Circulating adiponectin levels are lower in men than in women and lower in advanced coronary artery disease, obesity, and type 2 but not type 1 diabetes. However, it is not known whether low ...adiponectin levels predict development of atherosclerosis independently of other cardiovascular risk factors.
Progression of coronary artery calcification (CAC) over an average of 2.6 years (range, 1.6 to 3.3) was assessed in a cohort of patients with type 1 diabetes and nondiabetic subjects 19 to 59 years of age. In this nested case-control substudy, plasma adiponectin levels were measured in 101 cases with significant CAC progression and in 205 controls. Controls were oversampled on the basis of age, gender, diabetes status, and presence of baseline CAC. In conditional logistic regression adjusted for baseline CAC volume and other significant predictors of CAC progression, adiponectin levels were inversely related to progression of CAC in diabetic (OR, 0.47; 95% CI, 0.24 to 0.94) and nondiabetic (OR, 0.15; 95% CI, 0.05 to 0.40 for a doubling in adiponectin levels) subjects. Adjustment for additional cardiovascular risk factors did not change this association. In conditional logistic regression models by quartiles of plasma adiponectin levels, the probability value for trend was statistically significant for all participants (P<0.001) and nondiabetic participants (P<0.001) and was borderline for type 1 diabetics (P=0.08).
Low plasma adiponectin levels are associated with progression of CAC in type 1 diabetic and nondiabetic subjects independently of other cardiovascular risk factors.
OBJECTIVE:--To compare the prevalence, awareness, treatment, and control of hypertension in a population-representative sample of adults with type 1 diabetes and comparable nondiabetic control ...subjects. RESEARCH DESIGN AND METHODS--In 2000-2002, the Coronary Artery Calcification in Type 1 Diabetes Study enrolled 1,416 individuals aged 19-56 years with no known history of coronary artery disease: 652 type 1 diabetic patients (46% male, mean age 37 years) and 764 nondiabetic control subjects (50% male, mean age 39 years). Subjects were asked if they had been told by a physician that they had hypertension or were on a blood pressure medication. Blood pressure was measured using standardized Joint National Committee (JNC) protocol. RESULTS:--Type 1 diabetic subjects, compared with nondiabetic subjects, had higher rates of hypertension prevalence (43 vs. 15%, P < 0.001), awareness (53 vs. 45%, P = 0.11), treatment (87 vs. 47%, P < 0.001), and control (55 vs. 32%, P < 0.001) for the JNC 6 goal (130/85 mmHg). Only 42% of all type 1 diabetic hypertensive subjects met the new JNC 7 goal (130/80 mmHg). Type 1 diabetic subjects had better blood pressure control (72 vs. 32%, P < 0.0001), using 140/90 mmHg as a common measure. The majority of treated subjects were on a single antihypertensive agent (75 vs. 64%). CONCLUSIONS:--Subjects with type 1 diabetes have higher rates of hypertension prevalence, treatment, and control than nondiabetic subjects. However, hypertension remains largely uncontrolled, even if treated in high-risk populations, such as type 1 diabetic subjects and undiagnosed individuals in the general population. Achieving more stringent blood pressure goals will require increased attention and may necessitate the use of multiple antihypertensive agents.
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Background: Malglycemia, defined as hypoglycemia, hyperglycemia, or glycemic variability is common in adult hematopoietic stem cell transplant (HSCT) recipients. It is associated with increased ...rates of infection, acute graft-versus-host disease (GVHD), organ dysfunction, time to engraftment, and mortality. Malglycemia in pediatric HSCT has not been well studied and may have unique incidence, risk factors and clinical implications. Therefore, this study aimed to identify the incidence of and risk factors for malglycemia inpediatric, adolescent and young adult (AYA) HSCT patients, and to characterize associated impacts on outcomes.
Methods: Medical records for 351 pediatric/AYA patients, age 0-26 years (average 8.0 years, interquartiles 3.0, 15.0; 59.3% male), who underwent first HSCT from 2007-2016 at Children's Hospital Colorado were retrospectively reviewed. Patients with pre-existing diabetes mellitus (n=5) and patients with inadequate blood glucose data (n=2) were excluded, resulting in a final cohort of 344 patients. The goal was to identify risk factors for malglycemia and to determine its association with clinically significant infection in the first 100 days after HSCT. Malglycemia was defined as presence of mean blood glucose ≥126 mg/dL and/or standard deviation ≥29 mg/dL for each patient, assessed for the following intervals: pre-HSCT (days -14 to 0), days 0-30, days 0-100, and overall (days -14 to +100).
