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Objectives: The study aimed to investigate the interaction of intraoperative stress hyperglycemia with monocyte functions and their impact on major adverse events (MAEs) in acute aortic dissection (AAD) patients who underwent open repair surgery. Methods: A total of 321 adults who underwent open surgery for AAD at two tertiary medical centers in China were enrolled in the study. The primary endpoint was defined as the incidence and characteristics of perioperative stress hyperglycemia. The secondary endpoints included the incidence of postoperative MAEs, postoperative monocyte counts and inflammatory cytokine expression. Multi-logistic, linear regression and receiver operating characteristic (ROC) curve analyses were used to establish relationships between intraoperative time-weighted average glucose (TWAG), day-one postoperative monocyte counts, serum inflammatory cytokines and postoperative outcomes. In addition, in vitro experiments were conducted to evaluate changes in the inflammatory features of monocytes under high glucose conditions. Results: Intraoperative hyperglycemia, as indicated by a TWAG level over 142 mg/dL, was associated with elevated postoperative monocyte counts and inflammatory cytokines, which correlated with extended intensive care unit (ICU) stays and worsened outcomes. In vitro, high glucose treatment induced mitochondrial impairment in monocytes, increased the release of inflammatory cytokines and the proportion of classical monocytes from AAD patients. Conclusions: Intraoperative stress hyperglycemia, in combination with day-one postoperative monocyte counts, were clinically significant for predicting adverse outcomes in AAD patients undergoing open repair surgery. Elevated glucose concentrations shaped the inflammatory features of monocytes in AAD by impairing mitochondrial functions. High glucose-driven mitochondrial functional impairment mediates a more pronounced monocytic inflammatory state in Stanford type-A AAD. [ABSTRACT FROM AUTHOR]

Purpose: The objective of this retrospective cohort study was to investigate the predictive value of stress-induced hyperglycemia parameters for delayed healing after tibial fracture post-surgery. Methods: A cohort of 108 participants who underwent surgical intervention for tibial fractures caused by trauma was included in this retrospective study. Data collected from electronic medical records encompassed demographic characteristics, bone healing assessments, stress-induced hyperglycemia parameters, inflammatory markers, and stress-related hormones. Comparative analyses, correlation analyses, univariate logistic regression analyses, and receiver operating characteristic (ROC) curve analyses were conducted to assess the predictive value of the studied parameters. Results: The delayed healing group exhibited higher levels of fasting blood glucose, postprandial glucose, and HbA1c, as well as elevated levels of inflammatory markers and stress-related hormones compared to the normal healing group. Correlation analysis and logistic regression demonstrated positive associations between stress-induced hyperglycemia parameters, inflammatory markers, stress-related hormones, and delayed union of tibial fractures (R2: 0.183 ~ 0.403;OR: 1.091 ~ 16.332). ROC curve analysis revealed high area under the curve (AUC = 0.911) values for stress-induced hyperglycemia parameters, indicating their potential as predictive markers for delayed healing. Multivariate regression analysis further substantiated the predictive capability of stress-induced hyperglycemia parameters. Conclusion: The study findings highlight the complex interplay between stress-induced hyperglycemia, inflammatory response, and bone healing outcomes in patients undergoing surgical intervention for tibial fractures. The identification of stress-induced hyperglycemia parameters as potential predictive markers for delayed healing after tibial fracture surgery offers insights for risk assessment and patient management, emphasizing the need for comprehensive understanding of these factors to optimize postoperative recovery in orthopedic patients. [ABSTRACT FROM AUTHOR]

Abstract Objectives The study aimed to investigate the interaction of intraoperative stress hyperglycemia with monocyte functions and their impact on major adverse events (MAEs) in acute aortic dissection (AAD) patients who underwent open repair surgery. Methods A total of 321 adults who underwent open surgery for AAD at two tertiary medical centers in China were enrolled in the study. The primary endpoint was defined as the incidence and characteristics of perioperative stress hyperglycemia. The secondary endpoints included the incidence of postoperative MAEs, postoperative monocyte counts and inflammatory cytokine expression. Multi-logistic, linear regression and receiver operating characteristic (ROC) curve analyses were used to establish relationships between intraoperative time-weighted average glucose (TWAG), day-one postoperative monocyte counts, serum inflammatory cytokines and postoperative outcomes. In addition, in vitro experiments were conducted to evaluate changes in the inflammatory features of monocytes under high glucose conditions. Results Intraoperative hyperglycemia, as indicated by a TWAG level over 142 mg/dL, was associated with elevated postoperative monocyte counts and inflammatory cytokines, which correlated with extended intensive care unit (ICU) stays and worsened outcomes. In vitro, high glucose treatment induced mitochondrial impairment in monocytes, increased the release of inflammatory cytokines and the proportion of classical monocytes from AAD patients. Conclusions Intraoperative stress hyperglycemia, in combination with day-one postoperative monocyte counts, were clinically significant for predicting adverse outcomes in AAD patients undergoing open repair surgery. Elevated glucose concentrations shaped the inflammatory features of monocytes in AAD by impairing mitochondrial functions. Graphical abstract High glucose-driven mitochondrial functional impairment mediates a more pronounced monocytic inflammatory state in Stanford type-A AAD.

Abstract Purpose The objective of this retrospective cohort study was to investigate the predictive value of stress-induced hyperglycemia parameters for delayed healing after tibial fracture post-surgery. Methods A cohort of 108 participants who underwent surgical intervention for tibial fractures caused by trauma was included in this retrospective study. Data collected from electronic medical records encompassed demographic characteristics, bone healing assessments, stress-induced hyperglycemia parameters, inflammatory markers, and stress-related hormones. Comparative analyses, correlation analyses, univariate logistic regression analyses, and receiver operating characteristic (ROC) curve analyses were conducted to assess the predictive value of the studied parameters. Results The delayed healing group exhibited higher levels of fasting blood glucose, postprandial glucose, and HbA1c, as well as elevated levels of inflammatory markers and stress-related hormones compared to the normal healing group. Correlation analysis and logistic regression demonstrated positive associations between stress-induced hyperglycemia parameters, inflammatory markers, stress-related hormones, and delayed union of tibial fractures (R2: 0.183 ~ 0.403;OR: 1.091 ~ 16.332). ROC curve analysis revealed high area under the curve (AUC = 0.911) values for stress-induced hyperglycemia parameters, indicating their potential as predictive markers for delayed healing. Multivariate regression analysis further substantiated the predictive capability of stress-induced hyperglycemia parameters. Conclusion The study findings highlight the complex interplay between stress-induced hyperglycemia, inflammatory response, and bone healing outcomes in patients undergoing surgical intervention for tibial fractures. The identification of stress-induced hyperglycemia parameters as potential predictive markers for delayed healing after tibial fracture surgery offers insights for risk assessment and patient management, emphasizing the need for comprehensive understanding of these factors to optimize postoperative recovery in orthopedic patients.

