Indian Dermatology Online Journal

: 2021  |  Volume : 12  |  Issue : 2  |  Page : 211--219

Polymorphous light eruption- An Indian Scenario

Kaliaperumal Karthikeyan1, Manju Aishwarya2,  
1 Department of Dermatology, Venereology and Leprosy, Sri ManakulaVinayagar Medical College and Hospital, Madagadipet, Pondicherry, India
2 Department of Dermatology, Venereology and Leprosy, Pondicherry Institute of Medical Sciences, Pondicherry, India

Correspondence Address:
Kaliaperumal Karthikeyan
Department of Dermatology, Venereology and Leprosy, Sri ManakulaVinayagar Medical College and Hospital, Madagadipet, Pondicherry


Polymorphous light eruption (PMLE) is the most common, idiopathic, acquired photodermatosis, characterized by abnormal, recurrent, and delayed reaction to sunlight. Polymorphous light eruption is common worldwide but the morphology, distribution, and pigmentary changes are unique in Indian skin which is discussed in this review. The prevalence of PMLE is around 10–20% in the general population. It commonly occurs in females between 20and 30 years of age. It is the most common photodermatosis in school-going children. Visible light sensitivity is an important phenomenon in PMLE. It typically presents as recurrent and chronic lesions over photoexposed sites. Initially, patchy erythema occurs with pruritus. Most of the Indians belong to type IV to type VI skin and pigmentary changes are commonly seen. The unique feature of PMLE in Indian skin is the pigmentary change which varies from hypopigmented to hyperpigmented lesions. These pigmentary changes may occur alone or in combination with erythematous or skin-colored lesions. The pigmentary lesions are seen in more than 50% of lesions. The histopathology of PMLE is characterized by the presence of hyperkeratosis, spongiosis with or without the presence of liquefactive degeneration in the epidermis. Dermal changes in the upper and mid dermis include the presence of dense perivascular lymphocytic infiltrate. The management of PMLE includes both preventive measures and medical management. Topical sunscreens, topical steroids, hydroxychloroquine and antioxidants play a very important role.

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Karthikeyan K, Aishwarya M. Polymorphous light eruption- An Indian Scenario.Indian Dermatol Online J 2021;12:211-219

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Karthikeyan K, Aishwarya M. Polymorphous light eruption- An Indian Scenario. Indian Dermatol Online J [serial online] 2021 [cited 2021 Apr 16 ];12:211-219
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 Polymorphous light eruption- an Indian Scenario

Polymorphous light eruption (PMLE) is the most common, idiopathic, acquired photodermatosis, characterized by abnormal, recurrent, and delayed reaction to sunlight. It is an immunologically mediated disease that occurs due to delayed hypersensitivity reactions.[1],[2],[3],[4] It is commonly known as “sunrash” and referred to as “sunallergy” by the patients even though there is no real allergy associated with its pathogenesis.[5] It was first described by Robert Willanin 1817 as“eczema solare.” The term “polymorphous light eruption” was coined by Carl Raschin 1990 and was again described as a common term for prurigo aestivalis and eczema solare by Haxthausenin1919.[6] It is also referred to as dermatographia photogenica, erythema perstans solare, and prurigo aestivalis.[7] Polymorphous light eruption is common worldwide but the morphology, distribution, and pigmentary changes are unique in Indian skin which is discussed in this review. Further, the treatment modalities and the role of sunscreens in Indian context is also discussed.


The prevalence of PMLE is around10−20% in the general population[8] with females between 20 and 30 years of age[6] and school-going children affected more commonly. PMLE frequently occurs in temperate climates due to a greater proportion of UVA to UVB in these regions. Though the disease is said to be more common in temperate regions, the prevalence of PMLE in India is similar to that reported in the world.[9] The proportion of cases varies between 2% and13.5% across different areas in India.[10],[11],[12],[13],[14],[15],[16],[17] Most of these studies are hospital-based and may not represent the community prevalence. This probably is an underestimate of the real prevalence.

