The importance of housing characteristics in determining house dust mite (derp1) levels in carpets in New Zealand
Background: A study done in 1994 in Wellington, New Zealand showed that having carpeted floors, carpets more than 1 year old, the autumn season and increasing family size were the most important determinants of house dust mite (Der p 1) levels. However, there were many unexplained variabilities between houses.
Objective: To determine to what extent housing characteristics might explain this variability in dust mite levels between houses.
Methods: A selection of houses were chosen from the 1994 study and a questionnaire was used to collect information on housing characteristics including:
" Building materials
" Insulation (to prevent heat loss) in walls, ceilings or under floors
" Condensation, damp and mould
" Hours of sun, position of living room in relation to other rooms in the house
" Vacuum cleaner - make, model, and motor size, frequency & recency of vacuuming
" Steam cleaning or shampooing
" Carpet & underlay material
" Type of carpet and age and Occupancy.
The sampling frame of the study was based on 355 houses. From this 78 houses were eligible for the study. Living room dust was sampled and Der p 1 levels were estimated by ELISA test and expressed as m g/g and m g/m2.
Temperature and relative humidity for each house was calculated.
Results: Houses with insulation or a room or garage below the living room had approximately half of the der p 1 concentration than houses without these features. Having more than 2 children was associated with higher levels of Der p 1.
Carpet underlay less than 8mm thick was associated with an almost 3-fold increase in m g/m2 in the whole room sample when compared with thicker carpet underlays.
Conclusion: The presence of insulation is the single most important characteristic explaining the between-house variability in der p 1 levels on carpeted living room floors.
Reference: Clinical and Experimental Allergy, 2001, Volume 31, pages 827-835
AAC Comments: This is a very good study by Wickens et al from the Wellington Asthma research group. Along with results of similar studies from other Western countries we can conclude that higher dust mite levels are related to:
" Presence of carpets vs. smooth floors
" Older carpets
" Older homes poor insulation
" Presence of damp in the home
" Increasing number of occupants
" Older mattress and bedding.
Diet high in polyunsaturated fats may increase risk of asthma in young children
Study: Asthma in preschool children: prevalence and risk factors
M M Haby et al, Royal Childrens Hospital, Melbourne, Australia
Background: The prevalence of asthma in children has increased in many countries over recent years. To plan effective intervention to reverse this trend we need a better understanding of the risk factors for asthma in early life. This study was undertaken to measure the prevalence of, and risk factors for, asthma in preschool children.
Methods: Parents of children aged 3-5 years living in two cities (Lismore, n=383; Wagga Wagga, n=591) in New south Wales, Australia, were surveyed by questionnaire to ascertain the presence of asthma and various proposed risk factors for asthma in their children. Recent asthma was defined as ever having been diagnosed with asthma and having cough or wheeze in the last 12 months. Atopy was measured by prick tests to six common allergens.
Results: The prevalence of recent asthma was 22% in Lismore and 18% in Wagga Wagga. Factors which increased the risk of recent asthma were: atopy, having a parent with a history of asthma, having had a serious chest infection in the first 2 years of life, and a high dietary intake of polyunsaturated fats. Breast feeding and having 3 or more older siblings decreased the risk of recent asthma.
Conclusion: Of the factors tested, those that have the greatest potential to be modified to reduce the risk of asthma are breast-feeding and consumption of polyunsaturated fats.
Reference: Thorax 2001; 56: 589-595 (August).
Does tobacco smoke prevent atopic disorder?
Background: Earlier studies have given conflicting results regarding the effect of tobacco smoke on atopic sensitisation.
Methods: A cross-sectional study of present and former smoking habits in relation to atopic disorders from data on 6909 adults (16-49yrs) and their 4472 children (3-15 years) from the Swedish Survey of Living Conditions in 1996-97.
