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1 gestive heart failure, hypoxia, and diabetic ketoacidosis.
2 nically ill pediatric patients with diabetic ketoacidosis.
3 in adult patients with a history of diabetic ketoacidosis.
4 a background for the development of diabetic ketoacidosis.
5 s causes early postnatal death from diabetic ketoacidosis.
6 erapy and resolution of hyperglycemia and/or ketoacidosis.
7 associated with newly diagnosed diabetes and ketoacidosis.
8 developed diabetes or were hospitalized for ketoacidosis.
9 diabetes and 88 (0.2%) were hospitalized for ketoacidosis.
10 develop early postnatal diabetes and die of ketoacidosis.
11 ed in 24-36 h after birth due to accelerated ketoacidosis.
12 type 1 diabetes rarely results in death from ketoacidosis.
13 to SGLT2is without a higher risk of diabetic ketoacidosis.
14 n SQ insulin treatment protocol for diabetic ketoacidosis.
15 ng, especially for the diagnosis of diabetic ketoacidosis.
16 c obstructive pulmonary disease and diabetic ketoacidosis.
17 ical stigma as they are involved in diabetic ketoacidosis.
18 1 diabetes, with dramatic hyperglycemia and ketoacidosis.
19 e 1 diabetes because of the risk of diabetic ketoacidosis.
20 onavirus disease (COVID-19) who had diabetic ketoacidosis.
21 be avoided where there is a risk of diabetic ketoacidosis.
22 cates the effect of dapagliflozin and causes ketoacidosis.
23 roughly six-times increased risk of diabetic ketoacidosis.
24 aloacetate deficiency, acetate overload, and ketoacidosis.
25 studies also showed the presence of diabetic ketoacidosis.
26 d fasting or streptozotocin-induced diabetic ketoacidosis.
27 Two children had diabetic ketoacidosis.
28 lled diabetes, including a model of diabetic ketoacidosis.
29 hypoglycemic event; no patients had diabetic ketoacidosis.
30 nderlying cause of death of coma or diabetic ketoacidosis.
31 rveillance programs effectively prevent most ketoacidosis(10-12) but require frequent evaluations who
32 0001), and were more likely to have diabetic ketoacidosis (11% [61/537] vs 0.3% [30/11 696]; p<0.0001
34 group and 4 in the BGM group), and diabetic ketoacidosis (3 participants with an event in the CGM gr
35 CI, -6.15 to -2.69]; P < .001) and diabetic ketoacidosis (3.64 vs 4.26 per 100 patient-years; differ
36 58.3% of all patients with NODM), comprising ketoacidosis (334, 8.1%), hyperosmolarity (131, 3.2%), r
38 of intensive care for patients with diabetic ketoacidosis, a common condition with a low risk of mort
39 n extreme conditions ketosis can progress to ketoacidosis, a dangerous and potentially life-threateni
41 is hospitalization for treatment of diabetic ketoacidosis, acute renal failure, and sepsis, he sudden
42 nt, hospitals with a high volume of diabetic ketoacidosis admissions admitted diabetic ketoacidosis p
44 Wild type (WT) mice developed fatal diabetic ketoacidosis after streptozotocin, whereas GcgR(-/-) mic
46 glucose <120 mg/dL), prevention of diabetic ketoacidosis and absence of cataract development, unlike
50 anisms by which these drugs cause euglycemic ketoacidosis and hyperglucagonemia and stimulate hepatic
51 erate-intensity insulin therapy for diabetic ketoacidosis and hyperosmolar hyperglycemic state result
54 quencing in a patient with recurrent, severe ketoacidosis and identified a homozygous frameshift muta
55 sed after 3 months of age and presented with ketoacidosis and marked hyperglycemia, which could have
57 dary outcomes were the frequency of diabetic ketoacidosis and parental psychological stress, assessed
59 lates its own production, thereby preventing ketoacidosis and promoting efficient use of fat stores.
60 sect the pathogenesis of mucormycosis during ketoacidosis and reinforce the importance of careful met
61 pant in the CGM plus MDI group, and diabetic ketoacidosis and severe hyperglycaemia occurred in one p
64 d about their potential to induce euglycemic ketoacidosis and to increase both glucose production and
65 er risks of severe hypoglycemia and diabetic ketoacidosis and with better glycemic control during the
66 c status of pediatric patients with diabetic ketoacidosis and, along with pulse oximetry, in lung-fun
67 caemic control (HbA1c), episodes of diabetic ketoacidosis, and all hospital admissions for acute comp
68 nabling earlier diagnosis, reducing diabetic ketoacidosis, and allowing timely introduction of diseas
69 ntribute to poor glycaemic control, diabetic ketoacidosis, and brittle diabetes in adolescents and yo
70 opulation-based newborn screening to prevent ketoacidosis, and enables individualized risk estimates
71 ain conditions, such as starvation, diabetic ketoacidosis, and ketogenic diets, play a potentially im
73 ice from neonatal death, preventing diabetes ketoacidosis, and normalizing life span and reproductive
74 rse events reported were diarrhoea, diabetic ketoacidosis, and pneumonitis (one patient each) in the
75 ight mediate vasogenic edema during diabetic ketoacidosis, and selective proteinase-3 antagonists may
76 , the effects of SGLT2 inhibition to promote ketoacidosis are independent from hyperglucagonemia.
