Selective Serotonin Re-uptake Inhibitors (SSRI)
| 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 and excretion |
| 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 Relevant 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 Test(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 interpretation |
| 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 effects |
| 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 |
| 9.5 Other |
| 9.6 Summary |
| 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), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES) |
Selective Serotonin Re-uptake Inhibitors
International Programme on Chemical Safety
Poisons Information Monograph G011
Pharmaceutical
This Monograph contains the following sections:
1. Name, 2. Summary, 3. Physico-chemical properties ,
7.1 Mode of Action, 9.Clinical Effects, 10.Management,
11.1 Case reports from the literature, 12.2 Other.
See also individual Monographs on Fluoxetine (PIM651) and Sertraline
(PIM177) for further information.
1. NAME
1.1 Substance
Selective Serotonin Re-uptake Inhibitors
1.2 Group
The members of this group contain:
alaproclate; citalopram;
fluoxetine; fluvoxamine;
paroxetine; sertraline;
zimeldine
1.3 Synonyms
SSRI
Citalopram: nitalapram
Zimeldine: zimelidine
1.4 Identification numbers
1.4.1 CAS number
Alaproclate hydrochloride 60719-83-7
Citalopram 59729-33-8
Citalopram hydrobromide 59729-32-7
Fluoxetine 54910-89-3
Fluoxetine hydrochloride 59333-67-4
Fluvoxamine 54739-18-3
Fluvoxamine maleate 61718-82-9
Paroxetine 61869-08-7
Paroxetine hydrochloride 78246-49-8
Sertraline 79617-96-2
Sertraline hydrochloride 79559-97-0
Zimeldine 56775-88-3
Anhydrous zimeldine dihydrochloride 60525-15-7
Zimeldine dihydrochloride monohydrate 61129-30-4
1.4.2 Other numbers
ATC Classification:
Psychoanaleptic, antidepressant, selective
serotonin reuptake inhibitor: N06AB
1.5 Main brand names, main trade names
1.6 Main manufacturers, main importers
2. SUMMARY
2.1 Main risks and target organs
When taken alone Selective Serotonin Re-uptake
Inhibitors (SSRIs) appear safer in overdose than most other
classes of antidepressants.
They are potent inhibitors of serotonin re-uptake by central
nervous system neurones and may interact with other drugs or
circumstances which cause serotonin release. The enhancement
of the serotonergic effects may produce a life-threatening
serotonin syndrome.
Drugs which can increase the serotonin level when taken in
combination with SSRIs include: tricyclic antidepressants,
monoamine oxidase inhibitors (MAOIs), carbamazepine, lithium
or serotonergic substances.
2.2 Summary of clinical effects
Drowsiness, tremor in upper extremities, lightheadness,
nausea, vomiting are the most common symptoms. Other symptoms
include: tachycardia (occasionally bradycardia),
hypo/hypertension, dilated pupils, agitation, dry mouth and
sweating.
Coma and convulsions may occur in large overdoses.
They are much less cardiotoxic than the conventional
antidepressants, though citalopram has caused nodal rhythm,
QT and QRS prolongation.
The combination of SSRIs with agents that increase serotonin
availability in the central nervous system can cause the
serotonin syndrome which is characterised by the presence of
at least 3 of the following symptoms: mental status changes
(confusion, hypomania), agitation, myoclonus, hyperreflexia,
sweating, shivering, tremor, diarrhoea, motor incoordination,
muscle rigidity and fever. Severe complications may occur,
including: severe hyperthermia, rhabdomyolysis, disseminated
intravascular coagulation (DIC), convulsions, respiratory
arrest and death.
2.3 Diagnosis
Diagnosis of SSRIs poisoning is clinical and based on
history of overdosssive supportive care including diazepam,
mechanical ventilation, external cooling and if necessary,
curarization.
2.4 First aid measures and management principles
Treatment is symptomatic and supportive, with diazepam
for sedation if necessary. Cardiac monitoring is recommended
in symptomatic cases.
If the patient presents within 2 hours, a dose of activated
charcoal should be given (50g in adults; 1g/kg in children).
Observation for 6 hours is recommended.
Treatment of the serotonin syndrome in more severe
intoxications or where there is a co-ingestion may require
more aggressive measures such as establishment of an airway,
ventilation, administration of intravenous fluids, control of
seizures, and control of hyperthermia may be necessary.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
3.2 Chemical structure
See individual Monographs for Fluoxetine and Sertraline.
Citalopram
Chemical names:
1-[3-(Dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-5-
isobenzofurancarbonitrile;
1-[3-(dimethylamino)propyl]-1-(4- fluorophenyl)- 5-
phthalancarbonitrile;
Molecular formula Citalopram: C20H21FN2O
Molecular weight Citalopram: 324.40.
