New-Onset Urticaria
New-Onset Urticaria
New-Onset Urticaria
New-onset urticaria
Author: Riccardo Asero, MD
Section Editors: Sarbjit Saini, MD, Jeffrey Callen, MD, FACP, FAAD
Deputy Editor: Anna M Feldweg, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2023. | This topic last updated: Jun 27, 2023.
INTRODUCTION
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CATEGORIZATION OF URTICARIA
Acute urticaria — Urticaria is considered acute when it has been present for less than six
weeks.
Chronic urticaria — Urticaria is considered chronic when it is recurrent, with signs and
symptoms recurring most days of the week, for six weeks or longer.
The period of six weeks is somewhat arbitrary and simply represents a timeframe in which
new cases of urticaria usually resolve. More than two-thirds of cases of new-onset urticaria
prove to be self-limited (acute) [2]. The lesions of acute and chronic urticaria are identical in
appearance, so when the problem first develops, it is not possible to differentiate the two
disorders [3].
EPIDEMIOLOGY
Urticaria affects up to 20 percent of the population at some point in their lives and occurs
across the age spectrum [1].
CLINICAL MANIFESTATIONS
Urticarial lesions are circumscribed, raised, erythematous plaques, often with central pallor (
picture 2). Lesions may be round, oval, or serpiginous in shape and vary in size from less
than 1 centimeter to several centimeters in diameter. They are intensely itchy. Pruritus may
disrupt work, school, or sleep. Symptoms often seem most severe at night.
Individual lesions are transient, usually appearing and enlarging over the course of minutes
to hours and then disappearing within 24 hours. Lesions may coalesce as they enlarge (
picture 3A-B). Urticarial lesions are not normally painful and resolve without leaving
residual ecchymotic marks on the skin, unless there is trauma from scratching. If lesions are
long-lasting, painful, or leave residual bruising, the diagnosis of urticarial vasculitis should be
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Any area of the body may be affected, although areas in which clothing compresses the skin
(eg, under waistbands) or skin rubs together (axillae) are sometimes affected more
dramatically. Typically, compressed areas become more severely affected once the restricting
clothing has been removed.
Angioedema, when associated with urticaria, usually affects the face and lips, extremities,
and/or genitals. Angioedema without urticaria should prompt consideration of other
angioedema disorders, such as drug-induced angioedema (eg, angiotensin-converting
enzyme [ACE] inhibitors), idiopathic angioedema, and hereditary and acquired C1 inhibitor
deficiency. (See "ACE inhibitor-induced angioedema" and "An overview of angioedema:
Pathogenesis and causes".)
PATHOPHYSIOLOGY
Urticaria is mediated by cutaneous mast cells in the superficial dermis. Basophils have also
been identified in lesional biopsies [4]. Mast cells and basophils release multiple mediators
upon activation including histamine (which causes itching) and vasodilatory mediators (which
cause localized swelling in the uppermost layers of the skin). The same process gives rise to
angioedema when mast cells deeper in the dermis and subcutaneous tissues are activated.
(See "Mast cells: Development, identification, and physiologic roles".)
ETIOLOGIES
The potential causes of new-onset urticaria are numerous, although no specific etiology can
be identified in many patients. Acute urticaria is more likely to have an identifiable etiology
compared with chronic urticaria. The different etiologies activate mast cells through various
mechanisms.
Infections — Viral, bacterial, and parasitic infections are associated with new-onset urticaria.
● Viral and bacterial infections – Acute urticaria may develop during or following a viral
or bacterial infection, particularly in children. Infections are associated with over 80
percent of cases of acute urticaria in some pediatric series [2,5-8]. Immune activation,
involving immune complex formation and/or complement activation, is a proposed
mechanism, although the exact pathogenesis is unclear.
• In one study, common viral illnesses and bacterial infections (eg, urinary tract
infections) were the leading identifiable trigger for acute urticaria in 57 children
between the ages of one and three years who presented to an emergency
department [5]. Many of these children had also received antibiotics, so it was not
clear in these patients if the infection, the drug, or the combination had triggered
urticaria.
