Association Between Hyper- and Hypoglycaemia and 2-Year All-Cause Mortality Risk in Diabetic Patients With Acute Coronary Events

2005 ◽  
Vol 14 (10) ◽  
pp. 4
Author(s):  
A.M. Svensson ◽  
D.K. McGuire ◽  
P. Abrahamsson ◽  
M. Dellborg
2005 ◽  
Vol 26 (13) ◽  
pp. 1255-1261 ◽  
Author(s):  
Ann-Marie Svensson ◽  
Darren K. McGuire ◽  
Putte Abrahamsson ◽  
Mikael Dellborg

2020 ◽  
Author(s):  
Chao-lei Chen ◽  
Lin Liu ◽  
Jia-yi Huang ◽  
Yu-ling Yu ◽  
Kenneth Lo ◽  
...  

Abstract Background The optimal blood pressure (BP) level for diabetic patients remains controversial, and population-based evidence on BP management for individuals with normoglycemia and prediabetes is insufficient. We aimed to investigate the associations between systolic blood pressure (SBP) and all-cause mortality among US adults with different glucose metabolism.Methods We used data from the 1999–2014 National Health and Nutrition Examination Survey (NHANES, n = 40,046) with comprehensive baseline examination and follow-up assessment. Restricted cubic spline was performed to examine dose-response relationship between continuous SBP and all-cause mortality. Cox regression models were used to estimate hazard ratios of all-cause mortality for SBP categories.Results Over 32,5450 person-years of follow-up (median 8.1 years), 4745 all-cause death (11.8%) were recorded, corresponding to an event rate of 14.58 per 1000 patient years. U-shaped associations between SBP and all-cause mortality were observed regardless of glucose status. The lowest mortality risk of optimal SBP (mmHg) by group was 115–120 (normoglycemia), 120–130 (prediabetes), and 125–135 (diabetes). Compared with the reference group, SBP < 100 mmHg was significantly associated with 49% (HR = 1.49, 95%CI: 1.13–1.96), 57% (1.57, 1.07–2.3), and 59% (1.59, 1.12–2.25) higher mortality risk in normoglycemia, prediabetes, and diabetes, respectively. The multivariable-adjusted HRs of all-cause mortality for SBP of 150–159 mmHg and ≥ 160 mmHg were 1.35 (1.08–1.70) and 1.61 (1.31–1.98), 1.44 (1.13–1.83) and 1.66 (1.33–2.08), and 1.29 (1.02–1.65) and 1.37 (1.09–1.72), respectively.Conclusions U-shaped relationships between SBP and all-cause mortality existed regardless of diabetes status. The optimal SBP range for the lowest mortality was gradually higher with worsening glucose status.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
wenhui zhao ◽  
Peter Katzmarzyk ◽  
Ronald Horswell ◽  
Yujie Wang ◽  
Jolene Johnson ◽  
...  

Background: Several prospective studies have evaluated the association between body mass index (BMI) and the risk of all-cause mortality among diabetic patients; however, the results are controversial. Aim: To investigate the association of BMI levels with all-cause mortality among patients with type 2 diabetes in the Louisiana State University Hospital-based Longitudinal study (LSUHLS). Methods: We performed a prospective cohort study (2000-2009) of diabetic patients including 19,785 African Americans and 15,534 whites. Cox proportional hazards regression models were used to estimate the association of BMI levels at baseline, during follow-up and at last visit with the risk of all-cause mortality. Results: During a mean follow up of 8.7 years, 4,206 deaths were identified. The multivariable-adjusted (age, sex, smoking, income and type of insurance) hazard ratios (HRs) of all-cause mortality associated with BMI levels (<23, 23-24.9, 25-29.9, 30-34.9 [reference group], 35-39.9, and ≥40 kg/m 2 ) at baseline were 2.53 (95% confidence interval [CI] 2.18-2.93), 1.76 (1.48-2.09), 1.23 (1.08-1.40), 1.00, 1.19 (1.02-1.38), and 1.22 (1.05-1.41) for African Americans, and 1.92 (1.63-2.27), 1.53 (1.28-1.82), 1.07 (0.95-1.21), 1.00, 1.07 (0.93-1.23), and 1.21 (1.06-1.39) for whites, respectively. When stratified by age, gender, smoking status or use of anti-diabetic drugs, a U-shaped association was still present. When we used an updated mean or last visit value of BMI, the U-shaped association of BMI with all-cause mortality risk did not change. Conclusions: The current study indicated a U-shaped association of BMI with all-cause mortality risk among African American and white patients with type 2 diabetes. A significantly increased risk of all-cause mortality was observed among African Americans with BMI<30 kg/m 2 and BMI ≥35 kg/m 2 , and among whites with BMI<25 kg/m 2 and BMI ≥40 kg/m 2 compared with patients with BMI 30-34.9 kg/m 2 .


