Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calorie restriction is widely used as a primary therapy for obese pregnant women with gestational diabetes. To better understand the metabolic consequences of marked calorie restriction, we performed a randomized prospective trial under metabolic ward conditions. Obese gestationally diabetic women were randomized to control (n = 5) and calorie-restricted (n = 7) groups. All patients consumed an approximately 2400-kcal/day diet during the 1st wk of the study, and at the end of the 1st wk, metabolic features of the two groups were statistically indistinguishable. During the 2nd wk, the control group continued to consume approximately 2400 kcal/day, whereas the calorie-restricted group consumed approximately 1200 kcal/day. Twenty-four-hour mean glucose levels remained unchanged in the control group (6.7 +/- 0.8 mM wk 1 vs. 6.8 +/- 0.8 mM wk 2), although they dropped dramatically in the calorie-restricted group (6.7 +/- 1.0 mM wk 1 vs. 5.4 +/- 0.5 mM wk 2, P less than 0.01). Fasting plasma insulin also declined in the calorie-restricted group (265 +/- 165 pM wk 1 vs. 145 +/- 130 pM wk 2), resulting in a significant change between groups (P less than 0.02). Surprisingly, fasting plasma glucose and glucose tolerance measured by the 3-h oral glucose tolerance test did not change within or between groups. Fasting levels of beta-hydroxybutyrate rose in the calorie-restricted group (290 +/- 240 microM wk 1 vs. 780 +/- 30 microM wk 2) but not in the control group (P less than 0.01). Finally, urine ketones increased significantly (P less than 0.02) in the calorie-restricted group, whereas they remained absent in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic effects of 1200-kcal diet in obese pregnant women with gestational diabetes. 222 31

Examined neurocognitive functions in 63 newly diagnosed pediatric patients with insulin-dependent diabetes mellitus (DM) at onset of illness (T0) and 1 year postdiagnosis (T1). Siblings (S) serving as controls were assessed at T0 only. Subjects were given age-appropriate tests of verbal and visuospatial abilities. In addition, DM were interviewed regularly during diabetes clinic to determine current diabetic control and different intervening glycemic-related events. Results revealed no differences between DM and S at T0, nor any specific impairment in DM predating illness. Also, DM did not demonstrate any acquired impairment after 1 year of illness. Children with early onset DM (less than 5 years) scored lower in spatial ability at T0 and T1 than children with later onset DM, who scored lower in verbal ability. Episodes of asymptomatic and mild chronic hypoglycemia correlated positively, not negatively, with improved outcome over time. There were no adverse effects of severe hypoglycemia. Ketonuria and hospitalizations were associated with lower performance IQs 1 year after onset, as was diabetic ketoacidosis at onset. Results are discussed in terms of critical periods of sensitivity of different brain regions to the effects of diabetes and the need for longer follow-up of these children.
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PMID:Intellectual characteristics of diabetic children at diagnosis and one year later. 228 80

A film test for the rapid detection of plasma/serum 3-hydroxybutyrate (3-OHB) has been developed. The film contains NAD, nitro blue tetrazolium, 3-OHB dehydrogenase, and diaphorase, and the surface is coated with modified biomembrane and can detect 50-1500 microM 3-OHB within 2-3 min. One drop or 50 microliters of plasma/serum or blood is applied to the film, and the violet color is read via reflectance meter after 2 min. Plasma/serum samples greater than 1500 microM 3-OHB can be measured by dilution with saline. In blood with 40% hematocrit, the color developed is 50% less than with plasma/serum, and this was adjusted in the reflectance meter. A good correlation (r = 0.99) was observed between results with automated and film methods and between visual methods and reflectance meter. In insulin-dependent diabetes mellitus, all 3 subjects with positive ketonuria (+ +), 8 of 12 subjects with mild ketonuria (+), and 7 of 25 subjects without ketonuria exhibited elevation of 3-OHB in blood greater than 200 microM. The results indicate that 3-OHB film is valuable not only in the emergency room for the differential diagnosis between ketoacidotic and nonketotic hypersomolar coma but also as a marker for insulin dependency, energy dependency on fatty acid compared with glucose, and metabolic control of diabetes.
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PMID:Development of stable film test for rapid estimation of blood or plasma 3-hydroxybutyrate. 235 Oct 30

