http://informahealthcare.com/pgm ISSN: 0032-5481 (print), 1941-9260 (electronic) Postgrad Med, 2015; Early Online: 1–6 DOI: 10.1080/00325481.2015.1045817
CLINICAL FOCUS: ADHD, ALLERGIES AND IMMUNIZATIONS ORIGINAL RESEARCH
Physical urticaria: Review on classification, triggers and management with special focus on prevalence including a meta-analysis Jordan Trevisonno1, Bhairavi Balram1, Elena Netchiporouk2 and Moshe Ben-Shoshan 3 Postgraduate Medicine Downloaded from informahealthcare.com by Nyu Medical Center on 06/01/15 For personal use only.
1
Department of Medicine, McGill University, Montreal, QC, Canada, 2Division of Dermatology, Montreal Children’s Hospital, Montreal, QC, Canada, and 3Department of Paediatrics, Montreal Children’s Hospital, Montreal, QC, Canada
Abstract
Keywords
Background. Physical urticaria (PU) is a subset of chronic urticaria (CU) induced by physical stimuli. To date, there is no consensus in the literature on the prevalence of PU among patients with CU. Objectives. Our objective was to review the clinical presentation, diagnosis and management of PU and to estimate the prevalence of PU in CU patients. Methods. We performed a narrative review of PU and conducted a systemic review and meta-analysis to determine the pooled estimates of the prevalence of PU among patients with CU in the literature up to September 2014. We searched four databases (PubMed, Ovid MEDLINE and Web of Science) of published work for which full text was available in English or French. Studies were eligible if they measured the prevalence of PU in adults or children with CU worldwide and ineligible if CU cases were not differentiated from total urticaria cases. Meta-analysis was conducted using Stata, version 12.0 (StataCorp, College Station, TX). In addition, the quality and validity of the articles included in the meta-analysis was assessed. Results. Ten studies were included in our meta-analysis. Sample sizes ranged from 202 to 4157 patients. The pooled prevalence estimate of PU including and excluding cholinergic forms among all cases of CU were 13.1% (95% CI: 12.5, 13.6) and 14.9% (95% CI: 14.3, 15.7), respectively. Conclusion. Our results must be viewed with circumspection because of the small number of eligible articles and heterogeneity among studies. Even so, the results suggest that PU is an important subset of CU and that physicians should be aware of this important condition in order to manage patients appropriately.
Chronic urticaria, cold induced urticaria, meta-analysis, physical urticaria, prevalence, urticaria.
Introduction Urticaria is more commonly referred to as hives, characterized by red, swollen, itchy areas of the skin of different sizes [1]. Chronic urticaria (CU) is defined when an individual presents with transient wheals lasting more than 6 weeks in duration almost daily [2,3]. In most cases of CU a trigger cannot be identified. These cases are defined as chronic spontaneous urticaria. The term inducible urticaria is used when a specific trigger can be linked to the development of CU e.g. contact urticaria [4-6]. Physical urticaria (PU) is a subtype of inducible urticaria that is associated with a specific physical trigger [6,7]. Given that certain forms of PU may have systemic symptoms and may result in fatality, increased awareness, appropriate diagnosis and management of are crucial.
Classification, pathogenesis and diagnosis PUs are classified according to the physical trigger and are diagnosed by the appropriate provocation test that induces wheals and/or angioedema [1,8]. Establishing the diagnosis
History Received 19 February 2015 Accepted 24 April 2015 Published online 9 May 2015
of PU with provocation tests is crucial given that almost a third of patients reporting history suggestive of PU may have negative challenge testing which allows discontinuation of medications and avoidance behavior [9]. The clinical characteristics, diagnostic approach and potential pathogenic mechanisms of the main forms of PU are enlisted below: 1. Dermatographism: Presents as skin whealing occurring at sites of trauma, friction with clothing or scratching [10]. The provocation test consists of moderate stroking of the skin with a blunt smooth object(e.g. closed ballpoint pen tip) and observation for wheals 10 minutes later (Figure 1a) [1]. The pathogenic mechanism is thought to be related to histamine degranulation due to a mechanoimmunologic trigger [11]. 2. Cold-induced urticaria: This form is characterized by localized or diffuse urticaria that could be accompanied by angioedema within minutes after exposure to a cold contact (object, air or liquid) [12]. It may evolve to systemic symptoms and anaphylaxis with extensive cold contact like swimming in cold water in up to one third of children.
Correspondence: Moshe Ben-Shoshan, Department of Paediatrics, Montreal Children’s Hospital, Montreal, QC, Canada. E-mail: [email protected] 2015 Informa UK Ltd.
