Materiały źródłowe

• #1 Polymorphic Light Eruption – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430886/

  Polymorphic light eruption is the most common form of immunologically mediated photosensitivity dermatoses. […] This activity reviews the pathophysiology of polymorphic light eruption and highlights the role of the interprofessional team in its management. […] The cause of polymorphic light eruption is unknown. It is postulated that there is a delayed hypersensitivity reaction to an endogenous antigen expressed after exposure to sunlight or artificial sources of ultraviolet (UV) radiation. […] Current theories involve two steps that lead to a polymorphous light eruption. An unknown photoantigen is rendered immunogenic on exposure to UV. This does not cause a problem in unaffected individuals because of UV-induced suppression. In patients with a polymorphic light eruption, Tcell function is not suppressed by UV radiation until photo-hardening has taken place. The putative antigen induced by UV radiation leads to a predominance of CD4+ T cells and the production of proinflammatory cytokines such as interleukin (IL) 1.

• #2 Polymorphous light eruptions – Indian Journal of Skin Allergy

  https://skinallergyjournal.com/polymorphous-light-eruptions/

  Polymorphous light eruption (PMLE) is the most common, immunologically acquired photo-dermatosis due to delayed hypersensitivity reaction to sunlight. This review article focuses on immunopathogenesis, clinical features, and treatment option of PMLE. […] Genetic susceptibility and environmental exposure play an important role in the pathogenesis of PMLE. […] The exact etiopathogenesis of polymorphous light eruption (PMLE) is still not well understood, but the disease is linked to a delayed-type (type IV) hypersensitivity reaction to one or more endogenous photo-antigens. […] In allergic contact dermatitis, interleukin (IL)-1 family of cytokines, especially IL-36 alpha and gamma, are increased, which is also observed in patients with PMLE. […] Dysregulation of AMPs is found in skin lesions of PMLE, which triggers the release of IL-31 from keratinocytes and is an important cytokine in the pathogenesis of pruritic lesions in these patients.

• #3 2013.3-29.Polymorphous – Our Dermatology Online

  https://www.odermatol.com/issue-in-html/2013-3-29-polymorphous/

  Polymorphous Light Eruption (PMLE), also termed Polymorphic Light Eruption, is the most common photodermatosis encountered in clinical practice. It is an idiopathic acquired disorder in which a delayed cutaneous response to ultraviolet radiation occurs in the form of skin eruptions consisting of papules, vesicles or plaques over the sun-exposed and rarely on partially covered areas. The reaction usually follows the brief spring or summer sun exposure and occurs after a latent period of hours to days. Polymorphous light eruption causes lot of psychological stress amongst those suffering from the disease especially in women with longstanding illness. […] Pathogenic mechanisms in PMLE have not been fully elucidated. An abnormal immunological response of Gell and Coombs type IV to a sunlight-induced cutaneous neoantigen, first proposed in 1942, because of the delayed reaction time and histological appearance, remains a favored hypothesis, although possible abnormalities of arachidonic acid metabolism have also been suggested as being responsible.

• #4 2013.3-29.Polymorphous – Our Dermatology Online

  https://www.odermatol.com/issue-in-html/2013-3-29-polymorphous/

  Most authors agree that PMLE results from delayed cell-mediated hypersensitivity to some unknown sunlight-induced antigen. Three commonly reported findings support this hypothesis: delay in onset of symptoms from 30 minutes to several days; dense perivascular infiltrate in the dermis resembling that observed in allergic contact dermatitis; and the pattern of adhesion molecule expression is similar to that seen in a delayed hypersensitivity response.

• #5 Polymorphous Light Eruption | Plastic Surgery Key

  https://plasticsurgerykey.com/polymorphous-light-eruption-3/

  Polymorphous light eruption is an immunologically mediated photodermatosis with high prevalence, particularly among young women in temperate climates, characterized by pruritic skin lesions of variable morphology, occurring in spring or early summer on sun-exposed body sites. A resistance to ultraviolet radiation (UVR)-induced immunosuppression and a subsequent delayed-type hypersensitivity response to a photoantigen have been suggested as key factors in the disease. […] A resistance to ultraviolet radiationinduced immunosuppression (ie, a physiologic phenomenon in healthy subjects) and a subsequent delayed-type hypersensitivity response to a photoantigen have been suggested as key factors in the disease. […] Molecular and immunologic disturbances associated with disease pathogenesis include a failure of skin infiltration by neutrophils and other regulatory immune cells on UVR exposure linked to a disturbed cytokine microenvironment.

