2012 AAAAI Annual Meeting

ORLANDO – Asthma-related visits to emergency departments spike in the spring, when grass and tree pollen levels are at their highest, according to investigators in two separate studies presented here at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Over a 9-year period, asthma-related ED visits at two hospitals in the Bronx borough of New York City tended to peak in May, coinciding with high tree pollen levels, reported Dr. Jennifer Toh and colleagues from Albert Einstein College of Medicine, New York, and Southern Methodist University in Dallas.

© ideeone/iStockphoto.com

On the other side of the world in Australia, ED visits for asthma care coincided with high grass pollen levels in November and early December, spring months in the antipodean calendar, reported Dr. Bircan Erbas of La Trobe University in Melbourne and colleagues.

"We have a growth corridor in Melbourne which has been predominantly used for grazing of cattle and sheep, and we’ve seen increases in admissions for asthma and allergies," Dr. Erbas said in an interview.

She noted that following several days of high winds and severe thunderstorms in Melbourne in November 2003, there was a peak in ED attendance of 70 visits per day, "consistent with thunderstorm-associated asthma related to the preceding extreme grass pollen days and strong winds."

In the Bronx, where there is a high prevalence of asthma, tree pollen spikes in the Northern Hemisphere’s spring seem to be related to increases in asthma-related ED visits, Dr. Toh said in an interview.

Dr. Toh and colleagues looked at day-by-day asthma-related emergency department visits, as identified by ICD (International Classification of Disease) codes, at two hospitals in the Bronx. They then matched those data to daily pollen counts collected at the nearest pollen trap, located in Armonk, N.Y., about 27 miles north of New York City.

From 2001 through 2008, the investigators noted distinct peaks of increased ED visits for asthma, one each in January, May, and November.

"For most of the years studied, the spring peak was most prominent and consistently overlapped with high tree pollen levels. In addition, our regression analysis [of excess vs. average daily asthma ED visits] revealed that the largest excess asthma-related emergency department visits consistently overlapped the larger tree pollen levels during the month of May every year," they wrote in a poster presentation.

The investigators did not have data on the type of tree pollen.

"I think that in the entire Northeast, tree pollen is the most relevant allergen in terms of severe seasonal allergies. We don’t have as many problems with grass or ragweed as we do with trees," said Dr. Bernard Silverman, of Mount Sinai Hospital in New York. Dr. Silverman commented on the study in an interview, but was not involved in it.

The height of the pollen traps and their distance from the city may have influenced the results, said another clinician not involved in the study. It is important when studying pollen levels to set pollen traps at the appropriate height for the question the investigators hope to address, said Dr. Karl-Christian Bergmann of Charité Hospital in Berlin. Traps lower to the ground are more useful for measuring the amount of pollen that individuals are likely to inhale at the local level, whereas as traps set at a height of about 15-25 m are more useful for gauging airborne pollen levels over a broader geographic area. Results also can be confounded by higher levels of airborne carbon particulates, such as those found in diesel exhaust, he said.

Dr. Erbas and colleagues noted that "lower levels of pollen may contribute to asthma symptoms, levels that are much lower than the current level of 50 g/m³ which is used as the trigger point for warning asthma patients to avoid nonessential outdoor activities and/or take additional asthma medication."

Both Dr. Toh’s and Dr. Erbas’ studies were supported by the participating institutions. Both clinicians reported having no relevant disclosures.

ORLANDO – Asthma-related visits to emergency departments spike in the spring, when grass and tree pollen levels are at their highest, according to investigators in two separate studies presented here at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Over a 9-year period, asthma-related ED visits at two hospitals in the Bronx borough of New York City tended to peak in May, coinciding with high tree pollen levels, reported Dr. Jennifer Toh and colleagues from Albert Einstein College of Medicine, New York, and Southern Methodist University in Dallas.