In Indian studies, a female preponderance was noted. The disease is seen in people who indulge in outdoor activities such as farmers and laborers. In certain studies, high incidence was noted in housewives probably because of household activities.[10],[11],[18]

 Seasonal Variation

The wide climatic and geographic variations in India lead to a range of seasonal variation. The PMLE peaks in the month of March and continues into early summer. These are the days when sunshine is longer. Some cases also occur during later winter from January onwards in Northern India probably because of the habit of sunbathing. The second peak was noted in September.[10],[11],[14],[17]

 Genetic Predisposition

Polymorphous light eruption occurs in family members in 12−46% of PMLE patients.[8] “Familial clustering” in PMLE suggests a genetic etiology.[10] In India family clustering was not observed.

 Pathogenesis of PMLE

PMLE occurs due to the interplay of genetic and environmental factors.[19],[20],[21],[22] The possible mechanisms involved in pathogenesis are given in the form of a chart [Figure 1] which incorporates various factors involved.[23],[24],[25],[26],[27]{Figure 1}

 Clinical Features


Visible light sensitivity is an important phenomenon in PMLE.[27] It typically presents over photo exposed sites within a few minutes of exposure to sunlight. Photosensitivity is the most common symptom that occurs in Indian patients but some experienced a burning sensation on exposure to the sun.

Morphological lesions

Initially, patchy erythema occurs with pruritus. The primary sites involved are upper chest, “V” area of the neck, upper arms, forearms, back of hands, thighs, and the sides of the face.[28],[29],[30],[31],[32],[33],[34] Improvement of lesions is noticed during the latter half of the summer season, which is called “hardening.”[32],[34] Due to repeated daily sun exposure, the face and hands undergo hardening.[35]

The action spectrum involves UVA, UVB, and visible light.[25],[36] There is also an interesting observation of PMLE preferentially involving the sites of hypopigmented scars.[37]

PMLE is typically characterized by transient, intermittent, and a delayed response at 30 minutes to several hours after UV light exposure resulting in an abnormal cutaneous response.[10],[15],[16] The eruption usually takes up to two weeks to resolve in the absence of further ultraviolet radiation.[17] A typical lesion of PMLE is a hyperpigmented plaque with a hypopigmented rim. Morphologically many variants have been described, hence the name “polymorphous.”[28] But one morphology usually predominates in an individual i.e., monomorphous.[38] The lesions usually resolve in about 2 weeks in the absence of UV radiation.

The clinical features of PMLE usually follow a characteristic sequence following sun exposure. It starts with itching followed by the appearance of a patchy erythema. Following this, distinct lesions appear which are sparsely distributed initially, which then coalesce to form densely aggregated lesions. Lichenification, scaling, and scarring usually occur as secondary lesions as a result of scratching and rubbing.

The morphological types of lesions noted in the Indian skin are macule, papule, plaque, vesicular, and plaques with lichenification; as isolated lesions or in combinations. In India, the sites of lesions are influenced by the clothing. In women, the forearm and back are exposed and they are commonly involved.[Figure 2] The external aspect of the arms and forearms were involved in most of the cases possibly because these parts are placed horizontally while sitting or traveling and receive the maximum exposure.[18] [Figure 3] On the other hand, the position of the face is vertical while walking or working and only rays fall on the cheek and nose which are affected. [Figure 4],[Figure 5],[Figure 6],[Figure 7]. Neck may be exposed to the sun if the person is bending forward. [Figure 8]. Covered areas were not affected irrespective of the type of clothing which suggests that it is probably preventable by all types of clothing.{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}{Figure 7}{Figure 8}

Various morphological types of PMLE have been reported. They are summarized in [Table 1].{Table 1}

The unique variants described include the pinpoint papular variant or micropapular variant of PMLE, which presents as multiple, monomorphic pinpoint, closely aggregated skin-colored to hypopigmented itchy lichenoid papules (1−2 mm) on sun-exposed areas[Figure 6].[39] Erythema multiforme like PMLE is a less common type of PMLE. It typically presents as target-like lesions in photo distributed areas. This type has to be differentiated from photosensitive erythema multiforme based on histopathology and phototesting results.[40],[41]

