ライフサイエンスコーパス: HbA1c

1 HbA1c contributed significantly to PD in women (P = 0.01

2 HbA1c is considered one of the primarily factor to disce

3 HbA1c is formed by the non-enzymatic glycation of termin

4 HbA1c levels reduced for TG1.

5 HbA1c levels, urinary albumin-creatinine ratio (p = 0.04

6 d a significant reduction in TG (p = 0.001), HbA1c (p = 0.019) and fasting plasma glucose (p = 0.019)

7 ding TyG-WC (SD -0.20; 95% CI -0.26, -0.15), HbA1c (SD -0.16; 95% CI -0.23, -0.10), weight (SD -0.12;

8 ssociation studies (GWAS) have identified 18 HbA1c-associated genetic variants.

9 ommon clinical practice, BMI >= 23 kg/m(2) + HbA1c >= 5.7% (AUROC = 0.70 [0.64-0.75]) and anthropomet

10 MI (0.7 mum; 95% CI, 0.4-1.0 per 5 kg/m(2)), HbA1c level (0.4 mum; 95% CI, -0.1 to 0.9 per 1%), and b

11 28), 3.6 SD-OCT tests (range, 2-10), and 8.3 HbA1c tests (range, 2-21).

12 nt differences for all 9 CGM metrics, 6 of 7 HbA1c outcomes, and none of the 15 cognitive and patient

13 Haemoglobin A1c (HbA1c) is a significant glycaemic marker for diabetes me

14 including disease duration, haemoglobin A1c (HbA1c) levels and urine albumin creatinine ratio.

15 suse, well-being, change in haemoglobin A1c (HbA1c), and smoking cessation.

16 f all recommended levels of haemoglobin A1c (HbA1c), BP, and cholesterol; risky prescribing levels; a

17 , and DCCT/EDIC mean updated hemoglobin A1c (HbA1c) (2-step progression: HR, 1.28; 95% CI, 1.03-1.58;

18 may fail to achieve adequate hemoglobin A1c (HbA1c) control despite metformin-sulfonylurea (Met-SU) d

19 nvestigated whether elevated hemoglobin A1c (HbA1c) is associated with the development of pancreatic

20 Hemoglobin A1c (HbA1c) is widely used to diagnose diabetes and assess gl

21 ], 1.7%-3.3% per 5 kg/m(2)), hemoglobin A1c (HbA1c) level (2.2%; 95% CI, 1.0%-3.5% per 1%), and preva

22 tcome was the change in mean hemoglobin A1c (HbA1c) levels estimated over three 12-month periods: pre

23 rolled blood glucose levels (hemoglobin A1c (HbA1c) levels of >7) also had intracellular HA, whereas

24 y insulin injections and had hemoglobin A1c (HbA1c) levels of 7.5% to 9.9%.

25 ed using a questionnaire and hemoglobin A1c (HbA1c) levels were measured.

26 Hemoglobin A1c (HbA1c) levels were recorded.

27 ype 1 diabetes and screening hemoglobin A1c (HbA1c) of 7.5% to 10.9%.

28 least 10 (range, 0-27); and hemoglobin A1c (HbA1c) of at least 8%, systolic blood pressure (SBP) of

29 glycemic status evaluated by hemoglobin A1c (HbA1c) on the risk of thromboembolism among patients wit

30 Measurement of hemoglobin A1c (HbA1c) provides an estimate of mean blood sugar levels a

31 sterol, triglycerides (TGs), hemoglobin A1c (HbA1c), and homeostasis model assessment of insulin resi

32 dynamic effects, assessed by hemoglobin A1c (HbA1c), body weight, and blood lipid concentrations, of

33 interview or measurements of hemoglobin A1c (HbA1c), fasting plasma glucose (FPG), and 2-hour plasma

34 , lipids, serum glucose, and hemoglobin A1c (HbA1c).

35 for the glycemic outcome of hemoglobin A1c (HbA1c).

