[Loss of an eye due to hyper-IgE syndrome after a corneal transplant].
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Biomedical subjects
Publications and source records attributed to A E Dubois.
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OBJECTIVE: To determine if a causal connection exists between food additives and various medical complaints. DESIGN: Literature study. METHOD: Medline over the period January 1966-January 1999 was searched for articles on the following substances not containing protein and lactose: monosodium glutamate (MSG), sulfites, azo-dyes (tartrazine, sunset yellow, azorubin, amarant, cochineal red), benzoates, sorbates, butylated hydroxyanisole/butylated hydroxytoluene (BHA/BHT), parabens, cinnamon and vanilla, in combination with key words regarding food and side effects. Of those studies purporting to demonstrate an effect, only double-blind randomized placebo-controlled studies with oral challenge were assessed further, unless the complaint was anaphylaxis. Of studies not demonstrating an effect the design was assessed. RESULTS: Only for sulfites as causative agents of asthma and anaphylaxis, methodologically adequate studies demonstrating a causal connection could be found. For azo-dyes, benzoates, MSG, sorbates and BHA/BHT, no link with medical symptoms was demonstrable. For parabens, cinnamon and vanilla there were insufficient or inadequate data to justify a conclusion.
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BACKGROUND: Exposure to cat and dog allergens is very common in the Western World and is a serious cause of asthma in sensitized subjects. OBJECTIVE: We sought to study the clinical effects of air cleaners in living rooms and bedrooms of asthmatic children sensitized to cat or dog allergens. METHODS: Twenty asthmatic children sensitized to pet allergens (cat/dog) and with an animal at home participated in a double-blind, placebo-controlled, cross-over study in which the effects of air cleaners placed in the living room and bedroom for 3 months were compared with the effects of sham air cleaners. Before and after each study period, lung function, airway hyperresponsiveness (adenosine monophosphate), and peak flow variation were recorded. Cat and dog allergen levels were assessed in the filters of the air cleaners. RESULTS: After a 3-month intervention with active air cleaners, airway hyperresponsiveness decreased significantly, showing a 1.2 doubling dose increase of PC(20 )adenosine (P =.003). Peak flow amplitude also decreased (P =. 045). Substantial amounts of airborne cat and dog allergen were captured by the air cleaners in living rooms and bedrooms as well. Allergen levels in floor dust were not changed. CONCLUSION: In young asthmatic patients sensitized and exposed to pets in the home, application of air cleaners in living rooms and bedrooms was accompanied by a significant improvement in airway hyperresponsiveness and a decrease in peak flow amplitude.
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The purpose of this study was to investigate whether preventive measures such as reduction of exposure and the introduction of the histamine provocation test (HPT) as a selection instrument resulted in a lower incidence of potroom asthma (PA) and a longer time lag between the commencement of employment and the occurrence of PA. Between 1970 and 1990, 179 cases of PA were diagnosed. This period was divided into three periods. During period 1 (1970-1975), no exposure data were available. Period 2 (1976-1981) is characterized by known exposure data obtained by means of fluoride determinations in urine. At the beginning of period 3 (1982-1990) the HPT was incorporated into the preemployment medical examination. We computed the incidence density (ID) in the three periods and analyzed the timelag in relation to the year of employment and confounding factors such as age, atopic history, blood eosinophil counts, lung function, smoking habits at preemployment, and exposure level. After introduction of the preemployment HPT the ID decreased, but cases continued to occur (ID 11.6 in period 2 versus 2.5 in period 3). The time lag was did not differ when subjects with bronchial hyperresponsiveness were screened out. The exposure level and an atopic history were factors associated with the period of employment and, therefore, confounded the results. The results of this study support the role of an atopic history as a risk factor for development of PA at lower exposure levels and suggest that potroom exposure not only incites asthmatic symptoms but also acts as an inducer of respiratory disease.