© ideeone/iStockphoto.com

On the other side of the world in Australia, ED visits for asthma care coincided with high grass pollen levels in November and early December, spring months in the antipodean calendar, reported Dr. Bircan Erbas of La Trobe University in Melbourne and colleagues.

"We have a growth corridor in Melbourne which has been predominantly used for grazing of cattle and sheep, and we’ve seen increases in admissions for asthma and allergies," Dr. Erbas said in an interview.

She noted that following several days of high winds and severe thunderstorms in Melbourne in November 2003, there was a peak in ED attendance of 70 visits per day, "consistent with thunderstorm-associated asthma related to the preceding extreme grass pollen days and strong winds."

In the Bronx, where there is a high prevalence of asthma, tree pollen spikes in the Northern Hemisphere’s spring seem to be related to increases in asthma-related ED visits, Dr. Toh said in an interview.

Dr. Toh and colleagues looked at day-by-day asthma-related emergency department visits, as identified by ICD (International Classification of Disease) codes, at two hospitals in the Bronx. They then matched those data to daily pollen counts collected at the nearest pollen trap, located in Armonk, N.Y., about 27 miles north of New York City.

From 2001 through 2008, the investigators noted distinct peaks of increased ED visits for asthma, one each in January, May, and November.

"For most of the years studied, the spring peak was most prominent and consistently overlapped with high tree pollen levels. In addition, our regression analysis [of excess vs. average daily asthma ED visits] revealed that the largest excess asthma-related emergency department visits consistently overlapped the larger tree pollen levels during the month of May every year," they wrote in a poster presentation.

The investigators did not have data on the type of tree pollen.

"I think that in the entire Northeast, tree pollen is the most relevant allergen in terms of severe seasonal allergies. We don’t have as many problems with grass or ragweed as we do with trees," said Dr. Bernard Silverman, of Mount Sinai Hospital in New York. Dr. Silverman commented on the study in an interview, but was not involved in it.

The height of the pollen traps and their distance from the city may have influenced the results, said another clinician not involved in the study. It is important when studying pollen levels to set pollen traps at the appropriate height for the question the investigators hope to address, said Dr. Karl-Christian Bergmann of Charité Hospital in Berlin. Traps lower to the ground are more useful for measuring the amount of pollen that individuals are likely to inhale at the local level, whereas as traps set at a height of about 15-25 m are more useful for gauging airborne pollen levels over a broader geographic area. Results also can be confounded by higher levels of airborne carbon particulates, such as those found in diesel exhaust, he said.

Dr. Erbas and colleagues noted that "lower levels of pollen may contribute to asthma symptoms, levels that are much lower than the current level of 50 g/m³ which is used as the trigger point for warning asthma patients to avoid nonessential outdoor activities and/or take additional asthma medication."

Both Dr. Toh’s and Dr. Erbas’ studies were supported by the participating institutions. Both clinicians reported having no relevant disclosures.

ORLANDO – Asthma-related visits to emergency departments spike in the spring, when grass and tree pollen levels are at their highest, according to investigators in two separate studies presented here at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Over a 9-year period, asthma-related ED visits at two hospitals in the Bronx borough of New York City tended to peak in May, coinciding with high tree pollen levels, reported Dr. Jennifer Toh and colleagues from Albert Einstein College of Medicine, New York, and Southern Methodist University in Dallas.

© ideeone/iStockphoto.com

On the other side of the world in Australia, ED visits for asthma care coincided with high grass pollen levels in November and early December, spring months in the antipodean calendar, reported Dr. Bircan Erbas of La Trobe University in Melbourne and colleagues.

"We have a growth corridor in Melbourne which has been predominantly used for grazing of cattle and sheep, and we’ve seen increases in admissions for asthma and allergies," Dr. Erbas said in an interview.

She noted that following several days of high winds and severe thunderstorms in Melbourne in November 2003, there was a peak in ED attendance of 70 visits per day, "consistent with thunderstorm-associated asthma related to the preceding extreme grass pollen days and strong winds."

