ライフサイエンスコーパス: hypoglycaemia

1 4 to 0.88; p=0.0131; 25.5%vs 33.6% had minor hypoglycaemia).

2 ey protective mechanism for the organ during hypoglycaemia.

3 ove glycaemic control and reduce the risk of hypoglycaemia.

4 on, inducing weight gain or posing a risk of hypoglycaemia.

5 that is dose-dependent but does not lead to hypoglycaemia.

6 young, type 1 (MODY1) and hyperinsulinaemic hypoglycaemia.

7 consequently, the risk of hyperglycaemia or hypoglycaemia.

8 ts with type 2 diabetes with minimum risk of hypoglycaemia.

9 a role in the counterregulatory response to hypoglycaemia.

10 and was well tolerated with minimum risk of hypoglycaemia.

11 reased weight gain, and high risk for severe hypoglycaemia.

12 r resistance increased in all fetuses during hypoglycaemia.

13 upling and lower the risk of weight gain and hypoglycaemia.

14 o respond to mitochondrial inhibition and to hypoglycaemia.

15 ed insulin secretion even in the presence of hypoglycaemia.

16 ate (measured as ) was almost doubled during hypoglycaemia.

17 e aged 75 years and older because of reduced hypoglycaemia.

18 ed adrenal responsiveness to insulin-induced hypoglycaemia.

19 c patients is limited by a high frequency of hypoglycaemia.

20 is crucial in the response to hypoxia and to hypoglycaemia.

21 who have difficulty recognising the onset of hypoglycaemia.

22 glucose metabolism in the liver with minimal hypoglycaemia.

23 more effective than BGAT at reducing severe hypoglycaemia.

24 foundation for management and prevention of hypoglycaemia.

25 on secretion, impaired glucose tolerance and hypoglycaemia.

26 ove insulin sensitivity and increase risk of hypoglycaemia.

27 of combined clinically significant or severe hypoglycaemia.

28 nd bodyweight at week 52 and a lower risk of hypoglycaemia.

29 ibitors probably increase the risk of severe hypoglycaemia.

30 stemic inflammatory response, accompanied by hypoglycaemia.

31 the resolution of T2DM and the induction of hypoglycaemia.

32 hypoglycaemia and no participants had severe hypoglycaemia.

33 ol and bodyweight, without increased risk of hypoglycaemia.

34 ) operation with a high risk of postprandial hypoglycaemia.

35 n people with type 1 diabetes predisposes to hypoglycaemia.

36 We also assessed incidence of severe hypoglycaemia.

37 g or stable rates of hospital admissions for hypoglycaemia.

38 reduce the burden of hospital admissions for hypoglycaemia.

39 ital mortality, and 1 month readmissions for hypoglycaemia.

40 for the global burden of hospitalisation for hypoglycaemia.

41 mpanied by reduced time spent by patients in hypoglycaemia.

42 .86; p=0.0157), fewer incidences of neonatal hypoglycaemia (0.45; 0.22 to 0.89; p=0.0250), and 1-day

43 on responsiveness to arginine was reduced by hypoglycaemia (0.98 +/- 0.11 ng ml(-1) in H vs. 1.82 +/-

44 se events (2.09, 1.85, to 2.36, p < 0.0001), hypoglycaemia (1.21, 1.06, to 1.38, p = 0.012), baseline

45 .0359), as were rates of nocturnal confirmed hypoglycaemia (1.4 vs 1.8 episodes per patient-year of e

46 glycaemic control while lowering the risk of hypoglycaemia(3).

47 recorded during infusion of insulin-induced hypoglycaemia (8-17 mIU kg(-1) min(-1) ) in Alfaxan-anae

48 Fetal pancreatic adaptations to relative hypoglycaemia, a characteristic of intra-uterine growth

49 In adults, hyperinsulinaemic hypoglycaemia accounts for 0.5-5.0% of cases of hypoglyc

50 However, biochemical hypoglycaemia also was increased in the study, which wil

51 During hypoglycaemia, an initial rise in fetal heart rate was f

52 nt for a range of acute conditions including hypoglycaemia, anaphylaxis and cardiac arrest.