• Ingestion of fish contaminated with the parasite Anisakis simplex can also cause
urticaria. Anisakis can be transmitted through the ingestion of sushi [18]. (See
"Seafood allergies: Fish and shellfish", section on 'Anisakis'.)
COVID-19 vaccines and boosters — Urticaria with or without angioedema has been
reported in association with coronavirus disease 2019 (COVID-19) messenger ribonucleic acid
(mRNA) vaccines and boosters, particularly the Moderna mRNA booster. In a study of over
800 patients in two cohorts with newly diagnosed urticaria that had occurred most days of
the week and persisted for weeks to months, 92 and 94 percent of cases were temporally
associated with receiving the Moderna vaccine or booster [19]. Onset of urticaria was
between 8 and 13 days after vaccination. In those patients with subsequent resolution, the
duration of symptoms ranged from two to six months. The author and editors of this topic
have also observed reactivation of chronic urticaria that had been quiescent for years.
medications, foods and food additives, insect stings and bites, latex, and blood products.
Allergic reactions may be limited to the skin or part of a systemic allergic reaction (eg,
anaphylaxis) ( table 2 and table 3). Generalized urticaria or angioedema following
exposure to a potential allergen should be interpreted as a systemic reaction with an
attendant risk of anaphylaxis upon subsequent exposure, and patients should be advised to
avoid the potential cause until further evaluated. (See 'Referral' below.)
● Stinging and biting insects – Stinging insects that can cause true urticarial lesions as
part of an allergic reaction include Hymenoptera (eg, bees, wasps, hornets, and
imported fire ants) and Triatoma (eg, kissing bugs).
Bedbugs, fleas, and mites can cause papular urticaria, usually on the lower extremities.
The lesions of papular urticaria resolve over the course of weeks. (See "Bee, yellow
jacket, wasp, and other Hymenoptera stings: Reaction types and acute management"
and "Reactions to bites from kissing bugs (primarily genus Triatoma)" and "Bedbugs".)
● Foods and certain food additives – Allergic reactions to foods can cause urticaria,
typically within 30 minutes of ingestion. Milk, eggs, peanuts, tree nuts, soy, and wheat
are the most common foods to cause generalized urticaria in children. In adults, fish,
shellfish, tree nuts, and peanuts are most often implicated [21]. In Mediterranean areas,
the most frequent cause of food-induced urticaria is the peach, due to sensitization to
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lipid transfer protein [22]. (See "Clinical manifestations of food allergy: An overview".)
● Contact with allergens – Physical contact with a number of agents may result in
urticaria, including plant products and resins, raw fruits and vegetables, or raw seafood.
People employed in food processing can develop contact urticaria from various
exposures [23]. Children sometimes develop urticaria upon contact with animal saliva, if
allergic to those allergens. In contrast, detergents, soaps, and lotions are more likely to
cause contact dermatitis than urticaria. (See "Clinical features and diagnosis of allergic
contact dermatitis" and "Allergic contact dermatitis in children".)
Direct mast cell activation — Certain drugs and plants can cause urticaria due to mast cell
degranulation through a non-IgE-mediated mechanism. The most frequently implicated are
narcotics, muscle relaxants, vancomycin, and radiocontrast media. Nettle plants are examples
of plants that cause direct mast cell activation. Some years ago "pseudoallergens" contained
in certain foods were considered as a possible co-factor in patients with chronic urticaria, and
this concept appeared in the European Academy of Allergy and Clinical Immunology (EAACI)
Guidelines for a while, but the lack of any convincing evidence has led to the exclusion of this
hypothesis in the most recent, revised versions of this document [24]. In these cases, urticaria
may develop variably within minutes to some hours after contact; in the case of drugs, this
may sometimes depend on the route of administration of a drug (eg, oral versus
intramuscular/intravenous). The wheal-and-flare response to stinging nettle is practically
immediate (a few seconds).
