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

In 21 patients, epilepsia partialis continua (EPC) was an early symptom of nonketotic hyperglycemia and occurred during an initial phase of hyponatremia and mild hyperosmolality. EPC persisted for an average of 8 days, and its duration correlated predominantly with the degree of hyponatremia. Depression of consciousness and cessation of seizures occurred with increasing severity of hyperglycemia and hyperosmolality. In 9 patients, EPC was the first symptom leading to the diagnosis of diabetes mellitus. Four patients died of serious associated illness. The majority of the patients had evidence of a localized structural cerebral lesion. Metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of EPC in areas of focal cerebral damage.
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PMID:Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical profile of 21 patients. 677 82

Abnormal electroencephalograms in patients with long-standing diabetes mellitus have been attributed to hypoglycemia. EEG changes in newly diagnosed patients or in patients during episodes of diabetic ketoacidosis have not previously been reported. We performed serial EEGs at one, 12, 24 hours and five days after initiation of treatment for DKA on 39 patients aged 11 months to 16 years with newly or previously diagnosed insulin-dependent diabetes mellitus. Twenty-seven patients were in ketoacidosis and 12 patients ketotic only. Abnormal EEGs were found in 30 patients on admission. The EEG changes at one hour, classified in order of increasing severity, correlated with the serum glucose, osmolality, bicarbonate, beta-hydroxybutyrate, and acetoacetate values, but not with pH or glycosylated hemoglobin. The rate of improvement of the EEGs was unaffected by the addition of phosphate to the intravenous fluids during therapy. EEG changes persisted in five of the seven children who had follow-up studies at two to five months, and in two of the six children one year after admission. We conclude that EEG changes are common in children with DKA or ketosis, the severity of the abnormalities being most closely associated with the degree of hyperosmolality rather than acidosis. These changes may persist in some cases, possibly accounting for the increased frequency of EEG abnormalities in diabetic children.
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PMID:Electroencephalographic changes in diabetic ketosis in children with newly and previously diagnosed insulin-dependent diabetes mellitus. 679 Jun 87

Diabetes mellitus was diagnosed in an aged bonnet macaque (Macaca radiata). Six months later the monkey was found comatose. Laboratory findings of extreme hyperglycemia, hyperosmolality, and glycosuria without ketonuria were consistent with a diagnosis of hyperosmolar, non-ketotic diabetic coma (NKC). Further laboratory studies disclosed very low levels of immunoreactive insulin and depressed free fatty acid values. Growth hormone and cortisol levels were within normal limits.
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PMID:Hyperosmolar non-ketotic diabetic coma in the nonhuman primate: a first report. 685 68

There appears to be an association between affective disorders and diabetes mellitus independent of the use of lithium in treatment. Prior studies have suggested that lithium treatment may impair glucose tolerance or produce frank diabetes in certain patients. Metabolic complications of the diabetic state, such as hyperosmolality and salt depletion increase lithium absorption and the risk of toxicity even at generally acceptable serum levels. The management of patients with diabetes and affective disorders on prophylactic lithium is discussed.
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PMID:Affective disorders, diabetes mellitus and lithium. 704 79

1. To investigate the mechanism of hepatic V1a vasopressin receptor down-regulation in streptozotocin-induced diabetes mellitus in the rat, we measured hepatic V1a receptor mRNA by in situ hybridization histochemistry using oligonucleotide probes to the V1a receptor and Northern blotting. 2. Diabetes mellitus caused hyperglycaemia, hyperosmolality and increased plasma vasopressin concentrations (P < 0.01). Hepatocyte V1a receptor mRNA was reduced by 76% in diabetic rats (P < 0.01) and by 53% in insulin-treated diabetic rats (P < 0.01) versus control rats, in parallel with reduced V1a radioligand binding and vasopressin-stimulated inositol phosphates production. There was a similar decrease in hepatic V1a/18S mRNA density ratio in the diabetic and diabetic+insulin groups (both P < 0.05 versus control). 3. These findings suggest that altered V1a mRNA transcription is responsible for the reduced hepatic V1a receptor density in diabetes mellitus.
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PMID:Down-regulation of vasopressin V1a receptor mRNA in diabetes mellitus in the rat. 763 50

Continuous partial epilepsy (CPE) is characterized by isolated, subintrant clonus focalized to a limited territory with critical focal electroencephalography in a concordant territory. CPE is observed in various cortical lesions but also in disorders of metabolism and notably decompensated diabetes mellitus. We report a case of CPE without focal lesion at MRI which revealed hyperglycaemia without ketosis. The 54-year old female patient was hospitalised for C.P.E.. Early CT and later MRI gave normal results. Biochemistry showed hyperglycaemia without kenoturia, acidosis or hyperosmolality. Insulin therapy rapidly brought glycaemia down to its normal level and the clonsism disappeared. Five months later, the patient had no other seizure and the EEG was normal. Epileptic seizures are frequent in hyperglycaemia without ketosis (25% of the cases) where they are mainly partial and motor (75 to 86% of the cases), rarely associated with a focal lesion (15% of the cases with CT scan). They are rare in patients with ketoacidosis. This apparent protective effect of ketoacidosis may be attributed to an increase of GABA bioavailability consecutive to acidosis. CPE is resistant to antiepileptic treatments. In CPE induced by hyperglycaemia without ketosis normalization of blood glucose level with insulin therapy is concomitant with a rapid cure of epilepsy. Thus glycaemia should be measured in all patients presenting with CPE, the aim being to diagnose hyperglycaemia without ketosis rapidly to avoid hyperosmolality and to prescribe an adequate treatment based exclusively on insulin and rehydration.
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PMID:[Continuous partial epilepsy disclosing diabetes mellitus]. 786 72