2021 ◽  
Author(s):  
Shanjie Wang ◽  
Ye Wang ◽  
Xin Wan ◽  
Junchen Guo ◽  
Yiying Zhang ◽  
...  

<a><b>Objective</b></a> Despite periodical monitoring of cobalamin (vitamin B12) in metformin-treated diabetic patients is recommended, the cobalamin-associated mortality benefits or risks remains unclear. We investigated the association between cobalamin intake and related biomarkers and mortality risk in diabetic adults using metformin or not. <p><b>Methods</b> This study included 3,277 adults with type 2 diabetes from NHANES and followed up until December 31, 2015. Weighted Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95% CIs for mortality risk.</p> <p><b>Results </b>Among 3,277 participants, 865 all-cause deaths occurred during a median follow-up of 7.02 years. There was no robust relationship between all-cause mortality and serum cobalamin, intakes from foods or cobalamin supplements regardless of metformin treatment (each p ≥0.120). The doubling of methylmalonic acid (MMA, a cobalamin-deficiency marker) was significantly associated with higher all-cause (HR 1.31 95%CI 1.18–1.45, p <0.001) and cardiac mortality (HR 1.38 95%CI 1.14–1.67, p =0.001). Cobalamin sensitivity was assessed by the combination of binary B12<sub>low/high</sub> and MMA<sub>low/high</sub> (cutoff values: cobalamin 400 pg/ml and MMA 250nmol/L). Patients with decreased cobalamin sensitivity (MMA<sub>high</sub>B12<sub>high</sub>) had the highest mortality risk. The multivariable-adjusted HRs (95%CIs) of all-cause mortality in MMA<sub>low</sub>B12<sub>low</sub>, MMA<sub>low</sub>B12<sub>high</sub>, MMA<sub>high</sub>B12<sub>low</sub>, and MMA<sub>high</sub>B12<sub>high</sub> groups were<sub> </sub>1.00 (reference), 0.98 (0.75–1.28), 1.49 (1.16–1.92), and 1.96 (1.38–2.78), respectively. That association was especially significant in metformin nonusers.</p> <p><b>Conclusions</b> Serum and dietary cobalamin were not associated with reduced mortality. Decreased cobalamin sensitivity was significantly associated with all-cause and cardiac mortality, particularly among metformin nonusers.</p>


2021 ◽  
Author(s):  
Shanjie Wang ◽  
Ye Wang ◽  
Xin Wan ◽  
Junchen Guo ◽  
Yiying Zhang ◽  
...  

<a><b>Objective</b></a> Despite periodical monitoring of cobalamin (vitamin B12) in metformin-treated diabetic patients is recommended, the cobalamin-associated mortality benefits or risks remains unclear. We investigated the association between cobalamin intake and related biomarkers and mortality risk in diabetic adults using metformin or not. <p><b>Methods</b> This study included 3,277 adults with type 2 diabetes from NHANES and followed up until December 31, 2015. Weighted Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95% CIs for mortality risk.</p> <p><b>Results </b>Among 3,277 participants, 865 all-cause deaths occurred during a median follow-up of 7.02 years. There was no robust relationship between all-cause mortality and serum cobalamin, intakes from foods or cobalamin supplements regardless of metformin treatment (each p ≥0.120). The doubling of methylmalonic acid (MMA, a cobalamin-deficiency marker) was significantly associated with higher all-cause (HR 1.31 95%CI 1.18–1.45, p <0.001) and cardiac mortality (HR 1.38 95%CI 1.14–1.67, p =0.001). Cobalamin sensitivity was assessed by the combination of binary B12<sub>low/high</sub> and MMA<sub>low/high</sub> (cutoff values: cobalamin 400 pg/ml and MMA 250nmol/L). Patients with decreased cobalamin sensitivity (MMA<sub>high</sub>B12<sub>high</sub>) had the highest mortality risk. The multivariable-adjusted HRs (95%CIs) of all-cause mortality in MMA<sub>low</sub>B12<sub>low</sub>, MMA<sub>low</sub>B12<sub>high</sub>, MMA<sub>high</sub>B12<sub>low</sub>, and MMA<sub>high</sub>B12<sub>high</sub> groups were<sub> </sub>1.00 (reference), 0.98 (0.75–1.28), 1.49 (1.16–1.92), and 1.96 (1.38–2.78), respectively. That association was especially significant in metformin nonusers.</p> <p><b>Conclusions</b> Serum and dietary cobalamin were not associated with reduced mortality. Decreased cobalamin sensitivity was significantly associated with all-cause and cardiac mortality, particularly among metformin nonusers.</p>


Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 638
Author(s):  
Elena Dozio ◽  
Simone Vettoretti ◽  
Lara Caldiroli ◽  
Silvia Nerini-Molteni ◽  
Lorenza Tacchini ◽  
...  

Advanced glycation end-products (AGE) can promote chronic kidney disease (CKD) progression and CKD-related morbidities. The soluble receptor for AGE (sRAGE) is a potential biomarker of inflammation and oxidative stress. Here, we explored the role of AGE, glycated albumin, sRAGE and its different forms, cRAGE and esRAGE, as prognostic factors for mortality in 111 advanced CKD patients. The median follow-up time was 39 months. AGE were quantified by fluorescence, sRAGE and its forms by ELISA. Malnutrition was screened by the Malnutrition Inflammation Score (MIS). The Cox proportional hazards regression model was used to assess the association of variables with all-cause mortality. Mean levels of sRAGE, esRAGE and cRAGE were 2318 ± 1224, 649 ± 454 and 1669 ± 901 pg/mL. The mean value of cRAGE/esRAGE was 2.82 ± 0.96. AGE were 3026 ± 766 AU and MIS 6.0 ± 4.7. eGFR correlated negatively with AGE, sRAGE, esRAGE and cRAGE, but not with cRAGE/esRAGE. Twenty-eight patients died. No difference was observed between diabetic and non-diabetic patients. Starting dialysis was not associated with enhanced risk of death. AGE, esRAGE and cRAGE/esRAGE were independently associated with all-cause mortality. AGE, esRAGE and cRAGE/esRAGE may help to stratify overall mortality risk. Implementing the clinical evaluation of CKD patients by quantifying these biomarkers can help to improve patient outcomes.


2007 ◽  
Vol 6 (1) ◽  
pp. 106-107
Author(s):  
J TEERLINK ◽  
L DELGADOHERRERA ◽  
R THAKKAR ◽  
B HUANG ◽  
R PADLEY

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 505-506
Author(s):  
Dominika Seblova ◽  
Kelly Peters ◽  
Susan Lapham ◽  
Laura Zahodne ◽  
Tara Gruenewald ◽  
...  

Abstract Having more years of education is independently associated with lower mortality, but it is unclear whether other attributes of schooling matter. We examined the association of high school quality and all-cause mortality across race/ethnicity. In 1960, about 5% of US high schools participated in Project Talent (PT), which collected information about students and their schools. Over 21,000 PT respondents were followed for mortality into their eighth decade of life using the National Death Index. A school quality factor, capturing term length, class size, and teacher qualifications, was used as the main predictor. First, we estimated overall and sex-stratified Cox proportional hazards models with standard errors clustered at the school level, adjusting for age, sex, composite measure of parental socioeconomic status, and 1960 cognitive ability. Second, we added an interaction between school quality and race/ethnicity. Among this diverse cohort (60% non-Hispanic Whites, 23% non-Hispanic Blacks, 7% Hispanics, 10% classified as another race/s) there were 3,476 deaths (16.5%). School quality was highest for Hispanic respondents and lowest for non-Hispanic Blacks. Non-Hispanic Blacks also had the highest mortality risk. In the whole sample, school quality was not associated with mortality risk. However, higher school quality was associated with lower mortality among those classified as another race/s (HR 0.75, 95% CI: 0.56-0.99). For non-Hispanic Blacks and Whites, the HR point estimates were unreliable, but suggest that higher school quality is associated with increased mortality. Future work will disentangle these differences in association of school quality across race/ethnicity and examine cause-specific mortality.


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