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Acute hypersensitivity reactions to drugs occur infrequently during anaesthesia and the peri-operative period. When clinical presentation includes the classical triad, erythema, cardiovascular abnormalities and increased airway pressure, the diagnosis is evident and the challenge is to prescribe a therapeutic regimen according to guidelines and to manage refractory signs in a timely manner. In many situations, however, the initial clinical signs are isolated, such as increased airway pressure or arterial hypotension. Rendering a differential diagnosis with causes and mechanisms other than acute hypersensitivity reactions (AHRs) is difficult, delaying treatment with possible worsening of the clinical signs, and even death, in previously healthy individuals. In these difficult diagnostic situations, clinical reasoning is mandatory, and guidelines do not explicitly explain the elements on which clinical reasoning can be built. In this article, based on clinical evidence whenever available, experimental data and pathophysiology, we propose algorithms that have been evaluated by experts. The goal of these algorithms is to provide explicit elements on which the differential diagnosis of AHRs can be made, accelerating the implementation of adequate therapy.

Introduction: Among allergic rhinitis (AR) symptoms, nasal obstruction particularly affects the quality of life. Antihistamines and intranasal corticosteroids are the most frequently prescribed symptomatic drugs, but their efficacy is often incomplete. Essential oils (EO) have shown an anti-inflammatory effect and potential in treating patients with AR. The aim of this study was to evaluate the effectiveness of a hypertonic EO-based nasal spray on perennial AR (PAR) symptoms. Methods: This prospective, open-label, non-randomized, multicentric trial included 43 patients with PAR sensitized to mites, not controlled for more than a year. All were treated with Puressentiel® Respiratory-Decongestant Nasal Spray for 30 days. Their usual treatment remained unchanged during the study period. Before and after treatment, each participant filled out a rhinitis questionnaire, the Allergic Rhinitis Control Test (ARCT). A nasal inspiratory peak flow (NIPF) was performed. Results: The mean ARCT was 16.4 and 20.5 at D0 and D30, respectively (p < 0.001); the mean increase between D0 and D30 was 4.1 (p < 0.001). The proportion of patients with controlled rhinitis after 30 days of treatment was 69.8 versus 14% before treatment (p < 0.001). The mean NIPF was 86.5 L/min and 105.1 L/min at D0 and D30, respectively (p < 0.001); the mean increase between D0 and D30 was 18.5 L/min. Conclusion: A hypertonic EO-based nasal spray could be a new and natural option in the management of PAR. It could also be used as an add-on therapy when nasal symptoms are not fully controlled.

International audience; The prevalence of asthma has increased rapidly since the early 1970s, and only changes in exposure to environmental factors; which go together with changes in lifestyle, are likely to explain such a rapid increase. Exposure to allergens is a risk factor for allergic sensitization, and allergic sensitization is a risk factor for allergic asthma. However, apart from indoor mold exposure as a risk factor for childhood asthma, there is insufficient evidence to conclude that the associations between allergen exposure and asthma development are causal. A new challenge for research is to analyze the huge amount of data derived from the metagenomic characterization of the environmental and human microbiome, to understand the role of interactions between viruses, bacteria and allergens in the development of asthma. It is recognized that prenatal and postnatal exposure to air pollution and maternal smoking increase the risk of developing asthma in children. In adults, the data are scarce and the results remain controversial as regards these exposures and asthma incidence. Further research is needed to appraise the effect of exposure to phenols, phthalates and perfluorinated compounds, which are widespread in the environment and may be associated with asthma, especially in children. Frequent use of chemicals for home cleaning especially in the form of sprays - which is a common practice at the population level - is a risk factor for the development of adult asthma. The domestic use of cleaning products might also be a risk factor for asthma in children exposed at home. The chemicals involved in these relationships are still to be identified. Occupational asthma is a major phenotype of adult asthma. A significant part of these asthma cases might relate to occupational exposure to cleaning products. While there is evidence of associations between diet during pregnancy or during childhood and the risk of developing asthma in children, the data in adults are insufficient. Beyond genetic factors, body composition is influenced by dietary choices and physical activity. Further research is needed to clarify the complex interplay between these nutritional factors and asthma development. The new challenge for research is to decipher the role of all the environmental factors to which the individual is exposed since conception ("exposome") in the development of asthma, using a holistic approach.

