integumentary system disease: part 1 · integumentary system disease: part i o principles and...

© Endeavour College of Natural Health endeavour.edu.au 1

NMDC221 Session 22:

Integumentary System Disease

Part I


Topic Summary

Integumentary System Disease: Part I

o Principles and considerations in nutritional medicine

management of the integumentary system

o Review anatomy & physiology of the integumentary

system

Nutritional management & consideration of drug-nutrient

interactions for:

o Eczema & Dermatitis


Integumentary System



o The integument (skin) is the largest organ of the body

when including its epidermal structures (nails, hair) it

constitutes the integumentary system

o It accommodates for protective and metabolic functions

in certain areas of the body

o Assists in homeostasis

(Tortora & Derrickson, 2009,p.170; Davidson & Haslett

2002,p.878)



Functions

o Protects the body from disease and personal injury

o Regulation of Body Fluids and Temperature

o Cutaneous Absorption

o Synthesis

o Sensory Reception

o Communication

o Vitamin D synthesis

(Tortora & Derrickson, 2009,p.170; Davidson & Haslett

2002,p.878)


Nutrient Dosage Therapeutic Actions

Vitamin A

Beta-carotene

5,000-

10,000iu (up

to 20,000iu)

15-30mg

Antioxidant, photo-protective agent, immuno-

protective agent. Required for appropriate cell

differentiation, growth and development of epithelium

and keratin formation

Vitamin B1

Vitamin B3

Vitamin B5

Vitamin B6

50-200mg

100-200mg

50-500mg

50-200mg

Deficiency presents with skin lesions

Deficiency presents with skin peeling

Cofactor of CoA, aids wound healing

Alters PG species lines

Vitamin C 500-5000mg Combined with iron hydroxylate lysine and proline in

collagen formation. Antioxidant.

Vitamin E 100-1000iu Stabilize cell membranes, inhibits lipid peroxidation,

anti-inflammatory (LOX)

Nutrients for the Integumentary System

(Osiecki 7thed,p.3; Kohlmeier,2003,p.465; Mahan & Escott-Stump,2012,p.59)




Lysine

Proline

Cysteine

500-3,000mg

500-2,000mg

200-500mg

Main structural amino acid components of collagen and

elastin

Biotin 0.5-15mg Combined with CoA is involved in the synthesis of amino

acids

Omega 3 1,000-5,000mg Deficiency presents in scaling and loss of cell

membrane integrity resulting in water loss. Anti-

inflammatory action

Copper 2-5mg Nutrient

Iron 15-80mg Combined with ascorbic acid hydroxylate lysine and

proline in collagen formation. Supports immune system

function.

(Osiecki 7thed,p.103,109; Kohlmeier,2003,p.350,356,404; Schlenker & Long, 2007;

Braun & Cohen,2010,p.677; Mahan & Escott-Stump,2012,p.41)




Manganese 2-20mg Required for the activation of prolidase, stimulating the

utilization of proline, for collagen formation in human skin

cells.

Silica 20-30mg Deficient states present with reduced formation of collagen

and poor wound healing. Aid in eosinophil formation

Zinc 20-

100mg

Required for utilization of EFAs, inhibit lipid peroxidation,

immune system modulation, high concentrations present in

the epidermis.

(Osiecki 7thed,p.161; Muszyska et al. 2001; Seaborn & Nielsen, 2002; Mahan & Escott-

Stump,2012,p.111)



Vitamin C

o Vitamin C stimulates collagen synthesis and increases

healing (500-1000mg) with rapid use at wound sites.

o Oral vitamin C reduces lipid peroxidation and quashing

reactive oxygen species.

o Topical vitamin C protects from photo-oxidation

(Coulston, 2001)


Integumentary SystemVitamin C

NF-kB plus AP-1 ratio play a key role in determining cell

survival or death after oxidative stress

UV-A irradiated cells respond to oxidative stress by

enhancing NF-kB binding activity.

