Relay-Version: version B 2.10 5/3/83; site utzoo.UUCP
Posting-Version: version B 2.10.2 9/5/84; site aecom.UUCP
Path: utzoo!decvax!genrad!panda!talcott!harvard!cmcl2!philabs!aecom!werner
From: werner@aecom.UUCP (Craig Werner)
Newsgroups: net.med
Subject: Aspirin vs. Tylenol
Message-ID: <2208@aecom.UUCP>
Date: Mon, 20-Jan-86 15:54:19 EST
Article-I.D.: aecom.2208
Posted: Mon Jan 20 15:54:19 1986
Date-Received: Wed, 22-Jan-86 02:26:27 EST
Distribution: na
Organization: Albert Einstein Coll. of Med., NY
Lines: 44


	The mechanism of Aspirin is at the end of this article.

	Aspirin has three actions tha make it ideal.  It is an analgesic -
it releives pain.  It is also an anti-inflammatory and anti-pyretic -- it
reduces swelling and fever, thus actually objectively lessens symptoms, in
addition to masking them by analgesia.
	Tylenol (Acetominophen) is purely an analgesic without anti-inflam
or anti-pyretic effects.  It has the advantage, however, of having less
short-term side effects, so is better tolerated.  Moreover, it is the belief
of the author that a large portion of its success is due to the fact that
most people don't have about the objective relief of signs, as long as the
pain/discomfort goes away.
	Phenacetin (Acetophenetidin) is an older drug, whose active metabolite
turns out to the Acetominophen.  It was used very extensively at one point, 
but it was found that heavy use or abuse causes permanent Kidney damage.  
It is no longer available in the US.


The mechanism of Aspirin:
	Aspirin mechanism is at least two fold.  In its original form,as
Acetylsalicylic Acid, it can permanently acetylate the enzyme Cyclooxygenase
which is the first step towards Prostaglandin synthesis.  This enzyme can
be reformed as soon as the Aspirin is degraded (about 15 minutes), except in
the platelets, where it is estimated 1 lick of 1 children's Aspirin will
destroy all Platelet cyclooxygenase for 2-3 days (as Platelets regenerate)
A second effect is caused by Salicylic Acid (sans Acetate) which blocks a
step towards Leukotriene formation, HPETE--> HETE, and the resulting
HPETE inhibits the Cyclooxygenase, and hence Prostaglandin formation. 
	Both Leukotrienes and Prostaglandins arise from an essential fatty
acid, Arachidonic Acid, so the pathways aren't as unlinked as it seems from
words.  Moreover, both Leukotrienes and Prostaglandins are mediators of
inflammation, and both (but particularly PG-E2) have something to do with
fever.
	Whether any of this has anything directly to do with Aspirin's
analgesic effect, I do not know.  Obviously, Tylenol is proof tha one can
be analgesic without being anti-anything.

	
-- 

				Craig Werner
				!philabs!aecom!werner
          "It's hard to argue with someone who knows what he's talking about."