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Phototherapy with Narrowband vs Broadband UVB
Mark Berneburg a; Martin Röcken a; Frauke Benedix a
a Department of Dermatology, Eberhard Karls University. Tuebingen. Germany
To cite this Article: Mark Berneburg, Martin Röcken and Frauke Benedix ,
'Phototherapy with Narrowband vs Broadband UVB', Acta Dermato-Venereologica,
To link to this article: DOI: 10.1080/00015550510025579
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Taylor and Francis 2007
Acta Derm Venereol 2005; 85: 98–108
Phototherapy with Narrowband vs Broadband UVB
Mark BERNEBURG, Martin RO
¨ CKEN and Frauke BENEDIX
Department of Dermatology, Eberhard Karls University, Tuebingen, Germany
Phototherapy with ultraviolet (UV) radiation of wavelengths
(v280 nm) is mostly absorbed in the stratum corneum,
between 280 and 320 nm (UVB) is a safe and effective
UVA (320–400 nm) shows deeper penetration than
treatment for a variety of diseases. In addition to standard
UVB (280–320 nm) (8–12). Thus, UVB is mainly
broadband UVB (bUVB), narrowband phototherapy with
absorbed by epidermal components including keratino-
fluorescent bulbs emitting near monochromatic UV around
cytes, melanin and Langerhans' cells (13). Biological
311 nm (nUVB) has become an important treatment for
effects of UV radiation are generated through interac-
diseases such as psoriasis, atopic dermatitis and vitiligo. In
tion with absorbing molecules called chromophores. In
addition to these indications, the number of diseases for which
the case of UVB, the most important chromophores
nUVB phototherapy is reported to be effective is continuously
are proteins such as keratin, melanin, collagen and
growing. The differential effects of nUVB phototherapy in
elastin, urocanic acid and DNA (14–16). Ultimately,
comparison to other UV wavelengths as well as established
the interaction of UV with chromophores can lead to a
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and new indications for this treatment modality are reviewed.
multitude of effects such as induction of oxidative
Key words: broadband UVB; narrowband UVB; phototherapy;
stress and activation of transcription factors, as well as
psoriasis; skin cancer; ultraviolet light.
induction of damage to the cell membrane and DNA
(Accepted October 4, 2004.)
Acta Derm Venereol 2005; 85: 98–108.
Induction of DNA damage
Dr Mark Berneburg, Department of Dermatology, Eberhard
UVB radiation leads directly to the generation of pre-
Karls University, Liebermeisterstrasse 25, DE-72076 Tuebingen,
mutagenic lesions, so-called photoproducts. Among
others, the most prevalent photoproducts induced byUV are cyclobutane pyrimidine dimers (CPD), pyrimidin-
While it has been known for more than 2000 years that
(6-4)-photoproducts (6-4PP) and Dewar isomers. Normally
several skin diseases improve upon exposure to the sun
these lesions are repaired by a highly conserved repair
(heliotherapy), the systematic investigation of photo-
mechanism called nucleotide excision repair (NER).
therapeutic modalities did not start until the beginning
This mechanism acts in a tightly regulated fashion
of the twentieth century. In 1903, Niels Finsen received
including recognition and processing of DNA damage,
the Nobel Prize for developing phototherapy as a
unwinding of DNA by helicases, excision of the
treatment for tuberculosis of the skin and 23 years later
Goeckerman (1) showed the beneficial effect of natural
DNA polymerase (17). If UVB-induced lesions are
sunlight in combination with tar for psoriasis vulgaris. In
not repaired, CRT and CCRTT transitions can occur
1953, Ingram (2) initiated the combination of UVB
as DNA mutations (18) representing initial events of
radiation, dithranol and tar-bathing for psoriasis (2).
multi-step carcinogenesis. These mutations are char-
Data from Fischer & Alsins (3) and Parrish & Jaenicke (4)
acteristic for UV exposure in potentially relevant genes
subsequently showed that wavelengths around 311 nm
such as tumour suppressor genes or oncogenes (19).
