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

The authors analyze a group of 121 patients with focal cerebral ischaemia, hospitalized at the Neurological Clinic in Kosice in 1987-1989. Forty-three patients were treated before the development of the vascular attack for diabetes. In the second group of patients, comprising 78, diabetes was newly detected in 26, i. e. in one third of the group. Glycaemic compensation of 40% of the treated diabetics, evaluated on the basis of glycaemic profiles and the concentration of glycohaemoglobin, was not satisfactory. High glycohaemoglobin levels in five patients with newly detected diabetes suggested that diabetes had persisted for a long time and was probably asymptomatic. The mortality from a cerebral attack was higher in diabetics than in non-diabetics. The highest mortality was recorded in a group of women with newly detected diabetes where of nine six died. In the authors' opinion it is particularly important that in patients with newly detected diabetes death occurred at a younger age as compared with non-diabetics and with treated diabetics. Based on these results the authors confirm the view that undiagnosed and untreated diabetes is a serious risk factor for the development of focal cerebral ischaemia and that it plays moreover an important role in its subsequent course and provides a poorer perspective of recovery in the affected patients.
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PMID:[Newly diagnosed diabetes mellitus in patients with focal cerebral ischemia]. 225 82

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct]. 239 9

The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.
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PMID:Platelet alpha granule secretion in cerebral ischemia: effect of short and long term low dose aspirin treatment. 245 69

Dichloroacetate (DCA) exerts multiple effects on pathways of intermediary metabolism. It stimulates peripheral glucose utilization and inhibits gluconeogeneis, thereby reducing hyperglycemia in animals and humans with diabetes mellitus. It inhibits lipogenesis and cholesterolgenesis, thereby decreasing circulating lipid and lipoprotein levels in short-term studies in patients with acquired or hereditary disorders of lipoprotein metabolism. By stimulating the activity of pyruvate dehydrogenase, DCA facilitates oxidation of lactate and decreases morbidity in acquired and congenital forms of lactic acidosis. The drug improves cardiac output and left ventricular mechanical efficiency under conditions of myocardial ischemia or failure, probably by facilitating myocardial metabolism of carbohydrate and lactate as opposed to fat. DCA may also enhance regional lactate removal and restoration of brain function in experimental states of cerebral ischemia. DCA appears to inhibit its own metabolism, which may influence the duration of its pharmacologic actions and lead to toxicity. DCA can cause a reversible peripheral neuropathy that may be related to thiamine deficiency and may be ameliorated or prevented with thiamine supplementation. Other toxic effects of DCA may be species-specific and reflect marked interspecies variation in pharmacokinetics. Despite its potential toxicity and limited clinical experience, DCA and its derivatives may prove to be useful in probing regulatory aspects of intermediary metabolism and in the acute or chronic treatment of several metabolic disorders.
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PMID:The pharmacology of dichloroacetate. 255 95

Severe head injury is associated with a stress response that includes hyperglycemia, which has been shown to worsen outcome before or during cerebral ischemia. To better define the relationship between human head injury and hyperglycemia, glucose levels were followed in 59 consecutive brain-injured patients from hospital admission up to 18 days after injury. The patients who had the highest peak admission 24-hour serum glucose levels had the worse 18-day neurologic outcome (p = 0.01). Patients with peak 24-hour admission glucose levels greater than 200 mg/dL had a two-unit increase in Glasgow Coma Scale score while patients with admission peak 24-hour serum glucose levels less than or equal to 200 mg/dL had a four-unit increase in Glasgow Coma Scale score during the 18-day study period (p = 0.04). There was a significant relationship between 3-month and 1-year outcome and peak admission 24-hour serum glucose level (p = 0.02 and p = 0.02, respectively). Those patients with admission peak 24-hour serum glucose levels less than or equal to 200 mg/dL had a greater percentage of favorable outcome at 18 days, 3 months, and 1 year than those with admission peak 24-hour glucose levels greater than 200 mg/dL (p = 0.0007, p = 0.03, and p = 0.005, respectively). A significant relationship between admission peak 24-hour Glasgow Coma Scale score and 18-day, 3-month, and 1-year outcomes was found (p = 0.0001, p = 0.0002, and p = 0.0002, respectively). Patients with mean admission peak 24-hour Glasgow Coma Scale scores of 3.5, 6, and 10 had mean admission 24-hour peak serum glucose levels of 252 +/- 23.5, 219.1 +/- 19, and 185.8 +/- 21, respectively (p = 0.05). These relationships were not significantly altered when confounding variables such as the amount of glucose given over the initial 24-hour postinjury period, the presence of diabetes or multiple injuries, and whether patients were given steroids, dilantin, or insulin were statistically incorporated. These data suggest that admission hyperglycemia is a frequent component of the stress response to head injury, a significant indicator of severity of injury, and a significant predictor of outcome from head injury.
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PMID:Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. 267 55

Experimental und clinical data suggest a negative influence of diabetes mellitus and hyperglycemia on the outcome of cerebral ischemia. In a retrospective analysis of 135 consecutive patients with cerebral ischemia we found more severe clinical defects in diabetics and patients with initial hyperglycemia but without previously known diabetes mellitus than in patients with initial normoglycemia. This was especially true for blood glucose above 10 mmol/l. Before drawing therapeutic conclusions, further prospective studies are necessary.
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PMID:[The effect of blood glucose on the course of cerebral ischemia]. 273 19

