Official reprint from UpToDate

www.uptodate.com 2014 UpToDate

Author
Herbert Hnigsmann, MD
Section Editor
Craig A Elmets, MD
Deputy Editor
Rosamaria Corona, MD,
DSc
UVB therapy (broadband and narrowband)
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2014. | This topic last updated: Jul 17, 2014.
INTRODUCTION Broadband ultraviolet B (UVB) radiation (280 to 320 nm), with or without topical tar, has
been used for the treatment of moderate to severe psoriasis for decades. In the early 1980s, the observation
that wavelengths around 311 nm were more effective than broad-spectrum UVB in clearing psoriasis led to a
major advancement in phototherapy with the development of fluorescent lamps emitting selective UVB
spectra in the range of 311 to 313 nm (narrowband UVB) [1,2].
Narrowband UVB has since become the type of phototherapy most frequently used for the treatment of
psoriasis and a wide range of skin diseases, including atopic dermatitis, vitiligo, early stages of mycosis
fungoides, and pruritic disorders (table 1) [3,4].
This topic will discuss the mechanism of action, treatment protocols, indications, and adverse effects of UVB
therapy. PUVA therapy and the use of UVB for the treatment of specific skin conditions are discussed
separately.
PRINCIPLES AND MECHANISMS UVB radiation (280 to 320 nm) is absorbed in the epidermis and
superficial dermis by molecules called chromophores, which include DNA, urocanic acid (a breakdown
product of histidine abundantly present in stratum corneum), keratin, and melanin. Although nuclear DNA is
the main chromophore in the skin, there is evidence that UVB also targets cytoplasm and cell membrane
components, including cell surface receptors, kinases, phosphatases, and transcription factors [5].
Photochemical reactions convert the chromophores into photoproducts that stimulate signal transduction
pathways leading to the activation of transcription factors, cytokine secretion, and a variety of cellular
responses, including cell cycle arrest and apoptosis [6].
Decreased cell proliferation, immunosuppression, and T cell apoptosis may contribute to the UVB-mediated
suppression of disease activity in inflammatory and lymphoproliferative skin disorders [7,8].
Effects on DNA The most important chromophore in the skin is nuclear DNA. The absorption of UVB by
nucleotides leads to the formation of cyclobutane pyrimidine dimers and pyrimidine (6-4)-photoproducts,
which play a key role in both UVB therapeutic effect and toxicity.
The majority of UV-induced DNA lesions are not translated into a mutation, because cells have a variety of

(See "Psoralen plus ultraviolet A (PUVA) photochemotherapy".)

