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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A critical analysis of the evolution during the first 24 hours was undertaken in 41 children and adolescents (age: 10.1 +/- 4.6 years) treated for diabetic ketoacidosis. Three of 4 children presented with ketoacidosis revealing diabetes. One of 4 was less than 6 years of age. Severe ketoacidosis (pH less than 7.15) concerned one third of children and were more frequent in the group of adolescents with already known diabetes. In these patients, ketoacidotic decompensation was attributed to psychosocial factors in most cases. Evolution was favorable in all cases, without complication. Blood glucose levels decreased from 28.7 mmol/l on arrival to 16.2 mmol/l after 2 hours of treatment and became stable at 10 mmol/l from the 12th to the 24th hours. The corrected blood sodium levels were stable, showing the adequacy of infusion solute osmolarities. Blood potassium was maintained at a normal level owing to early potassium supplementation. Ketoacidosis was corrected after about 12 hours, without bicarbonate administration when pH was greater than 7.15. Average perfused volumes were 3 l/m2/24 hours. Insulin doses were 2 UI/kg/24 hours and were inversely correlated with the admission pH (r = -0.6; p = 0.0001). This study shows the efficacy of a treatment taking into account the pathophysiology of diabetic ketoacidosis and the knowledge of the complication risk factors, by foreseeing the adjustments to be done with respect to individual and/or at risk situations. These precise descriptive data, collected on a large group of patients, establish a reference basis to follow evolution in the course of the treatment of diabetic ketoacidosis in children.
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PMID:[Critical study of diabetic ketoacidosis in children. Initial description and course during the first 24 hours of treatment]. 161 Feb 73

The influence of clinical and laboratory findings on the two-year survival prognosis was investigated in 558 geriatric patients admitted to permanent institutional care. The patients surviving for two years (52%) were somewhat younger (79 vs 82 years, p less than 0.01), and on admission had significantly higher diastolic blood pressure (p less than 0.001), serum thyroxin (p less than 0.05), serum albumin (p less than 0.01) and blood haemoglobin (p less than 0.05), but lower treatment score (p less than 0.001), serum creatinine (p less than 0.001), and fasting plasma glucose (p less than 0.05). Decreased survival prognosis was also found in patients with abnormal serum sodium, chloride, and potassium (p less than 0.05 or less). However, an excess mortality of patients with abnormal laboratory data occurred within the first month after admission. Stepwise logistic regression analysis disclosed that the three-month survival prognosis was significantly impaired by low blood pressure (less than 110/70 mmHg), high treatment score (greater than 22), elevated serum creatinine (greater than 150 mumol/L), use of digitalis and atrial fibrillation. Poor two-year survival was further associated with the use of diuretics, and diabetes mellitus. The risk for death was lowest in patients with elevated blood pressure (greater than 160/95 mmHg). These data verify the significance of the clinically common diseases and indicators of homeostasis in the assessment of geriatric hospital patients, and demonstrate the nature of "terminal decline" in geriatric practice.
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PMID:Survival prognosis in geriatric patients admitted to permanent institutional care. 162 79

Six cases of acute renal failure (ARF) due to rhabdomyolysis were experienced between 1984 and 1989. Patients' ages ranged from 33 to 92 years old (average ages 61) and all were male. The causes of rhabdomyolysis were as follows: one crush syndrome, one acute arterial occlusion, one diabetic hyperosmolar nonketotic coma and three cases of malignant syndrome due to neuroleptica (mainly haloperidol). Underlying diseases included, one case of abdominal aneurysm, two cases of diabetes mellitus, two cases of schizophrenia and one case of reactive psychosis. Dehydration was considered as an important factor in the onset of rhabdomyolysis and ARF, because it was observed in 4 of the cases in this study. In all cases, the serum levels of potassium, phosphorus and uric acid as well as myoglobin and myogenic enzymes increased markedly. In patients with myoglobinuric ARF, severe metabolic acidosis and hypocalcemia in the oliguric phase and hypercalcemia in the diuretic phase were prominent. Muscle biopsy showed myolytic degeneration in 2 of 4 cases. Five cases were treated with hemodialysis and one case was managed conservatively. All 6 cases had relatively good prognosis. However, 3 cases with malignant syndrome showed outcomes more severe than in the other 3 cases without such syndrome.
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PMID:[Acute renal failure due to rhabdomyolysis--clinical investigation on our 6 cases]. 163 34