Results: The prevalence of allergic asthma and allergic rhino conjunctivitis decreased, in a dose-response manner, with increasing exposure to tobacco smoke in the adult study population. This pattern was not affected much when potential cofounders (sex, age, education, domicile, country of birth) were entered into a multivariate analysis. Former smokers had a tendency for a slightly lower risk. In a multivariate analysis, children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for suffering from, asthma, eczema, allergic rhinitis and food allergy, compared to children of mothers who had never smoked. Children of fathers who smoked at least 15 cigarettes a day had a similar tendency.
Conclusion: This study demonstrates an association between current exposure to tobacco smoke and a low risk for atopic disorders in smokers themselves and a similar tendency in their children. There is now the need for a prospective study to certify the causal effect of this association.
Reference: Clinical and Experimental Allergy, 2001, Volume 31, pages 908-914
AAC Comment: This is only an association at this stage and there could be several explanations for this. Is the gene for addiction protective of allergies? Are smokers more likely to live in dirty environments? Are families with a history of asthma less likely to smoke? Are smokers less likely to perceive atopic symptoms? (This was a subjective study)
This article was chosen mainly because of its controversial message, but also to highlight my earlier point about how quickly Allergy views change. This study might also shed some more light on the mystery of why allergies are increasing.
Even before we can identify the reason for the association, the message to asthmatics should be the same as always "Smoking is a trigger for asthma and should be avoided".
Depot corticosteroid treatment for hay fever causing avascular necrosis of both hips BMJ, June 30: Lesson of the week
Consider immunotherapy rather than depot corticosteroid treatment for hay fever
S M S Nasser, senior registrar, P W Ewan, consultant, Dept of Allergy and Clinical Immunology, Addenbrookes Hosp., Cambridge
The British Society for Allergy and Clinical Immunology published guidelines on the management of rhinitis recommend that when allergen avoidance measures are insufficient, oral or topical antihistamines should be used as required or topical sodium cromoglycate used regularly. If these treatments are ineffective, intranasal steroids should be taken regularly, with antihistamines added if required. If this stepped care approach is adhered to, the vast majority of patients will respond and systemic steroids are very rarely required.
Case report
A 42-year old man developed hay fever at 21 years of age, but his symptoms became severe and disabling at age 27. Every year in mid-April he developed severe rhino conjunctivitis with incessant sneezing and blocked nose. Symptoms would continue until mid July, consistent with tree and grass pollen allergy. His symptoms were severe enough to prevent him from going to work. For the past eight years he also got seasonal asthma.
He had used antihistamines, and a number of intranasal steroids, including beclomethasone, budesonide and fluticasone, but without relief of symptoms; therefore his GP resorted to depot steroids. From 1987 to 1997 he was given 16 injections of depot steroids: 9 of Kenalog (triamcinalone) 40mg and 7 of Depo-Medrone (methylprednisolone) 80mg. His symptoms were relieved for up to 6 weeks after his injections.
He had no other atopic disease. He was a non-smoker, did not drink alcohol, and had no history of substance abuse or previous musculoskeletal problems.
In August 1997 he developed a limp, with pain in his right hip, and a few months later developed similar symptoms in his left hip. Plain radiographs showed abnormalities in both hip joints. MRI scans arranged by an Orthopaedic Surgeon showed avascular necrosis of both femoral heads (right worse than left).
It was thought that he would require total hip replacement at some stage in the future.
Reference: BMJ 2001; 322: 1589-1591 (30 June).
Comments: Avascular necrosis is an uncommon, though serious complication of corticosteroid treatment. This has not been previously described in hay fever or with the use of depot steroids.
Avascular necrosis of the hip is associated with steroid therapy, but there is no direct relationship with the total steroid dosage. It has been reported to develop after as little as 2 weeks of steroid therapy, but no susceptibility factors have been identified.
Avascular necrosis affects patients in their 30s or early 40s, corticosteroids being the leading cause, although alcohol and substance abuse have been implicated. Patients who develop avascular necrosis at an early age must undergo total hip replacement, which carries a poor long-term prognosis.
