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A case of isolated rice allergy

Allergy

June 2003
58(5):456-7

DOI:10.1034/j.1398-9995.2003.00132.x

Source
PubMed

Authors:

Bulent Enis Sekerel

Hacettepe University

Content uploaded by Bulent Enis Sekerel

Content may be subject to copyright.

A 50-year-old man began experiencing

nausea, breathing diﬃculty, and hives on

his back and buttocks 10 min after eating

Quorn.

Those anecdotal reports are supported

by other data. Marlow Foods Ltd.,

Quorn’s producer, receives about 100

adverse-reaction reports (including sev-

eral IgE food-allergy reactions) annually

(1). An ‘idiosyncratic responseof vom-

iting and diarrhoea occurred in 10 com-

plainants (2). Two complainants had a

skin-prick test response to mycoprotein

>2 mm. Food challenges were not

conducted.

In a company-sponsored, double-blind

study, 200 volunteers ate up to 15 g (dry

weight) of mycoprotein up to eight times

over 4 weeks (3). Another 100 volunteers

ate foods without mycoprotein. Six peo-

ple in the test group vomited a total of

seven times. Three of those people agreed

to rechallenges (up to four), with one

person vomiting again (4). One person in

the control group vomited, but was not

rechallenged. In contrast, another com-

pany-sponsored study did not detect

symptoms that the researchers ascribed

to the test material (5).

Research is needed to ﬁnd the mech-

anism(s) by which mycoprotein causes

symptoms. Regardless of the mechanism,

physicians should be aware that Quorn

may cause illnesses. Acceptance by gov-

ernment agencies (6) of Quorn as being

safe raises questions about the adequacy

of those agenciespremarket reviews and

postmarket monitoring of novel ingredi-

ents.

Center for Science in the Public Interest 1875

Connecticut Ave. NW Suite 300 Washington,

DC, USA

Tel: 202-777-8328

Fax: 202-265-4954

E-mail: mjacobson@cspinet.org

Accepted for publication 2 January 2003

Allergy 2003: 58:455–456

ISSN 0105-4538

References

1. Food and Drug Administration, FDA.

GRAS Notification for Mycoprotein,

Marlow Foods Ltd., 30 Nov 2001. (On file

at the US FDA).

2. Tee RD, Gordon DJ, Welch JA, Newman

Taylor AJ. Investigation of possible

adverse allergic reactions to mycoprotein

(‘Quorn). Clin Exper Allergy 1992;23:

257–260.

3. R.H.M. Research Limited.Large scale

volunteer trial on mycoprotein (A3/5).

R. H. M. Research Limited, High

Wycombe, Buckinghamshire: 1977.

(On ﬁle at the FDA.)

4. R.H.M. Research Limited.Supplementary

studies on subjects who consumed A3/5 my-

coprotein in a large scale volunteer trial

conducted November/December 1977.R.H.

M. Research Limited, High Wycombe,

Buckinghamshire: 1978. (On ﬁle at the

FDA.)

5. Udall JN, Lo,CW,Young VR,

Scrimshaw NS. The tolerance and nutri-

tional value of two microfungal foods in

human subjects. Am J Clin Nutr

1984;40:285–292.

6. Agency Response Letter, GRAS Notice

No. GRN 000091, Office of Food Additive

Safety, Center for Food Safety and Applied

Nutrition, US Food and Drug Adminis-

tration, 7 Jan 2002. (http://www.cfsan.

fda.gov/rdb/opa-g091.html; accessed

23 Dec. 2002).

A case of isolated rice allergy

F. Orhan, B. E. Sekerel*

Key words: food allergy; gastrointestinal symptoms;

rice; urticaria.

Rice (Oryza sativa) belongs to the sub-

family of Oryzoidea which is a member of

the Graminea

family. Although

rice is one of the

most common

cereals produced

and consumed

around the

world, there have been only a few reports

on rice allergy most of which deﬁne

contact urticaria caused by raw rice (1, 2).