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● Narcotics – Opiate analgesics, such as morphine and codeine, cause direct mast cell
activation. Dextromethorphan, an opiate derivative ingredient in cough suppressant
syrups, can also cause urticaria [25].
● Vancomycin – Vancomycin infusion reaction is seen after rapid vancomycin infusion and
presents as diffuse erythema or flushing, sometimes with accompanying urticaria. The
concomitant use of opiates and vancomycin may increase the likelihood of a reaction.
(See "Vancomycin hypersensitivity".)
● Stinging nettle – The nettle plant (Urtica dioica), after which the disorder "urticaria" was
named, is a common weed found in Europe, North and South America, and parts of
Africa that causes hives and a stinging sensation immediately following contact with the
skin [26-28]. These symptoms may be due to histamine in the nettle plant itself, in
addition to mediators that cause pain [29].
● Allergic – A specific NSAID can also cause acute urticaria in patients who are allergic to
that one agent. These reactions are presumed to represent true, immunologic allergy.
(See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions", section on
'Allergic reactions (presumed IgE-mediated)'.)
Both allergic and pharmacologic reactions to NSAIDs may occur within minutes after taking
the drug, although pharmacologic reaction may frequently take longer (up to one to two
hours). Both pharmacologic and allergic reactions to NSAIDs can be severe. However, the
management differs. (See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions",
section on 'Management'.)
Scombroid syndrome — The ingestion of poorly preserved fish (tuna in most cases, but
sometimes mackerel or sardines) containing large amounts of histamine may cause acute
symptoms that resemble those of an IgE-mediated allergic reaction characterized by flushing,
urticaria, diarrhea, headache, and sometimes bronchospasm. In this case also, symptoms
may appear from a few minutes up to one to two hours after ingestion depending on the
concentration of histamine in the fish, the quantity ingested, and the association with other
foods. (See "Scombroid (histamine) poisoning".)
● Physical stimuli – Physical urticarial syndromes are forms of chronic urticaria that are
triggered by specific physical factors, such as cold exposure, sudden changes in body
temperature, pressure or vibration against the skin, exercise, exposure to sunlight, or
other stimuli. These disorders are reviewed separately. (See "Physical (inducible) forms
of urticaria" and "Cold urticaria".)
● Mastocytosis – Mastocytosis and mast cell disorders are rare conditions in which
patients present with apparent allergic reactions and anaphylaxis to a variety of triggers.
Characteristic skin findings are helpful in diagnosis. These disorders are reviewed
separately. (See "Mastocytosis (cutaneous and systemic) in adults: Epidemiology,
pathogenesis, clinical manifestations, and diagnosis".)
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● Cutaneous small vessel vasculitis – Some forms of cutaneous small vessel vasculitis
can appear urticarial during early stages. Urticarial lesions that are persistent in a single
location for >24 hours, have bruising, are painful, or are accompanied by systemic
symptoms (eg, fever) should raise a concern for vasculitis.
• Patients with lupus may also develop urticarial lesions that persist and become
vasculitic. Skin biopsy may show evidence of vasculitis. (See "Overview of cutaneous
lupus erythematosus".)
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The urticaria associated with systemic disorders is usually recurrent, persistent, and relatively
difficult to treat, so patients with these disorders typically present with chronic urticaria.
Clinical features that can help distinguish these disorders from uncomplicated chronic
urticaria are reviewed separately. (See "Chronic spontaneous urticaria: Clinical manifestations,
diagnosis, pathogenesis, and natural history", section on 'Differential diagnosis'.)
Urticaria is diagnosed clinically, based upon a detailed history and physical examination
confirming the presence of characteristic skin lesions [37-40].
● Were there other signs and symptoms of a generalized allergic reaction or anaphylaxis?
Patients may fail to report more subtle symptoms unless specifically asked. The clinician
should ask about chest tightness or difficulty breathing, hoarse voice or throat
tightness, nausea, vomiting, crampy abdominal pain, lightheadedness, and other
symptoms of anaphylaxis ( table 2). (See "Anaphylaxis: Emergency treatment".)
