Background: The global COVID-19 pandemic was initiated by the appearance of the novel coronavirus SARS-CoV-2 in 2019, presenting a spectrum of clinical manifestations from asymptomatic cases to severe pneumonia and multi-organ dysfunction, with some cases leading to death induced by hyperinflammatory responses. Neurological manifestations have been reported in more than one-third of COVID-19 patients, particularly in severe instances. While vaccines are pivotal in combating infectious diseases and enhancing public health, reports have linked Guillain-Barré syndrome (GBS) to COVID-19 vaccination and infection. This study seeks to analyze four cases of GBS associated with COVID-19.
Methods: Clinical and demographic data were collected from all patients diagnosed with GBS from a biobank, including patients with severe COVID-19 and those with autoimmune conditions resulting from COVID-19 infection or vaccination, who were referred to Alzahra University Hospital in Isfahan, Iran, between October 2020 and December. 2023.
Results: Clinical and demographic data of affected patients are presented. This includes a unique family case involving a daughter who passed away due to GBS following AstraZeneca vaccination, her mother who succumbed to post-COVID-19 GBS, and her father who passed away from severe COVID-19 a year earlier.
Conclusions: These cases provide valuable insights into investigating potential genetic or epigenetic influences on GBS and hyperinflammation. Furthermore, the occurrence of GBS following exposure to COVID-19 and vaccination suggests shared pathways of autoimmunity induction by SARS-CoV-2 and vaccines.
{"title":"Guillain-Barré syndrome (GBS) after severe/critical COVID-19 or COVID-19 vaccination.","authors":"Samira Bahrami, Behnaz Ansari, Leyla Norouzi-Barough, Bahram Bagherpour, Farzin Khorvash, Kiana Shirani, Saeed Abbasi, Roya Sherkat","doi":"10.1186/s40001-025-02378-w","DOIUrl":"10.1186/s40001-025-02378-w","url":null,"abstract":"<p><strong>Background: </strong>The global COVID-19 pandemic was initiated by the appearance of the novel coronavirus SARS-CoV-2 in 2019, presenting a spectrum of clinical manifestations from asymptomatic cases to severe pneumonia and multi-organ dysfunction, with some cases leading to death induced by hyperinflammatory responses. Neurological manifestations have been reported in more than one-third of COVID-19 patients, particularly in severe instances. While vaccines are pivotal in combating infectious diseases and enhancing public health, reports have linked Guillain-Barré syndrome (GBS) to COVID-19 vaccination and infection. This study seeks to analyze four cases of GBS associated with COVID-19.</p><p><strong>Methods: </strong>Clinical and demographic data were collected from all patients diagnosed with GBS from a biobank, including patients with severe COVID-19 and those with autoimmune conditions resulting from COVID-19 infection or vaccination, who were referred to Alzahra University Hospital in Isfahan, Iran, between October 2020 and December. 2023.</p><p><strong>Results: </strong>Clinical and demographic data of affected patients are presented. This includes a unique family case involving a daughter who passed away due to GBS following AstraZeneca vaccination, her mother who succumbed to post-COVID-19 GBS, and her father who passed away from severe COVID-19 a year earlier.</p><p><strong>Conclusions: </strong>These cases provide valuable insights into investigating potential genetic or epigenetic influences on GBS and hyperinflammation. Furthermore, the occurrence of GBS following exposure to COVID-19 and vaccination suggests shared pathways of autoimmunity induction by SARS-CoV-2 and vaccines.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"131"},"PeriodicalIF":2.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate the relationship between the geriatric nutritional risk index (GNRI) and sepsis in elderly critically ill patients.
Methods: We extracted data from the MIMIC-IV database for patients aged 65 and older who were first-time admissions to the Intensive Care Unit. The GNRI, derived from serum albumin, height, and weight, served as the exposure variable. The main outcome was the occurrence of sepsis. We utilized multivariable logistic regression to evaluate the association between GNRI and sepsis. Additionally, we employed restricted cubic splines to evaluate the potential nonlinear relationship between GNRI and the incidence of sepsis.
Results: The study included 3,535 elderly patients, with 2,005 (56.7%) developing sepsis. Septic patients had significantly lower GNRI values (median: 99 vs. 101, P = 0.021) and a higher prevalence of malnutrition risk (GNRI ≤ 98) (47.5% vs. 43.5%, P = 0.018). The analysis employing restricted cubic splines identified a U-shaped association between GNRI and sepsis (P for non-linearity = 0.004), with an inflection point at 105.4. To the left of this inflection point, GNRI was significantly negatively associated with sepsis (OR = 0.987, 95% CI 0.978-0.996, P = 0.005), while the right side showed a positive correlation (OR = 1.011, 95% CI 1.000-1.022, P = 0.044).
Conclusion: The study reveals a U-shaped association between GNRI and sepsis in elderly critically ill patients. Both low and high GNRI values are associated with increased sepsis risk, with a turning point at 105.4. These findings highlight GNRI's utility as a screening tool for identifying sepsis risk in elderly ICU patients.
