This study revealed demographic information regard-
ing matched dermatology applicants and the many fac-
tors involved in the rank process. Program directors,
through the Association of Professors of Dermatology,
could collect more data in a serial fashion to effectively
manage the application process. Such data should help
guide both applicants and program directors in their pur-
suit of the “perfect match.”
Jennie T. Clarke, MD
Jeffrey J. Miller, MD
Jennifer Sceppa, MD
Lowell A. Goldsmith, MD
Erin Long, MD
Correspondence: Dr Clarke, Department of Dermatol-
ogy, Milton S. Hershey Medical Center, Pennsylvania State
University, 500 University Dr, Hershey, PA 17033
(jclarke1@psu.edu).
Financial Disclosure: None reported.
1. Nuthalapaty FS, Jackson JR, Owen J. The influence of quality-of-life, aca-
demic, and workplace factors on residency program selection. Acad Med. 2004;
79:417-425.
2. Flynn TC, Gerrity MS, Berkowitz LR. What do applicants look for when se-
lecting internal medicine residency programs? a comparison of rating scale
and open-ended responses. J Gen Intern Med. 1993;8:249-254.
3. Rutkow IM, Imbembo AL, Zuidema GD. The application and interviewing
process for surgical house officership. Surgery. 1979;85:184-190.
4. Stringer SP, Cassisi NJ, Slattery WH. Otolaryngology residency selection pro-
cess: medical student perspective. Arch Otolaryngol Head Neck Surg. 1992;
118:365-366.
5. Wass CT, Rose SH, Faust RJ, Offord KP, Harris AM. Recruitment of house
staff into anesthesiology: factors responsible for house staff selecting anes-
thesiology as a career and individual training program. J Clin Anesth. 1999;
11:150-163.
6. Association of American Medical Colleges Web site. www.aamc.org/programs
/eras/statistics/residency/derm.htm. Accessed January 2004.
A Clinician’s View of Urticarial Dermatitis
I believe the term urticarial dermatitis caught on
quickly with clinicians in Australia because the clini-
cal picture of patients with the histologic features
reported by Kossard et al1 has urticarial and eczematous
features that vary in intensity over time, creating an oxy-
moronic quality that the name they coined captures nicely.
The authors mention contact sensitivity as a mecha-
nism capable of producing urticarial plaques, and Fung2
described a case of contact dermatitis to nickel that pro-
duced a solitary urticarial plaque with the histologic traits
of a dermal hypersensitivity reaction that he termed ur-
ticarial papulosis. Kossard et al1 acknowledge that Fung2
has described the same process. More than 20 patients
with such symptoms have been referred to me for patch
testing, and I have yet to find a relevant contact allergen
to account for the condition. The histologic traits in the
cases I have evaluated have been more consistent with
Fung’s description2 of virtually no epidermal involve-
ment and no neutrophils, just superficial and midder-
mal lymphohistocytic infiltration accompanied by eo-
sinophils. Some of these patients have abnormally high
eosinophil counts in their blood and meet the criteria for
having hypereosinophilic syndrome (⬎1500 eosinophils/
mL3 for more than 6 months without other explana-
tion). That syndrome was described in 1978 by Kazmie-
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©2006 American Medical Association. All rights reserved.
rowski et al, 3 who reported skin lesions that were
erythematous and pruritic, papules and nodules, or ur-
ticaria and angioedema. It was pointed out that these skin
changes may be the only manifestation of the hypere-
osinophilic syndrome.3 When urticarial dermatitis has
been accompanied by systemic eosinophilia, I have con-
sidered it to be a benign, cutaneous form of the hypere-
osinophilic syndrome, and when the same eruption was
present without systemic eosinophilia, I have previ-
ously used the term subacute prurigo. I find the term ur-
ticarial dermatitis far more descriptive. However, it should
be noted that this same eruption has also been reported
not only using these terms and those listed in the article
by Kossard et al1, but also as grouping prurigo by Ofuji
and Ogino4 and Ofugi precursor eruption by Fujii et al.5
The clinical features of this entity are urticarial patches
that remain for days to weeks and are commonly accom-
panied by erythematous papules that are excoriated, cre-
ating an eczematous dermatitis-like picture at times and
a more urticarial picture at other times. The trunk is com-
monly involved in a symmetrical fashion, as are the sa-
crum and proximal extremities. Pruritus is unrelieved by
treatment with antihistamines and topical corticoste-
roids. Whatever this disease is to be called, it is poorly
understood and is by no means rare.
