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)

Diabetes in childhood is essentially represented by the type 1 or insulin-dependent diabetes mellitus (IDDM). Classical symptoms (polyuria, polydipsia, asthenia, weight loss) are usually present at the first consultation and allow an immediate diagnosis at the physician's office by performing capillary (finger-prick) blood glucose measurement (> or = 200 mg/dL) and urine-stripe test (detection of glucosuria and ketonuria). A diagnosis performed at this stage of the disease leads to the admission of the child at hospital, in order to institute the insulintherapy without delay. This attitude should permit to avoid the rapid development of diabetic keto-acidosis, which is at present too much frequent at diagnosis (50% of the cases) and which is associated with potential risks of severe complications in children. In case of incidental detection of hyperglycemia without ketonuria in childhood, the differential diagnoses of early IDDM are the rare form of familial non insulin-dependent diabetes with onset in childhood (MODY: maturity-onset diabetes of the young) and the transient hyperglycemia in childhood. Finally, diabetes could also develop in the course of an other chronic disease (i.e. cystic fibrosis) or as part of genetical syndroms.
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PMID:[Diagnosis of diabetes mellitus in children]. 881 19

Prospective registry of newly diagnosed cases of insulin-dependent diabetes mellitus in subjects under 20 years began in 1988 in Aquitaine, Lorraine, Basse- and Haute-Normandie (population base = 2,288,018 inhabitants under 20). The registry gave a complete coverage of the population as the capture-recapture method gave a 98% yield. The mean annual incidence was 7.6/100,000 for the period 1988-1990. A specific survey aimed at describing clinical and biological presentation at diagnosis. The main symptom was polyuria in 98% of the cases, fatigue in 58% and weight loss in 44%. Abdominal pain was reported in 34% of the cases. Diagnosis was ascertained by measurement of plasma glucose, which was > or = 11 mmol/l in 95% of the cases and associated with ketonuria in 84% of the children. Coma in 13% of the children and acidosis (total CO2 < or = 18 mmol/l) in 48% showed the severity at diagnosis. Ketonuria and acidosis were significantly more frequent in the younger age group (0-4 yr). Diagnosis was made by a general practitioner in the majority of the cases; conversely insulinotherapy was initiated at the hospital in 95% of the cases. Initial insulin treatment was 2 daily injections. Following the French experience the collaborative network EURODIAB ACE has undertaken the same survey among the European Registries. Important geographical variations in incidence rates of IDDM in children has been reported across Europe but it is not known whether this interferes with presentation at diagnosis of the disease.
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PMID:[Diagnosis of insulin-dependent diabetes in children: data from the incidence registry]. 893 70

Clinical and laboratory data of 1248 newly diagnosed diabetic children at the time of diagnosis were analysed. All children were admitted to the University Children's Hospital in Sofia, 45.9% before first their insulin injection. Symptoms preceding the diagnosis and laboratory data (plasma glucose and ketonuria) were analysed, respectively for 1100 and 1022 children. Blood pH (mainly arterialized) was available in 558 ketonuria positive children and in other 82 acidotic breathing was reported. Mother's education was noted in the 1226 hospital records. Among the children with known urinanalysis 13.5% were without ketonuria (148 patients), 12 of them with fasting blood glucose < or = 6.4 mmol/1 (115 mg/dl). Eighteen-point-two percent of all children were hospitalized in a state of severe ketoacidosis (blood pH < or = 7.2 or reported acidotic breathing). The average duration of thirst and polyuria was 28 +/- 33 days. Ketonuria negative children with plasma glucose < or = 6.4 mmol/l showed a significantly shorter period of symptoms, compared to those with plasma glucose > 6.4 mmol/1 (17 +/- 25 vs. 25 +/- 31 days; P = 0.0991). The cases with severe ketoacidosis, compared to those with mild ketoacidosis (blood pH 7.21 - 7.34) showed shorter period of symptoms too (P = 0.0658). Moderate positive relation existed between the age at diagnosis and duration of symptoms (chi 2 = 43.28, D.F. = 8, P = 0.0000). The percentage of severe ketoacidosis is higher in the younger age groups. Febrile illness, preceding the start of the symptoms was more common in the groups with shorter duration of symptoms (up to 1 month), but did not change the proportion of severe ketoacidosis. No significant difference was found between the level of mother's education and duration of the symptoms before diagnosis (P = 0.9782). We conclude that the level of metabolic disturbances at the diagnosis of IDDM among children was not influenced by the duration of the preceding symptoms. The severity of clinical picture was possibly dependent on the degree of insulinopenia, i.e. the rate of beta-cell destruction. Clinical heterogeneity was possibly dependent on genetical heterogeneity related to HLA class II genes.
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PMID:Clinical and laboratory characteristics of type I (insulin dependent) diabetes mellitus at presentation among Bulgarian children. 901 86

