MICRO NUTRIENTS AND SKIN

1)ZINC

*Trace element which has catalytic, structural, and regulatory function.

📌Why do we need Zinc?

*Required by 300 enzymes

*Growth & development

*wound healing

*immune function

*collagen synthesis.

*Key ion in zinc finger proteins, play an important role in the formation and maintenance of all tissues including the skin

📌Zinc containing foods - Animal products, Legumes, Whole grains, Dairy products, nuts

📌Vegetarian diet can cause  zinc deficiency.

📌Cereal grains contain phytates which chelates zinc and prevents absorption.

📌Zinc absorption greater in human breast milk than bovine milk.

📌REQUIREMENT OF ZINC

*RDA ( recommended daily allowance )

Adults – 15.5 mg

Infants less than six months – 3 – 5 mg

6 months to 1 year old – 5 mg

pregnant and lactating women – 20 – 25 mg

📌CLASSIFICATION  OF  ZINC DEFICIENCY

*Genetic

*Acquired

*Acute

*chronic

📌ACRODERMATITIS  ENTEROPATHICA

📍Term coined by Danbolt and Closs 1942

📍Thore brandt 1st described the condition.

📍Autosomal recessive condition - – SLC39A4 on chromosome 8q243 encoding the ZIP4 – 4

transporter on enterocytes in the small intestine.

📍Symptoms usually appear when the infant is weaned from the breast feeding.

📍Manifest early in formula fed infants (4th and 10th).

📍Breast milk contains a zinc ligand binding protein

📍CLINICAL FEATURES

*Classical clinical triad

-Diarrhea + Alopecia +Periorificial and acral dermatitis

*Periorificial findings - Relative sparing of upper lip giving the horse shoe shaped or U shaped configuration.

*Psoriasiform or eczematous lesions with vesicles, bullae and peripheral crusting – symmetrically in the acral, periorificial areas and bony prominence 

*Vitiligo like depigmentation

*Superinfection by bacteria such as staphylococcous aureus, and yeast such as candida albicans.

*Hair- Dry and brittle with areas of alopecia and may show alternating dark and light bands on polarized light microscopy.

*Ophthalmic – blepharitis, conjunctivitis, photophobia and nyctalopia

*General condition – irritable child, stops smiling

📌ACQUIRED ZINC DEFICIENCY

📍Causes:-

*Premature infants – inadequate zinc stores, decreased absorptive capablity, and high fecal loss.

*Full term infant – low zinc content of either breast milk or bottle milk.

*Pregnancy

*Intestinal parasitic infestations

*Malabsorption

*Intestinal bypass operation

*Cystic fibrosis

*Chronic alcoholism

*Alcoholic pancreatitis

*Liver cirrhosis

*Nephrotic syndrome

*Chronic renal failure

*Diabetes mellitus

*Malignancy

*Severe burns

*Collagen vascular disease

*HIV infection

*Anorexia nervosa

*Excess ingestion of coffee or tea

*DRUGS CAUSING ZINC DEFICIENCY:-

-Therapy with chelating agents

-Antimetabolites

-Cancer chemotherapy in children with leukemia

-Diuretics

-Sodium valproate

-Oral contraceptives

-Total parentral nutrition devoid of zinc

-Dialysis

📌ACUTE ZINC DEFICIENCY

📍Palmoplantar, periorificial, anogenital dermatitis and angular stomatitis

📍Flat greyish vesiculo bullous lesion surrounded by reddish brown erythema are seen on the creases of palms and fingers.

📍Paronychia of finger nails and toe nails

📍Diffuse progressive thinning of scalp hair leading to total alopecia

📍General symptoms – septicaemia, photophobia, and mental depression

📌CHRONIC ZINC DEFICIENCY

📍Initial lesions are seen in perioral and anogenital areas

📍Perleche, glossitis, and stomatitis are seen.

📍Eczematous, vesiculobullous, pustular, erosive, crusted lesions develop.

