Curr Allergy Asthma Rep (2017) 17:36
DOI 10.1007/s11882-017-0705-2
ALLERGIC SKIN DISEASES (L FONACIER, SECTION EDITOR)
Photodermatitis for the Allergist
Samuel L. Coffin 1 & Jake E. Turrentine 1 & Ponciano D. Cruz Jr. 2,3
# Springer Science+Business Media New York 2017
Abstract
Purpose of Review The photodermatoses represent a group of
disorders of sensitivity to light that continue to pose difficul-
ties in diagnosis and management. Photodermatoses are of
interest to allergists because many photosensitive skin disor-
ders have immunologic underpinnings, and patients often
present to clinic complaining of “allergy” to the sun. We pro-
vide a concise reference for allergists on the clinical recogni-
tion and management of photodermatitis.
Recent Findings New developments in the understanding of
immunomodulatory effects of light have demonstrated nor-
mally immunosuppressive responses in the skin to light expo-
sure, and a blunted immunosuppressive response in the path-
ogenesis of many photodermatoses. Vitamin D plays an im-
portant role in immunomodulation and itself may be affected
by photodermatoses due to the impact of photoprotective
treatment strategies on circulating vitamin D levels.
Summary The elucidation of the immunological basis of
many photodermatoses may provide guidance for developing
This article is part of the Topical Collection on Allergic Skin Diseases
* Jake E. Turrentine
JakTurrentine@augusta.edu
Samuel L. Coffin
SCoffin@augusta.edu
Ponciano D. Cruz, Jr.
Ponciano.Cruz@utsouthwestern.edu
1
Division of Dermatology, Augusta University, 1004 Chafee Ave,
FH-100, Augusta, GA 30904, USA
2
Department of Dermatology, The University of Texas Southwestern,
5323 Harry Hines Blvd, Dallas, TX 75390-9069, USA
3
North Texas Veterans Affairs Medical Center, Dallas, TX, USA
new treatment modalities. Further research is necessary to
determine the optimal management of vitamin D metabolism
in patients with photodermatoses.
Keywords Photodermatoses . Photodermatitis .
Photoimmunosuppression . Regulatory T cell . Vitamin D .
Photoprotection
Introduction
Dermatitis provoked by light (photodermatitis) is a common
complaint from patients, and it can pose diagnostic and ther-
apeutic challenges. Photodermatitis encompasses skin erup-
tions caused or exacerbated by electromagnetic radiation with-
in ultraviolet (UV) and visible spectra. Specific wavelengths
triggering the disease vary depending on the underlying con-
dition and may include UVB (290–320 nm), UVA (320–
400 nm), and less commonly, visible light (400–700 nm). In
this review, the photodermatoses are categorized into immu-
nologically mediated (formerly known as “idiopathic”) and
exogenous (phototoxic or photoallergic) subtypes, and we
briefly discuss systemic conditions that cause photosensitivity.
Also covered are controversies surrounding sunlight and vita-
min D, which are issues frequently raised by patients with
photosensitivity disorders.
Immunologically Mediated (Idiopathic)
Photodermatoses
Polymorphic light eruption (PMLE) is the most common idi-
opathic photodermatosis, especially among patients younger
than 40 years, and more commonly in women than men.
Classically, PMLE manifests in springtime (or following the
36 Page 2 of 7
first major exposure to sunlight in a given year). As the term
polymorphic denotes, the clinical presentation may vary, with
the most common manifestation being grouped pruritic pap-
ules limited to or beginning on sun-exposed areas such as the
arms, face, and chest. The lesions do not develop immediately,
but may take hours to days after sun exposure and persist
afterwards.
The pathogenesis of PMLE remains unclear but likely in-
volves an altered form of delayed hypersensitivity reaction to
an unknown antigen produced by exposure to UVB light.
Unaffected individuals typically respond to UVB radiation
with immunosuppressive responses that includes upregulated
IL-10 expression, emigration of Langerhans cells from the
epidermis, and proliferation of suppressor macrophages—all
of which were absent in some patients with PMLE [1].
As with all photosensitivity disorders, patients with PMLE
should practice photoprotection, including use of protective
clothing and sunscreens. In mild cases, topical corticosteroids
are sufficient for symptomatic relief. Topical calcipotriol (vi-
tamin D) has also been used to reduce symptom severity [2].
More severe cases may require short courses of oral predni-
sone, thalidomide, and/or antimalarial agents. More novel
strategies include topical DNA repair enzymes and
afamelanotide to induce melanization [3].
Many cases of PMLE tend to improve naturally from in-
creased exposure to sunlight as spring evolves into summer.
This observation has led to the concept of “hardening”, which
has been invoked in prophylactically treating patients with
predictable PMLE flares (before springtime or a sunny vaca-
tion) with phototherapy. Such phototherapy was shown to
increase proliferation and the function of regulatory T cells
in the skin, thereby reversing PMLE patients’ lack of an im-
munosuppressive response to UVB radiation [4••].
Juvenile spring eruption is a variant of PMLE that also
occurs in the springtime, but is limited to children, with boys
affected more commonly than girls. Lesions are similar to
those of PMLE, but with a higher propensity for ear involve-
ment. This gender predilection may occur because boys typi-
cally have shorter hair and thus less protection from sunlight
on their ears [5]. Both sun exposure and cold weather are
thought to be relevant to the pathophysiology [6]. Treatment
is primarily symptomatic since most cases remit after several
years of seasonal recurrence.
Actinic prurigo differs from PMLE in several ways. Eroded
or ulcerated nodules are the most characteristic lesions and
these may arise in areas not directly exposed to the sun.
Cheilitis or inflammation of the lips is often present [7].
Actinic prurigo is seen most frequently in patients of Native
American or mestizo (mixed European and Native American)
descent. The disease is associated with the major histocom-
patibility (MHC) haplotype HLA DR4 or DRB1*0047 [8].
Treatment requires strict photoprotection. Topical steroids or
calcineurin inhibitors like tacrolimus are the mainstay of
Curr Allergy Asthma Rep (2017) 17:36
therapy [9]. In severe cases, thalidomide is often successful
for alleviating pruritus and preventing erosions and ulceration
[10].
Solar urticaria is distinct from the conditions already
discussed in its morphology, kinetics after sun exposure, and
pathogenicity. As denoted by its name, solar urticaria presents
as urticarial papules and plaques, manifesting within seconds
to minutes after sun exposure. Finally, it is mediated by IgE
and therefore considered a type I hypersensitivity reaction
[11]. Like other forms of urticaria, solar urticaria presents as
erythematous and pruritic wheals but is restricted to sun-
exposed areas. However, like PMLE, episodes may begin or
peak in the spring and decrease through the summer, consis-
tent with the concept of hardening discussed earlier for PMLE
[12].
Given the urticarial morphology and immediate onset after
sun exposure, the diagnosis can be arrived at purely on clinical
grounds. This can be confirmed by phototesting, with the
action spectrum for solar urticaria varying within the UVA,
UVB, or even visible light range. Identifying the action spec-
trum for a given patient will provide specific guidance regard-
ing which wavelengths to avoid [13].
Protection from sunlight is again the mainstay of therapy.
Initial treatment may consist of use of protective clothing and
sunscreen plus daily antihistamines. Chemical sunscreens
may be ineffective in patients whose action spectrum is in
the visible range. These patients will require physical sun-
blocks containing titanium and/or zinc oxide to block visible
light. As in cases of PMLE, patients with solar urticaria may
benefit from prophylactic phototherapy to induce hardening
[14]. New treatment modalities include omalizumab and in-
travenous immunoglobulin (IVIG) [15•, 16].
Hydroa vacciniforme is a rare photodermatosis of child-
hood that may be linked to infection with the Epstein-Barr
virus (EBV). Lesions include pruritic papules or vesicles on
sun-exposed areas that arise hours after sun exposure [17].
Presence of EBV RNA within lesion-associated T lympho-
cytes supports a role for EBV in pathophysiology. Because
hydroa vacciniforme may cause pockmark scarring, it can be
confused with the inherited disorder, erythropoietic
protoporphyria, but the absence of laboratory abnormalities
relevant to the porphyrin pathway readily distinguishes
hydroa vacciniforme from protoporphyria [18]. In addition
to aggressive photoprotection, current management options
include UVB phototherapy and immunosuppressant agents
[19].
Chronic actinic dermatitis primarily affects older male pa-
tients, with eczematous papules and plaques on sun-exposed
skin [20]. The disorder is uncommon for patients younger than
50 years and for those living in the tropics. Many cases present
with a very sharp demarcation between lesional and unaffect-
ed skin, corresponding to the borders of clothing or skin folds
[21]. Chronic actinic dermatitis is associated with previous
Curr Allergy Asthma Rep (2017) 17:36 Page 3 of 7 36

