FIGURE 19.1 Pathomechanism of sensitive skin.
AD and ACD are both common skin diseases having an immune pathogenesis (9). AD is a common skin condition, characterized by a complex, heterogeneous pathogenesis, including skin barrier dysfunctions and significant pruritus. Recently, the skin barrier dysfunction induced by the FLG mutation has been demonstrated in AD. The barrier dysfunction shifts Th1 to Th2 response. Th2 cells produce IL-31, which provokes pruritus, and Th2 cytokines decrease filaggrin expressions by keratinocytes. These findings suggest that the evolution of a Th2 response lead to pruritus and barrier dysfunctions in patients with AD (10,11).
There is some similarity between sensitive skin and AD. It is likely that the same factors that play a role in the development of sensitive skin are also operative in AD. The most common and an important factor is skin-barrier dysfunction. There may also be differences among neural thresholds. Some patients have an abnormal response to mediators such as histamine. In some, exposure to histamine generates a significant wheal, whereas in others, there is only an insignificant response or none at all. This differing response can be due to their diverse neural threshold.
Atopic Diathesis and Sensitive Skin
It was thought that patients with AD were unable or less likely to develop contact dermatitis. In various studies, patients with AD stimulated with strong allergens failed to develop sensitization at rates similar to patients without AD. However, recent literature evidence from the United States and Europe has shown that patients with AD have similar if not higher rates of positive patch test results to common contact allergens, than in patients without AD (12).
There are studies supporting the link between sensitive skin and an atopic diathesis (13). It was first suggested by Thiers that features of atopic diathesis could explain sensitive skin syndrome (SSS) (14).
In a survey from the United Kingdom, only 49% of persons with sensitive skin had atopic diathesis concurrently. Hence, all cases with sensitive skin cannot be attributed to underlying atopic diathesis (15).
Clinical Features
The most practical, functional clinical description of sensitive skin is the one that reacts to cosmetic products. That is the hallmark feature of sensitive skin. It is mainly diagnosed by the subjective perceptions of the patient or from patient observation.
The usual complaints with which the patients approach the dermatologists are “I applied that moisturizer and it irritated me so much” or “I cannot find a sunscreen that feels good” or “Everything I apply to my skin burns and stings,” and so on. These are the clues toward the diagnosis of sensitive skin. Demonstrable clinical signs are rare or none in these patients. Only identifiable clinical features may be less hydrated and less supple skin (1). Subjective, sensorial signs, such as stinging, burning, and itching sensations on an apparently normal-looking skin are the clinching points for the diagnosis of sensitive skin (16). The face is the main target of cosmetic use and, hence, the main body part affected. However, sensitive skin may as well involve other locations, such as the hands or scalp (5). In contrast, all the eczematous dermatoses have specific clinical signs and symptoms, specific distribution or body site predilection, and well-defined diagnostic criteria.
People with sensitive skin may identify and mention various aggravating factors for their condition; these include environmental factors such as cold, wind, sun, heat, humid weather, pollution, and exposure to water during showers and in swimming pools (17). Such triggering factors may be part of various eczematous disorders, such as AD, and may even be misdiagnosed as rosacea.
Diagnosis
