kronik idiopatik urtikaria

doi: 10.1111/j.1346-8138.2007.00276.x Journal of Dermatology 2007; 34: 294–301

294 © 2007 Japanese Dermatological Association

Blackwell Publishing AsiaORIGINAL ARTICLE

Chronic idiopathic urticaria: prevalence and clinical course

Kanokvalai KULTHANAN, Sukhum JIAMTON, Narumol THUMPIMUKVATANA, Sumruay PINKAEWDepartment of Dermatology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkoknoi, Bangkok, Thailand

ABSTRACT

The purpose of our study was to assess the prevalence and clinical course of patients with chronic idiopathicurticaria (CIU), as well as possible causes or associated findings, laboratory findings and the duration of thedisease in patients with chronic urticaria (CU). We retrospectively reviewed the 450 case record forms of patientswith CU and/or angioedema who attended the Department of Dermatology, Siriraj Hospital, during the period2000–2004. Of 450 patients with CU, 337 patients (75%) were diagnosed as CIU. Forty-three patients (9.5%)had physical urticaria, while 17 patients (3.8%) had infectious causes. Other possible causes were food, thyroiddiseases, atopy, drugs, dyspepsia and collagen vascular diseases. In eighty-nine percent of patients, no abnormalitieswere detected at the time of physical examination. The most common abnormal laboratory finding was minimalelevation of the erythrocyte sedimentary rate (42%). In 61 patients, autologous serum skin tests had been done.Fifteen patients (24.5%) had positive results i.e. autoimmune urticaria. Anti-thyroglobulin and anti-microsomalantibodies were positive in 16 % and 12% of CIU patients respectively. After 1 year from the onset of the symptoms,34.5% of CIU patients were free of symptoms and after 1.2 years from the onset of the symptoms, 56.5% ofautoimmune urticaria patients were free of symptoms. The median disease duration of CIU and autoimmuneurticaria were 390 days and 450 days respectively. Our study provided an overview of CU and CIU in a large seriesof Thai patients, based on etiological aspects and clinical courses.

Key words: chronic idiopathic urticaria, course, prevalence.

INTRODUCTION

Chronic urticaria (CU) is defined as any pattern ofrecurrent urticaria occurring at least twice a week forat least 6 weeks.1 The pathogenesis of CU is notcompletely understood. However, mast cell degran-ulation and histamine release has been thought toplay a central role.2 Most patients with CU have nospecific allergic trigger for mast cell activationand when no causes can be identified, the finaldiagnosis is chronic idiopathic urticaria (CIU).3

This condition is thought to affect at least 0.1% ofthe population.4

The concept of autoimmune urticaria as one of thecauses of CIU has evolved over the past decade.5 Thisis a subset of patients with CIU who processedfunctional antibodies against the high affinity immu-noglobulin (Ig)E receptor, or less commonly IgE intheir blood. These autoantibodies were estimated tobe present in at least 30–50% of patients with CIU.6

There were some reports of immunogenetic differencesbetween Oriental and Caucasian populations, result-ing in differences in the clinical presentation andfrequency of autoantibodies detected in someautoimmune diseases.7–8 Moreover, different dietaryhabits between Asian and Western countries as well

Correspondence: Kanokvalai Kulthanan, M.D., Department of Dermatology, Faculty of Medicine, Siriraj Hospital, Mahidol University, 2 Prannok Road,Bangkoknoi, Bangkok 10700, Thailand. Email address: [email protected] 26 June 2006; accepted 16 November 2006.

Chronic idiopathic urticaria

© 2007 Japanese Dermatological Association 295

as the socioeconomic status may cause differentallergen sensitization. Most of the studies aboutchronic urticaria were reported from Western coun-tries. It is interesting to know the prevalence andclinical features of Asian patients with CU.

The purpose of our study was to assess the prev-alence and clinical course of CIU patients, as well aspossible causes or associated findings, laboratoryfindings and the duration of the disease in Thaipatients with CU.