International audience; Background: Essential oils are volatile compounds of plant origin increasingly used by allergic and/or asthmatic subjects to purify indoor air. The active compounds of essential oils belong to terpenes, the most widespread biogenic volatile organic compounds (VOC). Although there is substantial literature showing associations between exposure to chemical VOCs and asthmatic symptoms and impaired respiratory function, the impact of essential oils in patients with asthma has never been studied. Objectives: To evaluate the safety of a purifying air spray containing 41 essential oils (PPAS) in patients with mild or moderate allergic asthma. Methods: This was a prospective open study in which 25 mild (19) and moderate (6) asthmatics were exposed to PPAS, one spray twice a day at 8 am and 8 pm in two different corners of a given subjects bedroom for 4 weeks. Before and after 4 weeks of exposure, fractional exhaled nitric oxide (FeNO), lung function and methacholine challenge (PD20) were performed and asthma control was assessed by the 5 questions of the Asthma Control Test (ACT). The spray was weighed after the 4-week exposure to assess compliance. Results: FeNO was the primary endpoint and was thus analyzed in all (N = 25) subjects irrespective of the level of airflow obstruction. The results apply to all (N = 25) subjects in which FeNO could be measured at D1 and D30 (17 subjects). Mean (SD) FeNO amounted to 37.4 (16.6) and to 33.1 (18.7) ppm before and after PPAS exposure, respectively (p = 0.09). No significant change in lung function and methacholine responsiveness was noted after PPAS exposure, the mean PD20 amounting to 1179 (1124.42) μg (range 100-3200) before and to 1226 (1189.8) μg (p = 0.06) after. The mean ACT before and after PPAS exposure amounted to 20.9 (4.2) and 21 (5.15), respectively (p = 0.80). The mean weight of the PPAS bottles was 211.4 g (DS:0) before the first use and 171.41 g (DS: 29.8) at the end of the study. The average amount of PPAS used was 40.0 g (29.8). In the subgroup of subjects who used the highest quantities of essential oils (>40 g), as assessed by the mean weight of the bottle at the end of the study, FeNO after 30 days of exposure decreased more than in the entire group: 7.9 ppm vs 4.2 ppm (p = 0.07). Conclusion: No difference was noted on airway inflammation, lung function or asthma control in mild and moderate allergic asthmatics after exposure twice a day for one month, to a spray containing a mixture of 41 essential oils.

We previously showed that patients with severe allergic asthma have high numbers of circulating ILC2s expressing CCR10.Herein, CCR10When compared to healthy controls, CCR10Frequencies of circulating CCR10

Telomere shortening is associated with COPD and impaired lung function in cross-sectional studies, but there is no longitudinal study. We used data from 448 participants recruited as part of the French follow-up of the European Community Respiratory Health Survey. We found no relationship between telomere length at baseline and FEV1 decline after 11 years of follow-up. However, heavy smoking was associated with an accelerated FEV1 decline in individuals with short telomeres, but not in subjects with longer telomeres (p for interaction p=0.08). Our findings suggest that short telomere length in peripheral leucocytes might be a marker for increased susceptibility to the effect of smoking.

Background: Nitrogen dioxide (NO2), a ubiquitous atmospheric pollutant, may enhance the asthmatic response to allergens through eosinophilic activation in the airways. However, the effect of NO2 on inflammation without allergen exposure is poorly studied. Objectives: We investigated whether repeated peaks of NO2, at various realistic concentrations, induce changes in airway inflammation in asthmatics. Methods: Nineteen nonsmokers with asthma were exposed at rest in a double-blind, crossover study, in randomized order, to 200 ppb NO2, 600 ppb NO2, or clean air once for 30 min on day 1 and twice for 30 min on day 2. The three series of exposures were separated by 2 weeks. The inflammatory response in sputum was measured 6 hr (day 1), 32 hr (day 2), and 48 hr (day 3) after the first exposure, and compared with baseline values measured twice 10–30 days before the first exposure. Results: Compared with baseline measurements, the percentage of eosinophils in sputum increased by 57% after exposure to 600 ppb NO2 (p = 0.003) but did not change significantly after exposure to 200 ppb. The slope of the association between the percentage of eosinophils and NO2 exposure level was significant (p = 0.04). Eosinophil cationic protein in sputum was highly correlated with eosinophil count and increased significantly after exposure to 600 ppb NO2 (p = 0.001). Lung function, which was assessed daily, was not affected by NO2 exposure. Conclusions: We observed that repeated peak exposures of NO2 performed without allergen exposure were associated with airway eosinophilic inflammation in asthmatics in a dose-related manner. Citation: Ezratty V, Guillossou G, Neukirch C, Dehoux M, Koscielny S, Bonay M, Cabanes PA, Samet JM, Mure P, Ropert L, Tokarek S, Lambrozo J, Aubier M. 2014. Repeated nitrogen dioxide exposures and eosinophilic airway inflammation in asthmatics: a randomized crossover study. Environ Health Perspect 122:850–855; http://dx.doi.org/10.1289/ehp.1307240

