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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?
Answer
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.
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.
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Link
to further Information on:
For
more information on neomycin allergy, see the eMedicine
articles Contact
Dermatitis, Allergic and Drug
Eruptions (within the Dermatology specialty).
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