Perdita Permaul
Harvard University
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Featured researches published by Perdita Permaul.
The Lancet | 2009
Michael E. Wechsler; Susan J. Kunselman; Vernon M. Chinchilli; Eugene R. Bleecker; Homer A. Boushey; William J. Calhoun; Bill T. Ameredes; Mario Castro; Timothy J. Craig; Loren C. Denlinger; John V. Fahy; Nizar N. Jarjour; Shamsah Kazani; Sophia Kim; Monica Kraft; Stephen C. Lazarus; Robert F. Lemanske; Amy Markezich; Richard J. Martin; Perdita Permaul; Stephen P. Peters; Joe W. Ramsdell; Christine A. Sorkness; E. Rand Sutherland; Stanley J. Szefler; Michael J. Walter; Stephen I. Wasserman; Elliot Israel
BACKGROUND Some studies suggest that patients with asthma who are homozygous for arginine at the 16th amino acid position of the beta2-adrenergic receptor (B16 Arg/Arg) benefit less from treatment with longacting beta2 agonists and inhaled corticosteroids than do those homozygous for glycine (B16 Gly/Gly). We investigated whether there is a genotype-specific response to treatment with a longacting beta2 agonist in combination with inhaled corticosteroid. METHODS In this multicentre, randomised, double-blind, placebo-controlled trial, adult patients with moderate asthma were enrolled in pairs matched for forced expiratory volume in 1 s and ethnic origin, according to whether they had the B16 Arg/Arg (n=42) or B16 Gly/Gly (n=45) genotype. Individuals in a matched pair were randomly assigned by computer-generated randomisation sequence to receive inhaled longacting beta2 agonist (salmeterol 50 microg twice a day) or placebo given in a double-blind, crossover design for two 18-week periods. Open-label inhaled corticosteroid (hydrofluoroalkane beclometasone 240 microg twice a day) was given to all participants during the treatment periods. The primary endpoint was morning peak expiratory flow (PEF). Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00200967. FINDINGS After 18 weeks of treatment, mean morning PEF in Arg/Arg participants was 21.4 L/min (95% CI 11.8-31.1) higher when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.0001). In Gly/Gly participants, morning PEF was 21.5 L/min (11.0-32.1) higher when participants were assigned to receive salmeterol than when assigned to receive placebo (p<0.0001). The improvement in PEF did not differ between genotypes (difference [Arg/Arg-Gly/Gly] -0.1, -14.4 to 14.2; p=0.99). In Gly/Gly participants, methacholine PC20 (20% reduction in forced expiratory volume in 1 s; a prespecified secondary outcome) was 2.4 times higher when participants were assigned to salmeterol than when assigned to placebo (p<0.0001). Responsiveness to methacholine did not differ between salmeterol and placebo in Arg/Arg participants (p=0.87). The 2.5 times higher genotype-specific difference in responsiveness to methacholine was significant (1.32 doubling dose difference between genotypes, 0.43-2.21, p=0.0038). Seven Arg/Arg participants (placebo, n=5; salmeterol, n=2) and six Gly/Gly participants (placebo, n=3; salmeterol, n=3) had an asthma exacerbation. Five serious adverse events were reported, one each during the pre-match and run-in phases on open-label inhaled corticosteroid, two during double-blind treatment with salmeterol/inhaled corticosteroid, and one during double-blind treatment with placebo/inhaled corticosteroid. None of the serious events was asthma-related or related to study drugs or procedures. INTERPRETATION In asthma patients with B16 Arg/Arg and B16 Gly/Gly genotypes, combination treatment with salmeterol and inhaled corticosteroid improved airway function when compared with inhaled corticosteroid therapy alone. These findings suggest that patients should continue to be treated with longacting beta2 agonists plus moderate-dose inhaled corticosteroids irrespective of B16 genotype. Further investigation is needed to establish the importance of the genotype-specific difference in responsiveness to methacholine. FUNDING National Institutes of Health.
Pediatric Allergy and Immunology | 2012
Perdita Permaul; Elaine Hoffman; Chunxia Fu; William J. Sheehan; Sachin N. Baxi; Jonathan M. Gaffin; Jeffrey P. Lane; Ann Bailey; Eva M. King; Martin D. Chapman; Diane R. Gold; Wanda Phipatanakul
To cite this article: Permaul P, Hoffman E, Fu C, Sheehan W, Baxi S, Gaffin J, Lane J, Bailey A, King E, Chapman M, Gold D, Phipatanakul W. Allergens in urban schools and homes of children with asthma. Pediatr Allergy Immunol 2012: 23: 543–549.
