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Our Dermatol Online. Online. 2013; 4(3): X-X
DOI: 10.7241/ourd.20133.??
Date of submission: 11.04.2012/acceptance: 16.05.2013
Conflicts of interest: None


Yogeesh Hosahalli Rajaiah, Kallappa C. Herkal

Department of Dermatology Venereology and Leprosy, Navodaya Medical College Hospital and Research Centre, Raichur, Karnataka, India

Corresponding author:  Ass. Prof. Yogeesh Hosahalli Rajaiah    e-mail: hryogesh@yahoo.com


Polymprhouos light eruption is the most common idiopathic photodermatosis. It is a sun induced cutaneous reaction characterized by onset itchy erathematous papules, plaques, vesicles or erythema multiforme type of lesions after brief exposure to sunlight. Sun-exposed areas of the body or rarely the partially covered areas are commonly involved. PLE is more common in temperate climates than in tropics. It begins usually at the onset of summer and moderates as the summer progresses. In most patients it usually runs a benign course. Diagnosis is mainly on clinical grounds. Therapy involves avoidance of sun-exposure and use of sunscreens. Cases not responding to simple measures require PUVA (Psoralen and Ultraviolet A) or UVB (ultraviolet B) therapy. Other alternative suggested therapies with variable success include oral hydroxychloroquine, beta-carotene, thalidomide and nicotinamide.

Key words: Polymorphous Light Eruption; UV-A radiation; UV-B radiation; Sunscreens; sun-induced reaction

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. It moderates as the summer progresses and usually subsides on absence of further sun exposure [1]. Polymorphous light eruption causes lot of psychological stress amongst those suffering from the disease especially in women with longstanding illness [2].
The first description of PMLE was probably that of Robert Wilson as reported by Bateman [3]. These authors used the term eczema solare to describe recurrent eczematous skin lesions that appeared on light-exposed body areas during the summer months. Jonathan Hutchinson introduced the term summer prurigo to describe a disorder that he observed in 13 Patients that probably represented a form of PMLE [4]. He described this disorder as a papular eruption that began at puberty and affected primarily the face and upper extremities. Hutchinson noted that it occurred in the summer and was related to sun exposure. Sellei and Liebner attempted to differentiate the eczema solare and the summer prurigo types of PMLE; they believed that the lesions of eczema solare are confined to exclusively sun-exposed parts of the body whereas the papules of summer prurigo appear on certain predisposed areas, such as forehead, the outer aspects of arms and ankles. In addition, they showed that, in one patient, sun exposure of a single body area not only produced local erythema in situ but also evoked the development of papular lesions in previously involved areas [5]. Lamb et al reviewed their experience with PMLE and called the condition solar dermatitis [6]. They noted that, in their patients from south western United States, plaques were the most common lesions, appearing in 75 percent of patients, and that vast majority of affected individuals were males. McGrae and Perry reviewed the Mayo clinic experience with PMLE and observed that persistent erythema should be included with eczema solare, summer prurigo and solar dermatitis as part of PMLE [7]. Magnus asserted that summer prurigo identified by Hutchinson is a disorder separate from PMLE [8]. Harber and Bickers opined that the terms summer prurigo, solar eczema, prurigo, plaques and persistent erythema (sun induced) to be included under a single term PMLE [9]. However, the current literature includes clinical lesions consisting of intermittent, delayed and transient cutaneous reaction to sun exposure as PMLE. The reaction is usually non-scarring, is pruritic and the lesions consist of either papules, vesicles, plaques, eczema, erythema multiforme-like lesions or insect bite reaction-like lesions as a spectrum of lesion in PMLE. Some authors do not include eczema, erythema-multiforme-like lesions or insect-bite like reactions as a part of spectrum since they are a source of confusion, and they may occur in conjunction with papules, plaques or vesicles at other sites in the body but not alone [10].
