1/30. lipids in the proximal tubules of the kidney in diabetic coma.Vacuolization of the renal tubular epithelial cells (the Armanni-Ebstein lesion) associated with diabetic hyperglycemia is usually regarded as an accumulation of glycogen. In a case of death of diabetic coma, the vacuoles were stained strongly for lipids. This observation may have both clinical and therapeutic consequences, and may increase our knowledge of the metabolism in diabetes.- - - - - - - - - - ranking = 1keywords = metabolism (Clic here for more details about this article) |
2/30. Recurrent hyperosmolar nonketotic episodes in a young diabetic.A 15-month-old girl was successfully treated for substantial hyperosmolarity in the absence of ketosis at the onset of permanent insulin-requiring diabetes mellitus. hypotonic solutions containing small amounts of glucose and subcutaneous administration of low doses of insulin were empolyed. Potassium was added to the hydrating solutions during the second hour of treatment. In the next three months, two recurrences of this syndrome were verified and successfully treated in a similar manner.- - - - - - - - - - ranking = 56.71330009865keywords = glucose (Clic here for more details about this article) |
3/30. Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.- - - - - - - - - - ranking = 56.71330009865keywords = glucose (Clic here for more details about this article) |
4/30. Repeated hypoglycemia and cognitive decline. A case report.OBJECTIVE: diabetes mellitus has a high incidence in general population and goes by high morbidity by specific micro vascular pathology in the retina, renal glomerul and peripheral nerves. In type 1 DM, intensive therapy can prevent or delay the development of long-term complications associated with DM but hypoglycaemia especially severe hypoglycaemia defined, as a low blood glucose resulting in stupor, seizure, or unconsciousness that precludes self-treatment is a serious threat. Hypoglycaemia that may preferentially harm neurons in the medial temporal region, specifically the hippocampus, is a potential danger for the brain cognitive function which several studies failed to detect any significant effects, whereas others indicated an influence on it. A young diabetic case presented here with severe cognitive defect. Great number of severe hypoglycaemic or hyperglycaemic attacks and convulsion episodes were described in his medical history. RESULTS and CONCLUSION: Neuroradiologic findings on CT and MRI, pointed that global cerebral atrophy that is incompatible with his age. brain perfusion studies (SPECT, (99m)Tc-labeled HMPAO) also showed that there were severe perfusion defects at superior temporal region and less perfusion defects at gyrus cingulum in frontal region. These regions are related with memory processing. Severe cognitive defect in this patient seems to be closely related these changes and no another reason was found to explain except the repeated severe hypoglycaemic episodes.- - - - - - - - - - ranking = 56.71330009865keywords = glucose (Clic here for more details about this article) |
5/30. Diabetic keto-acidotic (DKA) coma following olanzapine initiation in a previously euglycaemic woman and successful continued therapy with olanzapine.We report the case of a euglycaemic woman whose glucose control rapidly decompensated following olanzapine initiation leading to diabetic coma. Hyperglycaemia has been associated with chronic psychotic disorders and antipsychotics for many years. However, it is unusual to see such rapid and life-threatening changes associated with treatment. The case highlights that changes in antipsychotic treatment may be associated with large changes in glucose tolerance, and that it is possible to continue antipsychotic treatment with appropriate diabetic care.- - - - - - - - - - ranking = 113.4266001973keywords = glucose (Clic here for more details about this article) |
6/30. Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. methods: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.- - - - - - - - - - ranking = 56.71330009865keywords = glucose (Clic here for more details about this article) |
7/30. Rapid onset of glycogen storage hepatomegaly in a type-2 diabetic patient after a massive dose of long-acting insulin and large doses of glucose.We present a case of rapid onset of glycogen storage hepatomegaly, caused by a massive dose of long-acting insulin and large doses of glucose, in a type-2 diabetic patient. A 41-year-old man was admitted to our hospital because of hypoglycemia and unconsciousness following subcutaneous administration of 180 units of insulin glargine in a suicide attempt. Despite continuous hypercaloric infusion with additional intravenous glucose injections, hypoglycemia persisted for 36 hours. Although the hepatic function was normal and no hepatomegaly was detected on admission, the liver function tests became abnormal and hepatomegaly was detected on hospitalization day 3. Plain abdominal computed tomography (CT) scanning confirmed liver enlargement, with hepatic CT attenuation markedly elevated at 83.7 HU. Liver biopsy revealed hepatocytic glycogen deposition with edematous degeneration. Based on these findings, the diagnosis was made as rapid onset glycogen storage hepatomegaly caused by administration of a massive dose of long-acting insulin and supplementation with large doses of glucose. With improved glycemic control, the liver function improved, the CT findings of hepatomegaly improved, and the hepatic CT attenuation decreased. Repeat liver biopsy also confirmed almost complete disappearance of glycogen deposits. When hepatic dysfunction or hepatomegaly is detected during treatment with insulin, the possibility of hepatic glycogen deposition should be considered. CT scanning and liver biopsy were useful in diagnosing this case.- - - - - - - - - - ranking = 396.99310069055keywords = glucose (Clic here for more details about this article) |
8/30. Glucose metabolism in a patient with insulinoma complicated by hyperosmolar non-ketotic state.A case of a patient with organic hyperinsulinism complicated by the development of hyperosmolar state is described. The hyperosmolar state was induced by vomiting and dehydration during an acute urinary tract infection. Impairment of glucose metabolism was confirmed by the finding of reduced tissue sensitivity to insulin during a euglycaemic clamp.- - - - - - - - - - ranking = 569.0996424701keywords = glucose metabolism, glucose, metabolism (Clic here for more details about this article) |
9/30. Coexisting bacterial pyelonephritis and bilateral ureteral fungus balls in a diabetic patient. Case report.Bacterial pyelonephritis is a common precipitating factor in the development of diabetic ketoacidosis. Prompt diagnosis and appropriate antimicrobial therapy usually result in resolution of constitutional symptoms and adequate control of serum glucose. However, occasional cases of presumed bacterial pyelonephritis may not respond to appropriate empiric antibiotic therapy, then causes should be sought such as obstruction or untreated fungal infections of the urinary tract. In this case a diabetic patient with classical pyelonephritis was found to have bilateral ureteral fungus balls as the underlying cause of refractory infection.- - - - - - - - - - ranking = 56.71330009865keywords = glucose (Clic here for more details about this article) |
10/30. Asymptomatic, nonketotic, severe hyperglycemia with hyponatremia.We describe five patients with asymptomatic, nonketotic, severe hyperglycemia (serum glucose concentrations between 45.8 and 92 mmol/L) in the face of renal insufficiency are described. As opposed to most of the previously described patients with hyperglycemic, nonketotic, hyperosmolar coma, our patients were hyponatremic. The lack of symptoms in our patients may be related to the absence of cerebral cellular dehydration. Aggressive treatment of hyperglycemia in such patients is unnecessary. attention to the serum sodium level as well as to the serum glucose concentration will allow recognition of this clinical entity.- - - - - - - - - - ranking = 113.4266001973keywords = glucose (Clic here for more details about this article) |
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