Stress-induced hyperglycemia (SIH) is common in patients with traumatic brain injury (TBI) and has been suggested to influence mortality rates. This meta-analysis aims to evaluate the impact of SIH on the mortality of TBI patients without preexisting diabetes mellitus (DM). A comprehensive search was performed in Medline, Web of Science, Embase, Wanfang, and CNKI databases up to May 15, 2024, to retrieve relevant studies. Observational studies reporting the incidence of all-cause mortality among TBI patients without preexisting DM, comparing those with and without SIH, were included. The association between SIH and all-cause mortality was analyzed using risk ratios (RR) and 95% confidence intervals (CI) with a random-effects model. Twelve cohort studies comprising 15 datasets with 16,387 TBI patients were included. The pooled analysis showed that SIH was associated with a higher risk of all-cause mortality (RR: 2.00, 95% CI: 1.72-2.33, p < 0.001), with mild heterogeneity (I² = 25%). Sensitivity analysis confirmed the robustness of these findings. Subgroup analyses indicated no significant differences based on study design, patient age, gender proportion, SIH definition, or follow-up duration. However, the association was slightly weaker but still significant in studies using multivariate analyses (RR: 1.76) compared to univariate analyses (RR: 2.69). In conclusion, SIH was associated with a higher risk of all-cause mortality in TBI patients without preexisting DM. Further research should explore the underlying mechanisms and optimal management strategies for SIH in this population.

Aim. To investigate the prevalence and some aspects of the carbohydrate metabolism pathology in patients with combat limb injuries. Materials and methods. 210 patients who suffered from combat injuries of the lower and/or upper extremities from 4 to 58 days (mean 15.9±8.7 days) before admission to the hospital were enrolled in the study. All study participants were men. The mean age of the patients was 36.0±8.4 years (19–59 years). Fasting venous blood glucose concentrations were determined in all patients. Patients with hyperglycemia underwent a study of the glycemic profile and HbA1c. Stress-induced hyperglycemia, estimated mean glucose level over the past 3 months (ADAG), and glycemic gap were calculated. Insulin in fasting blood plasma was determined and the HOMA-IR insulin resistance index was calculated. Results. The incidence of hyperglycemia was 23.3%. In the general group of patients, the mean glucose concentration was 5.5±1.0 mmol/l (3.1–9.73 mmol/l). In the group of patients with hyperglycemia, the mean blood glucose level reached 6.7±0.9 mmol/l, in patients with normal glucose concentration – 5.1±0.5 mmol/l (p

Abstract Background Stress hyperglycemia ratio (SHR), associated with adverse outcomes in patients with ST-segment elevation myocardial infarction (STEMI), has several definitions. This study aims to assess the prognostic value of SHR, derived from hemoglobin A1c (HbA1c) or glycated albumin (GA), to mortality. Methods The study comprised 1,643 STEMI patients who underwent percutaneous coronary intervention (PCI) in two centers. SHR1 was calculated using fasting blood glucose (FBG)/GA, while SHR2 was calculated using the formula FBG/(1.59*HbA1c-2.59). The primary endpoints were in-hospital death and all-cause mortality, with a median follow-up duration of 1.56 years. Results Higher SHR1 and SHR2 values are associated with increased risks of in-hospital death and all-cause mortality. Each standard deviation increase in SHR1 corresponded to a 39% and 22% escalation in in-hospital death and all-cause mortality, respectively. The respective increases for SHR2 were 51% and 26%. Further examinations validated these relationships as linear. Additionally, the areas under the curve (AUC) for in-hospital death were not significantly different between SHR1 and SHR2 (p > 0.05). Incorporating SHR1 or SHR2 into the base model significantly improved the discrimination and risk reclassification for in-hospital and all-cause mortality. A subgroup analysis revealed that the effects of SHR1 and SHR2 were more pronounced in patients with hypercholesteremia. Conclusion SHR1 and SHR2 have emerged as robust and independent prognostic markers for STEMI patients undergoing PCI. The SHR calculation based on either HbA1c or GA can provide additional predictive value for mortality beyond traditional risk factors, helping to identify high-risk STEMI patients.

Background: Stress hyperglycemia ratio (SHR), associated with adverse outcomes in patients with ST-segment elevation myocardial infarction (STEMI), has several definitions. This study aims to assess the prognostic value of SHR, derived from hemoglobin A1c (HbA1c) or glycated albumin (GA), to mortality. Methods: The study comprised 1,643 STEMI patients who underwent percutaneous coronary intervention (PCI) in two centers. SHR1 was calculated using fasting blood glucose (FBG)/GA, while SHR2 was calculated using the formula FBG/(1.59*HbA1c-2.59). The primary endpoints were in-hospital death and all-cause mortality, with a median follow-up duration of 1.56 years. Results: Higher SHR1 and SHR2 values are associated with increased risks of in-hospital death and all-cause mortality. Each standard deviation increase in SHR1 corresponded to a 39% and 22% escalation in in-hospital death and all-cause mortality, respectively. The respective increases for SHR2 were 51% and 26%. Further examinations validated these relationships as linear. Additionally, the areas under the curve (AUC) for in-hospital death were not significantly different between SHR1 and SHR2 (p > 0.05). Incorporating SHR1 or SHR2 into the base model significantly improved the discrimination and risk reclassification for in-hospital and all-cause mortality. A subgroup analysis revealed that the effects of SHR1 and SHR2 were more pronounced in patients with hypercholesteremia. Conclusion: SHR1 and SHR2 have emerged as robust and independent prognostic markers for STEMI patients undergoing PCI. The SHR calculation based on either HbA1c or GA can provide additional predictive value for mortality beyond traditional risk factors, helping to identify high-risk STEMI patients. [ABSTRACT FROM AUTHOR]

Background: Major surgeries cause metabolic stress and insulin resistance, leading to postoperative hyperglycemia and increased morbidity and mortality in diabetic patients. Therefore, this study aimed to assess blood sugar level changes in diabetic patients undergoing elective surgery and its confounding factors. Methods: A cross-sectional study compared blood sugar levels (BS) in 100 diabetic patients undergoing elective surgeries. Demographic data, medical history, surgery type, and anesthetic technique were documented. Laboratory assessments included fasting blood sugar (FBS) and glycosylated hemoglobin (HbA1C). Statistical analysis used SPSS software and nonparametric tests. Results: Postoperative blood sugar levels significantly increased compared to preoperative levels (mean change 11.40 ± 14.356 mg/dL). Age over 60 and general anesthesia were significant factors associated with elevated blood sugar. Conclusion: This study reveals a significant postoperative increase in blood glucose levels in diabetic patients, particularly those aged over 60 and under general anesthesia.

The aim of this study was to systematically evaluate the incidence of stress-induced hyperglycemia (SIH) in acute ischemic stroke (AIS). Studies that reported SIH incidence in AIS and examined risk factors for SIH and non-SIH patients were systematically searched in PubMed, Embase, Cochrane Library, and Web of Science from the inception of each database to December 2021. Article screening and data extraction were performed by two independent reviewers according to the inclusion and exclusion criteria. The quality of the included studies was assessed using the Newcastle–Ottawa Scale (NOS), and meta-analysis was performed using Stata. A total of 13 studies involving 4552 patients (977 in the SIH group and 3575 in the non-SIH group) were included. Meta-analysis showed that the incidence of SIH was 24% (95% CI: 21–27%) in the total population, 33% (14–52%) in North America, 25% (20–29%) in Europe, and 21% (12–29%) in Asia. Subgroup analysis by year of publication revealed that the pooled incidence of SIH was 27% (22–32%) in studies published before 2010 and 19% (14–24%) in those published after 2010. SIH is relatively common in AIS and poses a serious public health problem. Therefore, more emphasis should be placed on the prevention and control of SIH in AIS. [ABSTRACT FROM AUTHOR]