36 Unfortunately, tests such as hemoglobin A1c (HbA1c)/fasting plasma glucose (FPG) alone fail to diagno

37 ycemia, and glucose control; hemoglobin A1c (HbA1c); and cognition and patient-reported outcomes, wit

38 1268 (34%) had prediabetes (hemoglobin A1c [HbA1c] 5.7-6.4%), and 606 (16%) had normoglycemia (HbA1c

39 with glycated hemoglobin (or hemoglobin A1c [HbA1c]) levels is unclear.

40 etic variation, may influence how accurately HbA1c reflects underlying glycemia.

41 ration clinical categories and 0.688 for ADA HbA1c clinical categories for all-cause mortality.

42 l concentration categories and 0.672 for ADA HbA1c clinical categories for atherosclerotic cardiovasc

43 ration clinical categories and 0.722 for ADA HbA1c clinical categories for peripheral arterial diseas

44 20 secondary outcomes, including additional HbA1c outcomes, CGM glucose metrics, and patient-reporte

45 esterol); percentage of patients who met all HbA1c, SBP, and LDL cholesterol targets; and mean reduct

46 y, incorporating BMI >= 23 kg/m(2) alongside HbA1c >= 5.7% into first-stage screening to identify hig

47 3.2% (12 of 19, 7.6% of total cohort) had an HbA1c >=5.7%.

48 e 1 diabetes for at least 2 years and had an HbA1c level of 6.0% to 12.0%.

49 fication of therapy for patients who have an HbA1c level lower than 6.5% and avoidance of HbA1c-targe

50 3.1 kg/m (-4.4 to -1.9) kg/m, P < 0.001] and HbA1c change [mean adjusted difference -0.5% (95% CI -0.

51 ons in glucose (17.02 mg/dL [p < 0.001]) and HbA1c (0.63% [p < 0.001]) levels were recorded.

52 e length and fasting glucose (P = 0.003) and HbA1c (P = 0.0008) were found.

53 Older age (p < 0.01) and HbA1c in the prediabetic range or higher (p = 0.01) were

54 a = 0.07; 95% CI: 0.01, 0.14; P = 0.025) and HbA1c (beta = 0.46; 95% CI: 0.06, 0.85; P = 0.02).

55 (hazard ratio, 1.49; 95% CI, 1.09-2.05) and HbA1c >58 mmol/mol (hazard ratio, 1.59; 95% CI, 1.13-2.2

56 ders, age (aOR 9.08, 95% CI 2.29-36.10), and HbA1c > 5.7% (aOR 5.82, 95% CI 1.50-22.54) remained asso

57 time was 8.1% +/- 2% (range, 5.5-15.6), and HbA1c fluctuation was 0.6% +/- 0.6% (range, 0-4.4).

58 atients with diagnosed DM had higher BMI and HbA1c, less severe TB, and more frequent comorbidities,

59 adjusting for baseline weight, TG, HDL-C and HbA1c (p = 0.002).

60 ary by biomarker, with total cholesterol and HbA1c showing the greatest intersectional variation.

61 y associated with glucose concentrations and HbA1c levels within the normal non-diabetic range indepe

62 ificant correlations between DM duration and HbA1c levels with the investigated OCT-A parameters.

63 onversation Map improved patient glucose and HbA1c levels.

64 WHR), glucose, insulin, HOMA-B, HOMA-IR, and HbA1c.

65 Data on 2-hour plasma glucose level and HbA1c concentration were not available, and the glycemic

66 randomized trials show less weight loss and HbA1c improvement compared with Roux-en-Y gastric bypass

67 A1c <=48 mmol/mol, HbA1c=49-58 mmol/mol, and HbA1c >58 mmol/mol.

68 between plasma organophosphate residues and HbA1c but no association with acetylcholine esterase was

69 umferences, 4-site skinfold thicknesses) and HbA1c z-scores with dysglycemia (fasting glucose >=6.1 m