In the Bronx, where there is a high prevalence of asthma, tree pollen spikes in the Northern Hemisphere’s spring seem to be related to increases in asthma-related ED visits, Dr. Toh said in an interview.

Dr. Toh and colleagues looked at day-by-day asthma-related emergency department visits, as identified by ICD (International Classification of Disease) codes, at two hospitals in the Bronx. They then matched those data to daily pollen counts collected at the nearest pollen trap, located in Armonk, N.Y., about 27 miles north of New York City.

From 2001 through 2008, the investigators noted distinct peaks of increased ED visits for asthma, one each in January, May, and November.

"For most of the years studied, the spring peak was most prominent and consistently overlapped with high tree pollen levels. In addition, our regression analysis [of excess vs. average daily asthma ED visits] revealed that the largest excess asthma-related emergency department visits consistently overlapped the larger tree pollen levels during the month of May every year," they wrote in a poster presentation.

The investigators did not have data on the type of tree pollen.

"I think that in the entire Northeast, tree pollen is the most relevant allergen in terms of severe seasonal allergies. We don’t have as many problems with grass or ragweed as we do with trees," said Dr. Bernard Silverman, of Mount Sinai Hospital in New York. Dr. Silverman commented on the study in an interview, but was not involved in it.

The height of the pollen traps and their distance from the city may have influenced the results, said another clinician not involved in the study. It is important when studying pollen levels to set pollen traps at the appropriate height for the question the investigators hope to address, said Dr. Karl-Christian Bergmann of Charité Hospital in Berlin. Traps lower to the ground are more useful for measuring the amount of pollen that individuals are likely to inhale at the local level, whereas as traps set at a height of about 15-25 m are more useful for gauging airborne pollen levels over a broader geographic area. Results also can be confounded by higher levels of airborne carbon particulates, such as those found in diesel exhaust, he said.

Dr. Erbas and colleagues noted that "lower levels of pollen may contribute to asthma symptoms, levels that are much lower than the current level of 50 g/m³ which is used as the trigger point for warning asthma patients to avoid nonessential outdoor activities and/or take additional asthma medication."

Both Dr. Toh’s and Dr. Erbas’ studies were supported by the participating institutions. Both clinicians reported having no relevant disclosures.

ORLANDO – Gastroesophageal reflux disease was associated with prior wheezing and greater severity of infant acute respiratory illness in a study involving 430 term, healthy infants presenting with acute respiratory illness due to bronchiolitis or upper respiratory infection.

New-onset gastroesophageal reflux disease (GERD) during bronchiolitis in previously health infants has been shown to increase the risk for respiratory failure (Acta Paediatr. 2007;96:1025-9). Bronchiolitis is a prominent risk factor for childhood asthma, and GERD is associated with worsened asthma severity (J. Asthma 2011;48:366-73). As yet unknown is whether preexisting GERD (clinically significant reflux) in infants modulates the severity of infant bronchiolitis or the diagnosis of childhood asthma, Dr. Robert S. Valet of Vanderbilt University, Nashville, Tenn., and his associates said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The 430 infants, aged 0-12 months, were enrolled in the Tennessee Children\'s Respiratory Initiative. The presence of infant GERD was defined by parental report with an answer of "yes" to the question, "Does your child have a history of gastroesophageal reflux disease?"

In all, 45 infants (10%) were reported to have GERD. They were more likely than those without GERD to be white and to have a family history of allergic rhinitis, but did not differ by age at illness, secondhand smoke (SHS) exposure, or family history of asthma. The group with GERD was significantly more likely to have previous treatment for wheeze (42% vs. 25%), and to have bronchiolitis (84% vs. 71%).

The median bronchiolitis severity score (range, 0-12; higher score indicates more severe disease, with a difference of 0.5 being clinically meaningful) in univariate analysis was 5.5 in the GERD group vs. 4.0 in infants without GERD. Adjusting for age, race, sex, and SHS, the increased bronchiolitis severity score in the GERD group persisted (odds ratio, 1.90). Although not significant, 11% of infants with GERD vs. 5% of non-GERD infants needed ICU care, Dr. Valet and his associates reported.

