CUTANEOUS

MANIFESTATION OF
NUTRITIONAL
DISTURBANCES

Dr. Khalid Alregaiey

• Dermatologic manifestations of nutrient deficiencies,
including protein-energy and micronutrient-related
malnutrition, vitamin and mineral deficiencies..
• The various nutrient deficiencies presented may share
common features. However, distinctive cutaneous
signs may prompt clinicians to consider a nutritional
cause and help distinguish a nutrient deficiency from
other common dermatologic conditions.
• NUTRITION: Nutrition is complex series of
events by which living organisms
Overview
consume and assimilate foods and other
nutrients to live, grow, and maintain
homeostasis.
• Malnutrition: A pathological state
resulting from :
• Relative or absolute deficiency, Excess of
one or more nutrient

• :Nutrients are the constituents of food

necessary to sustain the normal function
of the body.
• 1. Macronutrients :CHO, protein, fat, Ca,
Na, K, Mg, C1 & PO4.
•
Disorders due to Macronutrient
Deficiency :
• Protein - Energy Malnutrition : refers to
a spectrum of disorders describing
varying degrees of protein and calorie
deficiency. Several types of PEM have
been defined on the basis of relative
deficiencies in protein and total calorie
intake.

• 1. Marasmus: Characterized by the wasting

of muscle mass and depletion of body fat
stores. It is the most common form of PEM
and is caused by inadequate intake of all
nutrient
Protein-energy malnutrition

• Marasmus, kwashiorkor, and marasmic kwashiorkor

• Marasmus occurs with prolonged inadequate intake of
protein and calories, leading to stunted growth. (Fig. 1
; Dipasquale et al., 2020). Marasmic kwashiorkor is an
overlap syndrome wherein the growth retardation of
marasmus and the edema of Kwashiorkor are both
present.
• In marasmus, loss of subcutaneous fat leads to dry,
loose, and wrinkled skin. On the face, loss of the
buccal fat pads results in a prematurely aged
appearance. Excess lanugo-like hair can be seen, as
well as fissured, poorly growing nails and thin hair (
Castellani, 1947). Unlike Kwashiorkor, there is no
edema or dermatitis.
 cutaneous findings of marasmus

• Dry, thin, loose, wrinkled skin resulting

from loss of subcutaneous fat with an
emaciated appearance.
• Hair growth slows and examination may
reveal easy hair loss, leading to thin,
fine, brittle, hair and alopecia.
Increased lanugo hair may also be
present.
• Nails may show signs of fissuring, with
impaired growth.
•
2. Kwashiorkor:
• Kwashiorkor, also known as wet malnutrition is
observed in infants and children who have
hypoproteinemia.
• Cutaneous findings: Cutaneous findings
is known as dermatosis of kwashiorkor
(DoK). DoK is described as initially
small black patches on extensor
surfaces of ankles, knees, above wrists
and on elbows. The character of the
thickened epidermis is described as a
'crazy pavement".
• Skin changes: thin, dry, peeling skin with areas
of hyperpigmentationand hyperkeratosis(flaky skin)
• Hair changes: dry, hypopigmented hairthat falls
out easily
• EFAs
3. are components
Essential of Deficiency
Fatty Acids cell :
membranes, mediators of inflammation
via synthesis of prostaglandins and
leukotrienes, and are building blocks
throughout the body. Fatty acids also
contribute to the permeability barrier of
the stratum corneum and, therefore, are
important mediators of skin barrier
function.
• treatment: Essential fattv acid
replacement.
depenaing severity .
• Topical, intravenous
• • correction of coexistingnutritional
deficiencies
Risk factors for EFA deficiency

• poor dietary intake, including alcoholics

and patients with anorexia nervosa, or
those with malabsorptive conditions
such as biliary disease, inflammatory
bowel disease, and
• post-GI surgery (e.g., bariatric surgery).
• Cutaneous findings: Xerosis; scaly,
diffuse erythema; and associated
intertriginous erosions.
• hyperpigmentation or hypopigmentation
of the hair.
• Skin changes: thin, dry, peeling skin with areas
of hyperpigmentationand hyperkeratosis(flaky skin)
• Hair changes: dry, hypopigmented hairthat falls
out easily
• Rounded cheeks (moon face)
Micronutrients Deficiency Disorder
• Micronutrients consist of vitamins and minera
• Vitamins are divided in two group: (i)Fat solub
(ii)Water soluble. Fat soluble vitamins are vit. A
K. All othersare water soluble.
• Minerals are inorganic elements or substance
required by the organism in very
• small amounts for maintenance of vital proces
essential for life.
• Principal elements/macrominerals
• K, Ca, Mg, Na, P, S and Cl.
• Trace elements/ microminerals
• Fe, Zinc, Copper, Selenium, Fluoride, lodine,
• Cobalt, Molybdenum, Silicon, Nickel, Tin,Crom
Vitamin A (Retinol) Deficiency

• Vitamin A is a fat-soluble vitamin

important in keratinization, epithelial
proliferation, and photoreceptor
production.
• Dietery sources: Vitamin A is present in
plant as well as animal sources.
• The primary causes of vitamin A
deficiency continue to be inadequate
intake, fat malabsorption states, and
liver disease.

