Thiamine and salts
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 ENTRY |
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 |
7.2 Toxicity |
7.2.1 Human Data |
7.2.1.1 Adults |
7.2.1.1 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 |
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 |
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) |
Thiamine and salts
International Programme on Chemical Safety
Poisons Information Monograph G015 (Group PIM)
Pharmaceutical
1. NAME
1.1 Substance
Thiamine
1.2 Group
This group includes:
Acetiamine Hydrochloride
Benfotiamine
Bisbentiamine
Bisbutiamine
Cetotiamine Hydrochloride
Cycotiamine
Fursultiamine
Octotiamine
Prosultiamine
Sulbutiamine
Thiamine Hydrochloride
Thiamine Nitrate
1.3 Synonyms
Acetiamine Hydrochloride (r INNM)
Acethiamine Hydrochloride
Diacethiamine Hydrochloride
Benfotiamine (r INN)
S-Benzoylthiamine O-Monophosphate
Bisbentiamine (r INN)
O-Benzoylthiamine Disulphide
Bisbutiamine
O-Butyrylthiamine Disulphide
Cetotiamine Hydrochloride (r INNM)
Dicethiam Hydrochloride
Cycotiamine (r INN)
CCT
Cyclorcabolthiamine
Fursultiamine (r INN)
Thiamine Tetrahydrofurfuryl Disulphide
TTFD
Octotiamine (r INN)
TATD
Thioctothiamine
Prosultiamine (r INN)
DTPT
Thiamine Propyl Disulphide
Sulbutiamine (r INN)
Bisibutiamine
O-Isobutyrylthiamine Disulphide
Thiamine Hydrochloride (BANM, INNM)
Aneurine Hydrochloride
Thiamin Hydrochloride
Thiamine Chloride
Thiamini Hydrochloridum
Thiaminii Chloridum
Vitamin B1
Thiamine Nitrate (BANM, INNM)
Aneurine Mononitrate
Thiamine Mononitrate
Vitamin B1 Mononitrate
1.4 Identification Numbers
1.4.1 CAS Number
Acetiamine Hydrochloride 299-89-8
Benfotiamine 2457-89-2
Bisbentiamine 2667-89-2
Bisbuntiamine 18481-23-7
Cetotiamine 137-76-8
Cetotiamine Hydrochloride 616-96-6
Cycotiamine 6092-18-8
Fursultiamine 804-30-8
Octotiamine 137-86-0
Prosultiamine 59-58-5
Sisbutiamine 3286-46-2
Thiamine Hydrochloride 67-03-8
Thiamine 59-43-8
Thiamine Nitrate 532-43-4
1.4.2 Other Numbers
1.5 Main brand names, main trade names
Monocomponent Products
Aneurin (Germany); Benerva (Eire, Italy, Spain, Sweden, UK,
Brazil); Bénerva (France, Switzerland); Betamin (Australia);
Betalin S (USA); Betabion (Germany); Betatabs (Australia);
Beta-Sol (Australia); Betaxin (Canada); Bewon (Canada);
Bisolvit (Italy) Invite B(1) (Australia);
Multicomponent Products
Alcacyl B1 (Switzerland); Alegrina (Spain); Algimax (France)
Antiadiposo (Italy);Banikol Vitaminé B1 (France); Benexol B1
B6; B12 (Spain); Bénexol (Switzerland); Benevit (Italy);
Benerva (UK); Cheihepan (Germany); Emazian B12 (Italy);
Milgamma (Germany); Neurobion (Germany);
1.6 Main manufacturers, main importers
Wander (Switzerland); Rorer (Australia); Lilly (USA); E.
Merck (Germany); Fawns & McAllan (Australia); Winthrop
(Canada); Wyeth (Canada); Nuovo (Italy); Nelson (Australia);
BioIndustria (Italy); Worwag (Germany); Roche (Switzerland,
Spain, UK); Salus (Italy); Steigerwald (Germany); Martinet
(France)
2. SUMMARY
2.1 Main risks and target organs
Hypersensitivity reactions have occurred, sometimes
progressing to death. Thiamine is relatively non-toxic and
poisoning usually follows a benign course.
