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Abstract
Keywords
hair; micronutrients; micronutrient deciencies; mineral deciency; nails; skin; vitamin deciency
Cutaneous Micronutrient
Manifestation Deciency Causes of Micronutrient Deciency
Hair
Diffuse alopecia Biotin, zinc, EFAs Biotin: Malabsorptive disorders, alcohol use disorder, biotinidase deciency,
consumption of large amounts of raw egg whites, pregnant and lactating
women
Acquired zinc deciency: Malabsorptive disorders, alcohol use disorder,
long-term parenteral supplementation, after GI surgery, chronic liver disease,
chronic renal disease, sickle cell disease, diabetes mellitus, pregnant and
lactating women, exclusively breastfed infants after 6 months of age.
Congenital zinc deciency: Autosomal recessive disorder
EFA: Malabsorptive disorders, pancreatic insufciency, severe cholestatic
(continued)
492 Nutrition in Clinical Practice 34(4)
Table 1. (continued)
Cutaneous Micronutrient
Manifestation Deciency Causes of Micronutrient Deciency
Vitamins
Vitamins are substances that are required for normal growth absorbed in the proximal small intestine and is metabolized
and metabolism, cannot be synthesized by humans, and by the liver or can be complexed to form avoproteins. 7,8
therefore require dietary intake. The exception is vitamin Commensal lactic acid bacteria present in the large intestine
D, which to some extent can be produced through exposure can also produce riboavin, which can be absorbed.1,8
to sunlight in addition to dietary intake. The vitamins are Insufciency can occur in patients who avoid dairy products,
divided into fat soluble (A, D, E, and K) and water soluble as this is a major source of the vitamin. 1,7,8 Deciency can
(B vitamins and C). Fat-soluble vitamins require adequate occur in patients with malabsorptive disorders, in alcohol
fat digestion and absorption and are stored in appreciable use disorder, and in patients with anorexia nervosa.1,7,8
amounts in the liver and adipose tissue. For this reason, Deciency of riboavin can manifest as changes to
excess intake can lead to toxicity. In contrast, water-soluble the mucous membranes, including pharyngitis, cheilitis
vitamins are minimally stored in tissues, and excess levels are (Figure 1), stomatitis (Figure 2), and glossitis (Figure 3). 1,7-9
rapidly excreted in urine. Toxicity is therefore uncommon, There is also an increased incidence of seborrheic dermatitis
except in patients with chronic kidney disease who are at risk in riboavin deciency (Figure 4).9 As an isolated nd-
of pyridoxine and folic acid toxicity. 5 Isolated deciencies of ing, seborrheic dermatitis may not trigger a consideration
just 1 of the water-soluble vitamins are also uncommon. As of vitamin deciency because of the ubiquitous nature
such, supplementation of all water-soluble vitamins is gen- of “dandruff.” Testing, however, should be considered in
erally warranted when a deciency of just 1 is diagnosed.1 patients who have extensive involvement of disease or are
resistant to treatment with over-the-counter dandruff med-
ications (selenium sulde, zinc pyrithione, and ketoconazole
B Vitamins shampoos).
Riboavin, Flavin Mononucleotide, and Flavin Testing for deciency is best assessed through the
erythrocyte glutathione reductase activity coefcient
Adenine Dinucleotide (Vitamin B2)
(EGRAC); however, it should be recognized that this test
Dietary sources substantial in riboavin include dairy, eggs, cannot be utilized in patients with glucose-6-phosphate
sh, meat, poultry, and fortied cereals. 6 Riboavin is dehydrogenase (G6PD) deciency.7,8 A level >1.4 is
DiBaise and Tarleton 493
Figure 14. Koilonychia associated with iron-deciency anemia (sodium ferric gluconate), and Feraheme (ferumoxytol).
Photo courtesy of CHeitz (Flickr). Hypersensitivity reactions can occur with any of these
preparations; therefore, they should be administered where
with malignancies, particularly colon cancer; in patients
the patient can be closely monitored with resuscitation
who have had GI surgeries; and patients with chronic
equipment and personnel trained to respond to an
heart failure.60 Iron deciency can lead to a microcytic,
anaphylactic reaction.62-66 There is currently no form of
hypochromic anemia with associated pallor along with fa-
parenteral iron that is suitable for addition to PN in the U.S.
