NUTRITIONAL DERMATOSES

Presentor : Dr. Sanjay Singh

FOOD

• Food is any substance which an individual takes, digests and assimilates to derive

nutritive requirement for maintaining growth and physical well being.

NUTRITION

• Dynamic process concerned with ingestion, digestion, absorption and assimilation of

food for nourishing the body.

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.

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

Either cannot be synthesized in body or cannot be synthesized in

adequate amount to meet the needs of the body.

1. Certain amino acids.

2. Certain fatty acids.

3. Vitamins.

4. Minerals.

Malnutrition

A pathological state resulting from :

Relative or absolute deficiency

Excess of one or more nutrient

Biomed Environ Sci 2001 ; 14(4):283-91

Forms of Malnutrition

1. Undernutrition : Marasmus

2. Overnutrition : Obesity, Hypervitaminoses

3. Specific Deficiency : Kwashiorkor, Hypovitaminoses, Mineral Deficiencies

4. Imbalance : Electrolyte Imbalance

• Community-based cross-sectional study :

• 71,591 preschool children were screened for ocular signs

• 3,291 preschool children and 6,616 adolescents screened for hemoglobin

Results :

Bitot's spots : 0.8%

Anemia : 67% in preschool children

69% in Adolescents

Prevalence and determinants of micronutrient deficiencies among rural children of eight states in India

Laxmaiah A, Arlappa N, Balakrishna N et al. Ann Nutr Metab. 2013;62(3):231-41

• Sample Size : 109, nonpregnant rural and tribal women (18-30 Y)

• Result -

Concurrent micronutrient deficiencies are prevalent in nonpregnant rural and tribal women from central India

Menon KC, Skeaff SA, Thomson CD et al. Nutrition. 2011 ;27(4):496-502

Anaemia 66%

Zinc 52%

Vitamin B12 34%

Retinol 4%

Folate 2%

Minerals

Minerals are inorganic elements or substances required by the organism in very

small amounts for maintenance of vital processes essential for life.

1. Principal elements/macrominerals

K, Ca, Mg, Na, P, S and Cl.

2. Trace elements/ microminerals

Iron , Zinc, Copper, Selenium, Fluoride, Iodine, Cobalt, Molybdenum, Silicon,Nickel, Tin, Cromium

Zinc Status in South Asian Populations—An UpdateSaeed Akhtar, J Health Popul Nutr. Jun 2013; 31(2): 139–149.

Prevalence of zinc deficiency in developing countries is very common, and 61% of the population is at an increased risk of low dietary zinc intake

52% non-pregnant women of central India suffered from zinc deficiency Cutoff level ≤65 μg/dL : reporting an overall zinc deficiency of 43.8% in children from

low socioeconomic group

Orissa : 51.3%

Uttar Pradesh : 48.1%

Gujarat : 44.2%

Madhya Pradesh : 38.9%

Karnataka : 36.2%

Cross sectional : 260 adolescent (schoolchildren, 114 males) in the age group of

11-18 years

Serum zinc was estimated using Inductively coupled plasma mass spectrometer.

49.4% children (50.8% males, 48.2% females) were found to have a deficient zinc nutriture

Zinc deficiency amongst adolescents in DelhiKapil U, Toteja GS, Rao S et al. Indian Pediatr. 2011;48(12):981-2

Zinc

Essential component of many metalloenzymes involved in a variety of

metabolic pathways and cellular functions

Adequate zinc levels are also important for wound healing and for T-cell,

neutrophil, and natural killer cell function

Meat & fish are best dietery sources

Human breast milk contains very high levels of zinc during the first 1 to 2

months of lactation

Also contains a zinc-binding ligand that increases the bioavailability

Total body zinc is stored primarily in the bones, skin, muscles and prostate,

there is no free exchange of stored zinc

Deficiency :

1. Hereditary type

2. Non-hereditary type Low grade, marginal, nonhereditary zinc deficiency is far more common

I. Early weaning

II. Excessive calcium intake

III. Phytate in diet

IV. Cutaneous burn, Exfoliative dermatitis

V. Nephrotic syndrome

Acrodermatitis Enteropathica

Classically presents during infancy on weaning from breast milk to formula or cereal, which have lower zinc bioavailability than breast milk

