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#1
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MDS misdiagnosis owing to excess zinc...
Today there is an interesting article posted in the MDS Beacon regarding MDS misdiagnosis owing to excess zinc...
http://www.mdsbeacon.com/news/2014/0...mes-diagnosis/
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Ric: Low-risk MDS (blasts <4%); 4 cycles Revlimid no positive response; PRBC transfusion dependent; so far, 392'units' over 8 3/4 years; BMB #4 (15/04/01) shows evolution to AML (blasts 20-30%) 47,XY,del(5) (q22q35),+21[24][cp24]/46,XY(1). |
#2
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Zinc/copper
riccd2001,
Interesting article. You have perhaps understood that a member, Chirley from Australia, has very low copper levels and initially a disease similar to MDS. Marlene informs all new members about how important it is to control the copper levels Before the dx MDS. Kind regards Birgitta-A |
#3
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During the initial testing phase and MDS dx, my mother had zinc level higher than normal and copper low-normal. The doctor confirmed the MDS dx.
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Mother age 79, dx MDS RCMD low risk del 20q April 2013, no response to EPO, Danazol. pRBC tx dependent - 2 units every 3-4 weeks, exjade Dec 2013 - Mar2014, restarted Dec 2014 |
#4
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Thanks for posting this. A very interesting link. Copper, zinc and iron need to be in balance. Too much or too little of one can really throw things off. There was time, not too long ago, denture creams containing zinc lead to excessive zinc in people resulting in neurological as well as hematological problems.
At some point, the first line of investigation in all disease will begin with a solid nutritional workup. I know I sound like a broken record but I have seen time and time again when B vitamins, minerals and vitamin D are optimized blood work improves and can normalize. One last word of caution on supplements. Many people take a daily and then add in other formulas to address other issues. It is important to look at the total amounts you are consuming across all your products. You may get the RDA of zinc in the multi and then take an anti-oxidant mix for eye health that also has zinc which, overtime, is probably going to be too much a good thing. Thanks again for posting.
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Marlene, wife to John DX w/SAA April 2002, Stable partial remission; Treated with High Dose Cytoxan, Johns Hopkins, June 2002. Final phlebotomy 11/2016. As of July 2021 HGB 12.0, WBC 4.70/ANC 3.85, Plts 110K. |
#5
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I haven't read the article but yes I have high zinc and low copper, however I also have a chromosome deletion and some gene mutations so the thinking is reversed in my case. I dont take excess zinc.
It is thought that the reason my zinc is high is because my copper is low (not the other way round) due to malabsorption, high urinary excretion and (potentially) disrupted intracellular copper transport. If you don't absorb enough copper through the enterocytes you absorb more zinc by default. I tried a low zinc diet but it's just about impossible to avoid zinc in foods. So now I just avoid foods that are known to have high zinc levels. My iron levels are whacky and I've never fully had them explained to me. Originally I was told I had iron deficiency anaemia and had iron infusions which never caused any increase in reticulocyte count. Then I became allergic to the iron infusions (anaphylaxis and ICU admission) so no more infusions for the following three years. Then suddenly my BMB went from no iron stores to increased iron deposits and ringed sideroblasts. My ferritin went from normal to over 5000 in the space of a month and a liver biopsy showed hepatitis from moderate iron overload. If anyone can figure out what's going on I'd be grateful. I was seeing a very respected Prof of Metabolic Medicine who was convinced it was due to a missing copper transport protein.
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Copper deficiency bone marrow failure (MDS RAEB 1), neuromyelopathy. FISH reported normal cytogenetics but gene testing showed Xq 8.21 mutation Xq19.36 mutation Xq21.40. mutation 1p36. Mutation 15q11.2 deletion |
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