ABSTRACT Hypokalaemia (defined as a plasma potassium concentration<3.5 mEq/L) is a common electrolyte abnormality in clinical practice. Drugs are a common cause of either asymptomatic or symptomatic hypokalaemia. Drug-induced hypokalaemia is an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic disease. Hypokalaemia can complicate the use of the drug in the therapeutic concentration range, and can also be precipitated with overdose or conditions leading to drug intoxication. Because the etiologies of hypokalaemia are numerous, the diagnosis of drug-induced hypokalaemia may be overlooked. Physicians should always pay close attention to this common side effect. Evaluation and management of a hypokalaemic patient should include a careful review of medications history to determine if a drug capable of causing or aggravating this electrolyte abnormality is present.
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ABSTRACT: Anorexia nervosa (AN) has serious negative effects on multiple organs and systems of the human body. As patients often do not make their eating disorder the subject of discussion, the physician is forced to rely on the physical examination and laboratory parameters as diagnostic hints. Obvious signs of AN are a body mass index (BMI) below 17.5 kg/m, dry and scaly skin, lanugo, edema, acrocyanosis, petechias, dental problems, and low blood pressure. However, because the often complex laboratory alterations can be difficult for the general psychiatrist to interpret, this article presents some useful guidelines. The plasma of patients with AN often shows alterations in laboratory parameters and appetite regulators, including electrolytes, liver enzymes, leukocyte count, hemoglobin (Hb), leptin, neuropeptide Y (NPY), triiodothyronine (T3), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, ghrelin, pancreatic polypeptide (PP), tumor necrosis factor-alpha (TNF-alpha), and cortisol. Medical problems secondary to AN or due to the treatment itself may lead to further laboratory abnormalities. To date, despite these associated laboratory alterations, the diagnosis of anorexia is a clinical one, based on weight and specific psychopathology.Journal of psychiatric practice. 03/2010; 16(2):82-92.
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ABSTRACT: Metal ion uptake is crucial for all living cells and an essential part of cellular bioenergetic homeostasis. In this study the uptake and the impact of the most abundant internal cation, potassium, were investigated in Actinobacteria, a group of high G+C Gram-positives with a number of prominent biotechnologically and medically important members. Genome analyses revealed a variety of different potassium uptake systems in this monophyletic group ranging from potassium channels common in virtually all Actinobacteria to different active carriers that were present predominantly in pathogenic members able to cope with various stress conditions. By applying Corynebacterium glutamicum as model system we provide experimental evidence that under optimal conditions a potassium channel is sufficient in bacteria for the maintenance of internal pH and membrane potential ensuring survival of cells under stress conditions. Under potassium limitation, however, viability of C. glutamicum was increased under acidic stress or during desiccation when a functional KtrAB potassium transporter from the pathogen Corynebacterium jeikeium was heterologously expressed. We provide experimental evidence that the KtrAB mediated enhanced potassium accumulation improved maintenance of internal pH and membrane potential. The results indicate that the occurrence of active potassium transport systems correlates with an improved potassium-dependent bioenergetic homeostasis and survival of bacterial cells under stress conditions.Biochimica et Biophysica Acta 02/2011; 1807(4):444-50. · 4.66 Impact Factor
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ABSTRACT: Acquired Bartter-like syndrome (BLS), characterized by hypokalemic metabolic alkalosis, hypomagnesemia, hypocalcemia, and normal kidney function, can be induced by diuretics or antibiotics. It is a very rare condition and only anecdotal cases mostly in adults were reported. Although tubulopathy associated with colistin was reported in adults, to the best of our knowledge, colistin-associated BLS neither in adults nor in children has been reported in the literature. We here report a-28-week, 740 g female preterm infant who developed BLS just after colistin treatment for Acinetobacter baumannii infection and recovered few days after the drug cessation, and discuss the possible association of colistin and tubulopathy. More research on colistin pharmacokinetics and pharmacodynamics in critically ill patients and preterm infants is needed to guide adequate colistin dosing at the least toxicity.Renal Failure 01/2013; · 0.94 Impact Factor
Current Drug Safety, 2009, 4, 55-61 55
1574-8863/09 $55.00+.00 © 2009 Bentham Science Publishers Ltd.