● Has the patient had hives previously in the past? Some children develop acute urticaria
repeatedly with infections. Adults may develop urticaria following nonsteroidal anti-
inflammatory drug (NSAID) ingestion but may not recognize the association until it has
occurred several times. Does the patient have other allergic disorders?
● Is a possible etiology apparent from the patient's history ( table 1)? (See 'Etiologies'
above.)
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• Was the patient in his/her usual state of health when the hives appeared or has the
patient been ill recently with viral or bacterial infections? Has the patient experienced
any recent health events, such as musculoskeletal injuries for which he/she was
taking NSAIDs or new diagnoses requiring unfamiliar medications or treatments?
• The patient should be asked to review events in the hours before the urticaria
appeared. What had the patient ingested (foods, beverages, candy)? Was the patient
involved in exercise or physical exertion? Was the patient exposed to extremes of
temperature or stung by an insect? The answers may reveal clues to allergic or
physical causes of urticaria.
• Inquiries should be made about recent travel (and symptoms of parasitic infection)
and sexual history. (See 'Infections' above.)
Physical examination — Lesions should be visualized directly in order to make the diagnosis
with certainty, since the term "hives" is used nonspecifically by patients. If the patient has no
lesions at the time of evaluation, showing patients photographs of urticaria and asking if their
lesions look similar can be helpful, although the diagnosis will need to be confirmed at some
point in the future ( picture 2).
Individual urticarial lesions usually appear and resolve completely within 24 hours. If the
patient is unsure of the duration of the lesions, a lesion can be circled with a pen and time to
resolution noted.
Laboratory studies — Laboratory studies are typically normal in patients who lack any
history or physical findings to suggest an underlying disease process [3].
● For patients presenting with new-onset urticaria (with or without angioedema) in whom
the clinical history and physical exam do not suggest an underlying disorder or urticarial
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vasculitis, international, European, and British practice parameters state that laboratory
testing is not indicated [45-47]. American practice parameters state that a limited
evaluation "may be considered" in such patients, primarily for the purpose of detecting
underlying disorders earlier in the one-third of patients in whom urticaria will prove
persistent (ie, initial presentation of chronic urticaria) [48]. In this setting, complete
blood count with differential, urinalysis, erythrocyte sedimentation rate, and liver
function tests are suggested. However, the author's approach is to obtain these tests in
patients with persistent symptoms.
Tests for allergic causes — An allergic cause is possible if the clinical history reveals a
specific trigger to which the patient was exposed shortly before the onset of symptoms
(usually within one to two hours). If the history does suggest a possible allergy, serum tests
for allergen-specific immunoglobulin E (IgE) antibodies are appropriate, if commercially
available. For example, if a patient who does not normally eat seafood but did so at a special
occasion develops hives within 10 minutes of eating a crab cake, it would be reasonable to
obtain a crab-specific IgE test, particularly if there were no other new foods ingested and the
patient is avoiding seafood for fear of a repeat reaction. However, the interpretation of allergy
tests can require some expertise. A positive result is suggestive, although not diagnostic, of
allergy, and a negative result does not exclude allergy. Because of this, we suggest that
patients suspected of having an allergy be referred to an allergist/immunologist for further
evaluation when possible. Skin tests with fresh food, which should be performed by an allergy
specialist, is probably the most convenient, inexpensive, and sensitive way to detect food
hypersensitivity. (See 'Referral' below and "Overview of in vitro allergy tests".)
DIFFERENTIAL DIAGNOSIS
The conditions discussed in this section are those that may mimic various features of urticaria
[49]. The presence or absence of pruritus is a helpful clinical feature that can be used to
narrow the differential.
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Pruritic conditions — Pruritic conditions that are more likely to be confused with urticaria
are discussed here. An overview of the causes of pruritic dermatoses is found separately. (See
"Pruritus: Etiology and patient evaluation".)