Background Neuromuscular blocking agents (NMBA) are responsible for most immediate hypersensitivity reactions during anesthesia, as a result of the presence of a quaternary ammonium ion. The aim of this study was to evaluate the diagnostic performance of a commercial immunoglobulin E (IgE) test (quaternary ammonium morphine [QAM]) for diagnosing sensitivity to NMBA. Methods We tested 168 patients exposed to NMBAs during anesthesia. Of those patients, 54 had an uneventful procedure and 114 had immediate hypersensitivity reactions, and 57 patients had positive skin tests to the administered NMBA, whereas 57 had negative skin tests. Specific IgE concentrations determined with the QAM method based on a morphine solid phase were compared with those obtained with a recommended experimental method with a choline solid phase. Results For the QAM test, a 0.35 kUA/l positivity cutoff was chosen from the receiver operating characteristics curve. QAM-specific IgE was found in 84.2% of skin test-positive reactors (80.7% with the recommended method; no significant difference), and binding was inhibited by the culprit NMBA in 80% of cases. The frequency of QAM-specific IgE positivity was significantly higher in skin test-negative reactors (24.6%) than in controls (9.3%), suggesting NMBA sensitivity. Conclusion Sensitivity of the QAM test (84.2%), together with its simplicity and suitability for routine laboratory use, makes it a valuable tool, in conjunction with skin tests, for diagnosing NMBA sensitivity in patients who react after NMBA injection. The QAM test is of particular interest when skin tests are not available or not reliable or give results poorly compatible with mediator release or clinical features.

BACKGROUND: Cross-sectional studies have reported a lower prevalence of sensitization in older adults, but few longitudinal studies have examined whether this is an aging or a year-of-birth cohort effect. OBJECTIVE: We sought to assess changes in sensitization and total IgE levels in a cohort of European adults as they aged over a 20-year period. METHODS: Levels of serum specific IgE to common aeroallergens (house dust mite, cat, and grass) and total IgE levels were measured in 3206 adults from 25 centers in the European Community Respiratory Health Survey on 3 occasions over 20 years. Changes in sensitization and total IgE levels were analyzed by using regression analysis corrected for potential differences in laboratory equipment and by using inverse sampling probability weights to account for nonresponse. RESULTS: Over the 20-year follow-up, the prevalence of sensitization to at least 1 of the 3 allergens decreased from 29.4% to 24.8% (-4.6%; 95% CI, -7.0% to -2.1%). The prevalence of sensitization to house dust mite (-4.3%; 95% CI, -6.0% to -2.6%) and cat (-2.1%; 95% CI, -3.6% to -0.7%) decreased more than sensitization to grass (-0.6%; 95% CI, -2.5% to 1.3%). Age-specific prevalence of sensitization to house dust mite and cat did not differ between year-of-birth cohorts, but sensitization to grass was most prevalent in the most recent ones. Overall, total IgE levels decreased significantly (geometric mean ratio, 0.63; 95% CI, 0.58-0.68) at all ages in all year-of-birth cohorts. CONCLUSION: Aging was associated with lower levels of sensitization, especially to house dust mite and cat, after the age of 20 years. Amaral receives research funding from the Medical Research Council. M. J. Abramson receives research support from E.H.Walters & M.Abramson, Pfizer, and Boehringer Ingelheim and receives consulting fees from AstraZeneca and travel support from Boehringer Ingelheim and Sanofi. P. Demoly receives consulting fees from ALK-Abell o, Circassia, Stallergenes, Allergopharma, Chiesi, Thermo Fisher Scientific, Medam Menarini, AstraZeneca, Pierre Fabra Mediacament, and DBV. R. Jogi receives research support from the Estonian Research Council and receives consulting and lecture fees from Boehringer, Novartis, and GlaxoSmithKline and travel support from GlaxoSmithKline and Boehringer. C. Neukirch receives consulting fees and travel support from ALKAbell o and Stallergenes. D. Nowak receives speaker fees from Mundipharma. I. Pin receives lecture fees from Novartis and MSD and travel support from GlaxoSmithKline, TEVA, and Novartis. R. van Ree receives consulting fees from HAL Allergy BV and speaker fees from Thermo Fisher Scientific. J.-P. Zock receives research support from FIS, Health Institute Carlos III, and the Spanish Ministry of Health. P. G. J. Burney serves on the Novartis Advisory Board. D. L. Jarvis receives research support from the Medical Research Council

