[Wiggler11]

Hey everyone I have been on phentermine for over a week now, the side effects are still there, and after researching it for the last couple of days, I came across this info. Its basically info for doctors, but most of the info EVERYONE taking phen or thinking about taking phen should read.

I found another study that said some people have the same reactions after taking one pill that some others who have taken mass quantities of phentermine have had.One important thing is that our bodies are all different and react to this medicine differently.

I wish I had known this before I started. I made the mistake of taking two pills at once not realizing how strong this medicine really was. I got so sick, and the left side of my face went numb for a day. After looking up some of the symptoms, I found that it could have been a sign of a stroke. There are so many other health problems that you can get from taking this medicine, all they tell you is the possible side effects, not what the side effects are telling you about what is going on in your body. I am going to try taking half a pill, and if I still have bad symptoms, I am going off phen completely.

This info refers to phentermine as an amphetamine, even though it is not technically one. The reason they do this is because even though it is only "like" an amphetamine, it still has the same side effects.

The link for this info is
http://www.inchem.org/documents/pims/pharm/pim415.htm

1. NAME

1.1 Substance

Phentermine

1.2 Group

ATC Classification

Antiobesity preparations, excl., diet products (A08A)
Centrally acting antiobesity products (A08A A)

1.3 Synonyms

Duromine; Ionamin; Linyl;
Lipopill; Mirapront;
Normephentermine; Omnibex;
Wilpo

1.4 Identification numbers

1.4.1 CAS numbers

Phentermine 122-09-8

1.4.2 Other numbers

Phentermine hydrochloride CAS 1197-21-3

Phentermine RTECS/NIOSH SH4025000

RCRA waste number P046

1.5 Main brand names, main trade names

1.6 Main manufacturers, main importers

2. SUMMARY

2.1 Main risks and target organs

Acute central nervous system stimulation, cardiotoxicity
causing tachycardia, arrhythmias, hypertension and
cardiovascular collapse. High risk of dependency and abuse.


2.2 Summary of clinical effects

Cardiovascular - Palpitation, chest pain, tachycardia,
arrhythmias and hypertension are common; cardiovascular
collapse can occur in severe poisoning. Myocardial ischaemia,
infarction and ventricular dysfunction are described.

Central Nervous System (CNS) - Stimulation of CNS, tremor,
restlessness, agitation, insomnia, increased motor activity,
headache, convulsions, coma and hyperreflexia are described.
Stroke and cerebral vasculitis have been observed.

Gastrointestinal - Vomiting, diarrhoea and cramps may occur.
Acute transient ischaemic colitis has occurred with chronic
methamphetamine abuse.

Genitourinary - Increased bladder sphincter tone may cause
dysuria, hesitancy and acute urinary retention. Renal failure
can occur secondary to dehydration or rhabdomyolysis. Renal
ischaemia may be noted.

Dermatologic - Skin is usually pale and diaphoretic, but
mucous membranes appear dry.

Endocrine - Transient hyperthyroxinaemia may be noted.

Metabolism - Increased metabolic and muscular activity may
result in hyperventilation and hyperthermia. Weight loss is
common with chronic use.

Fluid/Electrolyte - Hypo- and hyperkalaemia have been
reported. Dehydration is common.

Musculoskeletal - Fasciculations and rigidity may be noted.
Rhabdomyolysis is an important consequence of severe
amphetamine poisoning.

Psychiatric - Agitation, confusion, mood elevation, increased
wakefulness, talkativeness, irritability and panic attacks
are typical. Chronic abuse can cause delusions and paranoia.
A withdrawal syndrome occurs after abrupt cessation following
chronic use.

2.3 Diagnosis

The diagnosis of acute amphetamine poisoning is made on
the history of exposure or abuse, and the characteristic
features of CNS and cardiovascular stimulation. The presence
of amphetamines in urine or blood can support the diagnosis
but is not helpful in management. Whilst some patients show
signs of toxicity at blood concentrations of 20 µg/L, chronic
abusers of amphetamine have been known to have blood
concentration of up to 3000 µg/L.


