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

UNICEF promotes the use of a very effective, inexpensive treatment of dehydration in developing countries: oral rehydration therapy (ORT), which is oral administration of a solution with equimolar concentrations of sodium and glucose (osmolality of about 300 mosmol). The solution is isotonic with respect to total body water when it reaches the small intestine. It expands the extracellular fluid without changing serum osmolality, thus, brain edema does not occur. Further, metabolic degradation of glucose eventually releases free water. On the other hand, intravenous rehydration with saline solution can be lethal, causing excess free water to expand shrunken cells and, thereby, causing brain swelling, rupture of blood vessels and hemorrhage. Yet, physicians and other health workers in developed countries have been quite sow to accept ORT. Leading conditions of dehydration include insensible loss of water and heat through evaporation from the respiratory tract and skin (common in dry air, hot environment, and fever), sensible loss of water and heat through perspiration (common in hot, humid environment and with warm and absorbent clothing), and irritation of the intestinal mucosa by allergies, infections, toxins, and intolerance to some nutrients, resulting in diarrhea. Diarrhea is indeed the main cause of dehydration. Other causes of dehydration are: failure of the hypothalamus to secrete antidiuretic hormone (ADH), kidney unresponsiveness to ADH, diabetes mellitus, protein-rich nutrition, catabolic states, and brush-border lactase after weaning. Physiological changes in dehydration consist of rigidity of the connective tissue (vascular system and lungs) and intracellular fluid loss to the extracellular spaces, resulting in dry mucous membranes, shrunken muscle cells in the lips and the tongue, soft eyes, and adverse effects to the central nervous system. Children become dehydrated more readily than adults, but they tolerate it better.
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PMID:Water: mechanism of oral rehydration, water deficiency = deficiency in salt. 150 31

Blood glucose, plasma sodium, bicarbonate (HCO3-), vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3- (r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P less than 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.
Diabetes 1992 May
PMID:Correlates of brain edema in uncontrolled IDDM. 156 33

The discovery that monoamine nerves end on the central microvessels of the choroid plexus, pia-arachnoid and parenchyma has prompted an intense investigation as to their physiological and neuropathological roles. The source of the monoamine fibers to the pial vessels and choroid plexus was shown to be the superior cervical ganglion. Ganglionic stimulation causes vasoconstriction or vasodilation of pial vessels, an event depending upon the functional ratio of alpha to beta adrenergic receptors. Moreover, stimulation of the superior cervical ganglion evokes an inhibition of cerebrospinal fluid formation in choroid plexus. The locus coeruleus is the site of adrenergic nerve supply to the parenchymal capillaries and stimulation of this nucleus increases capillary permeability to small molecules and water. Neurotransmitter receptors (adrenergic, histamine, adenosine, dopamine, prostacyclin, prostaglandins and specific amino acids or neuropeptides) have been identified on microvessels and in many instances these transmitter actions are coupled to cyclic AMP synthesis. Moreover, cyclic AMP has been shown to increase the rate of capillary endothelial pinocytosis and produce brain edema. In small vessels containing smooth muscle cells cyclic AMP production improves cerebral blood flow via an initiation of vasodilatory processes. The presence of receptors for serotonin and acetylcholine have likewise been demonstrated to occur on cerebral microvessels. Limited information is available as to the receptor coupled actions of these two transmitters, but cholinergic mechanisms may act to restrict catecholamine-induced formation of cyclic AMP. Altered sensitivity of microvessels to neurotransmitters has been demonstrated following conditions of stroke, hypertension, aging, diabetes and X-irradiation.
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PMID:Neurochemical coupled actions of transmitters in the microvasculature of the brain. 287 36

This study examines the immediate and long-term results of surgical treatment for intracranial meningioma in patients aged 65 and over. Average patient age was 69 years. The most frequent localizations were the convexity (29.8%) and the sphenoid wing (20.1%). Preoperative risk factors included hypertension (16.1%), cardiopathies (16.1%), diabetes (12.9%) pneumopathies (12.9%) and peripheral vascular diseases (9.6%). All patients were assessed according to the Karnofsky Performance Status (KPS). Operative mortality was 18.5% (23 cases). At long term follow up (minimum 4 months, maximum 12 years, average 5 years) 31.5% of patients were cured, 32.3% had improved and 4% had worsened. The risk factors that mainly influenced results included poor preoperative clinical condition as expressed by low KPS, while the most frequent medical postoperative complications that increased the rate of operative mortality were brain edema, infections and lung embolism.
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PMID:Meningiomas in elderly patients. Clinico-therapeutic considerations. 847 51

During the last 10 years, five children were treated at Childrens Hospital Los Angeles for acute, persistent neurologic loss during diabetic ketoacidosis (DKA). Four were transferred from local hospitals after the neurologic crisis. Computed tomography (CT) studies showed one or more areas of brain infarction in each patient, and none had evidence of diffuse cerebral edema. As three of the five patients had been treated for cerebral edema before their CT, brain edema may have been present initially. Our findings emphasize the importance of brain infarction as a cause of persistent neurologic loss in children with DKA.
J Diabetes Complications
PMID:Brain infarction in children with diabetic ketoacidosis. 877 28

