Muscle paresis and hypokalemia after treatment with duogastrone.

Forshaw, J.

doi:10.1136/bmj.2.5658.674

Cited by 22 publications

(12 citation statements)

References 6 publications

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“…She has remained well at all times when avoiding the drug, while trial exposure to it under controlled circumstances provoked hypokalaemia, with potassium loss and sodium retention. Myoglobinuria in her initial severe illness was almost certainly due to hypokalaemic-induced myopathy, as has been reported previously in association with both liquorice (Gross et al, 1966) and carbenoxolone (Mohammed, Chapman and Crooks, 1966;Forshaw, 1969) administration.…”

Section: Discussionsupporting

confidence: 74%

Severe hypokalaemia with paralysis induced by small doses of liquorice

A¹,

Boddy²,

Brown³

et al. 1980

Postgraduate Medical Journal

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SummaryA patient, who presented with a flaccid quadriplegia due to profound hypokalaemia, is described. Hypokalaemia and myoglobinuria were caused by the ingestion of small amounts of liquorice contained in a laxative preparation. Subsequent controlled administration of small amounts of this preparation induced marked hypokalaemia. This was associated with sodium retention and potassium loss confirming a mineralocorticoid-like action. The sodium retention was associated with suppression of plasma levels of renin and aldosterone. IntroductionLiquorice extracts are prepared from the root of the plant Glycyrrhiza glabra, and contain a principal glycyrrhizic acid which has an action resembling that of mineralocorticoids. The effects of liquorice ingestion may therefore include hypertension, hypokalaemia, hypernatraemia and a fall in plasma renin and aldosterone (Molhuysen et al

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Section: Discussionsupporting

confidence: 74%

Severe hypokalaemia with paralysis induced by small doses of liquorice

A¹,

Boddy²,

Brown³

et al. 1980

Postgraduate Medical Journal

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“…A number of aldosterone-like side effects of this drug have been reported (Doll, Hill & Hutton, 1965;Horwich & Galloway, 1965;Turpie & Thomson, 1965;Mohammned, Chapman & Crooks, 1966;Forshaw, 1969). During carbenoxolone therapy, Baron et al (1969) reported suppression of aldosterone secretion although in contrast to the present study and that of Conn et al (1968) they did not find suppression of the plasma renin.…”

Section: Discussioncontrasting

confidence: 68%

Pseudohyperaldosteronism induced by habitual ingestion of liquorice

Holmes

Young

Marrott

et al. 1970

Postgraduate Medical Journal

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“…Carbenoxolone therapy may give rise, in about 20% of patients, to mineralocorticoid-like side-effects resulting in oedema and, less frequently, to more severe effects of hypertension, sodium retention and hypokalaemia (Doll et al 1968;Forshaw, 1969;Muir, Laithwaite & Wood, 1969). Baron & Nabarro (1968), reviewing liquorice and its principal derivatives, glycyrrhizic and glycyrrhetic acids, concluded that the metabolic effects of carbenoxolone sodium (the sodium hemisuccinate of 18ß-glycyrrhetic acid) were essentially identical to the parent compounds and strongly resembled those of aldosterone.…”

Section: Discussionmentioning

confidence: 99%

Effect of Carbenoxolone on the Concentrations of Aldosterone in Rat Plasma and Kidney

Humphrey¹,

Lindup²,

Chakraborty³

et al. 1979

Journal of Endocrinology

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The renal subcellular distribution of various subcutaneous doses (10\ m=-\ 10\ p=n-\ 10\ m=-\ 8mol) of [3H]aldosterone has been investigated in adrenalectomized rats pretreated with carbenoxolone.Carbenoxolone increased the concentration of plasma [3H]aldosterone, but the uptake of [3H]aldosterone into the kidney nuclear and cytosol fractions was decreased. Pretreatment ofrats with carbenoxolone at low doses of aldosterone (0\ m=. \ 4 \ m=x\10\m=-\10 and 1\ m=. \ 5\ m=x\10\m=-\10mol) decreased both the amount of [3H]aldosterone bound to the 50% (NH4)2SO4 precipitate, and that present in the supernatant fraction, of a Tris\p=n-\CaCl2 extract of the kidney nuclear fraction. Carbenoxolone also decreased the rate of biliary excretion of metabolites of aldosterone.When [3H]aldosterone and carbenoxolone were incubated with Tris\p=n-\CaCl2 extracts of a kidney nuclear fraction in vitro, the carbenoxolone did not decrease the [3H]aldosterone bound to the 50% (NH4)2SO4 precipitate, although the [3H]aldosterone bound to the 50% (NH4)2SO4 supernatant was significantly decreased by carbenoxolone at concentrations known to occur in the kidney in vivo.These results indicate that displacement of aldosterone from binding sites, with a concomitant potential increase in the amount ofhormone available to specific receptors may be part of the mechanism by which carbenoxolone potentiates aldosterone action in toad skin in vitro. However, in rat kidney, such a mechanism is unlikely to play a significant role in the manifestation by carbenoxolone of aldosterone-like effects. Data are presented to indicate that carbenoxolone may affect the normal distribution and metabolism of aldosterone, and it is possible that potentiation of aldosterone action may involve receptors in other tissues, such as the gastrointestinal tract which is the major site of action of carbenoxolone.

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Muscle paresis and hypokalemia after treatment with duogastrone.

Cited by 22 publications

References 6 publications

Severe hypokalaemia with paralysis induced by small doses of liquorice

Severe hypokalaemia with paralysis induced by small doses of liquorice

Pseudohyperaldosteronism induced by habitual ingestion of liquorice

Effect of Carbenoxolone on the Concentrations of Aldosterone in Rat Plasma and Kidney

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