2.4 First aid measures and management principles

Management of amphetamine and its complications is
essentially supportive.
The initial priority is stabilisation of the airway,
breathing and circulation. Monitoring of pulse, blood
pressure, oxygenation, core temperature and cardiac rhythm
should instituted. Supplemental oxygen should be
administered. Specific supportive care measures that may be
necessary include: maintenance of hydration, control of
seizures, relief of agitation, control of hyperthermia,
control of hypertension, management of rhabdomyolysis.

Decontamination with oral activated charcoal is appropriate
if the patient is conscious.

There are no suitable methods of enhancing elimination of
amphetamine and no specific antidotes.

3. PHYSICO-CHEMICAL PROPERTIES

3.1 Origin of the substance

Synthetic

3.2 Chemical structure

Phentermine

Chemical name:

1,1-Dimethyl-2-phenylethylamine

Other chemical names:

2-Amino-2-methyl-1-phenylpropane
2-Phenyl-tert-butylamine
alpha,alpha-Dimethyl-beta-phenylethylamine
alpha,alpha-Dimethylphenethylamine
Benzeethanamine, alpha,alpha-dimethyl (9CI)
1,1-Dimethyl-2-phenyl-ethanamine

Molecular formula: C10H15N
Molecular weight: 149.2

Phentermine hydrochloride

Chemical name:

Molecular formula: C10H15N,HCl
Molecula weight: 185.7


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

Store in airtight containers. Refrigeration
unnecessary.

4. USES

4.1 Indications

4.1.1 Indications

Antiobesity preparation (not diet product)
Centrally acting antiobesity product

4.1.2 Description

Indications

Appetite suppressant (anorectic) for benzphetamine,
diethypropion, phendimetrazine, phenmetrazine and
phenteramine.

Misuse:

Performance enhancement
Relief of fatigue

Abuse:

Abuse either orally or by injection is extremely
common.

(Dollery, 1991; Reynolds, 1996)

4.2 Therapeutic dosage

4.2.1 Adults

4.2.2 Children


4.3 Contraindications

Anorexia, insomnia, psychopathic personality disorders,
suicidal tendencies, Gilles de la Tourette syndrome and other
disorders, hyperthyroidism, narrow angle glaucoma, diabetes
mellitis and cardiovascular diseases such as angina,
hypertension and arrythmias (Dollery, 1991; Reynolds, 1996).

Amphetamine interacts with several other drugs (see 7.6).

5. ROUTES OF EXPOSURE

5.1 Oral

Readily absorbed from the gastro-intestinal tract and
buccal mucosa. It Is resistant to metabolism by monoamine
oxidase.

5.2 Inhalation

Amphetamine is rapidly absorbed by inhalation and is
abused by this route (Brust, 1993).

5.3 Dermal

No data available.

5.4 Eye

No data available.

5.5 Parenteral

Frequent route of entry in abuse situations.

5.6 Other

No data available.

6. KINETICS

6.1 Absorption by route of exposure

Amphetamine is rapidly absorbed after oral ingestion.
Peak plasma levels occur within 1 to 3 hours, varying with
the degree of physical activity and the amount of food in the
stomach. Absorption is usually complete by 4 to 6 hours.
Sustained release preparations are available as resin-bound,
rather than soluble, salts. These compounds display reduced
peak blood levels compared with standard amphetamine
preparations, but total amount absorbed and time to peak
levels remain similar (Dollery, 1991).


6.2 Distribution by route of exposure

Amphetamines are concentrated in the kidney, lungs,
cerebrospinal fluid and brain. They are highly lipid soluble
and readily cross the blood-brain barrier. Protein binding
and volume of distribution varies widely, but the average
volume of distribution is 5 L/kg body weight (Dollery, 1991).

6.3 Biological half-life by route of exposure

Under normal conditions, about 30% of amphetamine is
excreted unchanged in the urine but this excretion is highly
variable and is dependent on urinary pH. When the urinary pH
is acidic (pH 5.5 to 6.0), elimination is predominantly by
urinary excretion with approximately 60% of a dose of
amphetamine being excreted unchanged by the kidney within 48
hours. When the urinary pH is alkaline (pH 7.5 to 8.0),
elimination is predominantly by deamination (less than 7%
excreted unchanged in the urine); the half-life ranging from
16 to 31 hours (Ellenhorn, 1997).

