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Best of Five MCQs for the Acute Medicine SCE$

Nigel Lane, Louise Powter, and Sam Patel

Print publication date: 2016

Print ISBN-13: 9780199680269

Published to Oxford Scholarship Online: November 2020

DOI: 10.1093/oso/9780199680269.001.0001

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Immunology and Allergy

Immunology and Allergy

Chapter:
(p.383) Chapter 14 Immunology and Allergy
Source:
Best of Five MCQs for the Acute Medicine SCE
Author(s):
Nigel Lane, Louise Powter, Sam Patel
Publisher:
Oxford University Press
DOI:10.1093/oso/9780199680269.003.0018

Abstract and Keywords

An 18-year-old Iranian man was brought to the emergency department unconscious. He was pyrexial, hypotensive, and had a petechial rash. A computerised tomography (CT) scan of head was normal and he was ventilated on intensive care. He was treated with intravenous ceftriaxone for presumed meningitis and recovered with persistent hearing loss. Blood cultures were positive for Neisseria meningitidis serogroup Y.

One year later he presented with a rash, headache, and neck stiffness. He was afebrile, conscious, and alert. He was treated with intravenous ceftriaxone for presumed meningitis and blood cultures confirmed Neisseria meningitidis (which was ‘not typable’ and therefore not serogroup A, B, or C).

Keywords:   acute anaphylaxis, biphasic allergic response, conjunctivitis, food allergies, hyper IgM syndrome, immunology, mast-cell tryptase, rhinorrhoea, wasp venom allergy

QUESTIONS

An 18-year-old Iranian man was brought to the emergency department unconscious. He was pyrexial, hypotensive, and had a petechial rash. A computerised tomography (CT) scan of head was normal and he was ventilated on intensive care. He was treated with intravenous ceftriaxone for presumed meningitis and recovered with persistent hearing loss. Blood cultures were positive for Neisseria meningitidis serogroup Y.

One year later he presented with a rash, headache, and neck stiffness. He was afebrile, conscious, and alert. He was treated with intravenous ceftriaxone for presumed meningitis and blood cultures confirmed Neisseria meningitidis (which was ‘not typable’ and therefore not serogroup A, B, or C).

What is the most appropriate investigation to confirm the most likely immunodeficiency?

  • Classical and alternative pathway complement haemolysis

  • Complement C1-inhibitor levels

  • Complement C3 and C4 levels

  • immunoglobulin G, A, and M levels

  • Lymphocyte subset analysis (T, B, and NK cell analysis)

(p.384) A 50-year-old British man presented to the acute medical unit with a cough productive of green sputum and pyrexia. He had a past medical history of right-sided pneumonia 20 years ago and mentioned that he was investigated by the immunology department at the time. On examination, he had bronchial breathing over the right hemi-thorax.

Figure 14.1 C

Immunology and Allergy

Figure. 14.1. Chest X-ray at presentation to the acute medical unit.

Investigations:

Previous immunological assessment (20 years ago): serum IgG 5.7 g/L

serum IgG

5.7 g/L

(6.0–13.0)

serum IgA

<0.07 g/L

(0.8–3.0)

serum electrophoresis normal

His immunological blood tests serum IgG serum IgA serum IgM

serum IgG

4.85 g/L

(6.0–13.0)

serum IgA

0.24 g/L

(0.8–3.0)

serum IgM

0.19 g/L

(0.4–2.5)

serum electrophoresis

no monoclonal protein

dentified

urine electrophoresis

normal

CD3

2.4 × 109/L, 89%

(1.1–1.7)

CD4

1.19×109/L, 44%

(0.7–1.1)

CD8

1× 109/L, 37%

(0.5–0.9)

CD19

0.16 × 109/L, 6%

(0.2–0.4)

lymphocyte count

2.7 × 109/L

(1.5–4.0)

serum C-reactive protein

143 mg/L

(<10)

serum alkaline phosphatase

240 U/L

(40–105)

haemoglobin

118 g/L

(130–180)

pneumococcal antibodies

9 U/mL

(>20)

(p.385) A CT scan of thorax revealed pleural thickening, bronchiectasis, consolidation of the right lung, and mediastinal lymphadenopathy. Bronchoscopy had easy contact bleeding but no other abnormalities and bronchoalveolar lavage cytology and microbiology was negative.

What is the most likely diagnosis?

