Association of preoperative blood glucose level with delirium after non-cardiac surgery in diabetic patients

Park Soo Jung,Oh Ah Ran,이종환,Yang Kwangmo,박정찬 대한마취통증의학회 2024 Korean Journal of Anesthesiology Vol.77 No.2

Background: Hyperglycemia has shown a negative association with cognitive dysfunction. We analyzed patients with high preoperative blood glucose level and hemoglobin A1c (HbA1c) level to determine the prevalence of postoperative delirium.Methods: We reviewed a database of 23,532 patients with diabetes who underwent non-cardiac surgery. Acute hyperglycemia was defined as fasting blood glucose > 140 mg/dl or random glucose > 180 mg/dl within 24 h before surgery. Chronic hyperglycemia was defined as HbA1c level above 6.5% within three months before surgery. The incidence of delirium was compared according to the presence of acute and chronic hyperglycemia.Results: Of the 23,532 diabetic patients, 21,585 had available preoperative blood glucose level within 24 h before surgery, and 18,452 patients reported levels indicating acute hyperglycemia. Of the 8,927 patients with available HbA1c level within three months before surgery, 5,522 had levels indicating chronic hyperglycemia. After adjustment with inverse probability weighting, acute hyperglycemia was related to higher incidence of delirium (hazard ratio: 1.33, 95% CI [1.10,1.62], P = 0.004 for delirium) compared with controls without acute hyperglycemia. On the other hand, chronic hyperglycemia did not correlate with postoperative delirium.Conclusions: Preoperative acute hyperglycemia was associated with postoperative delirium, whereas chronic hyperglycemia was not significantly associated with postoperative delirium. Irrespective of chronic hyperglycemia, acute glycemic control in surgical patients could be crucial for preventing postoperative delirium.

Hyperglycemia during Adjuvant Chemotherapy as a Prognostic Factor in Breast Cancer Patients without Diabetes

안하림,강상율,윤현조,정성후 한국유방암학회 2020 Journal of breast cancer Vol.23 No.4

Purpose: Breast cancer treatments, including chemotherapy, administered in combination with glucocorticoids can induce hyperglycemia. This study aimed to investigate the effect of hyperglycemia during adjuvant chemotherapy on the prognosis of breast cancer patients without a known history of diabetes. Methods: In this study, 936 patients who underwent breast cancer surgery from 2010 to 2015 were initially selected as participants. Chemotherapy-related hyperglycemia was defined as fasting plasma glucose levels ≥ 100 mg/dL or random blood glucose levels ≥ 140 mg/dL during 2 or more cycles of adjuvant chemotherapy. After dividing the patients into the euglycemia and hyperglycemia groups, univariate and multivariate analyses were performed, and survival outcomes were analyzed by propensity score matching. Results: The mean age of the patients was 47.4 ± 7.7 years, and the median follow-up period was 70.1 months. Eighty-two patients (19.4%) were diagnosed as having hyperglycemia. There were significant differences between the euglycemia and hyperglycemia groups with respect to age, hypertension, body mass index, axillary surgery extents, nodal stage, and total steroid dosage. T stage, vascular invasion, and hyperglycemia were identified as prognostic factors of relapse-free survival (RFS). The 5-year RFS rates were 92.0% and 82.3% in the euglycemia and hyperglycemia groups, respectively, and there was a statistically significant difference between the 2 groups (p = 0.011). The 5-year overall survival rates were 94.6% and 92.0% in the euglycemia and hyperglycemia groups, respectively, showing no statistically significant difference between the 2 groups (p = 0.113). Conclusion: These data suggest that hyperglycemia during adjuvant chemotherapy is a prognostic factor for RFS in breast cancer patients without diabetes.

Acute Hyperglycemia Associated with Anti-Cancer Medication

황보율,이은경 대한내분비학회 2017 Endocrinology and metabolism Vol.32 No.1

Hyperglycemia during chemotherapy occurs in approximately 10% to 30% of patients. Glucocorticoids and L-asparaginase are wellknown to cause acute hyperglycemia during chemotherapy. Long-term hyperglycemia is also frequently observed, especially in patientswith hematologic malignancies treated with L-asparaginase-based regimens and total body irradiation. Glucocorticoid-inducedhyperglycemia often develops because of increased insulin resistance, diminished insulin secretion, and exaggerated hepatic glucoseoutput. Screening strategies for this condition include random glucose testing, hemoglobin A1c testing, oral glucose loading, andfasting plasma glucose screens. The management of hyperglycemia starts with insulin or sulfonylurea, depending on the type, dose,and delivery of the glucocorticoid formulation. Mammalian target of rapamycin (mTOR) inhibitors are associated with a high incidenceof hyperglycemia, ranging from 13% to 50%. Immunotherapy, such as anti-programmed death 1 (PD-1) antibody treatment,induces hyperglycemia with a prevalence of 0.1%. The proposed mechanism of immunotherapy-induced hyperglycemia is an autoimmuneprocess (insulitis). Withdrawal of the PD-1 inhibitor is the primary treatment for severe hyperglycemia. The efficacy of glucocorticoidtherapy is not fully established and the decision to resume PD-1 inhibitor therapy depends on the severity of the hyperglycemia. Diabetic patients should achieve optimized glycemic control before initiating treatment, and glucose levels should bemonitored periodically in patients initiating mTOR inhibitor or PD-1 inhibitor therapy. With regard to hyperglycemia caused by anticancertherapy, frequent monitoring and proper management are important for promoting the efficacy of anti-cancer therapy and improvingpatients’ quality of life.

