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Hypoglycaemia insulin-induced

Hypoglycaemia remains the most frequent complication of insulin administration to diabetics. It usually occurs due to (a) administration of an excessive amount of insulin (b) administration of insulin prior to a mealtime, but with subsequent omission of the meal or (c) due to increased physical activity. In severe cases this can lead to loss of consciousness, and even death. Although it may be treated by oral or i.v. administration of glucose, insulin-induced hypoglycaemia is sometimes treated by administration of glucagon. [Pg.305]

Recombinant glucagon Insulin-induced hypoglycaemia emergency treatment for severe hypogycaemic reactions... [Pg.60]

Deacon SP, Barnett D. Comparison of atenolol and propranolol during insulin-induced hypoglycaemia. BMJ 1976 2(6030) 272-3. [Pg.663]

Steil GM, Rebrin K, Hariri F, Jinagonda S, Tadros S, Darwin C, Saad MF. Interstitial fluid glucose dynamics during insulin-induced hypoglycaemia. Diabetologia 2005, 48, 1833-1840. [Pg.314]

The long tetracosactride test (see later) or measurements of plasma corticotropin concentration may be used to assess recovery of adrenal responsiveness, but a positive result should not be taken to indicate full recovery of the patient s ability to respond to stressful situations the latter is best shown by an adequate response to insulin-induced hypoglycaemia (which additionally tests the hypothalamic/pituitary capacity to respond). [Pg.674]

Insulin-induced hypoglycaemia can also be used as a test of anterior pituitary function (growth hormone and corticotropin are released). [Pg.681]

A rebound hyperglycaemia, caused by counter-regulatory hormones provoked by insulin-induced hypoglycaemia, is called the Somogyi phenomenon (Gerich, 1988). Attvall etal. (1987) have shown that prolonged... [Pg.12]

Insulin-induced hypoglycaemia decreases luteinizing hormone (LH) secretion (Koivisto and Felig, 1978). The effect is prevented by the intravenous infusion of glucose, suggesting that neuroglycopenia and not a direct action of insulin is the cause of reduced LH secretion (Koivisto and Felig, 1978). [Pg.57]

Bin-Jaliah 1, Maskell PD, Kumar P. 2004. Indirect sensing of insulin-induced hypoglycaemia by the carotid body in the rat. J Physiol Online 556 255-266. [Pg.222]

H42. Hilsted, J., Bonde-Peterson, F., and Norgaard, M. B., Haemodynamic changes in insulin-induced hypoglycaemia in normal man. Diabetologia 26, 328-332 (1984). [Pg.368]

H55. Howie, A. F., Patrick, A. W., Fisher, B. M., Collier, A., Frier, B. M., and Beckett, G. J., Plasma hepatic glutathione S-transferase concentrations after insulin-induced hypoglycaemia in normal subjects and diabetic patients. Diabetic Med. 6, 224-227 (1989). [Pg.369]

Cushing s syndrome is the most likely diagnosis in this case. One can be confident of the diagnosis in view of the increased urinary cortisohcreatinine ratio, the absent diurnal rhythm, failure to suppress with low-dose dexamethasone and the failure of the insulin-induced hypoglycaemia to stimulate cortisol secretion. [Pg.72]

Growth hormone deficiency may be present from birth or due to later pituitary-failure. A variety of stimulation tests have been used to evaluate GH deficiency. Seram GH concentrations rise in response to exercise, and this may be u.sed as a preliminary screening test. They also rise during sleep, and high concentrations in a nocturnal sample may exclude GH deficiency. The lack of GH response to clonidine, a potent stimulant of GH secretion, isdiagnostic. Some centres have now abandoned the use of insulin-induced hypoglycaemia as a diagnostic test in children because of its hazards. [Pg.142]

Failure of the serum cortisol to rise after insulin-induced hypoglycaemia is also a characteristic feature of Cushing s syndrome. Since patients with cortisol overproduction will be insulin-resistant, adequate hypoglycaemia may not be achieved with O.l, ) units of insulin/kg body weight. A higher dose may have to be u.sed. In normal individuals a fall of blood glucose concentration to less than... [Pg.154]

A study in 16 healthy subjects found that a single 600-microgram dose of eprosartan did not significantly affect adrenaline (epinephrine) release in response to insulin-induced hypoglycaemia, but the eprosartan tended to blunt some of the haemodynamic responses to hypoglycaemia. Theoretically, therefore, hypoglycaemic symptoms could be reduced in some diabetic patients. [Pg.476]

Christensen M, Ibsen H, Worck R. Effect of eprosartan on catecholamines and peripheral haemodynamics in subjects with insulin-induced hypoglycaemia. Clin Sci (2005) 108,113-19. [Pg.476]

Newman RJ. Comparison of propranolol, metoprolol, and acebutolol on insulin-induced hypoglycaemia. BMJ (1976) 2,447-9-... [Pg.482]

Hedeland H, Djmling J-F, Holrfelt B. Pharmacological inhibition of adrenaline secretion following insulin induced hypoglycaemia in man the effect of Catapresan. Acta Endocrinol (Copenh) (1971) 67, 97-103. [Pg.485]

Glucagon 30 amino adds Bovine or porcine pancreas or synthetic Reversal of insulin induced hypoglycaemia... [Pg.555]

Airey CM, Williams DR, Martin PG, Bennett CM, Spoor PA. Hypoglycaemia induced by exogenous insulin— human and animal insulin compared. Diabet Med 2000 17(6) 416-32. [Pg.416]

INSULIN VASODILATOR ANTIHYPERTENSIVES-DIAZOXIDE May t insulin requirement Diazoxide causes hyperglycaemia by inhibiting insulin release and probably by a catecholamine-induced extrahepatic effect. Used in the treatment of hypoglycaemia due to insulinomas Larger doses of insulin are often required, and there is a need to monitor blood sugar until adequate control of blood sugar is achieved... [Pg.409]


See other pages where Hypoglycaemia insulin-induced is mentioned: [Pg.422]    [Pg.687]    [Pg.133]    [Pg.11]    [Pg.49]    [Pg.56]    [Pg.57]    [Pg.57]    [Pg.58]    [Pg.227]    [Pg.139]    [Pg.481]    [Pg.475]    [Pg.646]    [Pg.92]    [Pg.81]    [Pg.117]    [Pg.538]    [Pg.182]    [Pg.306]    [Pg.117]    [Pg.538]    [Pg.407]    [Pg.411]   
See also in sourсe #XX -- [ Pg.685 , Pg.686 ]




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