  • Bronchiectasis secondary to previous infection

  • Common variable immunodeficiency

  • Hyper IgM syndrome

  • secondary antibody deficiency

  • selective igA deficiency

A 35-year-old British woman presented to the acute medical unit with a three-day history of intense pruritus and rash. The rash consisted of raised pale patches on an erythematous base. She described the patches as ‘coming and going’ all over her body. She noticed the pruritus on waking, while in bed. She was well without any rash when she went to bed the night before. She did not have any unusual contact during the night and had not changed any of the products used in the house. She did not take any medications regularly.

On further questioning, she recalled episodes of a similar rash that was controlled with antihistamines when she was younger.

She had recently separated from her husband due to domestic abuse and the legal proceedings were due to start next week. Her observations, full blood count, and renal and liver function were all normal.

What is the most likely diagnosis?

  • Allergic urticaria

  • Chronic idiopathic urticaria

  • Erythema multiforme minor

  • idiopathic anaphylaxis

  • Urticaria pigmentosa

(p.386) A 23-year-old British man attended the emergency department in July with rhinorrhoea, conjunctivitis, and wheeze. The symptoms started in May with rhinorrhoea and conjunctivitis. He had been taking non-sedating antihistamines and intranasal corticosteroids regularly, on the advice of his GP, without significant benefit. His symptoms had occurred on every day over the last two months and had impacted on his sleep and daytime concentration. He had missed ten days of work during the last two months. Today, he developed tightness in his chest and therefore presented to the emergency department. He had no past medical history and had never experienced these symptoms before. His two sisters and his mother had eczema and hay fever.

He was treated with inhaled salbutamol and his wheeze improved. His peak expiratory flow rate returned to the normal predicted for age and height.

Investigations:

total IgE

120 kU/L

(<120)

mixed grass-specific IgE

90 kU/L

(0 to 0.4)

mixed tree-specific IgE

>0.4 kU/L

(0.0.4)

cat-specific IgE

>0.4 kU/L

(0–0.4)

dog-specific IgE

>0.4 kU/L

(0–0.4)

house dust mite-specific IgE

>0.4 kU/L

(0–0.4)

What is the most appropriate long-term treatment to consider?

  • Allergen-specific immunotherapy

  • As required bronchodilator

  • Intramuscular corticosteroids before each summer

  • oral corticosteroids during the pollen season

  • Regular oral antihistamines and intranasal corticosteroids

A 25-year-old British man presented to the acute medical unit in September following a collapse while walking with his parents in the countryside. They had been picking blackberries from the hedges. Immediately prior to collapsing he mentioned his hand being pricked by a thorn and he developed shortness of breath and became flushed. Paramedics arrived promptly and administered intramuscular adrenaline. The emergency department administered a further dose of intramuscular adrenaline as he was hypotensive, dyspnoeic, and had significant upper-airway angioedema on arrival. He received high-flow oxygen and intravenous fluids throughout. Antihistamines and corticosteroids were administered later.

What is the most appropriate next step in management?

  • Discharge with oral antihistamines and corticosteroids

  • He is safe to be discharged with general practice follow-up

  • He should be admitted to complete 24 hours’ observation

  • He should receive an adrenaline auto-injector and referral to the allergy clinic

  • Mast-cell tryptase blood tests should be sent for analysis

(p.387) An 18-year-old student presented having become acutely unwell at lunch during freshers’ week. He had a history of allergy to peanuts, and had adrenaline auto-injectors, which he’d left at home.

On examination, he was unwell and struggling to breathe. His heart rate was 120 beats per minute, blood pressure 90/55 mmHg, and oxygen saturation 86% breathing room air. He was treated with high-flow oxygen and intravenous crystalloid.

Which of the following drugs should be administered immediately?

  • 0.5 mL of 1:1,000 adrenaline intramuscularly

  • 0.5 mL of 1:1,000 adrenaline intravenously

  • 10 mg chlorphenamine intravenously

  • 200 mg hydrocortisone intramuscularly

  • 200 mg hydrocortisone intravenously

An 18-year-old student who suffered a nut-induced episode of anaphylaxis at lunchtime was admitted for overnight observation on the acute medical unit. At 22:00 hours he was mistakenly given intravenous amoxicillin prescribed for the patient in the next bed. There was no previous history of penicillin allergy. At 04:00 hours the following morning he was found in extremis with severe respiratory compromise and hypotension.

The most likely cause of his deterioration is:

  • Biphasic allergic response

  • Inadvertent peanut consumption

  • Missed peanut aspiration

  • Previously undiagnosed asthma

  • severe type 1 hypersensitivity to amoxicillin

A 32-year-old heavily pregnant woman was brought collapsed to the acute medical unit by her husband. She had a history of wasp venom allergy and had been due to start immunotherapy when she discovered she was pregnant.