provoke fewest erythema while being most effective for
The fact that defective NER in the autosomal recessive
clearing psoriasis. According to these results a fluorescent
disease xeroderma pigmentosum is associated with a
bulb was developed (TL-01), emitting a major peak at 311
strong increase of DNA mutations, photosensitivity
(¡ 2 nm) and a minor peak at 305 nm. This treatment
and development of skin cancer further underscores the
was later called narrowband UVB (nUVB) and following
central role of DNA damage and its repair in the
its introduction several studies were published on its
process of multi-step photocarcinogenesis (20, 21).
superior efficacy in phototherapy of psoriasis (5–7).
UV radiation and its effects on the immune system
UV radiation alters immunological function (22) andUVB can increase the production of pro-inflammatory
Interaction between UV radiation and the skin
UV radiation that reaches the skin is either reflected
necrosis factor (TNF), as well as the production of
or absorbed by structures of the skin. While UVC
Acta Derm Venereol 85
# 2005 Taylor & Francis. ISSN 0001-5555
Phototherapy with narrowband UVB
a-melanocyte stimulating hormone (MSH) and PGE2.
The most important indications will be discussed in
UVB down-regulates the expression of intercellular
detail below.
adhesion molecule (ICAM)-1 (13). With regard towavelength, reduction of the density and function of
Langerhans' cells in the skin and their migration to thedraining lymph nodes is more pronounced with bUVB
Monotherapy with nUVB. According to Feldman et al.
than with nUVB (23). Infiltrating epidermal T cells as
(39), with regard to efficacy, safety and cost-effectiveness,
well as mast cells are susceptible to UVB-induced
UVB phototherapy appears to be the best first-line
apoptosis (24–26) and depletion of T lymphocytes from
treatment for the control of generalized psoriasis and
psoriatic lesions seems to be greater after nUVB than
there is a large body of evidence indicating that nUVB
after bUVB irradiation (27). Moreover, nUVB appears
is more effective than bUVB as a monotherapeutic
to have a more immunosuppressive effect than bUVB
agent in the treatment of psoriasis even in children (5,
on natural killer cell activity, cytokine responses and
40–42). Whereas bUVB is considered to be most effec-
of peripheral blood
tive close to the minimal erythema dose (MED), nUVB
mononuclear cells (23, 28) and photo-isomerization of
trans- to cis-urocanic acid is more effective with nUVB
erythemogenic doses (27). However, Diffey (43) could
than with bUVB (23), with urocanic acid photoconver-
show in a mathematical model that clearance of pso-
sion being mainly induced by wavelengths between 310
riasis plaques is achieved faster with higher MED rates.
and 340 nm (29). Therefore, the immunomodulatory
Furthermore, nUVB has been shown to be more
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effects of nUVB appear to be more pronounced than
effective than bath-PUVA with trimethoxsalen (41, 44),
and according to some studies it was as effective as
nUVB suppresses the production of interferon (INF)-
systemic PUVA therapy (45–47), although this evalua-
c, IL-2 and IL-12 and increases that of IL-4 and IL-10,
tion was dependent on the type of psoriasis. In a study
which together could account for a shift of the immune
by van Weelden et al. (46), the therapeutic result differeddepending on the treated body site, with lesions on the
trunk responding better to nUVB and lesions on the
responses (30–32). The shift from an IFN-c-dominated
extremities responding better to PUVA. Other studies
Th1 to an IL-4 dominated Th2 response appears to be
showed that PUVA is more effective for psoriasis than
one of the major factors determining the therapeutic
nUVB alone (48) and systemic PUVA remains an
efficacy of nUVB phototherapy as well as that of many
important therapeutic modality for patients with high
systemic treatments such as IL-4 (33), not altering
PASI scores, especially those who do not respond
plasma antibody concentrations (34).
adequately to nUVB.