{"title":"Relationship between the geriatric nutritional risk index and sepsis in elderly critically ill patients: a retrospective cohort study.","authors":"Yujiao Jin, Tianyun Zhou, Chenshu Hou, Huihui Zhang, Binbin Xu","doi":"10.1186/s40001-025-02389-7","DOIUrl":"10.1186/s40001-025-02389-7","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the relationship between the geriatric nutritional risk index (GNRI) and sepsis in elderly critically ill patients.</p><p><strong>Methods: </strong>We extracted data from the MIMIC-IV database for patients aged 65 and older who were first-time admissions to the Intensive Care Unit. The GNRI, derived from serum albumin, height, and weight, served as the exposure variable. The main outcome was the occurrence of sepsis. We utilized multivariable logistic regression to evaluate the association between GNRI and sepsis. Additionally, we employed restricted cubic splines to evaluate the potential nonlinear relationship between GNRI and the incidence of sepsis.</p><p><strong>Results: </strong>The study included 3,535 elderly patients, with 2,005 (56.7%) developing sepsis. Septic patients had significantly lower GNRI values (median: 99 vs. 101, P = 0.021) and a higher prevalence of malnutrition risk (GNRI ≤ 98) (47.5% vs. 43.5%, P = 0.018). The analysis employing restricted cubic splines identified a U-shaped association between GNRI and sepsis (P for non-linearity = 0.004), with an inflection point at 105.4. To the left of this inflection point, GNRI was significantly negatively associated with sepsis (OR = 0.987, 95% CI 0.978-0.996, P = 0.005), while the right side showed a positive correlation (OR = 1.011, 95% CI 1.000-1.022, P = 0.044).</p><p><strong>Conclusion: </strong>The study reveals a U-shaped association between GNRI and sepsis in elderly critically ill patients. Both low and high GNRI values are associated with increased sepsis risk, with a turning point at 105.4. These findings highlight GNRI's utility as a screening tool for identifying sepsis risk in elderly ICU patients.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"130"},"PeriodicalIF":2.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-24DOI: 10.1186/s40001-025-02367-z
Yang Xiao, Ran Guo, Haitao Yang, Xiaoyong Geng
Background: Lower extremity deep venous thrombosis (LEDVT) is a serious and potentially fatal complication with a high incidence following liver transplantation, significantly affecting patient prognosis. This study aimed to investigate the characteristics and risk factors associated with LEDVT post-transplantation and to develop an effective clinical prediction model.
Methods: A retrospective analysis was conducted on 298 liver transplant recipients at Hebei Medical University Third Hospital between January 2021 and April 2024. The cohort was randomly divided into a training set and a validation set in a 7:3 ratio. Baseline variables, including demographics, smoking history, comorbidities, surgical data, and biochemical indicators at admission, were collected. The training set data were used to construct the predictive model. Relevant predictors were identified using non-parametric rank-sum tests, chi-square tests, and least absolute shrinkage and selection operator (LASSO) regression. A multivariate logistic regression model was then developed to optimize these predictors and generate a nomogram. Model performance was assessed through receiver operating characteristic (ROC) analysis, calibration curve analysis, and decision curve analysis (DCA). Validation of the model was conducted using the independent validation set.
Results: LEDVT occurred in 28 (13.5%) of the 208 patients in the training cohort. LASSO regression identified smoking history, hyperlipidemia, intraoperative blood loss, and elevated D-dimer levels as independent predictors of LEDVT after liver transplantation. A nomogram was constructed based on these predictors, with risk scores assigned to each variable (as depicted in Fig. 3). Higher total scores were associated with an increased likelihood of LEDVT. The predictive model demonstrated satisfactory discrimination and calibration, with an area under the ROC curve (AUC) indicating good predictive accuracy. The calibration plot, Hosmer-Lemeshow test, and DCA further confirmed the model's clinical utility.
Conclusions: The developed prediction model exhibited excellent performance in identifying patients at high risk for LEDVT following liver transplantation. Early identification of at-risk individuals allows for timely intervention, potentially reducing LEDVT incidence and improving patient outcomes. Furthermore, this model has significant implications for reducing healthcare costs and optimizing resource allocation.
