NUTRITIONAL

DERMATOSES
 VITAMIN A
Important in
Retinal photoreceptor function
Epithelial proliferation
Keratinization

The two most clinically important metabolites of vitamin A are

Retinal: key component of rhodopsin generation
Retinoic acid: regulates cell differentiation
Dietary sources:

Plant sources(beta-carotene):
Dark, green, leafy vegetables, red palm oil, and brightly colored
fruits such as papaya, mango, carrots, tomatoes, apricots.

Animal sources(retinyl esters):

Egg yolk, liver, fish, fortified milk, and other dairy products.
VITAMIN A DEFICIENCY
The most common cause of preventable blindness in children,
according to the WHO.

Etiology and Pathogenesis

Inadequate intake
Fat malabsorption states
Liver disease
Chronic intestinal parasitic infection
Gastric bypass surgery
Manifestations of Vitamin A Deficiency
Ocular
Impaired dark adaption
Xerophthalmia
Corneal xerosis, ulceration, keratomalacia
Corneal perforation, blindness
Cutaneous, Mucocutaneous
Xerosis
Skin fissuring (dermatomalacia)
Phrynoderma
Xerostomia
Hypotonia
Hypogeusia
Laboratory Testing:
Normal serum levels: 20 and 50 mcg/dL
Assessment for the hydrolysis of retinoyl glucuronide
to retinoic acid.

Treatment:
RDA:
700 mcg (adult females)
900 mcg(adult males)

Recommended treatment: 600 to 3000 mcg of vitamin A daily

till symptom resolves.
 VITAMIN A TOXICITY
Acute toxicity: excessive amounts of vitamin A are
ingested over a period of several hours or days.

Intake exceeds 20 times the RDA in a child or 100 times the

RDA in an adult.

Chronic toxicity:
Daily ingestion of
>25,000 IU for >6 years or
>100,000 IU for >6 months
At risk patients:

Taking vitamin A derivatives for the treatment of dermatologic

conditions such as acne, psoriasis, and ichthyosis.

Other includes vitamin food faddists who consume large

quantities of nonprescription vitamin A supplements.
Manifestations of Vitamin A Toxicity:

Dry, scaly skin with desquamation

Peeling of palms and soles, follicular hyperkeratosis
Cheilitis, fissuring of lips and angles of mouth
Alopecia
Anorexia, nausea, vomiting
Myalgias, arthralgias
Blurred vision, pseudotumor cerebri
Skeletal changes: premature closure of the epiphyses,
spontaneous one fractures
Laboratory Testing:
Elevated levels of calcium and alkaline phosphatase
Cirrhosis ; the most significant effect of long-term vitamin A
toxicity.

Treatment:
Discontinuation of the excess vitamin intake.
CAROTENEMIA AND CAROTENODERMA
Characterized by yellow-orange skin pigmentation.

Etiology and Pathogenesis:

Thyroid hormone
Pancreatic lipase
Bile acid concentrations
Processing of foods
Dietary fat and fiber content.
Clinical Findings:
Yellow discoloration of skin
First on the face--progresses to manifest diffusely.

Laboratory Testing:
Serum levels >250 mcg/dL, and is detectable 4 to 7 weeks
following initiation of a carotenoid-rich diet.

Treatment:
Discontinuation of excessive carotene intake
 VITAMIN D CALCITRIOL
Regulation of calcium and phosphorus metabolism.

Dietary sources : fortified milk, fish oil, and fish such as salmon,
sardines, herring, tuna, cod, and shrimp.

Synthesis in the skin from exposure to ultraviolet light.

The most common disorder:

vitamin D-deficient rickets
Type I
AR
Defect in renal vitamin D–1- hydroxylase
Treated with supplements of 1,25-hydroxyvitamin D.