Chaker Ben Salem*,1, Houssem Hmouda2 and Kamel Bouraoui1
1Department of Clinical Pharmacology, Faculty of Medicine of Sousse, Sousse, Tunisia
2Medical Intensive Care Unit, Sahloul University Hospital, Sousse, Tunisia
Abstract: Hypokalaemia (defined as a plasma potassium concentration <3.5 mEq/L) is a common electrolyte abnormality
in clinical practice. Drugs are a common cause of either asymptomatic or symptomatic hypokalaemia. Drug-induced hy-
pokalaemia is an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic dis-
ease. Hypokalaemia can complicate the use of the drug in the therapeutic concentration range, and can also be precipitated
with overdose or conditions leading to drug intoxication. Because the etiologies of hypokalaemia are numerous, the diag-
nosis of drug-induced hypokalaemia may be overlooked. Physicians should always pay close attention to this common
side effect. Evaluation and management of a hypokalaemic patient should include a careful review of medications history
to determine if a drug capable of causing or aggravating this electrolyte abnormality is present.
tion <3.5 mEq/L) is one of the most common electrolyte
abnormality found in clinical practice. Mild hypokalaemia is
usually well tolerated in healthy people, but hypokalaemia
can be lifethreatening when severe. The risks of morbidity
and mortality are increased in the elderly, patients with car-
diovascular, hepatic or renal disease. Patients with underly-
ing cardiovascular disease including myocardial infarction
have an increased risk of ventricular dysrhythmias which is
almost linearly related to the degree of hypokalaemia. In
fact, the catecholamine surge that accompanies acute myo-
cardial infarction causes redistributional hypokalaemia and
hyperpolarizes non-ischemic myocardium, producing electri-
cal inhomogeneity and ventricular arrhythmias . Hy-
pokalaemia seems also to be an independent predictor of
mortality in heart failure. In a recent study serum potassium
<4 mEq/L was associated with increased mortality, with a
trend towards increased hospitalization in wide spectrum of
ambulatory patients with chronic, mild to moderate systolic
and diastolic heart failure . Potassium depletion can lead
to muscle cramps and other symptoms. However, the elderly
are less likely to have classic symptoms since they are less
active, and their symptoms may be confused with other
medical problems. In addition, they are predisposed to be-
coming potassium depleted because of possible inadequate
dietary intake of potassium, and greater number of medica-
tions that may lead to potassium depletion . Potassium
depletion causes a decrease in acetylcholine levels due to
diminished choline acetylase activity. This effect can depress
neuromuscular function causing decreased intestinal motility
and even paralytic ileus, contributing to the precipitation of
hepatic coma in patients with hepatic insufficiency. In addi-
tion, hypokalaemia can contribute to the development, or
aggravates the symptoms of hepatic encephabopathy by in-
creasing proximal tubule ammoniagenesis. In hepatic
Hypokalaemia (defined as a plasma potassium concentra-
*Address correspondence to this author at the Departement de Pharmacolo-
gie Clinique, Faculté de Médecine de Sousse, Avenue Mohamed Karoui,
4002 Sousse, Tunisia; Tel: 00 216 98 240 775; Fax: 00 216 73 224 899;
E-mail: email@example.com or firstname.lastname@example.org
insufficiency, the increased systemic burden of ammonia
resulting from increased renal ammoniagenesis can be suffi-
cient to cause the development or worsen the symptoms of
hepatic encephabopathy .
the diagnosis of drug-induced hypokalaemia may be over-
looked. Only systematic review of medications history al-
lows recognition and prompt treatment.
Below, we provide an exhaustive review of drug-induced
hypokalaemia, and discuss the underlying mechanisms and
consequent relevant issues for clinical practice.
Because the etiologies of hypokalaemia are numerous,
between January 1966 to June 2008, regardless of the lan-
guage. The approach used was: hypokalaemia and potassium
disorders as keywords with the subheading “drug-induced”,
and certain drugs were inserted as keywords.
