Reduced Serum Zinc Levels Research Articles

Association of serum zinc with mineral stress in chronic kidney disease.

The excessive cardiovascular mortality of patients with chronic kidney disease (CKD) could be linked to mineral stress, the biological consequence of calcium-phosphate nanoparticle exposure. This study investigated whether zinc is associated with mineral stress markers in CKD. Zinc and T50 (serum calcification propensity) as well as hydrodynamic radius of secondary calciprotein particles (CPP2) were measured in blood donors and CKD patients with/out dialysis. Serum zinc concentrations and T50 were reduced, while CPP2 radius was increased in CKD patients. Serum zinc levels positively correlated with T50 and inversely correlated with CPP2 radius. In a hierarchical linear regression model, T50 was associated with age, calcium, phosphate, magnesium and albumin. Addition of zinc significantly improved prediction of the model, confirming an additional contribution of zinc to T50. Similar observations were made for the association of zinc and CPP2 radius, but spiking experiments indicated that zinc may stronger modify T50 than CPP2 radius. Also, urinary zinc excretion was increased in patients with kidney disease and correlated to T50 and CPP2 radius. Serum zinc further correlated with markers of arterial stiffness in blood donors and CKD patients, but these associations did not remain significant in a multivariate linear regression model. Reduced serum zinc levels in CKD appear directly linked to lower T50 and associated with larger CPP2 radius. Further studies on the associations of zinc and mineral stress as well as putative therapeutic benefits of zinc supplementation are required.

Evaluation of Serum Zinc Levels in Children of 6 Months to 5 Years of Age Diagnosed with Simple Febrile Seizures

Background: Febrile seizures are defined as seizures associated with a febrile illness that developed without central nervous system infection or acute electrolyte imbalance, intoxication, trauma, and metabolic disorder in children aged 1 month to 5 years without previous afebrile seizures. Various studies show a relationship between zinc levels and febrile seizures. Objectives: The purpose of this study was to examine the relationship between serum zinc levels and febrile seizures. Methods: This prospective, cross-sectional, and descriptive study was conducted from 04/10/2021 to 04/02/2022. A total of 85 children aged 6 months to 5 years admitted to the pediatric emergency service of the Republic of Turkey Ministry of Health Cemil Taşcıoğlu City Hospital were included in the study. The patients who met the inclusion criteria and whose consent was obtained were included in the study. Complex and febrile status patients were not included in the study due to the small number of patients. The cases included in the study were divided into 2 groups of patients and healthy controls. The patients with fever were divided into 2 groups, including those with and without febrile seizures. The levels of zinc and complete blood count parameters were measured in the blood samples taken from all the patients. IBM SPSS 22 package software was used for the statistical examination of the data. Results: When the cases included in this study were divided according to gender, 33 (38.8%) and 52 (61.2%) patients were female and male, respectively. The mean age of the cases was 29.2 ± 15.9 months (range: 6 - 60). Of the 85 participating cases, 30 patients had febrile seizures, 30 were only febrile patients, and 25 were healthy controls. When zinc levels were compared between the groups, the plasma zinc levels of the febrile seizures and febrile groups were observed to be lower than the healthy control group (P < 0.05). Conclusions: In this study, the group consisting of patients with febrile seizures and the groups of patients who had a fever but did not have febrile seizures during the study had reduced serum zinc levels than the control group consisting of healthy patients without fever.

Can Oral Zinc Supplementation Reduce Relapses in Childhood Steroid-Sensitive Nephrotic Syndrome? A Systematic Review.

Frequent relapses and steroid dependence are common treatment challenges of steroid-sensitive nephrotic syndrome (SSNS) in children. Acute respiratory infection (ARI) is the most frequently reported trigger of relapse. Given the role of zinc supplementation in preventing ARI, some studies show that this targeted intervention may reduce relapses in childhood SSNS. This systematic review aimed to determine if oral zinc supplementation can significantly reduce relapses in this disease. We searched the PubMed and Google Scholar electronic databases for interventional and observational analytical studies without limiting their year or language of publication. We selected studies with primary data that met our inclusion criteria, screened their titles and abstracts, and removed duplicates. We used a preconceived structured form to extract data items from selected studies and conducted a quality assessment of randomized controlled trials (RCTs) and non-randomized studies with the Cochrane collaboration tool and the Newcastle Ottawa Scale, respectively. We qualitatively synthesized the extracted data to validate the review's objective. Eight full-text articles were selected, comprising four RCTs and four observational analytical studies. Two of the RCTs had a high risk of bias in three parameters of the Cochrane collaboration tool, while three non-randomized studies had low methodological quality. A total of 621 pediatric patients with SSNS were investigated in the eight studies: six participants dropped out in one study. Three RCTs indicate that zinc supplementation may lead to sustained remission or reduction in relapse rate. Similarly, three observational analytical studies suggest a significant relationship between reduced serum zinc levels and disease severity. Despite the association of zinc deficiency with increased morbidity in SSNS and the reduction of relapse rates with zinc supplementation, there is no robust evidence to recommend its use as a therapeutic adjunct. We recommend more adequately-powered RCTs to strengthen the current evidence.