Formaldehyde is a well-known airborne contaminant causing eye, nose, and throat irritation as well as airway irritation and slight neuropsychologic changes (Hester and Harrison 1998; Samet et al. 1988). The major indoor sources of formaldehyde are off-gassing from urea–formaldehyde foam insulation, particle board, paneling, plywood, some carpets and furniture, and, to a lesser extent, tobacco smoke and indoor combustion sources. Indoor concentrations of formaldehyde can vary between different countries (Sakai et al. 2004). In a Japanese study, formaldehyde concentrations ranged between 91.25 and 290 μg/m3 (Minami et al. 2002), whereas in the United Kingdom, the highest level measured in 876 homes was much lower (median = 24 μg/m3) (Brown et al. 2002). Indoor formaldehyde concentrations measured in mobile homes in the United States ranged from nondetectable values to 575 μg/m3 (Liu et al. 1991). Indoor concentrations generally exceed those outdoors, and studies on formaldehyde levels in homes have demonstrated higher formaldehyde concentrations in newer compared with older dwellings, with higher levels in buildings built after 1970 (Gilbert et al. 2005). Formaldehyde is an etiologic factor in occupational asthma. However, although formaldehyde may cause asthma in some individuals, this occurs relatively rarely (Nordman et al. 1985; Paustenbach et al. 1997). Whether nonoccupational exposure to formaldehyde is related to asthma is still subject to discussion (Delfino 2002; Institute of Medicine 2000). In murine models, formaldehyde exposure has been shown to enhance the allergic eosinophilic airway inflammation in sensitized mice (Sadakane et al. 2002). In a part of the European Community Respiratory Health Survey, asthma prevalence was greater for newly painted homes, consistent with greater differences in formaldehyde exposure (Wieslander et al. 1997). A relationship between physician-diagnosed asthma and indoor concentration of formaldehyde was reported even at low levels of exposure in children (Rumchev et al. 2002). Franklin et al. (2000) reported that exposure to formaldehyde in homes could produce a subclinical inflammatory response in the airways of healthy children. A possible association between exposure to formaldehyde and allergic sensitization to common aeroallergens has been suggested by another cross-sectional study in children (Garrett et al. 1999). Human exposure studies can provide valuable data for assessing more specifically the acute effects of air pollutants, particularly the airway response to allergen (Sandstrom 1995). The hypothesis that formaldehyde enhances asthmatic response to allergen has not yet been investigated in controlled conditions in humans. To test this hypothesis, we carried out this controlled human study to investigate the effect of a short exposure to 500 μg/m3 formaldehyde on asthmatic response to inhaled allergen.

Background: Seasonal allergic rhinitis could predispose to the development of chronic bronchial inflammation as observed in asthma. However, direct links between nasal inflammation, bronchial inflammation and airway responsiveness in patients with seasonal allergic rhinitis and without asthma are not fully understood. The aim of this study was to analyse the changes induced by allergic nasal challenge outside the pollen season in airway responsiveness and bronchial inflammation of patients with seasonal allergic rhinitis. Methods: Nine patients were evaluated after either grass pollens or placebo nasal challenge in a randomized cross-over double-blinded trial. Nasal parameters were recorded hourly and airway responsiveness was assessed by methacholine challenge. Cytological examinations and cytokine measurements were performed in nasal lavage and induced sputum. Eosinophil activation was investigated by eosinophil-cationic protein expression and secretion. Results: Airway responsiveness was increased after allergic nasal challenge. Total eosinophils and eosinophils expressing eosinophil-cationic protein were increased in induced sputum after allergic nasal challenge. Both eosinophil number and eosinophil-cationic protein concentration in induced sputum were correlated to methacholine responsiveness. Conclusions: These results suggest that eosinophils participate to the bronchial inflammation in patients with seasonal allergic rhinitis following allergic nasal challenge outside the pollen season and might explain changes in airway responsiveness.

