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112 Textbook of Diagnostic and Therapeutic Procedures in Allergy
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profile for each patient with a serum or plasma sample of only 30 μL. The Microtest Allergy System
(Microtest Diagnostics), another automated microarray platform for allergy diagnostics, has recently
become available. Using a 100 μL serum or plasma sample, specific IgE against 19 extracts and
16 components of 22 common allergen sources can be identified (Williams et al. 2016; Onell
et al. 2017).
In clinical practice, when CRD is performed, it is usually through single test assays, and
clinicians decide which allergen component should specifically be looked at. While CRD by means of
microarrays is reprimanded to be too complex and detailed. SPT, on the other hand, is advantageous
in terms of providing information on the biological function of the antibody in question.
In recent years, the development of allergen panels oriented to different types of allergies
(e.g., food vs. respiratory allergy), age (e.g., pediatric vs. adult), and geographic region
(e.g., northern vs. southern Europe) has become the subject of discussion. Such an approach has
already, to some extent, been adopted by commercial providers, although mainly focusing on
extracts rather than individual molecular components.
Indications of CRD
CRD is of little use when there is a convincing history of IgE-mediated allergy and a positive SPT
or specific IgE to the relevant whole food allergen, as this information is already enough to make a
diagnosis. However, CRD is useful in the following situations:
1) when there are low abundant and/or labile food proteins in conventional allergy tests;
2) to provide information on risk or severity associated with molecules;
3) to provide indicators of food-related cross-reactivity;
4) markers of genuine (species-specific) sensitization;
5) to predict the outcome of oral immunotherapy for food (under research).
Other indications in which CRD may be useful include idiopathic anaphylaxis, delayed red
meat anaphylaxis and wheat-dependent exercise-induced anaphylaxis to differentiate between
high versus low-risk molecules from foods giving rise to food-induced anaphylaxis (peanuts, nuts,
shrimps, etc.), baked egg or milk allergy (ovomucoid, casein), etc.
The European Academy of Allergy and Clinical Immunology (EAACI) recently proposed
the so-called “U-shaped” approach: start with the patient’s clinical history, physical examination,
and SPT or specific extract-based IgE testing. CRD should be performed for allergen components
of sources to which the previous diagnostics have detected a clinically relevant sensitization.
Additionally, when IgE sensitization to highly cross-reactive allergens had been found, (a) CRD
diagnostics should be broadened to include molecules of the same family and (b) clinical history
should be expanded by actively investigating for the presence of possible symptoms caused by other
allergen sources of the index protein family (EAACI 2016).
CRD in Food Allergy
CRD has been used in the diagnosis of FA and in specific cases, like soy, peanut and hazelnut
allergy, CRD is able to determine the risk of severity of an allergic reaction. Commonly used food
proteins that have been identified are in the TABLE below.
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Table 3. Commonly used CRP in food allergy.
Food Component Cut-O Level
COW’S MILK
EGG WHITE
PEANUT
* Predicts a severe reaction
Cow’s milk
Bos d 8 (casein)
Egg white
Gal d 1 (ovomucoid)
Gal d 2 (ovalbumin)
Peanut
Ara h 2
Ara h 6
> 24 kU/L for reactivity to baked milk
> 6.6 kU/L for reactivity to baked milk
> 30.7 kU/L for reactivity to boiled egg
> 7.3 kU/L for reactivity to raw egg
> 10.8 kU/L for reactivity to boiled egg
> 5.2 kU/L for reactivity to raw egg
> 29.3 kU/L for reactivity to boiled egg
> 9.8 kU/L for reactivity to raw egg
> 14.9 kU/L
> 1.0 kU/L for severity pf reaction*
> 0.8 kU/L for the severity of reaction
Other Examples
• Ovomucoid and omega-5 gliadin seem to be good diagnostic markers for egg allergy and wheat
allergy respectively.
• The severity of the allergic reaction can be predicted in peanut allergy with Ara h 2.
• In tree nut allergy it was found that other storage proteins, such as Jug r 1 (walnut), Ana o
e (cashew), Ses I 1 (sesame), and Fag e 3 (buckwheat) seem to be better markers of allergic
reactions than the whole allergen extract (Sato et al. 2018).
However, age and geographic differences affect CRD results, and they should always be utilized
in the context of clinical history. In the future, clinical phenotypes may be differentiated with larger
prospective studies utilizing food challenges (Tuano 2015).
