Diagnostics and treatment of urticaria

Laboratory and instrumental diagnostic algorithm

The scope of diagnostic measures directly depends on the form of the disease.

• Acute spontaneous urticaria: Routine laboratory testing is not indicated. During the first six weeks (the acute period), an in-depth search for triggers is not performed, as the main task at this stage is the pharmacological control of symptoms. In the absence of obvious causes, tests often remain within normal limits, and the patient is diagnosed with "Unspecified urticaria".
• Chronic spontaneous urticaria: Performing basic tests is mandatory — a complete blood count (CBC) and C-reactive protein (CRP) level determination. If necessary, the spectrum of investigations is expanded.

Areas for extended investigation in the chronic form:

1. Infections and parasites: detection of infestations and testing for Helicobacter pylori (with possible upper endoscopy/EGD).
2. Endocrinology and allergy: atopy markers, thyroid panel (hormones and anti-thyroperoxidase antibodies), thyroid ultrasound.
3. Exclusion of severe pathology: D-dimer assay, antinuclear antibodies (ANA), complement fractions (C3/C4), protein electrophoresis, and skin biopsy.

Differential diagnosis and red flags

The main task when examining a patient with an urticarial rash is to exclude systemic autoimmune processes, primarily urticarial vasculitis. The absence of a response to antihistamines and the onset of general symptoms — headache, fever, intoxication, and joint pain — indicate a systemic disease.

Characteristic signs of vasculitis upon examination:

• Lesions do not migrate; an individual wheal persists in the same place for more than a day.
• After the elements disappear, characteristic marks remain on the skin — hemorrhages or hyperpigmentation.

Identification of inducible forms of urticaria

The diagnosis of physical (inducible) urticaria requires mandatory provocative testing to confirm the induction of wheals by a specific factor:

• Cold contact: provocation with an ice cube or exposure to cold water/wind. The sensitivity threshold is determined. Additionally, cryoproteins, CBC, and CRP are investigated.
• Pressure: test with calibrated pressure.
• Heat contact: provocation with warm water with assessment of the sensitivity threshold.
• Solar: irradiation of the skin with ultraviolet and visible light of different spectra. Differential diagnosis with photodermatoses is required.
• Dermographic: mechanical stroking irritation of the skin (elicitation of urticarial dermographism).

Criteria for the autoimmune nature of the disease

According to the guidelines of the European Academy of Allergy and Clinical Immunology (EAACI), autoimmune urticaria is confirmed using special markers:

• In vivo tests: positive intradermal test with the patient's own (autologous) serum.
• In vitro tests: functional assays for autoantibody activity — assessment of histamine release by basophils or detection of their activation markers (CD63, CD203c) by flow cytometry.
• Serology: detection of specific autoantibodies to the high-affinity IgE receptor (anti-FcεRIα).

Treatment principles and lifestyle modification

Since histamine is the main inflammatory mediator and the cause of wheal formation, non-sedating H1-antihistamines (2nd generation) serve as the basis of fundamental therapy.

Key management approaches:

• Trigger elimination: It is recommended to avoid tight and warm clothing to minimize skin friction and heat. If food allergy is suspected, an elimination diet is prescribed for exactly 1 month. If there is no effect, the diet is discontinued.
• Systemic glucocorticosteroids (sGCS): Reserved for severe cases. Used in a short course (from 3 to 10 days) at a dose of 1 mg/kg body weight, but not more than 40 mg per day.
• Sedating antihistamines (1st generation): Their use is limited. Permitted in infants during the first 6 months of life, as well as in injectable form in a hospital setting for urgent conditions (e.g., to relieve an exacerbation combined with angioedema).

The chronic form requires stepwise therapy. Despite the fluctuating course, progressive worsening is atypical, and about half of patients eventually achieve spontaneous remission.

Class and exam questions

What else to study on this topic

• Mechanisms of histamine release and pathogenesis of urticarial inflammation
• Stepwise pharmacotherapy of chronic spontaneous urticaria
• Differential diagnosis of hereditary angioedema (the role of the C1 esterase inhibitor)
• Interpretation of autologous serum skin test results

Other topics in "Chapter 5. Allergic Diseases"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.