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Info on the PBT pills we took...

n/an/a Member Posts: 168,427
edited September 2006 in US Military Veteran Forum
PYRIDOSTIGMINE BROMIDE Tablets, USP
30 mg
Rx only
CAUTION!
PYRIDOSTIGMINE BROMIDE IS FOR USE AS A PRETREATMENT FOR
EXPOSURE TO THE CHEMICAL NERVE AGENT SOMAN. PYRIDOSTIGMINE
ALONE WILL NOT PROTECT AGAINST EXPOSURE TO SOMAN. THE
EFFICACY OF PYRIDOSTIGMINE IS DEPENDENT UPON THE RAPID USE OF
ATROPINE AND PRALIDOXIME (2-PAM) AFTER SOMAN EXPOSURE.
PRIMARY PROTECTION AGAINST EXPOSURE TO CHEMICAL NERVE
AGENTS IS THE WEARING OF PROTECTIVE GARMENTS INCLUDING MASKS,
HOODS AND OVERGARMENTS DESIGNED SPECIFICALLY FOR THIS USE.
INDIVIDUALS MUST NOT RELY SOLELY UPON PRETREATMENT WITH
PYRIDOSTIGMINE AND THE ANTIDOTES ATROPINE AND PRALIDOXIME (2-
PAM) TO PROVIDE COMPLETE PROTECTION FROM POISONING BY THE
CHEMICAL NERVE AGENT SOMAN.
PYRIDOSTIGMINE MUST NOT BE TAKEN AFTER EXPOSURE TO SOMAN. IF
PYRIDOSTIGMINE IS TAKEN IMMEDIATELY BEFORE EXPOSURE (E.G.,
WHEN THE GAS ATTACK ALARM IS GIVEN) OR AT THE SAME TIME AS
POISONING BY SOMAN, IT IS NOT EXPECTED TO BE EFFECTIVE, AND MAY
EXACERBATE THE EFFECTS OF A SUB-LETHAL EXPOSURE TO SOMAN.
FOR MILITARY COMBAT MEDICAL USE ONLY
DESCRIPTION
Pyridostigmine bromide tablets, USP 30 mg. Pyridostigmine bromide is an orally active
cholinesterase inhibitor. Its chemical name is: 3-hydroxy-1-methylpyridinium bromide
dimethylcarbamate.
CAS registration number is 101-26-8.
White tablet each imprinted with letters "PBT".
Pyridostigmine bromide has a molecular formula of C9H13BrN202, a molecular weight of
261.12, and the following molecular structure:
The inactive ingredients included in the tablet formula are: colloidal silicon dioxide, lactose
anhydrous, and stearic acid or, alternatively; lactose, starch, silica precipitated, talc, and
magnesium stearate.
ANIMAL PHARMACOLOGY
Evidence of the effectiveness of pyridostigmine as a pre-treatment for Soman poisoning was
obtained from studies in animals alone, because it is clearly unethical to perform such studies
in humans. While the results of these animal studies cannot be extrapolated to humans with
certainty, the extrapolation is supported by the reasonably well understood pathophysiologic
mechanisms of the toxicity of Soman and the mechanism of the protective effect of
pyridostigmine pre-treatment, as examined in various animal species. In addition, the results
of these animal studies establish that pyridostigmine is reasonably likely to produce clinical
benefit in humans. The section below explains the current understanding of the mechanism of
Soman toxicity and the beneficial effect of pyridostigmine pre-treatment, as well as the basis
for extrapolating the animal findings to humans.
Pyridostigmine pretreatment has been shown in animals to decrease the lethality of the nerve
agent Soman, provided atropine and pralidoxime (2-PAM) are administered immediately after
exposure to Soman. The mechanism of Soman induced death is reasonably well-understood;
death is believed to result primarily from respiratory failure due to irreversible inhibition of
the enzyme acetylcholinesterase and the consequent increase in the level of the
neurotransmitter acetylcholine 1) at nicotinic receptors at the neuromuscular junction,
resulting in pathological stimulation and ultimate failure of the muscles of respiration, 2) at
muscarinic receptors in secretory glands and smooth muscle, resulting in excessive respiratory
secretions and bronchoconstriction, and 3) at cholinergic receptors in the brain, resulting in
central respiratory depression. The effect of pyridostigmine is presumed to result from its
reversible inhibition of a critical number of acetylcholinesterase active sites in the peripheral
nervous system, protecting them from irreversible inhibition by Soman. (Pyridostigmine is
not thought to enter the brain in significant amounts.) When the pyridostigmine-induced
inhibition of the enzyme is subsequently reversed, there is a small residual amount of enzyme
activity that is adequate to sustain life (provided atropine and 2-PAM are subsequently
administered). An implication of this presumed mechanism is that it is not helpful to give
pyridostigmine either just before or during exposure to Soman.
Rhesus monkeys were given oral doses of pyridostigmine every 8 hours for a total of 6 doses,
and were challenged with Soman given intramuscularly 5 hours after the last pyridostigmine
dose. Two dosage groups of pyridostigmine were used: a low dose group given 1.2 mg/kg for
all 6 doses, and a high dose group given 1.2 and 1.8 mg/kg for the first and second doses,
respectively, and 2.4 mg/kg for the final 4 doses. These animals were also given atropine and
2-PAM after exposure to Soman. An untreated control group, and a group given atropine and
2-PAM (but not pyridostigmine), were also used. The primary endpoint in this study was a
decrease in the lethality of Soman expressed as an increase in the LD 50 (the dose of Soman
that killed 50 % of the animals). The atropine/2-PAM control group showed a small but
statistically significant 1.6 fold increase in the Soman LD 50 compared to the untreated
control group. The groups given pyridostigmine as well as atropine and 2-PAM showed
increases in the Soman LD50 of at least 40 fold compared to the untreated control group and
at least 25 fold compared to the atropine/2-PAM group. The two dose levels of
pyridostigmine showed similar effectiveness.
Additional studies in rhesus monkeys and guinea pigs also showed effectiveness of
pyridostigmine (in the presence of post-Soman administration of atropine and 2-PAM). The
magnitude of effect in guinea pigs was smaller than that in monkeys (Soman LD 50 increased
4-7 fold compared to untreated control and 2-4 fold compared to atropine/2-PAM alone).
Pyridostigmine produced only small and inconsistent effects in studies in rats, mice and
rabbits. It is thought that the effect of pyridostigmine in rats and mice is masked by high
blood levels of the enzyme carboxylesterase, which eliminates Soman from blood and makes
those species highly resistant to Soman. In a study in which rats were given an inhibitor of
carboxylesterase, pretreatment with pyridostigmine plus atropine increased the LD 50 of
Soman 8.5 fold compared to untreated controls. Humans have little or no carboxylesterase in
blood.
Animal studies have shown that pyridostigmine pretreatment was effective only when animals
were given atropine and 2-PAM after exposure to Soman.
CLINICAL PHARMACOLOGY
Pharmacokinetics
Pyridostigmine bromide is poorly absorbed from the gastrointestinal tract with an absolute
bioavailability of 10-20%. Following a single oral dose of 30 mg pyridostigmine bromide in
the fasting state, the TMAX was 2.2 ? 1.0 hours. The pharmacokinetics of pyridostigmine
bromide is linear over the dose range of 30-60 mg. Following multiple doses of
pyridostigmine bromide (30 mg every 8 hours for 21 days), the average steady-state trough
concentration of pyridostigmine was about ? of the peak concentration after a single dose.
The volume of distribution was about 19 ? 12 liters, indicating that pyridostigmine distributes
into tissues. No information on protein binding of pyridostigmine is available.
Pyridostigmine undergoes hydrolysis by cholinesterases and is metabolized in the liver. It is
excreted in the urine both as unchanged drug and its metabolites. The systemic clearance of
pyridostigmine bromide is 830 mL/min and the elimination half-life of pyridostigmine
bromide is approximately 3 hours.
Renal Dysfunction
In anephric patients (n=4), the elimination half-life increased 3 fold and the systemic
clearance decreased by 75%. Therefore caution should be observed when administering
pyridostigmine bromide to patients with impaired renal function.
Hepatic Impairment
No information is available on the pharmacokinetics of pyridostigmine in hepatic impaired
patients.
Gender
The clearance of pyridostigmine bromide is not influenced by gender.
Elderly
In a pyridostigmine study in the elderly (71-85 years), the elimination half-life of
pyridostigmine was similar to the half-life in the young (21-51 years). However, the systemic
plasma clearance was 30% lower in the elderly.
INDICATIONS AND USAGE
Pyridostigmine bromide is indicated for prophylaxis against the lethal effects of soman nerve
agent poisoning. Pyridostigmine is intended to be used in conjunction with protective
garments, including a gas mask, and immediate atropine and pralidoxime therapy at the first
sign of nerve agent poisoning. Pyridostigmine should be stopped at the first sign of nerve
agent poisoning.
The evidence for the effectiveness of pyridostigmine as prophylaxis against Soman-induced
toxicity was derived from animal studies alone. (see ANIMAL PHARMACOLOGY)
CONTRAINDICATIONS
Pyridostigmine bromide is contraindicated in mechanical intestinal or urinary obstruction.
Do not administer to personnel with known hypersensitivity to anticholinesterase agents
WARNINGS (see CAUTION at beginning of this label)
Pyridostigmine pretreatment offers no benefit against the nerve agent Soman unless the
nerve agent antidotes atropine and pralidoxime are administered once symptoms of
poisoning appear. Pyridostigmine should be discontinued at the first sign of nerve agent
poisoning since it may exacerbate the effects of a sub-lethal exposure to Soman.
Pyridostigmine should be used with caution in patients with bronchial asthma, chronic
obstructive pulmonary disease, bradycardia, cardiac arrhythmias, and people being treated for
hypertension or glaucoma with beta adrenergic receptor blockers.
Caution should be taken when administering pyridostigmine bromide to individuals with
known bromide sensitivity. The risks and benefits of administration must be weighed against
the potential for rash or other adverse events in these individuals.
PRECAUTIONS
General
If personnel experience serious side effects such as difficult breathing, severe dizziness, or
loss of consciousness as a result of ingestion of pyridostigmine bromide, they should be
advised to temporarily discontinue use of product and seek immediate medical attention.
Serious adverse events should be reported to their commander and responsible medical
officer.
Information for Patients
See Patient Information Sheet.
Drug Interactions
A potential interaction between the antimalarial drug mefloquine and pyridostigmine bromide
exists through a possible additive effect on the gastrointestinal tract. The most common
complaint about both drugs is loose bowels. It has been reported that simple additive effects
on the atrial rate occur when mefloquine and pyridostigmine bromide are combined.
Because anticholinesterase drugs are often used in the treatment of glaucoma, the use of
pyridostigmine bromide in such situations may have an additive effect that may cause or
exacerbate problems with night vision.
The bradycardia associated with the use of narcotics may exacerbate pyridostigmine-induced
bradycardia.
Particular caution should be observed in the administration of depolarizing neuromuscular
blocking agents (e.g., succinylcholine) during surgery since the degree of neuromuscular
blockade that ensues may be enhanced by previously administered pyridostigmine bromide.
Doses of non-depolarizing neuromuscular blocking agents (e.g., pancuronium bromide) may