• #6 Low Incidence of Polymorphous Light Eruption in Renal Transplant Recipients | HTML | Acta Dermato-Venereologica

  https://www.medicaljournals.se/acta/content/html/10.2340/00015555-0248

  Polymorphous light eruption (PLE) is the most common form of photodermatosis and is estimated to affect 15% of healthy people in the UK. The pathogeny of PLE remains unclear, however, despite plenty of recent research. PLE is characterized by a recurrent, delayed cutaneous reaction appearing a few hours after exposure to ultraviolet (UV) radiation, mostly from the sun, in susceptible individuals. Although the prime mechanism of PLE remains unknown, it has been suggested that a delayed-type hypersensitivity response to autologous antigens generated by ultraviolet radiation (UVR) is involved. […] It has been postulated that this immunosuppression prevents autoimmune responses to UVR-damaged skin, in particular to photo-antigens. It is thus hypothesized that, in patients with PLE, there is a partial failure of UVR-induced immunosuppression, causing an abnormal response to these antigens. There is some evidence of the role of immune response in patients with PLE.

• #7

  https://link.springer.com/article/10.1007/s00403-004-0508-x

  Despite the fact that polymorphous light eruption (PLE) is the most common photodermatosis, affecting 15% of healthy people in the UK, its pathogeny remains unclear. […] The mechanism of PLE is under active research as shown by recent results, and it is hypothesized that in PLE patients, there is a partial failure of ultraviolet radiation-induced immunosuppression, causing an abnormal response to autologous antigens generated by ultraviolet radiation (UVR). […] The recent demonstration that the female hormone, 17-estradiol prevents UVR-induced suppression of the contact hypersensitivity response caused by the release of immunosuppressive cytokines (IL-10) from keratinocytes might thus explain why the risk of PLE is higher in females than in males and why the risk decreases in women after the menopause.

• #8 Polymorphic Light Eruption: A Clue to Pathogenesis?logo-32logo-40logo-60NEJM Journal WatchnejmJW_1L_RGB-b

  https://www.jwatch.org/jd199909010000007/1999/09/01/polymorphic-light-eruption-clue-pathogenesis

  Polymorphic light eruption (PLE), the most common idiopathic photodermatosis, affects up to 20% of some Caucasian populations. When exposed to ultraviolet (UV) light, PLE patients develop a pruritic photoexposed site eruption. High-dose UV irradiation is believed to induce a wide range of neoantigens, and UV-induced suppression via clearance of Langerhans cells may be the reason why normal skin does not overreact. […] Langerhans cells disappeared with MED irradiation in normal subjects but not in the 10 PLE patients, suggesting that the persisting Langerhans cells may be available for antigen presentation and production of a delayed hypersensitivity response. […] Nevertheless, if the finding is confirmed, it will represent a step toward improved understanding of the pathogenesis of PLE.

• #9 Polymorphous Light Eruption: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1119686-overview

  The production of neoantigens, failure to induce apoptosis, poor immune tolerance, delayed hypersensitivity reaction, and skin microbiome dysregulation are important factors in the pathogenesis of PMLE. […] The action spectrum is primarily UVA light but can include UVB light. Some patients even react in the visible light spectrum. It has also been shown that UVC can cause PMLE. […] Delayed hypersensitivity reaction of PMLE is supported by the study of timed biopsy samples of PMLE lesions. The CD4 subtype of T cells seen very early after exposure is replaced by CD8 lymphocytes 72 hours after irradiation. […] Klgen et al noted that the reduced expression of tumor necrosis factor (TNF)-, interleukin (IL)-4, and IL-10 in the UVB-irradiated skin of patients with PMLE. The reduction of these cytokines seems linked to a relative neutropenia and is a manifestation of decreased Langerhans cell migration and reduced TH2 skewing.

