Decreased Epinephrine Excretion in Idiopathic Hypoglycemia

Goodall, McChesney; Cragan, Mary; Sidbury, James

doi:10.1001/archpedi.1972.02110120093009

Cited by 4 publications

(2 citation statements)

References 14 publications

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“…The explanation of the failure of adrenaline response has until recently remained a puzzle. Goodall, Cragan and Sidbury (1972) thought that delayed maturation of the adrenal medulla was a likely explanation but clearly this is now unacceptable since the abnormality persists until after puberty. Tietze et al (1972) favoured a central neurological hypothalamic explanation but again no convincing evidence of such an abnormality is available.…”

Section: Discussionmentioning

confidence: 99%

Ketotic hypoglycaemia of childhood

Pierides

Anderson

Stansfeld

1975

Postgraduate Medical Journal

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Summary A patient with recurrent convulsions in childhood and associated ketotic hypoglycaemia is described. Hypoglycaemic attacks started at the age of 3 years and 4 months and continued until 9. At present (aged 15) the patient is mentally retarded, has epilepsy, high tone deafness and a major behaviour disturbance. Prednisone therapy failed to prevent hypoglycaemic convulsions and eventually irreversible brain damage. Intramuscular glucagon and adrenaline were ineffective in raising the blood glucose during acute hypoglycaemic attacks. Investigations at 3 years and 7 months and at 14 years showed a persistent and markedly abnormal sensitivity to a small dose of exogenous insulin with severe hypoglycaemia with convulsions, absence of clinical hyperadrenalism during hypoglycaemia, and a metabolic block in gluconeogenesis. The demonstration of a persistent biochemical abnormality of glucose metabolism at the age of 14 strongly suggests that ketotic hypoglycaemia of childhood is not another aspect of nutritional deprivation, as recently suggested (Buist, 1974), but the result of a defect in glucose homeostasis.

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Section: Discussionmentioning

confidence: 99%

Ketotic hypoglycaemia of childhood

Pierides

Anderson

Stansfeld

1975

Postgraduate Medical Journal

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“…The vast majority of these children present a fairly characteristic disorder called ketotic hypoglycemia (7,15). A significant proportion of these children have a reduced urinary output of epinephrine during insulin-induced hypoglycemia, first described by Broberger & Zetterstrom ( 2 , 3) and later verified by many investigators (4, 9,13,18).…”

mentioning

confidence: 98%

Plasma Adrenalin in a Child With Ketotic Hypoglycemia and Calcifications of the Suprarenal Glands

1975

Acta Paediatrica

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Urinary excretion of adrenalin has been reported to be reduced during insulin-induced hypoglycemia in a significant proportion of children having ketotic hypoglycemia. By employing a sensitive double-isotope derivative technique, plasma adrenalin and plasma noradrenalin were determined in a boy 6 years 9 months old who had had ketotic hypoglycemia with intermittent hypoglycemic symptoms from the age of 10 months. Bilateral calcifications of the suprarenal glands were present. The adrenocortical function was normal. The plasma adrenalin response to hypoglycemia were practically absent, being only 4% of the value obtained in healthy children. The results were related to previous findings of a low plasma adrenalin response in patients with ketotic hypoglycemia without adrenal calcifications and support the assumption that ketotic hypoglycemia is associated with hypoadrenalinemia.

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Sympatho-adrenal response to hypoglycaemia in infants

Stanek

Lischka

Hörtnagl³

et al. 1988

Eur J Pediatr

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The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.

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Decreased Epinephrine Excretion in Idiopathic Hypoglycemia

Cited by 4 publications

References 14 publications

Ketotic hypoglycaemia of childhood

Ketotic hypoglycaemia of childhood

Plasma Adrenalin in a Child With Ketotic Hypoglycemia and Calcifications of the Suprarenal Glands

Sympatho-adrenal response to hypoglycaemia in infants

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