On examination, she was unwell with widespread urticaria and angioedema, limited to her face. Her pulse was 135 beats per minute, blood pressure 70/45 mmHg, respiratory rate 28 breaths per minute, and oxygen saturation 89% breathing room air. She received oxygen, intravenous crystalloid fluids, and adrenaline followed by hydrocortisone and chlorphenamine.

The correct position to nurse the patient in is:

  • Lay flat on the bed with legs elevated at 45°

  • Lay on her left-hand side at 15°

  • Lay on her right-hand side at 15°

  • Lay on the bed with head down tilt at 25°

  • sat up in bed at 60°

(p.388) A 58-year-old man was admitted to the acute medical unit having attended the emergency department the night before with swelling to his face, mouth, tongue, and neck. He had suffered approximately six similar, although milder, episodes over the past 18 months but had not previously sought medical attention. His past medical history revealed hypertension, monoclonal gammopathy of undetermined significance, and mild osteoarthritis. His regular medication was atenolol and paracetamol.

The day before presentation he had taken his atenolol before lunch.

His lunch consisted of beef lasagne and salad (lettuce, tomatoes, and cucumber). Four hours after his lunch he developed swelling of his face. The swelling gradually increased over the following eight hours until he presented to the emergency department. In the emergency department he received adrenaline, chlorphenamine, and hydrocortisone with little improvement so had been admitted for observation. He reported that the swelling to his mouth and tongue had improved while waiting to be seen.

On examination, he was maintaining his own airway, and although it had been difficult due to his swollen tongue, he had been able to swallow two paracetamol tablets he brought with him. His Early Warning Score was zero.

The most likely diagnosis is:

  • Acquired angioedema

  • Allergy to atenolol

  • Angiotensin converting enzyme inhibitor related angioedema

  • Food allergy

  • Hereditary C1 inhibitor deficiency

A 56-year-old man was admitted with sudden onset severe hypotension, widespread urticaria, and angioedema following a wasp sting. Anaphylaxis was suspected and treated appropriately according to the Resuscitation Council guidance. One of the nurses took some extra blood while inserting a spare cannula during resuscitation and asks you if you want any tests done.

Which blood test should be taken as soon as possible during the management of acute anaphylaxis?

  • Mast-cell tryptase

  • serum histamine

  • specific IgE

  • specific IgG

  • Total IgE

(p.389) ANSWERS

A. Classical and alternative pathway complement haemolysis

This patient has had recurrent meningococcal infections with unusual serogroups of meningococcus. Complement deficiency is the most likely immunodeficiency in cases of recurrent meningococcal infection, although antibody deficiency can occasionally be the cause. non-immunological causes include anatomical defects (including skull-base abnormalities). Guidelines from the Clinical Working Party of the european society for immunodeficiencies in 2006 suggest excluding antibody deficiency and complement deficiency in patients with recurrent meningococcal disease. Complement deficiency in this context requires the testing of the integrity of the entire complement cascade, which is performed on fresh serum by assessing the haemolytic pathways (alternative and classical). terminal complement (C5, C6, C7, C8, and C9) deficiency, which causes dysfunction of the membrane attack complex, is detected as absent haemolysis on both classical and alternative pathways.

the lifetime risk of meningococcal disease is 1,000 to 10,000 times greater in individuals with terminal complement defects than in the healthy population. relapse and recurrence of meningococcal disease is 10 and 150 times more likely respectively in terminal complement deficient individuals as compared with healthy controls. Disease tends to occur in older age groups (median age of onset is 3 in healthy controls and 17 in complement deficiency) and is caused by unusual serogroups of meningococcus (W135, X, Y, and non-typable) in complement deficiency.

De Vries E. Clinical Working Party of the European Society for Immunodeficiencies (ESID). Patientcentred screening for primary immunodeficiency: a multi-stage diagnostic protocol designed for non-immunologists. Clinical … Experimental Immunology 2006; 145: 204–214.

Walport MJ. Complement. First of two parts. New England Journal of Medicine 2001; 344: 1058–1066.