• #10 Polymorphous Light Eruption

  http://www.thedoctorsdoctor.com/diseases/pmle.htm

  Disturbances in UV-induced Langerhans cell migration and T helper (T(H)) 2 cell responses could be early steps in the pathogenesis of PLE. […] The reduced expression of TNF-alpha, IL-4, and IL-10 in the UV-B-irradiated skin of patients with PLE appears largely attributable to a lack of neutrophils, and is indicative of reduced Langerhans cell migration and reduced T(H)2 skewing. An impairment of these mechanisms underlying UV-B-induced immunosuppression may be important in the pathogenesis of PLE. […] Histological examination of biopsies performed 1 h, 5 h, 24 h, 72 h and 144 h post-irradiation revealed onset within 5 h of perivascular cellular infiltration. The infiltrate was dominated by lymphocytes in both early and established lesions, without evident epidermal pathology. […] These findings are consistent with a delayed type hypersensitivity response underlying the pathogenesis of polymorphic light eruption.

• #11 Polymorphic Light Eruption: What’s New in Pathogenesis and Management

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6139322/

  The immunological mechanisms involved in PLE, with mediators from the innate and adaptive immune system, are very similar, either from the histological or the biochemical point of view, to the ACD ones. […] Recently, to reinforce this concept, some of the inflammatory mediators involved in ACD have been demonstrated also in PLE. […] The increase of IL-36s in skin and peripheral blood of PLE patients indicates the activation of local and systemic immune response, as found in multiple inflammatory skin conditions. […] As largely examined in multiple skin inflammatory processes, these mediators, named as defensins, cathelicidin, ribonuclease 7, and psoriasin, in light of the imbalance induced by UVR on keratinocytes and skin microbiome, have also been investigated in PLE. […] The first line of treatment for PLE includes sun avoidance, sunscreens and topical corticosteroids.

• #12 Polymorphous Light Eruption: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1119686-overview

  An increase in the IL-1 family of cytokines (in particular, IL-36 gamma) in skin lesions and peripheral blood of PMLE patients indicates an enhanced focal and systemic immune response. […] Apoptotic keratinocytes produce photoneoantigens, and failure to clear these antigens leads to an increased immune response. In photoprovocated skin samples of PMLE patients, gene expression of apoptotic cell clearance C1S and SCARB1 are reduced. […] Regarding microbiome dysregulation, UV-induced changes to the skin microbiome in PMLE patients was proposed as an initiating or provoking factor in the inflammatory cascade, via antimicrobial peptide (AMP) release and activation of the innate immune system. […] In a study by Muhlbauer et al, intravascular and focal perivascular deposits of fibrin were detected in biopsy samples of PMLE papules.

• #13 Polymorphic Light Eruption: What’s New in Pathogenesis and Management

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6139322/

  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. […] In a recent genome-wide expression analysis, only 16 genes were differentially expressed between PLE and healthy controls after UV irradiation respect to control. Of these genes, 14 showed lower expression in PLE patients, whereas two resulted over-expressed. […] It has been supposed that protein modification during apoptotic cell clearance could lead to potential auto-antigen formation. […] This partial failure of the apoptosis contributes, together with the inadequate immunosuppression after UV exposure, to the antigen recognition and presentation, leading to the clinical manifestation typical of PLE patients.

• #14 Photodermatoses in India – Indian Journal of Dermatology, Venereology and Leprology

  https://ijdvl.com/photodermatoses-in-india/

  The cause of PMLE is not known, although an immunologic basis has been demonstrated. […] There appears to be a delayed type hypersensitivity (DTH) response to undefined endogenous, cutaneous photoinduced antigens as a result of inherited abnormality in the reduction of normal UVR-induced immunosuppression, thereby resulting in enhanced response to photoantigens and development of clinical lesions. […] The action spectrum is unclear, although it is most commonly 290-365 and rarely visible light.

• #15 Polymorphic Light Eruption – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK430886/

  The hardening effect, where further exposure to UV prevents the eruption, is not fully understood and could involve tanning, hyperkeratosis, and acanthosis of the epidermis, and/or the development of immunological tolerance. […] Twin studies indicate a polygenic model may explain familial clustering. Sunburn reaction in patients affected by polymorphous light eruption is normal.

• #16 Polymorphic light eruption – GPnotebook

  https://gpnotebook.com/pages/dermatology/polymorphic-light-eruption

  Polymorphic light eruption is a common idiopathic photosensitive disorder which is frequently mis-diagnosed with miliara („prickly heat”). It occurs in about 10-20% of the population with females affected more frequently than males in the ratio of 4:1. Presentation is usually in late adolescence and young adulthood, often early in the summer following exposure to ultraviolet (A and B wavelengths), intermittent eruption of non-scarring, erythematous itchy papules, plaques or vesicles induced by UV irradiation of sun-exposed skin. Also is a genetic component – appears to cluster in families: it has been estimated that the prevalence of PLE was 21 and 18% in monozygotic and dizygotic twins, respectively. First line of treatment for polymorphic light eruption includes sun avoidance, sunscreens and topical corticosteroids. New generation broad-spectrum sunscreens, with high sun protection factor for UVB (SPF), together with longer wavelength UVA protection, have been reported to confer total or partial protection in up to 90% of patients. Second line therapies includes systemic corticosteroids and photo(chemo)therapy.

