Amiloride Hydrochloride
| 1. NAME |
| 1.1 Substance |
| 1.2 Group |
| 1.3 Synonyms |
| 1.4 Identification numbers |
| 1.4.1 CAS number |
| 1.4.2 Other numbers |
| 1.5 Main brand names, main trade names |
| 1.6 Main manufacturers, main importers |
| 2. SUMMARY |
| 2.1 Main risks and target organs |
| 2.2 Summary of clinical effects |
| 2.3 Diagnosis |
| 2.4 First aid measures and management principles |
| 3. PHYSICO-CHEMICAL PROPERTIES |
| 3.1 Origin of the substance |
| 3.2 Chemical structure |
| 3.3 Physical properties |
| 3.3.1 Colour |
| 3.3.2 State/Form |
| 3.3.3 Description |
| 3.4 Other characteristics |
| 3.4.1 Shelf-life of the substance |
| 3.4.2 Storage conditions |
| 4. USES |
| 4.1 Indications |
| 4.1.1 Indications |
| 4.1.2 Description |
| 4.2 Therapeutic dosage |
| 4.2.1 Adults |
| 4.2.2 Children |
| 4.3 Contraindications |
| 5. ROUTES OF EXPOSURE |
| 5.1 Oral |
| 5.2 Inhalation |
| 5.3 Dermal |
| 5.4 Eye |
| 5.5 Parenteral |
| 5.6 Other |
| 6. KINETICS |
| 6.1 Absorption by route of exposure |
| 6.2 Distribution by route of exposure |
| 6.3 Biological half-life by route of exposure |
| 6.4 Metabolism |
| 6.5 Elimination by route of exposure |
| 7. PHARMACOLOGY AND TOXICOLOGY |
| 7.1 Mode of action |
| 7.1.1 Toxicodynamics |
| 7.1.2 Pharmacodynamics |
| 7.2 Toxicity |
| 7.2.1 Human data |
| 7.2.1.1 Adults |
| 7.2.1.2 Children |
| 7.2.2 Animal Data |
| 7.2.3 Relevant in vitro data |
| 7.3 Carcinogenicity |
| 7.4 Teratogenicity |
| 7.5 Mutagenicity |
| 7.6 Interactions |
| 7.7 Main adverse effects |
| 8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS |
| 8.1 Material sampling plan |
| 8.1.1 Sampling and specimen collection |
| 8.1.1.1 Toxicological analyses |
| 8.1.1.2 Biomedical analyses |
| 8.1.1.3 Arterial blood gas analysis |
| 8.1.1.4 Haematological analyses |
| 8.1.1.5 Other (unspecified) analyses |
| 8.1.2 Storage of laboratory samples and specimens |
| 8.1.2.1 Toxicological analyses |
| 8.1.2.2 Biomedical analyses |
| 8.1.2.3 Arterial blood gas analysis |
| 8.1.2.4 Haematological analyses |
| 8.1.2.5 Other (unspecified) analyses |
| 8.1.3 Transport of laboratory samples and specimens |
| 8.1.3.1 Toxicological analyses |
| 8.1.3.2 Biomedical analyses |
| 8.1.3.3 Arterial blood gas analysis |
| 8.1.3.4 Haematological analyses |
| 8.1.3.5 Other (unspecified) analyses |
| 8.2 Toxicological analyses and their interpretation |
| 8.2.1 Tests on toxic ingredient(s) of material |
| 8.2.1.1 Simple qualitative tests(s) |
| 8.2.1.2 Advanced qualitative confirmation test(s) |
| 8.2.1.3 Simple quantitative method(s) |
| 8.2.1.4 Advanced quantitative method(s) |
| 8.2.2 Tests for biological specimens |
| 8.2.2.1 Simple qualitative test(s) |
| 8.2.2.2 Advanced qualitative confirmation test(s) |
| 8.2.2.3 Simple quantitative method(s) |
| 8.2.2.4 Advanced quantitative method(s) |
| 8.2.2.5 Other dedicated method(s) |
| 8.2.3 Interpretation of toxicological analyses |
| 8.3 Biomedical investigations and their interpretation |
| 8.3.1 Biochemical analysis |
| 8.3.1.1 Blood, plasma or serum |
| 8.3.1.2 Urine |