In the case of psoriasis, nUVB seems to clear plaques
For treatment of psoriasis with nUVB, three rather
through local rather than systemic effects, as unexposed
than two or five radiations a week are effective (49, 50)
plaques cleared significantly less than directly exposed
and low incremental regimens are sufficient according
plaques (35). However, it has also been hypothesized
to Wainwright et al. (51), who showed this regimen to
that clearing of psoriasis is a combination of local and
be as effective as high incremental regimens but less
systemic effects (36).
Combination therapies for psoriasis. In order to reduce
INDICATIONS FOR NARROWBAND UVB
cumulative UV doses and to enhance clearance of
Phototherapy with bUVB or nUVB has been reported
psoriasis lesions, combination therapies with topical as
to be effective and safe for the treatment of a large
well as systemic agents have been established:
number of skin diseases. In addition to psoriasis, atopic
nUVB plus dithranol (Ingram): In many studies the
dermatitis (AD) and vitiligo, various other skin diseases
efficacy of dithranol combined with UVB (broadband
can be treated successfully with nUVB phototherapy,
or narrowband) could be shown (7, 52, 53). As dithranol
like parapsoriasis, initial mycosis fungoides (MF), graft-
is difficult to handle, this therapy is mainly reserved for
versus-host disease and pruritus, as well as acquired
hospital settings.
perforating dermatosis, lichen planus, lichen simplexchronicus, lymphomatoid papulosis, generalized granu-
UVB plus vitamin D3 analogues: Vitamin D3 analogues
loma anulare, nummular dermatitis, pityriasis liche-
inhibit proliferation, induce terminal differentiation of
noides chronica, pityriasis rosea, pityriasis rubra pilaris,
human keratinocytes and exhibit immunomodulating
pruritic folliculitis of pregnancy, seborrhoeic dermatitis,
properties (54). Several studies showed that calcipotriol
Schnitzler's syndrome and Sneddon-Wilkinson disease
as well as calcitriol and tacalcitol are efficacious, safe
(as reviewed in refs 37, 38). Table I depicts newer
and can be used on a long-term basis for psoriasis (55–
studies reporting efficacy and possible combinations of
58). Vitamin D3 analogues, when used after nUVB
nUVB phototherapy with other treatment modalities.
Acta Derm Venereol 85
M. Berneburg et al.
Table I. Recent studies (published since 1999) involving narrowband UVB (nUVB) shown with regard to patient number (n), studydesign and response rate (in some cases descriptive values in results have been calculated from the studies original data to facilitatecomparison between studies)
PsoriasisPasic (42)
>90% PASI reduction: 45%
84% (PUVA), 63% (nUVB);6 month remission: 35% (PUVA),12% (nUVB)
PASI reduction: 84% (nUVB); 89%
non-randomized (25)
Half-side, randomized,
100% (nUVB), 70% (bath-PUVA)
observer-blinded (10)
Half-side, randomized
PASI reduction: 77% (nUVB); 45%
Open, randomized,
Treatments to clear: 25; days to clear:
67 (nUVB), 66 (PUVA)
Half-side, open (12)
PASI reduction: 67.8% (nUVB),
Multicentre (280)
71.4% improvement
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PASI reduction: 83.9 ¡ 15.6%
Prospective, randomized,
Significant higher PASI reduction
with calcipotriol
w95% response: 90.0% (withcalcipotriol), 61.1% (no calcipotriol)
Half-side, controlled (10)
CR: 100% both groups
PASI only on arms
Half-side, open (10)
PASI reduction 48% (nUVB):64% (nUVB/tazarotene),
CR: after 19 treatments on
w50% response: 38% (tacalcitol)
After 6 weeks equal
86% (tacalcitol/nUVB),
Retrospective (40)
w75% response: 72.5%
Recalcitrant psoriasis
Atopic dermatitisPasic (42)
>90% SCORAD reduction: 45.4%;
70–90% reduction: 22.7%
Response: 81%; CR: 43%,
(87)Reynolds (89)
Randomized, controlled
Reduction of activity:
83% (nUVB), 47% (UVA),47% (Visible light)
Pruritus reduction: significant
Half-side, open (9)
Reduction of Costa and Leister score:40% and 50% (nUVB), 33% and30% (UVA1); pruritus: 67% (nUVB),34% (UVA1)
Half-side, randomized,
SCORAD reduction: 65.7%
(bath-PUVA), 64.1% (nUVB)
SCORAD: 63.3% (CsA);
relapses treated with nUVB led tofurther SCORAD-reduction (total59.9%)
Mycosis fungoides (MF) and parapsoriasisGathers (93)
Retrospective (24)
CR: 54.2%; PR: 29.2%; 30% of CR
relapse after 12.5 weeks
CR: 75%; relapse after 20 months
CR: 95%; relapses: 100% within a
SPP and early-stage MF
Retrospective (56)
CR: 81% (nUVB), 71% (PUVA);
remission in months: 24.5 (nUVB),22.8 (PUVA)
Acta Derm Venereol 85
Phototherapy with narrowband UVB
Table I. (Continued.)