Type II
hereditary vitamin D–resistant rickets (Rare)
AR end-organ resistance to 1,25-hydroxyvitamin D.
Supplementation with high doses of 1,25-hydroxyvitamin D and
calcium may overcome this resistance.
vitamin D deficiency is associated with

Increased systolic blood pressures,

Fasting plasma glucose
Insulin concentrations
Risk of cardiovascular disease
Risk of hip fractures in postmenopausal women
Colon cancer mortality
Vitamin D–deficient rickets is A/W:
Congenital ichthyoses, such as lamellar ichthyosis, nonbullous
ichthyosiform erythroderma, X-linked ichthyosis
Epidermolytic hyperkeratosis
Photosensitive disorders such as xeroderma pigmentosum.

Factors contributing to vitamin D deficiency:

Avoidance of sun exposure
Excessive transepidermal calcium loss
Defective vitamin D synthesis in affected skin
Decreased intestinal calcium absorption secondary to systemic
retinoid therapy.
Vitamin D: antiproliferative properties - may influence the
development of skin cancer.

Clinical Findings:
Rachitic rosary
Craniotabes, frontal bossing
Lateral bowing of lower extremities
Widening of wrists, scoliosis, fractures
Dental defects
Rarely hypocalcemic seizures
Laboratory Testing:
Elevated alkaline phosphatase levels
Low serum 25-hydroxyvitamin D levels

Treatment:
RDA: 5 to 10 mcg
TREATMENT - 200 to 400 mcg/day until resolution of symptoms
(approximately 2 to 3 months)
 VITAMIN E TOCOPHEROL
Found in oils, fortified grains, dark-green leafy vegetables,
legumes, nuts, avocado, and small fishes - herring and sardines.

Fat-soluble vitamin, excessive intake may augment the effects of

anticoagulant medications leading to purpura and propensity
for hemorrhage.

Deficiency states are rare.

 VITAMIN K PHYTONADIONE
Necessary cofactor in the carboxylation of glutamate residues
on coagulation factors II, VII, IX, and X, and proteins C and S.

Dietary vitamin K
Phylloquinone
Green, leafy vegetables, certain legumes, soybeans, cereals, and
beef liver.

Half is synthesized by GI flora as menaquinones.

Clinical Findings
Impaired coagulation and hemorrhage
In neonates= hemorrhagic disease of the newborn (HDN)

Neonates: prone to vitamin K deficiency due to poor

transplacental transfer, low dietary intake, and a sterile bowel.

It can present as
Ecchymoses
Cephalohematomas
Nasal, subgaleal, umbilical, intestinal, or intracranial
hemorrhages.
Vitamin K deficiency in older children and adults
Purpura, ecchymoses, gingival bleeding, and GI, genitourinary,
and retroperitoneal hemorrhage.

Laboratory Testing:
Elevations in PT/APTT
Serum vitamin K level
Treatment:
Neonatal prophylaxis - a single intramuscular dose of 0.5 to 1.0
mg vitamin K.

Acute treatment- FFP to replace deficient coagulation factors.

Vitamin deficiency can also be treated with parenteral or

intramuscular 5 to 10 mg vitamin K per day to correct severe
deficiency.
 VITAMIN B1 THIAMINE
Thiamine is an essential coenzyme for 3 separate enzymes
involved in
Nicotinamide adenine dinucleotide phosphate synthesis,
Carbohydrate metabolism,
Deoxyribose and ribose synthesis.

Sources: whole grains, enriched bread products, dried peas

and beans, potatoes, and fish.

Polished rice eliminates the thiamine- containing husk and

predisposes to thiamine deficiency.
Beriberi refers to a thiamine deficiency state

Predisposing factors for pediatric

unsupplemented parenteral nutrition, breastfed infants of thiamine-
deficient mothers, congestive heart failure and severe malnutrition.

In adults
chronic alcoholism,bariatric surgery,food refusal in severedepression,
renal disease,congestive heart failure, lymphoma
Clinical Findings

Early signs include irritability, apathy, restlessness, and vomiting

As the disease progresses, neurologic signs of Wernicke

encephalopathy may develop,
ophthalmoplegia, ataxia, nystagmus

Adult beriberi: dry and wet forms.

Dry beriberi: symmetric distal peripheral neuropathy involving

both sensory and motor systems.

