Endogenous insulin fluctuations during glucose-induced paralysis in patients with familial periodic hypokalemia

Johnsen, Torsten

doi:10.1016/0026-0495(77)90110-x

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…In the study of one of our patients we found a 24 h binding curve almost identical with that in normals. During long-lasting glucose stimulation and induction of paralysis the insulin concentration does not change signifi¬ cantly (Johnsen 1977 ). This finding was expected, as it has been demonstrated that insulin is able to regulate its own receptor by a negative feed-back mechanism (Gavin et al 1974).…”

Section: Discussionmentioning

confidence: 58%

Insulin Receptors, Insulin Secretion, and Glucose Disappearance Rate in Patients With Periodic Hypokalaemic Paralysis

Johnsen

Beck‐Nielsen

1979

Acta Endocrinologica

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In a study of 6 male patients with periodic hypokalaemic paralysis (PHP), we found reduced insulin binding to monocytes as compared with a group of 25 normal subjects (P < 0.1). The decreased insulin binding was caused by the decreased binding affinity. During induction of paralysis by a prolonged oral glucose load, one patient showed 24-h variations in the insulin binding to monocytes not differing from those observed in normals. After iv administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P < 0.1). However, the iv glucose tolerance tests revealed normal glucose disappearance rates. We conclude that changes in insulin receptor binding do not appear to be of pathophysiological significance for eliciting the parese attacks in PHP. However, the increased insulin response, following carbohydrate intake, might be of significance in the generation of paralytic attacks in patients with PHP.Familial periodic hypokalaemic paralysis (PHP) is a rare muscle disease characterised by attacks of flaccid paresis lasting from a few hours to several

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Section: Discussionmentioning

confidence: 58%

Insulin Receptors, Insulin Secretion, and Glucose Disappearance Rate in Patients With Periodic Hypokalaemic Paralysis

Johnsen

Beck‐Nielsen

1979

Acta Endocrinologica

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“…High insulin levels were reported immediately before a spontaneous paralytic attack in two patients with the variant form of thyrotoxic periodic paralysis [19]. Johnsen [20] studied the en dogenous insulin production in patients with familial periodic hypokalemic paralysis. Af ter a prolonged glucose administration, he found no difference in the response of the serum insulin between patients with this dis order and normal subjects.…”

Section: Discussionmentioning

confidence: 99%

Hormonal Changes during a Spontaneous Attack of Hypokalemic Periodic Paralysis

Keyser¹,

Smitz²,

Malfait³

et al. 1987

Eur Neurol

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We studied the hormonal changes during a spontaneous attack of hypokalemic periodic paralysis in a 20-year-old man, before and after treatment with potassium chloride. During paralysis, we observed high circulating levels of insulin, epinephrine, norepinephrine, growth hormone, ACTH and Cortisol, most likely reflecting a condition of stress. Normalization of all these hormones occurred with recovery. Plasma aldosterone concentrations were normal. The increased plasma levels of insulin, but also of catecholamines and growth hormone, created a condition promoting potassium uptake in muscle cells. We suggest that stress may play a role in the pathophysiology of the paralytic attacks in this disorder.

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Insulin-mediated hypokalemia and paralysis in familial hypokalemic periodic paralysis

Minaker

Meneilly

Flier

1988

The American Journal of Medicine

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Endogenous insulin fluctuations during glucose-induced paralysis in patients with familial periodic hypokalemia

Cited by 4 publications

References 27 publications

Insulin Receptors, Insulin Secretion, and Glucose Disappearance Rate in Patients With Periodic Hypokalaemic Paralysis

Insulin Receptors, Insulin Secretion, and Glucose Disappearance Rate in Patients With Periodic Hypokalaemic Paralysis

Hormonal Changes during a Spontaneous Attack of Hypokalemic Periodic Paralysis

Insulin-mediated hypokalemia and paralysis in familial hypokalemic periodic paralysis

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