C-reactive protein (CRP), a marker of systemic inflammation, is a powerful predictor of adverse cardiovascular events. Respiratory impairment is also associated with cardiovascular risk. Although some studies have found an inverse relationship between lung function and markers of systemic inflammation, only one study has reported a relationship between lung function and CRP levels. In contrast, little is known about the relationship between bronchial hyperresponsiveness (BHR) and systemic inflammation. The association between lung function and CRP and between BHR and CRP has been investigated.As part of the European Community Respiratory Health Survey follow up study serum CRP levels, forced expiratory volume in 1 second (FEV(1)), and BHR to methacholine (/=20% decrease in FEV(1) to4 mg methacholine) were measured in 259 adults aged 28-56 years free of cardiovascular disease or respiratory infection.Mean (SD) FEV(1) (adjusted for age, sex, height, and smoking status) was lower in subjects with a high CRP level (high tertile) (3.29 (0.44) l/s v 3.50 (0.44) l/s; p0.001) and BHR was more frequent (41.9% v 24.9%; p = 0.005) than in subjects with lower CRP levels (low+middle tertiles). Similar results were obtained when the potential confounding factors were taken into account. Similar patterns of results were found in non-smokers and in non-asthmatic subjects.Increased CRP levels are strongly and independently associated with respiratory impairment and more frequent BHR. These results suggest that both respiratory impairment and BHR are associated with a systemic inflammatory process.

Background— Respiratory alterations have been associated with subsequent coronary heart diseases in numerous population-based studies. The underlying mechanisms remain largely unknown. The objective of this study was to examine the association between bronchial hyperresponsiveness (BHR) to methacholine (which reflects local inflammation in the bronchus) and common carotid intima-media thickness (CCA-IMT). Methods and Results— As part of the European Community Respiratory Health Survey follow-up, in Paris Center, we assessed BHR to methacholine (≥20% decrease in FEV1 for a maximum methacholine dose of 4 mg) and measured CCA-IMT by ultrasonography in 255 adults free of cardiovascular diseases aged 29 to 56 years (123 men, 132 women; mean age 44.5 years, 43.5% never smokers). In men, CCA-IMT mean value was higher in subjects with BHR than in those without (0.68±0.11 versus 0.62±0.09 mm, P =0.002). No association was found in women. Multivariate analysis confirmed the independent association between BHR and CCA-IMT in men (adjusted odds ratio for a 0.10-mm increase in CCA-IMT=2.1, 95% confidence interval: 1.1 to 4.3; P =0.02). These results remained similar after exclusion of asthmatic subjects (n=11). In each strata of smoking status (nonsmoker, ex-smoker, and current smokers), CCA-IMT mean values tended to be higher in subjects with BHR than in those without, although the difference between the 2 groups was more pronounced in current smokers. Conclusions— The results of the present study suggest that BHR is independently associated with CCA-IMT in men. The interrelationships between cardiovascular and respiratory alterations should be further investigated.

Background Although asthma and rhinitis often occur together, the reason for this common comorbidity is still a matter of debate. Objective We sought to assess whether the coexistence of asthma and rhinitis could be explained by common risk factors. Methods International cross-sectional study of representative samples of young adults, who completed a detailed questionnaire and underwent lung function tests, bronchoprovocation challenge, IgE measurements, and skin prick tests. Results In all countries, asthma and bronchial hyperreactivity were more frequent in subjects with rhinitis than in those without (odds ratio [OR], 6.63; 95% CI, 5.44-8.08; and OR, 3.02 95% CI, 2.66-3.43, respectively). Seventy-four percent to 81% of subjects with asthma reported rhinitis, depending on sensitization to specific allergens. Conversely, the risk of asthma increased from 2.0% in subjects without rhinitis to 6.7% in subjects with rhinitis only when exposed to pollen, 11.9% in subjects with rhinitis when exposed to animals, and 18.8% in subjects with rhinitis either when exposed to pollen or to animals. The association between rhinitis and asthma remained significant after adjustment for total IgE, parental history of asthma, and allergen sensitization (OR, 3.41; 95% CI, 2.75-4.2 suggesting that the coexistence of asthma and rhinitis is not solely due to atopic predisposition to these 2 diseases. Conclusions Although there were some variations in the association between asthma and rhinitis according to sensitization to individual allergens, the strong association between asthma and rhinitis was not fully explained by shared risk factors, including atopy. Our findings are consistent with the hypothesis that rhinitis might increase the risk of asthma.

