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CLINICAL INFORMATION for Rice

Clinical History

Number of Studies:
6-10
Number of Patients:
6-10
Symptoms:

Immediate nausea, abdominal pain and diarrhea were experienced in a 9 year old girl after ingestion (Orhan and Sekerel, 2003 [737]). She also suffered from urticaria-angioedema after inhalation in a kitchen as rice was being prepared.

Fiocchi et al. (2003) [1095] report a case of a boy with atopic dermatis who at age 6 showed a positive response, eczema after 24 hours, on rice DBPCFC. At age 8 he suffered a severe anaphylatic reaction, cardiopulmonary collapse and generalized urticaria, following inhalation of rice. At age 11, he was tolerant to ingestion by DBPCFC but double blind challenge by inhalation caused a urticarial rash and laryngeal stridor.

Rhinitis, itching of the scalp and asthma initially with acute urticaria on subsequent exposure and dyspnea in a single patient (Wütherich et al. 2002 [738]).

Severe bronchial asthma in a single patient (Arai et al 1998 [740])

Single cases of rice dependent exercise induced anaphylaxis are described by Guinnepain et al. (1996) [741] and Caffarelli et al. (1997) [742]. Romano et al. (2001) [1039] also noted one case with symptoms with rice.

Intestinal symptoms and dyspnea after consumption of rice in a single patient (Musken et al. 1991 [1094]).

Atopic dermatitis due to rice has been reported (Uenishi et al (2003) [750]; Ikezawa et al 1992 [746]; Uehara et al 1992 [747]). These are not included in the number of cases above because only some of the >1000 cases were associated with rice and the involvement of IgE mediated hypersensitivity is not clear.

Skin Prick Test

Number of Studies:
1-5
Food/Type of allergen:

Commercial extract and prick-prick (Orhan and Sekerel, 2003 [737]

Commercial extract (Fiocchi et al. 2003) [1095].

Commercial extracts (two suppliers) and prick-prick with cooked rice (Wütherich et al. 2002 [738]).

Protocol:
(controls, definition of positive etc)
Not described
Number of Patients:

Orhan and Sekerel (2003) [737], Fiocchi et al. (2003) [1095], Wütherich et al. (2002) [738], Arai et al (1998) [740], Caffarelli et al. (1997) [742] and Musken et al. (1991) [1094] each tested one patient.

Romano et al. (2001) [1039] tested 54 patients.

Varjonen et al. (1995) [225] tested with rice 16/34 children with atopic dermatitis who already had given a positive SPT with wheat.

Summary of Results:

Strongly positive wheal and flare reaction was observed to rice and not to wheat, barley, oat and lentil or common aeroallergens both with extracts and prick-prick tests (Orhan and Sekerel, 2003 [737]).

Fiocchi et al. (2003) [1095] report positive skin prick test results for a boy for rice and peanut at age 6 (3 mm and 4 mm diameter wheals respectively) and at age 8 (6 and 4 mm diameter wheals respectively).

A single patient had a positive prick-prick test with cooked rice, and a commercial extract (Bencard) but negative SPTs with common inhalant and food allergens (Wütherich et al. 2002 [738]).

Romano et al. (2001) [1039] found that 28/54 patients were SPT positive to rice.

Caffarelli et al. (1997) [742] report a positive SPT for rice and peanut in a single patient.

Some correlation was seen between the wheal sizes for wheat and rice in the children with atopic dermatitis. 11/16 children gave positive SPTwith rice (Varjonen et al. 1995) [225].

Musken et al. (1991) [1094] reported an individual had a positive prick-prick test with both raw and cooked rice.

IgE assay (by RAST, CAP etc)

Number of Studies:
6-10
Food/Type of allergen:

Commercial extracts

IgE protocol:

CAP-FEIA (Orhan and Sekerel, 2003 [737]; Fiocchi et al. 2003 [1095]; Wütherich et al. 2002 [738]; Romano et al. 2001 [1039]; Caffarelli et al. 1997 [742]).

Guinnepain et al. (1996) [741] used CAP-RAST

Shibasaki et al. (1979) [514], Musken et al. (1991) [1094] and Urisu et al. (1991) [535] used RAST.

Number of Patients:

Orhan and Sekerel (2003) [737], Fiocchi et al. (2003) [1095], Wütherich et al. (2002) [738], Arai et al (1998) [740] and Musken et al. (1991) [1094] each used sera from 1 patient.

Guinnepain et al. (1996) [741] used sera from 1 patient with food dependent exercise induced anaphylaxis.

Urisu et al. (1991) [214] and [535] used sera from 31 rice allergic individuals.

Limas et al. (1990) [1099] used sera from 4 patients suspected of allergy to cereals.

Matsuda et al. (1988) [108] used sera from 3 rice allergic individuals.

Shibasaki et al. (1979) [514] used sera from 6 rice allergic individuals.

