Allergen avoidance

Allergen avoidance and nasal topical corticosteroid in children with allergic rhinitis. Its effect on mild asthma

 

Ataualpa P. Reis, MDa, Liliane L. Reis, BScb, José Augusto N. Machado, PhDa  Belo Horizonte, Minas Gerais, Brazil

 

 

 

 

 

 

 

 

From a  Santa Casa de Misericórdia de Belo Horizonte, Department of  Biomedicine and Immunology, Minas Gerais, Brazil.
b  Metropolitan Faculty of Belo Horizonte, Minas Gerais, Brazil
Supported  by institutional funding: Santa Casa de Misericórdia de Belo Horizonte(Brazil)
Reprint requests: Ataualpa P. Reis, MD, 1764 Bandeirantes Ave. Belo Horizonte, MG,  30315.000. Brazil
Author: Ataualpa P. dos Reis. Avenida Bandeirantes 1764 - Belo Horizonte-CEP 30315-000 – Minas Gerais, Brazil. Tel: (5531) 3221 9900, Fax: (5531) 3221-8476. E-Mail: apreis@uai.com.br
Total words:

 

 

 

 

 

 

Abstract

 

Background:  Home exposure to high level of house allergens has been demonstrated  to be related to rhinitis and asthma; allergen control as well as the use of corticosteroids can reduce both conditions.
Objectives:  The purpose of the study was to identify environmental allergens and perform aggressive home control measures as well as the simultaneous use of intranasal steroids in children with persistent allergic rhinitis (AR), in order to verify if this approach could reduce mild asthma.
Methods: Children (30) with clinical persistent rhinitis and mild persistent asthma (FEV1>80% of the predicted) were randomly allocated to an aggressive house dust avoidance treatment group (16) and to a control group with no intervention (14).The aggressive intervention for the environment control consisted in the use of mite impermeable covers for mattress and beds, dusting and vacuuming, regular laundered linen, avoidance of carpets and upholstered furniture, avoidance of toys in the bedroom, avoidance of pets in the bedroom, maximal exposure of home to sunlight and control of dampness.
 All patients in both groups used continuously a triamcinolone nasal spray  throughout the study period. We tested whether the intervention and the nasal spray had any effect on the expected percentage of FEV1  (FEV 1%) and on the Peak Flow parameters (PEFR), asthma symptoms and medication usage during a period of six months, as well as the determination of home antigen levels.
Results: Significant improvements were observed in the symptoms scores of the treatment group, and Peak Flow measurements in association with the reduction of antigen determination in their homes. FEV1% determination did not improve; a minor improvement was observed in the control group for the symptom scores and PEFR, but no reduction of antigens was observed.
Conclusion: The results indicate that aggressive dust mite avoidance intervention and the simultaneous use of intranasal steroid in patients with persistent AR and mild persistent asthma had a positive impact on the asthma condition.

Key words:  environment control, asthma, rhinitis, nasal corticosteroid

 

 

 

 

 

 

 

Abbreviation used

FEV1%:   Percent of the predicted FEV1
AR:         Allergic rhinitis
PEFR:      Peak expiratory flow rate

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Introduction

 

   Asthma is the most common chronic disease in children and its most frequent cause is allergy to environmental mites and to other allergens at home 1-3. Several studies have demonstrated the relationship between the exposure to home allergens, e.g. mites, and the development of a respiratory allergic condition 4-6. Furthermore, the correlation between levels of exposure and asthma symptoms, as well as the seriousness of the disease, has also been demonstrated 4, 7-8.
   On the other hand, the inflammation of the upper and lower airways has been strongly associated, as stated in  “ARIA Workshop Report (Allergic Rhinitis and Its Impact on Asthma)” 9, indicating that 80% to 90% of patients suffering from asthma also suffered from allergic rhinitis (AR) at the same time and about 40% to 50% of patients suffering from AR also suffered from asthma, as has been clinically demonstrated 10 .
   We were interested in confirming that intervention on the upper airways may favorably affect the lower airways, and that the long-time use of an intranasal corticosteroid may protect against the exacerbations of asthma 11, as well as reduce bronchial hyperreactivity and improve asthmatic symptoms 12-14.
   We conducted a study including an aggressive intervention on the home environment of patients suffering from allergy, intending to reduce the patients’ exposure to allergens, and  associating the simultaneous, long-time use, for six (6) months of a nasal corticosteroid in children suffering from persistent and mild to moderate AR; we wanted to know if this combination could alter the presence and manifestations of mild asthma.