Although H1 antihistamine compounds (H1) are highly effective in the treatment of allergic rhinitis (AR), their role in the treatment of asthma is still controversial. Because a strong association between AR and bronchial hyperresponsiveness (BHR) has been reported, this study was designed to assess the effect of a new H1 anti histamine, cetirizine (C), on nonspecific BHR in patients with AR. Twelve patients were included in a double-blind, crossover, placebo-controlled trial. All patients had positive skin tests for common allergens and showed BHR to inhaled methacholine after specific nasal allergenic challenge. After a washout period of 1 week to ensure the stability of the BHR, the patients received, by crossover randomization, C 10 mg daily or placebo (P) for 2 weeks. After each treatment period, BHR and nasal blocking index (NBI) were measured 1 and 6 h after nasal challenge. Bronchial responsiveness was expressed as methacholine PD20, the provocation dose of methacholine causing a 20% decrease in FEV1. Measurements were then performed after 2 weeks of C and after 2 weeks of P. Baseline values of PD20 (median) measured before challenge showed no difference after cetirizine or after placebo (1.36 mg). Results 1 h after allergen did not show significant differences between C (methacholine PD20=0.522 mg) and placebo (methacholine PD20=0.455 mg). By contrast, 6 h after challenge, methacholine PD20 was 0.918 mg for C and 0.483 mg for P (P=0.042). Similarly, NBI showed no change between C and P 1 h after challenge, whereas the difference was significant 6 h after challenge (P=0.011 ). These data demonstrate a protective nasal effect of C against BHR measured 6 h after nasal allergen challenge in patients with AR. They suggest that C may be useful in patients with asthma associated with AR.

Quality of life has been found to be impaired both in patients with asthma and in patients with allergic rhinitis, but the relative burden of these diseases has not been investigated. We analyzed answers to the SF-36 questionnaire from 850 subjects recruited in two French centers participating in the European Community Respiratory Health Survey, a population-based study of young adults. Both asthma and allergic rhinitis were associated with an impairment in quality of life. However, 78% of asthmatics also had allergic rhinitis. Subjects with allergic rhinitis but not asthma (n = 240) were more likely than subjects with neither asthma nor rhinitis (n = 349) to report problems with social activities, difficulties with daily activities as a result of emotional problems, and poorer mental well-being. Patients with both asthma and allergic rhinitis (n = 76) experienced more physical limitations than patients with allergic rhinitis alone, but no difference was found between these two groups for concepts related to social/mental health. As asthma was not found to further impair the quality of life in subjects with allergic rhinitis for concepts related to mental disability and well-being, and as subjects with asthma often also suffer from allergic rhinitis, further studies on quality of life in asthma should ensure that the impairment in quality of life attributed to asthma could not result from concomitant allergic rhinitis.

It has been recognized recently that theophylline possesses anti-inflammatory effects that could be of clinical interest in patients with airway inflammatory diseases such as asthma and allergic rhinitis (AR). The aim of the present study was to explore the effect of theophylline on the nasal eosinophilic inflammatory response following allergen challenge in patients with AR. Fourteen subjects suffering from seasonal rhinitis with an early reaction after nasal allergen provocation were challenged outside the pollen season after pretreatment for 3 weeks with placebo or slow-release theophylline (Euphylong in a randomized double-blind, cross-over study. Nasal blocking index (NBI), nasal airway resistance and symptoms were recorded before, and 1 and 5 h after challenge; additionally, nasal lavage fluid was collected before, as well as 1 and 5 h after challenge. Eosinophil cationic protein (ECP) was measured in the lavage as well as the number of eosinophils before, and 1 h and 5 h after allergen challenge. After 3 weeks of treatment, baseline concentrations of ECP in nasal lavage amounted to 826+/-329 ng x L(-1) (placebo) and 936+/-351 ng x L(-1) (theophylline). The ECP levels did not increase during the early phase response. Five hours after challenge, ECP in the placebo group increased markedly (p

