Allergy & Immunology — GCC Nursing Guide

Clinical Reference

Gell & Coombs Hypersensitivity Classification

TypeMechanismMediatorsOnsetExamples
Type I
IgE-mediated
IgE bound to mast cells; allergen cross-links IgE → degranulationHistamine, tryptase, leukotrienes, prostaglandinsMinutes (immediate)Anaphylaxis, allergic rhinitis, food allergy, urticaria
Type II
Cytotoxic
IgG/IgM binds cell-surface antigen → complement/ADCC lysisComplement, NK cellsHoursHaemolytic anaemia (penicillin), transfusion reaction, Goodpasture's
Type III
Immune-complex
Antigen-antibody complexes deposit in tissues → complement activationComplement, neutrophilsHours–daysSerum sickness, SLE, Farmer's lung, post-strep GN
Type IV
Delayed (T-cell)
Sensitised T-cells release cytokines/cause cytotoxicityIFN-γ, IL-2, TNF24–72 hContact dermatitis, TB skin test, transplant rejection, Stevens-Johnson

Type I IgE-Mediated Mechanism

Sensitisation Phase

  1. First allergen exposure → antigen-presenting cells process allergen
  2. Th2 cytokines (IL-4, IL-13) drive B-cell class switching to IgE production
  3. IgE binds high-affinity FcεRI receptors on mast cells and basophils
  4. No clinical symptoms during sensitisation — patient is "primed"

Elicitation Phase

  1. Re-exposure to allergen → cross-links IgE molecules on mast cells
  2. Mast cell degranulation releases pre-formed mediators (histamine, tryptase, heparin)
  3. Arachidonic acid cascade → leukotrienes (LTC4/D4/E4), prostaglandin D2
  4. Late-phase reaction (4–8 h) — eosinophil and basophil infiltration

Mast Cell Degranulation — Clinical Effects

  • Histamine H1: pruritus, bronchoconstriction, vasodilation, urticaria
  • Histamine H2: gastric acid, cardiac tachycardia
  • Leukotrienes: prolonged bronchoconstriction, mucus secretion
  • Tryptase: rises within 15–60 min, peaks at 1–2 h — diagnostic marker for mast cell activation
  • PAF: platelet aggregation, bronchoconstriction

Common Allergens

Food Allergens (Big-9)

  • Milk, eggs, peanuts, tree nuts
  • Fish, shellfish, wheat, soy
  • Sesame (added 2023, USA)

Drug Allergens

  • Beta-lactams (penicillin, cephalosporins)
  • NSAIDs, aspirin (COX-1 inhibition)
  • Contrast media, muscle relaxants
  • Biologics (hypersensitivity infusion reactions)

Insect Venom

  • Honeybee (Apis mellifera)
  • Yellow jacket / wasp (Vespula)
  • Fire ant (common in some GCC areas)

Latex

  • Hevea brasiliensis proteins (Hev b 1–13)
  • Cross-reacts with banana, avocado, kiwi, chestnut

GCC-Specific Allergens

Desert & Arid Environment Allergens

  • Date Palm Pollen (Phoenix dactylifera): Major sensitiser in GCC — high season Feb–April; cross-reacts with grass pollens; responsible for much of "Ramadan rhinitis" in some years
  • Desert Dust / Sand Storms (Haboob): Particulate matter <10µm; carries mould spores, pollen fragments, endotoxin; exacerbates asthma and rhinitis
  • Aspergillus flavus / fumigatus: Thrives in irrigated areas, construction sites; allergic bronchopulmonary aspergillosis (ABPA) reported in GCC asthma patients
  • Salsola kali (Russian thistle): Dominant weed pollen in arid zones; cross-reacts with Chenopodium
  • Bermuda grass (Cynodon dactylon): Dominant grass pollen in GCC lawns and parks

Animal Allergens

  • Camel dander (Cam d 1): Occupational exposure — camel farms, racing events, Ramadan markets; serum-specific IgE available
  • Goat, sheep, horse dander — pastoral workers
  • Cockroach (Blattella germanica) — high sensitisation in older GCC urban housing
  • House dust mite — lower in desert but significant in coastal cities (Dubai, Abu Dhabi, Bahrain, Jeddah)

Food — Region-Specific

  • Sesame (Sesamum indicum) — very high consumption in Gulf cuisine (tahini, hummus)
  • Lupin flour — used in some artisanal breads
  • Camel milk — emerging food allergen, cross-reactivity with cow's milk debated

⚠ FIRST-LINE TREATMENT: ADRENALINE (EPINEPHRINE)

Antihistamines and corticosteroids are ADJUNCTS only. Adrenaline is the ONLY life-saving drug in anaphylaxis. Do NOT delay it.

