SEMINAR ON NUTRITIONAL DISORDERS OF SKINSEMINAR 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
INTRODUCTIONINTRODUCTION
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.
FOODFOOD
Food is any substance which an individual Food is any substance which an individual
takes, digests and assimilates to derive takes, digests and assimilates to derive
nutritive requirements for maintaining nutritive requirements for maintaining
growth and physical well – being.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 NUTRITIONSOME 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 NUTRIENTSESSENTIAL 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.
VITAMINSVITAMINSVitamins are organic nutrients that Vitamins are organic nutrients that are required in small quantities for a are required in small quantities for a variety of biochemical functions and variety of biochemical functions and which, generally, can not be which, generally, can not be synthesized by the body and must synthesized by the body and must therefore be supplied bytherefore be supplied bythe diet.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 MINERALSTYPES OF MINERALS1. 1. Principal elements/macromineralsPrincipal elements/macrominerals K, Ca, Mg, Na, P, S and Cl.K, Ca, Mg, Na, P, S and Cl.2. 2. Trace elements/ micromineralsTrace elements/ microminerals
Iron , Copper, Fluoride, Iodine, Iron , Copper, Fluoride, Iodine, Cobalt, Cobalt, Zinc, Molybdenum,Zinc, Molybdenum,
Selenium, Selenium, Silicon,Silicon, Nickel, Nickel, Tin, Cromium, Vanadium.Tin, Cromium, Vanadium.
NUTRITIONAL DISORDERNUTRITIONAL DISORDERCLASSIFICATIONCLASSIFICATION
1.1. Undernutrition. Undernutrition. 2.2. Malnutrition.Malnutrition.3.3. Nutrient excess.Nutrient excess.4.4. Obesity.Obesity.5.5. Effect of toxicants in foods.Effect of toxicants in foods.
DISORDERS DUE TO VITAMIN DISORDERS DUE TO VITAMIN DEFICIENCYDEFICIENCY
Vitamin AVitamin A Phrynoderma, xerophthalmia, Phrynoderma, xerophthalmia, night blindness,keratomalacia.night blindness,keratomalacia.
Vitamin DVitamin D Rickets, osteomalaciaRickets, osteomalacia
Vitamin EVitamin E Haemolytic anaemia, ataxiaHaemolytic anaemia, ataxia
Vitamin KVitamin K Purpura, haemorrhage, Purpura, haemorrhage, ecchymosis.ecchymosis.
DISORDERS DUE TO VITAMIN DISORDERS DUE TO VITAMIN DEFICIENCY (Contd.)DEFICIENCY (Contd.)
Thiamin (Vitamin B1)Thiamin (Vitamin B1) Beri-beriBeri-beri
Riboflavin Riboflavin (VitaminB(VitaminB22))
Oro-ocular-genital Oro-ocular-genital syndrome (glossitis, syndrome (glossitis, stomatitis etc.)stomatitis etc.)
Niacin (Vitamin BNiacin (Vitamin B33)) Pellagra.Pellagra.
Vitamin BVitamin B6 6
(Pyridoxine)(Pyridoxine)PolyneuropathyPolyneuropathy
BiotinBiotin Dermatitis, alopecia,Dermatitis, alopecia,paraesthesiae.paraesthesiae.
DISORDERS DUE TO VITAMIN DEFICIENCY (Contd.)
Folate Anaemia
Vitamin B12 (Cobalamin)
Glossitis, hyperpigmentation, canitis.
Vitamin-C (Ascorbic acid)
Scurvy
DISORDERS DUE TO DISORDERS DUE TO MINERAL DEFICIENCYMINERAL DEFICIENCY
IronIron Anaemia, glossitis, Anaemia, glossitis, cheilosis, cheilosis, koilonychia.koilonychia.
ZincZinc Acrodermatitis Acrodermatitis enteropathicaenteropathica
ESSENTIAL AMINO ACID AND ESSENTIAL AMINO ACID AND ESSENTIAL FATTY ACID ESSENTIAL FATTY ACID DEFICIENT DISORDERSDEFICIENT DISORDERS
MarasmusMarasmus Sprue Sprue
Kwarshiorkor Kwarshiorkor CarotenemiaCarotenemia
Pellagra Pellagra LycopenemiaLycopenemia
DISORDERS DUE TO NUTRIENTS DISORDERS DUE TO NUTRIENTS EXCESSEXCESSVitamin A Liver damage, bone
damage, teratogenesisVitamin D Hypercalcaemia
Vitamin B6
(pyridoxine)Subepidermal vesicular dermatitis, sensoryperipheral 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 ACRODERMATITIS ENTEROPATHICAENTEROPATHICA
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.
EpidemiologyEpidemiology:: No geographical, racial or genderNo geographical, racial or gender
predilection.predilection.