{"title":"Analysis of risk factors and construction of prediction model for lower extremity deep vein thrombosis after liver transplantation.","authors":"Yang Xiao, Ran Guo, Haitao Yang, Xiaoyong Geng","doi":"10.1186/s40001-025-02367-z","DOIUrl":"10.1186/s40001-025-02367-z","url":null,"abstract":"<p><strong>Background: </strong>Lower extremity deep venous thrombosis (LEDVT) is a serious and potentially fatal complication with a high incidence following liver transplantation, significantly affecting patient prognosis. This study aimed to investigate the characteristics and risk factors associated with LEDVT post-transplantation and to develop an effective clinical prediction model.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on 298 liver transplant recipients at Hebei Medical University Third Hospital between January 2021 and April 2024. The cohort was randomly divided into a training set and a validation set in a 7:3 ratio. Baseline variables, including demographics, smoking history, comorbidities, surgical data, and biochemical indicators at admission, were collected. The training set data were used to construct the predictive model. Relevant predictors were identified using non-parametric rank-sum tests, chi-square tests, and least absolute shrinkage and selection operator (LASSO) regression. A multivariate logistic regression model was then developed to optimize these predictors and generate a nomogram. Model performance was assessed through receiver operating characteristic (ROC) analysis, calibration curve analysis, and decision curve analysis (DCA). Validation of the model was conducted using the independent validation set.</p><p><strong>Results: </strong>LEDVT occurred in 28 (13.5%) of the 208 patients in the training cohort. LASSO regression identified smoking history, hyperlipidemia, intraoperative blood loss, and elevated D-dimer levels as independent predictors of LEDVT after liver transplantation. A nomogram was constructed based on these predictors, with risk scores assigned to each variable (as depicted in Fig. 3). Higher total scores were associated with an increased likelihood of LEDVT. The predictive model demonstrated satisfactory discrimination and calibration, with an area under the ROC curve (AUC) indicating good predictive accuracy. The calibration plot, Hosmer-Lemeshow test, and DCA further confirmed the model's clinical utility.</p><p><strong>Conclusions: </strong>The developed prediction model exhibited excellent performance in identifying patients at high risk for LEDVT following liver transplantation. Early identification of at-risk individuals allows for timely intervention, potentially reducing LEDVT incidence and improving patient outcomes. Furthermore, this model has significant implications for reducing healthcare costs and optimizing resource allocation.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"127"},"PeriodicalIF":2.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-24DOI: 10.1186/s40001-025-02377-x
Shujuan Hu, Xuan Liu, Yiting Ding, Jun Chen, Xianwang Wang
Carboxylesterase 1 (CES1) and inflammatory factors play important roles in regulating lipid metabolism and maintaining glucose homeostasis. Exercise and walnut oil have anti-inflammatory effects, but the effects of exercise and walnut oil on CES1 and inflammatory factors in type 2 diabetes mellitus (T2DM) remain to be revealed. 8-week-old SD male rats were randomly divided into normal control group (NC group, N = 12) and high fat group (HFD group, N = 28) after 1 week of adaptive feeding. HFD rat models were established by high-fat diet and one-time injection of streptozocin. The successfully constructed rats were randomly divided into diabetes control group (T2DM-NC group, N = 6), the diabetes plus moderate intensity exercise group (T2DM-MED group, N = 6), the diabetes plus high intensity intermittent exercise group (T2DM-HIIT group, N = 6), and the diabetes plus walnut oil group (T2DM-WO group, N = 6). After 6 weeks of intervention, ELISAs were used to determine the blood glucose and lipid-related indices of the rats. Histomorphologic changes in the liver were observed by hematoxylin‒eosin staining. The mRNA expression levels of CES1 and inflammatory cytokines were determined by real-time quantitative PCR. The protein expression levels of CES1 and inflammatory factors were determined by immunofluorescence staining. Compared with those in the NC group, in the T2DM-NC group, FBG, TG, LDL-C and HOMA-IR were increased (P < 0.01), FINS activity was decreased (P < 0.01), liver morphology was more disorganized, and CES1 and inflammatory cytokines were highly expressed in the liver tissue (P < 0.05 or P < 0.01). After 6 weeks of intervention, TG levels were significantly decreased (P < 0.05 or P < 0.01), whereas FINS levels were increased (P < 0.05 or P < 0.01), liver morphology was significantly ameliorated, and the CES1, TXNIP and IL-1β expression levels were decreased (P < 0.05 or P < 0.01) in the T2DM-MED, T2DM-HIIT and T2DM-WO groups when compared with those in the T2DM-NC group. The T2DM rats presented abnormal blood glucose and lipid levels, and CES1, TXNIP and IL-1β were highly expressed in the liver. Exercise and walnut oil intervention ameliorated the glycolipid metabolism and liver morphology, and reduce the expression of CES1, TXNIP and IL-1β in the liver.
{"title":"Effects of exercise and walnut oil on CES1 and inflammatory factors in the liver of type 2 diabetic rats.","authors":"Shujuan Hu, Xuan Liu, Yiting Ding, Jun Chen, Xianwang Wang","doi":"10.1186/s40001-025-02377-x","DOIUrl":"10.1186/s40001-025-02377-x","url":null,"abstract":"<p><p>Carboxylesterase 1 (CES1) and inflammatory factors play important roles in regulating lipid metabolism and maintaining glucose homeostasis. Exercise and walnut oil have anti-inflammatory effects, but the effects of exercise and walnut oil on CES1 and inflammatory factors in type 2 diabetes mellitus (T2DM) remain to be revealed. 8-week-old SD male rats were randomly divided into normal control group (NC group, N = 12) and high fat group (HFD group, N = 28) after 1 week of adaptive feeding. HFD rat models were established by high-fat diet and one-time injection of streptozocin. The successfully constructed rats were randomly divided into diabetes control group (T2DM-NC group, N = 6), the diabetes plus moderate intensity exercise group (T2DM-MED group, N = 6), the diabetes plus high intensity intermittent exercise group (T2DM-HIIT group, N = 6), and the diabetes plus walnut oil group (T2DM-WO group, N = 6). After 6 weeks of intervention, ELISAs were used to determine the blood glucose and lipid-related indices of the rats. Histomorphologic changes in the liver were observed by hematoxylin‒eosin staining. The mRNA expression levels of CES1 and inflammatory cytokines were determined by real-time quantitative PCR. The protein expression levels of CES1 and inflammatory factors were determined by immunofluorescence staining. Compared with those in the NC group, in the T2DM-NC group, FBG, TG, LDL-C and HOMA-IR were increased (P < 0.01), FINS activity was decreased (P < 0.01), liver morphology was more disorganized, and CES1 and inflammatory cytokines were highly expressed in the liver tissue (P < 0.05 or P < 0.01). After 6 weeks of intervention, TG levels were significantly decreased (P < 0.05 or P < 0.01), whereas FINS levels were increased (P < 0.05 or P < 0.01), liver morphology was significantly ameliorated, and the CES1, TXNIP and IL-1β expression levels were decreased (P < 0.05 or P < 0.01) in the T2DM-MED, T2DM-HIIT and T2DM-WO groups when compared with those in the T2DM-NC group. The T2DM rats presented abnormal blood glucose and lipid levels, and CES1, TXNIP and IL-1β were highly expressed in the liver. Exercise and walnut oil intervention ameliorated the glycolipid metabolism and liver morphology, and reduce the expression of CES1, TXNIP and IL-1β in the liver.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"128"},"PeriodicalIF":2.8,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143491357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-22DOI: 10.1186/s40001-025-02387-9
Yangjuan Jia, Ning Han, Hui Guo, Hongling Li, Yunlei Du, Cancan Li, Jianguo Li
Objective: This study aimed to evaluate the effects of coma on the prognosis and delayed encephalopathy in patients with acute carbon monoxide poisoning (DEACMP) and to analyze the predictive factors affecting the prognosis of these patients.
