Reprint, Acta Derm
Hydrogen Peroxide Cream
for the Prevention of
White Pressure Areas in UVA Sunbeds
EVA TEGNER and ALF BJÖRNBERG
Department of Dermatology, Lund University Hospital, Lund Sweden
(Accepted August 3, 1989)
Acta Derm Venereol (Stockh) 1990;70:75-76.
F. Tegner, Department of Dermatology, Lasarettet, S-22185 Lund, Sweden.
A single application of 1%
hydrogen peroxide in a stabilized lipid cream during 2 min before UVA
exposure prevents white spots in anoxic pressure areas in sunbed use,
causing an almost normal pigmentation. During maintenance exposure with
UVA once a week this pigmentation will remain unchanged if the pressure
areas are pretreated with hydrogen peroxide before each irradiation.
White spots will appear 3-4 weeks after finishing hydrogen peroxide
pretreatment in the pressure areas thus exposed to UVA alone.
Pressure areas on the
back(scapular region and medial sacral region) remain unpigmented on the
reclining subject upon exposure to UVA from sunbeds, probably due to a
lack of oxygen(1,2). It has earlier been demonstrated that the
application of a stabilized hydrogen peroxide cream prior to UVA
exposure could induce delayed tanning on the pressure areas, while the
placebo-treated contralateral sites remained unpigmented(3). This
finding provides evidence for the role of oxygen in delayed pigmentation
by UVA(4). The hydrogen peroxide cream was used ad libitum with repeated
applications during a half hour period before exposure to UVA(3). The
aim of the present study was to evaluate the pigment promoting effect of
a single application of the cream a short time before exposure to UV
light and to study pigmentation during maintenance treatment with UVA
with and without hydrogen peroxide.
MATERIALS, AND METHODS
individuals, 18 men and 3 women, in the age range 23 -35 years, who tan
easily in the summer sun (skin types III and IV), were selected for the
A Phillips sunbed was used
(Phillips TI. 85 W/09T) with an emission spectrum of 310-420 nm and a
peak emission at 355 nm. The skin was exposed for 30 min per day, 4-5
times per week(6-12 exposures in all during the initial treatment phase)
and then during the maintenance treatment phase once a week.
The two active creams
contained 2% and 1% hydrogen peroxide in a stabilized lipid cream base
of 21% Monomyristin, 7% Monolaurin and 70% water. The two creams used in
series II were not identifiable by appearance or smell and were supplied
in identical tubes with a code sign and marked "left" and "right".
Series I: Comparison 2 and 5
min application of 2% h2O2 cream. The subjects were irradiated with UVA
from below while reclining fairly still on the hard acrylic surface of
the sunbed. Before each sunbed session the 2% H2O2 cream was applied to
symmetrical areas known to remain hypopigmented after exposure to UVA on
sunbeds (scapular areas and sacro-gluteal areas) during periods of 5 min
and 2 min before irradiation, randomly on the left and right sides. The
cream was washed off with lukewarm water just before light exposure.
Series II: Comparison 2% and
1% H2O2 cream. In this study 2% and 1% hydrogen peroxide creams were
applied with a double-blind technique on the selected symmetrical
areas (scapular and sacro-gluteal areas) 2 min before irradiation. The
cream was washed off just before light exposure.
Series III: Maintenance
treatment. After the provocation of delayed tanning with H2O2 and UVA on
the pressure sites, maintenance treatment followed once a week. Before
each irradiation one side was pretreated with 2% H2O2 cream 2 min before
exposure while the contralateral side was not treated. The cream was
washed off with water just before light exposure.
After 6-12 initial treatment
sessions (H2O2 cream + UVA) delayed tanning was observed on the pressure
areas. However, compared with the "normal" delayed UVA tanning on
non-pressure areas, the pigmentation of the pressure sites was delayed
by a few days and was also somewhat uneven, with a slight variation in
pigmentation, often with a semilunar hyperpigmentation at the periphery
of the pressure site. It was also noted that it was more difficult to
obtain even pigmentation on the scapular region than on the medical
In series I there was no
difference in the pigmentation on the sides pretreated for 5 and 2 min.
In series II there was no difference in the pigmentation between the
sides pretreated with 2% and 1% H2O2cream. Series III. When pretreatment
with H2O2 cream was stopped, the white spots appeared after 3-4 weeks of
UVA light alone (maintenance treatment once a week). When, however, one
side was pretreated 2 min before irradiation during the maintenance
treatment the pigmentation remained unchanged during the whole
observation period (3-6 weeks).
During the initial
pigmentation phase with 4-5 exposures/week, one patient experienced
soreness on the side treated with 2% but not with 1% H2O2 cream after 7
exposures when the pressure areas were almost "normally" pigmented. A
acute skin reaction with redness and later hyperpigmentation was
observed in this area, being more pronounced at the periphery. The
condition was clinically similar to a toxic or phototoxic exposure.
Biopsy was not permitted. The UV exposure was stopped and the
inflammatory reaction slowly subsided during the next few days, leaving,
however, a marginal hyperpigmentation for several days.
It has earlier been shown
that repeated applications of 2% hydrogen peroxide in a stabilized lipid
cream base can restore the UVA pigmentation in oxygen-deficient pressure
areas of the skin associated with the use of sunbeds(3). The present
study shows that a single application of 1% hydrogen peroxide cream
applied for a period of 2 min before each UV exposure is sufficient to
prevent the white pressure areas associated with commercial UVA sunbeds.
During a maintenance period with UVA-treatment once a week the
pigmentation remains unchanged in the pressure areas pretreated with
hydrogen peroxide before each irradiation. On the other hand, white
spots will appear 3-4 weeks after finishing hydrogen peroxide
pre-treatment in the pressure areas thus exposed to UVA alone. One
patient suffered a local inflammation skin reaction in the pressure area
with the 2% but not the 1% hydrogen peroxide cream. The reaction was
similar to a toxic or phototoxic skin response.
Acknowledgment The hydrogen
peroxide creams were supplied by Biogram AB, Malmo, Sweden.
1. Tegner E, Rorsman H,
Rosengren F. 3-S-Cysteinyldopa and pigment response to UVA light. Acta
Derm Venereol (Stockh) 1983;63:21-25.
2. Tegner E, Tissue anoxia prevents inflammation and pigmentation caused
by UVA but not by UVB and PUVA., Photoderinatology 1984;1:311-312.
3. Tegner E, Hjörnberg A. Induction of UVA pigmentation in pressure
areas by hydrogen peroxide. Acta Derm Venereol (Stockh) 1986;66:65-67.
4. Auletta M, Gange W, Tan OT, Matzinger E. Effect of cutaneous hypoxia
upon erythema and pigment responses to UVA, UVB and PUVA (8-MOP + UVA)
in human skin. J Invest Ermatol 1986;86:649-652.