📍Seborrheic dermatitis like changes

📍Hair growth is poor and sparse.

📌OTHER FEATURES OF ZINC DEFICIENCY

📍Delayed wound healing

📍Stomatitis

📍Photophobia

📍Conjunctivitis

📍Irritablity

📍Emotional lability

📍Growth retardation

📍Lack of secondary sexual and genital development in boys

📍Men – sperm production reduced

📍Women – abnormal oogenesis occur

📍Pregnant women – increased maternal morbidity, prolonged gestation, inefficient labor, atonic bleeding, increased fetal risk, and congenital malformation.

📍Deficiency of biotin and zinc in maternal diet – infantile seborrheic dermatitis.

📌LAB INVESTIGATIONS

📍Plasma zinc levels

📍Zinc level – < 70 mg/dl - deficiency

📍Measurement of zinc dependent enzymes such as alkaline phosphatase (ALP)

📍Albumin level in serum

📌HISTOPATHOLOGY OF SKIN LESIONS IN ZINC DEFICIENCY

📍Early lesion- Focal parakeratosis and vacuolization of the granular cell layer

📍Acute zinc deficiency with vesiculobullous dermatitis, Spongiosis and suprabasal clefts, Horny layer is seperated or lost

📍Later lesions- Confluent parakeratosis, Extensive vacoulization of upper epidermal cells and

psoriasiform acanthosis, Tortousity of papillary vessels and a perivascular mononuclear cell infiltrate

📌TREATMENT OF ZINC DEFICIENCY

📍Zinc replacement therapy

*3mg/kg/day of elemental zinc

*0.5 – 1 mg/kg in children

*15-30 mg/day in adults

📍Therapeutic uses of zinc:-

Rosacea, hidradenitis suppurativa, seborrheic dermatitis, necrolytic

acral erythema, hand eczema and cutaneous ulcers

📌ZINC TOXICITY

📍Tolerable upper intake level for adults – 40 mg/day

📍Clinical features – epigastric pain, dizziness, nausea, vomiting and diarrhea

📍Less common side effects – gastric erosions, promotion of tumor growth, genitourinary complication.

📍Renal failure, sideroblastic anemia, neutropenia and leukopenia.

📌ZINC INDUCED COPPER DEFICIENCY

📍Competitive absorption between zinc and copper in enterocytes of small intestine

📍Clinical features- Myelopathy, demyelination, numbness, weakness, spastic gait, ataxia and

significant dorsal coloumn deficit.

COPPER

📍Copper is an essential trace elements

📍Required for production of melanin, collagen and elastin

📍It stimulates proliferation of keratinocytes and fibroblast .

📍In plasma 90% copper - with ceruloplasmin

      rest - linked to other plasma proteins

📍RDA of copper – 340 ug/day for young children

📍Requirement of copper- 900 ug/day for adults

📍CAUSES OF ZINC DEFICIENCY

*Acquired copper deficiency is rare

*Reported in infants – diet/milk low in copper

*Protein energy malnutrition

*Excessive zinc intake

📍MENKES DISEASE (KINKY HAIR DISEASE)

*X – linked recessive condition

*Defect – due to mutation in the ATP7A gene which encodes copper transporting ATPase

*Defective copper absorption with low copper levels in blood , liver, and hair.

*Failure to thrive, lethargy, hypothermia, hypotonia, seizures, mental retardation, anemia is also common.

*Characteristics facies – pudgy cheeks, a cupid’s bow of upper lip and horizontal eyebrows

*Abnormalities due to immature elastin ( as detected by ultrastructural studies)

*HAIR – 180 degree twist of hair (pili torti)

*Segmental shaft narrowing (monilithrix)

*Brush like swelling of hair shaft ( trichorrhesis nodosa )

*Hairs – light in color, sparse, fragile and kinky

*Decrease activity of several enzymes including cytochrome c oxidase in the brain. – SEVERE

TRUNCAL HYPOTONIA WITH POOR HEAD CONTROL. Increased tone in the extremities,

exaggerated deep tendon reflexes and developmental delay

*Bony abnormalities – scalloping of posterior vertebral bodies

- subperiosteal new bone formation

- ossification of sutures

- metaphyseal widening

- lateral spur formation

*Arteriography – tortuosity and elongation of arteries

📍COPPER TOXICITY

*Acquired – ingestion of excess amount of copper ( eg, milk boiled in eroded copper plates )

*Lethal dose 10 – 20 gm

*Inherited forms – Wilson’s disease

WILSON'S DISEASE

-Due to dysfunction of ATP7B gene

-Clinical hallmark – liver disease, kayser fleischer corneal rings

-Neurological symptoms – dysarthria, dyspraxia, ataxia and parkinsonian like extrapyramidal signs

📍LAB DIAGNOSIS  OF COPPER DEFICIENCY

*Estimation of plasma ceruloplasmin

*Value less than 125 mg/dl indicates deficiency

📍TREATMENT OF COPPER DEFICIENCY

*Desirable intake of copper for adults is 2.2 mg/day

SELENIUM

📍Selenium present in all tissues in the body and is important for tissue repair.

📍Photoprotective, antioxidant, and anti – inflammatory effects

📍Antioxidant properties are due to glutathione peroxidase activity in vivo

📍Selinium is found in soil

📍RDA – 70 microgram

📍Pregnant and lactating mothers – additional 10 -15 microgram/day

📍Wheat, nuts, red meat, egg yolk, grains, sea food are rich source of selenium

📍CLINICAL MANIFESTATIONS OF SELENIUM DEFICIENCY

*Selinium deficiency – Keshan disease

Highest incidence in China

Cardiomyopathy, muscle pain and weakness

Loss of pigment of skin, and hair, white nails - pseudoalbinism

Elevated serum creatinine kinase and transaminase levels are also seen

Low plasma selenium levels and glutathione peroxidase activity demonstrate selenium deficiency

📍Protective role of selenium – psoriasis, rheumatological disorders, cancer ( eg. melanoma ) and cardiovascular disease

📍TREATMENT OF SELENIUM DEFICIENCY

*Selenium 2mg/kg/day

*Selenium along with antioxidants are useful in the treatment of severe erythroderma or arthropathic psoriasis

*Selenium sulfide shampoo – seborrheic dermatitis and pityriasis versicolor

*Use on large areas of eroded or ulcerated skin may lead to excessive absorption with loss of appetite and tremor.

MANGANESE

📍It is required for the synthesis of proteins, DNA and RNA

📍It is required for superoxide dismutase, a key enzyme in the antioxidant defence mechanism

📍The daily requirement 2.5 – 7 mg

📍Clinical features of manganese deficiency

*Transient dermatitis, discoloration and slow growth of hair

*Nausea, vomiting and weight loss

 IRON

📍Sources of iron – red meat, egg yolk, green leafy vegetables, dried fruits, nuts etc

📍It is required for the formation of hemoglobin, the transport of oxygen and for the various

oxidation reduction reactions in the tissues.

📍Essential for cellular processes including synthesis of DNA, RNA and protein.

📍CAUSES OF IRON DEFICIENCY

*Inadequate dietary intake

*Increased need in growing children

*Pregnant women

*Chronic blood loss

*Parasitic infections

*Ankylostomiasis and malaria

📍RDA OF IRON:-

*MEN – 10 mg

*WOMEN – 18mg

📍CLINICAL FEATURES OF IRON DEFICIENCY:-

*Hypochromic microcytic anemia

*Chronic generalized pruritis

*Increased hair loss

*Telogen loss with sederopenia with or without anemia

*Koilonychia

*Angular stomatitis

*Cheilosis

*Glossitis

📍CLINICAL FEATURES OF IRON DEFICIENCY

*Atrophy of the filiform papillae of the tongue

*Pica

*Cell mediated immunity is grossly impaired

*Increased susceptibility to bacterial and fungal infection particularly candida albicans

📍PLUMMER VINSON SYNDROME

*Precancerous condition results from advanced iron deficiency

*Occurs in middle aged woman

*Clinical features-:

-Lips are thin and opening of mouth becomes smaller

-Skin is dry and wrinkled

-Microcytic hypochromic anemia with dysphagia, glossitis, cheilosis and koilonychia

-Condition respond to treatment with iron and vitamins

📍Lab diagnosis:-

Routine hemogram – serum ferritin

📍TREATMENT OF IRON DEFICIENCY

*Therapeutic dose

-Ferrous sulphate or gluconate 300 mg TID + vitamin supplements and treatment of the cause

-Green leafy vegetables, pulses and meat products which are rich in iron

-Consumption of vitamin c rich food such as orange, guava and amla promotes iron absorption

📍IRON OVERLOAD

*Hemosiderosis – greater than normal deposition of iron within the body tissues is called hemosiderosis

*Hemochromatosis – when such deposition is associated tissue injury with total body iron more than 15g it is known as hemochromatosis.

*Clinical features:-

-Bronze pigmentation of the skin ( bronze diabetes)

-Cirrhosis of the liver

FLUORIDE

📍Fluoride is an essential element for mineralization of bones and formation of dental enamel.

📍RDA

Adults – 2.5 mg

0.5 to 0.8 mg /liter of water is a safe limit

Sources:-Drinking water, sea foods, and pulses such as red gram and bengal gram

Tea leaves, betel nut and tobacco

Absorbed fluoride – stored in bones, teeth, hair, nail and soft tissues

Small amount are excreted in sweat

Large amount of fluoride ( 2-3 ppm ) causes dental, skeletal and neurological manifestations

📍CLINICAL FEATURES

Abnormal calcification of teeth, bones, and ligaments

Dental caries mottled teeth and osteoporosis

Pruritis, urticaria, and dermatitis

Conjunctival edema and migraine like headache

SULFUR

📍Dietary thionine and cysteine are the main precursors for the synthesis of sulfur components of the body

📍Sulfur component of the amino acid methionine and cysteine which have a role in keratinization

📍Chondroitin sulfate – formation of dermal collagen

.📍Clinical features of sulfur deficiency:=

-Impaired keratinization leading to tissue paper scars and sparse fair hair

-In conditions with increased epidermopoiesis as in exfoliative psoriasis there is sulfur depletion

-Diversion of sulfur containing amino acids for the formation  of skin protein instead of hair keratin causes hair loss

IODINE

📍Iodine deficiency or excess may indirectly produce cutaneous change of hypo or hyperthyroidism

respectively by an effect on thyroid function

📍HYPOTHYROIDISM:-

-Dryness and coarseness of the skin

-Hypohidrosis

-Carotenemia

-Diffuse or partial alopecia

-Lateral superciliary madrosis ( hertog’s sign )

-Generalized myxedema

📍HYPERTHYROIDISM:-

-Warm moist feel of the skin

-Palmar erythema and telengiectasia

-Diffuse hyperpigmentation

-Hair is fine and friable

-Nails are often soft and friable

-Alopecia areata and scleromyxedema

PROTEIN ENERGY MALNUTRITION

📍Malnutrition - quantitative and qualitative deficiencies in the intake or metabolism of the nutrients resulting in inadequate body weight or developmental and physiological changes

📍Primary or Exogenous malnutrition – due to inadequate intake

📍Secondary or Endogenous malnutrition – due to malabsorbtion or defective metabolism

📍Exist in three major forms:-

1) Marasmus

2) Kwashiorkar

3) Marasmus kwashiorkar

📍MARASMUS

*Starvation - chronic nutrient deficiency

*Decreased intake of all micronutrients ( carbohydrates, protiens and fats) decreased insulin production and unopposed catabolism .