Wet beriberi: neuropathy and signs of cardiac involvement,

including cardiomegaly, cardiomyopathy, CHF, peripheral edema
and tachycardia.
Laboratory Testing:

Erythrocyte thiamine transketolase or blood thiamine concentration

Normal up to 15%

Treatment:
RDA:0.5 mg per 1000 kcal

Treatment : initiated with IV or im thiamine of 50 -100 mg/day for 7

to 14 days;

oral supplementation is then provided until full recovery is

documented
 VITAMIN B2 RIBOFLAVIN
Riboflavin is used in 2 coenzymes:

flavin mononucleotide (FMN) and flavinadenine dinucleotide

Involved in oxidation-reduction reactions in cellular respiration
and oxidative phosphorylation

Sources: dairy products, nuts, meat, eggs, whole grain and

enriched bread products, fatty fish, and green leafy vegetables
Deficiency states can be caused by
Decreased intake
Inadequate absorption
Phototherapy
Alcoholics

Clinical Findings
Acute
Erythema
Epidermal necrolysis
Mucositis
Chronic
Angular stomatitis ,Glossitis
Cheilosis with erythema, xerosis, and fissuring
Seborrheic dermatitis-like dermatitis affecting typical sites and flexures
Photophobia and conjunctivitis
Laboratory Testing:
A normochromic, normocytic anemia may be observed.
Erythrocyte glutathione reductase activity:
screening test.

Treatment:
RDA: 0.6 mg per 1000 kcal.
Treatment of infants and children: 1 to 3 mg per day, and
For adults: 10 to 20 mg per day
 VITAMIN B3 NIACIN
Niacin is a vitamin cofactor, obtained for the diet or synthesized
endogenously from the essential amino acid tryptophan.

Sources: whole grains and enriched bread products, nuts, dairy

products, liver, animal meat, mushrooms, and dried beans

Deficiency of niacin results in pellagra

Francesco Frapoli coined- pellagra after the Italian words “pelle,”

meaning skin, and “agra,” meaning rough
Corn and maize contain bound niacin, so without hydrolysis, it is
unavailable for absorption

Other Predisposing Factors:

GI diseases like jejunoileitis, gastroenterostomy, prolonged

diarrhea, chronic colitis, ulcerative colitis, cirrhosis, Crohn
disease, and subtotal gastrectomy
Alcoholics
Hartnup disease
Medications like isoniazide, 5 FU, phenytoin, chloramphenicol,
azathioprine, sulfonamides, and antidepressants
Clinical Manifestations of Pellagra:

Painful pruritic dermatitis in photoexposed areas

May be vesicular, crusted, and develops into scaly, keratotic
plaques
Dorsum of hands (“gauntlet”), neck (“Casal’s necklace”), dorsa of
feet (“gaiter” of pellagra); butterfly distribution in face
Angular stomatitis, cheilitis, glossitis
Diarrhea, nausea, vomiting, abdominal pain, anorexia
Insomnia, fatigue, nervousness, apathy, impaired memory,
depression, psychosis, dementia
Laboratory Testing:
clinical grounds and through a rapid response to vitamin
supplementation

Skin biopsies: depletion of Langerhans cells whose absence are

thought to allow for more prolonged inflammation at these sites.

Treatment:
RDA: 15 to 20 mg of niacin or approximately 60 mg of exogenous
tryptophan.

Treatment with 500 mg per day of nicotinamide or nicotinic acid is

given over several weeks.
 VITAMIN B6 PYRIDOXINE
Vitamin B6 describes 3 interchangeable molecules: pyridoxine,
pyridoxamine, and pyridoxal

Sources: Meats, whole grains, vegetables, and nuts are the best
sources for vitamin B6.

The most common form existing is pyridoxal-5-phosphate

Deficiency is due to:
Inadequate intake
Alcoholics
Malabsorption
Medication: isoniazid, hydralazine, penicillamine, and oral
contraceptives.