Diabetes mellitus with onset during childhood usually presents as overt ketoacidemia. Pediatricians now inquire specifically about diabetes mellitus in children with nonspecific signs of illness and perform urinary dipstick testing. The present study was therefore performed to assess the possible influence of this strategy on the initial presentation and management of diabetes mellitus. The charts of 61 consecutive children with newly diagnosed diabetes mellitus (positive glucosuria and ketonuria and capillary glucose >14 mmol/l), who had been admitted between 1991 and 1996 at the Department of Pediatrics, University of Bern, Switzerland, were therefore reviewed. Twenty-six out of the 61 patients were nonacidemic (blood pH 7.36 or more). Children with and without acidemia did not differ with respect to age, history of polydipsia and polyuria, plasma glucose and circulating glycated hemoglobin A1c. The degree of dehydration and the amount of fluid required for its correction and the total insulin dosage were more prominent in the group of patients with acidemia. The study demonstrates that childhood diabetes mellitus is nowadays often recognized as nonacidemic hyperglycemia and that in these patients a reduced initial fluid repair and total insulin dosage is recommended.
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PMID:Childhood insulin-dependent diabetes mellitus: initial presentation and management in the nineties. 970 68

A 9-month-old bull was presented with a history of runting and glucosuria. The bull showed major signs of diabetes mellitus, such as polyuria, polydipsia, polyphagia, emaciation, glucosuria, and ketonuria, but persistent hyperglycemia was missing. Because in an intravenous glucose tolerance test glucose disappearance was only insignificantly more rapid in a non-diabetic age-matched control than in the diabetic bull a butyrate-stimulated insulin response test was performed. Insulin response to butyrate infusion was markedly impaired in the diabetic bull compared with the non-diabetic bull. At necropsy hepatic cirrhosis was noticed and suggestive signs for diabetes mellitus were seen in liver and kidneys.
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PMID:Diagnosis of diabetes mellitus in a bull by means of butyrate infusion. 971 60

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.
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PMID:Transient clinical diabetes mellitus in cats: 10 cases (1989-1991). 1005 60

Diabetes mellitus is uncommon in infancy and newborn period. The two common forms seen are the transient and permanent forms of diabetes mellitus of the newborn. They have to be differentiated from the transient hyperglycemic states (Blood sugar > 125 mg/dl) seen in newborns who receive parenteral glucose infusions and in those with septicemia and CNS disorders. Transient diabetes mellitus of the newborn (TDNB) is defined as hyperglycemia occurring within the first month of life lasting at least 2 weeks and requiring insulin therapy. Most of these cases resolve spontaneously by 4 months. It has a reported incidence of 1 in 45,000 to 60,000 live births. The most likely etiology is a maturational delay of cAMP mediated insulin release. The clinical features include small for datedness, proneness for birth asphyxia, open-eye alert facies, dehydration, emaciation, polyuria and poydipsia. These children are prone to septicemia and urinary tract infections. They have hyperglycemia, glucosuria, absent or mild ketonuria, low basal insulin, C-peptide and IGF-1 levels. Treatment consists of hydration and judicious administration of insulin with close monitoring. Thirty percent of these children are likely to develop permanent neonatal diabetes. Compared to transient form, permanent diabetes mellitus is uncommon. It is usually due to pancreatic dysgenesis often associated with other malformations and rarely due to type 1 diabetes mellitus. The diagnosis is based on the demonstration of both exocrine and endocrine pancreatic dysfunction. These children are managed as type 1 diabetes mellitus. They are prone to develop the vascular complications of diabetes at an earlier date.
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PMID:Diabetes mellitus in newborns and infants. 1093 65