| 8.3.1.3 Other fluids |
| 8.3.2 Arterial blood gas analyses |
| 8.3.3 Haematological analyses |
| 8.3.4 Interpretation of biomedical investigations |
| 8.4 Other biomedical (diagnostic) investigations and their interpretations |
| 8.5 Overall interpretation of all toxicological analyses and toxicological investigations |
| 8.6 References |
| 9. CLINICAL EFFECTS |
| 9.1 Acute poisoning |
| 9.1.1 Ingestion |
| 9.1.2 Inhalation |
| 9.1.3 Skin exposure |
| 9.1.4 Eye contact |
| 9.1.5 Parenteral exposure |
| 9.1.6 Other |
| 9.2 Chronic poisoning |
| 9.2.1 Ingestion |
| 9.2.2 Inhalation |
| 9.2.3 Skin exposure |
| 9.2.4 Eye contact |
| 9.2.5 Parenteral exposure |
| 9.2.6 Other |
| 9.3 Course, prognosis, cause of death |
| 9.4 Systematic description of clinical effect |
| 9.4.1 Cardiovascular |
| 9.4.2 Respiratory |
| 9.4.3 Neurological |
| 9.4.3.1 Central Nervous System (CNS) |
| 9.4.3.2 Peripheral nervous system |
| 9.4.3.3 Autonomic nervous system |
| 9.4.3.4 Skeletal and smooth muscle |
| 9.4.4 Gastrointestinal |
| 9.4.5 Hepatic |
| 9.4.6 Urinary |
| 9.4.6.1 Renal |
| 9.4.6.2 Other |
| 9.4.7 Endocrine and reproductive systems |
| 9.4.8 Dermatological |
| 9.4.9 Eye, ear, nose throat: local effects |
| 9.4.10 Haematological |
| 9.4.11 Immunological |
| 9.4.12 Metabolic |
| 9.4.12.1 Acid base disturbances |
| 9.4.12.2 Fluid and electrolyte disturbances |
| 9.4.12.3 Others |
| 9.4.13 Allergic reactions |
| 9.4.14 Other clinical effects |
| 9.4.15 Special risks: pregnancy, breast-feeding, enzyme deficiencies |
| 9.5 Other |
| 10. MANAGEMENT |
| 10.1 General principles |
| 10.2 Life supportive procedures and symptomatic/specific treatment |
| 10.3 Decontamination |
| 10.4 Enhanced elimination |
| 10.5 Antidote treatment |
| 10.5.1 Adults |
| 10.5.2 Children |
| 10.6 Management discussion |
| 11. ILLUSTRATIVE CASES |
| 11.1 Case reports from literature |
| 12. ADDITIONAL INFORMATION |
| 12.1 Specific preventive measures |
| 12.2 Other |
| 13. REFERENCES |
| 14. AUTHOR(S), REVIEWER(S) DATA (INCLUDING EACH UPDATING), COMPLETE ADDRESSES |
AMILORIDE HYDROCHLORIDE
International Programme on Chemical Safety
Poisons Information Monograph 026
Pharmaceutical
1. NAME
1.1 Substance
Amiloride Hydrochloride
1.2 Group
ATC code: C03DB01 Cardiovascular system, diuretics,
other potassium-sparing agents
1.3 Synonyms
Guanamprazine; Amipramidin; Amipramizide
1.4 Identification numbers
1.4.1 CAS number
2609-46-3
1.4.2 Other numbers
None
1.5 Main brand names, main trade names
Midamor, MSD. Moduretic (amiloride and hydrochlothiazide),
MSD
1.6 Main manufacturers, main importers
MSD-Merck Sharp & Dohme
2. SUMMARY
2.1 Main risks and target organs
The major potential toxic effect is hyperkalemia which
can cause life-threatening cardiac arrhythmias.
2.2 Summary of clinical effects
The signs and symptoms of hyperkalemia include cardiac
dysrrhythmias and arrest. Fatigue, weakness, gastrointestinal
distress, and paresthesia.
2.3 Diagnosis
Based primarily on history of ingestion, serum potassium
levels, and signs and symptoms of hyperkalemia.
