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From: werner@aecom.UUCP (Craig Werner)
Newsgroups: net.med
Subject: Re: Re: Aspirin vs. Tylenol
Message-ID: <2227@aecom.UUCP>
Date: Wed, 29-Jan-86 23:58:52 EST
Article-I.D.: aecom.2227
Posted: Wed Jan 29 23:58:52 1986
Date-Received: Fri, 31-Jan-86 02:27:01 EST
References: <2208@aecom.UUCP> <346@muddcs.UUCP>
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Organization: Albert Einstein Coll. of Med., NY
Lines: 29

> >         Moreover, both Leukotrienes and Prostaglandins are mediators of
> >inflammation, and both (but particularly PG-E2) have something to do with
> >fever.
> >
> Prostaglandin-E is produced as a response to endogenous pyrogen and causes
> the hypothalamus to increase the body's temperature set point, resulting in 
> fever.  Aspirin and acetaminophen block this prostaglandin synthesis, causing
> the hypothalamus to re-establish the normal set point; they also cause 
> increased heat dissipation (by cutaneous vasodilatation and increased 
> sweating).
>                                      Lydia Uribe

	The above by L. Uribe is wrong in one respect.
	Yes, I did say Acetominophen was a pure analgesic without 
anti-imflammatory or anti-pyretic properties.  Yes, it does in fact have
anti-Pyretic properties (that was a misreading on my part)  But, NO, Tylenol
has no effect in inhibiting Prostaglandin synthesis. It is the only available
analgesic that has this effect, which is why it is so easy on the stomach.
Tylenol (Acetominophen) still lacks Anti-inflammatory properties.
	PG-E is only one of many endogenous pyrogens and does not directly cause
fever if injected into the hypothalamus but is neccessary for the development
of fever (put another way, it's necessary, but NOT sufficient).
	I do not know how Tylenol lowers fever, but it does not do it by
blocking PG-E2 synthesis, as Aspirin does. Maybe it's a direct effect?
-- 

				Craig Werner
				!philabs!aecom!werner
                     "The end. 94. 95. The very, very, very end."