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.

Department of Dermatology, MMCH. & SK+F

Organized by :

INTRODUCTION
A large number of disorders in relation to nutrition are being found in our profession. If we want to know about them well 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. 2. Macronutrients
CHO, protein, fat, Ca, Na, K, Mg, Cl & PO4.

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. 2. 3. Certain amino acids. Certain fatty acids. 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. 2. Principal elements/macrominerals
K, Ca, Mg, Na, P, S and Cl.

Trace elements/ microminerals

Iron , Copper, Fluoride, Iodine,
Cobalt, Zinc, Molybdenum,

Selenium,

Silicon,

Nickel,

Tin, Cromium, Vanadium.

NUTRITIONAL DISORDER CLASSIFICATION

1.
2.

Undernutrition.
Malnutrition.

3.
4.

Nutrient excess.
Obesity.

5.

Effect of toxicants in foods.

DISORDERS DUE TO VITAMIN DEFICIENCY

Vitamin A Phrynoderma, xerophthalmia, night blindness,keratomalacia.

Vitamin D
Vitamin E Vitamin K

Rickets, osteomalacia
Haemolytic anaemia, ataxia Purpura, haemorrhage, ecchymosis.

DISORDERS DUE TO VITAMIN DEFICIENCY (Contd.)

Thiamin (Vitamin B1) Beri-beri Riboflavin (VitaminB2) Niacin (Vitamin B3) Oro-ocular-genital syndrome (glossitis, stomatitis etc.) Pellagra.

Vitamin B6 (Pyridoxine) Biotin

Polyneuropathy Dermatitis, alopecia, paraesthesiae.

DISORDERS DUE TO VITAMIN DEFICIENCY (Contd.)

Folate Vitamin B12 (Cobalamin) Anaemia Glossitis, hyperpigmentation, canitis.

Vitamin-C Scurvy (Ascorbic acid)

DISORDERS DUE TO MINERAL DEFICIENCY

Iron Anaemia, glossitis, cheilosis, koilonychia. Acrodermatitis enteropathica

Zinc

ESSENTIAL AMINO ACID AND ESSENTIAL FATTY ACID DEFICIENT DISORDERS

Marasmus
Kwarshiorkor Pellagra

Sprue
Carotenemia Lycopenemia

DISORDERS DUE TO NUTRIENTS EXCESS

Vitamin A Vitamin D Liver damage, bone damage, teratogenesis 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). - 5mg/day. - 10mg/day. mother, - 19 mg/day - 16 mg/day

Infants Children Lactating

1-6 months > 6 months

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 bioavailability 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 expression, genitic and stability, cell gene 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 periorificialpathognomic). - Diarrhea. - Alopecia (Generalized). - Crying baby.

 OTHER MANIFESTATION:
Perlechecommon early sign and a sign heralding relapse.

Superficial
lesions.

oral

aphthouslike

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 subepidermal blister formation. Neutrophils typically present. with

LABORATORY DIAGNOSIS
Serum Zinc levels (80-120gm/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
: Gastric irritation. Nausea. Vomiting. Gastric heamorrhage. Chronic: Reduced growth rates. Reduced rate of reproduction. Anemia. Hypo cupremia.
Acute

PHRYNODERMA
Other

names: A.

Hypovitaminosis

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

INTRODUCTION (CONTD.)
About

90% of the bodys 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 Specially in Asia & Africa &

In such region most common cause

children in developing countries.

of blindness.

INCIDENCE & PREVALENCE

It is rare in developed countries & most malabsorption syndrome ,

oil laxative abuse & oil laxative abuse &

commonly associated with

Fat

Mineral Mineral

ASSOCIATED DISORDERS OF VITAMIN A DEFICIENCY:

Diseases of fat malabsorption syndrome Crohns disease Celiac disease

Cystic fibrosis
Cholestatic liver disease

 Inflammatory Diarrhea, Pneumonia

ASSOCIATED DISORDERS OF VITAMIN A DEFICIENCY (CONTD.)

disorders

CAUSES OF VITAMIN A DEFICIENCY

Principal

cause is inadequate diet(chiefly in

3rd world countries)

Fat

malabsorption
damage

Liver

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.

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

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 Follicular Severe

Hyperkeratosis

plugging in the upper portion of the hair follicle,

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
The Also

of vitamin A deficiency is usually based on

typical clinical findings & aided by determining of serum vitamin A level (normal 30-65 mg/dl).

DIFFERENTIAL DIAGNOSIS OF PHRYNODERMA:

Keratosis pilaris Dariers 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 23 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.