Methods

 

Subjects

 

   A total of 36 children  (age group 5-15), with persistent AR and also with persistent mild asthma were included in the randomized, prospective, parallel study for six (6) months. The study protocol was designed in accordance with the Helsinki Declaration. All patients and/or their parents were carefully informed and did accept to participate in the research group, through verbal consenting declarations or written documents from the parents or legal guardians before joining the study group and all documents were approved by an Ethics Committee. The inclusion criteria were based on the clinical diagnosis of persistent mild to moderate AR as described in  the classification of the “Brazilian Consensus on Rhinitis”15, puncture positive cutaneous tests to two or more environmental allergens (mainly mites), presence of mild persistent asthma (with FEV1> 80% of the predicted value), in accordance with the classification criteria under the  “Guidelines for the Diagnosis and Management of Asthma-2002” and of the III Brazilian Consensus in the Care of  Asthma-2002 16-17. Subjects using any medication besides short-acting b2 – agonists as needed for their asthma, with an FEV1 below 80%, or clinically unstable, were excluded from the study. Also, subjects with troublesome nasal symptoms that interfered with their daily activities, or with sleep problems at the time of the study, or who were using or had used nasal, oral, inhaled or intramuscular  corticosteroids during the last 4 weeks before recruitment, were excluded. No other medication for the treatment of asthma, except short-term b 2 - agonists, was allowed during the study. Upper respiratory tract infection, sinus infection, or asthma exacerbation within 4 weeks of recruitment or during the study were considered exclusion criteria.

Study design

 

   After an initial screening visit, subjects were enrolled in a 1-week run-in period when nasal and asthma symptoms, frequency and the amount of use of short-term b2  - agonist, pulmonary function and PEFR, were recorded. Patients were re-evaluated at the end of this run-in period and, if stable, were allocated in randomized, two-blinded parallel fashion to the treatment period. After inclusion, the children were divided into 2 groups: an active group with 20 children to whom   aggressive environmental control measures were applied, and a control group (16 children) without aggressive environmental control. All children were treated with the corticosteroid  triamcinolone throughout the study at  a dose of 1 spray  (55mcg) into each nostril at night. The use of oral rescue inhaled bronchodilating medication was also allowed (salbutamol- SOS) vs asthmatic episodes.

Measurements

 

   The active group was instructed to accept the aggressive measures of environmental control, and was asked to report their symptoms on a diary . They were also instructed on the use of the nasal corticosteroid, and of the rescue medication. The control group was given the same instructions except for the environmental control. Measurements were carried out at a 2-month interval until the end of the study.
   Aggressive measures for environmental control in the active group were conducted according to the “practical allergen avoidance” recommendations of WAO (World Allergy Organization) and included: the use of impermeable covers of mattresses and pillows,   house cleaning with a wet  cloth, removal of rugs and carpets, exclusive use of impermeable   sofas, easy chairs and other pieces of furniture , weekly laundry of bedding  with hot (  56o C) water , maximum exposure of the environment to sunlight, avoidance of cloth or furry toys, keeping  pets outdoors, application of  5% ammonia solution in places where  humidity was obvious.
   Samples of house dust were collected (for mite allergens) according to a collecting protocol, using an Electrolux vacuum cleaner, model Vac. A-10, applied onto the surface of the room, mattresses, TV room, rugs and carpets. The vacuuming was performed during two (2) minutes in an area of one (1) square meter. The material collected in an adequate collecting device, using a fine filter of 40 µm, was then mixed to 10 ml of extracting liquid ( 1% BSA-PBS-T), and  sealed. This solution was then shaken and extracted for five (5) minutes and stored in a refrigerator at 4oC until assaying the allergens by the specific semi quantitative  “Rapid Test for Dust Mite” (Indoor Biotechnologies, Ltd., UK-USA) 19. The results were reported as negative, low (less than 0.2 micrograms/g of dust), moderate (0.2-1.0 micrograms/g of dust), or high level (one (1) or more micrograms/g of dust.). 
    The skin tests were performed using disposable plastic pricking devices and glycerinated  extracts purchased from IPI-ASAC do Brasil S/A (International Pharmaceutical Immunology). The allergens used included Dermatophagoides pteronyssinus, Dermatophagoides farinae, Blomia tropicalis, dog epithelium (Canis familiares), cat epithelium (Felis domesticus), fungi of the Penicillium nonatum species, Alternaria alternata, Aspergillus fumigatus and  cockroaches (Blatella germanica and Periplaneta americana). All allergens used were standardized in biological units, and the pricking technique was standardized according to Dreborg and Frew 18. We considered a test to be positive if the papula had a largest diameter equal to or above 3mm, with a negative control using a saline solution equal to zero, and positive control with histamine (10mg) above 3mmD.
   Spirometry was performed in all patients in the run-in period, and on each two subsequent (2) months using the spirographer  Spiromatic Vitatrace VT 130 SL version 3.2 (Pro Médico Ltda.) and interfaced with a Dell Dimension-Pentium 2.400 computer with 1.80 GHZ, using the software developed by the company Engelógica- Engenharia de Sistemas Ltda. A technician was trained by a specialized team, and was the only person in charge of the pulmonary evaluations .She was also responsible for the peak measurements of expiratory flow (PEFR), using a Wright Peak Flow Meter. Three (3) evaluations were done and the best, calculated after temperature and barometric room pressure correction, was recorded.

