ライフサイエンスコーパス: ketoacidosis

1 develop early postnatal diabetes and die of ketoacidosis.

2 ed in 24-36 h after birth due to accelerated ketoacidosis.

3 type 1 diabetes rarely results in death from ketoacidosis.

4 aloacetate deficiency, acetate overload, and ketoacidosis.

5 studies also showed the presence of diabetic ketoacidosis.

6 d fasting or streptozotocin-induced diabetic ketoacidosis.

7 lled diabetes, including a model of diabetic ketoacidosis.

8 hypoglycemic event; no patients had diabetic ketoacidosis.

9 nderlying cause of death of coma or diabetic ketoacidosis.

10 gestive heart failure, hypoxia, and diabetic ketoacidosis.

11 nically ill pediatric patients with diabetic ketoacidosis.

12 in adult patients with a history of diabetic ketoacidosis.

13 a background for the development of diabetic ketoacidosis.

14 s causes early postnatal death from diabetic ketoacidosis.

15 erapy and resolution of hyperglycemia and/or ketoacidosis.

16 associated with newly diagnosed diabetes and ketoacidosis.

17 developed diabetes or were hospitalized for ketoacidosis.

18 diabetes and 88 (0.2%) were hospitalized for ketoacidosis.

19 0001), and were more likely to have diabetic ketoacidosis (11% [61/537] vs 0.3% [30/11 696]; p<0.0001

20 CI, -6.15 to -2.69]; P < .001) and diabetic ketoacidosis (3.64 vs 4.26 per 100 patient-years; differ

21 58.3% of all patients with NODM), comprising ketoacidosis (334, 8.1%), hyperosmolarity (131, 3.2%), r

22 of intensive care for patients with diabetic ketoacidosis, a common condition with a low risk of mort

23 nt, hospitals with a high volume of diabetic ketoacidosis admissions admitted diabetic ketoacidosis p

24 episodes of severe hypoglycemia or diabetic ketoacidosis after randomization.

25 Wild type (WT) mice developed fatal diabetic ketoacidosis after streptozotocin, whereas GcgR(-/-) mic

26 increased risks of adverse outcomes such as ketoacidosis and bone fracture.

27 diabetes with numerous episodes of diabetic ketoacidosis and frequent hypoglycemic episodes.

28 quencing in a patient with recurrent, severe ketoacidosis and identified a homozygous frameshift muta

29 sed after 3 months of age and presented with ketoacidosis and marked hyperglycemia, which could have

30 lates its own production, thereby preventing ketoacidosis and promoting efficient use of fat stores.

31 sect the pathogenesis of mucormycosis during ketoacidosis and reinforce the importance of careful met

32 pant in the CGM plus MDI group, and diabetic ketoacidosis and severe hyperglycaemia occurred in one p

33 Diabetic ketoacidosis and severe hypoglycemia are acute complicat

34 ildren with diabetes remain at high risk for ketoacidosis and severe hypoglycemia.

35 er risks of severe hypoglycemia and diabetic ketoacidosis and with better glycemic control during the

36 c status of pediatric patients with diabetic ketoacidosis and, along with pulse oximetry, in lung-fun

37 caemic control (HbA1c), episodes of diabetic ketoacidosis, and all hospital admissions for acute comp

38 ntribute to poor glycaemic control, diabetic ketoacidosis, and brittle diabetes in adolescents and yo

39 ain conditions, such as starvation, diabetic ketoacidosis, and ketogenic diets, play a potentially im

40 ice from neonatal death, preventing diabetes ketoacidosis, and normalizing life span and reproductive

41 ight mediate vasogenic edema during diabetic ketoacidosis, and selective proteinase-3 antagonists may

42 er rates of severe hypoglycemia and diabetic ketoacidosis are lower with insulin pump therapy compare

43 ffect of hyperglycemia, hypoinsulinemia, and ketoacidosis, as well as the role of various mediators o

44 additional groups of children with diabetic ketoacidosis but without cerebral edema were also identi

45 died in the late infant period due to severe ketoacidosis, clearly suggesting the requirement of incr

46 ol for treating adult patients with diabetic ketoacidosis decreases intensive care and hospital lengt

47 bo, while an increased incidence of diabetic ketoacidosis (DKA) (n = 16) was seen in SGLT-2 inhibitor

48 -threatening complication of severe diabetic ketoacidosis (DKA) and its treatment.

49 ot known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH).

50 Patients with diabetic ketoacidosis (DKA) are uniquely predisposed to mucormyco

51 e (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by strong cl

52 of AKI in children hospitalized for diabetic ketoacidosis (DKA) has not been previously examined.

53 Most often, diabetic ketoacidosis (DKA) in adults results from insufficient i

54 ce, despite a significant degree of diabetic ketoacidosis (DKA) in all 14 animals.

55 a life-threatening complication of diabetic ketoacidosis (DKA) in children.

56 ly life-threatening complication of diabetic ketoacidosis (DKA) in children.

57 mechanism by which leptin reverses diabetic ketoacidosis (DKA) is unknown.

58 Diabetic ketoacidosis (DKA) may cause brain injuries in children.

59 R1 is expressed during infection in diabetic ketoacidosis (DKA) mice.

60 at oxidative stress associated with diabetic ketoacidosis (DKA) of T1DM might have measurable brain s

61 le serum iron, including those with diabetic ketoacidosis (DKA), are uniquely susceptible to mucormyc

62 Diabetic ketoacidosis (DKA)-induced hypertriglyceridemia causing

63 oped during the treatment of severe diabetic ketoacidosis (DKA).

64 re rates of severe hypoglycemia and diabetic ketoacidosis during the most recent treatment year.