● Contact dermatitis – Contact dermatitis refers to any dermatitis arising from direct skin
exposure to a substance. The dermatitis may either be allergic or irritant-induced. The
latter is more common. Contact dermatitis is an erythematous, papular dermatitis, often
with areas of vesiculation ( picture 9). It is distributed in the areas of direct contact.
(See "Allergic contact dermatitis in children" and "Irritant contact dermatitis in adults"
and "Common allergens in allergic contact dermatitis".)
● Insect bites – Insect bites produce individual lesions that persist for days in most cases
(see "Insect and other arthropod bites"). However, the stings of some insects can cause
true urticaria as part of a systemic allergic reaction. (See 'IgE-mediated allergic reactions'
above.)
● Bullous pemphigoid – In older adults, bullous pemphigoid may start with pruritus, with
or without urticarial lesions. Blistering usually becomes evident eventually. (See "Clinical
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● Plant-induced reactions – Poison ivy and poison oak can present with urticaria-like
lesions initially that evolve into vesicular lesions. (See "Poison ivy (Toxicodendron)
dermatitis".)
Nonpruritic conditions — Nonpruritic conditions that may resemble acute urticaria include
viral exanthems, the skin changes of auriculotemporal syndrome, and Sweet syndrome.
● Viral exanthems – Viral exanthems are common in children and can occur with many
different infections, including erythema infectiosum (fifth disease), Epstein-Barr virus,
enteroviruses, and measles. However, viral exanthems are generally not pruritic and
usually consist of erythematous maculopapular eruptions that persist for days. Fever is
often present. The macules are relatively fixed compared with urticarial lesions, which
continually change, with new lesions appearing as older lesions resolve. (See topic
reviews on specific infections.)
TREATMENT
Initial treatment of new-onset urticaria (with or without angioedema) should focus on the
short-term relief of pruritus and angioedema, if present. Approximately two-thirds of cases of
new-onset urticaria will be self-limited and resolve spontaneously. The literature on
management of acute urticaria is sparse, probably because the condition is so often self-
limited [52]. The agents discussed below have mostly been evaluated in the treatment of
chronic urticaria, and in some cases, their use in acute urticaria is extrapolated from those
studies, which are presented separately. (See "Chronic spontaneous urticaria: Standard
management and patient education".)
efficacy studies'.)
Some patients require higher than standard doses (shown below in parentheses) for control
of urticarial symptoms and may experience drowsiness at these higher doses. Caution is
therefore warranted until effects upon the individual are understood. The higher doses may
have better efficacy in some adults, although this has not been conclusively demonstrated.
Studies of higher-dose antihistamines for chronic urticaria are reviewed separately. (See
"Chronic spontaneous urticaria: Standard management and patient education", section on
'H1 antihistamines'.)
Treatment with H1 antihistamines results in clearance of the lesions in some patients, but in
others, treatment may only achieve flattening of the lesions and reduction in pruritus, with
persistence of erythematous macules. Patients in the latter group can begin to reduce
medications after the erythematous lesions clear.
● Cetirizine – Cetirizine demonstrates a rapid onset of action and some mast cell-
stabilizing activity. It can be mildly sedating, in a dose-dependent manner, although less
so than first-generation agents. It is available in both intravenous (in some countries)
and oral formulations, and the dosing is similar for either route of administration.
Intravenous doses should be administered over one to two minutes. The standard oral
or intravenous dose of 10 mg once daily is appropriate for adults and children aged 12
years and older (and may be increased to 10 mg twice daily in adults if needed).
Children six years of age and older can receive 5 mg or 10 mg. The usual dose for
children aged two to five years is 5 mg once daily. Smaller children aged six months to
two years may be given 2.5 mg once daily (can be increased to 2.5 mg twice daily in
children one year and older if needed). The maintenance dose for patients with
significant renal and/or hepatic insufficiency should be reduced by one-half.
Levocetirizine is unlikely to be effective as an alternative for patients who did not have
an adequate response to cetirizine, and its sedative effects are similar to those of other
second-generation antihistamines [60]. Dose reductions are necessary in renal
insufficiency.