Preexisting GERD was associated with increased bronchiolitis severity and increased recurrent wheezing illness at 2 years, at which time 69% of infants with GERD and 46% of those without GERD had experienced wheeze since initial study enrollment (OR, 2.35; P = .006). And although not statistically significant, 52% with GERD vs. 40% without had used albuterol in this time period (P = .13). However, there was no difference in asthma diagnosis at age 2 years; 24% of infants with GERD were diagnosed with asthma by age 2, compared with 22% of those without GERD (P = .76).

This is the first time that preexisting infant GERD has been associated with increased bronchiolitis severity, Dr. Valet noted. Future study could investigate whether treating infant GERD decreases both bronchiolitis and asthma severity. "These findings should be replicated using a more rigorous assessment of GERD," he concluded.

The study was funded by the Thrasher Research Fund. Dr. Valet said he had no relevant financial disclosures.

ORLANDO – Gastroesophageal reflux disease was associated with prior wheezing and greater severity of infant acute respiratory illness in a study involving 430 term, healthy infants presenting with acute respiratory illness due to bronchiolitis or upper respiratory infection.

New-onset gastroesophageal reflux disease (GERD) during bronchiolitis in previously health infants has been shown to increase the risk for respiratory failure (Acta Paediatr. 2007;96:1025-9). Bronchiolitis is a prominent risk factor for childhood asthma, and GERD is associated with worsened asthma severity (J. Asthma 2011;48:366-73). As yet unknown is whether preexisting GERD (clinically significant reflux) in infants modulates the severity of infant bronchiolitis or the diagnosis of childhood asthma, Dr. Robert S. Valet of Vanderbilt University, Nashville, Tenn., and his associates said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The 430 infants, aged 0-12 months, were enrolled in the Tennessee Children\'s Respiratory Initiative. The presence of infant GERD was defined by parental report with an answer of "yes" to the question, "Does your child have a history of gastroesophageal reflux disease?"

In all, 45 infants (10%) were reported to have GERD. They were more likely than those without GERD to be white and to have a family history of allergic rhinitis, but did not differ by age at illness, secondhand smoke (SHS) exposure, or family history of asthma. The group with GERD was significantly more likely to have previous treatment for wheeze (42% vs. 25%), and to have bronchiolitis (84% vs. 71%).

The median bronchiolitis severity score (range, 0-12; higher score indicates more severe disease, with a difference of 0.5 being clinically meaningful) in univariate analysis was 5.5 in the GERD group vs. 4.0 in infants without GERD. Adjusting for age, race, sex, and SHS, the increased bronchiolitis severity score in the GERD group persisted (odds ratio, 1.90). Although not significant, 11% of infants with GERD vs. 5% of non-GERD infants needed ICU care, Dr. Valet and his associates reported.

Preexisting GERD was associated with increased bronchiolitis severity and increased recurrent wheezing illness at 2 years, at which time 69% of infants with GERD and 46% of those without GERD had experienced wheeze since initial study enrollment (OR, 2.35; P = .006). And although not statistically significant, 52% with GERD vs. 40% without had used albuterol in this time period (P = .13). However, there was no difference in asthma diagnosis at age 2 years; 24% of infants with GERD were diagnosed with asthma by age 2, compared with 22% of those without GERD (P = .76).

This is the first time that preexisting infant GERD has been associated with increased bronchiolitis severity, Dr. Valet noted. Future study could investigate whether treating infant GERD decreases both bronchiolitis and asthma severity. "These findings should be replicated using a more rigorous assessment of GERD," he concluded.

The study was funded by the Thrasher Research Fund. Dr. Valet said he had no relevant financial disclosures.

ORLANDO – Gastroesophageal reflux disease was associated with prior wheezing and greater severity of infant acute respiratory illness in a study involving 430 term, healthy infants presenting with acute respiratory illness due to bronchiolitis or upper respiratory infection.