Singh et al. described a distinctive pseudovesicular, monomorphic micropapular eruption predominantly involving the nose and adjoining cheeks that affects young to middle-aged people with no gender predilection. It may be photoaggravated in some cases and runs a chronic course. They proposed the term lichenoid pseudovesicular papular eruption of the nose for this condition. This may be variant of PMLE seen in India.[46]

 Pigmentary Changes and PMLE

In fairer skin types, the lesions are mostly erythematous papules or plaques and pigmentary changes are unknown.[38] Most of the Indians belong to type IV to type VI skin and pigmentary changes are commonly seen which varies from hypopigmented to hyperpigmented lesions. [Figure 7] and [Figure 8] These pigmentary changes may occur alone or in combination with erythematous or skin-coloured lesions. The pigmentary lesions are seen in more than 50% of lesions.[18]

The pigmentary chnges may persist after the lesions subside and have to be differentiated from other causes of hypopigmentation.

 Differential Diagnosis

The important differential diagnosis is Lupus erythematosus. There are also a few reports that show that PMLE patients are associated with high titres of ANA and severe photosensitivity progressing into lupus erythematosus.[47] The difference between PMLE and LE are summarized in [Table 2].{Table 2}

The differential diagnosess for hypopigmented macular PMLE lesions are pityriasis alba, pityriasis versicolor, indeterminate leprosy, previtiligo, post-inflammatory

Hypopigmentation, and nevus anemicus.[48],[49] In India, dermatophytosis is also an important mimic of PMLE.[50]

The infiltrated plaques have to be differentiated from sarcoidosis, Borderline leprosy, Jesse's lymphocytic infiltrate, lupus vulgaris, granuloma annulare, and granuloma multiforme. Another important photodermatosis which has to be differentiated from PMLE is actinic prurigo.

 PMLE in Children

PMLE is the most common photodermatosis in childhood.[35] It occurs in children during the summer. They are commonly seen over the face, the “V” area of the chest, the back of the neck, and the dorsolateral aspects of the forearms. The face is the common site of occurrence in children. [Figure 6] and [Figure 7] The morphological patterns observed include grouped papules, plaques, vesicles, and eczematous plaques.

 Histopathology of PMLE

The histopathology of PMLE is characterized by the presence of hyperkeratosis, spongiosis with or without the presence of liquefactive degeneration in the epidermis. Dermal changes in the upper and mid dermis include the presence of dense perivascular lymphocytic infiltrate. The dermal infiltrate is composed primarily of T lymphocytes. Sunburn cells are notably sparse or absent.[25] The histopathology varies depending upon the morphological type. Histopathological differential diagnoses for polymorphous light eruption includes reticular erythematous mucinosis, Jessener's lymphocytic infiltrate, lupus erythematosus, and actinic reticuloid. The histopathology of PMLE can be graded as follows [Table 3].[17]{Table 3}


In an Indian study, phototesting of patients with PMLE showed that UVB rays were the most relevant wavelength. This increased sensitivity could be due to the geographical conditions, heat, and humidity in the subtropical climate. Photo-patch testing is not helpful indiagnosing PMLE.[51]

 Management of PMLE

The management of PMLE includes both preventive measures and medical management.

Physical protection plays a very important role. The use of an umbrella can be very useful. The patients should wear a dress covering the exposed areas to provide sun protection. Light-colored clothing is preferred over darker shades. Cotton fabric is recommended for people who work in sun. The patient advice pamphlet is given in [Table 4]. The various lines of management available are listed in [Table 5].{Table 4}{Table 5}

Treatment should be based on the age, sex, occupation, and site of involvement. In Indian context, economic conditions also should be considered. The management designed individually to suit the patients can be successful in the treatment and prevention of the disease.

