SEMINAR ON NUTRITIONAL DISORDERS OF SKIN

Chairperson : Professor (Dr.) C.N. Sarker

Head of the department
Department of Medicine, MMC.

Speakers : 1. Dr. Md. Nazrul Islam,

MCPS,DDV,FCPS (Part-II)
2. Dr. Mohammed Saiful Islam Bhuiyan,
MD (Part-II), FCPS (Part-II)
Medical Officers,
3. Dr. Mohammad Assaduzzaman
MCPS, FCPS (Part-II)
Assistant Registrar
Department of Dermatology, MMCH.

Date & Time : 15th May, 2005 at 1.30 pm.

Organized by : Department of Dermatology, MMCH.

&
SK+F
 INTRODUCTION

A large number of disorders in relation to

nutrition are being found in our profession.
If we want to know about them we’ll have to
go through some basic terms.
 FOOD

Food is any substance which an individual

takes, digests and assimilates to derive
nutritive requirements for maintaining
growth and physical well – being.
 NUTRITION

Nutrition is a dynamic process

concerned with ingestion , digestion,
absorption and assimilation of food
for nourishing the body.
SOME SIGNS OF GOOD NUTRITION

 Smooth shiny skin.

 Glossy hair.
 Well developed muscles, bones and
teeth.
 Strong built and energetic to look at.
 NUTRIENTS

Nutrients are the constituents of food

necessary to sustain the normal function of
the body.
1. Macronutrients
CHO, protein, fat, Ca, Na, K, Mg, Cl & PO4.
2. Micronutrients
Vitamins, trace elements.
ESSENTIAL NUTRIENTS

Essential nutrients are those that

either cannot be synthesized in
the body or cannot be synthesized
in adequate amount to meet the
needs of the body.
THE ESSENTIAL NUTRIENTS

1. Certain amino acids.

2. Certain fatty acids.
3. Vitamins and
4. Minerals.
 VITAMINS
Vitamins are organic nutrients that are
required in small quantities for a variety
of biochemical functions and which,
generally, can not be synthesized by the
body and must therefore be supplied by
the diet.
TYPES OF VITAMINS

1. Fat soluble vitamins.

- Vitamin A, D, E & K.

2. Water soluble vitamins.

- Vitamin B –Complex and C.
 MINERALS

Minerals are inorganic elements or

substances required by the organism in very
small amounts for maintenance of vital
processes essential for life.
 TYPES OF MINERALS
1. Principal elements/macrominerals
K, Ca, Mg, Na, P, S and Cl.
2. Trace elements/ microminerals
Iron , Copper, Fluoride, Iodine,
Cobalt, Zinc, Molybdenum,
Selenium, Silicon, Nickel,
Tin, Cromium, Vanadium.
 NUTRITIONAL DISORDER
CLASSIFICATION

1. Undernutrition.
2. Malnutrition.
3. Nutrient excess.
4. Obesity.
5. Effect of toxicants in foods.
 DISORDERS DUE TO VITAMIN
DEFICIENCY
Vitamin A Phrynoderma, xerophthalmia,
night blindness,keratomalacia.
Vitamin D Rickets, osteomalacia

Vitamin E Haemolytic anaemia, ataxia

Vitamin K Purpura, haemorrhage,

ecchymosis.
 DISORDERS DUE TO VITAMIN
DEFICIENCY (Contd.)
Thiamin (Vitamin B1) Beri-beri
Riboflavin Oro-ocular-genital
(VitaminB2) syndrome (glossitis,
stomatitis etc.)
Niacin (Vitamin B3) Pellagra.
Vitamin B6 Polyneuropathy
(Pyridoxine)
Biotin Dermatitis, alopecia,
paraesthesiae.
 DISORDERS DUE TO VITAMIN
DEFICIENCY (Contd.)
Folate Anaemia
Vitamin B12 Glossitis,
(Cobalamin) hyperpigmentation,
canitis.