Bimoclomol (BRLP-42) is a novel antiischemic compound acting against peripheral vascular complications of diabetes mellitus (neuropathy, retinopathy, and nephropathy). In the present study the activity of bimoclomol was tested in experimental subarachnoid hemorrhage (SAH) and arachidonic acid (AA)-induced brain edema in rats to elucidate whether the compound may also have beneficial effect in cerebrovascular disturbances. For comparison, a neuroprotective AMPA antagonist, GYKI-52466, was examined. Injury caused by autologous intracranial blood injection or sodium-arachidonate was evaluated by the damage of blood-brain barrier (BBB) reflected in the extravasation of Evans blue dye into the cerebral tissue. Bimoclomol (2 x 2 mg/kg IV) markedly reduced, while GYKI-52466 (2 x 2 mg/kg IV) moderately diminished the extravasation produced by SAH (39.9%, p < 0.01 and 26.7%, p > 0.05, respectively). In the case of AA-induced brain edema, bimoclomol showed less pronounced (19.6%, p < 0.05) inhibitory action, and GYKI-52466 seemed to be more effective (34.2%, p < 0.05). These results suggest that bimoclomol may be active not only in peripheral micro- and macroangiopathy, but also in some types of cerebrovascular disorders.
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PMID:Bimoclomol protects against vascular consequences of experimental subarachnoid hemorrhage in rats. 944 34

The acute complications of diabetic ketoacidosis in children and adolescents are well recognized but not completely understood. Clinical studies have focused primarily on brain edema. We have investigated the prevalence and course of interstitial pulmonary edema in patients with severe diabetic ketoacidosis all of whom had uneventful clinical courses. High resolution computed tomography scans of the lungs were analyzed by determining the Hounsfield attenuation level and then converting to physical density values. All seven patients had evidence of interstitial pulmonary edema on the first scan, which was performed within 1 h of hydration and prior to receiving insulin; six of the seven patients had increased pulmonary density 6-8 h into treatment, and all had complete resolution of the interstitial changes at discharge. Our study suggests that subclinical interstitial pulmonary edema may be a frequent occurrence in children and adolescents with severe diabetic ketoacidosis and may very well be present prior to treatment. The study also supports the philosophy of cautious rehydration and the close monitoring of children and adolescents with diabetic ketoacidosis until a more complete understanding of this pathophysiologic event is achieved.
J Diabetes Complications
PMID:Interstitial pulmonary edema in children and adolescents with diabetic ketoacidosis. 987 65

Cerebral vascular accidents are one of the causes of morbidity and mortality in children with diabetic ketoacidosis. We investigated the possible occurrence of asymptomatic cerebrovascular infarcts and the course of subclinical brain edema in six patients. Neurologic examinations and computer analysis of magnetic resonance imaging were performed immediately after, and again at 14 days after, correction of DKA. None of the patients had clinical evidence of a neurologic deficit. Neither radiologic evaluation nor computer analysis of MRI identified changes indicating asymptomatic ischemic events. However, a computer analysis of the MRI identified a significant increase of the total ventricle area between Day one and Day 14. Our study does not establish whether this change is a return to the baseline prior to DKA or a new baseline, representing an early manifestation of diabetic encephalopathy.
J Diabetes Complications
PMID:Computer analysis of magnetic resonance imaging of the brain in children and adolescents after treatment of diabetic ketoacidosis. 1061 55

Diabetes mellitus is a metabolic disorder associated with central nervous system impairments. Recent studies implicate oxidative stress mediated by reactive oxygen species (ROS) in the pathogenesis of diabetic complications. ROS have been shown to play role in the pathophysiology of brain injury. In the present study, closed head injury (CHI) was induced in diabetic rats to test the hypothesis that chronic oxidative stress exacerbates brain damage following CHI. Neurological recovery, edema, levels of low molecular weight antioxidants (LMWA), and markers of lipid peroxidation were determined at different intervals after injury. Diabetic rats (4 weeks after induction with streptozotocin) were subjected to CHI. Brain edema (percent water) and clinical status (neurological severity score) were assessed during 7 days. Brain LMWA were determined using cyclic voltammetry (CV) and HPLC-EC. In addition, conjugated dienes and thiobarbituric acid reactive substances (TBARS) were measured. Diabetic-CHI rats exhibited a lower rate of recovery and greater and more sustained edema (p < 0.01), as compared with the controls. At all times diabetic rats had higher levels of TBARS and conjugated dienes and lower concentrations of LMWA, and of vitamins C and E, suggesting chronic oxidative stress. At 5 min of CHI, the amounts of LMWA in control-CHI brains decreased (approximately 50%, p < 0.01) and returned to normal by 48 h and 7 days. In the diabetic-CHI brain only one class of LMWA slightly declined but remained low for 7 days. The present results support the hypothesis that diabetic rats are under chronic oxidative stress, and suffer greater neurological dysfunction, associated with further lipid peroxidation following CHI.
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PMID:Neurological recovery from closed head injury is impaired in diabetic rats. 1110 Dec 5

Activated peripheral T-lymphocytes are increased in both pre-insulin-dependent diabetes mellitus (IDDM) patients and in recently diagnosed IDDM patients, as well as in various forms of acute stress. We studied the in vivo T-lymphocyte activation in six patients in severe diabetic ketoacidosis (DKA) prior to treatment, after 24 h of treatment and > or =5 days after admission. Five of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05). There was no correlation to the admission serum glucose, osmolality, or electrolytes. Serum pH showed a trend toward an inverse correlation, but was not statistically significant. We speculate that T-lymphocyte activation plays a role in the progression of the acute complications of subclinical brain edema and interstitial pulmonary edema of DKA. This process could also be another factor in the progression of the chronic complications of IDDM in addition to the well-established effects of hyperglycemia and hypertension.
J Diabetes Complications
PMID:Acute activation of peripheral lymphocytes during treatment of diabetic ketoacidosis. 1135 83


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