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Polymorfe lichteruptie bij huidaandoeningen

Andere soorten huidreacties (veroorzaakt door de zon)

Ook bepaalde medicijnen kunnen de gevoeligheid voor zonnestraling verhogen.

Terwijl PLE naar verwachting tot wel 90% van de mensen met huidreacties (veroorzaakt door de zon) treft, bestaan er andere aandoeningen met vergelijkbare tekenen.

Acne aestivalis (Mallorca-acne) wordt niet alleen veroorzaakt door UV-straling, maar verschijn pas na interactie met bepaalde bestanddelen van cosmeticaproducten of zonnebrandmiddelen, zoals bepaalde emulgatoren. Dit treft het meest vrouwen van de leeftijd tussen 25 en 40 jaar van wie velen met een verleden van acne in de puberteit. De klinische tekenen lijken sterk op die van PLE.

Introduction

We are most probably dealing with polymorphic light eruption (PLE) and, following the requests of our patients, medical research has mainly been focused on prevention strategies become nowadays quite satisfactory. On the other side, the second and certainly less explored question remains unclear, unless multiple pieces have been added to this rather complicate puzzle. Aim of this brief review is to resume the most recent advances in PLE possible mechanisms and the most used protocols for prevention or treatment.

PLE is the commonest photosensitive disorder, characterized by an intermittent eruption of non-scarring pruritic erythematous papules, vesicles or plaques (Figure ​ (Figure1) 1 ) that develop within hours of ultraviolet radiation (UVR) exposure of patient skin. The disease is dependent on genetic susceptibility, as well as environmental component, such as type of exposure. PLE appears to cluster in families: it has been estimated that the prevalence of PLE was 21 and 18% in monozygotic and dizygotic twins, respectively (1). Moreover, a positive family history of PLE in first-degree relatives was present in 12% of affected twin pairs respect to 4% of unaffected twin pairs (p < 0.0001). The probandwise concordance in monozygotic was superior than in dizygotic twin pairs (0.72 vs. 0.30, respectively), demonstrating a strong genetic effect (1). Many genes of potential interest in the pathogenesis of PLE have been investigated with generally unrewarding results. Using segregation analysis, it has been estimated that 72% of the UK population carry a low penetrance PLE susceptibility allele (2).

Clinical picture of polymorphic light eruption in a young woman.

The failure of apoptosis: the possible photo-induced neo antigens

In a recent genome-wide expression analysis, only 16 genes were differentially expressed between PLE and healthy controls after UV irradiation respect to control (3). Of these genes, 14 showed lower expression in PLE patients, whereas two resulted over-expressed. Among the 14 genes with lower expression in PLE are: complement 1s subunit (C1s), scavenger receptor B1 (SCARB1) fibronectin (FN1), immunoglobulin superfamily member 3 (IGSF3), caspase-1 (CASP1) and paraoxonase 2 (PON2), all genes associated with apoptotic cell clearance. It has been supposed that protein modification during apoptotic cell clearance could lead to potential auto-antigen formation (4). Then, the reduced expression in PLE patients of genes connected to this process might represent a possible auto-antigen source, as well as a crucial phase in the initiation of the autoimmune process that promotes the disease (3). In accordance to these findings, Kuhn et al. showed accumulation of apoptotic cells in PLE patients irradiated either with 1.5 Minimal Erythema Dose (MED) of UVB, or 60–100 J/cm 2 of UVA1, compared to controls (5).

Abstract

Polymorphic light eruption is the commonest photosensitive disorder, characterized by an intermittent eruption of non-scarring erythematous papules, vesicles or plaques that develop within hours of ultraviolet radiation exposure of patient skin. Together with the lesions, a terrible itch starts and increases with the spreading of the disease, sometimes aggravated by a sort of burning sensation. Clinical picture and symptoms can improve during the rest of the summer with further solar exposures. In the last years many advances have been performed in the knowledge of its pathogenesis and some news have been proposed as preventive, as well as therapeutic options. All this has been discussed in the current mini review.

Keywords: polymorphic light eruption, photosensitive disorders, phototherapy, apoptosis, delayed type hypersensitivity reaction

References

1. Millard TP, Bataille V, Snieder H, Spector TD, McGregor JM. The heritability of polymorphic light eruption . J Invest Dermatol . (2000) 115 :467–70. 10.1046/j.1523-1747.2000.00079.x [PubMed] [CrossRef] [Google Scholar]

2. McGregor JM, Grabczynska S, Vaughan R, Hawk JL, Lewis CM. Genetic modelling of abnormal photosensitivity in families with polymorphic light eruption and actinic prurigo . J Invest Dermatol . (2000) 115 :471–6. 10.1046/j.1523-1747.2000.00080.x [PubMed] [CrossRef] [Google Scholar]

3. Lembo S, Hawk JLM, Murphy GM, Kaneko K, Young AR, McGregor JM, et al.. Aberrant gene expression with deficient apoptotic keratinocyte clearance may predispose to polymorphic light eruption . Br J Dermatol . (2017) 177 :1450–3. 10.1111/bjd.15200 [PubMed] [CrossRef] [Google Scholar]

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Zonneallergie kind

Bij kindjes zit de zonneallergie vaak alleen op of achter de oren (de lente-oren). Met name jongens hebben hier in het voorjaar last van. Als je kindje last heeft van zonneallergie is het belangrijk om ervoor te zorgen dat de zon even gemeden wordt. Verder kan het fijn zijn om de huid te koelen met natte handdoeken.

Wat je ik afraad is het smeren van aftersun. Vaak zitten er namelijk irriterende ingrediënten in aftersun producten. Die de huidklacht alleen maar erger maken.. Wat je wél kunt doen is je kindje in een bad met zemelen (haver) doen.

Zemelen hebben namelijk een kalmerend en jeukstillend effect op de huid. Vul een oude panty met zes tot acht schepjes haver en leg dit vervolgens in een bad. Grote kans dat de allergie, en bijhorende jeuk, snel afnemen!


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