There are only two reports in the litera-

ture describing immediate hypersensitiv-

ity reactions after ingestion of rice (3, 4).

A 9-year-old girl was admitted to our

asthma clinic for routine follow-up visit

and had been under regular follow-up

during the last 2 years. She had been found

allergic to grass pollens through intrader-

mal but not epidermal tests. However, her

history was not suggestive of any seasonal

symptoms. Her skin prick tests (SPTs)

with other common inhalant (ALK,

Horsholm, Denmark) (mites, weeds, trees,

animal dander, and molds) and food

allergen extracts (Allergopharma,

Reinbek, Germany) (hen’s egg, milk, soy,

wheat, ﬁsh, and peanut), and her speciﬁc

IgE to grass pollens had also been found

negative. During that visit, her parents

informed that she ‘dislikesfoods consti-

tuting rice and avoided eating them for the

last 3 years. A couple of attempts to feed

her with rice resulted in immediate nausea,

abdominal pain and diarrhea. On one

occasion, she had suﬀered urticaria–angi-

oedema in the kitchen when her mother

was sorting rice.

We performed SPT (Allergopharma,

Reinbek, Germany) and prick–prick tests

with various cereals including rice, wheat,

barley, oat and lentil, and demonstrated a

(++++) wheal and ﬂare reaction only

to rice with both tests. The total IgE

concentration was 165 kU/l, and IgE

speciﬁc to rice (CAP-FEIA, Pharmacia,

Uppsala, Sweden) was 13.2 kU/l

(Class 3). For a more deﬁnitive diagnosis

we performed a double-blind, placebo-

controlled food challenge which result in

nausea, abdominal pain and diarrhea

after 10 min of ingestion.

Although our patient demonstrated

positive response to grass pollens through

intradermal skin tests, her SPT response

and speciﬁc IgE to grass pollens were

negative, and her asthma symptoms were

perennial rather than seasonal. It has

been pointed out that the presence of a

positive intradermal skin test response in

the presence of a negative SPT response

does not indicate the presence of a

clinically signiﬁcant sensitivity (5). Thus,

we excluded grass pollen sensitivity.

Cereal grains may show cross-reactivity

with grass pollens and each other. Our

patient had no problems when eating

other cereals. Her SPTs and prick–prick

tests with available cereals were also

negative. Therefore, it seems rice allergy

in our patient is isolated instead of being

a co-sensitization to grass pollens or

other cereals.

Rice allergy may lead

to urticarial lesions via

inhalation.

456

ALLERGY Net

Our patient exhibits the symptoms of

two diﬀerent systems by two diﬀerent

routes of exposure of two diﬀerent forms

of rice. The ﬁrst is ingestion of cooked

rice resulted in acute gastrointestinal

symptoms. The second is urticaria–angi-

oedema while her mother was sorting

rice, possibly caused by inhalation of

minute particles of raw rice. Inhalation of

foodstuﬀs in aerosol forms may cause

allergic food reactions. Also, inhalant

allergens may solely provoke urticaria

without associated allergic rhinitis or

asthma (6). To our knowledge, however,

IgE-mediated allergic symptoms limited

to skin following inhalation of food

allergens have not been reported to date.

Hacettepe University Faculty of Medicine

Department of Pediatric Allergy & Asthma

Sihhiye 06100 Ankara, Turkey

Tel: +90 312 3051700

Fax: +90 312 3112357

E-mail: b_sekerel@yahoo.com

Accepted for publication 22 January 2003

Allergy 2003: 58:456–457

ISSN 0105-4538

References

1. Yamakawa Y, Ohsuna H, Aihara M,

Tsubaki K, Ikezawa Z. Contact urticaria

from rice. Contact Dermatitis 2001;44:

91–93.