70 Healthcare provision included annual HbA1c, renal function (estimated glomerular filtration r

71 Undiagnosed diabetes was defined as HbA1c 6.5% or greater, FPG 126 mg/dL or greater, or 2hPG

72 Diabetes was defined as HbA1c of >=6.5% and/or current diabetes medication.

73 Average HbA1c mean was 7.1% +/- 1.1% (range, 5.4-11.7), peak HbA

74 On average, HbA1c levels overestimate the mean glucose concentration

75 f cardiovascular disease, BMI, age, baseline HbA1c, and baseline estimated glomerular filtration rate

76 thod of insulin administration, and baseline HbA1c.

77 ferent combinations of conditions), baseline HbA1c, and all-cause mortality in T2D.

78 analyzed as a continuous variable, baseline HbA1c did not significantly modify the benefits of empag

79 Outcomes of interest were baseline HbA1c and all-cause mortality.

80 rically greater among patients with baseline HbA1c >/=7.5% than those with HbA1c <7.5% (interaction p

81 Because HbA1c levels were registered annually at routine visits,

82 t gain was associated with marginally better HbA1c outcomes only among patients with near normal HbA1

83 There was no association between HbA1c and duration of diabetes with nerve fibre paramete

84 lly significant differences in 3 of 7 binary HbA1c outcomes, 8 of 9 CGM metrics, and 1 of 4 patient-r

85 Baseline BMI, HbA1c, and diabetes-duration were similar between groups

86 ticipants with HbA1c 6.8% or higher, or both HbA1c less than 6.8% and Short Form Health Survey (SF-36

87 The performance of current point-of-care HbA1c analyzers available on the market are also compare

88 , patients were divided into the categories: HbA1c <=48 mmol/mol, HbA1c=49-58 mmol/mol, and HbA1c >58

89 for sex, age, diabetes duration, concurrent HbA1c and hypertension, neither haplogroups H1, H2, UK,

90 ntinuous insulin treatment, or 2 consecutive HbA1c >=8.5% while on >=2 oral glucose-lowering drugs (O

91 patients were diabetologically conspicuous (HbA1c >= 5.7%), including those with already known DM.

92 In non-MetS, strategies to control HbA1c and SBP should be prioritised as these have the la

93 edication given ("treated"), and controlled (HbA1c < 8.0% or equivalent).

94 patient with long-standing T2D and a current HbA1c level of 7.8%.

95 placebo, ranolazine significantly decreased HbA1c by 0.42 +/- 0.08% (adjusted mean difference +/- SE

96 Age, duration of diabetes, HbA1c, BMI, BCVA, and CST had no impact on the ability t

97 m plasma glucose >= 11.1 mmol/l (200 mg/dl), HbA1c >= 6.5%, or reporting to be taking medication for

98 itiation contributed time until clinical DM (HbA1c >=6.5%, initiation of DM-specific medication, or n

99 ough routinely measured, the impact of donor HbA1c levels on pancreas graft outcomes has not been rep

100 t organization use of HbA1c shows that donor HbA1c levels between 3.5 and 6.2 in otherwise transplant

101 sociation between increased age and elevated HbA1c (p < 0.01).

102 HRIs with elevated HbA1c were more likely to have pancreatic cysts compared

103 itial surveillance in patients with elevated HbA1c.

104 We evaluated HbA1c, body weight, BMI, body composition parameters, bl

105 All analyses, except HbA1c, were associated with moderate/high heterogeneity.

106 t intensification, nonwhite groups had fewer HbA1c measurements than white groups.