Adults: Adrenaline 1:1000 — 0.5 mg (0.5 mL) IM into outer mid-thigh (anterolateral)

Children <12 years: 0.01 mg/kg IM (max 0.5 mg) — see paediatric calculator below

Repeat every 5 minutes if no improvement. Auto-injector: EpiPen 0.3 mg (adult), EpiPen Jr 0.15 mg (child)

WAO/EAACI Diagnostic Criteria for Anaphylaxis

Anaphylaxis is highly likely when ANY ONE of the following three criteria is met:

Criterion 1 — Acute onset, skin/mucosal involvement PLUS at least one of:

  • Respiratory compromise (dyspnoea, wheeze, stridor, reduced PEF, hypoxia)
  • Reduced BP or associated symptoms (hypotonia, syncope, incontinence)

Criterion 2 — Two or more of the following after likely allergen exposure:

  • Skin/mucosal involvement (urticaria, angioedema, flushing, pruritus)
  • Respiratory compromise
  • Reduced BP or associated symptoms
  • Persistent GI symptoms (cramping, vomiting)

Criterion 3 — Reduced BP after exposure to a KNOWN allergen:

  • Adults: systolic BP <90 mmHg or >30% drop from baseline
  • Infants & children: age-specific low systolic BP

Emergency Management Protocol

StepActionDetail
1Call for helpActivate emergency team; GCC emergency: Saudi 911 / UAE 999 / Qatar 999 / Kuwait 112 / Bahrain 999 / Oman 9999
2Adrenaline IM0.5 mg (0.5 mL of 1:1000) anterolateral mid-thigh. Repeat q5 min PRN
3PositionSupine + legs elevated (unless respiratory distress → semi-recumbent). Lateral position if vomiting. Do NOT allow patient to stand/sit upright — risk of "empty ventricle" death
4OxygenHigh-flow O₂ 10–15 L/min via non-rebreather mask; target SpO₂ >95%
5IV accessLarge-bore IV (×2); bloods: FBC, U&E, serum tryptase (within 1–2 h of reaction, and repeat at 24 h)
6IV fluids0.9% NaCl 500–1000 mL bolus IV (adults); 20 mL/kg in children. Repeat PRN for hypotension
7AntihistamineChlorphenamine 10 mg IV/IM (adult) — for skin symptoms ONLY, does NOT treat hypotension/bronchospasm
8CorticosteroidHydrocortisone 200 mg IV (adult) — may reduce late-phase reaction; NOT first-line
9BronchospasmSalbutamol 2.5–5 mg nebulised + adrenaline IM repeated
10Refractory shockIV adrenaline infusion (specialist); glucagon 1–2 mg IV if on beta-blockers

Biphasic Reaction Risk

Second wave of anaphylaxis occurs 8–12 hours after initial reaction (range 1–72 h) in 3–20% of cases. Observe ALL anaphylaxis patients for minimum 4–6 hours (8–12 h if severe/biphasic risk factors).

Biphasic risk factors: unknown trigger, large allergen dose, delayed adrenaline, severe initial reaction, previous biphasic reactions.

Discharge Criteria & Auto-Injector Training

Safe Discharge Requires ALL of:

  • Symptom-free for minimum observation period (4–6 h minimum)
  • Vital signs stable, no recurrence of symptoms
  • Allergen identified or follow-up with allergist arranged
  • 2 × adrenaline auto-injectors prescribed and demonstrated
  • Written anaphylaxis action plan provided
  • Medical alert bracelet recommended
  • Allergy clinic referral arranged (SCIT/avoidance counselling)

Auto-Injector Instructions (EpiPen)

  1. Remove blue safety cap
  2. Hold orange tip toward outer mid-thigh (can inject through clothing)
  3. Press firmly until click heard — hold 10 seconds
  4. Remove, massage injection site 10 seconds
  5. Go to nearest Emergency Department immediately — call ambulance
  6. Second injection can be given 5–15 minutes later if no improvement

Skin Prick Testing (SPT)

Principle

Standardised allergen extracts placed on forearm skin → single lancet prick through drop → IgE on dermal mast cells cross-linked → local wheal-and-flare if sensitised.