Epidemiological Aspects
Several population-based prevalence surveys have been conducted, and the results of these studies suggested that the prevalence of PMLE is 10-20 % in North America populations [11]. Berg interviewed 809 randomly selected office workers from four Swedish cities, and observed that 100 (12.4%) had a history consistent with PMLE [12]. In this study, there was a predominance of women with a history of PMLE. Pao et al interviewed 182 subjects in England and 368 subjects in Australia and found that the prevalence of PMLE to be 14.8% in London and 4.3% in Australia [13]. They suggested that the prevalence of PMLE may be higher in regions further away from the equator because of variations in the proportions of UVA and UVB radiation at different latitudes. Morison and Stern interviewed 271 random individuals entering a medical library in Massachusetts. Ten percent of this sample reported a history consistent with PMLE, and the reported prevalence was higher among females than males (14% VS 7%) [14]. Only 15% of individuals with a history consistent with PMLE had sought previous medical attention for their symptoms. Morrison and stern compared the PMLE patients identified from their survey of 38 patients with PMLE who presented to the photosensitivity clinic at General Hospital, Massachusetts. Only one significant difference between the two groups was observed; clinic patients required a mean exposure of 30 minutes to induce symptoms compared to a mean exposure of 3 hours among survey cases [15]. Ros and Wennernstern interviewed 397 workers in a Swedish pharmaceutical company and found 21% had a history consistent with PMLE. Their sample study primarily included women (86%) and so after adjusting, a prevalence estimate of 7.4% was reported. Only 3% of these patients had sought medical attention for their symptoms [16]. The results of these prevalence studies suggest that PMLE is a relatively common condition in North America and European populations. PMLE is more common in temperate climates than nearer equator. The explanation for this is unknown, but lesion development may be inhibited by UVB-induced immunological reactivity in sunnier climates. In addition, variations in the proportions of UVA and UVB in terrestrial sunlight at different latitudes may play a role, as UVA appears to be important in lesion induction. Thus, the greater proportion of UVA to UVB in temperate climates may cause more PMLE than in tropical regions. Furthermore, greater UVA exposure may also occur because of a slower rate of sun burning [13]. Jansen observed 138 PMLE cases in Finland during the early 1970s. 62% of these were women, 51% reported seasonal hardening effect, and 60% reported symptom development with 30 min of sun exposure [16]. 57% were able to identify the exact onset of their first symptoms. The mean age of onset was 36.6 years, and a mean duration of symptoms prior to clinical presentation was 10.5 years. Petzelbaner et al studied 198 patients and reported that the mean age at onset of symptoms was 35 years and the mean duration of PMLE prior to diagnosis was 12 years [17]. Lesional morphologies reported in these series include urticaria-like plaques (25.1%), blistering (36%), papular lesions (25%) and lesions with scales or crusts (6%) [17]. In a study of 110 patients by Boonstra et al, average age onset of disease in men was 46 yrs as compared to 28 yrs in females [18]. The mean duration of complaints before they came to the clinic was 9.2 years. The course of disease activity during the period (from 1985 to 1991) was progressive in 86 patients, stationary in 19, and unknown in 5. The morphology of lesions, according to patient history and clinical inspection, was papular (61 Patients), papulovesicular (27 patients), eczematous (18 patients), or erythematous with infiltration of the skin (4 patients). The Minimum Erythema Doses (MEDs) for UVB and UVA were lowered in 43% and 37% respectively in men. In women only 4% and 11% MEDs were reduced for UVB and UVA respectively [18]. The photoprovocation tests showed a pathologic reaction to both UVB and UVA in 88% of the men and in 52% of the women. In the remaining patients they found pathologic reactions to UVB alone (3% men, 24% women). Abnormal reactions to visible light were mostly observed in those patients who reacted pathologically to UVB and UVA [19].