2. Lezaun A, Igea JM, Quirce S, Cuecas M,

Parra F, Alonso MD, Martin JA,

Cano MS. Asthma and contact urticaria

caused by rice in a housewife. Allergy

1994;49:92–95.

3. Wu

¨thrich B, Scheitlin T, Ballmer-

Weber B. Isolated allergy to rice. Allergy

2002;57:263–64.

4. Arai T, Takaya T, Ito Y, Hayakawa K,

Toshima S, Shibuya C, Nomura M,

Yoshimi N, Shibayama M, Yasuda Y.

Bronchial asthma induced by rice. Intern

Med 1998;37:98–101.

5. Nelson HS, Oppenheimer J, Buchmeier A,

Kordash TR, Freshwater LL. An

assessment of the role of intradermal skin

testing in the diagnosis of clinically relevant

allergy to timothy grass. J Allergy Clin

Immunol 1996;97:1193–1201.

6. Lee IW, Ahn SK, Choi EH, Lee SH.

Urticarial reaction following the inhala-

tion of nicotine in tobacco smoke.

Br J Dermatol 1998;138:486–488.

Type I sensitization towards

patent blue as a cause of

anaphylaxis

K. Forschner, A. Kleine-Tebbe, T. Zuberbier, M. Worm*

Key words: anaphylaxis; patent blue; lymphography.

Detection and excision of sentinel lymph

nodes is an established technique for

early staging and

treatment of not

only malignant

melanoma, but

also of other

cancers (1, 2).

Allergic reactions to patent blue were

ﬁrstly reported in the 1960s and 1970s

(3, 4). Recently a few cases of anaphy-

laxis to patent blue after lymph node

mapping were published (5–7). We report

a 37-year-old female patient with a

superﬁcial spreading malignant

melanoma who underwent lymph

node mapping. The patient was sedated

with midazolam (Dormicum



) and

received anaesthesia with articain

(Xylonest



1%).

Five minutes after intralymphatic

injection of 1 ml patent blue (Guerbet



)

the patient developed a generalized

urticaria and angiooedema. A few

minutes later, the patient became

hypotensive (50/40 mmHg) and lost

consciousness. The anaphylactic reaction

was treated immediately with adrenaline

(0.2 mg), prednisone (500 mg) and

dimetindenmaleat (8 mg) intravenously

and the patient recovered completely

within 30 min. The patient’s history

revealed neither other allergic diseases

like atopic dermatitis, allergic rhinitis or

allergic asthma nor previous anaphylaxis.

Accordingly, the total serum IgE anti-

bodies were normal (19.7 kU/l), speciﬁc

IgE to latex was negative (>0.35 kU/l)

and no speciﬁc serum IgE was found

regarding the most frequent inhalant

allergens (SX1). Also the tryptase level

was normal (4.79 lg/l).

Three weeks postoperatively a skin

prick test (SPT) was performed. All used

drugs were tested. The SPT using articain

(1%), diazepam and midazolam was

negative. By contrast, a strong positive

SPT towards patent blue 1 : 100 was

found (Fig. 1). In ﬁve control individuals

SPT with patent blue (dilution 1 : 100)

was negative. These ﬁndings indicate a

type I allergy towards patent blue in this

patient as a cause of the perioperative

anaphylaxis.

Patent blue is a widely used agent in

textile, paper, agriculture industries,

cosmetic and medical products. In the

past, a frequency of type I sensitization

towards patent blue of 2.7% has been

reported (8). A recent review revealed

adverse reactions to injection of isosulfan

blue dye during sentinel lymph node

mapping in breast cancer patients in

1.6% of documented allergic reactions

(n¼2392) (1). Most reactions produced

urticaria and pruritus (69%) but only

0.5% of the patients showed hypotensive

reactions. As the procedure of sentinel

lymphnode biopsy becomes more fre-

quent the risk of an increased incidence

of adverse reactions to patent blue may

be expected. The value of preoperative

performed SPT to rule out preexisting

type I sensitization towards patent blue

will need to be clariﬁed by prospective

controlled studies.

