Micronutrients

BY: Basant Helmi Hassan

Assisstant lecturer of pediatrics
 The dietary micronutrients: Vitamins and trace minerals
 The dietary micronutrients , are essential for growth and
development and contribute to a host of physiologic functions
 Food fortification is an effective strategy to prevent some nutrient
deficiencies and has been successfully implemented to prevent iodine
and folate deficiency.
Water soluble
vitamins
 Vitamin B Complex Deficiencies
and
Excess
 B-complex vitamins serve as coenzymes in many metabolic pathways.
Consequently, a lack of one of the vitamins has the potential to interrupt a
chain of many chemical reactions, and ultimately produce diverse clinical
manifestations.
 Because diets deficient in any one of them are often poor sources of
other B vitamins, manifestations of several vitamin B deficiencies
usually can be observed in the same person. Therefore evidence of
deficiency of a specific B vitamin should be treated with the entire
B-complex group.
 1-Thiamine (Vitamin B1 )
function
 Thiamine diphosphate, the active form of thiamine,
serves as a cofactor for several enzymes involved in
carbohydrate catabolism
 These enzymes also play a role in the hexose
monophosphate shunt that generates nicotinamide
adenine dinucleotide phosphate (NADP) and
pentose for nucleic acid synthesis.
 synthesis of acetylcholine (ACh) and γ- aminobutyric
acid (GABA), which have important roles in nerve
conduction.
 dietary
sources of thiamine.

 Rice, oat, wheat, and legumes. Most ready-

to-eat breakfast cereals
 Pork (especially lean), fish, and poultry are
good non vegetarian dietary sources
 The breast milk of a well-nourished
mother provides adequate thiamine;
breastfed infants of thiamine-deficient
mothers are at risk for deficiency.
Thiamine Deficiency

1. Decreased intake, severely malnourished states, including malignancy

and following surgery.
2. Thiamine antagonists (coffee, tea) and thiaminases (fermented fish) may
contribute to thiamine deficiency
3. Thiamine-responsive megaloblastic anemia (TRMA) syndrome is a
rare AR disorder characterized by megaloblastic anemia, DM, and SNHL,
responding in varying degrees to thiamine treatment due to to abnormal
thiamine transportation and cellular vitamin deficiency
4. Another dependency state, biotin and thiamine–responsive basal
ganglia disease , presents with lethargy, poor contact, and poor
feeding in early infancy; and responds to combined treatment with
biotin and thiamine
Clinical Manifestations

 Develop within 2-3 mo of a deficient intake.

 Early symptoms: nonspecific, such as fatigue, apathy,

irritability, depression, drowsiness, poor mental concentration,
anorexia, nausea, and abdominal discomfort.

 As the condition progresses, more-specific manifestations

of beriberi develop.
 Eye: ptosis and atrophy of the optic nerve.
 Hoarseness or aphonia caused by paralysis of the laryngeal nerve
is a characteristic sign.
 CNS: Muscle atrophy and tenderness of the nerve trunks are
followed by ataxia, loss of coordination, and loss of deep sensation.
tingling, burning, paresthesias of the toes and feet), decreased deep
tendon reflexes, tenderness and cramping of the leg muscles
 Later signs include increased intracranial pressure, meningismus,
and coma.
 The clinical picture of thiamine deficiency is usually divided into a
dry (neuritic ) type and a wet (cardiac ) type depending on the
amount of fluid that accumulates in the body because of cardiac
and renal dysfunction, even though the exact cause for this edema
is unknown.
 Many cases of thiamine deficiency show a mixture of both
thiamine deficiency with cardiopathy and peripheral
neuropathy .
 Death from thiamine deficiency usually is secondary to cardiac
involvement. The initial signs are cyanosis and dyspnea,These
changes, rapidly revert to normal with treatment, but without
prompt treatment HF can develop rapidly
Diagnosis