6.4 Metabolism

The major metabolic pathway for amphetamine involves
deamination by cytochrome P450 to para-hydroxyamphetamine and
phenylacetone; this latter compound is subsequently oxidised
to benzoic acid and excreted as glucuronide or glycine
(hippuric acid) conjugate. Smaller amounts of amphetamine are
converted to norephedrine by oxidation. Hydroxylation
produces an active metabolite, O-hyroxynorephedrine, which
acts as a false neurotransmitter and may account for some
drug effect, especially in chronic users (Dollery, 1991).

6.5 Elimination and excretion

Normally 5 to 30% of a therapeutic dose of amphetamine
is excreted unchanged in the urine by 24 hours, but the
actual amount of urinary excretion and metabolism is highly
pH dependent (Dollery, 1991).

7. PHARMACOLOGY AND TOXICOLOGY

7.1 Mode of action

Amphetamine appears to exert most or all of its effect
in the CNS by causing release of biogenic amines, especialy
norepinephrine and dopamine, from storage sites in nerve
terminals. It may also slow down catecholamine metabolism by
inhibiting monoamine oxidase (Hardman, et al., 1997).


7.2 Toxicity

7.2.1 Human data

7.2.1.1 Adults

The toxic dose varies considerably
due to individual variations and the
development of tolerance. Fatalities have
been reported following ingestion of doses as
low as 1.3 mg/kg, while tolerance has been
developed to 1,000 mg at a time and up to 5 g
in a day.

7.2.1.2 Children

Children appear to be more
susceptible than adults and are less likely
to have developed tolerance.

7.2.2 Relevant animal data

Adult monkeys have an LD50 of 15 to 20 mg/kg,
whereas for young monkeys the LD50 is only 5 mg/kg.

7.2.3 Relevant in vitro data

Not relevant

7.3 Carcinogenicity

To be completed

7.4 Teratogenicity

The use of amphetamine for medical indications does not
pose a significant risk to the fetus for congenital anomalies
(Briggs, 1990). Amphetamines generally do not appear to be
human teratogens. Mild withdrawal symptoms may be observed in
the newborn, but the few studies of infant follow-up have not
shown long-term sequelae, although more studies of this
nature are needed.

Illicit maternal use or abuse of amphetamine presents a
significant risk to the foetus and newborn, including
intrauterine growth retardation, premature delivery and the
potential for increased maternal, fetal and neonatal
morbidity.


These poor outcomes are probably multifactorial in origin,
involving multiple drug use, life-styles and poor maternal
health. However, cerebral injuries occurring in newborns
exposed in utero appear to be directly related to the
vasoconstrictive properties of amphetamines. Ericksson et al.
(1989) followed 65 children whose mothers were addicted to
amphetamine during pregnancy, at least during the first
trimester. Intelligence, psychological function, growth, and
physical health were all within the normal range at eight
years, but those children exposed throughout pregnancy tended
to be more aggressive.

7.5 Mutagenicity

No relevant data

7.6 Interactions

Acetazolamide - administration may increase serum
concentration of amphetamine.

Alcohol - may increase serum concentration of amphetamine.

Ascorbic acid -lowering urinary pH, may enhance amphetamine
excretion

Furazolidone - amphetamines may induce a hypertensive
response in patients taking furazolidone.

Guanethidine - amphetamine inhibits the antihypertensive
response to guanethidine.

Haloperidol - limited evidence indicates that haloperidol may
inhibit the effects of amphetamine but the clinical
importance of this interaction is not established.

Lithium carbonate - isolated case reports indicate that
lithium may inhibit the effects of amphetamine.

Monoamine oxidase inhibitor - severe hypertensive reactions
have followed the administration of amphetamines to patients
taking monoamine oxidase inhibitors.

Noradrenaline - amphetamine abuse may enhance the pressor
response to noradrenaline.

Phenothiazines - amphetamine may inhibit the antipsychotic
effect of phenothiazines, and phenothiazines may inhibit the
anorectic effect of amphetamines.

Sodium bicarbonate - large doses of sodium bicarbonate
inhibit the elimination of amphetamine, thus increasing the
amphetamine effect.


Tobacco smoking - amphetamine appears to induce dose-related
increases in cigarette smoking.

Tricyclic antidepressants - theoretically increases the
effect of amphetamine, but clinical evidence is lacking.

