SKIN MANIFESTATIONS of

NUTRITIONAL DISORDERS
 Food ingestion ~ health
skin condition
 Nutritional deficiencies  alterations in
photoprotection, immune function and
homeostasis
 Mucocutaneous changes  most frequent
manifestations of malnutrition
Protein-energy malnutrition

 Comprises quantitative and qualitative

defects in the ingestion and / or utilization
of nutrients
 Inadequate body weight
 Developmental and physiological
alterations
 Classification

 Marasmus
- failure in weight gain, leading to emaciation
- skin  dry, thin, pale lax & wrinkled
- subcutaneous fat disappears
- muscles  considerable loss in volume
- basal metabolism is diminished
- body temperature is low
 Kwashiorkor
- wet malnutrition
- oedema, failure to thrive
- loss of muscle mass
Cutaneous manifestations

 Marasmus
- Skin  thin, lax or wrinkled, scaly &
hyperpigmented
- excess lanugo-like hair
- loss of buccal fat pads  monkey faces,
aged appearance
- hair  brittle
- nail  thin & fissured
- angular cheilitis, pale & atrophic tongue
Nail Changes During PCM - Note
Brittle Nail Being Replaced by
Normal Nail as Client Fed
 Kwashiorkor
- hyperpigmentation & occasional fissuring
in areas subject to pressure
- erythema, desquamation, thinning,
ptechiae, ecchymosis and purpura
- shiny varnished-like skin (64%), dark
erythemateous pigmented macules (48%),
xerotic ‘crazy-paving’ skin (28%), residual
hypochromia (21%), large-scale desquamation
(18%)
 Superimposed bacterial & mycotic (candida)
 Hair  sparse, thin & depigmented
 Periodic episodes  ‘flag sign’
Management

 Multidisciplinary approach
 Skin lesions regress as soon as receives
adequate dietary intake
 Acute phase  lubricating ointments
 Bacterial infections  AB
 Candida infection  topical agents
Fatty acid deficiency

 Low-fat diets, severe malabsorption, long

term parenteral nutrition, in association
with PEM
 Skin  dry, scaly, underlying erythema,
intertriginous erosions, alopecia
 Treatment : EFA replacement
Vitamin A deficiency

 Follicular papules with a central keratotic

plug, primary on the extensor extremities
 Skin  dry, scaly
 Hair  sparse & fragile
Follicular Hyperkeratosis of
Vitamin A Deficiency
Hypervitaminosis A

 Most cases due to oral therapy

 Erythema, skin fragility, desquamation,
mucosal dryness, diffuse alopecia
 Carotenoderma 
- orange-yellow skin pigmentation due to
high intake of ß-carotene
- disappear when dietary habits are regulated
Vit B2 (riboflavin) deficiency

 Cheilitis, depapillated glossitis, pruritus,

seborrhoeic-like desquamation, scrotal
dermatitis
 Keratitis, conjunctivitis, photophobia,
tearing
 Mild cases  3 – 10 mg /d/o
 Severe cases  parenteral
 Vitamin B3 deficiency

 Pellagra  classic clinical menifestation 

dermatitis, diarrhoea, dementia
 Associated with :
- nutritional deprivation
- rich maize diet
- alcoholism
- impaired absorption of tryptophan
- GI disease, psychiatric disturbances
 Cutaneous manifestation : symmetrical
erythema on light exposed area (hands,
neck, face)  scarlet, hyperpigmented,
desquamating, crusted
 Mucosal  cheilitis, red, atrophic glossitis,
perianal & vaginal inflmmation, pain
 Prolonged patients  neurological
manifestations
 Treatment :
- 300 mg / o niacin
- 100 mg / iv
- adequate well-balanced diet
Vitamin B6 (pyridoxine)

 Skin lesions :
- cheilosis
- glossitis
- conjunctivitis
- periorificial seborrhoeic-like dermatitis
 Treatment :
- 20 – 100 mg /d/o
- 100 mg / im in cases of convulsions
Vitamin B12 (cyanocobalamin)

 Mucocutaneous alterations are rare 

hyperpigmentation of flexural areas, palms,
soles, nails, oral cavity
 Th/ : 1 mg vit B12 once/month/im
Biotin (vitamin H)

 Biotin deficiency may be genetic or

acquired
 Ingestion of raw egg white (avidine) and
malabsorption  main causes
 Periorificial erythematous, scaling
dermatitis, pallor, atrophic papilla of the
tongue, diffuse alopecia with
hypopigmented hair
 Acquired biotin deficiency : eczema.
Alopecia, conjunctivitis, parasthesiae,
muscle pain
 Th/: 10 – 30 mg biotin /o/d
Vitamin C (Ascorbic acid)

 Clinical manifestation : scurvy 

irritability, pseudoparalysis of the legs
(frog position), osseous alterations,
haemorrhage, anemia
 Bluish-purple and painful swellings of the
gum, follicular hyperkeratosis,
haemorrhages in the skin range from
ptechia to ecchymoses
 Th/ : 150 mg/d of ascorbic acid
Patient With Multiple Deficiencies
exhibits cheilosis, glossitis, and
scorbutic gums
Selenium

 Hypopigmentation of the skin, hair & nails

(white nails).
 Selenium supplementation 2 mg/kg/d
 Se sulphide shampoo  used in pityriasis
capitis, pityriasis vesicolor, seborrhoeic
dermatitis
 Excessive absorption through damaged skin
may cause tremor and loss of appetite
Zinc

 Factors in the pathogenesis of deficiency :

- low zinc content in the diet
- consumption of substances that interfere
with zinc bioavailability (phytate)
- homeostatic incapacity of the individual
to retain zinc
- increased need for zinc (pregnancy)
 Acrodermatitis enteropathica  classic
condition due to Zn deficiency  triad of
dermatitis, diarrhoea and alopecia
 Cutaneous lesion : periorificial
erythematous, scaling plaques, erosion
 Frequently complicated by candidiasis
Anorexia nervosa / bulimia

 Dry skin, hyperpigmentation, skin

roughness, generalized lanugo-like hair,
diffuse alopecia, brittle hair & nails
 Ecchymoses due to vitamin K deficiency
 Advanced cases  scurvy & pellagra
Obesity

 Cutaneous alterations are related to

friction, accumulated moisture,
overheating, oversweating in fat skinfolds
 Friction between skin surfaces leads to
hyperpigmentation