107 For HbA1c, however, the association with obesity duration pe

108 the American Diabetes Association to aim for HbA1c levels less than 7% for many nonpregnant adults an

109 han White individuals to have monitoring for HbA1c (OR 1.10, 95% CI 1.01-1.20; p = 0.023) and eGFR (O

110 The future perspectives for HbA1c detection and diabetes management are proposed.

111 we report the label-free affinity sensor for HbA1c based on the chemiresistor-type field-effect trans

112 White individuals to have annual testing for HbA1c (OR 0.89, 95% CI 0.79-0.99; p = 0.04) and retinopa

113 her IMD quintiles to have annual testing for HbA1c, BP, eGFR, retinopathy, and neuropathy.

114 st association with obesity duration was for HbA1c: HbA1c levels in those with obesity for <5 years w

115 ively correlated with fasting blood glucose, HbA1c and diastolic blood pressure (DBP), and positively

116 d cardiometabolic markers including glucose, HbA1c, insulin, C-peptide, HOMA-IR, triglycerides, and b

117 poorly controlled diabetes (glycohemoglobin [HbA1c] >=8.0%) was unexpectedly associated with better T

118 ycerides <=1.7 mmol/L, glycated haemoglobin (HbA1c) <=53 mmol/mol (<=7.0%), systolic blood pressure <

119 lood glucose (RBS), or glycated haemoglobin (HbA1c) were reported.

120 Mean changes in glycated haemoglobin (HbA1c), and mean changes in fasting blood sugar (FBS) le

121 etween multimorbidity, glycated haemoglobin (HbA1c), and mortality in people with T2D have been studi

122 age, sex, deprivation, glycated haemoglobin (HbA1c), body mass index (BMI), smoking status, comorbidi

123 olesterol (HDL-C), and glycated haemoglobin (HbA1c).

124 o-hip ratio (WHR), glycosylated haemoglobin (HbA1c), diabetes duration, retinopathy, nephropathy, chr

125 iglycerides [TGs], and glycated haemoglobin [HbA1c]).

126 ciation with obesity duration was for HbA1c: HbA1c levels in those with obesity for <5 years were rel

127 nce in postintervention glycated hemoglobin (HbA1c) between the arms (P = 0.007).

128 -peptide, and increased glycated hemoglobin (HbA1c) compared with sham-operated controls.

129 The level of Glycated hemoglobin (HbA1c) is accordingly examined for checking diabetes mel

130 Glycated hemoglobin (HbA1c) is used to diagnose type 2 diabetes (T2D) and ass

131 rs with DM duration and glycated hemoglobin (HbA1c) levels were evaluated among patients with type 1

132 T (SD-OCT) tests, and 2 glycated hemoglobin (HbA1c) measures over time with a minimum follow-up of 6

133 imated using laboratory glycated hemoglobin (HbA1c) or fasting plasma glucose in TB patients.

134 oassay for detection of glycated hemoglobin (HbA1c) that can reveal a patient's average level of bloo

135 ic control (assessed by glycated hemoglobin (HbA1c) values) in patients from the Kaiser Permanente No

136 ucose, fasting insulin, glycated hemoglobin (HbA1c), and homeostasis model assessment of insulin resi

137 d with low-fat dairy on glycated hemoglobin (HbA1c), body weight, and cardiovascular disease risk fac

138 tatus, fasting glucose, glycated hemoglobin (HbA1c), fructosamine, glycated albumin), and a latent va

139 , fasting glucose (FG), glycated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric acid, C-react

140 associated with higher glycated hemoglobin (HbA1c), insulin, HOMA-IR, triglycerides, liver fat, and

141 fasting blood glucose, glycated hemoglobin (HbA1c), triglyceride levels, triglycerides and glucose (

142 OR15+years = 3.99), glycosylated hemoglobin (HbA1c) (OR6.5-6.9% = 1.33, OR7-7.9% = 1.86, OR8%+ = 3.22

143 Measurement of glycosylated hemoglobin (HbA1c) is a gold standard procedure for assessing long t

144 ation of DM and the glycosylated hemoglobin (HbA1c) levels of the patients in the DM group were recor

145 lood glucose [FBG], and glycated hemoglobin [HbA1c]) and survival in all lung transplant (LTx) recipi

146 was associated with extremes of BMI and high HbA1c.