PATIENTS AND METHODS

This study was conducted at the outpatient Depart-ment of Dermatology, Siriraj Hospital, MahidolUniversity, Thailand in 2005. The study had beenapproved by the ethical committee on researchinvolving human subjects of Siriraj Hospital. We ret-rospectively reviewed case record forms of patientswho attended the urticaria clinic during the period2000–2004. All consecutive patients aged more than15 years with a diagnosis of CU and/or angioedemaof at least 6 week duration were included. Thefollowing data were collected: demographic data,type of CU (i.e. chronic continuous urticaria; whealsoccurring continuously for long periods or daily fora few days and then not for a week or two, chronicrecurrent urticaria; continuous urticarial activitypunctuated by gaps of several weeks or months),9

a complete history of possible causes, physicalexamination, provocative tests for physical urticaria,laboratory investigation and duration of treatment.To evaluate dermographism, firm stroking of the skinwas performed using a dermographometer with apressure of 4900 gm/cm2, which induced linear itchywheals within minutes.10 The test for delayed pres-sure urticaria was performed using sandbags joinedby a rope weighing 15 lb each placed over oneshoulder for 15 min, which resulted in a palpablewheal at the application site 2–8 h later.11 Diagnosisof cold urticaria was made by application of an icecube in a thin plastic bag to the skin of the forearmfor 20 min which caused whealing to occur within15 min at the test site, on rewarming the skin.12 Forassessment of cholinergic urticaria, the patient wasasked to run on the spot to the point of perspiration.A positive response was defined by subsequentpruritic erythematous punctuate whealing, within

5–15 min.13 Adrenergic urticaria was confirmed byintradermal injection of noradrenaline (3–10 ng in0.02 mL saline), a small red papule in a halo ofblanched skin was considered positive.14 Solar urti-caria was diagnosed by phototest and confirmedby exposure to natural sunlight.15 Screening for foodallergy or intolerance was investigated by an eli-mination diet for 3 weeks. All suspected drugs usedwere discontinued or replaced with chemicallyunrelated drugs. Skin prick testing, drug provocationtests and oral food challenge tests were performedif necessary. Laboratory investigation included com-plete blood counts, urinalysis, erythrocyte sedimentaryrate (ESR), stool examination and other investiga-tions that were necessary for the individuals, that is,urea nitrogen (BUN), creatinine, aspartate ami-notransferase (AST), alanine transferase (ALT), alkalinephosphatase (ALP), bilirubins, total protein, albumin,hepatitis B surface antigen (HBsAg), anti-hepatitis Cvirus (HCV), free T3, free T4, thyroid stimulatinghormone (TSH), antithyroid autoantibodies (i.e. anti-thyroglobulin and anti-microsomal antibodies;passive hemagglutination test; Hausen Bernstein,USA), antinuclear antibodies (ANA), cryoglobulins,serum complement level, chest and sinus X-ray studies.In addition to these, Helicobacter pylori infectionwas investigated in those with chronic gastric com-plaints. The autologous serum skin test (ASST) wasperformed as previously described.16 Briefly, 50 µL ofundiluted autologous serum was injected intrader-mally into the volar aspect of the forearm togetherwith simultaneously injected controls includingsaline and histamine 10 µg/mL. The test is positiveat 30 min if the serum-injected site manifests awheal with a diameter at least 1.5 mm greater thanthat of the saline wheal.

The mainstay of treatment was oral antihistamine.Other medication included oral corticosteroids, anti-leukotrienes, disodium chromoglycate, sulfasalazine,chloroquine and cyclosporin among others.

After a follow-up period of at least 12 monthsafter stopping the medication, patients were askedwhether they had any remaining symptoms andwhether they still used antihistamines or other drugsfor their urticarial symptoms or not, by interviewingthe patients at the outpatient department or bytelephone inquiry. Repeated laboratory tests wereperformed, if necessary. When the patients were

K. Kulthanan et al.


free of symptoms for at least 12 months, they weredefined as in remission.

Descriptive statistics (e.g., mean, median, minimum,maximum, frequency and percentages) were usedto describe the demographic data, possible causesand laboratory findings. Because some patients werelost to follow up, to determine the probability ofsymptom resolving at each time point, the Kaplan–Meier survival curve which showed the probability ofremission was applied. All statistical data analyseswere performed using SPSS for Windows version 10(SPSS, Chicago, IL, USA).

RESULTS

Patients with chronic urticariaOf the 450 patients diagnosed with CU, 94 weremale (21%) and 356 were female (79%) (Table 1).Their mean age was 35 years with a range of 15–80 years. Two-thirds of the patients had urticariaalone. Most of the patients (76%) had chroniccontinuous urticaria which is defined as havingalmost daily wheals, whereas 107 patients (24%)had chronic recurrent urticaria which had disease-free time intervals. The common associated atopicconditions were mainly allergic rhinitis and asthma.