A 35-year-old patient received omalizumab (300 mg twice a month) for 2 years for a severe atopic keratoconjunctivitis (AKC) in order to reduce the risk for steroid-induced keratitis. After 4 months, quality of life and ocular symptoms improved, and the use of oral steroids was strongly reduced. The treatment was well tolerated. This observation suggests that omalizumab may be a good option for the treatment of severe AKC, especially to avoid side effects of immunosuppressive treatments, as suggested for other allergic diseases. Specific trials should be designed for allergic eye diseases.

International audience; BACKGROUND: A close relation between asthma and allergic rhinitis has been reported by several epidemiological and clinical studies. However, the nature of this relation remains unclear. We used the follow-up data from the European Community Respiratory Health Survey to investigate the onset of asthma in patients with allergic and non-allergic rhinitis during an 8.8-year period. METHODS: We did a longitudinal population-based study, which included 29 centres (14 countries) mostly in western Europe. Frequency of asthma was studied in 6461 participants, aged 20-44 years, without asthma at baseline. Incident asthma was defined as reporting ever having had asthma confirmed by a physician between the two surveys. Atopy was defined as a positive skin-prick test to mites, cat, Alternaria, Cladosporium, grass, birch, Parietaria, olive, or ragweed. Participants were classified into four groups at baseline: controls (no atopy, no rhinitis; n=3163), atopy only (atopy, no rhinitis; n=704), non-allergic rhinitis (rhinitis, no atopy; n=1377), and allergic rhinitis (atopy+rhinitis; n=1217). Cox proportional hazards models were used to study asthma onset in the four groups. FINDINGS: The 8.8-year cumulative incidence of asthma was 2.2% (140 events), and was different in the four groups (1.1% (36), 1.9% (13), 3.1% (42), and 4.0% (49), respectively; p

Strong data are lacking on the cross-reactivity between individual carbapenems. We describe a 48-year-old woman with ventilator-associated Pseudomonas aeruginosa pneumonia who received an 8-day course of imipenem-cilastatin and experienced a delayed (i.e., nonimmediate) hypersensitivity reaction, evidenced by an extensive erythematous macular morbilliform rash and an increased eosinophil count. Eight days after completion of therapy, the pneumonia returned, and it was decided to avoid using imipenem-cilastatin; she was administered a 14-day course of meropenem. To our knowledge, this is the first report of a nonimmediate hypersensitivity reaction to imipenem-cilastatin without cross-reactivity to meropenem. This suggests that if carbapenem therapy is unavoidable, meropenem may be cautiously administered in patients with a known allergy to imipenem-cilastatin.

Some patients with imperative cardiologic indications for combination therapy with aspirin and clopidogrel (stent placement and/or acute coronary syndrome 1,2 ) have a history of allergy to aspirin. In other patients, symptoms of aspirin hypersensitivity may develop in the days after stenting, at which time discontinuation of aspirin carries a risk of catastrophic stent thrombosis. 3 We challenged 16 such patients using rapidly escalating low doses of aspirin. In 14 patients, reintroduction was immediately successful, and 11 underwent uneventful stent placement. Two patients developed transient allergic reactions, 1 of whom was successfully rechallenged 48 hours later. No late allergic reactions or adverse cardiac events were seen after a mean follow-up of 14 months. A rapid challenge-desensitization procedure may allow introduction of aspirin at therapeutic doses within a few hours.

An association between impaired lower respiratory function and cardiovascular risk factors, such as hypertension, is often reported but it is unknown whether there is a relationship between upper airway disorders and cardiovascular risk factors, despite evidence that upper and lower respiratory tract disorders are closely linked. Our objective was to assess whether rhinitis is associated with arterial blood pressure and hypertension. In a population-based study of 330 adults aged 28-56 years, as part of the European Community Respiratory Health Survey, rhinitis was assessed by means of a questionnaire, and cardiovascular data were obtained using a questionnaire and by measuring blood pressure. Systolic blood pressure (SBP) was higher in men with rhinitis than in men without rhinitis (130.6 +/- 12.7 mm Hg versus 123.5 +/- 13.9 mm Hg; p = 0.002), and it was still the case after adjustment for cardiovascular and respiratory confounding factors. Hypertension was more frequent in men with rhinitis than in men without rhinitis, even after multivariate adjustment (odds ratio = 2.6, 95% confidence interval = [1.14-5.91]). The observation of SBP levels according to whether men have no rhinitis, seasonal rhinitis, or perennial rhinitis was compatible with a dose-response relationship (p for trend = 0.02). In conclusion, rhinitis is strongly associated with SBP and hypertension in men. Blood pressure should be regularly checked in men with rhinitis.