Etiology and Pathogenesis
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 [20,21]. Far et al studied the effects of indomethacin on UVB and UVA induced erythema in patients with PMLE [22]. They found that topical application of indomethacin inhibited UVB but not UVA erythema in 13 of 23 patients. In the remaining 10 patients there was an augmented response to both UVA and UVB. This finding indicates that PMLE embraces two or more disease states- the more severe group, perhaps associated with the abnormal metabolism of arachidonic acid in response to UV irradiation, and a milder form [22]. In some PMLE lesions induced by UV-A, keratinocytes were found to express intercellular adhesion molecule 1 (ICAM-1) [23,24]. Induction of ICAM-1 occurs either directly by effects of UV on ICAM-1 gene or indirectly by effect of interferon gamma produced by activated lymphocytes in the lesions. Intravascular deposits of fibrin, C3 and Immunofglobulin-M were noted in certain patients suggesting the possible role of vascular injury and ensuing activation of clotting cascade in the pathogenesis. Immunohistochemical analysis by Schornagel et al in 2004 showed a significant decreased neutrophil infiltration in PMLE skin after UV-B irradiation compared with healthy case control subjects (P < .05) [25]. The authors concluded that PMLE is marked by an altered immune response resulting in decreased skin infiltration of neutrophils after UV-B irradiation. Induction of PMLE: Difficulty in reliable laboratory induction of clinical lesions has frustrated investigators into the pathogenesis of PMLE. No particular wavelength induces lesions consistently. In most series, however, UVA has been more reliable effective in inducing lesions than UVB [26]. Although chromopheres for PMLE have not been identified, the induction of lesions by a UVA sun-bed in the non-tanning sacral pressure area suggests that UV absorption, at least some patients, may be oxygen independent [27,28]. The reported percentage of patients with family history of photosensitivity ranges from 15% to 56%. Several authors have speculated that PMLE is inherited as an autosomal dominant gene with reduced penetrance. Some published studies have investigated the genetics of PMLE in greater detail, and the results of these studies suggest that a polygenic model can also explain PMLE inheritance. Millard et al examined 420 adult female twins enrolled in a twin registry in England. The prevalence of PMLE was 23% in monozygotic twins and 18% in dizygotic twins [29]. Both a polygenic model of inheritance and a dominant single gene model explained these data. Although results of the genetic studies suggest that environmental factors, other than UV radiation, may be involved in the pathogenesis of PMLE. Oral contraceptive use was evaluated in one small case series. 3 out of 87 women in this study noted some improvement in their PMLE symptoms after discontinuation of oral contraceptives, but this alleviation of symptoms was only temporary [29]. 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 [30].
The histological features of PMLE are characteristic but not pathognomonic and vary with the different clinical presentations. There is a moderate to intense, tight perivascular infiltrate in the upper dermis and mid-dermis in all clinical types, the infiltrate consisting predominantly of T cells; although neutrophils are also present. Eosinophisls are infrequent [31].
Epidermal changes may be absent or variable in severity [31].
Epidermal spongiosis occurs along with perivascular infilitration and dermal edema. In older lesions dermal edema and perivascular infiltrate may extend into deep dermis. Acanthosis and parakeratosis can occur along with epidermal spongiosis [12]. Occasional dyskeratosis, exocytosis may be seen [1]. Sunburn cells are notably absent. The liquefactive degeneration at the dermo-epidermal interface, commonly observed in cutaneous lupus erythematosus, may also be seen in PMLE [32]. Dermal edema may be accompanied by perivascular edema and endothelial swelling [31].
Influence of time
The manifestations of a normal sunburn response must be considered in the description of abnormal findings in the epidermis of a skin biopsy from a patient with PMLE. For example necrosis of epidermal cells which is not a specific feature of PMLE, but is response seen in normal skin 24 hours after irradiation with UVB, may be seen in lesions of PMLE [9].
Influence of site
Biopsy specimens obtained from light-exposed areas, such as the face and the arms, may show chronic degenerative changes due to repetitive actinic damage; among them are hyperkeratosis, epidermal atrophy and solar elastosis [9]. The dermal infiltrate is composed primarily of lymphocytes. CD4+T cells dominate in the first 5 hours after irradiation, while CD8+T cells dominate 72 hours after exposure. Delayed Langerhan’s cell depletion has been observed in PMLE. In normal skin CD11b+ cells decrease in the dermis following UV exposure. In PMLE patients, CD11b+ cells increase in both epidermis and dermis after UV exposure [33]. Most histopathological studies have focused papular type lesions; other lesion type may have slightly varied appearances. For example, spongiotic vesicles and subepidermal blisters are often formed in vesiculobullous lesions and, in plaque lesions, the dermal infiltrate tends to be lichenoid and spongiosis is widespread [34]. The picture may resemble that seen in early lesions of subacute cutaneous lupus erythematosus (SCLE), except that the infiltrate is periadnexal in case of SCLE and perivascular in case of PMLE [31].
