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Brief Reports

Indian Pediatrics 2005; 42:362-366 

Avoidance of Food Alleggens in Childhood Asthma

 

S.R. Agarkhedkar, H.B. Bapat and B.N. Bapat

From the Allergy Research Institute, Sinhagad Road, Vadgaon Budruk, Pune, 411 051, India and Department of Pediatrics, MIMER Medical College,Talegaon Dabhade, Pune, India.

Correspondence to :Dr. H.B.Bapat, Allergy Research Institute, Sinhgad Road,Vadgaon Budruk, Pune 411 051, Maharashtra, India. E-mail: [email protected] 

Manuscript received: November 18, 2003, Initial review completed: March 1, 2004;
Revision accepted: October 19, 2004.

Abstract:

Twenty-four patients of moderate persistent perennial asthma with documented aggravation to severe persistent asthma, during monsoon season in the past two years, were put on specific elimination diet during August and September. The diet was based on results of in-vitro allergy tests for a selected food panel. On specific elimination diet, five patients improved to mild persistent asthma and twelve patients improved to mild persistent asthma with occasional exacerbations . Six patients remained at moderate persistent asthma and only one patient deteriorated to severe persistent asthma. These results indicate that food avoidance may help in asthma control in children.

Key words: Allergy, Asthma, Food-allergens.

Allergic bronchial asthma is caused by exposure to environmental and dietary allergens. Allergen avoidance is considered to be an important aspect of management of allergic asthma(1). Many studies show the beneficial effect of environmental allergen avoidance(2). Regarding avoidance of food allergens, studies are available only for neonates and infants in relation to later risk of asthma(3). There is paucity of evidence dealing specifically with avoidance of food allergens in the clinical management of childhood asthma.

The purpose of this study was to evaluate possible effect of a specific elimination diet (i.e., avoidance of food items for which serum IgE titers were raised) in pediatric asthmatics having seasonal aggravation.

Subjects and Methods

This study was carried out in pediatric patients of bronchial asthma, attending the out patient department of a general teaching hospital. Age of the children was in the range of 3 to 15 years. There were 14 males and 10 females.

All children had moderate perennial asthma. Fifteen patients were receiving Step 2 and nine patients were receiving Step 3 treatment as per GINA guidelines(4). Previous two years records showed that all of them deteriorated to severe persistent asthma during the peak monsoon months of August and September and needed upgradation to Step 4 treatment.

Total IgE levels and specific IgE titers for all foodstuffs listed in the Table I were measured in all children. The test was performed on clear serum separated from 5 mL venous blood. Total serum IgE was measured by a two stage enzyme immuno-assay sandwich technique. The enzyme lable used was penicillinase manufactured by Hindustan Antbiotics, India. The iodometric method of penicillinase assay introduced by Pollock(5) and modified by Ghosh and Borkar(6) was employed to measure bound enzyme. Penicillin, starch, iodine, gelatin and phosphate buffer formed the substrate mixture. Time taken for decolorisation of substrate mixture was plotted against different dilutions of IgE standards to get a reference curve.

For Specific IgE Titers (Allergy Research Institute Specific IgE Titers: ARISIT), extracts of foods were prepared at Allergy Research Institute, Pune as per standard methods(7). Fractions having maximum molecular weight were collected by passing extracts through a ceralose 6 B column (bead size 40 to 190 microns). ELISA was carried out, employing penicillinase enzyme for conjugate.

Sandwich technique was used and iodometric method mentioned above was followed with penicillin, starch, iodine, gelatin and phosphate buffer forming the substrate mixture. Specific IgE titre was calculated from the time taken in seconds for decolorisation of iodine in the substrate for two different dilutions of serum, a ratio serving as an index of binding of antigen and corresponding specific IgE if present in the serum. At our institute mean specific IgE titers in asymptomatic, non-atopic individuals for each antigen included in the food panel was 1.07 with standard deviation of .002. Specific IgE titers higher than 1.085 were considered positive.

Patients were asked to avoid all food items, which tested positive and parents were asked to maintain a food diary. The tests were carried out in middle of July and patients were asked to start food avoidance immediately.

All patients were called for 8 follow up visits during study period, i.e., weekly. They were instructed to contact for any aggravation of symptoms. If they could not contact the doctor they were asked to make a written note of aggravation and medication required to control the aggravation.