1. A high index of suspicion in children presenting with unexplained

cardiac failure may sometimes be lifesaving.
2. The biochemical diagnostic criteria : low erythrocyte transketolase
activity and high thiamine pyrophosphate effect (normal range: 0–
14%).
3. Urinary excretion of thiamine or its metabolites after an oral
loading dose of thiamine may also be measured to help identify
the deficiency state.
4. MRI changes of thiamine deficiency
Prevention

 A maternal diet with sufficient amounts of thiamine in breastfed

infants, and infant formulas provide recommended levels of intake.
 Adequate intake during complementary feeding,
 Improvement in cooking techniques, such as not discarding the
water used for cooking, minimal washing of grains, and
reduction of cooking time helps to minimize the thiamine losses
during the preparation of food.
 Thiamine supplementation should be ensured during total
parenteral nutrition (TPN).
Treatment

 Children with cardiac failure, convulsions, or coma should

be given (IM) or (IV) daily for the 1st wk.
 followed (PO) for at least 6 wk (In the absence of GI
disturbances)
 The response is dramatic in predominantly cardiovascular
manifestations, whereas the neurologic response is slow and
often incomplete
Riboflavin (Vitamin B2 )
function

 Riboflavin is part of the structure of the coenzymes flavin adenine

dinucleotide (FAD) and flavin mononucleotide, which participate
in
1. Oxidation-reduction (redox) reactions in numerous metabolic
pathways
2. Energy production via the mitochondrial respiratory chain.
dietary sources

 Riboflavin is stable to heat but is destroyed by

light.
 Milk, eggs, organ meats, legumes, and
mushrooms . Most commercial cereals, flours,
and breads are enriched with riboflavin.
Riboflavin
Deficiency(ariboflavinosis )
 Malnourished and malabsorptive states
 Some drugs, such as probenecid, phenothiazine, or oral
contraceptives (OCs).
 The side chain of the vitamin is photochemically destroyed during
phototherapy for hyperbilirubinemia.
 Rare dependency states: Isolated complex II deficiency , a
rare mitochondrial disease in infancy and childhood. Brown-
Vialetto-Van Laere syndrome (BVVLS) , a rare AR, potentially
lethal, rapidly progressive neurologic disorder with respiratory
insufficiency, responds to treatment with high doses of riboflavin
if treated early in the disease course.
Clinical Manifestations

 Cheilosis begins with pallor at the angles of

the mouth, thinning and maceration leading to
fissures extending radially into the skin
 Glossitis, the tongue becomes smooth, with
loss of papillary structure
 keratitis, conjunctivitis, photophobia,
lacrimation, corneal vascularization, and
seborrheic dermatitis
 Normochromic, normocytic anemia because of
the impaired erythropoiesis
Diagnosis

1. Clinical suspicion: angular cheilosis in a malnourished child, who

responds promptly to riboflavin supplementation.
2. functional test : measuring the activity of erythrocyte glutathione
reductase (EGR), with and without the addition of FAD.
3. An EGR activity coefficient (ratio of EGR activity with added FAD
to EGR activity without FAD) of >1.4 is used as an indicator of
deficiency.
4. Urinary excretion of riboflavin <30 μg/24 hr also suggests low
intakes.
Prevention

 Adequate consumption of milk, milk products, and eggs prevents riboflavin

deficiency.
 Fortification of cereal products is helpful for those who follow vegan diets or
who are consuming inadequate amounts of milk products for other reasons.
Treatment
Niacin (Vitamin B3 )
function

 Niacin (nicotinamide or nicotinic acid) forms part of two cofactors,

nicotinamide adenine dinucleotide (NAD) and NADP, which are
important in several biologic reactions, including the
respiratory chain, fatty acid and steroid synthesis, cell
differentiation, and DNA processing.
 Dietary sources

 Meat, fish, and poultry for

nonvegetarians and cereals, legumes,
and green leafy vegetables for
vegetarians.
 Enriched and fortified cereal products
also are major contributors.
 Milk and eggs contain little niacin but
are good sources of tryptophan, which
can be converted to NAD (60 mg
tryptophan = 1 mg niacin).
Niacin Deficiency