•
• Cutaneous lesions caused by VAD consist of follicular
papules with a central keratotic plug, primarily located
on the extensor extremities. This finding, referred to
as phrynoderma, must not be confused with keratosis
pilaris. The skin may also be dry and scaly, and the
hair sparse and fragile.
Cutaneous findings : Result of
abnormal keratinization.
• Mild deficiency may manifest as xerosis
and scaling.
• Severe deficiency may result in deep
skin fissuring referred to as
dermomalacia.
• Squamous metaplasia of the salivary
glands as well as the nasal and oral
mucosa may occur, leading to
xerostomia, hyposmia, and hypogeusia.
Laryngeal, bronchial, and vaginal
mucosa can also become involved.
• Phrynoderma, meaning "toad skin," is
typically associated with vitamin A
deficiency. These keratotic follicular
• Cutaneous manifestation Dry, thickened skin
(toad skin)
• Hair: Follicular hyperkeratosis (phrynoderma)
secondary to blockage of hair follicles with plugs
of keratin.
• Nail: Broken fingernails
• ocular manifestations include conjunctival
and corneal xerosis (drying), keratomalacia
(corneal necrosis/ulceration), nyctalopia (night
blindness), and Bitot spots (conjunctival lesions).
 Treatment

• : The recommended daily allowance

(RDA) of vitamin A is between 1000 and
5000 IU, with younger individuals
requiring a lower intake of vitamin A.
Recommended treatment for vitamin
deficiency disorder is 100,000 to
300,000 IU of oral vitamin A daily until
symptoms resolve and serum levels
normalize.
Vitamin K (phytomenadione)

• Functions
• Cofactor for γ-carboxylation of glutamate residues
on vitamin-K-dependent proteins involved in:
• Coagulation: maturation of factors II (prothrombin),
VII, IX, and X, protein C, protein S
• Bone formation: osteocalcin (bone Gla protein),
matrix Gla protein
• Vitamin K deficiency Causes
• Liver failure- Fat malabsorption
• Prolonged broad-spectrum antibiotic therapy
• Vitamin K antagonists (e.g., warfarin)
• Neonatal deficiency
• The neonatal intestine is sterile (no flora to
synthesize vitamin K).
• Cutaneous features VKD
• Hemorrhage (e.g., petechiae, ecchymoses)
•
 WATER-SOLUBLE VITAMIN DEFICIENCIES

• •The hydrosoluble vitamins are a group of

organic substances necessary in humans to prevent
disorders of metabolism.
• •The B group vitamins include thiamin (vitamin B1),
riboflavin (vitamin B2), niacin or niacinamide (vitamin
B3), pantothenic acid (vitamin B5), pyridoxine
or pyridoxal (vitamin B6) and cobalamin (vitamin B12).
Vitamin B2 (riboflavin)

• Riboflavin is a hydrosoluble vitamin that is abundant

in foods of animal origin, green leafy vegetables and
yeasts.
• is a member of naturally occurring
compounds known as flavins. Flavins have a
critical role in numerous biochemical reactions,
primarily those that are classified as oxidation-
reduction reactions, otherwise referred to as
redox reactions.
•
•
• (vit-B2) deficiency is characterized classically
by angular stomatitis, glossitis (magenta
tongue) (picture 3),
• seborrheic dermatitis around the nose and
scrotum, and vascularization of the cornea
• ●The dermatitis is localized to sun-exposed
areas of the body. The skin is dry, cracked,
hyperkeratotic, and hyperpigmented.
 Riboflavin deficiency
• Skin and mucous membrane findings
predominate. Initially, angular
stomatitis manifests as small papules
at the corners of the mouth
• cheilosis with erythema, xerosis, and
vertical fissuring of lips can occur.
• Early glossitis appears as prominent
lingual papillae, but after these papillae
are lost, the tongue becomes smooth,
swollen, and magenta in color.
• seborrheic dermatitis it involves the
nasolabial folds, nostrils, nasal bridge,
forehead, cheeks, and posterior
auricular regions.
• vitamin B2 (riboflavin) deficiency include breastfed
infants of mothers with deficiency and patients who
have undergone bariatric surgery. Deficiency can also
be seen in the setting of alcohol use disorder,
hypothyroidism, phototherapy for neonatal
hyperbilirubinemia, and medications such as
chlorpromazine, probenicid, and
tricyclic antidepressants (Miller, 1989). Acute vitamin
B2 deficiency, which may be induced by acute borate
ingestion (Yan and Jen, 2012), presents with deep-red
erythema, epidermal necrolysis, and mucositis. These
findings may resemble the clinical features of
Kwashiorkor.
The dermatitis of riboflavin deficiency

