Effect of zinc supplementation on incidence of infections and hospital admissions in sickle cell disease (SCD)

Abstract

Zinc deficiency is a common nutritional problem in adult sickle-cell disease (SCD) patients. Hyperzincuria and increased requirement of zinc due to continued hemolysis in SCD are probable bases for zinc deficiency in these patients. Zinc deficiency affects adversely T-helper 1 (TH 1) functions and cell mediated immunity and interleukin (IL)-2 production is decreased in zinc deficient subjects. We hypothesized that zinc supple-mentation will improve T-helper 1 function and decrease incidence of infections in patients with SCD. We tested this hypothesis in 32 SCD subjects who were divided in three groups (Grs A, B, and C). Grs A (n = 11) and B (n = 10) were zinc deficient based on cellular zinc criteria and Gr C (n = 11) were zinc sufficient. Gr A subjects were observed for 1 year (baseline), following which they received zinc acetate (50 to 75 mg of elemental zinc orally daily) for 3 years. Gr B subjects were observed for 1 year (baseline), following which they received placebo for 1 year and then switched to zinc supplementation (50 to 75 mg of elemental zinc orally daily) for 2 years. Gr C subjects did not receive any intervention inasmuch as they were zinc sufficient. Prolonged zinc supplementation resulted in an increase in lymphocyte and granulocyte zinc (P = 0.0001), and an increase in interleukin-2 production (P = 0.0001), decreased incidence of documented bacteriologically positive infections (P = 0.0026), decreased number of hospitalizations and decreased number of vaso-occlusive pain crisis (P = 0.0001). The predominant pathogens isolated were staphylococci and streptococci involving the respiratory tract and aerobic gram-negative bacteria , particularly Escherichia coli, involving the urinary tract. Further confirmation of our observations will require prospective studies of zinc supplementation in a larger number of SCD patients. Am.

Pharmacotherapeutical strategies in the prevention of acute, vaso-occlusive pain in sickle cell disease: a systematic review

“…1968 and 2016, of which 15 trials were published before the year 2000 37,[42][43][44][45][46][47][48][49][50][51][52][53][54][55] and 8 in the last 5 years. [56][57][58][59][60][61][62][63] Three studies did not use a placebo intervention for their control group.…”

“…[56][57][58][59][60][61][62][63] Three studies did not use a placebo intervention for their control group. 43,54,56 A majority of studies were performed in North America (n 5 10), 33,46,47,51,61,62,[64][65][66][67][68] Africa (n 5 9), 38,42,52,55,56,59,[69][70][71] and Latin America (n 5 8). 40,44,48,49,53,54,57,72 Four studies were performed on multiple continents.…”

“…[75][76][77] A large, placebo-controlled study in India (N 5 130) demonstrated a significant decrease in the number of sickle-cell-related crises (including nonpain events) in the zinc sulfate group, but no effect on length of hospital stay (Table 1; supplemental Table 3). 50 Prasad et al 47 compared zinc acetate supplementation with routine care and placebo and did not observe any differences between treatments arms (N 5 32). Data from an additional study by this group did not allow post hoc comparison of the number of VOCs between the treatment arms (N 5 36).…”

Efeitos da suplementação com zinco sobre o crescimento, sistema imunológico e diabetes

“…Os efeitos da suplementação com zinco sobre o sistema imunológico de adultos portadores de anemia falciforme foram objeto do estudo realizado por Prasad et al 19 . Para tanto, 32 pacientes receberam, via oral, uma suplementação com acetato de zinco (50 a 75mg/dia de zinco elementar) durante dois ou três anos.…”

Zinc supplement greatly improves the condition of parkin mutant Drosophila

“…Zinc is not redox-active, but nevertheless toxic when in excess (Beyersmann and Haase, 2001). Acute zinc toxicity is rare but has been reported (Duncan et al, 1992;Whittaker, 1998;Prasad et al, 1999). If the extracellular concentration of zinc exceeds the capacity of zinc homeostasis mechanisms, it becomes cytotoxic and an excess of free intracellular zinc can trigger apoptosis (Choi et al, 1988;Duncan et al, 1992;Kim et al, 1999;Beyersmann and Haase, 2001;Wilhelm et al, 2001;Beyersmann, 2002;Walther et al, 2003).…”