 Decreased intake: chiefly in populations where corn (maize),

a poor source of tryptophan, is the major foodstuff.
 A severe dietary imbalance, such as in anorexia nervosa and
in war or famine conditions.
 disturbed tryptophan metabolism
Clinical Manifestations

 Pellagra , the classic niacin deficiency disease,

 The early symptoms of pellagra are vague: anorexia,
lassitude, weakness, burning sensation, numbness, and
dizziness.
 After a long period of deficiency, the classic triad of
dermatitis, diarrhea, and dementia appears.
 Symmetric, Sharply demarcated areas of
erythema on exposed surfaces, resembling
sunburn, might go unrecognized.
 A glove or stocking appearance
 Casal necklace
 In some cases, vesicles and bullae develop
(wet type).
 there may be suppuration beneath the
scaly, crusted epidermis;
 Followed by desquamation.
 The healed parts might remain pigmented
 The cutaneous lesions may be preceded by or
accompanied by stomatitis, glossitis, vomiting,
and diarrhea.
 Nervous symptoms include depression,
disorientation, insomnia, and delirium.
 The classic symptoms of pellagra usually are not well developed
in infants and young children, but anorexia, irritability, anxiety,
and apathy are common.
Diagnosis

 Physical signs of glossitis, GI symptoms, and a symmetric dermatitis.

 Rapid clinical response to niacin is an important confirmatory test.
 A decrease in niacin metabolites in urine provide biochemical evidence
of deficiency and can be seen before the appearance of overt signs of
deficiency.
 Histopathologic changes from the affected skin include dilated blood
vessels without significant inflammatory infiltrates, ballooning of the
keratinocytes, hyperkeratosis, and epidermal necrosis.
Prevention
Treatment
Vitamin B6 (Pyridoxine)
function

 pyridoxine,pyridoxal, pyridoxamine, and their phosphorylated

derivatives. Pyridoxal 5′- phosphate (PLP) and, to a lesser
extent, pyridoxamine phosphate function as coenzymes for
many enzymes involved in amino acid metabolism,
neurotransmitter synthesis, glycogen metabolism, and steroid
action.
food sources

 Fortified ready-to-eat cereals, meat,

fish, poultry, liver, bananas, rice, and
certain vegetables.
 The vitamin B6 content of human milk
and infant formulas is adequate.
 Large losses can occur during high-
temperature processing of foods or
milling of cereals.
Vitamin B6 Deficiency

 Medications that inhibit the activity of vitamin B6 (e.g.,

isoniazid, penicillamine, corticosteroids, phenytoin,
carbamazepine),oral progesterone-estrogen OCs
 Maintenance dialysis.
Clinical Manifestations

 In infants: are listlessness, irritability, seizures, vomiting, and

failure to thrive.
 Peripheral neuritis in adults but is not usually seen in children.
 Electroencephalogram(EEG) abnormalities have been
reported in infants as well as in young adults.
 Skin lesions include cheilosis, glossitis, and seborrheic dermatitis
around the eyes, nose, and mouth.
 Microcytic anemia can occur in infants but is not common.
 Oxaluria, oxalic acid bladder stones
Diagnosis

 Clinical evaluation
 measurement of serum pyridoxal phosphate being used more
often,
 AST, ALT, low in vitamin B6 deficiency;
 Abnormally high xanthurenic acid excretion after tryptophan
ingestion also provides evidence of deficiency
Prevention
Biotin
Biotin deficiency.

 Avidin found in raw egg whites acts as a biotin antagonist,

biotin deficiency have been demonstrated in persons who
consume large amounts of raw egg whites over long periods.
 Enteral and parenteral nutrition formula that lack biotin.
 valproic acid may result in a low biotinidase activity and/or biotin
deficiency.
 Biotin-responsive basal ganglia disease or biotin and
thiamine–responsive basal ganglia disease is a rare
childhood neurologic disorder characterized by encephalopathy,
seizures, extrapyramidal manifestations,
The clinical findings

 Scaly periorificial dermatitis,

conjunctivitis, thinning of hair, and
alopecia.
 Central nervous system(CNS)
abnormalities are lethargy, hypotonia,
seizures, ataxia, and withdrawn
behavior
Folate(B9)
function

 coenzymes in amino acid and nucleotide metabolism.