In New Zealand some GPs use annual depot steroids for hay fever. With the options of good non-sedating antihistamines, intranasal steroids and immunotherapy widely available there should be no need to use regular depot steroids.
Does pine pollen cause hay fever?
Study: Pinus pollen aerobiology and clinical sensitisation in northwest Spain
Background: Pinus Pollen has been generally considered to be a rare and clinically insignificant allergen. In their geographical area in northwest Spain, pinus pollen constitutes one of the most prevalent pollen. Pinus pinaster and Pinus radiata are the main species.
Objective: This study aimed to determine the atmospheric fluctuations and the existence of patients monosensitized to pinus pollen in their region
Method: Patients attending their outpatient clinic in the last 4 years with positive skin prick test to pinus pollen and with respiratory symptoms were selected. They were skin tested with commercial extracts of a battery of inhalants including pine pollen. RASTtype testing using Pharmacia CAP was also performed. Airborne pine pollen counts were obtained for a 5-year period (1995 to 1999).
Results: 10 patients were presented with sensitivity to pine pollen and with respiratory symptoms coinciding with pine pollen season (February to April). Most of these patients were monosensitised to pine pollen and suffered from seasonal rhino conjunctivitis. Pine pollen is present in their area in large amounts in February to April with a peak pollen count in March and April.
Conclusion: Pine pollen may be an important allergen since it causes allergic rhinitis in patients monosensitised to pine pollen. Therefore, the researchers think, "It must be taken into account in patients living in areas with high pine pollen concentration and with seasonal respiratory disease".
AAC Comment: New Zealand has plenty of pine trees, but this pollen has generally not been considered to be a serious allergenic hazard. Some of the reasons proposed for the hypoallergenicity of pine pollen include: the large size of the grain and an assumed poor penetration of the respiratory tract, its low protein content, and also its hydrophobic nature because of its waxy coat. The large size of the pollen also prevents it from travelling long distances. David Fountain, Massey University and Cornford studied the allergenicity of Pinus radiata pollen and they detected 5 allergenic proteins, but they proved that the release of proteins from Pinus pollen in an aqueous medium was much lower than that obtained from grass pollen subjected to equivalent conditions.
In New Zealand most allergy sufferers will know when it is the pine pollen season, because of the yellow sheen covering cars and ponds in the mornings. Patients will also describe hay fever symptoms, and I would put it down to the well-known irritant effect of pine pollen. Also, when skin prick tests were routinely done for hay fever, it was very rare to get a strongly positive result to pine. Based on this study, we should rethink our approach to pine pollen allergy.
Are oats harmful in coeliac disease?
Study: Immunologic evidence of no harmful effect of oats in coeliac disease
Antonio Picarelli et al, St Paul Hospital, Rome
Background: It was recently shown that antiendomysial antibodies (EMAs), which are highly sensitive and specific for coeliac disease, are produced by intestinal mucosa. Furthermore, EMAs were detected previously in supernatant fluid from cultured duodenal mucosa specimens collected from treated coeliac disease patients and in culture media of biopsy specimens collected from treated coeliac disease patients after an in vivo challenge with gliadin. Moreover, it was recently shown in vivo that oats are not toxic to coeliac disease patients, suggesting the safety of oats in gluten-free diet.
Objective: To define the role of oats in coeliac disease.
Design: An in vitro model was used to test whether oats induced EMA production in supernatant fluid from cultured duodenal mucosa specimens collected from 13 treated coeliac disease patients. The biopsy specimens were cultured with and without peptic-tryptic digest (PT) of gliadin and avenin (from oats) and in medium alone. Samples from 5 of the 13 patients were cultured with the C fraction of PT-avenin. Indirect immunofluorescence was used to detect EMAs.
Result: EMAs were detected in specimens from all 13 patients after the challenge with gliadin but not after culture in medium alone. By contrast, no EMAs were detected in any of the specimen cultured with PT-avenins (from oats) and its C fraction.