For children aged 6 to 11 years, the dose is 2.5 mg once daily, and for those aged 1 to 5
years, the dose is 1.25 mg once daily. A lower dose of 1 mg once daily is approved in the
United States for small children aged 6 months to 1 year. For patients with significant
renal and/or hepatic insufficiency, the usual dose is administered every other day.
There are additional nonsedating antihistamines that are available in many countries,
although not in the United States:
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● Hydroxyzine – The dose in adults is 25 to 50 mg deep IM administration in adults every
six hours as needed. Do not administer intravenously. Children may receive 0.5 to 1
mg/kg (up to 50 mg per dose) IM every six hours as needed.
Pregnant and lactating patients — Pregnant patients may be treated initially with
loratadine (10 mg once daily) or cetirizine (10 mg once daily). There are reassuring human
data for each of these drugs in a large number of pregnant patients [68]. The first-generation
agent chlorpheniramine, 4 mg orally every four to six hours, may also be safely used in
pregnancy [69,70]. Safety issues surrounding the use of antihistamines in pregnancy are
reviewed separately. (See "Recognition and management of allergic disease during
pregnancy", section on 'Oral antihistamines'.)
Lactating patients may be treated with either cetirizine or loratadine (both are dosed at 10 mg
once daily), which are minimally excreted in breast milk and should not cause sedation or
poor feeding in the infant. (See "Pharmacotherapy of allergic rhinitis", section on
'Breastfeeding'.)
H2 antihistamines — There are very few data examining the use of H2 antihistamines for
acute urticaria, but the practice is supported by one randomized trial of 91 adults presenting
to an emergency department with acute allergic reactions [71]. Subjects received 50 mg IV
diphenhydramine with either placebo or 50 mg IV ranitidine. At two hours, the number of
patients in whom urticaria had resolved was statistically greater in the ranitidine group
compared with the placebo group (25 of 29 and 13 of 24, respectively). Options for H2
antihistamines include nizatidine, famotidine, ranitidine (no longer available in the US), and
cimetidine, although caution should be used with cimetidine, since it can increase levels of
other drugs. (See "Antiulcer medications: Mechanism of action, pharmacology, and side
effects".)
Studies of the use of H2 antihistamines in chronic urticaria are conflicting and are reviewed
elsewhere [72-74]. (See "Chronic spontaneous urticaria: Standard management and patient
education", section on 'H2 antihistamines'.)
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A small number of trials have examined the utility of glucocorticoids in the management of
acute urticaria [75-77]. In the largest study, the addition of prednisone to levocetirizine did
not speed resolution of acute urticaria. In this randomized trial, 100 adults presenting to the
emergency department with urticaria of ≤24 hours duration without angioedema,
anaphylaxis, or fever, were treated with the H1 antihistamine levocetirizine (5 mg once daily
for five days) plus either placebo or prednisone (40 mg once daily for four days) and followed
by phone for several days [77]. The primary endpoint was complete relief of itching two days
after the start of therapy, and secondary endpoints included resolution of skin lesions,
relapses, and adverse events. Most subjects had resolution of itch by day 2, with a slightly
lower percentage itch-free in the prednisone group (79 versus 67 percent). Similarly, by day 2,
skin lesions had resolved entirely in 78 and 70 percent of those in the placebo and prednisone
groups, respectively. Thus, the addition of prednisone to levocetirizine did not speed
resolution of acute urticaria. Between one-quarter and one-third of patients experienced
relapse in both groups, generally within the first few days of therapy. Another smaller
randomized trial found that glucocorticoids were helpful when added to antihistamines,
although the antihistamine regimen used in that study (hydroxyzine 25 mg orally every four
to eight hours) may have been more difficult to adhere to [75].