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Postgrad Med, 2015; Early Online:1–6
a
b
c
d
Figure 1. (a) Dermatographism. (b) Hand swelling and hives after cold exposure. (c) Positive ice cube test on same patient. (d) Hives developing 6 hours after pressure applied on shoulder.
Given that fatality has been reported in several cases, prompt diagnosis is crucial [12,13]. The diagnosis is established when wheals reproduce after contact for 5 minutes with an ice cube (in a thin plastic bag) placed on the volar aspect of the arm (Figure 1b and c). More accurate provocation testing could be conducted with the aid of computer-aided thermoelectric Peltier device [14]. Rare hereditary (autosomal-dominant) autoinflammatory conditions may present with cold-induced whealing (with negative ice cube test) [15,16] including rare cases of phospholipase Cg2 gene mutations and mutations in coldinduced auto-inflammatory syndrome-1 gene [17-20]. It is suggested that an autoimmune mechanism involving interaction of IgE autoantibodies with a cold-dependent skin antigen plays a major role in the development of coldinduced urticaria [12]. In addition, it was shown that patients with active cold-induced urticaria have circulating histamine-releasing factors and positive autologous serum skin test (ASST) [21]. 3. Solar urticaria: This is a less common form of urticaria that occurs following exposure to light. It is hypothesized that a photo allergen produced by sun exposed skin cross-reacts with IgE located on mast cells and leads to the release of histamine and other inflammatory mediators. Some forms of solar urticaria can be diagnosed by exposure to visible light (projector) for 15 minutes [8], although other forms may require more sophisticated testing [22]. 4. Vibratory urticaria: Vibratory urticaria is defined by the presence of skin swellings and itching after exposure to vibration at the contact site. This form can be diagnosed with the use of a vortex vibrator for 10 miniutes (1000 r.p.m.) [16]. 5. Delayed pressure urticaria: this type of PU is characterized by wheals/angioedema that develop 4 to 6 h after applying any type of pressure such as wearing tight clothing, hammering, walking or sitting down [23]. The diagnosis is
confirmed when wheals develop about 6 hours after suspension of 7 kg weight (3 cm strap width) over the shoulder (Figure 1d). It has been suggested that non-immunologic mechanisms and several mediators beyond histamine, such as proinflammatory cytokines may play a role in mast cell activation. 6. Heat contact urticaria is diagnosed when wheals develop 10 minutes after contact with a heat source (450C) for 5 minutes. 7. Aquagenic urticaria: Wheals generally affect the upper part of the body and are induced by water. The pathogenic mechanisms are not known [24,25]. Aquagenic challenge test (applying a water-drenched compress at bodily temperature during 20 minutes) is used to establish the diagnosis [24]. Cholinergic urticaria, an inducible form of CU presenting as itchy pinpoint lesions measuring 1–3 mm (Figure 2) [26], was previously classified as PU. However, recently the EAACI/GA2LEN (European Academy of Allergology and Clinical Immunology, the Global Allergy and Asthma European Network) task force consensus report defines cholinergic urticaria as a separate entity of inducible urticaria given that it is triggered by elevated core body temperature and not necessarily by an exogenous trigger (Figure 2) [27-29]. The diagnosis is established when lesions occur reproducibly with exercise and with passive warming and rest, such as might occur in a steam bath or hot pool [15]. It has been suggested that certain forms of cholinergic urticaria result from impaired muscarinic cholinergic receptors [30].
Figure 2. Cholinergic urticaria manifestation as pinpoint lesions after exercise.
Physical urticaria
DOI: 10.1080/00325481.2015.1045817
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The prevalence of physical urticaria To assess the prevalence of PU, we conducted a systematic review with a meta-analysis for relevant studies assessing the prevalence of PU among all cases of CU and evaluating the effect of environmental temperatures on the prevalence of cold induced urticaria.
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Methods A search of the literature was conducted using electronic literature databases PubMed, OVID Medline and Web of Science all from inception (without date limitations) through 1 July 2014, using the following terms: ‘PU’, ‘inducible urticaria’ and ‘prevalence’. Studies in English and French were included. Studies that were included provide a quantitative assessment of the prevalence of PU and/or the types of PU in children and/adults. A meta-analysis was conducted of studies that report the prevalence of PU among those with CU, and the prevalence of the different subtypes of PU. Prevalence data were extracted from the article’s tables or text. Additional data that were collected include the author name, study location, sample size, sample collection period and collecting method. A 95% confidence interval was calculated and the I2 value (the variation in effect size that is attributable to heterogeneity) was calculated as well. Univariate and mutivariate linear regression was used to assess potential confounders and evaluate the association between the average January temperature, latitude and the prevalence of cold forms. All coefficients are presented with 95% CIs. A two-sided p-value < 0.05 was considered statistically significant. Stata, version 12.0. and R version 2.12.0 (2010-10-15) were used to conduct all statistical analysis. In order to assess the quality of the aforementioned studies, we employed a standardized measure specifically tailored to this systematic review, based on the Newcastle-Ottawa Scale [31] and in compliance with PRISMA guidelines for systematic reviews. This approach included the appraisal of external and internal validity. We have aimed to assess specifically if the study was representative of the population and whether the participation rate of the study was disclosed. In addition, we evaluated if biases common to observational studies specific to CU were assessed including the use of clear definitions of PU and physical triggers, the completeness of the study, selection biases (age, sex, presence of atopy, the presence of an autoimmune disease and use of ASST or basophil activation [32,33] to assess autoreactivity). The independent reviewers (JT and MBS) evaluated study quality separately, and resolved differences in opinion by consulting a third reviewer (EN).