B. Common variable immunodeficiency

Common variable immunodeficiency (CVID) is the most common clinically significant antibody deficiency disease (1 in 36,000). Patients present with recurrent sinopulmonary infections and often with structural lung and sinus disease. the delay to diagnosis often exceeds two years. the diagnostic criteria for probable CVID include:

  • igG below reference range (2 SD below mean for age)

  • Marked decrease in igA and/or igM

  • Absent/impaired responses to polysaccharide vaccine

  • onset after 2 years of age

  • Exclusion of defined causes of hypogammaglobulinaemia

exclusion of secondary and defined causes of hypogammaglobulinaemia is advised by the Clinical Working Party of the european society forimmunodeficiencies (ESID). the alternative causes includemedications (immunosuppression, anticonvulsants, antipsychotics),genetic disorders, (p.390) infectious diseases (HIV, CMV, rubella, EBV), malignancy (haematological and thymoma), and increased losses (proteinuria, diarrhoea).

This patient has all of the clinical and laboratory features of CVID and the alternative causes have been excluded on clinical features or investigation.

selective igA deficiency (igAD) is the most common antibody deficiency (1 in 600). igAD is usually asymptomatic but can be associated with infections, autoimmunity, allergy, and transfusion reactions. the other immunoglobulin proteins are normal in igAD as are responses to vaccination. Hyper igM syndrome is a rare antibody deficiency syndrome caused by defective communication between B and T lymphocytes. the most common mutation involves the CD40 ligand molecule and is an X-linked condition. Classically, young boys present with recurrent infections and unusual infections (including pneumocystis). the igM level is within the normal range or high with low levels of igG and igA.

specific antibody deficiency is similar in presentation to CVID but immunoglobulin levels are normal. the condition is diagnosed by absent response to vaccination with a polysaccharide vaccine (usually the pneumococcal polysaccharide vaccine).

CVID diagnostic criteria. http://esid.org/Working-Parties/Clinical/Resources/Diagnostic-criteria-for-PID2#Q3

Differential diagnosis of hypogammaglobulinaemia. http://esid.org/Working-Parties/Clinical/Resources/Diagnostic-criteria-for-PID2#Q6

Wood P Primary antibody deficiency syndromes. Annals of Clinical Biochemistry 2009; 46: 99-108.

B. Chronic idiopathic urticaria

She describes a classical urticarial rash. Urticaria can arise (with or without angioedema) secondary to allergy, infection, related to medications, or without clear cause (spontaneous or idiopathic). Her features are not consistent with anaphylaxis, which is defined as a severe, life-threatening, gen-eralized, or systemic hypersensitivity reaction. similarly, type 1 hypersensitivity is not likely as the symptoms started without any related exposure. type 1 hypersensitivity reactions, including allergic urticaria, usually occur within an hour of exposure to an allergen. in her case, the urticaria could also be precipitated by asymptomatic infection or stress.

Johansson S, Hourihane J, Bousquet J et al. EAACI (the European Academy of Allergology and Clinical Immunology) nomenclature task force. A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force. Allergy 2001; 56: 813–824.

Powell R, Du Toit L, Siddique N et al. British Society for Allergy and Clinical Immunology (BSACI). BSACI guidelines for the management of chronic urticaria and angio-oedema. Clinical … Experimental Allergy 2007; 37: 631–650.

A. Allergen-specific immunotherapy

this patient has allergic rhinitis and has presented with an episode of wheeze. He should be treated with antihistamines and intranasal steroids for his rhinitis. As the pharmacological therapy has failed to control his symptoms and there is clear evidence of grass pollen allergy, he is a good candidate for allergen specific immunotherapy. inhaled bronchodilators may be necessary currently due to the wheeze. systemic steroid therapy should be avoided, where possible, in the treatment of allergic rhinitis, particularly intramuscular corticosteroids as the side effects can include avascular necrosis of the femoral neck.

ARIA. http://www.whiarorg/

Walker S, Durham S, Till S et al. British Society for Allergy and Clinical Immunology Immunotherapy for allergic rhinitis. Clinical … Experimental Allergy 2011; 41: 1177–1200.

(p.391) D. He should receive an adrenaline auto-injector and referral to the allergy clinic

The most appropriate next step is referral to the local allergy clinic for further assessment and advice. He may have insect venom allergy. Mast-cell tryptase blood tests should be taken immediately, 1–2 hours post event and 24 hours post event. Prolonged observation is not required in patients that have recovered completely, but they should be advised of the possibility of a biphasic reaction. Recent NICE guidelines (CG134) recommend an adrenaline auto-injector is given to all patients presenting with suspected anaphylaxis with advice on how and when to use it.

Soar J, Pumphrey R, Cant A, et al. Emergency treatment of anaphylactic reactions - guidelines for healthcare providers. Resuscitation 2008;77:157–69.283.