 Folate is important for CNS development during
embryogenesis
 Prevents megaloblastic anemia
Dietary sources

 Rice and cereals are rich

dietary sources of folate,
especially if enriched.
 Beans, leafy vegetables,
and fruits such as oranges
and papaya are good
sources
Folate Deficiency

Because of folate's role in protein, DNA, and RNA synthesis, the risk
of deficiency is increased during periods of rapid growth or
increased cellular metabolism.
 poor nutrient content in diet,
 inadequate absorption (celiac disease, inflammatory bowel
disease),
 Increased requirement (sickle cell anemia, psoriasis,
malignancies, periods of rapid growth as in infancy and
adolescence)
 Inadequate utilization (long-term treatment with high-dose
NSAIDS; anticonvulsants; methotrexate).
 Rare causes : hereditary folate malabsorption, inborn errors of
folate metabolism
Diagnosis

 CBC film :macrocytosis with low folate. Levels of RBC folate are
a better than serum level.
 BM: hypercellular, and megaloblastic changes are prominent.
 Large, abnormal neutrophilic forms (giant metamyelocytes)
with cytoplasmic vacuolation also are seen.
Treatment

 Orally or parenterally at 0.5-1.0 mg/day for 3-4 wk or until a

definite hematologic response has occurred.
 Maintenance therapy with 0.2 mg of folate is adequate
Vitamin B12 (Cobalamin)

 functions as a cofactor in lipid and carbohydrate

metabolism.
 Methylcobalamin is another circulating form of vitamin B12 and
is essential for conversion of homocysteine to methionine.
 important for protein and nucleic acid biosynthesis
 B12 is important for hematopoiesis, CNS myelination, and
mental and psychomotor development
Dietary sources

 almost exclusively from animal foods.

 Organ meats, muscle meats, seafood
(mollusks, oysters, fish), poultry, and egg
yolk are rich sources.
 Fortified ready-to-eat cereals, milk
and their products are the important for
vegetarians.
 Human milk is an adequate source for
breastfeeding infants if the maternal
serum B12 levels are adequate.
Vitamin C (Ascorbic Acid)
Function

 Vitamin C is important for synthesis of collagen

 It is also involved in neurotransmitter metabolism (conversion of
dopamine to norepinephrine and tryptophan to serotonin),
 cholesterol metabolism (conversion of cholesterol to steroid
hormones and bile acids), biosynthesis of carnitine.
 Vitamin C functions to maintain the iron and copper atoms.
 Antioxidant (electron donor.
 Vitamin C enhances non heme iron absorption and thus can affect
the cellular and immunologic functions of the hematopoietic system.
Dietary Sources of Vitamin C
Vitamin C Deficiency

Decreased intake: predominantly heat-treated (ultrahigh-

temperature or pasteurized) milk or unfortified formulas, or not
receiving fruits and fruit juices and children on highly restrictive
diets devoid of most fruits and vegetables
Clinical Features (scurvy)

 In scurvy, there is defective formation of connective

tissues and collagen in skin, cartilage, dentine, bone,
and blood vessels, leading to their fragility.

 Early manifestations irritability, loss of appetite, low-grade fever,

musculoskeletal pain, and tenderness in the legs
 Followed by leg swelling—most marked at the knees and the
ankles—and pseudoparalysis . The infant might lie with the
hips and knees semiflexed and the feet rotated outward.
 Sub periosteal hemorrhages in lower-limb bones sometimes
acutely increase the swelling and pain, that might mimic acute
osteomyelitis or arthritis
 A “rosary” at the costochondral
junctions and depression of the
sternum are other typical features.
 The angulation of scorbutic beads is
usually sharper than that of a rachitic
rosary.
 Gum changes as bluish purple,
spongy swellings of the mucous
membrane, especially over the upper
incisors
 Anemia, related to impaired iron absorption and
coexistent hematopoietic nutrient deficiencies,
including iron, vitamin B12 , and folate.
 poor wound and fracture healing, hyperkeratosis of
hair follicles, arthralgia, and muscle weakness.
 Hemorrhagic manifestations of scurvy
include petechiae, purpura, and
ecchymoses at pressure points;
epistaxis; gum bleeding; and the
characteristic perifollicular
hemorrhages
Diagnosis

the
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a ra ct i c a
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The typical radiographic changes

