uvb therapy (broadband and narrowband)

Official reprint from UpToDate www.uptodate.com ©2014 UpToDate

AuthorHerbert Hönigsmann, MD

Section EditorCraig A Elmets, MD

Deputy EditorRosamaria 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, hasbeen used for the treatment of moderate to severe psoriasis for decades. In the early 1980s, the observationthat wavelengths around 311 nm were more effective than broad-spectrum UVB in clearing psoriasis led to amajor advancement in phototherapy with the development of fluorescent lamps emitting selective UVBspectra 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 ofpsoriasis and a wide range of skin diseases, including atopic dermatitis, vitiligo, early stages of mycosisfungoides, and pruritic disorders (table 1) [3,4].

This topic will discuss the mechanism of action, treatment protocols, indications, and adverse effects of UVBtherapy. PUVA therapy and the use of UVB for the treatment of specific skin conditions are discussedseparately.

PRINCIPLES AND MECHANISMS — UVB radiation (280 to 320 nm) is absorbed in the epidermis andsuperficial dermis by molecules called chromophores, which include DNA, urocanic acid (a breakdownproduct of histidine abundantly present in stratum corneum), keratin, and melanin. Although nuclear DNA isthe main chromophore in the skin, there is evidence that UVB also targets cytoplasm and cell membranecomponents, including cell surface receptors, kinases, phosphatases, and transcription factors [5].

Photochemical reactions convert the chromophores into photoproducts that stimulate signal transductionpathways leading to the activation of transcription factors, cytokine secretion, and a variety of cellularresponses, including cell cycle arrest and apoptosis [6].

Decreased cell proliferation, immunosuppression, and T cell apoptosis may contribute to the UVB-mediatedsuppression 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 bynucleotides 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

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(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 suppressorgene p53 has a central role in the regulation of the cellular responses to DNA damage, which include cellcycle arrest, DNA repair, and apoptosis [9].

DNA lesions that are not repaired may lead to cytosine-thymine transition mutations, which represent theinitial event in skin carcinogenesis, or to cell death. Severely damaged cells (“sunburn cells”) undergoapoptosis as the result of a “cellular proofreading” mechanism in which p53 erases aberrant cells throughthe activation of the death receptor Fas and proapoptotic effector proteins Bax (Bcl-2–associated 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 orepidermis. T-cells apoptosis is the main mechanism underlying the depletion of the neoplastic infiltrate inmycosis fungoides.

Effects on the immune system — UVB radiation induces the release of a variety of proinflammatory andimmunosuppressive 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 ofcutaneous infections, with the exception of reactivation of Herpes simplex infection. Studies suggest thatUVB radiation may induce keratinocyte-derived antimicrobial peptides that prevent skin colonization bypathogens [15].

DEVICES FOR BROADBAND AND NARROWBAND UVB — Devices for broadband UVB therapy utilizefluorescent lamps emitting a wide range of wavelengths. Approximately two-thirds of the output is in the UVBrange (280 to 320 nm) and the rest is primarily in the UVA range (320 to 400 nm) (figure 1) [16]. Devices fornarrowband 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. Smallerdevices, 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 particularfor narrowband UVB, include moderate to severe psoriasis that is unresponsive to topical therapy, severeatopic dermatitis, and vitiligo [17,18]. Narrowband UVB is also indicated for the prevention of polymorphouslight 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].

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

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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 theindividual patient must be determined. The starting dose can be established by determining the minimalerythema dose (MED) with phototesting or by using an empirical method based upon the patient’s skinphototype (table 2).

The patient’s MED is determined by exposing six small template areas (eg, circles of 1 cm diameter) ofnonexposed skin (lower back, buttocks) to an incremental series of UVB irradiations. Increases are made byfixed values (eg, 10 mJ/cm ) or by a fraction (eg, 40 percent) of the previous dose. The MED is defined asthe lowest dose that causes a minimally perceptible erythema reaction 24 hours after irradiation. Sunbathingor 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 isimportant to document the type of lamp used for MED determination, since values obtained with broadbandor narrowband sources are markedly different (table 3). Narrowband UVB is approximately 10 times lesserythemogenic than broadband UVB. Thus, MEDs determined by using narrowband UVB devices areconsiderably higher than those determined with broadband sources.