National Institute for Health and Care Excellence. Clinical Guideline 134. Anaphylaxis: assessment and referral after emergency treatment. December 2011.

A. 0.5 mL of 1:1,000 adrenaline intramuscularly

Adrenaline is key to immediate treatment in acute anaphylaxis. The European Resuscitation Council guidance from 2015 emphasizes early treatment with adrenaline and a repeated dose after 5 minutes if no clinical improvement in the patient's condition.

Adrenaline used during anaphylaxis is at a concentration of 1:1,000.

In adults (and in children over the age of 12) the dose is 0.5 mg (a volume of 0.5 mL of the 1:1,000 solution).

Adrenaline for anaphylaxis should be given intramuscularly (IM) by all except for anaesthetists/intensivists experienced in intravenous use. There is a much higher risk of causing harm if intravenous adrenaline is used.

Hydrocortisone 200 mg IM or slow IV and chlorphenamine 10 mg IM or slow IV should be given after the initial resuscitation.

Soar J, Pumphrey R, Cant A, et al. Emergency treatment of anaphylactic reactions - guidelines for healthcare providers. Resuscitation 2008;77:157–69.283.

(p.392) Truhlar A, Deakin C, Soar J et al. European Resuscitation Council Guidelines for Resuscitation 2015 Section 4. Cardiac arrest in special circumstances ; Resuscitation 95 (2015) 148–201.

National Institute for Health and Care Excellence. Clinical Guideline 134. Anaphylaxis: assessment and referral after emergency treatment. December 2011.

A. Biphasic allergic response

The European Resuscitation Council recommends all patients treated for anaphylaxis are observed for at least 6 hours, and in some cases up to 24 hours (e.g. in patients with a severe asthmatic component, previous history of biphasic reactions or patients initially presenting at night). NICE guidance suggests observing adults for 6–12 hours and warning patients about biphasic responses prior to discharge.

The frequency of biphasic reactions is not clear, but may be as high as 20%. They are generally unpredictable, although if there is a history of biphasic reactions, the risk is thought high for future biphasic responses. These can be severe and may result in death.

A review within the resuscitation council guidance found fatal anaphylaxis occurred soon after contact, and never occurred more than six hours after allergen exposure.

Soar J, Pumphrey R, Cant A, et al. Emergency treatment of anaphylactic reactions - guidelines for healthcare providers. Resuscitation 2008;77:157–69.283.

Truhlár A, Deakin C, Soar J et al. European Resuscitation Council Guidelines for Resuscitation 2015 Section 4. Cardiac arrest in special circumstances ; Resuscitation 95 (2015) 148–201 .

National Institute for Health and Care Excellence. Clinical Guideline 134. Anaphylaxis: assessment and referral after emergency treatment. December 2011.

B. Lay on her left-hand side at 15°

Pregnant patients beyond 20 weeks’ gestation should lie on their left side to prevent caval compression by the pregnant uterus. the european Resuscitation Council guidance recommends a left lateral tilt of 15°.

Truhlár A, Deakin C, Soar J et al. European Resuscitation Council Guidelines for Resuscitation 2015 Section 4. Cardiac arrest in special circumstances ; Resuscitation 95 (2015) 148–201.

A. Acquired angioedema

This is angioedema alone, and there are no other features to suggest this is allergy. Additionally, he

did not eat food or take atenolol in the period immediately before onset. With episodes starting in his mid-50s, he is unlikely to have hereditary angioedema (hereditary C1 inhibitor deficiency).

He is not on an angiotensin converting enzyme inhibitor (ACE-I) for his hypertension. He is in the age range for presentation of acquired angioedema, and has a history of monoclonal gammopathy of undetermined significance (MGUS), one of the major conditions associated with acquired angioedema (AEE).

Allergy—food or drug

igE-mediated allergy causes immediate allergy. symptoms include urticaria, angioedema, wheeze secondary to bronchospasm, dizziness secondary to hypotension, and gastrointestinal disturbance. typically, symptoms appear within minutes of intravenous drug administration and within 30 minutes of food or oral drug ingestion, and may be life-threatening (anaphylaxis).

Cross-linking of the allergen to mast-cell-bound igE receptors causes mast-cell degranulation, releasing preformed mediators (e.g. histamine, tryptase, and heparin) and newly formed thromboxane, prostaglandin D2, and leukotriene C4. these cause the signs and symptoms of an allergic reaction.

