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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


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

• 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
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

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


• Result -
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 Update
Saeed 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%
Zinc deficiency amongst adolescents in Delhi
Kapil U, Toteja GS, Rao S et al. Indian Pediatr. 2011;48(12):981-2

 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
 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 Water Soluble Vitamins


Vitamin A, D, E, K 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 Chronic intoxication
 Dry, scaly skin, with large  Early cutaneous sign is
areas of desquamation and dryness of the lips
fissuring of the lips and
angles of the mouth.  Diffuse, dry, pruritic, scaly
skin with peeling of palms
 Infants: nausea & vomiting, and soles,
drowsiness or irritability with
signs of increased ICP  Alopecia, follicular
hyperkeratosis, and
 Adults: drowsiness, hyperpigmentation of the
irritability, headache & face and neck.
vomiting
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 • Deep red erythema, epidermal
deficiency necrolysis, and mucositis
• Angular stomatitis
Chronic • Cheilosis with erythema
deficiency • Vertical fissuring of lips
• Bald swollen tongue (magenta in
color)
• Seborrheic dermatitis
• Scrotal or vulvar dermatosis

Ocular • Corneal vascularization


changes • Photophobia
Treatment
 Riboflavin 3–10 mg/day orally

 In refractory cases, 2 mg IM TID

Circumcorneal vascularization
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 : Systemic findings :

• Alopecia • Depression, lassitude

• Seborrheic dermatitis • Anorexia, nausea & vomiting

• Nummular eczema • Paresthesias

• Blepharitis, conjunctivitis • Hypotonia, muscle pain

• Erythroderma in neonatal form • Developmental delay, hearing loss


• Juvenile form may resemble • Seizures, ataxia
acrodermatitis enteropathica
 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
EFA deficiency

Causes :
 Malabsorbtion

 Long term parenteral nutrition

without lipid supplementation

 Low dietery intake

 Nephrotic sydrome
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 Study
S 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 <3mm

2. Mid-arm muscle circumference


<15cm

3. Most hair bulbs are in the telogen


phase

4. Abundant broken hairs

5. Creatinine height index <60% of


standard

6. Serum albumin Normal


7. Urinary urea/gram creatinine

N or low
8. Low zinc & cholesterol levels

9. 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