VitiligoScherschun (99)
Retrospective (7)
75% response: 71.4%; rest:
Response depended on
50–40% response
75% response: 53%; stable disease:
Children; localization
(100% repigmentation: 92%; equal
response with FA and vitamin B12
PruritusBaldo (107)
Polymorphous light eruptionDummer (113)
Response: 80% (nUVB), 66.6%
nUVB effective after
ineffective UVA/UVB
Retrospective (5)
Spontaneous clearing:
CR: 70%; significant improvement:
Pityriasis lichenoidesPasic (42)
>90% reduction: 33.3%; 70–90%
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Lichen planusSaricaoglu (123)
CR: 100% (30–51 radiations)
CR: 100%; Remission: >5–21 months
Oral lesions: noresponse
Seborrhoeic dermatitisPirkhammer (124)
CR: 33.3%, PR: 66.6%; pruritus: 100%
All relapsed after 21 d
CR, complete remission; PR, partial remission; MF, mycosis fungoides; SPP, small plaque parapsoriasis; SCORAD, Severity Scoring of AtopicDermatitis; PUVA, psoralen with UVA; PASI, Psoriasis Area and Severity Index.
Furthermore, clearing of plaques occurs faster if vitamin
nUVB (73, 74). A multicentre study with 280 psoriasis
D is applied (59–61). Vitamin D3 derivatives may be
patients describes a PASI reduction of 71.4% when
used up to 2 h before phototherapy (62, 63) or after UV
patients are irradiated with nUVB in the presence of
application, as they are unstable under UV irradiation
Dead Sea salt solution (75). These are encouraging data,
(64). One study showed that pretreatment with tacalcitol
but controlled comparative trials are needed to support
accelerated the response to nUVB (65).
these results.
Hofmann et al. (66) found no difference in the efficacy
Combination of UVB and systemic therapy: UVB plus
of the combination of nUVB with dithranol versus
systemic retinoids (isotretinoin and acitretin) can
nUVB with calcipotriol in a half-side trial. However,
improve the efficacy of nUVB, almost reaching the
studies with higher patient numbers are necessary to
effectiveness of PUVA (76). In patients refractory to
confirm this finding.
other treatments, the combination of low-dose acitretin
UVB plus topical retinoids: In clinical studies, tazarotene
and nUVB results in greater improvement than mono-
0.1% gel in combination with nUVB showed faster and
therapy with either acitretin or nUVB (77) and retinoids
significantly greater reduction of psoriasis plaques with
may protect against development of squamous skin
significantly lower median cumulative UV exposure
cancer (78–81). Thus, combination of nUVB with
than UVB alone (67, 68). Mild irritations like erythema,
systemic retinoids is a possible alternative to avoid large
peeling, dryness, burning and pruritus do occur but
cumulative PUVA doses.
