of the dorsal hands
elicited by thermal
L. Stransky and V. Broshtilova
Department of Dermatology and
Venereology, Faculty of Medicine, Medical
University, Sofia, Bulgaria
Key words: burns; neutrophilic dermatosis
of the dorsal hands; thermal injury.
Neutrophilic vascular reactions range
histologically from fully developed
leukocytoclastic vasculitis to mild
(1). Limited forms of neutrophilic
dermatosis that show no vascular
involvement have been termed as
localized Sweet’s syndrome (2). The
term pustular vasculitis of the dorsal
hands was first introduced in 1995 to
describe an eruption of papules and
plaques localized to the radial sides
of the hands, which histologically
(3). Later, this condition was recog-
nized as neutrophilic dermatosis of
the dorsal hands (NDDH) and as
demonstrating a spectrum of vascular
A 54-year-old woman with well-
controlled, insulin-dependent diabetes
presented with a chronic dermatosis
of the dorsal hands induced by ther-
mal injury. The onset of the disease in
1998 followed a minor burn to the
dorsum of the right hand where a
firm, bluish-red plaque with peri-
pheral vesicles and an elevated well-
accompanied by nocturnal pain. The
lesion rapidly responded to systemic
corticosteroid and healed without
5 years later, 2 weeks after a burn
to the left hand, a similar bluish indu-
rated plaque developed, localized to
the radial side plus the first 3 digits.
Subsequently, a bulla appeared in the
centre of this plaque.
Based on the clinical findings and
a dense band-like neutrophilic der-
mal infiltrate with leukocytoclastic
vasculitis histologically, a diagnosis
of NDDH was made. Immunofluor-
escence showed immunoglobulin G
(IgG) and C3 complement fragments
within the affected vessel walls, con-
firming vasculitis. No evidence of
neoplasia was detected.
Once again, the lesion responded
rapidly to systemic corticosteroid and
healed within a month without scar-
ring. No relapse had occurred at a
3 patients with haemorrhagic bullae,
plaques and pustules, restricted to the
dorsal hands, were described by
Galaria et al. in 2000, biopsies
demonstrating a neutrophilic infil-
trate and leukocytocylasis (4). The
condition was termed as NDDH.
NDDH has to date been described
in 19 patients: 3 men and 16 women
NDDH bears some clinical and
histopathological resemblance to pre-
viously described neutrophilic derma-
and erythema elevatum diutinum
(6, 7). Controversy remains as to the
categorization of this spectrum of
diseases (8, 9). In contrast to Sweet’s
syndrome (10, 11), NDDH does not
appear to be associated with leukae-
mia. Nor does it seem to be triggered
A recently published report sug-
gested that a localized neutrophilic
dermatosis had been elicited by weld-
ing burns (12). Our case lends some
further credence to this aetiology,
though further published cases are
required to confirm it.
1. Callen J P. Neutrophilic dermatoses.
Dermatol Clin 2002: 20: 409–419.
2. Malone J C, Slone S P, Wills-Frank L
A et al. Vascular inflammation (vas-
culitis) in Sweet syndrome. Arch
Dermatol 2002: 138: 345–349.
3. Strutton G, Weedon D, Robertson I.
Pustular vasculitis of the hands. J Am
Acad Dermatol 1995: 32: 192–198.
4. Galaria N A, Junkins-Hopkins J M,
Kligman D, James W D. Neutrophi-
lic dermatosis of the dorsal hands:
pustular vasculitis revisited. J Am
Acad Dermatol 2000: 43: 870–874.
5. Cohen P R. Skin lesions of Sweet
syndrome and its dorsal hand variant
contain vasculitis: an oxymoron or an
2002: 138: 400–403.
6. Di Caudo D J,ConnollyS M. Neutro-
philic dermatosis (pustular vasculitis)
of the dorsal hands: a report of seven
cases and review of literature. Arch
Dermatol 2002: 138: 361–365.
7. YianniasJ A,
Gibson L E. Erythema elevatum
diutinum: a clinical and histopatho-
logic study of 13 patients. J Am Acad
Dermatol 1992: 26: 38.
8. Ayoub N & Tomb R. Neutrophilic
dermatosis of the dorsal hands: a vari-
ant of erythema elevatum diutinum?
Arch Dermatol 2003: 139: 102.
9. James W D. Newer neutrophilic
dermatoses. Arch Dermatol 2003:
10. Nishie W, Kimura T, Kanagawa M.
recurrent erythema nodosum in a
patient with myelodysplastic syn-
drome. J Dermatol 2002: 29: 91–95.
11. Astudillo L, Loche F, Reynish W,
Rigal-Huguet F, Lamant L, Pris J.
Sweet’s syndrome associated with
retinoic acid syndrome in a patient
with promyelocytic leukemia. Ann
Hematol 2002: 81: 111–114.
12. Lack M D & Weingold DH. Loca-
lized neutrophilic dermatosis follow-
ing welding burns. J Occup Environ
Med 2002: 44: 491–492.
Prof L. Stransky, MD, PhD
1 Sn Georgi Sofiisky Street
Tel: þ359 2 9230684
Fax: þ359 2 9522774
CONTACT DERMATITIS 2003 49: 42–52
COPYRIGHT#BLACKWELL MUNKSGAARD 2003
ALL RIGHTS RESERVED
CONTRIBUTIONS TO THIS SECTION WILL NOT UNDERGO PEER REVIEW, BUT WILL BE REVIEWED BY THE EDITOR
dermatitis – a
Saumya Panda and Subrata Malakar
Rita Skin Foundation, Kolkata, India
Key words: allergic contact dermatitis;
chromate; lichen nitidus; occupational;
propylene glycol; talc.
Lichen nitidus (LN) is an idiopathic
granulomatous reaction manifested
by multiple tiny, shiny non-pruritic
papules with a flat surface (1).
During the last year, we studied
112 cases of palmar allergic contact
dermatitis. Of these, 4 cases exhibited
the morphology and the histopatho-
logical characteristics of LN. All the
cases presenting with palmar lesions
in the clinic (n¼1289) were subjected
to patch testing either with the Indian
standard series or with the standard
series plus the implicated allergens in
(e.g. talc), 20 volunteers without a his-
were selected to rule out false-positive
irritant reactions. All patch test results
were read according to the ICDRG
grading at 3 days.
The LN-like cases represented 3%
of the study population (n¼112). All
were males. 3 were characterized by
widespread distribution of the lesions
over the extremities and trunk; only
in 1 case were the lesions confined to
the palms. In none of the patients
were penile lesions observed. There
were morphological variations in the
form of pompholyx-like lesions (n¼2),
confluent hyperkeratosis (n¼1) and
discrete papules (n¼1).
were also marked. 2 of the cases
showed patch test positivity to potas-
sium dichromate 0?5% pet., 1 to talc
0?5% aq. and 1 to propylene glycol
5% aq. The reaction gradings were þ
and þþ for potassium dichromate, þ
for talc and þþ for propylene glycol.