The present study was designed to examine the effect of chronic type 2 (noninsulin-dependent) diabetes mellitus on cerebral blood flow and metabolism during cerebral ischemia induced by bilateral carotid artery occlusion in spontaneously hypertensive rats. Diabetes was produced by streptozotocin treatment in 2-day neonates and the experiment was performed at the age of 5 months. The level of mean arterial pressure was not different between diabetic and nondiabetic rats. At 1 h after ischemia, cerebral blood flow was decreased to 1% of the resting value and supratentorial lactate was increased by 8-fold of control, being virtually the same in both groups of rats. In contrast, reduction of cerebral ATP was much less in diabetic rats (1.64 +/- 0.15 mmol/kg) than in nondiabetic rats (0.74 +/- 0.07 mmol/kg) (p less than 0.001); ATP in nonischemic control is 2.80-2.85 mmol/kg. These results could not be explained by the difference in cerebral blood flow between the groups during ischemia. The results suggest that chronic mild hyperglycemia exerts rather a protective effect on the brain against ischemic insult. Effective utilization of metabolites, such as glucose and ketone bodies, may play an important role to minimize metabolic derangements in the ischemic brain in type 2 diabetic-hyperglycemic rats.
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PMID:Cerebral ischemia in spontaneously hypertensive rats with type 2 (noninsulin-dependent) diabetes mellitus, cerebral blood flow and tissue metabolism. 279 88

Focal cerebral ischemia was induced by occlusion of the middle cerebral artery in rats. The volumetric assessment of infarcted tissue, 2 days following occlusion, was calculated from the examination of eight preselected coronal sections. Five differing rat strains were examined. A small and variable infarcted volume was seen in Wistar-Kyoto rats; Sprague-Dawley rats had a relatively large, but still variable, infarcted volume. Of the normotensive rat strains, the most reproducible volume of infarcted tissue was seen in Fischer-344 rats; also the absolute value of the infarcted volume did not vary from one series to another in this strain. Chronic arterial hypertension, studied in both normal and stroke-prone spontaneously hypertensive rats, was associated with significantly larger infarction volumes. Age does not change the volume of necrosis: Fischer-344 rats were studied at 3, 9, and 20 months of age, and no significant differences were noted between these ages. Experimental diabetes was induced by the administration of streptozotocin 3 days prior to middle cerebral artery occlusion. Severe hyperglycemia (greater than 400 mg/dl) was associated with a considerably increased volume of infarction. The variability of the resultant lesion is high in the most commonly studied strains, but our results suggest that, for studies in normotensive rats, the use of the Fischer-344 strain produces a standardized and repeatable infarction that may be significantly modified by experimental interventions. Age is not a factor that affects the occlusion-induced infarction; in contrast, both chronic arterial hypertension and experimental diabetes aggravate the histological consequences of middle cerebral artery occlusion in the rat. We conclude that quantitative histological evaluation of infarct size allows a meaningful assessment of the gravity of focal cerebral ischemia.
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PMID:The quantification of cerebral infarction following focal ischemia in the rat: influence of strain, arterial pressure, blood glucose concentration, and age. 296 87

A review of 15 cases of pancreas transplantation at the Presbyterian University Hospital in Pittsburgh showed that all of the neurologic complications occurred outside of the pancreas transplantation surgery itself. Major CNS complications included hypoxic encephalopathy (20 per cent), cerebral and spinal-cord infarction (7 per cent), and seizures (13 per cent). These appeared to be closely associated with cardiovascular collapse or cardiac arrest that often occurred following septic, hemorrhagic, or additional surgical-anesthetic stresses, removed in time from the transplantation. When patients who died of sudden cardiorespiratory arrest were included, the overall frequency of global cerebral ischemia was 33 per cent. The occurrence of herpes zoster neuritis (13 per cent) was contrasted with the lack of CNS infections. The possible associations of visual hallucinations with cyclosporine therapy (7 per cent), CSF pleocytosis with OKT3 therapy (7 per cent), and compressive neuropathy with operative-anesthetic monitoring (7 per cent) were discussed in relation to previous reports in the literature. Randomized controlled clinical studies were suggested to distinguish more clearly the complications due to pancreas transplantation from those due to the natural history of the underlying diabetes and to distinguish the beneficial and adverse effects of pancreas transplants from those of coexisting renal transplants.
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PMID:Neurologic complications of pancreas transplants. 304 46

Occlusion of the common and internal carotid arteries in a patient with symptomatic severe cerebral ischemia, with or without contralateral carotid disease, portends a poor prognosis. The present study has described our experience with subclavian and external carotid artery revascularization for symptomatic severe cerebral ischemia from common and internal carotid artery occlusion. Nine patients (five men and four women) with a mean age of 62 (range 41 to 82 years) were diagnosed as having symptomatic severe cerebral ischemia. All patients had ipsilateral hemispheric symptoms, seven had amaurosis fugax, and two had associated syncope. Four patients (three men and one woman) were hypertensive, four (two men and two women) had diabetes, eight smoked, and all had a history of coronary artery disease. All of the patients had noninvasive laboratory studies and preoperative angiography, and three had postoperative angiography. Five patients were successfully revascularized to a patent external carotid artery despite nonvisualization by angiography. Six patients had unilateral and three bilateral occlusion of the common and internal carotid arteries appropriate to their symptoms. Using regional anesthesia, four patients underwent a subclavian-external carotid bypass with polytetrafluoroethylene; saphenous vein was used in five; and three had concomitant axilloaxillary bypass grafting with polytetrafluoroethylene. Neurologic improvement (that is, no subsequent deficit and no progression of symptoms) was noted in all nine patients with a follow-up of 4 to 28 months (mean 11.2 months). Two patients died from myocardial infarction 4 and 7 months after operation. Subclavian-external carotid artery bypass is a safe addition to the options for the treatment of symptomatic severe cerebral ischemia with occlusion of the common and internal carotid arteries, visualization of a superior thyroid collateral vessel on the recipient end, and nonvisualization of the external carotid artery.
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PMID:Subclavian-external carotid bypass for symptomatic severe cerebral ischemia from common and internal carotid artery occlusion. 335 78


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