Cases reported "Hyperglycemia"

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1/28. theophylline intoxication mimicking diabetic ketoacidosis in a child.

    A 5-year-old boy presented with abdominal pain, nausea and vomiting of blood. Twelve hours after admission, "diabetic ketoacidosis" was diagnosed on the basis of elevated glycaemia, glycosuria, ketonuria and a low bicarbonate blood level, which led to treatment with fluids and regular insulin infusion. Over a 36-hour period, insulin was progressively decreased and finally stopped because of the rapid fall and normalization of blood glucose concentration. Drug poisoning was suspected on the basis of persistent tachycardia in the absence of other signs of dehydration. Salicylate intoxication was excluded, and theophylline was finally incriminated. This compound, used by adults in the child's home, had caused accidental theophylline poisoning, mimicking diabetic ketoacidosis. Pre-diabetic immune markers were repeatedly negative, and no diabetes has developed after four years of follow-up. Thus, the transient increase in blood glucose was not related to a pre-diabetic status. A diagnosis of masked theophylline poisoning should be considered in similar situations involving a rapid decrease of insulin requirements.
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2/28. Absence of maternal A3243G mtDNA mutation and reversible hyperglycemia in a patient with melas syndrome.

    We report the unusual features of a female patient who had MELAS-specific A3243G mutation in mitochondrial dna (mtDNA) and diabetes mellitus (DM). The patient showed mitochondrial myopathy, encephalopathy, lactic acidosis, and deafness but lacked the stroke-like episode. Acute hyperglycemia was noted after one attack of status epilepticus. Molecular genetic analysis demonstrated a heteroplasmic A3243G point mutation in the mtDNAs of muscle, blood cells and hair follicles. glucagon stimulation test exhibited marked depression of pancreatic beta-cell function. However, in a further study neither this mutation, nor melas syndrome or DM, was found in all of her maternal relatives. A series of follow-up studies for beta-cell function also showed gradual improvement. The pedigree study led us to believe that this A3243G mutation arose from the germ line cells or occurred later in somatic tissues of the patient. We also suggest that the A3243G mutation of mtDNA may elicit the pathogenesis of a subtype of DM. Nevertheless, environmental stress may be another important factor for provocation of the disease.
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3/28. Status-like recurrent pilomotor seizures: case report and review of the literature.

    A diabetic 66 year old man who presented with pilomotor seizures in his right hemibody is described. The seizures recurred with an increasing frequency, leading to a status-like condition associated with Korsakoff's syndrome. An EEG was performed and several electroclinical seizures were recorded. brain MRI was negative. The patient, who was treated with carbamazepine, became seizure free after 1 week. memory and behaviour gradually returned to normal within 3 weeks. There was no further neurological episode during an 8 year follow up. Hyperosmolar, non-ketotic hyperglycaemia was considered to be the cause of the seizures. The pathophysiology of pilomotor seizures is discussed and the literature on the subject reviewed.
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4/28. Presentation of striatal hyperintensity on T1-weighted MRI in patients with hemiballism-hemichorea caused by non-ketotic hyperglycemia: report of seven new cases and a review of literature.

    Recent studies have shown unique clinicoradiologic characteristics in patients with hemiballism-hemichorea (HB-HC) caused by non-ketotic hyperglycemia; however, there is still a limited number of patients being reported. We report 7 patients (3 males and 4 females) with this type of dyskinesia, whose ages ranged from 60 to 84 years. brain CT of these patients showed hyperdensity in the contralateral striatum, corresponding with MRI studies that showed an increased signal intensity on T1-weighted images and a decreased signal on T2-weighted images. After metabolic control had been achieved, the hyperkinetic state of these patients abruptly ceased. Follow-up neuroimaging studies in 2 patients documentied complete resolution of the striatal hyperintensity on brain CT and MRI after 3 months and 6 months, respectively. A review of patients with HB-HC caused by non-ketotic hyperglycemia reported formerly and in the present study shows that the dyskinesia tends to occur in aged diabetic patients. The age of patients with dyskinesia secondary to cerebral infarction is generelly much lower. We also found that 86% (30 out of 35 cases) patients reported with HB-HC caused by non-ketotic hyperglycemia were Asians. The prognosis of the dyskinesia was excellent, and the radiological abnormalities are completely reversible.
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ranking = 4296.0361133577
keywords = dyskinesia
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5/28. pancytopenia, hyperglycemia, shock, coma, rhabdomyolysis, and pancreatitis associated with acetaminophen poisoning.