• #17 Polymorphous light eruption: Pictures and treatments

  https://www.medicalnewstoday.com/articles/polymorphous-light-eruption

  Polymorphous light eruption (PLE) is a common skin rash that occurs due to sunlight exposure. […] Researchers are not sure what causes PLE, but they believe it may occur due to a reaction by the immune system. […] It is possible that people with PLE have some resistance to this UV-induced immunosuppression, which could result in skin inflammation, a 2022 review of research suggests. […] There may also be a link with estrogen, according to the 2022 review. This hormone may prevent UV radiation from suppressing the skin’s immune responses. […] In up to 50% of cases, people with PLE have family members who also have the condition. This may suggest a genetic component, but researchers have not proven this.

• #18 Polymorphous light eruption – Wikipedia

  https://en.wikipedia.org/wiki/Polymorphous_light_eruption

  Polymorphous light eruption (PLE) presents with itchy red small bumps on sun-exposed skin, particularly face, neck, forearms and legs. […] It is a non-life-threatening and potentially distressing skin condition that is triggered by sunlight and artificial UV exposure in a genetically susceptible person, particularly in temperate climates during the spring and early summer. […] The cause of PLE is not yet understood, but several factors may be involved. It is thought to be due to a type IV delayed-type hypersensitivity to an allergen produced in the body following sunlight exposure, in a genetically susceptible person. […] It has been suggested that an undefined endogenous or exogenous photo-allergen may trigger a delayed immune reaction resulting in PLE. […] Oxidative stress and the modification of the redox status of the skin has been implicated in the expression of PLE. […] Half of patients have a family history of PLE, demonstrating a clear genetic influence. […] The preponderance in women with a decline in severity following menopause has been thought to be associated with oestrogen effects.

• #19 Polymorphous Light Eruption: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1119686-overview

  In some PMLE lesions induced by UVA, keratinocytes were found to express ICAM-1. […] The demonstration that the female hormone 17beta-estradiol prevents UV radiationinduced suppression of the contact hypersensitivity response caused by the release of immunosuppressive cytokines (IL-10) from keratinocytes might explain why the risk of PMLE is higher in females than in males and why the risk decreases in women after menopause. […] It has been suggested that glutathione S-transferases (GSTs) act to protect against PMLE; however, a study of the isoenzymes of the GST genes GSTM1, GSTT1, and GSTP1 found no protective relationship of these isoenzymes to PMLE.

• #20 Polymorphic Light Eruption (PMLE): Causes and Treatment

  https://patient.info/doctor/polymorphic-light-eruption-pro

  A polymorphic light eruption (PMLE) occurs in response to sunlight after a period of time in which the skin has been covered and scarcely exposed to the sun. It is caused by ultraviolet A (UVA) light or visible light. […] The cause of PMLE is likely to be multifactorial. It is thought to be caused by an immunological reaction to a compound in the spring, but the precise nature is unknown. Findings are consistent with a type IV delayed hypersensitivity reaction. […] UV exposure causes a contact hypersensitivity response – this is normally suppressed by the release of immunosuppressive cytokines from keratinocytes. It has been suggested that 17-estradiol somehow prevents this response, thus leading to PMLE. This theory would account for the increased prevalence of PMLE in adult women and its tendency to wane after the menopause.

• #21 Polymorphous light eruptions – Indian Journal of Skin Allergy

  https://skinallergyjournal.com/polymorphous-light-eruptions/

  In PMLE, failure of this UV-induced immunosuppression leads to reduced production of neutrophil-derived TNF-, IL-4, and IL-10, failure of Langerhans cell migration, and lack of neutrophil infiltration. […] In patients with PMLE, these T cells are decreased, leading to a loss of immune tolerance resulting in autoimmunity. […] In patients of PMLE, reduced expression of these genes may lead to partial failure of apoptosis, leading to the accumulation of apoptotic cells, which acts as a potential trigger for the formation of autoantigens, thereby promoting the disease process. […] A deficiency of Vitamin D3 is considered a risk factor to increase disease susceptibility by impairing immune function and increasing inflammation. […] PMLE being more in females is possibly due to the hormone 17-estradiol, which prevents the UVR-induced immunosuppression and inhibits the release of immunosuppressive cytokines (IL-10) from keratinocytes, thus triggering the inflammation.

