Zhonghua wei zhong bing ji jiu yi xue最新文献

Objective: To identify independent predictors of in-hospital mortality in elderly patients with acute pancreatitis (AP) and to develop and validate a nomogram prediction model.

Methods: A retrospective cohort study was conducted, including patients aged ≥ 60 years admitted to the Affiliated Hospital of Zunyi Medical University with a diagnosis of AP from January 2015 to December 2024. Based on in-hospital outcomes, patients were divided into survival and death groups and were then randomly allocated to a training set and a validation set in a 7 : 3 ratio. Predictors were initially screened using Lasso regression and subsequently entered into multivariate Logistic regression analysis to identify independent risk factors for constructing the nomogram. Model discrimination, calibration, and clinical utility were evaluated using the receiver operator characteristic curve (ROC curve), calibration curve, and decision curve analysis (DCA), respectively.

Results: A total of 2 569 elderly AP patients were enrolled, with 2 323 survivors and 246 deaths in the hospital. The training set contained 1 801 patients (177 deaths, 9.8%), and the validation set contained 768 patients (69 deaths, 9.0%). Lasso regression identified five candidate variables including age, Ranson score, aspartate aminotransferase (AST), acute respiratory distress syndrome (ARDS), and use of vasoactive agents. Multivariate Logistic regression showed that age [odds ratio (OR) = 1.076, 95% confidence interval (95%CI) was 1.054-1.099, P < 0.001], Ranson score (OR = 1.318, 95%CI was 1.215-1.429, P < 0.001), AST (OR = 1.001, 95%CI was 1.000-1.001, P < 0.001), ARDS (OR = 3.782, 95%CI was 2.495-5.732, P < 0.001), and use of vasoactive agents (OR = 4.850, 95%CI was 3.192-7.370, P < 0.001) were independent predictors of in-hospital mortality. The nomogram prediction model was constructed based on the above five factors, ROC curve analysis shows that, the area under the curve (AUC) was 0.817 (95%CI was 0.784-0.851) in the training set and 0.823 (95%CI was 0.775-0.871) in the validation set, indicating good discriminative ability. Calibration plots demonstrated good agreement between predicted and observed probabilities, and DCA showed favorable net clinical benefit across a wide range of threshold probabilities.

Conclusions: The nomogram incorporating five independent predictors-age, Ranson score, AST, ARDS, and use of vasoactive agents-demonstrated good predictive performance for in-hospital mortality among elderly AP patients. This model provides a practical tool for individualized prognostic assessment and for informing clinical decision-making in this population.

The initial management of septic shock necessitates adequate fluid resuscitation to restore tissue perfusion. However, excessive or sustained fluid administration may precipitate fluid accumulation syndrome (FAS), significantly exacerbating the risk of organ dysfunction and mortality. Consequently, proactive prevention and management of FAS are paramount for optimizing patient outcomes. With the continuous optimization of fluid resuscitation strategies in the treatment of septic shock, de-resuscitation, as a key stage for preventing or correcting FAS, provides an important opportunity to improve patient prognosis. Recent studies have shown that during the later phase of septic shock resuscitation, active de-resuscitation combined with hemodynamic monitoring, adjustment of vasoactive drugs and other comprehensive intervention measures can help reduce fluid positive balance, lower the risk of organ dysfunction, shorten the length of intensive care unit (ICU) stay, and improve patient prognosis. Currently, the timing of de-resuscitation, volume assessment methods, the development of individualized treatment protocols, and the prevention and control of related complications have become the focus of research, while the search for reliable biomarkers to guide de-resuscitation strategies will become a future hot direction. In this article, we review the pathophysiology and clinical diagnosis of FAS, as well as the clinical strategies, controversies and challenges of de-resuscitation in septic shock, and explore the future research directions of de-resuscitation strategies, with the aim of providing theoretical basis and practical guidance for optimizing fluid management in patients with septic shock.

The persistent spread of multidrug-resistant bacteria (MDR) infections has become a major challenge in global public health, severely limiting treatment options with traditional antimicrobial drugs and leading to a significant increase in patient mortality. Antimicrobial peptides, as small-molecule effectors within the innate immune system, demonstrate significant potential in combating MDR infections due to their unique membrane-disrupting mechanisms, broad-spectrum antimicrobial activity, and low propensity to induce resistance. However, the monotherapy of antimicrobial peptides still faces challenges such as poor stability, rapid degradation in vivo, and potential resistance risks. To overcome these limitations, recent research has increasingly focused on combination strategies for antimicrobial peptides. By synergistically combining antimicrobial peptides with traditional antibiotics, other antimicrobial peptides, nanomaterials, or phage lysins, these approaches aim to enhance bactericidal effects and delay the development of resistance. This systematic review summarizes the latest research advances in antimicrobial peptides combination therapy for infection control, emphasizing synergistic mechanisms. Current challenges and future directions are discussed to provide a theoretical foundation and practical insights for developing novel anti-infective treatment regimens.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection, characterized by high morbidity and mortality. Acute lung injury (ALI) is one of the earliest and most frequent complications of sepsis. Inflammatory response, oxidative stress, and ferroptosis are important pathogenic mechanisms in sepsis-induced ALI. Nuclear factor E2-related factor 2 (Nrf2), an essential antioxidant transcription factor, plays a pivotal role in alleviating lung injury by regulating multiple signaling pathways. This review systematically elaborates on the structure of Nrf2 and its protective role in sepsis-induced ALI, with a focus on how the Nrf2/heme oxygenase-1 (HO-1), Kelch-like ECH-associated protein 1 (Keap1)/Nrf2, silent information regulator 1 (Sirt1)/Nrf2, and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/Nrf2 pathways collaboratively alleviate oxidative stress, suppress the release of inflammatory factors, and inhibit ferroptosis by regulating downstream target genes such as HO-1, glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11). Furthermore, the article summarizes the lung-protective effects demonstrated by various agents, including β-globin, curcumin, and hyperoside, through the specific activation of these pathways, providing a solid experimental basis for optimizing related treatment strategies and developing new drugs. This review aims to offer a deeper understanding of the biological significance of Nrf2 in sepsis-induced ALI and to provide theoretical support and research insights for future targeted clinical therapies.

Sepsis-associated acute kidney injury (SAKI) is a life-threatening complication of sepsis, whose pathogenesis involves the intricate interplay of multiple factors, including dysregulated host immune-inflammatory responses, microcirculatory disturbances, and metabolic dysfunction. Aberrations in epigenetic modifications, including DNA methylation and histone acetylation, dynamically modulate gene expression networks, thereby influencing cellular metabolic reprogramming, activation of pro-inflammatory signaling pathways, and disruption of microvascular barrier integrity, are closely associated with adverse clinical outcomes in SAKI patients. As a central regulatory hub of gene expression, epigenetic modifications profoundly participate in key pathological processes of SAKI, including immune homeostasis imbalance, metabolic dysregulation, and microcirculatory dysfunction, through remodeling chromatin architecture and non-coding RNA expression profiles. Although emerging evidence suggests that targeting epigenetic regulation may mitigate SAKI-related pathological damage, the precise molecular mechanisms remain incompletely elucidated. This review systematically summarizes the regulatory roles and molecular mechanisms of epigenetic modifications in SAKI, aiming to provide a theoretical foundation for advancing the understanding of SAKI pathogenesis and developing novel therapeutic strategies.