(See "Treatment of psoriasis", section on 'Ultraviolet light'.)
(See "Management of severe refractory atopic dermatitis (eczema)", section on 'Phototherapy'.)
(See "Vitiligo", section on 'Ultraviolet light'.)
(See "Polymorphous light eruption", section on 'Phototherapy'.)
(See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Phototherapy'.)
(See "Pityriasis lichenoides chronica", section on 'Phototherapy'.)
(See "Lymphomatoid papulosis", section on 'Phototherapy'.)
(See "Parapsoriasis (small plaque and large plaque parapsoriasis)", section on 'Phototherapy'.)
(See "Pruritus: Overview of management", section on 'Phototherapy'.)
(See "Prurigo nodularis", section on 'Phototherapy'.)
antimutagenic mechanisms that prevent mutation formation at sites of DNA damage. The tumor suppressor
gene p53 has a central role in the regulation of the cellular responses to DNA damage, which include cell
cycle arrest, DNA repair, and apoptosis [9].
DNA lesions that are not repaired may lead to cytosine-thymine transition mutations, which represent the
initial event in skin carcinogenesis, or to cell death. Severely damaged cells (sunburn cells) undergo
apoptosis as the result of a cellular proofreading mechanism in which p53 erases aberrant cells through
the activation of the death receptor Fas and proapoptotic effector proteins Bax (Bcl-2associated X protein),
Bak, Bid, and PUMA [10].
Apoptosis of UVB-damaged cells occurs not only in keratinocytes but also in T-cells infiltrating the dermis or
epidermis. T-cells apoptosis is the main mechanism underlying the depletion of the neoplastic infiltrate in
mycosis fungoides.
Effects on the immune system UVB radiation induces the release of a variety of proinflammatory and
immunosuppressive cytokines from keratinocytes and T-cells. Proinflammatory cytokines (eg, interleukin
[IL]-1, IL-6, IL-8, and TNF-alpha) play an important role in local and systemic sunburn reaction [5]. (See
"Sunburn", section on 'Pathogenesis'.)
The mechanisms involved in UVB-induced immunosuppression are complex and only partially understood.
They involve:
Despite its immunosuppressive effects, UVB phototherapy is not associated with an increased risk of
cutaneous infections, with the exception of reactivation of Herpes simplex infection. Studies suggest that
UVB radiation may induce keratinocyte-derived antimicrobial peptides that prevent skin colonization by
pathogens [15].
DEVICES FOR BROADBAND AND NARROWBAND UVB Devices for broadband UVB therapy utilize
fluorescent lamps emitting a wide range of wavelengths. Approximately two-thirds of the output is in the UVB
range (280 to 320 nm) and the rest is primarily in the UVA range (320 to 400 nm) (figure 1) [16]. Devices for
narrowband UVB therapy use the TL-01 fluorescent lamps that emit UVB in the range of 311 to 313 nm [3].
Different phototherapy devices are designed to treat the whole body, localized regions, or only lesional skin.
Those used for large body surface areas resemble booths that patients enter for each treatment. Smaller
devices, including small handheld units, are used to treat limited areas (eg, palms, soles, scalp).
CLINICAL INDICATIONS FOR UVB THERAPY Most common indications for UVB therapy, in particular
for narrowband UVB, include moderate to severe psoriasis that is unresponsive to topical therapy, severe
atopic dermatitis, and vitiligo [17,18]. Narrowband UVB is also indicated for the prevention of polymorphous
light eruption. Additional indications for UVB phototherapy are summarized in the table (table 1).
The use of UVB phototherapy for the treatment of specific skin conditions is discussed separately.
Downregulation of interferon (IFN)-gamma, IL-2, and IL-12 and increased secretion of IL-4 and IL-10
[5,8,11,12].

Functional impairment of epidermal Langerhans cells and dermal dendritic cells and reduced
expression of ICAM-1 and other adhesion molecules, resulting in a reduced capacity of antigen
presentation to effector T cells [13].

Reduced activation of effector and memory T cells [14].