Data were identified from MEDLINE from the period
describe the same topic, only English or French articles were
analysed. However, in our review, pertinent informations in
articles written in other languages (such as Danish or Chi-
nese) has been extracted from the abstract in MEDLINE.
Identified articles were evaluated to determine whether any
of their references contained additional relevant publications.
We excluded the articles with insufficient clinical or labora-
If there were relevant articles in many languages which
lyte abnormality [5,6], and can induce either mild and as-
ymptomatic disorder or severe, even lethal hypokalaemia.
Patients with mild hypokalaemia usually have no symptoms.
If serum potassium level decreases further, nerves and mus-
cles are predominantly affected, causing weakness, fatigue,
leg cramps, myalgias, fasiculations, constipation and ileus
. In severe cases, rhabdomyolysis, ascending paralysis and
respiratory failure may occur. Other manifestations may be
associated such as atrial flutter, paroxysmal atrial tachycar-
dia, ventricular tachycardia and fibrillation, metabolic alka-
losis, nephrogenic diabetes insipidus, and enhanced renal
Medications constitute a common cause of this electro-
56 Current Drug Safety, 2009, Vol. 4, No. 1 Ben Salem et al.
hypokalaemia in hospitalised patients. Hypokalaemia has
been reported in over 20% of hospitalised patients (potas-
sium level <3.6 mmol/l), and a level < 3 mmol/l was found
in almost 3.5 to 5% in these studies [6,8,9]. Profound hy-
pokalaemia, defined as a serum potassium level of less than
2.5 mmol/l, is rare and occurred in less than 1% of hospital-
ised patients [9,10]. Mortality in the hypokalaemic popula-
tion was 10-fold higher than the general hospitalised popula-
tion. Drugs accounted for a consequent proportion in the
pathogenesis of this electrolyte abnormality in these hospi-
talised patients. In a recent study, drug-induced hypokalae-
mia is found in 2.5% of a population of the very old elderly
(subjects aged ?75 years) . Hence, it is important to ap-
propriately detect and treat hypokalaemia.
Several studies have examined the incidence and cause of
two major mechanisms. Hypokalaemia may result from re-
distribution between extracellular and intracellular compart-
ments, or an increased potassium loss through the gastroin-
testinal tract or kidney.
TRANSCELLULAR POTASSIUM SHIFTS
Drugs can decrease serum potassium concentration by
extracellular compartment to cells but the total body potas-
sium remains usually normal. Consequently, hypokalaemia
may be sometimes apparently minor, but should not be un-
derestimated . Indeed, clinicians should be aware that the
extent and consequences of hypokalaemia may vary in clini-
cal practice depending on factors such as co-morbidity, co-
prescribed medications, self-medications, drug dosage or
Numerous drugs can cause a shift of potassium from the
the Na+-K+-ATPase pump, leading to a shift of extracellular
potassium to the intracellular space . Conventional intra-
venous or inhaled doses of selective ?2-agonists reduce se-
rum potassium by 0.4-1.2 mmol/l in a dose dependent man-
ner [13,14]. Indeed, profound hypokalaemia (less than 2.5
mmol l-1) has been described when ?2-agonists are used in
higher doses and in self poisoning . Patients with severe
asthma, taking also theophylline and corticosteroids that also
decrease potassium level, appear to be more likely to de-
velop severe hypokalaemia when treated with ?2-agonists
. Serum potassium levels should therefore be monitored.
More interestingly, the hypokalaemic effect of ?2-agonists is
used in some cases to treat hyperkalaemia. Indeed, albuterol
was prescribed as adjunctive therapy to insulin and glucose
to manage hyperkalaemia.
?2-agonists may precipitate hypokalaemia by activating
Inhibitors of Uterine Contraction
patients treated with intravenous ritodrine or terbulatine .
The stimulation of cellular potassium uptake by these drugs
underlies the decrease of serum potassium level with a
maximum decrease in plasma potassium occurring few hours
of drug infusion. Changes in plasma aldosterone, renal po-
tassium excretion or acid-base homeostasis do not contribute
to ritodrine-or terbutaline-induced hypokalaemia. Careful
Various degrees of hypokalaemia have been described in
monitoring of electrolytes and cardiac rhythm during toco-
lytic therapy with ritodrine or terbutaline are mandatory.
are potent stimulants of the Na+-K+-ATPase activity .