53 nhibit mTORC1, which coincides with profound hypoglycaemia and a decrease in plasma amino-acid concen

54 estigated individuals with hyperinsulinaemic hypoglycaemia and biochemical or genetic evidence to sug

55 oglycaemia accounts for 0.5-5.0% of cases of hypoglycaemia and can be due either to beta-cell tumours

56 Higher rates of combined level 2 or level 3 hypoglycaemia and greater incidence of severe hypoglycae

57 linically, GSDIa is characterized by fasting hypoglycaemia and hepatic glycogen and triglyceride over

58 endocrine tumour who presented with reactive hypoglycaemia and hyperglycaemia, but who was subsequent

59 the p85 alpha isoform are viable but display hypoglycaemia and increased insulin sensitivity correlat

60 o the observations for K(ATP) currents, both hypoglycaemia and inhibition of mitochondrial function e

61 timum diabetes control to reduce the risk of hypoglycaemia and its consequences in advanced type 2 di

62 abetic patients against episodes of profound hypoglycaemia and make the achievement of normoglycaemia

63 ally-occurring fruit-based toxins that cause hypoglycaemia and metabolic derangement.

64 There were no reports of severe hypoglycaemia and no deaths during the study.

65 in and placebo groups, with low incidence of hypoglycaemia and no emergence of new safety signals.

66 and biochemical endogenous hyperinsulinaemic hypoglycaemia and no evidence for metastatic disease on

67 inically significant (<54 mg/dL [<3 mmol/L]) hypoglycaemia and no participants had severe hypoglycaem

68 eight, and safety outcomes, including severe hypoglycaemia and pulmonary toxicity.

69 t long-term trends in hospital admission for hypoglycaemia and subsequent outcomes in England to help

70 nd severe hypoglycaemia can increase fear of hypoglycaemia and the risk of subsequent hypoglycaemic e

71 The safety endpoints included hypoglycaemia and uncontrolled hyperglycaemia leading to

72 ed, phrenic neural activity increased during hypoglycaemia and was associated with a significant incr

73 t inhaled insulin has a lower risk of severe hypoglycaemia and weight gain.

74 ds to greater reductions in HbA(1c), weight, hypoglycaemia, and blood pressure than does glimepiride.

75 ell excitability, insulin hypersecretion and hypoglycaemia, and in humans lead to the clinical condit

76 s because it is associated with weight gain, hypoglycaemia, and the need for subcutaneous injections.

77 We demonstrate that hyper- and hypoglycaemia are common at the time of admission and re

78 tes, especially when weight loss and risk of hypoglycaemia are major considerations.

79 m glycaemia without promoting weight gain or hypoglycaemia, are not being undertaken.

80 ted data for all hospital admissions listing hypoglycaemia as primary reason of admission between Jan

81 cacy with low risk of clinically significant hypoglycaemia at any stage in the natural history of typ

82 Median [IQR] severe hypoglycaemia at baseline was 5[2-12] per patient/year,

83 HbA(1c) reduction with a lower incidence of hypoglycaemia at week 52.

84 Hypoglycaemia attenuates cyanide-mediated transcription

85 positive impact on cognitive barriers around hypoglycaemia avoidance and on diabetes-related and gene

86 severe hypoglycaemia complicated by impaired hypoglycaemia awareness or glycaemic lability, or who al

87 abetes technologies, were randomised to the "Hypoglycaemia Awareness Restoration Programme despite op

88 , p = 0.64 respectively), nor for changes in hypoglycaemia awareness scores or fear.

89 of combined clinically significant or severe hypoglycaemia (baseline to week 26) was statistically si

90 79 172 people had 101 475 admissions for hypoglycaemia between 2005 and 2014, of which 72 568 (72

91 Insulin (0.4 Ukg(-1)min(-1))-induced hypoglycaemia (blood glucose reduced by ca 50% to 3.4 +/

92 rated, improves glucose control, and reduces hypoglycaemia burden.

93 K(ATP) currents are observed not only during hypoglycaemia, but also in response to mitochondrial inh

94 r the ventilatory hyperpnoea observed during hypoglycaemia by an augmented carotid body and whole bod

95 In a subset of patients, post-bariatric hypoglycaemia can develop months to years after surgery,

96 Hypoglycaemia unawareness and severe hypoglycaemia can increase fear of hypoglycaemia and the

97 Hypoglycaemia caused an increase in the counter-regulato

98 oximately 80% of neurones did not respond to hypoglycaemia (changing artificial cerebrospinal fluid (

99 ative for those patients who have had severe hypoglycaemia complicated by impaired hypoglycaemia awar

100 ant-negative CREB inhibitor, exhibit fasting hypoglycaemia [corrected] and reduced expression of gluc

101 Adults with T1D, IAH and severe hypoglycaemia despite structured education in insulin ad

102 Because profound hypoglycaemia does not inhibit mTORC1 in RagA(GTP/GTP) n

103 ducing the chances of experiencing hyper- or hypoglycaemia during exercise.