Vitamin C exerts positive modulatory effects by

synergistically enhancing NF-kB activation in irradiated

keratinocytes

The ability of keratinocytes to accumulate Vitamin C can

prevent two effects of UV-B exposure:

o The increase of peroxide levels

o The induction of cell death

(Catani et al, 2005)



o “Human keratinocytes possess efficient systems to

maintain intracellular high levels of Vitamin C.

Keratinocytes transport inside the cytoplasm both the

reduced and oxidised form of Vitamin C and recycle the

reduced form through specific enzymatic systems. The

efficiency of systems involved in Vitamin C maintenance

is crucial to ameliorate the intracellular antioxidant state

in the skin” (Catani et al, 2005)


The role of Vitamin C in keratinocytes to

counteract oxidative stress

1. Act directly by scavenging ROS generated by several

stresses

2. Prevent ROS mediated cell damage by modulating

gene expression

3. Regulate the commitment to keratinocytes

differentiation maintaining a balanced redox state

4. Promote cell cycle arrest and apoptosis in response to

DNA damage

(Catani et al, 2005)



Digestive Tract Dysfunction

o Research suggests a link between low stomach acid and

skin conditions with hypochlorhydria occurring in up to

87% of acne rosacea and 74% of eczema cases.

(Osiecki 2004,p.637)

o In vivo research found an inverse relationship between

low CYP2C activity, an isozyme of hepatic cytochrome

P450, and psoriasis. (Helsby et al. 1998)

o Phase II detoxification also plays a role in deactivating

allergen metabolites and increasing their excretion.

(Lutz et al. 2001)


Eczema & Dermatitis


Eczema / Dermatitis

Dermatitis is defined as inflammation of the dermal layer.

Eczema is derived from the Greek word meaning ‘boiling’.

This refers to the presentation of inflammation and weeping

of the skin.

These words are used interchangeably.

Dermatitis can be classified into;

o Eczematous (eczema)

o Non-eczematous (contact).

An assigned prefix denotes the perceived cause.

(Bennett, 1999; Kumar & Clark,2009,p.1282)


Eczema / Dermatitis

Eczema / Dermatitis is characterized by;

o Redness, heat and inflammation.

o Pruritis with potential excoriation. Chronic scratching

leads to secondary thickening of the skin (lichenification).

o Oedema in the acute stages which separates the

keratinocyte (spongiosis) producing intradermal vesicles.

o Oozing with / without vesicles. Initially there may be

crusting followed by scaling & fissuring in chronic stages.

o Increased potential for secondary infection.

(Kumar & Clark 2009,p.1282)


Eczema/Dermatitis

Presentation With Age

o Infantile Eczema: erythema, weeping or scaling around

the mouth & cheeks when the infant is a few months old

o Flexural / childhood eczema: facial eczema may persist

with presentation in skin folds of toddlers & older

children. Climatic factors exacerbate (sunlight, low

humidity).

o Adult eczema: continuation into adult life may involve the

flexures at the neck, elbow, wrist, ankle or knee and

possibly the limbs. Chronic eczematous changes are

common on the face, though any site may be involved.

(Kumar & Clark, 2009,p.1282)


Eczema/Dermatitis

Atopic Endogenous Eczema

o Atopy is a predisposition to form allergen induced Th2

characterized by raised levels of IL-4 and IgE. This leads

to a generalized and prolonged hypersensitivity.

o Atopic individuals manifest one or more of a group of

diseases that includes asthma, hay fever, Urticaria, food

& other allergies, and eczema

o These atopic conditions tend to run true to type within

each family.

(Davidson & Haslett 2002)


Eczema/Dermatitis

o Atopic eczema is an intrinsic hyper-reactivity to common

environmental factors, genetic predispositions or even a

potential for defective skin barrier function.

(Leung et al. 2004)

o May be caused by CD4-type T Helper 2 cells infiltrating

the skin and producing certain cytokines: IL-2 & IL-4 and

Interferon-gamma. Serum levels of IgE are raised.

(Kumar & Clark, 2009,p.1283; Ahuja, Land & Barnes 2003)


Eczema/Dermatitis

o Reduced hypothalamic-pituitary-adrenal (HPA) axis

responsiveness has been found to present.