Methods: Patients with acute carbon monoxide poisoning were divided into comatose and non-comatose groups. The primary outcomes included clinical cure and the occurrence of DEACMP. Multivariate logistic regression analysis was performed to identify independent predictors of clinical outcome.
Results: Multivariate analysis indicated that coma (clinical cure: adjusted odds ratio [aOR] 0.24, 95% CI 0.12-0.47; DEACMP: aOR 42.5, 95% CI 7.99-789), longer the time from onset to the first HBOT (clinical cure: aOR 0.43, 95% CI 0.24-0.77; DEACMP: aOR 3.21, 95% CI 1.56-6.78) and abnormal chest CT findings (clinical cure: aOR 0.23, 95% CI 0.12-0.45; DEACMP: aOR 5.36, 95% CI 2.41-12.60) were associated with a lower rate of clinical cure and a higher proportion of DEACMP; and lower age was an independent predictor of clinical cure (aOR 0.96, 95% CI 0.94-0.98), but not of DEACMP (aOR 0.99, 95% CI 0.96-1.01). In comatose patients, both the duration of coma and abnormal chest CT findings were an independent factor for clinial cure (aOR 0.96, 95% CI 0.93-0.99; aOR 0.34, 95% CI 0.15-0.74) and DEACMP (aOR 1.09, 95% CI 1.06-1.14; aOR 4.93, 95% CI 1.67-16.30).
Conclusion: Coma and the duration of coma were significant predictors of clinical cure and DEACMP in patients; the older the patient, the longer the duration of coma, and the longer the time from onset to the first hyperbaric oxygen therapy (> 6 h), indicating that the patient's prognosis is often worse; abnormal chest CT manifestations were also an independent risk factor for a poor patient's prognosis.
{"title":"Hyperbaric oxygen therapy for acute carbon monoxide poisoning patients with coma onset.","authors":"Yangjuan Jia, Ning Han, Hui Guo, Hongling Li, Yunlei Du, Cancan Li, Jianguo Li","doi":"10.1186/s40001-025-02387-9","DOIUrl":"10.1186/s40001-025-02387-9","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the effects of coma on the prognosis and delayed encephalopathy in patients with acute carbon monoxide poisoning (DEACMP) and to analyze the predictive factors affecting the prognosis of these patients.</p><p><strong>Methods: </strong>Patients with acute carbon monoxide poisoning were divided into comatose and non-comatose groups. The primary outcomes included clinical cure and the occurrence of DEACMP. Multivariate logistic regression analysis was performed to identify independent predictors of clinical outcome.</p><p><strong>Results: </strong>Multivariate analysis indicated that coma (clinical cure: adjusted odds ratio [aOR] 0.24, 95% CI 0.12-0.47; DEACMP: aOR 42.5, 95% CI 7.99-789), longer the time from onset to the first HBOT (clinical cure: aOR 0.43, 95% CI 0.24-0.77; DEACMP: aOR 3.21, 95% CI 1.56-6.78) and abnormal chest CT findings (clinical cure: aOR 0.23, 95% CI 0.12-0.45; DEACMP: aOR 5.36, 95% CI 2.41-12.60) were associated with a lower rate of clinical cure and a higher proportion of DEACMP; and lower age was an independent predictor of clinical cure (aOR 0.96, 95% CI 0.94-0.98), but not of DEACMP (aOR 0.99, 95% CI 0.96-1.01). In comatose patients, both the duration of coma and abnormal chest CT findings were an independent factor for clinial cure (aOR 0.96, 95% CI 0.93-0.99; aOR 0.34, 95% CI 0.15-0.74) and DEACMP (aOR 1.09, 95% CI 1.06-1.14; aOR 4.93, 95% CI 1.67-16.30).</p><p><strong>Conclusion: </strong>Coma and the duration of coma were significant predictors of clinical cure and DEACMP in patients; the older the patient, the longer the duration of coma, and the longer the time from onset to the first hyperbaric oxygen therapy (> 6 h), indicating that the patient's prognosis is often worse; abnormal chest CT manifestations were also an independent risk factor for a poor patient's prognosis.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"125"},"PeriodicalIF":2.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11847349/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-22DOI: 10.1186/s40001-025-02340-w
Shiyong Xu, Yirou Cai, Haizhen Hu, Changlin Zhai
Background: Visceral adiposity index (VAI) and diets are associated with the risk of cardiovascular disease (CVD). It is unclear how well VAI and diet predict CVD.
