Transcript nutritional disorders

Nutritional Dermatoses
Stages of nutritional deficiency syndrome

Stage I
Intake falls below daily requirement but the
reserves maintain normal blood values

Stage II
Blood levels decrease but patient is
asymptomatic

Stage III
Development of clinical signs and symptoms
Causes of deficiencies
Decreased intake
Increased requirement

Poverty

During growth

Ignorance

Pregnancy

Food faddism

Lactation

Crash diets

Fever

Anorexia nervosa

Hyperthyroidism
Stages of nutritional deficiency syndrome
Decreased absorption and utilization

GI - mucosal disturbances: Malabsorption
syndrome

Dietary factors: High dietary phytate, TPN,
alcoholism

Trauma: Burns , Post surgical procedures

Malignancy

Renal disorders

Infections: Parasitic, bacterial, viral

Miscellaneous: Collagen vascular disease, HIV
Nutritional deficiencies

Fat soluble vitamins (A,D,E,K)

Water soluble vitamins
(B-complex, Niacin, Pantothenic acid, Biotin, Vit C)

Minerals

Trace elements (Zinc, Iron)

Essential fatty acids (EFA)

PEM (Protein energy malnutrition)
Important Points
1. Water soluble vitamins
◦ Not stored in body
◦ Excessive consumption
No toxicity
2. Fat soluble vitamins (A, D, E, K)
◦ Stored in liver
◦ Excessive consumption
toxicity
Vitamin A (Retinol) deficiency
Rich source

Animal fats, fish liver oils, milk, butter, eggs, liver ,
kidneys
Provitamin A (Beta carotene)

Green and yellow parts of plants (spinach, drum
sticks, spring onions, cabbage, pumpkin, carrots,
tomato)

Fruits – mango, papaya
Clinical features
Skin manifestations:

Infants, very young children
Extensive xerosis - an earliest manifestation

Adults: Follicular hyperkeratosis

Sites: extensor of extremities; spreads to
shoulder, face, chest, abdomen, back , buttocks.
Dry, firm brown follicular papule with keratotic
plug covered with loosely adherent scale
On removal of plug, a pit is seen
Clinical features
Skin manifestations:

Phrynoderma (Toad skin)
Mild follicular hyperkeratosis, limited distribution

Mixed deficiencies of Vit.A, Vit.E, B - complex,
Vit.C and EFA
Clinical features
Eye Manifestations:
Common cause of blindness in developing
countries
 Earliest symptoms:
◦ Nyctalopia (night blindness)
◦ Hemeralopia (inability to see bright light)

Xerophthalmia:
◦ Conjunctival xerosis
◦ Bitot’s spot
◦ Corneal xerosis
◦ Corneal ulceration
◦ Keratomalacia
◦ Phthisis bulbi, scarring, blindness
Treatment
Normal requirements:
 Infants, children < 4 yrs - 1500 IU of Vit. A
> 4 yrs - 5000 IU of Vit. A
Prophylactic Treatment:
 Vit. A (2 lacs IU) every 6 months to pre-school
children (Orally retinyl palmitate in oil)
 Good quality protein diet + vitamins
 Education of local community
Contd…
Treatment

Dose of 1-3 lacs IU of Vit. A for 1-3 days
(Stop in case of headaches)

Supplements: Vit. B complex and EFAs

Diet to include eggs, milk, butter, green leafy
vegetables

Treatment of underlying cause
(especially protein and zinc deficiency)
Vitamin D

Vit. D is a group of antirachitic sterol derivatives,
considered as a hormone

Skin: Role in synthesis, storage and release of
Vit. D
Source of Vit. D and Chemistry

Plants
ergosterol
ergocalciferol (Vit D2)

Animal and dairy products (Eggs, liver, butter,
codliver oil)
7 dehydrocholesterol (human skin)
UVB
Cholecalciferol (Vit. D3)
Liver
25 hydroxy cholecalciferol
Kidney
1, 25 di-hydroxy cholecalciferol (Calcitriol)
Clinical features and treatment
Children:
 Rickets, Tetany
Adults:
 Osteomalacia
 Type I Vit.D dependent rickets : No skin lesions
 Type II Vit.D resistant rickets : Progressive
alopecia
Treatment:
 Normal daily requirement: 400 IU
 In rickets : 5000 IU oral Vit D for 3 to 5 weeks
 Exposure to sunlight
Vitamin B Complex

