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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 > > > %%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%%