 Sun avoidance and Sun Protection

Sun avoidance is the only definitive way of preventing PMLE. But this is not possible in a largely agricultural country like India. Sun protection may be a useful alternative. Sun protection should be advised as a preventive measure during summer months with sun avoidance between 11.00 am and 3.00 pm accompanied by regular application of sunscreens. Patients should also be advised regarding the use of protective clothing and should be informed that a tight and wet fabric increases the transmission of UV light.[33]


Broad-spectrum sunscreens of the new generation have high SPF and they also provide protection against longer wavelength UVA. Hence, their regular use will provide partial or complete protection against PMLE in almost 90% of patients. In contrast, the old generation sunscreens protect primarily against UVB and does not protect against UVA can provoke PMLE. Patient education regarding proper application technique, quantity to be used, and the necessity to cover all sun-exposed sites including temples, ears, lateral and posterior neck.

In India, most of the sunscreens available are combination products which include physical and chemical sunscreens. They are available in a wide range of sun protection factors. Sunscreens are useful in the prevention of PMLE in patients. But it has been observed that most individuals are not aware of sunscreens and they do not apply sunscreens properly.[52],[53],[54]

Further application is necessary after sweating. In the Indian subcontinent where humidity is high and most of the patients are laborers, the role of sunscreen is debatable.

 Topical Corticosteroids

High potent topical steroids can be used in patients with mild episodes of PMLE to relieve itch. When used in combination with phototherapy or photo-chemotherapy, they help in reducing the severity and incidence of rash associated with treatment. Further in localized lesions occurring in specific areas, topical steroids are particularly useful.[4]

 Topical Antioxidants

A combination of topical antioxidants like alphaglycosylrutin, ferulic acid, and tocopherol acetate was found useful in PMLE. This protects against the inflammation reactions that are most likely to be mediated by the generation of free radicals in the skin.[54]

 Systemic Corticosteroids

Systemic steroids are indicated in acute and severe cases. Daily prednisolone in the dosage of 25 mg for 4−5 days at the onset may help to settle the attacks. Prednisolone 1 mg/kg for 1−2 weeks may be initiated during acute and severe exacerbations. Prolonged courses of prednisolone must be avoided due to its potential long term side effects. Therefore, it can be cautiously used in patients with occasional, symptomatic attacks of PMLE.[55]


The frequency and severity of PMLE decreases with summer progression as a result of desensitization phenomenon called “hardening.” This phenomenon is used in the treatment of PMLE. For mild cases, a self-conditioning programme by graduated exposure to sunlight is recommended. For severe cases, medically supervised conditioning is preferential. In Indian context, with increasing summer, the hardening occurs as a natural phenomenon.[55]

The mechanism of induction of photoprotection is probably due to the following reasons:

induction of melanizationinduction of epidermal thickeningUV induced immunomodulatory and anti-inflammatory effects


Hydroxychloroquine 400 mg daily for the first month followed by 200 mg daily for 12 weeks has shown to have a mild benefit in PMLE with a reduction in the severity of the rash. Its membrane stabilizing properties cause proteolytic enzyme inhibition. Hydroxychloroquine 400 mg/day has to be started a few days prior to exposure and it should be reduced to 200 mg/day after optimal drug levels have been reached. In an Indian study, the efficacy of hydroxychloroquine in PMLE has been demonstrated in the trial showing reduction in eruption. Short-term treatment courses with hydroxychloroquine seem to be well-tolerated with a minimized risk of ocular lesions.[56],[57],[58],[59]

 Systemic Immunosuppression

Systemic immunosuppressants like azathioprine may be recommended in PMLE in the following situations:

extreme sun sensitivityintolerance to phototherapypatients in whom sunscreens are ineffective

The azathioprine was used in the dose of 50mg to 150mg and was effective in a small series of patients but it takes few weeks to act. Cyclosporine has also been found to act in severe cases of PMLE.[60]

Thalidomide has been used with some success in certain cases, but the serious adverse side-effects associated with this medication have limited its use.[61]


