. In addition to several well-characterized immune cell-specific markers, we identified a set of 181 marker genes that were enriched in biological pathways associated with human immunodeficiency virus (HIV) replication. Notably, ISG15, IFITM3, PLSCR1, HLA-DQB1, CCL3L1, and DDX5, which have been demonstrated to influence HIV replication through their interaction with viral proteins, emerged as significant monocyte marker genes. Furthermore, the differentially expressed genes in natural killer cells were also enriched in biological pathways associated with HIV replication.

We generated an atlas of immune cell transcriptomes in HIV-infected IRs and INRs. Host genes associated with HIV replication were identified as markers of, and were found to be differentially expressed in, different types of immune cells.

Distinguishing between primary clear cell carcinoma of the liver (PCCCL) and common hepatocellular carcinoma (CHCC) through traditional inspection methods before the operation is difficult. This study aimed to establish a Faster region-based convolutional neural network (RCNN) model for the accurate differential diagnosis of PCCCL and CHCC.

In this study, we collected the data of 62 patients with PCCCL and 1079 patients with CHCC in Beijing YouAn Hospital from June 2012 to May 2020. A total of 109 patients with CHCC and 42 patients with PCCCL were randomly divided into the training validation set and the test set in a ratio of 4:1. The Faster RCNN was used for deep learning of patients’ data in the training validation set, and established a convolutional neural network model to distinguish PCCCL and CHCC. The accuracy, average precision, and the recall of the model for diagnosing PCCCL and CHCC were used to evaluate the detection performance of the Faster RCNN algorithm.

A total of 4392 images of 121 patients (1032 images of 33 patients with PCCCL and 3360 images of 88 patients with CHCC) were uesd in test set for deep learning and establishing the model, and 1072 images of 30 patients (320 images of nine patients with PCCCL and 752 images of 21 patients with CHCC) were used to test the model. The accuracy of the model for accurately diagnosing PCCCL and CHCC was 0.962 (95% confidence interval [CI]: 0.931–0.992). The average precision of the model for diagnosing PCCCL was 0.908 (95% CI: 0.823–0.993) and that for diagnosing CHCC was 0.907 (95% CI: 0.823–0.993). The recall of the model for diagnosing PCCCL was 0.951 (95% CI: 0.916–0.985) and that for diagnosing CHCC was 0.960 (95% CI: 0.854–0.962). The time to make a diagnosis using the model took an average of 4 s for each patient.

The Faster RCNN model can accurately distinguish PCCCL and CHCC. This model could be important for clinicians to make appropriate treatment plans for patients with PCCCL or CHCC.

Thymic carcinomas (TCs) and thymic neuroendocrine neoplasms (TNENs) are two aggressive subtypes of thymic malignancy. Traditional therapy for advanced TCs and TNENs has limited outcome. New genomic profiling of TCs and TNENs might provide insights that contribute to the development of new treatment approaches.

We used gene panel sequencing technologies to investigate the genetic aberrations of 32 TC patients and 15 TNEN patients who underwent surgery at Shanghai Chest Hospital between 2015 and 2017. Patient samples were sequenced using a 324-gene platform with licensed technologies. In this study, we focused on clinically relevant genomic alterations (CRGAs), which are previously proven to be pathogenic alterations, to identify the pathology-specific mutational patterns, prognostic signatures of TCs and TNENs.

The mutational profiles between TCs and TNENs were diverse. The genetic alterations that ranked highest in TCs were in CDKN2A, TP53, ASXL1, CDKN2B, PIK3C2G, PTCH1, and ROS1, while those in TNENs were in MEN1, MLL2, APC, RB1, and TSC2. Prognostic analysis showed that mutations of ROS1, CDKN2A, CDKN2B, BRAF, and BAP1 were significantly associated with worse outcomes in TC patients, and that mutation of ERBB2 indicated shortened disease-free survival (DFS) and overall survival (OS) in TNEN patients. Further investigation found that the prognosis-related genes were focused on signal pathways of cell cycle control, chromatin remodeling/DNA methylation, phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), and receptor tyrosine kinase (RTK)/RAS/mitogen-activated protein kinase (MAPK) signaling.

We profiled the mutational features of 47 Chinese patients with thymic malignancy of diverse pathologic phenotypes to uncover the integrated genomic landscape of these rare tumors, and identified the pathology-specific mutational patterns, prognostic signatures, and potential therapeutic targets for TCs and TNENs.