Mostly combined deficiencies occur due to
insufficient proteins or other essential nutrients
(Zinc, EFA)
Vitamin B1 (Thiamine, Aneurin)
Sources

Yeast (richest source), unmilled cereals, pulses,
nuts
Beriberi Dry

Peripheral neurologic syndrome, atrophic skin,
red burning tongue

Korsakoff's psychosis,Wernicke's encephalopathy
Beriberi Wet

High output cardiac failure
Skin is warm before CCF and cold, edematous,
cracked later
Diagnosis and treatment
Diagnosis

Urinary excretion of < 50 mcg of thiamine after
1 mg injection
Treatment:

Dietary requirement - 0.5 mg /1000 kcal, 0.5 to
2 mg

Beriberi - 10 to 100 mg / day

If severe - add manganese (corrects thiamine
resistance)

B - complex vitamins are supplemented

Local application of zinc oxide ointment ,
mineral oil (for cracked skin)
Riboflavin deficiency (Vit. B2):
(Oro - Oculo - Genital syndrome)
Sources of Vit. B2:

Milk, milk products, eggs, liver, cereals, pulses,
green leafy vegetables

Deficiency of Vit.B2 affects metabolism of free
fatty acids, tryptophan, folic acid

Presents as overlapping manifestations
Clinical features

Seen after 3-5 months of inadequate diet
It is also known as “pellagra sine pellagra”

Oral manifestations:

Angular stomatitis (perleche) with candidiasis

Cheilosis : lip involvement with vertical fissuring

Glossitis : magenta coloured tongue
atrophic filiform papillae
enlarged fungiform papillae
Clinical features
Skin manifestations:

Seborrheic dermatitis like rash; dyssebacea
Fine greasy scales with erythema over nasolabial
folds, ala nasi, nasal bridge, forehead, eyelids,
earlobes

Dysriboflavinosis
Dyskeratotic follicular papules with scaly
erythema

Patchy alopecia with scaling on scalp and
eyebrows
Clinical features

Genitals: Earliest manifestation (scrotum, vulva)
Early - Patchy redness, fine powdery
desquamation
Late - Lichenification
Severe - Raw areas over shaft of penis, inner
thighs

Eyes: Photophobia, lacrimation, blepharospasm,
conjunctivitis, decrease in visual acuity, corneal
vascularization

CNS: Psychomotor, intellectual development
impaired in children
Diagnosis and treatment
Diagnosis

Urinary excretion < 30 mcg of vit.B2 / gm of
creatinine
Treatment:

Normal requirement : 1-2 mg / day mg

Therapeutic dose:
Infants : 1-3 mg
Adults : 10-30 mg

Correct the associated tryptophan, FA, EFA
deficiency
Vitamin B3
(Nicotinic acid, Nicotinamide, Niacin )
Pellagra (deficiency of Niacin)

Italian word pelle - skin, agra - rough

First described in 1735 by Casal in Spain

Niacin includes both nicotinic acid and
niacinamide

Niacinamide is active form and is converted to
coenzymes NAD, NADP

Plays a vital role in cell, fatty acid, carbohydrate
metabolism
Sources

Meat, fish, eggs

Milk, cheese

Cereals, grains, legumes

Coffee and tea

Endogenous production
60 mg of tryptophan
1mg of niacin
Etiology

Staple diet of maize and jowar with less animal
proteins

Maize - poor source of nicotinic acid and
tryptophan
- niacin is present but not bio-available

Jowar - high content of leucine
Imbalance in leucine and isoleucine
of NAD
Tryptophan
Niacin

Chronic alcoholics - unbalanced diet

Malabsorption
inhibition
Clinical features

This disease is characterized by 4 “D’s”
◦ Dermatitis
◦ Dementia
◦ Diarrhea
◦ Death

Prodrome - weakness, fatigue
Clinical features
Skin:

Photo exposed areas

Erythema - well demarcated patches with
pruritus and burning, slight edema

Blisters, dry brown scales

Pressure sites, shoulder, elbow, buttocks, knee

Intertriginous area - redness, maceration
Clinical features

Pellagrins nose
Dull erythema, butterfly rash with scaling on
bridge of nose

Casal's necklace
Sharply demarcated lesion on upper central
chest, neck

Cravat
Anterior continuation of necklace on chest

Scrotal erythema
Symmetrical lesions, clear line of demarcation
Clinical features