(Buske-Kirschbaum & Hellhammer 2003).

o Psychological stress increases eosinophils, while

reducing cortisol levels in atopic eczema patients,

compared to healthy controls. (Raap et al. 2003)

o Research has examined the role of food allergy, e.g.

cow's milk and hen's eggs, and inhaled allergens.

(Werfel & Breuer 2004).


Eczema/Dermatitis

Atopic Eczema is characterized by the presentation of itchy

skin and at least 3 of the following:

o History of itch in skin creases (or cheeks if < 4 years)

o History of asthma/hay fever (or in first degree relative if <

4years). Atopy presenting in one or both parents

predisposes the infant to a greater chance of

presentation (20-50%)

o Dry skin (xeroderma)

o Visible flexural eczema (cheeks, forehead, outer limbs if

<4 years)

o Onset in first 2 years of life.

(Davidson & Haslett 2002)


Eczema/Dermatitis

Vitamin C & Vitamin E

o A study found a small positive association between

maternal vitamin C intake during pregnancy and atopic

eczema in the 2nd year of life

o The same study found that maternal vitamin E intake

was negatively associated with eczema in the second

year

(Sheelagh et al, 2005)


Eczema/DermatitisMaternal Diet

o A maternal diet during pregancy that had healthy

amounts of green and yellow vegetables, citrus fruit, and

β-carotene this may afford some protection against the

development of eczema in the infant.

o Conversely excessively high intakes of n-6 PUFA,

especially linoleic acid, during pregnancy may increase

the risk of childhood eczema

o Maternal intake of vitamin E, α-linolenic acid and

docosahexaenoic acid intake during pregnancy reduced

the chances of the development of infantile wheeze.

(Miyake et al. 2009, 820; Miyake et al. 2010, pp. 758, 764)


Eczema/Dermatitis

Fish

o “Children's consumption of fish during the first year of life

was more important than maternal consumption of fish

during pregnancy in preventing eczema at 2 years of

age.”

(Øien et al. 2010, p.124)

Food Intolerance Triggers

o Kojima et al. 2003 found that “T-cells, especially those

expressing CLA, play an important role in food-induced

atopic eczema…hen’s egg is the most common cause of

food-related AD in early childhood” (p. 537)


Eczema/Dermatitis

Food Additives and sensitives:-

Low Histamine Diet

o Removal of histamine foods from the diet Atopic eczema

(AE) patients led to a regeneration of the diaminoxidase-

producing jejunal enterocytes and therefore an increase

of enzyme activity.

o After two weeks on a histamine-free diet, participants

were challenged with histamine rich food.

o The participants “…reported an aggravation of eczema

as well as development of systemic reactions like flush,

headache, or dizziness…” (Maintz et al, 2006, p. 1110).


Vaso-active amines Salicylates

Meat, poultry and seafood

All cured meat especially pork products e.g.

ham, salami, pepperoni, game, bacon,

sausages, fresh pork, fresh or canned tuna,

canned sardines, anchovies, mackerel,

salmon, herring, processed fish products

(fish pastes, smoked, dried or pickled fish),

fish sauce

Milk and eggsBlue cheese, parmesan, brie, camembert,

emmenthal, old gouda, cheddar cheese and

other hard cheeses

FruitsOranges, bananas, tangerines, pineapple,

grapes, strawberries

Granny smith apples, cherries, strawberries,

currants, raisins, kiwi, Gala melon, peaches

and nectarines, raspberries

Vegetables, nuts, seeds

and savoury snacksTomatoes, pickled cabbage, aubergine,

spinach, broad beans, peanuts, tree nuts

Asparagus, sweet corn, raw tomatoes,

tomato puree

Condiments and

miscellaneousFermented soy products including miso and

tempeh

Ginger, mixed herbs, mustard, oregano,

curry powder, black pepper, cardamom

pods, cinnamon, cumin, fenugreek, mint,

nutmeg, paprika, rosemary, thyme, turmeric,

liquorice, peppermint, Worcestershire

sauce, honey, tomato ketchup

DrinksGreen tea, champagne, coffee, cocoa,

chocolate, wine, beer, fresh fruit juices,

smoothies

Coffee, pineapple juice, cider, Benedictine

liqueur, lemon tea, black tea, apple juice,

cranberry juice, orange juice, tomato juice,

fizzy drinks, Drambui liqueur, wine, rum

(Skypala I, Williams M, Reeves L 2015)

Foods likely to contain high levels of vasoactive amines and salicylates


Eczema/Dermatitis

Discord/Nummular Eczema

o Presentation of irritant vesicles, demarcated scaly

patches that form plaques.

o Commonly affects the sides of the fingers, palms, the

toes or soles of the feet.

o Common in adults

o May be atopic/ non-atopic

o Staphyloccocus aureus infection commonly presents.

(Kumar & Clark,2009,p.1285)


Eczema/Dermatitis

Seborrheic Eczema

o This condition is characterized by a red scaly rash and

inflammation (with little itch present).

o Overgrowths of Pityrosporum ovale yeast produces

inflammation and scaling in areas that are rich in

sebaceous glands. These include the scalp (dandruff),

central face, naso-labial folds, eyebrows and central

chest.

o An infantile form presents as ‘cradle cap.’ This may also

present on the torso and around the nappy area.

(Kumar & Clark,2009,p.1262; Davidson & Haslett, 2002)


Seborrhoeic eczema

Seborrheic eczema, viewed 23rd Oct 2007

http://health.yahoo.com/media/mayoclinic/images/image_popup/ans

7_seb_dermatitis.jpg


Eczema / Dermatitis Exogenous Eczema

Localized or unusual eczema presentation.

This may occur through;

o Direct irritation

o Allergic reaction (type IV hypersensitivity reaction)

Usually no personal or familial history of atopic disease.

( Kumar & Clark,2009,p.1286)


Eczema / Dermatitis

Allergic contact

o Occurs through exposure to an irritant / chemical that

stimulates a cell mediated allergic immune reaction.

o T – lymphocytes are sensitized to the antigen some time

after the first contact. Langerhans cells in the dermis of

the skin present the Ag to T – lymphocytes. Sensitivity to

the antigen lasts for life. Second exposure stimulates a

magnified reaction.

(Kumar & Clark,2009,p.1286)


Eczema / Dermatitis

Characteristics include;

o Intense pruritus (excoriation with scratching),

inflammation, heat, swelling.

o Pattern and distribution are suggestive of direct contact.

Ongoing irritation can see the symptoms spread.

Common irritants in allergic contact dermatitis include;

o Nickel (jewellery), Chromate (cement), Latex, Perfume,

Specific species of plants

(McKoy, 2009)


Eczema/ Dermatitis

Irritant contact

o Non-specific inflammatory reaction that occurs after

repeated exposure to an irritant. There is no immune

system activation.

Characteristics include;

o Pain and inflammation with mild pruritus.

o There may be mild erythema to haemorrhage, crusting,

erosion, pustules, bullae, and oedema.

Common irritants include;

o Chemicals, soaps, plants, body fluid.

(McKoy, 2009)


Eczema/ Dermatitis

Investigations

o Presentation of an unusual pattern of rash with clear-cut

demarcation or odd- shaped areas of erythema &

scaling.

o Exploration of history especially environmental changes

and the timing of those changes may indicate a cause.

o Skin patch test: back is most commonly used. Tested

substance is left on for 24 hours, removed & underlying

skin is examined.

o Causative agent may not be clearly defined.

(Kumar & Clark,2009,p1286; McKoy, 2009)


Eczema/Dermatitis

Drug Risk Factors: Paracetamol

o Studies found that eczema rates were higher than

normal in 6-7 year olds that had no previous medical

history of asthma or rhino-conjunctivitis that had

paracetamol in their first year of life. This was thought to

reduce glutathione levels.

o Lowered glutathione is linked to chronic inflammation.

The healthy skin of eczema patients commonly presents

with chronic inflammatory markers = increased

cutaneous antioxidant defense levels

o Low glutathione favours a Th2 allergic pathway when an

allergen presents that sustains this reaction.

(Garcia-Marcos et al. 2010, p. 1040).


Eczema/Dermatitis

Drug Risk Factors: Antibiotics

o Antibiotics taken in the first year of life is associated with

eczema presentation in 6-7 year old children with no

prior history of asthma or rhino-conjunctivitis.

(Garcia-Marcos et al. 2010, p. 1040)

o Children that had been in contact with antibiotics by 6

months old presented more frequently with flexural

eczema (Callard et al. 2002, p. 991)

o The “hygiene hypothesis” put forward for this is that gut

flora disruption causes an imbalance in Th1/Th2 and a

subsequent Th2 dominance

(Garcia-Marcos et al. 2010, p. 1040)


Eczema/Dermatitis

Treatment Aims

o Identify & remove risk factors and triggers (allergens,

environment)

o Reduce inflammation in the skin

o Improve hydrochloric acid secretion

o Balance gut microbiome status

o Rebalance and regulate blood sugar levels

o Minimizing over heating of the skin

o Wearing cotton clothes

o Maintain hydration and moisture of the skin

(Stollery, 2007; Kumar & Clark,2009,p.1286; Sarris &

Wardle,2010,p.479)


Eczema/Dermatitis


Glutathione

Cysteine

Glutamine

Glycine

100-500mg

200-500mg

500-3000mg

4-30gm

Glutathione is able to stop the production of

cytokines when they are being produced in the

excessive amounts. Assists within liver phase 1

and 2 detoxification pathways.

Alpha

Linolenic Acid

(Omega 3)

1000-6000mg Alpha-Linolenic Acid (LNA) suppresses the

inflammatory response. This is due to its action on

enhancing PGE 3 response thereby down

regulating PGE 2 production. High PGE2 stimulate

mast cell hyper-excitability

Vitamin E 100-1000iu Due to its action as an antioxidant of lipid

peroxides or alternatively in diminishing PGE 2

activity.

(Coulston 2003; Jamison 2003; Pizzorno & Murray 2006,p.1093; Sarris & Wardle,2010,p.545)


Eczema/Dermatitis


Vitamin A 5000-10000iu Antioxidant, deficiency presents with increases in

the severity of atopic eczema.

Vitamin C 500-5,000mg Antioxidant, Collagen repair, stabilizing mast cell

hyper-excitability

Zinc 10-100mg Collagen Repair, enhances antioxidant activity

rebalances Th2 dominance

Lysine 300-3000mg Collagen Repair

Proline 500-1000mg Collagen Repair

Lactobacillus

rhamnosus

10-40 Billion Maternally from 36 weeks to post natal for 2 years

is linked to reduced presentation of atopy in

genetically predisposed individuals

(Wickens et al. 2008; Gropper et al. 2009,p.488; Sarris &Wardle, 2010,p.474)


Eczema/Dermatitis

Drug Action Side Effects Interaction

Topical

Corticosteroids:

hydrocortisone,

methyl-

prednisolone,

betamethasone.

Anti-

inflammatory,

antipruritic,

immuno-

suppressant

action.

Skin atrophy, striae,

burning, dryness,

itching, loss of

pigmentation,

hirsutism, folliculitis.

Proportion is

systemically

absorbed

(dependent on the

size of area and the

frequency of

application) which

may result cortisol

excess symptoms.

Aloe vera: beneficial in

combination.

Green tea: concurrent

consumption has

presented with significant

skin lesion healing

Zinc & Biotin:

Co-administration of oral

doses have seen

reduced requirements for

topical applications of

corticosteroids.

(Stargrove et al, 2008,p.635; Bryant & Knight,2011,p.862)


Eczema/Dermatitis

Drug Action Side Effects Interaction

Vitamin A

Analogue:

Alitretinoin

Topical retinoid

that binds to and

then stimulates

intracellular

retinoid

receptors. Anti-

inflammatory

and immuno-

modulatory

effects.

Skin irritation

– burning,

itching & heat.

Alitretinoin

CYP3A4 Inhibitors

Alitretinoin is metabolised by

cytochrome P450 3A4, so CYP3A4

inhibitors (grapefruit juice) can raise

plasma levels of alitretinoin.

Vitamin A

Patients should not take vitamin A

supplements or other retinoids while

being treated with alitretinoin, to avoid

the risk of hypervitaminosis A.

(Kumar & Clark, 2009)


Eczema/Dermatitis

Drug Action Side Effects Interactions

Rituximab Antibody that destroys B

cells that have a specific

protein (CD20) on their

surfaces. Utilized in

conditions with overactive

or malfunctioning B cells.

Up to half of clients

experience fever.

Less commonly chills,

headache and

abdominal pain.

Severe side effects of

alterations of blood

levels of neutrophils,

white blood cells and

red blood cells.

None listed

(Hosli et al. 2008, p. 126)


Eczema/Dermatitis

Other Topical Preparations

o Oatmeal baths to reduce itching

o Bath oils/ soap substitutes

o Emollients – changes in skin moisture reduces the

barrier function and allowing triggers and allergens to

penetrate the skin. Dry skin can increase itching which in

turn creates physical damage. Can potentially reduce the

requirement for corticosteroids

o Emollients can be used as soap alternatives.

o Occlusive treatment can be used if the site is wet,

exuding or inflamed. (Bennett, 1999)


Class Discussion

6 year old boy

Presenting symptoms

o Eczema present in the creases of the elbows, knees,

ankles and webbing of the fingers. Eczema presents as

red, dry, slightly raised and weeping in the folds.

o It is very itchy and the child has been scratching it. He says

that it is far worse after a bath and in bed.

o Initially presented at 6 months old – the eczema was milder

and presented as a diffuse dry rash

o Was contained with steroid cream and oil additive in the

bathwater.

o Has flared up recently. Boy has started at a new school.


Discussion

Medications / Supplements

o Hydrocortisone cream 1%

o Ego QV bath oil – fragrance free

Family History

o Mother: eczema, asthma as a child

o Father: eczema, nervous disposition

Past Medical History

o Infant: Natural birth, breastfed until 15 months old. Food

was introduced at 5 months. Fully vaccinated.


Discussion

System Presentation

o Immune: Ran a high fever (39.5ºC) when he was 5.5

months old. It lasted for 6 hours. Was given Panadol &

the fever improved. There was no skin rash or URTI

symptoms.

o Has had a cold 4-5 times. Gets over them quickly, within

2-3 days. Only runny noses.

o GIT: craves fresh fruit: strawberries, oranges, rock

melon. Also craves dried fruits: dates, sultanas, figs.

Eats a varied diet.


Discussion

Physical Examination Results

o Nails: pink, good capillary return, all fingers have moons,

white spots present on 2 fingers, soft, peel easily

o Skin: elbows & heels dry

o Tongue: pale & flabby, white coat, central crack, quiver

o Appearance: slim build, slightly agitated and fidgety

o Height: 98cm Weight: 20.5kg


Discussion

Time Daily Dietary Intake

7am Muesli topped with fresh banana & yoghurt (pot set). Milk added.

10am Box sultanas

Rice crackers – cheese flavoured

12.30pm Vegetable pastie & tomato sauce

Apple

Orange juice

3.15pm Cheese & tomato sandwich (multigrain)

6pm Beef lasagne: beef, tomato, onion, mushroom, zucchini

Water: 500ml


Group Discussion

o Cover the development of complementary diagnosis and

formulation of goals, application of goals to specific

actions, identifying the nutrients related to each action,

and developing a nutritional prescription.

o Consider individual nutrient dosage with clinical

decisions, integrative management of each condition

giving mechanisms of actions relevant for nutrient-drug

interactions.

o Discuss findings in the class with critical discussion.


References

o Ahuja A, Land K, & Barnes CJ 2003, ‘Atopic dermatitis.’ South medical

journal, Vol. 96, No. 11, pp. 1068-1072 Viewed 23/03/11:

http://www.ncbi.nlm.nih.gov/pubmed/14632353

o Alan, C & Clemetson, B 1980, ‘Histamine and ascorbic acid in human

blood.’ The Journal of nutrition, Vol. 110, No. 4, pp. 662-668. Viewed

23/03/11: http://jn.nutrition.org/content/110/4/662.full.pdf+html

o Bennett, A 1999, Managing eczema and dermatitis.’ Nursing standard. Vol.

13. no. 42, pp. 67-72. Viewed 23/03/11:

http://proquest.umi.com.ezp01.library.qut.edu.au/pqdweb?index=0&did=436

50911&SrchMode=1&sid=1&Fmt=6&VInst=PROD&VType=PQD&RQT=309

&VName=PQD&TS=1300694374&clientId=14394

o Braun L, Cohen M. 2010. Herbs and Natural Supplements, An Evidence-

based Guide, 3rd ed. Churchill Livingstone Elsevier

o Bryant B & Knights K 2O11, Pharmacology for Health Professionals. 3RD ed.

Mosby Elsevier Australia

http://www.ncbi.nlm.nih.gov/pubmed/14632353


References

o Buske-Kirschbaum, A. & Hellhammer, D.H. 2003, ‘Endocrine and immune

responses to stress in chronic inflammatory skin disorders’, Annuals of the

New York academy of science, Vol. 992, pp. 231-240.

o Callard, RE Hamvas, R Chatterton, C Blanco, C Pembrey, M Jones, R

Sherriff, A & Henderson, J 2002, ‘An interaction between the IL-4Rα gene

and infection is associated with atopic eczema in young children.’ Clinical

and experimental allergy, Vol 32, No. 7, pp. 990-993. Viewed 23/03/11:

http://onlinelibrary.wiley.com.ezp01.library.qut.edu.au/doi/10.1046/j.1365-

2222.2002.01414.x/full

o Catani MV 2005, ‘Biological role of vitamin C in keratinocytes.’ Nutrition

Reviews Washington, Vol. 63, No. 3; pp. 81-90.


References

o Clark, C 2009, ‘New treatment for patients with chronic hand eczema.’

Clinical dermatology, Vol. 25, No. 1, pp. 6.Viewed 23/03/11:

http://find.galegroup.com.ezp01.library.qut.edu.au/gtx/retrieve.do?contentSe

t=IAC-

Documents&resultListType=RESULT_LIST&qrySerId=Locale%28en%2CUS

%2C%29%3AFQE%3D%28ti%2CNone%2C52%29New+treatment+for+pati

ents+with+chronic+hand+eczema+%3AAnd%3AFQE%3D%28da%2CNone

%2C4%292009%3AAnd%3AFQE%3D%28iu%2CNone%2C1%291%3AAnd

%3AFQE%3D%28pu%2CNone%2C20%29Clinical+Dermatology%3AAnd%

3AFQE%3D%28vo%2CNone%2C2%2925%24&sgHitCountType=None&in

PS=true&sort=DateDescend&searchType=AdvancedSearchForm&tabID=T

002&prodId=HRCA&searchId=R1&currentPosition=1&userGroupName=qut

&docId=A202706132&docType=IAC


References

o Coulston, A Rock, C Monsen, E 2001, Nutrition in the Prevention and

Treatment of Disease, Academic Pree, London.

o Davidson, S Haslett, C 2002, Davidson’s Principles and Practice of

Medicine, 19th ed, Churchill Livingstone, United States.

o Garcia-Marcos L, Gonzalez-Dıaz C, Garvajal-Uruen AL, Pac-Sa MR,

Busquets-Monge RM, Suarez-Varela MM, Batlles-Garrido J, Blanco-Quiros

A, Varela A LS, Garcıa-Hernandez G, Aguinaga-Ontoso I. 2010, ‘Early

exposure to paracetamol or to antibiotics and eczema at school age:

modification by asthma and rhino conjunctivitis.’ Pediatric allergy and

immunology, Vol. 21, pp. 1036–1042.

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