(Stockley, 1994; Dollery, 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 test(s)

8.2.1.3 Simple qualitative 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 test(s)

8.2.2.3 Simple qualitative 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

8.3.1.1.1 Basic analyses

8.3.1.1.2 Dedicated analyses

8.3.1.1.3 Optional analyses

8.3.1.2 Urine

8.3.1.2.1 Basic analyses

8.3.1.2.2 Dedicated analyses

8.3.1.2.3 Optional analyses

8.3.1.3 Other fluids

8.3.2 Arterial blood gas analyses


8.3.3 Haematological analyses

8.3.3.1.1 Basic analyses

8.3.3.1.2 Dedicated analyses

8.3.3.1.3 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

Sample collection

Creatinine, urea, and electrolyte measurement are important
to establish whether renal impairment or hyperkalaemia is
present. Measurements of serum creatine kinase, aspartate
transaminase and myoglobin can help to establish if there is
rhabdomyolysis, and myoglobin can be detected in urine.

Liver function tests are relevant, since hepatitis can occur.

A full blood count and coagulation studies can be helpful,
with measurement of fibrinogen and of fibrin degradation
products, in establishing a diagnosis of disseminated
intravascular coagulation.

Biomedical analysis

Temperature, blood pressure, and pulse rate should be
monitored frequently. A temperature above 40°C, and marked
hypertension and tachycardia are seen in severe poisoning.

An electrocardiogram can be useful in detecting myocardial
ischaemia or arrhythmia. Electrocardiographic monitoring can
be helpful in patients with arrhythmia.

Toxicological analysis

Urine or serum analysis for amphetamine can help to confirm
exposure, but cannot be used to establish poisoning, because
of difference in individual tolerance to amphetamines.

8.6 References


9. CLINICAL EFFECTS

9.1 Acute poisoning

9.1.1 Ingestion

Effects are most marked on the central nervous
system, cardiovascular system, and muscles. The triad
of hyperactivity, hyperpyrexia, and hypertension is
characteristic of acute amphetamine overdosage.

Agitation, confusion, headache, delirium, and
hallucination, can be followed by coma, intracranial
haemorrhage, stroke, and death.

Chest pain, palpitation, hypertension, tachycardia,
atrial and ventricular arrhythmia, and myocardial
infarction can occur.

Muscle contraction, bruxism (jaw-grinding), trismus
(jaw clenching), fasciculation, rhabdomyolysis, are
seen leading to renal failure; and flushing, sweating,
and hyperpyrexia can all occur. Hyperpyrexia can cause
disseminated intravascular coagulation.

(Brust, 1993; Derlet et al., 1989)

9.1.2 Inhalation

The clinical effects are similar to those after
ingestion, but occur more rapidly (Brust, 1993).

9.1.3 Skin exposure

No data available

9.1.4 Eye contact

No data available

9.1.5 Parenteral exposure

Intravenous injection is a common mode of
administration of amphetamine by abusers. The euphoria
produced is more intense, leading to a "rush" or
"flash" which is compared to sexual orgasm (Brust,
1993). Other clinical effects are similar to those
observed after ingestion, but occur more rapidly.

9.1.6 Other

No data available


9.2 Chronic poisoning

9.2.1 Ingestion

Tolerance to the euphoric effects and CNS
stimulation induced by amphetamine develops rapidly,
leading abusers to use larger and larger amounts to
attain and sustain the desired affect.

Habitual use or chronic abuse usually results in toxic
psychosis classically characterised by paranoia,
delusions and hallucinations, which are usually
visual, tactile or olfactory in nature, in contrast to
the typical auditory hallucinations of schizophrenia.
The individual may act on the delusions, resulting in
bizarre violent behaviour, hostility and aggression,
sometimes leading to suicidal or homicidal actions.
Dyskinesia, compulsive behaviour and impaired
performance are common in chronic abusers. The chronic
abuser presents as a restless, garrulous, tremulous
individual who is suspicious and anxious.

9.2.2 Inhalation

As for 9.2.1.

9.2.3 Skin exposure

No relevant data.

9.2.4 Eye contact

No relevant data.

9.2.5 Parenteral exposure

As for 9.2.1.

9.2.6 Other

Vaginal exposure, as for 9.2.1.