allergic contact dermatitis, especially to sesquiterpene lactone
(from plants belonging to the Compositae family) and to para-
phenylenediamine (found in black dye) [22, 23]. Therefore,
patch testing and photopatch testing are important aspects in
evaluating patients with suspected chronic actinic dermatitis
[24].
Treatment for chronic actinic dermatitis follows a similar
strategy as in other photodermatoses with photoprotection be-
ing paramount. Symptomatic treatment includes topical ste-
roids or tacrolimus. Severe cases may require systemic immu-
nomodulators such as mycophenolate mofetil, azathioprine, or
methotrexate. Antimalarial agents have been used with some
success [25]. More recently, janus kinase signaling was shown
to be relevant to the pathogenesis of chronic actinic dermatitis,
prompting use of the janus kinase inhibitor tofacitinib in re-
fractory cases [26].
Chronic actinic dermatitis can rarely evolve into actinic
reticuloid, which is considered a variant of cutaneous T cell
lymphoma. This possibility highlights the importance of es-
tablishing the diagnosis via skin biopsy and may include spe-
cial T cell analyses to exclude the latter. Table 1 provides the
key characteristics of the immune-mediated photodermatoses.
Exogenous Causes of Photosensitivity
Photodermatitis due to exogenous drugs and substances can
be classified into phototoxic vs. photoallergic reactions.
Phototoxic reactions arise from direct cellular damage caused
by the culprit substances’ interaction with UV light, without
involvement of the immune system. Photoallergic reactions,
on the other hand, are delayed-type hypersensitivity reactions
produced in collaboration with UV light exposure [27].
Photoallergic reactions can be confirmed by photopatch
testing. Because most drugs causing photoallergy do so in
collaboration with UVA wavelengths, the latter spectrum is
(for practical purposes) the only one used for phototesting
suspected photoallergic patients [28].
The most common drugs causing phototoxicity are antibi-
otics including tetracyclines, fluoroquinolones, and sulfon-
amides. The most common drugs causing photoallergy in-
clude hydrochlorothiazide, amiodarone, and chlorpromazine
[29]. In particular, doxycycline can cause both phototoxicity
and photoallergy, with the former effects being dose-
dependent [30].
Plants containing furocoumarins (psoralens) are a very com-
mon cause of phototoxic dermatitis, known as
phytophotodermatosis [31]. Furocoumarins are an ubiquitous
ingredient in many common fruits (fig, lemon, lime) and veg-
etables (celery, fennel, parsley, parsnip). A usual clinical pre-
sentation is linear streaks on pruritic dermatitis on sun-exposed
sites. Depending on the degree of exposure to the culprit sub-
stance, painful blisters may develop, followed later by marked
hyperpigmentation. Among the most frequent presentations are
dermatitis or hyperpigmented streaks arising from spilled lem-
on or lime juice on the hands and arms of bartenders [32].