Induction of T cells with regulatory/suppressive activity [6].
Apoptosis of dermal T cells.
(See "Treatment of psoriasis", section on 'Ultraviolet light'.)
(See "Management of severe refractory atopic dermatitis (eczema)", section on 'Phototherapy'.)
(See "Vitiligo", section on 'Ultraviolet light'.)
(See "Polymorphous light eruption", section on 'Phototherapy'.)
DOSIMETRY AND TREATMENT PROTOCOLS
Determination of the initial dose Before initiating phototherapy, the initial irradiation dose for the
individual patient must be determined. The starting dose can be established by determining the minimal
erythema dose (MED) with phototesting or by using an empirical method based upon the patients skin
phototype (table 2).
The patients MED is determined by exposing six small template areas (eg, circles of 1 cm diameter) of
nonexposed skin (lower back, buttocks) to an incremental series of UVB irradiations. Increases are made by
fixed values (eg, 10 mJ/cm ) or by a fraction (eg, 40 percent) of the previous dose. The MED is defined as
the lowest dose that causes a minimally perceptible erythema reaction 24 hours after irradiation. Sunbathing
or exposure to solaria must be avoided before phototesting.
Treatment is generally started with an initial dose of UVB equal to 50 to 70 percent of the MED. It is
important to document the type of lamp used for MED determination, since values obtained with broadband
or narrowband sources are markedly different (table 3). Narrowband UVB is approximately 10 times less
erythemogenic than broadband UVB. Thus, MEDs determined by using narrowband UVB devices are
considerably higher than those determined with broadband sources.
The determination of the initial dose based upon the patients skin phototype may not reflect the actual
sensitivity of a particular individual. However, this method is used for practical reasons in many phototherapy
centers, particularly in the United States. The initial irradiation doses of broadband and narrowband UVB for
the treatment of psoriasis recommended by the American Academy of Dermatology are listed in the table
(table 4) [19].
Treatment initiation, frequency, and dose increments Treatment is generally started with an initial
dose equal to 70 percent of the MED for broadband UVB and 50 percent of the MED for narrowband UVB or
according to the Fitzpatrick skin type (table 4). Doses are then gradually increased to the maximum tolerated
dose or 2000 to 5000 J/cm , whichever is lower [19]. Treatments are given two to five times per week. The
duration of each treatment ranges from several seconds (at the beginning of treatment) to several minutes,
depending upon the type of irradiation unit used.
Since UVB-induced erythema peaks at 24 hours after exposure, the radiation dose should not be increased
on consecutive days for patients receiving more than three treatments per week. The dose increase is
determined based upon the effects of the previous treatment (ie, presence and intensity of erythema). Dose
increments usually vary between 10 and 40 percent of the last used dose.
The goal of dose increment is to achieve a minimally perceptible erythema, which is the clinical indicator of
optimal dosimetry. As an example, in a patient receiving three treatments per week, the UVB dose can be
increased by 40 percent if the patient has no evidence of erythema from the previous treatment. In contrast,
if a mild erythema is noticeable, the dose increase should be limited to 20 percent of the previous dose. If a
mild erythema persists even with smaller dose increments, the dose should be maintained until erythema
subsides.
In a patient receiving five treatments per week, smaller dose increments should be given every other session
(30 percent in the absence of erythema; 15 percent if mild erythema is noted; no increase if there is
persistent erythema).
In patients who develop intense or painful erythema, irradiation is stopped until the symptoms subside and
then resumed. Treatment is continued until complete remission is achieved or no further improvement can
be obtained with continued phototherapy.
(See "Treatment of early stage (IA to IIA) mycosis fungoides", section on 'Phototherapy'.)
(See "Pityriasis lichenoides chronica", section on 'Phototherapy'.)
(See "Lymphomatoid papulosis", section on 'Phototherapy'.)
(See "Parapsoriasis (small plaque and large plaque parapsoriasis)", section on 'Phototherapy'.)
(See "Pruritus: Overview of management", section on 'Phototherapy'.)
(See "Prurigo nodularis", section on 'Phototherapy'.)
2
2
Guidelines for the use of narrowband UVB therapy for the treatment of psoriasis and other skin disorders
have been published in Europe and in the United States [19-22].
Maintenance therapy Maintenance therapy may prolong remission. However, the optimal maintenance
schedules for specific diseases have not been determined. For the treatment of cutaneous T-cell lymphoma,
most therapists perform maintenance treatment for several months to a year. (See "Treatment of early stage
(IA to IIA) mycosis fungoides", section on 'Phototherapy'.)
For the treatment of psoriasis, some centers advocate a two-month maintenance phase with twice-weekly
exposures for one month and once-weekly exposures for another month. The last effective UVB dose is
given throughout the maintenance phase. If relapses occur during the maintenance phase, treatment
frequency and UVB dose are increased until clearing is achieved.
In a small randomized trial, 46 patients with psoriasis who had achieved a 75 percent reduction of the
psoriasis area and severity index (PASI) after 12 weeks of narrowband UVB therapy were assigned to
maintenance treatment or observation for two months [23]. More patients in the maintenance group than in
the observation group (12 of 22 versus 8 of 24) remained in remission after two months, although the
difference was not statistically significant.
Combination therapies Both topical and systemic agents can be used in conjunction with UVB
phototherapy to improve its efficacy, reduce the cumulative UVB dose, and minimize long-term side effects.
TARGETED PHOTOTHERAPY WITH 308 NM DEVICES Lasers and lamps emitting monochromatic
excimer light at 308 nm wavelength have a clinical use similar to narrowband UVB therapy. (See "Principles
of laser and intense pulsed light for cutaneous lesions", section on 'Excimer laser'.)
Excimer lasers emit a higher amount of radiation over a shorter period of time than conventional narrowband
UVB devices and are particularly useful for the treatment resistant psoriasis plaques that are unresponsive
to other treatments or located in difficult areas (eg, scalp, palms, soles, knees, and elbows) [41]. Excimer
lamps may be used to treat large body areas, but have a lower power density than lasers.
Targeted phototherapy may be a treatment modality for stable vitiligo, localized chronic dermatoses (eg,
granuloma annulare, lichen planus, lichen simplex chronicus, alopecia areata) [42-44].
Emollients (eg, petrolatum, salicylic acid ointments) increase the transmission of UV radiation by
altering the optical properties of the stratum corneum [24]. Application of a thin layer of emollient such
as petrolatum before UVB exposure is used in some institutions. However, the benefits of emollients
before UVB exposure have not been evaluated in randomized trials.