9.3 Course, prognosis, cause of death

Symptoms and signs give a clinical guide to the severity
of intoxication as follows (Espelin and Done, 1968):

Mild toxicity - restlessness, irritability, insomnia, tremor,
hyperreflexia, sweating, dilated pupils, flushing;

Moderate toxicity - hyperactivity, confusion, hypertension,
tachypnoea, tachycardia, mild fever, sweating;


Severe toxicity - delirium, mania, self-injury, marked
hypertension, tachycardia, arrhythmia, hyperpyrexia,
convulsion, coma, circulatory collapse.

Death can be due to intracranial haemorrhage, acute heart
failure or arrhythmia, hyperpyrexia, rhabdomyolysis and
consequent hyperkalaemia or renal failure, and to violence
related to the psychiatric effects (Kalant & Kalant, 1975).

9.4 Systematic description of clinical effects

9.4.1 Cardiovascular

Cardiovascular symptoms of acute poisoning
include palpitation and chest pain. Tachycardia and
hypertension are common. One third of patients
reported by Derlet et al. (1989) had a blood pressure
greater than 140/90 mmHg, and nearly two-thirds had a
pulse rate above 100 beats per minute.

Severe poisoning can cause acute myocardial ischaemia,
myocardial infarction (Carson et al., 1987; Packe et
al., 1990), and left ventricular failure (Kalant &
Kalant, 1975). These probably result from vasospasm,
perhaps at sites of existing atherosclerosis. In at
least one case, thrombus was demonstrated initially
(Bashour, 1994).

Chronic oral amphetamine abuse can cause a chronic
cardiomyopathy; an acute cardiomyopathy has also been
described (Call et al., 1982).

Hypertensive stroke is a well-recognised complication
of amphetamine poisoning (see 9.4.3).

Intra-arterial injection of amphetamine can cause
severe burning pain, vasospasm, and gangrene (Birkhahn
& Heifetz, 1973).

9.4.2 Respiratory

Pulmonary fibrosis, right ventricular
hypertrophy and pulmonary hypertension are frequently
found at post-mortem examination.

Pulmonary function tests usually are normal except for
the carbon monoxide diffusing capacity. Respiratory
complications are sometimes caused by fillers or
adulterants used in injections by chronic users. These
can cause multiple microemboli to the lung, which can
lead to restrictive lung disease.


Pneumomediastinum has been reported after amphetamine
inhalation (Brust, 1993).

9.4.3 Neurological

9.4.3.1 Central nervous system (CNS)

Main symptoms include agitation,
confusion, delirium, hallucinations,
dizziness, dyskinesia, hyperactivity, muscle
fasciculation and rigidity, rigors, tics,
tremors, seizures and coma.

Both occlusive and haemorrhagic strokes have
been reported after abuse of amphetamines.
Twenty-one of 73 drug-using young persons
with stroke had taken amphetamine (Kaku &
Lowenstein, 1990), of whom six had documented
intracerebral haemorrhage and two had
subarachnoid haemorrhage. Patients with
underlying arteriovenous malformations may be
at particular risk (Selmi et al., 1995).

Stroke can occur after oral, intravenous, or
nasal administration. Severe headache
beginning within minutes of ingestion of
amphetamine is usually the first symptom. In
more than half the cases, hypertension which
is sometimes extreme, accompanies other
symptoms. A Cerebral vasculitis has also been
observed (Brust, 1993).

Dystonia and dyskinesia can occur, even with
therapeutic dosages (Mattson & Calverley,
1968).

Psychiatric effects, particularly euphoria
and excitement, are the motives for abuse.
Paranoia and a psychiatric syndrome
indistinguishable from schizophrenia are
sequelae of chronic use ( Hall et al., 1988;
Flaum & Schultz, 1996; Johnson & Milner,
1966).

9.4.3.2 Peripheral nervous system

No relevant data


9.4.3.3 Autonomic nervous system

Stimulation of alpha-adrenergic
receptors produces mydriasis, increased
metabolic rate, diaphoresis, increased
sphincter tone, peripheral vasoconstriction
and decreased gastrointestinal motility.

Stimulation of ß-adrenergic receptors
produces increased heart rate and
contractility, increased automaticity and
dilatation of bronchioles.