Figure 3. Flow chart for studies included. Abbreviations: CU = Chronic urticaria; PU = Physical urticaria.
the first estimate included participants with cholinergic urticaria and the second excluded cases of cholinergic urticaria (Figure 4a and b) [34-40]. The pooled estimate of the prevalence of PU using the fixed effects model (including cholinergic urticaria) was calculated to be 13.1% (95% CI: 12.5, 13.6). For cases of PU excluding cholinergic forms the pooled estimate was 14.9% (14.3, 15.7). The I2 (the variation in effect size that is attributable to heterogeneity) was 98.8% and 98.2%, respectively. The majority of these studies failed a
b
Findings Ten studies fulfilled the inclusion criteria of our search and were included in the study (Figure 3). Sample sizes ranged from 202 to 4157 patients. Given that early studies have considered cholinergic urticaria as a form of PU, we have conducted two separate pooled prevalence estimates of PU;
Figure 4. (a) Prevalence (in percentage) of physical urticaria (PU) in patients with chronic urticaria (CU) (including cholinergic froms). (b) Prevalence (in percentage) of PU in patients with CU (excluding cholinergic froms).
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Table 1. Methodological quality of studies. External validity
Internal validity
Detection
Attrition
Selection bias/control for confounding factors
Study
Exclusion Representative Participation Clear rate definition of cases without of PU identifiable trigger
Presence Completeness Age Sex Presence of Presence of Use of autoimmune autoreactivity* of atopy validated diseases measure to define PU
Champion Ferrer Katsarou-Katsari Kozel Kulthanan Nettis Sibbald Silpa-archa Small Zhong
ü ü ü ü ü ü ü ü ü ü
NS ü ü ü ü ü ü ü NS NS
NS NS NS NS NS NS NS NS NS NS
ü ü ü ü ü ü ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
NS NS NS NS NS NS NS NS NS NS
ü ü ü ü
ü ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
*Defined by the use of autologous serum skin test (ASST) or basophil activation [32,33] to assess autoreactivity. Abbreviation: NS = Not specified. Table 2. Cold-induced urticaria among all cases of PU. Study Country City
Latitude
Average temperature in January
Percent of cold urticaria among all PU cases
SE
Champion Ferrer Kozel Kulthanan Nettis Sibbald Silpa-archa Small
52.12 42.45 52.22 13.45 41.07 43.42 13.45 45.3
4.45 5 3.4 27.6 8.8 -4 27.6 -9.2
13.8 28.2 14.3 20.5 7.9 18.6 25.0 100.0
1.8 7.2 3.8 6.5 3.1 4.7 4.8 0
UK Spain Netherland Thailand Italy Canada Thailand Canada
Cambridge Navarra Amsterdam Bangkok Bari Toronto Bangkok Montreal
*Excluding studies not limited to one geographic location and studies not differentiating cholinergic from other PU forms.