Conclusion: Because the in vitro challenge with PT-avenin and its C fraction did not induce EMA production in treated coeliac disease patients, it appears that oats have no harmful effects on coeliac disease. Therefore oats can be safely included in a gluten-free diet.
Reference: American Journal of Clinical Nutrition, Vol. 74. No. 1, 137-140, July 2001.
AAC Comments: Hopefully this will put to rest the ongoing uncertainty as to whether oats are harmful in coeliac disease.
Mustard cross-reacts with pollen and may aggravate hay fever.
Study: A prospective study of mustard allergy in allergic rhinitis cases
DM Tripathi et al, ENT and allergy Centre, Chandigarh, Bombay, India
Background: Mustard plant belongs to the family Brassicaceae and two species ie. Brassica nigra and Brassica juncea, are extensively cultivated in India. Mustard powder is used for spice and mustard oil is used for cooking. Mustard allergy is common in France & India. Both countries introduce mustard in the diet at an early age. Cross-reactions with pollens and fruits are well known in the oral allergy syndrome. A cross-reaction between pollens and mustard is not as well known.
Objective: To ascertain that mustard avoidance in patients with mustard sensitivity and pollen allergy leads to symptomatic improvement in hay fever.
Method: 78 consecutive patients suffering from allergic rhinitis were recruited and interviewed with a questionnaire. They were skin prick tested with commercial extracts of foods and inhalants and fresh extracts of Brassica nigra and Brassica juncea.
Results: 78% of the patients were allergic to mustard, followed by pollen extract of the mustard family (74%). Bengal gram (chana) showed 66% reactivity. Other food allergens like eggs did not show significant reactions.
73% of the subjects were allergic to house dust mites.
Maximum skin reactivity was observed with pollen extract of Brassica species (mustard pollen) as high as 78.2%.
Significant cross-reactivity among pollen extract of mustard plant and mustard seed powdered extract was observed. Patients, who showed skin sensitivity to pollen extract and mustard powder extract, were also found to be allergic to fresh extract of mustard powder.
Conclusion: Mustard allergy is very common in hay fever sufferers in India (78% in this study). There seems to be strong cross-reactivity between mustard seeds and pollen extract of mustard plant (Brassicaceae family).
Also it would seem as if patients who are sensitive to both pollen and mustard allergens had significant symptomatic relief when they avoided ingesting mustard in their diet. The degree of symptomatic relief was as high as 60%.
Reference: Bombay Hosp J
AAC Coments: Mustard is a cause of anaphylaxis and can be difficult to diagnose, as mustard is a common hidden ingredient. I had personal experience with a 6 yr old boy with multiple anaphylactic episodes, which were finally traced to a commercial food product. With the existing food labelling laws for spices, mustard does not have to be declared if it is less than 2% of the final food product.
The necessity for dual food intake to provoke food-dependent exercise-induced anaphylaxis (FEIAn): A case report of FEIAn with simultaneous intake of wheat and umeboshi
Yukoh Aihara et al, Yokohama, Japan
Background: Food-dependent exercise-induced anaphylaxis (FEIAn) is classified among the physical allergies. Many different food allergens have been reported, but the pathophysiology of FEIAn remains unknown. Furthermore, provocation tests with a suspected food do not always confirm the diagnosis of FEIAn.
Objective: They sought to clarify and investigate causative foods and mechanisms of FEIAn in a 14-year-old boy. In addition, they tested in vivo and in vitro effects of cromolyn sodium in the same patient.
Methods: They used open challenge tests for the provocation of FEIAn and measured changes in plasma histamine levels and FEV1. In addition, they investigated the mechanism of FEIAn in this case with in vitro histamine release testing.
Results: The patient was diagnosed as having FEIAn by provocation testing with a simultaneous intake of wheat and umeboshi (A Japanese condiment), but not when each food was eaten singly, followed by exercise. In addition, his serum histamine level increased transiently and FEV1, expressed as a change from baseline decreased significantly. A synergistic effect on in vitro histamine release testing with the 2 foods was shown. Administration of cromolyn sodium proved to be effective on both the in vitro and in vivo tests.