Intentional ingestion of large amounts of pseudoephedrine
and the abuse of ephedrine used in some cough mixture can
cause severe hypokalaemia . The association of corticos-
teroids with these decongestants can aggravate hypokalae-
mia. Physicians should be aware of the potential for these
drug-combinations to cause hypokalaemia.
In experimental studies, pseudoephedrine and ephedrine
pamine and dobutamine can cause hypokalaemia [20,21]. At
dosages of epinephrine > 80 ng/kg/min, hypokalaemia is
common . Catecholamines shift the potassium of ex-
tracellular space to the intracellular space via stimulation of
the ?2-adrenoceptors and enhancement of insulin secretion.
They may lead to arrhythmias and rhabdomayolysis in se-
vere cases . Therefore, potassium levels must be moni-
tored during and after high doses infusion of epinephrine
particularly during cardiac arrest .
Catecholamines such as adrenaline, noradrenaline, do-
toxication but it can also be seen with therapeutic doses .
A linear concentration-response relationship was docu-
mented between serum theophylline concentration and hy-
pokalaemia . Theophylline increases Na+-K+-ATPase
activity by inhibiting cellular phosphodisesterase with a re-
sultant trans-cellular shift of potassium which may aggravate
the theophylline-induced arrhythmia. Consumption of large
quantities of caffeine, present in some drinks, can lead to
severe hypokalaemia by stimulating cell membrane Na+-K+-
Severe hypokalaemia was noted with theophylline in-
pathogenesis of hypokalaemia remains equivocal . Cal-
cium-channel blockers alter potassium transport to cells .
Their possible hypokalaemic effect may be due in a part to
the enhancement of the adrenaline-induced intracellular
transfer of potassium from the extracellular space . Long
term treatment with nifedipine and nitrendipine may reduce
serum potassium concentrations in hypertensive patients
. Verapamil does not usually lead to hypokalaemia when
serum verapamil levels are therapeutic; however, intentional
ingestion of excess amounts of verapamil, can significantly
reduce plasma potassium levels .
The implication of calcium-channel blockers in the
can lead to hypokalaemia. Exogenous insulin always causes
a transient reduction in serum potassium but severe hy-
pokalaemia can occur during the treatment of diabetic ke-
toacidosis or in intentional overdose of insulin . Insulin
tolerance test may also be responsible for severe hypokalae-
mia with cardiac arrhythmias . Insulin increases cellular
potassium uptake in the liver, muscle, and adipose tissue by
activating the cellular Na+-K+-ATPase pump. The fall in
Insulin promotes transfer of potassium to the cells and
Drug-Induced Hypokalaemia Current Drug Safety, 2009, Vol. 4, No. 1 57
potassium level is independent of plasma aldosterone and
epinephrine levels .
large amounts of chloroquine . It seems due to a potas-
sium shift from extracellular space to cells. The decrease of
potassium serum is closely correlated with chloroquine con-
centration. Profound hypokalaemia (< 2mmol/l) has been
reported in 11% of cases after acute chloroquine intoxica-
tion. Patients who died from chloroquine overdose had sig-
nificantly lower serum potassium than survivors, but this
disorder could not be directly considered as the cause of
death in most cases . Potassium supplementation can be
used for the treatment of severe chlorquine-induced hy-
pokalaemia; however aggressive replacement can lead to
hyperkalaemia which potentially could contribute to the car-
diotoxic effects of this drug .
Hypokalaemia was frequently noted after ingestion of
lowing anaesthesia. The cause of this decrease is uncertain. It
may be due to the adrenergic stimulation or hyperventilation
during surgery. Thiopental sodium may induce severe hy-
pokalaemia . The exact mechanism of thiopental-induced
hypokalaemia is not elucidated, but seems secondary to the
movement of potassium between the extracellular and intra-
cellular compartments . Hypokalaemia was also noted
with supra-normal levels of lidocaine .