Statistical analysis

 

   Statistical analysis was performed using  “t” Student Test at the conventional limit of 5% for the paired results, and with  standard average deviation, always compared to   the base line. For the results expressed in percentage without the standard deviation, the Q-square test was used. The correlation coefficient between the expiratory flow peak measurements (PEFR) and the allergen level found at the residences of the patients was also analyzed, using the Spearman method. For these statistical evaluations we used the computer programs SPSS version 10.0 and the Minitab.LNK version 13.0.

Results

 

    A limited number of patients were excluded from the study.  In the active group, four (4) patients were excluded because they did not fulfill the requirements for the aggressive  environmental control, and two (2) patients of the control group were excluded from the study because they had episodes of repeated infections, used other medications, and/or suspended the use of the nasal corticosteroid for long periods of time. The patients’ characteristics (Caucasian) were similar with the variables’ parameters normally  distributed, i.e. the two (2) groups did not show any significant differences between  them (table I).
   We also analyzed  the  total symptom scores for rhinitis and the individual symptom scores for nasal obstruction, itching, rhinorrhea and sneezing. We also analyzed the nasal peak inspiratory flow ( nPIF). AR symptoms remarkably improved through the six (6) months in both groups after the use of the nasal corticosteroid in correlation with the effects on asthma symptoms, but the scores  of obstruction  and the nPIF were consistently and significantly even more improved( manuscript in preparation).

Effects on asthma symptoms

 

   Asthmatic symptoms were analyzed using Borg`s score table20 on breathlessness, wheezing, coughing, and disturbed sleep; in our study, all patients had mild asthma-according to the classification of the 3rd Brazilian Consensus in the Care of Asthma 17, with  an FEV1 above 80% of the expected value. At baseline the symptoms scored an average of 3.1 ±  0.3 SD  and  2.6 ±  0.2 SD;  2.1 ±  0.4 SD; 1.7 ±  0.3 SD during the following months in the active group and 2.9 ±  0.2 SD; 2.4 ±  0.3 SD; 2.3 ±  0.2 SD  for the control group (Fig.1). The statistical analysis for months 2, 4, and 6 in the active group when compared to  baseline, suggests that the treatment provided  a  significant improvement starting at month 2, and continued  until the end of the treatment ( months 4 and 6) at  p< 0.01 . The control group also showed a significant improvement, but at month 2 at p< 0.05; however, at months 4 and 6 it   was p< 0.01. In  summary , asthmatic symptoms in the active group significantly  improved  at months 2, 4, 6 and proved to be consistent; a similar improvement was observed in  the control group  though with a lesser significance at month 2, but with better results on  months 4 and 6.

Effects on PEFR and FEV1 %

   The PEFR was significantly improved: while baseline was - 290 ± 49 SD L/min it changed to 305 ± 38 SD L/min at month 2; 312 ± 32 SD L/min at month 4; and 324 ± 38 SD L/min at month 6 in the active group. In the control group baseline was  - 282 ± 34 SD L/min;   290 ± 28 SD L/min at month 2; 294 ± 30 SD L/min at month 4; and 310 ± 26 SD L/min at month 6 (Fig.2). A significant improvement was observed in the active group at month 6 (p<0.05); significant improvements were also observed at months 2 and 4, but did not reach statistical significance .It is important to note that although improvement was lower in the control group, the improvement was significant  (p< 0.05). There was  improvement of PEFR in both the active and control groups.
   The spirometry (FEV1%) was also performed at these same intervals in all patients both in   the active and the control groups. When compared to baseline there was no significant improvement (in both groups).  FEV1% of the active group was- 84% ± 3 SD at baseline, while the one of the control group was 87% ± 4 SD. At month 6 the average was 85 % ± 3 SD, and 84 ± 2 SD respectively.