 Distal ends of the long bones and particularly

common at the knees.
 Ground -glass appearance because of trabecular
atrophy.
 The cortex is thin and dense, giving the appearance of
pencil outlining of the diaphysis and epiphysis.
 The white line of Fränkel, an irregular but thickened
white line at the metaphysis, represents the zone of well-
calcified cartilage.
 The epiphyseal centers of ossification also have a
ground-glass appearance and surrounded by a sclerotic
ring
 Pelkan spur is also seen at the cortical end.
Prevention &Treatment
Fat soluble
vitamins
 Vitamin A
Function
The term vitamin A is generally used to refer to a group of compounds
that possess the biologic activity of all trans retinol.
 Essential for normal vision, reproduction, cell and tissue
differentiation, and functions of the immune system.
 Vitamin A plays critical roles in neonatal development.
 It is required for normal embryonic development,
hematopoiesis, immune response, metabolism, and growth
and differentiation of many types of cells.
 Many studies show that vitamin A reduces morbidity and
mortality from various infectious diseases, including
measles
 Diatry sources of vitamin A

 preformed vitamin A (retinyl

esters, such as retinyl palmitate)
primarily in foods of animal origin.
Organ meats (especially liver,
kidney).
 several provitamin A
carotenoids, which are found
naturally in many fruits and
vegetables, especially yellow-
orange vegetables (pumpkin,
squash, sweet potato), and leafy
green vegetables (chard, spinach,
broccoli).
Vitamin A Deficiency

 In many developing countries often associated with global

malnutrition.
 Chronic disorders or diseases. in children is uncertain but
likely significant in acute infectious diseases such as
measles, and possibly in chronic inflammatory conditions such
as cystic fibrosis.
 dietary habits can be important risk.
 Neonates begin life with low levels of vitamin A compared with
adults (especially in developing countries, low-birthweight
infants and in preterm newborns).
Clinical Manifestations of
Vitamin A Deficiency

The most obvious symptoms of vitamin A deficiency are associated with

changes in epithelial cell morphology and functions.
 In the intestines & respiratory tract : mucus secreting goblet
cells are affected. loss of an effective barrier against pathogens can
cause diarrhea or RTI.
 Characteristic epithelial changes including proliferation of basal
cells, hyperkeratosis, and formation of stratified squamous
epithelium.
 Squamous metaplasia of the renal pelvis, ureters, vaginal
epithelium, pancreatic and salivary ducts can lead to increased
infections in these areas
 In the skin, vitamin A deficiency manifests as dry, scaly,
hyperkeratotic patches, typically on the arms, legs,
shoulders, and buttocks.


The combination of the above ( defective epithelial barriers

to infection, low immune response, and lowered response
to inflammatory stress), can cause poor growth and
serious health problems in children.
 The most characteristic and specific signs are eye lesions.
 Early:
1. delayed dark adaptationas a result of reduced resynthesis of
rhodopsin; this may progress to night blindness .
2. Photophobia is a common symptom.
3. The retinal pigment epithelium (RPE), the structural element of
the retina, undergoes keratinization.
When the RPE degenerates, the rods and cones have no support
and eventually break down, resulting in blindness.
As vitamin A deficiency progresses, the
corneal and conjunctival epithelial tissues
become severely altered.
Stages in vitamin A deficiency include
 corneal keratinization and opacity,
susceptibility to infection, and formation of
dry, scaly layers of cells (xerophthalmia ).
 The conjunctival membrane keratinization and
develop foamy appearing plaques (Bitôt
spots).
 Irreversibly (keratomalacia and corneal
ulceration ), resulting in irreversible
blindness.
 Treatment with vitamin A, up to the stage of keratomalacia, is
effective in rapidly repleting the individual and saving vision
Diagnosis