Clinical Findings:
Seborrheic-like dermatitis of the face, scalp, neck, shoulders,
buttocks, and perineum.
Clinical features overlap those of niacin deficiency including
features of photodermatitis, glossitis, and cheilitis
Neurologic signs include somnolence, peripheral neuropathy,
paresthesias, weakness, and confusion.
Laboratory Testing:
Plasma pyridoxal-5- phosphate

Treatment:
RDA:
Adult males require at least 2 mg per day
Adult females require at least 1.6 mg per day
Infants require approximately 0.3 mg per day

Treatment involves discontinuation of inciting medication and

initiating replacement therapy of 100 mg of pyridoxine per day
 VITAMIN B9 FOLATE
Folate : almost all foods, particularly in liver, wheat bran and
other grains, leafy green vegetables, and dried beans.

Tetrahydrofolate, the coenzyme form of folate.

Predisposing factors for deficiency:

Poor diets of alcoholics
Malabsorption
Medications (methotrexate, trimethoprim, oral contraceptives,
and pyrimethamine)
Clinical Findings:

Primary manifestation is hematologic: hypersegmented

neutrophils, followed by macrocytosis and megaloblastic anemia.

Mucocutaneous findings:
Glossitis with atrophy of the filiform papillae, angular cheilitis
Mucosal ulceration, perirectal ulcerations,
Perineal seborrheic dermatitis
Diffuse brown hyperpigmentation concentrated in the palmar
creases and flexures
Laboratory Testing:
Macrocytic and megaloblastic anemia with hypersegmentation
of neutrophils is suggestive.

Diagnostic confirmation can be accomplished through

measurement of serum folic acid levels.

Treatment:
Discontinuation of antifolate agents is recommended if involved.

Treatment involves 1 to 5 mg of folic acid per day

 VITAMIN B12 COBALAMIN
Vitamin B12 is an important coenzyme for 2 biochemical
pathways in humans.

1. methylcobalamin as a coenzyme for methyltransferase to

methylate homocysteine to methionine, which is used in DNA,
protein, and lipid metabolism.
2.

3. 5-adenosylcobalamin to catalyze the reaction by methylmalonyl

coenzyme A (CoA) mutase to convert methylmalonic acid to
succinyl-CoA, which is used in fat and carbohydrate metabolism.
Sources: animal products, with liver, eggs, milk, beef, and organ
meats being excellent sources.

Deficiency due to:

Inadequate intake: Elderly individuals and psychiatric patients
with poor diets (including anorexia nervosa), and strict
vegetarians and their breastfed infants.

Malabsorption: decreased gastric acid states, decreased

intrinsic factor, microbial competition in the gut (bacterial
overgrowth), impaired absorption.
Clinical Findings:
Mucocutaneous: glossitis, angular cheilitis, hair depigmentation,
and cutaneous hyperpigmentation.

Hair depigmentation may be localized or diffuse.

Hyperpigmentation can be diffuse and symmetric or few scattered

macules.

The greatest concentration: on the hands, nails, and face, with the
most commonly- palmar creases, flexural regions and pressure
points.
Laboratory Testing:

The hematologic findings: macrocytic anemia and hypersegmented

neutrophils.
Bone marrow biopsy: hypercellular marrow.
serum cobalamin levels less than 200 pg/mL indicating definite B12
deficiency
200 to 300 pg/mL being borderline low.

Treatment:
RDA 2.4 mcg
Treatment dose: cynocobalamine 1 mg/week/month
 VITAMIN C ASCORBIC ACID
Essential cofactor in
several biologic reactions, including collagen biosynthesis,
prostaglandin metabolism, fatty acid transport, and norepinephrine
synthesis.

Humans are unable to synthesize ascorbic acid because they lack

gulonolactone oxidase.

Dietary source: fruits and vegetables, like potatoes, tomatoes,

berries, citrus fruits, and green vegetables
Depletion of body stores occurs after 1 to 3 months of a deficient
diet.

Vitamin C deficiency results in scurvy.

Causes of scurvy include insufficient vitamin C intake, increased

vitamin requirement, and increased loss.