Annals of Allergy Asthma & Immunology | 2012
Lisa M. Bartnikas; William J. Sheehan; Elaine Hoffman; Perdita Permaul; Anahita F. Dioun; James Friedlander; Sachin N. Baxi; Lynda C. Schneider; Wanda Phipatanakul
BACKGROUND Cows milk allergy is the most common food allergy in childhood. Many children with IgE-mediated cows milk allergy may tolerate baked milk products, but few data exist on predictors of outcomes of baked milk challenges. OBJECTIVE To determine the relation of milk protein allergen specific IgE (sIgE) levels and skin prick test (SPT) wheal size with baked milk challenge outcomes. METHODS A retrospective medical record review was conducted of 35 baked milk challenges. SPT results, sIgE levels, demographic characteristics, and food challenge results were analyzed. RESULTS Thirty-five children underwent open challenges to baked milk and 29 (83%) passed. Of those who failed, 3 (50%) passed the initial clinic challenge but developed symptoms to ongoing exposure at home, days to months later. One child who ultimately failed at home required epinephrine. Compared with those who passed, children who failed were younger (median age, 8.9 and 3.7 years, respectively; P = .02). Children with a milk SPT wheal less than 12 mm were more than 90% likely to pass a baked milk challenge, and no child with a milk SPT wheal less than 7 mm failed a baked milk challenge. We were also able to establish more than 90% predictive values for passing baked milk challenges with a casein SPT wheal of 9 mm, a milk sIgE level of 1.0 kU/L, and a casein sIgE level of 0.9 kU/L. CONCLUSION Most children allergic to cows milk tolerated baked milk. Milk protein SPT wheal may be more reliable than sIgE level in predicting outcomes of baked milk challenges. It is important to be aware of the possibility of late reactions to ongoing baked milk exposure.
Immunologic Research | 2009
Perdita Permaul; Anupama Narla; Jason L. Hornick; Sung-Yun Pai
Hypomorphic mutations in nuclear factor kappa B essential modulator (NEMO) cause X-linked ectodermal dysplasia with immunodeficiency (X-ED-ID). Clinical manifestations in boys with X-ED-ID apart from ectodermal dysplasia and immunodeficiency include osteopetrosis, lymphedema, and colitis. Further description of atypical findings in this disorder is needed. Treatment with allogeneic hematopoietic stem cell transplantation (HSCT) is in its infancy, and how or whether non-immune manifestations of defective NEMO function are impacted by HSCT is poorly described. We report an interesting case of a boy with NEMO mutation who had symptoms reminiscent of Omenn’s syndrome and small intestinal villous atrophy with features reminiscent of tufting enteropathy. We describe his treatment course as well as reconstitution of immune function and correction of osteopetrosis post-HSCT, and review the cases of allogeneic HSCT reported to date in the literature.
Journal of Asthma | 2011
Wanda Phipatanakul; Anne Bailey; Elaine Hoffman; William J. Sheehan; Jeffrey P. Lane; Sachin N. Baxi; Devika R. Rao; Perdita Permaul; Jonathan M. Gaffin; Christine A. Rogers; Michael L. Muilenberg; Diane R. Gold
Background. Children spend a significant amount of time in school. Little is known about the role of allergen exposure in school environments and asthma morbidity. Objectives. The School Inner-City Asthma Study (SICAS) is a National Institutes of Health (NIH)-funded prospective study evaluating the school/classroom-specific risk factors and asthma morbidity among urban children. Methods/results. This article describes the design, methods, and important lessons learned from this extensive investigation. A single center is recruiting 500 elementary school-aged children, all of whom attend inner-city metropolitan schools. The primary hypothesis is that exposure to common indoor allergens in the classroom will increase the risk of asthma morbidity in children with asthma, even after controlling for home allergen exposures. The protocol includes screening surveys of entire schools and baseline eligibility assessments obtained in the spring prior to the academic year. Extensive baseline clinical visits are being conducted among eligible children with asthma during the summer prior to the academic school year. Environmental classroom/school assessments including settled dust and air sampling for allergen, mold, air pollution, and inspection data are collected twice during the academic school year and one home dust sample linked to the enrolled student. Clinical outcomes are measured every 3 months during the academic school year. Conclusion. The overall goal of SICAS is to complete the first study of its kind to better understand school-specific urban environmental factors on childhood asthma morbidity. We also discuss the unique challenges related to school-based urban research and lessons being learned from recruiting such a cohort.