Introduction: Admission hyperglycemia is a common finding after spontaneous intracerebral hemorrhage (ICH) secondary to pre-existing diabetes mellitus (DM) or stress-induced hyperglycemia (SIH). Studies of the causal relationship between SIH and ICH outcomes are rare. Aim: We aimed to identify whether SIH or pre-existing DM was the cause of admission hyperglycemia associated with ICH outcomes. Methods: Admission glycosylated hemoglobin (HbA1c), glucose levels, and comorbidity data from the prospective, multicenter cohort, Chinese Cerebral Hemorrhage: Mechanisms and Intervention Study (CHEERY), were collected and analyzed. According to different admission blood glucose and HbA1c levels, patients were divided into nondiabetic normoglycemia (NDN), diabetic normoglycemia (DN), diabetic hyperglycemia (DH), and SIH groups. Modified Poisson regression models were used to analyze ICH outcomes in the different groups. Results: In total, 1372 patients were included: 388 patients with admission hyperglycemia, 239 with DH, and 149 with SIH. In patients with hyperglycemia, SIH was associated with a higher risk of pulmonary infection [risk ratios (RR): 1.477, 95% confidence interval (CI): 1.004–2.172], 30-day (RR: 1.068, 95% CI: 1.009–1.130) and 90- day mortality after ICH (RR: 1.060, 95% CI: 1.000–1.124). Conclusions: Admission hyperglycemia is a common finding after ICH, and SIH is a sensitive predictor of the risk of pulmonary infection and all-cause death after ICH. [ABSTRACT FROM AUTHOR]

Objective: This study assesses whether stress-induced hyperglycemia is a predictor of poor outcome at 3 months for patients with acute ischemic stroke (AIS) treated by endovascular treatment (EVT) and impacted by their previous blood glucose status. Methods: This retrospective study collected data from 576 patients with AIS due to large vessel occlusion (LVO) treated by EVT from March 2019 to June 2022. The sample was composed of 230 and 346 patients with and without diabetes mellitus (DM), respectively, based on their premorbid diabetic status. Prognosis was assessed with modified Rankin Scale (mRS) at 3-month after AIS. Poor prognosis was defined as mRS>2. Stress-induced hyperglycemia was assessed by fasting glucose-to-glycated hemoglobin ratio (GAR). Each group was stratified into four groups by quartiles of GAR (Q1-Q4). Binary logistic regression analysis was used to identify relationship between different GAR quartiles and clinical outcome after EVT. Results: In DM group, a poor prognosis was seen in 122 (53%) patients and GAR level was 1.27 ± 0.44. These variables were higher than non-DM group and the differences were statistically significant (p < 0.05, respectively). Patients with severe stress-induced hyperglycemia demonstrated greater incidence of 3-month poor prognosis (DM: Q1, 39.7%; Q2, 45.6%; Q3, 58.6%; Q4, 68.4%; p = 0.009. Non-DM: Q1, 31%; Q2, 32.6%; Q3, 42.5%; Q4, 64%; p < 0.001). However, the highest quartile of GAR was independently associated with poor prognosis at 3 months (OR 3.39, 95% CI 1.66-6.96, p = 0.001), compared to the lowest quartile in non-DM patients after logistic regression. This association was not observed from DM patients. Conclusion: The outcome of patients with acute LVO stroke treated with EVT appears to be influenced by premorbid diabetes status. However, the poor prognosis at 3-month in patients with DM is not independently correlated with stressinduced hyperglycemia. This could be due to the long-term damage of persistent hyperglycemia and diabetic patients' adaptive response to stress following acute ischemic damage to the brain. [ABSTRACT FROM AUTHOR]

Stress-induced hyperglycemia (SIH) generally occurs in critical illness. Recently, glycemic gap (GAP) has been considered to be a superior indicator of SIH. However, data on the association between GAP and prognosis in ST-segment elevation myocardial infarction (STEMI) is limited. This observational study aimed to estimate the prognostic value of GAP mean , defined as the difference between mean blood glucose level (MGL) within 24 h after admission and A1c-derived average glucose (ADAG), in patients with acute STEMI. A total of 4952 patients with acute STEMI were included in the final analysis, and they were divided into four groups according to GAP mean quartiles and diabetes mellitus (DM). The primary outcomes were all-cause mortality and major adverse cardiovascular events (MACEs). Cox proportional hazards regression analysis and net reclassification improvement (NRI) analysis were performed. At 30 days of follow-up, 324 (6.5%) deaths and 569 (11.5%) MACEs occurred. With the elevation of GAP mean , the incidence of all-cause mortality (4.0%, 5.6%, 6.5%, and 10.1%) and MACEs (7.3%, 9.6%, 11.4%, and 17.7%) significantly increased. Receiver operating characteristic curve analysis demonstrated that GAP mean was superior to admission blood glucose (ABG) and GAP adm (defined as the difference between ABG and ADAG) to detect adverse outcomes. Multivariate Cox regression analysis revealed that elevated GAP mean was independently associated with all-cause death and MACEs. With the first quartile as a reference, the hazards ratios (HRs) for all-cause death in the second, third, and fourth quartiles were 1.49 (95% CI 1.02–2.18), 1.58 (95% CI 1.09–2.30), and 2.11 (95% CI 1.48–3.02), respectively, and the HRs for MACEs were 1.40 (95% CI 1.05–1.86), 1.60 (95% CI 1.21–2.11), and 2.17 (95% CI 1.66–2.83), respectively, which were independent of DM status. Continuous NRI analysis revealed that GAP mean significantly improved risk stratification for all-cause mortality and MACEs by 21.6% and 19.8%, respectively. The glycemic gap between MGL within 24 h after admission and ADAG was independently associated with 30-day all-cause mortality and MACEs in patients with acute STEMI, which was not affected by DM status. Further, the glycemic gap provided incremental accuracy in the risk stratification of STEMI. [Display omitted] • Elevated GAP mean is independently related to 30-day all-cause death and MACEs in STEMI, independent of the status of DM. • GAP mean is superior to admission blood glucose and GAP adm in the prediction of all-cause death and MACEs in STEMI. • GAP mean can provide additional accuracy in risk stratification of STEMI beyond that provided by conventional risk factors. [ABSTRACT FROM AUTHOR]

Background: Early randomized controlled trials have demonstrated the benefits of tight glucose control. Subsequent NICE-SUGAR study found that tight glucose control increased mortality. The optimal glucose target in diabetic and nondiabetic patients remains unclear. This study aimed to evaluate the relationship between blood glucose levels and outcomes in critically ill patients with or without diabetes. Methods: This was a retrospective analysis of the eICU database. Repeat ICU stays, ICU stays of less than 2 days, patients transferred from other ICUs, those with less than 2 blood glucose measurements, and those with missing data on hospital mortality were excluded. The primary outcome was hospital mortality. Generalised additive models were used to model relationship between glycemic control and mortality. Models were adjusted for age, APACHE IV scores, body mass index, admission diagnosis, mechanical ventilation, and use of vasopressor or inotropic agents. Results: There were 52,107 patients in the analysis. Nondiabetes patients exhibited a J-shaped association between time-weighted average glucose and hospital mortality, while this association in diabetes patients was right-shifted and flattened. Using a TWA glucose of 100 mg/dL as the reference value, the adjusted odds ratio (OR) of TWA glucose of 140 mg/dL was 3.05 (95% confidence interval (CI) 3.03–3.08) in nondiabetes and 1.14 (95% CI 1.08–1.20) in diabetes patients. The adjusted OR of TWA glucose of 180 mg/dL were 4.20 (95% CI 4.07–4.33) and 1.49 (1.41–1.57) in patients with no diabetes and patients with diabetes, respectively. The adjusted ORs of TWA glucose of 80 mg/dL compared with 100 mg/dL were 1.74 (95% CI 1.57–1.92) in nondiabetes and 1.36 (95% CI 1.12–1.66) in patients with diabetes. The glucose ranges associated with a below-average risk of mortality were 80–120 mg/dL and 90–150 mg/dL for nondiabetes and diabetes patients, respectively. Hypoglycemia was associated with increased hospital mortality in both groups but to a lesser extent in diabetic patients. Glucose variability was positively associated with hospital mortality in nondiabetics. Conclusions: Time-weighted average glucose, hypoglycemia, and glucose variability had different impacts on clinical outcomes in patients with and without diabetes. Compared with nondiabetic patients, diabetic patients showed a more blunted response to hypo- and hyperglycemia and glucose variability. Glycemic control strategies should be reconsidered to avoid both hypoglycemia and hyperglycemia. [ABSTRACT FROM AUTHOR]