Conclusion: This is the first report of FEIAn provoked by simultaneous intake of 2 kinds of food. This case might in part explain negative challenge test results in patients with FEIAn.
Reference: J Allergy and Clinical Immunology 2001; 107: 1100-5.
AAC Comments: In my practice, wheat-dependent exercise-induced anaphylaxis is very common. Occasionally patients will need other Co-factors for the reaction to take place, like being on aspirin or NSAID. Now the necessity of 2 foods needs to be considered as well.
New Allergy Treatment Update
Anti-IgE Treatment
IIgE plays a central role in allergic disease and participates in the inflammatory process. Presently the most effective treatments for allergic diseases are directed towards regulation of the inflammatory process with corticosteroids. An exciting new approach is anti-IgE, which regulates the allergic process.
Anti-IgE, also known as Rhumab-E25 or olizumab, is a recombinant humanized monoclonal antibody to IgE that was developed to interfere early in the allergic process by targeting the source of the allergy symptoms.
Anti-IgE neutralizes IgE in the blood (by attaching to the area of the molecule that interacts with the IgE receptors) and prevents it from binding to the mast cells and basophils, thereby blocking the consequent release of inflammatory mediators. To avoid the problems of antigenicity associated with chronic administration of Murine antibodies, the anti-IgE monoclonal antibody was humanized (E25).
Numerous studies show that direct interference with the IgE response leads to a decrease or elimination of the allergic symptoms of rhinitis, asthma and atopic dermatitis.
The role of Anti-IgE in Asthma
In a phase III clinical trial, olizumab was shown to be highly effective in improving asthma symptoms and pulmonary function in adult patients with allergic asthma, according to Professor William Busse from the University of Wisconsin Hospital and Clinics, Madison, US.
Anti-IgE was given intravenously or subcutaneously every 2 to 4 weeks over a period of 5-7 months to over 500 patients. The level of IgE in their blood was reduced by more than 95%. Symptoms such as chest tightness, coughing and wheezing improved by 42% in people receiving high doses of anti-IgE and by 40% in those receiving a low dose. Most patients were either able to significantly reduce their corticosteroid dosage or eliminate its use completely.
Upper respiratory infections and viral infections were the most frequently reported adverse events in this study.
Treating seasonal allergic rhinitis with Anti-IgE
There have been two clinical trials performed to evaluate the efficacy and safety of anti-IgE humanized monoclonal antibody (Olizumab) in the treatment of seasonal allergic rhinitis. One study involved ragweed-induced allergic rhinitis. The other study evaluated treatment for birch pollen-induced allergic rhinitis. The improvement is related to the reduction in serum total IgE levels. The lowest reduction in IgE was associated with the greatest reductions in nasal symptoms and rescue medication use.
In both studies the anti-IgE was given either intravenously or subcutaneously every 2-4 weeks. Total IgE levels decreased in both studies, but significant clinical efficacy was seen in the birch allergic patients only. Urticaria has been reported in a few patients. No serious adverse effects have occurred, including anaphylactic or anaphylactoid episodes. Olizumab does not stimulate antibody production or formation of immune complexes.
Where are we at with Anti-IgE?
The drug was due to be released by Novartis as an asthma treatment next year in the US, under the trade name Xolair. However, Federal regulators on the 3rd July 2001 said they want more information about side effects.
Xolair (Olizumab), genetically engineered using mouse genes grafted onto human antibodies, blocks the ability of IgE to trigger inflammation. It was hoped that this would be the new "wonder drug" for treating allergies.
I do not believe we should hold out too much hope for this drug as a therapeutic option for allergic rhinitis, because it will have to be given as an injection, and efficacy is not much better than what is presently available.
Theoretically, the drug should be very useful for those very atopic patients (with very high IgE levels & multiple sensitivities) with asthma, eczema, allergic rhinitis and food allergy. I suspect, when it does become available, side effects will be a real issue and it won't be cheap.
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