• seborrheic dermatitis in that it involves

the nasolabial folds, nostrils, nasal
bridge, forehead, cheeks, and posterior
auricular regions. Flexural areas of the
limbs may also be affected. Plugging of
the sebaceous glands (dyssebacia) may
be observed around the nose.
• The dermatitis can affect the genitalia,
more often to a greater extent in males
than in females.
• A red, confluent, crusty, or lichenified
dermatitis of the scrotum often spreads
to involve the inner thighs.
• In general, the dermatitis is worse in
areas of chafing or trauma. Infants
frequently manifest the dermatitis in
theinguinal areas. In older individuals,
the dermatitis is often more pronounced
in facial creases and wrinkles, and, if
incontinent, can involve the perianal
and buttock areas.
• Management : Measurement of
erythrocyte glutathione reductase
activity can be used as a screening
test. Treatment for deficient infants and
children is 1 to 3 mg per day, and for
adults, 10 to 20 mg.
3. Vitamin B3 (vitamin PP, nicotinamide, niacin)

• is an essential nutrient involved in the

synthesis and metabolism of carbohydrates,
fatty acids, and proteins.
• Niacin deficiency causes pellagra, which is
characterized by a photosensitive pigmented
dermatitis (typically located in sun-exposed
areas), diarrhea, and dementia, and may
progress to death; the "4 Ds"
• In resource-rich countries, pellagra tends to
occur in those with alcohol use disorder and
has been reported as a complication of
bariatric surgery or anorexia nervosa.
Clinical Findings
• 3 typical features of severe vitamin
B3 Deficiency: Dermatitis, Diarrhea,and Dementia.
• Dermatitis Characteristic dermatitis
• Circular broad collar rash on the neck (Casal
necklace); affects dermatomes C3 and C4
• Diarrhea and vomiting
• Neurologic:symptoms; dementia, depression,hallucin
ations
• Mucous membrane manifestations
cheilitis, angular stomatitis, glossitis,
and ulceration of the buccal mucosa
and vulva.
Management Vitamin B3 (Niacin)
deficiency

• Treatment of pellagra consists of 300 mg of oral niacin or

intravenous niacin, and an ongoing, adequate well‐balanc
• Treatment with 500 mg per day of nicotina
acid is given over several weeks.
• Neuropsychiatric symptoms may remit afte
of treatment, but skin lesions often take 3
clear.
• Treatment of pellagra consists of 300 mg of oral niacin
or 100 mg of intravenous niacin, and an ongoing,
adequate well‐balanced diet.
• Treatment with 500 mg per day of
nicotinamide or nicotinic acid is given
over several weeks.
• Nicotinamide is preferred over nicotinic
acid because nicotinic acid is
frequently associated with headache
and flushing.
• Neuropsychiatric symptoms may remit
after 24 to 48 hours of treatment, but
skin lesions often take 3 to 4 weeks to
clear.
VITAMIN B6 (PYRIDOXINE)
• CausesMalnutrition
• Heavy drinking
• Chronic renal failure
• Chronic hepatitis
• Drug interactions