2.4 First aid measures and management principles
Evaluate airway, breathing and circulation. Consider
gastrointestinal decontamination with activated charcoal or
ipecac syrup. Obtain serum potassium level, electrocardiogram,
and signs and symptoms of hyperkalemia.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
Amiloride is a pyrazine carbonyl-quanidine
derivative.
3.2 Chemical structure
Structural name: 3,5-Diamino-N-(aminoiminomethyl)-6-
chlorpyrazine carboxamide
Molecular formula: C6H8ClN7O
Molecular weight of amiloride: 229.65
Molecular weight of chlorhydrate salt: 302.12
3.3 Physical properties
3.3.1 Colour
Yellow to greenish yellow
3.3.2 State/Form
Solid-crystal
3.3.3 Description
Odourless
Solubility in water: 0.52 g/100 mL; in alcohol
1.96
g/100 mL at 25°C; practically insoluble in ether
pKa 8.7; at room temperature solid;
melting point 240.5 to 241.5°C
pH (0.5% solution in water) 3.8 to 5.2
3.4 Other characteristics
3.4.1 Shelf-life of the substance
36 months. No known toxic products are produced.
3.4.2 Storage conditions
Store in well-closed containers ideally between
15 to 30°C. Avoid freezing or a temperature greater
than 40°C. Protect from light.
4. USES
4.1 Indications
4.1.1 Indications
4.1.2 Description
Hypokalemia induced by kaliuretic diuretic
(potassium-wasting diuretic) unresponsive to potassium
supplements, or in patient who cannot tolerate
potassium supplements.
Edema associated with congestive heart failure,
hepatic cirrhosis, or hyperaldosteronism. Amiloride
generally should not be used alone, without other more
potent diuretics.
Hypertension. Though amiloride has mild hypotensive
activity, the medication is generally used
concurrently with a thiazide or a loop diuretic to
prevent or treat diuretic-induced hypokalemia.
Hyperaldosteronism. Amiloride has been effectively
used to treat both primary and secondary
hyperaldosteronism, such as with hepatic cirrhosis
although spironolactone is generally considered more
effective.
4.2 Therapeutic dosage
4.2.1 Adults
Antihypertensive: 5 to 10 mg daily, up to 20 mg per
day.
Diuretic: 5 to 20 mg daily
4.2.2 Children
None identified
4.3 Contraindications
Hyperkalemia. Amiloride should be used with extreme
caution in patients with impaired renal function, diabetes
mellitus, or in the elderly.
5. ROUTES OF EXPOSURE
5.1 Oral
Most common.
5.2 Inhalation
Not available.
5.3 Dermal
Not available.
5.4 Eye
Not available.
5.5 Parenteral
Not available.
5.6 Other
No data
6. KINETICS
6.1 Absorption by route of exposure
Mean 50% when taken without food (range 15 to 90%); mean
30% when taken with food. Information on other routes is not
available.
6.2 Distribution by route of exposure
The apparent volume of distribution is 350 to 380 L
(estimate 5L/kg). This suggests the drug has a large
extravascular distribution. Protein binding is minimal.
6.3 Biological half-life by route of exposure
Based on limited data, the elimination half-life is
reportedly 6 to 9 hours. In patients with reduced renal
function (creatinine clearance ranging between 5 to 46
mL/minute), the half-life is prolonged from 21 to 144
hours.
6.4 Metabolism
Amiloride does not appear to be significantly
metabolized.
6.5 Elimination by route of exposure
Of an oral dose, up to 50% is eliminated unchanged in
urine, and up to 40% is eliminated unchanged in the stool by
72 hours.
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
Although amiloride is usually given with a
saliuretic, hyperkalemia may occur when the drug is
given with potassium supplementation or an ACE-
inhibitor or the patient has renal insufficiency,
diabetes or is elderly. An increase in serum potassium
causes depolarization of cardiac and skeletal muscle
cells. Such depolarization is particularly harmful to
cardiac cells, leading to abnormal impulse conduction.
Specifically hyperkalemia effects electrical
myocardial conductance causing arrhythmias,
bradycardia and hypotension. When used alone,
amiloride is also uricosuric. It also increases
urinary excretion of aldosterone, and plasma renin
concentrations.