TPN 투여되는 내과계 중환자에서 고혈당증 발생여부에 의한 치료 결과의 비교

박지원,정주원,김재연,송영천 한국병원약사회 2008 병원약사회지 Vol.25 No.4

Hyperglycemia is common in critically ill patients, even in those without diabetes mellitus. The importance of balancing the serum blood glucose in critically ill patients is also well known. However, there are some reports that patients receiving total parenteral nutrition(TPN) have higher risk of hyperglycemia. This study was designed to observe the incidence of hyperglycemia and evaluate the treatment outcomes of hyperglycemic patients on TPN in a medical ICU. We conducted the retrospective study on the patients who were hospitalized from Jan 2007 to June 2007 in Asan Medical Center, who were on TPN for more than 5 days. The data was collected by medical chart review. We analyzed the components of TPN, total daily calories, serum glucose, liver function test, serum albumin, protein and infection during the initial 7 days of TPN administration. Hyperglycemia was defined as serum glucose level exceeding 150mg/dl for 3 consecutive days in this study. All 147 patients who were administered TPN were analyzed. The patients with diabetes mellitus were excluded(n=31, 21%). The incidence of hyperglycemia within the initial 7 days was 56%(65/116). There were no significant differences in gender, initial APACHE II score, nutritive conditions before receiving TPN, use of mechanical ventilator, administration of insulin and the amount of TPN supply between the hyperglycemic group(n=65) and non-hyperglycemic group(n=51). However, the patients in hyperglycemic group were significantly older than those in non-hyperglycemic group(p=0.005), and initial serum glucose level before receiving TPN was also higher in hyperglycemic group(p=0.021). The infection rates with hyperglycemia showed a tendency to increase in hyperglycemic group(p=0.077). ICU mortality rate was significantly higher in hyperglycemic group, compared to non-hyperglycemic group(p=0.041). In conclusion, hyperglycemia occurred highly in critically ill patients, and the association between TPN and hyperglycemia was not statistically significant. However, it might also be associated with increased mortality

TPN 투여 환자에서 고혈당증 조절을 위한 Insulin 투여량

이수연,최수안,남궁형욱,이병구,한호성,신완균 한국병원약사회 2005 병원약사회지 Vol.22 No.3

Hyperglycemia is a common complication related to TPN administration. Because uncontrolled hyperglycemia results in electrolyte imbalance, decrease of immune function, increase of muscle protein catabolism, nonketogenic coma and increase of mortality, it is an obstacle of effective nutritional support. If stable blood sugar level maintain through appropriate administration of insulin, we can plan safe nutritional support for the critically ill patient needed to TPN administration. Objectives of this study were to yield appropriate insulin dose needed to control TPN-induced hyperglycemia and analysis the risk factor affected to hyperglycemia. EMR of 40 patients using insulin due to TPN induced hyperglycemia was reviewed from May of 2003 to Sep. of 2004. Exclusion criteria is not NPO state, concurrent oral intake, using NPH, unstable blood sugar level. In stable blood sugar level after administration insulin, yield insulin requirement per glucose, analysis the effect of risk factor on hyperglycemia. Insulin requirement per glucose is in total patient group, in DM patient, in non-DM patient 0.141 IU/g, 0.162 IU/g, 0.118 IU/g. In all patient group ICU patient, GIR, sepsis increase the insulin requirement. (α=0.05)

Post-stroke Hyperglycemia in Non-diabetic Ischemic Stroke is Related With Worse Functional Outcome: A Cohort Study

윤진아,신용일,김덕용,Min Kyun Sohn,Jongmin Lee,Sam-Gyu Lee,Yang-Soo Lee,Eun Young Han,Min Cheol Joo,Gyung-Jae Oh,Minsu Park,장원혁,Yun-Hee Kim 대한재활의학회 2021 Annals of Rehabilitation Medicine Vol.45 No.5

