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Eczema Treatment



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Dermatologists use the interchangeable terms "dermatitis" or "eczema" to refer to a specific group of inflammatory skin diseases. Dermatitis presents with pruritic, erythematous macules, papules, vesicles, or plaques with or without distinct margins. Lesions pass through acute (vesicular). Subacute (scaling and crusting ) and chronic ( acanthotic with thick epidermis ) phases. Oozing, crusting, scaling, fissuring and lichenification altogether accompany the primary lesions. Up to 25 % of all patient presents new skin diseases have a form of dermatitis. Patients typically suffer from intense pruritus that distracts them their daily activities. Including sleep and they are desperate for relief.

The prevalence of atopic dermatitis in six –and seven-year-old children varies from less than 2 % Iran and China to 10% to 20% in the united states. United Kingdom, Australia, and Scandinavia. The incidence was only 2% in those born before 1960. The increased time and difference over time and difference between more and less developed nations has been explained by the "hygiene hypothesis". This postulates that a reduction in the frequency of children infections results in an increased incidence of various allergic and autoimmune diseases including atopic dermatitis, asthma, allergic rhinitis, childhood insulin dependent diabetes mellitus and Crohn's diseases.

At least 50% patient with moderate to severe atopic dermatitis have a defect in the gene coding for filaggrin, a protein essential to maintain the barrier function of stratum corneum then allows various irritants, microbes or allergens to penetrate to the skin surface, elicit cytokine release from keratinocytes, and initiate an immune responses acutely that leads to the clinical manifestations of diseases and increased IgE levels. In chronic atopic patient cannot yet be ruled out because bone marrow stem cell transplants from atopic patients have transferred atopic dermatitis to recipients.

Terui T is an analysis of the mechanism for the development of an allergic skin inflammation the application for its treatment: an overview of the pathophysiology of atopic dermatitis.

The neural and chemical mechanism is involved. When the epidermis and its nerve fibers are stripped from skin, pruritus is abolished. Keratinocytes and mast cells release high levels of nerve growth factor (NGF), which increases the sensitivity of cutaneous pruritus receptors. These sensitized nerve endings demonstrate an increased capacity to transmit signals that are perceived as pruritus ( telekinesis ). Chemical mediators associated with itch including serine proteases, interleukins 2 and 31, opioids, acetylcholine, prostanoids, and substance P. Histamine may play in a limited role in the pruritus of atopic dermatitis. These mediators act either on nerve endings or directly on keratinocytes. They are produced by mast cells, keratinocytes. T cells, and nerve fibers.

Probably, in mice, various stressors can produce atopic dermatitis skin lesions, possibly due to an upregulation of substance P sensitive nerve fibers. Transepidermal water has an increase in humans who are under mental stress compared to control subjects. Such water loss is an indicator of a defective epidermal barrier.

Atopy is derived from the Greek word atopos, meaning "out-of-place," and refer to the predisposition to develop dermatitis, asthma, and allergic rhinitis. The surface the body contact the surface external environment is overreactive (the lover airways in asthma, the upper airways, and conjunctiva in allergic rhinoconjunctivitis, and the skin in atopic dermatitis ).

Atopic dermatitis is not an allergic disease, but a skin disease with allergies "( Jon Hannifin, dermatology, foundation clinical symposia 2007); upper airways allergic rhinitis ) or lower airways ( allergic asthma ), for example, atopic dermatitis typically improves in the spring when allergic rhinitis is at its peak.

Three or four following features must be present;

  • pruritus – the primary symptoms, and even referred to as the "primary lesion" by some
  • typical morphology and distribution of lesions forage.
  • chronic or chronically relapsing course.
  • personal or family history of asthma, allergic rhinitis, atopic dermatitis.

The itch, atopic dermatitis is "an itch, which, when scratched, erupts. " atopic dermatitis is pruritus enfleshed.

Scratching suppresses areas of the brain associated with a negative experience of pruritus and activates pleasure centers of the brain. In other words, there is an emotional reward for scratching. Unfortunately, scratching damages the skin and worsens dermatitis so that it itches even more. Therefore, people scratch more and get caught in an "itch-scratch cycle " that they cannot exist without medical help or supreme levels of self –restraint.

  • wool clothing; the size of wool fibers stimulated intense itching via allokinesis
  • clothing made of blended or synthetic fabrics and shirt collar tags.
  • prolonged bathings/hot water bathing: both promote transepidermal water loss.
  • soaps with a high ( basic ) PH.
  • Infection; Staphylococcus aureus colonizing skin disease superantigens that dermatitis flares
  • climate extremes: heat, cold, low humidity, and high humidity.
  • food: food antigens appears to play a minor role in the cause of atopic dermatitis.

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