Pediatric Allergy and Immunology | 2013
Sachin N. Baxi; Michael L. Muilenberg; Christine A. Rogers; William J. Sheehan; Jonathan M. Gaffin; Perdita Permaul; Lianne S. Kopel; Peggy S. Lai; Jeffrey P. Lane; Ann Bailey; Carter R. Petty; Chunxia Fu; Diane R. Gold; Wanda Phipatanakul
Students spend a large portion of their day in classrooms which may be a source of mold exposure. We examined the diversity and concentrations of molds in inner‐city schools and described differences between classrooms within the same school.
Allergy and Asthma Proceedings | 2012
Catherine F. Cortot; William J. Sheehan; Perdita Permaul; James Friedlander; Sachin N. Baxi; Jonathan M. Gaffin; Anahita F. Dioun; Elaine Hoffman; Lynda C. Schneider; Wanda Phipatanakul
Previous studies suggest that children with egg allergy may be able to tolerate baked egg. Reliable predictors of a successful baked egg challenge are not well established. We examined egg white-specific IgE levels, skin-prick test (SPT) results, and age as predictors of baked egg oral food challenge (OFC) outcomes. We conducted a retrospective chart review of children, aged 2-18 years, receiving an egg white-specific IgE level, SPT, and OFC to baked egg from 2008 to 2010. Fifty-two oral baked egg challenges were conducted. Of the 52 challenges, 83% (n = 43) passed and 17% (n = 9) failed, including 2 having anaphylaxis. Median SPT wheal size was 12 mm (range, 0-35 mm) for passed challenges and 17 mm (range, 10-30 mm) for failed challenges (p = 0.091). The negative predictive value for passing the OFC was 100% (9 of 9) if SPT wheal size was <10 mm. Median egg white-specific IgE was 2.02 kU/L (range, <0.35-13.00 kU/L) for passed challenges and 1.52 kU/L (range, 0.51-6.10 kU/L) for failed challenges (p = 0.660). Receiver operating characteristic (ROC) curve analysis for SPT revealed an area under the curve (AUC) of 0.64. ROC curve analysis for egg white-specific IgE revealed an AUC of 0.63. There was no significant difference in age between patients who failed and those who passed (median = 8.8 years versus 7.0 years; p = 0.721). Based on our sample, SPT, egg white-specific IgE and age are not good predictors of passing a baked egg challenge. However, there was a trend for more predictability with SPT wheal size.
JAMA Pediatrics | 2017
William J. Sheehan; Perdita Permaul; Carter R. Petty; Brent A. Coull; Sachin N. Baxi; Jonathan M. Gaffin; Peggy S. Lai; Diane R. Gold; Wanda Phipatanakul
Importance Home aeroallergen exposure is associated with increased asthma morbidity in children, yet little is known about the contribution of school aeroallergen exposures to such morbidity. Objective To evaluate the effect of school-specific aeroallergen exposures on asthma morbidity among students, adjusting for home exposures. Design, Setting, and Participants The School Inner-City Asthma Study was a prospective cohort study evaluating 284 students aged 4 to 13 years with asthma who were enrolled from 37 inner-city elementary schools in the northeastern United States between March 1, 2008, and August 31, 2013. Enrolled students underwent baseline clinical evaluations before the school year started and were then observed clinically for 1 year. During that same school year, classroom and home dust samples linked to the students were collected and analyzed for common indoor aeroallergens. Associations between school aeroallergen exposure and asthma outcomes during the school year were assessed, adjusting for home exposures. Exposures Indoor aeroallergens, including rat, mouse, cockroach, cat, dog, and dust mites, measured in dust samples collected from inner-city schools. Main Outcomes and Measures The primary outcome was maximum days in the past 2 weeks with asthma symptoms. Secondary outcomes included well-established markers of asthma morbidity, including asthma-associated health care use and lung function, measured by forced expiratory volume in 1 second. Results Among 284 students (median age, 8 years [interquartile range, 6-9 years]; 148 boys and 136 girls), exposure to mouse allergen was detected in 441 (99.5%) of 443 school dust samples, cat allergen in 420 samples (94.8%), and dog allergen in 366 samples (82.6%). Levels of mouse allergen in schools were significantly higher than in students’ homes (median settled dust level, 0.90 vs 0.14 µg/g; P < .001). Exposure to higher levels of mouse allergen in school (comparing 75th with 25th percentile) was associated with increased odds of having an asthma symptom day (odds ratio, 1.27; 95% CI, 1.05-1.54; P = .02) and 4.0 percentage points lower predicted forced expiratory volume in 1 second (95% CI, –6.6 to –1.5; P = .002). This effect was independent of allergic sensitization. None of the other indoor aeroallergens were associated with worsening asthma outcomes. Conclusions and Relevance In this study of inner-city students with asthma, exposure to mouse allergen in schools was associated with increased asthma symptoms and decreased lung function. These findings demonstrate that the school environment is an important contributor to childhood asthma morbidity. Future school-based environmental interventions may be beneficial for this important public health problem.