Objective To investigate long-term and serial functional outcomes in ischemic stroke patients without diabetes with post-stroke hyperglycemia. Methods The Korean Stroke Cohort for Functioning and Rehabilitation (KOSCO) is a large, multi-center, prospective cohort study of stroke patients admitted to participating hospitals in nine areas of Korea. From KOSCO, ischemic stroke patients without diabetes were recruited and divided into two groups: patients without diabetes without (n=779) and with post-stroke hyperglycemia (n=223). Post-stroke hyperglycemia was defined as a glucose level >8 mmol/L. Functional assessments were performed 7 days and 3, 6, and 12 months after stroke onset. Results There were no significant differences in baseline characteristics between the groups, except in the age of onset and smoking. Analysis of the linear correlation between the initial National Institutes of Health Stroke Scale (NIHSS) score and glucose level showed no significant difference. Among our functional assessments, NIHSS, Fugl-Meyer Assessment (affected side), Functional Ambulatory Category, modified Rankin Scale, and Korean Mini-Mental State Examination (K-MMSE) showed statistically significant improvements in each group. All functional improvements except K-MMSE were significantly higher in patients without post-stroke hyperglycemia at 7 days and 3, 6, and 12 months. Conclusion The glucose level of ischemic stroke patients without diabetes had no significant correlation with the initial NIHSS score. The long-term effects of stress hyperglycemia showed worse functional outcomes in ischemic stroke patients without diabetes with post-stroke hyperglycemia.

Effect of the Concomitant Use of Subcutaneous Basal Insulin and Intravenous Insulin Infusion in the Treatment of Severe Hyperglycemic Patients

임예지,온정훈,정주,류지원,김선욱,조재호,박희선,김혜원,이종찬,김은선,김낙현,조유환,장학철 대한내분비학회 2022 Endocrinology and metabolism Vol.37 No.3

Background: No consensus exists regarding the early use of subcutaneous (SC) basal insulin facilitating the transition from continuous intravenous insulin infusion (CIII) to multiple SC insulin injections in patients with severe hyperglycemia other than diabetic ketoacidosis. This study evaluated the effect of early co-administration of SC basal insulin with CIII on glucose control in patients withsevere hyperglycemia. Methods: Patients who received CIII for the management of severe hyperglycemia were divided into two groups: the early basal insulin group (n=86) if they received the first SC basal insulin 0.25 U/kg body weight within 24 hours of CIII initiation and ≥4 hoursbefore discontinuation, and the delayed basal insulin group (n=79) if they were not classified as the early basal insulin group. Rebound hyperglycemia was defined as blood glucose level of >250 mg/dL in 24 hours following CIII discontinuation. Propensityscore matching (PSM) methods were additionally employed for adjusting the confounding factors (n=108). Results: The rebound hyperglycemia incidence was significantly lower in the early basal insulin group than in the delayed basal insulin group (54.7% vs. 86.1%), despite using PSM methods (51.9%, 85.2%). The length of hospital stay was shorter in the early basal insulin group than in the delayed basal insulin group (8.5 days vs. 9.6 days, P=0.027). The hypoglycemia incidence did not differbetween the groups. Conclusion: Early co-administration of basal insulin with CIII prevents rebound hyperglycemia and shorten hospital stay withoutincreasing the hypoglycemic events in patients with severe hyperglycemia.

Telmisartan mitigates hyperglycemia-induced vascular inflammation by increasing GSK3β-Ser⁹ phosphorylation in endothelial cells and mouse aortas

Song, Kee-Ho,Bae, Sun-Ju,Chang, Jiyeon,Park, Jung-Hyun,Jo, Inho,Cho, Kae Won,Cho, Du-Hyong Elsevier 2017 Biochemical and biophysical research communication Vol.491 No.4