The aim of this study was to systematically evaluate the incidence of stress-induced hyperglycemia (SIH) in acute ischemic stroke (AIS). Studies that reported SIH incidence in AIS and examined risk factors for SIH and non-SIH patients were systematically searched in PubMed, Embase, Cochrane Library, and Web of Science from the inception of each database to December 2021. Article screening and data extraction were performed by two independent reviewers according to the inclusion and exclusion criteria. The quality of the included studies was assessed using the Newcastle–Ottawa Scale (NOS), and meta-analysis was performed using Stata. A total of 13 studies involving 4552 patients (977 in the SIH group and 3575 in the non-SIH group) were included. Meta-analysis showed that the incidence of SIH was 24% (95% CI: 21–27%) in the total population, 33% (14–52%) in North America, 25% (20–29%) in Europe, and 21% (12–29%) in Asia. Subgroup analysis by year of publication revealed that the pooled incidence of SIH was 27% (22–32%) in studies published before 2010 and 19% (14–24%) in those published after 2010. SIH is relatively common in AIS and poses a serious public health problem. Therefore, more emphasis should be placed on the prevention and control of SIH in AIS.

Background: Admission hyperglycemia is defined as any blood glucose (BG) level greater than 140 mg/dL (>7.8 mmol/L) in critical care unit (CCU) according to American Diabetes Association 2015. Stress hyperglycemia is related to multiple factors and can lead to insulin resistance and high hepatic glucose output. Aim: To determine the frequency, in-hospital mortality, and length of stay in a cohort of patients with admission hyperglycemia in unselected acute medically ill patients admitted to medical intensive care units (ICUs) (medical ICU and CCU) attending Internal Medicine Department, Assiut University Hospital, Assiut, Egypt, and to evaluate whether admission hyperglycemia or other comorbid conditions are responsible for outcome of critical ill patients. Subjects and Methods: This prospective, observational study involved 170 patients admitted at ICU unit of Internal Medicine Department at Assiut University Hospital between July and December 2016. Measurement of BG on admission to ICU was as following: normoglycemic if less than 140 mg/dL and hyperglycemic if more than 140 mg/dL. Then, follow up BG every 8h till either discharge or death or maximum 4 days in addition to fasting, postprandial BG, HbA1C, complete blood count and kidney function tests, serum sodium, serum potassium, arterial blood gases, and acute physiologic assessment and chronic health score were carried out. Results: This study included 170 patients, 35.3% were normoglycemic and 64.7% were hyperglycemic, which were further subdivided into 43% known diabetics, 14.1% stress hyperglycemia, and 7.6% newly discovered diabetics. Percentage of survivors was 72.9% versus non-survivors, which was 27.1%. Median hospital stay for all patients was 6 (4–28) days with in-hospital mortality of 46 (27.1%) patients. It was noticed that frequency of non-survivors was higher in patients with hyperglycemic versus that of survivors. Conclusion: Stress hyperglycemia and diabetes were independent predictors for in-hospital mortality in patients with admission hyperglycemia attending ICU.

Background: Acute Type A Aortic Dissection (AAAD) is one of the most life-threatening diseases, often associated with transient hyperglycemia induced by acute physiological stress. The impact of stress-induced hyperglycemia on the prognosis of ST-segment elevation myocardial infarction has been reported. However, the relationship between stress-induced hyperglycemia and the prognosis of AAAD patients remains uncertain., Methods: The clinical data of 456 patients with acute type A aortic dissection were retrospectively reviewed. Patients were divided into two groups based on their admission blood glucose. Cox model regression analysis was performed to assess the relationship between stress-induced hyperglycemia and the 30-day and 1-year mortality rates of these patients., Results: Among the 456 patients, 149 cases (32.7%) had AAAD combined with stress-induced hyperglycemia (SIH). The results of the multifactor regression analysis of the Cox model indicated that hyperglycemia (RR = 1.505, 95% CI: 1.046-2.165, p  = 0.028), aortic coarctation involving renal arteries (RR = 3.330, 95% CI: 2.237-4.957, p  < 0.001), aortic coarctation involving superior mesenteric arteries (RR = 1.611, 95% CI: 1.056-2.455, p  = 0.027), and aortic coarctation involving iliac arteries (RR = 2.034, 95% CI: 1.364-3.035, p  = 0.001) were independent influences on 1-year postoperative mortality in AAAD patients., Conclusion: The current findings indicate that stress-induced hyperglycemia measured on admission is strongly associated with 1-year mortality in patients with AAAD. Furthermore, stress-induced hyperglycemia may be related to the severity of the condition in patients with AAAD.

Background and Aim: To investigate the short-term dynamic changes and the factors associated with regression of glucose metabolism disorders in patients with hepatitis flare of chronic hepatitis B virus (HBV) infection. Methods: In this study, 118 patients with severe hepatitis flare of chronic HBV infection were prospectively studied. Oral glucose tolerance test was performed on admission and during follow-up to evaluate dynamic changes in glucose metabolism disorders. The factors associated with regression of glucose metabolism disorders were identified using univariate and multivariate logistic regression analyses. Results: The prevalence of diabetes was significantly higher in 70 (47.1%) patients with liver cirrhosis than that in 48 (16.8%) patients without liver cirrhosis. The prevalence of impaired glucose tolerance in patients with liver cirrhosis (35.7%) was significantly lower than that in patients without liver cirrhosis (47.8%). After a follow-up of 20.0 ± 18.7 days, 28 of 31 (90.3%) patients without liver cirrhosis experienced regression of glucose metabolism disorders. Additionally, 30 (54.5%) patients with liver cirrhosis experienced regression of glucose metabolism disorders after 42.0 ± 36.2 days. In patients with liver cirrhosis, those with regression of glucose metabolism disorders had significantly higher levels of homeostasis model assessment-β-cell function, albumin (ALB), and a significantly lower level of fibrosis-4 score. ALB was identified as an independent factor associated with the regression of glucose metabolism disorders in patients with liver cirrhosis. Conclusion: Severe acute liver inflammation aggravates glucose metabolism disorders in patients with hepatitis B-related liver cirrhosis and high ALB level is associated with regression of glucose metabolism disorders upon resolution of acute liver inflammation. [ABSTRACT FROM AUTHOR]

Background and AimTo investigate the short-term dynamic changes and the factors associated with regression of glucose metabolism disorders in patients with hepatitis flare of chronic hepatitis B virus (HBV) infection.MethodsIn this study, 118 patients with severe hepatitis flare of chronic HBV infection were prospectively studied. Oral glucose tolerance test was performed on admission and during follow-up to evaluate dynamic changes in glucose metabolism disorders. The factors associated with regression of glucose metabolism disorders were identified using univariate and multivariate logistic regression analyses.ResultsThe prevalence of diabetes was significantly higher in 70 (47.1%) patients with liver cirrhosis than that in 48 (16.8%) patients without liver cirrhosis. The prevalence of impaired glucose tolerance in patients with liver cirrhosis (35.7%) was significantly lower than that in patients without liver cirrhosis (47.8%). After a follow-up of 20.0 ± 18.7 days, 28 of 31 (90.3%) patients without liver cirrhosis experienced regression of glucose metabolism disorders. Additionally, 30 (54.5%) patients with liver cirrhosis experienced regression of glucose metabolism disorders after 42.0 ± 36.2 days. In patients with liver cirrhosis, those with regression of glucose metabolism disorders had significantly higher levels of homeostasis model assessment-β-cell function, albumin (ALB), and a significantly lower level of fibrosis-4 score. ALB was identified as an independent factor associated with the regression of glucose metabolism disorders in patients with liver cirrhosis.ConclusionSevere acute liver inflammation aggravates glucose metabolism disorders in patients with hepatitis B-related liver cirrhosis and high ALB level is associated with regression of glucose metabolism disorders upon resolution of acute liver inflammation.