77 er rates of severe hypoglycemia and diabetic ketoacidosis are lower with insulin pump therapy compare
78 ence of historical inquiry delayed notice of ketoacidosis as an adverse reaction, which could have re
79 ffect of hyperglycemia, hypoinsulinemia, and ketoacidosis, as well as the role of various mediators o
81 included hospitalized patients with diabetic ketoacidosis at 21 hospitals between January 1, 2010, an
83 s cohort study assesses the risk of diabetic ketoacidosis at the diagnosis of type 1 diabetes among c
84 t of side effects: genitourinary infections, ketoacidosis, bone fractures, amputations, acute kidney
85 additional groups of children with diabetic ketoacidosis but without cerebral edema were also identi
87 died in the late infant period due to severe ketoacidosis, clearly suggesting the requirement of incr
88 ol for treating adult patients with diabetic ketoacidosis decreases intensive care and hospital lengt
89 of diabetes admissions were due to diabetic ketoacidosis (DKA) (90%) compared to the pre-war period
90 bo, while an increased incidence of diabetic ketoacidosis (DKA) (n = 16) was seen in SGLT-2 inhibitor
92 body, anti-CotH C2, which protected diabetic ketoacidosis (DKA) and neutropenic mice from mucormycosi
93 ot known in hyperglycemic crises of diabetic ketoacidosis (DKA) and nonketotic hyperglycemia (NKH).
96 e (0.1 U/kg per hour) of insulin in diabetic ketoacidosis (DKA) guidelines is not backed by strong cl
97 of AKI in children hospitalized for diabetic ketoacidosis (DKA) has not been previously examined.
100 ry data to compare the frequency of diabetic ketoacidosis (DKA) in children and adolescents at time o
101 of acute kidney injury (AKI) during diabetic ketoacidosis (DKA) in children, raising the question of
109 at oxidative stress associated with diabetic ketoacidosis (DKA) of T1DM might have measurable brain s
110 ications of severe hypoglycemia and diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (
111 lin-days), glucose variability, and diabetic ketoacidosis (DKA) recurrences were compared for hospita
116 actures, falls, genital infections, diabetic ketoacidosis (DKA), acute kidney injury (AKI), and lower
117 le serum iron, including those with diabetic ketoacidosis (DKA), are uniquely susceptible to mucormyc
127 9 (95% CI 2.88 to 3.77); high certainty) and ketoacidosis due to diabetes (OR 2.08 (1.45 to 2.99); hi
128 re rates of severe hypoglycemia and diabetic ketoacidosis during the most recent treatment year.
130 n increased risk of postoperative euglycemic ketoacidosis (eKA) and acute kidney injury (AKI) among p
134 n of the clinical manifestations of diabetic ketoacidosis, followed by appropriate, timely treatment
135 he numbers of amputations, cases of diabetic ketoacidosis, fractures, and major hypoglycemic events w
136 sis, bone fractures, lower limb amputations, ketoacidosis, genital infections, or symptomatic hypovol
137 risks of SGLT2 inhibitors include euglycemic ketoacidosis, genital mycotic infections, and volume dep
138 rican persons with new diagnoses of diabetic ketoacidosis have clinical, metabolic, and immunologic f
139 tients with posttransplant diabetes included ketoacidosis, hyperosmolar coma or precoma, and sensorim
140 bit normal prenatal development, all develop ketoacidosis, hypoglycemia, and reduced plasma lactate c
141 , 4.33, 4.49) in hyperlipidemia, neuropathy, ketoacidosis, hypothyroidism and PCOS, respectively.
