Zinc Nasolabial

5.5.3.1. Zinc Deficiency. Prasad et al. (218) first described zinc deficiency as "adolescent nutritional dwarfism," documenting the nutrient's role in growth and sexual maturity. While the early syndrome occurred with iron deficit, identification of an autosomal recessive defect causing acrodermatitis enteropathica (219) produced a clear phenotypic presentation of zinc deficiency alone. Skin lesions with predictable distribution around body orifices and extremities predominate, with functional deficits of diarrhea, compromised T-cell function, and altered central nervous function. The pivotal role of zinc in gene expression, cellular growth, and differentiation is the underlying cause of generalized metabolic impairment in deficiency (220).

Subjects without kidney disease enrolled in well-controlled, induced zinc depletion studies show classic dermatitis around the mouth, nose, inflammation of the mucosal membranes (221), and structural changes in hair bulb formation (222)—signs that appear as plasma zinc falls.

Drug/Nutrient Interactions:

ACE Inhibitors (270) Loop/Thiazide Diuretics (233-235) Corticosteroids (271) Exogenous Estrogen (27i)

Iron supplements, Ca++ phosphate > 1,360 mg/day, and high phytate, milk casein, nucleic acid intake decrease absorption.

Absorption is higher in animal PRO versus plant diets.

Zinc, Riboflavin are required to phosphorylate, activate V-B 6.

Ca Acetate inhibits Zinc absorption in hemodialysis patients (272).

Zinc is used to inhibit copper absorption in Wilson's disease (273).

Zinc is necessary to mobilize V-A from liver stores (274).

Biochemical Evaluation:

Serum Zinc - Pre-breakfast > 70 mcg/dL sign of deficit.

Plasma Zinc preferable with reduced contamination from erythrocytes.

Endogenous Zinc Excretion can also be used (221).

Substantial diurnal, postprandial variation in plasma zinc concentrations (plasma nadir in early PM ~ 12% below AM peak level) (277).

Function/Absorption/Elimination: Function: Catalytic enzyme activity, creation of "zinc finger-like" structure for protein folding, regulatory of gene expression. Absorbed: Exogenous absorption via Albumin-bound, saturable trans-cellular process in small intestine (jejenum).

Elimination: Major: Secretion into, excretion from intestine; Minor: Kidney, integument, semen, menses. Endogenous intestinal zinc losses best correlate with absorbed

Medical

Diagnoses/Comorbidities: Malabsorption Syndromes

Sprue, Crohn's, Short bowel syndrome (Supplement 12.2 mg/L small intestine fluid; 17.1 mg/Kg stool or ileostomy output (278). Long-term Alcohol Consumption Reduced absorption, increased urinary excretion (279). Sickle Cell Disease (280) Chronic Renal Disease Increased fecal losses (272, 226, 227).

Food Sources: (> 3 mg/svg) Red meats, liver, dark turkey, oysters, bran cereal, and wheat germ.

US Diet Sources: >3% total intake Beef, hamburger, pork, hot dogs, milk, bread, and eggs (275). RDA: 11 mg Male 8 mg Female

Upper Limit: 40 mg cut-off for reduced copper status, assessed by Erythrocyte Copper-Zinc Superoxide Dismutase activity.

Total Body Store: 1.5-2.5 g with 85% in skeletal muscle, bone; Tissues with highest concentrations bone, prostate, choroid of eye (276).

Physical Findings/Functional Deficits: DEFICIENCY : Acrodermatits Enteropathica

Oral: Circumorificial dermatitis (221) Eye: Dermatitis on lateral canthus Hair: Alopecia, Defective hair sheaths, atrophied dyspigmented bulbs (222). Skin: Patchy dry skin, Scrotal dermatitis (221 ). Nails: Leukonychia (281) Gastronintestinal: Diarrhea, Poor intake, Reduced taste acuity (237). Compromised ethanol metabolism (270). Growth: Delayed in children Hematologic: Reduced retinol-binding protein, albumin, and pre-albumin.

Hormonal: Reduced testosterone, free T4, and IGF-1 Immunologic: Altered innate, cellular, and humoral immunity; Delayed hypersensitivity skin tests (282). Sexual: Delayed maturation, impotence.

Visual: Abnormal dark adaptation (283) TOXICITY : Epigastric pain, nausea, vomiting, loss of appetite, abdominal cramps, diarrhea, and headaches; Anemia, leukopemia, neutropenia from copper deficit (251, 252); Myelopathy (spastic gait)/sensory Atakia (284).

Fig. 9. Comprehensive zinc assessment in renal failure. If not annotated otherwise, data cited from ref. (230).

Use of plasma/serum zinc as an indicator of zinc status was criticized in early studies, but more recent kinetic research suggests that plasma zinc concentration may be a valid indicator of whole-body zinc status in the absence of infection or stress (221), particularly when levels are low.