Table 1 Key characteristics of

the immune-mediated Immune- Etiology Clinical presentation Treatment
photodermatoses mediated
dermatoses

Polymorphous Failure of innate UV Grouped pruritic papules on Photoprotection,

light immunosuppression,
eruption possible type IV
hypersensitivity reaction
Juvenile spring Similar to PMLE
eruption
Actinic prurigo Suspected association with
HLA types particularly
common in Native
Americans and mestizos
Solar urticaria Type I hypersensitivity
Hydroa Suspected relationship to
vaccinifor- EBV
me
Chronic actinic May be associated with a
dermatosis previous allergic contact
dermatitis
sun-exposed areas developing corticosteroids,
hours after exposure topical calcipotriol,
phototherapy as
“hardening”
Similar to PMLE but occurring Similar to PMLE,
on the superior surface of the primarily
ears symptomatic control
PMLE-like presentation but may Photoprotection,
also present with nodules, corticosteroids,
scarring lesions, and lesions topical tacrolimus,
not in sun-exposed areas thalidomide
Urticarial lesions within minutes Photoprotection,
to hours of sun exposure antihistamines,
omalizumab, IVIG
Pruritic papules or vesicles on Phototherapy, systemic
sun-exposed regions immunosuppression
Eczematous lesions, patches, Photoprotection,
plaques with sharp margins on systemic
areas of sun exposure and immunosuppression,
covering antimalarials
36 Page 4 of 7 Curr Allergy Asthma Rep (2017) 17:36