Antigen content of dust samples

 

   The study of allergens from environmental mites using the Rapid Test for Dust Mite was ranked as low (0.2 µ/g of collected dust); moderate (0.2 a 1.0 µg/g of collected dust); and high (> de 1.0 µg/g of collected dust). Decrease to a lower category occurred in 50 % in the active group, while 21.42 % of the control group moved to a higher category at the end of month 2, when compared to baseline. 75 % of the active group moved to a lower category while- 14.29 % in the control group moved to a higher category at month 4.  75 % of - the active group were still in  a lower category at month 6 while- 14.29% of the control group were in a higher category ; other 14.29 % moved to the lower category (p < 0.05 on month 2; p< 0.01 on months 4 and 6,  both for the active group). There was no statistically significant alteration among the categories in the control group (p> 0.05).  Decreases in dust level were observed as early as month 2 (50%) , decreasing until month 6 (75%), in the active group; conversely,  decrease in the control was only observed  at month 6 (14.29%)- and was not statistically significant. Some increase in dust level was observed  in the control group(21.42%) at month 2 and month 4 (14.29%) but did not reach significance. In conclusion, aggressive intervention reduced allergen levels ; this was not observed in houses without intervention (figures 3 and 4).

Salbutamol SOS and correlation of PEFR and dust mite concentration

 

   The analysis of the use of - rescuing salbutamol- vs - asthma episodes showed that, in average, there was no difference between the active and control groups. The use of β- 2 agonist as person-days during the first 2 months was 3.6% vs 4.3% (p=0.64) in the active and control group respectively, and did not vary throughout the study period.
   The coefficient of correlation of PEFR numbers and of allergen levels in houses with  high concentration  of allergen  did show  a strong negative correlation ( r= - 0.949,  p< 0.05) , demonstrating  that aggressive intervention measures at the homes of allergic children may result in improving their pulmonary function.

Discussion

 