Dermographism associated with ordinary wheals ofurticaria was found in 52% of CU patients.

In 89% of the patients, no abnormalities weredetected at the time of physical examination. Thepossible causes of CU have been shown in Table 2.Of 450 patients, 337 (75%) patients causes couldnot be identified and therefore CIU was diagnosed.Forty-three patients (9.5%) had physical causes, themost common was symptomatic dermographism.Seventeen patients (3.8%) had infectious causes,that is, dental caries, stool parasitic infection, hepa-titis, sinusitis, vaginal infection and herpes simplexinfection. In 50% of patients with dental caries, theCU symptom improved after the infection was elimi-nated, but it was not completely cured. Regardingthe other infections, after treatments were given, theurticarial symptom did not improve. This impliedthat these might be coincidental symptoms. In fivepatients with dyspepsia, investigations for H. pyloriinfection revealed negative results. Approximately4% of patients suspected that ingested food was anetiology of urticarial symptoms. The reactions usually

Table 1. Demographic data of chronic urticaria group(n = 450)

Characteristic No. (%)

SexMale 94 (21)Female 356 (79)

Type of urticariaChronic continuous urticaria 343 (76)Chronic recurrent urticaria 107 (24)Urticaria alone 292 (65)Urticaria with angioedema 153 (34)Angioedema alone 5 (1)

Personal history of atopy 110 (24.4)Allergic rhinitis 90 (20)Asthma 20 (4.4)Allergic conjunctivitis 6 (1.3)Atopic dermatitis 0 (0)

Family history of atopy 144 (32)Allergic rhinitis 84 (18.7)Asthma 57 (12.7)Allergic conjunctivitis 2 (0.4)Atopic dermatitis 1 (0.2)

Table 2. Possible causes and associated factors ofchronic urticaria

Possible causes and associating factors No. (%)

Idiopathic urticaria 337 (75)Physical urticaria 43 (9.5)

Symptomatic dermographism 17 (3.8)Cold urticaria 8 (1.8)Delayed pressure urticaria 7 (1.6)Adrenergic urticaria 6 (1.3)Cholinergic urticaria 4 (0.9)Solar urticaria 1 (0.2)

Infection 17 (3.8)Dental caries 4 (0.8)Parasitic infestation 3 (0.6)Hepatitis 2 (0.4)Sinusitis 2 (0.4)Miscellaneous 6 (1.3)

Food 16 (3.6)Thyroid diseases 15 (3.3)

Hyperthyroidism 12 (2.6)Hypothyroidism 3 (0.6)

Dyspepsia 5 (1.1)Atopy† 5 (1.1)Drugs 5 (1.1)Collagen Vascular diseases 5 (1.1)Others 2 (0.4)

†Urticaria wheals were frequently accompanied by an exacerbation of asthma, allergic rhinitis or atopic dermatitis



occurred within 2 h of the same food ingestion. Ofthese, the most common food causes were seafood,preserved food, wheat and beer. Drugs suspectedto aggravate chronic urticaria were antibiotics,non-steroidal anti-inflammatory drugs (NSAIDs), andherbal medication. All patients with collagen vas-cular diseases were lupus erythematosus (LE). A smallpercentage of patients mentioned that factors suchas stress (3%) and menstruation (6%) aggravatedtheir urticaria.

The most common abnormal laboratory findingwas a minimal increase in the ESR (42%; mean34 mm/h, range 21–94; Table 3). However, only 2%revealed associated infection. The common con-ditions were dental caries and parasitic infestation.Positive ANA, mostly at the low titer, was found in17% of the patients, and only 1.2% of them hadbeen diagnosed as LE. Eight percent of our CUpatients had positive HBsAg, and 4% had positiveanti-HCV antibodies. However, no clinical correla-tion with urticarial symptoms was established. Mildabnormality of urinalysis was detected in 7.6% ofthe patients without significant correlation withurticaria. Six percent of patients had abnormal stoolexamination, and 1.2% of them had parasitic infes-tation, mostly Blastocystis hominis and Giardialambdia cyst. As with dental caries infection, afteranti-helminthic administration, the urticarial sym-ptoms were partially improved in less than half ofthe patients. Leukocytosis was found in 5% andeosinophilia was found in only 1.1%. However, nosignificant clinical correlation was established.