7.1.2 Pharmacodynamics
Amiloride inhibits directly Na/K exchange in
the distal tubule of the nephron.
Amiloride decreases sodium reabsorption in the distal
tubule by inhibiting cellular sodium transport
mechanism such as the conductive sodium influx pathway
and possibly the sodium-hydrogen exchange system.
Amiloride's effect on sodium transport results in a
lower transtubular electrical potential difference
which inhibits passive distal tubular potassium
secretion.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
Toxic acute and chronic dosages have
not been established.
7.2.1.2 Children
Toxic acute and chronic dosages have
not been established.
7.2.2 Animal Data
Oral LD50 of amiloride in mice is 56 mg/kg;
in rats, 36 to 86 mg/kg; and in dogs, 40 mg/kg
Relevant animal data
Amiloride has been observed to cross the placenta in
modest amounts in rabbits and mice.
7.2.3 Relevant in vitro data
None available.
7.3 Carcinogenicity
No human data is available.
7.4 Teratogenicity
In humans, only one case report of exposure to amiloride
during pregnancy was located. The infant was exposed to
captopril and propranolol as well as amiloride. The child
had a major limb anomaly. In rats, traces of radiolabeled
amiloride has been shown to cross the placenta. Rabbits and
mice given 20 and 25 times the maximum daily human dose,
respectively, during pregnancy showed no teratogenic effects.
Rats and rabbits given comparable doses (up to 8 mg/kg/day),
however, have shown both reduced maternal and fetal growth
rate. (Briggs et al., 1986).
7.5 Mutagenicity
No human data are available. Various strains of
Salmonella typhimurium exposed to amiloride did not develop
mutagenesis.
7.6 Interactions
Hyperkalemia is more likely to occur if amiloride is
used concurrently with other potassium sparing agents
(spironolactone, triamterene), angiotensin-converting enzyme
inhibitors (captopril, enalapril), or potassium-containing
medications including potassium supplements.
Hypotension can occur if amiloride (a mild anti-
hypertensive) is used with other antihypertensive agents.
Nonsteroidal anti-inflammatory agents may decrease the
diuretic, natriuretic, and hypotensive effect of amiloride by
inhibition of prostaglandin synthetase.
The renal clearance of lithium is reduced by amiloride
which increases the risk of lithium toxicity.
Concomitant use of digoxin and amiloride can alter the
clinical response to digoxin, hence patients should be
carefully monitored if the use of both drugs is
necessary.
The alterations of response can occur by several mechanisms.
First, amiloride increases renal clearance but decreases
extrarenal clearance of digoxin. This usually results in
elevated digoxin levels. Second, amiloride inhibits positive
inotropic effects of digoxin, probably by increasing serum
potassium.
7.7 Main adverse effects
Hyperkalemia.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
Amiloride concentrations in serum,
blood or urine are not well established and
not clinically relevant.
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological analyses and their interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple qualitative tests(s)
8.2.1.2 Advanced qualitative confirmation test(s)
8.2.1.3 Simple quantitative method(s)
8.2.1.4 Advanced quantitative method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple qualitative test(s)
8.2.2.2 Advanced qualitative confirmation test(s)
8.2.2.3 Simple quantitative method(s)
8.2.2.4 Advanced quantitative method(s)
8.2.2.5 Other dedicated method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
Close monitoring of serum
electrolyte and urea are essential.
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
In severe cases, determine arterial pH to check
for metabolic acidosis.
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
Patients with hyperkalemia (serum potassium
greater than 5.5 mEq/L) should be continuously
monitored by electrocardiogram and treated
appropriately.
8.4 Other biomedical (diagnostic) investigations and their
interpretations
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Expected route since only commercially
available forms are oral tablets. Hyperkalemia due to
acute ingestion is the principal potential life-
threatening effect of amiloride. Elevated serum
potassium levels occur as a result of amiloride
potassium-sparing effects on the distal nephron
tubule. Hyperkalemia occurs most commonly in patients
who also take potassium supplements, or potassium
containing medicines, ACE-inhibitors, in patients with
renal failure, diabetes mellitus or elderly.
9.1.2 Inhalation
No data available
9.1.3 Skin exposure
No data available
9.1.4 Eye contact
No data available
9.1.5 Parenteral exposure
No data available
9.1.6 Other
Not applicable.