Procedure

  1. Antihistamines withheld 3–7 days prior (depends on generation); beta-blockers noted (relative contraindication — impairs adrenaline response if systemic reaction occurs)
  2. Patient positioned comfortably; forearm cleaned with alcohol, dried
  3. Allergen drops placed 2–3 cm apart on volar forearm
  4. Positive control: histamine (10 mg/mL) — confirms mast cell reactivity
  5. Negative control: saline (diluent) — confirms no dermatographism
  6. Single-use lancet through each drop at 90° — do not wipe
  7. Read at 15–20 minutes: measure largest wheal diameter in mm

Interpretation

  • Positive: Wheal ≥3 mm greater than negative control AND >50% of positive control wheal
  • Histamine control must be ≥3 mm — if not, test invalid (suppression by drugs)
  • Saline wheal ≥3 mm → dermatographism; test unreliable
  • SPT sensitivity ~85%, specificity ~77% for food allergens
  • A positive SPT = sensitisation, NOT necessarily clinical allergy — correlate with history

Contraindications

  • Severe eczema at test site, active urticaria
  • Anaphylaxis within past 2 weeks (unstable mast cells)
  • Pregnancy (relative — avoid in first trimester)
  • Severe or poorly controlled asthma (FEV1 <70% predicted)

Intradermal Testing (IDT)

More sensitive but less specific than SPT. Used when SPT negative but clinical suspicion high (drug allergy, venom allergy).

  • 0.02–0.05 mL allergen injected intradermally → raised bleb 3 mm
  • Positive: wheal growth ≥3 mm at 15–20 minutes
  • More risk of systemic reaction — performed only in specialist setting with resuscitation available
  • Not used for food allergens (high false-positive rate)

Patch Testing — Contact Dermatitis

Assesses Type IV delayed hypersensitivity. Used for suspected allergic contact dermatitis (ACD).

  1. Standard European/North American Baseline Series applied to upper back (Finn chambers or TRUE Test)
  2. Patches removed at 48 hours — first reading
  3. Second reading at 72–96 hours (some reactions peak at 96 h)
  4. Grading: Negative (–), Doubtful (?+), Weak positive (+), Strong positive (++), Extreme (+++), Irritant reaction (IR)

Common culprits in GCC healthcare workers: Nickel (jewellery, buckles), fragrance mix, rubber accelerators (latex gloves), preservatives (methylisothiazolinone in hand sanitisers), chromate (cement).

Specific IgE Testing (RAST / ImmunoCAP)

ClasskU/L (ImmunoCAP)Interpretation
0<0.35No detectable IgE — negative
10.35–0.70Very low — equivocal
20.71–3.50Low sensitisation
33.51–17.5Moderate sensitisation
417.6–50High sensitisation
550.1–100Very high
6>100Extremely high

Component-Resolved Diagnostics (CRD)

Identifies specific allergenic molecules — important for risk stratification:

  • Peanut: Ara h 2 (storage protein) = high risk for severe reactions; Ara h 8 (PR-10) = cross-reactive, usually mild oral allergy syndrome
  • Date palm: Pho d 2 (profilin), Pho d 3 (polcalcin) — cross-reactive with other pollens
  • Cat: Fel d 1 — major allergen; Fel d 4 (lipocalin) — relevant for systemic reactions
  • HDM: Der p 1, Der p 2 — major allergens, predictive of immunotherapy response

Subcutaneous Immunotherapy (SCIT)

Mechanism

Repeated escalating doses of allergen → immune tolerance via: increased Treg cells (IL-10, TGF-β), IgG4 "blocking antibodies", reduced Th2 response, mast cell and basophil hypo-responsiveness.

Build-Up Phase

  • Duration: 3–6 months (conventional) or 6–8 weeks (cluster/rush protocols in specialised centres)
  • Injections given 1–2× per week with increasing allergen concentration
  • Starting dose typically 1:1,000,000 weight/volume, escalating to maintenance
  • Nurse role: verify injection schedule, document lot numbers, administer and monitor

Maintenance Phase

  • Monthly injections for 3–5 years once maintenance dose reached
  • Efficacy persists 3–7 years after completion
  • Indications: moderate-severe allergic rhinitis/conjunctivitis, allergic asthma (controlled), insect venom allergy

30-Minute Observation Rule

ALL patients MUST remain in clinic for 30 minutes post-injection. Systemic reactions peak within 20–30 minutes. Never allow early departure. Resuscitation equipment including adrenaline MUST be immediately available.

