Cases reported "Hyperglycemia"

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1/7. 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.
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keywords = hypoglycaemia
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2/7. Fatal self-induced hyperinsulinaemia: a delayed post-mortem analytical detection.

    The inconspicuous number of cases of self-induced hyperinsulinaemia reported in the literature may suggest that many are obscure enough to escape their detection. A case of fatal suicidal hyperinsulinaemia in a non-diabetic is reported here, and in whom only a retrospective biochemical analysis provided an explanatory cause of death. A quantitative radioimmuno assay (RIA) estimation of the refrigerated postmortem blood sample stored at 4 degrees C for three weeks gave a positive insulin yield. It reiterates the need, in forensic cases, for a very low threshold of suspicion and a good back-up for the appropriate body fluid analysis or tissue microexamination, especially when full details of the circumstances surrounding the death are not available at the autopsy. A brief resume on insulin is presented as a background to the current forensic interest in the apparent increase in sudden deaths in young diabetics amidst the controversy about the bio-designed 'human' insulin and subjective unawareness of severe hypoglycaemia.
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3/7. blood glucose changes in diabetic children and adolescents engaged in most common sports activities.

    Circulating insulin levels decrease and substrate glycogenolysis-mediated conversion into glucose increases just a few minutes after normal subjects start exercising, but during sustained physical activity muscles massively utilize blood glucose, thus causing glycogenolysis to increase further until the end of the session. After that, in order to get liver and muscle glycogen stores up to pre-exercise levels again, blood glucose is mostly utilized, thus causing late-onset hypoglycaemia in the absence of any extra carbohydrate supply and rebound hyperglycaemia after a while. This and other patho-physiological mechanisms are dealt with in the present paper, and practical hints are provided to the clinician to cope with children-specific adaptation phenomena to exercise in t1DM.
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4/7. Cyclical disturbance of diabetic control in girls before the menarche.

    Seven diabetic girls who presented with cyclical disturbance of diabetic control before the menarche are described. In six girls cyclical hyperglycaemia occurred and in one cyclical hypoglycaemia. The index case is described in detail, and is then included in a description of the main clinical features of all seven cases. Cyclical disturbance of diabetic control may present in diabetic girls from age 9 years onwards. Home blood glucose monitoring records may reveal cyclical disturbance, usually hyperglycaemia, and usually occurring at 21-34 day intervals and lasting for two to five days. Serious illnesses and hospital admission can be averted by educating parents to make appropriate changes to insulin regimen or diet. Our hypothesis is that the disturbance of diabetic control is caused by the onset of cyclical hormonal changes, a 'menstrual' cycle before menstruation. The precise mechanism for the changes in carbohydrate tolerance is unknown.
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keywords = hypoglycaemia
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5/7. Hyperglycaemia associated with lactic acidaemia in a renal allograft recipient with type I glycogen storage disease.

    Renal disease is a frequent and serious complication of type I glycogen storage disease. A type I glycogen storage disease patient with focal segmental glomerulosclerosis and progressive renal insufficiency underwent a renal allograft transplantation. Despite the same cornstarch therapy, the post-transplantation course was complicated by worsening of the metabolic control manifested by exacerbated lactic acidaemia and hyperlipidaemia. This lactic acidaemia was remarkable for its association with hyperglycaemia. Hyperglycaemia accompanied by lactic acidaemia is strikingly unusual in type I glycogen storage disease, since this is a disease characterized by hypoglycaemia and an inverse relationship between blood glucose concentration and lactate levels. Both fasting insulin and c-peptide levels in the patient were greater than similar age-matched type I glycogen storage disease controls, indicating hyperinsulinaemia. The most likely mechanism responsible for the combined hyperglycaemia and lactic acidaemia was insulin resistance due to glucocorticoid treatment, instituted for immunosuppression. The hyperglycaemia associated with the lactic acidaemia was transient and resolved with steroid tapering. The exacerbated hyperlipidaemia, however, persisted after renal transplantation. Type I glycogen storage disease patients may be prone to glucocorticoid-induced insulin resistance, since the cellular metabolism in these patients may already be compromised with ineffective insulin action and/or reduced insulin output.
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keywords = hypoglycaemia
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6/7. Metabolic disorders presenting as stroke.

    In a series of 1460 consecutive patients admitted to an "acute" stroke unit, 10 patients (0.7%) were found to have a metabolic encephalopathy which mimicked stroke. Of these, three had hypoglycaemia, four had hyperglycaemia, three had hyponatraemia, and one had suffered from hypoxia. Metabolic disorders should be excluded in all patients with a diagnosis of suspected stroke, especially if the presentation is associated with a confusional state or focal seizures. The conventional symptoms and signs of the metabolic disorders may be minimal or absent. The relative rarity of these disorders among patients with suspected stroke is overshadowed by the importance of early recognition and treatment, in order to minimize morbidity and mortality.
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7/7. Transient focal neurological deficits in patients with hypoglycaemia and hyperglycaemia: report of four cases.

    A case of hypoglycaemia and three cases of hyperglycaemia presenting with focal neurological deficits are presented. The focal presentations were hemiparesis and focal convulsion that returned to normal upon correction of the blood sugar. Elderly patients not uncommonly present with transient focal neurologic deficits related to abnormalities in blood sugar levels. In these patients correction of blood sugar levels per se may ameliorate symptoms and signs making it unnecessary to investigate for cerebrovascular disease. In diabetic patients on insulin or oral hypoglycaemic agents focal neurologic deficit should alert the clinician on the possibility of hypoglycaemia.
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keywords = hypoglycaemia
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