Defect in intestinal zinc transporter, the human ZIP4 protein

Genetic locus for acrodermatitis entropathica on chromosome 8q24.3

Clinical findings Classic features include alopecia, diarrhea, lethargy, and an acute eczematous and erosive

dermatitis favoring acral areas—perioral, periocular, anogenital, hands, and feet

Bullae and erosions can develop with a characteristic peripheral crusted

border

Delayed wound healing, acute paronychia, conjunctivitis, blepharitis, and

photophobia may also be observed

Predisposition to infection with Candida and bacterial infections

Chronic deficiency : psoriasiform dermatitis involving the hands and feet

and, occasionally, the knees

Growth retardation, hypogonadism, dysguesia, impaired dark adaptation

Management

Low plasma zinc level is the gold standard for diagnosis

If plasma zinc level is equivocal and the diagnosis is uncertain, skin biopsy may

be helpful

Biopsy : Psoriasiform hyperplasia with confluent parakeratosis, spongiosis and

pallor of the upper epidermis, focal dyskeratosis, and variable epidermal atrophy

Treatment :

0.5 to 1.0 mg/kg of elemental zinc given as one to two daily doses

Patients with AE require lifelong treatment

Iron Used in several biologic pathways, including heme synthesis, oxidation-

reduction reactions, collagen synthesis, and as a co-factor for various enzymes

Animal sources, dried fruits, green leafy vegetables, jaggery are best sources

Iron deficiency remains an international problem that crosses socioeconomic and ethnic divide

Groups at high risk include infants, menstruating females, and individuals with chronic GI bleeds

Clinical Findings :

Nails :

Fragile, longitudinally ridged,

lamellated, or brittle nails

Thinning, flattening or spoon shaped

Koilonychia resolves slowly even after

replacement therapy

Hairs :

Lusterless, brittle, dry, and focally narrow or split hair shafts, likely caused by

impaired keratin production

Heterochromia of black scalp hair with alternating segments of dark brown,

white, and silver bands

Role of iron deficiency in hair loss : A controversy

J Am Acad Dermatol 2006 ;54(5):824-44

Mucous membrane manifestations include aphthous stomatitis, angular stomatitis, glossodynia, and absent or atrophied tongue papillae.

Generalized pruritus of variable severity has been reported in some individuals with iron deficiency

Treatment involves appropriate iron supplementation.

Hemochromatosis

Hyperpigmentation (brownish bronze or slate gray) and ichthyosis-like changes of

the skin are seen.

Cutaneous hyperpigmentation is seen in more than 90% of patients with idiopathic

hemochromatosis

Hyperpigmentation is one of the earliest signs of the disease, tends to be most

pronounced on sun-exposed skin.

1/3 shows external genital hyperpigmentation and 1/5 shows flexural folds, scars,

and nipple areolae hyperpigmentation

Associated findings are cirrhosis of the liver, diabetes mellitus, and

cardiomyopathy

Chelation therapy and phlebotomy mainstay of treatment.

Vitamins

Vitamins are biologically active organic compounds, which are indispensable for the

normal functions of the body.

No direct function as an energy source or as structural tissue components.

Act as coenzymes in various enzyme systems.

Fat Soluble Vitamins

Vitamin A, D, E, KWater Soluble Vitamins

Vitamin B & C

Vitamin A

Active forms: retinol, retinaldehyde & retinoic acid

Retinal, the aldehyde form, functions in vision

Retinoic acid, the physiologically most important vitamin A metabolite,

regulates many genes involved in biologic activities of cells

Functions :1. Retinal is in photosensitive pigment in both rods (rhodopsin) & cones (iodopsin)

2. Needed for lysosomal membrane stability

3. Involved in keratinization, cornification, bone development & cell growth &

reproduction

Dietary sources :

Pre-formed vitamin A : animal derived (liver, fish, eggs, milk, butter)

Carotenoids (e.g., beta-carotene) : yellow and leafy green vegetables

(carrots, squash and spinach)

Deficiency : Poor absorption as in low-fat diet, malabsorption syndromes, etc.