147 In non-MetS, higher HbA1c, SBP, and number of MetS components were linked to

148 th <1 serving/mo) was associated with higher HbA1c (6.5%; 95% CI: 1.9, 11.3; P-trend = 0.007); howeve

149 etes mellitus duration of >=10 years, higher HbA1c levels were not associated with a higher risk of t

150 RETATION: Semaglutide significantly improved HbA1c and bodyweight in patients with type 2 diabetes co

151 The primary outcome was change in HbA1c from baseline to 26 weeks.

152 The primary outcome was change in HbA1c from randomisation to 34 weeks' gestation in pregn

153 The primary outcome was change in HbA1c levels at 3 months.

154 nce (gain, loss, or no change) and change in HbA1c value, adjusting for individual- and area-level at

155 luding alcohol misuse, well-being, change in HbA1c, and smoking cessation.

156 e were no differences in the mean changes in HbA1c, body weight, BMI, body composition or lipid param

157 We assessed changes in HbA1c, triglycerides, HDL cholesterol and BMI in a mixed

158 th T2D only, the mean difference (95% CI) in HbA1c was -0.82% (-0.88, -0.76) p < 0.001.

159 Difference in HbA1c between weeks 26 and 69 for the 2 treatments.

160 We found a small difference in HbA1c in pregnant women using CGM (mean difference -0.19

161 ding factors, mean, peak, and fluctuation in HbA1c levels were not significantly associated with rate

162 Notably, improvements in HbA1c were akin to those observed in landmark trials.

163 duration was associated with an increase in HbA1c (0.02% per hour [95% CI 0.00 to 0.05]; P = 0.045).

164 Increase in HbA1c over time was statistically significant when sever

165 duction of at least 0.5 percentage points in HbA1c, 5 mm Hg in SBP, or 10 mg/dL in LDL cholesterol.

166 ot significantly correlate with reduction in HbA1c and TG.

167 lsartan had a greater long-term reduction in HbA1c than those receiving enalapril.

168 ntrol of blood sugar level (20% reduction in HbA1c) and weight control than daily injection of free l

169 0 score, >=0.5-percentage point reduction in HbA1c, >=5-mm Hg reduction in SBP, >=10-mg/dL reduction

170 ted with DMAb show significant reductions in HbA1c as compared to patients treated either with bispho

171 g, or canagliflozin 300 mg had reductions in HbA1c of 0.81%, 0.82%, and 0.93%, respectively, at 1 yea

172 graphic information, clinical data including HbA1c, and imaging results.

173 e evaluated at 0, 6, and 12 weeks, including HbA1c, body weight, body composition by dual-energy X-ra

174 Increasing HbA1c levels were associated with the study's secondary

175 data indicate that the impact of increasing HbA1c and SBP on DR probability is incrementally the sam

176 Correcting for age, sex, body mass index, HbA1c and statin therapy, an increase in 25(OH)D of 1 nm

177 ddition to a recommendation to individualize HbA1c target levels, the ACP proposed a level between 7%

178 n (lean or fat mass); fasting serum insulin; HbA1c; glucose dynamics during glucose tolerance testing

179 -0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), HbA1c [-10 g/L (95% CI: -12.90, -7.10 g/L; impaired gluc

180 ed with a small increase in population-level HbA1c.

181 ride, low-density lipid, high-density lipid, HbA1c (glycosylated hemoglobin), serum creatinine, eosin

182 (HRQOL), blood pressure, biomarkers (lipids, HbA1c, CRP) and 24-hour Holter monitoring were obtained

183 lower plasma glucose (p = 0.043), and lower HbA1c (p = 0.008) compared with CON animals.

184 Empagliflozin did not lower HbA1c in patients with prediabetes or normoglycemia and

185 imorbidity counts were associated with lower HbA1c and increased mortality in both datasets.