The determination of the initial dose based upon the patient’s skin phototype may not reflect the actualsensitivity of a particular individual. However, this method is used for practical reasons in many phototherapycenters, particularly in the United States. The initial irradiation doses of broadband and narrowband UVB forthe 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 initialdose equal to 70 percent of the MED for broadband UVB and 50 percent of the MED for narrowband UVB oraccording to the Fitzpatrick skin type (table 4). Doses are then gradually increased to the maximum tolerateddose or 2000 to 5000 J/cm , whichever is lower [19]. Treatments are given two to five times per week. Theduration 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 increasedon consecutive days for patients receiving more than three treatments per week. The dose increase isdetermined based upon the effects of the previous treatment (ie, presence and intensity of erythema). Doseincrements 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 ofoptimal dosimetry. As an example, in a patient receiving three treatments per week, the UVB dose can beincreased 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 amild erythema persists even with smaller dose increments, the dose should be maintained until erythemasubsides.

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 ispersistent erythema).

In patients who develop intense or painful erythema, irradiation is stopped until the symptoms subside andthen resumed. Treatment is continued until complete remission is achieved or no further improvement canbe 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'.)●

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Guidelines for the use of narrowband UVB therapy for the treatment of psoriasis and other skin disordershave been published in Europe and in the United States [19-22].

Maintenance therapy — Maintenance therapy may prolong remission. However, the optimal maintenanceschedules 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-weeklyexposures for one month and once-weekly exposures for another month. The last effective UVB dose isgiven throughout the maintenance phase. If relapses occur during the maintenance phase, treatmentfrequency 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 thepsoriasis area and severity index (PASI) after 12 weeks of narrowband UVB therapy were assigned tomaintenance treatment or observation for two months [23]. More patients in the maintenance group than inthe observation group (12 of 22 versus 8 of 24) remained in remission after two months, although thedifference was not statistically significant.

Combination therapies — Both topical and systemic agents can be used in conjunction with UVBphototherapy 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 monochromaticexcimer light at 308 nm wavelength have a clinical use similar to narrowband UVB therapy. (See "Principlesof 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 narrowbandUVB devices and are particularly useful for the treatment resistant psoriasis plaques that are unresponsiveto other treatments or located in difficult areas (eg, scalp, palms, soles, knees, and elbows) [41]. Excimerlamps 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 byaltering the optical properties of the stratum corneum [24]. Application of a thin layer of emollient suchas petrolatum before UVB exposure is used in some institutions. However, the benefits of emollientsbefore UVB exposure have not been evaluated in randomized trials.

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

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

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

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

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SAFETY MEASURES — Safety measures for patients undergoing UVB phototherapy include:

SHORT- AND LONG-TERM ADVERSE EFFECTS — Short-term adverse effects of UVB phototherapyinclude 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 carcinogenicpotential of narrowband phototherapy has not been determined. A systematic review of the carcinogenic riskassociated with PUVA and narrowband UVB therapy for psoriasis suggests that narrowband UVB therapydoes 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 of50+ or a cloth barrier

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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 ofmoderate 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.)

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The main cytochemical target of UVB is nuclear DNA. The UVB-induced DNA damage stimulatessignal 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.)

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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 fornarrowband UVB therapy use the TL-01 fluorescent lamps that emit UVB in the range of 311 to 313nm. (See 'Devices for broadband and narrowband UVB' above.)

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

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

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The most common indications for UVB therapy, in particular for narrowband UVB, include moderate to●

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REFERENCES

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7. Hönigsmann H. Phototherapy for psoriasis. Clin Exp Dermatol 2001; 26:343.8. Nickoloff BJ. Cracking the cytokine code in psoriasis. Nat Med 2007; 13:242.9. Bhana S, Lloyd DR. The role of p53 in DNA damage-mediated cytotoxicity overrides its ability to

regulate nucleotide excision repair in human fibroblasts. Mutagenesis 2008; 23:43.10. Raj D, Brash DE, Grossman D. Keratinocyte apoptosis in epidermal development and disease. J

Invest Dermatol 2006; 126:243.11. Walters IB, Ozawa M, Cardinale I, et al. Narrowband (312-nm) UV-B suppresses interferon gamma

and interleukin (IL) 12 and increases IL-4 transcripts: differential regulation of cytokines at the single-cell level. Arch Dermatol 2003; 139:155.

12. Berneburg M, Röcken M, Benedix F. Phototherapy with narrowband vs broadband UVB. Acta DermVenereol 2005; 85:98.

13. el-Ghorr AA, Norval M. Biological effects of narrow-band (311 nm TL01) UVB irradiation: a review. JPhotochem Photobiol B 1997; 38:99.

14. Rana S, Byrne SN, MacDonald LJ, et al. Ultraviolet B suppresses immunity by inhibiting effector andmemory T cells. Am J Pathol 2008; 172:993.