Vitamin-C Scurvy
(Ascorbic acid)
 DISORDERS DUE TO
MINERAL DEFICIENCY

Iron Anaemia, glossitis,

cheilosis,
koilonychia.
Zinc Acrodermatitis
enteropathica
ESSENTIAL AMINO ACID AND
ESSENTIAL FATTY ACID
DEFICIENT DISORDERS

Marasmus Sprue

Kwarshiorkor Carotenemia

Pellagra Lycopenemia
DISORDERS DUE TO NUTRIENTS
EXCESS
Vitamin A Liver damage, bone
damage, teratogenesis
Vitamin D Hypercalcaemia
Vitamin B6 Subepidermal vesicular
(pyridoxine) dermatitis, sensory
peripheral neuropathy

Iron Haemosiderosis
KERATOMALACIA
ANGULAR STOMATITIS
PELLAGRA
SCURVY
MARASMUS
KWARSHIORKOR
PHRYNODERMA
ACRODERMATITIS ENTEROPATHICA
OBESITY

 An alarming issue.
 A nutritional & metabolic disorder.
 Results from excessive intake of food
& insufficient exercise.
 It is said “rich people of poor countries
& poor people of rich countries” are the
sufferers.
 OBESITY

“EXCESS OF ANYTHING IS BAD”

ACRODERMATITIS
ENTEROPATHICA
 ACRODERMATITIS
ENTEROPATHICA
Acrodermatitis enteropathica (AE) is a
rare inherited disorder transmitted
as an autosomal recessive trait,
caused by defective intestinal
absorption of Zn, characterized by a
triad of acral dermatitis, alopecia and
diarrhea.
Epidemiology:
 No geographical, racial or gender
predilection.

Etiology:
 Genetic – autosomal recessive, defect in
intestinal zinc absorption.
 CONDITIONS MAY CAUSE
ZINC DEFICIENCY
 Reduced intake
Anorexia nervosa.

Bulimia.

Faddish weight reduction.

Prolong total parenteral nutrition.

High dietary phytate.

CONDITIONS MAY CAUSE ZINC
DEFICIENCY (Contd.)

Reduced absorption.
Mucosal disease.

Malabsorption syndromes.

Pancreatic disorders.
CONDITIONS MAY CAUSE
ZINC DEFICIENCY (Contd.)
 Increased loss
Malabsorption syndrome.
Blind-loop syndrome.
Renal tubular disease.
Nephrotic syndrome.
Dialysis.
Diabetes mellitus.
CONDITIONS MAY CAUSE ZINC
DEFICIENCY (Contd.)
 Increased Catabolism
Malignancy.
Burns.
Postsurgical procedure.
Antimetabolite drug therapy.
 Increased Demand
Pregnancy.
Lactation.
SOURCE OF ZINC

 Meat.
 Liver.
 Egg.
 Seafood.
 BIOCHEMISTRYOF ZINC
METABOLISM:

 Adult body contains 2-3 gms of

zinc, which is about half the iron
content, 10-20 times more than
other essential trace elements.
 BIOCHEMISTRYOF ZINC
METABOLISM(Contd.)
 Recommend dietary allowance:
 Adult - 15 mg/day (elemental).
Infants - 5mg/day.
Children - 10mg/day.
Lactating mother,
1-6 months - 19 mg/day
> 6 months - 16 mg/day
ZINC METABOLISM (CONTD.)
Normally about 30% of daily intake is
absorbed.
 All body tissue contain zinc.
 Richest Stores: Muscle, bone and prostate.
 Incorporation: > 300 metalloenzymes.
 Free radical scavenger: protect against
oxidative damage.
 TYPES OF ZINC DEFICIENCY

1. Hereditary type.

2. Non-hereditary type.

 Low grade, marginal, nonhereditary

zinc deficiency is far more common

than the hereditary form.

PATHOGENESIS:

The defect in AE is somewhere in the

early stages of zinc absorption.

Zn absorption is partially reduced in

AE.
 PATHOGENESIS (Contd.)
Bioavailability of zinc is more in human
milk than bovine milk.

In AE, genetic defect in different zinc

transporter (Zn T-1 to T-4) as well as
intestinal zinc transporter.
 PATHOGENESIS (Contd.)

Biologically active Zinc is highly

charged species that cannot cross cell
membrane by passive diffusion but the
process can greatly enhanced when
zinc is complexed with zinc binding
ligands (ZBL).
 PATHOGENESIS (Contd.)
Zinc in human milk is preferentially
bound to lower molecular-weight
ligands (~10,000) than bovine milk.

Total protein of human milk

(5.3mg/ml) compared with bovine
milk (29mg/ml) influence the bio-
availability of zinc in an unknown
mechanism.
 PATHOGENESIS (Contd.)

Metallothioneines regulates the transport of zinc

into the circulation and then to the liver and
kidneys.
Zinc is component of some peptidases, important
for digestion of proteins in GIT.
PATHOGENESIS (Contd.)
Keratinosome contain several zinc-
dependent enzyme systems, the
metabolism of which may be affected in
zinc deficiency.

