> According to wikipedia, some of the COX-2 inhibitors are still
> available in the US. It refers to only one, Vioxx (rofecoxib), as being wihdrawn.

Etoricoxib
Widely used internationally.
Not approved in US.

   http://en.wikipedia.org/wiki/Etoricoxib

Rofecoxib/Vioxx, Bextra, Celebrex discussion

       http://en.wikipedia.org/wiki/Coxibs#Adverse_drug_reactions_and_withdrawal_of_Vioxx

Valdexib/Bextra.
Withdrawn in USA in 2005

    http://en.wikipedia.org/wiki/Valdecoxib

Celebrex / Celebra / Onsenal / Celecoxib / Coxib / Celecoxx
Shonky research papers. FDA black box warnings.
YMMV.

    http://en.wikipedia.org/wiki/Celebrex

__________________________

> Do you mean a 1000mg dose of paracetamol? That's the standard maximum
> strength dose here in the US as an over-the-counter drug (two 500mg
> tablets). I was unable to find a statement saying that the FDA
> considered this beyond the max recommended dose. Instead, wikipedia
> once again says that 1000mg IS the maximum recommended dose to be
> taken at one time, and a total of 4000mg in 24 hours.

My original comments were correct, but they do appear to have been
having a bit of a running battle.

>From -     http://en.wikipedia.org/wiki/Acetaminophen

"In June 2009 an FDA advisory committee recommended that new
restrictions should be placed on paracetamol to help protect people
from the potential toxic effects.[65] [66]"

Some details from that page quoted at end.

Along the way:

    http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm165107.htm

    http://www.fda.gov/downloads/Drugs/DrugSafety/InformationbyDrugClass/UCM171901.pdf

    http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/psn/transcript.cfm?show=87#8

    http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/psn/transcript.cfm?show=87#9


________________

FWIW / FYI:

    http://en.wikipedia.org/wiki/Acetaminophen

Toxicity

Main articles: Paracetamol toxicity and Analgesic nephropathy
Excessive use of paracetamol can damage multiple organs, especially
the liver and kidney. In both organs, toxicity from paracetamol is not
from the drug itself but from one of its metabolites,
N-acetyl-p-benzoquinoneimine (NAPQI). In the liver, the cytochrome
P450 enzymes CYP2E1 and CYP3A4 are primarily responsible for the
conversion of paracetamol to NAPQI. In the kidney, cyclooxygenases are
the principal route by which paracetamol is converted to NAPQI.[61]
Paracetamol overdose leads to the accumulation of NAPQI, which
undergoes conjugation with glutathione. Conjugation depletes
glutathione, a natural antioxidant. This in combination with direct
cellular injury by NAPQI, leads to cell damage and death.[62]

Paracetamol hepatotoxicity is, by far, the most common cause of acute
liver failure in both the United States and the United Kingdom.[6][63]
Paracetamol overdose results in more calls to poison control centers
in the US than overdose of any other pharmacological substance.[64]
Signs and symptoms of paracetamol toxicity may initially be absent or
vague. Untreated, overdose can lead to liver failure and death within
days. Treatment is aimed at removing the paracetamol from the body and
replacing glutathione. Activated charcoal can be used to decrease
absorption of paracetamol if the patient presents for treatment soon
after the overdose. While the antidote, acetylcysteine, (also called
N-acetylcysteine or NAC) acts as a precursor for glutathione helping
the body regenerate enough to prevent damage to the liver, a liver
transplant is often required if damage to the liver becomes severe.[3]

In June 2009 an FDA advisory committee recommended that new
restrictions should be placed on paracetamol to help protect people
from the potential toxic effects.[65] [66]




     Russell
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