Zinc and Immunocompetence in Protein-Energy Malnutrition

Golden, Michael; Harland, P. S. E. G.; Golden, Barbara E.; Jackson, A. A.

doi:10.1016/s0140-6736(78)92463-7

Cited by 226 publications

(48 citation statements)

References 20 publications

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“…A significant (38) and profound T cell immunodeficiency (39), the recent evidence that zinc deficiencies may account for the cell-mediated immunodeficiencies in protein/calorie malnutrition syndromes of man seems attractive (40). The present findings would be consistent with this view.…”

Section: Resultssupporting

confidence: 87%

Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice

Fernandes

Nair

Onoé

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

284

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Section: Resultssupporting

confidence: 87%

Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice

Fernandes

Nair

Onoé

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

284

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“…The absolute numbers of circulating T cells are reduced, and the rela tive number of suppressor cells seem to be increased [1]. Various hypotheses have attributed the damage of the T cell function to vitamin D and B6 deficiency [2,3], low ered blood zinc level [4], and the presence of 'middle molecules' [5]. This depressed immunity is believed to be responsible for an increased incidence of infections and malignancies in CRF [6,7], For example, the inci dence of hepatitis B virus (HBV) infection is high among dialysis patients [8,9].…”

Section: Introductionmentioning

confidence: 99%

Cell-Mediated Immunity in Patients on Hemodialysis: Relationship with Hepatitis B Carrier Status

Lee

Yap²,

Tan³

et al. 1991

Am J Nephrol

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We compared cell-mediated immune responses in two groups of patients on hemodialysis. One group of patients were chronic carriers of hepatitis B virus (HBV), and the patients of the other group were HBV antigen negative. Our results show that despite the presence of normal numbers of T cells and an increased CD4/CD8 ratio in both groups of patients compared to healthy controls (p < 0.0001), only the group of patients who were chronic HBV carriers showed depressed lymphoproliferative responses to phytohemagglutinin (p < 0.001) and concanavalin A (p < 0.0001). In contrast, a control group of healthy adult HBV carriers showed normal T cell subsets and lymphoproliferative responses to mitogens, indicating that HBV infection per se did not result in depressed lymphoproliferative responses. These results further substantiate the notion that depressed cell-mediated immunity in chronic renal failure is an important factor in predisposing patients to HBV infection with subsequent development of the chronic carrier state.

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“…poor wound healing, and reduced cellular immunitythat have been ascribed to zinc deficiency [3][4][5][6][7], Profound zinc depletion occurs most commonly in association with chronic inflammatory bowel disease, prolonged parenteral nutrition, hepatic cirrhosis, and protein-caloric malnutrition [4. 6.…”

Section: Introductionmentioning

confidence: 99%

Zinc Metabolism in Patients on Maintenance Hemodialysis

Muirhead¹,

Kertesz²,

Flanagan³

et al. 1986

Am J Nephrol

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Recent studies have focused attention on the possible role of zinc depletion in the pathogenesis of uremic symptoms such as dysgeusia and impotence. The present studies were undertaken to evaluate the prevalence of zinc deficiency and abnormalities of zinc metabolism in patients with end-stage renal disease. A total of 43 stable chronic hemodialysis patients were screened for evidence of zinc deficiency by measurement of fasting predialysis leukocyte and plasma zinc. The results were compared with those from 30 healthy volunteers. Seventeen of these 43 patients had ⁶⁵Zn absorption measured, and in 9 the rate of disappearance of ⁶⁵Zn from the body was also measured. The results were compared with those obtained in 20 healthy controls. The nutritional status of these 17 patients was estimated by global nutritional assessment and calculation of the Quetelet index while 9 of 17 had dietary zinc intake calculated from a diet history. The mean plasma zinc level was lower in the hemodialysis patients (11.7 ± 2.3μmol/lvs. 13.3 ± 2.9 μmol/l in controls; p < 0.05). The mean leukocyte zinc level was 0.81 ± 0.27 μmol/g dry weight in dialysis patients and 0.81 ± 0.22 μmol/g in controls (p > 0.2). The mean ⁶⁵Zn absorption in the patients was 49 ± 14% and in controls 53 ± 12% (p > 0.2). Mean turnover of body ⁶⁵Zn was 0.47 ± 0.11 %/day in patients and 0.43 ± 0.18%/day in controls (p > 0.1). The mean ⁶⁵Zn half-life was 154 ± 29 days in patients and 187 ± 75 days in controls (p > 0.05). Nine patients were regarded as undernourished. The mean leukocyte zinc level in these patients was 0.53 ± 0.21 μmol/g and 0.64 ± 0.29 μmol/g in the 8 well-nourished patients (p < 0.05). The mean ⁶⁵Zn absorption in the undernourished patients was 44 ± 18% and 53 ± 10% in the well-nourished patients (p > 0.1). Dietary zinc was normal (10.2 ± 4.8 mg/day) and did not correlate with plasma zinc, leukocyte zinc, or ⁶⁵Zn absorption.

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Zinc and Immunocompetence in Protein-Energy Malnutrition

Cited by 226 publications

References 20 publications

Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice

Impairment of cell-mediated immunity functions by dietary zinc deficiency in mice

Cell-Mediated Immunity in Patients on Hemodialysis: Relationship with Hepatitis B Carrier Status

Zinc Metabolism in Patients on Maintenance Hemodialysis

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