9.4.3.4 Skeletal and smooth muscle

Myalgia, muscle tenderness, muscle
contractions, and rhabdomyolysis, leading to
fever, circulatory collapse, and
myoglobinuric renal failure, can occur with
amphetamines (Kendrick et al., 1977).

9.4.4 Gastrointestinal

Most common symptoms are nausea, vomiting,
diarrhoea, and abdominal cramps. Anorexia may be
severe. Epigastric pain and haematemesis have been
described after intravenous amphetamine use. A case of
ischaemic colitis with normal mesenteric arteriography
in a patient taking dexamphetamine has been described
(Beyer et al., 1991).

9.4.5 Hepatic

Hepatitis and fatal acute hepatic necrosis have
been described (Kalant & Kalant, 1975).

9.4.6 Urinary

9.4.6.1 Renal

Renal failure, secondary to dehydration
or rhabdomyolysis may be observed.

9.4.6.2 Other

Increased bladder sphincter tone may
cause dysuria, hesitancy and acute urinary
retention. This effect may be a direct result
of peripheral alpha-agonist activity.


Spontaneous rupture of the bladder has been
described in a young woman who took alcohol
and an amphetamine-containing diet tablet
(Schwartz, 1981).

9.4.7 Endocrine and reproductive systems

Transient hyperthyroxinaemia may result from
heavy amphetamine use (Morley et al., 1980).

9.4.8 Dermatological

Skin is usually pale and diaphoretic, but
mucous membranes appear dry. Chronic users may display
skin lesion, abscesses, ulcers, cellulitis or
necrotising angiitis due to physical insult to skin,
or dermatologic signs of dietary deficiencies, e.g.
cheilosis, purpura.

9.4.9 Eye, ear, nose, throat: local effects

Mydriasis may be noted.
Diffuse hair loss may be noted.
Chronic users may display signs of dietary
deficiencies.

9.4.10 Haematological

Disseminated intravascular coagulation is an
important consequence of severe poisoning ( Kendrick
et al., 1980).
Idiopathic thrombocytopenic purpura may occur.

9.4.11 Immunological

No relevant data.

9.4.12 Metabolic

9.4.12.1 Acid-base disturbance

No relevant data

9.4.12.2 Fluid and electrolyte disturbance

Increase metabolic and muscular activity
may result in dehydration.

9.4.12.3 Others

No data available


9.4.13 Allergic reactions

No relevant data

9.4.14 Other clinical effects

No relevant data

9.4.15 Special risks

Pregnancy: Eriksson et al. (1989) followed 65
children whose mother were addicted to amphetamine
during pregnancy, at least during the first trimester.
Intelligence, psychological function, growth, and
physical health were all within the normal range at
eight years, but those exposed throughout pregnancy
tended to be more aggressive.

A case report describes a normal female infant born to
mother who took up to 180 mg/day of dexamphetamine for
narcolepsy throughout pregnancy (Briggs et al., 1975).

Breast-feeding: Amphetamine is passed into breast
milk and measurable amounts can be detected in
breast-fed infant's urine. Therefore lactating mothers
are advised not to take or use amphetamine.

9.5 Other

Amphetamine withdrawal syndrome: Abrupt discontinuance
following chronic use is characterised by apathy, depression,
lethargy, anxiety and sleep disturbances. Myalgias, abdominal
pain, voracious appetite and a profound depression with
suicidal tendencies may complicate the immediate
post-withdrawal period and peak in 2 to 3 days. To relieve
these symptoms, the user will often return to use more
amphetamine, often at increasing doses due to the tolerance
which is readily established. Thus a cycle of
use-withdrawal-use is established (Kramer et al., 1967; Hart
& Wallace, 1975). Physical effects are not life threatening
but can lead to a stuporose state (Tuma, 1993); the
associated depression can lead to suicide. It may take up to
eight weeks for suppressed REM (rapid eye movement ) sleep to
return to normal (Brust 1993).

"Overamped": When the intravenous dosage is increased too
rapidly the individual develops a peculiar condition referred
to as "overamped: in which he or she is conscious but unable
to speak or move. Elevated blood pressure, temperature and
pulse as well as chest distress occurs in this setting. Death
from overdose in tolerant individuals is infrequent.