Limitations of CRD in Food Allergy
However, in daily practice, CRD has some limitations and is still mainly a research subject. The
main limitations include:
a) Not all allergenic molecules of food proteins are commercially available.
b) Positive results for certain allergenic molecules only suggest the severity of a potential reaction,
but it does not predict it with certainty.
c) Testing positive for specific allergenic molecules does not imply a certain clinical reaction. As
for high positive SPT or high specific IgE for a certain food, the results are only associated with
a higher probability of an allergic reaction after an oral food challenge but do not predict the
results of the challenge.
d) Diagnostic methods can yield different results. The singleplex method provides quantitative
results and it tends to be more precise with respect to the multiplex ones. The latter provides
semi-quantitative results, that could be conflicting, depending on the methodology used
(Calvani 2020).
Conclusion
At present, allergy diagnostics largely rely on clinical history, physical examination, and in vivo
SPT. However, although still a subject of intense research, CRD testing is currently finding its way
into the clinical routine and can offer additional information on the patient’s sensitization profile,
prediction of outcome and treatment responsiveness, mainly on specific immunotherapy.
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Glossary of Abbreviations
SPT – Allergy Skin Prick Test
CRD – Component-Resolved Diagnosis
RIST – Radio-Immunosorbent
FA – Food Allergy
RAST – Radio-Allergosorbent Test
WAO – World Allergy Organization
OFC – Office Food Challenge
OIT – Oral Immunotherapy
Ku/L – Kilo Units Per Liter
References on CRD (Part: II)
Calvani, M., Anania, C., Caffarelli, C., Martelli, A., Miraglia del Giudice, M., Cravidi, C. et al. 2020. Food
allergy: an updated review on pathogenesis, diagnosis, prevention, and management. Acta Biomed.
91(Supplement 11): e202001.
Eiringhaus, K., Renz, H., Matricardi, P. and Skevaki, C. 2019. Component-resolved diagnostics in allergic rhinitis and
asthma. J. Appl. Lab Med. 03(05): 883–898.
European Academy of Allergy and Clinical Immunology. EAACI molecular allergology user’s guide. Pediatric
allergy and immunology. Zurich (Switzerland): EAACI; 2016.
Onell, A., Whiteman, A., Nordlund, B., Baldracchini, F., Mazzoleni, G., Hedlin, G. et al. 2017. Allergy testing in
children with persistent asthma: comparison of four diagnostic methods. Allergy 72: 590–597.
Sato, S., Yanagida, N. and Ebisawa, M. 2018. How to diagnose food allergy? Curr. Opinion Allergy Clin. Immunol.
18: 214 0–221.
Tuano, K. S. and Davis, C. M. 2015. Utility of Component-Resolved Diagnostics in food allergy. Curr. Opinion
Allergy Clin. Immunol. 15(6): 32.
Williams, P., Onell, A., Baldracchini, F., Hui, V., Jolles, S. and El-Shanawany, T. 2016. Evaluation of a novel automated
allergy microarray platform compared with three other allergy test methods. Clin. Exp. Immunol. 184: 1–10. 32.
Chapter 4D
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Eosinophilic Oesophagitis
Marion M. Aw
Introduction
Eosinophilic oesophagitis (EoE) is a chronic disorder of the oesophagus first described in the
mid-1990s. Published data from the West has shown a significant increase in prevalence over the
last two decades with current estimates of 1/2,000 and a male predominance of approximately 3:1
(Mansoor 2016). While EoE is not as prevalent in Asia, there is emerging evidence that EoE would
also be a clinically important condition here.
Pathogenesis
EoE is believed to be triggered by environmental factors in a genetically predisposed individual.
Familial studies demonstrate that concordance in monozygotic twins is 58%, whereas the figure is
closer to 36% in dizygotic twins and only 2.4% in non-twin siblings (Alexander et al. 2014). Twin
cohort analysis reveals a more significant contribution by environmental factors (81%) compared to
genetics (14.5%) (Alexander et al. 2014).
As the normal oesophagus is devoid of eosinophils, EoE is believed to result from a trigger
which leads to inflammation and the migration of eosinophils into the oesophagus. It is not
surprising that genes involved in allergen sensitisation and disruption of epithelial barrier function
have been implicated in this process. Here Th2 cytokines (IL-5 and IL-13), TSLP (thymic stromal
lymphopoietin) and CAPN14 (calpain 14) are thought to have key roles (Kitajima et al. 2011; Litosh
et al. 2017; O’Shea et al. 2018).