• Marginal deficiencies may be more common,

manifested as nonspecific stomatitis, glossitis,
cheilosis, irritability, confusion, and
depression, and possibly peripheral
neuropathy (table 3) [3,113]. Severe deficiency
is associated with seborrheic dermatitis,
 Vitamin B7 deficiency (biotin deficiency)
• Biotin is a is an essential nutrient that plays key roles in the
metabolism of glucose, amino acids, and fatty acids..
• Causes
• Prolonged use of antibiotics (destruction of intestinal
flora)
• Excessive consumption of raw egg white:
contains avidin → binds biotin in the intestinal lumen
→inhibition of biotin resorption
• The classic clinical manifestations
of biotin deficiency include dermatitis around the
eyes, nose, and mouth; conjunctivitis; alopecia;
and neurologic symptoms, including changes in
mental status, lethargy, hallucinations, and
paresthesias
• The first symptoms are usually
associated with the skin and hair[29]
and may include:
• Dry skin
• Seborrheic dermatitis
• scaly, red rash, around eyes, nose,
mouth, and perineum
• Fine and brittle hair
• brittle nails
• Hair loss or total alopecia
• An erythematous, scaling, and crusting
dermatitis usually begins around the
eyes, nose, and mouth and continues to
involve multiple periorificial areas,
including the perianal region.
• Alopecia, conjunctivitis, and glossitis
have also been associated.
• Management : Dietery history should be
taken. If dietary history does not
adequately explain findings suggestive
of biotin deficiency, evaluation for
inborn errors of metabolism is
recommended. Acquired deficiency is
treated with 150 ug of biotin per day
until resolution of symptoms.
• Vitamin B6 deficiency presents as a
seborrheic-like dermatitis of the face,
scalp, neck, shoulders, buttocks, and
perineum. Clinical features resemble
niacin deficiency, including
photodermatitis, glossitis, and cheilitis.
• Glossitis appears as redness, burning,
and ulceration of the tongue,
 Clinical features
• Cheilosis, glossitis, stomatitis
• Sideroblastic anemia
• Irritability, seizures, peripheral neuropathy
• Seborrheic dermatitis
• M
• Treatment involves discontinuation of
inciting medication where relevant and
initiating replacement therapy with 100
mg of pyridoxine per day. Oral lesions
resolve in days, skin and hematologic
changes resolve in weeks, and
neurologic symptoms over several
months.
5. Vitamin B9 ( Folic acid ) :
• Folate can be found in almost all foods,
particularly in liver, wheat bran and
other grains, leafy green vegetables,
and dried beans.
• Cutaneous findings : Mucocutaneous
findings include glossitis with atrophy
of the filiform papillae, angular cheilitis,
mucosal ulceration, perirectal
ulcerations, perineal seborrheic
dermatitis, and diffuse brown
hyperpigmentation concentrated in the
palmar creases and flexures.
• Management: Folic acid
supplementation is typically curative.
Discontinuation of antifolate agents
6. Vitamin B12 ( Cobalamin) :
• Vitamin B12 is an important coenzyme
for two biochemical pathways in
humans.
• Mucocutaneous manifestations of
vitamin B12 deficiency include glossitis,
angular cheilitis, hair depigmentation,
and cutaneous hyperpigmentation.
• Glossitis is characterized by an
atrophic, red, and painful tongue with
atrophy of the filiform papillae, which is
referred to as Hunter glossitis. Hunter's
glossitis (or Moeller-Hunter) is the most
classic form. Hunter's glossitis, which
presents in up to 25% of cases.
• The most common cutaneous manifestation of vitamin
B12 deficiency is hyperpigmentation. This is typically
accentuated on the face, palmar creases, and flexures (
Brescoll and Daveluy, 2015), similar to what is
observed in Addison disease. Pigmentation in the nails
may appear as longitudinal hyperpigmented streaks (
Noppakun and Swasdikul, 1986). Depigmentation of
the hair and skin (vitiligo) may also be seen (
Brescoll and Daveluy, 2015).
Management

• For vitamin B12 deficiency in adults,

supplementation with 30 mg
administered via the intramuscular or
subcutaneous route for 5 to 10 days,
followed by 100 to 200 ug per month is
recommended.
Vitamin C deficiency
• ●Ascorbic acid – Vitamin C (ascorbic acid) is
essential for a variety of processes including
collagen synthesis, where it serves as a
reducing agent. Vitamin C deficiency, known as
scurvy, is characterized by ecchymoses,
bleeding gums (picture 4), petechiae, coiled
hairs, hyperkeratosis (picture 3A-B), Sjögren's
syndrome, arthralgias, and impaired wound
healing, as well as constitutional symptoms.
Evidence does not support the use of vitamin C
supplementation for disease prevention.
(See 'Vitamin C (ascorbic acid)' above.)
7. Vitamin C (Ascorbic Acid ) :
• Vitamin C is an antioxidant and essential
co-factor in several biologic reactions,
including collagen biosynthesis,
prostaglandin metabolism, fatty acid
transport, and norepinephrine synthesis.
• Vit-Cdeficiency is responsible for scurvy, which
is characterized by prominent cutaneous signs
(petechiae, perifollicular hemorrhage, and
bruising), gingivitis, arthralgias, and impaired
wound healing, appearing within a few months
of a vitamin C-deficient diet.
• Causes: severe malnutrition (e.g., due to alcoholism,
illicit drug use, and/or psychiatric illness)
• Cutaneous findings : The earliest
cutaneous sign of scurvy is
phrynoderma-enlargement and
keratosis of hair follicles (coiled
“corkscrew” hair) especially on the
posterolateral aspect of the arms,
resembling keratosis pilaris.
• The clinical deficiency syndrome known as
scurvy is largely due to impaired collagen
synthesis and disordered connective tissue.
 MINERAL AND TRACE ELEMENT
Minerals: are inorganic
•DEFICIENCIES
elements or substances required by
the organism in very
• small amounts for maintenance of
vital processes essential for life.

