Journal Information
Vol. 109. Issue 10.
Pages 929-932 (December 2018)
Vol. 109. Issue 10.
Pages 929-932 (December 2018)
Case and Research Letters
DOI: 10.1016/j.adengl.2018.10.007
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Urticarial Dermatitis. A Cutaneous Reaction Pattern
Dermatitis urticante. Un patrón de reacción cutánea
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M.C. García del Pozoa,
Corresponding author
sakuragarciadelpozo@hotmail.com

Corresponding author.
, I. Povedab, P. Álvarezb, J.F. Silvestreb
a Servicio de Dermatología, Complejo Hospitalario Universitario de Albacete, Albacete, España
b Servicio de Dermatología, Hospital General de Alicante–ISABIAL, Alicante, España
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Table 1. Descriptive Data: Patient Characteristics, Clinical Presentation, and Treatment.
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In 2006, Kossard and coworkers coined the term urticarial dermatitis (UD) to describe a histological skin reaction pattern with a broad clinical spectrum. UD is primarily characterized by the presence of urticarial, erythematous, pruritic papules or plaques and eczematous lesions.1 Biopsy of urticarial areas reveals a normal stratum corneum, minimal spongiosis, and perivascular lymphocytic infiltrate of the papillary dermis with eosinophils (with or without neutrophils)1 (Fig. 1). In this descriptive observational study we describe the clinical and histological findings in 6 patients with a diagnosis suggestive of UD who were treated at the Eczema Unit of the Dermatology Service of a tertiary hospital in 2015 and 2016. Table 1 shows corresponding data on epidemiology, comorbidities, clinical presentation, initial clinical suspicion, diagnostic tests, final diagnosis, disease duration at the time of diagnosis, follow-up period, treatment, and progression.

Figure 1.

Normal epidermis and dense perivascular lymphocytic infiltrate with abundant eosinophils. Preserved dermoepidermal junction (hematoxylin-eosin, original magnification ×20).

(0.17MB).
Table 1.

Descriptive Data: Patient Characteristics, Clinical Presentation, and Treatment.

Sex  Female  Male  Female  Male  Female  Female 
Age, y  71  88  62  77  45  77 
Comorbidities  DM
Dyslipidemia
Essential hypertension 
BPH  Dyslipidemia
DM 
DM
BPH
Ischemic heart disease 
N/A  DM
Osteoporosis
WM
Ovarian teratoma 
Dermographism 
Initial clinical suspicion  Scabies
Eczema
BP
UD
CSU 
BP
Eczema
UD
CSU 
UD
CSU
Urticaria-vasculitis 
Allergic contact dermatitis
UD
BP
DR 
Scabies
Eczema
CSU
Dermatitis herpetiformis 
CSU
Urticaria-vasculitis DR
BP 
Histology  Normal epidermis
Superficial dermal perivascular, lymphocytic, and eosinophilic infiltrate with presence of eosinophils
DIF– 
Focal parakeratosis, mild eosinophilic spongiosis, and poor vacuolization of the basement membrane Superficial perivascular lymphocytic infiltrate
Interstitial lymphocytic and eosinophilic infiltrate
DIF– 
Normal epidermis
Superficial dermal perivascular, lymphocytic, and eosinophilic infiltrate with interstitial eosinophils

DIF– 
Normal epidermis
Superficial dermal perivascular, lymphocytic, and eosinophilic infiltrate
DIF– 
Normal epidermis
Superficial dermal perivascular, lymphocytic, and eosinophilic infiltrate with interstitial eosinophils
DIF– 
Normal epidermis
Mild dermal edema, superficial and interstitial dermal perivascular, lymphocytic, and neutrophilic infiltrate without eosinophils
No signs of vasculitis
DIF– 
Other diagnostic tests  BT (IgE, 260 IU/mL;
eosinophils, 0.86 × 103/μL) 
N/A  N/A  Patch test (negative)  BT:
normal 
BT (glucose, 195mg/dL; GF, 52 mL/min; CBC, normal) 
Final diagnosis  UD (DR secondary to vildagliptin)  CSU
 
CSU
 
UD (DR secondary to silodosin)  CSU
 
Schnitzler syndrome 
Treatment  Permethrin
OA
OC
TC
MTX
Vildagliptin (interrupted) 
OA
OC
TC

 
OA
OC
NSAIDs (interrupted)
 
OA
OC
TC
Silodosin (interrupted)
 
Permethrin
OA
OC
TC
Montelukast Omalizumab 
OA
OC
TC
MTX 
Treatment response  Good  Good  Good  Good  Good  Poor
 
Delay between onset and diagnosis, mo  10  13 
Follow-up, mo  13  20  10  13 

Abbreviations: BP, bullous pemphigoid; BPH, benign prostatic hyperplasia; BT, blood test; CBC, complete blood count; CSU, chronic spontaneous urticaria; DIF, direct immunofluorescence; DM, diabetes mellitus; DR, drug reaction; GF, glomerular filtrate; MTX, methotrexate; N/A, not applicable; NSAIDs, non-steroidal anti-inflammatory drugs; OA, oral antihistamines; OC, oral corticosteroids; TC, topical corticosteroids; UD, urticarial dermatitis; WM, Waldenström macroglobulinemia.

The mean age at UD onset was 70 years (range, 45–88 years). None of the patients had a personal or family history of atopy, urticaria, or any other skin disease. All patients reported having pruritus and in all cases physical examination confirmed the presence of urticarial papules or plaques and clinical signs of dermatitis (Fig. 2A). Dermographism was detected in 4 patients (Fig. 2B). The initial clinical suspicions included UD, chronic spontaneous urticaria (CSU), bullous pemphigoid, and eczema. Other clinical entities included in the differential diagnosis were drug reactions, urticaria-vasculitis, scabies, and dermatitis herpetiformis.