Effect of Bacterial Diarrhoea on Serum Zinc Levels in Children with Special Reference to Different Bacterial Pathogens: A Cross-sectional Study

Introduction: Diarrhoea significantly leads to morbidity and mortality in under-five children, particularly in developing countries. Reduced serum zinc levels in acute non infectious diarrhoea has an impact on the frequency, severity and duration. However, evidence is still evolving on the status of zinc level in bacterial diarrhoea. Aim: To assess serum zinc level in bacterial diarrhoea and compare the serum zinc level in children with the different bacterial pathogens. Materials and Methods: This cross-sectional study was conducted in Department of Paediatrics at Federal Medical Centre, Owerri, Imo State, Nigeria, from August 2015 to February 2016, including 201 children aged 6 to 59 months with diarrhoea. Stool specimens were isolated for bacteria, using conventional culture techniques, while serum zinc levels were determined using atomic absorption spectrometry. Serum zinc level <65 µg/dL was regarded as zinc deficiency. The data collected was analysed using the Statistical Package for Social Sciences (SPSS) version 19.0. Results: Out of 201, 58 (28.9%) of the children with diarrhoea had bacteria in the stool. The most common organism isolated was Escherichia coli (33,16.4%) followed by Salmonella (13, 6.5%). All of the children with positive stool culture, irrespective of the type of microbial agent, had zinc deficiency with significant association between infective diarrhoea and zinc deficiency (χ2 =15.437; p-value=0.004). Children with shigella diarrhoea had the lowest mean serum zinc level, compared to other bacterial agents (33.6±4.4 µg/dL, p-value <0.001). Conclusion: Bacterial pathogens contribute significantly to the cause of diarrhoea in under-five Nigerian children, and are significantly associated with zinc deficiency. Thus, reinforcing the need for zinc supplementation and food fortification programs within the population, and maybe for longer in children with identified bacterial diarrhoea.

Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells

In diabetic patients, medial vascular calcification is common and associated with increased cardiovascular mortality. Excessive glucose concentrations can activate the nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-kB) and trigger pro-calcific effects in vascular smooth muscle cells (VSMCs), which may actively augment vascular calcification. Zinc is able to mitigate phosphate-induced VSMC calcification. Reduced serum zinc levels have been reported in diabetes mellitus. Therefore, in this study the effects of zinc supplementation were investigated in primary human aortic VSMCs exposed to excessive glucose concentrations. Zinc treatment was found to abrogate the stimulating effects of high glucose on VSMC calcification. Furthermore, zinc was found to blunt the increased expression of osteogenic and chondrogenic markers in high glucose-treated VSMCs. High glucose exposure was shown to activate NF-kB in VSMCs, an effect that was blunted by additional zinc treatment. Zinc was further found to increase the expression of TNFα-induced protein 3 (TNFAIP3) in high glucose-treated VSMCs. The silencing of TNFAIP3 was shown to abolish the protective effects of zinc on high glucose-induced NF-kB-dependent transcriptional activation, osteogenic marker expression, and the calcification of VSMCs. Silencing of the zinc-sensing receptor G protein-coupled receptor 39 (GPR39) was shown to abolish zinc-induced TNFAIP3 expression and the effects of zinc on high glucose-induced osteogenic marker expression. These observations indicate that zinc may be a protective factor during vascular calcification in hyperglycemic conditions.