Topical dithranol, vitamin D derivatives, and retinoids in conjunction with narrowband UVB
phototherapy have been reported as beneficial in a few small uncontrolled studies [25-29].

Systemic retinoids such as acitretin increase the efficacy of phototherapy, particularly in patients with
chronic plaque psoriasis [30]. Retinoids hasten and enhance the response to phototherapy and reduce
treatment frequency, duration, and cumulative UVB doses [19,31]. However, despite its many
advantages, retinoid-UVB therapy is infrequently used. (See "Treatment of psoriasis", section on
'Retinoids'.)

Methotrexate may have a synergistic effect with UVB therapy for the treatment of psoriasis. In a small
randomized trial, patients treated with methotrexate and narrowband UVB achieved a >90 percent
reduction of the baseline psoriasis area and severity index (PASI) more rapidly than patients treated
with placebo plus narrowband UVB (median time 4 weeks versus >24 weeks) [32]. However, further
studies are needed to confirm the efficacy of this combination therapy and evaluate potential short- and
long-term adverse effects.

Several reports suggest that narrowband UVB phototherapy may enhance the therapeutic response to
biologics [33-37]. However, long-term safety data on these combinations are not available and there is
concern that concurrent treatment with anti-TNF agents and narrowband phototherapy may increase
the risk of photocarcinogenesis [35,38-40].

SAFETY MEASURES Safety measures for patients undergoing UVB phototherapy include:
SHORT- AND LONG-TERM ADVERSE EFFECTS Short-term adverse effects of UVB phototherapy
include erythema, skin dryness, pruritus, blistering, and increased frequency of recurrent herpes simplex
(table 5).
Long-term adverse effects include photoaging and the possibility of photocarcinogenesis. The carcinogenic
potential of narrowband phototherapy has not been determined. A systematic review of the carcinogenic risk
associated with PUVA and narrowband UVB therapy for psoriasis suggests that narrowband UVB therapy
does not increase the risk of skin cancer [45]. However, there is a need for larger studies with longer follow-
up time to assess the risk of skin cancer among patients treated with narrowband UVB phototherapy.
CONTRAINDICATIONS Absolute contraindications for UVB phototherapy are:
Relative contraindications to UVB therapy include:
SUMMARY AND RECOMMENDATIONS
Wearing UV-blocking goggles to protect the eyes and prevent conjunctivitis and photokeratitis
Protecting the face (if not involved in the disease process) either by using a sunscreen with an SPF of
50+ or a cloth barrier

Protecting the genitalia (if not involved in the disease process) by wearing underwear
Avoiding concurrent natural sun exposure
Xeroderma pigmentosum
Lupus erythematosus
History of photosensitivity diseases (eg, chronic actinic dermatitis, solar urticaria)
History of melanoma
History of nonmelanoma skin cancer
History of treatment with arsenic or ionizing radiation because of the increased risk for skin cancer
Immunosuppression for organ transplant patients
Narrowband UVB (311 to 313 nm) is the type of phototherapy most frequently used for the treatment of
moderate to severe psoriasis and a wide range of skin diseases, including atopic dermatitis, vitiligo,
early stages of mycosis fungoides, and pruritic disorders (table 1). (See 'Introduction' above.)

The main cytochemical target of UVB is nuclear DNA. The UVB-induced DNA damage stimulates
signal transduction pathways leading to the activation of transcription factors, cytokine secretion,
immunosuppression, and a variety of cellular responses, including cell cycle arrest and apoptosis. (See
'Principles and mechanisms' above.)

Devices for broadband UVB therapy utilize fluorescent lamps emitting a wide range of wavelengths,
mostly in the UVB range (280 to 320 nm) and, in part, in the UVA range (figure 1). Devices for
narrowband UVB therapy use the TL-01 fluorescent lamps that emit UVB in the range of 311 to 313
nm. (See 'Devices for broadband and narrowband UVB' above.)

Treatment is generally started with an initial dose of UVB equal to 50 to 70 percent of the minimal
erythema dose (MED) or at a dose determined by the patients phototype (table 4). It is important to
document the type of lamp used for MED determination, since values obtained with broadband or
narrowband sources are markedly different (table 3). (See 'Dosimetry and treatment protocols' above.)