    It is known that 80 to 90 % of patients suffering from asthma have AR, and 40 to 50% of patients with AR suffer from asthma 10. The reason why some patients with AR develop bronchial hyperresponsiveness , while others do not, is not known. One hypothesis was  that high exposure to allergens may be an important inductive factor. Under natural conditions bronchial hyperresponsiveness may be induced by seasonal exposure to allergens in patients who only have AR21. This phenomenon may also be reproduced in the laboratory. In a study involving sixteen (16) patients with AR and no bronchial hyperreactivity (<20% of reduction in FEV1 reduction after inhaling 75mg/ml of metacholine), 4 patients developed hyperreactivity of the lower airways within the asthmatic standard22. We now know that there is a link between AR and asthma, due to physical contiguity and the same immunopathological mechanisms, mucous ciliary  transport, basal membrane, capillary system, mucous glands, goblet cells and innervation, resulting in  the concept of CARAS (Combined Allergic Rhinitis and Asthma Syndrome) or ARIA (Allergic Rhinitis and its Impact on Asthma)9,23. A nasal challenge test with a specific allergen (with no deposition in the bronchial airways) may trigger bronchial hyperreactivity12. Many patients suffering from AR and who do not suffer from asthma, show abnormal responses with the bronchial challenge, either during the early or late phase, to challenge with metacholine, histamine, or cold air24.
    A great number of scientific papers have consistently reported that treatment of AR is beneficial - vs asthma. Even though antihistamines are not considered to be active to treat asthma, the study ETAC (Early Treatment of the Atopic Child) in which cetirizine was administered for eighteen (18) months to atopic children in the age group 1-2 y, with positive skin tests to mites and pollens, resulted in an approximate 50% reduction of asthma incidence 25. Several studies have confirmed the efficacy of   nasal topical corticosteroids in patients with seasonal AR and mild asthma. Welsh et al.,(1987) already demonstrated  that patients with AR using beclomethasone or topical flunisolide had a significant improvement of their asthma symptoms 26. Corren et al. examined the effect of intranasal beclomethasone on bronchial hyperreactivity in patients with AR and mild asthma, and demonstrated , using metacholine challenge, a significant improvement in bronchial hyperreactivity 27. Other studies have addressed the effect of intranasal corticosteroids in patients with perennial AR and mild asthma. The first of them studied the use of intranasal budesonide and confirmed a reduction of objective nasal obstruction, asthma symptoms, and exercised-induced bronchospasm 28. Watson et al. confirmed the effect of intranasal beclomethasone on asthmatic symptoms and bronchial response to metacholine challenge, with a reduction of   asthmatic symptoms, and  metacholine-induced reactivity 29. Furthermore, these authors reported that, at the end of their study, only 2% of radio-labeled intranasal beclomethasone was found in the pulmonary area, confirming that the effects of the corticosteroid were achieved through the nasal mucosa and not directly in the lungs. Recently, Brazilian and Canadian authors demonstrated that intranasal triamcinolone is capable of reducing the inflammatory markers of the lower airways, when used as treatment of AR in patients   with concomitant asthma 30.
   We report, in this article, on the use of intranasal triamcinolone that did statistically significantly improve the symptoms of mild asthma. Remediation had a rather large effect in the active group, but also in the control group who only used the nasal corticosteroid (Fig 1). When we measured the expiratory peak flow (PEFR) we found significant improvement in the treated group, as well as in the control group, with the exclusive use of    the nasal corticosteroid for a period of six months, but this improvement was obvious only at month 6 of the study (Fig 2). The effects of the nasal topical corticosteroid could also explain why there was no increase of asthmatic symptoms in the control group when the level of allergens was higher as observed  during the  second and fourth months (Fig. 4)   Since  the  bioavailability of nasal triamcinolone is low, it is  unlikely that our results are due to the systemic activity of this medication; the action of the corticosteroid is more likely an anti- inflammatory one  on the inflammatory cells  and locally produced cytokines that affect all the respiratory airways, a functional entity.
  In accordance with the International and the Brazilian Consensus on the diagnosis and treatment of asthma, the treatment of mild asthma must include environmental control, use of beta 2 agonists, as needed, and eventually an inhaled corticosteroid in persistent asthma 16-17. The last Brazilian Consensus about Rhinitis, has recommended as treatment of persistent AR a combination of environmental control, the use of antihistamines, and either topical or oral corticosteroid15. In our study, we evaluated the results of a classical set of procedures in the treatment recommended for patients suffering from persistent AR and mild asthma; we included environmental control, the use of beta 2 - agonists as needed, and a nasal corticosteroids for a prolonged period. We observed positive results and improvement not only of AR, but also of the concomitant mild asthma, affecting our  patients. The environmental control was a critical component of our strategy. Allergy to environmental mites is the most common cause of allergic asthma in children, and environmental control is a logical approach for treating children with respiratory allergy related to mites. The medical literature supporting this statement is rather large31-38. Custovic et al. described the correlation between exposure to mites, reactivity to metacholine, and reduction of  FEV1 in adults39. Chang -Yeung et al. observed that children with asthma, sensitive to mites, showed a positive correlation between asthmatic symptoms and the environmental allergen level, and a negative correlation between PEFR and the level of mites40. Australian researchers have demonstrated that changes in the allergenic concentration in beds correlated positively with bronchial hyperreactivity to histamine and asthmatic symptoms33. European researchers have reported that the use of impermeable covers to mites in beds, combined with the use of filters, improved the bronchial hyperreactivity, even though no improvement had been observed in FEV 1, PEFR or asthmatic symptoms34. Murray and Ferguson, studying children with asthma and undergoing environmental control where they included the use of impermeable pillow encasing and mattress covers, the removal of carpets and plush toys and other items that keep dust, observed less symptoms of asthma, reduction of medication, and improvement in PEFR36. Walshaw and Evans, evaluating adults with asthma in a controlled environment, using impermeable covers, weekly washing of bedclothes, cleaning or removal of carpets, removal of upholstered arm chairs and sofas, observed improvement in PEFR, FEV 1/ FVC ratio, bronchial hyperreactivity to histamine, but not in isolated FEV1, when compared with the control group37.
  In this study, exposure to environmental mites was measured as antigenic concentration in µg/g of dust. This method was recommended at the last three international workshops and has been successfully used with several assays 37,41,42. Methods based on the ELISA technology ( immunoenzymatic assays with a monoclonal antibody)  provide highly  valid rates of antigenic exposure, while semi- quantitative methods, such as the one we used in this  study,  can be  used by clinics, physicians’ offices,  and even by patients to control and monitor the level of allergen concentration at their home.43. Allergens are measured in dust samples collected with a vacuum cleaner in an area of 1 square meter for 2 minutes in three or four areas of the house, mainly in bedrooms, TV rooms, rugs and carpets, showing a  good correlation between the amount of allergens and the exposure rating. The test is rapid and provides the investigator, or the patient, means to reckon the amount in high, moderate or low by simple color  coding that correlates with mite allergens’ group 2 as measured by ELISA.
   The final conclusion of this study is that environmental control and the use of nasal topical corticosteroids in children with AR, for a period of 6 months, are capable of reducing the symptoms of mild asthma, improve the expiratory peak flow (PEFR), and decrease the allergen concentration at the home of patients, supporting the hypothesis of a link between allergic inflammation of the upper and lower airways, and improvement of the asthmatic condition when therapeutic measures are addressing allergic rhinitis.

