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)

Two Type 1 diabetic patients with brittle diabetes were successfully treated using continuous SC octreotide (Sandostatin) infusion (200 micrograms 24-h-1) for 6 months and 12 months. When the analogue was discontinued, rapid deterioration in glucose control and ketonuria recurred in one patient and diabetic ketoacidosis in the other. These were corrected after reinstitution of the analogue.
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PMID:The use of continuous subcutaneous octreotide infusion in brittle type 1 diabetic patients. 183 Feb 62

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.
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PMID:A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate. 184 65

This is a case of a 15-month-old child suffering from Fanconi-Bickel syndrome, characterized with Fanconi syndrome manifestations (glycosuria, amino aciduria and phosphaturia), and the build-up of glycogen in the liver in a similar manner as seen in cases of glycogenesis type Ia. Due to the presence of liver glycogenosis, the patient also has a tendency towards hypoglycemia, ketonuria, hypercholesterolemia and hypertriglyceridemia. The glycogenosis seen in the patients with the Fanconi-Bickel syndrome, does not depend on a defect in the activity of the glucose-6-phosphatase enzyme, but in fact is due to a defect in the transporter which mobilizes glucose and galactose in the liver and in the basolateral membrane of the proximal tubule of the kidney.
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PMID:[The Fanconi-Bickel syndrome]. 186 46

Although the hourly intramuscular insulin regimen has been used in the management of diabetic ketoacidosis (DKA) in Ethiopia for over 7 years, continuous intravenous (IV) insulin infusion has never been previously used. In Tikur Anbessa Hospital, Addis Abeba, in 198788, we used the ordinary IV plastic bag and tubings alone to concurrently infuse the low-dose insulin and hydration solution in the management of 15 episodes of DKA in 13 patients, 5 males and 8 females. Initial blood glucose was over 400 mg/dl and urine ketones 4+ in all, and the level of consciousness ranged from drowsy to coma. Initially, 5 to 10 units of crystalline zinc insulin (CZI) was given IV directly to all but 2 patients. Then CZI was added to the normal saline IV bag and the dose of insulin was adjusted according to fluid requirements while at the same time maintaining the insulin rate at 5 to 10 units/hour until the blood glucose dropped to 250 mg/dl or lower. At this point the IV fluid was changed to 5% dextrose and the insulin infusion was reduced to 2 to 4 units/hour. The mean insulin requirement until the dextrose infusion was initiated was 33.2 +/- 7.3 units, IV fluid requirement was 3.5 +/- 0.8 litres and mean duration of treatment 4.4 +/- 1.6 hours. There was one death which was not due to insulin resistance, while all other patients fully recovered. The study demonstrates that insulin infusion using the ordinary IV plastic bag and tubings is safe, simple, and convenient in the management of DKA and hence should be used whenever indicated and feasible.
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PMID:The management of diabetic ketoacidosis by continuous infusion of low-dose insulin using the ordinary intravenous plastic bag and tubing. 190 Apr 69

This article reviews diagnosis and management of infants with diabetes. These infants present with signs and symptoms confused with other more common illnesses in this age group. A physician examining an ill-appearing dehydrated infant, without any obvious cause for the dehydration, should quickly screen the urine for glucose and ketones. Diagnosis of diabetes is a problem when an infant has only hyperglycemia or ketonuria. Febrile illnesses, convulsions, and dehydration can cause these laboratory abnormalities. Once the diagnosis of diabetes is made in the infant, management is complicated by the difficulty in administering small doses of insulin, monitoring blood glucose, complementing insulin administration with feedings, and hypoglycemia. The potential for brain damage with unrecognized episodes of hypoglycemia is always a concern in infants. This article offers suggestions for treating hypoglycemia as well as guidelines for making insulin adjustments when the infant is ill. The physician should be aware of the psychosocial issues involving the family of an infant with diabetes. Optimism and ongoing support should be provided to the family, so that the infant can grow up healthy and possibly benefit from research on the cure of diabetes.
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PMID:Diabetes in infancy: diagnosis and current management. 192 May 10

A modification of the urine osmolal gap was evaluated as an estimate of urine [NH4+]. We proposed that: Urine [NH4+] = Urine osmolality - [2(Na+ + K+) + urea + glucose]/2 Spot urine samples were collected from normal volunteers and from individuals with ketonuria; the modified urine osmolal gap as well as two other previously described estimates of urine [NH4+] were compared with measured urine [NH4+]. There was a significant positive linear correlation between the urine [NH4+] and the modified urine osmolal gap in normal volunteers (r = 0.81; p less than 0.01) and in individuals with ketonuria (r = 0.93; p less than 0.001). The originally described urine osmolal gap greatly overestimated the urine [NH4+] but also showed a significant correlation. The urine anion gap was not a valid estimate of urine [NH4+] within the range of values measured in our subjects. The modified urine osmolal gap is an improvement over previously described estimates of urine [NH4+] and can be used as a single calculation in place of the other two.
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PMID:A modification of the urine osmolal gap: an improved method for estimating urine ammonium. 208 Jul 86