Pre-Injection Assessment (WITHHELD if ANY present)

  • Asthma exacerbation, wheeze, PEF <80% predicted
  • Active infection / fever
  • Large local reaction at previous injection site
  • New beta-blocker prescription (impairs adrenaline rescue)
  • Pregnancy (new — maintenance doses may continue)
  • Recent vaccination within 48 h

Sublingual Immunotherapy (SLIT)

Daily sublingual drops or tablets; home-administered. First dose given in clinic with 30-min observation.

  • Licensed tablets: Grazax® (grass pollen), Acarizax® (HDM), Ragwitek® (ragweed)
  • Hold under tongue 1–2 minutes, then swallow
  • Fewer systemic reactions than SCIT; local oral pruritus common initially
  • Patient compliance critical — daily use for 3 years
  • Nurse education: when to stop (acute illness, oral surgery, ulcers), store refrigerated

Systemic Reaction Management During SCIT

GradePresentationAction
1 — LocalWheal >25 mm at injection site; local pruritusMonitor; oral antihistamine; reduce next dose
2 — Mild systemicGeneralised urticaria, rhinitisAntihistamine IM + consider adrenaline; withold next injection
3 — Moderate systemicUrticaria + bronchospasm or mild hypotensionAdrenaline 0.5 mg IM immediately; IV access; monitor 1 h+
4 — AnaphylaxisSevere bronchospasm, hypotension, loss of consciousnessFull anaphylaxis protocol; emergency services; ICU

After any systemic reaction: reduce dose by 50% when re-starting; allergist review required.

Food Immunotherapy & Biologics

Oral Immunotherapy (OIT) — Food Allergy

  • Increasing doses of food protein orally (peanut, milk, egg) to achieve desensitisation
  • Palforzia® (peanut OIT) — FDA/EMA approved for ages 4–17
  • Nurse role: observe 30 min post-dose escalation; recognise and treat reactions
  • Goal: partial desensitisation/tolerance — does not "cure" food allergy

Biologic Adjuncts

  • Omalizumab (Xolair®): Anti-IgE; approved for severe allergic asthma, chronic spontaneous urticaria, food allergy (2024 FDA approval as adjunct to OIT); reduces systemic reaction risk during immunotherapy build-up
  • Dupilumab (Dupixent®): Anti-IL-4Rα; approved for atopic dermatitis, eosinophilic asthma, allergic rhinitis with nasal polyps, EoE

Allergic Rhinitis — ARIA Classification & Step Therapy

ARIA CategoryDurationSeverityFirst-Line Treatment
Intermittent Mild<4 days/wk OR <4 wksNo sleep/activity impairmentOral or intranasal antihistamine PRN
Intermittent Moderate/Severe<4 days/wk OR <4 wksSleep/activity impairedIntranasal corticosteroid (INS) + antihistamine
Persistent Mild≥4 days/wk AND ≥4 wksNo impairmentINS or antihistamine
Persistent Moderate/Severe≥4 days/wk AND ≥4 wksImpaired sleep/activitiesINS (first-line) ± antihistamine; consider SCIT

Intranasal corticosteroids (INS): Mometasone, fluticasone furoate — most effective monotherapy. Teach correct technique: tilt head forward, aim away from nasal septum to prevent epistaxis.

Allergen immunotherapy (SCIT/SLIT): Modifies disease — consider in patients not controlled with pharmacotherapy, or those wishing to reduce long-term medication burden.

Allergic Asthma — GINA Step Therapy

GINA StepController TherapyReliever
Step 1 (Mild intermittent)As-needed low-dose ICS-formoterolICS-formoterol PRN
Step 2 (Mild persistent)Low-dose ICS daily OR as-needed ICS-formoterolICS-formoterol PRN
Step 3 (Moderate)Low-dose ICS-LABAICS-formoterol PRN
Step 4 (Severe)Medium/high-dose ICS-LABAICS-formoterol PRN
Step 5 (Very severe)Step 4 + biologic (Omalizumab, Mepolizumab, Dupilumab) ± OCSICS-formoterol PRN

Note: SABA-only treatment (old Step 1) is no longer recommended by GINA 2023 — ICS should accompany every reliever.

