scholarly journals Relationship between plasma zinc concentrations and clinical signs of zinc deficiency (1043.9)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
K. Ryan Wessells ◽  
Janet King ◽  
Kenneth Brown
Keyword(s):  
Zinc Deficiency ◽  
Clinical Signs ◽  
Plasma Zinc ◽  
Zinc Concentrations

Relationships between Plasma Zinc Concentrations and Clinical Signs of Zinc Deficiency

2015 ◽  
Vol 5 (5) ◽  
pp. 1015-1016
Author(s):  
K. Wessells ◽  
Janet King ◽  
Kenneth Brown
Keyword(s):  
Zinc Deficiency ◽  
Clinical Signs ◽  
Plasma Zinc ◽  
Zinc Concentrations

Enteropathic acrodermatitis in children

2021 ◽  
Vol 11 (2) ◽  
pp. 21-28
Author(s):  
V.P. Novikova ◽  
◽  
A.A. Pokhlebkina ◽  
D.V. Zaslavsky ◽  
A.I. Khavkin ◽  
...  
Keyword(s):  
Zinc Deficiency ◽  
Topical Therapy ◽  
Clinical Manifestations ◽  
Skin Lesions ◽  
Knee Joints ◽  
Zinc Metabolism ◽  
Plasma Zinc ◽  
Significant Treatment ◽  
Zinc Concentrations ◽  
Erythematous Plaques

Enteropathic acrodermatitis is a rare hereditary form of zinc deficiency, characterized by periorial and acral dermatitis, alopecia and diarrhea. Refers to congenital disorders of zinc metabolism, inherited as an autosomal recessive disease resulting from mutations in the gene for the zinc transporter SLC39A4. The prevalence ranges from 1 to 9:1,000,000, with an overall incidence of 1:500,000 newborns. The disease usually manifests itself in infancy, within a few weeks of stopping breastfeeding and switching the baby to a cow's milk-based formula, or in the first days of life if artificially fed from birth. The classical clinical manifestations of acrodermatitis enteropathic are characterized by the triad: acral and periofital dermatitis, alopecia and diarrhea, but all three signs together occur only in 20% of cases. Diarrhea may develop concurrently with skin symptoms, may precede or occur later. Characteristic signs of skin lesions include sharply demarcated, dry, scaly erythematous plaques or edematous foci with vesicles and pustules on the skin of the elbow and knee joints, distal extremities, genitals, in the inguinal folds, which are usually symmetrically distributed, have sharp boundaries and irregular outlines. The course of the skin syndrome is long, as it progresses, non-healing erosive and ulcerative areas appear. Plasma zinc deficiency is the gold standard for diagnosis. Most infants with AE have low plasma zinc concentrations (<500 mcg/L or <50 mcg/dl), but a level of less than 70 mcg/L on an empty stomach or less than 65 mcg/dl in older non-dieting children is considered diagnostically significant. Treatment for this disease usually includes enteral or parenteral zinc administration, at a dose of 1-3 mg/kg/day. for elemental zinc. A clinical response is observed within 5–10 days. Supportive zinc therapy is necessary throughout the patient's life, although periods of remission have been reported. Topical therapy is also used: Dexpanthenol in the form of a cream, applied 3 times a day in the area of dermatitis, can enhance re-epithelialization. There is no significant evidence of improvement with topical zinc application. No activity restrictions are required for patients with acrodermatitis enteropathic. Key words: zinc deficiency, enteropathic acrodermatitis, children

Zinc Deficiency and Edema

PEDIATRICS ◽  
1986 ◽  
Vol 77 (1) ◽  
pp. 132-133
Author(s):  
MICHAEL H. N. GOLDEN ◽  
BARBARA E. GOLDEN
Keyword(s):  
Developing Countries ◽  
Zinc Deficiency ◽  
Premature Infants ◽  
Zinc Concentration ◽  
Clinical Presentation ◽  
Plasma Zinc ◽  
Plasma Zinc Concentration ◽  
Clear Association ◽  
Zinc Concentrations

To the Editor.— Kumar and Anday1 describe three premature infants presenting with edema and hypoproteinemia—the classical signs of kwashiorkor—between 5 and 9 weeks of age. Such cases are not uncommon in developing countries. Kumar and Anday's patients had low plasma zinc concentrations (43, 37, and 42 µg/dL). On this basis the authors claim that edema and hypoproteinemia is a clinical presentation of zinc deficiency not previously reported. We reported2 a clear association between "nutritional" edema and a low plasma zinc concentration in 1979; our subsequent experience has confirmed that edema of this type is always associated with a low plasma zinc concentration, as indeed Kumar and Andays' cases demonstrate.

