Hypocupraemia-induced anaemia, sensory ataxia and cognitive impairment secondary to zinc-containing dental adhesive

2021 ◽  
Vol 14 (7) ◽  
pp. e239375
Author(s):  
Rayyan Jamal ◽  
Omar Walid Dihmis ◽  
Liam Stuart Carroll ◽  
George Pengas

A 67-year-old man presented with 5 months of worsening memory impairment and sensory gait ataxia on the background of symptomatic anaemia. He experienced falls, agitation and became socially withdrawn over 3 weeks, resulting in hospital admission. On examination, he had sensory gait ataxia consistent with a dorsal column syndrome. He scored 13/30 on the Montreal Cognitive Assessment. Serum analysis showed normocytic anaemia and leucopenia, severe hypocupraemia, reduced caeruloplasmin and normal zinc levels. Overuse of zinc-containing denture cream was the cause of excess zinc ingestion and resultant copper deficiency, leading to blood dyscrasia and myelopathy. The cream was withdrawn and intravenous and then oral copper supplementation was implemented. Direct questions with regard to excess zinc in the diet and serological testing of copper and zinc should be considered in any patient with a dorsal column syndrome, particularly with concurrent anaemia. Copper deficiency may also have a role in exacerbating pre-existing cognitive impairment.

2020 ◽  
Vol 12 (3) ◽  
pp. 466-471
Author(s):  
Giulia Grigioni ◽  
Christian Saleh ◽  
Phillip Jaszczuk ◽  
Dorothea Wand ◽  
Stefanie Wilmes ◽  
...  

Fragile-X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative disorder that manifests with intention tremor, progressive gait ataxia, and cognitive impairment. The disease is genetically characterized by a premutation of the <i>FMR1</i>gene on the X-chromosome manifesting with a CGG triplet expansion between 55 and 200. Given the phenotypical variety of this disease, diagnosis is frequently delayed. We present and discuss a male patient whose diagnosis of FXTAS was delayed due to his concomitant alcohol abuse.


2021 ◽  
pp. 167-175
Author(s):  
Stephanie Munie ◽  
Pairach Pintavorn

Excessive intake of zinc is a known but often forgotten cause of copper deficiency, and its consequences in the context of end-stage renal disease (ESRD) are not widely discussed. Zinc-induced copper deficiency (ZICD) can result in erythropoietin (EPO)-resistant anemia and may not be considered as a possible etiology when conducting the work-up. We present a case wherein an ESRD patient had been receiving excess zinc for several months and subsequently experienced EPO-resistant anemia. Our patient’s GI work-up was negative, and increased doses of iron and EPO-stimulating agent were ineffective. She underwent a bone marrow biopsy and more serological testing. She was ultimately diagnosed with ZICD, and cessation of her zinc supplement and initiation of copper replacement proved effective in restoring EPO responsiveness. Awareness of ZICD as a possible factor in EPO-resistant anemia could lead to an expedited diagnosis and avoid an unnecessary and extensive work-up.


1967 ◽  
Vol 18 (1) ◽  
pp. 169 ◽  
Author(s):  
GI Alexander ◽  
JM Harvey ◽  
JH Lee ◽  
WC Stubbs

Four experiments described determined the effect of copper and cobalt therapy on the growth and productivity of cattle on the marine plains of central coastal Queensland. Copper was administered by subcutaneous injections of copper glycinate, and cobalt by dosing per os with heavy cobalt pellets. The growth of weaned cattle was significantly improved by copper, particularly from June to October when limited palatable feed on the high ground forced the animals to forage on the para grass swamps. During the same period, 2-year-old heifers also showed a growth response to copper. Their conception rate increased after 19 months of copper therapy but not after 10.5 months. The growth rate of their calves bas significantly increased by copper supplementation. Liver copper concentrations were always low in untreated cattle. Copper therapy maintained these reserves at higher levels, which varied according to the season and the rate of growth of the animals. Calves born to treated cows had higher initial liver copper reserves than those from untreated cows, but in the absence of copper therapy these reserves declined to low and comparable levels in all calves at weaning. Pasture analyses suggest that the copper deficiency revealed was due to interference with copper metabolism rather than to a low copper status in the diet; this interference did not appear to be due to molybdenum. Weaned cattle appeared to respond to cobalt during 1960 but not subsequently, while the cows and calves showed no response. The vitamin B12 status in liver and serum appeared adequate in both treated and untreated cattle.


2014 ◽  
Vol 121 ◽  
pp. 17-18 ◽  
Author(s):  
S. Zittel ◽  
F. Ufer ◽  
C. Gerloff ◽  
A. Münchau ◽  
M. Rosenkranz

BDJ ◽  
2011 ◽  
Vol 210 (11) ◽  
pp. 523-525 ◽  
Author(s):  
K. Doherty ◽  
M. Connor ◽  
R. Cruickshank

2001 ◽  
Vol 26 (2) ◽  
pp. 429-432 ◽  
Author(s):  
N. R. Kendall ◽  
D. V. Illingworth ◽  
S. B. Telfer

AbstractSigns of clinical copper deficiency in ruminant animals include infertility. Blood copper concentrations alone are not an adequate indicator of copper status, as they take no account of the thiomolybdate challenge to the animal. The use of the ratio of caeruloplasmin activity to plasma copper concentration should provide a better indicator of molybdenum induced copper problems. The objectives of this study were to obtain veterinary feedback on the University of Leeds Trace Element Laboratory's (ULTEL) assessment of copper status and responses to any recommended supplementation. Blood samples from 713 female cattle from 114 herds were assessed for copper status, including plasma copper concentrations, serum caeruloplasmin activities and the ratio between the caeruloplasmin and plasma copper (CP/PlCu ratio). On the basis of only plasma copper analysis 95.0 % of the cattle were classified as being of normal copper status using Veterinary Laboratory Agency reference ranges. However, when the CP/PlCu ratio was also considered only 35.6 % of the cattle would be classed as having normal copper status. Appropriate copper supplementation would be required by 30.7 % of the cattle and a further 27.8 % could also benefit from additional copper. Veterinary responses to a questionnaire (80 % returned) indicated that infertility was a major problem in their clients’ herds. Where copper supplementation was recommended and administered an increase infertility was observed. In herds showing poor or lack ofoestrous behaviour/ later embryo loss (signs of clinical copper deficiency), 91.7 % reported that these signs were reduced by copper supplementation. The relevance of the CP/PlCu ratio as a diagnostic aid in the identification of copper responsive infertility has been supported by the responses of the veterinary surgeons.


2000 ◽  
Vol 2000 ◽  
pp. 88-88
Author(s):  
A.M. Mackenzie ◽  
S Evans ◽  
J.N.C. Lynn ◽  
D.V. Illingworth ◽  
R.G. Wilkinson

Clinical copper deficiency is the second most common mineral deficiency in the world, the main cause being high dietary levels of molybdenum, sulphur and iron. Phillippo et al, (1987) reported that clinical signs of deficiency resulted from high dietary Mo and S. However, Fe and S resulted in hypocupraemia but did not induce clinical signs of deficiency. Therefore is was concluded that clinical copper deficiency was due to a direct effect of dietary Mo and S on copper metabolism in ruminants. Mackenzie et al. (1997) reported that plasma copper levels were not an accurate indicator of copper status and unlikely to predict animals requiring copper supplementation. Caeruloplasmin is large copper enzyme and accounts for 88% of plasma copper and Mackenzie et al. (1997) proposed that a caeruloplasmin to plasma copper ratio may provide a more accurate biochemical indicator of copper status. This trial was designed to investigate the effect of dietary Mo, S and Fe on the copper status of the lambs.


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