Potassium depletion corticosteroids

In addition to the diuretics, other agents can cause potassium depletion. Prolonged therapy with cathartics and corticosteroids can cause potassium depletion, although this is not likely to occur as quickly or to the same extent as with diuretics. 

Potassium depletion, for example due to diuretics or corticosteroids, potentiates the effects of cardiac glycosides on the myocardium and may also have a small effect in reducing the renal tubular secretion of digoxin (211,212). 

Chlorothiazide is used in the treatment of oedema associated with congestive heart failure and renal and hepatic disorders. It is also employed in hypertension, either alone or in conjunction with other antihypertensive agents. It is also used in oedema associated with corticosteroid therapy thereby increasing the potassium-depleting action of the latter. 

Increased risk of toxicity with drugs that alter serum electrolytes (potassium -depleting diuretics, corticosteroids, thiazide and loop diuretics, amphotericin B, quinidine, amiodarone). Blockers of p adrenergic receptors, calcium channels, or acetylcholinesterase increase risk of complete AV block. Drugs which alter Gl absorption may alter bioavallabillty. 

The combined use of drugs that can cause hypokalaemia (e.g. amphotericin B, corticosteroids, thiazide and ioop diuretics, and stimuiant iaxatives) and drugs that proiong the QT intervai (e.g. ciass la and ciass in antiarrhythmics see Tabie 9.2 , (above)) shouid be well monitored because hypokalaemia increases the risk of torsade de pointes arrhythmias. There appear to be only a few reports of this interaction, for example, see Beta blockers + Potassium-depleting drugs , p.8S2. ... 

The use of potassium-depleting diuretics can precipitate the development of potentially life-threatening torsade de pointes arrhythmias in patients taking sotalol unless potassium levels are maintained. This would also be expected with other potassium-depleting drugs such as corticosteroids, some laxatives, and intravenous amphotericin. Chlortalidone and hydrochlorothiazide may reduce the bioavailability of celiprolol, but the evidence for this is sparse. 

Systemic corticosteroids can increase the loss of potassium, particularly those that are naturally occurring (cortisone, deoxycortone, hydrocortisone) whereas the synthetic derivatives (betamethasone, dexametha-sone, methylprednisolone, prednisolone, prednisone, triamcinolone) have much less mineralocorticoid activity. There is therefore the possibility of potassium depletion, particularly when corticosteroids are used long-term, which may increase the risk of digitalis toxicity. These corticosteroids also cause sodium and water retention, resulting in oedema and hypertension, which can lead to cardiac failure in some individuals. 

The greatest potassium loss occurs with the naturally occurring corticosteroids such as cortisone and hydrocortisone. Corticotropin (ACTH), which is a pituitary hormone, and tetracosactrin (a synthetic polypeptide) stimulate corticosteroid secretion by the adrenal cortex and can thereby indirectly cause potassium loss. Fludrocortisone also causes potassium loss. The synthetic corticosteroids (glucocorticoids) have a less marked potassium-depleting effect and are therefore less likely to cause problems. These include betamethasone, dexamethasone, prednisolone, prednisone and triamcinolone. 

The potassium-depleting diuretics (i.e. loop diuretics or thiazide and related diuretics) are listed in Table 26.1 , (p.944). Acetazolamide, a weak diuretic, has also been predicted to cause hypokalaemia in the presence of corticosteroids. However, hypokalaemia seen with acetazolamide is rarely clinically significant, and therefore the risks are lower... 

Beta agonists (e.g. fenoterol, salbutamol (albuterol), terbutaline) can cause hypokalaemia. This can be increased by other potassium-depleting drugs such as the corticosteroids, diuretics (e.g. bendroflumethiazide, furosemide) and theophylline. The risk of serious cardiac arrhythmias in asthmatic patients may be increased. 

No interactions are expected at standard therapeutic doses. At higher doses or with long-term use, licorice may potentiate potassium depletion of high-ceiling loop diuretics and thiazide diuretics, stimulant laxatives (Mills and Bone 2005), and corticosteroids such as prednisolone (Cheng et al. 2004 De Smet 1993), and may potentiate the action of cardiac glycosides such as digoxin (Kelly 1990). 

Since both corticosteroids and the loop or thiazide diuretics can cause potassium loss, severe depletion is possible if they are used together. 

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