Figure 2.

A, Excoriated erythematous papules on the back of a patient. B, Use of the Fric test to confirm dermographism on the back of a patient with prurigo lesions at different stages of progression.

(0.13MB).

In all cases, a final diagnosis was established based on the results of diagnostic tests (CSU in 3 patients, drug reaction in 2 patients, and Schnitzler syndrome in 1 patient). The mean time from disease onset to final diagnosis was 7 months (range, 3–13 months) and the mean duration of follow-up was 11.3 months (range, 5–20 months). All patients were initially treated with oral antihistamines and corticosteroids. Improvement was observed in only 2 patients, both of whom were later diagnosed with CSU. All but 1 patient responded well to targeted treatment once the definitive diagnosis had been established.

UD is not a discrete disorder, but a group of skin diseases that share similar clinical and histological manifestations. In many patients with clinically suspected UD a clinical-pathological correlation can be reached through accurate diagnostic assessment,2 although this can take several months. Pathologists have used the term dermal hypersensitivity reaction pattern to describe UD, despite the absence of a clinical or histological correlation between these presentations.1,3 All cases in this series initially posed a diagnostic challenge, as none could be classified as a specific inflammatory disorder. Ultimately, a final diagnosis was established in all cases. The most common diagnosis was CSU, followed by drug reaction. Our results differ from those previously reported in the literature: Kossard and coworkers found that the most frequent clinical associations were eczema and drug reactions,1 while 47% of the cases in the series by Hannon and coworkers were of idiopathic origin.2 Certain histological clues may facilitate the establishment of a more specific diagnosis,2 particularly if observed in earlier disease stages when the lesions are more edematous and less excoriated. The presence of spongiosis supports a diagnosis of eczema, while its absence is suggestive of urticaria or lesions secondary to either drug reaction or urticaria.1 Because UD can constitute the initial signs of bullous pemphigoid,1,2 it is advisable to perform direct immunofluorescence studies.

UD typically affects elderly patients, especially women.2,4 Because many patients are polymedicated, it can be difficult to identify the causative agent in cases of suspected drug-induced UD. UD lesions have a polymorphous appearance, and exhibit features of urticaria and concomitant or simultaneous dermatitis.4 Eczematous lesions may be caused in part by the use of home remedies to relieve itching. In our study, physical examination revealed dermographism in some patients. Although dermographism is typical of drug reaction, scabies and, above all, CSU, its presence can be particularly helpful in the diagnosis of UD.

UD may involve a T helper 2 (Th2) lymphocyte reaction, which precedes a dominant T helper 1 (Th1) cytokine profile, particularly in cases of atopic dermatitis.1,5 This induces the production of interleukin (IL)-4, IL-5, and IL-10, all of which can give rise to eosinophilia and urticarial reactions.5

The therapies most commonly used to treat UD include oral antihistamines, topical and systemic corticosteroids, narrowband ultraviolet B radiation, and topical calcineurin inhibitors, usually with unsatisfactory results.1,2,4 Some reports have described good responses to treatment with other therapeutic agents, including cyclosporins, mycophenolate mofetil, azathioprine, dapsone, and hydroxyurea.3,6

In conclusion, UD is a common manifestation of several distinct skin diseases that appear to share a similar pathophysiological mechanism. A final diagnosis can be established after exhaustive evaluation of the information obtained from anamnesis, histology, and other additional tests. The detection of dermographism in the physical examination may help orient the diagnosis towards UD. However, this finding should not be considered a specific sign of any condition in particular. In our opinion, UD is a useful term to describe a skin reaction mainly observed in the elderly, the clinical characteristics of which mimic those of several skin diseases. In many cases, a definitive diagnosis can only be established after long-term follow up.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

References
[1]
S. Kossard, I. Hamann, B. Wilkinson.
Defining urticarial dermatitis. A subset of dermal hypersensitivity reaction pattern.
Arch Dermatol, 142 (2006), pp. 29-34
[2]
G.R. Hannon, D.A. Wetter, L.E. Gibson.
Urticarial dermatitis: Clinical features, diagnostic evaluation, and etiologic associations in a series of 146 patients at Mayo Clinic (2006-2012).
J Am Acad Dermatol, 70 (2014), pp. 263-268
[3]
M.A. Fung.
The clinical and histopathologic spectrum of “dermal hypersensitivity reactions” a nonspecific histologic diagnosis that is not very useful in clinical practice, and the concept of a “dermal hypersensitivity reaction pattern”.
J Am Acad Dermatol, 47 (2002), pp. 898-907
[4]
P. Banan, G. Butler, J. Wu.
Retrospective chart review in a cohort of patients with urticarial dermatitis.
Australas J Dermatol, 55 (2014), pp. 137-139
[5]
T. Thepen, E.G. Langeveld-Wildschut, I.C. Bihari, D.F. van Wichen, F.C. van Reijsen, G.C. Mudde, et al.
Biphasic response against aeroallergen in atopic dermatitis showing a switch from an initial TH2 response to a TH1 response in situ: An immunocytochemical study.
J Allergy Clin Immunol, 97 (1996), pp. 828-837
[6]
C. Chaptini, S. Sidhu.
Mycophenolate mofetil as a treatment of urticarial dermatitis.
Australas J Dermatol, 55 (2014), pp. 275-278

Please cite this article as: García del Pozo MC, Poveda I, Álvarez P, Silvestre JF. Dermatitis urticante. Un patrón de reacción cutánea. Actas Dermosifiliogr. 2018;109:929–932.

Copyright © 2018. Elsevier España, S.L.U. and AEDV
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