Polymorphous light eruption is a common disease with varied presentation in the Indian skin. Large scale studies are sparse in this largely neglected disease. It has to be differentiated from its close mimics and appropriately managed. A concord in management between the patient and treating physician is cornerstone for successfully overcoming this disease.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Gruber-Wackernagel A, Byrne SN, Wolf P. Polymorphous light eruption. Clinic aspects and pathogenesis. Dermatol Clin2014;32:315–34.
2Moncada B, Gonzdlez-Amaro R, Baranda ML, Loredo C, Urbina R. Immunopathology of polymorphous light eruption: T lymphocytes in blood and skin. J Am Acad Dermatol 1984;10:970-3.
3Medeiros VL, Lim HW. Sunscreens in the management of photodermatoses. Skin Therapy Lett 2010;15:1-3.
4Boonstra HE, van Weelden Toonstra HJ, van Vloten WA. Polymorphous light eruption: A clinical, photobiologic, and follow-up study of 110 patients. J Am Acad Dermatol 2000;42:199-207.
5Hönigsmann H. Polymorphous light eruption. Photodermatol Photoimmunol Photomed 2008;24:155–61.
6Ling TC, Gibbs NK, Rhodes LE. Treatment of polymorphic light eruption. Photodermatol Photoimmunol Photomed 2003;19:217–27.
7Epstein S.Studies in Abnormal Human Sensitivity to Light, I Prurigo Aestivalis, Eczema Solare and Urticaria Photogenica; II Light Sensitivity in Prurigo Aestivalis, Eczema Solare and Urticaria Photogenica; III Passive Transfer of Light Hypersensitivity in Prurigo Aestivalis; IV Photoallergic Concept of Prurigo Aestivalis. J Invest Dermat 1942;5:187—96, 225—41, 285—7, 289—95.
8Ibbotson S, Dawe R. Cutaneous Photosensitivity Diseases. In: Griffiths CEM, Barker J, Bleiker T, Chalmers R, Creamer D, editors. In Rook's Textbook of Dermatology. 9th ed. John Wiley & Sons; 2016.p. 127.1-127.35.
9Wadhwani AR, Sharma VK, Ramam M, Khaitan BK. A clinical study of the spectrum of photodermatoses in dark-skinned populations. ClinExp Dermatol 2013;38:823–9.
10Verma K, Rokde R, Singh U. A clinic epidemiological and histo-pathological study of polymorphic light eruptions in malwa region. Indian J Clin Exp Dermatol 2019;5:24-9.
11Deshmukh AR, Pathrikar SS, Khedkar MY, Mahajan KR, Sherasiya BS.Clinic epidemiological study of polymorphous light eruption in Marathwada region. Int J Recent Trends Sci Technol 2015;17:128-30.
12Srinivas CR, Sekar CS, Jayashree R. Photodermatoses in India. Indian J Dermatol Venereol Leprol 2012;78:1-8.
13Kuruvila M, Dubey S, Gahalaut P. Pattern of skin diseases among migrant construction workers inMangalore. Indian J Dermatol Venereol Leprol 2006;72:129-33.
14Agarwa S, Sharma P, Gupta S, Ojha A. Pattern of skin diseases in Kumaun region of Uttarakhand. Indian J Dermatol Venereol Leprol 2011;77:603-4.
15Murthy PS, Kar PK, Grover S, Rajagopal S. Polymorphous light eruption in ground crew Ind J Aerospace Med 2006;50:39-42.
16Prasad PV, Kaviarasan K, Sidhu U.A clinico-pathological study of poly morphous light eruption. J Cosmet Dermatol Sci Appl 2012;2:219-23.
17Grover S, Ranyal RK, Bedi MK. A cross section of skin diseases in rural Allahabad.Indian J Dermatol 2008;53:179-81.
18Sharma L, Basnet A. A clinicoepidemiological study of polymorphic light eruption. Indian J Dermatol Venereol Leprol 2008;74:15–7.
