Allergy Testing: Skin Prick vs Specific IgE

Allergy testing investigates suspected IgE-mediated (type I) allergy. Identifying the trigger + planning treatment (allergen avoidance, immunotherapy, medication) requires it.

Main indications: allergic rhinitis (seasonal or perennial — nasal obstruction, discharge, sneezing, itch), asthma (atopic component), atopic dermatitis (especially suspected food trigger), anaphylaxis (food, drug, insect), chronic urticaria (limited yield), eosinophilic oesophagitis (food).

Right patient selection: symptoms + exposure history + family atopy — all three together makes testing useful. Pure "do I have allergies?" screening is not recommended (no clinical question, no test).

Atopic triad (rhinitis + asthma + atopic dermatitis) is highly probable allergic. Child with family atopy history + early skin symptoms (atopic eczema) + years later rhinitis/asthma — classic story.

Trigger types: (1) inhalant — house dust mite (Dermatophagoides), pollen (tree, grass, weed — regional variation), mould spores (Alternaria, Cladosporium), animal dander (cat Fel d 1, dog Can f 1), cockroach; (2) food — milk, egg, peanut, tree nuts, fish, shellfish, soy, wheat; (3) insect venom — bee, wasp; (4) drug — penicillin, cephalosporin, NSAID, latex; (5) contact (type IV) — nickel, cosmetics, latex.

Turkey-prevalent allergens: house dust mite (year-round, 60-70% of rhinitis), grass pollens (Phleum, Lolium — May-June), olive pollen (Mediterranean — April-May), Alternaria (summer-autumn), cat dander, food allergy in children to milk/egg/peanut.

Cost-benefit: SPT panel (10-15 allergens) is low-cost and quick; broad trigger panel feasible. Specific IgE charged per allergen — broad panel expensive. Clinical suspicion guides — unjustified broad testing (for "peace of mind") is poor value. Related overview: our general ENT services.

Skin prick test (SPT) is the oldest and most widely used skin allergy test. Defined in 1865; modern standard practice.

Technique: allergen drops (commercial extracts) placed on forearm or back, surface scratched with sterile lancet (no bleeding, epidermis only). Positive control — histamine (10 mg/mL), negative control — saline. Read at 15-20 minutes: wheal (raised) and flare (redness) measured.

Positivity criterion: wheal ≥3 mm beyond negative control, positive histamine control ≥3 mm (confirms skin reactivity). Wheal size does not predict clinical severity — only confirms sensitisation.

Standard panel: inhalants — house dust mite (Dermatophagoides pteronyssinus, D. farinae), grass pollen mix (5-grass), tree pollen mix, weed pollen mix, Alternaria, Cladosporium, cat, dog, cockroach; foods — milk, egg white, peanut, tree nuts, fish, shellfish, soy, wheat.

Preparation: antihistamines stopped 5-7 days before (sertraline, paroxetine, hydroxyzine; cetirizine, loratadine, fexofenadine; TCA 5-7 days), oral steroids usually do not affect results but high-dose chronic use may suppress. Beta-blockers reduce adrenaline response in anaphylaxis — some protocols recommend stopping.

Side effects: mild itch + local swelling (commonest), rare systemic reaction (anaphylaxis <0.01%, higher risk in food and venom testing). Test setting must have epinephrine + emergency readiness.

Contraindications: active eczema or extensive skin disease (no test area), dermographism (reaction without trigger — false positive), severe uncontrolled asthma or anaphylaxis, pregnancy (relative — anaphylaxis risk), infant <6 months (weak cutaneous response, difficult to interpret).

Interpretation pitfalls: positive test = sensitisation, not clinical allergy; 20-30% population is sensitised without symptoms. Clinical allergy = positive test + symptoms + trigger-exposure linkage. Screening in asymptomatic subjects not recommended.

Is a negative test reliable? Sensitivity 85-95% (with good standardised extracts); negative test largely rules out allergy. False negative causes: poor extract, medication effect (antihistamine), low cutaneous reactivity (elderly), systemic suppressant during test (steroid).

Specific IgE (allergen-specific IgE) measures allergen-specific IgE antibodies in blood. Older RAST (RadioAllergoSorbent Test); current methods are ImmunoCAP, Immulite (enzyme immunoassays) — higher sensitivity, numerical results.