• #22 Patients with polymorphic light eruption have decreased serum levels of 25-hydroxyvitamin-D3 that increase upon 311 nm UVB photohardening – Photochemical & Photobiological Sciences (RSC Publishing)

  https://pubs.rsc.org/en/content/articlelanding/2012/pp/c2pp25188d

  Polymorphic light eruption (PLE) is a very common condition whose pathogenesis may involve immunological abnormalities. Vitamin D sufficiency is thought to be important for normal immune function. PLE patients have low 25(OH)D serum levels. 311 nm UVB phototherapy that prevented PLE symptoms increased those levels. Thus, we speculate that boosting levels of vitamin D may be important in ameliorating PLE.

• #23 Polymorphic Light Eruption | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/34016

  The cause of polymorphic light eruption is unknown. It is postulated that there is a delayed hypersensitivity reaction to an endogenous antigen expressed after exposure to sunlight or artificial sources of ultraviolet (UV) radiation. Theories must account for increased prevalence in women and for the hardening effect of on-going exposure to ultraviolet radiation. […] Current theories involve two steps that lead to a polymorphous light eruption. An unknown photoantigen is rendered immunogenic on exposure to UV. This does not cause a problem in unaffected individuals because of UV-induced suppression. In patients with a polymorphic light eruption, Tcell function is not suppressed by UV radiation until photo-hardening has taken place. The putative antigen induced by UV radiation leads to a predominance of CD4+ T cells and the production of proinflammatory cytokines such as interleukin (IL) 1. Vitamin D insufficiency, the role of estrogen in preventing UV-induced immune suppression, and dysregulated antimicrobial factors may be relevant. […] The hardening effect, where further exposure to UV prevents the eruption, is not fully understood and could involve tanning, hyperkeratosis, and acanthosis of the epidermis, and/or the development of immunological tolerance.

• #24 Polymorphic Light Eruption: What’s New in Pathogenesis and Management

  https://pmc.ncbi.nlm.nih.gov/articles/PMC6139322/

  New generation broad-spectrum sunscreens, with high sun protection factor for UVB, together with longer wavelength UVA protection, have been reported to confer total or partial protection in up to 90% of PLE patients. […] The mechanisms by which phototherapy induces photoprotection are not fully understood. […] However, in the last years many advances have been performed. […] Summarizing, photohardening works in PLE by restoring the normal UV immune suppressive pathway, involving multiple cell types.

• #25 Polymorphous Light Eruption Symptoms, Causes, and Treatment

  https://www.healthline.com/health/polymorphous-light-eruption

  Gradual hardening is one form of treating PMLE. This can be done through careful and measured exposure to sunlight, or it can be achieved through the use of phototherapy. […] After the rash has already appeared, a doctor may prescribe corticosteroids to help alleviate itchiness or burning. […] Your skin can build up a tolerance to UV light throughout the summer, but this will go away during the winter.

• #26 Immune Responses in Polymorphic Light Eruption: A Double-Edged Swordlogo-32logo-40logo-60NEJM Journal WatchnejmJW_1L_RGB-b

  https://www.jwatch.org/jd201011120000002/2010/11/12/immune-responses-polymorphic-light-eruption

  Ultraviolet radiation usually causes an immunosuppressive response that is muted in patients with PLE, which could protect them from skin cancer. […] Mechanisms of immunity have been proposed to play a part in PLE pathogenesis. […] One theory of PLE pathogenesis proposes that the T-cell–mediated immune response to UV-induced endogenous antigens is suppressed in healthy people but not in those with PLE. As a result, a skin rash follows UV exposure in PLE patients. […] Because suppressed immune response following UV exposure is thought to facilitate the growth and development of UV-induced skin cancers, the findings may explain why PLE patients have a lower incidence of skin cancer than the general population. If PLE patients are less likely to develop suppressed immune responses following UV exposure, they may retain T-cell immunity to antigens on UV-induced tumors, destroying cells that could become clinically apparent skin cancers.

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