*Department of Dermatology and Allergy

Charite

´, Humboldt University

Schumannstrasse 20/21

D-10117 Berlin Germany

Tel: 04930450518105

Fax: 04930450518958

E-mail: margitta.worm@charite.de

Accepted for publication 17 January 2003

Allergy 2003: 58:457–458

ISSN 0105-4538

Figure 1. Positive skin prick test with patent blue

at 1 : 100 dilution.

Patent blue is

frequently used for

lymphnode mapping.

457

ALLERGY Net

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Purpose of review To summarize the current understanding and important aspects of anaphylaxis related to cereal grains. Recent findings Skin applied products have recently shown to be associated with cereal anaphylaxis; advances in wheat antigen investigation are discussed; new evidence of cereal cross-reactivity; and oral immunotherapy has been attempted with some success. Summary Cereal grains have been shown to cause anaphylaxis. Recent investigation into wheat antigens has led to identification of possible markers for WDEIA and wheat allergy. Cereal cross-reactivity has been noted, which is clinically relevant when treating cereal anaphylaxis.

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The literature supports the notion that carbohydrate epitopes, on their own, do not contribute significantly to the induction of allergic reactions. They bind weakly to IgE antibodies and have been termed as cross reactive carbohydrate determinants. These epitopes cause confusion in in vitro IgE testing through nonspecific cross-reactivity. Coincident with the rising trends in food allergy prevalence, there has recently been reports of anaphylaxis induced by carbohydrate epitopes. There are two distinct groups, each with unique characteristics and geographical distribution. Anaphylaxis and acute allergic reactions related to the carbohydrate galactose-α-1,3-galactose (α-Gal) epitope that are present in the monoclonal antibody, cetuximab and red meat have been described in the United States and Europe populations where tick bites have been found to be the primary sensitizer. Another carbohydrate inducing anaphylaxis is galacto-oligosaccharides in commercial milk formula which has been described in the several Asian populations including Singapore. The latter is unique in that the allergen is a pure carbohydrate. We summarize the current literature on carbohydrate-induced food allergy, and evaluate the two new groups of carbohydrate allergy that have defied previous findings on carbohydrates and their role.

Allergic reactions to foods by inhalation in children

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This article focuses on hypersensitivity reactions after inhalation of food particles as primary cause for food allergy. This is an increasingly recognized problem in children. Reactions are commonly diagnosed in children who develop symptoms when the food is ingested. Some children tolerate the food when it is eaten but they experience reactions to airborne food particles such as peanut, cow's milk, and fish. The exposure can be trivial, as in mere smelling or being in the vicinity of the food. Usually, respiratory manifestations include rhinoconjunctivitis, coughing, wheezing, and asthma, but in some cases even anaphylaxis has been observed. Practical approaches concerning diagnosing clinical reactivity including skin tests, serum IgE antibodies, specific provocation tests, and management have been identified. Studies are warranted to establish the accuracy of diagnostic tests as well as incidence, prevalence, and natural history of food allergy through inhalation route.

Rice Allergy Demonstrated by Double-Blind Placebo-Controlled Food Challenge in Peach-Allergic Patients Is Related to Lipid Transfer Protein Reactivity