Molecular formula Citalopram Hydrobromide: C20H21FN2O.HBr
Fluvoxamine
Chemical names:
(E)-5-Methoxy-1-[4-(trifluoromethyl)phenyl]-1-pentanone O-(2-
aminoethyl)oxime;
5-methoxy-4'-(trifluoromethyl)valerophenone (E)-O-(2-
aminoethyl)oxime
Molecular formula Fluvoxamine: C15H21F3N2O2
Molecular weight Fluvoxamine: 318.34
Molecular Fluvoxamine Maleate C15H21F3N2O2.C4H4O4,
Paroxetine
Chemical names:
(3S-trans)-3-[(1,3-Benzodioxol-5-yloxy)methyl]-4-(4-
fluorophenyl) piperidine;
(-)-trans-4-(p-fluorophenyl)-3-[[3,4 (methylenedioxy)
phenoxy] methyl]piperidine;
Molecular formula Paroxetine: C19H20FNO3;
Molecular weight Paroxetine: 329.37.
Molecular formula Paroxetine Hydrochloride: C19H20FNO3.HCl
Molecular formula Paroxetine Hydrochloride hemihydrate:
C19H20FNO3.HCl. 1/2 H2O
Zimeldine
Chemical names:
(Z)-3-(4-Bromophenyl)-N,N-dimethyl-3-(3-pyridinyl)-2-propen-
1-amine;
(Z)-3-(4'-bromophenyl)-3-(3''-pyridyl)dimethylallylamine;
Molecular formula Zimeldine: C16H17BrN2;
Molecular weight Zimeldine: 317.23.
Molecular formula Zimeldine dihydrochloride monohydrate:
C16H17BrN2.2HCl.H2O
3.3 Physical properties
3.3.1 Colour
3.3.2 State/Form
3.3.3 Description
Citalopram hydrobromide
Melting point: 182 to 183°C
Fluvoxamine Maleate
Melting point 120 to 121.5°C
Paroxetine Hydrochloride
Melting point 118°C
Paroxetine Hydrochloride hemihydrate
melting point 129 to 131°C
Zimeldine dihydrochloride monohydrate
melting point 193°C
(Budavari, 1996)
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
SSRIs are used in the treatment of depression.
They are also used in panic disorder, obsessive
compulsive disorder and bulimia nervosa.
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 and excretion
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of action
7.1.1 Toxicodynamics
SSRIs are potent inhibitors of serotonin
re-uptake by central nervous system neurones and may
interact with other drugs or circumstances which cause
serotonin release. The enhancement of the serotonergic
effects may produce a life-threatening serotonin
syndrome.
SSRIs can inhibit in vitro and in vivo the hepatic
isoenzyme 2D6 of the cytochrome P450 system (CYP2D6),
which is involved in the oxidative metabolism of
numerous drugs. Caution should be used when combining
a SSRI with CYP2D6 substrates (desipramine,
nortriptyline, haloperidol, thioridazine, flecainide,
codeine, propranolol, metoprolol), as the SSRI can
cause a significant increase in the serum
concentrations of these drugs.
7.1.2 Pharmacodynamics
SSRIs specifically inhibit central nervous
system neuronal re-uptake of serotonin, thus
increasing the concentration of the serotonin at the
synapse and enhancing of serotonergic neuronal
transmission. A deficiency of serotonin is thought to
play a major role in depression, therefore increasing
the availability of serotonin would be expected to
improve the clinical signs of depression.
SSRIs have no direct effect on the re-uptake of
noradrenaline, dopamine or GABA. Unlike tricyclic
antidepressants, they have no significant affinity for
alpha1-adrenergic, H1-histamine, and muscarinic
receptors. The selectivity of SSRIs may account for
the lower incidence of some adverse effects such as
sedation, orthostatic hypotension, and anticholinergic
effects.
7.2 Toxicity
7.2.1 Human data
7.2.1.1 Adults
7.2.1.2 Children
7.2.2 Relevant animal data
7.2.3 Relevant in vitro data
7.3 Carcinogenicity
7.4 Teratogenicity
7.5 Mutagenicity
7.6 Interactions
Co-administration of drugs increasing the level of
serotonin: tricyclic antidepressants, MAOIs, reversible
inhibitors of monoamine oxidase, lithium, may cause a
serotonin syndrome.
A minimum 2 week wash-out period should be observed between
stopping a monoamine oxidase inhibitor (MAOI) and starting a
SSRI. Conversely, a MAOI should not be started for at least a
week after a SSRI has been stopped (at least 5 weeks for
fluoxetine; at least 2 weeks for paroxetine and
sertraline.