186 variant of TMPRSS6 was associated with lower HbA1c levels (P = 8.66 x 10-10).

187 tic cysts compared to individuals with lower HbA1c on initial imaging in a pancreatic surveillance pr

188 an-Americans, MAF = 2% in Hispanics) lowered HbA1c (-0.88% in hemizygous males, -0.34% in heterozygou

189 Mean HbA1c change from baseline to 28 weeks was 0.3% (SD 0.9;

190 Mean HbA1c decreased in the CGM group compared with the stand

191 Mean HbA1c levels were significantly higher in group-1 than g

192 Mean HbA1c reduction from baseline was 1.1% at 12 weeks and 1

193 Mean HbA1c was 8.9% at baseline and 8.5% at 26 weeks in the C

194 mean furosemide dose, 49.6+/-31.3 mg/d; mean HbA1c, 7.9+/-3.8%) were recruited.

195 raftment but with significant different mean HbA1c levels of 5.5 +/- 0.4% for SPK and 8.3 +/- 1.5% fo

196 <0.001% [95% CI, -0.008% to 0.010%]) of mean HbA1c compared with the intervention period (P = .09 and

197 The mean HbA1c level was 9.1% in black persons and 8.3% in white

198 The mean HbA1c levels were higher in group A (P <0.01) than group

199 The mean HbA1c levels were significantly higher among CS (P <0.01

200 The mean HbA1c was 8.46% (95% CI, 8.40%-8.52%) at baseline and de

201 ears; 52% female; 53% insulin pump use; mean HbA1c, 7.5% [SD, 0.9%]), 83% used CGM at least 6 days pe

202 uration of diabetes 4 [IQR: 1-9] years; mean HbA1c 7.4% +/- 1.7%; mean body mass index [BMI] 25.3 +/-

203 nce in change in central-laboratory-measured HbA1c level from baseline to 24 weeks.

204 d cons of different techniques for measuring HbA1c are outlined.

205 an 300 different assay methods for measuring HbA1c which leads to variations in reported values from

206 Median HbA1c in TB-DM patients ranged from 7.4% (Romania) to 11

207 ed into the categories: HbA1c <=48 mmol/mol, HbA1c=49-58 mmol/mol, and HbA1c >58 mmol/mol.

208 Nonetheless, HbA1c was lower in overweight men and women in the resve

209 utcomes only among patients with near normal HbA1c values at baseline.

210 5.7-6.4%), and 606 (16%) had normoglycemia (HbA1c <5.7%).

211 n heterozygous females) and explained 23% of HbA1c variance in African-Americans and 4% in Hispanics.

212 In the meta-analysis of HbA1c from 35 of the included studies, the mean differen

213 The analysis of HbA1c tends to be complicated because there are more tha

214 0 total participants in the meta-analysis of HbA1c when accounting for the design effect of cluster R

215 litus is largely determined by assessment of HbA1c (glycated hemoglobin A1c) levels, which poorly ref

216 HbA1c level lower than 6.5% and avoidance of HbA1c-targeted treatment for patients with a life expect

217 diabetes status and across the continuum of HbA1c.

218 ys including biosensors for the detection of HbA1c.

219 d models were used to estimate the effect of HbA1c on rates of change in SAP mean deviation (MD) and

220 follow-up became null with the exception of HbA1c.

221 the product of the proteolytic hydrolysis of HbA1c.

222 sociated with greater postpartum increase of HbA1c (beta = 0.08%; P = 0.03) and 2-hour OGTT glucose c

223 The level of HbA1c reflects the mean blood glucose level over the pri

224 pe 2 diabetes mellitus, increasing levels of HbA1c were associated with a higher risk of thromboembol

225 n diabetes control, as measured by levels of HbA1c, and rates of visual field or RNFL loss over time

226 e to intensify treatment within 12 months of HbA1c >7.5% [58 mmol/mol]), were estimated using multiva

227 center/organ procurement organization use of HbA1c shows that donor HbA1c levels between 3.5 and 6.2

228 Values of HbA1c were summarized for each patient as mean, peak, an

229 n; there was no effect of nut consumption on HbA1c or fasting glucose.