Colorectal carcinogenesis and progression are related to the gut microbiota and the tumor immune microenvironment. Our previous clinical trial demonstrated that berberine (BBR) hydrochloride might reduce the recurrence and canceration of colorectal adenoma (CRA). The present study aimed to further explore the mechanism of BBR in preventing colorectal cancer (CRC).

We performed metagenomics sequencing on fecal specimens obtained from the BBR intervention trial, and the differential bacteria before and after medication were validated using quantitative polymerase chain reaction. We further performed Apc^Min/+ animal intervention tests, RNA sequencing, flow cytometry, immunohistochemistry, and enzyme-linked immunosorbent assays.

The abundance of fecal Veillonella parvula (V. parvula) decreased significantly after BBR administration (P = 0.0016) and increased through the development from CRA to CRC. Patients with CRC with a higher V. parvula abundance had worse tumor staging and a higher lymph node metastasis rate. The intestinal immune pathway of Immunoglobulin A production was activated, and the expression of TNFSF13B (Tumor necrosis factor superfamily 13b, encoding B lymphocyte stimulator [BLyS]), the representative gene of this pathway, and the genes encoding its receptors (interleukin-10 and transforming growth factor beta) were significantly upregulated. Animal experiments revealed that V. parvula promoted colorectal carcinogenesis and increased BLyS levels, while BBR reversed this effect.

BBR might inhibit V. parvula and further weaken the immunomodulatory effect of B cells induced by V. parvula, thereby blocking the development of colorectal tumors.

ClinicalTrials.gov, No. NCT02226185.

随着联合抗逆转录病毒疗法（cART）的发展，人类免疫缺陷病毒（HIV）感染在过去二十年中已经从一种通常致命的疾病转变为一种可控制的慢性疾病。^[1]cART提供对HIV的快速控制和免疫功能的部分恢复，从而预防各种HIV相关并发症。然而，这并不意味着艾滋病毒携带者（PLWH）在接受cART后完全恢复健康。接受长期cART的HIV感染个体患重大心血管疾病（CVD）的风险仍然高于未感染个体。^[2]动脉粥样硬化性心血管疾病（ASCVD）涉及心肌梗死（MI）、中风和心源性猝死，目前是PLWH死亡的主要原因之一。血脂异常是PLWH CVD的主要危险因素，约占总体CVD风险的50%。^[3]不仅心血管风险增加，PLWH的血脂异常也可能与非酒精性脂肪性肝病（NAFLD）和二型糖尿病的风险增加有关。此外，PLWH的血脂异常不同于普通人群，因为HIV治疗不仅可能诱导血脂异常，还可能与降脂剂相互作用。因此，PLWH人群血脂异常和CVD风险的管理具有挑战性，需要多学科专业团队的合作才能提供适当的护理。

人类免疫缺陷病毒（HIV）感染是全世界公共卫生的一个重大而紧迫的问题。^[1]20世纪90年代中期，抗逆转录病毒疗法（ART）的广泛使用导致了艾滋病毒感染管理的重大范式转变，从而将其预后从威胁生命的疾病改变为慢性和可管理的健康状况。根据以前的研究，目前正在接受抗逆转录病毒疗法的艾滋病毒感染者（PLWH）与艾滋病毒感染相关的发病率和死亡率都有所下降，同时将病毒传播给他人的风险也有所降低。^[2,3,4,5]整合酶链转移抑制剂（INSTIs）是最新的ART药物类别，表现出强效力、高耐药性屏障、最小的药物相互作用和优异的耐受性。^[6,7]2009年，中国食品药品监督管理总局（CFDA）批准雷替拉韦（RAL）用于治疗HIV/获得性免疫缺陷综合征（AIDS）的首个INSTI，随后分别于2015年、2018年、2019年和2023年批准了多替拉韦（DTG）、艾替拉韦（EVG）、比替拉韦（BIC）和卡博特拉韦（CAB）。自2018年以来，根据中国国家艾滋病毒/艾滋病诊断和治疗指南，基于INSTI的方案被建议作为首选的一线抗逆转录病毒疗法。^[8]然而，INSTIs的使用在中国大陆的大多数地区受到限制，因为它们的成本很高。因此，中国>80%的PLWH在国家免费抗逆转录病毒治疗计划（NFATP）下接受免费替诺福韦/齐多夫定+拉米夫定+依法韦仑治疗。^[8,9]自2020年以来，EVG、DTG和BIC等Insti的费用逐步下降，目前已纳入中国医疗保险。主要城市的当地医疗保险可以覆盖50-90%的费用，提供了实质性的报销政策；因此，越来越多的PLWH选择了基于INSTI的方案。截至2022年底，天津市近一半的PLWH正在接受机构收容治疗。INSTI的使用显著增加，导致INSTI相关耐药突变的稳定出现。中国有限的调查表明，在北京和深圳等大城市，未接受抗逆转录病毒治疗的PLWH中，INSTI耐药性水平相对较低。^[10,11]然而，天津未接受治疗的个体中INSTI耐药性的患病率仍然未知。本研究评估了中国天津未接受ART的HIV-1感染个体中INSTI相关耐药性的患病率。