2.2 Summary of clinical effects
Adverse effects are highly unusual.
Headache, irritability, tremors, nausea, vomiting, anorexia
and palpitations may occur.
Eczematus reactions and precipitation of episodes of herpes
zoster were reported.
Anaphylactoid reactions: anxiety, pruritus, respiratory
distress, nausea, abdominal pain, angioneurotic edema and
cardiovascular collapse were noted.
2.3 Diagnosis
Diagnosis is based on the above mentioned clinical signs
and symptoms.
Vomitus or gastric aspirate may be collected in clean bottles
for identification.
Blood levels are not needed for diagnosis.
2.4 First aid measures and management principles
Induced vomiting and gastric lavage may be indicated but
must be carefully considered.
Activated charcoal may be useful.
Most cases can be managed with the basic symptomatic and
supportive care.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substance
It is obtained either naturally from rice husk, cereal
grains, liver, yeast, eggs, green beans, milk, tubers and
roots; vegetables, plants, meat and fish . It may also be
obtained synthetically.
(Budavari, 1996; Reynolds, 1996).
3.2 Chemical structure
C12 H17 CIN4 OS - Thiamine Hydrochloride
C12 H17 N5 O4 S - Thiamine Nitrate
Molecular weight
Thiamine Hydrochloride 337.3
Thiamine Nitrate 327.4
Chemical names
Thiamine Hydrochloride
3 - (4 - Amino - 2 - methyl-pyrimidin - 5 - ylmethyl)
5 - (2 - hydroxyethyl) - 4 - methylthiazolium chloride
hydrochloride
Thiamine Nitrate
3 - (4 - Amino - 2 - methylpyrimidin - 5 - ylmethryl)
5 - (2 - hydroxyethyl) - 4 - methylthiazolium nitrate
3.3 Physical Properties
3.3.1 Colour
Thiamine Hydrochloride
Colourless or white (crystals)
White or almost white (powder)
Thiamine Nitrate
Colourless or white (crystals)
White or almost white (powder)
3.3.2 State / Form
Thiamine Hydrochloride
Solid / crystals
Solid / powder
Thiamine Nitrate
Solid / crystals
Solid / powder
3.3.3 Description
Thiamine Hydrochloride
Slight thiazole odour
Bitter Taste
Melting point about 248°C
Soluble in 1 in 1 of water and 1 in 100 of ethanol;
practically insoluble in dehydrated alcohol and ether;
soluble in methanol.
The vitamin is stable in the dry form.
pH of a 0.1% w/v solution in water 3.58
pH of a 1% w/v solution in water 3.13
Thiamine Nitrate
Slight characteristic odour.
Affected by light.
A 2% solution in water has a pH of 6.0 to 7.6.
Soluble in water 2.7 g /100 mL at 25° and
approximately
30 g /100 mL at 100°.
Sparingly soluble in water, freely soluble in boiling
water, slightly soluble in alcohol and in methyl
alcohol.
p.k.a. 4.8 (20°)
(Moffat et al, 1986; Reynolds, 1996).
3.4 Other characteristics
3.4.1 Shelf-life of the substance
No data available
3.4.2 Storage Conditions
Store in airtight, nonmetallic containers.
Protect from light.
4. USES
4.1 Indications
4.1.1 Indications
4.1.2 Description
Thiamine is a water-soluble vitamin that is
used in the treatment and prevention of thiamine
deficiency (Franco, 1982; Gilman et al., 1990).
4.2 Therapeutic Dosage
4.2.1 Adults
Thiamine is usually given by mouth, but may
also be administered by the intramuscular or
intravenous routes.
Mild chronic deficiency
Doses of up to 30 mg daily in single or divided have
been recommended.
Severe deficiency
Doses up to 300 mg daily have been given.
Alcoholic Neuropathy
Doses of 40 mg may be administered by the oral route.
Wernicke - Korsakoff Syndrome
Doses of at least 100 mg should be given, preferably
intravenously.
(Gilman et al., 1990; Goldfrank et al., 1990;
Reynolds, 1996).