Results

Twenty four patients having documented deterioration in control of their perenial asthma during months of August and September in two previous years were selected for the study. Their ages ranged from 3 yrs to 15 yrs and there were 14 males and 10 females.

Normal range of total Ige at our Allergy Research Institute has been found to be 150 ng/mL to 400 ngm/mL (with mean of 232 ng/mL and SD 34.7 ngm/mL). Total IgE level in all patients was more than 1500 ng/mL.

The result of specific IgE titers against different food items is presented in Table I.

TABLE I

Specific  IgE Titers in Study Subjects Against Different Food Stuffs.
Food Item IgE raised
n
Food item
 
IgE raised
n
Food item IgE raised
n
Food Item IgE raised
n
Cereals
Rice 20 (83%) Wheat 12 (50%) Maida 9 (38%) Maize 7(29%) 
Jowar 4 (17%)
Pulses
Tur  Dal 11(46%) Chana Dal 19 (79%) Masoor Dal 4 (17%) Moong Dal 19(79%)
Udid Dal 23(96%) Soyabean 5 (21%) Back-eyed
beans  
19(79%)
Beverages
Tea 1 (4%) Coffee 2 (8%) Cocoa 5 (21%)
Vegetables
Carrot 21 (88%) Potato 20(83%) Navalkol 18(75%) Cauliflower 19(79%)
Cabbage 8(33%) Cucumber 21(88%) Tondli 15(63%) Onions 6(25%)
Ridge-gourd 17(71%) Cluster-beans 18(75%) Red-pumpkin 11(46%) White-
pumpkin
 21(88%)
Brinjal 22(92%) French-beans 18(75%)
Fruits
Apple 21(88%) Banana 20(83%) Mosambi 19(79%) Lemon 19(79%)
Tomato 2(8%) Grapes 21(88%) Orange 4(17%) Pineapple 19(79%)
Papai 7(29%) Kokam 19(79%) Guava 19(79%) Sugarcane 18(75%)
Water-melon 19 (79%) Musk-melon 23(96%) Alphonso 19(79%) Chikku 18(75%)
Oils  
Groundnut 10 (42%) Coconut 5 (21%) Til 9(29%) Safflower 8(33%)
Mustard 9(29%) Cotton-seed 8(33%) Sunflower 9(29%)
Non-Vegetarian
Egg  4(17%) Mutton 19(79%) Chicken 20 (83%) Prawns 15 (75%)
Pomphret 17(71%) Rohu 14 (58%) Surmai 19(79%)
Milk Products
Milk 6(25%) Cheese 20 (83%) Curd 17 (71%) Butter 6 (25%)
Ghee 6(25%)
Spices 
Garlic 14 (58%) Ginger 11(46%) Red Chilly 3 (12.5 %) Green Chilly 8 (33%)
Turmeric 12 (50%) Jira 20 ( 83%) Coriander 20 (83%) Black-pepper 22 (92%)
Hing 15 (63%)
	

Majority (83%) of children had raised specific IgE titers against rice whereas only four (17%) children had raised antibodies against jowar. Among the pulses in vitro hypersensitivity against masoor dal was present in only 17% as compared to 96% and 79% against udid dal and chana dal or moong dal respectively. In the vegetable category, most children were allergic to brinjal while only 25% were allergic to onions. Among the fruits all but one child had raised titer against musk melon while only two had raised titer against tomato. In the cooking oil group antibody titer for groundnut oil was seen to be positive in 42% of children while corresponding figure for coconut oil was 21%. Among non-vegetarian items antibody titer against chicken was positive in 83% but egg was positive in only 17% children.

After elimination diet patients were classified on basis of their clinical status as per GINA guidelines(4) and their clinical status in August and September of current year was compared with that of previous two years during same months.

During August and September of previous two years, all patients had deterioration of asthma control to severe persistent asthma (Group IV).

During August and September of current year while on specific elimination diet five patients had mild persistent asthma with no aggravation (Group I ) and twelve had mild persistent asthma with occasional aggravation controlled with beta agonist (Group II ). Six patients did not deteriorate to severe persistent asthma and remained in Group III. Only one patient deteriorated to severe persistent asthma during current year while on specific elimination diet.

