In chronic Zinc deficiency, decreased Alkaline Phosphatase will be a
notable feature. It will be interesting tp know the Alkaline phosphatase
levels in Dr.Gordon Challand's patient.
Vivek
On Mon, 28 Sep 1998, Nick Miller wrote:
> To make my contribution to the replies to Gordon Challand's query
> from last week about low serum copper and caeruloplasmin in a
> patient on TPN, which I've just picked up on.
>
> One scenario is that the low Cu and CPL are caused by zinc
> deficiency, especially in a burns patient, which may or may not be
> evident from the serum Zn. The hepatocyte Zn concentration is one
> of the factors controlling protein synthesis; when Zn is deficient
> CPL synthesis slows down and serum Cu falls. At the same time
> Cu may actually be accumulating in the liver. If the serum Zn is
> very low (less than 9 umol/L) (ref. interval 11.5 - 20 umol/L) this is
> the most likely explanation and the remedy is to replenish body Zn
> stores.
>
> Alternatively both Zn and Cu may be low (as well as serum CPL).
> Genuine Cu deficiency in these circumstances is much more
> dangerous because it's most unlikely to diagnosed and causes,
> among other problems, an "iron deficiency" anaemia that does not
> respond to the adminstration of iron. Such a Cu deficiency
> anaemia, if treated continuously with Fe, will give rise to an
> aplastic anaemia and, ultimately, death.
>
> Part of the problem is that Zn, Cu and Fe share the same GIT route
> for absorption. However the two scenarios can be distingished by
> giving a loading dose of Zn (50 mg) and seeing if that raises the
> serum Cu and CPL (by restoring hepatic CPL synthesis).
>
> So the answer to Gordon Challand's question is - "it depends on
> what happens to the serum and intra-hepatic zinc".
>
> Nick Miller,
>
> London
>
>
>
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