Comparison of serum zinc level in acute improved and chronic cutaneous leishmaniasis

Background: Zinc is an effective factor in the immune response against infectious agents; its effect on the course of cutaneous leishmaniasis (CL) is unknown. This study aimed to compare the serum zinc level in patients with acute and chronic CL. Methods: A descriptive study was conducted on 120 CL cases and controls. This included 30 cases of acute CL (less than one year of lesion recovery), 30 cases of chronic CL (period of illness over one year), and 60 healthy subjects with age and gender proportional to the patients. Volunteers entered the study with knowledge and consent. The serum zinc level was measured by atomic absorption spectrophotometry. Results: The percentages of people with reduced serum zinc levels in the healthy, acute, and chronic groups were 13.3, 50, and 43.3%, respectively, whereby there was a significant difference between the leishmaniasis groups (acute and chronic) and the control group (p <0.001). However, the mean serum zinc level did not differ significantly between the acute (75.36 ± 15.72 µg/dl) and chronic (73.96 ± 17.98 µg/dl) leishmaniasis groups (P=0.94). Conclusions: A reduced serum zinc level is associated with symptomatic CL, but does not affect the clinical outcome and recovery.

274 Biotin Is required for the zinc homeostasis in the skin

Patients with biotin deficiency present symptoms that are similar to those in patients with acrodermatitis enteropathica (inherent zinc deficiency). However, the association between biotin and zinc deficiency remains unknown. We have previously shown that epidermal keratinocytes of mice fed zinc-deficient (ZD) diets secreted more adenosine triphosphate (ATP) than those of mice fed zinc-adequate (ZA) diets and that epidermal Langerhans cells are absent in ZD mice. Langerhans cells highly express CD39, which potently hydrolyzes ATP into adenosine monophosphate (AMP). Thus, a lack of Langerhans cells in ZD mice leads to non-hydrolysis ofATP, thereby leading to the development of ATP-mediated irritant contact dermatitis. In this study, we examined if biotin-deficient (BD) mice showed the same underlying mechanisms as those in ZD mice. BD mice showed reduced serum zinc levels, disappearance of epidermal Langerhans cells, and enhanced ATP production in the skin. Consequently, irritant contact dermatitis was significantly enhanced and prolonged in BD mice. In conclusion, the findings of our study showed that biotin deficiency leads to zinc deficiency because of which patients with biotin deficiency show similar symptoms as those with acrodermatitis enteropathica.

Coenzyme Q10, Zinc and MDA levels in verruca vulgaris

Background/aim Verruca vulgaris is a benign disease characterized with papillomas on the skin and mucosa. The aim of this study was to investigate the serum levels of coenzyme Q10, MDA, and zinc as well as the lipid profile of verruca vulgaris patients and examine the relationship between these parameters and clinical manifestations of the disease.Materials and methods The study included 49 verruca vulgaris patients (mean age: 32.01 ± 14.20 years; 22 males, 27 females) and 40 healthy volunteers (mean age: 31.63 ± 8.98 years; 21 males and 19 females). Coenzyme Q10 levels were assessed by using an enzyme-linked immunosorbent assay. Serum MDA levels were measured spectrophotometrically. Zinc levels were measured using a Perkin Elmer AAnalyst 800 atomic absorption spectrometer with a deuterium background correction and additional standard techniques. Results The coenzyme Q10 levels were found to be higher in the verruca vulgaris group compared to the healthy volunteers. However, this increase was not statistically significant (P = 0.195). Zinc levels were significantly lower in the verruca vulgaris group compared to the healthy volunteers (P = 0.002). In the patient group, MDA levels and HDL levels were significantly higher compared to the healthy volunteers (P = 0.023 and P = 0.004, respectively). Additionally, there was no statistically significant difference between the groups in the CoQ10/Total cholesterol ratio (P = 0.433).Conclusion Reduced serum zinc levels and increase of oxidative stress in verruca vulgaris may be a factor responsible for development of verruca vulgaris.

Biotin Is Required for the Zinc Homeostasis in the Skin.

Patients with biotin deficiency present symptoms that are similar to those in patients with acrodermatitis enteropathica (inherent zinc deficiency). However, the association between biotin and zinc deficiency remains unknown. We have previously shown that epidermal keratinocytes of mice fed zinc-deficient (ZD) diets secreted more adenosine triphosphate (ATP) than those of mice fed zinc-adequate (ZA) diets and that epidermal Langerhans cells are absent in ZD mice. Langerhans cells highly express CD39, which potently hydrolyzes ATP into adenosine monophosphate (AMP). Thus, a lack of Langerhans cells in ZD mice leads to non-hydrolysis of ATP, thereby leading to the development of ATP-mediated irritant contact dermatitis. In this study, we examined if biotin-deficient (BD) mice showed the same underlying mechanisms as those in ZD mice. BD mice showed reduced serum zinc levels, disappearance of epidermal Langerhans cells, and enhanced ATP production in the skin. Consequently, irritant contact dermatitis was significantly enhanced and prolonged in BD mice. In conclusion, the findings of our study showed that biotin deficiency leads to zinc deficiency because of which patients with biotin deficiency show similar symptoms as those with acrodermatitis enteropathica.