to control for potential confounds such as presence of autoreactivity and have failed to report the use of validated measures to define PU (Table 1). Given the potential life-threatening nature of cold-induced forms, we assessed specifically the prevalence of cold induced forms (Table 2). The prevalence of cold urticaria among patients with PU varied greatly with some studies citing a prevalence of less than 10% and others of almost 100%. Further, studies conducted in countries with similar climate conditions did not report comparable prevalence estimates of cold induced urticaria (Table 2). Multivariate regression analysis adjusting for latitude and average January temperature revealed that lower average temperatures in January were associated with higher prevalence of cold urticaria (adjusted b= -0.034(95% CI: -0.068, -0.001). Management of PU Treatment for all cases of PU is based primarily on removal or avoidance of causes and/or aggravating factors of urticaria. In addition, medications mainly second-generation anti-histamines may help control symptoms when complete avoidance is impossible [41]. In contrast to spontaneous forms of CU, certain forms of cold induced PU may be life-threatening and require prescription of an epinephrine auto-injector [42,43]. Although no fatalities were described with aquagenic urticaria, its management is especially challenging. Treatment with antihistamines, ultraviolet therapy or application of
protective hydrophobic barrier creams may be effective [25]. Recent case reports suggest that some forms of PU may respond to Omalizumab, a monoclonal anti-IgE antibody. However, larger randomized controlled trials are needed to establish its effect [23,44]. Although avoidance of the physical triggers often provides adequate control of PU, studies suggest that PU is less likely to resolve over time compared to chronic spontaneous forms (16% after 1 year versus almost 50%) [45,46]. Conclusion and future directions PU is the most common form of CU of known etiology [47], and is associated with poor quality of life, substantial psychosocial morbidity [35,48,49] and life threatening reactions [42]. Our review is the first to assess the pooled estimate of PU. Our results reveal that PU affects 6% to 30% of all patients with CU and that 8% to 100% of PU cases are triggered by cold. However, heterogeneity of studies (as reflected by high I2) precludes conclusive estimates. Recently, the World Allergy Organization, recognizing the importance of PU, has published a position paper for the diagnosis and management of all form of urticaria [8]. Given that cold-induced urticaria may be life-threatening and require the use of an epinephrine auto-injector [42,43,50], it is especially important to diagnose this form of PU. Extreme weather conditions are expected to contribute to the development of cold urticaria [36]. Indeed the highest prevalence of
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DOI: 10.1080/00325481.2015.1045817
cold-induced forms was reported in Montreal (that has the lowest average temperature in January compared to other cities in this analysis) and we have found a significant reverse association between the average January temperature and the prevalence of cold-induced forms. Our meta-analysis has some potential limitations. An evident weakness of this study is that there are very few papers discussing PU in the literature. In addition, over the last decade, methodologies and diagnostic approaches regarding the diagnosis of PU have changed substantially and could have resulted in misclassification bias. Hence earlier studies that have not used recently published confirmatory tests for the diagnosis of PU [1] might have over or underestimated the prevalence of PU. It is also possible that the prevalence of PU among all cases of CU is underestimated because less severe cases may not come to medical attention or may be treated by primary care providers and thus under-reported. However, we expect this misclassification to be nondifferential. Finally, the association we have found between cold urticaria and temperature may be related to ecological fallacy that occurs when conclusions about individuals are based only on analyses of group data [51]. Hence, it is possible that individual exposure to cold stimuli such as swimming regardless of the weather conditions may trigger cold-induced forms. Given that appropriate clinical history is the first essential step in the diagnosis of PU and given the fatality potential of PU, high level of awareness of family physicians, general practitioners and pediatricians, that are likely to have the first encounter with the patient as well as dermatologists and allergists (to which these patients are usually referred), is crucial. An accurate initial assessment of PU can aid to obtain a better symptom control, improve patients’ quality of life, contribute to patient education and enhance accessibility to more effective therapies. Increased awareness to this subset of potentially debilitating conditions can be of particular importance for the management of children and adults living in northern latitudes given the extremes of weather conditions and given that individuals engaged in winter sports such as ice-hockey players and speed skaters [52], are especially prone to the development of certain types of PU [12,53].
Declaration of interest M Ben-Shoshan is the recipient of the Emerging Clinician Scientist award and the Fonds de la recherche en sante du Quebec (FRSQ) junior 1 award and the emerging clinician scientist fellowship awarded by the Allergy, Genes, and Environment Network of Centres of Excellence (AllerGen NCE). M Ben-Shoshan serves as a consultant for Sanofi and Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