Etiology:Etiology:
Genetic – autosomal recessive, defect inGenetic – autosomal recessive, defect in
intestinal zinc absorption.intestinal zinc absorption.
CONDITIONS MAY CAUSE CONDITIONS MAY CAUSE ZINC DEFICIENCYZINC DEFICIENCY
Reduced intake Reduced intake Anorexia nervosa.Anorexia nervosa.Bulimia.Bulimia.Faddish weight reduction.Faddish weight reduction.Prolong total parenteral nutrition.Prolong total parenteral nutrition.High dietary phytate.High dietary phytate.
FF
CONDITIONS MAY CAUSE CONDITIONS MAY CAUSE ZINC DEFICIENCY (Contd.)ZINC DEFICIENCY (Contd.)
Reduced absorption.Reduced absorption.Mucosal disease.Mucosal disease.
Malabsorption syndromes.Malabsorption syndromes.
Pancreatic disorders.Pancreatic disorders.
CONDITIONS MAY CONDITIONS MAY CAUSE ZINC CAUSE ZINC
DEFICIENCY (Contd.)DEFICIENCY (Contd.)Increased lossIncreased lossMalabsorption syndrome.Malabsorption syndrome.Blind-loop syndrome.Blind-loop syndrome.Renal tubular disease.Renal tubular disease.Nephrotic syndrome.Nephrotic syndrome.Dialysis. Dialysis. Diabetes mellitus.Diabetes mellitus.
CONDITIONS MAY CAUSE ZINC CONDITIONS MAY CAUSE ZINC DEFICIENCY (Contd.)DEFICIENCY (Contd.)
Increased Catabolism Increased Catabolism Malignancy.Malignancy.Burns.Burns.Postsurgical procedure.Postsurgical procedure.Antimetabolite drug therapy.Antimetabolite drug therapy. Increased DemandIncreased Demand Pregnancy.Pregnancy.Lactation.Lactation.
SOURCE OF ZINC
Meat.
Liver.
Egg.
Seafood.
BIOCHEMISTRYOF ZINC BIOCHEMISTRYOF ZINC METABOLISM:METABOLISM:
Adult body contains 2-3 gms ofAdult body contains 2-3 gms of zinc, zinc, which iswhich is about half the ironabout half the iron content, 10-20 times more than content, 10-20 times more than other essential trace elements. other essential trace elements.
BIOCHEMISTRYOF ZINC BIOCHEMISTRYOF ZINC METABOLISM(Contd.)METABOLISM(Contd.)
Recommend dietary allowance: Recommend dietary allowance: AdultAdult - 15 mg/day (elemental). - 15 mg/day (elemental).Infants Infants - 5mg/day. - 5mg/day.ChildrenChildren - 10mg/day.- 10mg/day.Lactating mother,Lactating mother, 1-6 months1-6 months- 19 mg/day- 19 mg/day > 6 months> 6 months - 16 mg/day- 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 DEFICIENCYTYPES OF ZINC DEFICIENCY
1.1. Hereditary type.Hereditary type.2.2. Non-hereditary type.Non-hereditary type.
Low grade, marginal, nonhereditaryLow grade, marginal, nonhereditaryzinc deficiency is far more commonzinc deficiency is far more commonthan the hereditary form.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.)PATHOGENESIS (Contd.)
Biologically active Zinc is highly Biologically active Zinc is highly charged species that cannot cross cell charged species that cannot cross cell membrane by passive diffusion but the membrane by passive diffusion but the process can greatly enhanced when process can greatly enhanced when zinc is complexed with zinc binding zinc is complexed with zinc binding ligands (ZBL).ligands (ZBL).
PATHOGENESIS (Contd.)PATHOGENESIS (Contd.)Zinc in human milk is preferentially Zinc in human milk is preferentially
bound to lower molecular-weight bound to lower molecular-weight ligands (ligands (~~10,000) than bovine milk.10,000) than bovine milk.
Total protein of human milk Total protein of human milk (5.3mg/ml) compared with bovine (5.3mg/ml) compared with bovine milk (29mg/ml) influence the bio-milk (29mg/ml) influence the bio-availability of zinc in an unknown availability of zinc in an unknown mechanism.mechanism.
PATHOGENESIS (Contd.)PATHOGENESIS (Contd.)
Metallothioneines regulates the transport of zinc Metallothioneines regulates the transport of zinc
into the circulation and then to the liver and into the circulation and then to the liver and
kidneys. kidneys.
Zinc is component of some peptidases, important Zinc is component of some peptidases, important
for digestion of proteins in GIT. 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 GENETICSZINC 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 IMMUNITYZINC AND IMMUNITY Reduced immune function specially cellular.Reduced immune function specially cellular.