• Principal elements/macrominerals:
K, Ca, Mg, Na, P, S and Cl.
• Trace elements/ microminerals: Fe+,
Zinc, Copper, Selenium, Fluoride,
lodine,
• Cobalt, Molybdenum, Silicon,
• Iron deficiency anemia (IDA) is the most common
form of anemiaworldwide and is caused by inadequate
intake, decreased absorption, increased demand ), or
increased loss
•
Brittle nails, koilonychia (spoon-like nail deformity)
• Angular cheilitis: inflammation and fissuring of the
corners of the mouth
• Atrophic glossitis: erythematous, edematous,
painful tongue with loss of tongue papillae (smooth,
bald appearance)
• Zinc is themZinc, a critical component of
the body's metalloenzymes, is an
essential trace element. Zinc-
dependent enzymes have important
roles in gene regulation, protein
synthesis, and immune cell function.
• Zinc — Zinc deficiency was originally described
in a group of children with low levels of zinc in
their hair, poor appetite, diminished taste
acuity, hypogonadism, and short stature.

• Now zinc deficiency is recognized to be

associated also with numerous other findings,
including alopecia, dermatitis, growth failure,
cognitive dysfunction, and increased
susceptibility to infection (table 5) [31-35].

•
• The inherited autosomal recessive form of zinc
deficiency, acrodermatitis enteropathica, is caused by a
mutation in an intestinal zinc transporter gene. This
disease often presents in infants shortly after
transitioning from breastmilk to formula due to the
higher absorption of zinc from human milk.
• The complete classic triad of periorificial and acral
dermatitis, diarrhea, and alopecia is seen in only 20%
of patients with acrodermatitis enteropathica (
Nistor et al., 2016).
• The inherited form of zinc deficiency
(acrodermatitis enteropathica),
classically presents during infancy on
weaning from breast milk to formula or
cereal, which have lower zinc
bioavailability than breast milk.
• Acquired zine deficiency may result
from states associated with inadequate
intake, impaired absorption, or
increased excretion, including
pregnancy, lactation, extensive
cutaneous burns, generalized exfoliative
dermatoses, food faddism, parenteral
nutrition, anorexia nervosa, and even
excessive sweating. Intestinal
malabsorption
Clinical findings Zinc deficiency
• Acrodermatitis enteropathica (A)
presents soon after weaning in affected
infants or during the fourth to tenth
week of life in infants who are not
breast-fed.
• The classic features of AE include
alopecia, diarrhea, lethargy, and an
acute eczematous and erosive
dermatitis favoring acral areas-perioral,
periocular, anogenital, hands, and feet.
• Zinc supplementation with either an
enteral or parenteral formulation is
appropriate.
Copper deficiency

• Copper deficiency was first reported in infants

recovering from protein-energy malnutrition
whose diet was based on cow's milk. It is seen
also in infants receiving total parenteral
nutrition without trace mineral
supplementation
• Clinical findings : Hypopigmentation of
hair and skin and bony abnormalities
(osteoporosis, fractures, periosteal
reaction, and flaring of anterior ribs).
Copper deficiency

• Copper deficiency is marked by sensory and motor

neuropathy.Copper
The primary
deficiencydermatologic feature is
hypopigmentation of the hair and skin because
tyrosinase, a key enzyme in melanin synthesis, is
copper-dependent (Finner, 2013).
selenium deficiency:

• . Selenium is found in seafood, red

meat, egg yolks, grain products, and
chicken.
• deficiency can cause dilated cardiomyopathy
with myocardial necrosis and fibrosis. This
condition, known as Keshan disease, occurs
primarily in children living in rural China [39].
• Sporadic cases have been reported in
individuals on long-term home parenteral
nutrition without trace mineral
supplementation
Cutaneous findings

• white nail beds, similar to those of

Terry's nails in hepatic cirrhosis, and
hypopigmentation of skin and hair
(pseudoalbinism).
• management Diagnosis of selenium
deficiency is through measurement of
plasma selenium levels and glutathione
peroxidase activity.
• Selenium supplementation is used for
both acute correction and long term
maintenance.