photosensitivity is not observed (69, 70). Comparison of
UVB plus psoralen: Psoralen is normally combined with
tazarotene plus nUVB versus calcipotriol plus nUVB in
UVA (PUVA). Anecdotal reports describe equal effi-
clinical studies revealed no significant therapeutic
cacy of psoralens in combination with nUVB when
difference (71). However, reduction of stratum corneum
compared to PUVA, although it is unclear to what
by retinoids increases UV erythemogenicity and a more
extent improvement was due to nUVB radiation alone
cautious increment of UV is recommended when
(82–84). The combination of bath-PUVA plus addi-
combined with tazarotene (72).
tional nUVB has also been described with nUVB
UVB plus salt: Balneophototherapy is a widely applied
enhancing the phototoxic and therapeutic activities of
treatment modality in combination with bUVB or
bath-PUVA (85).
Acta Derm Venereol 85
M. Berneburg et al.
Atopic dermatitis
now there has been no clinical evidence suggesting thatUVB treatment promotes progression of MF.
There is a large body of evidence indicating that nUVBis effective in the treatment of atopic dermatitis (86). In
a recent study, Pasic et al. (42) combined nUVB withUVA for AD in children and showed >90% reduction
No randomized controlled trials investigating the efficacy
of the SCORAD index in 45.4% and 70–90% reduction
of nUVB in the treatment of vitiligo have been published
in another 22.7% of patients. Hudson-Peacock et al. (87)
so far. However, several clinical studies report that nUVB
described a response rate of 81% with complete
can achieve up to w75% repigmentation in about two-
clearance in 43% for nUVB twice weekly. The first
thirds of patients after at least 1 year of treatment (98,
randomized investigator-blinded, half-side comparison
99). Repigmentation w90% can even be observed (100).
study on the efficacy of 8-methoxypsoralen bath-PUVA
nUVB seems to be more effective than bUVB, local
versus nUVB in patients with severe chronic AD found
steroids or PUVA (101) and this wavelength also appears
equal effectiveness after a mean duration of 40 days
to be effective in children (102). Body areas with good
when used three times a week in equi-erythemogenic
responses (w75%) include face, neck, trunk and proximal
doses (88). Another randomized, controlled, double-
extremities, whereas distal extremities as well as genital
blind study with 73 patients treated with nUVB, bUVB/
areas respond very modestly (v25%) or not at all. nUVB
UVA or visible light twice a week showed nUVB to be
seems to be safe as regards photocarcinogenicity, as up to
most effective with respect to the following end points:
now only two patients with vitiligo have been reported to
disease activity and ability to sleep for up to 3 months
develop squamous cell carcinoma after prolonged PUVA
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after cessation of therapy (89). Furthermore, nUVB
therapy (103, 104).
was shown to be as effective as medium-dose UVA1in clearing chronic AD and better in reducing pruritus
Combination of nUVB phototherapy with cyclo-
Phototherapy of pruritus can be effective due to treatment
sporin A (CsA) has been reported to be effective in the
of the underlying disease, such as AD, lichen planus or
treatment of AD. Patients with severe AD were treated
lymphoma. Symptomatic improvement can also be
with oral short-term CsA for 4 weeks. Then CsA was
achieved by phototherapy in pruritus associated with
washed out for 4–6 weeks followed by nUVB photo-
uraemia, primary biliary cirrhosis, macular amyloidosis
therapy applied three times a week for up to 2 months.
and Hodgkin's lymphoma (105). According to Hsu &
This regimen showed good clinical response. However,
Yang (106) uraemic pruritus responds only to bUVB but
the study did not investigate long-term effects of this
not to nUVB. Baldo et al. (107) showed nUVB to be
protocol (91) and this combination has to be viewed
effective for treatment of pruritus associated with poly-
cythaemia vera. One open trial study showed that thecombination of initial thalidomide followed by nUVB for
Early stage mycosis fungoides and parapsoriasis en
prurigo nodularis leads to an excellent response after an
average of 12 weeks (108).
