Lichenification, excoriation, and erosion or crusting on the trunk may indicate secondary infection. Flexural distribution with ill-defined edges with or without hyperlinearity on the wrist, finger knuckles, ankle, feet, and hands are also commonly seen. Causes
The cause of AD is not known, although  some evidence indicates genetic, environmental, and immunologic factors. Climate
Low humidity, and low temperature increase the prevalence and risk of flares in patients with atopic dermatitis. Genetics
Many people with AD have a family history or a personal history of atopy. Atopy is an immediate-onset allergic reaction (type-1 hypersensitivity reaction mediated by IgE) that may manifest as asthma, food allergies, AD, or hay fever. Up to 80% of people with atopic dermatitis have elevated total or allergen-specific IgE levels.About 30% of people with atopic dermatitis have mutations in the gene for the production of filaggrin (FLG), which increase the risk for early onset of atopic dermatitis and developing asthma. Hygiene hypothesis
According to the hygiene hypothesis, early childhood exposure to certain microorganisms (such as gut flora and helminth parasites) protects against allergic diseases by contributing to the development of the immune system. This exposure is limited in a modern "sanitary" environment, and the incorrectly developed immune system is prone to develop allergies to harmless substances. Some support exists for this hypothesis with respect to AD. Those exposed to dogs while growing up have a lower risk of atopic dermatitis. Also, epidemiological studies support a protective role for helminths against AD.
Likewise, children with poor hygiene are at a lower risk for developing AD, as are children who drink unpasteurized milk. Allergens
In a small percentage of cases, atopic dermatitis is caused by sensitization to foods. Also, exposure to allergens, either from food or the environment, can exacerbate existing atopic dermatitis. Exposure to dust mites, for example, is believed to contribute to ones risk of developing AD. A diet high in fruits seems to have a protective effect against AD, whereas the opposite seems true for fast foods. Atopic dermatitis sometimes appears associated with celiac disease and nonceliac gluten sensitivity, and the improvement with a gluten-free diet (GFD) indicates that gluten is a causative agent in these cases. Role of Staphylococcus aureus
Colonization of the skin by the bacterium S. aureus is extremely prevalent in those with atopic dermatitis. Abnormalities in the skin barrier of persons with AD are exploited by S. aureus to trigger cytokine expression, thus aggravating the condition. Hard water
Atopic dermatitis in children may be linked to the level of calcium carbonate or "hardness" of household water, when used to drink. So far, these findings have been supported in children from the United Kingdom, Spain, and Japan. Pathophysiology
Excessive type 2 inflammation underlies the pathophysiology of atopic dermatitis.Disruption of the epidermal barrier is thought to play an integral role in the pathogenesis of AD. Disruptions of the epidermal barrier allows allergens to penetrate the epidermis to deeper layers of the skin.