Pailin Puangpet

MD
consultant dermatologist
Institute of dermatology, Thai... · contact and occupational dermatology

Publications

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    ABSTRACT: The ability to be sensitized to experimental contact allergens declines significantly with increasing age, from as early as age 40 years. In contrast, the rate of contact allergy to chemical allergens (haptens) in cosmetic products significantly increases with age. This has been explained previously on the basis of greater cumulative exposure in the older age groups. However, outbreaks of contact allergy to preservatives in cosmetic products recorded soon after their introduction to the market have also shown a significantly higher rate among older adult age groups. This association with increasing age cannot be readily explained by exposure history or pattern, and is not compatible with a sensitizing/stimulatory reaction that degrades with age as the sole immune response. From this, the existence of a second, tolerizing/regulatory arm to the immune response to cutaneous haptens that possibly becomes less effective with age at a higher rate than the sensitizing/stimulatory arm can be inferred. This reinforces the view that current clinical and experimental observations of allergic contact dermatitis are best explained by an immune system with the functional ability to produce both sensitizing/stimulatory and tolerizing/regulatory responses.
    Contact Dermatitis 09/2013; 69(3):129-37. · 2.93 Impact Factor
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    ABSTRACT: One explanation for the large increase in the prevalence of atopic disease during the last 50 years in developed countries is the 'hygiene hypothesis'. This proposes that a reduced exposure to pathogenic microorganisms at a key period(s) during development result in the maintenance or acquisition of an atopic phenotype. Alternatively, or additionally, we have postulated that increased exposures to chemicals generally, and to irritant/haptenic chemicals in particular, during critical windows of pregnancy/ early life development have also contributed to changes in the prevalence of atopic disease. Having previously reviewed the potential roles of oral and cutaneous exposures to chemicals on the subsequent diagnosis of atopic disease, we here consider possible evidence of a role for exposure to airborne chemicals as a contributory factor in acquired susceptibility to atopic allergy. After controlling for known confounders five specific maternal occupations during pregnancy have been implicated as being associated with subsequent atopic disease in offspring. Each of these occupations is characterised by high and persistent exposure to airborne chemicals. High level exposure to volatile organic compounds in the domestic environment either during maternal pregnancy or in early life, is also associated with development of childhood atopic disease. Similarly, sustained exposure to airborne chlorinated chemicals from swimming pools during childhood has been associated with the development of atopic allergy. A possible immunological basis for these associations is that exposure to certain airborne chemicals, even at low levels, can result in the delivery of 'danger' signals that, in turn, bias the immune response toward the selective induction or maintenance of preferential Th2-type immune responses consistent with the acquisition of allergic sensitisation. This article is protected by copyright. All rights reserved.
    British Journal of Dermatology 08/2013; · 3.76 Impact Factor
  • Pailin Puangpet, Joey Lai-Cheong, John P McFadden
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    ABSTRACT: Background. Although atopic disease is associated with protein allergy, its relationship with chemicals (haptens/contact allergens and irritants) is less clearly defined. The 'hapten-atopy' hypothesis, whereby significant hapten and irritant exposure during times of natural T helper (Th)2 bias (pregnancy and first year of life) promotes the development of atopy and atopic disease in the resulting child, has been previously proposed. Supporting evidence includes the practice of repeated cutaneous application of haptens in generating animal models of atopic dermatitis, and the observation of a significant increase in atopic disease in children born to mothers with occupations associated with high chemical exposure during pregnancy. Objectives. To observe the relationship between personal chemical exposure and atopic disease in a particular case series. Methods. We report a case series of exacerbation of atopic dermatitis after repeated cutaneous chemical exposure. Results. Most of the patients had atopic dermatitis in young childhood that had resolved. However, after repeated chemical exposure, either occupationally as an adult or after starting to use cosmetics as a teenager, there was clear exacerbation of atopic dermatitis. Patch tests gave negative results in most cases. Conclusions. We propose that repeated exposure to chemicals in patients with an atopic background can occasionally lead to reactivation of atopic dermatitis.
    Contact Dermatitis 04/2013; 68(4):208-13. · 2.93 Impact Factor
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    ABSTRACT: The skin immune system's propensity to produce allergic contact dermatitis (ACD) to harmless chemicals, whilst otherwise being an efficient defence system, represents a dermatological paradox. We postulate that a major role in signaling in ACD is played by Toll-like receptor (TLR) 2 and TLR4 that arises from their activation by extracellular DAMPs (danger associated molecular patterns). Ligand activation of TLR4/2 results in the expression of interleukins (IL) IL-1β, IL-6, IL-12, IL-18 and IL-23, tumour necrosis factor-α (TNF-α) and interferon-α (IFN-α). These cytokines promote acquisition of sensitisation, and facilitate elicitation of contact allergy, via multiple mechanisms, including the recruitment of CD4+ T helper (Th) cells, Th1 and Th17 cells. As Th1 cells secrete large amounts of Danger Associated Molecular Pattern molecules (DAMPs), a DAMP immune circuit (positive feedback loop) is created. This is an important driver of skin sensitisation and skin inflammation. Pathogenic extracellular bacteria, but not commensal bacteria, produce PAMPs (Pathogen-Associated Molecular Pattern molecules), that stimulate the expression of Th1 and Th17-promoting cytokines via TLR 2 and 4. This also induces an immune circuit. The ability of the skin immune system to activate host defence mechanisms and to distinguish between pathogenic bacteria and commensals provides an explanation why skin sensitisation and ACD develops; processes that rely on the same biological pathways. These pathways may also shed light on pathogenesis of chronic pustular inflammatory dermatoses (e.g. acne vulgaris). The existence of safety signals from commensal bacteria that prevent initiation of these pathways may represent opportunities for novel therapeutic approaches to the treatment of inflammatory skin diseases.
    British Journal of Dermatology 02/2013; · 3.76 Impact Factor
  • Contact Dermatitis 12/2012; 67(6):375-376. · 2.93 Impact Factor

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