Increased vitamin C requirements are encountered with certain

drugs, including aspirin, tetracycline, oral contraceptives,
corticosteroids, and tobacco smoking.
Clinical Manifestations of Scurvy
Skin
Follicular keratotic plugging
Corkscrew hairs
Perifollicular purpura
Lower-extremity edema with ecchymosis
Poor wound healing and dehiscence
Mucosa
Swelling, ecchymoses, and bleeding of gingiva
Hemorrhagic gingivitis, necrosis, loss of teeth
Other
Hemorrhagic intraarticular, subperiosteal, intramuscular, organs
disruption of growth plates, bowing of bones, depressed sternum
Epistaxis, hematuria, GI, and cerebral hemorrhage
Laboratory Testing:
Leukocyte ascorbate level: less than 75 mg/L

Treatment:

RDA: 40 to 60 mg of ascorbic acid.

Therapeutic doses of 100 to 300 mg/ daily.

 BIOTIN
Biotin is an essential cofactor for 4 carboxylating enzymes:

(a) Acetyl-CoA carboxylase in fatty acid synthesis and lipogenesis

(b) Pyruvate carboxylase in gluconeogenesis
(c) Propionyl-CoA carboxylase
(d) 3-methylcrotonyl-CoA carboxylase in amino acid
catabolism

Sources: Eggs, liver, milk, peanuts, mushrooms, chocolates, and

hazelnut
Avidin, a protein found in egg whites, binds free biotin in the
bowel, prevent absorption of both dietary and synthesized
biotin.

Deficiency due to:

Long-term parenteral nutrition without biotin supplementation

Anticonvulsants, such as valproic acid, carbamazepine, and
phenytoin
Clinical Findings:
Symptoms can develop 3 to 6 months after initiation of
unsupplemented parenteral nutrition or a raw-egg-white-rich
diet.

Erythematous, crusting, scaly dermatitis around eyes, nose,

mouth, and other periorificial areas

Alopecia, glossitis, conjunctivitis

Irritability, lethargy, paresthesias, hypotonia, developmental

delay
Laboratory Testing:
Evaluate for inborn errors of metabolism is recommended in
children
Biotinidase levels, serum amino acids, urine organic acids,
carnitine studies, and ammonia may be helpful

Treatment:
RDA: 30 mcg in neonates
100 to 200 mcg in adults.

Treatment 150 mcg of biotin/ day

Patients with biotinidase deficiency are treated with 5 to 10 mg

MINERALS
 COPPER
Copper is an essential component of several metalloenzymes,
including tyrosinase and lysyl oxidase.

Copper is found in fish, whole grains, beef and pork liver,

chocolate, eggs, and raisins.

Copper deficiency result from:

Malnutrition, malabsorptive states, chronic unsupplemented
parenteral nutrition, infants with a strictly cow’s-milk diet, and
excessive intake of antacids, zinc, iron, or vitamin C, that can
interfere with absorption.
Clinical Findings:
Hypopigmentation of hair and skin
Bony abnormalities (osteoporosis, fractures, periosteal reaction,
and flaring of anterior ribs).
Myeloneuropathy (If untreated, optic nerve involvement may
occur, with permanent vision loss).

Laboratory Testing:
Microcytic anemia, neutropenia, hypocupremia, and
hypoceruloplasminemia can be observed.

Treatment:
Treatment is with supplemental copper in the
diet
 COPPER AND MENKES DISEASE
Menkes disease, also known as kinky hair disease.

Mutations in MNK gene.

Clinical Features :

Depressed nasal bridge, ptosis, and reduced facial movements

Loss of developmental milestones, hypotonia, seizures,
hypothermia,and failure to thrive
Steel wool appearance of hair: short, sparse lusterless, tangled,
and depigmented.
Microscopically: pili torti, trichorrhexis nodosa
Follicular hyperkeratosis, inelastic depigmented skin at nape of
neck, axillae, and trunk
Arched palate, delayed tooth eruption
Severe neurologic deficits
Bony and renal changes, including bone fractures and subdural
hematomas

Laboratory Testing:
Diagnosis is through the clinical history, physical examination,
and reduced levels of serum ceruloplasmin and copper.

Treatment:
Early treatment with copper histidinate has resulted in good
outcomes, including normal neurodevelopment.
 SELENIUM
Selenium is an essential component of glutathione peroxidase.