Results: Malglycemia occurred in 43.9% of patients, with 22.3% experiencing malglycemia in the two weeks prior to HSCT, 22.3% in the first 30 days post-HSCT, and 22.6% in the first 100 days post-HSCT. In univariate analysis, the rate of malglycemia was higher among patients who underwent allogeneic than autologous transplant (pre-HSCT 35.6% vs 8.4%, p<0.001; days 0-30 25.8% vs 16.1%, p=0.056; days 0-100 27.6% vs 13.6%, p=0.004). In multivariate analysis, age ≥12 years was a risk factor for pre-HSCT malglycemia (p<0.0001), and post-HSCT steroids and treatment with tacrolimus were risk factors for post-HSCT (day 0-100) malglycemia (p<0.0001, p=0.034). Additional factors that did not have an association with malglycemia in multivariate analysis included body mass index, underlying diagnosis category (malignant vs non-malignant), pre-HSCT treatment with insulin, asparaginase, steroids, or radiation, HSCT type (autologous vs allogeneic), preparative regimen, post-HSCT treatment with total parenteral nutrition or radiation. Malglycemia at any time was associated with increased infection (p=0.008-0.042). After adjusting for age, pre-HSCT radiation, HSCT type, GVHD diagnosis (grades II-IV and/or chronic) and post-HSCT steroids, for each 10 mg/dL increase in pre-HSCT glucose, there was a 29.3% increase in any post-HSCT infection (p=0.007) and specifically a 28.8% increase in serious bacterial infection (SBI) (p<0.0001) and a 29.7% increase in viremia/viruria (p=0.002); similar findings existed at other time intervals analyzed (Table 1). Additionally, after adjusting for HSCT type and presence of GVHD, for every 10 mg/dL increase in mean glucose over days 0-100, the average number of hospitalized days from 0-100 increased by 2.7 days (p<0.0001) and days in the intensive care unit (ICU) increased by 1 day (p<0.0001). Similarly, patients with malglycemia during days 0-100 averaged 12.9 more hospital days (p<0.0001) and 3.9 more ICU days (p<0.0001) in the first 100 days post-HSCT than patients without malglycemia, regardless of HSCT type or GVHD diagnosis.
Conclusion : Malglycemia occurs frequently in the pediatric/AYA HSCT population and is more common in adolescent patients. When controlling for HSCT type, presence of GVHD and treatment with steroids, malglycemia is an independent risk factor leading to increased rates of serious bacterial infections and viremia/viruria. Mechanistically, the temporal relationship between pre-HSCT mean glucose increases and higher rates of infection support a causal link. The underlying pathophysiology by which malglycemia may influence outcomes such as infection is likely multifactorial, but data suggests that hyperglycemia drives immune system impairment and supports a pro-inflammatory state. Understanding the morbidities associated with malglycemia, and the underlying pathophysiology, should inform future studies evaluating the utility of intensive glucose control in improving pediatric/AYA HSCT outcomes.
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No relevant conflicts of interest to declare.
The objective of this study was to compare tobacco smoke exposure in mothers and their healthy children less than 3 years old using hair cotinine (HC) levels as an objective long-term measure of ...exposure. Hair samples were obtained from mother/child pairs recruited from the Columbus Children's Hospital Primary Care Center, and were analyzed by radioimmunoassay to compare HC levels. Mothers were both self-reported smokers and nonsmokers. Contributing and confounding variables were assessed based on questionnaires completed by participants. Exclusion criteria for children were prematurity and presence of chronic cardiopulmonary disease. Hair samples and questionnaires were obtained from 104 mother/child pairs. Child and maternal HC levels were correlated for both self-reported maternal smokers (R2=.13, p<.013) and self-reported maternal nonsmokers (R2=.54, p<001). Child HC levels were higher than maternal HC levels (1.18 ng/mg vs. .78 ng/mg, p<.001). Children of nonsmokers had higher HC levels than their mothers (.77 ng/mg vs. .35 ng/mg, p<.001), while HC levels of smokers and their children were no different (1.91 ng/mg vs. 1.92 ng/mg, p=.978). The relationship between child and maternal HC did not differ by child age, gender, or race. In conclusion, environmental tobacco smoke exposure in young children as reflected by HC is higher than expected based on prior studies of biomarkers and passive tobacco smoke exposure in adult nonsmokers.
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