Several studies indicate the beneficial effect of nUVB for
Polymorphous light eruption
patch-stage MF (Ia/Ib) and parapsoriasis (92, 93). Timesto reach complete remissions range from 6 weeks (92) up
Polymorphous light eruption (PLE) is mainly provoked
to 66 months (94). The time to relapse after complete
by UVA and to a lesser extent by a combination of
responses after photochemotherapy with PUVA ranges
UVA/UVB or UVB alone and a light-hardening effect
between 6 and 43 months (95). For nUVB prolonged
can be seen. For patients with severe forms of PLE
remission up to 20 months has been described (96).
effective photo-hardening in spring with nUVB has been
Diederen et al. (94) describes even higher complete
described as equally effective as with PUVA, UVA1 or
remissions rates and longer mean relapse-free intervals
bUVB (109, 110). Photohardening with nUVB has also
when comparing nUVB with PUVA (81% vs 71% resp.
been used for actinic prurigo, idiopathic solar urticaria,
24.5 vs 22.8 months). Some authors propose a main-
tenance phototherapy once a week after complete
sensitivity, congenital erythropoietic protoporphyria,
clearing of MF. As p53 mutations were described in
homozygous variegate porphyria or hydroa vacciniforme,
tumour stage MF with a mutation spectrum strikingly
even when patients showed abnormal photosensitivity in
similar to that reported in non-melanoma skin cancer
the UVB spectrum (86, 111, 112). PLE lesions provoked
and characteristic for DNA damage caused by UVB
by UVA and UVB may respond to photohardening with
radiation, precautions regarding long-term photother-
nUVB, even in patients where UVA/UVB treatment was
apy have to be taken (97). Even though treatment of MF
inefficient. On the other hand, if PLE lesions are induced
with UVB still raises the issue of carcinogenicity, until
by bUVB, correct application of nUVB might be
Acta Derm Venereol 85
Phototherapy with narrowband UVB
impossible. In these very rare cases PUVA therapy has
Late side effects
been reported to be a valid alternative (113).
Chronic exposure to UV radiation induces prematureaging (photoaging) of the skin, showing typical clinical
signs of leathery appearance, wrinkling, reduced recoil
The first-line treatment for graft-versus-host disease
capacity and increased fragility of the skin (128, 129).
(GvHD) is photochemotherapy (PUVA), especially
Both wavelengths UVA and UVB are capable of
when the skin involvement is severe. Moreover,
inducing the different metabolic changes that result in
Grundmann-Kollmann et al. (114) reported 10 patients,
enhanced skin aging (128, 130). The relative influence of
resistant to combinations of immunosuppressive drugs,
nUVB in comparison to UVA or bUVB has not yet been
of which seven patients showed complete clearance after
treatment with nUVB five times a week over 3–5 weeks.
More important than photoaging after chronic UVB
After clearing of cutaneous GvHD, radiation was
exposure is the risk of skin tumour induction. While the
continued as maintenance therapy for at least 4 weeks
role of PUVA in the induction of skin tumours is
and no patient relapsed during a follow-up of 4–18
undisputed, in humans the role of UVB phototherapy in
months. As nUVB phototherapy is a non-aggressive
skin carcinogenesis is less clear. No significant increase
treatment that may be of benefit for patients who
in the risk of developing squamous cell carcinoma or
are receiving higher doses of immunosuppressive
basal cell carcinoma has been associated with long-
drugs, including CsA or FK506, this form of photo-
term exposure of patients with psoriasis to bUVB
therapy may be an alternative to systemic and topical
phototherapy in older and recent studies (131–133),
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PUVA in mild cases or during onset of the disease
even in combination with crude coal tar over 25 years
(134). At present it is not clear whether nUVB or bUVBis more carcinogenic. Several animal studies found
Rare diseases and other indications
that nUVB has a higher carcinogenic potency thanbUVB (135–137), while others did not confirm this
There are anecdotal reports of using nUVB in various
(4, 5, 138–140). Macve & Norval (141) showed that
other diseases. Thus nUVB has been successfully used
tumour outgrowth is enhanced by bUVB, but not
for subcorneal pustular dermatosis (Sneddon-Wilkinson
by nUVB or UVA1. Remarkably, cis-urocanic acid
disease) (116, 117), acquired perforating dermatosis
seemed not to be important for tumour induction,
(118) and pruritic folliculitis of pregnancy (119).