Summary of Results:

The total IgE concentration was 165 kU/l, and rice specific IgE (CAP-FEIA, Pharmacia, Uppsala, Sweden) was 13.2 kU/l (Class 3) (Orhan and Sekerel, 2003 [737]).

A CAP class 4 was obtained to both rice and peanut at age 6 in the patient of Fiocchi et al. (2003) [1095]. At age 8, specific IgE to rice was 18.50 UI/mL.

The total IgE concentration was 55 kU/l, and IgE specific to rice (CAP-FEIA, Pharmacia, Uppsala, Sweden) was 4.6 kU/l (Class 3) (Wütherich et al. 2002 [738]).

Romano et al. (2001) [1039] found that 24/54 patients were CAP positive to rice (32 were either CAP or SPT positive).

Caffarelli et al. (1997) [742] found a single patient had a positive CAP for rice and peanut.

Guinnepain et al. (1996) [741] reported a specific IgE of 16.4 kU/l for rice in a single patient.

Urisu et al. (1991) [535] found that sera from 31 patients which showed positive RAST values for rice grain extract were also RAST positive for RP16KD. In 17 subjects leukocyte histamine releases was also triggered by RP16KD.

Musken et al. (1991) [1094] reported a positive RAST with raw rice but negative with cooked rice in a single patient..

Limas et al. (1990) [1099] reported the 4 sera gave positive RAST (class 2-4).

Matsuda et al. (1988) [108] reported IgE binding to a purified 16 kDa protein, RAP, by ELISA using each serum at 4 dilutions (1/100 to 1/800).

Shibasaki et al. (1979) [514] investigated the lymphocyte-stimulating properties of rice glutelin and globulin fractions. All fractions were found to be reactive with specific IgE antibody, and two of three fractions from gel filtration revealed lymphocyte-stimulating activity. RAST inhibition revealed considerable cross-reactivity of IgE antibody with the glutelin and globulin fractions.

Immunoblotting

Immunoblotting separation:
Usui et al. (2001) [217] ground samples of each rice tissue (seeds, stem and leaves) to fine pieces in a blender and suspended them in 10 ml/g phosphate buffered saline containing 5mM EDTA and 1mM phenylmethylsulfonyl fluoride. After being kept at 4°C with gentle shaking for 14h and treated with ultrasonication for 1min on ice, the tissue sample was passed through a piece of gauze and centrifuged at 15,000×g for 15min. The supernatant was dialyzed against distilled water and then freeze-dried. The crude extracts and purified proteins were separated by SDS-PAGE, 12% acrylamide, under reducing conditions.

Limas et al. (1990) [1099] defatted rice endosperm with petroleum ether and extracted the flour with chloroform/ethanol (2/1, v/v). The dried residual flour was extracted with 0.5 M NaCl (2 X 10 volumes, 1 hour, 4°C) and proteins precipitated with trichloracetic acid (to 15%). The precipitate was washed with cold acetone and dried. Samples of this extract and of purified proteins were separated by 1-D SDS-PAGE.

Immunoblotting detection method:

Usui et al. (2001) [217] transfered proteins by electrophoretic blotting onto a polyvinylidene difluoride membrane. After being blocked with 1% polyvinylpyrrolidone (Mr 40,000) in phosphate buffered saline (PBS) or 3% BSA in PBS, the membrane was incubated with serum 8 times diluted with 1% BSA in PBS, at 20 °C for 3 h. The membrane was washed with PBS with Tween 20 and incubated with peroxidase-labeled anti-human IgE diluted with 1% BSA in PBS. Activity staining for peroxidase was done with either an enhanced chemiluminescence (ECL) detection kit (Amersham Pharmacia) or 4-chloro-1-naphthol.

Limas et al. (1990) [1099] transfered proteins by electrophoretic blotting onto two nitrocellulose sheets. The sheets were incubated in 20 mM Tris/HCl buffer, pH 7.5, 500 mM NaCl, 0.5% (w/v) BSA and 0.5% (v/v) Triton X-100 (TBS-T) for 2 hours. The sheets were then shaken overnight with pooled sera from the 4 patients (1:9 diluted in TBS-T) and then washed with TBS-T for 30 minutes.

One sheet was shaken for 3 hours with 1:4000 diution of anti-human IgE labelled with alkaline phosphatase followed by 4 washes with TBS-T. Binding was revealed with 5-bromo-4-chloro-3-indolyl phosphate p-toluidine salt and p-nitro blue tetrazolium chloride (30 minutes, room temperature). The second sheet was incubated with iodine 125–labeled anti-human IgE antiserum diluted 1:5(v/v) in TBS-T for 10-18 hours and then washed four times as above. The dried nitrocellulose was exposed on autoradiography film for 10-15 days.

Immunoblotting results:
Fiocchi et al. (2003) [1095] report that immunoblotting with rice showed an IgE binding 16-kDa (suggested to correspond to a member of the alpha-amylase/trypsin inhibitor protein family) and a 25-kD protein band.