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INT ARCH ALLERGY IMM

Background: The risk factors for sensitisation to rice and the involved allergens are still partially unknown. In this study we evaluated the clinically relevant aspects of rice allergy in DBPCF-positive patients, the major rice allergens, the severity of peach- and rice-induced symptoms in respect to Pru p 3 sensitisation and the role of anti-rPru p 3 IgE levels as a risk factor for rice allergy. Methods: In 148 peach-allergic subjects, patients with allergic reactions to rice and rice-positive serum IgE were selected. Symptoms were verified by double-blind placebo-controlled food challenges (DBPCFCs), performed at a maximum dosage of 25 g. Rice allergens, identified by IgE immunoblotting, were characterised by N-terminal amino acid sequencing. The relationship between anti-rPru p 3, 1 and 4 IgE levels and rice symptoms were statistically analysed. Results: Eight out of 10 recruited rice-allergic patients had positive DBPCFCs, while 2 patients were not challenged due to their previously documented severe reactions. All patients with rice-induced symptoms were Pru p 3 positive and presented with higher anti-rPru p 3 levels than the rice-sensitised but tolerant patients. A 9-kDa lipid transfer protein, which was highly homologous to Pru p 3, was identified as the major rice allergen and elicited a positive response in all of the patients. Five patients reacted to a putative 15- to 17-kDa rice allergenic protein, and 3 patients reacted to an [alpha]-amylase/subtilisin inhibitor that was approximately 20 kDa. Conclusion: Rarely, allergic reactions to rice can arise in patients with peach allergies who are sensitised to Pru p 3, particularly in patients with high anti-rPru p 3 IgE levels.

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Identification of Rice Proteins Recognized by the IgE Antibodies of Patients with Food Allergies

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J AGR FOOD CHEM

Similarity among food allergens is a great problem affecting the specificity of diagnosis and treatment of allergic patients. We have observed that 80% of patients with food (including wheat) and pollen allergies have increased IgE antibodies against rice proteins. By immunoblotting, we documented that boiling decreased solubility and IgE reactivity of PBS-extracted rice and wheat proteins, yet in SDS extracts this reactivity was only slightly changed. The sera of patients highly positive on the IgE immunoblot and positive in basophil activation and skin prick test with boiled rice components were used for characterizing the IgE-binding proteins separated by 1D or 2D electrophoresis. Using mass spectrometry, we identified 22 rice SDS soluble proteins. Six of them were new thermostable potential rice allergens: glutelin C precursor, granule-bound starch synthase 1 protein, disulfide isomerase-like 1-1 protein, hypothetical protein OsI_13867, putative acid phosphatase precursor 1, and a protein encoded by locus Os02g0453600. All of the identified rice proteins differed from known wheat allergens, except proteins belonging to the α-amylase/trypsin inhibitor family. Furthermore, we would suggest that in patients with high IgE reactivity to wheat and rice components, the IgE immunoblot and skin prick test with boiled rice proteins could be beneficial before diet recommendation.

A case of rice allergy in a patient with baker's asthma

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Oct 2012

A case of rice allergy in a patient with bakers asthma is described. On ISAC 112 IgE reactivity to wheat alpha-amylase/trypsin inhibitor (nTri a aA_TI) and lipid tranfer protein (rTri a 14) was found. We hypothesize that the reaction by oral ingestion was elicited by homologous molecules in rice seeds.

Allergen of the Month—Rice

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Feb 2012

Richard W Weber

Rice-Induced Anaphylaxis: IgE-Mediated Allergy against a 56-kDa Glycoprotein

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Dec 2011
INT ARCH ALLERGY IMM

Although rice (Oryza sativa) is one of the most common cereals produced and consumed around the world, there have been only a few reports on immediate hypersensitivity reactions after ingestion of rice. Few clinical studies on rice allergy in Asia have been reported concerning rhinitis, asthma and atopic dermatitis. In this case study, we identify allergens presumably responsible for anaphylaxis after ingestion of rice in a German patient. Prick-to-prick tests, determination of specific IgE and the basophil activation test (BAT) were performed to confirm IgE-mediated allergy. IgE reactivity was further analyzed by immunoblotting of protein extracts from cooked commercial rice products. Rice allergens were purified, subjected to N-terminal sequencing and characterized by IgE binding and IgE inhibition assays using additional sera from 8 subjects with sensitization to rice and/or a history of hypersensitivity symptoms after rice ingestion. Prick-to-prick tests were positive to raw and cooked rice (basmati rice and long-grain rice) and preparations of different rice extracts. Specific IgE against rice (f9) was 1.87 kU(A)/l. The BAT showed specific IgE-mediated activation of basophils after stimulation with rice extracts. Four IgE-reactive rice proteins with an apparent molecular weight of 49, 52, 56 and 98 kDa were identified. Interestingly, only binding to the 56-kDa glycoprotein was at least partially independent from cross-reactive carbohydrate determinants (CCD), whereas IgE binding to the other rice proteins was completely inhibited by pre-incubation with the CCD MUXF derived from bromelain. Yet unidentified high-molecular-weight allergens from rice seeds, predominantly a 56-kDa glycoprotein, seem to be responsible for anaphylaxis after consumption of rice in a German patient.