The occupations ranged from painting
and construction work (potassium
dichromate) to school teaching (talc)
and refrigeration work (propylene
glycol). However, the test sites demon-
strated only erythema and papules and
Unlike idiopathic LN, all cases
Although the study population is very
small and no statistical significance
can be attached, the sex bias in favour
of males may also be noted. The
distribution of lesions corresponding
to the sites of allergenic exposure is
significant in these cases. The histo-
similar in that all of the cases demon-
strated granulomatous reaction and
the presence of Langerhans’ cells. A
deep parakeratotic plug, distinguish-
ing the lesions from palmar lichen
cells were not noticeable, which may
be taken as a point of histological
departure from idiopathic LN (3). It
is also interesting to note, in view of
the fact that chromate is the major
allergen in these cases (50%), that
titis due to chromium and other metal
salts has already been described (4),
though none of these have shown the
morphological characteristics of LN.
All the 4 cases responded toavoidance
tamine and a potent topical cortico-
steroid for 2–4 weeks.
To the best of our knowledge, this
is the 1st report of LN developing
secondarily to contact allergy and also
the 1st report of talc as an allergen.
The authors acknowledge the con-
tribution of Dr Enam Murshed
Khan, MD, MRCPath, who helped
in the evaluation and interpretation
of the histopathological slides.
1. Black M M. Lichen planus and
lichenoid disorders. In: Rook/Wilkin-
son/Ebling Textbook of Dermatology,
Champion R H, Burton J L, Burns D A,
Breathnach S M (eds), 6thedition.
Vol. 3. 1925.
2. Coulson I H, Marsden R A, Cook M G.
Purpuric palmar lichen nitidus: an
unusual though distinctive eruption.
Clin Exp Dermatol 1988: 13: 347–349.
3. Eisen R F, Stenn J, Kahn S M,
Bhawan J. Lichen nitidus with plasma
cell infiltrate. Arch Dermatol 1985: 121:
4. Ngyen L Q, Allen H B. Reactions to
manganese and cadmium in tattoos.
Cutis 1974: 23: 71–72.
Saumya Panda, MD
122/4, Dr Jiban Ratan Dhar Road
allergens in a violinist
Marcy S. Alvarez1and Ronald R. Brancaccio2
1New York College of Osteopathic Medicine,
Old Westbury, and2Ronald O. Perelman
Department of Dermatology, New York
School of Medicine, New York, NY 10016,
Key words: allergic contact dermatitis;
colophonium; ebony; fiddler’s fingers; hand
dermatitis; musician; nickel; rosin; violin.
String players have presented with a
variety of distinct clinical signs of
allergic contact dermatitis (1, 2). Most
dermatitis induced by exotic woods,
metallic components or varnishes on
the instrument’s chin rest (3). ‘Fiddler’s
fingers’ is induced by allergy both to
colophonium (rosin) and, less often, to
metals in the strings (4). Fingerboards
composed of ebony wood are also a
source of sensitization. Contact allergy
to propolis, a sensitizer found in violin
varnish, has been reported in a violin
referred with a 6-month history of an
eruption on the fingertips of her
left hand. Various strength topical
corticosteroids and topical tacrolimus
provided little help. She did report a
personal history of atopy. As a profes-
sional violinist, she has been using the
same antique 1836 Rivolta violin for
Clinically, the fingertips on the left
hand showed an eczematous dermatitis
with the strings and fingerboard. Her
CONTACT POINT 43
right hand and the remainder of her
skin were normal.
Patch testing was performed to 54
allergens (Chemotechnique Diagnos-
tics, Malmo ¨ , Sweden), based on the
NACDG Screening Series, and to her
own violin rosin. Readings were taken
according to the methodology of the
ICDRG after 2 and 4 days. Positive
reactions were noted to nickel sulfate,
cobalt chloride, colophonium, her own
rosin, neomycin sulfate, formaldehyde
tives (quaternium-15, imidazolidinyl
urea and diazolidinyl urea). Further
testing was negative to propolis and to
but positive (þþ) to shavings from
the patient’s metal E string proved
dimethylgloxime spot test positive,
confirming the release of nickel.
Occupational dermatitis in string
players presents a difficult manage-
ment problem. This patient presents
a particular challenge because of her
multiple sensitivities. Rosin is used
on the strings and is necessary to
induce friction that influences the
production of sound and stabilizes
bow contact. The fingerboard itself
is made of ebony wood. The strings,
depending on the note, are composed
of nickel, aluminium, chrome, gold
or silver. Her E string contained
nickel. Although it is relatively simple
for her to avoid the preservatives and
topical antibiotic allergens, the patient
is continuously exposed to rosin, the
nickel in the E string and the ebony
wood on the fingerboard.
experiencing occupational dermatitis is
of the utmost importance, but finding
suitable substitutes proves difficult. A
substitute for rosin proves the most
challenging. A modification of ingredi-
ents adversely affects the quality of
rosin, instrumental tone and adhesive
friction. However, there are synthetic
brands available that warrant trial
(e.g. Clarity1rosin, Shar Products
Company, Ann Arbor, MI, USA).
Although there are pure gut strings
sition poses a problem in that it can
cause an unacceptable change in tone
or quality of sound. Changing the
ebony fingerboard to a different type
of wood fingerboard can more easily
These problems that our violinist
faces have, and may continue to have,
a significant impact on her musical
career. Since there are various causes
of allergic contact dermatitis in violin-
ists, it is important to test for all of
these potential allergens.
1. Fisher A. Allergic contact dermatitis
from musical instruments. Cutis 1993:
2. Rimmer S, Spielvogel R L. Dermato-
logic problems of musicians. J Am
Acad Dermatol 1990: 22: 657–663.
3. Moreno J C, GataI M, Garcia-Bravo B
et al. Fiddler’s neck. Am J Contact
Dermat 1997: 8: 39–42.
4. Buckley D A, Roger A. ‘‘Fiddler’s
fingers’’: violin-string dermatitis. Con-
tact Dermatitis 1995: 32: 46–47.
5. LiebermanH D,
Ramsay D L et al. Allergic contact
dermatitis to propolis in a violin maker.
J Am Acad Dermatol 2002: 46: 30–31.
Ronald R. Brancaccio, MD
67 Perry Street
NY 10014, USA
reaction to cloxacillin
A´lvaro Moreno-Ancillo1, Carmen Domı ´nguez-
Noche1, Ana Carmen Gil-Adrados2and
Pedro M. Cosmes1
1Allergy Unit, Hospital Virgen del Puerto,
Plasencia, Ca ´ceres, and2Centro de Salud,
Castillo de Bayuela, Toledo, Spain
Key words: antibiotics; betalactams;
cloxacillin; cutaneous adverse drug
reactions; delayed hypersensitivity; lack of
cross-sensitivity; medicaments; patch
Reports of cell-mediated allergy to
betalactams have become increasingly
frequent in recent years (1–3). Patch
testing is useful in such cases (1–5).