9.6 Summary

10. MANAGEMENT

10.1 General principles

General supportive measures should be used. These
should include stabilisation of the airway, breathing, and
circulation; relief of agitation, adequate hydration, and
control of core temperature. Convulsions, hyperthermia, and
rhabdomyolysis may require specific treatment. Activated
charcoal may be helpful for decontamination after oral
ingestion. Ipecacuanha is contra-indicated because of its
stimulant properties. There are no effective methods of
enhancing elimination and no antidote.

Agitation and convulsion can be treated with diazepam. If
agitation is severe, then chlorpromazine may have specific
advantages over other major tranquillisers (Espelin & Done,
1968; Klawans, 1968). Parenteral dosages of 0.5 to 2
milligrams per kilogram have been used in Infants (Espelin &
Done, 1968).

Severe hyperthermia (core temperature greater than 40°C)
requires forced cooling by fans, tepid sponging or other
means, and may also require the administration of diazepam or
dantrolene or both agents in order to eliminate muscle
activity.

Rhabdomyolysis associated with muscle overactivity can cause
hyperkalaemia or renal failure, and should be treated
conventionally. Dialysis may be needed if renal failure
supervenes.

Acute severe hypertension (diastolic blood pressure greater
than 100 mmHg) can be controlled by infusion of sodium
nitroprusside by continuous intravenous infusion at an
initial rate of 3 mcg/kg/min, titrated to achieve the desired
response.

Patients who are addicted to amphetamines may develop the
withdrawal syndrome described in 9.5.

10.2 Life supportive procedures and symptomatic/specific
treatment

Treatment is supportive. Administration of
supplemental oxygen, establishment of intravenous access and
monitoring of vital signs including core temperature, and
cardiac rhythm are recommended. The following may be
necessary according to clinical indication:


-Maintenance adequate airway and ventilation
-Rehydration with intravenous fluids
-Control of seizures
-Control of agitation with benzodiazepines
-Control of severe hypertension (diastolic blood pressure
greater than 110 mmHg)
-Control of hyperthermia
-Treatment of hyperkalaemia
-Cardiac intensive care for ischaemia or arrhythmia

10.3 Decontamination

No regime of oral decontamination has been demonstrated
to improve outcome. Ipecacuanha is contra-indicated. Oral
activated charcoal may be helpful following oral overdosage.

10.4 Enhanced elimination

No regime of decontamination has been demonstrated to
improve outcome. Forced acid diuresis has been abandoned as a
decontamination procedure. Neither haemodialysis nor charcoal
haemoperfusion is likely to be of benefit.

10.5 Antidote treatment

10.5.1 Adults

There is no antidote to amphetamine poisoning.

10.5.2 Children

There is no antidote to amphetamine poisoning.

10.6 Management discussion

There are differences between dexamphetamine and
related compounds such as 3,4-methylenedeoxymetamphetamine
("ecstacy"); for example, hyperthermia appears to be more of
a problem with the latter, and this may be because of the
association between use and frenetic physical activity
("rave" dancing) (Henry et al., 1992).

In the past, energetic gastric decontamination procedures
were suggested (Espelin & Done, 1968). There is no evidence
that such procedures improve outcome in amphetamine
poisoning, and they are potentially hazardous.

Oral activated charcoal is probably the safest option for
decontamination, but is only likely to bind drug in the
stomach if a substantial oral dose of amphetamine has been
taken, and the charcoal is given within an hour or two of
ingestion. If should only administered to patients in whom
swallowing and gag reflexes are intact. In drug smugglers who

have swallowed supposedly inert packages of amphetamines
("stuffers" or "packers"), and who develop symptoms because
of leakage from the packages, then repeated doses of oral
activated charcoal with a cathartic are likely to be
worthwhile.

Forced acid diuresis has now been abandoned as an elimination
treatment, because it is intrinsically difficult and
potentially dangerous.

Treatment of agitation in amphetamine poisoning is required
when a patient is a danger to himself or herself, or to
others. Because poisoning is associated with sympathetic
overactivity, and chlorpromazine has alpha-adrenoreceptor
antagonist actions, chlorpromazine has been recommended as
the sedative treatment of choice (see 10.1). There is no
study to demonstrate that chlorpromazine is in fact superior
to benzodiazepine.