Possible role of biotin in AE, particularly

in premature infants with Zn deficiency.
 ZINC AND GENETICS
 Genetic locus for acrodermatitis entropathica
on chromosome 8q24.3.
 Nuclei are rich in Zinc, critically involved in
maintaining genitic stability, gene
expression, and cell proliferation,
defferentiation and death.
 ZINC AND IMMUNITY
 Reduced immune function specially cellular.
 In Acrodermatitis enteropathica thymic
atrophy causing depressed thymocyte and
cellular immune function, particularly T-cell.
 Neutrophil, peripheral blood monocytes,
tissue macrophages and mast cells require
optimal concentration of zinc for normal
function.
CLINICAL MANIFESTATION
 Age of onset:
 Infants with bovine milk- 4-10 weeks,
 Breast fed baby – after weaning.
 Prominent feature:
- Dermatitis (Acral and periorificial-
pathognomic).
- Diarrhea.
- Alopecia (Generalized).
- Crying baby.
  OTHER MANIFESTATION:

Perleche- common early sign

and a sign heralding relapse.

Superficial oral aphthous–like

lesions.

Photophobea.
 CLINICAL MANIFESTATION
(CONTD.)

 Paronychia and brightly erythematous

dermatitis of the palmer and finger

creases.

 Nail dystrophy.
 CLINICAL MANIFESTATION
(CONTD.)

Secondary infection with bacteria



and Candida albicans.

 Delayed wound healing
 Patients are irritable and
emotionally labile.
 CLINICAL MANIFESTATION
(CONTD.)

 Anorexia,
 hypogeusia,
 hyposmia and anemia
LONG TERM SEQULAE OF ZN
DEFICIENCY
 Growth reterdation and dwarfism.
 Delayed puberty.
 Hypogonadism in male adolescent.
 Continuing dermatitis.
LONG TERM SEQULAE (CONTD.)

 Frequent infection.
 Lower fertility.
 Lower fertility and congenital
malformation occurs in children of
mothers with AE.
 DIFFERENTIAL DIAGNOSIS

Candidiasis.
Diaper dermatitis.
Pellagra.
Necrolytic migratory erythema.
HISTOLOGY

 Vacuolation at upper str. malphigi.

 Vacules become confluent forming a
subcorneal bulla.
 Total epidermal necrosis with
subepidermal blister formation.
 Neutrophils typically present.
 LABORATORY DIAGNOSIS
 Serum Zinc levels (80-120gm/dl).
-is reduced.
-most accurate, earliest, commonly used.
 Erythrocyte and leukocyte zinc level
-is reduced
-quite sensitive to early minor changes in
total body Zn, but expensive.
 LABORATORY
DIAGNOSIS(Contd.)
Urine level (200-500 mg/24 hrs.).
- is reduced.
Serum alkaline phosphatase
- is reduced.
- moderately sensitive.
Hair Zn level – long term Zn status.
 TREATMENT

 Dietary or intravenous supplimentation with

zinc salt – 3mg/kg/day life long.
 ZINC TOXICITY

 Acute : Gastric irritation.

Nausea.
Vomiting.
Gastric heamorrhage.
 Chronic: Reduced growth rates.
Reduced rate of reproduction.
Anemia.
Hypo cupremia.
 PHRYNODERMA

 Other names:

Hypovitaminosis –A.

Toad skin,
 DEFINITION

Phrynoderma is a condition
characterized by
–Excessive dryness ,
–Wrinkling
–Scaling of skin
–Follicular hyperkeratosis.
 DEFINITION (CONTD.)
•Due to deficiency of Vitamin- A.
•May be associated with deficiency of
- Vitamin – B-Complex.
- Vitamin – C.
- Vitamin – E.
- Essential Fatty acids.
- Calories.
INTRODUCTION

• Other names of vitamin A are retinol , anti

infective vitamin
• Vitamin A is found in 2 forms animal food
as retinol & vegetables as beta carotene
• Daily requirement of retinol -750
microgram in adult.
 INTRODUCTION (CONTD.)
 1 microgram of retinol =6 microgram of
beta carotene
 Vitamin A is measured in international unit
where 1 IU=0.3 microgram retinol
 About 90% of the body’s vitamin A reserve
is found in the perisinusoidal stellate (Ito)
cells in the liver.
 INTRODUCTION
(CONTD.)

 About 90% of the body’s vitamin A

reserve is found in the perisinusoidal
stellate (Ito) cells in the liver.