9.2 Chronic poisoning
9.2.1 Ingestion
Most commonly expected route. Hyperkalemia due
to chronic ingestion is the principal potential life-
threatening effect of amiloride. Elevated serum
potassium levels occur as a result of amiloride
potassium-sparing effects on the distal nephron
tubule. Hyperkalemia occurs most commonly in patients
who also take potassium supplements, or potassium
containing medicines, ACE-inhibitors, in patients with
renal failure, diabetes mellitus or elderly.
9.2.2 Inhalation
No data
9.2.3 Skin exposure
No data
9.2.4 Eye contact
No data
9.2.5 Parenteral exposure
No data
9.2.6 Other
No data
9.3 Course, prognosis, cause of death
Prognosis based on amiloride dose or amiloride blood
levels has not been established. Determination of the
severity of intoxication is based on serum potassium levels.
Death secondary to hyperkalemia is due to cardiac
arrest.
9.4 Systematic description of clinical effect
9.4.1 Cardiovascular
Signs and symptoms described secondary to
hyperkalemia. There are no direct effects from
amiloride. Electrocardiographic abnormalities include
tall, peaked T waves, low voltage R waves, increased
depth of the S wave, widening or absence of the P
wave, progressive widening of the QRS complex,
prolongation of the PR interval, or depression of the
ST segment.
9.4.2 Respiratory
No direct complications.
9.4.3 Neurological
9.4.3.1 Central Nervous System (CNS)
Headache reportedly occurs in 3 to
8% of patients receiving amiloride.
Other adverse symptoms occurring in 1 to 3%
of patients include fatigue, dizziness,
tinnitus, vertigo and encephalopathy.
9.4.3.2 Peripheral nervous system
Paresthesias.
9.4.3.3 Autonomic nervous system
No effects.
9.4.3.4 Skeletal and smooth muscle
Weakness and flaccid paralysis occur
secondary to hyperkalemia. Muscle cramps
occur in about 1 to 3% of patients receiving
amiloride.
9.4.4 Gastrointestinal
Symptoms include nausea, vomiting, anorexia,
flatulence, dyspepsia, diarrhoea, or constipation,
abdominal pain, and gastrointestinal bleeding.
9.4.5 Hepatic
Jaundice has been reported in less than 1% of
patients receiving amiloride. Transient mild
abnormalities of liver function tests has reportedly
occurred with amiloride use.
9.4.6 Urinary
9.4.6.1 Renal
Transient elevations in BUN or serum
creatinine have been reported. No
significant renal dysfunction has been
reported.
9.4.6.2 Other
Polyuria, dysuria, increased urinary
frequency or bladder spasms have occurred in
1 to 3%. Mild proteinuria and transient
glycosuria rarely occur.
9.4.7 Endocrine and reproductive systems
Impotence, gynecomastia.
9.4.8 Dermatological
Erythematous rash, pruritus, and alopecia has
occurred in less than 1% of patients; rash has been
reported in 3 to 8% of patients taking
amiloride.
9.4.9 Eye, ear, nose throat: local effects
Dryness of mouth, taste alteration and
increased thirst occur in less than 1% of patients.
Tinnitus, vertigo, and nasal congestion occur
rarely.
9.4.10 Haematological
Eosinophilia, leukopenia, neutropenia, and
aplastic anemia have rarely been reported with
amiloride use. A causal relationship has not been
established.
9.4.11 Immunological
No data.
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Metabolic acidosis has been
reported in several patients receiving
amiloride. Severity and frequency of
occurence does not seem to be related to
dose.
9.4.12.2 Fluid and electrolyte disturbances
Hyperkalemia. In general, amiloride
does not cause clinically significant
hyponatremia or hypochloremia. Diuresis can
result in a decreased intravascular volume.
9.4.12.3 Others
No data.
9.4.13 Allergic reactions
No data.
9.4.14 Other clinical effects
No data.
9.4.15 Special risks: pregnancy, breast-feeding, enzyme
deficiencies
Reported experience with its use during
pregnancy in humans is limited, and there is no
evidence of teratogenic effects in animals. Fetal
growth rates were diminished in high-dose animal
studies. Amiloride is distributed into the milk of
lactating animals; it is not known if this occurs in
humans.