Clinical Features
The eruption typically begins in each spring often moderating as summer progresses. It rarely occurs in winter except after exposure to UVR reflected from snow. Individual susceptibility varies considerably; the period of sunexposure needed to trigger the eruption usually begin from 30 min to several hours, occasionally more or less. Following exposure, new lesions appear after a latent period of hours to days, but not less than 30 minutes, although pruritus may develop sooner. In the absence of further exposure, these lesions subside completely, usually without scarring, over 1 to 7 days or occasionally longer. In any one patient, PMLE always tends to occur on the same areas, although the distribution may gradually spread or recede overall. Lesions generally occur symmetrically and usually affect only some exposed sites, often those covered in winter such as the upper chest and arms. Associated systemic symptoms are rare, but chills, headache, fever and nausea are possible [15]. Over 7 years, 64 of 114 patients (57%) reported diminution in their sun sensitivity, including 12 (11%) that totally cleared [14]. PMLE has been subdivided into several morphologic variants, namely papular, papulovesicular, plaque, vesiculobullous, eczematous, insect bite-like, and erythema multiforme-like forms, with one type of lesions usually predominating in a given individual [1]. In some patients only pruritus occurs without any lesions. “Polymorphic light eruption sine eruption” is used to describe such an entity in patients. They probably represent milder form of PMLE or subclinical of PMLE [35]. The papular form is the most common followed by papulovesicular and plaque variants, while the rare vesiculobullous, eczematous, insect bite like, and erythema multiforme-like forms are controversial and are a source of confusion. They are excluded altogether by many authors. It is unlikely that such variants represent true subgroups, because lesion of different as morphology may occur at different skin areas in the same patient. Diffuse facial erythema and swelling, for example, may accompany typical papular lesions at other sites. A variation in susceptibility of exposed skin areas to PMLE is an important distinguishing characteristic feature of the disorder from other photodermatoses, and juvenile spring eruption [36]. Juvenile spring eruption commonly affects boys aged 5 to 12 years, apparently represents this phenomenon. This condition is a self limiting eruption of pruritic grouped papules and vesicles confined to the light exposed helices of the ears and histopathology is similar to that seen in PMLE. Sometimes a patient having PMLE lesions elsewhere can have lesions involving the helices of ears, similar to those seen in juvenile spring eruption. The most commonly affected sites include ‘V’area of the neck and forearms. The face and hands of PMLE cases may be spared, because these sites often receive daily sun exposure and thus undergo hardening [11]. The onset of PMLE usually occurs in second to third decades, but symptoms may begin in early childhood or late adulthood. PMLE is reported to occur in all skin types; however, fair-skinned individuals are most commonly affected. Women are more often affected than men, usually in 2:1 or 3:1 ratio. The observed gender differences in PMLE occurrence probably reflects differences in underlying genetic and hormonal pathways, and possibly differences in the daily and seasonal patterns of sun exposure between men and women. Women may also be more cognizant of their skin symptoms and are more likely to seek medical attention than men, which could result in an over representation of women in clinical studies [11].