Ten young adult cystic fibrosis (CF) patients over 16 years of age (average 21.4 years) began nighttime enteral feedings as a method of nutritional rehabilitation to regain and maintain body weight. Patients received nighttime feedings of 1,000 kcal/M2 of a low- (Pulmocare), medium- (Ensure Plus), or high-carbohydrate (Vivonex) formula for at least 2 nights each with pancreatic enzyme therapy. Five of ten young adult CF patients developed nocturnal hyperglycemia (serum glucose greater than 300 mg/dl) and glucosuria (1-3% glucose) with varying degrees of polyuria during enteral feedings. No patient developed ketonuria despite serum glucoses at times greater than 600 mg %. There was no difference between the hyperglycemic and normoglycemic groups in median age, percent of ideal body weight, NIH score, Brasfield scores, pulmonary function tests, or family history of diabetes. All normoglycemic and four of five hyperglycemic patients had normal fasting blood sugars. The percent hemoglobin A1c was greater in the glucose intolerant group than the normoglycemic patients (11.2 +/- 0.8% vs. 6.8 +/- 1.1%, mean +/- SE, p less than 0.005). Twelve to 15 units of NPH insulin prior to initiation of feedings provided adequate therapy in most hyperglycemic patients. There was no apparent difference in the elevation of early morning serum glucoses with the low- medium- and high-carbohydrate formulas. We concluded that hyperglycemia requiring insulin therapy was common in young adult CF patients using nighttime enteral feedings. A hemoglobin A1c appeared to be a useful screening test before initiating such therapy.
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PMID:Glucose intolerance with low-, medium-, and high-carbohydrate formulas during nighttime enteral feedings in cystic fibrosis patients. 249 15

In order to characterize Type I diabetes at its clinical onset in French children, we studied HLA-DR alleles, beta-cell function and autoantibodies to islet-cell antigens and insulin in 115 patients aged 1.8-17 years. Beta-cell function was markedly impaired, but with an unexpectedly wide range of individual variations. These variations showed no correlation with HLA alleles or circulating autoantibodies, as opposed to observations made by others. Age, however, had a clear influence on the degree of impairment of residual insulin secretion, the younger children having the more deteriorated beta-cell secretory capacity conditioning the severity of clinical manifestations (weight loss, ketonuria, ketoacidosis) and initial hyperglycemia.
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PMID:[Clinical and biological data affecting insulin-dependent diabetes in French children at the time of its diagnosis]. 250 Jan 9

The classic presentation of DKA, consisting of hyperglycemia, anion gap acidosis, and ketonuria, is readily recognized. The diagnosis may be missed, however, in the patient who is euglycemic, has a negative nitroprusside test for ketones, or has a nonanion gap metabolic acidosis. Treatment includes replacement of fluid and electrolytes lost through osmotic diuresis. Failure to recognize the magnitude of total-body potassium depletion and to begin replacement despite an initially normal serum potassium level may lead to fatal cardiac arrhythmia. Serum glucose must be monitored closely to avoid hypoglycemia; dextrose should be added to the infusion once the serum glucose falls to 250 mg per dl. Insulin is required to reverse ketoacid production by the liver; low-dose therapy is recommended. Ketogenesis may be reversed inadequately unless insulin treatment is continued until the anion gap has normalized. Failure to recognize precipitating causes may result in increased morbidity and mortality from underlying infection or myocardial infarction as well as rapid relapse of ketoacidosis.
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PMID:Diabetic ketoacidosis. 250 98

The epidemiology of uncontrolled diabetes mellitus was studied in an 11.2% sample of the Danish population (574,696 inhabitants) during a 24-month period. Some 175 admissions in ketoacidosis (heavy ketonuria and plasma bicarbonate below 21 mmol/l) were recorded. Based on prevalence rates from a socio-economically and ethnically comparable Danish county, the annual incidence rate was calculated to be 0.045 per diabetic. The incidence rate of moderate and severe episodes (bicarbonate less than 16 mmol/l) was 0.032 and of severe episodes only (bicarbonate less than 10 mmol/l) 0.017 per diabetic. The major risk group was female teenagers. The total annual frequency of recurrence was 8.7%: 48% of the male episodes were ketoacidosis (DKA) associated with onset of diabetes, against 30% of the female episodes (P = 0.02). All Danish diabetics were at the time of the survey (1978-79) treated with conventional insulin treatment. Annual incidence rate in these established diabetics was 0.028, i.e. three to five times less than reported during treatment with continuous subcutaneous insulin infusion. Mortality of DKA was low, 3.4%, and dependent upon age and precipitating factor but not upon the degree of acidosis. The overall annual mortality rate was 1.5 per 100 diabetics.
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PMID:Diabetic ketoacidosis in Denmark: epidemiology, incidence rates, precipitating factors and mortality rates. 250 23