19Rhodes L, Durham BH, Fraser WD, Friedmann PS. Dietary fish oil reduces basal and ultraviolet B-generated PGE2 levels in skin and increases the threshold to provocation of polymorphic light eruption. J Invest Dermatol 1995;105:532-5.
20Norris PG, Morris J, McGibbon DM, Chu AC, Hawk JLM. Polymorphic light eruption: An Immunopathological study of evolving lesions. Br J Dermatol 1989;120:173-83.
21Ren G, Su J, Zhao X, Zhang L, Zhang J, Roberts AI.Apoptotic cells induce immunosuppression through dendritic cells: Critical roles of IFN-gamma and nitric oxide.J Immunol2008;181:3277–84.
22Millard TP, Bataille V, Snieder H, Spector TD, McGregor JM. The heritability of polymorphic light eruption. J Invest Dermatol 2000;115:467–70.
23Elmets CA, Cala CM, Xu H. Photoimmunology. Dermatol Clin 2014;32:277–90.
24Hosahalli RY, Herkal KC. Polymorphous light eruption-A review. Our Dermatol Online 2013;4:375-9.
25Lal BM, Devi AS, Suhasini K. The study of clinical variations and histopathological findings in polymorphous light eruption. J Evid Based Med Healthc 2016;3:2899-904.
26Vandergriff TW, Bergstresser PR. Abnormal Responses to Ultraviolet Radiation: Idiopathic, Probably Immunologic, and Photoexacerbated in Fitzpatrick's Dermatology in General Medicine. 8th ed.. Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K, editors. McGraw-Hill; 2012. p. 1050-1.
27Wolf P, Byrne SN, Gruber-wackernagel A. New insights into the mechanisms of polymorphic light eruption: Resistance to ultraviolet radiation-induced immune suppression as an aetiological factor. Exp Dermatol 2009;18:350–6.
28Tutrone WD, Spann CT, Scheinfeld N, Deleo VA. Polymorphic light eruption. Dermatol Ther 2003;16:28-39.
29Singh M, Sharma E. Novel and secure trend for photo protection-A Hallmark of plant metabolites as UV filters. Int J Rec Sci Res 2014;5:322-5.
30AlJasser MI, Lui H, Ball NJ, Kalia S. Persistent polymorphous light eruption after ultraviolet A1 phototherapy. Photodermatol Photoimmunol Photomed 2013;29:52-4.
31Rai R, Shanmuga SC, Srinivas CR. Update on photoprotection. Indian J Dermatol 2012;57:335-342.
32Lehmann P, Schwarz T. Photodermatoses: Diagnosis and treatment. Dtsch Arztebl Int 2011;108:135–41.
33Naleway AL. Polymorphous light eruption. Int J Dermatol 2002;41:377-83.
34Schleyer V, Weber O, Yazdi A, Benedix F, Dietz K, Röcken M, et al. Prevention of polymorphic light eruption with a sunscreen of very high protection level against UVB and UVA radiation under standardized photo diagnostic conditions. Acta DermVenereol2008;88:555-60.
35Inamdar AC, Palit A. Photosensitivity in children: An approach to diagnosis and management. Indian J Dermatol Venereol Leprol 2005;71:73-9.
36Holzle E, Plewlg G, Hofmann C, Roser-Maass E.Polymorphous light eruption. J Am Acad Dermatol1982;7:111-25.
37Balasubramanian P, Jagadeesan S, Sekar L, Thomas J. An interesting observation of polymorphous light eruption occurring on hypopigmented scars.IndianDermatolOnlineJ 2015;6:294-6.
38Dover JS, Hawk JLM. Polymorphic light eruption sine eruption.Br J Dermatol1988;118:73-6.
39Isedeh P, Lim HW. Polymorphous light eruption presenting as pinhead papular eruption on the face. J Drugs Dermatol2013;12:1285-6.
40Rodríguez-Pazos L, Gómez-Bernal S, Rodríguez-Granados MT, Toribio J. Photodistributed erythema multiforme. Actas Dermo-Sifiliográficas 2013;104:645-53.