Dietary Zinc Intake and Plasma Zinc Concentrations in Children with Short Stature and Failure to Thrive

2016 ◽  
Vol 69 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Nadine Yazbeck ◽  
Rima Hanna-Wakim ◽  
Rym El Rafei ◽  
Abir Barhoumi ◽  
Chantal Farra ◽  
...  
Keyword(s):  
Short Stature ◽  
Zinc Deficiency ◽  
Growth Parameters ◽  
Medical Center ◽  
Failure To Thrive ◽  
Plasma Zinc ◽  
Dietary Zinc ◽  
Zinc Intake ◽  
Significant Difference ◽  
Zinc Concentrations

Background: The burden of zinc deficiency on children includes an increased incidence of diarrhea, failure to thrive (FTT) and short stature. The aim of this study was to assess whether children with FTT and/or short stature have lower dietary zinc intake and plasma zinc concentrations compared to controls. Methods: A case-control study conducted at the American University of Beirut Medical Center included 161 subjects from 1 to 10 years of age. Results: Cases had a statistically significant lower energy intake (960.9 vs. 1,135.2 kcal for controls, p = 0.010), lower level of fat (30.3 vs. 36.5 g/day, p = 0.0043) and iron intake (7.4 vs. 9.1 mg/day, p = 0.034). There was no difference in zinc, copper, carbohydrate and protein intake between the 2 groups. The plasma zinc concentration did not differ between the cases and controls (97.4 vs. 98.2 μg/dl, p = 0.882). More cases had mild-to-moderate zinc deficiency when compared to controls with 10.3 vs. 3.6%, p = 0.095. Conclusion: Our study did not show statistically significant difference in dietary zinc intake and plasma zinc concentrations between children with FTT and/or short stature compared to healthy controls. A prospective study is planned to assess the effect of zinc supplementation on growth parameters in FTT children.

scholarly journals Bovine Hereditary Zinc Deficiency: Lethal Trait a 46

1996 ◽  
Vol 8 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Margo Machen ◽  
Tim Montgomery ◽  
Robert Holland ◽  
Emmett Braselton ◽  
Robert Dunstan ◽  
...  
Keyword(s):  
Zinc Deficiency ◽  
Autosomal Recessive Disorder ◽  
Skin Lesions ◽  
Acrodermatitis Enteropathica ◽  
Plasma Zinc ◽  
Serum Samples ◽  
Secondary Complications ◽  
Bull Calf ◽  
Zinc Concentrations

Bovine hereditary zinc deficiency, also referred to as Adema disease, is an autosomal recessive disorder which results in inadequate amounts of zinc being absorbed from the gastrointestinal tract and leads to a number of clinical abnormalities. Using semen from a homozygous affected bull and obligate heterozygote cows in embryo transfer studies, 7 offspring were obtained. These included 5 affected calves and 1 heterozygous carrier; the seventh calf died within 48 hours of birth undiagnosed. One unaffected, unrelated bull calf was raised as a control. All the calves were raised and maintained under similar management conditions designed to minimize secondary complications that would obscure the clinical and biochemical observations of a zinc deficient state. The first clinical manifestation of zinc deficiency was diarrhea, followed by skin lesions, poliosis, and a decreased ability to sustain a suckle reflex. Trace mineral analysis of plasma blood samples revealed that plasma zinc concentrations of all the calves were normal at birth; however, they gradually declined in affected calves over the course of 3–8 weeks postpartum to below 0.5 ppm. Biochemical analysis of serum samples showed alkaline phosphatase activity consistently paralleled changes in the plasma zinc concentrations. The oral administration of zinc acetate caused a reversal of all clinical, biochemical, and histologic abnormalities in affected calves. The study of these affected calves allows further insight into the biological role of zinc as well as provides an animal model for the continued investigation of the human homologue acrodermatitis enteropathica.