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 Test(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
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.2 Urine
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
"Basic analyses"
"Dedicated analyses"
"Optional analyses"
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
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
Nausea, vomiting, abdominal pain, diarrhea,
tremor, confusion, agitation, drowsiness, blurred
vision, and in rare cases, seizures and coma.
Significant cardiovascular toxicity is unusual (except
citalopram). Effects have included mild hypo or
hypertension, tachycardia and ventricular
dysrrhythmia.
More serious toxicity may be expected with the
co-ingestion of tricyclic antidepressants and/or MAOIs
and may result in a life-threatening serotonin
syndrome.
9.1.2 Inhalation
Not relevant
9.1.3 Skin exposure
Not relevant
9.1.4 Eye contact
No data
9.1.5 Parenteral exposure
No data
9.1.6 Other
No data
9.2 Chronic poisoning
9.2.1 Ingestion
A case of sertraline abuse has been reported
with high doses, almost daily, for a period of 6
months. Effects include: relaxation, euphoria, then
intense excitement, marked tremor and visual and
auditory hallucinations.
9.2.2 Inhalation
Not relevant
9.2.3 Skin exposure
Not relevant
9.2.4 Eye contact
Not relevant
9.2.5 Parenteral exposure
Not relevant
9.2.6 Other
Not relevant
9.3 Course, prognosis, cause of death
Pure SSRIs overdoses usually have a fairly benign
course. However, a few deaths are reported in the literature,
most involving a co-ingestion and/or very high doses.
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Significant cardiovascular toxicity is unusual.
Effects have included mild hypo or hypertension,
tachycardia and ventricular dysrrhythmia (citalopram).
9.4.2 Respiratory
No data
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
Drowsiness, headache, restlessness,
delirium, insomnia, ataxia, extrapyramidal
syndrome, coma and convulsions.
9.4.3.2 Peripheral nervous system
Blurred vision.
9.4.3.3 Autonomic nervous system
Hypotension, hypertension,
tachycardia, profuse sweating.
9.4.3.4 Skeletal and smooth muscle
Myoclonus, hyperreflexia.
9.4.4 Gastrointestinal
Nausea, vomiting, diarrhea
9.4.5 Hepatic
Mild liver enzyme disturbances.
9.4.6 Urinary
9.4.6.1 Renal
No data
9.4.6.2 Other
No data
9.4.7 Endocrine and reproductive systems
Hyperglycemia
9.4.8 Dermatological
Pruritus, rashes, urticaria have been reported
9.4.9 Eye, ear, nose, throat: local effects
9.4.10 Haematological
No data
9.4.11 Immunological
Skin rashes have been reported
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data
9.4.12.2 Fluid and electrolyte disturbances
No data
9.4.12.3 Others
No data
9.4.13 Allergic reactions
No dara
9.4.14 Other clinical effects
No data
9.4.15 Special risks
9.5 Other
SSRI can cause adverse effects after withdrawal, either
from a reduction in dosage or from the abrupt cessation of
the drug. The most frequent symptoms include vertigo,
dizzines, paresthesia (shock-like sensations, tingling and
burning sensations); less frequent symptoms include
irritability, anxiety, headache, orthostatic hypotension,
sleep disturbances. The symptoms usually occur within 48
hours after stopping the SSRI and they last about 2 weeks.
9.6 Summary
10. MANAGEMENT
10.1 General principles
The primary management of SSRI overdose consists of the
institution of careful observation of vital signs and
neurological status and supportive care until signs and
symptoms resolve.
In more severe intoxications or where there is a
co-ingestion, more aggressive measures such as establishment
of an airway, ventilation, administration of intravenous
fluids, control of seizures, and control of hyperthermia may
be necessary.
10.2 Life supportive procedures and symptomatic/specific
treatment
In pure SSRI overdoses, intensive supportive care is
rarely required. Measures that may be required based on the
clinical presentation include: endotracheal intubation and
assisted ventilation if coma is present, intravenous fluid
resuscitation if hypotension is present, pharmacological
control of seizures, cooling if hypirthermia is
present.
10.3 Decontamination
Gastrointestinal decontamination by administration of a
single oral dose of activated charcoal may be indicated.
Gastric lavage followed by activated charcoal should be
advocated in patients who have ingested large doses and/or
when there has been a significant co-ingestion.
10.4 Enhanced elimination
There are no effective method known to enhance elimination.
10.5 Antidote treatment
10.5.1 Adults
There is no antidote
10.5.2 Children
There is no antidote
10.6 Management discussion
No prospective studies have been performed to evaluate
the treatment of the serotonin syndrome, and treatment
strategies are primarily based on case reports. Non specific
serotonin receptor antagonists such as methysergide and
cyproheptadine have been used successfully. Propranolol which
blocks serotonin 1A receptors has also been used.