Mucous membrane
◦ Angular stomatitis, cheilitis
◦ Scarlet glossitis with imprint of teeth
◦ Tongue is red, smooth, atrophy of filiform
papillae, erosions, ulcerations, fissures
◦ Swelling of parotid gland, increased salivation

GIT: Anorexia, nausea, vomiting, abdominal pain,
bloody diarrhoea

CNS: Depression, psychosis
Treatment
Daily requirement - 10 to 20 mg / day
Therapeutic dose:

300 - 500 mg niacinamide orally or intramuscular
in divided doses (amide preferred because it
does not precipitate flushing, itching, burning)

Supplement with B complex, animal proteins
eggs, milk

Balanced diet

Reduce alcohol
Vitamin B6 deficiency (Pyridoxine)

Animal sources:
Liver, egg yolk, meat

Vegetable sources:
Pulses, cereals, peas, soya beans

Pyridoxine deficiency occurs during
administration of drugs like:
INH
Hydralazine
Cycloserine
Penicillamine
Clinical features

Children: convulsion, anemia

Adults: seborrheic dermatitis like rash, cheilitis,
angular stomatitis, glossitis, peripheral neuritis

Chinese restaurant syndrome :
(Inability to metabolize monosodium glutamate)
Headache, sensation of pressure in chest,
palpitation, feeling of warmth, tingling, numbness
Diagnosis and treatment
Diagnosis

Serum Pyridoxal phosphate levels < 20 mcg / ml
Treatment:

Daily requirement: 1.5 - 2.5 mg

Therapeutic dose: 30 -100 mg / day orally
Vit B12 deficiency
(Cobalamin, Cyanocobalamin)

Sources:
◦ Liver, kidney, heart - richest
◦ Meat, fish, cheese, eggs, milk
◦ Vegetables, fruits, legumes - nil; but present if
contaminated by bacteria

Vit B12 is synthesized in colon (low bioavailability)
Cause of deficiency of Vit.B12

Strict vegetarian diet

Gastric atrophy (achlorhydria) and decreased
intrinsic factor (pernicious anemia)

Diphyllobothrium latum infestation

Malabsorption syndromes (sprue, intestinal TB,
Whipple’s disease)

Elderly individuals, chronic alcoholism
Clinical features

Skin
Symmetrical generalized hyperpigmentation
(greyish - brown)

Mucous membrane
Hyperpigmentation, cheilitis, glossitis with beefy
red tongue, glossodynia, aphthae like lesions

Nails: Pigmented streaks
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Hair: Premature graying, canities

Other manifestations: Megaloblastic, pernicious
anemia, peripheral neuritis, poor memory
Diagnosis

Serum Vit. B12 <150 pg/ml

Hemogram

Bone marrow examination

Schilling’s test - measures radioactive Vit. B12
with and without intrinsic factor
Treatment

Daily requirement :1 mcg

Dose : 1000 mcg / week for 1 month;
1000 mcg / month thereafter

Also add folic acid 1- 5 mg

Course:

Cutaneous changes improve within 1 year

In pernicious anemia Vitamin B12 given life long
Folic acid (Vit. B9)
(Pteroyl - glutamic acid, folacin)
Sources:

Liver, meat, green leafy vegetables, milk

Produced by colonic bacteria (inadequate)
Folic acid and Vit. B12 are interdependent,
therefore the deficiencies occur simultaneously
Vit C

Folic Acid
Folinic acid (active form)
Clinical features

Skin:
Diffuse hyperpigmentation

Mucous membrane:
Glossitis, superficial erosions, cheilitis

Others:
Megaloblastic anemia
Diagnosis and treatment
Diagnosis
Serum folate < 3 ng/ml (normal > 6 ng/ml)
Treatment

Daily requirement : 50 -100 mcg

In pregnancy : 400 mcg
Therapeutic dose: 1- 5 mg / day; also correct Vit.
B12 deficiency
Vitamin C (Ascorbic acid)

Scurvy: Deficiency of Vitamin C
Sources:

Fresh fruits - oranges, grapes, lemons

Fresh vegetables - Green leafy vegetables,
potatoes, cabbage
Functions:

Role in collagen and ground substance formation,
wound healing, immune response

Required for iron absorption
Causes

Diet poor in Vitamin C (elderly men, alcoholics)

Gastro-intestinal diseases

Malnourished children with scurvy (Barlow's
disease)

Seen in cigarette smokers
Clinical features
Skin

Follicular hyperkeratosis : Earliest change, cork
screw hair (swan neck deformity) - due to
reduced disulfide bond