need to be increased in patients previously administered pyridostigmine. Atropine antagonizes
the muscarinic effects of pyridostigmine, and this interaction is utilized to counteract the
muscarinic symptoms of pyridostigmine toxicity. Anticholinesterase agents are sometimes
effective in reversing neuromuscular block induced by aminoglycoside antibiotics. However,
aminoglycoside antibiotics, local and some general anesthetics, antiarrhythmic agents, and
other
drugs that interfere with neuromuscular transmission should be used cautiously, if at all.
Theoretically, drugs such as dexpanthenol, which are converted to pantothenic acid in vivo,
may have additive effects with pyridostigmine by increasing production of acetylcholine.
Carcinogenesis, Mutagenesis, Impairment Of Fertility
Carcinogenicity: No long-term studies to evaluate carcinogenicity have been performed in
animals.
Mutagenicity: Pyridostigmine was mutagenic and clastogenic in an in vitro mammalian gene
mutation assay in mouse lymphoma cells, in the presence of metabolic activation only.
Pyridostigmine was not mutagenic in an in vitro bacterial reverse mutation assay (Ames Test)
and in an in vitro mammalian gene mutation assay in Chinese hamster ovary cells, and was
not clastogenic in an in vitro assay in Chinese hamster ovary cells or in an in vivo mouse
micronucleus assay.
Impairment of Fertility: Pyridostigmine did not impair fertility in male and female rats given
oral doses of up to 45 mg/kg/day (5 times the recommended human daily dose of 90 mg on a
mg/m2 basis) beginning at 10 (males) or 2 (females) weeks prior to mating.
Pregnancy Pregnancy Category B
Pyridostigmine produced no teratogenic effects in rats given up to 30 mg/kg/day and in
rabbits given up to 45 mg/kg/day orally during the period of organogenesis. These doses are 3
and 10 times, respectively, the recommended human dose of 90 mg on a mg/m2 basis. In rats,
a slight degree of delayed skeletal ossification was seen at 30 mg/kg, a dose which caused
maternal toxicity, and a slight increase in the incidence of hydronephrosis was seen at all dose
levels (lowest dose tested was 3 mg/kg). In rabbits, a slight increase in the incidence of
hydronephrosis was seen at 45 mg/kg, a dose which caused maternal toxicity, and increased
incidences of blood vessel variations were seen at all doses (lowest dose tested was 5 mg/kg).
There are no adequate and well-controlled studies in pregnant women. Because animal
reproduction studies are not always predictive of human response, this drug should be used
during pregnancy only if clearly needed.
Nursing Mothers
It is not known whether this drug is excreted in human milk. Because many drugs are excreted
in human milk caution should be exercised when pyridostigmine is administered to a nursing
woman.
Pediatric Use
Safety and effectiveness in pediatric patients have not been established.
Geriatric Use
Clinical studies of pyridostigmine did not contain sufficient numbers of subjects aged 65 and
over to determine whether they respond differently from younger subjects. In general, dose
selection for an elderly patient should be cautious, reflecting the greater frequency of
decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug
therapy.
In the elderly (71-85 years of age) the elimination half-life, volume of distribution (central
and steady state) were comparable with the young (21-51 years of age). However the systemic
plasma clearance was significantly lower in the elderly compared to the young (6.7 ? 2.2 vs.
9.5 ? 2.7 ml/min/kg).
This drug is known to be substantially excreted by the kidney, and the risk of toxic reactions
to this drug may be greater in patients with impaired renal function. Because elderly patients
are more likely to have decreased renal function, care should be taken in dose selection, and it
may be useful to monitor renal function.
ADVERSE REACTIONS
The side effects of pyridostigmine bromide are typically of two varieties, muscarinic and
nicotinic. Muscarinic side effects include abdominal cramps, bloating, flatulence, diarrhea,
emesis, increased peristalsis, nausea, hypersalivation, urinary incontinence, increased
bronchial secretion, diaphoresis, miosis, and lacrimation. Nicotinic side effects are comprised
chiefly of muscle cramps, fasciculations, and weakness.
Pyridostigmine is a quaternary ammonium compound and does not readily cross the bloodbrain
barrier. Compared to the peripheral effects of pyridostigmine bromide, central nervous
system manifestations are less frequent and less serious, primarily consisting of headache and
vertigo, with minor and clinically insignificant changes in heart rate, blood pressure, and
respiratory function.
Extremely high doses may produce CNS symptoms of agitation, restlessness, confusion,
visual hallucinations, and paranoid delusions. Electrolyte abnormalities, possibly resulting
from high serum bromide concentrations, also have been reported. Death may result from
cardiac arrest or respiratory paralysis and pulmonary edema.
In a controlled study of 90 healthy volunteers comparing pyridostigmine 30 mg every 8 hours
to placebo for 21 days, the following incidence of adverse events was reported.
Table 1: Incidence of Adverse Events - 2%
Event: %
Pyridostigmine
N = 60
%
Placebo
N = 30
Diarrhea 7 0
Abdominal Pain 7 0
Dysmenorrhea 5 0
Twitch 3 0
Myalgia 2 0
Dry Skin 2 0
Urinary Frequency 2 0
Epistaxis 2 0
Amblyopia 2 0
Hypesthesia 2 0
Neck Pain 2 0
Other less common adverse events seen during controlled and uncontrolled clinical trials for
pyridostigmine include the following:
Pulmonary : Exacerbation of acute bronchitis and asthma
Cardiovascular: Elevated blood pressure, decreased heart rate (4-6 beats per
minutes), chest tightness
Eyes: Change in vision, eye pain
Neurologic: Headache, hypertonia, difficulty in concentrating, confusion,
disturbed sleep, tingling of extremities, numbness of the tongue
Skin: Increased sweating, rash, alopecia
Digestive: Vomiting, borborygmi, nausea, bloating, flatulence
General: Warm sensation, lethargy/drowsiness, depressed mood
During safety studies at the recommended dosage, there were two reports of loss of
consciousness, one of which also included urinary and fecal incontinence, stiffness of the
upper torso and arms, post syncopal skin pallor, post syncopal confusion, and post syncopal
weakness (suggesting a seizure event).
As with any compound containing bromide, a skin rash may be observed in an occasional
patient, which usually subsides promptly upon discontinuance of the medication.
DRUG ABUSE AND DEPENDENCE
Although the abuse potential of pyridostigmine has not been specifically assessed, no abuse
of, tolerance to, withdrawal from, or drug-seeking behavior was observed in patients who
received pyridostigmine in clinical trials. Cholinesterase inhibitors are not believed to be
associated with drug abuse.
OVERDOSAGE
As is true of all cholinergic drugs, overdosage of pyridostigmine bromide may result in
cholinergic crisis, a state characterized by increasing muscle weakness that, through
involvement of the muscles of respiration, may lead to death. Overdosage with
pyridostigmine must be differentiated from the acute manifestations of nerve agent poisoning
which may also be characterized by a cholinergic crisis. Atropine should be used to treat
pyridostigmine overdosage.
In the treatment of pyridostigmine overdosage, maintaining adequate respiration is of primary
importance. Tracheostomy, bronchial aspiration, and postural drainage may be required to
maintain an adequate airway; respiration can be assisted mechanically if required.
Supplemental oxygen may be necessary. Pyridostigmine should be discontinued immediately
and 1-4 mg of atropine sulfate administered i.v. Additional doses of atropine may be given
every 5-30 minutes as needed to control muscarinic symptoms. Atropine overdosage should
be avoided, as tenacious secretions and bronchial plugs may result. It should be kept in mind
that unlike muscarinic effects, the skeletal muscle effects and consequent respiratory paralysis
(nicotinic effects) which can occur following pyridostigmine overdosage are not alleviated by
atropine.
DOSAGE AND ADMINISTRATION
PYRIDOSTIGMINE BROMIDE IS FOR USE AS A PRETREATMENT FOR
EXPOSURE TO THE CHEMICAL NERVE AGENT SOMAN. PYRIDOSTIGMINE
ALONE WILL NOT PROTECT AGAINST EXPOSURE TO SOMAN. THE
EFFICACY OF PYRIDOSTIGMINE IS DEPENDENT UPON THE RAPID USE OF
ATROPINE AND PRALIDOXIME (2-PAM) AFTER SOMAN EXPOSURE.
PRIMARY PROTECTION AGAINST EXPOSURE TO CHEMICAL NERVE
AGENTS IS THE WEARING OF PROTECTIVE GARMENTS INCLUDING MASKS,
HOODS AND OVERGARMENTS DESIGNED SPECIFICALLY FOR THIS USE.
INDIVIDUALS MUST NOT RELY SOLELY UPON PRETREATMENT WITH
PYRIDOSTIGMINE, AND THE ANTIDOTES ATROPINE AND PRALIDOXIME (2-
PAM) TO PROVIDE COMPLETE PROTECTION FROM POISONING BY THE
CHEMICAL NERVE AGENT SOMAN.
PYRIDOSTIGMINE MUST NOT BE TAKEN AFTER EXPOSURE TO SOMAN. IF
PYRIDOSTIGMINE IS TAKEN IMMEDIATELY BEFORE EXPOSURE (E.G.,
WHEN THE GAS ATTACK ALARM IS GIVEN) OR AT THE SAME TIME AS
POISONING BY SOMAN, IT IS NOT EXPECTED TO BE EFFECTIVE, AND MAY
EXACERBATE THE EFFECTS OF A SUB-LETHAL EXPOSURE TO SOMAN.
The dose of pyridostigmine is one 30 mg tablet every 8 hours to be started at least several
hours prior to exposure to Soman. At the first sign of nerve agent poisoning, pyridostigmine
should be discontinued and treatment with atropine and pralidoxime should be instituted
immediately.
There is no known advantage to taking pyridostigmine just prior to or concurrent with Soman
exposure. According to the mechanism of action of pyridostigmine described above (see
ANIMAL PHARMACOLOGY section), pyridostigmine should be effective when it is given
sufficiently in advance of Soman poisoning to provide a pool of protected enzyme. Therefore,
it is expected that pyridostigmine will not be effective if administered just prior to or during
exposure to Soman.
The effects of use beyond 14 consecutive days have not been definitively established,
therefore, continued use beyond 14 consecutive days should be evaluated in the context of the
likelihood of exposure to Soman nerve agent.
HOW SUPPLIED
NSN 6505-01-178-7903 * Immediate Container. Twenty-one (21) tablets individually sealed
in a blister or strip package which is supplied in a protective sleeve.
*The NSN refers to the actual unit that is ordered from supply (if someone orders 1 of this stock number they will get one mylar
bag as a unit of issue (or one package of 10 blister packs). The exterior carton lists the NSN and the description of the product that
the NSN applies to and lists 10 PG (packages) as the quantity within the carton.
STORAGE
Store refrigerated between 2 and 8 0 C (36-46 0 F). Protect from light.
Do not dispense the content of unit packages (10 blister packs) and shipping containers (10
packages of 10 each blister packs) after removal from refrigeration for more than a total of 3
months. Do not use after the 10 year expiration date provided on the package. Military
personnel should be advised to discard the contents of the individual unit packages of
pyridostigmine 3 months after issue.
For Military Use Only
Distributed by: Defense Supply Center, Philadelphia
Medical Directorate
700 Robbins Ave
Philadelphia, PA 19111
For: Office of The Surgeon General
U.S. Army Medical Research
and Materiel Command (MCMR-RCQ-RA)
504 Scott Street
Fort Detrick, MD 21702-5012
Package Insert Revised: February 5, 2003