230 e maintaining energy intake has no effect on HbA1c, body weight, body composition, lipid profile, or

231 h professionals leads to a greater effect on HbA1c, weight, and LDL cholesterol.

232 of Physicians (ACP) published a guideline on HbA1c targets for nonpregnant adults with T2D.

233 The optimal HbA1c target level among various persons with T2D is a s

234 ose (-0.02 mg/dL; 95% CI, -0.12 to 0.08), or HbA1c levels (-0.0002 mg/dL; 95% CI, -0.0021 to 0.0016).

235 L; 95% CI: -1.43, 0.38 mg/dL; I2 = 53.4%) or HbA1c (WMD: 0.02%; 95% CI: -0.01%, 0.04%; I2 = 51.0%).

236 usly associated with T2D, fasting glucose or HbA1c were nominally (P < 0.05) associated with fasting

237 effects were observed for fasting glucose or HbA1c.

238 (AUROC = 0.71 [0.65-0.76]) both outperformed HbA1c >= 5.7% alone (AUROC = 0.61 [0.57-0.65]).

239 tions with dysglycemia but none outperformed HbA1c (OR = 4.09 [2.81-5.94]).

240 ld have stronger discriminative ability over HbA1c alone in detecting dysglycemia (diabetes and predi

241 the start of the intervention and an overall HbA1c level increase of 0.14% (95% CI, 0.05%-0.23%; P =

242 an was 7.1% +/- 1.1% (range, 5.4-11.7), peak HbA1c over time was 8.1% +/- 2% (range, 5.5-15.6), and H

243 h was 13.2% in women with a periconceptional HbA1c level below 6.5% (adjusted risk ratio [aRR] vs. wo

244 irth was strongly linked to periconceptional HbA1c levels.

245 groups (IMD quintiles 1 and 2) showed poorer HbA1c than the least deprived (IMD quintile 5).

246 adjusted means showed that postintervention HbA1c was lower on resveratrol (35.8 +/- 0.43 mmol/mol)

247 Preoperative HbA1c levels were examined as a continuous and categoric

248 eased readmission, but elevated preoperative HbA1c was not.

249 coronary artery disease, C-reactive protein, HbA1c, height, obesity, smoking status, triglycerides, t

250 t circumference, blood pressure, heart rate, HbA1c, blood glucose, LDL-to-HDL cholesterol ratio, C-re

251 On the basis of the most recent HbA1c measurement before an incident atrial fibrillation

252 increasing multimorbidity count and reduced HbA1c alongside increased mortality in people with T2D a

253 uivalent efficacy as comparators in reducing HbA1c by 0.05% (95% CI: -0.21 to 0.11) and greater effic

254 inical observation of a GABAA-R PAM reducing HbA1c levels in diabetic patients.

255 Guidelines regarding HbA1c targets have yielded differing recommendations.

256 score, Patient Health Questionnaire-9 score, HbA1c, SBP, and LDL cholesterol.

257 64.7%, GADA (>=35 U/mL) in 54.1%, and serum HbA1c > 48 mmol/mol in 94.3% of the individuals.

258 were analyzed including assessments of serum HbA1c levels and GADA titers.

259 Haematological tests (blood sugar, HbA1c and lipid profile, 31.8%), OCT (27.4%), refraction

260 Thirty-nine patients with uncontrolled T2D (HbA1c >7.5%) and 24 age- and sex-matched healthy control

261 Intensive glycemic control (IGC) targeting HbA1c fails to show an unequivocal reduction of macrovas

262 12 and 24 months who met treatment targets (HbA1c <7.0%, SBP <130 mm Hg, LDL cholesterol <100 mg/dL

263 biomarkers-LDL, HDL, total cholesterol, TG, HbA1c, Apo AI, Apo AII, Apo B, CRP, TNF-alpha, glucose,

264 No significant effects were observed for TG, HbA1c, CRP, ALT, and AST.

265 especially for the low concentrations of the HbA1c obtained from electrokinetic mixing assisted and c

266 lucose levels (p = 0.005) and 0.34% in their HbA1c levels (p < 0.001).