Introduction: The relationship between critical care mortality and combined impact of malglycemia remains undefined., Methods: We assessed the risk-adjusted relationship (n = 4790) between hospital mortality with malglycemia, defined as hypergycemia (hours Glycemic Ratio ≥ 1.1, where GR is quotient of mean ICU blood glucose (BG) and estimated average BG), absolute hypoglycemia (hours BG < 70 mg/dL) and relative hypoglycemia (excursions GR < 0.7 in those with HbA1c ≥ 8%)., Results: Each malglycemia was independently associated with mortality - hyperglycemia (OR 1.0020/h, 95%CI 1.0009-1.0031, p = 0.0004), absolute hypoglycemia (OR 1.0616/h, 95%CI 1.0190-1.1061, p = 0.0043), and relative hypoglycemia (OR 1.2813/excursion, 95%CI 1.0704-1.5338, p = 0.0069). Absolute (7.4%) and relative hypoglycemia (6.7%) exposure dominated the first 24 h, decreasing thereafter. While hyperglycemia had lower risk association with mortality, it was persistently present across the length-of-stay (68-76% incidence daily), making it the dominant form of malglycemia. Relative contributions in the first five days from hyperglycemia, absolute hypoglycemia and relative hypoglycemia were 60%, 21% and 19% respectively., Conclusions: Absolute and relative hypoglycemia occurred largely in the first 24 h. Relative to all hypoglycemia, the associated mortality from the seemingly less potent but consistently more prevalent hyperglycemia steadily accumulated with increasing length-of-stay. This has important implications for interpretation of study results., (Copyright © 2023. Published by Elsevier Inc.)

Background/purpose: Associations between the disturbances in glucose homeostasis and prognosis in patients with hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF) remain unclear. This study was conducted to investigate the clinical characteristics of disturbances in glucose homeostasis and their associations with 90-day mortality in patients with HBV-related ACLF. Methods: Ninety-six patients with HBV-related ACLF without pre-existing diabetes were prospectively included. Glucose abnormalities were diagnosed based on fasting plasma glucose and oral glucose tolerance test results on admission and during follow-up. Homeostasis model assessment was used to establish insulin resistance (HOMA2-IR), insulin sensitivity (HOMA2-IS) and HOMA2-β-cell function (HOMA2-β). Multivariate Cox proportional hazards analysis was used to identify independent risk factors for death within 90 days after admission. Results: Among 96 patients with ACLF, 51 (53.1%) had diabetes, 29 (30.2%) had impaired glucose tolerance (IGT), and 17 (17.7%) had hypoglycemia. Patients with diabetes had significantly lower levels of HOMA2-β than did patients with normal glucose tolerance. Of 22 patients with diabetes or IGT and without anti-hyperglycemic treatment, 8 (36.4%) exhibited regression of their glucose metabolism disorders after a follow-up of 32.8 ± 28.8 days, and higher platelet levels were associated with regression. Twenty-five patients (25.0%) with ACLF died of liver failure within 90 days. Diabetes [odds ratio (OR) 3.601, 95% confidence interval (CI) 1.342–9.661] and age (OR 1.045, 95% CI 1.010–1.082) were the independent risk factors associated with mortality. Conclusion: Impaired pancreatic β-cell function is related to diabetes development, and diabetes is associated with high mortality in patients with chronic HBV-related ACLF. [ABSTRACT FROM AUTHOR]

Objective: Stress-induced hyperglycemia is associated with poor outcomes in nearly all critical illnesses. This acute elevation in glucose after injury or illness is associated with increased morbidity and mortality, including multiple organ failure. Stress-induced hyperglycemia is often attributed to insulin resistance as controlling glucose levels via exogenous insulin improves outcomes, but the mechanisms are unclear. Forkhead box O (FOXO) transcription factors are direct targets of insulin signaling in the liver that regulate glucose homeostasis via direct and indirect pathways. Loss of hepatic FOXO transcription factors reduces hyperglycemia in chronic insulin resistance; however, the role of FOXOs in stress-induced hyperglycemia is unknown. Methods: We subjected mice lacking FOXO transcription factors in the liver to a model of injury known to cause stress-induced hyperglycemia. Glucose, insulin, glycerol, fatty acids, cytokines, and adipokines were assessed before and after injury. Liver and adipose tissue were analyzed for changes in glycogen, FOXO target gene expression, and insulin signaling. Results: Stress-induced hyperglycemia was associated with reduced hepatic insulin signaling and increased hepatic FOXO target gene expression while loss of FOXO1, 3, and 4 in the liver attenuated hyperglycemia and prevented hyperinsulinemia. Mechanistically, the loss of FOXO transcription factors mitigated the stress-induced hyperglycemia response by directly altering gene expression and glycogenolysis in the liver and indirectly suppressing lipolysis in adipose tissue. Reductions were associated with decreased IL-6, TNF-α, and follistatin and increased FGF21, suggesting that cytokines and FOXO-regulated hepatokines contribute to the stress-induced hyperglycemia response. Conclusions: This study implicates FOXO transcription factors as a predominant driver of stress-induced hyperglycemia through means that include cross-talk between the liver and adipose, highlighting a novel mechanism underlying acute hyperglycemia and insulin resistance in stress.

Introduction: The relationship between critical care mortality and hypoglycemia, both relative (>30% below average preadmission glycemia) and absolute (blood glucose (BG) <70 mg/dL (<10 mmol/L)) requires further definition., Methods: We assessed the risk-adjusted relationship between hospital mortality with relative hypoglycemia using the Glycemic Ratio (GR), and with absolute hypoglycemia using BG in a retrospective cohort investigation (n = 4790)., Results: Relative hypoglycemia excursions below GR 0.7 with a of 24-h non-exposure period between excursions in those with HbA1c ≥ 8% were independently associated with mortality (n = 373, OR 2.49, 95% CI 1.54-4.04, p = 0.0002) but not those with HbA1c < 8% (n = 4417, OR 0.98 95% CI 0.89-1.08, p = 0.70). Hours below GR 0.7 (1.0037, 0.9995-1.0080, 0.0846) or minimum GR (0.0896, 0.0030-2.6600, 0.1632) were not independently associated with outcome. Absolute hypoglycemia occurred across the HbA1c spectrum in a U-shaped pattern. There was no difference in mortality associated with exposure to BG < 70 mg/dL for HbA1c ≥ 6.5% vs <6.5% (29.7% vs 24.3%, p = 0.77). Hours below 70 mg/dL demonstrated strongest association with outcome, while minimum BG, and excursions below 70 mg/dL were also independently associated., Conclusions: Relative hypoglycemia represented by excursions below GR 0.7 in those with HbA1c ≥ 8% occurred commonly and was independently associated with mortality. Absolute hypoglycemia had similar association with mortality regardless of HbA1c., Competing Interests: Declaration of Competing Interest Drs. Krinsley is a consultant for Dexcom. Dr. Hirsch's institution received funding from Insulet, and Beta Bionics; he disclosed that he is a consultant for Abbott, Roche, Lifescan, and GWave. Dr. Umpierrez institution received funding from Dexcom, Abbott, and Baxter. The remaining authors have disclosed that they do not have any potential conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