The prevalence of sensitization to the storage mites Acarus siro (AS), Tyrophagus putrescentiae (TP), and Lepidoglyphus destructor (LD) was studied in 250 sera of patients with different degrees of sensitization to the house-dust mite Dermatophagoides pteronyssinus (DP) by measuring IgE binding to extracts of the storage mites. Additionally, allergenic cross-reactivity between DP and the storage mite species was studied by RAST inhibition with five individual sera (and a pool of these sera) with moderate IgE levels to all three storage mites and to DP. Increased serum IgE to storage mites was found in 46% of the 200 patients sensitized to DP. Increased prevalence rates of IgE titers to storage mites were associated with higher IgE levels to DP. In 50 sera without sensitization to DP, only five sera showed increased IgE to one of the storage mites. Extracts of TP almost completely inhibited the IgE binding to AS, and vice versa. DP inhibited IgE binding to all storage mites up to 60%, whereas IgE binding to DP was only minimally inhibited by extracts of storage mites. In conclusion, cosensitization to storage mites is a frequent finding in patients sensitized to DP. Although this is largely the result of cross-reactivity between different mite species, it may nevertheless be of clinical significance in patients exposed to storage mites.
Exposure to house-dust-mite allergens is an important cause of allergic reactions in sensitized patients. In community-based studies, sensitization to house-dust mites, as ascertained by a positive skin test or by an increased allergen-specific IgE level in serum, is associated with both diminished lung function and enhanced airway hyperresponsiveness. Sensitization to house-dust mites is an independent risk factor for the development of asthma, especially in areas which favor the growth of house-dust mites. In studies with asthmatic patients, however, the relationship between sensitization to mites and lung function or airway hyperresponsiveness is less clear. The selection of asthmatic individuals (with sensitization to other inhalant allergens) and the use of medication such as inhaled steroids may interfere with the demonstration of a possible association between mite allergy and lung function or airway hyperresponsiveness in asthmatic patients.
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BACKGROUND: The degree of airway hyperresponsiveness in allergic asthmatic patients may be influenced by changes in environmental exposure to inhalant allergens. OBJECTIVE: This study investigates the relationship between seasonal changes in exposure to house dust mite (HDM) allergens and non-specific airway hyperresponsiveness in asthmatic patients with multiple sensitizations to inhaled allergens. METHODS: In 43 asthmatic patients sensitized to several inhalant allergens, lung function (FEV1), airway hyperresponsiveness (PC20 histamine), serum total IgE, house dust mite (HDM) specific IgE and number of peripheral blood eosinophils were measured during autumn 1990 (September-November) and spring 1991 (March-May). During each season, floor dust samples were collected twice from living- and bedrooms and the concentration of the HDM allergens Der p 1 and Der p 2 determined. RESULTS: More severe airway hyperresponsiveness (lower PC20 histamine) during autumn was only found in patients sensitized to HDM (n = 32; autumn: 2.05 mg/mL, spring: 4.51 mg/mL (geometric means), P < 0.01), whereas in patients not sensitized to HDM (n = 11) similar values were observed in both seasons (3.44 and 4.52 mg/mL, respectively, P = 0.56). More severe airway hyperresponsiveness of HDM sensitized patients in autumn was significantly associated with higher Der p 1 concentrations in floor dust. Aside from airway hyperresponsiveness, seasonal changes in serum total IgE and number of peripheral blood eosinophils were seen in patients sensitized to HDM. CONCLUSIONS: In allergic asthmatic patients, airway hyperresponsiveness may increase during autumn, depending on sensitization to HDM and an increase of exposure to HDM allergen.
This double-blind, placebo-controlled study investigated whether the application of an acaricide (Acarosan) on mattresses and on textile floor coverings in living rooms and bedrooms can contribute to improvement in lung function and airway hyperresponsiveness in 40 adult asthmatic patients sensitized to house-dust mite. In a second group of 19 patients who refused chemical intervention, the clinical effects of application of allergen-impermeable mattress encasings were studied. In all three treatment groups, Der p 1 levels in mattress dust were statistically significantly decreased after 12 months. However, this decrease was much greater in the group who received mattress encasings (final mean level 430 ng/g) than in groups with acaricide- or placebo-treated mattresses (final mean levels 1730 and 2100 ng/g, respectively). Treatment of textile floors with either Acarosan or placebo chemical caused a statistically significant decrease in the level of the house-dust-mite allergen Der p1 in floor dust. In the group with mattress encasings, no significant changes of floor dust Der p 1 were found. Airway hyperresponsiveness (as measured by the PC20 histamine) improved significantly in the mattress cover group after 6 months. The Acarosan group also showed a small but statistically significant improvement after 12 months.