In Acrodermatitis enteropathica thymic In Acrodermatitis enteropathica thymic
atrophy causing depressed thymocyte and atrophy causing depressed thymocyte and
cellular immune function, particularly T-cell. cellular immune function, particularly T-cell.
Neutrophil, peripheral blood monocytes, Neutrophil, peripheral blood monocytes,
tissue macrophages and mast cells require tissue macrophages and mast cells require
optimal concentration of zinc for normal optimal concentration of zinc for normal
function. function.
CLINICAL MANIFESTATIONCLINICAL MANIFESTATIONAge of onset: Age of onset:
Infants with bovine milk- 4-10 weeks,Infants with bovine milk- 4-10 weeks, Breast fed baby – after weaning.Breast fed baby – after weaning.
Prominent feature:Prominent feature:- Dermatitis (Acral and periorificial- Dermatitis (Acral and periorificial-
pathognomic).pathognomic).- Diarrhea.Diarrhea.- Alopecia (Generalized).Alopecia (Generalized).- Crying baby.Crying baby.
OTHER MANIFESTATION:OTHER MANIFESTATION:
Perleche- common early sign Perleche- common early sign and a sign heralding relapse.and a sign heralding relapse.
Superficial oral aphthous–like Superficial oral aphthous–like lesions.lesions.
Photophobea.Photophobea.
CLINICAL MANIFESTATION CLINICAL MANIFESTATION (CONTD.)(CONTD.)
Paronychia and brightly erythematous
dermatitis of the palmer and finger
creases.
Nail dystrophy.
CLINICAL MANIFESTATION CLINICAL MANIFESTATION (CONTD.)(CONTD.)
Secondary infection with bacteria Secondary infection with bacteria and Candida albicans. and Candida albicans. Delayed wound healing Delayed wound healing Patients are irritable and Patients are irritable and emotionally labile.emotionally labile.
CLINICAL MANIFESTATION CLINICAL MANIFESTATION (CONTD.)(CONTD.)
Anorexia,Anorexia, hypogeusia, hypogeusia, hyposmia and anemia hyposmia and anemia
LONG TERM SEQULAE OF ZN LONG TERM SEQULAE OF ZN DEFICIENCYDEFICIENCY
Growth reterdation and dwarfism.Growth reterdation and dwarfism.
Delayed puberty.Delayed puberty.
Hypogonadism in male adolescent.Hypogonadism in male adolescent.
Continuing dermatitis.Continuing dermatitis.
LONG TERM SEQULAE (CONTD.)LONG TERM SEQULAE (CONTD.)
Frequent infection.Frequent infection.
Lower fertility.Lower fertility.
Lower fertility and congenital Lower fertility and congenital
malformation occurs in children of malformation occurs in children of
mothers with AE.mothers with AE.
DIFFERENTIAL DIAGNOSISDIFFERENTIAL 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 DIAGNOSISLABORATORY 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 LABORATORY DIAGNOSIS(Contd.)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.
TREATMENTTREATMENT
Dietary or intravenous supplimentation Dietary or intravenous supplimentation with zinc salt – 3mg/kg/day life long.with zinc salt – 3mg/kg/day life long.
ZINC TOXICITYZINC TOXICITY
Acute : Acute : Gastric irritation.Gastric irritation.Nausea.Nausea.Vomiting.Vomiting.Gastric heamorrhage.Gastric heamorrhage.
Chronic: Chronic: Reduced growth rates.Reduced growth rates.Reduced rate of reproduction.Reduced rate of reproduction.Anemia.Anemia.Hypo cupremia.Hypo cupremia.
PHRYNODERMAPHRYNODERMA
Other names: Other names: Hypovitaminosis –A. Hypovitaminosis –A. Toad skin,Toad skin,
DEFINITION DEFINITION
Phrynoderma is a condition characterized by–Excessive dryness , –Wrinkling –Scaling of skin –Follicular hyperkeratosis.
DEFINITION (CONTD.)DEFINITION (CONTD.)•Due to deficiency of Vitamin- A.Due to deficiency of Vitamin- A.•May be associated with deficiency of May be associated with deficiency of
- Vitamin – B-Complex.- Vitamin – B-Complex.- Vitamin – C.- Vitamin – C.- Vitamin – E.- Vitamin – E.- Essential Fatty acids.- Essential Fatty acids.- Calories. - 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 INTRODUCTION (CONTD.)(CONTD.)
1 microgram of retinol =6 microgram 1 microgram of retinol =6 microgram of beta caroteneof beta carotene
Vitamin A is measured in Vitamin A is measured in international unit where 1 IU=0.3 international unit where 1 IU=0.3 microgram retinolmicrogram retinol
About 90% of the body’s vitamin A About 90% of the body’s vitamin A reserve is found in the perisinusoidal reserve is found in the perisinusoidal stellate (Ito) cells in the liver. stellate (Ito) cells in the liver.