4.2.2 Children
Mild chronic deficiency
A dose of 10 to 50 mg given orally 3 times a day
Severe deficiency
A dose of 10 to 25 mg given parenterally 3 times a
day.
4.3 Contraindications
No data available.
5. ROUTES OF ENTRY
5.1 Oral
This is the preferred route (Reynolds, 1996).
5.2 Inhalation
No data available.
5.3 Dermal
No data available.
5.4 Eye
No data available.
5.5 Parenteral
May be administered by the intramuscular or intravenous
routes.
With Wenickeœs encephalopathy thiamine should be given,
preferably intravenously, to ensure adequate absorption.
5.6 Other
No data available.
6. KINETICS
6.1 Absorption by route of exposure
It is well absorbed from the gastrointestinal tract by
Na+ dependent active transport. Absorption is generally
limited to a maximal daily amount of 8 to 15 mg. However,
this amount can be exceeded by oral administration in divided
doses with food.
It is rapidly absorbed after intramuscular administration
(Moffat, 1986; Gilman et al., 1990; Baumgartner, 1991;
Reynolds, 1996).
6.2 Distribution by route of exposure
It is widely distributed throughout the body and appears
in breast milk. Thiamine is not stored to any appreciable
extent in the body.
Within the cell it is present as the diphosphate
(Moffat,1986; Gilman et al., 1990; Reynolds, 1996).
6.3 Biological half-life by route of exposure
No data available.
6.4 Metabolism
About 1 mg. of thiamine is metabolized in the body
daily.
Thiamine pyrophosphate functions in carbohydrate metabolism
as a coenzyme in the decarboxylation of alpha - keto acids,
such as alpha - keto glutarate and pyruvate, and in the
utilization of pentose in the hexose monophosphate shunt. The
latter function involves the thiamine pyrophospate-dependent
enzyme, transketolase (Moffat, 1986; Gilman et al., 1990).
6.5 Elimination and excretion
When intake is at a low level, little or no thiamine is
excreted in the urine. Amounts ingested in excess of the
minimal requirement are excreted in the urine as intact
thiamine or as pyrimidine. As the intake of thiamine is
further increased, more of the excess is excreted unchanged
(Moffat, 1986; Gilman et al., 1990).
7. PHARMACOLOGY AND TOXICOLOGY
7.1 Mode of Action
The physiologically active form of thiamine is the
thiamine pyrophosphate. In the carbohydrate metabolism, it
functions as a coenzyme in the decarboxylation of alpha -
keto acids such as pyruvate and alpha - keto glutarate, and
in the hexose monophosphate shunt. The latter function
involves the thiamine pyrophosphate-dependent enzyme
transketolase. Thiamine also may serve as a modulator of a
neuromuscular transmission. It binds to isolated nicotinic
cholinergic receptors(Gilman et al., 1990).
7.2 Toxicity
7.2.1 Human Data
7.2.1.1 Adults
Thiamine is relatively non-toxic and
adverse reactions are highly unusual with
rare fatalities (Wrenn et al., 1989;
Baumgartner, 1991). Untoward effects of
thiamine therapy may be either purely
allergic, or similar to a thyrotoxic state
(Leitner, 1943).
7.2.1.1 Children
No data available.
7.2.2 Relevant animal data
The direct application of thiamine to a
mammalsœ cortex (dogs) causes seizures (Dias, 1947;
Snodgrass 1992).
Large doses of intravenous injections produce
respiratory failure and death in dogs (Smith et al,
1948; Snodgrass, 1992).
The lethal dose of thiamine hydrochloride by
intravenous injection into rabbits is approximately
126 mg./kg (Halley & Flesher, 1946).
7.2.3 Relevant in vitro data
No data available.
7.3 Carcinogenicity
No data available.
7.4 Teratogenicity
No data available.
7.5 Mutagenicity
No data available.
7.6 Interactions
The risk of an allergic reaction is thought to be
negligible when it is administered together with other B
vitamins (Baumgartner, 1991).
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
Sample collection
Collect sample of lavage, vomitus, blood, and urine for
analysis. Blood levels are not needed to diagnose or treat
the patient.