The radiation dose is then gradually increased by 10 to 40 percent of the previous dose. The goal of
dose increment is to achieve a minimally perceptible erythema, which is the clinical indicator of optimal
dosimetry. Treatment is continued until complete remission is achieved or no further improvement can
be obtained with continued phototherapy. The role for maintenance therapy is uncertain. (See
'Treatment initiation, frequency, and dose increments' above.)

The most common indications for UVB therapy, in particular for narrowband UVB, include moderate to
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severe psoriasis that is unresponsive to topical therapy, severe atopic dermatitis, and vitiligo. (See
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During UVB phototherapy, the eyes must be protected with UV-blocking goggles. The face, genital
area, and skin that is not involved must be protected with an SPF 50+ sunscreen or a cloth barrier.
(See 'Safety measures' above.)

Short-term adverse effects of UVB phototherapy include erythema, skin dryness, pruritus, blistering,
and increased frequency of recurrent herpes simplex (table 5). Long-term adverse effects include
photoaging and photocarcinogenesis, although the carcinogenic potential of narrow band UVB is less
established. (See 'Short- and long-term adverse effects' above.)

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Topic 13745 Version 4.0
GRAPHICS
Clinical indications for UVB phototherapy
Indication Broadband Narrowband
Psoriasis + ++
Atopic dermatitis + ++
Pruritus, prurigo + +
Parapsoriasis en plaques + +
Mycosis fungoides (patch
stage)
+ +
Polymorphous light eruption
(prophylaxis)
+ ++
Vitiligo ++
Pityriasis lichenoides + +
Lymphomatoid papulosis + +
Seborrheic dermatitis + +
HIV-associated pruritic
eruptions
+ X
+: recommendable; ++: superior; : low efficacy; X: no experience.
Graphic 87494 Version 1.0
Spectrum of broad band and narrow band UVB lamps
Courtesy of James Ferguson, Dundee, Scotland.
Graphic 87492 Version 1.0
Fitzpatrick skin phototypes
Skin type Unexposed skin color Reaction to sun exposure*
I White Always burns, never tans
II White Always burns, minimal tan
III White to olive Burns minimally, gradually tans
IV Light brown Burns minimally, tans well
V Brown Very rarely burns, tans profusely
VI Dark brown to black Never burns, tans deeply
Note: Slight variations on the definitions of the phototypes appear in the literature.
* After the first one hour of sun exposure on untanned skin on the first day of spring.
Graphic 60541 Version 3.0
Determination of the minimal erythema dose (MED) with
broadband or narrowband UVB sources
Exposure doses (mJ/cm )
Broadband UVB 20 40 60 80 100 120
Narrowband UVB 200 400 600 800 1000 1200
Graphic 87493 Version 1.0
2
UVB phototherapy: Recommended initial doses according to skin
phototype
Skin phototype
Initial BB-UVB dose
(mJ/cm )
Initial NB-UVB dose
(mJ/cm )
I 20 130
II 25 220
III 30 260
IV 40 330
V 50 350
VI 60 400
Graphic 88228 Version 1.0
2 2
Short-term and long-term adverse effects of UVB phototherapy
Acute
Sunburn or phototoxic reaction if overdosed ++
Phototoxic reaction from accidental intake of a photosensitizer
Conjunctivitis, keratitis (if no eye shielding is used) ++
Provocation of photodermatoses (eg, polymorphous light eruption) +
Chronic
Lentigines +
Photoaging ++
Actinic keratosis, nonmelanoma skin cancer +/
Melanoma ?
: no risk; ++: high risk; +: medium risk; : low risk; ?: possible, insufficient data.
Most photosensitizing substances absorb in the UVA range. Thus, exposure to UVB after the
accidental ingestion of a photosensitizer does not induce a phototoxic reaction.
Graphic 87496 Version 2.0
Disclosures: Herbert Hnigsmann, MD Nothing to disclose. Craig A Elmets, MD Consultant:
Brickell Biotech, Inc. [skin cancer prevention (UAB30)]; Vaxin [influenza (topical vaccines)].
Consultant/Grant Recipient: Ferndale Laboratories, Inc. [Photoprotection (Polypodium leuketomos)].
Other: Astellas Pharma US, Inc. [Atopic Dermatitis (Topical Tacrolimus)]. Rosamaria Corona, MD,
DSc Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
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