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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

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stages of nutritional deficiency syndrome
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
Causes of deficiencies
  • Increased requirement
  • During growth
  • Pregnancy
  • Lactation
  • Fever
  • Hyperthyroidism

Decreased intake

  • Poverty
  • Ignorance
  • Food faddism
  • Crash diets
  • Anorexia nervosa
stages of nutritional deficiency syndrome1
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
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
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
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
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 features1
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 features2
Clinical features

Eye Manifestations:

Common cause of blindness in developing countries

  • Earliest symptoms:
    • Nyctalopia (night blindness)
    • Hemeralopia (inability to see bright light)
  • Xerophthalmia:
    • Conjunctivalxerosis
    • Bitot’s spot
    • Corneal xerosis
    • Corneal ulceration
    • Keratomalacia
    • Phthisis bulbi, scarring, blindness
treatment
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 retinylpalmitate in oil)

  • Good quality protein diet + vitamins
  • Education of local community

Contd…

treatment1
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
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
Source of Vit. D and Chemistry
  • Plants ergosterolergocalciferol (Vit D2)
  • Animal and dairy products (Eggs, liver, butter, codliver oil)

7 dehydrocholesterol (human skin)

UVB

Cholecalciferol (Vit. D3)

Liver

25 hydroxycholecalciferol

Kidney

1, 25 di-hydroxycholecalciferol (Calcitriol)

clinical features and treatment
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
Vitamin B Complex
  • Mostly combined deficiencies occur due to insufficient proteins or other essential nutrients

(Zinc, EFA)

vitamin b1 thiamine aneurin
Vitamin B1 (Thiamine, Aneurin)

Sources

  • Yeast (richest source), unmilled cereals, pulses, nuts

Beriberi Dry

  • Peripheral neurologic syndrome, atrophic skin, red burning tongue
  • Korsakoff'spsychosis,Wernicke's encephalopathy

Beriberi Wet

  • High output cardiac failure

Skin is warm before CCF and cold, edematous, cracked later

diagnosis and treatment
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
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 features3
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 features4
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 features5
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 treatment1
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
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
Sources
  • Meat, fish, eggs
  • Milk, cheese
  • Cereals, grains, legumes
  • Coffee and tea
  • Endogenous production

60 mg of tryptophan 1mg of niacin

etiology
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 inhibition of NAD

Tryptophan Niacin

  • Chronic alcoholics - unbalanced diet
  • Malabsorption
clinical features6
Clinical features
  • This disease is characterized by 4 “D’s”
    • Dermatitis
    • Dementia
    • Diarrhea
    • Death
  • Prodrome - weakness, fatigue
clinical features7
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 features8
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 features9
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
treatment2
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
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 features10
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 treatment2
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
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 bio-availability)
cause of deficiency of vit b12
Cause of deficiency of Vit.B12
  • Strict vegetarian diet
  • Gastric atrophy (achlorhydria) and decreased intrinsic factor (pernicious anemia)
  • Diphyllobothriumlatuminfestation
  • Malabsorption syndromes (sprue, intestinal TB, Whipple’s disease)
  • Elderly individuals, chronic alcoholism
clinical features11
Clinical features
  • Skin

Symmetrical generalized hyperpigmentation (greyish - brown)

  • Mucous membrane

Hyperpigmentation, cheilitis, glossitis with beefy red tongue, glossodynia, aphthae like lesions

  • Nails: Pigmented streaks
  • Hair: Premature graying, canities
  • Other manifestations: Megaloblastic, pernicious anemia, peripheral neuritis, poor memory
diagnosis
Diagnosis
  • Serum Vit. B12 <150 pg/ml
  • Hemogram
  • Bone marrow examination
  • Schilling’s test - measures radioactive Vit. B12 with and without intrinsic factor
treatment3
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
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

  • Folic Acid Folinic acid (active form)

Vit C

clinical features12
Clinical features
  • Skin:

Diffuse hyperpigmentation

  • Mucous membrane:

Glossitis, superficial erosions, cheilitis

  • Others:

Megaloblastic anemia

diagnosis and treatment3
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
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
Causes
  • Diet poor in Vitamin C (elderly men, alcoholics)
  • Gastro-intestinal diseases
  • Malnourished children with scurvy (Barlow's disease)
  • Seen in cigarette smokers
clinical features13
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 features14
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
treatment4
Treatment
  • Daily requirement

Adult: 50 mg

Children: 25 mg

  • Therapeutic dose: 100 - 300 mg / day
minerals and trace elements
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
Zinc deficiency

Genetic

  • Acrodermatitisenteropathica

Acquired

  • Acquired zinc deficiency
acrodermatitis enteropathica
Acrodermatitisenteropathica
  • Transmitted as autosomal recessive trait
  • First described by Danbolt and Class in 1943
  • Etiology:
  • Deficient zinc binding protein called zinc ligand binding (ZLB)
clinical features15
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 treatment4
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

treatment5
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
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
  • Hypochromicmicrocytic anemia
  • Plummer-Vinson syndrome
treatment6
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
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
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
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 features16
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
treatment7
Treatment
  • High protein, high caloric diet
  • Topical zinc paste, oral zinc supplements
  • Correction of other associated deficiency
  • Treatment of infection and infestation