致编辑：人类免疫缺陷病毒（HIV）流行病对全球公共卫生构成重大挑战。截至2022年，全球约有3900万人感染了艾滋病毒。^[1]随着联合抗逆转录病毒疗法（cART）的不断发展，HIV感染已经转变为一种需要长期治疗的可控慢性疾病。在各种类型的抗逆转录病毒（ARV）药物中，以效力和耐受性而闻名的基于整合酶链转移抑制剂（INSTI）的方案已成为全球主要的治疗方式。下一代INSTI bictegravir（BIC）于2018年获得美国食品药品监督管理局（FDA）批准，作为单片方案（STR），含有BIC（50 mg）/恩曲他滨（FTC，200 mg）/替诺福韦艾拉酚胺（TAF，25 mg），每日一次。它已被主要指南认可为初治患者的首选，包括2021年版的中国获得性免疫缺陷综合征（AIDS）诊疗指南。^[2]在中国，为HIV感染者（PLWH）提供了灵活的cART选择，包括国家报销药品目录（NRDL）、自费药品和免费药品。自2021年纳入国家医保目录以来，BIC/FTC/TAF在越来越多的患者中受到欢迎。

致编辑：即使在抗逆转录病毒治疗（ART）时代，人类免疫缺陷病毒（HIV）患者患非霍奇金淋巴瘤（NHL）的风险也会增加。^[1]HIV相关NHL（HIV-NHL）的具体机制仍不清楚。目前认为HIV主要通过慢性免疫激活和增加感染肿瘤病毒的风险引起淋巴瘤。此外，HIV可能还有其他一些直接促成淋巴瘤发生的机制。^[2]

致编辑：涉及人类缺陷病毒1型（HIV-1）的耐药突变（DRMs）降低了当前抗逆转录病毒治疗（ART）方案的疗效，导致治疗失败。更好地了解导致ART失败的当地DRM的患病率可以为临床和政府层面的决策提供有价值的数据。基于对2018年6月至2022年4月郑州市第六人民医院PLWH血浆样本的分析，评估了ART难治性HIV（PLWH）（病毒载量>200拷贝/mL）感染者的DRM状态。此外，扩增、测序和分析部分聚合酶(pol)和完整整合酶基因编码序列以鉴定DRM。本研究经郑州市第六人民医院机构伦理委员会批准（编号：2019-04）。所有参与者在样本采集前签署了书面知情同意书。

致编辑：先前的研究已经证明了比替格拉韦（B）、恩曲他滨（F）和替诺福韦艾拉酚胺（TAF）在人类免疫缺陷病毒（HIV）感染患者中实现病毒学抑制的功效。病毒学抑制可受多种因素影响，基线HIV-1 RNA是关键考虑因素。指南常将基线HIV RNA水平>500,000拷贝/mL作为药物选择的主要参考指标。^[1]然而，先前关于B/F/TAF有效性的研究并没有专门分析基线HIV RNA>500,000拷贝/mL的患者。在住院HIV感染者中晚期HIV患病率超过70%的中国重庆，^[2]在我们的研究中，高达25%的患者基线HIV-1 RNA>500,000拷贝/mL，许多患者存在机会性感染。在这种复杂的医疗环境中，使用B/F/TAF的患者的病毒学抑制率仍然不确定。

致编辑：与健康人群相比，携带人类免疫缺陷病毒（PLWH）的人更有可能患癌症，具有更严重的癌症临床病程，并且具有更高的死亡率。由于联合抗逆转录病毒疗法（cART）疗效和预期寿命的改善，用于癌症的标准治疗和免疫疗法（如免疫检查点抑制剂（ICIs））越来越多地用于治疗PLWH的非获得性免疫缺陷综合征定义的癌症。^[1]恶性肿瘤细胞引发免疫检查点的抑制并促进免疫抑制状态，这有利于免疫系统的逃避和肿瘤的生长。ICIs通过激活T细胞和其他先天细胞和适应性细胞来阻断抑制途径来发挥作用，从而导致生产性抗肿瘤免疫应答。美国食品药品监督管理局批准用于人用的ICI包括程序性细胞死亡受体1（PD-1）和程序性细胞死亡受体1配体（PD-L1）。^[2]

