Journal of Internal Medicine最新文献

To the editor,

We recognize the suggestion displayed by Famularo [1] and by Wu et al.[2] and appreciate the editor's opportunity to clarify our evidences. In our cross-sectional paper, we suggested the occurrence of a specific heart impairment in patients with Paget's disease of bone (PDB), namely, Pagetic heart disease, characterized by systo-diastolic dysfunction with higher left ventricular filling pressures, lower ejection fraction, concentric left ventricular remodeling, and a higher prevalence of cardiac valve sclerosis and calcifications.[3] One of the strengths of the study was the strict inclusion and exclusion criteria, which ruled out common cardiovascular diseases.[3]

Dr. Famularo suggested that our findings can be affected by bias, such as other unrecognized cardiac conditions, like transthyretin cardiac amyloidosis (TTA). However, it must be noted that all PDB patients underwent a Tc-99m–methylene diphosphonate (MDP) scintigraphy, both to diagnose and classify the condition.[4] Currently, non-biopsy diagnostic criteria for TTA include Tc-99m–MDP scintigraphy in diagnostic algorithm,[5] because its 100% negative predictive value.[6] Consequently, TTA could be excluded according to negative results in cardiac accumulation of Tc-99m–MDP during scintigraphy.

To further address Dr. Famularo's concerns and support the evidence of a Pagetic heart disease, we conducted an analysis of a small cohort of our patients diagnosed with transthyretin amyloidosis (TTA) and compared their clinical characteristics with PDB patients’ (Table 1), age- and sex-matched. As reported in the position statement of the ESC Working Group on Myocardial and Pericardial Diseases,[7] there are established echocardiographic criteria for non-invasive diagnosis of TTA as unexplained left ventricular thickness (≥12 mm) plus more than two of the following echocardiography findings: Grade 2 or worse diastolic dysfunction; reduced tissue Doppler systolic, early diastolic, and late diastolic wave velocities (<5 cm/s); and decreased global longitudinal left ventricular strain (absolute value < −15%). These features closely resemble those observed in our cohort of patients with TTA, whereas none of our patients with PBD exhibited such characteristics, despite presenting with a specific form of cardiac involvement.

In the second letter, Wu et al. raised some concerns, such as hint for predictive values and cut-off parameters for the Pagetic heart disease to look for in prospective studies; the contradiction in the found significance in the left ventricle ejection fraction but not in the global longitudinal strain in Table 3 [3]; and lastly, the suggestion for evaluation of segmental strain and myocardial work.

We greatly appreciated the first comment, as it gives us the opportunity to introduce the work we are currently con

This review elucidates the critical role of inter-organ crosstalk in systemic health, focusing on the kidney's interactions with the heart, bone marrow, lung, liver, intestine, bone-vascular, and nervous system. These interactions are vital for maintaining physiological homeostasis and are mediated by hormones, cytokines, and metabolites. The kidney's role in these networks is pivotal, as dysfunction can exacerbate systemic diseases, highlighting the need for integrated therapeutic strategies. Chronic kidney disease and acute kidney injury serve as key examples of how kidney dysfunction impacts other organs, leading to complex disease states. The central idea is that the kidney functions within a network of physiological processes, influencing and being influenced by other organs. This review provides an overview of the mechanisms underlying kidney-related inter-organ communication, emphasizing the significance of these interactions in disease progression. We explore how advanced computational models and multi-omics approaches can enhance our understanding of these complex networks, paving the way for precision medicine. The insights derived from this work underscore the potential for future research in developing innovative treatments that target these intricate pathways. By fostering interdisciplinary collaboration and leveraging emerging technologies, we aim to address the multifaceted nature of systemic diseases, offering new avenues for therapeutic intervention. This review represents a paradigm shift from reductionist to integrative approaches, emphasizing the importance of systemic balance and adaptation in human health, and sets the stage for future exploration into the interconnectedness of body systems.

Dear Editor,

We read with enthusiasm the article [1] comparing standard and advanced (speckle-tracking) echocardiographic parameters measured in patients with Paget's disease of bone (PDB) and would like to bring the following comments.

First, Giaquinto et al. present a multicenter case–control study of patients with PDB and normal controls who underwent very detailed echocardiographic analyses. Although the analyses are detailed, these findings are mainly descriptive and do not necessarily guide practice. The authors may need to evaluate the predictive value of outcomes and prognosis independently among the standard and advanced echocardiographic parameters in the populations [2]. The optimal cut-off value for myocardial work and speckle-tracking parameters in receiver operating characteristic curve analysis should also be applied to help come up with predictive parameters [3].

Second, no significant difference was observed in global longitudinal strain, whereas the left ventricle ejection fraction (LVEF) was significantly lower between the groups in Table 3 (p < 0.05). However, left ventricle global longitudinal strain is a more sensitive method than LVEF for diagnosing mild systolic dysfunction, applying to patients suspected of having heart failure with normal LVEF [4], which is inconsistent with the results in the study.

In addition, global longitudinal strain and global work efficiency were significantly lower in patients with PDB than those in controls. In fact, left ventricle was divided into 18 segments for the exploration of the distribution of regional, however, segmental strain and myocardial work were not evaluated, which added value to explore the distribution of myocardial impairment [4, 5].

Huihui Wu and Dong Wang: Conception and design. Huihui Wu and Lihong Wang: Writing of the manuscript. All authors have reviewed and approved the final version of the manuscript.

The authors declare no conflicts of interest.

Yen FS, Hung YM, Huang JY, Hsu CC, Cheng WY, Hwu CM, et al. Effects of SGLT2 inhibitors on transplant survival and key clinical outcomes in heart transplant recipients with diabetes. J Intern Med. 2025;297(5):532-542. https://doi.org/10.1111/joim.20077

In the originally published article, the affiliation for Jing-Yang Huang was incorrectly listed.

The incorrect affiliation was:

“6 Institute of Medicine, Chung Shan Medical University, Taichung City, Taiwan”

The correct affiliations for Jing-Yang Huang are:

“6 Institute of Medicine, Chung Shan Medical University, Taichung, 402, Taiwan; Department of Medical Research, Chung Shan Medical University Hospital, Taichung, 402, Taiwan.”

We apologize for this error.

Although outcomes for newly diagnosed acute myeloid leukaemia (AML) have been incrementally improved over the last decades, management of relapsed and refractory (R/R) AML remains a medical challenge. A curative intent for R/R AML usually involves chemotherapy (with or without targeted therapy) with subsequent consolidation, including allogeneic haematopoietic stem cell transplantation. Despite this, long-term survival rates of R/R AML only reach approximately 10% in adults and 40% in children. Given this great unmet clinical need, this review outlines the current and emerging paradigms for preventing and treating R/R AML. Somatic mutations, gene expression, and functional drug testing are important for the selection of small molecule inhibitors of oncogenic signalling pathways (e.g., FLT3), menin inhibitors that disrupt leukemogenic programmes, inhibitors of isocitrate dehydrogenases to restore oncometabolic homoeostasis, and proapoptotic Bcl-2 homology 3 (BH3) mimetics, such as venetoclax. Targeting the recently identified resistance factor SAMHD1 promises to overcome resistance to cytarabine and fludarabine. Given the growing number of potential combinatorial drug regimens and the genetic heterogeneity of AML, real-time ex vivo drug response profiling to guide individualized treatment decisions will become an important complement. We argue that better outcomes for R/R AML critically depend on being guided by precision oncology to define the best combination of chemotherapy, targeted therapy, and immunological therapy informed by phenotypic and genotypic patient- and disease-specific parameters.