Antidiabetic sulfonylureas act through receptors coupled to ATP-dependent potassium channels. Using the binding of [3H]glibenclamide, a highly potent sulfonylurea, to rat brain membranes to follow the purification procedure, we extracted from ovine brain, purified, and partially characterized two peptides that are endogenous ligands for the central nervous system sulfonylurea receptors. These peptides, referred to as alpha and beta endosulfine, differ by their isoelectric points, the beta form being more basic. Each form of endosulfine is recognized equally by the sulfonylurea receptors from the central nervous system and from insulin-secreting beta cells. In the same concentration range that is active on the receptors, beta endosulfine releases insulin from a beta-cell line. Endosulfine is a good candidate for being implicated in the physiology of beta cells and their disorders (e.g., type II diabetes) and in certain pathologies related to modifications of ion fluxes.
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PMID:Endosulfine, an endogenous peptidic ligand for the sulfonylurea receptor: purification and partial characterization from ovine brain. 163 Nov 65

We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old - 65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i.e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome. The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed. Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing's syndrome and those with Cushing's disease. Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease. Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Forty-one cases of Cushing's syndrome: a comparison between Cushing's syndrome (adrenal adenoma) and Cushing's disease (adrenal hyperplasia)]. 163 31

Chemically induced diabetes has been reported to induce profound changes in bile formation, but possible toxic effects of the streptozotocin or alloxan used cannot be excluded totally. This study was undertaken to evaluate biliary function in spontaneously diabetic female biobreeding rats with a diabetes duration of 2 wk and compare them with nondiabetic littermates. Diabetic animals evidenced glycosuria, hyperglycemia and hypoinsulinemia. Biliary concentration and secretion of bile acids, cholesterol and phospholipids were significantly increased, with no enhancement in the lithogenic index of bile. Bile flow and the biliary secretion of sodium, potassium, chloride and bicarbonate were significantly reduced despite the increased bile acid secretion. The cholestatic condition was confirmed by an increased serum concentration of bile acids and a higher activity in serum of the alkaline phosphatase liver isoenzyme. Biliary calcium concentration increased without any change in its serum concentration. A linear relationship was observed between biliary calcium and bile acid secretion. Serum concentration of unconjugated and of conjugated bilirubin was increased 1.6-fold and 8-fold, respectively, with a 1.5-fold enhanced biliary secretion of bilirubins despite the cholestasis; this points to an enhanced bilirubin production. An increased proportion of conjugated bilirubin was found in serum together with an enhanced bilirubin diconjugate/monoconjugate ratio in bile. A higher UDP-glucuronyltransferase activity and a delayed transit of bilirubin could account for these effects. Administration of insulin to diabetic animals tended to reverse the above reported changes. The spontaneously diabetic biobreeding rat thus represents a model of bile acid-independent cholestasis with enhanced biliary bile acid and calcium secretion and with presumably an enhanced bilirubin production.
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PMID:Spontaneously diabetic biobreeding rats and impairment of bile acid-independent bile flow and increased biliary bilirubin, calcium and lipid secretion. 163 53

Improved blood glucose control by insulin treatment in patients with Type 2 (non-insulin dependent) diabetes mellitus increases the risk for hypoglycaemic episodes. Our objective was to investigate if hypoglycaemia causes electrocardiographic changes and cardiac arrhythmias in patients with Type 2 diabetes. Six insulin-treated patients with Type 2 diabetes and no known cardiac disease took part in the study. Hypoglycaemia was induced by insulin infusion aiming at a plasma glucose less than or equal to 2.0 mmol l-1 or hypoglycaemic symptoms. All patients experienced hypoglycaemic symptoms. The median lowest arterial plasma glucose was 2.0 mmol l-1. Arterial plasma adrenaline concentration increased from 0.4 +/- 0.1 (mean +/- SE) to 6.9 +/- 0.3 nmol l-1 (p less than 0.001) while serum potassium was lowered from 4.1 +/- 0.3 mmol l-1 to 3.5 +/- 0.2 mmol l-1 (p less than 0.001). The heart rate increased significantly during hypoglycaemia except in one patient who developed hypoglycaemic symptoms and a severe bradyarrhythmia at a plasma glucose of 4.4 mmol l-1. One patient developed frequent ventricular ectopic beats during hypoglycaemia while four patients showed no arrhythmia. ST-depression in ECG leads V2 and V6 was observed during hypoglycaemia in five patients (p less than 0.05) and four patients developed flattening of the T-wave. In conclusion, the study supports the hypothesis that hypoglycaemia in patients with Type 2 diabetes may be hazardous by causing cardiac arrhythmias.
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PMID:Hypoglycaemia and cardiac arrhythmias in patients with type 2 diabetes mellitus. 164 1

