Atopic dermatitis (AD) or eczema is a chronic inflammatory itchy skin disease which starts early in life. Genetics, barrier function, immunity, and environmental factors all play key roles in the development of AD. Although genetics is a risk factor, the increase of AD over the past few decades are faster than any possible change in gene pool and shows that there must be a role for exogenous factors. These are likely to be multiple and also largely unavoidable.
Eczema can begin in childhood, adolescence, or adulthood – and it can range from mild to severe. Eczema typically flares up when individuals are exposed to triggers. Some can experience prolonged periods of flare-ups that can last many days or even several weeks. Symptoms include dry skin, itchy skin, red rashes, bumps on skin, swelling, and scaly/leathery patches of skin.
Barrier function has long been known to be reduced in the skin of patients with AD. Epidermal barrier defects are the initial step in the development of AD. The role of barrier dysfunction in the pathogenesis of AD and the development of further atopic disease is key. This is due to the increased trans-epidermal water loss in patients with eczema. The initial water loss can begin the breakdown of the skin’s barrier but inflammation and cellular responses drive the continuous breakdown. Filaggrin (FLG), a protein important in the structure of the epidermis, is downregulated by inflammatory molecules which further disrupts the ability of the skin to effect barrier dysfunction. The breakdown of the skins barrier allows antigen to enter the body and triggers an immune response.
Mutations in the genes that code FLG are a significant risk factor not only for AD but also for all aspects of atopy (allergic rhinitis, asthma, and food allergies). This supports the role of skin barrier dysfunction as a key driver of allergic disease and AD as the first point in this inflammatory cascade. This leads to a model of disease where initial barrier problems lead to exposure of skin to allergens which can then drive inflammation and a skewed immune response.
There are abnormalities in both adaptive and innate immunity in children with AD. AD is often associated with elevated serum level of immunoglobulin E (IgE) and a personal or family history of atopy. Even in children without FLG mutations, contact with an allergen that the immune system recognizes as foreign, directs local inflammation and synergistically drives a strong TH2 inflammatory response. Total IgE is often elevated, and many children have specific IgE elevated to ubiquitous environmental allergens, for example, house dust mite, grass, cat, dog, pollen. Whether genetic or acquired, once established, inflamed skin and a defective barrier in AD permit penetration of allergens that further trigger immune response and can lead to IgE-mediated allergies. According to Traditional Chinese Medicine (TCM), loss of water, skin barrier breakdown and elevated IgE levels is viewed as Blood Heat.
Increased Stress and Stress Response: Accumulating evidence indicates that AD patients exhibit elevated levels of stress and anxiety. AD patients also exhibit impaired hypothalamic-pituitary-adrenal (HPA) axis responses and excessive sympathetic-adrenal medullary responses to psychological stress. The HPA axis is responsible for communication between the brain and skin. Corticotropin-releasing hormone (CRH) is released from the hypothalamus and stimulates the pituitary to secrete adrenocorticotropic hormone (ACTH) release to the blood, which then triggers glucocorticoid (GC) (cortisol in humans) release from the adrenal cortex. High concentrations of GC can cause neuronal damage, decreased neurogenesis, and apoptosis in the hippocampus, which is involved in stress and anxiety. In the skin, mast cells are important players in the pathogenesis of AD and can be activated by stress hormones like CRH. Previous studies have suggested CRH might activate mast cells to release pro-inflammatory mediators, such as IL-8, tumor necrosis factor (TNF), and vascular endothelial growth factor (VEGF), which are known to contribute to skin inflammation in AD.2 According to TCM, the elevated levels of stress and the increased stress hormone (CRH) secretion in response to stress is viewed Liver Yin deficiency.
Food Allergy: Upwards of 80% of individuals who suffer from eczema also develop food allergies. It has been hypothesized that eczema "landscapes" the body for an allergy, in part, by diminishing the barrier function of the skin. As the structure of skin cells collapses, it not only causes the loss of moisture but allows allergens and irritants to infiltrate vulnerable tissues. This, in turn, triggers an immune response in the form of inflammation. It is believed that this hypersensitizes the immune system to the various allergens it encounters on the skin, causing an exaggerated response when those allergens are later either eaten or inhaled. Even though not all cases of eczema cause food allergies, food allergy especially in children, are likely to trigger other related allergic diseases. It can also trigger a worsening of existing eczema symptoms. The process by which flares are triggered can vary by the type of food eaten as well as the immunologic response of the individual. Food allergens cause cross-linking of IgE and activation of mast cells and basophils which release histamines and cause allergy symptoms. According to TCM, food allergies caused by eczema is viewed as Stomach Yin and Real Kidney Yin deficiencies.
Anemia Rash: Aplastic anemia is one of the most common causes of anemia rashes. Aplastic anemia occurs when the body’s bone marrow doesn’t make enough new blood cells. The rashes resemble patches of pinpoint red or purple spots, known as petechiae. These red spots may be raised or flat on the skin. They can appear anywhere on the body but are more common on the neck, arms, and legs. Iron deficiency anemia is one of the most common types of anemia. People with iron deficiency of any kind may develop pruritus, which is the medical term for itchy skin. When the itchy skin being scratched, it can cause redness and bumps that look like rashes. According to TCM, anemia is viewed as a Blood Deficiency.
Skin Rash Caused by Infections: Skin infections are common in people with eczema. The alterations in the barrier function of the skin increase the potential for skin infection. Infections that develop because of the underlying condition of eczema are often described as secondary infections.
Staphylococcus aureus is the bacterium that is most commonly responsible for secondary infection of eczema.4 It is often associated with hair follicle infections (folliculitis), boils and abscesses. ‘Impetiginized eczema’ is another label or name given to eczema infected with Staph. aureus. When the bacteria penetrate the epidermis, an immune reaction can be triggered, which aggravates the eczema and brings about a flare. Overt bacterial infection is easily recognized by the appearance of weeping lesions, honey-colored crusts and pustules.4 Other types of atypical bacteria can also cause infection on the skin. Gram-negative bacteria and mycobacteria are widespread throughout the environment, including water and soil. Typically, only causing infection in those who are immunocompromised.
Viral infections such as herpes simplex virus (HSV) can cause a skin rash. One of the main symptoms is a rash of blisters that doctors sometimes refer to as a herpes rash. A herpes rash usually develops on the genitals or around the mouth, but it can occur nearly anywhere on the body. It is typically painful and itchy and appear as small red bumps or tiny white blisters.
Contact dermatitis is an itchy rash caused by direct contact with a substance or an allergic reaction to it. The rash isn't contagious, but it can be very uncomfortable. Many substances can cause this reaction, such as cosmetics, fragrances, jewelry and plants. The rash often shows up within days of exposure. Some people react to strong irritants after a single exposure. Others may develop a rash after repeated exposures to even mild irritants, such as soap and water. And some people develop a tolerance to the substance over time. Contact dermatitis can lead to an infection if you repeatedly scratch the affected area, causing it to become wet and oozing. This creates a good place for bacteria or fungi to grow and may cause an infection.