There were no significant differences betweenpatients with chronic continuous urticaria and patientswith chronic recurrent urticaria regarding the causesand laboratory abnormalities.

Patients with chronic idiopathic urticariaOf the 337 patients with CIU, 66 were male (20%)and 271 were female (80%). Their mean age was34 years with a range of 15–80 years. In 61 patients,autologous serum skin tests had been done to detectthe presence of autoantibodies to a high affinity IgEreceptor (FCε RIα) on the mast cell surface. Fifteenpatients (24.5%) had positive autologous serum skintest (ASST) results, so we gave them a diagnosis ofautoimmune urticaria. We also investigated for thepresence of thyroid autoantibodies (anti-thyroglobulin, Ta

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K. Kulthanan et al.


and anti-microsomal antibodies). Anti-thyroglobulinantibodies were positive in 16% and anti-microsomalantibodies in 12% of our CIU patients.

After 1 year from the onset of the symptoms,34.5% of CIU patients were free of symptoms (Fig. 1)and after 1.2 years from the onset of the symptoms,56.5% of autoimmune urticaria patients were freeof symptoms (Fig. 2). The median disease duration ofCIU and autoimmune urticaria were 390 days and450 days, respectively.

DISCUSSION

As to the etiology, 75% of our CU patients were idi-opathic urticaria which was similar to other studies(70–82%17–20). Some cases of our CU patientshad an urticarial wheal concomitantly with allergicsymptoms (i.e. allergic rhinitis and asthma of atopiccause; 1.3%). These were suspected of being anIgE-mediated mechanism. Previous studies revealedlittle evidence to suggest that allergy is an importantfactor in CU. However, allergy is more important inacute urticaria than chronic urticaria. In our country,Tuchinda et al. reported in 1978 that the prevalence

of allergic rhinitis and asthma in Thai universitystudents was 23.6% and 2.3% respectively.21 In2001, Vichayanond et al. found that the prevalenceof allergic rhinitis and asthma in Thai university stud-ents was 26.3% and 8.8%.22 In the present study,the personal history of allergic rhinitis and asthma inCU patients was 20% and 4.4% respectively. Thesedata implied that the prevalence of atopy was notincreased in our patients with CU.

Dermographism occurs in 1.5–4.2% of the gen-eral population. There were reports of an increasedincidence of dermographism in patients with CU from8–22%.23 Dermographism associated with ordinarywheals of urticaria was found in half of our CU cases(data not shown). However, symptomatic dermogra-phism was found in only 3.8%.

Various infections have been reported to be theassociating factors of CU including parasitic infec-tion, hepatitis and H. pyroli infection. However, theprimary role of infection is controversial, although itis undeniable that concurrent infections can exacer-bate the condition.24 A possible association betweenH. pyroli gastritis and chronic urticaria remains to beconfirmed by a double-blinded study of eradicationtherapy.24 However, Erel et al. reported that treatingthe H. pyroli had no significant effect on the courseof their CU patients.25 An indirect role for H. pyroli of

Figure 1. A Kaplan–Meier curve demonstrating durationof the disease in patients with chronic idiopathic urticaria(n = 337). After 1 year from the onset of the symptoms,34.5% of patients were free of symptoms.

Figure 2. A Kaplan–Meier curve demonstrating durationof the disease in patients with autoimmune urticaria(n = 15). After 1.2 years from the onset of the symptoms,56.5% of patients were free of symptoms.



evoking autoantibody production through molecularmimicry has been proposed.26 In our study, dentalcaries, stool parasitic infection, hepatitis, sinusitis,vaginal infection, and herpes simplex infection wereoccasionally found. In most cases, after treatmentswere given, the urticarial symptoms did not improveor were not completely cured. This implied thatthese might be co-incidental symptoms. The find-ings in our study were similar to those of Wedi whoreported in 2004 that the prevalence of infectionwas not increased in CU.24

