Disease relevance of Diabetic Ketoacidosis

• Death from diabetic ketoacidosis after cessation of octreotide in acromegaly [1].
• Long-term intensive blood glucose control significantly reduces the risk of diabetic retinopathy and nephropathy progression but long-term continuous subcutaneous insulin infusion was associated with an increased incidence of diabetic ketoacidosis, and intensive therapy may cause more severe hypoglycaemic reactions [2].
• The effect of low-dose insulin treatment (5-10 U/h) on hepatic glucose production (HGP) and peripheral glucose disposal was determined in 5 insulin-dependent diabetes mellitus (IDDM) subjects who were admitted with diabetic ketoacidosis (DKA; plasma glucose 598 +/- 50 mg/dl, blood pH 7.20 +/- 0.06, plasma bicarbonate 12 +/- 2 meq/L) [3].
• Prevention of hypophosphatemia by phosphate infusion during treatment of diabetic ketoacidosis and hyperosmolar coma [4].
• Plasma vasopressin was measured in seven insulin-treated diabetics during 24 h of insulin withdrawal to determine: 1) if abnormalities of the neurohypophysial-renal axis contribute to the dehydration of uncontrolled diabetes mellitus; and 2) the factors causing elevated levels of vasopressin in diabetic ketoacidosis [5].

Psychiatry related information on Diabetic Ketoacidosis

• CASE: We review the relevant literature and describe a case with central nervous system involvement presenting with typical manifestations of Wernicke's encephalopathy, apparently precipitated by a combination of hyperemesis gravidarum, diabetic ketoacidosis, and intravenous glucose administration [6].
• Two had sensorineural hearing loss and mild mental retardation, while the other developed diabetic ketoacidosis (DKA) at 14 yr and was treated with insulin from onset of diabetes [7].

High impact information on Diabetic Ketoacidosis

• BACKGROUND: Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children [8].
• Isolation of a virus from the pancreas of a child with diabetic ketoacidosis [9].
• Thereafter, there were no significant differences in the rate of decline of plasma glucose or ketones nor in the time required for glucose to reach 250 mg per deciliter or for complete recovery from diabetic ketoacidosis [10].
• We investigated the importance of glucagon in the development of diabetic ketoacidosis by withholding insulin from six patients with juvenile-type diabetes and four totally pancreatectomized subjects [11].
• Prevention of human diabetic ketoacidosis by somatostatin. Evidence for an essential role of glucagon [12].

Chemical compound and disease context of Diabetic Ketoacidosis

• Diabetic ketoacidosis appearing as carbon monoxide poisoning [13].
• Thyroid storm with normal serum triiodothyronine level during diabetic ketoacidosis [14].
• The ketogenic models studied were streptozotocin-induced diabetic ketoacidosis, 48 h of starvation, and after growth hormone administration [15].
• It is concluded that during diabetic ketoacidosis, starvation, and growth hormone administration, there is (a) no alteration in hepatic mitochondrial function; (b) no change in the intrinsic capacity of hepatic mitochondria to oxidize fatty acids; and (c) no change in the specific activity of mitochondrial carnitine palmitoyltransferase [15].
• Blood concentrations of pancreatic glucagon, cortisol, noradrenaline, adrenaline, and growth hormone have been measured during the first 41 hours of insulin deprivation in six insulin-dependent diabetics to assess the importance of these hormones in the pathogenesis of diabetic ketoacidosis [16].

Biological context of Diabetic Ketoacidosis

• Metabolic effects of low-dose insulin therapy on glucose metabolism in diabetic ketoacidosis [3].
• To determine whether a physiological increase in plasma cortisol, similar to that observed in diabetic ketoacidosis and other stress conditions, stimulates lipolysis, palmitate kinetics were measured in seven nondiabetic volunteers on two occasions with [1-14C]palmitate as a tracer [17].
• Subcutaneous terbutaline infusion may precipitate transient insulin resistance and diabetic ketoacidosis in women with diabetes [18].
• Production of prostaglandin (PG)E(2) (PGE(2)) and prostacyclin (PGI(2)), two potent vasodilators, by adipose tissue is increased in severe insulin deficiency, eg, diabetic ketoacidosis (DKA), explaining the decreased peripheral vascular resistance in DKA [19].
• The relationship between plasma insulin level, prostaglandin production by adipose tissue, and blood pressure in normal rats and rats with diabetes mellitus and diabetic ketoacidosis [19].

Anatomical context of Diabetic Ketoacidosis

• It has been suggested that the hemodynamic derangements present in diabetic ketoacidosis are the results not only of profound volume depletion but also of the effects of increased production of vasodilating prostaglandins (PGs), principally PGI2, released by adipose tissue [20].
• The relation between serum and red blood cell (RBC) inorganic phosphate levels, RBC 2,3-diphosphoglycerate (2,3-DPG) levels, RBC nucleotide phosphate (Pn), and RBC total phosphate (Pt) levels were studied during the early phases of treatment and recovery from diabetic ketoacidosis (DKA) [21].
• The mechanism of activation of glutamine production by the hindlimb during diabetic ketoacidosis (DKA) was investigated in rats [22].
• 2. Insulin and exercise, induced by sciatic-nerve stimulation, enhanced glucose uptake about tenfold in fed and starved rats, but were without effect in rats with diabetic ketoacidosis [23].
• This effect was associated with the correction of blood/plasma/serum biochemical variables (beta-hydroxybutyrate, acetoacetate, triacylglycerol) directly related to diabetic ketoacidosis, and of others (cholesterol, creatinine, creatine kinase and aspartate transaminase) which are not directly related to this metabolic abnormality [24].

Gene context of Diabetic Ketoacidosis

• Insulin receptor (IR)-deficient pups rapidly become hyperglycemic and hyperinsulinemic and die of diabetic ketoacidosis within a few days [25].
• These findings do no suggest a role for prolactin in the development of diabetic ketoacidosis [26].
• Urinary excretion of aquaporin-2 water channel in diabetic ketoacidosis [27].
• The distribution of the CTLA-4 polymorphism between patients did not show any significant difference according to diabetic ketoacidosis at onset [28].
• These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition [12].

Analytical, diagnostic and therapeutic context of Diabetic Ketoacidosis

• The patients were referred from throughout the United States because their physicians had been unable to establish the reason for recurrent hospitalizations for diabetic ketoacidosis or coma [29].
• AIMS/HYPOTHESIS: An early diagnosis of sepsis in patients with diabetic ketoacidosis and hyperosmolar non-ketotic coma is crucial and could save lives [30].
• INTERVENTIONS: Patients with diabetic ketoacidosis were monitored with an oral/nasal carbon dioxide (CO2) sampling cannula while in the emergency department [31].
• Hydroxy- and oxomonocarboxylic acids in urine of healthy individuals and of patients with diabetic ketoacidosis are analysed as methyl esters and methyl esters/O-methyloximes, respectively, by gas chromatography and gas chromatography-mass spectrometry [32].
• Concepts of fluid therapy in diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma [33].

References