Zinc in schizophrenia: A meta-analysis.

The role of zinc homeostasis in various psychopathologies is an emerging area of interest. Zinc is strongly implicated in depressive disorders but is inadequately studied in schizophrenia, despite growing evidence of abnormal zinc transporters associated with schizophrenia. A meta-analysis of serum zinc concentrations in persons with schizophrenia was conducted to address this gap. PubMed and Embase were searched for all articles published through February 2018 that reported serum zinc concentrations in individuals with schizophrenia and in comparison subjects. A random-effects meta-analysis was carried out to compare mean serum zinc concentrations between the groups in terms of the weighted mean difference. The current meta-analysis combined 10 studies, including a total of 658 schizophrenia patients and 1008 controls. Serum zinc concentration was significantly lower in individuals with schizophrenia than controls (12.81 μg/dl (1.96 μmol/l), t = -2.59, 95% CI: -22.50 to -3.12, p < 0.05). The reduction in zinc levels was more pronounced among inpatients and newly diagnosed, drug-naïve patients. The current meta-analysis supports a disturbance of zinc homeostasis in individuals with schizophrenia compared to healthy controls, although the relationship between reduced serum zinc levels and psychotic symptoms remains unknown. Altered serum zinc might be linked to defective transporters and/or inflammation that impact the brain's glutamatergic system.

Zinc Inhibits Phosphate-Induced Vascular Calcification through TNFAIP3-Mediated Suppression of NF-κB

Background The high cardiovascular morbidity and mortality of patients with CKD may result in large part from medial vascular calcification, a process promoted by hyperphosphatemia and involving osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Reduced serum zinc levels have frequently been observed in patients with CKD, but the functional relevance of this remains unclear.Methods We performed experiments in primary human aortic VSMCs; klotho-hypomorphic (kl/kl), subtotal nephrectomy, and cholecalciferol-overload mouse calcification models; and serum samples from patients with CKD.Results In cultured VSMCs, treatment with zinc sulfate (ZnSO4) blunted phosphate-induced calcification, osteo-/chondrogenic signaling, and NF-κB activation. ZnSO4 increased the abundance of zinc-finger protein TNF-α-induced protein 3 (TNFAIP3, also known as A20), a suppressor of the NF-κB pathway, by zinc-sensing receptor ZnR/GPR39-dependent upregulation of TNFAIP3 gene expression. Silencing of TNFAIP3 in VSMCs blunted the anticalcific effects of ZnSO4 under high phosphate conditions. kl/kl mice showed reduced plasma zinc levels, and ZnSO4 supplementation strongly blunted vascular calcification and aortic osteoinduction and upregulated aortic Tnfaip3 expression. ZnSO4 ameliorated vascular calcification in mice with chronic renal failure and mice with cholecalciferol overload. In patients with CKD, serum zinc concentrations inversely correlated with serum calcification propensity. Finally, ZnSO4 ameliorated the osteoinductive effects of uremic serum in VSMCs.Conclusions Zinc supplementation ameliorates phosphate-induced osteo-/chondrogenic transdifferentiation of VSMCs and vascular calcification through an active cellular mechanism resulting from GPR39-dependent induction of TNFAIP3 and subsequent suppression of the NF-κB pathway. Zinc supplementation may be a simple treatment to reduce the burden of vascular calcification in CKD.

Serum Zinc Concentrations in Children with Acute Bloody and Watery Diarrhoea.

The role of zinc in the pathogenesis of diarrhoea is controversial. This study was conducted to compare serum zinc levels in children with acute diarrhoea to those found in healthy children. This case-control study was carried out at the Qazvin Children's Hospital in Qazvin, Iran, between July 2012 and January 2013. A total of 60 children with acute diarrhoea (12 children with bloody diarrhoea and 48 children with watery diarrhoea) and 60 healthy children were included. Zinc levels for all subjects were measured using a flame atomic absorption spectrophotometer and data were analysed and compared between groups. Mean serum zinc levels in the patients with acute bloody diarrhoea, acute watery diarrhoea and the control group were 74.1 ± 23.7 μg/dL, 169.4 ± 62.7 μg/dL and 190.1 ± 18.0 μg/dL, respectively (P = 0.01). Hypozincaemia was observed in 50.0% of children with acute bloody diarrhoea and 12.5% of those with acute watery diarrhoea. None of the patients in the control group had hypozincaemia (P = 0.01). Children with acute bloody diarrhoea had significantly reduced serum zinc levels in comparison to healthy children. However, a study with a larger sample size is needed to examine the significance of this trend.

