Randomized double-blinded placebo-controlled intra-individual trial on topical treatment with a 1,25-dihydroxyvitamin D3 analogue in polymorphic light eruption

Gruber‐Wackernagel, Alexandra; Bambach, Isabella; Legat, Franz J.; Hofer, Angelika; Byrne, Scott N.; Quehenberger, Franz; Wolf, Peter

doi:10.1111/j.1365-2133.2011.10333.x

Cited by 59 publications

(42 citation statements)

References 61 publications

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“…This is intriguing as we have recently shown that photohardening raises low baseline vitamin D3 levels in PLE patients (27). Moreover, a short-term topical pretreatment course over 1 week with the 1,25-dihydroxyvitamin D analogue calcipotriol diminished PLE symptoms after subsequent experimental photoprovocation (28). However, Schwarz et al (29) have recently reported from a murine study that 1,25-dihydroxyvitamin D exerted similar immunosuppressive effects as UV, but was dispensable for local UVinduced immunosuppression.…”

Section: Discussionmentioning

confidence: 64%

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

Wolf

Gruber‐Wackernagel

Bambach

et al. 2014

Experimental Dermatology

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The pathogenesis of polymorphic light eruption (PLE) has been linked to a lack of UV-induced immune suppression. To determine the role of Langerhans cells (LC), mast cells and regulatory T cells, biopsies from PLE patients were taken from exposed sites in spring before and after photohardening with 311 nm or PUVA as well as again in summer. Skin sections were assessed for the presence of Langerin/CD1a+ LC and CD3+, CD4+, CD25+ or FoxP3+ T cells and mast cells. Photohardening transiently decreased the density of epidermal LC and significantly increased a low baseline mast cell density in the papillary dermis of PLE patients. Baseline T cell numbers in the skin were low, and there was no difference in PLE patients among any time point. This suggests that LC suppression together with recruitment of mast cells into photohardened skin may be a key cellular event underlying the mechanism by which phototherapy protects from PLE.

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Section: Discussionmentioning

confidence: 64%

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

Wolf

Gruber‐Wackernagel

Bambach

et al. 2014

Experimental Dermatology

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“…In contrast, vitamin D3 has been shown to upregulate cathelicidin peptide LL‐37 in normal skin and 311 nm UVB treatment increased serum LL‐37 levels in patients with psoriasis . To that end, calcipotriol pretreatment of non‐lesional, apparently normal skin in patients with PLE significantly reduced the severity of PLE symptoms at subsequent experimental photoprovocation, although the mechanism remained elusive. Similar to photosensitive rosacea, in which LL‐37 increases UVB‐triggered inflammasome activation, this AMP may also play a role in PLE‐koebnerized psoriasis as we found it to be significantly increased in blood vessels in the dermis of lesional PLE skin compared to healthy skin (Fig.…”

Section: Initiators Of Photosensitive Psoriasismentioning

confidence: 99%

Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

Wolf

Weger

Patra

et al. 2016

Experimental Dermatology

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Psoriasis commonly responds beneficially to UV radiation from natural sunlight or artificial sources. Therapeutic mechanisms include the proapoptotic and immunomodulating effects of UV, affecting many cells and involving a variety of pro-and anti-inflammatory cytokines, downregulating the Th17/IL-23 response with simultaneous induction of regulatory immune cells. However, exposure to UV radiation in a subset of psoriasis patients leads to exacerbation of the disease. We herein shed light on the predisposing factors of photosensitive psoriasis, including genetics (such as HLACw*0602 or CARD14), gender and coexisting photodermatoses such as polymorphic light eruption (PLE) in the context of potential molecular mechanisms behind therapeutic photoresponsiveness or photoaggravation. UV-induced damage/pathogenassociated molecular patterns, damage to self-coding RNA (signalling through Toll-like receptors), certain antimicrobial peptides and/or inflammasome activation may induce innate immunity, leading to psoriasis at the site of UV exposure when there is concomitant, predisposing resistance against UV-induced suppression of the adaptive immune response (like in PLE) that otherwise would act to reduce psoriasis. K E Y W O R D S

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“…Finally, a randomized, double-blind right/left comparison study of calcipotriol and placebo creams in patients with polymorphous light eruption showed that twice daily application of calcipotriol for 7 days prior to UV irradiation significantly decreased pruritus compared to placebo. 43 …”

Section: Topical Vitamin D Modulatorsmentioning

confidence: 99%

Topical Therapies for Pruritus

Elmariah¹,

Lerner²

2011

Seminars in Cutaneous Medicine and Surgery

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Itch, or pruritus, is the predominant symptom associated with acute and chronic cutaneous disease and in some cases, may be debilitating. To date, there is no single universally effective anti-itch treatment. As the pathophysiology of itch in most cutaneous or systemic disorders remains unclear, anti-pruritic therapy is often directed against a variety of targets, including the epidermal barrier, immune system, or the nervous system. Topical therapy is the mainstay of dermatologic management of acute or localized itch or in patients with contraindications to systemic therapies. This review will summarize current topical therapies to treat pruritus and discuss potential future therapies.

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Randomized double-blinded placebo-controlled intra-individual trial on topical treatment with a 1,25-dihydroxyvitamin D3 analogue in polymorphic light eruption

Abstract: These results suggest a potential therapeutic benefit of topical 1,25-dihydroxyvitamin D₃ analogues as prophylactic treatment in patients with PLE.

Cited by 59 publications

References 61 publications

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

Topical Therapies for Pruritus

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