The optimal agent and dose have not been determined for acute urticaria, but we typically
administer:
● In adults – Prednisone 30 to 60 mg daily, with tapering of the dose over five to seven
days
● In children – Prednisolone 0.5 to 1 mg/kg/day (maximum 60 mg daily), with tapering of
the dose over five to seven days
Antihistamine therapy should be continued during and after the course of glucocorticoids
because some patients experience an exacerbation as the glucocorticoids are tapered or
discontinued. If symptoms do not recur over several days after stopping glucocorticoids, then
antihistamines can be discontinued also. For patients whose symptoms recur when
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medications are discontinued, antihistamines should be reinstituted and used at the lowest
effective dose. Repeated courses of glucocorticoids should be avoided, as the risks of adverse
effects outweigh the benefit for most patients (see 'Referral' below). The decision of
prescribing gastrointestinal prophylaxis (eg, a proton pump inhibitor) during a systemic
corticosteroid treatment depends essentially on the duration of therapy (that in this case
should be as brief as possible) and the specific conditions of the patient (eg, prior chronic
gastritis, gastric ulcers).
REFERRAL
Patients who are suspected of having an allergic etiology causing new-onset urticaria, such as
a food or medication allergy, should be referred to an allergy specialist who will evaluated for
possible causes and equip the patient with epinephrine for self-injection when indicated.
These issues are discussed in detail separately. (See "Anaphylaxis: Emergency treatment",
section on 'Discharge care'.)
PROGNOSIS
It should be explained to patients that about one-third of cases of new-onset urticaria will
prove persistent and that if they continue to have ongoing symptoms after several weeks,
they should seek re-evaluation in a primary care setting. Patients with difficult-to-control
symptoms may also be referred to a dermatology or allergy specialist.
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Urticaria and
angioedema (excluding hereditary angioedema)".)
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UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and
who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles on
a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Beyond the Basics topic (see "Patient education: Hives (urticaria) (Beyond the Basics)")
● Acute versus chronic – Urticaria is classified as either acute or chronic. Acute urticaria is
defined as periodic outbreaks of urticarial lesions that resolve within six weeks. Urticaria
that persists beyond six weeks may represent the beginning of chronic urticaria, a
disorder that is reviewed in detail separately. (See 'Categorization of urticaria' above and
"Chronic spontaneous urticaria: Clinical manifestations, diagnosis, pathogenesis, and
natural history".)
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● Possible triggers for new-onset urticaria – A presumptive trigger, such as common
viral and bacterial infections, medications, food ingestion, or insect sting, can
sometimes be identified for new-onset urticaria. (See 'Etiologies' above.)
● Systemic disorders that can involve urticaria – Occasionally, urticaria may be the
presenting feature of another systemic disorder, such as urticarial vasculitis,
mastocytosis, or systemic lupus erythematous. There are specific clinical features that
should prompt an evaluation for these conditions. (See 'Systemic disorders that may
include urticaria' above.)
• Other pruritic disorders that could be confused with urticaria include insect bites,
atopic dermatitis, contact dermatitis, morbilliform drug eruptions, bullous
pemphigoid, erythema multiforme minor, and plant-related dermatoses (eg, poison
ivy). (See 'Pruritic conditions' above.)
• Nonpruritic conditions that may resemble acute urticaria include viral exanthems,
the skin changes of auriculotemporal syndrome, and Sweet syndrome. (See
'Nonpruritic conditions' above.)
than standard doses (eg, cetirizine 10 mg twice daily). In patients at low risk of
complications from anticholinergic side effects (ie, healthy adults), use of a sedating
H1 antihistamine at bedtime and a nonsedating H1 antihistamine during the day is a
reasonable alternative. (See 'H1 antihistamines' above.)
ACKNOWLEDGMENT
The UpToDate editorial staff acknowledges Clifton O Bingham, III, MD, who contributed to
earlier versions of this topic review.
REFERENCES
1. Kaplan AP. Urticaria and angioedema. In: Middleton's Allergy: Principles and practice, 7th,
Adkinson NF, Bochner BS, Busse WW, Holgate ST, Lemanske RF, Simons FER (Eds), Mosby,
St Louis, MO 2009. Vol 2, p.1063.
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