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Ketosis

A condition characterized by an abnormally elevated concentration of KETONE BODIES in the blood (acetonemia) or urine (acetonuria). It is a sign of DIABETES COMPLICATION, starvation, alcoholism or a mitochondrial metabolic disturbance (e.g., MAPLE SYRUP URINE DISEASE).
Also Known As:
Acetonemia; Acetonuria; Ketoacidemia; Ketoaciduria; Ketonemia; Ketonuria; Acetonemias; Acetonurias; Ketoacidemias; Ketoacidoses; Ketoacidoses, Metabolic; Ketoacidosis, Metabolic; Ketoacidurias; Ketonemias; Ketonurias; Ketoses, Metabolic; Ketosis, Metabolic; Metabolic Ketoacidoses; Metabolic Ketoses; Ketoacidosis; Metabolic Ketoacidosis; Metabolic Ketosis
Networked: 2424 relevant articles (95 outcomes, 162 trials/studies)

Relationship Network

Disease Context: Research Results

Related Diseases

1. Hyperglycemia
2. Ketosis
3. Hypoglycemia (Reactive Hypoglycemia)
4. Acidosis
5. Type 1 Diabetes Mellitus (Autoimmune Diabetes)

Experts

1. Umpierrez, Guillermo E: 11 articles (11/2014 - 03/2004)
2. Wang, Zhe: 9 articles (03/2015 - 03/2008)
3. Fukao, Toshiyuki: 8 articles (02/2015 - 12/2004)
4. Cunnane, Stephen C: 8 articles (04/2013 - 01/2002)
5. Liu, Guowen: 7 articles (03/2015 - 12/2010)
6. Kitabchi, Abbas E: 7 articles (04/2010 - 03/2004)
7. Balasubramanyam, Ashok: 6 articles (09/2015 - 05/2007)
8. Jain, Sushil K: 6 articles (03/2015 - 07/2002)
9. Gautier, Jean-François: 6 articles (01/2015 - 03/2004)
10. Li, Xiaobing: 6 articles (06/2014 - 12/2010)

Drugs and Biologics

Drugs and Important Biological Agents (IBA) related to Ketosis:
1. Insulin (Novolin)FDA Link
2. Glucose (Dextrose)FDA LinkGeneric
3. Blood Glucose (Blood Sugar)IBA
4. C-PeptideIBA
5. 3-Hydroxybutyric Acid (beta-Hydroxybutyric Acid)IBA
6. Glucagon (Glukagon)FDA Link
7. HormonesIBA
8. KetonesIBA
9. Monensin (Coban)IBA
10. Hemoglobins (Hemoglobin)IBA
12/01/2000 - "four groups of patients were studied, comprising 19 patients with DKA, massive ketonuria and plasma standard bicarbonate levels below 16 mmol/l (group 1); 20 patients with poorly controlled diabetes, glycated hemoglobin (HbA1c) above 8% and plasma bicarbonate levels above 16 mmol/l (group 2); 11 patients with well-controlled diabetes and HbA1c below 8% (group 3); and 10 non-diabetic, non-obese control subjects (group 4). "
04/01/1996 - "A highly significant inverse correlation was observed between the change from baseline condition to ketosis of the ratio C20:4/C20:3, the product/precursor ratio for the reaction catalyzed by delta5-desaturase, and the values of hemoglobin A1c,(r = -0.855; P = 0.0015). "
03/17/1988 - "The major differences between the 27 patients with remission and the 13 without remission were the duration of symptoms before diagnosis (26.8 vs. 48.0 days, P less than 0.01), the degree of weight loss (3.2 vs. 10 percent of body weight, P less than 0.001), the initial hemoglobin A1c level (10.7 vs. 13.2 percent, P less than 0.001), and the frequency of ketoacidosis (11 vs. 61.5 percent, P less than 0.001). "
01/01/2006 - "Insulin pump therapy is effective in lowering glycated hemoglobin levels without higher risk of severe hypoglycaemia and ketoacidosis. "
08/01/2015 - "A serum chemistry panel, a glycated hemoglobin test, and urinalysis performed at presentation revealed elevated blood glucose and glycated hemoglobin (HbA1c) levels (727 mg/dL and 10.1%, respectively), glucosuria, and ketonuria. "

Therapies and Procedures

1. Ketogenic Diet
2. Diet Therapy (Therapy, Diet)
01/01/2007 - "A consistently strong ketosis (beta-hydroxybutyrate of >3 mmol/L) seemed to be important for maintaining the efficacy of the diet therapy. "
11/01/1999 - "Diet therapy improved ketosis without insulin therapy in a case of anti-GAD65+ diabetes."
02/01/2000 - "Subjects included 18 nondiabetic obese adolescents, 12 obese adolescents with type 2 diabetes on diet therapy, 10 obese adolescents with type 2 diabetes manifesting ketosis at onset or with a history of treatment with hypoglycemic agents, and 26 non-obese adolescent control subjects. "
05/01/2004 - "Compared with patients using insulin therapy, patients using oral hypoglycemic drugs or diet therapy showed higher BMI (at onset of ketosis (25.69+/-2.66) kg/m2 vs. (22.64+/-3.75) kg/m2, P=0.001; during follow-up period (26.19+/-3.11) kg/m2 vs. (22.29+/-2.97) kg/m2, P=0.000), higher post-load serum insulin level (at onset of ketosis (32.39+/-35.87) mU/L vs. (18.53+/-14.43) mU/L, P=0.017; during follow-up period (67.34+/-68.42) mU/L vs. (36.40+/-45.39) mU/L, P=0.004), lower HbA 1C (at onset of ketosis (10.76+/-1.25) percent vs. (12.04+/-1.99) percent, P=0.006; during follow-up period (6.97+/-1.31)percent vs. (9.36+/-3.18) percent, P=0.000), higher percentage of ICA and GAD positivity (at onset of ketosis, ICA positive rate was 18.52 percent vs. 0, P=0.030, GAD positive rate was 18.52 percent vs. 0, P=0.030; during follow-up period, ICA positive rate was 7.41 percent vs. 0, P=0.111, GAD positive rate was 14.81 percent vs. 0, P=0.022). "
3. Parenteral Nutrition
4. Injections
5. Cesarean Section (Caesarean Section)