104 d orexin neurones in the LH are activated by hypoglycaemia during fasting.

105 We did not observe an increased rate of hypoglycaemia during prone ventilation and the adequacy

106 (18%) people had more than one admission for hypoglycaemia during the study period.

107 (<54 mg/dL; 3.0 mmol/L) or level 3 (severe) hypoglycaemia during the treatment period were similar f

108 are important goals, as there is no risk of hypoglycaemia during this period and the adherence burde

109 These cells respond to brief hypoglycaemia either with a K(ATP) channel-mediated hype

110 control participants, with comparable severe hypoglycaemia episodes (18 CGM and 21 control) and time

111 in this study is for diagnosing the cases of hypoglycaemia especially in suppression tests of insulin

112 <54 mg/dL [<3.0 mmol/L]) or level 3 (severe) hypoglycaemia events from baseline to week 78 occurred a

113 Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea

114 ion of the cholyl-insulins was the amount of hypoglycaemia following infusion into the small intestin

115 U kg(-1) orally delivered insulin sustaining hypoglycaemia for a few hours longer than a 1 U kg(-1) d

116 stprandial glucose response to a mixed meal; hypoglycaemia frequency and severity; pulmonary function

117 The percentage of participants with hypoglycaemia (glucose <54 mg/dL or severe) was lower wi

118 .5%; -6.9% [-9.8% to -3.9], p<0.0001) and in hypoglycaemia (glucose concentration <3.9 mmol/L; 1.7% v

119 Combined level 2 hypoglycaemia (glucose concentration <54 mg/dL [<3.0 mmo

120 te advances in diabetes mellitus management, hypoglycaemia has continued to affect the majority of th

121 s associated with a decreased risk of severe hypoglycaemia (HR 0.76 [0.65-0.90]; p=0.001).

122 Impaired awareness of hypoglycaemia (IAH) is a major risk for severe hypoglyca

123 safety profile of glibenclamide and included hypoglycaemia in 15 (6%) of 259 patients in the glibencl

124 on was associated with: greater awareness of hypoglycaemia in 9 patients, significantly more intense

125 yperglycaemia was reduced without increasing hypoglycaemia in adolescents and young adults with type

126 lucose control while alleviating the risk of hypoglycaemia in adults with HbA1c below 7.5% (58 mmol/m

127 dy mass can safely reduce mean glycaemia and hypoglycaemia in adults with type 1 diabetes who were li

128 We assessed rates of hypoglycaemia in all treated patients.

129 -loop systems could reduce risk of nocturnal hypoglycaemia in children and adolescents with type 1 di

130 ent hepato-centric insulin action and blunts hypoglycaemia in dogs in response to overdosing.

131 ic assessment and enhances the prevention of hypoglycaemia in high-risk hospitalized patients.

132 a role in the counterregulatory response to hypoglycaemia in humans.

133 poglycaemia (IAH) is a major risk for severe hypoglycaemia in insulin treatment of type 1 diabetes (T

134 ay contribute to the development of neonatal hypoglycaemia in macrosomic babies of diabetic mothers.

135 s to week-long normoglycaemia and negligible hypoglycaemia in mice and minipigs with type 1 diabetes.

136 e most common cause of severe and persistent hypoglycaemia in neonates and children.

137 ypoglycaemia and greater incidence of severe hypoglycaemia in participants treated with efsitora comp

138 y explains the transient hyperinsulinism and hypoglycaemia in some IUGR infants.

139 n order to decrease the risk of postprandial hypoglycaemia in this specific cohort.

140 of cortisol response was by insulin-induced hypoglycaemia in three cases, by short tetracosactrin te

141 vernight glucose control and reduced risk of hypoglycaemia in type 1 diabetes.

142 ts against neuronal damage caused by hypoxia-hypoglycaemia in vitro and both global and focal cerebra

143 ydrochloride, NCC1048) in a model of hypoxia-hypoglycaemia in vitro and in a gerbil model of global a

144 Hypoglycaemia in vivo induces a counter-regulatory respo

145 Simulated ischemic conditions (hypoxia-hypoglycaemia) in vitro enhanced glutamate efflux from r

146 red for survival, but not for development of hypoglycaemia, in mice lacking p85 alpha.