A decrease in serum potassium levels has occurred fol-
Increased Loss of Potassium
Loss from Gastrointestinal Tract
In addition, sodium wasting in diarrhoeal stool can aggravate
potassium loss from both gut and kidney by secondary aldos-
teronism. Laxatives abuse causes excessive potassium loss in
the stool and may result in hypokalaemia, sometimes severe
resulting in rhabdomayolysis . Phenolphthalein and
docusate sodium has been found empirically to cause more
potassium loss than other laxatives such as sorbitol or so-
dium sulphate . In all cases of hypokalaemia, a laxative
abuse must be looked for in the patient history. Phosphate
enemas, used in bowel clearance before radiology, endo-
scopy and surgery, are associated with significant hy-
pokalaemia , and should be used cautiously in children
Drug-induced chronic diarrhoea can cause hypokalaemia.
with severe diarrhoea leading to hypokalaemia . Chemo-
therapy which induces diarrhoea and vomiting can also lead
to hypokalaemia . Diarrhea is the most common cause of
hypokalaemia in patients treated by capecitabine . Cyclo
3 fort, used in the treatment of chronic venous insufficiency,
can cause chronic diarrhoea with hypokalaemia . Diace-
tylrhein, a chondroprotective agent, can also cause severe
diarrhoea with hypokalaemia.
Persistent vomiting complicating drug therapy could lead
to hypokalaemia which is generally due to metabolic alkalo-
sis and hyperaldosteronism. For example, recreational drug-
induced vomiting can lead to severe hypokalaemia and
metabolic alkalosis . Vomiting-induced by quinine in-
toxication can cause severe hypokalaemia, potentiating the
Some antibiotics can cause pseudomembranous colitis
risk of quinine-induced arrhythmias . Vomiting due to
digitalis toxicity can aggravate an existing lack of potassium.
Even, at therapeutic dose, digitalis-induced arrhythmias can
be observed when hypokalaemia is present. Potassium deple-
tion must be corrected in patients taking digoxin.
Loss from Kidney
of potassium by various mechanisms. The main mechanisms
include renal tubular damage, increased delivery of sodium
or an excessive anion load to the distal tubule, and an inap-
propriate increase of sodium potassium exchange in the
Many classes of drugs may cause excessive kidney loss
of drug-induced hypokalaemia . Loop diuretics seem to
produce less average fall of potassium concentration com-
pared with thiazides . However, the potassium depletion
is usually mild and severe hypokalaemia (less than
3.0mmol/l) is uncommon with diuretics. The prevalence of
diuretic-induced hypokalaemia varies from a study to an-
other and with the used dosage. A recent study found that
diuretic-induced hypokalaemia was the most prevalent ad-
verse drug reaction in an elderly hospitalised population both
during hospitalisation and at the time of admission . In a
retrospective study, 33% of elderly patients taking fu-
rosemide alone were hypokalaemic as compared to 4% of
those receiving furosemide in combination with potassium
supplementation . In a recent observational study, hy-
pokalaemia occured in 8.5% of patients treated with low
doses of thiazide diuretics but in only about 1% did the po-
tassium level fall to less than 3 mmol/l . The risk of hy-
pokalaemia with thiazide is dose dependent and is greater
when dietary sodium intake is higher . There was no
significant association with age and no association with gen-
der. Diuretics affect the potassium serum levels by a variety
of mechanisms. Loop and thiazide diuretics block chloride-
associated sodium reabsorption in the loop of Henle and in
the early distal tubule respectively, resulting in an increased
sodium delivery to the distal tubule channel. Sodium is se-
lectively reabsorbed via the amiloride-sensitive sodium
channel creating a favourable gradient for potassium secre-
tion via potassium channels leading to hypokalaemia.