A patient with a typical clinical picture
of bacterial endocarditis was admitted
to our hospital. Empirical treatment,
with intravenous ampicillin and genta-
micin, was initially given for 3 days.
from blood cultures and the finding of
fibrinous clots forming on ulcerated
phy, cloxacillin was started and the
other antibiotics discontinued. Clinical
symptoms improved notably, but after
erythematous maculopapular rash and
malaise. New blood cultures were set
up, and gentamicin was again added.
The clinical picture worsened progres-
sively, with toxic haematological values,
hepatic and renal function and progres-
sion of the skin lesions to purple blisters
and subsequent desquamation. After 5
days, gentamicin and cloxacillin were
discontinued, and vancomycin, predni-
sone and antihistamines were started.
No bacterium was isolated in later
blood cultures. A skin biopsy showed a
eosinophils and neutrophils. After 1
week, he progressively felt better until
complete skin recuperation after 3
2 months later, prick testing and
intradermal testing were performed
with intravenous preparations of
the antibiotics vancomycin (Lilly,
Madrid, Spain), ampicillin (Medea
S.A., Barcelona, Spain), cloxacillin
(Normon, Madrid, Spain) in their own
diluents. Prick tests with vancomycin
1% (10mg/ml), ampicillin 2% (20mg/
ml), cloxacillin 2% (20mg/ml) and
1% (10mg/ml), ampicillin 0?2 and 2%
(2 and 20mg/ml) and gentamicin 0?4%
(4mg/ml) were negative. Intradermal test
with cloxacillin 0?2% (2mg/ml) was
negative on immediate reading at 20min,
but clearlypositiveat2 and4days.Patch
tests with gentamicin (0?4%, 4 and 5%
pet. and aq.) and ampicillin (0?2%,
0?5%, 2% and 5% pet. and aq.) were
negative. Patch tests with cloxacillin
(0?2 and 2% pet. and aq.) were clearly
positive at D2 and D4, with stronger
reactions at the higher concentrations:
0?2% pet. and aq. D2þ/D4þ; 2%
pet. D2þþ/D4þþ; 2% aq. D2þþ/
A RAST assay was performed in
our laboratory to assess specific
immunoglobulin E (IgE) to cloxacil-
lin and gentamicin. Specific IgE to
penicillin, ampicillin and amoxicillin
was investigated by the CAP-FEIA
system (Pharmacia, Uppsala, Sweden).
We could not detect specific IgE to
penicillin or gentamicin in the serum.
Skin biopsies performed in the
positive patch-tested area showed a
clear T-lymphocyte, CD4þinfiltrate,
thus confirming the occurrence of a
A challenge test was proposed to
assess the tolerance of gentamicin,
informed consent having been obtained
beforehand: repeated therapeutic doses
acillin provocation was not performed
because cloxacillin was considered the
causal agent of this severe delayed
Cell-mediated allergy to betalactams,
mainly aminopenicillins, has been
reported with increasing frequency
in recent years, though severe delayed
hypersensitivity reactions exclusively
due to cloxacillin are extremely rare
(1–5). In our case, cloxacillin pro-
voked a severe hypersensitivity reac-
tion. The involvement of other drugs
was not demonstrated. Despite the
negativity of patch tests with ampicil-
lin, we considered that the severity of
the reaction ruled out provocation
with other betalactams. With regard
to the specificity of patch testing (5),
such provocation might be performed
if absolutely necessary in the future.
Patch tests were very useful for diag-
nosis and further clinical treatment of
this patient, helping to identify safe
alternative antibiotics that could be
Larocca L M, Nucera E, Milani A.
tests in the diagnosis of cell-mediated
allergy to betalactams. Ann Allergy
Asthma Immunol 1999: 83:257–266.
2. Romano A, Quaratino D, Di Fonso M,
Papa G, Venuti A, Gasbarrini G.
A diagnostic protocol for evaluating
nonimmediate reactions to aminopeni-
cillins. J Allergy Clin Immunol 1999:
3. Terrados S, Blanca M, Garcı´a J et al.
Nonimmediate reactions to betalactams
prevalence and role of the different
penicillins. Allergy 1995: 50: 563–567.
4. Alonso Gomez A, Barranco Sanz P,
Caban ˜ as C, Lo ´ pez Serrano M C.
Erythema multiforme from betalactams
with positive cutaneous tests. J Investig
Allergol Clin Immunol 1999: 9: 401–402.
5. Gamboa P, Jauregui I, Urrutia I,
Gonzalez G, Antepara I. Contact sen-
sitization to cloxacillin with oral toler-
ance to other betalactam antibiotics.
Contact Dermatitis 1996: 34: 75–76.
Alvaro Moreno Ancillo, MD
Unidad de Alergologı´a
Hospital Virgen del Puerto
Paraje de Valcorchero s/n
dermatitis from a
fatty acids in a
Charlotte Devantier Jensen and Klaus Ejner
Department of Dermatology, Odense
University Hospital, University of Southern
Denmark and National Allergy Research
Centre, Gentofte, Denmark
Key words: allergic contact dermatitis; boric
acid compounds; metalworking fluids;
A 37-year-old male mechanic had
worked at a factory manufacturing
domestic and industrial ball valve
products for 9 months, when he
developed an itchy eczema on the
hands and arms. The eczema was
related to his work on a computer
machine, where the patient was daily
exposed to a mist of a water-based
spread rapidly to the neck and face,
causing swelling and reddening of the
eyelids. Use of gloves during work
had little or no protective effect.
Patch testing was performed with
the European standard series (TRUE
Hoersholm, Denmark), supplemented
with petrolatum-based patch test pre-
parations (Chemotechnique, Malmo ¨ ,
Sweden) in Finn Chambers (Epitest
Oy, Helsinki, Finland) on Scanpor
The constituents of the metalwork-
ing fluid were kindly supplied by the
manufacturer for further testing.
The patient showed a þþ reaction
at D3 to a 1% dilution in water of a
condensate of boric acid, monoetha-
nolamine (MEA) and fatty acids,
present in the fluid concentrate at
21%. The patient changed job and
the eczema disappeared. 26 consecu-
tive patients were tested as controls
with the condensate at a 5? higher
concentration (5%). 3 showed doubt-
ful (?þ) reactions and 2 showed irri-
TMpanels 1 and 2, AlkAbello,
Several of the components of metal-
working fluids have the potential to
cause irritant and/or allergic contact
dermatitis. Boric acid compounds are
often used as components in metal-
working fluids due to good corro-
fatty acid amides function as coemul-
sifiers and also ascorrosion inhibitors.