Acknowledgements

 

   We thank Georges M. Halpern, MD, PhD, for the extensive revision of the
manuscript.
   We thank Alessandro Henrique de Souza Miake and Cristiano Moravia Soares de Matos, from the Institute of Exact Sciences of the Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil, for their contribution to statistical analyses.

 

 

 

 

 

References

 

  1. Peat  JK, Tovey E, Toelle BG, Haby MM, Gray EJ, Mahmic A. House dust mite allergens. A major risk factor for childhood asthma in Australia. Am J Respir Crit Care Med 1996;153:141-6.     
  2. Boulet LP, Turcotte H, Laprise C, Lavertu C, Bedard PM, Lavoie A. Comparative degree  and type of sensitization to common indoor and outdoor allergens in subjects with allergic rhinitis and/or asthma. Clin Exp Allergy 1997; 27: 52-9.
  3. Reis AP. Controle ambiental nas Doenças Alérgicas -prós e contras. Rev Bras Alergia Imunopatol  1998; 21: 112-21.
  4. Host A, Halken  S. The role of allergy in childhood asthma. Allergy 2.000; 55: 600-8.
  5. Wickman M, Nordvall SL, Pershagen G, Sundell J, Schwartz B. House dust mites sensitization in children and residential characteristics in a temperate region. J Allergy Clin Immunol 1991; 88: 89-95.
  6. Huss K, Adkinson NF Jr, Eggleston PA, Dawson C, Van Natta ML, Hamilton RG. House dust mite and cockroach exposure are strong risk factors for positive allergy skin test responses in the Childhood Asthma Management Program. J Allergy Clin Immmunol 2001; 107: 48-54.
  7. Vervloet D, Charspin D, Haddi E, Nguyen A, Birnbaum J, Soler M. Medication requirements and house dust exposure in mite-sensitive asthmatics. Allergy 1991; 46: 554-58.
  8. Sporik R, Platts-Mills TA, Cogswell JJ. Exposure to house dust mite allergen of children admitted to hospital with asthma. Clin Exp Allergy 1993; 23: 740-6.
  9. Bousquet J & ARIA Workshop Group. Allergic Rhinitis and its Impact on Asthma. J Allergy Clin Immunol 2001; 108(Suppll.): S1-333.
  10. Leynaert B, Neukirch F, Demoly P, Bousquet J. Epidemiologic evidence for asthma and rhinitis co morbidity. J Allergy Clin Immunol 2.000; 106: S201-05.
  11. Adams RJ, Fuhlbrigge AL, Finkelstein JA, Weiss ST. Intranasal steroids and the risk of emergency department visits for asthma. J Allergy Clin Immunol 2002; 109: 636-42.
  12. Corren J, Adinoff AD, Irvin CG. Changes in bronchial responsiveness following nasal provocation with allergen. J Allergy Clin Immunol 1992; 89: 611-18.
  13. Watson WTA, Becker AB, Simons FE. Treatment of allergic rhinitis with intranasal corticosteroids in patients with mild asthma: effect on lower airway responsiveness. J Allergy Clin Immunol 1993; 91: 97-101.
  14. Reis AP, Machado JAN, Reis LL. Allergen avoidance and nasal topical corticosteroid in children with allergic rhinitis and mild asthma. Allergy Clin Immunol Int:J World Allergy Org 2003; Suppl:5.
  15. Consenso sobre Rinites 1999. Revista Brasileira de Otorrinolaringologia 1999; 66(Suppl): 1-34.
  16. Guidelines for the Diagnosis and Management of Asthma. Update Selected Topics 2002. J Allergy Clin Immunol 2002; 110(Suppl): S142-219.
  17. III Consenso Brasileiro no Manejo da Asma 2002. J Pneumol 2002; 28(Suppl): S1-28.
  18. Dreborg S, Frew A. Position Paper: Allergen standardization and skin tests. Allergy 1992; Suppl: 49-82.
  19. Chapman MD, Vailes LD, Ichikawa K.Immunoassays for indoors allergens. Clin Rev Allergy  Immunol 2.000; 18: 285-300.
  20. Borg GAV. Psychophysical bases of perceived exertion. Med Sc Sports Exerc 1982; 14: 377-81.
  21. Madonini E, Briatico-Vaganosa G, Pappacoda A, Maccagni G, Cardoni A, Saporiti F. Seasonal increase of bronchial reactivity in allergic rhinitis. J Allergy Clin Immunol 1987; 79: 358-363.
  22. Papiris S, Asi W, Windom H, Liu M, Permutt S, Brennan-Diemer F, Togias A. Strong association of late phase reactions with asthma (Submitted) Eur Resp J.