Sources: seafood, red meat, egg yolks, grain products, and chicken.

An area with low soil selenium is Keshan, China, where selenium

deficiency in humans is endemic.
 SELENIUM DEFICIENCY
Deficiency due to:
Low soil selenium, restricted protein diets, unsupplemented
parenteral nutrition, malabsorption states, and increased losses.

Clinical Findings:
Keshan disease
Acute or chronic insufficiency of cardiac function, cardiomegaly,
arrhythmias, and electrocardiographic abnormalities
Muscle pain and weakness
Cutaneous findings : white nail beds, similar to those of Terry’s
nails in hepatic cirrhosis, and hypopigmentation of skin and hair.
Keshin-Beck disease is an osteoarthropathy that affects the
epiphyseal and articular cartilage.

Laboratory Testing:
Measurement of plasma selenium levels and glutathione
peroxidase activity

Treatment:
Selenium supplementation is used for both acute correction and
long-term maintenance
 IRON
Iron is used in several biologic pathways:
Heme synthesis, oxidation-reduction reactions, collagen synthesis,
and as a cofactor for enzymes such as succinic dehydrogenase,
monoamine oxidase.

Sources: red meats, egg yolks, dried beans, nuts, dried fruits, green
leafy vegetables, and enriched grain products
 IRON DEFICIENCY
Deficiency due to: inadequate intake or chronic blood loss

Cutaneous Features of Iron Deficiency

Nails : Fragile, longitudinally ridged Lamellated brittle nails
thinning, attening of nail plate, koilonychia
Hair: Lusterless, dry, focally narrow and split hair shafts,
heterochromia of black hair; hair loss
Mucous membranes: Aphthous stomatitis, angular stomatitis,
atrophied tongue papillae
Blue sclerae
Pruritus
Iron deficiency in a microcytic anemia:
measurement of serum iron levels, ferritin, total iron binding
capacity, transferrin saturation.

Treatment involves appropriate iron supplementation

 ZINC
An essential component of many metalloenzymes involved in
metabolic pathways and cellular functions.

Also important for wound healing and for T-cell, neutrophil, and
natural killer cell function.

Dietary sources: meat, fish, shellfish, eggs, dairy products, and

legumes
The highest and most bioavailable forms of zinc found in meats,
fish, and shellfish.
 ZINC DEFICIENCY
Populations at risk:
Include patients with intestinal malabsorption syndromes liver
disease, anorexia nervosa or food faddism, extensive cutaneous
burns, and nephritic syndrome.

Inherited: AE (AR disorder of zinc absorption)

Acquired: AZD.
AE: Defect in an intestinal zinc transporter, the human ZIP4
protein encoded on the SLC39A4 gene.

Classically presents during infancy on weaning from breastmilk to

formula or cereal.

Clinical Features:
Eczematous and erosive dermatitis
Preferentially localized to perioricial and acral areas
Alopecia
Diarrhea
Lethargy, irritability
Superinfection with Candida albicans and
Staphylococcus aureus
AZD:
Secondary to impaired absorption of zinc, inadequate intake, or
excessive renal or intestinal losses

May result in a clinical picture that resembles AE and occurs also

in adults.

Chronic or subacute form:

Cutaneous manifestation: usually less striking and present
predominantly as a psoriasiform dermatitis involving the hands
and feet and, occasionally, the knees.
Laboratory Testing:
A low plasma zinc level: gold standard for diagnosis.
Normal plasma zinc levels: 70 to 250 mcg/dL.
Serum alkaline phosphatase—a zinc-dependent enzyme- rapid
indicator of zinc status

Treatment:

In children, 0.5 to 1.0 mg/kg of elemental zinc given as 1 to 2

daily doses: for mild to- moderate zinc deficiency.

In adults, 15 to 30 mg of elemental zinc per day.

 NOMA
Necrotizing ulcerative stomatitis, stomatitis gangrenosa, or
cancrum oris)

Devastating gangrenous condition that destroys soft and hard

tissue of the face

Children between the ages of 1 to 7 years.