9.5 Other
No data.
10. MANAGEMENT
10.1 General principles
Prompt evaluation for signs and symptoms of
hyperkalemia including monitoring of vital signs and the
electrocardiogram. Analysis of serum potassium, sodium,
chloride and bicarbonate should be performed. If evidence of
clinical signs and symptoms of hyperkalemia are observed
and/or hyperkalemia is identified, prompt medical treatment
should be undertaken.
10.2 Life supportive procedures and symptomatic/specific treatment
Evaluate and provide support for airway, breathing, and
circulation.
Treatment varies based on severity of hyperkalemia.
Mild Hyperkalemia: normal ECG or with peaked T waves,
normal vital signs, and no other symptoms; stop amiloride and
any sources of potassium.
Moderate Hyperkalemia: only T wave peaking on ECG, normal
vital signs, and no symptoms; treatment described above for
mild hyperkalemia plus: intravenous glucose and insulin;
consider intravenous sodium bicarbonate; cation exchange
resin.
Severe Hyperkalemia: absent P waves, widened QRS or
ventricular arrhythmias, bradycardia, hypotension, or other
symptoms associated with hyperkalemia; treatment as outlined
with above plus: intravenous calcium gluconate and consider
hemodialysis, especially with renal failure.
10.3 Decontamination
Gastrointestinal decontamination is indicated for
recent substantial oral ingestions. If patient is awake and
alert, ipecac (adult 30 mL; child 1 to 12 yrs 15 mL) may be
given. Alternately charcoal may be given alone (1 mg/kg body
weight). Charcoal may be mixed with water or sorbitol 70%, 1
to 2 mL/kg body weight.
10.4 Enhanced elimination
Hemodialysis: It has not been established whether
amiloride is dialyzable, but dialysis may be necessary to
remove potassium if signs and symptoms of severe hyperkalemia
persist despite aggressive and maximal supportive treatment,
especially if the patient has decreased renal function.
10.5 Antidote treatment
10.5.1 Adults
No antidote available
10.5.2 Children
No antidote available
10.6 Management discussion
Prompt evaluation and treatment of hyperkalemia is
essential. Aggressiveness of therapy should be based on the
severity of the signs and symptoms of hyperkalemia.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
No data available
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
No data available
12.2 Other
No data available
13. REFERENCES
Briggs GC, Freeman RK, Yaffe SJ (1986) Amiloride. Drugs in
pregnancy and lactation. Baltimore, MD, Williams and Wilkins.
Brumwald E (1987) Fluids and Electrolytes. Harrison's Principles
of Internal Medicine, Eleventh Edition. New York, McGraw-Hill
Books.
Budavari S (1989) Amiloride. The Merck Index. Rahway NJ, Merc and
Co.
Ellenhorn MJ, Barceloux DG (1988) Potassium-Sparing Diuretics.
Medical Toxicology: Diagnosis and treatment of human poisoning.
New York, Elsevier.
McEvoy GK (1989) Potassium-Sparing Diuretics. The American
Hospital Formulary Service. Bethesda, MD, American Society of the
Hospital Pharmacists.
Reynolds JEF (1989) Amiloride. Martindale: the extra
pharmacopoeia. London, Pharmaceutical Press.
West JB (1985) Potassium balance and the regulations of potassium
excretion. Best and Taylors physiological basis of medical
practice, eleventh edition. Baltimore, Williams and Wilkins.
14. AUTHOR(S), REVIEWER(S) DATA (INCLUDING EACH UPDATING), COMPLETE
ADDRESSES
Author: Dr M.A. McGuigan
Poisons Control Centre
Hospital for Sick Children
555, University Avenue
Toronto, Ontario M5G 1X8
Canada
Tel: 416 598 5823
Fax: 416 598 7489
Reviewer: J Szajewski, August 1997
Peer review: INTOX-10 Meeting, Rio,Brazil, 4 September, 1997
(M Kowalczyk, L Lubomirov, R McKneown, P Rosen, J Szajewski, W
Watson)
Finalization/Edition: Drs MO Rambourg Schepens & M Ruse
October, 1997