Reduced serum zinc levels while improving growth of underweight school children in trial of zinc-fortified milk in Indonesia

Background Most children in low-income countries haveinadequate dietary zinc. The study was aimed to demonstrate theeffect of iron-zinc fortified milk in improving zinc status amongunderweight school children in Indonesia.Objective To evaluate the effects of milk fortification with zinc onserum zinc levels in underweight Indonesian school children.Methods A double-blind, randomized, controlled, communitybasedstudy was conducted on 426 underweight children aged 7to 9 years in several low economic income level elementary schoolsin Jakarta and Solo. Subjects were randomly allocated to receiveeither zinc-fortified milk (n= 217) or standard milk (n=209) for6 months. The fortified milk provided an 2.38 mg zinc per dayand the standard milk provided 0.88 mg zinc per day.Results Among underweight children, the prevalence of stuntingwith a height-for-age z-score &lt; - 2.0 SD was 39.7%. Almost allsubjects (98%) had zinc intake ofless than 60% of the Indonesianrecommended daily allowance (RDA) for that particular agegroup. After receiving the milk intervention, mean serum zincconcentration declined significantly in both groups (from 13 .50±3.05 μmol/Lat baseline to 10.59±1.93 μmol/L, P&lt; 0.05), butgrowth parameters (weight and height) improved.Conclusion Reduced mean serum zinc levels were observed inchildren who received standard milk, as well as those who receivedzinc-fortified milk. These reduction in serum zinc levels may be apart of homeostatic control mechanim for improving the negativezinc balance in zinc pools, as a negative effect on linear growthwas not observed. Larger clinical trials of adequate sample sizeneed to be conducted in order to provide better understandingon zinc regulation among underweight school children. [Paediatrlndones. 2012;52:118-24).

Reduced serum zinc levels while improving growth of underweight school children in trial of zinc-fortified milk in Indonesia

Reduced serum zinc levels while improving growth of underweight school children in trial of zinc-fortified milk in Indonesia

Zinc regulates DNA synthesis and IL‐2, IL‐6, and IL‐10 production of PWM‐stimulated PBMC and normalizes the periphere cytokine concentration in chronic liver disease

Zinc (zinc ions and/or chelated zinc) plays an important role in the maintenance of immune function. Patients with chronic liver disease, particularly liver cirrhosis, frequently have endotoxemia, increased serum concentrations of cytokines, e.g., interleukin-6 (IL-6), and reduced serum zinc levels. The aim of the present study was to investigate the effects of zinc (ZnCl2, ZnO, ZnSO4) on DNA synthesis and cytokine production (IL-2, IL-6, IL-10) in pokeweed mitogen (PWM)-stimulated peripheral blood mononuclear cells (PBMC). In addition, we examined the effect of long-term zinc supplementation (zinc-hydrogenaspartate; UNIZINK 50; 3 × 1 = 29.76 mg/day) on IL-6 and IL-10 serum levels in patients with chronic liver disease (n = 16), all with reduced serum zinc levels. It could be shown that zinc concentrations up to 0.1 mM stimulate DNA synthesis and cytokine production by PWM-stimulated PBMC, whereas higher concentrations (0.2–0.4 mM) have a strongly inhibitory effect. Zinc concentrations exceeding 0.5 mM were found to have a toxic effect on these immune cells. Interestingly, in most patients with chronic liver disease (n = 10), zinc supplementation decreased IL-6, and to a lesser extent, IL-10 serum levels, and normalized the serum zinc concentrations. We conclude that zinc plays a regulatory role in DNA synthesis and cytokine production by PBMC. The critical zinc concentration for immune cells lies in the range of 0.5 mM, which is equivalent to a daily dose of ∼45 mg zinc salt. Furthermore, zinc supplementation in chronic liver disease with reduced serum zinc levels appears to normalize IL-6 and IL-10 production. J. Trace Elem. Exp. Med. 10:19–27, 1997. © 1997 Wiley-Liss, Inc.