Methods: Data were obtained from the National Health and Nutrition Examination Survey (NHANES 2017-2018). Demographic data, diets, biochemical examination, and questionnaire information were collected. VAI was calculated using body mass index, waist circumference, triglycerides, and high-density lipoprotein cholesterol. Binary logistic regression was adopted to examine the correlation of VAI and diets with CVD. A decision tree model was developed to predict CVD risk according to different factors.
Results: 2104 participants (mean age: 50.87 ± 17.35 years, 48.38% males) were included. Participants with high levels of VAI (≥ 2.18) had an elevated risk of CVD compared to those with low levels of VAI (≤ 0.76) (OR = 1.654, 95% CI: 1.025-2.669, P = 0.039). Compared with the low protein intake level (≤ 50.34 g), the upper intermediate (72.10-99.92 g) (OR = 0.445, 95% CI: 0.257-0.770, P = 0.004) and high (≥ 99.93 g) levels of protein intake (OR = 0.450, 95% CI: 0.236-0.858, P = 0.015) reduced CVD risk. The decision tree model unveiled that VAI, protein intake, and dietary fiber intake were predictors for CVD.
Conclusion: VAI and protein intake levels are independently associated with CVD risk and have predictive power for CVD. These findings can provide insights into the development of appropriate lifestyle and treatment strategies for patients to reduce the incidence of CVD.
{"title":"Correlation of visceral adiposity index and dietary profile with cardiovascular disease based on decision tree modeling: a cross-sectional study of NHANES.","authors":"Shiyong Xu, Yirou Cai, Haizhen Hu, Changlin Zhai","doi":"10.1186/s40001-025-02340-w","DOIUrl":"10.1186/s40001-025-02340-w","url":null,"abstract":"<p><strong>Background: </strong>Visceral adiposity index (VAI) and diets are associated with the risk of cardiovascular disease (CVD). It is unclear how well VAI and diet predict CVD.</p><p><strong>Methods: </strong>Data were obtained from the National Health and Nutrition Examination Survey (NHANES 2017-2018). Demographic data, diets, biochemical examination, and questionnaire information were collected. VAI was calculated using body mass index, waist circumference, triglycerides, and high-density lipoprotein cholesterol. Binary logistic regression was adopted to examine the correlation of VAI and diets with CVD. A decision tree model was developed to predict CVD risk according to different factors.</p><p><strong>Results: </strong>2104 participants (mean age: 50.87 ± 17.35 years, 48.38% males) were included. Participants with high levels of VAI (≥ 2.18) had an elevated risk of CVD compared to those with low levels of VAI (≤ 0.76) (OR = 1.654, 95% CI: 1.025-2.669, P = 0.039). Compared with the low protein intake level (≤ 50.34 g), the upper intermediate (72.10-99.92 g) (OR = 0.445, 95% CI: 0.257-0.770, P = 0.004) and high (≥ 99.93 g) levels of protein intake (OR = 0.450, 95% CI: 0.236-0.858, P = 0.015) reduced CVD risk. The decision tree model unveiled that VAI, protein intake, and dietary fiber intake were predictors for CVD.</p><p><strong>Conclusion: </strong>VAI and protein intake levels are independently associated with CVD risk and have predictive power for CVD. These findings can provide insights into the development of appropriate lifestyle and treatment strategies for patients to reduce the incidence of CVD.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"123"},"PeriodicalIF":2.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11847326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The association between periodontitis (PT) and rheumatoid arthritis (RA) is well-established; however, the molecular mechanisms underlying this relationship remain poorly understood. This study aims to delineate shared genetic and molecular features between PT and RA to uncover potential common pathways involved in their pathogenesis.
Methods: Gene expression data sets for PT and RA were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and co-expressed gene modules were identified using weighted gene co-expression network analysis (WGCNA) and the DESeq2 package. Enrichment analyses, including KEGG and Gene Ontology (GO) pathways, as well as immune cell infiltration profiling, were performed to explore shared biological pathways. A protein-protein interaction (PPI) network was constructed to pinpoint key genes linking PT and RA. Functional assays were conducted by overexpressing the identified core gene, PTPRC, in MH7A cells via lentiviral transfection, followed by cell viability (CCK-8), migration, and invasion assays. In addition, transcription factor enrichment and connectivity map (cMAP) analyses were employed to identify common transcriptional regulators and potential therapeutic targets for both conditions.
Results: WGCNA and DESeq2 analyses revealed 154 shared DEGs between PT and RA, predominantly enriched in immune and inflammatory response pathways. PTPRC emerged as a pivotal shared gene, exhibiting significantly higher expression in PT patients compared to controls. In vitro assays confirmed that PTPRC overexpression enhanced fibroblast proliferation, migration, and invasion. Furthermore, transcription factor enrichment analysis and cMAP identified overlapping transcriptional regulators and potential pharmacological agents for both diseases.