The major goal for the develop-
ment of metalworking fluids is to
obtain good technical performance.
Further, economical and safety con-
siderations are important. The metal-
working fluid industry often uses
technical grade ingredients with the
desired properties, because the use of
more well-defined chemistry is both
expensive and valueless to the manu-
facturer, and exact knowledge of the
chemical structures contained in the
ingredients is not always available.
In this case, the allergen was
shown to be a component of a con-
densate produced by heating a mix-
ture of boric acid, MEA and tall oil
may be present in such condensates,
these being condensation products of
boric acid and mono-, di-, or trietha-
nolamine, and used as corrosion
metalworking fluids. Cases of allergic
contact dermatitis from these com-
pounds have been described (1), how-
ever, it is not known if the allergen(s)
in the present case is the same as
previously reported. Extensive che-
mical analysis and subsequent testing
with fractions would be needed to
answer this question.
1. Bruze M, Hradil E, Eriksohn I L,
Gruvberger B, Widstrom L. Occupa-
tional allergic contact dermatitis from
alkanolamineborates in metalworking
fluids. Contact Dermatitis 1995: 32:
Charlotte Devantier Jensen
Department of Dermatology
Odense University Hospital
Sdr. Boulevard 29
5000 Odense C
dermatitis due to
glycyrrhizic acid as an
ingredient of a hair
SE´RGIO F. CABRITA, RAQUEL sILVA AND MIGUEL P.
Clı ´nica Universita ´ria de Dermatologia-
Hospital de Santa Maria, 1699 Lisboa Codex,
Key words: allergic contact dermatitis;
androgenetic alopecia; glycyrrhizic acid;
A 40-year-old female kindergarten
teacher, with long-term androgenetic
alopecia, was referred to our clinic.
No personal or family atopic history
was reported. 2 months earlier, she
had started topical daily application
of 5% minoxidil. On the 5th day
erythema and micropapules, with
burning and itching, appeared locally
leading to cessation of the treatment.
After a month of oral antihistamine
and topical corticosteroid therapy,
with complete resolution of the pre-
vious signs of local irritation, alter-
native treatment was started with
topical application of another hair
restorer, mainly consisting of Ruscus
auleatus, glycyrrhizic acid and Ser-
enoa serrulata. 2 weeks later, she
again noticed erythematous papules,
scaling and itching on her scalp,
which once more led to therapeutic
withdrawal. Patch testing with the
Portuguese standard series, 5% min-
oxidil (in the commercial form used
by the patient) and the hair restorer
mentioned above was performed.
Positivity (þþ) was shown at 2 and
4 days to the latter hair restorer, with
no reaction at all to minoxidil.
The manufacturer then supplied
the 10 components (coded) of the
hair restorer and further patch test-
ing was carried out. Once more we
found positivity (þþ) to the hair
restorer as a whole, this time with a
similar reaction (þþ) to glycyrrhizic
acid (0.3% aq.), 20 controls were
Treatments for androgenetic alope-
cia, range from non-hormonal ther-
experimental use of anti-androgens
and various combinations of medical
and surgical treatments (1). Both
allergic and irritant contact derma-
titis from minoxidil
already been described (2), and its
components as well allergic contact
dermatitis from Serenoa repens and
sensitization occurring after previous
treatment with minoxidil (3). How-
ever, we could find no previous
report from glycyrrhizic acid, as in
this case, though there have been a
few cases of contact allergy to enox-
Enoxolone is derived from glycyr-
rhizic acid. Licorice root, a plant of
the Glycyrrhiceae family, has two
(glycyrrhizic acid) and triterpenes.
Glycyrrhizin occurs as a mixture of
potassium and calcium salts. On
D-glucuronic acid and glycyrrhretinic
acid (enoxolone) are released. It also
contains complex B and E vitamins,
pantothenic acid, biotin, phosphorus,
lecithin, iodine, chromium and zinc.
Triterpenes are similar to adrenal
Glycyrrhizic acid has been used
as cough suppressant, and in the
treatment of adrenal insufficiency
and gastrointestinal diseases. It has
an aldosterone-like effect (7) and
it was recently demonstrated to
inhibiting 17b-hydroxysteroid dehy-
enzymesresponsiblefor the conversion
of 17-hydroxyprogesterone to andros-
tenedione. Androstenedione is nor-
mally converted to testosterone (8).
1. Sawaya M E. Biochemistry and con-
trol of hair growth. In: Cutaneous
Medicine and Surgery-An Integrated
Leboit, Robinson, Wintroub (eds):
1996, Vol. 2, 1245–1257.
2. FriedmanE S,
Cohen D E, Washenik K. Allergic
contact dermatitis to topical minoxidil
solution: etiology and treatment. JAm
Acad Dermatol 2002: 46: 309–312.
3. Sinclair R D, Mallari R S, Tate B.
Sensitization to saw palmetto and
minoxidil in separate topical extem-
poraneous treatments for androgenetic
alopecia. Australas J Dermatol 2002:
4. Fernandez J C, Gamboa P, Jauregui I,
Gonzalez G, Antepara I. Concomitant
sensitization to enoxolone and mafe-
nide in a topical medicament. Contact
Dermatitis 1992: 27: 262.
5. Martinez F V, Badas A J, Goitia J F G,
Aguirre I. Sensitization to oral enoxo-
lone. Contact Dermatitis 1994: 30: 124.
6. Tanaka S, Otsuki T, Matsumoto Y,
Hayakawa R, Sugiura M. Allergic
contact dermatitis from enoxolone.
Contact Dermatitis 2001: 44: 192.
7. Hulisz D, Plant R. Popular Herbal
Remedies: Examining their effective-
ness and potential for drug inter-
actions and adverse reactions. A review
for pharmacy technicians 2000: 29–30.
(University Family Medicine Founda-
tion-11100 Euclid Avenue. Cleveland,
Ohio 44106: E-mail: email@example.com.
8. Armanini D et al. Reduction of serum
testosterone in men by licorice. N Engl
J Med 1999: 341: 1158.
Se´rgio F. Cabrita
Clı´nica Universita´ria de Dermatologia
Hospital de Santa Maria
1699 Lisboa Codex
pustulosis induced by
Mar Blanes Martı ´nez, Juan Francisco
Silvestre Salvador, Gloria Vergara Aguilera,
Isabel Betlloch Mas and Jose Carlos Pascual
Department of Dermatology, Hospital
General Universitario of Alicante, Alicante,
Key words: acute generalized
exanthematous pustulosis; cutaneous
adverse drug reaction; positive patch test;
A 53-year-old man presented with an
extensive erythematous and pustular
eruption of sudden onset. He had no
personal or family history of skin dis-
ease. 10 days before, the patient had
been started on ranitidine hydro-
chloride 300mg oral daily. Other-
wise, he had
atorvastatine and clopidogrel for the
last 2 years. Examination revealed an
erythematous eruption, studded with
smaller than 5mm in diameter, over
the trunk and the extremities. There
was also oedema of the left hand.
were noted in some areas. Palms,
soles and visible mucosa were spared.