  23. Geller M. Vias aéreas unidas:a atopia como processo sistêmico and continuo. Rev Bras Alergia Imunopatol  2002; 25: 74-80.
  24. Aubier M.Liu K. The upper and lower airways. An Allergy Asthma Immunol 1999; 83: 431-34.
  25. Warner J O et ETAC Study Group. A double-blinded, randomized, placebo-controlled trial of cetirizine in preventing the onset of asthma in children with atopic dermatitis-18 months’ treatment and 18 months’ post treatment follow-up. J Allergy Clin Immunol 2001;108:929-937.
  26. Welsh PW, Stricker EW, Chu-Pin C. Efficacy of beclomethasone nasal solution, flunisolide and cromolyn in relieving symptoms of ragweed allergy. Mayo Clin Proc 1987; 62: 125-34.
  27. Corren J, Adinoff AD, Buchmeier AD, Irvin CG. Nasal beclomethasone prevents the seasonal increase in bronchial responsiveness in patients with allergic rhinitis and asthma. J Allergy Clin Immunol 1992; 90: 250-6.
  28. Henriksen JW, Wenzel A. Effect of an intranasally administered corticosteroid(budesonide) on nasal obstruction, mouth breathing and asthma. Am Rev Resp Dis 1984; 130:1014-8.
  29. Watson WTA, Becker AB, Simons FER. Treatment of allergic rhinitis with intranasal corticosteroid in patients with mild asthma: effect on lower airway responsiveness. J Allergy Clin Immunol 1993; 91: 97-101.
  30. Sandrini A, Ferreira IV, Jardim JR, Zamel N, Chapman KR. Effect of nasal triamcinolone acetonide on lower airway inflammatory markers in patients with allergic rhinitis. J Allergy Clin Immunol 2003; 11: 313-20.
  31. Platts-Mills TAE. Dust mite allergens and asthma-a worldwide problem. J Allergy Clin Immunol 1989; 83: 416-27.
  32. Platts-Mills TAE, Woodfolk JA, Chapman MD, Heymann PW. Changing concepts of allergic disease: the attempt to keep up real changes in lifestyle. J Allergy Clin Immunol 1996; 98: S297-306.
  33. Marks GB, Tovey ER, Green W, Shearer M, Salome CM, Woolcock AJ. The effect of changes in house dust mite allergen exposure on the severity of asthma. Clin Exp Allergy 1995; 25: 114-18.
  34. van der Heide S, Kauffman HF, Dubois AE, de Monchy JER. Allergen reduction measures in houses of allergic asthmatic patients: effects of air cleaners and allergen impermeable mattress covers. Eur Respir J 1997; 10: 1217-23.
  35. Korsgaard J. Mite asthma and residency. A case-control study on the impact of exposure to house dust mites in dwellings. Am Rev Resp Dis 1983; 128: 231-5.
  36. Murray AB, Ferguson AC. Dust-free bedrooms in the treatment of asthmatic children with house dust mite allergy: a controlled trial. Pediatrics 1983; 71: 418-22.
  37. Walshaw MJ, Evans CC. Allergen avoidance in house dust mite sensitive adult asthma. Q J Med 1986; 58: 199-215.
  38. Halken S, Host A, Niklassen U, Hansen LG, Nielsen F, Pedersen S, et al. Effect of mattress and pillow encasings on children with asthma and house dust mite allergy. J Allergy Clin Immunol 2003; 111: 169-76.
  39. Custovic A, Toggard SCV, Francis HC, Chapman MD, Woodcock A. Exposure to house dust mite allergens and the clinical activity of asthma. J Allergy Clin Immunol 1996; 98: 64-72.
  40. Chan-Yeung M, Manfredo J, Dimich-Ward H, Lam J, Ferguson A, Warren P et al. Mite and cat allergen levels in homes and severity of asthma. Am J Resp Crit Care Med 1995; 152: 1085-11.
  41. Ehnert B, Lau-Shadendorf S, Weber A, Buettner P, Schou C, Wahn U. Reducing domestic exposure to dust mite allergen reduces bronchial hypersensitivity in sensitive children with asthma. J Allergy Clin Immunol 1992; 90:135-8.
  42. Platts-Mills TAE, Vervloet D, Thomas WR, Aalberse RC, Chapman MD.. Report of the Third International Workshop in Indoor Allergens and Asthma. J Allergy Clin Immunol 1999; 100: S1-S24.
  43. Chapman MD, Tsay A, Vailes LD. Home allergen monitoring and control: improving clinical practice and patients benefits. Allergy 2001; 56: 604-10.

