Re: Urinary catecholamines
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
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.
New Children's Hospital,
Sydney, NSW, Australia
>>> "Michael Freemantle" <[log in to unmask]> 17/May/1999
I am trying to come up with a comment to send with results showing
marginal elevations (NA <1000 nmol/d and A <200 nmol/d) in urinary free
catecholamines (method = HPLC - ECD with cation exchange/alumina
cleanup ). In particular I am interested in an up to date list of drugs known
to increase catecholamine excretion eg the list so far includes
Sinemet/Madopar - dopamine invariably increased.
Adrenalin - administered during the collection can increase adrenaline
Can MAOI and the newer COMTI drugs cause increased
I believe most drugs that increase noradrenaline levels do so by either
blocking reuptake or increasing release but do any cause increases in
both NA and A ?
Aldomet and Labetalol metabolites are well resolved in our assay.
Thanks in advance for your opinion on this matter.
Sullivan Nicolaides Pathology
PO Box 344
ph +61 (0)7 33778638
fax +61 (0)7 38705989
home page http://www.powerup.com.au/~mfreeman