As to treatment, the use of topical corticosteroids and
oral antihistamines has been disappointing, as has been
treatment with narrow-band UV-B. Results from treat-
ment with low dosages of prednisone (7.5 mg/d or less)
combined with either dapsone (50-100 mg/d) or hy-
droxyurea (500-1000 mg/d) have been very gratifying.
Robert L. Rietschel, MD
Correspondence: Dr Rietschel, Southern Arizona VA
Health Sciences Center, 3601 S 6th Ave, 1-11M, Tuc-
son, AZ 85723 (Robert.Rietschel@med.va.gov).
Financial Disclosure: None reported.
1. Kossard S, Hamann I, Wilkinson B. Defining urticarial dermatitis, a subset of
dermal hypersensitivity reaction pattern. Arch Dermatol. 2006;142:29-34.
2. Fung MA. The clinical and histologic spectrum of “dermal hypersensitivity
reactions”: a nonspecific histologic diagnosis that is not very useful in clini-
cal practice, and the concept of a “dermal hypersensitivity reaction pattern.”
J Am Acad Dermatol. 2002;47:898-907.
3. Kazmierowski JA, Chusid MJ, Parrillo JE, Fauci AS, Wolff SM. Dermatologic
manifestations of the hypereosinophilic syndrome. Arch Dermatol. 1978;
114:531-535.
4. Ofuji S, Ogino A. Grouping prurigo. J Dermatol. 1988;15:60-64.
5. Fujii K, Kanno Y, Konishi K, Ohgou N. Relapsing coalescent papular derma-
tosis of elderly patients: a precursor or an abortive lesion of Ofuji
papuloerythroderma. Eur J Dermatol. 2003;13:272-275.
In reply
We appreciate the comments of Dr Rietschel on his experi-
ence with patients who had a clinical presentation of urti-
carial dermatitis and patch test results that were negative
for contact allergens.
The term urticarial dermatitis may not be an oxymoron
as we do not consider the reaction pattern to be simply due
to the combination of physical or allergic urticaria com-
bined with dermatitis but rather to be a genuine reaction
pathway. The urticarial appearance may reflect the pres-
ence of T cells with a helper type 2 phenotype-producing cy-
tokine (eg, interleukin [IL] 4, IL-5, and IL-10) that may
WWW.ARCHDERMATOL.COM
induce eosinophilia and urticarial reactions. There is ini-
tial evidence, not only in reports of atopic dermatitis1 but
also of systemic contact allergies2 and pemphigoid gesta-
tionis,3 that T-helper type 2 lymphocyte mediators can be
demonstrated in each of these conditions that may present
clinically as urticarial dermatitis.
The superficial nature of the urticarial component in ur-
ticarial dermatitis may reflect that it is an initial phase of
an epidermal reaction pathway. Investigative studies are
needed to establish whether urticarial dermatitis in other
settings (particularly when it is the sole reaction pattern)
is also associated with a similar T-helper type 2 cytokine
cascade. Whether this reaction is modulated by the emer-
gence of a T-helper type 1 phenotype pattern commonly linked
to dermatitis remains to be demonstrated. The clinical rec-
ognition and definition of urticarial dermatitis may help such
studies select a suitable subset of patients.
The term urticarial dermatitis is not synonymous with
prurigo or the broader group of pruriginous dermatoses. Pru-
rigo is linked with multiple eponyms and is usually domi-
nated by papules rather than the urticarial plaques seen in
cases urticarial dermatitis. Subacute prurigo is often papu-
lovesicular and excoriated and more often shares features
with papular urticaria.
We hope that the recognition of urticarial dermatitis as
a reaction pattern may help to define further settings in which
this can be found, including the association with hypere-
osinophilia that Dr Rietschel has observed. Assessment of
IgE levels and the relationship to atopic dermatitis in adults
also remains to be explored.
Steven Kossard, FACD
Ian Hamann, FACD
Correspondence: Dr Kossard, Skin and Cancer Foun-
dation Australia, 277 Bourke St, Darlinghurst 2010 Syd-
ney, NSW, Australia (skossard@scfa.edu.au).