Moreover, Volume depletion caused by diuretics activates
renin-angiotensin-aldosterone pathway. Therefore, increased
production of aldosterone stimulates the reabsorbtion of so-
dium and water and promotes excretion of potassium via the
secretory potassium channels in the collecting ducts leading
to hypokalaemia . In addition, aldosterone can cause
metabolic alkalosis which can worsen the diuretic-induced
hypokalaemia by increasing potassium shift into cells. Hy-
pokalaemia can also contribute to the maintenance of a
metabolic alkalosis by enhancing bicarbonate absorption and
increasing chloride excretion in the kidney. Aldosterone also
has an extrarenal activity by stimulating cellular Na+-K +-
ATPase pump activity. Loop and, occasionally, thiazide diu-
retics may cause hypomagnesemia. The coexistent hyomag-
nesemia can promote renal potassium wasting and increase
the potential for arrhythmias. In fact, any magnesium deficit
should be detected and corrected with magnesium supple-
mentation. Magnesium is important for potassium uptake
Loop and thiazide diuretics are the most common cause
58 Current Drug Safety, 2009, Vol. 4, No. 1 Ben Salem et al.
and for the maintenance of intracellular potassium levels,
particularly in the myocardium. Combined deficiency may
potentiate the risk of cardiac arrhythmias .
tolerance. It has been also implicated as a cause of new onset
diabetes and in theory in a possible reduction in benefice of
diuretic therapy. However, the new onset diabetes that oc-
curs during diuretic treatment has not been shown to increase
cardiovascular disease, either in clinical trials, or during
longer observational studies . The exact mechanism by
which hypokalaemia may cause glucose intolerance is still
unclear. It seems related to the inhibition of insulin secretion
by the beta cells, and reductions in extracellular fluid volume
and cardiac output. In addition, the evidence linking ar-
rhythmias or cardiac death to the diuretic-induced hy-
pokalaemia remains an area of controversy. Some studies
suggest that hypokalaemia-induced arrhythmias, torsades de
pointes and cardiac arrest have been involved as a cause of
the deleterious effect of diuretics on cardiovascular risk, es-
pecially in patients at greatest risk such as history of left ven-
tricular hypertrophy, heart failure or myocardial infarction
[58-60]. However, several studies have shown no increase in
the cardiac arrhythmias or in the mortality [61,62]. Even
though the evidence linking arrhythmias and cardiac death to
the diuretic-induced hypokalaemia remains an area of con-
troversy; this latter is undoubtedly associated with a risk of
serious arrythmias when diuretics are co-administrated with
drugs that prolong the QT interval. Therefore, caution should
be taken when diuretics are co-administrated with drug-
inducing QT interval prolongation.
Diuretic-induced hypokalaemia may lead to glucose in-
increase of the delivery of sodium and bicarbonate to the
distal nephrons leading to potassium excretion. During long-
term therapy with this drug, hypokalaemia is not common
due to a compensatory potassium retention secondary to aci-
Acetazolamide can causes hypokalaemia. It causes an
sium excretion by increasing sodium delivery to the distal
nephron and by acting as nonreabsorbable anions in the dis-
tal renal tubule, which enhances the secretion of potassium
and hydrogen ion and results in hypokalaemia and metabolic
alkalosis . In a series of 16 patients treated with ticarcil-
lin, the risk of hypokalaemia appeared greatest among pa-
tients who received higher doses (>18g/day) . Oxacillin,
dicloxacillin, flucloxacillin and piperacillin can also cause
severe hypokalaemia . Meropenem , outdated tetra-
cycline, neomycin, polymyxin B, colistin and bacitracin have
also been reported to cause hypokalaemia .
Large doses of penicillins may promote urinary potas-
tassium wasting by inducing depletion of magnesium. These
drugs can cause Bartter-like syndrome, which associated
hypokalaemic metabolic alkalosis, hypomagnesemia, and
hypocalcemia. NSAIDs are beneficial in some situations;
however, in one of the cases, electrolyte abnormalities were
unaffected by indomethacin treatment but were partially cor-
rected by large doses of spironolactone . In a more recent
case, gentamicin therapy induced a marked hypokalaemia
and hypomagnesaemia associated with excessive kaliuresis
and magnesiuria. Hypokalaemia was corrected with potas-
Aminoglycosides and capreomycin can induce renal po-
sium and magnesium supplements and the use of diclofenac
. The frequency of hypokalaemia ranges from 4 to 15%
of patients receiving capreomycin therapy for 6 to 26
months. In a cohort study, among 44 patients taking capreo-
mycin, 30 (68.2%) developed hypokalaemia (defined as se-
rum potassium below 3.3 meq/l) . Capreomycin-induced
hypokalaemia seems to be more common in patients with
low initial body weight or malnutrition. The exact mecha-
nism of the urinary loss of potassium and magnesium due to
aminoglycoside is not entirely elucidated. It may be due to
aminoglycoside-induced hyperaldosteronism and tubular
toxicity. Chou and colleagues  hypothesize that gentami-
cin, stimulates calcium-sensing receptors on the thick as-
cending loop of Henle and distal tubule leading to renal
wasting of potassium, sodium and magnesium. Close moni-
toring of serum potassium in patients who receive aminogly-
coside especially capreomycin and/or high doses of penicil-
lins is mandatory.