Discussion

In the present study the distribution of clinical status during August and September of the current year with specific elimination diet was compared to that during August and September of the previous years when none of the patients were on specific elimination diet and had deteriorated. The results indicated that deterioration could be prevented in most patients with specific food avoidance in the vulnerable period. There were certain limitations of the present study.The study was based on speculation that the children would have progressed to severe persistent asthma during August and September without specific elimination diet.However the records of these children showed that they had worsened during these months in the last two years.There was no other obvious reason that they should have not deteriorated this year while age advanced only by one year. Another limitation of the study was lack of control group and a small sample size which precluded any valid statistical interpretation

The beneficial effect of food avoidance in our cases could possibly be explained by the concept of Total Allergen Load introduced by Feinberg(8) and later highlighted by Sheldon (9). Sheldon observed that in comparison with sensitivity to inhalants, sensitivity to foods is more common in infants and children and it is therefore important not to overlook food allergy. Food allergies need not be perennial and patients may manifest symptoms only during seasons when these foods are available or consumed in large amount affecting the allergen load(9). Symptoms occur when mediators are released on degranulation of mast cells. Degranulation results from binding of the double bond of antigen-specific IgE receptors,present for that particular antigen on the mast cells. Thus, degree of response is directly related to product of the dose of antigen with number of antigen-specific IgE receptors.

Each individual antigen on its own may not be able to produce much reaction since number of antigen-specific receptors for that particular antigen are few. The simultaneous exposure to a number of such antigens, however, would bind enough antigen-specific IgE receptors on a greater number of mast cells and result in symptoms(10).

Overall the results of this study suggested, that children with asthma having seasonal exacerbation have evidence of in-vitro hypersensitivity to a wide variety of food antigens and the use of a specific elimination diet might prevent the seasonal exacerbation. These preliminary results should be confirmed by large well-designed controlled trials.

Acknowledgement

Authors are grateful to Dean, M.I.M.E.R. Medical College, Talegaon, Dabhade, Pune, India for the permission to conduct study and for providing other facilities

Contributors: BNB provided the concept and framework of the study. SRA conducted the study with HBB and drafted the manuscript. SRA shall act as guarantor.

Funding: None.

Competing interest: None.

 

Key Messages


• Children with seasonal asthma have evidence of in-vitro hypersensitivity to wide variety of food antigens

• Use of specific elimination diet might help in better control asthma in these children.
 

 

 References

 

1. British Thoracic Society, National Asthma Campaign, Royal College of Physicians of London. The British guidelines on asthma management, 1995: Review and position statement. Thorax 1997; 52: 1-27.

2. Custovic A, Simpson A, Chapman MD, Woodcock A. Allergen avoidance in the treatment of asthma and atopic disorders. Thorax 1998; 53: 63-72.

3. Zeigar RS, Heller S. The development and prediction of atopy in high-risk children: follow-up at age seven years in a prospective randomized study of combined maternal and infant food allergen avoidance. J Allergy Clin Immunol 1995; 95: 1179-1190.

4. National Heart Lung and Blood Institute. Global Strategy for Asthma Management and Prevention. NHLBI / WHO Workshop report. NIH PUBLICATION No. 95. National Heart Lung and Blood Institute, 1995; p. 36-59.

5. Pollock MR. A Simple Method for the production of high titer penicillinase. J Pharmacol 1968; 9: 609-611.

6. Ghosh C, Borkar DS. Studies on penicillinase: A modified rapid iodometric method of assay. Hindustan Antibiotics Bull,1 961; 3: 85-91.

7. Phillips GL. Preparation of allergenic extracts for testing and treatment. In: Sheldon JM, Lovel RD, Mathews KP, editors. A Manual of Clinical Allergy, 2nd edn. Philadelphia: W.B. Saunders & Co. 1967; p. 507-531.

8. Feinberg SM. Allergy in Practice. 2nd edn. Chicago: The Yearbook Publishers Inc., 1946; p. 85-86.

9. Sheldon JM. Food Allergy and gastrointestinal allergy. In: Sheldon JM , Lovel RD, Mathews KP editors.A Manual Of Clinical Allergy. 2nd edn. Philadelphia: W.B. Saunders & Co. 1967; p.196-225.

10. Frick OL. Immediate hypersensitivity. In: Stites DP, Stobo JO, Fudenberg HH, Wells JV, eds. Basic & Clinical Immunology. 6th edn. Singapore: Lange Medical Publications ; 1987. p. 197-227.

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