INTRODUCTION INTRODUCTION (CONTD.)(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 INCIDENCE & PREVALENCE
Vitamin A deficiency is common in Vitamin A deficiency is common in children in developing countries.children in developing countries.Specially in Asia & Africa & Specially in Asia & Africa & In such region most common cause In such region most common cause of blindness.of blindness.
INCIDENCE & PREVALENCE INCIDENCE & PREVALENCE
It is rare in developed countries & It is rare in developed countries & most commonly associated with most commonly associated with Fat malabsorption syndrome , Fat malabsorption syndrome , Mineral oil laxative abuse &Mineral oil laxative abuse & 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 ASSOCIATED DISORDERS OF VITAMIN A DEFICIENCY VITAMIN A DEFICIENCY
(CONTD.)(CONTD.)Inflammatory disorders –Inflammatory disorders –
Diarrhea, Diarrhea, PneumoniaPneumonia
CAUSES OF VITAMIN A CAUSES OF VITAMIN A DEFICIENCYDEFICIENCY
►Principal cause is inadequate Principal cause is inadequate diet(chiefly in 3diet(chiefly in 3rdrd world countries) world countries)
►Fat malabsorptionFat malabsorption►Liver damageLiver damage
PATHOLOGY & PATHOLOGY & PATHOGENESISPATHOGENESIS
• Vitamin A deficiency involves-•Visual system• Immune system•Skin •GIT•Respiratory system•Urinary system
SITES OF INVOLVEMENT SITES OF INVOLVEMENT IN SKININ SKIN
• 80%cases limited to – Arms – Arround elbows & knees
SITES OF INVOLVEMENT IN SITES OF INVOLVEMENT IN SKINSKIN
20% cases20% casesanterolateral aspect of thigh , anterolateral aspect of thigh , posterolateral aspect of posterolateral aspect of
superior forearm , superior forearm , the extensor surface of upper the extensor surface of upper
& lower extremities , & lower extremities , the shoulders , the shoulders , back back abdomen & abdomen & buttockbuttock
CLINICAL FEATURES IN SKINCLINICAL FEATURES IN SKIN
Skin becomes
–Dry
–Wrinkled,
–Covered with fine scale,
CLINICAL FEATURES IN CLINICAL FEATURES IN SKIN (CONTD.)SKIN (CONTD.)
Morphology of the lesion is variable Morphology of the lesion is variable may range from filiform papule to may range from filiform papule to small conical papule to large papule small conical papule to large papule with large horny centre ,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 INVOLVEMENT OF VISUAL SYSTEM (CONTD.)SYSTEM (CONTD.)
Dryness of the conjunctiva Dryness of the conjunctiva
(xeropthalmia) & development Bitot spot (xeropthalmia) & development Bitot spot
( small white patches on conjunctiva) ( small white patches on conjunctiva)
are early signs.are early signs.
INVOLVEMENT OF VISUALSYSTEM (CONTD.)
Keratomalacia ulceration & necrosis of the cornea, perforating endopthalmitis & blind ness are late manifestation .
HISTOPATHOLOGICAL HISTOPATHOLOGICAL FINDINGSFINDINGS
In adults :In adults :Follicular Hyperkeratosis Follicular Hyperkeratosis Follicular plugging in the upper Follicular plugging in the upper
portion of the hair follicle, portion of the hair follicle, Severe atrophy of the Severe atrophy of the
sebaceous gland.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 HISTOPATHOLOGICAL FINDINGS(CONTD.)FINDINGS(CONTD.)
• In infants & young adults –
(before pilosebaceous gland mature fully)–Simple xerosis or xeroderma is usually
characteristic feature
DIAGNOSIS DIAGNOSIS
Diagnosis of vitamin A Diagnosis of vitamin A deficiency is usually based on deficiency is usually based on The typical clinical findings & The typical clinical findings & Also aided by determining of serum Also aided by determining of serum vitamin A level (normal 30-65 mg/dl).vitamin A level (normal 30-65 mg/dl).
DIFFERENTIAL DIAGNOSIS OF PHRYNODERMA:
Keratosis pilarisDarier’s diseasePityriasis rubra pilarisAcne vulgaris Lichen planopilaris.
MANAGEMENTMANAGEMENT General management – General management –
improvement of diet. improvement of diet. Antibiotic if there is infection.Antibiotic if there is infection.
Special –Special –Treatment with vitamin A in Treatment with vitamin A in
deficient cases. deficient cases. Treatment with other specific Treatment with other specific
vitamins according to need. 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 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.