15. Schwarz T. The dark and the sunny sides of UVR-induced immunosuppression: photoimmunologyrevisited. J Invest Dermatol 2010; 130:49.

16. Cafardi JA, Pollack BP, Elmets CA. Phototherapy. In: Fitzpatrick's Dermatology in General Medicine,8th Edition, Goldsmith LA, Katz SI, Gilchrest BA, et al. (Eds), 2012.

17. Tanew A, Radakovic-Fijan S, Schemper M, Hönigsmann H. Narrowband UV-B phototherapy vsphotochemotherapy in the treatment of chronic plaque-type psoriasis: a paired comparison study. ArchDermatol 1999; 135:519.

18. Yones SS, Palmer RA, Garibaldinos TT, Hawk JL. Randomized double-blind trial of the treatment ofchronic plaque psoriasis: efficacy of psoralen-UV-A therapy vs narrowband UV-B therapy. ArchDermatol 2006; 142:836.

19. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis andpsoriatic arthritis: Section 5. Guidelines of care for the treatment of psoriasis with phototherapy and

severe psoriasis that is unresponsive to topical therapy, severe atopic dermatitis, and vitiligo. (See'Clinical indications for UVB therapy' above.)

During UVB phototherapy, the eyes must be protected with UV-blocking goggles. The face, genitalarea, and skin that is not involved must be protected with an SPF 50+ sunscreen or a cloth barrier.(See 'Safety measures' above.)

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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 includephotoaging and photocarcinogenesis, although the carcinogenic potential of narrow band UVB is lessestablished. (See 'Short- and long-term adverse effects' above.)

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photochemotherapy. J Am Acad Dermatol 2010; 62:114.20. Ibbotson SH, Bilsland D, Cox NH, et al. An update and guidance on narrowband ultraviolet B

phototherapy: a British Photodermatology Group Workshop Report. Br J Dermatol 2004; 151:283.21. Beani JC, Jeanmougin M. [Narrow-band UVB therapy in psoriasis vulgaris: good practice guideline

and recommendations of the French Society of Photodermatology]. Ann Dermatol Venereol 2010;137:21.

22. Spuls PI, Tuut MK, van Everdingen JJ, et al. [The practice guideline 'Photo(chemo)therapy andsystemic therapy in severe chronic plaque-psoriasis']. Ned Tijdschr Geneeskd 2004; 148:2121.

23. Boztepe G, Karaduman A, Sahin S, et al. The effect of maintenance narrow-band ultraviolet B therapyon the duration of remission for psoriasis: a prospective randomized clinical trial. Int J Dermatol 2006;45:245.

24. Lebwohl M, Martinez J, Weber P, DeLuca R. Effects of topical preparations on the erythemogenicity ofUVB: implications for psoriasis phototherapy. J Am Acad Dermatol 1995; 32:469.

25. Hofmann UB, Eggert AA, Bröcker EB, Goebeler M. Calcitriol vs. dithranol in combination with narrow-band ultraviolet B (311 nm) in psoriasis. Br J Dermatol 2003; 148:779.

26. Carrozza P, Häusermann P, Nestle FO, et al. Clinical efficacy of narrow-band UVB (311 nm) combinedwith dithranol in psoriasis. An open pilot study. Dermatology 2000; 200:35.

27. Behrens S, Grundmann-Kollmann M, Schiener R, et al. Combination phototherapy of psoriasis withnarrow-band UVB irradiation and topical tazarotene gel. J Am Acad Dermatol 2000; 42:493.

28. Goktas EO, Aydin F, Senturk N, et al. Combination of narrow band UVB and topical calcipotriol for thetreatment of vitiligo. J Eur Acad Dermatol Venereol 2006; 20:553.

29. Ada S, Sahin S, Boztepe G, et al. No additional effect of topical calcipotriol on narrow-band UVBphototherapy in patients with generalized vitiligo. Photodermatol Photoimmunol Photomed 2005;21:79.

30. Green C, Lakshmipathi T, Johnson BE, Ferguson J. A comparison of the efficacy and relapse rates ofnarrowband UVB (TL-01) monotherapy vs. etretinate (re-TL-01) vs. etretinate-PUVA (re-PUVA) in thetreatment of psoriasis patients. Br J Dermatol 1992; 127:5.

31. Lebwohl M, Drake L, Menter A, et al. Consensus conference: acitretin in combination with UVB orPUVA in the treatment of psoriasis. J Am Acad Dermatol 2001; 45:544.