147 d Charlson comorbidity score) admissions for hypoglycaemia; in admissions for hypoglycaemia per total

148 Severe hypoglycaemia incidence was higher with efsitora (35 [10

149 Advances in the field of hyperinsulinaemic hypoglycaemia include use of rapid molecular genetic tes

150 10 years, hospital admissions in England for hypoglycaemia increased by 39% in absolute terms and by

151 ent models of absence epilepsy, we show that hypoglycaemia increases the occurrence of spike-wave sei

152 tumour secreting GLP-1 and causing reactive hypoglycaemia, indicates a potential adverse effect of G

153 ageing population, and costs associated with hypoglycaemia, individual and national initiatives shoul

154 measured at baseline, and during acute fetal hypoglycaemia induced by maternal insulin infusion at 12

155 We show that the hypoglycaemia-induced increase in ventilation and CO2 se

156 eceptor function, is a significant driver of hypoglycaemia-induced spike-wave seizures.

157 is revealed that mitochondrial inhibition or hypoglycaemia inhibited an openly rectifying K+ conducta

158 without changes in body-mass index, rate of hypoglycaemia, insulin dose, or circulating concentratio

159 In hyperinsulinaemic hypoglycaemia, insulin secretion becomes dysregulated (i

160 l reports indicate that an increased risk of hypoglycaemia is associated with some GK activators.

161 I cells are direct physiological sensors of hypoglycaemia is challenged by the finding that the basa

162 Hypoglycaemia is counteracted by release of hormones and

163 s and prompt management of hyperinsulinaemic hypoglycaemia is essential to avoid hypoglycaemic brain

164 ously suspected, whereas a history of severe hypoglycaemia is perhaps less injurious.

165 Hyperinsulinaemic hypoglycaemia is the most common cause of severe and per

166 f GLP-1 to treat diabetes, since the risk of hypoglycaemia is thought to be low.

167 atment rate ratio 0.448, p<0.0001) and minor hypoglycaemia less frequent with liraglutide than with e

168 ostic of early dumping syndrome, and a nadir hypoglycaemia level <50 mg/dl is diagnostic of late dump

169 high (hyperglycaemia) or low blood glucoses (hypoglycaemia) levels.

170 or a person with diabetes, including fear of hypoglycaemia, loss of glycaemic control, and inadequate

171 The risk of inducing hypoglycaemia (low blood glucose) constitutes the main c

172 Hypoglycaemia (low plasma glucose) is a serious and pote

173 evertheless, homozygous mice still displayed hypoglycaemia, lower insulin levels and increased glucos

174 ssive hyperglycaemia (>10 mmol/L) and severe hypoglycaemia (<2.2 mmol/L) should be avoided in critica

175 8.0 mmol/L) (15.9%, 10.7-21.0; p<0.0001) and hypoglycaemia (<3.9 mmol/L) (median 0.9, IQR 0.2-2.2; p=

176 rate glycaemic control), while avoiding mild hypoglycaemia (<3.9 mmol/L), is a reasonable strategy in

177 Hypoglycaemia (<54 mg/dL or severe) was reported in five

178 The most common adverse events were hypoglycaemia (observed in ten [13%] of 77 participants

179 aximum femoral artery blood flow response to hypoglycaemia occurred earlier in PI50 and PI40 compared

180 Hypoglycaemia occurred in 13 patients (9%) in the sitagl

181 mg, and placebo groups, respectively; severe hypoglycaemia occurred in 21 (8%), 19 (6%), and 19 (7%)

182 Hypoglycaemia occurred in 220 (79%), 235 (79%), and 207

183 Severe hypoglycaemia occurred in one participant in the CGM plu

184 Symptoms of hypoglycaemia occurred in similar proportions of patient

185 ed in either group and one episode of severe hypoglycaemia occurred in the multiple daily injection g

186 No episodes of major hypoglycaemia occurred.

187 ; three trials) and a smaller risk of severe hypoglycaemia (odds ratio 0.61, 95% CI 0.35-0.92; five t

188 om a child with persistent hyperinsulinaemic hypoglycaemia of infancy and been engineered in culture

189 f-function mutations cause hyperinsulinaemic hypoglycaemia of infancy.