267 ed whether adding anthropometric measures to HbA1c would have stronger discriminative ability over Hb

268 80 [95%CI 0.75-0.85]) performed similarly to HbA1c alone (AUROC = 0.79 [0.74-0.84]).

269 thropometry trio) as continuous variables to HbA1c (AUROC = 0.80 [95%CI 0.75-0.85]) performed similar

270 = 0.70 [0.64-0.75]) and anthropometry trio + HbA1c >= 5.7% (AUROC = 0.71 [0.65-0.76]) both outperform

271 tia following identification of uncontrolled HbA1c.

272 ong participants with SCT when defined using HbA1c values (29.2% vs 48.6% for prediabetes and 3.8% vs

273 s suggest that prediabetes definitions using HbA1c were more specific and provided modest improvement

274 All participants were screened for DM using HbA1c and fasting plasma glucose at TB treatment and aft

275 The most frequently used threshold was HbA1c<42 mmol/mol (6.0%) in 47 (20%) definitions.

276 Blood-based biomarkers were HbA1c, total cholesterol and C-reactive protein.

277 While HbA1c, mean glucose and median percent time hypoglycemic

278 ing the risk of hypoglycaemia in adults with HbA1c below 7.5% (58 mmol/mol).

279 ), we confirmed five regions associated with HbA1c (GCK in Europeans and African-Americans, HK1 in Eu

280 d 60 common genetic variants associated with HbA1c.

281 s) and detected significant association with HbA1c when aggregating rare missense variants in G6PD.

282 er studies in large multiethnic cohorts with HbA1c, glycemic, and erythrocytic traits are required to

283 B1 level was also positively correlated with HbA1c and negatively correlated with nitric oxide (NO) i

284 mes and, despite an overall correlation with HbA1c, was elevated in some low-BMI individuals with nor

285 nefit was reported in those individuals with HbA1c > 7%.

286 In a sub-group analysis of participants with HbA1c > 7%, larger reductions in glucose (17.02 mg/dL [p

287 event over 9.6 years among participants with HbA1c 6.8% or higher, or both HbA1c less than 6.8% and S

288 73%, p=0.038) By contrast, participants with HbA1c less than 6.8% and baseline SF-36 general health s

289 Compared with patients with HbA1c <=48 mmol/mol, we observed a higher risk of thromb

290 risk of thromboembolism among patients with HbA1c=49-58 mmol/mol (hazard ratio, 1.49; 95% CI, 1.09-2

291 derdiagnosed for diabetes when screened with HbA1c.

292 , 95% CI: 1.72% to 3.78%), and in those with HbA1c <6.5% at baseline (3.08%, 95% CI: 2.47% to 3.69%).

293 with baseline HbA1c >/=7.5% than those with HbA1c <7.5% (interaction p = 0.07).

294 lso had intracellular HA, whereas those with HbA1c of <7, did not.

295 Women with HbA1c levels consistent with recommended target levels a

296 nsulin levels, of CDK5 tv1 positively with % HbA1c levels, while in controls, elevated levels of TSPA

297 People of Black ethnicity had worse HbA1c than those of White ethnicity.

298 Supermarket loss was associated with worse HbA1c trajectories for those with good, moderate, and po

299 % females, diabetes duration 13.2 +/- 8.3 y, HbA1c 8.09 +/- 0.96%) who consumed <3 servings of dairy/

300 ars, duration of diabetes-9.1 +/- 2.7 years, HbA1c-75.66 +/- 2.53 mmol/mol [9.1 +/- 1.8%]) and 48 age