32. Asawanonda P, Nateetongrungsak Y. Methotrexate plus narrowband UVB phototherapy versusnarrowband UVB phototherapy alone in the treatment of plaque-type psoriasis: a randomized,placebo-controlled study. J Am Acad Dermatol 2006; 54:1013.

33. Kircik L, Bagel J, Korman N, et al. Utilization of narrow-band ultraviolet light B therapy and etanerceptfor the treatment of psoriasis (UNITE): efficacy, safety, and patient-reported outcomes. J DrugsDermatol 2008; 7:245.

34. Wolf P, Hofer A, Legat FJ, et al. Treatment with 311-nm ultraviolet B accelerates and improves theclearance of psoriatic lesions in patients treated with etanercept. Br J Dermatol 2009; 160:186.

35. Calzavara-Pinton PG, Sala R, Arisi M, et al. Synergism between narrowband ultraviolet Bphototherapy and etanercept for the treatment of plaque-type psoriasis. Br J Dermatol 2013; 169:130.

36. Wolf P, Hofer A, Weger W, et al. 311 nm ultraviolet B-accelerated response of psoriatic lesions inadalimumab-treated patients. Photodermatol Photoimmunol Photomed 2011; 27:186.

37. Gambichler T, Tigges C, Scola N, et al. Etanercept plus narrowband ultraviolet B phototherapy ofpsoriasis is more effective than etanercept monotherapy at 6 weeks. Br J Dermatol 2011; 164:1383.

38. Hönigsmann H. Synergism between narrowband ultraviolet B phototherapy and etanercept for thetreatment of plaque-type psoriasis. Br J Dermatol 2013; 169:4.

39. Richard EG, Hönigsmann H. Phototherapy, psoriasis, and the age of biologics. PhotodermatolPhotoimmunol Photomed 2014; 30:3.

40. Inzinger M, Legat FJ, Hofer A, et al. Short- to intermediate-term follow-up in patients treated with thecombination of 311-nm ultraviolet B phototherapy and biological agents. Br J Dermatol 2014.

41. Köllner K, Wimmershoff MB, Hintz C, et al. Comparison of the 308-nm excimer laser and a 308-nmexcimer lamp with 311-nm narrowband ultraviolet B in the treatment of psoriasis. Br J Dermatol 2005;152:750.

42. Nicolaidou E, Antoniou C, Stratigos A, Katsambas AD. Narrowband ultraviolet B phototherapy and308-nm excimer laser in the treatment of vitiligo: a review. J Am Acad Dermatol 2009; 60:470.

43. Welsh O, Herz-Ruelas ME, Gómez M, Ocampo-Candiani J. Therapeutic evaluation of UVB-targeted

phototherapy in vitiligo that affects less than 10% of the body surface area. Int J Dermatol 2009;48:529.

44. Aubin F, Vigan M, Puzenat E, et al. Evaluation of a novel 308-nm monochromatic excimer lightdelivery system in dermatology: a pilot study in different chronic localized dermatoses. Br J Dermatol2005; 152:99.

45. Archier E, Devaux S, Castela E, et al. Carcinogenic risks of psoralen UV-A therapy and narrowbandUV-B therapy in chronic plaque psoriasis: a systematic literature review. J Eur Acad DermatolVenereol 2012; 26 Suppl 3:22.

Topic 13745 Version 4.0

GRAPHICS

Clinical indications for UVB phototherapy

Indication Broadband Narrowband

Psoriasis + ++

Atopic dermatitis + ++

Pruritus, prurigo + +

Parapsoriasis en plaques + +

Mycosis fungoides (patchstage)

+ +

Polymorphous light eruption(prophylaxis)

+ ++

Vitiligo – ++

Pityriasis lichenoides + +

Lymphomatoid papulosis + +

Seborrheic dermatitis + +

HIV-associated pruriticeruptions

+ 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.


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.


Determination of the minimal erythema dose (MED) withbroadband or narrowband UVB sources

Exposure doses (mJ/cm )

Broadband UVB 20 40 60 80 100 120

Narrowband UVB 200 400 600 800 1000 1200


2

UVB phototherapy: Recommended initial doses according to skinphototype

Skin phototypeInitial 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


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 theaccidental ingestion of a photosensitizer does not induce a phototoxic reaction.


Disclosures: Herbert Hönigsmann, 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, theseare addressed by vetting through a multi-level review process, and through requirements forreferences to be provided to support the content. Appropriately referenced content is required of allauthors and must conform to UpToDate standards of evidence.Conflict of interest policy

Disclosures

uvb therapy (broadband and narrowband)

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