No fever was present.
Laboratory examination showed a
mild leukocytosis with neutrophilia
and eosinophilia. Cultures for bac-
teria and fungi of the pustular con-
tents were negative. A punch biopsy
of an affected area showed a subcor-
necrosis and a mild dermal perivas-
cular infiltrate of lymphocytes with
findings consistent with acute gener-
alized exanthematous pustulosis. The
patient was admitted to hospital and
all medication was discontinued. The
acute eruption resolved within a
week, followed by postinflammatory
2 months after the cutaneous reac-
tion, patch tests were performed with
GEIDC standard series and a tablet
of ranitidine hydrochloride dispersed
in pet. Only the ranitidine test gave a
positive (þþ) reaction, manifesting
as a pustular eruption on an erythe-
matous base. Patch testing with
ranitidine hydrochloride in pet. was
also performed in 15 controls, with
pustulosis (AGEP) is an uncommon
reaction pattern characterized by the
sterile pustules on an erythematous
background, fever and elevated num-
bers of blood neutrophils. Target-like
lesions may be associated (1, 2). Most
cases are related to drugs, mainly to
antibiotics. Other causes have occa-
sionally been described, such as acute
infections with enteroviruses or hyper-
sensitivity to mercury (1, 2). The main
psoriasis: AGEP is a reaction pattern
potentially favoured by a psoriatic
background, though histologically dif-
ferent from pustular psoriasis (1, 3).
Patch testing has been variably
useful in identifying the aetiologic
agent in cases of AGEP. Approxi-
mately 50% of AGEP cases demon-
strate positive patch test results,
eruption both clinically and histo-
logically (2). Thesecasesarguestrongly
for a Type IV-delayed hypersensitivity
reaction as the
mechanism of AGEP (4, 5).
We have found other cases of
AGEP caused by ranitidine (6), but
our review of the literature failed to
identify any reports of AGEP related
to ranitidine intake confirmed by
patch testing. There are previous
dermatitis in pharmaceutical manu-
facturing plant employees exposed
to ranitidine compounds, with posi-
tive patch tests to 1–5% ranitidine
hydrochloride in pet. (7). It has been
suggested that the furan ring may be
the main sensitizing moiety (7, 8).
1. Rojeau J C, Bioulac-Sage P, Borseau C
et al. Acute generalized exanthematous
pustulosis. Analysis of 63 cases. Arch
Dermatol 1991: 127: 1333–1338.
2. Beylot C, Doutre M S, Beylot-BarryM.
Acute generalized exanthematous pus-
tulosis. Semin Cutan Med Surg 1996:
Pustular eruption after drug exposure:
is it pustular psoriasis or a pustular
drug eruption? Br J Dermatol 1994:
4. Barbaud A. The use of skin testing in
from pathophysiology to the results
of skin testing. Therapie 2002: 57:
et al. Patch testing in severe cutaneous
adverse drug reactions, including Ste-
epidermal necrolysis. Contact Dermatitis
1996: 35: 234–236.
6. Shawney R A, Dubin D B, Otley C C,
Kwan T H, Bowers K E. Generalized
exanthematous pustulosis induced by
medications. Int J Dermatol 1996: 35:
7. Ryan P J, Rycroft R J, Aston I R.
occupational exposure to ranitidine
2003: 48: 67–68.
8. Goh C L, Ng S K. Allergic contact
Dermatitis 1984: 11: 252.
Mar Blanes Martı´nez
Service of Dermatology
Avd/Pintor Baeza s/n
M. Angeles Gonzalo-Garijo1, Remedios
Pe ´rez-Caldero ´n1, Diego De Argila2and Isabel
1Department of Allergology, and2Department
of Dermatology, Infanta Cristina University
Hospital, Carretera de Portugal s/n, 06080
Key words: acute generalized
exanthematous pustulosis; cutaneous
adverse drug reactions; dipyrone; lack of
cross-sensitivity; metamizole; positive patch
pustulosis (AGEP) is a rare, but
well recognized, drug-induced hyper-
sensitivity reaction. Most cases of
AGEP are associated with antibiotics.
We report a case of AGEP due to
A 58-year-old man presented a diffuse
pruritic eruption of 1–2mm pustules
on an erythematous background over
the trunk with malaise. There was no
adenopathy. The patient had been
operated 48h earlier for a ruptured
tendon with mepivacaine and bupi-
vacaine, and concurrent medications
included cefazoline, metamizole and
enoxaparin. He had no known aller-
gies, no history of drug or food reac-
tions nor contact hypersensitivity.
Laboratory testing showed a neu-
trophilia. Erythrocyte sedimentation
rate, urinalysis, biochemistry (liver
and renal function tests and electro-
lytes) and coagulation studies were
within normal limits. Histologic exam-
ination of the skin showed spongiform
pustules, papillary dermal oedema and
a perivascular lymphohistiocytic and
neutrophilic infiltrate. Microbiological
cultures of pustules were negative.
continued, and the eruption resolved
without sequelae after 1 week of treat-
ment with oral dexclorpheniramine
and prednisone, with emollients.
3 months after the adverse reac-
tion, we carried out patch tests. Only
metamizole was positive (Table1).
Controlled administration of cefazo-
line, mepivacaine and bupivacaine
was well tolerated after the reaction,
and the patient has taken other
NSAIDs without problems.
AGEP is an uncommon cutaneous
eruption that is most often provoked
by drugs, by acute infections with
acterized by acute, extensive forma-
tion of non-follicular sterile pustules
fever and an elevated number of
blood neutrophils. The drugs most
frequently associated with develop-
ment of AGEP are macrolide and
b-lactam antibiotics. Other agents
reported to cause AGEP, more rarely,
nifedipine, diltiazem, ciprofloxacin,
terbinafine and itraconazole (1).
The eruption frequently begins on
the face with rapid spread to the trunk
and extremities. Onset occurs within
2–21 days of initiation of the provok-
ing drug, followed by desquamation,
approximately 2 weeks later. Follow-
ing discontinuation of the offending
drug, the eruption resolves without
serious sequelae. Diagnosis may be
aided by patch testing. Avoidance of
the causative drug is recommended (2).
(1) To our knowledge, this is the first
case reported of AGEP induced by
(2) Patch tests have been useful in
with other NSAIDs.
Bourseau C et al. Acute generalized
exanthemathous pustulosis. Analysis
of 63 cases. Arch Dermatol 1991: 127:
2. del Rosso J Q. Skin manifestations of
drug reactions. Curr Allergy Asthma
Rep 2002: 2: 282–287.