致编辑：由严重急性呼吸系统综合症冠状病毒2（新型冠状病毒）引发的2019冠状病毒病（COVID-19）已表现为一场可怕的全球大流行，引发了重大的经济影响并导致广泛的死亡。与此同时，由人类免疫缺陷病毒（艾滋病毒）引起的获得性免疫缺陷综合症（艾滋病）流行病仍然是一个突出的全球卫生紧急情况。截至2022年底，艾滋病相关病理累计造成约4040万人死亡，全球现存艾滋病毒人口约3900万艾滋病毒感染者（PLWH），作为一个潜在的免疫功能低下人群，在新冠肺炎研究领域受到的关注有限。大多数现有研究将接受HIV治疗的受试者与HIV阴性的受试者进行了比较。在全球艾滋病毒病例总数中，估计有920万未接受抗逆转录病毒治疗（ART）的PLWH人可能比接受ART的人面临更明显的免疫缺陷风险。^[1]ART经验和ART初治PLWH之间新冠肺炎严重程度和临床表现的差异尚未得到全面了解。有鉴于此，我们的研究试图通过回顾性病例对照分析阐明接受过ART和未接受ART的PLWH之间新冠肺炎严重程度的差异。

致编辑：通过常规耐药性测定检测到的高频耐药性（通常≥15-25%的病毒准种）长期以来一直与抗逆转录病毒疗法（ART）抑制病毒复制的失败有关，^[1]但是预先存在的低频耐药性对病毒学反应的影响是有争议的。既往研究表明，在开始抗病毒治疗后，已有低频耐药突变的患者，尤其是含非核苷类逆转录酶抑制剂（NNRTIs）的初级ART方案，病毒学应答失败的可能性增加。^[2]然而，一些研究得出了不同的结论，表明预先存在的低频耐药突变与病毒应答失败无关。^[3]这可能与检测预先存在的低频耐药突变的方法有关。

致编辑糖尿病的流行在世界范围内构成了主要的公共健康威胁。在美国，2型糖尿病（T2D）的患病率影响了13.9%的成年人，并且将继续增加。^[1]饮食是T2D的主要生活方式风险因素之一，在过去的20年里，膳食铁引起了人们的极大兴趣。^[2,3]需要注意的是，膳食维生素A、B₂, B₆据报道，叶酸、E、C和叶酸会影响体内铁的吸收或氧化。^[4]然而，这些膳食维生素是否在铁相关的T2D中发挥作用仍不清楚。需要进一步的研究来揭示这些膳食维生素在铁和T2D之间的关系中的整体作用，这将为降低铁相关的T2D的风险提供重要的指导。本研究旨在在国家健康和营养检查调查（NHANES）中检查膳食铁和T2D之间的关系，并评估整体膳食维生素是否影响这种关系。

致编辑：糖尿病并发症的发生率随着糖尿病发病率的增加而增加。糖尿病周围神经病变（DPN）是糖尿病患者最常见的并发症之一。DPN危害很大，是糖尿病足和截肢的重要原因。DPN患者的截肢率比非糖尿病患者高10-20倍。每隔30秒，在世界的某个地方，就会有一名患者的下肢或部分下肢因DPN而被手术截肢。^[1]DPN严重干扰患者的身心健康。同时，高昂的治疗和康复护理费用也给患者造成巨大的经济压力。因此，在早期或超早期识别、诊断和预防DPN尤为重要。

致编辑：高血压是糖尿病和缺血性脑卒中发病和预后的重要危险因素。糖尿病和缺血性中风都是常见的疾病，经常一起发生，高达约34%的急性缺血性中风患者还患有糖尿病。^[1]先前的研究表明，伴有高血糖或糖尿病的卒中患者表现出卒中复发、不良神经结局和死亡率的风险增加。然而，很少有研究探讨缺血性卒中和糖尿病患者的收缩压（SBP）水平或SBP轨迹与临床结局之间的关系。

作者声明，在《可切除食管癌的治疗：从传统全身治疗到免疫治疗》一文中^[1]发表在卷。135，第18期，第2143-2156页中华医学杂志，第一作者阎焱的隶属关系应更正为“上海交通大学医学院附属瑞金医院胸外科，中国上海200025”。作者对由此造成的任何不便深表歉意。