This study was conducted to document temporal patterns of blood glucose level changes during the first 10-day critical period and to identify factors that influence stress-induced hyperglycemia development in brain injury patients. The medical records of 190 brain injury patients were retrospectively reviewed. Blood glucose levels in the poor recovery group were significantly higher than in the good recovery group, particularly during the first 72 hr (158-172 mg/dl). The poor recovery group showed persistent, fluctuating hyperglycemia, whereas the good recovery group exhibited hyperglycemic peaks during the first 3 days that subsequently reduced linearly to normal. Gender, preexisting hypertension, disease severity at admission, total calorie intake, and steroid use were found to influence stress-induced hyperglycemia development significantly. In conclusion, close monitoring and adjustment are required to maintain safe blood glucose levels and the development of protocols for safe glycemic management is essential to improve critical care in brain injury patients. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the association between diabetes and stress-induced hyperglycemia with skeletal muscle gene expression of INSR of critically ill patients. Skeletal muscle biopsies were prospectively taken from the vastus muscle, and the expression level of INSR was analyzed using RT-qPCR. Fifty patients were included from April 2018 to September 2018. No significant differences in skeletal muscle gene expression were found between patients with or without diabetes. Similarly, there were no differences in gene expression between groups according to the presence of hypoglycemia 〈 70 mg/dl or hyperglycemia 〉 140 mg/dl. Patients with glycemic variability ≥ 40 mg/dl exhibited a downregulation of INSR compared to those with glycemic variability < 40 mg/dl (1.3 [0.01–5] vs. 2.1 [0.7 - 3.4] fold-changes, P = 0.045). The same pattern was observed when glycemic gap threshold of 80 mg/dl was used (1.4 [0.25–5] vs 1 [0.01 - 2.3] fold-changes in patients with glycemic gap < 80 mg/dl and glycemic gap ≥ 80 mg/dl respectively, P = 0.015). In conclusion, INSR was downregulated in the skeletal muscle of critically ill patients with stress-induced hyperglycemia. [ABSTRACT FROM AUTHOR]

Abstract Background Vitamin D level is inversely associated with tuberculosis (TB) and diabetes (DM). Vitamin D could be a mediator in the association between TB and DM. We examined the associations between vitamin D, TB and DM. Methods Consecutive adults with TB and sex- and age-matched volunteers were included in a case-control study in Dar es Salaam, Tanzania. Glycemia and total vitamin D (25(OH)D) were measured at enrolment and after TB treatment in cases. The association between low 25(OH)D (

Introduction: Stress-induced hyperglycemia (SIH) is conventionally represented by Blood Glucose (BG) although recent evidence indicates the Glycemic Ratio (GR, quotient of mean BG and estimated preadmission BG) is a superior prognostic marker. We assessed the association between in-hospital mortality and SIH, using BG and GR in an adult medical-surgical ICU., Methods: We included patients with hemoglobin A1c (HbA1c) and minimum four BGs in a retrospective cohort investigation (n = 4790)., Results: A critical SIH threshold of GR 1.1 was identified. Mortality increased with increasing exposure to GR ≥ 1.1 (r 2  = 0.94, p = 0.0007). Duration of exposure to BG ≥ 180 mg/dL demonstrated a less robust association with mortality (r 2  = 0.75, p = 0.059). In risk-adjusted analyses, hours GR ≥ 1.1 (OR 1.0014, 95%CI (1.0003-1.0026), p = 0.0161) and hours BG ≥ 180 mg/dL (OR 1.0080, 95%CI (1.0034-1.0126), p = 0.0006) were associated with mortality. In the cohort with no exposure to hypoglycemia however, only hours GR ≥ 1.1 was associated with mortality (OR 1.0027, 95%CI (1.0012-1.0043), p = 0.0007), not BG ≥ 180 mg/dL (OR 1.0031, 95%CI (0.9949-1.0114), p = 0.50) and this relationship remained intact for those who never experienced BG outside the 70-180 mg/dL range (n = 2494)., Conclusions: Clinically significant SIH commenced above GR 1.1. Mortality was associated with hours of exposure to GR ≥ 1.1 which was a superior marker of SIH compared to BG., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Objective: To investigate the relationship between stress glucose elevation and the risk of 28 d all-cause mortality in intensive care unit (ICU) patients, and to compare the predictive efficacy of different stress glucose elevation indicators., Methods: ICU patients who met the inclusion and exclusion criteria in the Medical Information Mart for Intensive Care Ⅳ (MIMIC-Ⅳ) database were used as the study subjects, and the stress glucose elevation indicators were divided into Q1 (0-25%), Q2 (>25%- 75%), and Q3 (>75%-100%) groups, with whether death occurred in the ICU and the duration of treatment in the ICU as outcome variables, and demographic characteristics, laboratory indicators, and comorbidities as covariates, Cox regression and restricted cubic splines were used to explore the association between stress glucose elevation and the risk of 28 d all-cause death in ICU patients; and subject work characteristics [receiver operating characteristic (ROC) and the area under curve (AUC)] were used to evaluate the predictive efficacy of different stress glucose elevation indicators, The stress hyperglycemia indexes included: stress hyperglycemia ratio (SHR1, SHR2), glucose gap (GG); and the stress hyperglycemia index was further incorporated into the Oxford acute severity of illness score (OASIS) to investigate the predictive efficacy of the improved scores: the AUC was used to assess the score discrimination, and the larger the AUC indicated, the better score discrimination. The Brier score was used to evaluate the calibration of the score, and a smaller Brier score indicated a better calibration of the score., Results: A total of 5 249 ICU patients were included, of whom 7.56% occurred in ICU death. Cox regression analysis after adjusting for confounders showed that the HR (95% CI ) for 28 d all-cause mortality in the ICU patients was 1.545 (1.077-2.217), 1.602 (1.142-2.249) and 1.442 (1.001-2.061) for the highest group Q3 compared with the lowest group Q1 for SHR1, SHR2 and GG, respectively, and The risk of death in the ICU patients increased progressively with increasing indicators of stressful blood glucose elevation ( P trend < 0.05). Restricted cubic spline analysis showed a linear relationship between SHR and the 28 d all-cause mortality risk ( P >0.05). the AUC of SHR2 and GG was significantly higher than that of SHR1: AUC SHR2 =0.691 (95% CI : 0.661-0.720), AUC GG =0.685 (95% CI : 0.655-0.714), and AUC SHR1 =0.680 (95% CI : 0.650-0.709), P < 0.05. The inclusion of SHR2 in the OASIS scores significantly improved the discrimination and calibration of the scores: AUC OASIS =0.820 (95% CI : 0.791-0.848), AUC OASIS +SHR2=0.832 (95% CI : 0.804-0.859), P < 0.05; Brier score OASIS =0.071, Brier score OASIS+SHR2 =0.069., Conclusion: Stressful glucose elevation is strongly associated with 28 d all-cause mortality risk in ICU patients and may inform clinical management and decision making in intensive care patients.