Low protein intake resulting in deficient carriers

Increased excretion as in cancer & UTI

Hypovitaminosis A

Cutaneous Findings :

• Follicular papules with central

keratotic plug; favors extensor

surfaces of extremities, buttocks

• Generalized xerosis

• Sparse, fragile hair

• Squamous metaplasia

Other Manifestations :

•  Night blindness

•  Xerophthalmia 

•  Bitot spots 

•  Keratomalacia 

•  Stunted growth

Corneal ulcer upto ¾ depth is one of characteristic finding

Treatment

•  Based on severity of ophthalmologic impairment

•  10000–50000 IU/day PO or IM in infants on days 1, 2 & 14

•  200000 IU/day PO or IM in children and adults on days 1, 2 & 14

•  Higher doses given if keratomalacia

Hypervitaminosis A

Toxicity typically results when intake exceeds 20 times the RDA in a child or 100

times the RDA in an adult.

Acute intoxication : excessively large single doses >300,000 IU

Chronic toxicity results from daily ingestion of >25,000 IU for more than 6 years or

>100,000 IU for more than 6 months of pre-formed vitamin A

Acute Intoxication

Dry, scaly skin, with large areas of desquamation and fissuring of the lips and angles of the mouth.

Infants: nausea & vomiting, drowsiness or irritability with signs of increased ICP

Adults: drowsiness, irritability, headache & vomiting

Chronic intoxication

Early cutaneous sign is dryness of the lips

Diffuse, dry, pruritic, scaly skin with peeling of palms and soles,

Alopecia, follicular hyperkeratosis, and hyperpigmentation of the face and neck.

Treatment

Discontinuation of excess intake

All symptoms reverse to normal except liver cirrhosis and

pseudotumor cerebri

Carotenoderma

Excessive intake of carotene

Characterized by yellow-orange

skin pigmentation

Spares mucous membranes

Fades after decreased intake of

carotene

Vitamin K Naturally occurring vitamin K abundant in pork, liver, soybeans & green

leafy vegetables

Synthesize by intestinal microorganisms

Required for normal clotting of blood

Vitamin K-dependent clotting factors:

● Prothrombin (Factor II)

● Proconvertin (Factor VII)

● Plasma thromboplastin component or PTC (Factor IX)

● Stuart-Prower factor (Factor X

Clinical Findings Hemorrhagic manifestations are the hallmark, leads to ecchymoses and

purpura

Bleeding in the newborn from the cord or circumcision site

GIT bleeding, hematuria & intracranial hemorrhage

Anemia & shock may ensue from severe blood loss

Treatment Acute treatment of vitamin K deficiency with hemorrhage is with fresh frozen

plasma to replace deficient coagulation factors.

Parenteral or intramuscular 5 to 10 mg vitamin K per day

Thiamine Cofactor to enzymes in energy metabolism

Obtained from whole grains, enriched bread products, dried peas and beans, potatoes, and fish

Polished rice eliminates the thiamine containing husk

Deficiency show up in quickly growing tissues such as epithelium and cells using lots of energy like nerve cells and cardiac muscles

Beriberi

Wet beriberi : generalized edema, acute cardiac symptoms and prompt

response to thiamine administration

Dry beriberi : peripheral neuritis with neurological disorders

Glossitis and glossodynia

Treated with 50-100mg IV or IM thiamine for 7-14 days

Riboflavin FMN and FAD involved in oxidation-reduction reactions in cellular respiration

and oxidative phosphorylation

Source : Dairy products, meat, nuts, eggs, whole grain and enriched bread

products, fatty fish, and green leafy vegetables

Visible light phototherapy causes photodecomposition of riboflavin

Chlorpromazine and other tricyclic drugs inhibit transport of riboflavin in the gastrointestinal tract

Acute deficiency

• Deep red erythema, epidermal necrolysis, and mucositis

Chronic deficiency

Ocular changes

• Angular stomatitis• Cheilosis with erythema• Vertical fissuring of lips• Bald swollen tongue (magenta in

color)• Seborrheic dermatitis• Scrotal or vulvar dermatosis

• Corneal vascularization• Photophobia

Circumcorneal vascularization

Treatment Riboflavin 3–10 mg/day orally

In refractory cases, 2 mg IM TID

Niacin

•  Vital oxidation–reduction reactions

•  Biosynthesis of epidermal lipids, e.g. ceramides

Deficiency :

Maize and Jowar rich diet

Carcinoid syndrome

Hartnup disease

Isoniazid

Clinical findings :