41Akarsu S, Ilknur T, Fetil E, Lebe B, Güneş AT. Erythema multiforme-like eruption localized to a sun-exposed area. Photodermatol Photoimmunol Photomed2010;26:101-3.
42Bansal I, Kerr H, Janiga JJ, Qureshi HS, Chaffins M, Lim HW, et al.Pinpoint papular variant
43of polymorphous light eruption: Clinical and pathological correlation. J Eur Acad Dermatol Venereol2006;20:406-10.
44Chiam LY, Chong WS.Pinpoint papular polymorphous light eruption in Asian skin: Avariant in darker-skinned individuals. Photodermatol Photoimmunol Photomed2009;25:71-4.
45Kontos AP, Cusack CA, Chaffins M, Lim HW. Polymorphous light eruption in African Americans: Pinpoint papular variant. Photodermatol Photoimmunol Photomed2002;18:303-6.
46Bylaite M, Grigaitiene J, Lapinskaite GS. Photodermatoses: Classification, evaluation and management. Br J Dermatol 2009;161:61–8.
47Singh S, Singh A, Mallick S, Arava S, Ramam M. Lichenoid pseudovesicular papular eruption on nose: A papular facial dermatosis probably related to actinic lichen nitidusor micropapular polymorphous light eruption. Indian J Dermatol Venereol Leprol 2019; 85:597-604.
48Tzaneva S, Volc-Platzer B, Kittler H, Hönigsmann H, Tanew A. Antinuclear antibodies in patients with polymorphic light eruption: A long-term follow-up study.Br J Dermatol 2008;158:1050–4.
49Pathania V, Shankar P, Shelley D, Baveja S, Sinha A. A case of Hansen's disease masquerading as polymorphous light eruption. J Mar Med Soc 2019;21:196-8.
50Tey HL. A practical classification of childhood hypopigmentation disorders.Acta Derm Venereol 2010;90:6-11.
51Dogra S, Narang T.Emerging atypical and unusual presentationsof dermatophytosis in India. Clin Dermatol Rev 2017;1:S12-8.
52Bejoy P, Srinivas CR, Shenoi SD.Phototesting in the idiopathic photodermatoses among Indians.Indian J Dermatol 1998;43:1-3.
53Latha MS, Martis J, Shobha V, Shinde RS, Bangera S, Krishnankutty B, et al. Sunscreening agents: A review.J Clin Aesthet Dermatol2013;6:16–26.
54Agarwal SB, Godse K, Patil S, Nadkarni N. Knowledge and attitude of general population toward effects of sun exposure and use of sunscreens. Indian J Dermatol 2018;63:285-91.
55Rai R, Srinivas CR. Photoprotection. Indian J Dermatol Venereol Leprol 2007;73:73-9.
56Hadshiew I, Stäb F, Untiedt S, Bohnsack K, Rippke F, Hölzle E. Effects of topically applied antioxidants in experimentally provoked polymorphous light eruption. Dermatology1997;195:362-8.
57Ling TC, Dawe RS, Gardener E, Rothwell E, Rhodes LE. Interventions for polymorphic light eruption. Cochrane Database Syst Rev 2005, Issue 1. Art. No.: CD005069.doi: 10.1002/14651858.CD005069.pub2.
58Murphy GM, Hawk JL, Magnus IA. Hydroxychloroquine in Polymorphic light eruption: A controlled trial with drug and visual sensitivity monitoring. J Dermatol 1987;116:379-86.
59Pareek A, Khopkar U, Sacchidanand S, Chandurkar N, Naik GS. Comparative study of efficacy and safety of hydroxychloroquine and chloroquine in polymorphic light eruption: A randomized, double-blind, multicentric study. Indian J Dermatol Venereol Leprol 2008;74:18-22.
60Norris PG, Hawk JL. Successful treatment of severe polymorphous light eruption with azathioprine.Arch Dermatol1989;125:1377–9.
61Shipley DRV, Hewitt JB. Polymorphic light eruption treated with Cyclosporin.Br J Dermatol 2001;144:446–7.