 

Table I.  Subject characteristics in each treatment group

Allergic rhinitis + mild asthma

 

Aggressive intervention

No intervention

Remarks

 

 

 

 

No. of patients

20

16

 

No. of patients completing the study

16

14

 

Age (years)

10.5 (SD: 5-15)

10.7 (SD: 5-15)

 

Sex

10 F/6M

9 F/5M

 

Atopy

16

14

 

Duration of AR diagnosis

 

 

 

1st year

05

04

 

2nd year

08

06

 

3rd year or longer

03

04

 

Duration of asthma diagnosis

 

 

 

1st year

04

03

 

2nd year

06

05

 

3rd year or longer

06

06

 

Skin test responses for persistent allergens

16

14

(at least 1 positive)

 

 

 

 

 

 

 

 

 

 

 

 

Figure Legends

 

Fig 1.  Average of total asthmatic symptoms scores .
Total Borg symptoms included to: breathlessness, wheezing , cough, and disturbed sleep.
Active group differed  significantly  at  months 2,4 and 6 from baseline ( p<0.01).
Control group also varied but less significantly at month 2 (p< 0.05) but was as significant as the active group at months 4 and 6 (p< 0.01) when compared to  the baseline.

 

Fig 2.   Changes from baseline in Peak Expiratory Flow Rate (PEFR-L/min) after intervention.
 Active =intervention + topical nasal corticosteroid (p< 0.05 month 6; N.S.   months 2 and 4)  Control=no intervention + topical nasal corticosteroid ( p< 0.05 month 6 and N.S months 2 and 4)

 

Fig.3   Changes in dust mite concentration levels-intervention group (h

igh > 1.0 µg/ g, moderate, 0.2 to 1.0 µg/g and low,< 0.2 µg/ g of dust). Changes from high to low at month 2: 50 % (p< 0.05); month 4: 75 % (p< 0.01) and month 6: 75 % (p< 0.01), when compared to the baseline.

 

Fig 4.   Changes in dust mite concentration levels- control group (h

igh > 1.0 µg/ g, moderate, 0.2 to 1.0 µg/g and low,< 0.2 µg/ g of dust). Changes from low to high at month 2: 21.42 % (p> 0.05); month 4: 14.29 % (p> 0.05); month 6: 14.29 % (p> 0.05) and change from high to low concentration: 14.29 % (p> 0.05), when compared to the baseline.
The change to a lower concentration range was significant in the intervention when compared to the control group ( p<0.03)

Notícias
  • Diretor Médico.
  • Professor Convidado de Pós Graduação da UFMG e Santa Casa de Belo Horizonte.
  • Doutor em Imunologia pela
  • Bioquímica da UFMG.
  • Ex-presidente da Soc. Brasileira de Alergia e Imunopatologia-MG.
  • Artigos