 A diet history is useful in suggesting low intake as a cause of

symptoms
 characteristic lesions of vitamin A deficiency
 For detection of less severe deficiency (marginal vitamin A
status), include conjunctival impression cytology, relative dose
response, and modified relative dose response tests
 Dark adaptation tests can be used in early-stage vitamin A
deficiency
 In children, plasma retinol <0.35 μmol/L is considered very
deficient, 0.35-0.7 μmol/L deficient, 0.7-1.05 μmol/L marginal,
and >1.05 μmol/L adequate.
 liver vitamin A concentration >20 μg/g is needed to support
a normal rate of secretion and therefore normal delivery to
peripheral tissues.
Vitamin A for Treatment of
Deficiency

 A daily supplement of 1,500 μg after which intake at the RDA

level should be the goal.
 Rates of morbidity and mortality, as from viral infections such as
measles, have been reduced by a weekly doses of vitamin A at
the RDA level.
 More often, higher doses of 30-60 mg of retinol
(100,000-200,000 IU/child) are given once or twice, under
careful monitoring to avoid toxicity
 Vitamin A is also used in preterm infants to improve
respiratory function and prevent development of chronic lung
disease.
Hypervitaminosis A
Hypervitaminosis A

Except for vitamin A, toxicity from excess intake of

vitamins is rare.
 Because there is no antidote for hypervitaminosis A, it is most important
to prevent toxicity.
 Symptoms may subside rapidly on withdrawal of the vitamin, but the
rate of improvement depends on the amount of vitamin A stored in
tissues.
 Extreme hypervitaminosis A is fatal.
 (early signs): Headache, vomiting, anorexia, dry itchy
desquamating and seborrheic lesions.
 In young children, signs of vitamin A toxicity include
vomiting and bulging fontanels, neither of which is
specific. Combined with anorexia, pruritus, and a lack of weight
gain, vitamin A toxicity should be considered.
 Less common symptoms include diplopia, papilledema, cranial
nerve palsies, and other symptoms suggesting pseudotumor
cerebri.
With chronic hypervitaminosis A(Excessive ingestion of
preformed vitamin A (retinol or retinyl ester), generally for
several weeks or months.
 Fissuring at the corners of the mouth, alopecia and coarsening of
the hair, bone abnormalities and swelling, HSM, Hypercalcemia
and/or liver cirrhosis
 diplopia, increased intracranial pressure, irritability, stupor,
limited motion, dryness of the mucous membranes, and
desquamation of the palms and soles
 Radiographs may show hyperostosis
affecting several long bones
 During the 1st trimester of pregnancy: severe congenital
malformations may occur . Teratogenicity. A high
incidence (>20%) of spontaneous abortions and birth
defects, including characteristic craniofacial
abnormalities
 Carotenoids, even in high doses, are not associated with
toxicity but can cause yellowing of the skin (carotenodermia ),
including palms of the hands, and high levels in serum
(carotenemia); this relatively benign state disappears slowly
when carotene intake is reduced.
 Vitamin E

 Vitamin E is a fat-soluble vitamin

and functions as an
antioxidant,
 The best dietary sources are
vegetable oils, seeds, nuts, green
leafy vegetables, and margarine
vitamin E deficiency

1. In premature infants
 Vitamin E deficiency can cause neurologic manifestations,
thrombocytosis, edema, and hemolysis, potentially causing
anemia.
  The risk of symptomatic vitamin E deficiency was increased by