although it is recognized as an initiator of UV-induced
For classical juvenile pityriasis rubra pilaris (PRP), a
good clinical result was observed with nUVB in
Throughout the UVB spectrum, the first DNA lesions
combination with acitretin (120). Notably, PRP can be
induced are pyrimidine dimers, but the number of
provoked by UV irradiation and painful and tense
dimers produced decreases dramatically with longer UV
lesional blistering has been described under nUVB.
wavelengths. For example, irradiation of human fibro-
Thus, phototesting prior to initiation of nUVB as well as
blasts with equal UVB energy produces 100 pyrimidine
discrete dose increments are mandatory (121). Patients
dimers at 302 nm, but only 1 dimer at 312 nm.
with lichen planus have successfully been treated with
Similarly, 60 functional mutations of the hypoxanthine
nUVB: pruritus responded early and a complete
flattening occurred within 30–51 radiations and no
302 nm, but only one is produced at 312 nm (142).
relapse was seen during follow-up of 20 months. Again,
These data were confirmed by Tzung & Runger (143)
photoaggravated lichen planus should be kept in mind
and Budiyanto et al. (144), who showed 10-fold higher
doses of nUVB yielding a similar amount of CPD and
Other diseases responding to treatment with nUVB
also a 1.5–3 times higher amount of oxidative DNA
include chronic pityriasis lichenoides in children, but not
damage compared with bUVB.
pityriasis lichenoides et varioliformis acuta (42) and
Data investigating the carcinogenic risks of nUVB
seborrhoeic dermatitis (124).
and bUVB are limited. When used in humans nUVBseems not to be associated with a higher carcinogenic
ADVERSE EFFECTS OF NUVB
risk when compared with bUVB, but a significantlyreduced risk compared with PUVA (145, 146). A first
Early side effects
long-term retrospective study by Weischer et al. (147)
Early side effects of nUVB include erythema and
during a follow-up of 10 years further supports the view
dryness of the skin. The maximum erythema occurs
that neither nUVB nor bUVB significantly increase the
8–24 h after irradiation (125, 126). As patients over 70
risk of skin cancer. Nevertheless, phototherapy must be
years show a prolonged nUVB-induced erythema, a
applied with due caution and patients possibly receiving
more cautious approach to dose increases is recom-
long-term phototherapy should be followed-up by a
mended in the elderly (127).
dermatologist on a regular basis.
Acta Derm Venereol 85
M. Berneburg et al.
cytotoxicity with the induction of specific photoproductsin T-lymphocytes and fibroblasts from normal human
Phototherapy with nUVB is a safe and effective
donors. Photochem Photobiol 1995; 61: 163–170.
treatment modality for a continuously increasing
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number of skin diseases. In addition to its low
and its functional consequences for skin ageing. Clin Exp
erythemogenicity and high therapeutic efficacy, its
Dermatol 2001; 26: 573–577.
major advantages are possible combination with other
16. Dalziel KL. Aspects of cutaneous ageing. Clin Exp
Dermatol 1991; 16: 315–323.
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17. Berneburg M, Krutmann J. Photoimmunology, DNA
effectiveness. More clinical trials are needed to investi-
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Source: http://www.lighting.philips.co.nz/b-dam/b2b-li/en_AA/products/special-lighting/phototherapy/downloads/uvb_narrowband_vs_buvb.pdf
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