Biomedical analysis
Arterial gases, electrolytes , routine blood may be useful in
mild to severe hypersensitivity cases.
Toxicological analysis
Thiamine levels are not clinically useful to manage patients.
8.6 References
9. CLINICAL EFFECTS
9.1 Acute Poisoning
9.1.1 Ingestion
Ingestion of supraphysiological doses has not
usually produced toxic effects (Snodgrass, 1992;
Reynolds, 1996).
However, an anaphylactic response may occur after
multiple administrations of the drug (Stephen et al.,
1992).
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
Hypersensitivity reactions have occurred.
Pruritus, respiratory distress, nausea, abdominal
pain, weakness, anxiety, shock and sudden death have
been described. The anaphylactic reactions, were most
often seen after multiple administrations of thiamine
(Leitner, 1943; Stephen et al., 1992).
9.1.6 Other
No data available.
9.2 Chronic Poisoning
9.2.1 Ingestion
After large doses, administered over a long
period of time a syndrome was described with the
following symptoms: hyperthyroidism, nausea and
vomiting, anorexia, headache, irritability, tremors,
and palpitations (Stephen et al., 1992).
9.2.2 Inhalation
No data available.
9.2.3 Skin Exposure
Eczamatous reactions to topical exposure in
pharmaceutical workers has also been observed (Larsen
et al., 1989; Stephen et al., 1992).
9.2.4 Eye Contact
No data available.
9.2.5 Parenteral Exposure
No data available.
9.2.6 Other
No data available.
9.3 Course, prognosis, cause of death
Poisoning in most patients follows a benign course.
Adverse effects are highly unusual.
Anaphylactic reactions have been described after parenteral
administration. The severity may be from very mild to rarely
fatal anaphylactic shock and death may result from
cardiovascular collapse (Baumgartner, 1991; Stephen et al.,
1992; Wrenn & Slovis, 1992).
9.4 Systematic description of clinical effects
9.4.1 Cardiovascular
Acute
No data available.
Chronic
Palpitations were described after oral administration of large doses (Stephen et al.,
1992; Bryson, 1996).
9.4.2 Respiratory
No data available.
9.4.3 Neurological
9.4.3.1 Central nervous system (CNS)
Acute
No data available.
Chronic
Headache, irritability and tremours occurred
after overdosing over a long period of time
(Stephen et al., 1992).
9.4.3.2 Peripheral nervous system
No data available.
9.4.3.3 Autonomic nervous system
No data available.
9.4.3.4 Skeletal and smooth muscle
No data available.
9.4.4 Gastrointestinal
Acute
No data available.
Chronic
Nausea, vomiting, and anorexia were reported after
large doses (Stephen et al., 1992).
9.4.5 Hepatic
No data available.
9.4.6 Urinary
9.4.6.1 Renal
No data available.
9.4.6.2 Other
No data available.
9.4.7 Endocrine and reproductive systems
No data available.
9.4.8 Dermatological
Acute
No data available.
Chronic
Eczematous reactions to topical exposure and
precipitation of episodes of herpes zoster were
reported (Steinberg , 1938; Larsen et al., 1989;
Stephen et al., 1992).
9.4.9 Eye, ear, nose, throat: local effects
No data available.
9.4.10 Haematological
No data available.
9.4.11 Immunological
No data available.
9.4.12 Metabolic
9.4.12.1 Acid-base disturbances
No data available.
9.4.12.2 Fluid and electrolyte disturbances
No data available.
9.4.12.3 Others
No data available.
9.4.13 Allergic Reactions
Acute
Anaphylactoid reactions have occurred after parenteral
administration. They included: respiratory distress,
nausea, abdominal pain, angioneurotic edema,
cardiovascular collapse, sometimes progressing to
death (Baumgartner, 1991; Bryson, 1996; Stephen et
al., 1992; Zanini et al.).
9.4.14 Other Clinical Effects
No data available.
9.4.15 Special Risks
High doses administered during a long period
may produce severe symptoms (Leitner, 1943).
Other
No data available.