Conclusions: This study provides novel insights into shared gene expression profiles and molecular mechanisms linking PT and RA, identifying PTPRC as a potential key regulator. These findings suggest that targeting PTPRC could offer therapeutic opportunities for RA driven by PT.
{"title":"Immunological landscape of periodontitis and rheumatoid arthritis and their molecular crosstalk.","authors":"Weimin Zhao, Chenxu Liu, Xiangzhi Cui, Qianjiang Chen","doi":"10.1186/s40001-025-02376-y","DOIUrl":"10.1186/s40001-025-02376-y","url":null,"abstract":"<p><strong>Background: </strong>The association between periodontitis (PT) and rheumatoid arthritis (RA) is well-established; however, the molecular mechanisms underlying this relationship remain poorly understood. This study aims to delineate shared genetic and molecular features between PT and RA to uncover potential common pathways involved in their pathogenesis.</p><p><strong>Methods: </strong>Gene expression data sets for PT and RA were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) and co-expressed gene modules were identified using weighted gene co-expression network analysis (WGCNA) and the DESeq2 package. Enrichment analyses, including KEGG and Gene Ontology (GO) pathways, as well as immune cell infiltration profiling, were performed to explore shared biological pathways. A protein-protein interaction (PPI) network was constructed to pinpoint key genes linking PT and RA. Functional assays were conducted by overexpressing the identified core gene, PTPRC, in MH7A cells via lentiviral transfection, followed by cell viability (CCK-8), migration, and invasion assays. In addition, transcription factor enrichment and connectivity map (cMAP) analyses were employed to identify common transcriptional regulators and potential therapeutic targets for both conditions.</p><p><strong>Results: </strong>WGCNA and DESeq2 analyses revealed 154 shared DEGs between PT and RA, predominantly enriched in immune and inflammatory response pathways. PTPRC emerged as a pivotal shared gene, exhibiting significantly higher expression in PT patients compared to controls. In vitro assays confirmed that PTPRC overexpression enhanced fibroblast proliferation, migration, and invasion. Furthermore, transcription factor enrichment analysis and cMAP identified overlapping transcriptional regulators and potential pharmacological agents for both diseases.</p><p><strong>Conclusions: </strong>This study provides novel insights into shared gene expression profiles and molecular mechanisms linking PT and RA, identifying PTPRC as a potential key regulator. These findings suggest that targeting PTPRC could offer therapeutic opportunities for RA driven by PT.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"124"},"PeriodicalIF":2.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11847375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aim: This study compared the effects of hypoglycaemic drugs on beta-cell function among type 2 diabetes mellitus (T2DM) patients through a network meta-analysis of randomized controlled trials (RCTs).
Methods: We searched the PubMed, EMBASE, and Cochrane Library databases for RCTs of different hypoglycaemic drugs as T2DM treatment from database inception to December 1, 2024. The primary outcome was homeostasis model assessment-β (HOMA-β), and the secondary outcome was glycated haemoglobin (HbA1c). Direct and indirect evidence types were combined to calculate weighted mean difference (WMD) and 95% confidence interval (CI) values for the change in (△) HOMA-β and △HbA1c, and to determine surface under the cumulative ranking curve (SUCRA) values.
Results: A total of 58 RCTs involving 16,345 T2DM patients were incorporated into this network meta-analysis. The mean patient age was 66.70 years, and 54.14% were male. For improving HOMA-β, the top treatments were glimepiride + rosiglitazone (WMD = 81.83, 95% CI 45.85-117.82) and glibenclamide + rosiglitazone (WMD = 79.51, 95% CI 40.66-118.36). Acarbose (WMD = 60.90, 95% CI 27.56-94.25) ranked third as monotherapy. For reducing HbA1c, glibenclamide + rosiglitazone was the most efficacious treatment (WMD = - 2.48, 95% CI - 3.67 to - 1.29), followed by metformin + exenatide (WMD = - 1.77, 95% CI - 2.25 to - 1.29) and liraglutide (WMD = - 1.77, 95% CI - 2.33 to - 1.21). The treatment with the highest SUCRA value for HOMA-β improvement was glimepiride + rosiglitazone (95.1%), followed by glibenclamide + rosiglitazone (94.9%). For HbA1c improvement, glibenclamide + rosiglitazone had the highest SUCRA value (97.6%).
Conclusions: The combination of glimepiride/glibenclamide and rosiglitazone was the most effective hypoglycaemic regimen for protecting beta-cell function and improving glycaemic control in T2DM treatment, possibly due to control of HbA1c and glycotoxicity.