The long-acting effect of a 10-min pulse infusion of the beta 2-adrenergic agonist fenoterol on oral glucose tolerance tests in controls and in normotensive patients with type 2 diabetes mellitus on diet was compared. During an oral glucose load starting 2 h after fenoterol control persons showed hyperglycemia (area: 25,950 +/- 467 vs. 22,650 +/- 410, P less than 0.01), hyperinsulinemia (area: 13,980 +/- 1050 vs. 8160 +/- 405, P less than 0.02) and a pronounced fall of serum potassium (area: 775 +/- 26 vs. 748 +/- 25, P less than 0.02). The patient group showed no late response to fenoterol: plasma glucose (area: 51,000 +/- 382 vs. 51,300 +/- 413, n.s.), serum insulin (area: 7215 +/- 233 vs. 8280 +/- 410, n.s.), serum potassium (area: 748 +/- 26 vs. 750 +/- 24, n.s.). The data show that there is a defect of the beta 2-adrenergic long-acting effect on glucose metabolism and on insulin release in type 2 diabetes mellitus.
Diabetes Res Clin Pract 1991 Aug
PMID:Lack of beta 2-adrenoceptor induced long-acting effect on glucose tolerance in type 2 diabetic patients. 166 46

Dietary boron, in concentrations similar to that found in human diets comprised mainly of fruits and vegetables, affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 mg B/kg; no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages for 6 days. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of mineral metabolism as expected. Plasma ionized calcium concentrations fell by approximately 10% in STZ-treated rats. Brain and heart mineral metabolism was spared from the toxic effects of STZ whereas spleen mineral metabolism was especially vulnerable to STZ. Supplemental dietary boron increased urinary excretion of calcium in the non-STZ rats but did not affect the plasma concentrations of alkaline phosphatase, ionized calcium or the concentration of calcium in the brains, lungs, kidneys and spleens of those animals. Supplemental dietary boron temporarily reduced the abnormally elevated renal excretion of albumin, potassium and sodium during the acute phase of diabetes mellitus. On the other hand, physiological amounts of dietary boron exacerbated the abnormally elevated rate of collagen breakdown in the STZ animal. Finally, boron may have indirectly affected heart mineral metabolism because dietary boron did not affect cardiac boron concentrations but did affect cardiac copper, calcium, manganese, molybdenum and phosphorus concentrations, primarily in non-STZ rats. The findings suggest that dietary boron has both protective and regulatory roles in mineral metabolism.
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PMID:Effects of dietary boron on calcium and mineral metabolism in the streptozotocin-injected, vitamin D3-deprived rat. 166 22

Methodological developments in recent years, particularly patch clamp technology and the techniques of molecular biology, have advanced our knowledge of the molecular basis of synaptic transmission. The review is a brief summary of some findings concerning the ion channels that respond to hormones transmitters, or change in cell membrane potential, and of advances in our understanding of transmitter storage and release. Ion channels have been found to be targets for several drugs in clinical use, including anaesthetics, bensodiazopines, so-called calcium antagonists and the sulphonylureas used in the treatment of diabetes. The latter drugs have been shown to interact specifically with a potassium channel regulated by ATP (adenosine triphosphate). In pancreatic beta-cells, this channel controls membrane potential and insulin release under physiological conditions; in several other cells, it is activated under hypoxic or ischaemic conditions.
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PMID:[Ion channels--the molecular background of neural transmission]. 171 16


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