Elevated glucose level on admission in the number of emergency conditions, including acute myocardial infarction (AMI), is linked to worse outcomes, regardless of the current treatment. The introduction of primary percutaneous coronary intervention (PPCI) in therapy of AMI patients with ST segment elevation (STEMI) has improved the treatment of these patients. However, there are contradictory evidences regarding the impact of stressinduced hyperglycemia on the treatment outcome. The present study is aimed to indentify the effect of stress-induced hyperglycemia on in-hospital prognosis of patients with STEMI treated with AIM-PPCI. Prospective study included 116 patients with a diagnosis of first AMI-STEMI treated with PPCI at the Department of Cardiovascular Diseases, Clinical Center Niš in the period 2010-2011. Immediately after establishing the diagnosis, the patients with adequate medicament preparation were transferred into the angiography room for the coronary stent implantation. Laboratory analysis of the whole blood samples were done immediately after admission and in the next 24 hours. Receiver operator characteristic (ROC) analysis revealed that stress-induced hyperglycemia (glucose 11.2 mmol / L, an area under the curve of 0.812) is a delimiting factor for distinguishing the outcome and survival of patients on admission. The group of patients without stress-induced hyperglycemia had mortality rate about five times less (1/79 -1.2%) than the group of patients with stress-induced hyperglycemia (5/37 -13.5%), p=0.041. Comparing these groups with the incidence of DM, stress-induced hyperglycemia had no significant effect on mortality in the group without DM (1/54 vs. 3/26, ns) and in the group with DM (1/25 vs. 1/11, ns). The cut-off value of glucose, obtained by ROC curve, is 11.2 mmol/L for stressinduced hyperglycemia in patients with STEMI treated with PPCI. This value could determine a significant gradient of risk: patients with glycemia

Diabetes mellitus (DM) is one of the most common chronic metabolic disorders worldwide, which increases the risk of common and opportunistic infections. Following the coronavirus disease 2019 (COVID-19) pandemic, a higher incidence rate, more severe forms of the disease, and exacerbation of hyperglycemia and its complications have been observed in patients with DM. Moreover, stress-induced hyperglycemia has been observed in many hospitalized nondiabetic patients after contracting COVID-19. Hyperglycemia worsens prognosis in both diabetic and nondiabetic patients. In this study, the mechanism of new-onset or exacerbation of hyperglycemia, the effect of the treatments used for COVID-19 on hyperglycemia, the importance and appropriate method of blood glucose (blood sugar (BS)) control during the disease, and the possible fate of new-onset hyperglycemia after recovery from COVID-19 to some extent is expressed., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Zahedi et al.)

Background: Vitamin D level is inversely associated with tuberculosis (TB) and diabetes (DM). Vitamin D could be a mediator in the association between TB and DM. We examined the associations between vitamin D, TB and DM. Methods: Consecutive adults with TB and sex- and age-matched volunteers were included in a case-control study in Dar es Salaam, Tanzania. Glycemia and total vitamin D (25(OH)D) were measured at enrolment and after TB treatment in cases. The association between low 25(OH)D (<75 nmol/l) and TB was evaluated by logistic regression adjusted for age, sex, body mass index, socioeconomic status, sunshine hours, HIV and an interaction between low 25(OH)D and hyperglycemia. Results: The prevalence of low 25(OH)D was similar in TB patients and controls (25.8 % versus 31.0 %; p = 0.22). In the subgroup of patients with persistent hyperglycemia (i.e. likely true diabetic patients), the proportion of patients with low 25(OH)D tended to be greater in TB patients (50 % versus 29.7 %; p = 0.20). The effect modification by persistent hyperglycemia persisted in the multivariate analysis (pinteraction = 0.01). Conclusions: Low 25(OH)D may increase TB risk in patients with underlying DM. Trials should examine if this association is causal and whether adjunct vitamin D therapy is beneficial in this population. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus (DM) increases tuberculosis risk while tuberculosis, as an infectious disease, leads to hyperglycemia. We compared hyperglycemia screening strategies in controls and patients with tuberculosis in Dar es Salaam, Tanzania.Methods: Consecutive adults with tuberculosis and sex- and age-matched volunteers were included in a case-control study between July 2012 and June 2014. All underwent DM screening tests (fasting capillary glucose [FCG] level, 2-hour CG [2-hCG] level, and glycated hemoglobin A1c [HbA1c] level) at enrollment, and cases were tested again after receipt of tuberculosis treatment. Association of tuberculosis and its outcome with hyperglycemia was assessed using logistic regression analysis adjusted for sex, age, body mass index, human immunodeficiency virus infection status, and socioeconomic status. Patients with tuberculosis and newly diagnosed DM were not treated for hyperglycemia.Results: At enrollment, DM prevalence was significantly higher among patients with tuberculosis (n = 539; FCG level > 7 mmol/L, 4.5% of patients, 2-hCG level > 11 mmol/L, 6.8%; and HbA1c level > 6.5%, 9.3%), compared with controls (n = 496; 1.2%, 3.1%, and 2.2%, respectively). The association between hyperglycemia and tuberculosis disappeared after tuberculosis treatment (adjusted odds ratio [aOR] for the FCG level: 9.6 [95% confidence interval {CI}, 3.7-24.7] at enrollment vs 2.4 [95% CI, .7-8.7] at follow-up; aOR for the 2-hCG level: 6.6 [95% CI, 4.0-11.1] vs 1.6 [95% CI, .8-2.9]; and aOR for the HbA1c level, 4.2 [95% CI, 2.9-6.0] vs 1.4 [95% CI, .9-2.0]). Hyperglycemia, based on the FCG level, at enrollment was associated with tuberculosis treatment failure or death (aOR, 3.3; 95% CI, 1.2-9.3).Conclusions: Transient hyperglycemia is frequent during tuberculosis, and DM needs confirmation after tuberculosis treatment. Performance of DM screening at tuberculosis diagnosis gives the opportunity to detect patients at risk of adverse outcome. [ABSTRACT FROM AUTHOR]

Background: Only a few information is available on the risk of stress hyperglycemia following acute myocardial infarction after statin use. We investigate the association of stress-induced hyperglycemia following statin use in patients with acute myocardial infarction. Methods:An observational analysis of 476 consecutive patients who suffered acute myocardial infarction was carried out. All selected patients were divided into diabetes mellitus and non-diabetes based on the presence or absence of diabetes. The cardiac incidence of in-hospital and stress-induced hyperglycemia was recorded. Results: Among patients with stress hyperglycemia in non-diabetes mellitus subgroups, the average fasting plasma glucose values in statin users were higher than in non-statin users (P < 0.05). But in diabetes mellitus subgroups, the average fasting plasma glucose did not have a significant difference between statin users and non-statin users (P > 0.05). In non-diabetes mellitus patients, the incidence of stress hyperglycemia with statin therapy was significantly higher than with non-statin therapy (P = 0.003). But in diabetes mellitus patients group, there is no significant difference in incidence of stress hyperglycemia between patients with statin therapy and patients without statin therapy (P = 0.902).The incidence of heart failure and in-hospital mortality of acute myocardial infarction in patients with stress-induced hyperglycemia was significantly higher than in non-hyperglycemia patients (P < 0.05). Conclusion: Statins are related to higher stress hyperglycemia and cardiac incidences after acute myocardial infarction. [ABSTRACT FROM AUTHOR]