This paper describes a 6-year-old Simmental bull with diabetes mellitus. The animal was referred to our clinic because of severe weight loss and chronic indigestion. Clinical examination revealed markedly disturbed general condition, impaired forestomach function and polyuria. There was aciduria, glucosuria and ketonuria. The most important biochemical findings were severe hyperglycemia, markedly increased activities of hepatic enzymes and severe metabolic acidosis. Plasma concentrations of insulin, insulin-like growth factor-I, thyroxine and 3,5,3'-triiodothyronine were lower than normal, whereas those of glucagon were higher than normal. Based on these findings, a diagnosis (secondary) diabetes mellitus was made. The bull was slaughtered and histological examination revealed mixed cell pancreatitis with severe degeneration of islet cells. Immunohistochemical examination of the pancreas showed that very few insulin-, glucagon-, somatostatin- and pancreatic polypeptide, insulin-like growth factor-I and adrenomedullin-producing islet cells were present.
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PMID:[Diabetes mellitus caused by pancreatitis in a bull]. 1123 31

This study was undertaken to determine which type 1 diabetes-associated autoantibodies and what clinical characteristics are most useful to identify patients with type 1(1/2) diabetes. We studied 125 patients, recently diagnosed clinically with type 2 diabetes for the presence of islet cell antibodies (ICA), insulin autoantibodies (IAA), antibodies to glutamic acid decarboxylase(GADAb), and IA-2a (IA-2Ab). Patients with a diagnosis of type 2 diabetes who met all of the following criteria at diagnosis were studied: age > or = 30 years, no history of ketonuria or ketoacidosis, and not requiring insulin treatment. Thirty-six patients (29%) were positive for at least 1 antibody. Thirty-two (26%) were ICA positive and 20 (16%) GADAb positive. Insulin autoantibodies and IA-2Ab occurred less frequently in 2 (1.6%) and 8 (6.4%) patients, respectively. There was no significant difference in the ages at diagnosis between the Ab(+) and Ab(-) patients, age in years (range) 47.2 (32 to 64) versus 51.2 (31 to 77), respectively, P =.06. Body mass index (BMI) was different in the 2 groups, with Ab(+) patients being less obese, BMI (range) 28.3 kg/m(2) (17.6 to 54.9) versus 32.0 kg/m(2) (19.2 to 68.8), respectively, P =.01. Clinical presentation of diabetes was more commonly symptomatic with polyuria and polydipsia in Ab(+) patients, while in Ab(-) patients, diagnosis was more often incidental, P =.002. However, more than 95% of patients overlapped in both age and BMI irrespective of antibody status. Similarly, 42% of Ab(+) patients had their diabetes diagnosed incidentally, while 29% of Ab(-) patients presented with polyuria and polydipsia. We therefore conclude that screening with antibodies, mainly ICA and GAD, but not age, BMI, or clinical presentation should be used to identify type 1(1/2) diabetes.
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PMID:Islet cell antibodies and glutamic acid decarboxylase antibodies, but not the clinical phenotype, help to identify type 1(1/2) diabetes in patients presenting with type 2 diabetes. 1155 30

The simultaneous occurrence of juvenile dermatomyositis (DMS) and diabetes mellitus is described in 2 pediatric patients. Both these patients presented with significant weight loss, polyuria, and polydypsia within a short time of being diagnosed with JDMS, while these patients were taking oral prednisone (40-60 mg/day in divided doses). Laboratory evaluation detected ketonuria, significant hyperglycemia (696 and 913 mg/dL) and low serum levels of insulin and C-peptide. Both these patients were treated with high doses of insulin. Islet cell and GAD65 antibodies were found to be positive in 1 of the patients, pointing toward a diagnosis of insulin-dependent diabetes mellitus. The other patient tested negative for these antibodies and required insulin therapy for approximately 6 months. Steroid-induced diabetes mellitus seemed highly likely in this case. We hypothesize that a common environmental trigger possibly a viral infection might have been responsible in causing 2 different autoimmune pathologies in these genetically predisposed individuals.
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PMID:Simultaneous occurrence of diabetes mellitus and juvenile dermatomyositis: report of two cases. 1286 53


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