Usui et al. (2001) [217] identify the 33-kDa allergen, Glb33, as a glyoxalase I. Recombinant Glb33 was shown to be as reactive as the native Glb33 with mouse IgG and patients' IgE antibodies to Glb33. Glb33 was also shown to be expressed in seeds, stem and leaves using a mouse monoclonal antibody.

Ikezawa et al. (1992) [742] note as unpublished data that the 16 and 50 kDa allergens are frequently detected as allergens by immunoblotting.

Urisu et al. (1991) [214] reported IgE binding to proteins of 14-16, 26, 33 and 56 kDa. The 14-16 kDa proteins were shown to be a family of alpha-amylase/trypsin inhibitors (Nakase et al. 1995 [128]).

Musken et al. (1991) [1094] reported IgE binding to allergens of 14.4 and 28 kDa. A band at 45 kDa was also seen with long grain rice. IgE bound to an IEF band at pH 6.45-6.55.

Limas et al. (1990) [1099] reported IgE binding to an unidentified protein of 12.5 kDa and to the rice alpha-globulin (28 kDa observed). Both proteins were purified and shown to bind IgE but both had blocked N-termini. The purified rice alpha-globulin was identified from its amino acid composition.

Oral provocation

Number of Studies:
1-5
Food used and oral provocation vehicle

Not described for oral challenges.

Fiocchi et al. (2003) [1095] described the inhalant challenge. They extracted rice and wheat proteins in phosphate buffered saline in an agitator for 60 hours at 4°C. The samples were centrifuged at 2500 rpm for 15 minutes and the supernatant dialyzed against deionized distilled water for 24 hours at 4°C. The resulting solutions of 1 mg/mL were used to prepare incremental doses of rice and wheat of 0.0625, 0.125, 0.25, 0.50, and 1 mg/mL in a saline vehicle. Placebo and allergen doses were planned for separate days over 5 hours at hourly intervals. The inhalation provocation tests were performed through use of a nebulizer attached to a dosimeter. The solutions were administered at room temperature as aerosols.

Blind?

Orhan and Sekerel (2003) [737]) and Fiocchi et al. (2003) [1095] were double blind.

Arai et al (1998) [740] was open.

Number of Patients?

Orhan and Sekerel (2003) [737]), Fiocchi et al. (2003) [1095] and Arai et al (1998) [740] each tested 1 patient

Dose response

300 g gave positive response (Arai et al 1998 [740]).

Fiocchi et al. (2003) [1095] reported a positive response to the second dose of aerosol (a cumulative dose of 0.085 mg).

Orhan and Sekerel (2003) [737] did not report a dose.

Symptoms

Nausea after 10 minutes, abdominal pain and diarrhea in a 9 year old girl (Orhan and Sekerel, 2003 [737]).

Fiocchi et al. (2003) [1095] report a positive response, eczema after 24 hours, on rice DBPCFC in a 6 year old boy. At age 11, he was tolerant to ingestion by DBPCFC but double blind challenge with rice as an inhalant caused a urticarial rash and laryngeal stridor.

Wheezing (Arai et al 1998 [740]). The patient could tolerate hypoallergenic rice (Watanabe et al. 1990 [743]).

Musken et al. (1991) [1094] reported a positive challenge with rice.

IgE cross-reactivity and Polysensitisation

Asero et al (2002) [667] reported 11/20 positive SPTs with rice in patients sensitised to Rosaceae LTPs. However, only one reported symptoms with rice as contact allergy

Lehrer et al. (1999) [1034] reported significant correlations between specific IgE to rice and to corn (maize) with r = 0.95 and to soy with r = 0.81 over 123 sera.

IgE cross reactivity with other cereals has been observed but without clinical symptoms (Yamada et al. 1995 [236]).

Varjonen et al. (1995) [225] also reported a correlation between SPT results for wheat and rice in children with atopic dermatitis.

Other Clinical information

Atopic dermatitis due to rice has been reported and RAST has shown a correlation with specific IgE to rice extract especially for severe cases (Ikezawa et al 1992 [746]; Uehara et al 1992 [747]; Uenishi et al 2003 [750]). The complex relationship between food allergy and atopic dermatitis has been reviewed by Sampson (2003) [751].

Rice has been reported as a contact and inhalant allergen. The pollen also includes an allergen, Ory s 1, which is an expansin-like protein.

Cavataio et al. (1996) [739] and Giombetti and Schwartz (1999) [749] describe reactions to ingestion of rice that may not involve IgE. Sicherer et al. (1998) [748] describes a delayed reaction to rice.

Several methods have been developed to produce hypoallergenic rice for the treatment of atopic determatis (Watanabe et al. 1990 [743]; Ikezawa et al. (1992) [742]; Nakamura & Matsuda, 1996 [126])


Reviews (0)

References (29)

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This record was last modified on 18-Oct-2006
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