The risk of copper deficiency in patients prescribed zinc supplements

2015 ◽  
Vol 68 (9) ◽  
pp. 723-725 ◽  
Author(s):  
Andrew Duncan ◽  
Calum Yacoubian ◽  
Neil Watson ◽  
Ian Morrison
Keyword(s):  
Zinc Deficiency ◽  
Copper Deficiency ◽  
Plasma Concentrations ◽  
Neurological Symptoms ◽  
Plasma Zinc ◽  
Reactive Protein ◽  
Plasma Copper ◽  
Zinc Concentrations ◽  
Zinc Supplements ◽  
High Doses

AimsIn high doses zinc may cause copper deficiency, a diagnosis that is often missed resulting in anaemia, neutropenia and irreversible neurological symptoms. The aim of this study was to assess if zinc deficiency is erroneously diagnosed by misinterpretation of plasma zinc concentrations and whether copper deficiency is induced in patients prescribed zinc.MethodsCasenotes of 70 patients prescribed zinc were scrutinised. Plasma concentrations of zinc, copper, C reactive protein and albumin were recorded from the laboratory database.Results62% of patients were prescribed zinc at doses sufficient to cause copper deficiency. In 48% of the patients, plasma zinc concentrations were low as a probable result of hypoalbuminaemia or the systemic inflammatory response rather than deficiency. Awareness of copper deficiency was lacking; it was only documented as a possible side effect in one patient and plasma copper was measured in only two patients prescribed zinc. 9% of patients developed unexplained anaemia and 7% developed neurological symptoms typical of copper deficiency.ConclusionsZinc deficiency is frequently misdiagnosed on the basis of low plasma zinc concentrations. The potential risk of copper deficiency developing in patients prescribed high doses of zinc is apparently infrequently considered. It is probable that a significant minority of patients prescribed with high doses of zinc develop iatrogenic copper deficiency.

scholarly journals Relationship Between Plasma Zinc, Angiotensin-converting Enzyme, Alkaline Phosphatase and Onset of Symptoms of Zinc Deficiency in the Rat

1988 ◽  
Vol 41 (3) ◽  
pp. 343 ◽  
Author(s):  
Colin L White
Keyword(s):  
Alkaline Phosphatase ◽  
Angiotensin Converting Enzyme ◽  
Zinc Deficiency ◽  
Protein Intake ◽  
Zinc Concentration ◽  
Clinical Signs ◽  
Plasma Zinc ◽  
Converting Enzyme ◽  
Plasma Zinc Concentration ◽  
Sequence Of Events

Recent evidence suggests that changes in plasma zinc concentration may play a central role in the development of early lesions of zinc deficiency. The aim of the following work was to better understand events occurring in plasma during the onset of zinc deficiency, and to investigate biochemical mechanisms by which plasma zinc may exert its effects. Fifty male weanling rats of 90 g weight were allocated to five treatment groups of ten rats each. Treatments were: 1, zinc deficient, mixed diet (1-2 mg Zn per kg): 2, zinc deficient, self-select diet; 3, zinc repleted; 4, control, pair fed; 5, control, ad libitum fed. With the exception of treatment 1, which consisted of a 25% casein diet, all rats were offered protein as a separate component of the diet. Control rats received zinc in the drinking water (100 mg I-I). The sequence of events following initiation of zinc deficiency were: reduced plasma zinc concentration (2 days), reduced plasma angiotensin-converting enzyme and alkaline phosphatase activities (3-4 days), reduced feed intake and growth (5-6 days) and reduced percentage protein intake (12 days). Plasma zinc concentration in the deficient rats was inversely correlated with the growth rate of the rat over the previous 24 h. Zinc repletion resulted in marked overshoot in plasma zinc concentration (300%) and converting-enzyme activity (150%) within 24 h, but a return to normal within 72 )1. Alkaline phosphatase activity responded likewise, albeit more slowly. Protein self selection had no effect on the manifestations of zinc deficiency, although reduced protein intake was associated with lower plasma zinc concentration. The results provide evidence of a role for plasma zinc in the development of early clinical signs of zinc deficiency, possibly acting biochemically through reduced activity of zinc-dependent peptidases such as angiotensin-converting enzyme.

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