Comments

  • n/an/a Member Posts: 168,427
    edited November -1
    Pyridostigmine (peer-id-oh-STIG-meen) is taken by mouth for protection against a nerve agent called soman. It should be used along with wearing protective clothing including a gas mask, hood and overgarment.

    It is very important that pyridostigmine use be stopped at the first sign of nerve agent poisoning. Atropine and pralidoxime [2-PAM] are medicines that must be taken at the first sign of nerve agent poisoning and immediately after pyridostigmine use has stopped. Atropine and 2-PAM are called antidotes and help the pyridostigmine work better against nerve agent poisoning.

    Pyridostigmine is to be administered to military personnel only by or under the immediate supervision of your chain of command or medical officer. It is available in the following dosage form:

    Oral
    Tablet (U.S.)



    Before Using This MedicineReturn to top
    In deciding to use a medicine, the risks of taking the medicine must be weighed against the good it will do. This is a decision you and your medical officer will make. For pyridostigmine, the following should be considered:

    Allergies-Tell your doctor if you have ever had any unusual or allergic reaction to pyridostigmine or any of the anticholinesterase agents (certain drugs used during surgery like physostigmine, edrophonium, neostigmine, and ambenonium). Also tell your medical officer if you are allergic to any other substances, such as foods, preservatives, or dyes.

    Pregnancy-Pyridostigmine has not been studied in pregnant women. However, pyridostigmine has not been shown to cause birth defects or other major problems in animal studies.

    Breast-feeding-It is not known if pyridostigmine passes into breast milk.

    Older adults-May medicines have not been studied specifically in older people. Therefore, it may not be known whether they work exactly the same way they do in younger adults or if they cause different side effects or problems in older people. There is no specific information comparing use of pyridostigmine in the elderly with use in other age groups.

    Other medicines-Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. Tell your health care professional if you are taking any other prescription or nonprescription (over-the-counter [OTC]) medicine.

    Other medical problems-The presence of other medical problems may affect the use of pyridostigmine. Make sure you tell your medical officer if you have any other medical problems, especially:
    Asthma (in the bronchial tubes) or
    Irregular or slowed heartbeat or
    Slowed rate of breathing-Pyridostigmine may make the condition worse
    Bladder blockage or
    Bowel blockage-Pyridostigmine should not be used if you have these medical problems
    Bromide allergy-Rash and other side effects may occur



    Proper Use of This MedicineReturn to top
    Dosing-

    Take this medicine exactly as directed. Do not skip, double up on your dose, or stop taking it unless directed by your medical officer. Taking pyridostigmine right before being exposed to soman nerve agent (e.g., when the gas attack alarm is given) or at the same time as poisoning by soman may not work. And, it may make the symptoms of an exposure to soman much worse.

    Pyridostigmine use must be stopped at the first sign of nerve agent poisoning. Tell your medical officer or chain of command if you think you may have symptoms of nerve agent poisoning such as weak muscles or trouble breathing.

    It is important that you wear protective clothes such as masks, hoods and overgarments designed to protect against nerve agent poisoning.

    The dose of pyridostigmine will be determined by your chain of command and/or medical officer based on the threat of soman nerve agent exposure. Follow your medical officer's directions about how much and when to take this medicine.. The following is the dosing information for pyridostigmine.

    For oral dosage form (tablets):
    For protection against soman nerve agent poisoning:
    Adults-The usual dose is one 30 mg tablet every 8 hours
    Missed dose-

    If you miss a dose of this medicine, take it as soon as possible. However, if it is almost time for your next dose, skip the missed dose and go back to your regular dosing schedule. Do not double doses.

    Storage-

    To store this medicine:

    Store in the refrigerator.
    Store away from direct light.
    Do not keep outdated medicine or medicine no longer needed. Ask your medical officer how you should dispose of any medicine you do not use. Be sure that any discarded medicine is out of the reach of children.


    Precautions While Using This MedicineReturn to top
    If you experience serious side effects such as difficulty breathing, severe dizziness, or loss of consciousness after taking pyridostigmine, you should contact your medical officer immediately.



    Side Effects of This MedicineReturn to top
    Side Effects of This Medicine
    Along with its needed effects, a medicine may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.