 Retinol is the transport & also the storage

form of vitamin A.
INCIDENCE & PREVALENCE

 Vitamin A deficiency is common in

children in developing countries.
 Specially in Asia & Africa &
 In such region most common cause
of blindness.
INCIDENCE & PREVALENCE

 It is rare in developed countries & most

commonly associated with
Fat malabsorption syndrome ,
Mineral oil laxative abuse &
Mineral oil laxative abuse &
ASSOCIATED DISORDERS OF
VITAMIN A DEFICIENCY:
• Diseases of fat malabsorption
syndrome
• Crohns disease
• Celiac disease
• Cystic fibrosis
• Cholestatic liver disease
 ASSOCIATED DISORDERS OF
VITAMIN A DEFICIENCY
(CONTD.)
 Inflammatory disorders –

 Diarrhea,

 Pneumonia
 CAUSES OF VITAMIN A
DEFICIENCY
►Principal cause is inadequate diet(chiefly in
3rd world countries)

►Fat malabsorption

►Liver damage
 PATHOLOGY &
PATHOGENESIS
• Vitamin A deficiency involves-
• Visual system
• Immune system
• Skin
• GIT
• Respiratory system
• Urinary system
 SITES OF INVOLVEMENT
IN SKIN

• 80%cases limited to

– Arms

– Arround elbows & knees

SITES OF INVOLVEMENT IN SKIN
 20% cases
 anterolateral aspect of thigh ,
 posterolateral aspect of superior
forearm ,
 the extensor surface of upper &
lower extremities ,
 the shoulders ,
 back
 abdomen &
 buttock
CLINICAL FEATURES IN SKIN

Skin becomes

– Dry

– Wrinkled,

– Covered with fine scale,

 CLINICAL FEATURES IN
SKIN (CONTD.)
 Morphology of the lesion is variable
may range from filiform papule to
small conical papule to large papule
with large horny centre ,
CLINICAL FEATURES IN SKIN
(CONTD.)
Color may similar to surrounding skin or
may be slightly hyper pigmented

Back ground skin in affected area is

wrinkled

Hands & feet are not involved.

INVOLVEMENT OF
VISUAL SYSTEM
In vitamin A deficiency eye findings
are prominent & often
pathognomonic.
• Delayed dark adaptation & night
blindness is the earliest
symptoms of vitamin A deficiency
 INVOLVEMENT OF VISUAL
SYSTEM (CONTD.)
 Dryness of the conjunctiva
(xeropthalmia) & development Bitot
spot ( small white patches on
conjunctiva) are early signs.
INVOLVEMENT OF VISUAL
SYSTEM (CONTD.)
 Keratomalacia ulceration &
necrosis of the cornea, perforating
endopthalmitis & blind ness are
late manifestation .
 HISTOPATHOLOGICAL
FINDINGS
In adults :
 Follicular Hyperkeratosis
 Follicular
plugging in the upper
portion of the hair follicle,
 Severe atrophy of the sebaceous
gland.
 HISTOPATHOLOGICAL
FINDINGS(CONTD.)

Squamous metaplasia of the secretory cells

of the eccrine sweat gland

Dermis is otherwise normal except for

perifollicular infiltrate.
 HISTOPATHOLOGICAL
FINDINGS(CONTD.)
• In infants & young adults –
(before pilosebaceous gland mature fully)
– Simple xerosis or xeroderma is usually
characteristic feature
 DIAGNOSIS

Diagnosis of vitamin A deficiency is

usually based on
The typical clinical findings &
Also aided by determining of serum
vitamin A level (normal 30-65 mg/dl).
DIFFERENTIAL DIAGNOSIS
OF PHRYNODERMA:
Keratosis pilaris
Darier’s disease
Pityriasis rubra pilaris
Acne vulgaris
Lichen planopilaris.
 MANAGEMENT
 General management –
 improvement of diet.
 Antibiotic if there is infection.
 Special –
 Treatment with vitamin A in deficient
cases.
 Treatment with other specific vitamins
according to need.
 TREATMENT (CONTD.)
Phrynoderma -

– Local application of 10-40 % Urea cream

&
– 50,000 units of Vitamin A twice a day
orally can make the lesion disappear in 2-
3 months.
 PREVENTION
• Oral dose of 60 mg retinol (200000 IU)
as palmitate given to preschool children

• Oral administration 4- 6 months

interval is sufficient to prevent serious
consequence of vitamin a deficiency.