Malnutrition, vitamin deficiencies, and immune dysregulation

create an environment for this rapidly progressive destructive
polymicrobial infection(Prevotella intermedia and
Fusobacterium necrophorum- Most frequent
organism)
Clinical Presentation of Noma:

Rapid progression of soreness of mouth

halitosis, purulent oral discharge, tenderness of
lips and cheeks

Necrotizing stomatitis starting at alveolar

margin and extending to mucosal surface of
cheek

Swelling and blue-black discoloration of cheek

cone-shaped black necrosis, tissue destruction,
and ulceration
Laboratory investigation:
Shows severe anemia, a high wbc, and hypoalbuminemia

Healing noma lesions are also difficult to manage because of

the extensive fibrous scars.

These scars can lead to strictures of the mouth, severe dental

malposition, defective speech, and even complete closure of
the mouth from contractures
PROTEIN ENERGY MALNUTRITION
PEM refers to a spectrum of disorders describing varying
degrees of protein and calorie deficiency.

In developing countries, malnutrition most commonly arises

as a result of inadequate dietary intake.

Other etiologies:
chronic illness, malabsorption, presumed food allergies, food
aversion, nutritional ignorance, and fad diets
Marasmus: with severe wasting and stunting and are at less
than 60% of expected body weight for age.

Kwashiorkor have body weights less than 60% to 80% of that

expected for age.

Because they are being fed grain-derived foods without

adequate accompanying protein or fat.
PATHOGENESIS
Clinical findings of Marasmus:

Affects infants younger than age 1 year

Failure to thrive
Dry, thin, loose, wrinkled skin
Hair loss; ne, brittle hair; alopecia
Fissuring and impaired growth of nails
Loss of subcutaneous fat
Loss of buccal fat (monkey facies)
Rectal prolapse, abdominal distension
Diarrhea, constipation
Angular cheilitis
Clinical Features of Kwashiorkor:

Affects children between 6 months and 5 years of age

Failure to thrive, edema
Irritability, lethargy, apathy
Generalized dermatitis likened to “aking enamel paint,”
“cracked pavement.
Increased pigmentation on arms and legs
Hair color changes (red tint gray-white; “ag sign”)
Distension of abdomen
LABORATORY TESTING
As recommended by the WHO: screening for hypoglycemia and
anemia, and an investigation into potential comorbid infectious
diseases.

Chest radiography: signs of bacterial pneumonia, tuberculosis,

heart failure, rickets, and fractures.

Patients with kwashiorkor will also demonstrate hypoproteinemia.

Elevated soluble CD14 levels

TREATMENT:

Severe PEM: require hospitalization because of the concurrent risks

of hypoglycemia, hypothermia, dehydration, and sepsis.

Care must be taken to avoid excessively rapid rehydration because of

the risks of congestive heart failure.

Severely malnourished children are relatively immunocompromised,

empiric antibiotic therapy.
 ESSENTIAL FATTY ACIDS
Patients at risk for EFA deficiency include those with:
poor dietary intake
Alcoholics
Patients with anorexia nervosa
Malabsorption (biliary disease, IBD, postgastrointestinal surgery)

EFAs represent a group of 18-carbon, 20-carbon, or 22-carbon

polyunsaturated fatty acids that cannot be synthesized de novo by
the human body.

Omega-6 series: vegetable oils, and is derived from linoleic acid.

Linoleic acid and -linoleic acid: precursors for other EFAs.

Arachidonic acid, a derivative of linoleic acid, is converted into

prostaglandins, eicosanoids, and leukotrienes.

Skin Manifestations:

Xerosis
Scaly erythema, intertriginous erosions
Traumatic purpura, poor wound healing
Brittle nails, alopecia
Hyperpigmentation and hypopigmentation of hair
LABORATORY TESTING:
Decreased levels of linoleic and arachidonic acids, and elevated
plasma levels of an abnormal intermediary, 5,8,11-eicosatrienoic
acid.

TREATMENT:
Topical application of sunflower seed and safflower oils that
contain linoleic acid may improve the clinical cutaneous findings.

Treatment typically consists of oral or intravenous

supplementation of EFA.
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