Atopic Dermatitis — SCORAD Assessment

SCORAD Components

  • A — Extent (0–100): Body surface area affected using rule of nines — score /5
  • B — Intensity (0–18): Six signs scored 0–3: erythema, oedema/papulation, oozing/crusting, excoriation, lichenification, dryness
  • C — Subjective (0–20): Pruritus (0–10) + sleep disturbance (0–10) — last 3 days/nights
  • Formula: SCORAD = A/5 + 7×B/2 + C
  • Mild: <25 | Moderate: 25–50 | Severe: >50

Nursing Management

  • Emollients: apply liberally ≥2× daily, within 3 minutes of bathing (soak and smear)
  • Topical corticosteroids (TCS): lowest effective potency; fingertip unit (FTU) guidance
  • Topical calcineurin inhibitors (tacrolimus, pimecrolimus): steroid-sparing, especially face/neck
  • Dupilumab: for moderate-severe atopic dermatitis not controlled with topicals; subcutaneous injection every 2 weeks
  • Trigger identification: sweat, wool, detergents, food (in young children), stress

Food Allergy — Anaphylaxis vs Intolerance vs Coeliac

FeatureIgE-Mediated Food AllergyFood IntoleranceCoeliac Disease
MechanismIgE / mast cellNon-immunological (enzyme deficiency, FODMAP, etc.)Autoimmune (anti-TTG IgA, HLA-DQ2/DQ8)
Onset after exposureMinutes–2 hoursHours–daysDays–years (chronic)
Dose dependenceSmall doses can triggerOften dose-dependentAll gluten must be avoided
Life-threateningYes — anaphylaxisNoYes if untreated (lymphoma, malnutrition)
DiagnosisSPT, specific IgE, OFCExclusion diet/food diaryAnti-TTG IgA, duodenal biopsy (Marsh grading)

Drug Allergy

Penicillin Allergy

  • ~10% of patients label themselves "penicillin allergic" — >90% can tolerate penicillin on formal testing
  • Cross-reactivity with cephalosporins: ~1–2% (previously overestimated at 10%)
  • Shared R1 side-chain similarity more important than beta-lactam ring in predicting cross-reactivity
  • Penicillin allergy delabelling (skin testing + oral challenge) recommended for low-risk labels

NSAID Hypersensitivity (AERD)

  • Aspirin-Exacerbated Respiratory Disease (AERD/Samter's triad): Asthma + nasal polyps + NSAID sensitivity
  • Mechanism: COX-1 inhibition → shunts arachidonic acid to leukotriene pathway
  • Management: NSAID/aspirin avoidance; aspirin desensitisation in specialist centres; montelukast; zileuton
  • Selective COX-2 inhibitors (celecoxib) generally tolerated in AERD patients

Drug Allergy Documentation — GCC Requirements

  • Document: drug name (generic + brand), reaction type, date, severity, investigation results
  • UAE (DHA/DOH): allergy field mandatory in Salama/NABIDH/Malaffi systems
  • Saudi Arabia (MOH): allergy documented in SEHA/SIHF unified record
  • Qatar (PHCC/HMC): CERNER allergy fields; "Allergy Review" flag alerts prescribers
  • Always distinguish true allergy from intolerance/side-effect in documentation

Urticaria & Angioedema

Urticaria Classification

  • Acute spontaneous: <6 weeks; often IgE-mediated (food, drug, infection)
  • Chronic spontaneous (CSU): >6 weeks; autoimmune (anti-FcεRI/IgE antibodies) in ~40%
  • Physical urticarias: dermographism, cold, pressure, solar, aquagenic, cholinergic
  • UAS7 score: Urticaria Activity Score over 7 days — monitor disease control (0–42; ≥28 = uncontrolled)

CSU Treatment Ladder

  1. 2nd-generation antihistamine (cetirizine, loratadine) regular dose
  2. Up-dose antihistamine ×4 (off-label but guideline-supported)
  3. Add omalizumab 300 mg SC monthly
  4. Cyclosporine (specialist use)

Angioedema

  • Allergic (histaminergic): urticaria + angioedema; responds to antihistamines/adrenaline
  • Hereditary Angioedema (HAE): C1-inhibitor deficiency; bradykinin-mediated; does NOT respond to antihistamines/adrenaline
  • ACE-inhibitor angioedema: Bradykinin accumulation; onset months–years after starting drug; tongue/larynx commonly involved — life-threatening

Laryngeal Angioedema

Stridor + voice change + throat tightness = impending airway obstruction. Give adrenaline 0.5 mg IM immediately. Prepare for intubation/surgical airway. HAE: icatibant 30 mg SC or C1-INH concentrate.