EoE has also been seen in association with genetic conditions, such as connective tissue
disorders with hypermobility (e.g., Ehlers-Danlos syndrome, Loeys-Dietz syndrome), autoimmune
conditions (e.g., Hashimoto’s thyroiditis, coeliac disease) and a number of other syndromes
(e.g., Hyper-IgE syndrome, severe atopy associated with metabolic wasting (SAM) syndrome,
Netherton’s syndrome) (O’Shea et al. 2018). The oesophageal inflammation in EoE leads to
remodelling and fibrosis, resulting in oesophageal rigidity and dysfunction. Untreated, EoE is a
progressive fibro stenotic condition with stricture formation as a complication (Dellon et al. 2014).
The diagnosis of EoE is a clinicopathological one (Dellon et al. 2018). That is the presence of
histologic criteria in a child with clinical features consistent with the disease. Symptoms
National University, Singapore.
Email: paesawm@nus.edu.sg
Clinical Presentation
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experienced are a result of oesophageal dysfunction. Typical clinical symptoms are similar to that
of gastroesophageal reflux disease (GERD) with vomiting and pain. Infants and young children
may also present with feeding difficulties, feed refusal and failure to thrive. The older child and
adolescent may manifest with dysphagia, epigastric or chest pain and PPI-dependent or resistant
GERD. The clinical presentation in the adolescent patient is closer to what one may encounter in
adult patients with EoE (Liacouras et al. 2005).
Often, one would need to take a careful feeding and/or eating history, as symptoms of dysphagia
may be subtle in children. These include selective or picky eating in order to avoid troublesome
foods, taking a long time to chew and swallow food and having to drink a fair amount of water or
liquid at mealtimes. As EoE is an immunologic disease associated with food allergy, the presence of
a personal history of atopy or a family history of atopic and allergic disease (such as eczema, asthma,
and allergic rhinitis) should raise the suspicion that EoE could be the underlying cause of what may
otherwise appear to be GERD in an infant or child. The physical examination in children with EoE
is often normal. Features of atopy (eczema and allergic rhinitis) and nutritional consequences (pallor
and poor growth) should be actively looked for.
Investigations for EoE
Discussions and referral to a paediatric gastroenterologist would be useful. As EoE is a
clinicopathological diagnosis, endoscopy with biopsy should be performed in any child suspected
to have EoE. There are typical endoscopic features of EoE. These include the appearance of white
exudates, linear grooves or furrows and concentric rings in the oesophagus (Hirano et al. 2013). As
the endoscopic appearance of the oesophagus may be normal in as many as 10–25% of children with
EoE and the histologic involvement patchy, multiple biopsies are usually taken. The endoscopist
would usually take biopsies from the lower, mid and upper oesophagus (Liacouras et al. 2011). The
presence of ≥ 15 eosinophils per high-power field, seen only in the oesophagus, is required to make a
diagnosis of EoE. Additional supportive histological features include eosinophilic micro-abscesses,
surface layering of eosinophils, extracellular eosinophilic granules, basal cell hyperplasia, dilated
intercellular spaces and lamina propria fibrosis (Liacouras et al. 2011). There are a number of other
clinical conditions that can result in oesophageal eosinophilia. These include parasitic infections,
hyper-eosinophilic syndrome and inflammatory bowel disease to name a few (Dellon et al. 2018).
In most instances, the clinical presentation and features would be distinguishable from those of EoE.
Treatment aims to induce remission of inflammation and prevent long-term complications. As food
allergy is thought to be a key trigger of EoE in children, elimination of the offending food would be
the mainstay of treatment. Other modalities include pharmacological therapy. When complications
of strictures occur, mechanical dilation of the oesophagus would be required.
Diet
There are several strategies for food elimination in children with EoE. These include the use of
an elemental diet, an empiric elimination diet or a targeted elimination diet. Infants in whom milk
can be the sole source of nutrition could be placed on an amino acid-based milk formula. Doing so
can achieve a high rate of clinical, endoscopic and histological improvement (Arias et al. 2014).
The challenge thereafter would be maintaining this remission when solids and other food are
reintroduced back into the diet.