Formulas for premature

infants had a high content of
Aggressive use of iron
(PUFAs) leading to a high content
supplementation; iron increases
of PUFAs in RBC membranes,
the production of oxygen
making them more susceptible
radicals.
to oxidative stress, which could
be ameliorated by vitamin E.
 Primary dietary deficiency is rare except in severe
generalized malnutrition& prematures.
 Fat malabsorption as bile acid needed for vitamin E
absorption as in cholestatic liver disease, cystic
fibrosis, celiac disease, short bowel syndrome,
and Crohn disease.
 Abetalipoproteinemia : AR disorder causes fat
malabsorption, and vitamin E deficiency is a common
complication).
 Ataxia with isolated vitamin E deficiency (AVED) , a rare
AR mutations in the gene for α-tocopherol transfer protein (TTPA
), so unable to incorporate vitamin E into lipoproteins before
their release from the liver, leading to reduced serum levels of
vitamin E with no associated fat or vitamin E malabsorption,
Clinical Manifestations

 Clinical manifestations do not appear until after 1 yr of age, even in

children with cholestasis since birth.
 A severe, progressive neurologic disorder :cerebellar, posterior
column dysfunction, and retinal disease.
 Ophthalmoplegia (limited upward gaze), nystagmus, Some patients
have pigmentary retinopathy. Visual field constriction can
progress to blindness.
 In premature infants, hemolysis typically develops during the 2nd
mo of life. Edema may also be present.
Prevention& treatment

In Premature infants
 less-aggressive use of iron, and provision of adequate
vitamin E
 with unexplained hemolytic anemia after the 1st mo of life,
especially if thrombocytosis is present, either should be
1. empirically treated with vitamin E through formula
2. or breast milk fortifier and formula without a high content of
PUFAs
3. or should have serum vitamin E and lipid levels measured.
Prevention& treatment

 Children with neurologic findings and a disease that

causes fat malabsorption should have:
1. their vitamin E status evaluated. and
2. given adequate vitamin E supplementation.
Vitamin K

 is a group of compounds:
 Phylloquinone , called vitamin K1 , is
present in green leafy vegetables, liver,
and certain legumes and plant oils having
the highest content.
 Vitamin K2 is called menaquinones , which
are produced by intestinal bacteria.
 The major function of the K vitamins is in the maintenance of
normal levels of the coagulation factors II, VII, IX, X and
protein C and protein S
 Unlike other fat-soluble vitamins,
1. there are limited body stores of vitamin K.
2. high turnover of vitamin K, and the vitamin K–dependent clotting
factors have a short half-life.
 Thus, symptomatic vitamin K deficiency can develop within weeks
when there is inadequate supply because of low intake or
malabsorption.
3 forms of vitamin K deficiency
bleeding (VKDB)

 Early VKDB was formerly called classic hemorrhagic disease of

the newborn and occurs at 1-14 days of age
 Late VKDB most often occurs at 2-12 wk of age, although cases
can occur up to 6 mo after birth
 The third form of VKDB of the newborn occurs at birth or
shortly thereafter. secondary to maternal intake of (warfarin,
phenobarbital, phenytoin) that cross the placenta and interfere
with vitamin K function.
Beyond infancy,

 low intake by itself never causes vitamin K deficiency.

However, the combination of poor intake and the use of broad
spectrum antibiotics that eliminate the intestine's vitamin K2 –
producing bacteria can cause vitamin K deficiency. This scenario
is especially common in ICU.
 Micronutrient Mineral
Deficiencies
 The dietary micronutrients: Vitamins and trace minerals
Micronutrient Mineral
Deficiencies

 By definition, a trace element is <0.01% of the body weight.

 Breast milk provides optimal intake of most nutrients,
including iron and zinc.
 Although present in lower amounts compared with infant
formula, iron and zinc are more bioavailable and are
sufficient to meet infant needs until approximately 4-6 mo of
age.
 After 4-6 mo, iron and zinc are required from complementary
foods, such as iron-fortified cereal
For a number of reasons, children are especially
susceptible to trace element deficiency

 First, growth creates an increased demand .