Epidemiology & Prevalence in the GCC

  • Atopy prevalence in GCC adults 30–45%; allergic rhinitis affects ~30% of population in Saudi Arabia, UAE, Kuwait
  • Asthma prevalence ~13–15% (higher than global average of ~8%)
  • Rapid urbanisation, air conditioning, hygiene hypothesis, diesel particulates = rising atopy
  • Haboob (sandstorm) season (March–June) dramatically increases ER attendances for asthma/rhinitis; fine particles carry endotoxin, fungal spores, metals
  • Aspergillus sensitisation higher in GCC than temperate climates — ABPA should be excluded in difficult-to-control asthma
  • High humidity in coastal cities (Dubai, Manama, Doha, Muscat) drives indoor HDM and mould sensitisation year-round

Latex Allergy in GCC Healthcare Settings

Occupational Risk — Surgical & Theatre Nurses

  • Repeated exposure to natural rubber latex (NRL) gloves → sensitisation, progressing from contact urticaria → rhinitis → anaphylaxis
  • Prevalence in healthcare workers: 8–17% sensitisation; higher in atopic individuals
  • Powdered gloves greatly increase airborne latex allergen exposure — WHO recommends phase-out
  • GCC hospitals increasingly latex-safe: use nitrile/vinyl gloves, latex-free environments
  • Known latex allergy: first on operating list (when environment cleanest), latex-free OR, latex-free IV equipment, alert bracelet
  • Cross-reactive foods: banana, avocado, kiwi, chestnut, papaya — advise avoidance

Drug Allergy Documentation — MOH / DHA / SCHS

AuthoritySystemKey FieldsNurse Responsibility
Saudi MOHHESN / Nphies / SIHFDrug name, reaction type (allergy/ADR/contraindication), severity, date, status (active/inactive)Verify allergy status before administration; document new reactions within same shift
UAE DHA (Dubai)Salama EMR / Malaffi HIEAllergen, reaction description, category, certaintyFlag unverified or self-reported allergies for pharmacist review
UAE DOH (Abu Dhabi)NABIDH / ShafafiyaAllergy type, reaction, onset, evidence typeMandatory allergy documentation before prescribing through system
Qatar MOPH (HMC/PHCC)Cerner / HAYATAllergy name, reaction, severity, statusAllergy reconciliation at admission and discharge
SCHS (Saudi private)Varies by hospital groupFollow facility SOPs; CBAHI accreditation standards require allergy fieldAllergy band on patient wrist; documented in nursing admission assessment

Halal / Haram Considerations in Allergy Medications

Key Medications to Verify

  • Gelatin capsules: Most standard capsules contain porcine gelatin — check with pharmacist for halal-certified alternatives or tab/liquid formulations; fatwa generally allows for medical necessity (“darura”)
  • Vaccines with porcine-derived materials: Some seasonal flu vaccines (cell-culture grown) use porcine trypsin — GCC Islamic authorities generally permit for medical need; discuss with patient
  • Alcohol-based oral solutions (antihistamines): Some liquid antihistamines contain ethanol as excipient; prefer tablet/syrup form for patients who request alcohol-free
  • Omalizumab (Xolair): Chinese hamster ovary cell derived — generally considered permissible; no porcine material
  • Heparin (used in some allergy testing buffers): May be porcine-derived — bovine heparin alternatives exist; clarify for strict observance
  • Nurse role: Never assume; consult hospital pharmacist; respect patient autonomy; document discussion; Islamic jurisprudence generally supports medical necessity principle