According to month of diagnosis, 165 children who developed Type 1 (insulin-dependent) diabetes mellitus at the age of 0-16.2 years (mean +/- SD, 7.6 +/- 4.1 years) could be divided into 69 patients diagnosed during peak seasons (epidemic cases) and 96 patients diagnosed during months of low incidence (non-epidemic cases). Seasonality of onset of symptoms and of diagnosis was observed in both sexes in all age groups. The patients diagnosed during peak seasons had shorter duration of symptoms (13.2 +/- 8.1 days) as compared to 22.9 +/- 10.3 days; p less than 0.001 in the patients diagnosed during months of low incidence. At diagnosis, 88.4% (61/69) of the epidemic group had ketonuria as compared to 71.9% (69/96); p less than 0.06 in the non-epidemic patients. The values of C-peptide, insulin antibodies, haemoglobin A1c and HLA-DR phenotype frequencies in the 69 epidemic patients were compared with those of the 96 non-epidemic patients. In the epidemic patients, the C-peptide values of 0.11 +/- 0.05 mmol/l at diagnosis had increased to 0.12 +/- 0.05 mmol/l at one month and 0.13 +/- 0.06 mmol/l at 3 months. These values were significantly lower (p less than 0.001) than in the non-epidemic patients at the same time points: 0.17 +/- 0.08 nmol/l; p less than 0.001, 0.23 +/- 0.11 nmol/l; p less than 0.001, and 0.22 +/- 0.10 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seasonality of type 1 (insulin-dependent) diabetes mellitus: values of C-peptide, insulin antibodies and haemoglobin A1c show evidence of a more rapid loss of insulin secretion in epidemic patients. 265 53

Many patients with Type 2 (non-insulin-dependent) diabetes mellitus are treated with insulin in order to control hyperglycaemia. We studied fasting plasma C-peptide, glucagon stimulated plasma C-peptide, and 24 h urinary C-peptide in relation to clinical type of diabetes in 132 insulin treated diabetic subjects. Patients were classified clinically as Type 1 (insulin-dependent) diabetic subjects in the presence of at least two of the following criteria: 1) significant ketonuria, 2) insulin treatment started within one year after diagnosis, 3) age of diagnosis less than or equal to 40 years, and 4) weight below 110% of ideal weight of the same age and sex. Eighty patients were classified as Type 1 and 52 as Type 2 diabetic subjects. A second classification of patients into 6 C-peptide classes was then performed. Class I consisted of patients without islet B-cell function. Class II-VI had preserved islet B-cell function and were separated according to the 20%, 40%, 60% and 80% C-peptide percentiles. The two classifications of patients were compared by calculating the prevalence of clinical Type 1 and Type 2 diabetes in each of the C-peptide classes. This analysis showed that patients with a fasting plasma C-peptide value less than 0.20 nmol/l, a glucagon stimulated plasma C-peptide value less than 0.32 nmol/l, and a urinary C-peptide value less than 3.1 nmol/l, or less than 0.54 nmol/mmol creatinine/24 h, or less than 5.4 nmol/24 h mainly were Type 1 diabetic patients; while patients with C-peptide levels above these values mainly were Type 2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fasting plasma C-peptide, glucagon stimulated plasma C-peptide, and urinary C-peptide in relation to clinical type of diabetes. 266 17

Circulating insulin antibodies at birth and the degree of maternal metabolic control were measured in 68 infants of insulin-treated diabetic mothers. Their correlation with neonatal B cell function and with the clinical features of the infants was evaluated in order to better understand their influence on fetal outcome. Maternal metabolic control was assessed on the basis of blood glucose levels, glycosuria and the occurrence of hypoglycemia and/or ketonuria. All infants were clinically evaluated for gestational age, macrosomia, hypoglycemia, hyperbilirubinemia, hypocalcemia, and respiratory distress syndrome. Cord blood plasma glucose, C peptide, and IgG insulin antibodies were also measured. It was shown that poor maternal metabolic control was associated with a higher prevalence of fetal morbidity as well as with signs of B cell hyperfunction. Also the presence of circulating insulin antibodies correlated well with higher C peptide levels and with several neonatal complications. B cell hyperfunction, indicated by high C peptide levels in the infants of diabetic mothers, may possibly play a causal role in the pathogenesis of fetal morbidity. In conclusion, a good fetal outcome in insulin-treated diabetic pregnancies was associated with and may have depended upon: (1) good maternal metabolic control, and (2) absence or low levels of circulating insulin antibodies.
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PMID:Influence of maternal metabolic control and insulin antibodies on neonatal complications and B cell function in infants of diabetic mothers. 269 30


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