effect on the renal tubule. It causes inhibition of hydrogen
ions secretion by collecting-duct cells as well as magnesium
depletion . Amphotericin-induced hypokalaemia is dose
dependent and generally occurs before renal failure. In com-
parison with amphotericin, the lipid formulation of ampho-
tericin causes less hypokalaemia . Hypokalaemia is sig-
nificantly less common with caspofungin than with ampho-
tericin . Amiloride may be beneficial in amphotericin-
induced hypokalaemia . Spironolactone may also pre-
vent amphotericin-related hypokalaemia in neutropenic pa-
tients . Itraconazole can induce severe hypokalaemia by
excessive urinary loss of potassium . In a recent study,
hypokalaemia represents the most common adverse effect of
itraconazole therapy . Hypokalaemia is also seen with
oral fluconazole . Patients who are treated with these
antifungal drugs should have their serum potassium level
Amphotericin promotes renal potassium wasting by toxic
Drugs Associated with Mineralocorticoid Effects
serum potassium and is occasionally accompanied by hy-
pokalaemia and severe metabolic abnormalities. Only a few
case reports about severe hypokalaemia have been described.
The maximum decrease in potassium serum levels is reached
in the first week of corticosteroids treatment . High
doses of hydrocortisone (> 100 mg/day) can induce severe
hypokalaemia by causing sodium retention and excessive
renal potassium loss secondary to their significant mineralo-
corticoid effect . Dexamethasone, methylprednisolone,
cortisol and prednisolone seem to be less likely to induce
hypokalaemia . Severe potassium depletion can occur
when these drugs are prescribed with concomitant diuretics
. Fludrocortisone, used in the treatment of Addison's
disease and orthostatic hypotension, can cause potassium
wasting and severe hypokalaemia especially in the elderly
population . It is proposed in the treatment of hy-
perkalaemia in patients undergoing hemodialysis.
Long-term therapy with corticosteroids slightly reduces
dependent hypokalaemia in 1% of users . Some patients
were reported to have chronic persistent hypokalaemia long
after cessation of gossypol treatment. Gossypol-induced hy-
Gossypol, a male contraceptive agent, can cause dose
Drug-Induced Hypokalaemia Current Drug Safety, 2009, Vol. 4, No. 1 59
pokalaemia is related, in part, to the inhibition of 11 ?-
hydroxysteroid dehydrogenase that causes an apparent min-
eralocorticoid excess leading to excessive potassium excre-
tion and sodium resorption. Carbenoxolone can cause also
hypokalaemia by inhibiting the renal enzyme ?11-
hydroxysteroid dehydrogenase. Hypokalaemia appears most
frequently in those receiving excessive doses of carbenox-
olone . Mifepristone, an antiprogestogenic steroid, has
also been incriminated as a possible cause of severe hy-
pokalaemia which is related to excessive cortisol activation
of the mineralocorticoid receptor .
Chemotherapy and Other Nephrotoxic Drugs
bolic alkalosis, hypomagnesaemia, and hypocalciuria resem-
bling Gitelman’s syndrome . The exact mechanism of
this drug’s nephrotoxicity is not elucidated, but it seems to
be due to a tubular necrosis, predominantly in the distal con-
voluted tubule and the collecting ducts, which may result in
salt wasting and stimulation of the renin-angiotensin-
aldosterone system, with consequent hypokalaemic meta-
Cisplatin has been associated with hypokalaemic meta-
secondary to proximal renal tubular dysfunction . The
lower weight, the concomitant association of ritonavir or
didanosine and the long duration of tenofovir use appear to
be risk factors for tenofovir-induced renal tubular disease
. Foscarnet may cause hypokalaemia by renal potassium
wasting probably by magnesium depletion .