142 tified including hyperlipidemia, neuropathy, ketoacidosis, hypothyroidism and polycystic ovary syndro
143 etes with complications: ICC, 0.36; diabetic ketoacidosis: ICC, 0.33; acute appendicitis without peri
144 ch leptin reverses fasting hyperglycemia and ketoacidosis in a rodent model of DKA versus the chronic
145 T2 inhibitor (SGLT2i) dapagliflozin promotes ketoacidosis in both healthy and type 2 diabetic rats in
149 standard-care group; 1 instance of diabetic ketoacidosis in each group; and 12 device-related advers
152 porter-2 inhibitors and the risk of diabetic ketoacidosis in patients with type 2 diabetes: a systema
155 k: SGLT2 inhibitors predispose to euglycemic ketoacidosis in those with type 2 diabetes and, largely
157 by age (<13 vs > or =13 years), the risk of ketoacidosis in younger children increased with higher h
158 ve care unit utilization for all nondiabetic ketoacidosis in-patients admitted diabetic ketoacidosis
161 and George Cahill) had described ketosis and ketoacidosis induced by administration of the phytochemi
162 sex-specific incidence patterns suggest that ketoacidosis is a challenge in adolescent girls while se
164 Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complication of i
167 Also, circulating S100A9 in patients with ketoacidosis is only marginally increased hence unveilin
169 rial septal defects, bronchiolitis, diabetic ketoacidosis, Kawasaki syndrome, mental health admission
170 In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted
171 athophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of cerebral au
173 Reported complications included diabetic ketoacidosis (n = 8), sepsis or septic shock (n = 9), an
174 The clinical phenotype includes often fatal ketoacidosis, neurological derangement, and mental retar
175 tabolic disorder associated with often-fatal ketoacidosis, neurological derangement, and mental retar
176 led type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated with a decreas
177 ho are immunocompromised because of diabetic ketoacidosis, neutropenia, organ transplantation, and/or
185 total of 7989 hospitalizations for diabetic ketoacidosis occurred, with 4739 (59.3%) occurring befor
186 ric type 1 diabetes patients; acute diabetic ketoacidosis or age-/sex-matched insulin-controlled.
188 of severe hypoglycemia and none of diabetic ketoacidosis or hyperosmolar hyperglycemic syndrome.
191 median age of 9 weeks, usually with diabetic ketoacidosis or marked hyperglycemia, was not associated
195 se solution; a history of diabetes, diabetic ketoacidosis, or diabetes insipidus; a need for renal re
196 events, including volume depletion, diabetic ketoacidosis, or renal events, were similar with dapagli
197 related to hospital admissions for diabetic ketoacidosis (p < 0.001) and all hospital admissions rel
198 ls in the use of intensive care for diabetic ketoacidosis patients that was not associated with diffe
199 ic ketoacidosis admissions admitted diabetic ketoacidosis patients to the intensive care unit less of
200 c ketoacidosis in-patients admitted diabetic ketoacidosis patients to the intensive care unit more fr
202 zurophilic enzymes were elevated in diabetic ketoacidosis patients, including human leukocyte elastas
204 had new-onset type 1 diabetes mellitus with ketoacidosis related to pembrolizumab and no patients re
206 an emerging syndrome of obesity, unprovoked ketoacidosis, reversible beta-cell dysfunction, and near
209 , only proteinase-3 correlated with diabetic ketoacidosis severity and potently degraded the blood-br
210 asma azurophilic enzyme levels with diabetic ketoacidosis severity, and to determine whether azurophi
211 ional status was found to be correlated with ketoacidosis severity, MCT1 protein levels, and transpor
212 MCT1 deficiency is a novel cause of profound ketoacidosis; the present work suggests that MCT1-mediat
213 ling may be useful in patients with diabetic ketoacidosis to allow for continuous monitoring of patie
214 ilic enzyme levels in children with diabetic ketoacidosis, to correlate plasma azurophilic enzyme lev
215 a protocol based on SQ insulin for diabetic ketoacidosis treatment was associated with significant d
216 (anno 1953) treating a youngster in diabetic ketoacidosis underscored our ignorance of the controls i
217 droxybutyrate (BHB)-a biomarker for diabetic ketoacidosis-using a commercial combination BHB/glucomet
219 1% in women) but death from diabetic coma or ketoacidosis was associated with the largest percentage
220 kocyte elastase and proteinase-3 in diabetic ketoacidosis was confirmed with buffy coat quantitative
223 7.0% with no severe hypoglycemia or diabetic ketoacidosis was larger in the group that received sotag
224 her cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral blood fl
227 c infections, volume depletion, and diabetic ketoacidosis were more common with sotagliflozin than wi
230 betes (two severe hypoglycemia, one diabetic ketoacidosis) were reported in the physician arm and non
231 iting and life-threatening, such as diabetic ketoacidosis, which appears to be more frequent than ini
233 rained ketogenesis leads to life-threatening ketoacidosis whose incidence is high in patients with di
234 ration estimated that one additional case of ketoacidosis will occur for every 26 patient-years of ex
236 p severe hyperglycemia, hypoinsulinemia, and ketoacidosis within 2 days and typically die within 5.
237 ldren who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebra