Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically. It may be accompanied by asthma or hay fever.

1. Atopic dermatitis

2. Atopic dermatitis
 Atopic dermatitis (AD) is a pruritic disease of unknown origin that usually starts in
early infancy (an adult-onset variant is recognized); it is characterized by pruritus,
eczematous lesions, xerosis (dry skin), and lichenification (thickening of the skin
and an increase in skin markings)
 AD may be associated with other atopic (immunoglobulin E [IgE]–associated)
diseases (eg, acute allergic reaction to foods, asthma, urticaria, and allergic
rhinitis

4.  AD is basically the inflammation of the skin due to allergic reaction, when
the immune system attacks the skin causing dry skin rashes ,which are
common among small children
 The skin rashes are found on the flexor surfaces of the body such as –
creases of the wrists, insides of the elbows, backs of knees
 It is due to TYPE 1 HYPERSENSITIVITY REACTION
1. Sensitization
2. Re- exposure

5. CASE STUDY
• Tom was admitted to hospital when he was 2 years old , because of his worsening
ECZEMA , in the week before admission he had developed many open skin
lesions(erosion) of the skin . Lesions oozed a clear fluid , which formed crust
around them. Tom had suffered from eczema since the age of two months when
he developed a scalyred rash over his cheeks, knees and his elbows . He was breast
fed until 3 months old, when he was given cows milk based formula . After 24
hours on the formula he started to vomit and to scratch his skin. A case in
hyrolyzate formula was substituted for milk and he tolerated this well but as new
foods were added to his diet the eczema worsened. At 9 months old he developed a
wheeze and was treated with bronchodilators. At 2 years old he had hives after
eating peanut butter. Toms mother suffers from hays fever and his father has atopic
dermatitis.The family lives in an old house. Tom slept on a 10 year old mattress
surrouned with lot of stuffed animals.

6. • Tom was evidently uncomfortable and scratched his skin continuously. His
temperature was 37.9 * C, pulse 96 beats per min , respiratory rate 24 per
min blood pressure 98/58mmHg weight 12kg , height 12cm .He was very
red, with large scales and with scratched and infected lesions on his face
trunkand extremities. Pustules were present on his arms and legs. There were
thick scales on his scalp , thickened plaques of skin( lichenification) with a
deep criss cross pattern were seen around the creases on the inside of his
elbows, knees and on his back of hand and feet. A skin culture was posiyive
for staphylococcus aureus and streptococcus pyrogenes group A .Tom was
treated with intravenous oxacillin, anti histamine, topical steroid . The
infection resolved and his skin heeled. The laboratory study during
hospitalization revealed wbc count of 9600 with 41% PMN leukocytes , 26%
lymphocytes and 25% eosinophil ( normal 0-5%), 13.1g/dl Hb and
haematocrit of 37.2%.

8. Epidemiology
 The prevalence rate for atopic dermatitis (AD) is 10-12% in children and 0.9%
in adults (US)
 The prevalence rate of AD is rising, and AD affects 15-30% of children and
2-10% of adults (international) The frequency is increased in patients who
immigrate to developed countries from underdeveloped countries.
 The male-to-female ratio for AD is 1:1.4.
 In 85% of cases, AD occurs in the first year of life; in 95% of cases, it occurs
before age 5 years. The incidence of AD is highest in early infancy and
childhood.

9. CAUSES
• Genetic
• A family history of atopic dermatitis (AD) is common. The strongest
known genetic risk factor for developing AD is the presence of a
loss-of-function mutation in filaggrin(helps in water retention).
These genes encodes proteins involved in epidermal proliferation
and differentiation or inflammatory cytokines.

10. Infection
 The skin of patients with AD is colonized by S. aureus. Clinical
infection with S aureus often causes a flare of AD, and S
aureus has been proposed as a cause of AD by acting as a
superantigen. Similarly, superinfection with herpes simplex
virus can also lead to a flare of disease and a condition
referred to as eczema herpeticum.

11. Aero Allergens
An aeroallergen (pronounced aer·o·al·ler·gen) is
any airborne substance, such as pollen or spores, which triggers
an allergic reaction.

13. Pathophysiology
Two main hypotheses have been proposed regarding the
development of inflammation that leads to AD. The first suggests a
primary immune dysfunction resulting in IgE sensitization, allergic
inflammation, and a secondary epithelial barrier disturbance. The
second proposes a primary defect in the epithelial barrier leading to
secondary immunologic dysregulation and resulting in inflammation.

14.  In healthy individuals, balance exists between important subsets of T cells (eg, Th1,
Th2, Th17, Th22). The primary immune dysfunction hypothesis invokes an imbalance
in the T cell subsets, with Th2 cells predominating; this results in the production of type
2 cytokines such as interleukin (IL)–4, IL-5, and IL-13, causing an increase in IgE from
plasma cells. Later, in persons with chronic AD, the Th1 cells have been shown to
predominate. More recently, Th17 cells have been found to be elevated in patients with
AD.Although primarily considered a Th2 cell‒associated cytokine-mediated disease,
the precise contributions of Th1 and Th17 cell responses remain to be fully define
 In addition to the role of T and B cells in AD, other innate immune cells have also been
implicated in the pathogenesis of AD, including eosinophils and mast cells. More
recently, basophils and newly identified innate immune cells called group 2 innate
lymphoid cells (ILC2s) have been shown to underlie the pathogenesis of AD. Together,
basophils and ILC2s are critical sources of the type 2 cytokines IL-4, IL-5, and IL-13. -
derived cytokines.

15.  Further, these cells appear to be potently regulated by a family of epithelial
cell‒derived cytokines directly released from damaged keratinocytes, including thymic
stromal lymphopoietin (TSLP), IL-25, and IL-33. Taken together, these studies
highlight a new paradigm in which, in addition to classical adaptive Th2 cells, innate
type 2 immune cells play critical roles in the etiology of AD through interactions with
epidermal
 The epidermal barrier dysfunction hypothesis suggests that AD patients develop AD
as a result of skin barrier defects that allow for the entry of antigens, resulting in the
production of inflammatory cytokines

16. SIGNS AND SYMPTOMS
• Erythema
• Crusted lesions on the face neck
• Erythematous macules that lichenifies with scratching
• Swelling
• Pruritis
• Weeping clear fluid
• Dry and itchy skin

17. Treatment
 There is no cure for AD
 Lifestyle changes –avoid soaps ,avoid allergy triggers
 Skin care –use oil based moisturisers
 Medications -such as oral corticosteroids or antihistamines, are taken as
pills, use of anti-inflammatory drugs