Benzodiazepines can reduce the muscular rigidity. Dantrolene
which is a direct skeletal muscle relaxant has also been
found to be useful. The efficacy of these agents has yet to
be evaluated.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
In 12 patients taking 10 to 100mg fluoxetine a day with
either phenelzine (30 to 60mg) or tranylcypromine (10 to
140mg), there was a high incidence (25 to 50%) of adverse
effects. These included hypomania, racing thoughts,
agitation, restlessness, confusion, myoclonus, hypertension,
tremor and diarrhoea (Feighner et al., 1990).
3 male patients aged 29, 34 and 41 died after taking
overdoses of moclobemide and citalopram concomitantly
(Neuvonen et al., 1993).
12. Additional information
12.1 Specific preventive measures
No data
12.2 Other
Useful references on the SSRIs:
Alderman CP & Cheum Lee P (1996) Serotonin syndrome
associated with combined sertraline-amitriptyline therapy.
Ann Pharmacother, 30: 1499-1500
Amsden GW & Georgian F (1996) Orthostatic hypotension induced
by sertraline withdrawal. Pharmacotherapy, 16 (4): 684-686
Brown DF & Kerr HD (1994) Serttraline overdose. Ann
Pharmacother, 28: 1307
Caracci G (1994) Unsuccessful suicide attempt by sertraline
overdose. Am J Psychiatry, 151:147
Coupland NJ, Bell CJ, Potokar JP (1996) Serotonin reuptake
inhibitor withdrawal. J Clin Pharmacol, 16: 356-362
D'Urso P (1996) Abuse of sertraline. J Clin Pharmacy and
Therapeutics, 21: 359-360
Frost L & Lal S (1995) Shock-like sensations after
discontinuation of selective serotonin reuptake inhibitors.
Am J Psychiatry, 152 (5): 810
Graber MA, Hoehns TB, Perry PJ (1994) Sertraline-phenelzine
drug interaction: a serotonin syndrome reaction. Ann
Pharmacother, 28 (6): 732-735
Klein-Schwartz W & Anderson B (1996) Analysis of sertraline-only overdoses. Am J Emerg Med, 23 (6):
1371-1374
Lappin RI & Auchincloss EL (1994) Treatment of serotonin
syndrome with cyproheptadine. N Engl J Med, 331: 1021-1022
Lejoyeux M, Ades J, Rouillon F (1994) Serotonin syndrome:
incidence, symptoms and treatment. CNS Drugs, 2 (2): 132-143
Mason BJ & Blackburn KH (1997) Possible serotonin syndrome
associated with tramadol and sertraline co-administration.
Ann Pharmacother, 31: 175-177
Myers LB, Dean BS, Krenzelok EP (1993) Sertraline(Zoloft)
overdose: assessment of a new antidepressant. In: Proceedings
of the International Congress of Clinical Toxicology, New
York City, 10-13 September 1993, Vet Hum Toxicol, 35 (5): 341
Personne M; Sjoberg G and Persson H 1997 Citalopram overdose
- Review of cases treated in Swedish hospitals. Clin.
Toxicol. 35 (3): 237-240.
Riesenman C (1995) Antidepressant drug interactions and the
cytochrome P450 system: a critical appraisal. Phamacotherapy,
15, supp 6, 84S-99s
Rosenstock HA (1996) Sertraline withdrawal in two brothers: a
case report. Int Clin Psychopharmacol, 11 (1): 58-59
Sternbach H 1991 The serotonin syndrome. Am. J. Psychiatry
148: 705-713
13. REFERENCES
Budavari S ed. (1996) The Merck Index: an encyclopedia of
chemicals, drugs and biologicals, 12th ed. Rahway, New Jersey,
Merck and Co., Inc.
Feighner JP; Boyer WF; Tyler DL and Neborsky RJ 1990 Adverse
consequences of fluoxetine-MAOI combination therapy. J. Clin.
Psychiatry 51: 222-225
Neuvonen PJ, Pohjola-Sintonen S, Tacke U and Vuori E 1993. Five
fatal cases of serotonin syndrome after moclobemide-citalopram or
moclobemide-clomipramine overdose. Lancet 342: 1419.
14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE
ADDRESS(ES)
Author: Medical Toxicology Unit,
Guyís and St Thomasí Trust
Avonley Road, London SE14 5ER, UK
November, 1997
Reviewers: R Ferner, A van Heijst, M Mathieu-Nolf, MO Rambourg
Schepens (coordinator)
London, March, 1998
Editor: Dr M.Ruse, September 1998