ライフサイエンスコーパス: diabetic ketoacidosis

1 boratory studies also showed the presence of diabetic ketoacidosis.

2 prolonged fasting or streptozotocin-induced diabetic ketoacidosis.

3 ly controlled diabetes, including a model of diabetic ketoacidosis.

4 a severe hypoglycemic event; no patients had diabetic ketoacidosis.

5 had an underlying cause of death of coma or diabetic ketoacidosis.

6 uding congestive heart failure, hypoxia, and diabetic ketoacidosis.

7 me in clinically ill pediatric patients with diabetic ketoacidosis.

8 pendence in adult patients with a history of diabetic ketoacidosis.

9 provide a background for the development of diabetic ketoacidosis.

10 receptors causes early postnatal death from diabetic ketoacidosis.

11 96]; p<0.0001), and were more likely to have diabetic ketoacidosis (11% [61/537] vs 0.3% [30/11 696];

12 4.42 [95% CI, -6.15 to -2.69]; P < .001) and diabetic ketoacidosis (3.64 vs 4.26 per 100 patient-year

13 the use of intensive care for patients with diabetic ketoacidosis, a common condition with a low ris

14 adjustment, hospitals with a high volume of diabetic ketoacidosis admissions admitted diabetic ketoa

15 , with no episodes of severe hypoglycemia or diabetic ketoacidosis after randomization.

16 Wild type (WT) mice developed fatal diabetic ketoacidosis after streptozotocin, whereas GcgR

17 ontrolled diabetes with numerous episodes of diabetic ketoacidosis and frequent hypoglycemic episodes

18 e participant in the CGM plus MDI group, and diabetic ketoacidosis and severe hyperglycaemia occurred

19 Diabetic ketoacidosis and severe hypoglycemia are acute

20 with lower risks of severe hypoglycemia and diabetic ketoacidosis and with better glycemic control d

21 metabolic status of pediatric patients with diabetic ketoacidosis and, along with pulse oximetry, in

22 tween glycaemic control (HbA1c), episodes of diabetic ketoacidosis, and all hospital admissions for a

23 ght to contribute to poor glycaemic control, diabetic ketoacidosis, and brittle diabetes in adolescen

24 nder certain conditions, such as starvation, diabetic ketoacidosis, and ketogenic diets, play a poten

25 inase-3 might mediate vasogenic edema during diabetic ketoacidosis, and selective proteinase-3 antago

26 ine whether rates of severe hypoglycemia and diabetic ketoacidosis are lower with insulin pump therap

27 Two additional groups of children with diabetic ketoacidosis but without cerebral edema were al

28 ry protocol for treating adult patients with diabetic ketoacidosis decreases intensive care and hospi

29 to placebo, while an increased incidence of diabetic ketoacidosis (DKA) (n = 16) was seen in SGLT-2

30 but life-threatening complication of severe diabetic ketoacidosis (DKA) and its treatment.

31 isks is not known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia

32 Patients with diabetic ketoacidosis (DKA) are uniquely predisposed to

33 ended dose (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by

34 requency of AKI in children hospitalized for diabetic ketoacidosis (DKA) has not been previously exam

35 Most often, diabetic ketoacidosis (DKA) in adults results from insuf

36 d-type mice, despite a significant degree of diabetic ketoacidosis (DKA) in all 14 animals.

37 edema is a life-threatening complication of diabetic ketoacidosis (DKA) in children.

38 potentially life-threatening complication of diabetic ketoacidosis (DKA) in children.

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

40 Diabetic ketoacidosis (DKA) may cause brain injuries in

41 w that FTR1 is expressed during infection in diabetic ketoacidosis (DKA) mice.

42 esized that oxidative stress associated with diabetic ketoacidosis (DKA) of T1DM might have measurabl

43 d available serum iron, including those with diabetic ketoacidosis (DKA), are uniquely susceptible to

44 Diabetic ketoacidosis (DKA)-induced hypertriglyceridemia

45 hat developed during the treatment of severe diabetic ketoacidosis (DKA).

46 tcomes were rates of severe hypoglycemia and diabetic ketoacidosis during the most recent treatment y

47 ecognition of the clinical manifestations of diabetic ketoacidosis, followed by appropriate, timely t

48 rican-American persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immu

49 Diabetic ketoacidosis in children is associated with vas

50 Acute diabetic ketoacidosis in children was associated with el

51 an uncommon but devastating complication of diabetic ketoacidosis in children.

52 The development of diabetic ketoacidosis in pregnancy is a medical emergenc

53 utes to long-term poor glycaemic control and diabetic ketoacidosis in this age group.

54 Treatment of the patient with diabetic ketoacidosis includes insulin therapy and caref

55 Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complica

56 Our results indicate that diabetic ketoacidosis is associated with systemic polymo

57 hat the pathophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of ce

58 atients who are immunocompromised because of diabetic ketoacidosis, neutropenia, organ transplantatio

59 Adjudicated definite diabetic ketoacidosis occurred in four (1%) patients in

60 Pediatric type 1 diabetes patients; acute diabetic ketoacidosis or age-/sex-matched insulin-contro

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

62 Patients with diabetic ketoacidosis or hyperosmolar nonketotic coma we

63 nds at a median age of 9 weeks, usually with diabetic ketoacidosis or marked hyperglycemia, was not a

64 reversible metabolic causes of coma such as diabetic ketoacidosis or uremia were excluded.

65 inversely related to hospital admissions for diabetic ketoacidosis (p < 0.001) and all hospital admis

66 s hospitals in the use of intensive care for diabetic ketoacidosis patients that was not associated w

67 of diabetic ketoacidosis admissions admitted diabetic ketoacidosis patients to the intensive care uni

68 ondiabetic ketoacidosis in-patients admitted diabetic ketoacidosis patients to the intensive care uni

69 Use of intensive care for diabetic ketoacidosis patients varied widely across hosp

70 Plasma azurophilic enzymes were elevated in diabetic ketoacidosis patients, including human leukocyt

71 PetCO2 monitoring of patients with diabetic ketoacidosis provides an accurate estimate of P

72 ed, only proteinase-3 levels correlated with diabetic ketoacidosis severity (p = 0.002).

73 examined, only proteinase-3 correlated with diabetic ketoacidosis severity and potently degraded the

74 relate plasma azurophilic enzyme levels with diabetic ketoacidosis severity, and to determine whether

75 tCO2 sampling may be useful in patients with diabetic ketoacidosis to allow for continuous monitoring

76 a azurophilic enzyme levels in children with diabetic ketoacidosis, to correlate plasma azurophilic e

77 n intern (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the c

78 e beta-hydroxybutyrate (BHB)-a biomarker for diabetic ketoacidosis-using a commercial combination BHB

79 human leukocyte elastase and proteinase-3 in diabetic ketoacidosis was confirmed with buffy coat quan

80 However, the rate of diabetic ketoacidosis was higher in the sotagliflozin gr

81 The rate of diabetic ketoacidosis was higher in the sotagliflozin gr

82 wer than 7.0% with no severe hypoglycemia or diabetic ketoacidosis was larger in the group that recei

83 mine whether cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral

84 Severe hypoglycemia and diabetic ketoacidosis were absent in patients with funct

85 Patients with diabetic ketoacidosis were monitored with an oral/nasal

86 Children with diabetic ketoacidosis who have low partial pressures of

87 ematemesis, abdominal distention, and severe diabetic ketoacidosis with hypotension.

88 ed 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in who