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[40] Sibbald RG, Cheema AS, Lozinski A, Tarlo S. Chronic urticaria. Evaluation of the role of physical, immunologic, and other contributory factors. Int J Dermatol 1991;30:381–6. [41] Zuberbier T, Bindslev-Jensen C, Canonica W, Grattan CE, Greaves MW, Henz BM, et al. EAACI/GA2LEN/EDF guideline: definition, classification and diagnosis of urticaria. Allergy 2006; 61:316–20. [42] Mazarakis A, Bardousis K, Almpanis G, Mazaraki I, Markou S, Kounis NG. Kounis syndrome following cold urticaria: the swimmer’s death. Int J Cardiol 2014;176:e52–3. [43] Kursbaum A, Spalter L, Ben-Assuly S. A dramatic presentation of primary idiopathic cold urticaria. Harefuah 1983;104:393–4. [44] Metz M, Altrichter S, Ardelean E, Kessler B, Krause K, Magerl M, et al. Anti-immunoglobulin E treatment of patients with recalcitrant physical urticaria. Int Arch Allergy Immunol 2011;154:177–80. [45] Kozel MM, Sabroe RA. Chronic urticaria: aetiology, management and current and future treatment options. Drugs 2004; 64:2515–36. [46] Silpa-Archa N, Kulthanan K, Pinkaew S. Physical urticaria: prevalence, type and natural course in a tropical country. J Eur Acad Dermatol Venereol 2010;25:1194–9. [47] Sackesen C, Sekerel BE, Orhan F, Kocabas CN, Tuncer A, Adalioglu G. The etiology of different forms of urticaria in childhood. Pediatr Dermatol 2004;21:102–8. [48] Weldon DR. Quality of life in patients with urticaria. Allergy Asthma Proc 2006;27:96–9. [49] Ben-Shoshan M, Blinderman I, Raz A. Psychosocial factors and chronic spontaneous urticaria: a systematic review. Allergy 2013;68:131–41. [50] Fernando SL. Cold-induced anaphylaxis. J Pediatr 2009;154:148. [51] Leon G. 14: From associations to Causation: Deriving Inferences from epidemiologic Studies. Epidemiology. 4 Edition. Philadelphia: Saunders; 2009;227-246. [52] Forward KE, Seabrook JA, Lynch T, Lim R, Poonai N, Sangha GS. A comparison of the epidemiology of ice hockey injuries between male and female youth in Canada. Paediatr Child Health 2014;19:418–22. [53] Tlougan BE, Mancini AJ, Mandell JA, Cohen DE, Sanchez MR. Skin conditions in figure skaters, ice-hockey players and speed skaters: part II - cold-induced, infectious and inflammatory dermatoses. Sports Med 2011;41:967–84.
CLINICAL FOCUS: ADHD, ALLERGIES AND IMMUNIZATIONS ORIGINAL RESEARCH
Physical urticaria: Review on classification, triggers and management with special focus on prevalence including a meta-analysis Jordan Trevisonno1, Bhairavi Balram1, Elena Netchiporouk2 and Moshe Ben-Shoshan 3 Postgraduate Medicine Downloaded from informahealthcare.com by Nyu Medical Center on 06/01/15 For personal use only.
1
Department of Medicine, McGill University, Montreal, QC, Canada, 2Division of Dermatology, Montreal Children’s Hospital, Montreal, QC, Canada, and 3Department of Paediatrics, Montreal Children’s Hospital, Montreal, QC, Canada
Abstract
Keywords
Background. Physical urticaria (PU) is a subset of chronic urticaria (CU) induced by physical stimuli. To date, there is no consensus in the literature on the prevalence of PU among patients with CU. Objectives. Our objective was to review the clinical presentation, diagnosis and management of PU and to estimate the prevalence of PU in CU patients. Methods. We performed a narrative review of PU and conducted a systemic review and meta-analysis to determine the pooled estimates of the prevalence of PU among patients with CU in the literature up to September 2014. We searched four databases (PubMed, Ovid MEDLINE and Web of Science) of published work for which full text was available in English or French. Studies were eligible if they measured the prevalence of PU in adults or children with CU worldwide and ineligible if CU cases were not differentiated from total urticaria cases. Meta-analysis was conducted using Stata, version 12.0 (StataCorp, College Station, TX). In addition, the quality and validity of the articles included in the meta-analysis was assessed. Results. Ten studies were included in our meta-analysis. Sample sizes ranged from 202 to 4157 patients. The pooled prevalence estimate of PU including and excluding cholinergic forms among all cases of CU were 13.1% (95% CI: 12.5, 13.6) and 14.9% (95% CI: 14.3, 15.7), respectively. Conclusion. Our results must be viewed with circumspection because of the small number of eligible articles and heterogeneity among studies. Even so, the results suggest that PU is an important subset of CU and that physicians should be aware of this important condition in order to manage patients appropriately.
Chronic urticaria, cold induced urticaria, meta-analysis, physical urticaria, prevalence, urticaria.
Introduction Urticaria is more commonly referred to as hives, characterized by red, swollen, itchy areas of the skin of different sizes [1]. Chronic urticaria (CU) is defined when an individual presents with transient wheals lasting more than 6 weeks in duration almost daily [2,3]. In most cases of CU a trigger cannot be identified. These cases are defined as chronic spontaneous urticaria. The term inducible urticaria is used when a specific trigger can be linked to the development of CU e.g. contact urticaria [4-6]. Physical urticaria (PU) is a subtype of inducible urticaria that is associated with a specific physical trigger [6,7]. Given that certain forms of PU may have systemic symptoms and may result in fatality, increased awareness, appropriate diagnosis and management of are crucial.