*Early gluconeogenesis is followed by fat breakdown as the body tries to preserve remaining muscle mass

*Children with marasmus weigh less than 60% of expected body weight without edema or hypoproteinemia

*DERMATOLOGICAL MANIFESTATIONS

-Loose, dry, wrinkled skin with fine scales due to

generalized loss of subcutaneous fat and muscle loss.

-Skin may be hyperpigmented

-Purpuric lesions may be seen

-Hair changes- Excess of lanugo like hair, Thin hair grows slowly and falls out easily

-Follicular hyperkeratosis and folliculitis in adults

-Nail changes- Impaired growth of nails and fissured nails

*LABORATORY INVESTIGATIONS

-Routine test like complete blood count, blood sugar levels to rule out anemia and hypoglycemia.

-Urine routine , blood smear, mantoux examination and chest x-ray to rule out infections

-Chest radiography – signs of bacterial pneumonia, tuberculosis, heart failure, rickets and fractures

-Electrolyte imbalance can complicate refeeding

*TREATMENT OF MARASMUS

-Hospitalization along with adequate protien – caloric intake

-Treat any underlying infection with broad spectrum antibiotics

-Correction of fluid and electrolyte imbalance

-Oral rehydration therapy to be initiated if diarrhea is present

-Oral refeeding is preferred

*Prognosis:-

-Decreased mortality in recent years

-10% dies due to diarrhoea or pneumonia

📍KWASHIORKAR

*Kwashiorkar also known as wet malnutrition

*At the time infants are weaned from the breast milk and shifted to a diet with inadequate protein and calorie

*Amino acid substrate inevitable for visceral protein synthesis

*Resultant hypoproteinemia – edema, diarrhoea, immuno suppression

*SKIN AND MUCOSAL CHANGES:-

-Characteristic flaky paint, crazy paving enamel paint dermatoses

-Dyschromias

-circumoral and lower extremity pallor due to distension of skin and loss of pigment.

-Thinning, erythema, petechiae, purpura and ecchymosis.

-Mucosal lesions – chelitis, xeropthalmia, and vulvovaginitis

*HAIR CHANGES:-

-Hair is sparse, dry, lusterless and brittle with a reddish tinge

-Bands of light and dark coloration ( flag sign ) reflect intermittent periods of malnutrition .

*Nail changes- Nails are soft and thin

*LABORATORY INVESTIGATIONS

-Routine test like complete blood count, blood sugar levels to rule out anemia and hypoglycemia.

-Urine r/e, blood smear, mantoux, stool examination and chest x – ray to rule out infections.

-Serum albumin level less than 2.5 g/dl

*TREATMENT

-Hospitalization to reduce the risk of hypoglycemia, hypothermia, dehydration and sepsis.

-Correction of electrolyte imbalances

-Complete and balanced diet with adequate protien and calorie intake

-Mineral and vitamin supplement

-Topical moisturizers and ointments

📍ESSENTIAL FATTY ACID DEFICIENCY

*Essential fatty acids are unsaturated fatty acids that cannot be synthesized by the body and must be obtained from the diet.

*Linoleic, linolenic and arachidonic acids are three major essential fatty acids

*FUNCTIONS-of fatty acids

-Serving as precursor to prostaglandins

-Reducing the fluidity within phospholipid membranes

-Energy storage

-Proper lamellar granule formation

*Isolated deficiency of essential fatty acids are uncommon, but can be seen in patients receiving parentral nutrition without lipid supplementation and with overtly aggressive low fat diet.

*SKIN AND MUCOSAL CHANGES:-

-Dry, scaly and leathery skin with underlying erythema

-Erosions in the intertriginous areas

-Other features include increased transepidermal water loss and petechiae

-Hair changes- Alopecia and more lightly pigmented hair

*LABORATORY INVESTIGATIONS

-Complete blood count to rule out anemia, thrombocytopenia.

-Low plasma levels of linoleic, linolenic and arachidonic acids

-Presence of 5,8,11 – icosatrienoic acid.

-Elevated levels of palmitoleic and oleic acids

*Treatment of EFA deficiency:-

Replacement of essential fatty acids