Perifollicular hemorrhage
Sites: upper arms, buttocks, shins, trunk, thighs

Petechiae, echhymosis

“Woody” edema of legs

Delayed wound healing
Clinical features
Oral Cavity:

Hemorrhagic gingivitis - spongy gum

Loosened teeth, foul odour
Internal hemorrhage :

Hematuria, epistaxis, malena, hematemesis
In infants:

Excessive crying

Pseudo paralysis

Scorbutic rosary
Treatment

Daily requirement
Adult: 50 mg
Children: 25 mg

Therapeutic dose: 100 - 300 mg / day
Minerals and Trace elements
Zinc :

It is metal moiety of important enzymes for
carbohydrate, protein, lipid and nucleic acid
metabolism

Role in immunological functions and wound
healing
Sources:

Shellfish, legumes, nuts, whole grains, green
leafy vegetables
Zinc deficiency
Genetic

Acrodermatitis enteropathica
Acquired

Acquired zinc deficiency
Acrodermatitis enteropathica

Transmitted as autosomal recessive trait

First described by Danbolt and Class in 1943

Etiology:

Deficient zinc binding protein called zinc ligand
binding (ZLB)
Clinical features
Disease occurs within few weeks after birth if bottle
fed or 4-6 weeks after weaning from breast milk

Perlèche : early sign; angular stomatitis, glossitis

Perioral and peri-orificial rash

Vesiculobullous and pustular lesions

Superadded infection with candida is common

Nails : paronychia, white spots

Hair : alopecia

Eyes : photophobia, conjunctivitis

Diarrhoea, growth failure, emotional and mental
disturbances
Diagnosis and treatment
Diagnosis

Serum zinc levels <80 mcg/dl (80 - 120 mcg/dl)
Treatment

Daily requirement:
Infants < 6months : 3 mg
6months - 1yr
: 5 mg
1 - 7 yrs
: 10 mg
> 7 yrs, adults
: 16 mg
Pregnant and lactating mothers : 20 -25 mg
Treatment
Dose

Oral zinc : 2mg/kg/day for 1- 2 weeks
30 to 55 mg of elemental Zn for 1-2 weeks
(220 mg ZnSo4 = 55 mg of elemental Zn)

Hereditary type requires life long treatment
Iron deficiency
Sources:

Green leafy vegetables, pulses, meat products

Vitamin C rich foods improve absorption; tea and
tamarind inhibits absorption
Clinical features:

Generalized pruritus, increased hair loss,
koilonychia

Angular stomatitis, cheilitis, glossitis

Hypochromic microcytic anemia

Plummer-Vinson syndrome
Treatment
Therapeutic dose:

Ferrous sulphate or gluconate 300mg thrice daily

Treat underlying cause: chronic blood loss,
parasitic infestations, malaria

Supplementation with Vitamin C

Supplementation during pregnancy
Protein Energy Malnutrition (PEM)

PEM is most common form of malnutrition

Age: 1-3 years, commonly seen during weaning
and post weaning period
Marasmus:

Patient with 60% of expected body weight without
edema
Kwashiorkor:

Patient who weighs 60 - 80 % of expected body
weight for that age with severe protein
malnutrition with relative carbohydrate excess
Marasmus: Clinical features
Skin
 Dry, inelastic, thin, wrinkled, loose
 Follicular hyperkeratosis (adults)
Hair
 Slow growth, lustreless
 Growth of lanugo hair occurs
Nails : Fissured
Facies :
 “Monkey facies”- wrinkled skin with loss of buccal
fat pad
 Child is alert
Kwashiorkor: Clinical features
Skin

“Flaky paint” or “crazy pavement” dermatoses,
extensive peeling of skin with erosions

“Enamel paint” dermatoses
Sites: pressure sites
Sharply demarcated hyperpigmented plaques
with burnt out appearance and waxy feel (spares
feet and dorsa of hands in contrast to pellagra)
Clinical features
Mucosae:

Cheilitis with fissuring on lips

Angular stomatitis, glossitis
Nails: Soft and thin
Hair :

Sparse, thin, brittle, easy pluckable

Dyschromotrichia : golden, blonde, rust (red boy)

Flag sign

Eyelashes : broomstick appearance
Treatment

High protein, high caloric diet

Topical zinc paste, oral zinc supplements

Correction of other associated deficiency

Treatment of infection and infestation
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