The first food eliminated is usually cow’s milk protein. However, a six-food elimination diet
(dairy, soy, eggs, wheat, peanuts/tree nuts and fish/shellfish) or a four-food elimination diet (dairy,
eggs, wheat and soy) can also be considered in infants and older children (Arias et al. 2014) in
Management
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whom there is no clear-cut offending food. In instances when a diet history may shed some light as
to possible offending foods, skin prick tests (SPT) and atopy patch tests (APT) may be performed
to help guide a targeted elimination diet approach. The choice of foods for the six- and four-food
elimination diets are based on the most common food triggers in Caucasian populations. As the
spectrum of food allergens may differ between countries and populations, the empiric elimination
diet would need to be tailored to take that into account. For example, in Spain, legumes were found
to be the fourth most common food allergen (Lucendo et al. 2013). Hence the four-food elimination
diet in Spain would include diary, eggs, wheat and legumes (which comprise beans, peas, peanuts
and soy). A study from Iran demonstrated that the most common sensitised foods on SPT were
sesame and walnut (Momen et al. 2018).
Drugs
The first line of pharmacology therapy would be the use of a Proton Pump Inhibitor (PPI),
which induces clinical and histologic remission in over 50% of patients (Lucendo et al. 2016).
PPI-responsive EoE (previously known as PPI-responsive oesophageal eosinophilia) is now
considered a sub-phenotype of EoE.
Other pharmacologic options include the use of topical corticosteroids (fluticasone propionate
delivered via metered dose inhaler or oral viscous budesonide) (Table 2) (Furuta and Katzka 2015).
A recent meta-analysis demonstrated the effectiveness of topical steroids in providing symptom
resolution and decreasing oesophageal eosinophilia (Murali et al. 2016). Patients should be
counselled not to eat or drink for 30–60 minutes following swallowing the medication. As symptoms
often recur on stopping medications, treatment is generally long-term. The principles for long-term
treatment include the use of the lowest possible doses of topical steroids with periodic endoscopic
assessment. A number of biologic agents (monoclonal antibodies against various cytokines) have
been trialled. However, none are sufficiently effective to be considered part of the therapeutic
armamentarium currently.
Table 1. EoE diagnostic criteria (Dellon et al. 2018).
1. Clinical symptoms of oesophageal dysfunction
2. Presence of concomitant atopic features
3. Typical or suggestive endoscopic appearance
4. ≥ 15 eosinophils per high-power eld, seen only in the oesophagus
5. Exclusion of other causes of oesophageal eosinophilia
Table 2.
Steroid therapy in EoE.
Topical Corticosteroid Age group Dose
Fluticasone via MDI Child 220–440 mcg bd
Adolescent 440–880 mcg bd
Oral viscous budesonide Child 0.25–0.5 mg bd
Adolescent 1–2 mg bd
Endoscopic Dilatation
Endoscopic dilation is reserved for when complications of oesophageal stenosis and stricture are
present. This would need to be coupled with management to prevent ongoing inflammation of the
oesophagus.
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Disease Monitoring
Symptom resolution usually indicates a reduction in oesophageal inflammation. However, this
may not always be so, and endoscopic assessment with biopsies would invariably be required to
determine the histologic resolution of oesophageal eosinophilia and inflammation. Children with
EoE often undergo multiple endoscopies. In order to maximise the clinical information obtained
at each procedure, the indication and timing would need to be discussed carefully between the
managing clinicians (paediatric gastroenterologist and allergist) as well as parents/patient.
Coeliac Disease in Children
Clinical Presentation
Coeliac disease (CD) is an immune-mediated chronic condition that occurs in genetically
predisposed individuals (Husby et al. 2020). It presents in many different ways with gluten exposure
being a prerequisite. Traditionally, children with CD manifest features of malabsorption dominated
by diarrhoea, steatorrhea, weight loss or failure to thrive. However, CD can also present with
gastrointestinal (GI) symptoms similar to that of irritable bowel syndrome (IBS) as well as non-GI
symptoms (Table 3).
The diagnostic challenge for clinicians is to distinguish CD from other gluten-related conditions
(Figure 1), particularly when the symptoms are not classic or typical. In addition, CD would also
need to be distinguished from children with functional bowel disorders (i.e., IBS). In general,
children with CD have more extra-intestinal manifestations (EIMs) (62%) than those with functional
disorders (33%). The most common EIMs in children with CD are poor growth (27%) and anaemia
(18%) (Nurminen et al. 2019).
Table 3. Symptoms of CD and indications for testing.
GI Symptoms Extra-Intestinal Symptoms Others
Typical
Chronic diarrhoea
Recurrent abdominal pain
Less Typical
Chronic constipation not
responding to usual treatment
Recurrent nausea, vomiting
Aphthous ulcers
Typical
Faltering growth
Short stature
Other Symptoms
Dermatitis herpetiformis
Iron deciency anaemia
Delayed puberty
Fatigue
Headaches
Irritability
Abnormal liver tests
Dental enamel defects
Figure 1. Gluten-related disorders.
First-degree relatives with CD
Autoimmune conditions
IgA deciency
Down syndrome
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Investigations for CD
Updated guidelines for the diagnosis of CD in children were published in 2020 (Husby et al. 2020).
Indications to considering testing for CD are shown in Table 1. First-line investigation (regardless of
symptoms) would be total IgA and anti-tissue transglutaminase (TGA) IgA, done whilst the child is
still taking a gluten-containing diet. Children, who have a high serum TGA-IgA (≥ 10x ULN) and a
positive Endomysial antibody (EMA)-IgA in a second blood sample, may be diagnosed to have CD
without the need to undergo a small bowel biopsy. This diagnostic approach without tissue biopsy
should be discussed with the parent/patient.
In children who are IgA deficient, an IgG-based test (DGP, deamidated gliadin peptide, EMA,
TGA) can be performed. Children with an elevated TGA-IgA (< 10x ULN) and IgA deficient
children with IgG-positive serological tests should undergo a small biopsy in order to make an
accurate diagnosis.
HLA-typing is not recommended as a test to “rule in” the diagnosis of CD. A negative
HLA-DQ2/DQ8 means the risk of CD is very low, whereas a positive result does not confirm the
diagnosis.
Management
The treatment for children with CD would be a gluten-free diet. Parents and patients need to be
taught to read food labels. Advice from a dietician would be helpful to ensure nutritional adequacy.
Follow up for children with CD is life-long.
Glossary of Abbreviations
ATP – Atopy Patch Tests
CD – Coeliac Disease
DGP – Deamidated Gliadin Peptide
EoE – Eosinophilic Oesophagitis
EMA – Endomysial Antibody
EIM – Extra-Intestinal Manifestations
GERD – Gastro-Oesophageal Reflux Disorder
HLA – Human Leucocyte Antigen
IBS – Irritable Bowel Syndrome
PPI – Proton Pump Inhibitor
SPT – Skin Prick Test
TGA – Transglutaminase
ULN – Upper Limits of Normal
References
Alexander, E. S., Martin, L. J., Collins, M. H., Kottyan, L., Sucharew, H., Hua He, M. S. et al. 2014. Twin and family
studies reveal strong environmental and weaker genetic cues explaining heritability of eosinophilic esophagitis.
J. Allergy Clin. Immunol. 134: 1084–92.
Arias, A., Gonzalez-Cervera, J., Tenias, J. M. and Lucendo, A. J. 2014. Efficacy of dietary interventions for
inducing histologic remission in patients with eosinophilic esophagitis: a systematic review and meta-analysis.
Gastroenterology 146: 1639–48.
Dellon, E. S., Kim, H. P., Sperry, S. L., Rybnicek, D. A., Woosley, J. T. and Shaheen, N. J. 2014. A phenotypic
analysis shows that eosinophilic esophagitis is a progressive fibrostenotic disease. Gastrointestinal Endoscopy
79: 577–85.
Dellon, E. S., Liacouras, C. A., Molina-Infante, J., Furuta, G. T., Spergel, J. M., Zevit, N. et al. 2018. Updated
International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE
Conference. Gastroenterology 155: 1022–1033.
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Furuta, G. T. and Katzka, D. A. 2015. Eosinophilic esophagitis. N Engl. J. Med. 2015 October 22;
373(17): 1640–1648.
Hirano, I., Moy, N., Heckman, M. G., Thomas, C. S., Gonsalves, N. and Achem, S. R. 2013. Endoscopic assessment
of the oesophageal features of eosinophilic oesophagitis: validation of a novel classification and grading system.
Gut 62: 489–495.
Husby, A., Koletzko, S., Korponay-Szabo, I., Kurppa, K., Mearin, M. L., Ribes-Koninckx, C. et al. 2020. European
society paediatric gastroenterology, hepatology and nutrition guidelines for diagnosing coeliac disease. J. Pediatr
Gastroenterol. Nutr. 70: 141–157.
Kitajima, M., Lee, H. C., Nakayama, T. and Ziegler, S. F. 2011. TSLP enhances the function of helper type 2 cells.
Eur. J. Immunol. 41: 1862–71.
Liacouras, C. A., Spergel, J. M., Ruchelli, E., Ruchelli, E., Verma, R., Mascarenhas, M. et al. 2005. Eosinophilic
esophagitis: A 10-year experience in 381 children. Clin. Gastroenterol. Hepatol. 3(12): 1198–1206.
