Normal noradrenaline and adrenaline output in the presence of raised
dopamine in patients with symptoms consistent with phaeochromocytoma has
been described by Otto Kuchel. So called pseudo-phaeochromocytoma, also
sometimes referred to as Page's syndrome. It is suggested that the elevated
dopamine arises as a result of hyperactivity of the sympathetic nervous
system plus or minus deficient conjugation of catecholamines following their
release. Presumably DOPA release on sympathetic activation followed by
decarboxylation to dopamine in the kidney could also lead to a rise in
urinary dopamine output. As an alternative explanation others have argued
that this syndrome arises because of failure of the gut sulphotransferases
to sulphate and deactivate dietary dopamine from such sources as bananas (a
single banana has been shown to raise circulating DA-so4 by 20-30 fold).
Cereal diets have been shown to increase urinary dopamine sulphate output by
a factor of 8 It is possible that reduced activity in these enzyme systems
in concert with increased intake of dopamine could give rise to elevated
urinary free dopamine outputs. Most of the circulating dopamine is
sulphated and may represent the sum of dietary sources and those produced in
vivo. It is interesting to note that dopamine sulphate rises in heart
failure and hypertension, and normalises on treatment. Some patients do
seem to have hypertensive episodes following food ingestion and it is
postulated that failure in the gut conjugation systems may allow passage of
hypertensive agents into the circulation. See also the issues surrounding
sulphotransferases and migraine headache.
There is an active sulphatase/sulphotransferase shuttle mechanism in the
kidney that may act upon dopamine (a known natriuretic factor) and be
subject to imbalances (a priori) leading to increased free dopamine in some
situations. Urinary dopamine appears to be elevated in later stages of
pregnancy and there have been some suggestions that elevations may be seen
in the latter half of the menstrual cycle during which there are effects on
the overall fluid and electrolyte economy. Dopamine output can certainly be
affected by changes in dietary salt intake.
Dopamine is associated with neural crest tumours. It has been proposed as an
indicator of malignancy in patients with phaeochromcytoma going on to follow
a malignant history. Elevations are seen in patients being treated for
Parkinson's. Thiazides can also push urinary free dopamine output up.
Cardiac arrhythmias have also been cited as a cause of increased dopamine
output.
Good review on Dopamine Sulphate by Eisenhoffer et al. Clin Exp Pharmac and
Physiolo 199:26(Suppl).S41-S53
Dr WA Bartlett
Consultant Clinical Scientist
Dept of Clinical Biochemistry & Immunology
Birmingham Heartlands Hospital
Birmingham Heartlands & Solihull NHS Trust (Teaching)
Bordesley Green East
Birmingham B9 5ST
-----Original Message-----
From: [log in to unmask] [mailto:[log in to unmask]]
Sent: 01 July 2002 14:50
To: [log in to unmask]
Subject: DOPAMINE
What is the significance of a raised urinary dopamine (in three 24 hr
collections)
when both adrenaline and noradrenaline normal in all 3?
Thanks
Rob L
Dr Robert Lord
Department of Clinical Biochemistry
Rotherham District General Hospital
Moorgate Road
Oakwood
Rotherham
S60 2UD
Tel 01709 820000
E mail [log in to unmask]
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