 Second, some organs are more likely to sustain
permanent damage because of trace element deficiency.
The developing brain is particularly vulnerable to the
consequences of certain deficiency states (iron, iodide).
Similarly, adequate fluoride is most critical for dental health
during childhood.
 Third, children are more prone to gastrointestinal disorders that
can cause trace element deficiencies as with short bowel
syndrome or malabsorption
 unusual diets or prolonged total parenteral nutrition
(TPN) without adequate delivery of a specific trace
element.
 Iron deficiency is the most common micronutrient deficiency
in the world and is associated with iron-deficiency anemia and
neurocognitive deficits in some children.
Zinc deficiency

Zinc deficiency affects millions of children and is associated with

 increased risk for impaired linear growth (stunting),
 impaired immune function,
 and increased risk for respiratory and diarrheal diseases.
often associated with malnutrition or other micronutrient
deficiencies (iron).
 Zinc deficiency

 Deficiency can occur from:

1. decreased intake, 1. Co-ingestion of phytates, calcium, and
phosphate
2. inability to absorb the micronutrient, 2. small bowel malabsorption: Crohn’s disease,
3. increased metabolic demand, SSS, hookworms, pancreatic insufficiency,
3. Exclusive parental nutrition, strict vegetarian
4. or excessive loss
diets, and anorexia nervosa.
4. Medications inhibit absorption. including
penicillamine, various diuretics, and sodium
valproate.
5. Acrodermatitis enteropathica
Acrodermatitis enteropathica

 Rare AR disorder caused by an inability to

absorb sufficient zinc from the diet.
 Initial signs usually occur in the 1st few
months of life,
 The cutaneous eruption: vesiculobullous,
eczematous, dry, scaly, or psoriasiform skin
lesions symmetrically distributed in the perioral,
acral, and perineal, cheeks, knees, and elbows.
 The hair often has a peculiar, reddish tint, and
alopecia of some degree is characteristic.
 Ocular manifestations include photophobia, conjunctivitis,
blepharitis, and corneal dystrophy detectable by slit-lamp
examination.
 Associated manifestations include chronic diarrhea,
stomatitis, glossitis, paronychia, nail dystrophy, growth
retardation, irritability, delayed wound healing, intercurrent
bacterial infections, and superinfection with Candida albicans .
 Lymphocyte function and free radical scavenging are
impaired.
 Without treatment the course is chronic and intermittent but
often progressive.
Diagnosis

 clinical findings and

 A serum zinc level less than 50 μg/dL is suggestive but not
diagnostic of acrodermatitis enteropathica.
 Levels of alkaline phosphatase, a zinc-dependent enzyme,
may also be decreased.
 Histopathologic changes in the skin are nonspecific
Treatment

 The cause of underlying malnutrition should be

addressed.
 Oral therapy is the treatment of choice.
 Inherited acrodermatitis enteropathica : elemental zinc, 3
mg/kg/24 hr, in the form of zinc sulfate, gluconate, or acetate.
 Supplementation is for life
Selenium

 Antioxidant activities that protect against reactive oxygen

species
 convert inactive thyroxine to active thyroid hormone, T3,
is selenium-dependent.
 Selenium plays a role in the immune system functioning
Selenium deficiency

 has been implicated in cardiovascular disease, infertility,

myodegenerative diseases, and cognitive decline.
 Keshan disease is congestive cardiomyopathy associated with
heart failure, cardiac enlargement, electrocardiogram (ECG)
abnormalities, gallop rhythm, and even cardiogenic shock
 Both Keshan disease and myopathy have been described in
patients on (TPN) who did not have selenium added to their
supplement. Symptoms described included intermittent myalgias
and tenderness as well as eventual white fingernail beds
 Recent evidence has highlighted that nutritional
supplementation play a supportive role in COVID-19 patients.
Administration of higher than recommended daily doses of
nutrients such as vitamins D, C, E, Zinc and omega-3 fatty acids
might have a beneficial effect, potentially reducing viral
load, length of hospitalization, the severity of symptoms
and delay disease progression.
 These nutrients are well-known for their antioxidant
properties, variety of potent immunomodulatory, anti-
inflammatory, and antiviral properties.
Finally, take home message

Prevention is
better than
cure