tigue, exertional dyspnea, koilonychia (spoon-shaped nails)
(Figure 14), and developmental delays in children.60
Deciency is generally considered in the setting of mi-
Copper
crocytic, hypochromic anemia determined by a complete Beef, soy, nuts, seeds, beans, shellsh, and mushrooms
blood count. 60 This is, however, not specic for iron de- are all good sources of dietary copper. 6 The RDA for
ciency, whereas iron studies that may include serum iron copper is 900 g/d for adult men and for nonpregnant
level, total iron binding capacity, transferrin, serum ferritin, adult women, with the UL being 10,000 g/d.58,59 Copper
and transferrin saturation will allow for a more specic is absorbed in the stomach and proximal small intestine
diagnosis of iron deciency.60 With inammatory reactions and is decreased in the presence of iron, zinc, and vita-
(acute-phase reaction), transferrin and serum iron levels min C.67 Copper is transported to the liver where it is
may decrease, whereas serum ferritin levels may increase. bound to ceruloplasmin for transport to tissues.67 Copper
This contradictory pattern of lab ndings should lead is eliminated in the GI tract, predominantly in bile. Copper
the provider to investigate for an underlying inammatory deciency can be found in patients who have undergone
process or infection. gastric bypass or gastrectomy, premature infants on milk
Oral iron supplementation is generally considered rst formulas without copper, in patients with chronic excess zinc
in the treatment of iron deciency. Iron sulfate is most ingestion, and in patients overtreated for Wilson’s disease.68
frequently used; however, iron gluconate and iron fumarate Wilson’s disease is a deciency in ceruloplasmin leading to
are also good alternatives. Recommended dosing for adults excessive copper deposits in multiple organs. Classic signs
is 100–200 mg of elemental iron. 61 Divided doses in between are azure lunula and Kayser-Fleischer rings of the eyes
meals with a vitamin C source will optimize absorption. (Figure 15).69 A rare X-linked disorder, Menkes disease,
Repletion of iron stores and normalization of serum ferritin results in copper deciency due to inability to absorb copper
will typically occur within 3–6 months of treatment. Adher- from the intestine. Copper deciency leads to abnormally
ence to treatment may be compromised by side effects such formed hair (kinky hair syndrome) (Figure 16), skin de-
as nausea, vomiting, constipation, and a metallic taste. If pigmentation (Figure 17), ataxia, myeloneuropathy, and
treatment with oral iron fails, including premature termi- hepatosplenomegaly.70 The signs and symptoms of Menkes
nation of treatment, lack of adequate adherence with the disease are similar to acquired copper deciency, except
regimen, or a refractory response to treatment, parenteral Menkes is more severe and diagnosed early in infancy with
iron should be initiated.61 associated developmental delay, epilepsy, and progressive
There are 5 forms of parenteral iron available in neurologic symptoms.70
the United States: INFeD (iron dextran), Venofer (iron Testing for deciency is accomplished by measurement
sucrose), Injectafer (ferric carboxymaltose), Ferrlecit of serum copper and ceruloplasmin levels; however, like
500 Nutrition in Clinical Practice 34(4)
Selenium
Poultry, nuts, seeds, wheat, barley, beef, and potatoes are all
good sources of selenium; however, there is variability of
selenium in food sources based on the amount of selenium
in the soil used to grow foods.6 The RDA for selenium
is 55 g/d for adult men and nonpregnant women, with
the UL being 400 g/d. 58,59 Selenium is absorbed in the
small intestine and is excreted in the urine.74 In areas of
the world where low levels of selenium exist in the soil,
Figure 17. Skin depigmentation associated with copper deciency is more common. This is particularly true for veg-
deciency Photo courtesy of
C A. Bueckert Adobe Stock
etarians living in selenium-decient areas. 74 Deciency may
images.
also occur in patients on long-term hemodialysis; receiving
long-term PN; having chylous loss, phenylketonuria, or
ferritin, both are also acute-phase reactants and can be malabsorption disorders; and in individuals with HIV.74-77
elevated in the presence of inammatory processes.69,70 Selenium deciency leads to whitened nailbeds (Figure 18),
Treatment of Wilson’s disease consists of avoidance of impaired immune function, and skeletal myopathy. Patients
high-copper foods and copper chelation.69 In early stages, receiving long-term PN without selenium supplementation
high doses of zinc may be effective in delaying the onset may develop cardiomyopathy.76
of symptomatic disease, as zinc competes with copper for Testing for deciency is generally accomplished through
absorption in the GI tract. Copper can be administered measurement of serum or plasma selenium levels, although
orally or intravenously for deciency; however, there are no selenium levels in hair and nails can provide a more accurate
set recommendations regarding dose, route, or monitoring long-term assessment of intake. The optimal dose and dura-
parameters. 71,72 The American Society for Metabolic and tion of selenium supplementation is not well established.77
DiBaise and Tarleton 501
Conclusion
Although MNDs are uncommon in the general population,
a number of conditions are at risk of these deciencies,
including those patients with restricted diets; chronic med-
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