    It is well recognized that acetaminophen overdose can cause severe hepatic injury. However, extra-hepatic manifestations may also develop following inappropriate use or ingestion of large amounts of acetaminophen. We present a 44-y-o female who manifested coma, metabolic acidosis, shock, hypothermia, hyperglycemia, rhabdomyolysis, hepatotoxicity, and renal insufficiency after suicidal ingestion of an unknown amount of acetaminophen. Although her consciousness and hemodynamic status gradually improved after treatment with N-acetylcysteine and other supportive measures, she was found to have pancytopenia, pancreatitis and hepatorenal failure during the hospitalization and eventually died 18 d post-admission. review of relevant literature reports and the clinical findings in our patient suggests that direct toxic effects mediated by acetaminophen or its metabolites were most likely responsible for most of the observed clinical features.
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6/28. Transient hemichorea/hemiballismus associated with new onset hyperglycemia.

    OBJECTIVE: To describe three patients suffering from transient hemichorea/hemiballismus associated with hyperglycemia, review previous reports and propose a possible pathophysiological explanation for this phenomenon. RESULTS: Our original cases and previously reported ones reveal a uniform syndrome: mostly female patients (F/M ratio of 11/2), 50-80 years old, usually with no previous history of diabetes mellitus (9/13), develop choreic or ballistic movements on one side of the body over a period of hours. serum glucose levels are elevated. In most of the patients, a lowering of the blood sugar level reverses the movement disorder within 24-48 hours. CONCLUSIONS: We believe that the combination of a recent or old striatal lesion (causing increased inhibition of the subthalamic nucleus) and hyperglycemia (causing decreased GABAergic inhibition of the thalamus) may be responsible for the appearance of this unilateral hyperkinetic movement disorder. Undiagnosed diabetes mellitus should always be suspected in patients who develop hemiballistic or hemichoreic movements. When hyperglycemia is detected and corrected, the movement disorder usually resolves within two days and may not require symptomatic therapy with dopamine receptor antagonists.
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ranking = 2770.0865430648
keywords = movement disorder, movement
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7/28. chorea due to nonketotic hyperglycemia.

    A 62 year old diabetic and hypertensive male presented with sudden onset generalized chorea. Investigations revealed uncontrolled diabetes with absent ketones and normal serum osmolality. achievement of euglycemia with insulin therapy abolished the involuntary movements completely within a day. The direct effect of hyperglycemia causing striatal neuronal dysfunction could be the pathogenesis of the chorea in our patient.
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ranking = 18.147515934976
keywords = movement
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8/28. reflex epilepsy and non-ketotic hyperglycemia.

    Epileptic seizures are paroxysmal events, and it is likely that many, if not most, of them are precipitated by known or unknown factors acting on a central nervous system that is predisposed to the production of epileptic discharges by the presence of an organic lesion, a genetically determined neuronal hyperexcitability, or both. Known precipitating influences are quite varied. We report the case of a 58 years-old patient, followed for non-ketotic hyperglycemia, who presented with focal seizures exclusively induced by specific, active or passive, postures and movements of the right arm or hand. MRI was normal. Following regulation of glucose blood levels the position-induced seizures stopped and antiepileptics were not prescribed. The seizures are kept under control by regulating blood glucose.
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ranking = 18.147515934976
keywords = movement
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9/28. Striatal hyperintensity on T1-weighted magnetic resonance images and high-density signal on CT scans obtained in patients with hyperglycemia and no involuntary movement. Report of two cases.

    The authors report on two patients in whom an increased signal on T1-weighted magnetic resonance images and a high-density signal on computerized tomography scans of the striatum were demonstrated, both of which were associated with nonketotic hyperglycemia. Involuntary movements, which have been present in all previously reported cases, were not observed in either patient at any time during the entire course of illness. One patient displayed hemiparesis, whereas the other had dementia, gait disturbance, and urinary incontinence. Clinical and radiological abnormalities improved on control of blood glucose levels. Invasive studies, including biopsy procedures, should be avoided on encountering this disease given the good prognosis that results from simple medical treatment.
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ranking = 90.737579674882
keywords = movement
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10/28. Adaptive bolus-based targeted glucose regulation of hyperglycaemia in critical care.

    Tight regulation of blood glucose can significantly reduce mortality in critical illness. Critically ill patients are extremely diverse in the dynamics of their hyperglycaemia. Hence, responses can vary significantly, due to variations in insulin levels, effective insulin utilization, glucose absorption and other factors. Consequently, fixed protocols and sliding scales can result in error, given this large variation in patient dynamics. A two-compartment glucose-insulin system model that accounts for time-varying insulin sensitivity and endogenous glucose removal, along with two different saturation kinetics, is developed and tested in preliminary proof-of-concept clinical trials for adaptive control of blood glucose levels. The adaptive control algorithm developed in this research monitors the physiological status of a critically ill patient, allowing real-time, tight glycaemic regulation. The bolus-based insulin administration provides a safe approach to glucose level management. The ability to track changing physiological status and account for insulin transport and effect saturation enabled targeted stepwise reduction in glycaemic levels in three test cases.
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