Dra. M. A´ngeles Gonzalo Garijo
Hospital Infanta Cristina
Servicio de Alergologı´a
Carretera de Portugal s/n
cheilitis from ricinoleic
acid in lipsticks
Yung-Hian Leow, Suat-Hoon Tan and
National Skin Centre, 1 Mandalay Road,
Singapore 308205, Singapore
Key words: cosmetics; lipsticks; pigmented
allergic contact cheilitis; ricinoleic acid.
A 30-year-old Chinese woman pre-
sented to our hospital, in June 2002,
with darkened lips and associated
itchy swelling for the past 1 year.
There was no personal or family his-
tory of atopy. She was previously
using commercial brands of lipsticks
but had also been using lipsticks pre-
scribed by a private general practi-
tioner. There had not been any
recent change in the brand of tooth-
paste, and there were no other
obvious triggering or precipitating
factors of significance.
Clinically, scaly erythema with
associated diffuse hyperpigmentation
was seen on the upper and lower lips
and the adjacent vermilion border.
There was no associated intraoral
hyperpigmentation or hyperpigmen-
tation elsewhere. The clinical differ-
pigmented contact dermatitis from
lipsticks and fixed drug eruption.
The latter diagnosis was thought to
be less likely, as there was no signifi-
cant drug history of note. She was
treated with topical corticosteroid.
She was patch tested subsequently
to the National Skin Centre (NSC)
which include ricinoleic acid 30%
pet., and also to her own commercial
lipsticks. At D3, there were þþ reac-
tions to ricinoleic acid and to an
unnamed lipstick preparation pro-
vided by her private general practi-
tioner. 2 weeks later, she was further
patch tested to the NSC-pigmented
contact dermatitis series, additional
commercial lipsticks and 2 cleansers
that she had not brought with her
previously. Numerous þ patch test
reactions were found to 3 of the com-
mercial lipsticks, and marked hyper-
pigmentation was noted on the patch
NSC lip series,
Table1. Patch test results
Drug Concentration (%)Vehicle Results (D2/D4)
*10 control patients were negative.
48 CONTACT POINT
test site of 1 of the commercial
brands of lipstick (Table1). The
patient stopped using all lipsticks for
the following 1 year, with complete
resolution of pruritus. There was
40% improvement in her condition,
with residual brown hyperpigmenta-
tion on her lower lip.
Allergic contact dermatitis from rici-
noleic acid in castor oil is a well
known entity, first reported by Sai
in 1983 (1). Sources of allergic con-
tact dermatitis from ricinoleic acid
and its derivatives range from deo-
dorants and lipsticks to a military
camouflage stick (2–6).
Pigmented contact dermatitis is
another well known entity, with var-
ious allergens previously reported,
notably azo dyes, deodorants, nickel,
However, pigmented contact cheilitis
from a lip preparation is not a com-
mon occurrence. Hemmer et al. (12)
reported a Philippina patient who
presented with hyperpigmentation of
her lips from the use of lipstick. This
patient’s condition improved with
avoidance, but exhaustive patch test-
ing failed to elucidate the exact aller-
gen and it was concluded that the
cheilitis occurred as a result of chem-
Our patient showed a distinct clin-
ical presentation suggestive of pig-
Patch testing demonstrated positive
reactions to various lipsticks and rici-
noleic acid. Hyperpigmentation was
also demonstrated on one of the
patch test sites with the patient’s
own commercial lipsticks. Ricinoleic
acid should be included as one of
the putative contact allergens in the
or pigmented contact
1. Sai S. Lipstick dermatitis caused by
castor oil. Contact Dermatitis 1983:
2. Tan B B, Noble A L, Roberts M E,
Lear J T, English J S C. Allergic con-
tact dermatitis from oleyl alcohol in
lipstick cross-reacting with ricinoleic
acid in castor oil and lanolin. Contact
Dermatitis 1997: 37: 41–42.
3. Inoue A, Shoh A, Aso S. Allergic lip-
stick cheilitis due to ester gum and
ricinoleic acid. Contact Dermatitis
1998: 39: 39.
4. Goon A T-J, Ng P P-L, Ng S K.
Allergic contact dermatitis from mili-
tary camouflage. Contact Dermatitis
1999: 40: 290–291.
5. Magerl A, Heiss R, Frosch P J. Aller-
gic contact dermatitis from zinc rici-
noleate in a deodorant and glyceryl
ricinoleate in a lipstick. Contact
Dermatitis 2001: 44: 119–121.
6. Sowa J, Suzuki K, Tsuruta K,
Akamatsu H, Matsunaga K. Allergic
contact dermatitis from propylene
glycol ricinoleate in lipstick. Contact
Dermatitis 2003: 48: 228–229.
7. Kozuka T, Tashiro M, Sano S,
Fujimoto K, Nakamura Y, Hashimoto
S,Nakaminami G. Brilliant Lake Red
matitis. Contact Dermatitis 1979: 5:
8. Pincelli C, Magni R, Motolese A.
Pigmented contact dermatitis from
deodorant. Contact Dermatitis 1993:
9. El Sayed F, Manzur F, Bazex J. Pig-
mented contact dermatitis from cos-
metics. Contact Dermatitis 1995: 32:
10. Valsecchi R, Di Landro A, Pansera B,
Cainelli T. Pigmented contact der-
matitis. 1995: 33: 70.
11. Trattner A, David M. Pigmented
contact dermatitis from topical min-
oxidil 5%. Contact Dermatitis 2002:
12. Hemmer W, Focke M, Gotz M,
Jarisch R. Pigmented contact derma-
titis of the lips from a lipstick. Con-
tact Dermatitis 1997: 37: 244.
National Skin Centre
1 Mandalay Road
Contact allergy to
various ingredients of
Chan Seok Oh and Jun Young Lee
Department of Dermatology, College of
Medicine, The Catholic University of Korea,
62 Youido-dong, Youngdeungpo-gu, Seoul,
Key words: asiatic acid; asiaticoside;
Centella asiatica; contact dermatitis;
madecassic acid; methylprednisolone
An 18-year-old woman presented
with a pruritic eczematous eruption
on the dorsum of the 4th proximal
Seoul, South Korea). Previously, she
had used various topical medica-
ments for the treatment of a burn
and had often experienced exacerb-
ations of her skin lesions after
applying Madecassol1ointment. A
provisional diagnosis of contact der-
matitis and autosensitization derma-
titis was made, and she was treated
with oral medication for 1 week, after
which Advantan1ointment (Schering
Pharmaceutical Co., Seoul, South
Korea) was tried. However, after
applying Advantan1ointment, her
skin lesion was abruptly aggravated.