Treatment depends on the severity of the reaction. For anaphylaxis, where potentially life-threatening features are present, adrenaline 0.5 mg intramuscular is essential. other immediate treatments include oxygen and intravenous fluids followed less urgently by hydrocortisone and chlorphenamine. For milder cutaneous-only reactions, oral antihistamines are usually adequate.

Hereditary angioedema (HAE) (hereditary C1 inhibitor deficiency)

C1 is the initiator of the classical complement pathway, and is made up of C1q, C1r, and C1s. on activation by binding to igM molecules or to igG bound to pathogen surface, C1q undergoes a conformational change allowing C1r to activate C1s. C1s then cleaves C2 and C4. Cleavage of C4 means C4 can be used as a screening test for over activation of C1 in this disorder. C1 inhibitor blocks C1 from becoming activated.

C1 inhibitor is also part of the kinin pathway from which bradykinin is produced. C1 inhibitor inhibits plasma kallikrein, which acts on high-molecular weight kininogen produced by the liver to release bradykinin. bradykinin is a vasoactive peptide that causes vasodilatation and increased vascular permeability via its constitutively expressed B2 receptors. this is the main cause of angioedema in C1 inhibitor deficiency.

(p.393) HAE is inherited in an autosomal dominant fashion. in females, it may first present around puberty or with commencement of combined oral contraceptives as oestrogen promotes at-tacks. Episodes may be with overt angioedema, but alternatively patients may present with recurrent episodes of abdominal pain, which may have been extensively investigated by surgical colleagues.

For the treatment of acute attacks of HAE in the UK consider the use of C1 inhibitor concentrate (from donor plasma) or icatibant, a bradykinin B2 receptor antagonist.

Acquired angioedema (AAE) (acquired C1 inhibitor deficiency)

This disorder is identical to HAE except for an older age of onset. it occurs most commonly secondary to MGUs, lymphproliferative disease, or sometimes in autoimmune diseases such as sLE. A proposed mechanism includes a blocking autoantibody against C1 inhibitor, thereby preventing its action. Higher doses of C1 inhibitor concentrate may be required than for HAE.

ACE-I induced angioedema

Angiotensin converting enzyme (ACE) acts on the renin-aldosterone system to convert angiotensin I to angiotensin II; however, it also acts to degrade bradykinin (Figure 14.2). Bradykinin is a vaso-active peptide that causes vasodilatation and increased vascular permeability via its constitutively expressed B2 receptors. ACE-I block bradykinin degradation, so increasing levels of bradykinin available.

Immunology and Allergy

Figure. 14.2 Figure showing pathway of ACE-I induced angioedema.

ACE-I associated angioedema is estimated at occurring in 0.1–0.2% of patients treated with ACE-I, although this is probably an underestimate. The frequency is higher in African Americans. It can appear at any time after starting an ACE-I, and has been reported to occur after patients have tolerated treatment for many years.

There is no universally agreed treatment for ACE-I angioedema and the main aim should be supportive care such as airway protection in laryngeal compromise. Some teams support the use of antihistamines and adrenaline, although these are of unproven benefit. The bradykinin B2 receptor antagonist icatibant, developed for HAE, has recently been reported to be useful and effective in ACE-I induced angioedema, although it is currently not licensed for this use.

ACE-I should be stopped and remain contraindicated for future use. In general, angiotensin II receptor blockers may be used as an alternative, although there have been rare reports of angioedema linked to these too.

Vasekar M, Craig T ACE inhibitor induced angioedema. Current Allergy and Asthma Reports. Springer 2011. doi: 10.1007/s11882-011-0238-z

(p.394) A. Mast-cell tryptase

Mast-cell tryptase is pre-formed in the granules of mast cells, and is released into circulation on cross-linking of allergen to mast-cell-bound-specific igE. it peaks in circulation between 30–120 minutes after onset, and with a half-life of approximately two hours, concentrations return to baseline within about eight hours.

Both the National institute for Health and Care excellence and the european Resuscitation Council guidance include measurement of mast-cell tryptase within their recommendations. Both recommend:

  • One sample as soon as possible on presentation (but not delaying resuscitation)

  • A second sample 1–2 hours after onset of symptoms

  • A convalescent sample more than 24 hours after the onset of symptoms

Importantly, the time should be noted on all samples to aid interpretation.

National Institute for Health and Care Excellence. Clinical Guidelines 134, Anaphylaxis: assessment and referral after emergency treatment. December 2011.

Truhlar A, Deakin C, Soar J et al. European Resuscitation Council Guidelines for Resuscitation 2015 Section 4. Cardiac arrest in special circumstances ; Resuscitation 95 (2015) 148–201.