Leading GCC Allergy & Immunology Centres

CountryCentreSpeciality
Saudi ArabiaKing Fahad Medical City (Riyadh) — Allergy & Immunology DeptComprehensive adult & paediatric allergy; SCIT programs
Saudi ArabiaKing Faisal Specialist Hospital & Research Centre (Riyadh)Primary immunodeficiency, severe asthma, transplant
Saudi ArabiaKing Abdulaziz University Hospital (Jeddah)Academic centre; allergy research; coastal allergen profiling
UAECleveland Clinic Abu Dhabi — Allergy & ImmunologyFull allergy workup, immunotherapy, biologic therapies
UAEAmerican Hospital Dubai — Allergy DeptPrivate sector; food allergy OIT protocols
UAEAl Jalila Children’s Specialty Hospital (Dubai)Paediatric allergy, eczema, food allergy, primary immunodeficiency
QatarHamad Medical Corporation — Allergy & ImmunologyNational referral; severe allergic asthma; immunodeficiency
KuwaitAl-Razi Hospital (Kuwait City) — Allergy UnitPollen allergy profiling; SCIT
BahrainSalmaniya Medical ComplexGovernment allergy services; drug allergy evaluation
OmanSultan Qaboos University Hospital (Muscat)Academic; allergy & clinical immunology research

⚡ Anaphylaxis Severity Grader

Select all signs and symptoms present, then click Grade Severity.

⚡ Paediatric Adrenaline Dose Calculator

Enter child’s weight to calculate IM adrenaline 1:1000 dose for anaphylaxis.

✍ Practice MCQs — Allergy & Immunology

10 questions with instant feedback. Click an answer to check.

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1. A patient develops urticaria, wheeze and hypotension 10 minutes after penicillin IV. What is the MOST appropriate IMMEDIATE action?
Adrenaline 0.5 mg IM is the first-line life-saving treatment. Antihistamines and corticosteroids are adjuncts only and must never precede or replace adrenaline.
2. Which immunoglobulin class mediates Type I hypersensitivity reactions?
IgE binds to high-affinity FcεRI receptors on mast cells and basophils. Cross-linking of IgE by allergen triggers immediate degranulation — the hallmark of Type I hypersensitivity.
3. A nurse administers SCIT. How long must the patient be observed post-injection?
All SCIT patients must remain in clinic for 30 minutes post-injection. The majority of systemic reactions occur within 20–30 minutes, making this the internationally recommended minimum observation period.
4. During skin prick testing, the histamine positive control produces a 1 mm wheal. What does this indicate?
The positive control (histamine) must produce a wheal ≥3 mm. A subthreshold response indicates mast cell suppression, usually from recent antihistamine use. The entire test must be considered invalid and repeated when medications are withheld.
5. Which GCC-specific allergen is a major cause of seasonal rhinitis due to pollination in February–April?
Date palm (Phoenix dactylifera) pollinates predominantly from February to April and is a major regional sensitiser in GCC countries. It cross-reacts with grass pollens. HDM is more relevant in humid coastal cities; Timothy grass and birch are temperate-region pollens.
6. A patient on long-term ACE inhibitor develops sudden tongue swelling without urticaria. Which medication is LEAST likely to be effective?
ACE inhibitor-induced angioedema is bradykinin-mediated, NOT histamine-mediated. Antihistamines are ineffective. Treatment options include stopping the ACE inhibitor, icatibant (bradykinin B2 antagonist), C1-inhibitor concentrate, or FFP. Adrenaline may help with airway oedema temporarily.
7. Patch testing is used to diagnose which type of hypersensitivity reaction?
Patch testing diagnoses Type IV (delayed) hypersensitivity — allergic contact dermatitis. Patches are read at 48 and 72–96 hours because T-cell mediated reactions develop over 24–72 hours, in contrast to immediate IgE reactions.
8. What is the recommended minimum observation period for a patient who has had anaphylaxis to assess for biphasic reaction?
Biphasic reactions occur in 3–20% of anaphylaxis cases, most commonly at 8–12 hours. Minimum observation is 4–6 hours for uncomplicated cases, extended to 8–12 hours for severe reactions, unknown triggers, delayed adrenaline, or history of previous biphasic reactions.
9. A nurse is about to give a SCIT injection and the patient says they have had a fever of 38.5°C since yesterday. What should the nurse do?
Active infection/fever is an absolute reason to withhold SCIT. Fever and infection increase the risk of systemic reactions to immunotherapy. The injection should be postponed until the patient is well, and this should be documented clearly in the notes.
10. Which component-resolved diagnosis (CRD) result for peanut allergy indicates the HIGHEST risk for a severe systemic reaction?
Ara h 2 is a heat-stable, digestion-resistant 2S albumin storage protein and is the most clinically significant peanut allergen associated with severe systemic reactions and anaphylaxis. Ara h 8 is a labile PR-10 protein cross-reactive with birch pollen, typically causing only oral allergy syndrome.