Contact urticaria from rice

Article

Feb 2001
CONTACT DERMATITIS

A 30-year-old man with atopic dermatitis had had erythema and itching of the hands after washing rice in water, though he had always eaten cooked rice without problems. Handling test with water used to wash regular rice was performed on abraded hands, and produced urticarial erythema after several minutes. Applications of water used to wash allergen-reduced rice were negative for urticarial reaction. Prick test with water used to wash regular rice was +++. However prick test reaction with water used to wash allergen-reduced rice was +. Histamine-release test of regular rice-washing water was grade 3 and that of allergen-reduced rice grade 1. In immunoblotting analysis with regular rice washing water, there were no bands with this patient. These results suggest that the allergen responsible for contact urticaria in this patient might be water-soluble, heat-unstable, and not contained in allergen-reduced rice.

Bronchial Asthma Induced by Rice

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Jan 1998

A 43-year-old patient with rice-induced bronchial asthma was first admitted to our hospital for developing bronchial asthma induced by mite and house dust. At that time, there was no sign of allergic response to rice. Two years later, he was readmitted in an emergency state, with a severe attack of bronchial asthma. This time, however, the result of immunoglobulin E (IgE)-radioallergosorbent test (RAST) for rice was positive, with those to mite and house dust were unexpectedly negative. The causative factors and pathological mechanisms of various kinds of food allergies still remain unknown. The patient is now followed up in an ambulatory setting, and has been eating hypoallergenic rice with no bronchial asthma-induced attack. The present case, being an adult patient with severe grain-induced bronchial asthma previously allergic to mite and house dust, seems to be rather rare in the literature.

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The tolerance of human subjects to two microfungal food products was studied in separate double-blind cross-over studies. As an addition to the subject's usual diets, cookies with and without 20 g of a product from Fusarium graminearium were fed to a group of 100 individuals daily. In a second study, cupcakes with and without 10 g of Paecilomyces variotii were given daily to 50 individuals. Mild rashes possibly related to one of the microfungal food products occurred in two individuals fed P variotii. Except for a decrease in serum cholesterol during the F graminearium study, no significant changes were noted in 17 serum constituents. During nutritive value studies, digestibility, biological value, and net protein utilization were calculated for the two microfungal proteins and for milk. The values for milk were 95, 85, and 80%, respectively. The values for F graminearium were 78, 84, and 65%, respectively. For P variotii corresponding figures were 81, 67, and 54%. On the basis of these results both microfungal foods may be deemed safe for human consumption at the levels tested.

Asthma and urticaria caused by rice in a housewife

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We report the case of an atopic housewife who presented with rhinoconjunctivitis-asthma and contact urticaria from handling rice and other cereals. She tolerated cooke cereals. Both skin prick tests with a rice extract (20% w/v) and a rub test with raw rice gave positive results. Bronchial challenge test with methacholine revealed a PC20 of 0.45 mg/ml. The challenge test with raw rice resulted in immediate and late clinical and spirometric responses; pretreatment with DSCG inhibited both responses. The histamine release test (HRT) with rice was positive, and we detected rice-specific IgE antibodies by REIA in the patient's serum. Skin prick tests, HRT, and RAST with a battery of cereals gave positive results. Finally, the rice REIA was inhibited by rice (75%), rye (63%), corn (64%), and wheat (51%) extracts.