• Photodistributed erythema

becomes hyperpigmented, with

scale-crust

• “Casal’s necklace” – well

demarcated band around neck

• Painful fissures of the palms & soles

• Peri-anal & oral inflammation &

erosions

• Cheilitis & glossitis (atrophic, red)

• Classic triad dermatitis, diarrhea &

dementia, can progress to death

• Peripheral neuropathy with 

dysesthesias, including burning

•  Lassitude

•  Dizziness

•  Irritability, disorientation

Treatment

•  Mild cases – nicotinic acid 50 mg TID orally

•  If symptomatic, nicotinic acid 25 mg TID IV

Pyridoxine

•  Cofactor for multiple enzymes involved in amino acid metabolism and

conversion of linoleic acid to arachidonic acid

•  Ceramide synthesis

•  Gluconeogenesis & heme biosynthesis

Deficiency :

•  Other vitamin or trace element deficiencies (metabolism of B6 is dependent 

on riboflavin, niacin & zinc)

•  Medications : isoniazid, anticonvulsants, penicillamine, hydralazine, oral 

contraceptives, corticosteroids

 

•  Periorificial seborrheic dermatitis-like lesions

•  Angular cheilitis, stomatitis

•  Glossitis – atrophic with ulceration

•  Conjunctivitis

•  Intertrigo

•  Neurologic symptoms including peripheral neuropathy, somnolence, confusion 

& seizures

Treatment : • Pyridoxine 50–100 mg/day PO to prevent neuropathy

•  100 mg/day IV in those with seizures

Biotin

•  Essential cofactor for several carboxylases involved in cellular metabolism

•  Plays role in gluconeogenesis

• Animal sources like liver, meat and eggs are best sources

• Synthesized in gut by bacterial flora

Deficiency :

Excessive raw egg white consumption

Chronic anticonvulsant therapy

Inborn error of metabolism

Cutaneous findings :

• Alopecia

• Seborrheic dermatitis

• Nummular eczema

• Blepharitis, conjunctivitis

• Erythroderma in neonatal form

• Juvenile form may resemble

acrodermatitis enteropathica

Systemic findings :

• Depression, lassitude

• Anorexia, nausea & vomiting

• Paresthesias

• Hypotonia, muscle pain

• Developmental delay, hearing loss

• Seizures, ataxia

Genetic forms can be fatal (Holocorboxylase and Biotinidase deficiency)

Treatment :

•  Infants & children – 5–20 mg/day PO or IM

•  Adults : 10 – 40 mg/day PO or IM

Vitamin B12 Methylcobalamin : For DNA, protein, and lipid metabolism

5 -Adenosylcobalamin : Required for myelination of nerve′ Present in animal sources

Deficiency :

Strict vegetarianism

Pernicious anemia

Bacterial overgrowth and fishworm infestation

Drugs : PPIs, H2receptor blockers, Metformin

Clinical findings :

•  Megaloblastic anemia with

neurological complications

•  Diffuse or patchy hyperpigmentation, 

including flexural areas, palms,soles, 

nails, oral cavity

•  Glossitis with fissures of the oral 

mucosa (early sign prior to anemia)

•  Painful, red, swollen tongue

Pernicious anemia : decrease in gastric intrinsic factor, associated with vitiligo, alopecia areata

Treatment Oral supplementation is not recommended due to poor absorption

30 μg administered via the IM or SC route for 5 to 10 days, followed by 100 to 200 μg per month is recommended

Vitamin C•  Collagen formation

•  Cofactor for several enzymes, e.g. lysyl hydroxylase

•  Antioxidant

•  Iron absorption

•  Folate metabolism (folic acid to active form folinic acid)

Dietery Source : Fresh fruits & vegetables

Deficient intake for as few as 3 months can lead to scurvy

Clinical findings :

• Spongy gingivae with bleeding & erosions

• Petechiae, ecchymoses

• Follicular hyperkeratosis

• Corkscrew hairs (flattened & curled) 

with perifollicular erythema or

hemorrhage

• Impaired wound healing

Clinical Findings :

•  Subperiosteal hemorrhage with “pseudoparalysis”, especially in children

•  Arthralgias, joint swelling, edema

•  Weakness, malaise, depression

•  Vasomotor instability

•  GI tract, cerebral & femoral sheath hemorrhages

Management :

• Positive Rumpel–Leede capillary fragility test

• Adults: 800 mg/day orally

• Children: 150 mg/day orally

Essential Fatty Acids

They are also called as poly unsaturated fatty acids (PUFA).