{"title":"Effects of different hypoglycaemic drugs on beta-cell function in type 2 diabetes mellitus: a systematic review and network meta-analysis.","authors":"ZhiFeng Guo, LingHong Huang, ZhengRong Jiang, XueFeng Bai, ZiTong Wang, HuiBin Huang","doi":"10.1186/s40001-025-02368-y","DOIUrl":"10.1186/s40001-025-02368-y","url":null,"abstract":"<p><strong>Aim: </strong>This study compared the effects of hypoglycaemic drugs on beta-cell function among type 2 diabetes mellitus (T2DM) patients through a network meta-analysis of randomized controlled trials (RCTs).</p><p><strong>Methods: </strong>We searched the PubMed, EMBASE, and Cochrane Library databases for RCTs of different hypoglycaemic drugs as T2DM treatment from database inception to December 1, 2024. The primary outcome was homeostasis model assessment-β (HOMA-β), and the secondary outcome was glycated haemoglobin (HbA1c). Direct and indirect evidence types were combined to calculate weighted mean difference (WMD) and 95% confidence interval (CI) values for the change in (△) HOMA-β and △HbA1c, and to determine surface under the cumulative ranking curve (SUCRA) values.</p><p><strong>Results: </strong>A total of 58 RCTs involving 16,345 T2DM patients were incorporated into this network meta-analysis. The mean patient age was 66.70 years, and 54.14% were male. For improving HOMA-β, the top treatments were glimepiride + rosiglitazone (WMD = 81.83, 95% CI 45.85-117.82) and glibenclamide + rosiglitazone (WMD = 79.51, 95% CI 40.66-118.36). Acarbose (WMD = 60.90, 95% CI 27.56-94.25) ranked third as monotherapy. For reducing HbA1c, glibenclamide + rosiglitazone was the most efficacious treatment (WMD = - 2.48, 95% CI - 3.67 to - 1.29), followed by metformin + exenatide (WMD = - 1.77, 95% CI - 2.25 to - 1.29) and liraglutide (WMD = - 1.77, 95% CI - 2.33 to - 1.21). The treatment with the highest SUCRA value for HOMA-β improvement was glimepiride + rosiglitazone (95.1%), followed by glibenclamide + rosiglitazone (94.9%). For HbA1c improvement, glibenclamide + rosiglitazone had the highest SUCRA value (97.6%).</p><p><strong>Conclusions: </strong>The combination of glimepiride/glibenclamide and rosiglitazone was the most effective hypoglycaemic regimen for protecting beta-cell function and improving glycaemic control in T2DM treatment, possibly due to control of HbA1c and glycotoxicity.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"121"},"PeriodicalIF":2.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: To compare the POD rates in patients undergoing non-cardiac surgery who received remimazolam perioperatively versus placebo or other sedatives.
Methods: We systematically searched four major databases (Cochrane Central Register of Controlled Trials, Web of Science, Embase, and PubMed) for relevant randomized controlled trials (RCTs) up to July 11, 2024. Literature quality evaluation was used the bias risk table in Review Manager 5.4. The primary outcome of interest was POD, and secondary outcomes were the hypotension risk, bradycardia and, nausea and vomiting.
Results: Across 11 trials involving 1985 participants, we recorded 309 cases of POD during follow-up. In trials where the control group received saline, remimazolam decrease the risk of POD significantly by 70% (RR 0.30, 95% CI [0.19, 0.46]; p < 0.00001). Statistical analysis did not show significant difference in the risk of POD between the remimazolam group and the groups receiving either dexmedetomidine (RR 1.23 [0.64, 2.37]; p = 0.53) or propofol (RR 0.83 [0.60, 1.16]; p = 0.28). Regarding adverse events, remimazolam significantly reduces the morbidity of hypotension compared to dexmedetomidine (RR 0.25 [0.10, 0.65]; p = 0.004) and propofol (RR 0.45 [0.33, 0.60]; p < 0.00001). In addition, there were no significant differences in the incidence of bradycardia (RR 0.85; 95% CI [0.34-2.12], p = 0.72) and nausea and vomiting (RR 1.06; 95% CI [0.74-1.51], p = 0.77) between remimazolam and the control group.
Conclusions: During the perioperative period, using remimazolam can lower POD risk after surgery for patients who had non-cardiac surgery, but remimazolam does not work better than dexmedetomidine or propofol. Compared with the dexmedetomidine and propofol, remimazolam also has apparent advantages in preventing intraoperative hypotension.