Objective: This study assesses whether stress-induced hyperglycemia is a predictor of poor outcome at 3 months for patients with acute ischemic stroke (AIS) treated by endovascular treatment (EVT) and impacted by their previous blood glucose status., Methods: This retrospective study collected data from 576 patients with AIS due to large vessel occlusion (LVO) treated by EVT from March 2019 to June 2022. The sample was composed of 230 and 346 patients with and without diabetes mellitus (DM), respectively, based on their premorbid diabetic status. Prognosis was assessed with modified Rankin Scale (mRS) at 3-month after AIS. Poor prognosis was defined as mRS>2. Stress-induced hyperglycemia was assessed by fasting glucose-to-glycated hemoglobin ratio (GAR). Each group was stratified into four groups by quartiles of GAR (Q1-Q4). Binary logistic regression analysis was used to identify relationship between different GAR quartiles and clinical outcome after EVT., Results: In DM group, a poor prognosis was seen in 122 (53%) patients and GAR level was 1.27 ± 0.44. These variables were higher than non-DM group and the differences were statistically significant ( p < 0.05, respectively). Patients with severe stress-induced hyperglycemia demonstrated greater incidence of 3-month poor prognosis (DM: Q1, 39.7%; Q2, 45.6%; Q3, 58.6%; Q4, 68.4%; p = 0.009. Non-DM: Q1, 31%; Q2, 32.6%; Q3, 42.5%; Q4, 64%; p < 0.001). However, the highest quartile of GAR was independently associated with poor prognosis at 3 months (OR 3.39, 95% CI 1.66-6.96, p = 0.001), compared to the lowest quartile in non-DM patients after logistic regression. This association was not observed from DM patients., Conclusion: The outcome of patients with acute LVO stroke treated with EVT appears to be influenced by premorbid diabetes status. However, the poor prognosis at 3-month in patients with DM is not independently correlated with stress-induced hyperglycemia. This could be due to the long-term damage of persistent hyperglycemia and diabetic patients' adaptive response to stress following acute ischemic damage to the brain., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Duan, Yun, Rajah, Che, Wang, Liu, Tong, Cheng, Cai, Geng and Ding.)

The authors consider the influence of carbohydrate metabolism disorders on postoperative period. Data on the influence of diabetes mellitus on morbidity are summarized. Mechanisms and significance of stress-induced hyperglycemia are described. The authors also discuss modern approaches to the treatment of hyperglycemic conditions in perioperative period.

Stress-induced hyperglycemia is a common problem in patients admitted to the Intensive Care Unit, even when glucose homeostasis has previously been normal. Hyperglycemia is a near-universal inding in persons suffering catabolic illnesses and may worsen prognosis. The presence of hyperglycemia is associated with an increased risk of infectious complications in surgical patients, and indirect evidence indicates that maintenance of euglycemia can reduce the risk of infection. The causes of stress hyperglycemia include the presence of excessive counterregulatory hormones (glucagon, growth hormone, catecholamine, and glucocorticoid, either endogenous or exogenous), high circulating or tissue levels of cytokine (in particular tumor necrosis factor-alpha [TNalpha] and interleukin-1). This metabolic milieu results in failure of insulin to suppress hepatic gluconeogenesis despite hyperglycemia; in addition, insulin-mediated glucose uptake into skeletal muscle is impaired. Patients given excessive nutritional support, especially by the intravenous route, are particularly likely to encounter hyperglycemia. Insulin remains the obvious treatment for hyperglycemia, although evidence documenting the clinical benefit of aggressive insulin therapy in the Intensive Care Unit is sparse. It has been beneficial for patients in the surgery Intensive Care Units. [ABSTRACT FROM AUTHOR]

Elevated glucose level on admission in the number of emergency conditions, including acute myocardial infarction (AMI), is linked to worse outcomes, regardless of the current treatment. The introduction of primary percutaneous coronary intervention (PPCI) in therapy of AMI patients with ST segment elevation (STEMI) has improved the treatment of these patients. However, there are contradictory evidences regarding the impact of stress-induced hyperglycemia on the treatment outcome. The present study is aimed to indentify the effect of stress-induced hyperglycemia on in-hospital prognosis of patients with STEMI treated with AIM-PPCI. Prospective study included 116 patients with a diagnosis of first AMI-STEMI treated with PPCI at the Department of Cardiovascular Diseases, Clinical Center Niš in the period 2010-2011. Immediately after establishing the diagnosis, the patients with adequate medicament preparation were transferred into the angiography room for the coronary stent implantation. Laboratory analysis of the whole blood samples were done immediately after admission and in the next 24 hours. Receiver operator characteristic (ROC) analysis revealed that stress-induced hyperglycemia (glucose 11.2 mmol / L, an area under the curve of 0.812) is a delimiting factor for distinguishing the outcome and survival of patients on admission. The group of patients without stress-induced hyperglycemia had mortality rate about five times less (1/79 -1.2%) than the group of patients with stress-induced hyperglycemia (5/37 -13.5%), p=0.041. Comparing these groups with the incidence of DM, stress-induced hyperglycemia had no significant effect on mortality in the group without DM (1/54 vs. 3/26, ns) and in the group with DM (1/25 vs. 1/11, ns). The cut-off value of glucose, obtained by ROC curve, is 11.2 mmol/L for stress-induced hyperglycemia in patients with STEMI treated with PPCI. This value could determine a significant gradient of risk: patients with glycemia <11.2 mmol/L on admission had almost five times lower risk of mortality in hospital than those with the level of glucose ≥ 1.2mmol/L. Stress-induced hyperglycemia has an equally bad effect on hospital survival in the groups with and without DM. [ABSTRACT FROM AUTHOR]

Stress-induced hyperglycemia is associated with poor outcomes in nearly all critical illnesses. This acute elevation in glucose after injury or illness is associated with increased morbidity and mortality, including multiple organ failure. Stress-induced hyperglycemia is often attributed to insulin resistance as controlling glucose levels via exogenous insulin improves outcomes, but the mechanisms are unclear. Forkhead box O (FOXO) transcription factors are direct targets of insulin signaling in the liver that regulate glucose homeostasis via direct and indirect pathways. Loss of hepatic FOXO transcription factors reduces hyperglycemia in chronic insulin resistance; however, the role of FOXOs in stress-induced hyperglycemia is unknown. We subjected mice lacking FOXO transcription factors in the liver to a model of injury known to cause stress-induced hyperglycemia. Glucose, insulin, glycerol, fatty acids, cytokines, and adipokines were assessed before and after injury. Liver and adipose tissue were analyzed for changes in glycogen, FOXO target gene expression, and insulin signaling. Stress-induced hyperglycemia was associated with reduced hepatic insulin signaling and increased hepatic FOXO target gene expression while loss of FOXO1, 3, and 4 in the liver attenuated hyperglycemia and prevented hyperinsulinemia. Mechanistically, the loss of FOXO transcription factors mitigated the stress-induced hyperglycemia response by directly altering gene expression and glycogenolysis in the liver and indirectly suppressing lipolysis in adipose tissue. Reductions were associated with decreased IL-6, TNF-α, and follistatin and increased FGF21, suggesting that cytokines and FOXO-regulated hepatokines contribute to the stress-induced hyperglycemia response. This study implicates FOXO transcription factors as a predominant driver of stress-induced hyperglycemia through means that include cross-talk between the liver and adipose, highlighting a novel mechanism underlying acute hyperglycemia and insulin resistance in stress. • Liver forkhead box O (FOXO) target gene expression is increased in critical illness. • Loss of FOXO1, 3, and 4 in the liver mitigates stress-induced hyperglycemia (SIH). • Hepatic FOXO drives SIH via direct and indirect means in the liver and adipose. [ABSTRACT FROM AUTHOR]