Zinc studies in kidney failure consistently reveal reduced serum concentrations (223-225). Metabolic research in patients receiving

A. Angular stomatitis Zinc 50 mcg/dL (R 50-150) ©Steve Castillo

C. Seborrheic-like dermatitis between eyebrows Zinc 50 mcg/dL (R 50-150) ©Steve Castillo

E. Circumorificial dermatitis Zinc 52 mcg/dL (R 50-150) ©David Giacalone

Dermatitis Circumorificial

B. Seborrheic-like dermatitis of the nasolabial fold Zinc 50 mcg/dL (R 50-150) ©Steve Castillo

D. Retroauricular dermatitis Zinc 50 mcg/dL (R 50-150) ©Steve Castillo

Zinc Nasolabial

F. Seborrheic-like dermatitis of the scalp Zinc 50 mcg/dL (R 50-150) ©Steve Castillo

Fig. 10. Nutrient-based lesions associated with laboratory validated zinc deficit. Photographs may not be reproduced, copied, projected, televised, digitized, or used in any manner without photographer's express written permission.

G. Alopecia Zinc 45 mcg/dL (R 50-150) ©Steve Castillo

H. Leukonychia Zinc 45 mcg/dL (R 50-150) ©David Giacalone

Acrodermatitis Enteropathica Beaus Lines

I. Beau's Lines R hand Hospitalization, bacteremia ©David Giacalone

  1. Beau's Lines L hand Hospitalization, bacteremia ©David Giacalone
  2. Beau's Lines Thumb Hospitalization, bacteremia ©David Giacalone
  3. 10. (Continued)

maintenance HD on fixed zinc intakes indicate increased fecal loss is a major contributor (226). Aluminum hydroxide gels and ferrous sulfate were shown to increase zinc losses (227). Calcium carbonate also binds zinc, but to a lesser degree than calcium acetate (228). Other factors that may contribute to zinc depletion in predialysis patients include reduced zinc intake with low protein diets (229-231) and increased urinary losses with angiotensin enzyme inhibitors (232) and loop/thiazide diuretics (233-235).

Functional studies in HD patients present conflicting reports on the ability of zinc to improve taste acuity, impotence, and immunity. Supplementation of 120 mg elemental zinc as sulfate post-HD treatment for 6 weeks was shown to improve taste acuity in 95% of cases (236); 50 mg zinc as acetate over a 6- to 12-week period was associated with significant improvement in taste thresholds for salt, sweet, and bitter (237). Matson et al. (238) failed to demonstrate improved taste acuity or increased serum zinc in HD patients or controls following 60 mg elemental zinc as sulfate, but poor response may have been related to the inability to normalize plasma zinc concentrations in this study. Indeed, research by Henkin et al. (239,240) in non-renal patients suggests salivary zinc concentration best correlates with reversal of taste dysfunction.

A double blind study by Mahajan et al. (241) showed improved potency, libido, and frequency of sexual intercourse by HD patient report, following a 6-month course of 50 mg elemental zinc. Later work by Rodger et al. (242) with supplementation up to 100 mg elemental zinc daily did not demonstrate improved potency using subjective measures of sperm count, nocturnal penile tumescence, testosterone, sex hormone binding globulin, and gonadotrophin concentration.

Ribeiro et al. (243) showed improved delayed hypersensitivity skin tests with Escherichia coli and phytohemagglutinin (PHA)-stimulated lymphocyte blastogenesis after 100 days of 15 mg elemental zinc as acetate twice daily, consistent with improved skin tests by Brodersen et al. (244), Bonomini et al. (245), and Antoniou et al. (246). Briggs et al. (247) did not find increased cellular lymphocyte blast formation in vitro with cells isolated from zinc-supplemented HD patients exposed to PHA, pokeweed, conconavalin A mitogens, or strepto-kinase/streptodornase soluble antigen.

A comprehensive zinc assessment is shown in Fig. 9; lesions observed in hypozincemic dialysis patients are shown in Fig. 10. Seborrheic-like dermatitis in the scalp, between the eyebrows, behind the ears, and along the nasolabial folds predominates; angular stomatitis, circumorificial dermatitis, alopecia, and leukonychia are also seen. Beau's Lines (248) were observed in the nails of a HD patient hospitalized with bacteremia complete probable zinc-related lesions.

5.5.3.2. Zinc Toxicity. Given research using zinc supplementation 3-10 times the RDA, concerns about zinc-induced copper deficiency is appropriate. Literature supports increased risk for copper deficiency with modest zinc supplementation, when the zinc to copper ratio is high (249). Monitored zinc to copper intake at 15:1 has shown limited effects on copper absorption (250) and is frequently used as the industry standard for nutritional supplements. Classic copper deficiency symptoms of anemia (normocytic and hypochromic), leukopenia, and neutropenia have been observed in patients receiving total parenteral nutrition (251) and jejunostomy feedings (252). Idiopathic myelopathy is recently described as a functional copper deficit that curiously mimics sensory ataxia and gait disturbances observed in V-B12deficiency (253). With consistent evidence that zinc deficit exists in kidney failure, the best advice may be to "start low and go slow." Copper indicators should be monitored if zinc supplementation continues for more than 90 days.

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