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ACB-CLIN-CHEM-GEN  1999

ACB-CLIN-CHEM-GEN 1999

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Subject:

Re: Interpretive comment for urine catecholamines

From:

"Michael Freemantle" <[log in to unmask]>

Reply-To:

<[log in to unmask]>

Date:

Fri, 25 Jun 1999 10:12:03 +1000

Content-Type:

text/plain

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----------
> From: John O'Connor <[log in to unmask]>
>
> We often find slightly elevated urine adrenaline and noradrenaline in
> patients who are under investigation for pheochromocytoma but do not have
> this condition. Usually the drug history indicates that the patient is
> taking some medication that is known to cause mild elevations in the
> catecholamines.
> 
> Our reference ranges are based on normotensive patients (should they be
as
> the majority of patients under investigation are hypertensive?)
> Our ranges are as follows
> Noradrenaline  male <640 nmol/24h; female <470 nmol/24h
	We use adult M/F <600 nmol/24h and consider up to 1000 nmol/24h a marginal
elevation. 
> Adrenaline male <100 nmol/24h; female <70 nmol/24h
	We use adult M/F <120 nmol/24h nd consider up to 200 nmol/24h a marginal
elevation.
   The problem with marginal elevation in urinary catecholamines when
investigating familial forms of phaeochromocytomas (MEN2    and VHL) is
well illustrated in a paper in the latest NEJM which recommends plasma
metanephrine and normetanephrine levels          for the  diagnosis of
these patients.	
> Our protocol is to collect *3, 24h collections on consecutive days. (is
this
> the best approach)
	We dont insist on consecutive days particularly where the symptoms may be
intermittent.  Something that I thought may take off was day / night
collection but alas we stick to our old ways.
> We do not routinely perform the Pentolinium suppression test. 
> Do many of you do this procedure, if so what are your decision
> making criteria?
 	We occasionally do clonidine suppression of plasma catecholamines
(referred) and no longer get requests for clonidine suppression of urinary
catecholamines. 
> Do any labs have 'canned' interpretative comments for catecholamines if
so
> what are they?.
This is the same questions I asked some time away and I am indebted to Dr
John Earl for the following reply
I think agonists like amphetamines, ephedrine etc do not necessarily
increase urinary catecholamines. In a large study we did some years
ago with ADHD children, neither amphetamine nor Ritalin resulted in
elevated urinary noradrenaline, adrenaline or VMA (HMMA). 

The effects of a drug will vary depending on whether therapy has just
commenced,  or has settled down into a steady state.  For example,
drugs which are taken up into neuronal stores can displace
catecholamines and cause an immediate rise in urinary levels but after
about ten days stores become depleted and urinary catecholamines and
metabolites will return to normal or sub-normal.  Tyramine from food or
arising from bacterial overgrowth can potentially do this. Reuptake
inhibitors will also cause an initial rise in apparent turnover but will
deplete neuronal stores over time and urinary metabolites will return to
normal.  

L-Dopa (as Maldopar, Sinemet etc) and dopamine infusion will of course
raise urinary dopamine and homovanillic acid, and adrenaline infusions
will raise adrenaline, metanephrine and VMA.  

Physiological/drug effects, stress and diet often affect noradrenaline but
rarely affect adrenaline. Improved chromatography often solves the
falsely raised adrenaline problem. MAO inhibitors wlll increase the ratio
of metanephrines to VMA but not necessarily raise noradrenaline.
COMTIs will reduce VMA, HVA and metanephrins but
3,4-dihydroxymandelic acid, DHPG and 3,4-dihydroxyphenylacetic acids
will rise. To detect neural crest tumour we are looking for an increased
turnover of catecholamines. Inhibitors are not altering the overall
turnover
so much as altering the pattern of metabolites. More importantly,
depending on what you measure, they may give rise to false negative
results  The problem should not be how to explain away the occasional
borderline result but to explain that the diagnostic test is questionable
under such circumstances and should be repeated off medication.  The
worst situation is where the patient is on a mixture of drugs, almost
anything may be happening with the metabolite pattern depending upon
the relative dosages/ pharmacokinetics and  the symptoms may (or may
not) be a side effect of the medication. 

John Earl
Neurochemistry Laboratory
New Children's Hospital,  
Sydney, NSW, Australia


With regards

Michael Freemantle 
Sullivan Nicolaides Pathology
PO Box 344
Indooroopilly   Q4068
Brisbane
Australia     4068

ph +61 (0)7 33778638
fax +61 (0)7 38705989
home page  http://www.powerup.com.au/~mfreeman
> 


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