Tenofovir can lead to nephrotoxicity and hypokalaemia
act mechanism is still unknown, but seems to be secondary
to a dysfunction of ion channels on skeletomuscular mem-
branes . Sirolimus has been shown to cause hypokalae-
mia by excessive urinary excretion of potassium, probably
secondary to tubular dysfunction. Potassium deficit is mild
and seems to be dose dependent and it can disappear when
doses are reduced. It can occur without associated metabolic
acidosis, hyperaldosteronism or Fanconi syndrome. Patients
with sirolimus-induced hypokalaemia respond well to potas-
sium supplements .
Methotrexate may induce severe hypokalaemia. The ex-
vere hypokalaemia and metabolic alkalosis, especially in
patients with impaired renal function . Hypokalaemia is
due to an excessive delivery of acid, sodium or bicarbonate
to distal tubule which stimulates distal tubular hydrogen ions
secretion and potassium secretion leading to hypokalaemia.
Sodium bicarbonate is also proposed in treatment of hy-
perkalaemia with metabolic acidosis . Salicylate intoxi-
cation can cause hypokalaemia, which may be aggravated
with forced alkaline diuresis used in this situation. Hpoka-
lemia may complicate poisoning with papaverine when there
is a lactic acidosis. The biochemical features of papaverine-
induced acid-base disturbance closely resemble those caused
by salicylates . Paracetamol overdose is associated with
dose-related hypokalaemia, and kaliuresis of short duration
(<24 h). A specific renal effect of paracetamol in overdose
possibly linked to cyclo-oxygenase inhibition, distinct from
any nephrotoxic effect of paracetamol, irrespective of N-
Excessive administration of bicarbonate may lead to se-
acetylcysteine administration and independent of whether
vomiting occurred has been suggested [98,99]. Vitamin D
intoxication induces potassium and water depletion and hy-
pernatraemia probably because of renal tubular damage
. The abuse of thyroxine can cause severe hypokalae-
mia . Indeed, animal studies show that the thyroid-
hormones stimulate the synthesis of Na+-K+-ATPase pump
. Overdose of risperidone and quetiapine, has also been
associated wih hypokalaemia . Symptomatic hy-
pokalaemia has also been reported with infliximab ,
ibuprofen , ondansetron , and meglumine antimo-
DRUGS INDUCING CELLULAR PROLIFERATION
during initial treatment. The presumed mechanism was an
increase in cellular proliferation with sudden production of
millions of new cells leading to a shift of potassium to cells
. In addition, such patients are probably chronically
hypoxic and predisposed to total body potassium depletion.
Massive leukocytosis after Granulocyte–macrophage colony-
stimulating factor therapy has also been associated with se-
vere hypokalaemia due to potassium shift to cells recently
Hydroxocobalamin may rarely precipitate hypokalaemia
and the presence of symptoms and ECG abnormalities. Cor-
rection of drug-induced hypokalaemia is generally not indi-
cated especially in the case of transcellular potassium shift.
This situation may not have significant total body potassium
deficit and when corrected rebound hyperkalaemia can occur
and should be kept in mind by the clinician. Withdrawal of
the offending drug is usually sufficient to restore a normal
level of serum potassium. However, severe hypokalaemia
should be corrected by intravenous infusion of potassium. In
moderate hypokalaemia, and in the absence of digoxin toxic-
ity or severe heart disease, oral administration of potassium
salts may be useful, but can cause gastrointestinal adverse
effects and contact irritation. The daily dose should be di-
vided into three to four doses to prevent these side effects.
When drug-induced hypokalaemia is predictable e.g with
prescription of diuretics, concomitant potassium supplements
should be provided to patients. In case of co-existent magne-
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Received: August 22, 2008
Revised: September 20, 2008 Accepted: September 30, 2008