{"title":"Effectiveness of perioperative remimazolam in preventing postoperative delirium: a systematic review and meta-analysis.","authors":"Mingzhen Wang, Jinhui Liu, Wenjie Liu, Xin Zhang, Gaofeng Zhang, Lixin Sun, Yanlin Bi, Hong Wang, Rui Dong","doi":"10.1186/s40001-025-02383-z","DOIUrl":"10.1186/s40001-025-02383-z","url":null,"abstract":"<p><strong>Background: </strong>To compare the POD rates in patients undergoing non-cardiac surgery who received remimazolam perioperatively versus placebo or other sedatives.</p><p><strong>Methods: </strong>We systematically searched four major databases (Cochrane Central Register of Controlled Trials, Web of Science, Embase, and PubMed) for relevant randomized controlled trials (RCTs) up to July 11, 2024. Literature quality evaluation was used the bias risk table in Review Manager 5.4. The primary outcome of interest was POD, and secondary outcomes were the hypotension risk, bradycardia and, nausea and vomiting.</p><p><strong>Results: </strong>Across 11 trials involving 1985 participants, we recorded 309 cases of POD during follow-up. In trials where the control group received saline, remimazolam decrease the risk of POD significantly by 70% (RR 0.30, 95% CI [0.19, 0.46]; p < 0.00001). Statistical analysis did not show significant difference in the risk of POD between the remimazolam group and the groups receiving either dexmedetomidine (RR 1.23 [0.64, 2.37]; p = 0.53) or propofol (RR 0.83 [0.60, 1.16]; p = 0.28). Regarding adverse events, remimazolam significantly reduces the morbidity of hypotension compared to dexmedetomidine (RR 0.25 [0.10, 0.65]; p = 0.004) and propofol (RR 0.45 [0.33, 0.60]; p < 0.00001). In addition, there were no significant differences in the incidence of bradycardia (RR 0.85; 95% CI [0.34-2.12], p = 0.72) and nausea and vomiting (RR 1.06; 95% CI [0.74-1.51], p = 0.77) between remimazolam and the control group.</p><p><strong>Conclusions: </strong>During the perioperative period, using remimazolam can lower POD risk after surgery for patients who had non-cardiac surgery, but remimazolam does not work better than dexmedetomidine or propofol. Compared with the dexmedetomidine and propofol, remimazolam also has apparent advantages in preventing intraoperative hypotension.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"122"},"PeriodicalIF":2.8,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-20DOI: 10.1186/s40001-025-02362-4
Hechen Shen, Peng Zhang
Introduction: The association between relative hyperglycemia and postoperative delirium (POD) following coronary artery bypass grafting (CABG) remains inadequately understood. This research aims to explore the correlation between the stress hyperglycemia ratio (SHR) and the occurrence of delirium in patients undergoing CABG.
Methods: This study analyzed the data from 9613 patients who underwent coronary artery bypass grafting (CABG) using information from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. To assess the association between SHR and POD following CABG, restricted cubic spline (RCS) models and logistic regression analyses were applied. Patients were categorized into high SHR (SHR ≥ 1.21) and low SHR (SHR < 1.21) groups based on optimal cut-off values derived from the receiver operating characteristic (ROC) curve. To evaluate the influence of diabetes mellitus (DM) on the outcomes, further classified of four groups of patients were conducted based on the presence or absence of DM and SHR levels. Subgroup analyses were subsequently applied to assess the relationship of POD and SHR within various patient groups.
Results: The average age of the enrolled patients was 67.62 ± 12.54 years, with 6284 (65.3%) males, higher SHR was associated with an increased incidence of postoperative delirium following CABG (OR 1.37, 95% CI 1.24-1.52, P < 0.001), even after adjusting for confounders (OR 1.55, 95% CI 1.32-1.79, P < 0.001). RCS analysis revealed a "J-shaped" relationship between the POD fowling CABG and SHR level. Logistic regression analysis further demonstrated that the association between SHR and POD may be higher than that of glucose or glycated hemoglobin levels alone. Among the stratified groups based on SHR and DM, the high-SHR/DM group exhibited the highest risk of developing POD. In conclusion, SHR is an independent risk factor that may have potential as a biomarker for assessing POD after CABG.
Conclusion: SHR serves as an independent risk factor and shows promise as a potential biomarker for predicting the risk of POD following CABG.
{"title":"The relationship between stress hyperglycemia ratio and the risk of delirium in patients after coronary artery bypass grafting.","authors":"Hechen Shen, Peng Zhang","doi":"10.1186/s40001-025-02362-4","DOIUrl":"10.1186/s40001-025-02362-4","url":null,"abstract":"<p><strong>Introduction: </strong>The association between relative hyperglycemia and postoperative delirium (POD) following coronary artery bypass grafting (CABG) remains inadequately understood. This research aims to explore the correlation between the stress hyperglycemia ratio (SHR) and the occurrence of delirium in patients undergoing CABG.</p><p><strong>Methods: </strong>This study analyzed the data from 9613 patients who underwent coronary artery bypass grafting (CABG) using information from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. To assess the association between SHR and POD following CABG, restricted cubic spline (RCS) models and logistic regression analyses were applied. Patients were categorized into high SHR (SHR ≥ 1.21) and low SHR (SHR < 1.21) groups based on optimal cut-off values derived from the receiver operating characteristic (ROC) curve. To evaluate the influence of diabetes mellitus (DM) on the outcomes, further classified of four groups of patients were conducted based on the presence or absence of DM and SHR levels. Subgroup analyses were subsequently applied to assess the relationship of POD and SHR within various patient groups.</p><p><strong>Results: </strong>The average age of the enrolled patients was 67.62 ± 12.54 years, with 6284 (65.3%) males, higher SHR was associated with an increased incidence of postoperative delirium following CABG (OR 1.37, 95% CI 1.24-1.52, P < 0.001), even after adjusting for confounders (OR 1.55, 95% CI 1.32-1.79, P < 0.001). RCS analysis revealed a \"J-shaped\" relationship between the POD fowling CABG and SHR level. Logistic regression analysis further demonstrated that the association between SHR and POD may be higher than that of glucose or glycated hemoglobin levels alone. Among the stratified groups based on SHR and DM, the high-SHR/DM group exhibited the highest risk of developing POD. In conclusion, SHR is an independent risk factor that may have potential as a biomarker for assessing POD after CABG.</p><p><strong>Conclusion: </strong>SHR serves as an independent risk factor and shows promise as a potential biomarker for predicting the risk of POD following CABG.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":"30 1","pages":"120"},"PeriodicalIF":2.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}