Annals of Allergy Asthma & Immunology | 2014
Perdita Permaul; Watcharoot Kanchongkittiphon; Wanda Phipatanakul
Obesity rates have increased significantly in children in many parts of the world, especially in North America.1 According to data from the most recent National Health and Nutrition Examination Survey, approximately 17% (or 12.5 million) of US children and adolescents 2 to 9 years old are obese.2 The impact that childhood obesity has on pediatric diseases has become a major prevention initiative by the Obama administration and several public health organizations. Children with obesity are at increased risk for developing asthma, one of the most common chronic diseases in children.3 Childhood asthma accounts for more than 14 million missed school days per year and is the primary cause of school absences in the United States.4 A relation between obesity and asthma is supported by prospective studies in adults and children suggesting that being overweight and obese can precede the onset of asthma5 and studies in adults showing alleviation of asthma symptoms with weight loss.6 Despite consistent evidence linking obesity to the incidence and prevalence of asthma and several postulated hypotheses to explain this association, a definitive mechanism remains a mystery. Genetic and Environmental Factors Asthma and obesity are likely to be connected in a multifactorial fashion. Although genetic susceptibility can contribute to the development of asthma and obesity, the rapid increase in a relatively short period suggests that changes in lifestyle, such as diet, physical activity, early life exposures, and other environmental interactions, also can play a role. Epigenetic mechanisms associated with obesity and asthma have been proposed. Obesity and asthma likely have their beginnings in utero and in early childhood. Diet and nutrition, especially prenatal and early infant diet, may play a part in these diseases. Greater consumption of fruits and vegetables, antioxidants, minerals and vitamins, fish, and legumes during pregnancy seems to confer protection against childhood asthma and wheeze7 and may influence the neonatal immune system and lung development.8 However, 1 study showed that fatty acid dietary supplementation during pregnancy did not lower the overall incidence of asthma.9 To further support the idea that intrauterine nutrition is important, associations between low birth weight and resulting obesity and asthma have been shown. In 1 study, low birth weight led to the development of asthma and excess body mass increased the risk.10 Rapid growth in body mass index (BMI) during the first 2 years of life increased the risk of asthma up to 6 years of age based on published data from 8 European birth cohorts.11
American Journal of Respiratory and Critical Care Medicine | 2013
Matteo Bonini; Perdita Permaul; Tejaswini Kulkarni; Shamsah Kazani; Alex Segal; Christine A. Sorkness; Michael E. Wechsler; Elliot Israel
RATIONALE β2-Agonists are the treatment of choice for exercise-induced bronchoconstriction (EIB) and act through specific receptors (ADRB2). Arg16Gly polymorphisms have been shown to affect responses to regular use of β2-agonists. OBJECTIVES To evaluate the influence of the Arg16Gly receptor polymorphism on salmeterol bronchoprotection in EIB and assess predictors of bronchoprotection. METHODS A prospective, genotype-blinded, randomized trial was performed in 26 subjects (12 Arg16Arg and 14 Gly16Gly) with EIB who were not on controller therapy. Subjects were administered salmeterol, 50 μg twice a day for 2 weeks, and underwent an exercise challenge 9 hours after the first and last drug dose. In addition to genotype, FEV1, response to salmeterol, degree of EIB, and exhaled nitric oxide (FE(NO)) at baseline were examined for their association with loss of bronchoprotection (LOB). MEASUREMENTS AND MAIN RESULTS The maximum exercise-induced FEV1 fall was 27.9 ± 1.4% during the run-in period, 8.1 ± 1.2% (70.3 ± 4.1% bronchoprotection) after the first salmeterol dose, and 22.8 ± 3.2% (18.9 ± 11.5% bronchoprotection) after 2 weeks of salmeterol (P = 0.0001). The Arg16Gly polymorphisms were not associated with the LOB in response to salmeterol. FeNO values at baseline were significantly related to the LOB (r = 0.47; P = 0.01). Mean change was a 74 ± 13% LOB in subjects with FE(NO) levels greater than 50 ppb and a 7 ± 16% gain in bronchoprotection in those with FE(NO) levels less than 25 ppb (P = 0.01). CONCLUSIONS The LOB that occurs with chronic long-acting β2-agonists use is not affected by ADRB2 Arg16Gly polymorphisms. High FE(NO) was associated with marked LOB. Use of long-acting β2-agonists before achieving a reduction in FeNO may need to be avoided. Clinical trial registered with www.clinicaltrials.gov (NCT 00595361).