Zinc metabolism and immune function in healthy elderly people

Changes in immune function have been described in the elderly, and zinc is known to influence immune parameters. Zinc supplementation has, however, produced contradictory results. We evaluated zinc metabolism and immunity in 15 healthy non-institutionalised elderly people on a self-selected diet and compared the results with those obtained from 10 young healthy subjects. The elderly subjects had reduced serum zinc levels and their zinc absorption values were lower than in the young subjects. Circulating immune parameters were within the normal range, while delayed immune response was altered in 8 of the 15 elderly subjects. Zinc supplementation (25 mg/day) did not result in a significant improvement in dermal hypersensitivity responses although some effect was seen in 5 cases. It is concluded that zinc supplementation is unnecessary in elderly healthy subjects even if they present zinc metabolism alterations, but may be indicated in the presence of disease.

Tumor necrosis factor induces skeletal muscle protein breakdown in rats

The metabolic response to infection includes loss of lean tissue and increased nitrogen excretion. The loss of muscle tissue during infection results in large part from accelerated skeletal muscle protein breakdown. Recent studies suggest that macrophage-derived products secreted during infection may signal increased muscle proteolysis. To test this, in the present report the ability of interleukin (IL-1) and tumor necrosis factor (TNF) to enhance muscle proteolysis was examined. Young rats were injected intravenously with either recombinant human IL-1 or TNF. For comparison some rats were injected with bacterial endotoxin. Eight hours after each treatment, the extensor digitorum longus muscles were isolated and incubated in vitro to assess muscle proteolysis by measuring tyrosine and 3-methyl-L-histidine release by the incubated muscles. Treatment of rats with either IL-1, TNF, or endotoxin all induced fever, increased serum lactate, and reduced serum zinc levels. Despite similar metabolic changes, muscle proteolysis responded differently. As expected, endotoxin treatment enhanced muscle protein breakdown, whereas IL-1 treatment was without effect. On the other hand, TNF was effective in accelerating muscle protein breakdown. TNF addition in vitro failed to enhance muscle proteolysis by incubated muscles, suggesting that its effects may be mediated in an indirect manner; however, a direct mode of action cannot yet be ruled out. Overall, the data indicate that the acute administration of TNF can signal increased muscle proteolysis similar to that observed during infection.

Spontaneous and interferon-induced natural cytotoxicity in Crohn's disease.

Natural killer cell (NK) activity and antibody-dependent cellular cytotoxicity (ADCC) exerted by peripheral blood mononuclear cells (PMNC) were investigated in 53 patients with Crohn's disease (CD). NK activity and ADCC were found to be significantly reduced in patients with CD (p less than 0.0005) as compared to healthy controls. Both effector cell functions increased after in vitro treatment of PMNC with gamma-interferon, but did not reach the levels found in controls (p less than 0.0005). Neither NK activity nor ADCC was significantly influenced by therapy with corticosteroids. Moreover, the reduced serum zinc levels in patients with CD, which have been shown to be associated with impaired immune function, did not influence the lytic effector cell mechanism assayed either. Finally, no association could be found between NK cell activity or ADCC and CD activity index, the extent of the disease and several laboratory parameters of inflammation. We conclude that patients with CD have a reduced lytic effector cell function which remains uninfluenced by corticosteroid treatment and seems to be present independently of disease activity.

Serum zinc levels in heterozygous carriers of the gene for acrodermatitis enteropathica

Three cases of acrodermatitis enteropathica (a.e.) from two nonrelated families are described. Two siblings had characteristic symptoms of a.e. in childhood. Both survived to adulthood without treatment, at which time the clinical picture became uncharacteristic of a.e. Even so, the serum zinc levels confirmed the diagnosis in both cases. The third case showed classic symptoms of a.e.; the patient had a greatly reduced serum zinc level and responded at once to treatment with zinc sulphate. Heterozygous carriers of the gene for a.e. have often had slightly reduced serum zinc levels. The value of this test could probably be improved by correcting the normal range of serum zinc for factors known to influence this, such as the patient's age and serum albumin level. The normal range ought also to be corrected for diurnal and postprandial variations of serum zinc.

Effect of oral zinc therapy in cirrhosis.

In 15 subjects with cirrhosis receiving oral zinc therapy at a dose of 90 mg. daily for 3 mo., no clinical response could be detected when comparison was made with control periods. In 12 subjects with cirrhosis, reduced serum zinc levels were observed, confirming previous studies. At variance with these results was the reduced urinary excretion of zinc. In 10 patients with cirrhosis a 1-wk. course of zinc elevated the serum zinc levels significantly but did not affect urinary excretion.