Patch tests were performed withthe
Korean standard series (Chemotech-
nique Diagnostics, Malmo0, Sweden),
a cosmetic series (Chemotechnique
Table1. Patch test results
Lipstick from medical clinic (red)
Own commercial lipstick 1
Own commercial lipstick 2
Own commercial lipstick 3
Lipstick from medical clinic (neutral)
NSC lip series
NSC-pigmented contact dermatitis series
NSC¼National Skin Centre.
CONTACT POINT 49
(as is), Madecassol1ointment (as is)
and Dermatop1ointment (Aventis,
Seoul, South Korea) (as is), using
Finn Chambers on Scanpor tape
(Epitest, Tuusula, Finland) on the
skin of her back. Patch tests were
read at 2 and 4 days after application.
Reactions were scored as recom-
mended by the International Contact
Dermatitis Research Group (ICDRG).
The Korean standard series showed
positive reactions to neomycin sulfate
(þþþD2/þþþD4) and balsam of
(þD2/þD4). In addition, she was
positive to Advantan1
þþþD4) and Madecassol1
quent patch tests were performed
with the individual ingredients of
ments, kindly provided by Dongkook
and Schering Pharmaceuticals Com-
pany, respectively (Table1). Hydro-
asiatica (þþD2/þþD4) among the
ingredients of Madecassol1ointment
and methylprednisolone aceponate
(þþD2/þþD4) among the ingredi-
ents of Advantan1ointment were
The reported frequency of contact
allergy to corticosteroids on patch
testing varies mainly between 0?2
and 4?8% (1), although the reported
rate has been as high as 13?3% (2).
Coopman et al. (3) classified cortico-
steroids into 4 groups, groups A–D,
based on the frequency of cross-
methylprednisolone aceponate (MPA),
which belong to Group D, cross-react
with group A corticosteroids because
of steroid metabolism. MPA is meta-
bolized to 6a-methylprednisolone-17-
propionate (group D), which is then
metabolized to methylprednisolone
(group A) (4). In our case, the patient
showed a positive reaction to both
hydrocortisone acetate and MPA,
and this is suspected to be the result
of cross-reaction between hydrocorti-
sone acetate and MPA, to which she
had not previously been exposed.
Centella asiatica is a species of the
Apiaceae family, called familiarly
centella, hydrocotyle, gotu kola or
Indian pennywort. Centella has been
to treat skin diseases such as leprosy
sores, slow-healing wounds, keloids,
striae distensae (5). The action of
promoting the epithelialization of
wounds and ulcers has been con-
firmed in an animal study (6). In
Korea, centella extracts have been
on the market for many years under
the trade name of Madecassol1. A
centella extract consists of 3 major
triterpenic acids (asiaticoside, made-
cassic acid and asiatic acid). Huriez
and Martin (7) suggested that asiati-
extract was a weak sensitizer (5).
The authors thank Schering Pharma-
ceutical Co., Ltd, for supplying the
aceponate ointment and Dongkook
Pharmaceutical Co., Ltd, for supply-
ing the ingredients of the centella
1. Burden A D, Beck M H. Contact
Br J Dermatol 1992: 127: 497–500.
2. Corazza M, Mantovani L, Maranini
C, Bacilieri S, Virgili A. Contact sensi-
tization to corticosteroids: increased
risk in long tern dermatoses. Eur J
Dermatol 2000: 10: 533–555.
3. Coopman S, Degreef H, Dooms-
Goossens A. Identification of cross-
reaction patterns in allergic contact
dermatitis from topical corticosteroids.
Br J Dermatol 1989: 121: 27–34.
4. Goossens A, Matura M, Degreef H.
Reactions to corticosteroids: some
new aspects regarding cross sensitivity.
Cutis 2000: 65: 43–45.
5. Hausen B M. Centella asiatica (Indian
pennywort), an effective therapeutic
but a weak sensitizer. Contact Derma-
titis 1993: 29: 175–179.
6. Lawrence J C. The effect of asiatico-
side on guinea pig skin. J Invest
Dermatol 1967: 49: 95–96.
7. Huriez C, Martin P. L’allergie de con-
tact a l’asiaticoside. G Ital Derm Min
1969: 44: 463–464.
Jun Young Lee, MD
Department of Dermatology
St. Mary’s Hospital
The Catholic University of Korea
Rafael L. P. Lijnen1and Linda de Graff2
1Laurentius Hospital, Monseigneur
Driessenstraat 6, 6043 CV Roermond,
2Netherlands Pharmacovigilance Centre,
Goudsbloemvallei 7, 5237 MH’s-
Hertogenbosch, The Netherlands
Key words: cutaneous adverse drug
reactions; systemic contact dermatitis;
blocker frequently used for symp-
tomatic relief of benign prostate
hyperplasia (BPH). The most fre-
quent adverse reactions are dizziness
and headache, orthostatic hypoten-
complaints and ejaculation disorders.
Table1. Patch test results
Hydrocortisone acetate (2% eth.)
Neomycin sulfate (20% pet.)
TECA (10% pet.)
Methylprednisolone aceponate (1% eth.)
Dehymuls E (as is)
Heavy liquid paraffin (as is)
White soft paraffin (as is)
TECA, titrated extract of Centella asiatica asiaticosideþfree genins (asiatic acid,
50 CONTACT POINT
Sometimes, hypersensitivity reactions
such as rash or pruritus occur (1).
A 46-year-old man presented with
itch and rash for 1 week. On exam-
ination, we found widespread erythe-
matous papules and plaques and on
both hands, vesicles. On 1 wrist and
on the neck, there were erythematous
patient was treated with triamcino-
lone acetonide 40mg/ml 1ml intra-
muscular with good result.
2 weeks before, he had started ther-
apy with tamsulosin 0.4mg oral, daily
for BPH. He had discontinued the
drug immediately after the appear-
ance of the first skin symptoms.
The patient had concomitantly
taken paroxetine 20mg oral, daily
for 3 years. He had a history of
eczema and hay fever. In the past
year, he had been free of skin disease,
with the exception of a persistent
patch of eczema on one wrist, which
was being treated with hydrocorti-
sone butyrate cream.
8 weeks later, patch tests were per-
formed with the European standard
series and tamsulosin as is. There was
a þþ reaction to tamsulosin at day 3.
Tamsulosin as is was tested in 20
control patients without any reaction
stronger than a slightly irritant reac-
tion (erythema) in 1 patient. 1 week
after the patch tests, a rechallenge
with tamsulosin was performed. The
eczema returned within 3 days.
Coombs classification (2), this eczema-
tous skin eruption is a type 4 allergic
reaction. Systemic type 4 skin reac-
tions with positive patch tests are
reported with several drugs, such as
zepam and pyrazolines. Calkin and
Maibach formulated 6 criteria for
the diagnosis of a systemic type 4
allergic drug reaction which are: a
history of drug ingestion, clinical
appropriate patch test controls, reso-
lution when drug is discontinued and
positive provocative drug challenge
(3). Our case fulfilled all these cri-
teria. To our knowledge, this is the
1st patient reported to have devel-
oped eczema associated with the
taking of tamsulosin.