    Check with your doctor immediately if any of the following side effects occur:

    Incidence not determined
    blue lips and fingernails; chest pain ; cough producing mucus or sometimes producing a pink frothy sputum; difficult, fast, noisy breathing, sometimes with wheezing; inability to breath without assistance; increased sweating; irregular heartbeat; loss of bladder control; loss of bowel control; loss of consciousness ; mood or mental changes; no blood pressure or pulse; numbness, tingling, pain, or weakness in hands or feet; pale skin; paleness of skin after fainting; seizures ; stiffness of upper body and arms; stopping of heart; swelling in legs and ankles; trembling; unconsciousness; weakness after fainting; weakness and heaviness of legs


    Other side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. However, check with your doctor if any of the following side effects continue or are bothersome:

    More common
    Cramps; diarrhea; pain; heavy bleeding; stomach pain


    Less common
    Bloody nose; burning feeling; change in vision; crawling, itching feeling; difficulty in moving; dry skin; impaired vision; increased need to urinate; joint pain; muscle aching or cramping; muscle pains or stiffness; neck pain; numbness; passing urine more often; "pins and needles" feeling; gentlemanling feeling; swollen joints; tingling feeling


    Incidence not determined
    Anxiety; bloated, full feeling; discouragement; dizziness; dry mouth; excess air or gas in stomach or intestines; excessive muscle tone; eye pain; feeling of constant movement of self or surroundings; feeling of sluggishness ; feeling sad or empty; hair loss; headache; hyperventilation ; irritability; lack of appetite; lightheadedness; loss of interest or pleasure; mental problems; muscle tension or tightness; nausea ; nervousness; no blood pressure or pulse; numbness of the tongue; passing gas; rash; restlessness; seeing things that are not there; seizures; sensation of spinning; shaking; stiffness of upper body and arms; swelling; thinning of hair; tingling of extremities; trouble concentrating; trouble sleeping; unusual dullness; vomiting; warm sensation; wheezing


    Symptoms of overdose
    Get emergency help immediately if any of the following symptoms of overdose occur

    blurred vision; diarrhea; frequent urge to urinate; increasing muscle weakness or paralysis, especially in the arms, neck, shoulders, and tongue; muscle cramps or twitching; nausea; shortness of breath; slow heartbeat; small pupils; stomach cramps or pain; sweating; tightness in chest; unusual tiredness or weakness; vomiting; watering of eyes or mouth; wheezing


    Other side effects not listed above may also occur in some patients. If you notice any other effects, check with your doctor.
  • n/an/a Member Posts: 168,427
    edited November -1
    49
    Chapter Four
    PB USE IN THE PERSIAN GULF WAR
    This chapter briefly reviews circumstances of use of PB in the PGW, including
    production and storage of PB, training of personnel with regard to PB use,
    decisions regarding use, and actual use of PB. (This does not include such circumstances
    of use as concurrent exposures, which are reviewed elsewhere-see
    Chapter Nine, "Interactions.") A review of the circumstances of use was undertaken
    to ascertain whether any irregularities in these circumstances might pertain
    to illnesses in PGW veterans and to evaluate ways in which circumstances
    may be improved in future deployments. This chapter relies heavily on non-
    peer reviewed sources (government reports and personal communication),
    because much information regarding circumstances of use is rare in the peerreviewed
    literature.
    PRODUCTION
    PB for use in the PGW was produced overseas. No 30 mg PB tablets are manufactured
    in the United States. Duphar BV in Holland and Roche Products, Ltd.,
    in England produced PB tablets used in Operation Desert Shield and Operation
    Desert Storm in the PGW (Brake, 1997). Discussion with FDA officials indicates
    that drugs manufactured overseas for use in the United States are required to
    meet the same criteria and are subject to the same oversight as drugs manufactured
    in the United States. PB was distributed in blister packs of 21 30 mg
    tablets (a one-week supply), each termed a Nerve Agent Pretreatment Pack
    (NAPP).
    PACKAGING
    The NAPP states the agent and dose (21 tablets PB USP 30 mg). Dutch packaging
    from 1990 contained the following directions:
    1. Commence taking only when ordered by your commander.
    2. Take one every eight hours.
    50 Pyridostigmine Bromide
    3. It is dangerous to exceed the stated dose.
    The PB packaged at Duphar in Amsterdam, the Netherlands, included the
    manufacture date and lot number.
    Current packaging (not that used in the Gulf War) on PB packaged at Roche
    Products Ltd., U.K., states "For Military Combat Use and Evaluation" and contains
    the following additional warning:
    Warning
    If you have asthma, are pregnant or are taking medications for high blood pressure
    or glaucoma, see your unit doctor before taking pyridostigmine.
    Pyridostigmine may cause stomach cramps, diarrhea, nausea, frequent urination
    or headaches.
    Seek medical attention if these or other symptoms persist or worsen.
    STORAGE
    Under Forces Command (FORSCOM) guidelines, following FDA/DSCP
    directives, PB in NAPP must be stored refrigerated in temperatures ranging
    from 2? to 8? C (35? to 46? F) to retain potency for the full shelf life. Those that
    have exceeded their expiration date or have remained unrefrigerated for more
    than six months are not to be used (FORSCOM, 1990; Field Manual, 1990).
    According to discussion with some in-theater personnel, PB, once overseas, was
    not refrigerated, although others report that PB that remained in the hands of
    the medical/logistics community was reputedly refrigerated (Clawson, 1999);
    nor was there any indication that PB required refrigeration during what proved
    to be a short conflict. Discussion with FDA officials indicates that no concerns
    regarding toxic products were related to a lapse in the refrigeration of PB (FDA,
    1997). PB is refrigerated only to ensure efficacy with extended storage. PB
    given in the PGW was primarily made for the PGW and manufactured shortly
    prior to it. Other PB was manufactured approximately five years earlier
    (Clawson, 1999). PB is on a "shelf life extension program" through the FDA. PB
    from 1985 has continued to undergo testing, and has continued to pass all tests,
    receiving successive one- to two-year shelf life extensions (Clawson, 1999).
    TRAINING AND EDUCATION
    As part of granting a waiver of informed consent to DoD for use of PB as a nerve
    agent pretreatment during the PGW, the FDA required DoD to disseminate
    information to all military personnel concerning the risks and benefits of PB
    (Federal Register, 1997; Friedman, 1997).
    PB Use in the Persian Gulf War 51
    Efforts were made to train medical personnel in the use of PB and in the
    recognition and treatment of side effects related to use of PB. According to
    FORSCOM regulations, unit medical personnel must be trained to recognize the
    signs and symptoms of PB overdose, allergic reactions, and side effects and to
    give emergency treatment if necessary (FORSCOM, 1990). A "Field Manual"
    was produced (and has since been updated) that describes the purpose of nerve
    agent pretreatment; the NAPP Tablet Set; effects of PB; principles of use;
    administration in an uncontaminated environment; signs and symptoms of
    overdose, adverse reactions, and contraindications; emergency medical
    treatment for PB's adverse side effects, allergic reactions, and overdose; and
    responsibilities of corps/division/wing commanders, the units, and the unit
    medical personnel (Field Manual, 1995; Field Manual, 1990).
    Evidence suggests there was wide variation in the education of personnel in the
    combat setting. A survey by DoD, of an unspecified number of military personnel,
    queried their views on the adequacy of the training and information they
    received regarding PB (Federal Register, 1997). Of 149 respondents, 43.7 percent
    responded to the question "Was training about pyridostigmine adequate?"
    in the negative. Most expressed the desire for more information on side effects,
    long-term effects, and the drug's mechanism of action. The following list is a
    sample of comments from those who felt the training was inadequate, and from
    those who felt it was adequate but could have been better (Federal Register,
    1997):
    "No standard side effects were given."
    "No training on side effects."
    "People were worried about the drug's side effects. Many people avoided
    taking it. Some people would double dose after missing one."
    "Combat lifesavers brief it and said it was FDA-approved."
    "Many soldiers didn't take the tablets due to the fact that they weren't FDA
    approved or thought not."
    "Didn't know what it did, what it was for. Disregarded instructions to take
    it."
    "Training was not enough in layman's terms. You would need to know
    more about nerve agents."
    Veterans made similar remarks regarding the adequacy of the information they
    received, at hearings before the Senate Committee on Veterans' Affairs and the
    Presidential Advisory Committee on Gulf War Veterans' Illnesses (Federal Register,
    1997).
    52 Pyridostigmine Bromide
    As part of a DoD survey of medical personnel (described in Chapter Three, subsection
    on "Side Effects"), 15 of 23 medical officers who returned the survey
    indicated that the information sheet on PB was not distributed to personnel
    instructed to take the drug. Two respondents said the information was distributed,
    and one, whose unit was not instructed to commence treatment with
    PB, indicated that he had the sheet available for distribution (Federal Register,
    1997). The FDA has expressed concern about several features of PB training.
    These include the high rate of dissatisfaction regarding education, the
    responses indicating that the Army's educational activities were uneven and
    possibly not targeted to the education level of all personnel; and the indication
    that the information sheet on PB was not provided and disseminated to military
    personnel in the Gulf as conditioned in the commissioner's letter granting the
    waiver of informed consent under the interim rule (Federal Register, 1997).
    (See also Rettig, 1999.)
    DECISION REGARDING USE
    Under FORSCOM guidelines, the corps or division commander determines
    whether to begin, continue, or discontinue the NAPP medication with advice
    from the intelligence officer or chemical officer and the surgeon (FORSCOM,
    1990). Unit commanders had discretion on whether and when to order use of
    PB and could delegate this authority to the lowest level of field command
    (Federal Register, 1997). Documentation does not exist on how far down the
    command chain the authority was delegated in each unit (Federal Register,
    1997). The decision to use PB was to be reevaluated each three days, and
    administration beyond 21 days was not recommended without a thorough
    evaluation of the situation (FORSCOM, 1990). There is no documentation
    regarding adherence to these directives.
    USE
    Some unit commanders reportedly advised troops to take more than the stated
    amount of PB. Veterans' self-reports of pills taken, based on telephone interviews
    conducted by the Office of the Special Assistant to the Deputy Secretary
    of Defense for Gulf War Illnesses (OSAGWI), range from one tablet daily to five
    tablets every four to six hours (Brake, 1997). The troops did not necessarily take
    PB as advised (Federal Register, 1997); monitoring was variable, ranging from
    strict enforcement, with pills taken while in formation, to use of the honor system
    (Brake, 1997). Some individuals report having taken more than 60 tablets
    in total (Zeller, 1997), or in one "Open Letter" on the Internet, 500 tablets over
    six months (Hamden, 1997).
    PB Use in the Persian Gulf War 53
    Although several reports states that "most" or "nearly all" or "a great majority"
    of U.S. troops received PB (Defense Science Board, 1994; National Institutes of
    Health, 1994) or that most allied coalition troops and Israeli civilians received
    PB pretreatment (De Fraites, 1996), the actual usage appears to be substantially
    less comprehensive. One estimate, in use by the Office of the Special Assistant
    for Gulf War Illnesses is that 250,000 to 300,000 U.S. personnel received some
    PB, an estimate based on number of tablets delivered but not returned in the
    system (Brake, 1997). (This estimate is subject to uncertainty based, among
    other factors, on uncertainty in average duration of use.) Tablets were taken
    primarily in January 1991 in preparation for the air war, and again in February
    1991 in preparation for the ground war (Brake, 1997). Based on the author's
    discussions with Israeli military personnel and leaders, conducted in concert
    with the OSAGWI, Israeli military but not civilians received PB during the PGW.
    There is no documentation on whether or when each unit issued orders to
    begin taking PB or on who took it (Federal Register, 1997).
    OTHER NATIONS
    PB nerve agent pretreatment was used by the United Kingdom and Canada as
    well as the United States; perhaps 45,000 U.K. troops received PB (Defense Science
    Board, 1994). The French evidently dispensed PB to their troops but did
    not issue the order to use it. However, not all PB was returned, and some
    French troops took PB. Saudi Arabian and Egyptian troops did not take it.
    PB TIMETABLE IN THE PGW
    The following timetable is adapted primarily from De Fraites (1996) with
    additional input. (The accuracy of the statements has not in each case been
    independently verified.)
    Aug. 2, 1990: Iraq invades Kuwait. At the onset of Operation Desert Shield,
    the threat of chemical weapons, including exposure to nerve agents is
    recognized.
    Aug. 7, 1990: FORSCOM message provides guidance for issue and use of PB,
    IAW FM 8-285 during Operation Desert Shield. PB tablet to be used when
    risk of imminent nerve agent exposure is evident, and only on direct order
    of division or corps commander.
    Oct. 11, 1990: U.S. Army Medical Research and Development Command
    identifies the need for FDA waiver for use of PB in Operation Desert Shield.
    Though PB has been licensed by FDA, it had not been specifically approved
    for use as NAPP.
    54 Pyridostigmine Bromide
    Dec. 21, 1990: FDA publishes interim regulation in Federal Register allowing
    waiver of informed consent for investigational new drugs (IND) for DoD
    use during Operation Desert Shield. This statement explains FDA position
    on specific waivers to DoD under circumstances when informed consent is
    considered unfeasible.
    Dec. 28, 1990: Assistant Secretary of Defense (Health Affairs) submits to
    FDA a specific request for waiver of informed consent for PB pretreatment
    for Operation Desert Shield.
    Jan. 8, 1991: FDA approves the waiver of informed consent for PB for
    Operation Desert Shield. The FDA's Informed Consent Waiver Review
    Group supports the DoD use of PB as the only potentially useful nerve agent
    pretreatment available. The group "had no specific safety concerns" with
    the dose of 30 mg each eight hours (only 15 percent of the dose often used
    to treat myasthenia gravis). The only substantial FDA concern expressed in
    this memo is that DoD instructional materials (Field Manual 8-285 and
    Training Manual 90-4) implies that PB pretreatment had been proven
    effective in human trials. FDA agreed with the text of a supplemental
    information sheet produced by DoD that stated that PB had been shown
    effective in animal studies.
    Jan. 16-17, 1991: Operation Desert Storm (air war) begins. PB use was
    ordered on at least two separate occasions in the subsequent 30 days. The
    soldier information sheet gets very limited distribution.
    Feb. 23, 1991: Ground war begins and concludes after 100 hours. Results of
    a survey involving 40,000 XVIII Corps (Airborne) soldiers conducted shortly
    after cessation of hostilities indicated that though minor symptoms such as
    abdominal cramps and frequent urination were quite common, only about
    1 percent of people taking PB sought medical care, and fewer than one in
    1,000 had to discontinue PB pretreatment.
    May 24, 1996: New Drug Application for PB use in NAPP filed with FDA.
    SUMMARY
    Circumstances of PB use were appropriate in several respects. A waiver of
    informed consent was obtained from the FDA prior to administration of PB to
    personnel without informed consent. Conservative strategies for use of PB with
    the threat of nerve agent exposure were devised, requiring repeated reevaluation
    of PB use every several days, with decisionmaking regarding use of PB by
    high-level commanders with medical, chemical, and intelligence consultation.
    A training manual was devised and training programs were implemented in an
    effort to ensure that medical and chemical personnel had knowledge regarding
    PB Use in the Persian Gulf War 55
    the use and side effects of PB. Agreement in principle was made to educate
    troops regarding the function and side effects of PB. No irregularities were
    identified in storage or delivery that would have altered the characteristics of PB
    to render it unexpectedly deleterious.
    The circumstances of PB use were suboptimal in several respects. Training in
    the use and side effects of PB was not in all cases reflected in practice in the
    field. The FDA's requirement of information distribution regarding PB to all
    military personnel as a condition of the waiver of informed consent was not
    upheld. Personnel perceived the education they received to be inadequate.
    Because of these problems, wide variations in de facto use occurred across and
    within units, with irregularities in orders given regarding dosage in some units
    and with some personnel electing to alter the dosing schedule or refrain from
    use of PB. Record-keeping to allow a determination of which units received PB,
    for how long, and when is not available; neither are records regarding which
    level of command made the decision regarding the use of PB.
    Overall, many circumstances of PB use-including its manufacture, transport,
    and storage-do not appear to have contributed materially to illnesses in PGW
    veterans. For instance, there is no evidence that manufacture was flawed and
    resulted in an inferior or toxic product; or that adverse storage conditions were
    present and led to toxic substances or byproducts of PB. Whether other types of
    "circumstances" of PB use_such as coexposure with other PGW exposures-
    could have been contributory is the subject of subsequent sections (e.g., Chapter
    Nine, "Interactions Between PB and Other Exposures").
    SCIENTIFIC RECOMMENDATIONS
    Scientific recommendations for the circumstances of PB use constitute policy
    recommendations, which are not the primary focus of the present report.
    However, certain recommendations can readily be made:
    Advance planning and training should be improved regarding education
    and the consent process.
    Medical personnel should instruct soldiers regarding PB side effects.
    Consistent strategies should be adopted for handling those who "decline"
    to take PB when ordered.1
    ______________
    1The military has held that refusal by personnel to take PB under orders, when the threat of
    chemical warfare is perceived, potentially compromises the welfare of the whole unit in the event of
    nerve agent attack and is therefore untenable. This position is made less persuasive by the limited
    corpus of evidence regarding benefits of PB in the event of nerve agent attack. Evidence of benefit
    vis-?-vis soman derives from only a few studies in primates: in one study, the effects of atropine and
    56 Pyridostigmine Bromide
    Careful planning should be undertaken to ensure accurate generation and
    coordinated maintenance of records regarding who received which agents,
    from what lots, in what doses, and when.
    Testing of PB pretreatment for nerve agents other than soman should be
    performed in primates. The effects of pralidoxime and atropine
    postexposure treatment should be compared with and without PB
    pretreatment to ensure that PB pretreatment does not in fact enhance
    lethality to an important degree.
    ________________________________________________________________________
    oxime postexposure treatment were tested with and without PB pretreatment to calculate
    protective ratios. Of more concern, there is no primate evidence regarding the effect of PB
    pretreatment in the event of nerve agent attack with other nerve agents. (That is, no studies have
    evaluated lethality with atropine and pralidoxime, with and without PB pretreatment.) The
    beneficial effect of PB pretreatment against soman occurs in other mammals but is magnified in
    primates. It is conceivable that the detrimental effect of PB on death from sarin and VX that is seen
    in other mammals is also magnified in primates, and there is no primate evidence to preclude this
    possibility. (Neither is there evidence from close primate relatives to humans that benefit against
    soman is preserved, though evidence from some other primate species suggests that primates may
    share similar characteristics related to aging of AChE-nerve agent complexes.) It is also possible,
    however, that PB provides benefit in primates against all nerve agent threats. Because neither the
    mechanism of benefit of PB for soman nor the mechanism of "harm" for sarin and VX are fully
    understood, this determination cannot be made without empirical testing. Thus, the existing state
    of knowledge is consistent with the possibility that refusal to take PB either compromises or
    enhances the viability of the unit in the event of nerve agent attack, particularly when the threat
    includes nonsoman nerve agents. It might be appropriate to consider this element of uncertainty in
    making judgments about the right of personnel to refuse the pretreatment drug.
  • n/an/a Member Posts: 168,427
    edited November -1
    39 days X 3 Pills a day...117 pills. It's hard to say what kind of damage they may have done.
  • amsptcdsamsptcds Member Posts: 679
    edited November -1
    talk about cya with gaggle of foofoo...

    NO ONE said any thing about it acting with and supplemented by atropine. This is after the fact bs in the paper. I say this because no one explained that or even tried to. Bowever one person, the colonel, did say that the drug was unproven.

    Read it again carefully and you will realize that it is a blocker. It is a blocker that works at the synaptic gap. Synaptic firing is dependent upon balanced bio chemicals at the potential site. A proper balance of sodium is crucial for a "normal" firing.

    A firing neuron must first reach a stage where the action potential is a plus .5 to 1.5, if I remember right (these are called "weights") in order to jump the gap. It puts the receptors in a receiving mode. If anything interferes with that bioelectric state, then completion of the process is, of course, not achievable.

    Atropine alone does this. It doesn't seem proper that we should have had another resident chemical in our system already performing the function. SO then we would have had a double dose of blocker by injecting atropine, which the latter only having effects possible lasting two hours, if it stimulared the bromide, then it would have continued to operate in the system, if it hadn't done so already.

    It probably is fair to note that in a real situation where nerve agent was encountered, and atropine administered, that it is possible that this double dose may have saved lives.

    The objection, I think, ought to be about:
    A the levels of the pb in our systems that were meant to be kept ata certain level over a period of, some say, 14 days, yet there are many vets told to continue the teatment.
    B whether such an unproven and speciously approved chemical ought to have been distributed for general use at all.

    I believe research would show that this chemical did in fact cause some damage, possibly irreversibly.

    Its a matter of getting these folks to be honest, but thst isn't going to happen. All this foofoo paper arises instead, which in my suspicions are probably faked documents if their dates supercede DS by so much as one day. THIS WOULDN'T BE THE FIRST TIME.

    Isn't it also amazing how they always claim it to be an ethical issue about testing on humans, until the military is concerned.

    swine flu vaccine
    anthax vacine
    pb pills

    They order you to take it and courtmartial you if you don't. Yep the ethics are clear.

    hey what was that "one time dose" for malaria that I took down in panama anyway?
  • n/an/a Member Posts: 168,427
    edited November -1
    quote:Originally posted by amsptcds
    talk about cya with gaggle of foofoo...

    NO ONE said any thing about it acting with and supplemented by atropine. This is after the fact bs in the paper. I say this because no one explained that or even tried to. Bowever one person, the colonel, did say that the drug was unproven.

    Read it again carefully and you will realize that it is a blocker. It is a blocker that works at the synaptic gap. Synaptic firing is dependent upon balanced bio chemicals at the potential site. A proper balance of sodium is crucial for a "normal" firing.

    A firing neuron must first reach a stage where the action potential is a plus .5 to 1.5, if I remember right (these are called "weights") in order to jump the gap. It puts the receptors in a receiving mode. If anything interferes with that bioelectric state, then completion of the process is, of course, not achievable.

    Atropine alone does this. It doesn't seem proper that we should have had another resident chemical in our system already performing the function. SO then we would have had a double dose of blocker by injecting atropine, which the latter only having effects possible lasting two hours, if it stimulared the bromide, then it would have continued to operate in the system, if it hadn't done so already.

    It probably is fair to note that in a real situation where nerve agent was encountered, and atropine administered, that it is possible that this double dose may have saved lives.

    The objection, I think, ought to be about:
    A the levels of the pb in our systems that were meant to be kept ata certain level over a period of, some say, 14 days, yet there are many vets told to continue the teatment.
    B whether such an unproven and speciously approved chemical ought to have been distributed for general use at all.

    I believe research would show that this chemical did in fact cause some damage, possibly irreversibly.

    Its a matter of getting these folks to be honest, but thst isn't going to happen. All this foofoo paper arises instead, which in my suspicions are probably faked documents if their dates supercede DS by so much as one day. THIS WOULDN'T BE THE FIRST TIME.

    Isn't it also amazing how they always claim it to be an ethical issue about testing on humans, until the military is concerned.

    swine flu vaccine
    anthax vacine
    pb pills

    They order you to take it and courtmartial you if you don't. Yep the ethics are clear.

    hey what was that "one time dose" for malaria that I took down in panama anyway?


    I've got so much medical crap going on now (Persian Gulf Related), and I would not be a bit suprized if these pill contributed to it. I kind of believe we were exposed to small doses of Nerve/Biological agents as well. We had chemical alarms going off non stop...after the bababooey hit the fan. They functioned fine up until then. Suposedly these were false alarms though. All I know is that my health is continuing to deteriorate. I just wish they would actively pursue treating us for what's wrong with us...and try to get us straightened out. Knowing what I know today, I'd still do it all over again...that's why I joined the Army...but I would be lying if I didn't say I'm a little disappointed with how the Gov't treats it's Vets.
  • amsptcdsamsptcds Member Posts: 679
    edited November -1
    ECC,
    I think you'll find that different VA hospitals actually act differently. Some where around here I ra about how some folks are happy with theirs and others aren't. Loma Linda, out here in crapifornia near San Bernardino, is a crap job, but on the other hand the one in Long Beach is excellent.

    But I think the pb pills are an embarrassment and have gone the way of flying saucers. I was shocked that all during that big hoodoo on TV about gulf war disease, that no one even mentioned them, and obviously possible source.

    Consider a permanent adjustment of neurological behavior in a person and consider that it could even modify genetics some what. Then think about those who had mishapen kids and etc after going home. I does make one wonder. I just wish the fedgov would cease being our enemy in these things and other political arenas.

    Oh by the way, there was rumored to be some dusty mustard in the sand also. To make things a little more spooky, I found an iraqi decon kit half buried in the sand at one pos. but among the piles of ammo, I didn't find any contaminants.

    My opinion of most VAs are that they are staffed by marginal snitbags that aren't up to the task that real hospitals present. The professionalism simply isn;t there at many,not all, of the sites.

    If ENOUGH of you guys that are suffering beat on your congressman and senators perhaps at least some independent pharmacutical company can test that chemical properly. Don't forget that for the Nam vets, it was hell to get agent orange (dioxin) recognised as the culprit of many of their ills.

    FOR ACTIVE DUTY GUYS IN IRAQ:

    Do any of you guys over there now have any contact with these anti nerve gas pills? Or did you initially?
  • wanted manwanted man Member Posts: 3,276
    edited November -1
    Yet another reason I do not advocate drug use, other than recreationally!
    Seriously, ECC, I feel for you and tend to believe that some of the things you were exposed to in the Gulf are at least partially to blame for your medical problems.
    As for the chemical alarms, I won't go into details, but let me say this: About a dozen of us were quite far from the rest of the "unit", well in advance of the onset(s) of both the air and ground campaign(s). On more than one occassion otherwise flawlessly functioning chemical alarms went off for no apparent reason and our NBC guy never did find contaminants upon testing.(Note this guy knew what he was doing; READ SUBJECT MATTER EXPERT!) AND, on more than one occassion one or two of us (not me, thank God!) who did not mask immediately, experienced what appeared to be MILD nerve agent symptoms.
    I don't kow about you, but I DID NOT have to "babysit" any oil wells, in fact I wasn't even exposed to being in CLOSE proximity to any burning wells, but I KNOW that that could only add to any health problems, underlying or otherwise.
  • jimkanejimkane Member Posts: 1,534 ✭✭✭✭✭
    edited November -1
    we had a guy shoot up with atropiene for fun over there, needless to say he wasn't the sharpest spoon in the drawer
  • ntwilleantwillea Member Posts: 3 ✭✭
    edited November -1
    I ran across a site a few months back and put in the NSN for the PB pills that you were talking about and low and behold they have them. I haven't got a clue as to why anyone would want to after reading all the "side effects" that the Gov't says it won't/doesn't cause. They don't have a lot of information on it but they list stocking numbers for related items in other countries and for NATO. The price is available by request only.


    http://www.iso-parts.com/Public/Search_NSN_Details.aspx?NSN=6505-01-178-7903


    I don't know if any of this helps but maybe you could have a lab analyze it for you if ISO will sell some to you. Just a thought.
  • n/an/a Member Posts: 168,427
    edited November -1
    quote:Originally posted by ntwillea
    I ran across a site a few months back and put in the NSN for the PB pills that you were talking about and low and behold they have them. I haven't got a clue as to why anyone would want to after reading all the "side effects" that the Gov't says it won't/doesn't cause. They don't have a lot of information on it but they list stocking numbers for related items in other countries and for NATO. The price is available by request only.


    http://www.iso-parts.com/Public/Search_NSN_Details.aspx?NSN=6505-01-178-7903


    I don't know if any of this helps but maybe you could have a lab analyze it for you if ISO will sell some to you. Just a thought.
    This has been done.

    The American Gulf War Veterans Association has a good web site that tells about alot of the research that has been done.
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