Cases reported "hyperglycemia"

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1/316. Blood brain barrier destruction in hyperglycemic chorea in a patient with poorly controlled diabetes.

    A case of hemichorea in a patient with poorly controlled diabetes is reported. T1-weighted magnetic resonance imaging (MRI) showed an unusual homogeneous high-intensity area in the corpus striatum. Of interest in the case was the fact that the globus pallidus, which was enhanced with gadolinium at the onset of hemichorea, showed homogeneous high-intensity on a subsequent T1-weighted image. This indicated that blood brain barrier destruction preceded the signal intensity change in the basal ganglia. As far as the authors could determine, this is the first reported case showing such enhancement during the course of diabetic hemichorea. ( info)

2/316. Insulin and type 2 diabetes. Last resort or rational management?

    BACKGROUND: Recent evidence indicates that lower glucose levels in people with type 2 diabetes result in fewer complications. People with diabetes generally have sub-optimal glycaemic control. The natural progression of diabetes is characterised by increasing glucose levels requiring increasing therapy. OBJECTIVE: This article explores the possible role of therapeutic insulin in the management of type 2 diabetes. Arguments for earlier use of insulin, illustrative cases and common dilemmas faced when introducing insulin are examined. DISCUSSION: Findings from the United Kingdom Prospective Diabetes Study (UKPDS) are reviewed. It suggests that active and aggressive management of type 2 diabetes in general practice can have a role to play in reducing complications from diabetes. It now appears that insulin has a role earlier in the management of type 2 diabetes. ( info)

3/316. Insulin receptor antibodies and insulin resistance.

    The presence of insulin receptor antibodies is a rare cause of insulin resistance. patients usually have a combination of hyperglycemia, insulin resistance, acanthosis nigricans, and autoimmune features. We report a patient with systemic lupus erythematosus and severe insulin resistance due to insulin receptor antibodies. The most striking aspect of the clinical presentation is the resistance to insulin therapy, with our patient unresponsive to doses of up to 154,075 units in a day. While on a low-dose glucocorticoid therapy, the patient had clinical improvement, and glucose levels subsequently became normal even without insulin and glucocorticoid. ( info)

4/316. Episodic hyperglycaemia in pregnant women with well-controlled Type 1 diabetes mellitus: a major potential factor underlying macrosomia.

    AIMS: To test the common assumption that pregnant women who are sufficiently motivated to achieve very good HbA1c levels will record home blood glucose data accurately. methods: A new device was used to download information from electronic blood glucose meters to assess the extent of selectivity in patient glucose diary-keeping. RESULTS: In an index case, a woman with excellent ambient HbA1c (5.9%; upper limit of normal 6.1%) was observed to have 68% of preprandial blood glucose readings above the target range of 3.5-6.5 mmol/l and a mean ( /- SD) level of 8.9 /-3.9 mmol/l in the corresponding period. No such impression was conveyed by the home monitoring diary. Six pregnant women with well controlled Type 1 diabetes (mean HbA1c 6.6 /-0.2%) exhibited between 42 and 68% of preprandial readings above the target range. CONCLUSIONS: The frequency of hyperglycaemia has hitherto been underestimated in well controlled pregnant women whose near-perfect home monitoring record is apparently corroborated by near-normal HbA1c levels. These observations provide a hypothesis for understanding of the disappointing continuance of macrosomia despite excellent HbA1c levels throughout pregnancy. ( info)

5/316. Unilateral macronodular adrenal hyperplasia as an unusual cause of Cushing's syndrome--a case study.

    To appraise clinicians of the problems that may be encountered in the diagnosis and management of Cushing's syndrome, we present a case report of a 20-year old female, who was admitted with a recently developed central obesity, ammenorrhea hirsuitism, proximal myopathy and depression. She was found to have multiple striae, thin skin, elevated blood pressure glycosuria and hyperglycaemia. Morning and mid-night plasma cortisol concentrations revealed elevated levels, with a loss of diurnal variation. There was a failure of the normal suppressibility of cortisol secretion by low doses of dexamethasone, while a significant suppression of plasma cortisol concentration was observed with high doses of dexamethasone. There were no significant abnormalities observed in the pituitary fossa on skull radiograph and on the cranial computerised tomographic scan. After a period of stabilisation, she had a bilateral adrenalectomy done, with a histopathological finding of a left adrenal macronodular hyperplasia, while the right adrenal gland was small and friable. There was an uneventful post-operative period, with a gradual return to normality of most of the presenting complaints. The hyperglycaemia and hypertension got controlled without medications, while her menstrual cycles resumed within three months of bilateral adrenalectomy. This case report illustrates that an adrenal-dependent Cushing's syndrome may mimic a pituitary-dependent one, especially as regards the suppressibility of plasma cortisol secretion by high doses of dexamethasone. ( info)

6/316. Non-ketotic hyperglycemia in a young woman, presenting as hemiballism-hemichorea.

    We report a 22-year-old girl presenting with acute onset left sided hemiballism-hemichorea (HH) and non-ketotic hyperglycemia (NKH). Initial brain CT revealed faint hyperdensities, sharply confined to the contralateral nucleus caudatus and putamen. Sequential MRI investigations yielded increasing hypersignal intensities on T1-weighted images and resolving hypodensities on T2-weighted images of the right striatum, leaving small sequelae in the head of the right caudate nucleus. NKH is an unusual cause of HH. The abnormalities seen in neuroimaging are rare, but seem to be quite specific to this syndrome. We give an update on current literature regarding the possible pathophysiological processes underlying this specific clinical entity. ( info)

7/316. The dietary treatment of hepatic glycogen synthetase deficiency.

    A child with glycogen synthetase deficiency has been treated for one year by more frequent feeding with a diet lower in carbohydrate and higher in protein than her previous diet. This treatment virtually abolished the overnight hyperketonaemia and daytime hyperglycaemia which occurred before treatment. On the new dietary regime the child has had no clinical symptoms of hypoglycaemia and her growth velocity has increased dramatically. ( info)

8/316. 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. ( info)

9/316. 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. ( info)

10/316. Post-transplant diabetic ketoacidosis--a possible consequence of immunosuppression with calcineurin inhibiting agents: a case series.

    Post-transplant diabetes mellitus, a complication due to corticosteroids and the calcineurin inhibitors, cyclosporine and tacrolimus (FK506), is commonly regarded as a form of type-2 (adult-onset) diabetes mellitus. diabetic ketoacidosis, which requires relative insulin deficiency to impair fatty acid metabolism, is a complication of type-1 diabetes mellitus. We report three patients who presented with diabetic ketoacidosis post-transplant. All three patients presented with severe hyperglycemia, significant ketosis and metabolic acidosis of variable severity. One patient was a renal transplant recipient on a cyclosporine-based regimen. The other two patients were liver transplant recipients receiving either cyclosporine or tacrolimus-based immunosuppression. Both of the liver transplant recipients were found to have moderate to high serum levels of calcineurin inhibitors on presentation. The liver recipient on cyclosporine (Neoral) had a 4 hour post-dose level of 388 ng/ml and the patient on tacrolimus was found to have a trough level of 21.2 ng/ml. Our experience suggests that post-transplant diabetes mellitus, in association with calcineurin inhibition, may result in ketoacidosis either secondary to relative beta cell dysfunction, peripheral insulin resistance, or a combination of the two effects. Post-transplant diabetes mellitus can be an atypical form of adult-onset diabetes with features of both type I and type II diabetes mellitus. ( info)
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