We quantitatively determined whether the selective phosphodiesterase (PDE) inhibitor, rolipram, inhibits changes in the adhesion molecules CD11b and L-selectin on platelet-activating factor (PAF)-stimulated human neutrophils and eosinophils in vitro. Incubations were performed in human whole blood obtained from healthy volunteers, to restrict activation by purification procedures and to simulate in vivo conditions, in which different cell types may interact, more closely. Receptor expression was measured after fixation of cells, using monoclonal antibodies and flow cytometry. Concentration-dependent inhibition of the PAF-induced CD11b expression and L-selectin shedding for neutrophils and eosinophils was observed with rolipram, dibutyryl cyclic adenosine monophosphate (cAMP), prostaglandin E2 (PGE2), and isoproterenol. However, these inhibitions did not exceed 50%. Preincubation with rolipram (10(-8) M) and subsequent incubation with isoproterenol (0.5x10(-8) M) or PGE2 (10(-8) M) induced a cumulative, but not synergistic, effect. Using the combination of rolipram with isoproterenol or PGE2, inhibition of PAF-induced L-selectin shedding from eosinophils was as high as 71+/-28 and 67+/-21%, respectively. Other inhibitions were below 50%. In conclusion, rolipram inhibits CD11b expression and L-selectin shedding of platelet-activating factor-stimulated neutrophils and eosinophils in whole blood in a concentration-dependent fashion. Inhibitions did not exceed 50%, even at high concentrations. The inhibition of platelet-activating factor induced shedding of L-selectin from eosinophils with a combination of rolipram and prostaglandin E2 or isoproterenol, however, was found to be approximately 70%. Inhibition of rolling adhesion of eosinophils may, therefore, be a mode of action of type IV phosphodiesterase inhibitors.
Recommendations for allergen avoidance or allergen reduction measures play an important part in the treatment of allergic asthmatic patients. The purpose of this study was to test recently developed air-cleaners with respect to their capacity to capture airborne allergen particles and to improve clinical parameters of asthmatic patients sensitized to aeroallergens. Forty five allergic asthmatic patients were studied in a double-blind procedure for 6 months. The patients were divided into three groups of 15 patients. In Group 1, the intervention consisted of the application of active air-cleaners in living-rooms and bedrooms. In Group 2, placebo air-cleaners were used in combination with allergen-impermeable mattress covers. In Group 3, the same intervention was performed as in Group 2 but with active air-cleaners. Allergen levels in mattress and floor dust were measured before, and 3 and 6 months after the interventions. After 6 months, the air-cleaners were dismantled and the filters were analysed for the amount of dust collected and allergen content. Immunological and lung function parameters were measured before, and 3 and 6 months after the interventions. Considerable amounts of airborne dust and allergenic particles were captured in the filters of the air-cleaners. Up to the 18.9 g of dust, 4,513 ng of house dust mite allergen, Der p 1, and 50,000 mU of cat allergen, Fel d 1, (in houses with cats) were collected by air-cleaners in living-rooms. Only in Group 3 (in which both active air-cleaners and mattress covers were used) was a small (less than 1 doubling dose) but statistically significant improvement of provocative concentration of histamine causing a 20% fall in forced expiratory volume in one second (PC20) observed (from 5.96 to 9.02 mg x mL(-1)). The amount of dust and house dust mite allergen collected in the filters was significantly correlated with an improvement of peak flow variation. In combination with other allergen avoidance measures, the examined air-cleaners can contribute to diminished allergen exposure and improvement of airway hyperresponsiveness in asthmatic patients.