Method: venous blood sample (5-10 mL); allergen-bound bead or solid-phase reacts with serum IgE; result reported numerically in IU/mL or kU/L. Result available within days.

Positivity threshold: <0.35 kU/L usually negative; ≥0.35 low positive; higher values with increasing clinical meaning. Thresholds vary by lab and allergen; some foods (egg, peanut) — high IgE values predict clinical reaction (e.g., peanut IgE >15 kU/L predicts 95% oral challenge positive).

Pros: no drug stop needed (antihistamines, TCAs OK), feasible in severe eczema or dermographism, child-friendly (single venepuncture), no anaphylaxis risk (in vitro), multiple allergens in one go, digital archive, high standardisation.

Cons: higher cost (3-5× SPT panel), days to result (vs 20 min for SPT), slightly lower sensitivity (SPT 85-95% vs IgE 80-90%), interpretation difficult at low values.

Interpretation: positive = sensitisation, not clinical allergy. Modest predictive value — symptoms may exist at low IgE and not at high. Always integrate with clinical picture.

Component-Resolved Diagnostics (CRD): IgE to specific molecular components. Example: peanut Ara h 2 positive → high reaction risk; Ara h 8 positive → oral allergy syndrome risk, low anaphylaxis risk; cross-reactivity (e.g., pollen-food syndrome) better understood. CRD is an important step in allergy risk stratification.

When IgE preferred? When SPT not feasible (skin condition, medication, dermographism, child anxiety, high anaphylaxis risk, pregnancy), severe allergy (anaphylaxis, eosinophilic oesophagitis, severe asthma), cross-reactivity investigation, component risk stratification.

Total IgE vs specific IgE: total IgE indicates atopic constitution (high value suggests atopy); does not identify specific trigger. Total IgE has no screening value; specific IgE is what clinical suspicion drives. More detail: sinusitis page.

Intradermal test: confirms when SPT negative but suspicion high. Drug allergy (penicillin, anaesthetic), insect venom. Technique: allergen extract (0.02 mL) injected intracutaneously; wheal at 15-20 minutes. More sensitive (100-1000× SPT) but more false positives + serious systemic reaction risk. Hospital-only with expert team.

Patch test: type IV (delayed) hypersensitivity — contact dermatitis. Standard baseline series (European — nickel, cobalt, chromium, formaldehyde, fragrance, colophony, rubber, cosmetic) applied to back, kept 48 hours. Read at 48, 72 and 96 hours. Positive: erythema + papule + vesicle + itch. Gold standard for contact dermatitis (jewellery allergy, drug-type dermatitis, cosmetic reaction).

Provocation (challenge) test: gold standard for food or drug allergy — suspect substance given in graduated doses, symptoms monitored. Hospital, epinephrine + emergency readiness. Double-blind placebo-controlled food challenge (DBPCFC) is the diagnostic gold standard. Drug provocation especially when history is unclear (years ago, mild reaction).

Total IgE: baseline serum IgE. Indicator of atopy — high value suggests atopic constitution, but no trigger identification. Not for screening. Very high (>500 IU/mL) suggests atopic dermatitis, parasitic infection, hyper-IgE syndrome, allergic bronchopulmonary aspergillosis.

Eosinophil count: blood eosinophilia (>500/µL) may indicate allergic state, parasite, malignancy, drug reaction, autoimmune disease. Non-specific — supportive.

Basophil activation test (BAT): allergen activation of blood basophils by flow cytometry. Useful in drug allergy (NSAID, beta-lactam); not routine, research lab.

Interpretation principles: a positive test alone is not a diagnosis — symptoms + trigger + positive test together. Value of negative test: negative SPT mostly rules out allergy; not for delayed drug reactions. CRD is the novel risk stratification. If clinical suspicion and test results disagree, additional testing (intradermal, provocation) or re-evaluation.

Test interpretation should be performed by an allergist or experienced clinician (ENT, immunology, dermatology, paediatrics). A lab value alone is not interpreted for the patient — treatment is not started without integrating with the clinical picture. We share patient experiences on our Istanbul ENT services.