This study was aimed at investigating the mechanisms of clinically important overt hyperkalemia in diabetes mellitus with underlying hyporeninemic hypoaldosteronism known as a classic model of the syndrome of hyporeninemic hypoaldosteronism (SHH). Rats (Sprague-Dawley, male) were streptozotocin-treated (60 mg/kg, ip) and used after 60 days. Rats with plasma glucose levels higher than 300 mg/dL (mean +/- SEM, 423 +/- 20 mg/dL, n = 8) were selected as the diabetic group. Age-matched normal rats served as control (mean plasma glucose, 88 +/- 2, mg/dL, n = 8). Serum potassium concentrations and osmolalities as well as serum creatinine levels were significantly higher in the diabetic than in the control group (5.07 +/- 0.09 vs. 4.68 +/- 0.11 mEq/L; 330 +/- 14 vs 290 +/- 3 mOsm/L; 0.40 +/- 0.03 vs 0.31 +/- 0.02 mg/dL, p < 0.05). Plasma renin activity (PRA) in the diabetic group was significantly lower than that in the control group (6.0 +/- 1.0 vs 12.1 +/- 1.1 ng Al/ml/h, p < 0.001). Plasma aldosterone concentration (PAC) was also significantly lower in the former than in the latter (368 +/- 30 vs 761 +/- 57 pg/ml, p < 0.001). Renomegaly, abnormal distal tubular cells with few organelles, and increased lipid droplets with pyknotic nucleus in zona glomerulosa of the adrenal glands were noted in the diabetic group. In conclusion, multifactorial causes including insulinopenia, hyperosmolality, elevated serum creatinine level and hypoaldosteronism with possible contribution of altered distal tubular response to aldosterone may have interacted to develop hyperkalemia in these diabetic rats.
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PMID:Mechanisms of hyperkalemia associated with hyporeninemic hypoaldosteronism in streptozotocin-induced diabetic rats. 798 85

Taurine, a product of sulfur amino acid metabolism, is important in cerebral osmoregulation. To understand the adaptive changes in transport which accompany different hyperosmolal states, we determined lipid composition and fluorescence anisotropy of synaptosomal liposomes from rats with chronic hypernatremic dehydration (CHD), streptozocin-induced (STZ) diabetes, and insulin treated diabetes. Induction of CHD increased serum osmolality, and enhanced in vitro synaptosomal taurine uptake (P < 0.01, n = 3, vs. control). Fluorescence anisotropy studies showed that the fluidity of lipids from CHD synaptosomes was higher than control (P < 0.05, n = 3). STZ-diabetes resulted in hyperglycemia, increased serum osmolality, and stimulated synaptosomal taurine uptake (P < 0.01, n = 3, vs. control). Insulin treatment of diabetic rats restored serum osmolality and taurine transport to control values. The fluidity of diabetic rat brain synaptosomal lipids was significantly higher than control (P < 0.05, n = 3); fluidity was normalized by insulin administration to diabetic rats. Total fatty acid, cholesterol, and cholesterol/phospholipid molar ratio of CHD, STZ, and insulin treated diabetic rats were similar to control. However, the ratio of saturated to unsaturated fatty acids was decreased in hyperosmolal states. This suggests that adaptive increases in cerebral taurine transport during hyperosmolality may result from a direct effect on membrane composition that alters fluidity and permits enhanced transmembrane flux of osmoprotective molecules.
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PMID:Increased lipid fluidity in synaptosomes from brains of hyperosmolal rats. 805 54

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

Sixty-two consecutive episodes of diabetic ketoacidosis (DKA) were studied at Aga Khan University Hospital, Karachi. Forty-four (71%) were type I and 18 (29%) type II diabetics. Mean age was 28.1 years and mean duration of diabetes 4.1 years. Infections were the most common precipitating factor accounting for 28 episodes (45.2%). Twenty-two patients (35.5%) had hyperosmolality (serum osmolality > 320 mosmol/L). Mean serum Na+ was 131.7 mmol/L and K+ 4.6 mmol/L. Twenty-three (37.1%) were hyperkalemic at presentation with seven patients (11.3%) being comatosed and 35 (56.5%) alert. Mean random blood glucose (RBG) was 624 mg/dl, mean pN 7.09, osmolality 316 mosmol/L and the neurological status correlated statistically significantly with mean RBG, pH and osmolality. A leukemoid response was seen in 83.9% episodes. Mortality rate was 8.0% in patients with DKA managed in this hospital.
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PMID:Diabetic ketoacidosis in a hospital based population in Pakistan. 823 Jun 67


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