Rarely, chemical sunscreen ingredients can cause DNA repair (e.g., xeroderma pigmentosa), and pellagra
photoallergic contact dermatitis and, thus, should be in the less-developed world [37]. Table 3 provides an
suspected when patients with photodermatitis fail to im- overview of genetic and systemic diseases to be consid-
prove or even worsen with continued use of sunscreens. ered in the differential diagnosis of photosensitivity.
Benzophenone 3, oxybenzone, and p-aminobenzoic acid
are the most frequent culprits implicated by photopatch
testing [33, 34]. Phototesting
Idiosyncratic drug reactions can also produce photosensi-
tivity, triggering reactions that resemble lupus erythematosus Although the technical details are out of the scope of this
or porphyria. Antihypertensive agents such as hydrochlorothi- review, photoprovocation and photopatch testing warrant a
azide and antifungal agents such as terbinafine have been most brief discussion. Most causes of photodermatitis are diag-
strongly associated with drug-induced subacute cutaneous lu- nosed by history, physical examination, laboratory testing,
pus erythematosus (DI-SCLE) [35]. Pseudoporphryia, which and/or skin biopsy. Photoprovocation testing is useful in select
clinically and histologically resembles porphyria (but lacks cases, especially when the patient does not have an active
porphyrins in the plasma/urine), can be triggered by dermatitis at the time of presentation. After determining a
NSAIDs. Pseudoporphyria particularly affecting the face has patient’s minimal erythema dose (MED) using a standard pro-
been found to occur in pediatric patients treated with tocol, photoprovocation testing may be performed by expos-
naproxen, and less commonly with indomethacin or ibupro- ing one body site to narrow band UVB (311-313 nm) and
fen, for juvenile idiopathic arthritis [36]. Table 2 provides an another body site to broad band UVA (320-400 nm) each at
overview of the common exogenous causes of phototoxic, approximately 1.5× the MED. Caution should be exercised in
photoallergic, and idiosyncratic photodistributed reactions. testing patients suspected of solar urticaria due to a small risk
of inducing anaphylaxis.
Diagnosis of photoallergic contact dermatitis requires
photopatch testing, a procedure in which two sets of patch
Systemic Conditions with Light Sensitivity
tests are performed in parallel, with only one set being ex-
posed to broad band UVA (5–10 J/cm2) after 24–48 h of con-
While our review focused on immunologically mediated and
tact with the skin, while the other set is protected from the light
exogenous causes of photodermatitis, one should always con-
source. If a reaction develops to an allergen only in the site
sider the possibility of a systemic, genetic, or nutritional con-
exposed to UVA light, but not the UV-protected site, then
dition as the cause of a photodistributed eruption. These dis-
photoallergic contact dermatitis (rather than allergic contact
orders include autoimmune diseases (e.g., systemic lu-
dermatitis) is diagnosed. If a reaction develops in both sites,
pus erythematosus, dermatomyositis), enzyme-deficient
a diagnosis of allergic contact dermatitis is favored.
disorders of the porphyrin pathway (e.g., porphyria
Additionally, in some patients, an allergen may elicit allergic
cutanea tarda; erythropoietic protoporphyria) or of
contact dermatitis without UV exposure yet demonstrate an
even stronger response in the presence of UV light—a situa-
Table 2 Common exogenous causes of phototoxic, photoallergic, and tion in which both allergic and photoallergic dermatitis may
idiosyncratic photodistributed reactions both be considered present (photoaugmented reaction).
Photosensitivity Photoallergic contact Idiosyncratic
reactions dermatitis photodistributed
reactions The Controversy About Vitamin D
Tetracyclines, esp. Sunscreen ingredients Hydrochlorothiazide
doxycycline (p-aminobenzoic acid, (DI-SCLE) With so many photosensitive diseases requiring sun avoidance
(phototoxicity) benzophenone-3, and photoprotection, patients often express concern about the
oxybenzone) potential for vitamin D deficiency. There is a rationale for this
Fluoroquinolones Ketoprofen Terbinafine concern, as UVB mediates the production of 25-
(phototoxicity) (DI-SCLE)
hydroxyvitamin D in the skin, which is converted internally
Sulfonamides Naproxen
(phototoxicity) (pseudoporphyria)
into its active form, 1,25-dihydroxyvitamin D. Vitamin D
Amiodarone Amiodarone
plays a well-known role in calcium homeostasis and skeletal
Hydrochlorothiazide
development, and recent research has recognized a role for
vitamin D in immunomodulation and immunosuppression.
Chlorpromazine
Studies of both cell lines and peripheral blood mononuclear
Furocoumarins, esp.
celery and lime cells have demonstrated that 1,25-dihydroxyvitamin D may
modulate toll-like receptors 2 and 4, as well as NFkB,
Curr Allergy Asthma Rep (2017) 17:36 Page 5 of 7 36