Cases of malnutrition-related diabetes mellitus conforming to the description of the protein deficient pancreatic diabetes type in Ethiopian patients were compared with Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic. Fourteen of 39 malnutrition-related diabetes mellitus patients had fat malabsorption compared with only two of ten Type 1 diabetic patients and one of nine control subjects. Xylose absorption was normal favouring a pancreatic cause for the malabsorption. Plasma C-peptide during oral glucose tolerance test was significantly lower than that in Type 2 diabetic patients and normal control subjects (p less than 0.01 to 0.001) and was also consistently but not significantly higher than in Type 1 diabetic patients. Glucagon secretion patterns were similar in malnutrition-related and Type 1 diabetic patients. Of 23 new malnutrition-related diabetic patients treated with glibenclamide after nutritional rehabilitation and insulin treatment, only three responded, 14 were unresponsive but remained ketosis free for over eight days while another six developed ketoacidosis or significant ketonuria within two to six days during the trial. Sixteen unselected Type 1 diabetic patients who discontinued their insulin therapy all developed frank ketoacidosis after a mean of 5.5 days. The similarity of the malnutrition-related and Type 1 diabetes mellitus in age of onset, insulin requirement for diabetic control and appearance of ketosis-proneness in some cases, together with the similarity of C-peptide and glucagon secretion patterns suggest that the protein deficient pancreatic diabetes variant of malnutrition-related diabetes mellitus may be Type 1 diabetes mellitus modified by the background of malnutrition rather than an aetiologically separate entity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical and hormonal (C-peptide and glucagon) profile and liability to ketoacidosis during nutritional rehabilitation in Ethiopian patients with malnutrition-related diabetes mellitus. 211

A case of isovaleric acidemia appearing as diabetic ketoacidosis with acute encephalopathy and pancytopenia was reported. A three-year-old male patient, with mild psychomotor retardation, had recurrent bouts of acute encephalopathy and pancytopenia after episodes of upper respiratory infection. At admission, he had vomiting associated with dehydration, acidosis, ketonuria, coma and a pungent, rather unpleasant odor. Laboratory features included hyperglycemia, hyperammonemia, hyperamylasemia, hypocalcemia, neutropenia, thrombocytopenia and subsequent anemia. Urine organic acid profiles showed profuse amount of 3-beta-hydroxyisovaleric acid (295 mg/ml) and isovalerylglycine (616 mg/ml) by gas chromatography-mass spectrometry. Levels of amino acids in the serum and urine were normal. The patient received treatment with rehydration and insulin, with rapid improvement. After the acute illness, blood glucose levels returned to normal. The patient was doing well on a low-protein diet in recent 3 months.
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PMID:Isovaleric acidemia: report of one case. 212 76

Although metabolic disorders are a frequent concern in cattle, they are not commonly recognized in bulls. The combination of hyperglycemia, acetonemia, ketonuria, and glycosuria in a bull was highly suggestive of diabetes mellitus. This uncommon diagnosis was confirmed by results of intravenous glucose tolerance testing. Results of the test and serum insulin values were further able to classify the disease in this bull as type-I diabetes mellitus.
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PMID:Type-I diabetes mellitus in a bull. 221 31

The mainstay of management for gestational diabetic women (GDM) has been dietary. If it is inadequate to sustain normoglycemia, insulin therapy must be initiated. We studied whether we could prevent macrosomia by insulin therapy based on four daily self blood glucose levels (SBG). Fifty GDM, ages 28-39 years were, recruited to the study. They were divided based on fasting glucose (FBS) level on the glucose tolerance test (GTT): those with FBS less than 90 mg/dl were managed by diet alone; those with FBS greater than 90 mg/dl were immediately started on insulin. The four SBG checks [FBS and 1 hour after each meal (lhpc)] correlated with the continuous glucose monitor with r = 0.91. The women were asked to perform a dipstick for ketones on their urine upon awakening and whenever a meal or snack had been missed. Insulin was initiated when the SBG monitoring indicated that: (1) the FBS was 80 mg/dl whole blood from fingerstick (WBG) or the plasma glucose (PG) greater than 90 mg/dl and/or (2) the lhpc was greater than 140 mg/dl WBG and/or (3) the patient had persistent ketonuria on the prescribed diet which cleared only when the caloric intake was increased to a point which precipitated postprandial hyperglycemia. The prescribed diet was calculated based on body weight to be 30 kcal/kg if the women were between 80 and 120% ideal body weight; or was calculated to be 24 kcal/kg if their weight was greater than 120% ideal body weight. The calories were divided such that 40% was carbohydrate, 20% protein, and 40% fat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary manipulation as a primary treatment strategy for pregnancies complicated by diabetes. 221 89


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