Differential Diagnosis
PMLE can be differentiated from actinic prurigo because the onset of actinic prurigo typically occurs in early childhood. Actinic prurigo lesions often persist for months even after cessation of UVR experience, and chelitis and scarring are common features [37]. Solar urticaria develops almost immediately after sunexposure and resolves within hours, lesions being wheals; lesion development and resolution in PMLE are less rapid [38]. Chronic actinic dermatitis primarily affects elderly men and is characterized by scaly or eczematous lesions [37,39], while PMLE lesions predominately affect women in early to mid adulthood. Other differential diagnosis that should be considered includes drug-induced photosensitivity, photocontact dermatititis, airborne contact dermatitis, hydroa vaccinforme, lupus erythematosus and porphyrias. Careful history, including questions about age at symptom onset, exposure to known photosenitizers, the time interval between the sunexposure and the onset of symptoms, family history of photosensitivity, sunscreen use and possible involvement of other organ system may aid in diagnosis. Sometimes subacute cutaneous lupus erythematosus may present with lesions similar to PMLE. In case of doubt, measurement of serum antinuclear factor, serum anti-Ro and anti-La would exclude SCLE. More persistent plaque-type PMLE must be differentiated from Jessner’s lympholytic infiltrate of the skin by histopathological examination of skin biopsy [40].
Studies of the natural history of PMLE have demonstrated that the course of this condition is highly variable, ranging from complete remission to development of debilitating symptoms and possibly other autoimmune disorders. After 38 years of follow-up, Ferguson and Ibbotson observed a 24% spontaneous remission rate in their cohort [41]. Jansen and Karvonen followed 114 patients for 7 years after diagnosis, and found that 57% improvement in their patients during the follow–up period [42]. After 4 years of follow up of 110 Dutch PMLE patients, symptoms worsened in 86, stayed the same in 19, and were unknown in 5. Hasan et al observed 24% of their patients went into complete resolution of lesions, 51% showed improvement of the conditions, and in 24% condition remained unchanged or worsened [43].
The mild disease of many patients is satisfactorily controlled by the moderation of sunexposure at times of high UV intensity and regular application of broad-spectrum sunscreens with a high protection factor particularly against UVA. Thus, the use of sunscreen protecting against mostly UVB may lead exacerbation of UVA-sensitive PMLE by permitting patients longer sunexposure without burning and should be avoided [44]. More severely affected subjects, however require courses of prophylactic low-dose photochemotherapy or phototherapy [45]. In a study of 42 patients of PMLE, Murphy et al found that 6 weeks of thrice weekly low-dose PUVA and UVB irradiation therapy in early spring were found to be excellent prophylactic treatments [45] PUVA was more effective than UVB from patients’ subjective reports and from clear clinical trend in that direction. In another study by Addo et al, 36 Patients with PMLE were treated with either UVB photo therapy or PUVA therapy during the spring and the early summer [46]. Both the forms of therapy were found to be effective in 90% of cases. Similar efficacies were found in other studies as well [47]. The UV exposure of prophylactic UVA or UVB may sometimes trigger the eruption, particularly in severely affected individuals, necessitating concurrent administration of systemic glucocorticosteroids on occasion. However, some patients are unsuitable for this or their disease remains uncontrolled, and therefore is inappropriate for further courses. Such PUVA – intolerant patients or those unable to commute for treatment may instead be tried on suggested alternative therapies such as hydroxychloroquine, thalidomide, beta-carotene and nicotinamide [47,48]. A study by Corbett et al reported that beta-carotene was effective in reducing erythema and irritation [47]. Chloroquine also reduced irritation and erythema. They concluded that they are only moderately effective in controlling the disease. Similarly Murphy et al reported only moderate improvement with hydroxychloroquine. Hence except for thalidomide, in cases of persistent case of PMLE, these are of only occasional or limited therapeutic value, and phototherapy-resistant cases thus pose a management problem [48]. Sometimes, short-term (less than a week) oral glucocorticoid therapy rapidly suppresses the eruption once developed although no controlled studies are undertaken. Thus glucocorticoids can be given for young, fit patients or in those who need only intermittent therapy for vacations or other occasional sun exposure [49]. Topical corticosteroids and oral antihistamines are effective in alleviating symptomatic relief but are of not much benefit [47]. There remain, however, a small proportion of patients, who are unsuitable for, or unable to tolerate, or not helped by any of these measures, and UV avoidance remains only safe and effective option. A further few of them are so sensitive that they are continuously affected in spite of all reasonable UV avoidance measures, and in these, short-term immuno- suppressive therapy with low-dose azathioprine may be appropriate, and has lead to marked clinical improvement in two such patients [50].
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