Classification, pathogenesis and diagnosis PUs are classified according to the physical trigger and are diagnosed by the appropriate provocation test that induces wheals and/or angioedema [1,8]. Establishing the diagnosis
History Received 19 February 2015 Accepted 24 April 2015 Published online 9 May 2015
of PU with provocation tests is crucial given that almost a third of patients reporting history suggestive of PU may have negative challenge testing which allows discontinuation of medications and avoidance behavior [9]. The clinical characteristics, diagnostic approach and potential pathogenic mechanisms of the main forms of PU are enlisted below: 1. Dermatographism: Presents as skin whealing occurring at sites of trauma, friction with clothing or scratching [10]. The provocation test consists of moderate stroking of the skin with a blunt smooth object(e.g. closed ballpoint pen tip) and observation for wheals 10 minutes later (Figure 1a) [1]. The pathogenic mechanism is thought to be related to histamine degranulation due to a mechanoimmunologic trigger [11]. 2. Cold-induced urticaria: This form is characterized by localized or diffuse urticaria that could be accompanied by angioedema within minutes after exposure to a cold contact (object, air or liquid) [12]. It may evolve to systemic symptoms and anaphylaxis with extensive cold contact like swimming in cold water in up to one third of children.
Correspondence: Moshe Ben-Shoshan, Department of Paediatrics, Montreal Children’s Hospital, Montreal, QC, Canada. E-mail: [email protected] 2015 Informa UK Ltd.
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a
b
c
d
Figure 1. (a) Dermatographism. (b) Hand swelling and hives after cold exposure. (c) Positive ice cube test on same patient. (d) Hives developing 6 hours after pressure applied on shoulder.
Given that fatality has been reported in several cases, prompt diagnosis is crucial [12,13]. The diagnosis is established when wheals reproduce after contact for 5 minutes with an ice cube (in a thin plastic bag) placed on the volar aspect of the arm (Figure 1b and c). More accurate provocation testing could be conducted with the aid of computer-aided thermoelectric Peltier device [14]. Rare hereditary (autosomal-dominant) autoinflammatory conditions may present with cold-induced whealing (with negative ice cube test) [15,16] including rare cases of phospholipase Cg2 gene mutations and mutations in coldinduced auto-inflammatory syndrome-1 gene [17-20]. It is suggested that an autoimmune mechanism involving interaction of IgE autoantibodies with a cold-dependent skin antigen plays a major role in the development of coldinduced urticaria [12]. In addition, it was shown that patients with active cold-induced urticaria have circulating histamine-releasing factors and positive autologous serum skin test (ASST) [21]. 3. Solar urticaria: This is a less common form of urticaria that occurs following exposure to light. It is hypothesized that a photo allergen produced by sun exposed skin cross-reacts with IgE located on mast cells and leads to the release of histamine and other inflammatory mediators. Some forms of solar urticaria can be diagnosed by exposure to visible light (projector) for 15 minutes [8], although other forms may require more sophisticated testing [22]. 4. Vibratory urticaria: Vibratory urticaria is defined by the presence of skin swellings and itching after exposure to vibration at the contact site. This form can be diagnosed with the use of a vortex vibrator for 10 miniutes (1000 r.p.m.) [16]. 5. Delayed pressure urticaria: this type of PU is characterized by wheals/angioedema that develop 4 to 6 h after applying any type of pressure such as wearing tight clothing, hammering, walking or sitting down [23]. The diagnosis is
confirmed when wheals develop about 6 hours after suspension of 7 kg weight (3 cm strap width) over the shoulder (Figure 1d). It has been suggested that non-immunologic mechanisms and several mediators beyond histamine, such as proinflammatory cytokines may play a role in mast cell activation. 6. Heat contact urticaria is diagnosed when wheals develop 10 minutes after contact with a heat source (450C) for 5 minutes. 7. Aquagenic urticaria: Wheals generally affect the upper part of the body and are induced by water. The pathogenic mechanisms are not known [24,25]. Aquagenic challenge test (applying a water-drenched compress at bodily temperature during 20 minutes) is used to establish the diagnosis [24]. Cholinergic urticaria, an inducible form of CU presenting as itchy pinpoint lesions measuring 1–3 mm (Figure 2) [26], was previously classified as PU. However, recently the EAACI/GA2LEN (European Academy of Allergology and Clinical Immunology, the Global Allergy and Asthma European Network) task force consensus report defines cholinergic urticaria as a separate entity of inducible urticaria given that it is triggered by elevated core body temperature and not necessarily by an exogenous trigger (Figure 2) [27-29]. The diagnosis is established when lesions occur reproducibly with exercise and with passive warming and rest, such as might occur in a steam bath or hot pool [15]. It has been suggested that certain forms of cholinergic urticaria result from impaired muscarinic cholinergic receptors [30].
Figure 2. Cholinergic urticaria manifestation as pinpoint lesions after exercise.