190 rate interventions given per participant for hypoglycaemia on days 1-5 (ie, glucose <3.9 mmol/L) was

191 iling and sustained hypoxaemia, acidaemia or hypoglycaemia on the fetal cardiovascular responses to a

192 In conclusion, the stimulant effect of hypoglycaemia on the hypoxic ventilatory response is con

193 levels of adrenaline mimicked the effect of hypoglycaemia on ventilation and CO2 sensitivity.

194 ients, grade 3), nausea (one [2%], grade 3), hypoglycaemia (one [2%], grade 3 and one [2%], grade 4),

195 ring exercise, which often results in either hypoglycaemia or hyperglycaemia as well as increased gly

196 No episodes of severe hypoglycaemia or hyperglycaemia with ketonaemia occurred

197 No episodes of severe hypoglycaemia or hyperglycaemia with ketonaemia occurred

198 at high risk of hypoglycaemia (recent severe hypoglycaemia or hypoglycaemia unawareness defined by a

199 No episodes of major hypoglycaemia or minor hypoglycaemia were reported.

200 No episodes of serious hypoglycaemia or other serious adverse events occurred.

201 either inhibit ATP production (e.g. hypoxia, hypoglycaemia) or that accelerate ATP consumption (e.g.

202 eprived of either oxygen (hypoxia), glucose (hypoglycaemia), or both oxygen and glucose (ischaemia).

203 g on changing cognitive barriers to avoiding hypoglycaemia, or the evidence-based "Blood Glucose Awar

204 carcinoma, and acute kidney injury [NSCLC], hypoglycaemia [other solid tumours], retinopathy [urothe

205 ol/L]), but also an increase in CGM-measured hypoglycaemia (p=0.0001 for <70 mg/dL [<3.9 mmol/L], p=0

206 ey outcomes, and key safety outcomes (severe hypoglycaemia, pancreatitis, and pancreatic cancer).

207 There was no increase in risk of severe hypoglycaemia, pancreatitis, or pancreatic cancer.

208 significant differences were seen in severe hypoglycaemia, pancreatitis, pancreatic cancer, or medul

209 Admissions for hypoglycaemia per 100 000 total hospital admissions incr

210 issions for hypoglycaemia; in admissions for hypoglycaemia per total hospital admissions and per diab

211 Rates of overall confirmed hypoglycaemia (plasma glucose <3.1 mmol/L or severe epis

212 Rates of overall confirmed hypoglycaemia (plasma glucose <3.1 mmol/L or severe) wer

213 ICIPANTS: Exploratory cohort analysis of the Hypoglycaemia Prevention With Oral Dextrose (hPOD) rando

214 ld improvements in management strategies and hypoglycaemia prevention.

215 glycaemic and severe hypoglycaemic events in hypoglycaemia-prone adults compared with use of continuo

216 (Medtronic MiniMed 640G with SmartGuard) in hypoglycaemia-prone adults with type 1 diabetes.

217 The hypoglycaemia rate was 0.34 (SE 1.44) and 0.52 (3.01) ev

218 Overall, combined level 2 and level 3 hypoglycaemia rates were similar between treatment group

219 -10.0% (40-86 mmol/mol), and at high risk of hypoglycaemia (recent severe hypoglycaemia or hypoglycae

220 day euglycaemic recovery period from chronic hypoglycaemia reestablished GSIS to normal levels, but t

221 Hypoglycaemia remains an important avoidable iatrogenic

222 men after 32 weeks, with significantly lower hypoglycaemia risk and better patient satisfaction.

223 to be efficacious but in many cases present hypoglycaemia risk due to activation of the enzyme at lo

224 mellitus improved glycaemic control without hypoglycaemia risk.

225 Rates of severe hypoglycaemia seemed similar (0.06 vs 0.05 episodes per

226 We have identified and characterized hypoglycaemia-sensitive neurones in the dorsal vagal com

227 model of type 1 diabetes without observable hypoglycaemia, showing promise for the safe and effectiv

228 Hypoglycaemia significantly augmented minute ventilation

229 Hypoglycaemia significantly decreased plasma insulin con

230 Across the two trials, rates of confirmed hypoglycaemia (SMBG <3.1 mmol/L or severe [needing assis

231 cells, contribute to the mechanisms by which hypoglycaemia stimulates glucagon release from pancreati

232 ycaemia suppressing the hypoxic response and hypoglycaemia stimulating it.