The association of impaired pulmonary function with cardiovascular morbidity and mortality has been reported in several prospective studies. The nature of this association and the mechanisms underlying it are unknown. Both atherosclerosis and central arterial stiffness might be involved. We recently reported, in a 4-yr longitudinal study, that reduced lung function predicts the development of carotid atherosclerotic plaques. In the present study, we report the associations of aortic stiffness with lung function measurements. One hundred and ninety-four men, aged 30 to 70 yr and free of coronary heart disease, who volunteered for a standard health examination were included. FEV(1) and FVC were used to assess lung function. Aortic stiffness was estimated from the carotid-femoral pulse-wave velocity (PWV), which increases proportionally with an increase in aortic stiffness. PWV was significantly and negatively associated with FEV(1) and FVC (partial correlation coefficients adjusted for age and height: -0.27 [p0.001] and -0.24 [p0.001], respectively). For every 1 SD increase in PWV (2.5 m/s), FEV(1) decreased by 195.2 +/- 50.1 ml (p0.001) in an age- and height-adjusted analysis. The corresponding decrease in FVC was 190.4 +/- 55.0 ml (p0.001). Further adjustment for cardiovascular risk factors (weight, smoking habits, hypercholesterolemia, diabetes, and hypertension) did not markedly alter these results. In addition, negative associations of PWV with lung function measurements were observed within each category of cardiovascular risk factors. This study suggests that reduced pulmonary function is independently associated with aortic stiffness in men. The interrelations between pulmonary and vascular alterations should be thoroughly investigated.

Background: Although clinical and experimental studies suggest that upper respiratory tract dysfunction may affect the lower airways, rhinitis is usually not studied as a potential risk factor for asthma. This is because both diseases share key elements of pathogenesis and are usually considered as different manifestations of the same underlying "atopic" state. Objective: We sought to assess whether asthma is associated with rhinitis in the absence of immunologic disorders in a population study. Methods: Data from 34 centers participating in the European Community Respiratory Health Survey were analyzed. Random samples of 20- to 44-year-old subjects were invited to complete a detailed questionnaire and undergo total and specific IgE measurements, skin prick tests to 9 allergens, and bronchoprovocation challenges with methacholine. Results: Subjects with perennial rhinitis (n = 1412) were more likely than control subjects (n = 5198) to have current asthma. After adjustment for sex, age, smoking habit, family history of asthma, geographic area, and season at the time of examination, asthma was strongly associated with rhinitis among atopic subjects (odds ratio [OR] = 8.1; 95% confidence interval [CI] = 5.4–12.1) but also among nonatopic subjects (OR = 11.6; 95% CI=6.2-21.9). Moreover, the association remained very strong when the analysis was restricted to nonatopic subjects with IgE levels of 80 kIU/L or less (OR = 13.3; 95% CI=6.7–26.5). In nonasthmatic subjects bronchial hyperresponsiveness was also more frequent in subjects with rhinitis than in those without rhinitis (OR = 1.7; 95%CI = 1.2-2.6 in nonatopic subjects with IgE levels of ≤80 kIU/L). Conclusion: The strong association between perennial rhinitis and asthma in nonatopic subjects with normal IgE levels is consistent with the hypothesis that rhinitis is an independent risk factor for asthma. (J Allergy Clin Immunol 1999;104:301-4.)

We report herein the case of an asymptomatic popliteal aneurysm due to fibromuscular dysplasia in a 39-year-old woman. The aneurysm was resected and arterial continuity restored by direct end-to-end anastomosis. Pathologic findings were consistent with fibromuscular dysplasia of the media. To the best of our knowledge, this is the fourth case documented by pathologic findings in the literature.