1. Thepen T, Langeveld-Wildschut EG, Bihari IC, et al. Biphasic response against
aeroallergens in atopic dermatitis showing a switch from an initialTh2 re-
sponse to a Th1 response in situ: an immunohistochemical study. J Allergy
Clin Immunol. 1996;97:828-837.
2. Jensen CS, Lisby S, Larsen JK, Veien NK, Menne T. Characterization of lym-
phocytic subpopulations and cytokine profiles in peripheral blood of nickel-
sensitive individuals with systemic contact dermatitis after oral nickel exposure.
Contact Dermatitis. 2004;50:31-38.
3. Fabbri P, Caproni M, Berti S, et al. The role of T lymphocytes and cytokines
in the pathogenesis of pemphigoid gestationis. Br J Dermatol. 2003;148:1141-
1148.
Targeted UV-B Phototherapy:
When and Why to Start
W e read with interest the article by Asawa-
nonda and colleagues1 on the use of tar-
geted UV-B phototherapy for plaque-type
psoriasis, in which the authors describe results reported
by our research team in a study dealing with similar treat-
ments.2 We totally agree that targeted UV-B photo-
therapy is safe and convenient for the treatment of some
skin disorders, including localized and recalcitrant pso-
riasis in plaques.
However, the assumption of the authors1 that we used
the 308-nm excimer laser is incorrect. In fact we treated
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our patients with a 308-nm monochromatic excimer light,
which was not generated by a laser but by a device re-
leasing a noncoherent light.2
In addition, Asawanonda et al1 speculate that, be-
cause UV-B radiation penetrates rather superficially into
the dermis, it might be of limited use in palmoplantar
psoriasis. This has not been the case with our patients.
Instead, we have seen that palmoplantar psoriasis is the
form that responds better to the 308-nm targeted UV-B
phototherapy.3
Furthermore, after treatment with the same 308-nm
targeted UV-B phototherapy, palmoplantar areas show
a longer time before relapse than any other areas af-
fected by psoriasis and treated with the same light source.3
We agree that there are no serious adverse events asso-
ciated with this treatment,1 but we would like to go further.
In fact, we think that this targeted phototherapy has some
more relevant advantages. The total irradiation targeted dose
is minimal, depending on the limited percentage of the body
surface affected, and it is always possible to irradiate dif-
ferent parts of the body (ie, hands and feet) with a dose even
5 or 6 times higher than the dose used for other parts (ie,
face or the genital area). This is not possible or convenient
with nontargeted methods, which increase the risk of de-
veloping photoaging or skin cancer in normal skin.
A further evolution of the technique, using UV-B nar-
rowband beam passing through an optical fiber to selec-
tively reach the affected skin, seems even more exciting.4-6
For this purpose we use different conical hoods of 0.5 to
5 cm in diameter, which can be applied at the end of the
optical fiber to obtain different light spot diameters. With
this device, the advantages of targeted phototherapy are
more evident: (1) the treatment does not increase the color
contrast between affected and non-affected skin and (2) it
is easy for the operator to vary the irradiation dose accord-
ing to the specific anatomic location of the areas under treat-
ment and their different responsiveness.
Not only psoriasis but also vitiligo (when localized on
less than 10% of the skin surface) and many other local-
ized recalcitrant skin disorders that respond to light
sources (not necessarily laser) of 308 to 315 nm should
more often be treated with targeted UV-B therapy. This
could well become the treatment of first choice and not,
as the authors suggest, used only for “localized, recalci-
trant disease for which other treatments have failed.”1
Why only when other treatments have failed?
Torello Lotti, MD
Riccardo Rossi, MD
Piero Campolmi, MD
Correspondence: Dr Lotti, University Unit of Dermatol-
ogy and Physiotherapy, School of Medicine, University
of Florence, Via Della Pergola 58, 50121 Florence, Italy
(torello.lotti@unifi.it).
Financial Disclosure: Dr Lotti has received honoraria from
Deka MELA, Calenzano, Italy, and Ratokderm Co, Mi-
lan, Italy, and has provided expert testimony for Bioskin
(Cropper Medical Inc, Ashland, Ore). Dr Rossi has served
as a university consultant and provided expert testi-
mony for Deka MELA. Dr Campolmi has provided ex-
pert testimony for Deka MELA.
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