Investigation of possible adverse allergic reactions to mycoprotein (‘Quorn’)

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Mycoprotein ('Quorn') is a food produced for human consumption from Fusarium graminearum. Crossreactivity studies showed that mycoprotein shared multiple common allergenic determinants with Aspergillus fumigatus and Cladosporium herbarum and some with Alternaria alternata. There is, therefore, a potential for mould allergic patients to react adversely to inhaled or ingested mycoprotein. Mycoprotein RAST screening of mycoprotein production workers was made during a 2 year period. Two of the production workers had specific RAST binding > or = 2% but none reported symptoms. Two of 10 patients referred to hospital following vomiting and diarrhoea after ingestion of mycoprotein had a mycoprotein skin-prick test weal > or = 2 mm but none had a significantly raised RAST. These largely negative results are important and reassuring because consumption of the product in the U.K. is now widespread and increasing.

An assessment of the role of intradermal testing in the diagnosis of clinically relevant allergy to timothy grass

Article

Jul 1996
J ALLERGY CLIN IMMUN

Immediate skin testing is generally the preferred method for establishing the presence of allergy in clinical practice. There is no agreement, however, as to whether intradermal testing should be routinely performed if skin prick test results are negative. The study was done to address the value of intradermal skin testing in the diagnosis of clinically significant sensitivity to grass pollen in patients exhibiting negative skin prick test responses to timothy extract. Four groups were studied. Group I had a history of seasonal allergic rhinitis, negative skin prick test responses to timothy and Bermuda grass, but positive intradermal skin test responses to timothy grass. Group II had a history of seasonal allergic rhinitis and positive skin prick test responses to timothy grass. Group III had a history of seasonal allergic rhinitis but had negative responses to both prick and intradermal testing with timothy and Bermuda grass. Group IV had no history of rhinitis, had negative responses to skin testing with a panel of locally important allergens, as well as Bermuda and timothy grass, and had a serum IgE value of less than 20 IU/ml. Clinical sensitivity to grass was assessed by two methods: (1) nasal challenge with threefold increasing amounts of timothy pollen performed out of the pollen season and (2) correlation of subjects' daily symptom and medication scores with daily grass pollen counts during the grass pollen season. On the basis of nasal challenge with timothy grass, pollen allergic reactions were present in 11% of group I, 68% of group II, 11% of group III, and 0% of group IV. As determined by correlation of symptoms during the grass pollen season with grass pollen counts, 22% of group I, 64% of group II, 21% of group III, and 0% of group IV were considered allergic. If both criteria were required for a diagnosis of clinical allergy to grass, the percent positive was 0 for group I, 46 for group II, 0 for group III, and 0 for group IV. Under the conditions of this study the presence of a positive intradermal skin test response to timothy grass (1000 AU/ml) in the presence of a negative skin prick test response to timothy grass (100,000 AU/ml) did not indicate the presence of clinically significant sensitivity to timothy grass, and by inference, to other cross-reacting grasses.

Urticarial reaction following the inhalation of nicotine in tobacco smoke

Article

Apr 1998

We report a patient with recurrent generalized itching and urticaria due to inhalation of nicotine in tobacco smoke. A skin prick test with nicotine base (1:10 w/v) was negative but an intradermal test with nicotine base (1:100 w/v) was strongly positive. Intradermal tests with nicotine base (1:100 w/v) performed on 10 healthy controls were negative. A provocation test with a nicotine patch showed the same symptoms and signs including generalized itching, weals and flares, and mild dyspnoea, which occurred when he was exposed to tobacco smoke. Nicotine in tobacco smoke can act as an inhalant allergen and induce urticaria in hypersensitive persons.

Contact urticaria from rice

Article