Atopic Eczema in Darker Skin: Epidemiology and Pathophysiology

00:01 Welcome to our lecture on eczema focusing mainly on atopic eczema.

00:07 So how do we classify eczema? We classify eczema into exogenous and endogenous eczema.

00:14 So this morning we're going to be talking about atopic dermatitis.

00:19 And you can see under endogenous eczema there's a whole lot of conditions.

00:24 But we'll focus on atopic eczema.

00:26 So what is atopic dermatitis or eczema.

00:29 And remember dermatitis and eczema are used synonymously.

00:34 It's a disorder of altered skin barrier integrity and immune dysregulation that presents as a chronic relapsing inflammatory skin disease.

00:43 So let's have a look at epidemiology of atopic eczema.

00:47 What is the prevalence of this condition.

00:50 It usually affects school-aged children.

00:52 And at about 17% that's the prevalence of atopic eczema.

00:58 In adults, the prevalence ranges from 2 to 10%.

01:03 So when we talk about the atopic triad, which occurs in about 30 to 50% of patients.

01:09 We're referring to the combination of atopic dermatitis, allergic rhinitis and asthma.

01:15 30% of patients develop asthma.

01:18 So what's the pathophysiology of atopic eczema? Well it's a combination of factors: genetic, environmental, immunologic as well as a dysfunction of the epidermal barrier.

01:34 So all of those four contribute to the development of atopic dermatitis.

01:39 As mentioned it's multifactorial in terms of etiology.

01:43 And listed there are the genetic factors, the environmental factors which include changes in the environment which can trigger further disruption of the skin barrier.

01:56 The microbiome is also another factor that has been talked about recently.

02:00 And of course, the immune factors that we've spoken about.

02:05 So the likely mechanism of how the environmental affects the environment, excuse me affects the organisms.

02:12 Cells are epigenetic changes.

02:15 And if we look at this diagram over here, you see on the left the list of all the epigenetic factors that impact on the DNA and eventually lead to the phenotype or the clinical presentation of atopic eczema. What about atopic dermatitis and food allergy? Is there a link? Can food trigger allergy? So we know that consistently, evidence has been found to show that a relationship between food allergy and atopic dermatitis in some children and up to 30% of children with severe atopic dermatitis experience IgE-mediated food allergy.

02:54 It's important that we confirm a allergy with a food challenge test before advising a restrictive diet, which could be harmful for the patient.

03:05 Actually, do remember that a couple of years ago, I had a young child who was about 3 or 4 years old, who was literally malnourished because the mother excluded all types of food because of the fear of creating or triggering allergies.

03:20 So it's very important that we teach our patients about this.

03:24 So younger children with atopic dermatitis frequently show sensitization to egg, milk or peanut, while older ones and adults are more often sensitized to environmental allergens such as house dust mite, molds and dander or pollens.

03:42 We mentioned the barrier dysfunction in patients with atopic dermatitis.

03:46 So if we focus on the barrier disturbance, it really plays a main role in the development of sensitization and allergy and newborn skincare with emollients and early introduction of food may actually help this particular trigger.

04:05 The three main phenotypes of food allergy in atopic dermatitis are immediate, delayed and mixed. Breastfeeding and introduction of solid foods at four months with hydrolyzed milk has been shown to prevent or minimize food allergy.

04:23 And of course, probiotics and vitamin D may be beneficial in patients with atopic eczema.

04:30 So if we look at the etiology of atopic eczema, again emphasizing the pathogenesis of atopic dermatitis as being multifactorial, involving genetic susceptibility, skin barrier dysfunction and inflammation, as well as microbial dysbiosis.

04:49 We do know that the costs of the disease can be modified by external exposures that interact with the above pathogenic pathways, and the biological response to such exposures is termed an individual's exposome.

05:03 So as we mentioned, it's multifactorial and not completely understood.

05:09 So if we look at genetics there's usually a family history of Atopy and Filaggrin.

05:15 Gene also has been mentioned as a contributing factor in the pathogenesis of atopic eczema.

05:25 Again looking at etiology, the second aspect being the immune defects, more so in the Th2 disease focusing on the T helper cells.

05:35 So we know that eczema is associated with predominance of Th2 immune responses and characterized by the release of cytokines such as 4, 5 and 13. And these cytokines promote allergic inflammation and IgE production.

05:53 So you do also find elevated cord blood IgE levels at birth.

05:58 And these are associated with an increased risk of developing eczema in infants.

06:03 So these are the prenatal factors that can also contribute to the etiology of atopic eczema.

06:09 As mentioned early childhood exposure to microbes and allergens may actually prevent atopy.

06:17 Now let's look at the pathogenesis and pathophysiology of atopic eczema.

06:21 So this is what happens. The inflammation disrupts the normal architecture of the epidermis causing swelling and separation of skin cells.

06:31 This swelling is often described as spongiosis or epidermal edema.

06:36 Spongiosis or epidermal edema contributes to the characteristic redness, swelling and itching that is seen in eczema lesions.

06:45 So as the fluid accumulates within the epidermis, it exerts pressure on the cells, leading to the breaking of intercellular attachments.

06:55 This disruption of cell to cell adhesion results in the formation of vesicles, which are small, fluid filled blisters that may be visible on the surface of the skin in eczema lesions. These vesicles can rupture, leading to oozing, crusting, and further inflammation.

07:14 All of these changes are also followed by an inflammatory response involving various inflammatory cells. In the dermis, the deeper layer of the skin, there is often an infiltration of lymphocytes.

07:27 As mentioned these are particularly the T cells.

07:31 So that's all about pathophysiology.

07:34 I hope that will help you understand the clinical presentation which is the next step of our discussion.