65 n of the clinical manifestations of diabetic ketoacidosis, followed by appropriate, timely treatment

66 rican persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic f

67 tients with posttransplant diabetes included ketoacidosis, hyperosmolar coma or precoma, and sensorim

68 bit normal prenatal development, all develop ketoacidosis, hypoglycemia, and reduced plasma lactate c

69 ch leptin reverses fasting hyperglycemia and ketoacidosis in a rodent model of DKA versus the chronic

70 Diabetic ketoacidosis in children is associated with vasogenic ce

71 Acute diabetic ketoacidosis in children was associated with elevated po

72 mon but devastating complication of diabetic ketoacidosis in children.

73 The development of diabetic ketoacidosis in pregnancy is a medical emergency, requir

74 ong-term poor glycaemic control and diabetic ketoacidosis in this age group.

75 lin results in oscillating hyperglycemia and ketoacidosis in type 1 diabetes.

76 by age (<13 vs > or =13 years), the risk of ketoacidosis in younger children increased with higher h

77 ve care unit utilization for all nondiabetic ketoacidosis in-patients admitted diabetic ketoacidosis

78 Treatment of the patient with diabetic ketoacidosis includes insulin therapy and careful fluid

79 In older children, the risk of ketoacidosis increased with higher HbA(1c) (RR, 1.43; 95

80 sex-specific incidence patterns suggest that ketoacidosis is a challenge in adolescent girls while se

81 Ketoacidosis is a potentially lethal condition caused by

82 Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complication of i

83 Our results indicate that diabetic ketoacidosis is associated with systemic polymorphonucle

84 If alcoholic ketoacidosis is suspected, dextrose-containing fluids ar

85 In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted

86 athophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of cerebral au

87 The disease is characterized by severe ketoacidosis, mental retardation, and neurological impai

88 The clinical phenotype includes often fatal ketoacidosis, neurological derangement, and mental retar

89 tabolic disorder associated with often-fatal ketoacidosis, neurological derangement, and mental retar

90 led type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated with a decreas

91 ho are immunocompromised because of diabetic ketoacidosis, neutropenia, organ transplantation, and/or

92 No ketoacidosis occurred in either group and one episode of

93 Adjudicated definite diabetic ketoacidosis occurred in four (1%) patients in the dapag

94 ric type 1 diabetes patients; acute diabetic ketoacidosis or age-/sex-matched insulin-controlled.

95 There were no episodes of diabetic ketoacidosis or hyperglycemia with ketosis.

96 Patients with diabetic ketoacidosis or hyperosmolar nonketotic coma were exclud

97 median age of 9 weeks, usually with diabetic ketoacidosis or marked hyperglycemia, was not associated

98 le metabolic causes of coma such as diabetic ketoacidosis or uremia were excluded.

99 related to hospital admissions for diabetic ketoacidosis (p < 0.001) and all hospital admissions rel

100 ls in the use of intensive care for diabetic ketoacidosis patients that was not associated with diffe

101 ic ketoacidosis admissions admitted diabetic ketoacidosis patients to the intensive care unit less of

102 c ketoacidosis in-patients admitted diabetic ketoacidosis patients to the intensive care unit more fr

103 Use of intensive care for diabetic ketoacidosis patients varied widely across hospitals (ad

104 zurophilic enzymes were elevated in diabetic ketoacidosis patients, including human leukocyte elastas

105 PetCO2 monitoring of patients with diabetic ketoacidosis provides an accurate estimate of PCO2.

106 an emerging syndrome of obesity, unprovoked ketoacidosis, reversible beta-cell dysfunction, and near

107 y infant periods, preventing a lethal fit of ketoacidosis (SAP(+)PCCA(-/-) mice).

108 proteinase-3 levels correlated with diabetic ketoacidosis severity (p = 0.002).

109 , only proteinase-3 correlated with diabetic ketoacidosis severity and potently degraded the blood-br

110 asma azurophilic enzyme levels with diabetic ketoacidosis severity, and to determine whether azurophi

111 ional status was found to be correlated with ketoacidosis severity, MCT1 protein levels, and transpor

112 MCT1 deficiency is a novel cause of profound ketoacidosis; the present work suggests that MCT1-mediat

113 ling may be useful in patients with diabetic ketoacidosis to allow for continuous monitoring of patie

114 ilic enzyme levels in children with diabetic ketoacidosis, to correlate plasma azurophilic enzyme lev

115 (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the controls i

116 droxybutyrate (BHB)-a biomarker for diabetic ketoacidosis-using a commercial combination BHB/glucomet

117 The incidence of ketoacidosis was 8 per 100 person-years and increased wi

118 1% in women) but death from diabetic coma or ketoacidosis was associated with the largest percentage

119 kocyte elastase and proteinase-3 in diabetic ketoacidosis was confirmed with buffy coat quantitative

120 The rate of diabetic ketoacidosis was higher in the sotagliflozin group than

121 However, the rate of diabetic ketoacidosis was higher in the sotagliflozin group.

122 7.0% with no severe hypoglycemia or diabetic ketoacidosis was larger in the group that received sotag

123 her cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral blood fl

124 Severe hypoglycemia and diabetic ketoacidosis were absent in patients with functioning gr

125 Patients with diabetic ketoacidosis were monitored with an oral/nasal carbon di

126 ts with alcohol use disorders, and alcoholic ketoacidosis were selected.

127 Children with diabetic ketoacidosis who have low partial pressures of arterial

128 s, abdominal distention, and severe diabetic ketoacidosis with hypotension.

129 p severe hyperglycemia, hypoinsulinemia, and ketoacidosis within 2 days and typically die within 5.

130 ldren who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebra