Hi, Jack,
I urge you to read the article. I can't do it justice here. I
found it fair and well-researched. One poor fellow who successfully
sued the maker for 8.5 million bucks lost his liver after taking some
Tylenol (I think) and a few drinks after dinner. The two in
combination can be deadly. Worse, the trouble is often not
diagnosed correctly, and the symptoms may resemble flu.
JBB
On Saturday, Oct 25, 2003, at 03:37 Asia/Tokyo, Jack Dayton wrote:
Jonathan B. Britten 10/22/03 1:20 AM Wrote:
List,
Please see this month's Esquire magazine to learn that Acetaminophen
is the
leading cause of liver failure in the USA today. Tens of
thousands of
people each year suffer serious, sometimes irreversible, sometimes
fatal toxic
reactions from this powerful and popular drug -- which of course is
approved
by the FDA.
I am busy and will stop here: if you read the entire article, you
will
understand clearly the grotesque contrast between the FDA tolerance
of toxic
OTC remedies from the big pharmaceutical companies, as opposed to
the FDA
attacks on effective, largely harmless non-pharmaceutical substances
and
devices,.
Read it and weep, or laugh bitterly, depending on your inclinations.
***************************
Hi Jon,
Man, Esquire is cheap -- you can,t read an article on-line without
paying.
BUT -- that turns out to be a good thing, because I then
went looking for supportive evidence of acetaminophen toxicity--
and I found it, but no normal person coming anywhere near the
recommended dosage would be in any danger of harm from the
use of acetaminophen; Esguire must have been hard-up for a
filler article.
The complete information can be found at:
http://www.emedicine.com/emerg/topic819.htm
a portion of the reference follows:
Pathophysiology: The maximum daily dose of APAP is 4 g in adults and 90
mg/kg in children. The toxic dose of APAP after a single acute
ingestion is
150 mg/kg or approximately 7 g in adults, although the at-risk dose
may be
lower in persons with alcoholism and other susceptible individuals.
When
dosing recommendations are followed, the risk of hepatotoxicity is
extremely
small.
Acetaminophen is rapidly absorbed from the stomach and small intestine
and
metabolized by conjugation in the liver to nontoxic agents, which then
are
eliminated in the urine.
In acute overdose or when maximum daily dose is exceeded over a
prolonged
period, the normal pathways of metabolism become saturated. Excess
APAP is
then metabolized in the liver via the mixed function oxidase P450
system to
a toxic metabolite, N-acetyl-p-benzoquinone-imine (NAPQI). NAPQI has an
extremely short half-life and is rapidly conjugated with glutathione, a
sulfhydryl donor, and removed from the system. Under conditions of
excessive
NAPQI formation or reduced glutathione stores, NAPQI is free to
covalently
bind to vital proteins and the lipid bilayer of hepatocytes; this
results in
hepatocellular death and subsequent centrilobular liver necrosis.
The antidote for APAP poisoning is N-acetylcysteine (NAC). NAC is
theorized
to work by a number of protective mechanisms. Early after overdose, NAC
prevents the formation and accumulation of NAPQI. NAC increases
glutathione
stores, combines directly with NAPQI as a glutathione substitute, and
enhances sulfate conjugation. NAC also functions as an
anti-inflammatory and
antioxidant and has positive inotropic and vasodilating effects, which
improve microcirculatory blood flow and oxygen delivery to tissues.
Vasodilating effects decrease morbidity and mortality once
hepatotoxicity is
well established.
The same thing was done to Ephedrin ( sp?) those athletes that had
trouble
were probably of the mind set -- If a little does good, then a lot
will do
gooder -- duh?
Jack
Be Nice
-- Be Nice
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