Physical urticaria
DOI: 10.1080/00325481.2015.1045817
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The prevalence of physical urticaria To assess the prevalence of PU, we conducted a systematic review with a meta-analysis for relevant studies assessing the prevalence of PU among all cases of CU and evaluating the effect of environmental temperatures on the prevalence of cold induced urticaria.
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Methods A search of the literature was conducted using electronic literature databases PubMed, OVID Medline and Web of Science all from inception (without date limitations) through 1 July 2014, using the following terms: ‘PU’, ‘inducible urticaria’ and ‘prevalence’. Studies in English and French were included. Studies that were included provide a quantitative assessment of the prevalence of PU and/or the types of PU in children and/adults. A meta-analysis was conducted of studies that report the prevalence of PU among those with CU, and the prevalence of the different subtypes of PU. Prevalence data were extracted from the article’s tables or text. Additional data that were collected include the author name, study location, sample size, sample collection period and collecting method. A 95% confidence interval was calculated and the I2 value (the variation in effect size that is attributable to heterogeneity) was calculated as well. Univariate and mutivariate linear regression was used to assess potential confounders and evaluate the association between the average January temperature, latitude and the prevalence of cold forms. All coefficients are presented with 95% CIs. A two-sided p-value < 0.05 was considered statistically significant. Stata, version 12.0. and R version 2.12.0 (2010-10-15) were used to conduct all statistical analysis. In order to assess the quality of the aforementioned studies, we employed a standardized measure specifically tailored to this systematic review, based on the Newcastle-Ottawa Scale [31] and in compliance with PRISMA guidelines for systematic reviews. This approach included the appraisal of external and internal validity. We have aimed to assess specifically if the study was representative of the population and whether the participation rate of the study was disclosed. In addition, we evaluated if biases common to observational studies specific to CU were assessed including the use of clear definitions of PU and physical triggers, the completeness of the study, selection biases (age, sex, presence of atopy, the presence of an autoimmune disease and use of ASST or basophil activation [32,33] to assess autoreactivity). The independent reviewers (JT and MBS) evaluated study quality separately, and resolved differences in opinion by consulting a third reviewer (EN).
Figure 3. Flow chart for studies included. Abbreviations: CU = Chronic urticaria; PU = Physical urticaria.
the first estimate included participants with cholinergic urticaria and the second excluded cases of cholinergic urticaria (Figure 4a and b) [34-40]. The pooled estimate of the prevalence of PU using the fixed effects model (including cholinergic urticaria) was calculated to be 13.1% (95% CI: 12.5, 13.6). For cases of PU excluding cholinergic forms the pooled estimate was 14.9% (14.3, 15.7). The I2 (the variation in effect size that is attributable to heterogeneity) was 98.8% and 98.2%, respectively. The majority of these studies failed a
b
Findings Ten studies fulfilled the inclusion criteria of our search and were included in the study (Figure 3). Sample sizes ranged from 202 to 4157 patients. Given that early studies have considered cholinergic urticaria as a form of PU, we have conducted two separate pooled prevalence estimates of PU;
Figure 4. (a) Prevalence (in percentage) of physical urticaria (PU) in patients with chronic urticaria (CU) (including cholinergic froms). (b) Prevalence (in percentage) of PU in patients with CU (excluding cholinergic froms).
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Table 1. Methodological quality of studies. External validity
Internal validity
Detection
Attrition
Selection bias/control for confounding factors
Study
Exclusion Representative Participation Clear rate definition of cases without of PU identifiable trigger
Presence Completeness Age Sex Presence of Presence of Use of autoimmune autoreactivity* of atopy validated diseases measure to define PU
Champion Ferrer Katsarou-Katsari Kozel Kulthanan Nettis Sibbald Silpa-archa Small Zhong
ü ü ü ü ü ü ü ü ü ü
NS ü ü ü ü ü ü ü NS NS
NS NS NS NS NS NS NS NS NS NS
ü ü ü ü ü ü ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
NS NS NS NS NS NS NS NS NS NS
ü ü ü ü
ü ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
ü ü ü ü
ü ü ü ü ü ü ü ü ü ü
*Defined by the use of autologous serum skin test (ASST) or basophil activation [32,33] to assess autoreactivity. Abbreviation: NS = Not specified. Table 2. Cold-induced urticaria among all cases of PU. Study Country City
Latitude
Average temperature in January
Percent of cold urticaria among all PU cases
SE
Champion Ferrer Kozel Kulthanan Nettis Sibbald Silpa-archa Small
52.12 42.45 52.22 13.45 41.07 43.42 13.45 45.3
4.45 5 3.4 27.6 8.8 -4 27.6 -9.2
13.8 28.2 14.3 20.5 7.9 18.6 25.0 100.0
1.8 7.2 3.8 6.5 3.1 4.7 4.8 0
UK Spain Netherland Thailand Italy Canada Thailand Canada
Cambridge Navarra Amsterdam Bangkok Bari Toronto Bangkok Montreal
*Excluding studies not limited to one geographic location and studies not differentiating cholinergic from other PU forms.
