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From: sdyer@bbnccv.UUCP (Steve Dyer)
Newsgroups: net.med
Subject: Re: Thiazide diuretics & blood lipid level
Message-ID: <765@bbnccv.UUCP>
Date: Sun, 17-Nov-85 15:54:25 EST
Article-I.D.: bbnccv.765
Posted: Sun Nov 17 15:54:25 1985
Date-Received: Tue, 19-Nov-85 03:24:13 EST
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Organization: Bolt Beranek and Newman, Cambridge, MA
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>>   Third if Steve has a reference for the increase blood lipid findings I'd
>> really like to get it.
> 	It's in the package insert (and required to be there) on all drugs that
> it is associated with, also on all the ads in Medical Journals.  Not to
> mention the PDR and Merck manual, which Steve Dyer is exquisitely consistent
> in consulting.

Actually, the Merck Manual doesn't mention thiazide-induced increases in
blood lipids, and I don't own a PDR.  The latest 1985 Goodman and Gilman
mentions this, and the references I posted were transcribed from a computerized
literature search on "Paperchase", Beth Israel's medical database service.

Regarding new diuretic agents which may not produce this increase in blood
lipids, they may eventually be welcomed into a doctor's armamentarium, but
as a medical consumer, you might want to ask yourself whether you'd prefer to
be treated with agents which have been in use for billions of patient-years,
instead of the "latest" drug, which of necessity is much less familiar and
which may have undiscovered side-effects.  (Provided that these older agents
are effective and do not cause you undesirable side-effects.)  Certainly
it is prudent to measure a patient's lipids if thiazides are being given,
but if the drug-induced increase is small, it doesn't necessarily follow
that one MUST change to a new diuretic.

I mention this specifically in the context of thiazide diuretics and their
well-known actions, because about 5 or 6 years ago, a new diuretic, ticrynafen,
was promoted as specifically avoiding another side-effect of thiazide therapy,
retention of uric acid, which may aggravate gout in susceptible individuals.
Indeed, it actually promoted the excretion of uric acid, much like some drugs
used only for gout.  Ticrynafen became quite popular when it was introduced
and many patients were treated with this drug, even though they might not have
been at risk for gout, and whose thiazide-induced hyperuricemia might have been
clinically insignificant (or non-existent, assuming that they went directly on
ticrynafen.)  It turned out that a significant proportion of those receiving
ticrynafen (0.01 - 0.1 %) suffered from varying degrees of liver toxicity, an
effect which wasn't uncovered until it was approved and in wide use.  It was
quickly withdrawn by the FDA, much to the chagrin of Smith, Kline and French
stockholders.

All this points to just a simple fact: that prescribing a therapy isn't
simple, that there are always tradeoffs which the physician and patient
have to come to terms with, and that the yet-unknown offers as many
uncertainties as the knowledge which we are developing.
-- 
/Steve Dyer
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