Alergic Dermatithis

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Allergic contact dermatitis due to neomycin allergy, also known as neomycin


sulphate allergy: Allergic contact dermatitis is a T cell–mediated, delayed skin
hypersensitivity reaction to a specific antigen, such as common metals, dyes,
rubber products, or cosmetics. Women are more commonly affected than men,
and nickel is the most common allergen. The risk of neomycin allergy is directly
related to the extent of use in a population. Neomycin is widely included as an
ingredient in topical creams, and it is a component of Neosporin, an antibiotic
product used to treat minor skin infections. The risk of contact dermatitis is
higher when this agent is used to treat chronic stasis dermatitis than when it is
used as a topical antibiotic, eg, applied to cuts in children. Chemically related
aminoglycoside antibiotics include gentamicin and tobramycin; these should be
avoided in individuals allergic to neomycin. Other cross-reactions involve
framycetin, kanamycin, puromycin, spectinomycin, and streptomycin. Neomycin
also co-reacts with bacitracin.

On physical examination, acute allergic contact dermatitis is characterized by


pruritic papules and vesicles on an erythematous base. The lesions are sharply
delineated. The reaction develops over 48 hours at the site of contact with the
allergen. The skin initially becomes pruritic, red, and swollen. Tiny blisters
develop and may rupture and leave ulcers, crusted vesicles, and scales. An
inflamed, weepy ulcerated rash can result. The skin thickens with repeated
exposure and can become increasingly erythematous and scaly. The skin may
darken and become leathery and cracked. Chronic allergic contact dermatitis
can manifest as lichenified, pruritic plaques.

Allergic contact dermatitis is a type IV or cell-mediated immune reaction. The


reaction is mediated by lymphocytes and not antibodies. First, an induction
phase occurs in which naïve lymphocytes are sensitized to an allergen.
Allergens can be chemicals or haptens and are typically weak allergens that
require several exposures for sensitization to occur. Langerhans cells and
dermal dendritic cells, the antigen-presenting cells of the skin, first recognize
the antigens. These cells then migrate through the lymph system to lymph
nodes, where they interact with naïve T cells. Production of memory T cells
results, and these T cells pass into general circulation by means of the
lymphatic system. The T cells are now considered sensitized.

Once sensitized, T lymphocytes react when they subsequently encounter the


antigen. On further exposure, the dendritic cells and Langerhans cells re-
express the antigen. The T cells then recognize the antigen and release
cytokines, interferon (IFN)-gamma, interleukin (IL)-8, and IL-2, which activate
and recruit lymphocytes. Inflammatory cells accumulate in the dermis and
epidermis, resulting in the elicitation phase of allergic contact dermatitis
reaction.

The ability of allergens to sensitize varies. Poison ivy, for example, sensitizes
after one exposure, whereas bricklayers who are exposed to chrome become
allergic to it after a mean of 10 years. Localized contact dermatitis can develop
into a generalized, symmetric reaction remote from the initial contact area. This
is also known as the id reaction.

Treatment involves prompt removal of the causative agent, in this case


neomycin. The allergic reaction is limited to the site of exposure and improves
within weeks after the allergen is removed. Management of acute dermatitis
includes the application of topical corticosteroids and emollients.

To diagnose neomycin allergy, a patch test is performed by using 20%


neomycin in petrolatum. A positive result is an indurated papule that appears
after 48 hours. If the result is negative, testing with an intradermal injection of
neomycin 1:1000 can be considered; a positive result is a papule appearing in
24-48 hours.

For more information on neomycin allergy, see the eMedicine articles Contact
Dermatitis, Allergic and Drug Eruptions (within the Dermatology specialty).

References
 Hogan D. Contact Dermatitis, Allergic. eMedicine Journal [serial online].
January 12, 2005. Available at:
http://www.emedicine.com/derm/topic84.htm.
 Hunter J, Savin J, Dahl M. Clinical Dermatology. 3rd ed. Malden, Ma:
Blackwell Publishing; 2002.
 Leyden JJ, Kligman AM. Contact dermatitis to neomycin sulfate. JAMA
1979 Sep 21;242(12):1276-8.

 Rietschel RL, Fowler JF, eds. Fisher's Contact Dermatitis. Philadelphia,


Pa: Lippincott Williams and Wilkins; 2001.

BACKGROUND
A 59-year-old man presents to the emergency department complaining of a
diffuse, painful rash. The rash first arose 3 months ago and resolved after a
course of oral prednisone. However, the rash recurred a month ago, manifesting
in its current state and affecting most of the surface of his upper and lower
extremities. No new drugs were added when the initial rash started, and he
received only tapered prednisone therapy before his most recent presentation.
At that time, he began applying an antibiotic ointment (Neosporin) on affected
areas, with subsequent worsening of his rash. A short course of fluocinonide
cream resulted in mild improvement. He is now taking only hydroxyzine for
symptomatic relief of severe pruritus. He denies having other complaints.

The patient's medical history is significant for allergic contact dermatitis and
hypertension. On physical examination, fissuring is present on the creases of
his palms and heels, and his nails are thin. An erythematous, macular, scaly
rash is observed on the patient's forearms and on the lateral aspects of both
thighs, with multiple excoriations and pale, superficial ulcerations. His vital signs
and the rest of the physical findings are unremarkable. A KOH preparation of a
sample obtained from a thigh lesion yielded negative results.
What is the diagnosis?

Hint
The patient continued using neomycin despite worsening of the rash.

Authors: Anusuya Mokashi,


Medical Student,
New York Medical College, Valhalla

Lynne H. Morrison, MD,


Associate Professor,
Department of Dermatology,
Oregon Health and Science University
(OHSU) Department of Dermatology

eMedicine
Editor: Erik D. Schraga, MD,
Department of Emergency Medicine,
Kaiser Permanente,
Santa Clara Medical Center, Calif

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