to control for potential confounds such as presence of autoreactivity and have failed to report the use of validated measures to define PU (Table 1). Given the potential life-threatening nature of cold-induced forms, we assessed specifically the prevalence of cold induced forms (Table 2). The prevalence of cold urticaria among patients with PU varied greatly with some studies citing a prevalence of less than 10% and others of almost 100%. Further, studies conducted in countries with similar climate conditions did not report comparable prevalence estimates of cold induced urticaria (Table 2). Multivariate regression analysis adjusting for latitude and average January temperature revealed that lower average temperatures in January were associated with higher prevalence of cold urticaria (adjusted b= -0.034(95% CI: -0.068, -0.001). Management of PU Treatment for all cases of PU is based primarily on removal or avoidance of causes and/or aggravating factors of urticaria. In addition, medications mainly second-generation anti-histamines may help control symptoms when complete avoidance is impossible [41]. In contrast to spontaneous forms of CU, certain forms of cold induced PU may be life-threatening and require prescription of an epinephrine auto-injector [42,43]. Although no fatalities were described with aquagenic urticaria, its management is especially challenging. Treatment with antihistamines, ultraviolet therapy or application of
protective hydrophobic barrier creams may be effective [25]. Recent case reports suggest that some forms of PU may respond to Omalizumab, a monoclonal anti-IgE antibody. However, larger randomized controlled trials are needed to establish its effect [23,44]. Although avoidance of the physical triggers often provides adequate control of PU, studies suggest that PU is less likely to resolve over time compared to chronic spontaneous forms (16% after 1 year versus almost 50%) [45,46]. Conclusion and future directions PU is the most common form of CU of known etiology [47], and is associated with poor quality of life, substantial psychosocial morbidity [35,48,49] and life threatening reactions [42]. Our review is the first to assess the pooled estimate of PU. Our results reveal that PU affects 6% to 30% of all patients with CU and that 8% to 100% of PU cases are triggered by cold. However, heterogeneity of studies (as reflected by high I2) precludes conclusive estimates. Recently, the World Allergy Organization, recognizing the importance of PU, has published a position paper for the diagnosis and management of all form of urticaria [8]. Given that cold-induced urticaria may be life-threatening and require the use of an epinephrine auto-injector [42,43,50], it is especially important to diagnose this form of PU. Extreme weather conditions are expected to contribute to the development of cold urticaria [36]. Indeed the highest prevalence of
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DOI: 10.1080/00325481.2015.1045817
cold-induced forms was reported in Montreal (that has the lowest average temperature in January compared to other cities in this analysis) and we have found a significant reverse association between the average January temperature and the prevalence of cold-induced forms. Our meta-analysis has some potential limitations. An evident weakness of this study is that there are very few papers discussing PU in the literature. In addition, over the last decade, methodologies and diagnostic approaches regarding the diagnosis of PU have changed substantially and could have resulted in misclassification bias. Hence earlier studies that have not used recently published confirmatory tests for the diagnosis of PU [1] might have over or underestimated the prevalence of PU. It is also possible that the prevalence of PU among all cases of CU is underestimated because less severe cases may not come to medical attention or may be treated by primary care providers and thus under-reported. However, we expect this misclassification to be nondifferential. Finally, the association we have found between cold urticaria and temperature may be related to ecological fallacy that occurs when conclusions about individuals are based only on analyses of group data [51]. Hence, it is possible that individual exposure to cold stimuli such as swimming regardless of the weather conditions may trigger cold-induced forms. Given that appropriate clinical history is the first essential step in the diagnosis of PU and given the fatality potential of PU, high level of awareness of family physicians, general practitioners and pediatricians, that are likely to have the first encounter with the patient as well as dermatologists and allergists (to which these patients are usually referred), is crucial. An accurate initial assessment of PU can aid to obtain a better symptom control, improve patients’ quality of life, contribute to patient education and enhance accessibility to more effective therapies. Increased awareness to this subset of potentially debilitating conditions can be of particular importance for the management of children and adults living in northern latitudes given the extremes of weather conditions and given that individuals engaged in winter sports such as ice-hockey players and speed skaters [52], are especially prone to the development of certain types of PU [12,53].
Declaration of interest M Ben-Shoshan is the recipient of the Emerging Clinician Scientist award and the Fonds de la recherche en sante du Quebec (FRSQ) junior 1 award and the emerging clinician scientist fellowship awarded by the Allergy, Genes, and Environment Network of Centres of Excellence (AllerGen NCE). M Ben-Shoshan serves as a consultant for Sanofi and Novartis. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
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