Three EFAs - Linoleic acid

- Linolenic acid

- Arachidonic acid

Functions of EFA

1. Synthesis of Ecosanoids

2. Maintenance of structural integrity of cells

3. Development of retina and brain

4. Antiatherogenic effect

Causes :

Malabsorbtion

Long term parenteral nutrition

without lipid supplementation

Low dietery intake

Nephrotic sydrome

EFA deficiency

Cutaneous findings :

Dry, scaly and leathery skin with

underlying erythema

Follicular Hyperkeratosis

Intertriginous erosions

Alopecia and more lightly pigmented

hair

Treatment

Essential fatty acid replacement, depending upon severity

Topical

Oral

Intravenous

Therapeutic Response of Vitamin A, VitaminB Complex, Essential Fatty Acids (EFA) and Vitamin E in the Treatment of Phrynoderma: A Randomized

Controlled StudyS R, Kumar V J, S B M et al. J Clin Diagn Res. 2014;8(1):116-8

Protein Energy Malnutrition

Trend in Nutritional Status of Children

1. Wellcome classification

Based on 2 criteria : weight loss (wt. for age %) & edema (present or

absent)

Wt. for Age% Edema No Edema

80 – 60 Kwashiorkor Undernutrition

<60 Marasmic-Kwashiorkor Marasmus

2. Waterlow Classification :

Distinguishes between deficits of weight for height % (wasting) & height

for age % (stunting)

Adopted by WHO

N Mild Mod Severe

Wt for Ht % >90 89-80 79-70 <70

Ht for Age % >95 95-90 90-80 <80

Marasmus

Common in the 1st year of life Balanced starvation

Clinical Manifestations:1. Dry , thin, pale , lax and wrinkled skin

2. Follicular hyperkeratosis and folliculitis

3. Hairs : lanugo hairs, which grows slowly

and falls out readily

4. Impaired growth of nails, fissured nails

5. Muscle wasting

6. Growth retardation

7. Mental changes

8. No edema

9. Variable-subnormal temp, slow PR, good

appetite, often with diarrhea, etc. Monkey Facies

Multiple purpuric spots

Diagnostic findings :1. Triceps skin fold <3mm2. Mid-arm muscle circumference

<15cm3. Most hair bulbs are in the

telogen phase4. Abundant broken hairs5. Creatinine height index <60% of

standard6. Serum albumin Normal

7. Urinary urea/gram creatinine N or low 8. Low zinc & cholesterol levels9. Glucose tolerance curves diabetic type

10. Bone growth delayed

11. Liver biopsy N or atrophic

Treatment Treat cautiously, slowly replacing proteins and calories, allowing

readaptation of metabolic and intestinal functions

Supplementation with linoleic acid and zinc

Monitor for hypophosphatemia and cardiorespiratory failure (associated with overly aggressive nutritional replacement)

Kwashiorkor

Between 1-3 yrs old

Etiology :

Very low protein but

with calories from CHO

In places where starchy

foods main staple

Clinical Findings :

1. Dyschromia

2. Pallor

3. Enamel paint spots and flaky

paint dermatosis.

4. Hair : sparse, dry, lusterless 

and brittle with a reddish tinge

5. Flag sign

Systemic findings :

• Relatively well-nourished appearance

• Edema or even anasarca

• Apathy, anorexia, irritability

• Failure to thrive (retardation of growth

and mental development)

• Superimposed bacterial and

fungal (e.g. candidal) infections

• Bilateral parotitis, hepatomegaly, 

diarrhea, loss of muscle mass

Diagnostic Findings

• Hypoalbuminemia (<2.5 g/dl)

•  Total iron-binding capacity <200 ɱg/dl

• Peripheral lymphocyte count <1500/ɱl•  Decreased number of anagen hair follicles and increased number of telogen

follicles• Structural abnormalities in anagen follicles – severe atrophy, shaft constriction,

depletion of pigment

Treatment

• Aggressive nutritional support is indicated to rapidly restore metabolic balance; correction of any electrolyte disturbances or hypoglycemia

• Institute diet with adequate protein and caloric

• Identify and attempt to treat underlying cause(s), including bacterial and parasitic disease

Thank You