Table 3 Genetic and systemic

diseases to be considered in the
differential diagnosis of
photosensitivity
Systemic disease
Systemic lupus erythematosus
Porphyrias, e.g., porphyria cutanea tarda
(PCT), erythropoietic protoporphyria (EPP)
Inheritable DNA repair deficiencies
Nutritional deficiency (e.g., pellagra)
Presentation
Range of presentations from scarring lesions specifically
aggravated by sun exposure to generalized erythema and
rash on sun-exposed regions
PCT: painful bullae, vesicles, or erosions, especially on the
dorsal surfaces and sun-exposed regions
EPP: painful erythema, edema, or vesicles in sun-exposed
areas
Xeroderma pigmentosum: severe sunburn-like lesions soon
after sun exposure
Pruritus and hyperpigmentation on sun-exposed areas

resulting in decreased production of pro-inflammatory cyto-
kines [38••]. Vitamin D may also play a role in promoting the
proliferation of regulatory T cells and anti-inflammatory cyto-
kines such as IL-10. Vitamin D has also been found to play a
role in the promotion of immune responses, particularly the
innate immune system. Macrophages, which produce
cathelicidin as part of the innate response to microbial inva-
sion, rely on vitamin D receptors as part of the signaling for
increased expression of cathelicidin [39].
In regard to the optimal level of vitamin D, particularly in
the photosensitive population, there does not yet exist a clear
guidance. A study of British patients with photodermatoses
found them to be at higher risk for continuous vitamin D
insufficiency, which in this study was defined as <20 ng per
milliliter of 25-hydroxyvitamin D, during both the summer
and winter months. These patients had decreased measured
UVB exposure and subsequent vitamin D levels compared
to a healthy control, due to standard photoprotective strategies
such as avoiding direct sunlight, limiting skin exposure, and
sunscreen use [40••].
The benefits of sun exposure in increasing serum vitamin D
levels must be balanced against the known risk of excessive
sun exposure. The variation in benefits versus risks for differ-
ent skin types should be considered in advising patients, both
healthy and with photodermatoses, in appropriate levels of sun
exposure. Additionally, in patients with severe photosensitiv-
ity, oral vitamin D supplementation may be able to provide
required amounts of vitamin D without sun exposure.
Guidelines for oral vitamin D supplementation were released
in 2011 by the Endocrine Society—for adults aged 19–50 not
presently deficient in vitamin D take in at least 600 IU/day of
vitamin D to maintain their recommended serum level of
>30 ng/mL. For deficient patients, replenishment consists of
50,000 IU/week for 8 weeks and subsequent maintenance of
1500–2000 IU/day [41]. However, the Institute of Medicine’s
2011 guidelines on vitamin D consider levels <20 mg/mL as
deficient [42]. While photoprotection is a mainstay of treat-
ment for all the photodermatoses described here, recently, the
possible adverse effect of photoprotection on vitamin D levels
has been more appreciated. Patients with photodermatoses
have been found to be at higher risk for continuous vitamin
D deficiency and may benefit from oral vitamin D supplemen-
tation with their treatment [43]. However, the recommended
serum levels and oral doses needed to maintain that level have
yet to be definitively established.
Conclusions
Photodermatitis has been recognized as a set of clinically rel-
evant disorders of the skin that may present to the allergist,
posing unique challenges in diagnosis and management. We
have reviewed the most common intrinsic and exogenous
photodermatoses, with a reminder to always consider photo-
sensitive systemic disorders in the differential diagnosis. It has
been demonstrated that light exposure leads to immunomo
dulation in human skin, and it is now better understood how
aberrances in these processes contribute to the development of
the photodermatoses. The role of the immune system in these
disorders makes photodermatoses of significant interest to al-
lergists. Additionally, a better understanding of vitamin D’s
specific role in this immunomodulation is included, particu-
larly because vitamin D is also clinically relevant when con-
sidering the management of photodermatoses. Further inves-
tigation may be able to tailor treatment modalities that employ
the immunomodulatory role of light exposure in the skin. The
role of vitamin D in the context of photodermatoses, particu-
larly guidance on the sufficient levels of vitamin D and the
need for supplementation in patients with photodermatoses
merits further investigation.
Compliance with Ethical Standards
Conflict of Interest The authors declare no conflicts of interest relevant
to this manuscript.
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
36 Page 6 of 7
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