Hi everyone,
I'll make this much shorter, since I didn't get any response from my post
titled "run-around from Glaxo on Ecotrin". I apologize for my long posts,
but I try to be specific so there are no misunderstandings.
Is it true that enteric coated aspirin will "topically" (i.e., by direct
contact) damage the duodenum mucosa (since it is designed to dissolve in the
duodenum in lieu of the stomach) just as bad as non-enteric coated aspirin
would "topically" damage the stomach mucosa, and if so what is the advantage
of taking it (in other words it "topically" damages your duodenum instead of
your stomach). The box (whether it is brand name or generic) says something
like "safely designed to dissolve in the small intestine".
I understand the systemic damage by prostaglandin blocking (which is the
mechanism by which NSAIDS work), but that is a separate issue which will
occur regardless of any coating on the NSAID. And based on my studies, the
prostaglandin blocking is more damaging to the stomach/duodenum than the
topical damage anyway - do you agree.
If what I am getting at is true, how does the FDA allow this crap (which in
my opinion is false advertising). I tried to get a response from Glaxo from
their scientific department and they never called me back (which I knew they
wouldn't - they don't care about one little guy like me - its a sad state of
affairs what the world has become).
There must be at least one pharmacist that can address my concern. Your
response would be greatly appreciated. Thanks.
Pete
P T - 23 May 2005 17:15 GMT
"Aspirin produces local GI damage by penetrating the protective mucous
and bicarbonate layers covering the gastric mucosa and permitting the
"back diffusion" of acid, casing cellular and vascular erosion.
Contributing mechanisms include inhibition of mucosal prostaglandin
synthesis, reduction and alteration of mucous secretion, and reduction
of bicarbonate secretion. (12) Endoscopic evaluation of healthy
volunteers showed that 650mg of aspirin produced multiple gastric
petechie and erythema within 1 hour in all subjects. A second group
taking 650mg aspirin every 6 hours for 24 hours showed multiple
antral erosions in all subjects and duodenal erosions and petechiae
in half the volunteers. (12) ... [endoscopy found] patients taking
aspirin (2.5 g per day) for >3 months, 20% had gastic ulcers, 40% had
gastric erosions, 75% had gastric erythema, and 4% had duodenal
ulceration. (12)"
Source: Chapter 5: Handbook of Nonprescription Drugs, 10th Edition
(1993) Publisher Am. Pharmaceutical Assn.
Pete - 24 May 2005 00:29 GMT
PT...thanks for all the good info, but you didn't answer my question. Did
you read anything I wrote.
Pete
"Aspirin produces local GI damage by penetrating the protective mucous
and bicarbonate layers covering the gastric mucosa and permitting the
"back diffusion" of acid, casing cellular and vascular erosion.
Contributing mechanisms include inhibition of mucosal prostaglandin
synthesis, reduction and alteration of mucous secretion, and reduction
of bicarbonate secretion. (12) Endoscopic evaluation of healthy
volunteers showed that 650mg of aspirin produced multiple gastric
petechie and erythema within 1 hour in all subjects. A second group
taking 650mg aspirin every 6 hours for 24 hours showed multiple
antral erosions in all subjects and duodenal erosions and petechiae
in half the volunteers. (12) ... [endoscopy found] patients taking
aspirin (2.5 g per day) for >3 months, 20% had gastic ulcers, 40% had
gastric erosions, 75% had gastric erythema, and 4% had duodenal
ulceration. (12)"
Source: Chapter 5: Handbook of Nonprescription Drugs, 10th Edition
(1993) Publisher Am. Pharmaceutical Assn.
rastapasta - 24 May 2005 22:21 GMT
> Hi everyone,
>[cut]
Wish I could help, but you may try X-posting this over in the NG
'alt.drugs.hard', 'alt.drugs.chemistry', 'alt.drugs', 'sci.med', etc.
MobiusDick is the brains on a.d.hard.