<P><B>Abstract</B></P> <P>Telmisartan, an angiotensin II type 1 receptor blocker (ARB), attenuates hyperglycemia-aggravated vascular inflammation by decreasing IκB kinase β (IKKβ) expression in endothelial cells. Because glycogen synthase 3β (GSK3β) is involved in inflammatory process by regulating nuclear factor-κB (NF-κB) activity, we investigated whether GSK3β mediates telmisartan-ameliorated vascular inflammation in hyperglycemia-treated endothelial cells and high-fat diet (HFD)-fed mice. Telmisartan remarkably induced GSK3β-Ser<SUP>9</SUP> phosphorylation in hyperglycemia-treated endothelial cells that accompanied a decrease in hyperglycemia-induced NF-κB p65-Ser<SUP>536</SUP> phosphorylation, vascular cell adhesion molecule-1 (VCAM-1) expression, and THP-1 monocyte adhesion. Ectopic expression of GSK3β-S9A, a constitutively active mutant of GSK3β, significantly restored complete telmisartan-inhibited NF-κB p65-Ser<SUP>536</SUP> phosphorylation, VCAM-1 expression, and THP-1 monocyte adhesion. In addition, it reversed telmisartan-repressed IKKβ expression. Among the ARB, including losartan and fimasartan, only telmisartan increased GSK3β-Ser<SUP>9</SUP> phosphorylation, and telmisartan-induced GSK3β-Ser<SUP>9</SUP> phosphorylation remained unchanged by pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor γ (PPARγ) antagonist. Finally, in the aortas of HFD-fed mice, telmisartan treatment significantly attenuated HFD-induced upregulation of NF-κB p65-Ser<SUP>536</SUP> phosphorylation, VCAM-1 expression, and IKKβ expression and downregulation of GSK3β-Ser<SUP>9</SUP> phosphorylation. Taken together, our findings demonstrated that telmisartan ameliorates hyperglycemia-exacerbated vascular inflammation, at least in part, by inducing GSK3β-Ser<SUP>9</SUP> phosphorylation, which consequently inhibits IKKβ expression, NF-κB p65-Ser<SUP>536</SUP> phosphorylation, and VCAM-1 expression in a PPARγ-independent manner.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Telmisartan inhibits GSK3β activity by inducing GSK3β-Ser<SUP>9</SUP> phosphorylation. </LI> <LI> Increased GSK3β-Ser<SUP>9</SUP> phosphorylation leads to a decrease in IKKβ expression. </LI> <LI> Reduced IKKβ expression attenuates NF-κB p65 phosphorylation and VCAM-1 expression. </LI> <LI> Finally, these mediate ameliorating effects of telmisartan on vascular inflammation. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Hemichorea- Hemiballismus Associated with Hyperglycemia: A Case Report

허영진,정해웅 대한영상의학회 2017 대한영상의학회지 Vol.76 No.4

Hemichorea-hemiballism (HCHB) associated with nonketotic hyperglycemia is the most common cause of unilateral chorea in patients with type 2 diabetes mellitus. T1-weighted MRI characteristically demonstrates hyperintensity in the contralateral corpus striatum. Here we describe a case of HCHB associated with nonketotic hyperglycemia and unusual brain involvement. A 51-year-old man presented with involuntary limb movements for several months. He had a history of diabetes mellitus and poorly controlled hyperglycemia. MRI demonstrated characteristic striatal hyperintensity, with involvement of the temporal lobe and midbrain. The patient’s hyperglycemia was controlled with medication. However, his involuntary movements were reduced in terms of severity, but not eliminated, by the time of discharge. HCHB associated with hyperglycemia usually resolves rapidly after correction of blood glucose levels; thus, early recognition and glycemic control are needed to prevent an irreversible outcome.

흰쥐의 일과성 전뇌허혈모델에서 허혈성 신경세포손상에 대한 저체온과 고혈당의 동반효과

오종배 대한뇌졸중학회 2000 Journal of stroke Vol.2 No.1

Background & Objectives : Hypothermia is used in patients undergoing cardiac surgery to protect the brain. Hyperglycemia aggravates neuronal damage in global and focal cerebral ischemia. However, it is not clear whether it is beneficial or harmful if both hypothermia and hyperglycemia coexist in transient global ischemia. Methods : We used forty male Sprague- Dawley rats. Rats were divided into four groups; 1) normoglycemic, normal temperature (NGNT), 2) normoglycemic, low temperature (NGLT), 3) hyperglycemic, normal temperature (HGNT), and 4) hyperglycemic, low temperature (HGLT). Hyperglycemia was induced by intraperitoneal injection of streptozotocin 3 days before ischemia or intraperitoneal injection of glucose solution 30 minutes before ischemia. Intraischemic body temperature was regulated as 32˚C for hypothermia and 37˚C for normothermia group. Transient global cerebral ischemia was induced by clipping both common carotid arteries and blood exsanguination. Pre- and postischemic blood pressure and preischemic physiologic parameters were measured. The numbers of viable neuron were counted at CA1 sector of hippocampus, 5 or 7 days after ischemia. Results : Mean glucose levels were significantly higher in HGNT and HGLT groups than in NGNT and NGLT groups. The number of viable neurons in NGLT group was significantly higher than that in NGNT group (p = 0.04). No significant differences were recognized between HGLT group and HGNT group (p = 0.71) and between NGNT group and HGLT group (p = 0.55). Conclusions : Hypothermia had protective effect against ischemia in case of normoglycemia, not in hyperglycemia. Our results suggest that avoidance of hyperglycemia is mandatory for the effective neuroprotection by hypothermia and that the harmful effect of hyperglycemia possibly overrides the protective effect of hypothermia in transient global ischemia. Korean Journal of Stroke 2000;2(1): 62~69