Summary
10. MANAGEMENT
10.1 General Principles
Supportive and symptomatic treatment is frequently all
that is needed.
Emesis may be carefully considered in recent substantial
ingestion. However, it is not necessary in most cases because
of the benign nature of thiamine.
Activated charcoal may be administered.
10.2 Life supportive procedures and symptomatic/specific treatment
Make a proper assessment of airway, breathing,
circulation and neurological status.
Maintain a clear airway.
Monitor vital signs.
Correct hypotension / hypertension as required.
10.3 Decontamination
Induced vomiting and gastric lavage is not usually
necessary because of the benign nature of the intoxication.
Activated charcoal may be administered.
10.4 Enhanced elimination
Because of the usually benign nature of the
intoxication, methods of elimination would not be expected to
change the course.
10.5 Antidote treatment
10.5.1 Adults
None available.
10.5.2 Children
None available.
10.6 Management discussion
Not relevant.
11. ILLUSTRATIVE CASES
11.1 Case reports from literature
After administration intravenously of 100 mg of
thiamine hydrochloride, a patient developed anxiety, diffuse
and intense erythema, confusion and sinus tachycardia. He was
discharged on the second day after admission (Stephen et al.,
1992).
In a prospective study evaluating the safety of intravenous
thiamine in emergency department , only one potentially
serious reaction (pruritus) was reported (Wrenn et al., 1989;
Wrenn & Slovis, 1992).
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
Thiamine has an extremely high safety profile. Caution
is advised in administering large doses over a long period of
time and multiple parenteral administrations.
12.2 Other
No data available.
13. REFERENCES
Baumgartner TG (1991) What the practicing nurse should know
about thiamine. J Intravennurs, 14(2): 130-135.
Bryson PD (1996) Comprehensive review in toxicology for emergency
clinicians, 3rd ed. London, Taylor & Francis. pp 404.
Budavari S ed. (1996) The Merck Index: An Encyclopedia of
Chemicals, Drugs, and Biologicals. 12th ed. Merck & Co., Inc,
Whitehouse Station, NJ.
Dias MV (1947) Action of thiamine applied directly to the cerebral
cortex. Science,105: 211-213.
Franco G (1982) Complexo B. In: Franco G. Nutriçœo texto básico e
tabela de composiçao química dos alimentos, Rio de Janeiro,
Livraria Atheneu. pp 31-36.
Gilman AG, Rall TW, Nies AS & Taylor P eds. (1990) Goodman and
Gilmanœs the pharmacological basis of therapeutics, 8th ed. New
York, Pergamon Press, pp 1530-1534.
Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA &
Kulberg AG eds. (1990) Goldfrankœs toxicologic emergencies,
Norwalk, Appleton - Century - Crofts.
Haley TJ & Flesher AM (1946) A toxicity study of thiamine
hydrochloryde.Science,104:567-568.
Larsen Al, Jepsen JR & Thulin H (1989) Allergic contact dermatitis
from thiamine. Contact Dermatitis, 20(5): 387-388.
Leitner ZA (1943) Untoward effects of vitamin B1. Lancet, 2:
474-475.
Moffat AC ed. (1986) Clarkeœs isolation and identification of
drugs in pharmaceuticals, body fluids, and post-mortem material.
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14. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES) COMPLETE
ADDRESS(ES)
Authors: Dr. Rita de Cássia Bomfim Leitœo Higa
Dr. Oscar Higa
Centro de Assistencia Toxicológica de Presidente
Prudente
Hospital Estadual Dr. Odilo Antunes Siqueira
Universidade do Oeste Paulista
Presidente Prudente - Sœo Paulo
Brazil
Address for correspondence:
Av. José Soares Marcondes, 3758
Bairro: Jardim Bongiovanni
Presidente Prudente - Sœo Paulo
CEP 19001-000
Brazil
Telephone: 55.18.221.44.22
55.18.221.90.55
email: ceatox@fipplx.unoeste.br
home page: http://www.unoeste.br/~ceatox
Date: July, 1997
Peer review: INTOX meeting, Rio, Brazil, September, 1997
Editor: Dr. M.Ruse (October, 1998)