Liacouras, C. A., Furuta, G. T., Hirano, I., Atkins, D., Attwood, S. E., Bonis, P. A. et al. 2011. Eosinophilic esophagitis:
Updated consensus recommendations for children and adults. J. Allergy Clin. Immunol. 128: 3–20.
Litosh, V. A., Rochman, M., Rymer, J. K., Porollo, A., Kottyan, L. C. and Rothenberg, M. E. 2017. Calpain-14 and its
association with eosinophilic esophagitis. J. Allergy and Clin. Immunol. 139(16): 1762–1771.
Lucendo, A. J., Arias, A., Gonzalez-Cervera, J., Yagüe-Compadre, J. L., Guagnozzi, D., Angueira, T. et al. 2013.
Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic
esophagitis: A prospective study on the food cause of the disease. Journal of Allergy and Clinical Immunology
131(3): 797–804.
Lucendo, A. J., Arias, A. and Molina-Infante, J. 2016. Efficacy of proton pump inhibitor drugs for inducing clinical
and histologic remission in patients with symptomatic esophageal eosinophilia: a systematic review and
meta-analysis. Clin. Gastroenterol. Hepatol. 14: 13–22.
Mansoor, E. and Cooper, G. S. 2016. The 2010–2015 prevalence of eosinophilic esophagitis in the USA:
A population-based study. Dig Dis Sci. 61: 2928–34.
Momen, T., Saneian, H. and Amini, N. 2018. Demographic, clinical, and allergic characteristics of children with
eosinophilic esophagitis in Isfahan, Iran. Iran J. Allergy Asthma Immunol. 17(6): 533–539.
Munoz-Persy, M. and Lucendo A. J. 2018. Treatment of eosinophilic esophagitis in the pediatric patient: an
evidence-based approach. Eur. J. Pediatr 2018 May; 177(5): 649–663.
Murali, A. R., Gupta, A., Attar, B. M., Ravi, V. and Koduru, P. 2016. Topical steroids in eosinophilic esophagitis:
systematic review and meta-analysis of placebo-controlled randomized clinical trials. J. Gastroenterol. Hepatol.
31(6): 1111–9.
Nurminen, S., Kivela, L., Huhtala, H., Kaukinen, K. and Kurppa, K. 2019. Extraintestinal manifestations were
common in children with coeliac disease and were more prevalent in patients with more severe clinical and
histological presentation Acta Paediatr. 2019 Apr; 108(4): 681–687.
O’Shea, K. M., Aceves, S. S., Dellon, E. S., Gupta, S. K., Spergel, J. M., Furuta, G. T. et al. 2018. Pathophysiology
of eosinophilic esophagitis. Gastroenterology 154(2): 333–345.
Chapter 5
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Acute and Chronic Urticaria/Angioedema
Vinay Mehta
Introduction
Urticaria is a common disorder with a lifetime prevalence of approximately 20% in the general
population (Greaves 1995). Acute urticaria (lasting < 6 weeks) is more common in children and
adolescents whereas chronic urticaria (lasting > 6 weeks) is more common in adults (Bernstein
et al. 2014). Chronic urticaria affects up to 1% of the general population, with women affected
twice as frequently as men, and the onset typically in the third to fifth decades of life (Zuberbier
et al. 2010). It is a potentially disabling condition that can lead to substantial impairment of quality
of life (O’Donnell et al. 1997). Furthermore, psychosocial factors such as anxiety, depression and
poor sleep are present in half of the population (Ben-Shoshan et al. 2013).
Hives are pruritic, circumscribed, raised, erythematous lesions, often with central pallor
(Photo 1). They can vary in size and shape. Hives are transient in duration, usually appearing over
minutes to hours, then disappearing within 24 hours. They may appear flattened if the patient is
taking antihistamines. Although there is a predilection for pressure-prone areas such as the waist,
axilla and groin, hives can occur anywhere on the skin.
Concurrent angioedema may occur and is characterized by subcutaneous or submucosal
swelling affecting nondependent areas, most commonly the lips, cheeks, eyelids, extremities and
genitals (Photo 2). Angioedema typically develops over minutes to hours and resolves over one to
three days. Affected areas typically feel painful, numb or tingling (Zuberbier et al. 2022).
Photo 1. Hives. Source: Attribution details, CC BY 4.0 via Wikimedia Commons; https://commons.wikimedia.org/wiki/
Allergy & Asthma Associates of Southern California, Irvine, CA, USA and Mission Viejo, CA, USA.
Email: drvinaymehta@gmail.com
File:Chronic_spontaneous_urticaria.jpg.
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