Relay-Version: version B 2.10 5/3/83; site utzoo.UUCP Posting-Version: version B 2.10.2 9/18/84; site muddcs.UUCP Path: utzoo!decvax!ittatc!dcdwest!sdcsvax!sdcrdcf!trwrb!scgvaxd!muddcs!uribe From: uribe@muddcs.UUCP (Lydia Uribe) Newsgroups: net.med Subject: Re: Aspirin vs. Tylenol Message-ID: <346@muddcs.UUCP> Date: Sat, 25-Jan-86 02:48:10 EST Article-I.D.: muddcs.346 Posted: Sat Jan 25 02:48:10 1986 Date-Received: Tue, 28-Jan-86 00:02:06 EST References: <2208@aecom.UUCP> Reply-To: uribe@muddcs.UUCP (Lydia Uribe) Distribution: na Organization: Harvey Mudd College, Claremont, CA Lines: 31 Summary: Tylenol *is* an effective antipyretic In article <2208@aecom.UUCP> werner@aecom.UUCP (Craig Werner) writes: > > 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. > Acetaminophen is indeed an effective antipyretic, of equal efficacy with aspirin. > >The mechanism of Aspirin: > 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). > > Craig Werner (Reference: American Pharmaceutical Association, _Handbook of Nonprescription Drugs_, 7th edition, Chapter 11) Lydia Uribe ...scgvaxd!muddcs!uribe