233 al and symptomatic responses during moderate hypoglycaemia suggest caffeine as a potentially useful t

234 nd cognitive function, and patients recorded hypoglycaemia symptoms on a visual analogue scale.

235 ptions to long-term medication, dehydration, hypoglycaemia, test delays or anxiety, and has no benefi

236 ec, which are associated with lower risks of hypoglycaemia than insulin glargine.

237 o the combined stress of perturbed redox and hypoglycaemia than wild-type cells.

238 der of unregulated insulin secretion despite hypoglycaemia that can occur in isolation or as part of

239 morbidities, the increased susceptibility to hypoglycaemia, the increased dependence on care and the

240 also reduced the proportion of time spent in hypoglycaemia: the proportion of time with glucose conce

241 al contributions of hypoxaemia, acidaemia or hypoglycaemia to mediating these responses can vary.

242 es in ventilation and CO2 sensitivity during hypoglycaemia to prevent a serious acidosis in poorly co

243 n anaesthetized rat model of insulin-induced hypoglycaemia to test the hypothesis that peripheral che

244 In healthy individuals, hypoglycaemia triggers glucagon secretion, which restore

245 Hypoglycaemia unawareness and severe hypoglycaemia can i

246 ypoglycaemia (recent severe hypoglycaemia or hypoglycaemia unawareness defined by a Clarke or Gold sc

247 For the patient with diabetes, hypoglycaemia unawareness--ie, the warning signs of fall

248 of combined clinically significant or severe hypoglycaemia versus glargine U100 in participants with

249 The rate of nocturnal confirmed hypoglycaemia was 25% lower with degludec than with glar

250 1, 95% CI: 1.48 to 3.31), though the risk of hypoglycaemia was absolutely lower (RR: 0.51, 95% CI: 0.

251 ation fetal cardiovascular response to acute hypoglycaemia was consistent with a redistribution of co

252 The rate of nocturnal confirmed hypoglycaemia was higher for IDeg 3TW(AM) than for IGlar

253 Minor hypoglycaemia was recorded in about 5% of participants i

254 Severe or blood glucose-confirmed hypoglycaemia was reported by 16 (4%) participants with

255 Severe hypoglycaemia was reported by two (<1%) participants wit

256 atient per year, respectively, and no severe hypoglycaemia was reported.

257 rse events were most common; no level 2 or 3 hypoglycaemia was reported.

258 Hypoglycaemia was the most common adverse event in both

259 The exposure-adjusted rate of overall hypoglycaemia was three times higher in patients given g

260 To mitigate the risk of hypoglycaemia, we sought to increase GK activity by bloc

261 and renal impairment) and the need to avoid hypoglycaemia, weight gain, and drug interactions furthe

262 ncentrations, and occurrence and severity of hypoglycaemia were also similar between groups.

263 ecognition of and physiological responses to hypoglycaemia were altered in patients with insulin-depe

264 2 (<54 mg/dL [3.0 mmol/L]) or level 3 severe hypoglycaemia were higher with efsitora compared with de

265 No episodes of severe hypoglycaemia were recorded.

266 ignificant (<54 mg/dL [<3 mmol/L]) or severe hypoglycaemia were reported with tirzepatide.

267 No episodes of major hypoglycaemia or minor hypoglycaemia were reported.

268 ponse) for counterregulatory hormones during hypoglycaemia were significantly suppressed by hyperoxia

269 t higher degree of glycaemic variability and hypoglycaemia when compared to multiple daily basal-bolu

270 ro-hormonal counterregulation blunted during hypoglycaemia when the carotid bodies were desensitized

271 Tight glycaemic control may result in hypoglycaemia, which in itself can be detrimental.

272 control while lowering the risk of nocturnal hypoglycaemia, which is a major limitation of insulin th

273 Hypoglycaemia, which occurs when blood levels of glucose

274 Expanding CGM to these groups could minimize hypoglycaemia while allowing efficient adaptation and es

275 s demonstrated to lead to protection against hypoglycaemia while partially covering glucose excursion

276 rior glycaemic control and increased risk of hypoglycaemia with IDeg 3TW compared with IGlar OD do no

277 dverse effects, and there was no increase in hypoglycaemia with metformin.

278 The improved mean glycaemia and reduced hypoglycaemia with the bionic pancreas relative to insul

279 nd in individuals with impaired awareness of hypoglycaemia would advance the effective use of this te

280 his variability, we believed that hyper- and hypoglycaemia would remain common in ICU care despite st