11. ILLUSTRATIVE CASES

11.1 Case reports from literature

Ingestion of 2.2g (28mg/kg) in a 21 year old man
resulted in severe toxicity (Ginsberg et.al., 1970).

An 18 month old male infant ingested an unknown amount of
amphetamine, subsequently detected in the urine. He had a
history of restlessness and vomiting for 10 hours and was
admitted to hospital with mild fever (38°C), pulse rate of
140 per minute and respiratory rate of 34 per minute. He
looked acutely unwell, hyperactive and combative and had
normal pupils with a bi-lateral light reflex. Some irregular
flushing was found over the skin of the trunk. He was given
diazepam 10mg intravenously, 10% chloral hydrate 10ml
rectally and haloperidol 20mg intravenously. After a sleep of
20 hours normal activity resumed and the patient was
clinically well and discharged (Soong et.al., 1991).

A 20-month-old male infant was admitted to hospital with a
history of being too restless, hyperactive and agitated to be
manageable for several hours, and had not responded to 10mg
diazepam given intravenously in a local medical clinic. He
had dilated pupils, doll's eyes and normal discs. Generalised
hypperreflexia and a mild clonus were noted, but no focal
neurological abnormalities could be found. His vital signs
were - blood pressure 130/90 mmHg, pulse rate 150/min,
respiratory rate 46/min and normal temperature. The clinical
status remained unchanged for a further 18 hours and the
patient then calmed down to sleep for 20 hours. Subsequently
the parents found amphetamine powder spread near the infant's
bed (Soong, et.al., 1991).


12. ADDITIONAL INFORMATION

12.1 Specific preventive measures

When prescribing amphetamines, due regard must be given
to its potential for misuse and addiction.

12.2 Other

No data available.

[kimmieq]

Thats was very interesting. Thanks for posting this. I wonder how many people will stop using phen after reading this....Thank God I havent had any of these problems, but I will definatly be a bit more careful. I have taken 2 pills total throughout a day, but never 2 at the same time. I am too scared..lol even more so now. I have used actual amphetamine before, and the effects were similar to the effects of phen, but way way more increased. I mean to the point where I could not even sit for 5 minutes. Thank God that the phen does not do that to me.

[real-sistah]

Thank you so much for posting that. I too, have never taken more than one pill a day. I take mine very early in the day and have only had dry mouth. Very thankful that I've never had any other side effects. But, truth is that a lot of us (myself included) are so anxious to lose weight and get control of our lives that we may ignore the side effects as long as the medicine is working. This is my second time on phen and it seemed to be the only thing that worked for me along with changing my eating habits. Good luck on your journey and thank you again for the post.

[usuallytiny]

narcan is a shot that paramedics carry,,, it is used on meth addicts as well as opiates and it makes you almost instantly sober if given a high dose a small dose counteracts the amphetimines in your system. they dont revive a person completely because the shock is too great to their system and they come up swinging i asked my dr and he said there is a large difference in phentermine and street drugs first in makeup and second in usage.... nobody sits around all day smoking phentermine.

[LosingIt4JessnAsh]

I agree with Tiny , Doctors would not perscribe it if it were anything like a street drug...There are risks and side effects with everything you do , and I feel that the risks and side effects of overeating and becoming obese are just as great as those from taking the phen...Obesity is a KILLER plain and simple..so i think with the phen the good outweighs the bad..if you stop and think about it , Obesity can cause diabetes , Heart disease , heart attack , stoke , sleep apneia , the list goes on and on..so I see no big difference myself...I would rather take the risk of losing the weight with the phen , than stay fat and slowly kill myself.....EITHER WAY , there are going to be side effects..but again this is JMO..and I do appreciate you posting your concerns...

[etadpole06]

My weight Dr sat me down in his office for over 2 hrs telling me everything I needed to know about this drug.. according to him it is VERY safe, one of the safest on the market today.. if I can't trust him, who can I trust? Another thing I have learned... to stop reading those kinds of reports on the internet... if you do it long enough, you'll have diagnosed yourself with every ailment known to mankind!

[mammaca2u]

It's important to know the side effects of any drug you are taking and those that go to a doctor for their Phen. are aware of this. However, there are many people that buy Phentermine from the internet and are not being monitored on a regular basis by a doctor. These are the ones that need to be aware of the side effects because serious problems could occur.