In 4% of our CU patients, food was implicated asa cause of urticarial symptoms. Food allergy is arecognized cause of acute urticaria, but the role offood components in CU is controversial.6 Pseudoal-lergic reactions to food additives and natural dietarysalicylates may have a role in some patients.27 InGreave’s routine use of placebo-controlled single-blinded challenge for food additive intolerance, overa period of 20 years, patients who can reproduciblybe shown to react to a food additive are extremelyrare.6 This is similar to the study of Mathews whostated that food allergy can only rarely be implicatedas a cause of CU or angioedema.28

Drugs suspected to aggravate chronic urticaria inour study were antibiotics, NSAIDs and herbalmedication. Ingested and parenteral drugs are acommon cause of urticaria, especially acute urticaria.The most commonly implicated drugs are penicillins,sulfonamides usually in combination with trimetho-prim and NSAIDs. Drug-induced urticaria may becaused by IgE, by circulating immune complexesand by non-immunological activation of effectorpathways.29 Drugs account for a minority of chronicurticaria.29 Kozel et al. reported that 9% of 220patients had chronic urticaria or angioedema causedby adverse drug reaction.30 However, it is commonto see exacerbation of chronic urticaria caused bymedication. Aspirin and other NSAIDs were reportedto aggravate chronic urticaria in 10–30% ofpatients.31–32

Various studies have reported that the prevalenceof autoimmune urticaria ranged 30–40%.33 In thispresent study, autoimmune urticaria was diagnosedin 24.5% by ASST. This is a subset of patients withCIU who processed functional antibodies againstthe high affinity IgE receptor, or less commonly IgE.There is now controversy about the distinctive

clinical features that enable autoimmune chronicurticaria to be distinguished from non-autoimmunetypes. Early studies reported the presence of auto-antibodies which indicated a subset of patients withmore severe CIU.34 However, later studies did notsupport this.34–35 Due to the limited number of ourpatients undergoing ASST, we could not demon-strate any significant difference between patientswith positive ASST and negative ASST regarding theseverity of the disease (wheal numbers, wheal size,itching scores and the extent of body involvement).However, identification of patients with autoimmuneurticaria is of some importance because immuno-therapy can be contemplated in severely affectedtreatment resistant patients.36

It has been generally accepted that the preva-lence of thyroid autoimmunity is more common inCU. Leznoff et al. reported that 12.1% of 624 CUpatients were found to have thyroid autoimmunity.Of these 7.4% were biochemically euthyroid.37

Similarly, Toubi et al. reported that 12% of 139 CUpatients had thyroid autoimmunity.38 Compared tothe study in a large normal population, only 5.6% of477 control patients had thyroid autoimmunity.39 Inthe present study, CIU patients had positive anti-thyroglobulin antibodies and anti-microsomal anti-bodies of 16% and 12% respectively. Most of themwere clinically euthyroid. The prevalence of thyroidantibodies among normal Thai volunteers was 9%.40

This implied an increased prevalence of thyroidautoimmunity in our CIU patients.

Currently, there is no recommended diagnosticlaboratory evaluation for chronic urticaria andangioedema. In this present study, we performed ascreening laboratory investigation where necessaryfor the individuals. We found that most patients hadnon-specific positive laboratory findings such as amild increase in ESR and so forth. However, thesehad no clinical relevance and the causes of CU stillcould not be identified. This is similar to the study ofKozel et al. who suggested that there is no need forroutine laboratory investigation, and history is the mostimportant factor in identifying the causes of CU.41

Only a few studies deal with the duration of treat-ment in CU and CIU. Kozel et al. reported 47% of 78patients with CIU had remission within 1 year.42

Quaranta et al. performed a study in 86 patientswith CIU where in 32% of them the symptoms were

K. Kulthanan et al.


resolved after a 3-year period. They also found thatthere was no difference in the natural course ofurticaria alone, angioedema alone or urticaria withangioedema.43 The study of Champion et al. in554 patients revealed that 45% of patients with CIUstill had symptoms after 1 year.20 In this present study,the Kaplan–Meier survival curve showed that 34.5%of CIU patients had symptom remission within 1 year.

The median disease duration of our patients withautoimmune urticaria was longer than patients withCIU. Toubi et al. studied 139 patients with CU andreported that CU lasted over 1 year in more than70% of cases and in 14% it still existed after 5 years.38

CU duration is associated with the presence ofangioedema, positive ASST and antithyroid antibodies.

In summary, our study provided an overview ofCU and CIU in a large series of Thai patients, basedon etiological aspects and clinical courses.

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