1. Summary of product characteristics of
2. Coombs R R A, Gell P G H. Classifi-
cation of allergic reactions responsible
for clinical hypersensitivity and dis-
ease. In: Clinical Aspects of Immun-
ology, Gell P G H, Coombs R R A,
Lachmann P J (eds): Oxford, Black-
3. Calkin J M, Maibach H. Delayed
diagnosed by patch testing. Contact
Dermatitis 1993: 29: 223–233.
Rafael L. P. Lijnen, MD
Monseigneur Driessenstraat 6
6043 CV Roermond
dermatitis from rectified
camphor oil in Earex1
Olivia E. Stevenson and Tracey M. Finch
Department of Dermatology, Solihull
Hospital, Solihull, West Midlands, UK
Key words: allergic contact dermatitis;
camphor oil; ear drops; medicaments.
A 64-year-old woman presented with
severe eczema of the ears, neck and
upper chest following the use of
Earex1ear drops (Seton Healthcare
Group, Oldham, UK). She had no
personal history of atopy, although
there was a previous history of sensitiv-
ity to toiletries.
Patch testing was performed with
cosmetics and the hairdressing series,
as well as with her own products
developed a þ reaction at D4 to
Euxyl K 400 (1.5% pet.) and þþ
reactions to thimerosal (0.1% pet.),
tea tree oil (5.0% pet.) and Earex1
ear drops (as is).
Earex1ear drops contain only
arachis oil BP, almond oil and recti-
fied camphor oil, and further testing
to these ingredients demonstrated a
þþ reaction on D2 and D4 to recti-
fied camphor oil (10% pet.) only.
ear drops. She
Subsequently, a further 30 patients
attending the patch test clinic were
tested to the same rectified camphor
oil as is. None developed positive
Camphor oil is used as a perfumery
ingredient in soaps, cosmetics and
deodorants. It is also used, though
more often in synthetic form, as a
solvent in paints, varnishes, waxes
and insecticides, as a masking agent
for unpleasant odours and in a few
require a camphoraceous odour.
The only previous reports related
to camphor allergy are from the use
of 4-methylbenzylidene camphor and
its derivatives. This substance is
derived from synthetic camphor and
used as a chemical sunscreen, which
has the ability to cause both allergic
and less commonly photoallergic
contact dermatitis (1). To our knowl-
edge, however, this is the first report
of allergic contact dermatitis from
rectified (i.e. purified) camphor oil,
though camphor has been described
as a cause of non-immunological
contact urticaria (2). This case there-
fore highlights camphor oil as a rare
cause of allergic contact dermatitis in
a topical medicament.
We thank Seton Healthcare Group
for providing the ingredients for
1. Schauder S, Ippen H. Contact and
photocontact sensitivity to sunscreens:
review of a 15-year experience and of
the literature. Contact Dermatitis 1997:
2. Branda ˜ o F M, Goossens A, Tosti A.
Topical drugs. In: Textbook of Contact
Dermatitis, Rycroft R J G, Menne ´ T,
Frosch P J, Lepoittevin J-P (eds), 3rd
edn. Berlin: Springer, 2001: 689–723.
Department of Dermatology
Clifford Bridge Road
Coventry CV2 2DX
Contact dermatitis from
geraniol in washing-up
Lesley-Ann Murphy and Ian R. White
St Johns Institute of Dermatology, St
Thomas’ Hospital, London SE1 7EH, UK
Key words: allergic contact dermatitis;
antimicrobials; fragrance mix; geraniol;
Fragrance mix (FM), a mixture of 8
alcohol, a-amyl cinnamal, cinnamal,
citronellal and oak moss), gives a posi-
tive reaction in 4–11% of patch-tested
patients. Fragrances can cause allergic
contact dermatitis as well as contact
We describe a 27-year-old male dentist,
with a personal and family history of
partly responsive to treatment with
very potent topical corticosteroid. The
dorsum of his hands was more severely
affected than the palm. He wore
non-powdered latex gloves during his
work and thought that this might have
worsened his hand dermatitis, though
there had been no improvement in his
symptoms during a 2-week period of
absence from work. There were no
other precipitants or exacerbating fac-
tors identified, but he had changed his
washing-up liquid in the months pre-
ceding presentation and admitted to
not usually wearing household gloves.
Patch testing to an extended stand-
ard, dental and nursing series was
negative except to FM and potassium
dichromate. When patch tested to
individual fragrance allergens, he had a
positive response (þ) to geraniol. Prick
forearm was negative. Geraniol was
up liquid that he used and as being
present for its antimicrobial properties.
and his hand eczema has since resolved.
Based on this, we concluded that his
hand eczema had been an allergic
contact dermatitis from geraniol. We
did not consider potassium dichromate
to be a currently relevant allergen.
Epidemiological studies have described
an increasing frequency of fragrance
allergy and an association with hand
tic and occupational products can be
relevant in terms of risk assessment for
that are intended for hand exposure. A
(GC-MS) concluded that geraniol
was one of the 5 most commonly
used fragrances in such products,
occurring in those analysed as part of
the study at a mean concentration
value of 234.4 p.p.m. (2). This did
not vary significantly from previously
published GC-MS data pertaining
to various cosmetic products and
perfumes. Additionally, this study
suggested that, when considering
potential contact allergy to these
product types, the investigator should
consider fragrance allergens other
than those included in FM, because
these may also occur in occupational
and domestic products with greater
frequency than in deodorants, fine
fragrances, skin care products and
urticaria from geraniol have both
previously been reported (3–5). This is
the first report of a hand dermatitis
occurring as a result of contact with
geraniol as a constituent of a domestic
product intended for hand exposure.
This emphasizes the need to consider
household products and the possibility
when assessing patients who present
with hand eczema.
1. Harvell J, Bason M, Maibach H I.
Contact urticaria and its mechanisms.
Food Chem Toxicol 1994: 32: 103–112.
2. Rastogi S C, Heydorn S, Johansen J D,
Basketter D A. Fragrance chemicals in
domestic and occupational products.
Contact Dermatitis 2001: 45: 221–225.
3. Chang Y C, Maibach H I. Pseudo-
flautist’s lip: allergic contact cheilitis
from geraniol. Contact Dermatitis 1997:
4. Vilaplana J, Romaguera C, Grimalt F.
Contact dermatitis from geraniol in
Bulgarian rose oil. Contact Dermatitis
1991: 24: 301.
5. Yamamoto A,Morita A, Tsuji T,Suzuki
K, Matsunaga K. Contact urticaria from
geraniol. Contact Dermatitis 2002: 46: 52.
St Johns Institute of Dermatology
St Thomas’ Hospital
London SE1 7EH
52 CONTACT POINT