New-onset gastroesophageal reflux disease (GERD) during bronchiolitis in previously health infants has been shown to increase the risk for respiratory failure (Acta Paediatr. 2007;96:1025-9). Bronchiolitis is a prominent risk factor for childhood asthma, and GERD is associated with worsened asthma severity (J. Asthma 2011;48:366-73). As yet unknown is whether preexisting GERD (clinically significant reflux) in infants modulates the severity of infant bronchiolitis or the diagnosis of childhood asthma, Dr. Robert S. Valet of Vanderbilt University, Nashville, Tenn., and his associates said in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

The 430 infants, aged 0-12 months, were enrolled in the Tennessee Children\'s Respiratory Initiative. The presence of infant GERD was defined by parental report with an answer of "yes" to the question, "Does your child have a history of gastroesophageal reflux disease?"

In all, 45 infants (10%) were reported to have GERD. They were more likely than those without GERD to be white and to have a family history of allergic rhinitis, but did not differ by age at illness, secondhand smoke (SHS) exposure, or family history of asthma. The group with GERD was significantly more likely to have previous treatment for wheeze (42% vs. 25%), and to have bronchiolitis (84% vs. 71%).

The median bronchiolitis severity score (range, 0-12; higher score indicates more severe disease, with a difference of 0.5 being clinically meaningful) in univariate analysis was 5.5 in the GERD group vs. 4.0 in infants without GERD. Adjusting for age, race, sex, and SHS, the increased bronchiolitis severity score in the GERD group persisted (odds ratio, 1.90). Although not significant, 11% of infants with GERD vs. 5% of non-GERD infants needed ICU care, Dr. Valet and his associates reported.

Preexisting GERD was associated with increased bronchiolitis severity and increased recurrent wheezing illness at 2 years, at which time 69% of infants with GERD and 46% of those without GERD had experienced wheeze since initial study enrollment (OR, 2.35; P = .006). And although not statistically significant, 52% with GERD vs. 40% without had used albuterol in this time period (P = .13). However, there was no difference in asthma diagnosis at age 2 years; 24% of infants with GERD were diagnosed with asthma by age 2, compared with 22% of those without GERD (P = .76).

This is the first time that preexisting infant GERD has been associated with increased bronchiolitis severity, Dr. Valet noted. Future study could investigate whether treating infant GERD decreases both bronchiolitis and asthma severity. "These findings should be replicated using a more rigorous assessment of GERD," he concluded.

The study was funded by the Thrasher Research Fund. Dr. Valet said he had no relevant financial disclosures.

ORLANDO – Budesonide/formoterol pressurized metered-dose inhaler demonstrated similar cardiovascular safety to that of budesonide treatment alone in a study of 742 black adolescents and adults with moderate to severe asthma.

There has been concern that regular long-acting beta₂-adrenergic agonist (LABA) therapy may increase the risk of mortality, including that from cardiac adverse events. An analysis of asthma trials suggested that formoterol does not increase cardiac-related serious adverse events or cardiac-related deaths (Eur. Respir. J. 2009;33:21-32).

And a recent study showed that budesonide/formoterol pressurized metered-dose inhaler (BUD/FM pMDI) was well tolerated and more effective for preventing exacerbations, compared with monotherapy BUD pMDI, in a black patient population (Am. J. Respir. Crit. Care Med. 2011;183:A1294).

However, data have been limited on the cardiovascular safety of combination inhaled corticosteroids (ICSs) and LABAs in specific racial/ethnic patient populations with asthma, Dr. Kathy L. Lampl of AstraZeneca and her associates reported in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

In a randomized, double-blind, parallel-group, multicenter, 52-week study, 742 patients with moderate to severe persistent asthma who self-reported their race as black were randomized 1:1 to receive BUD/FM pMDI (160/4.5 mcg × 2 inhalations, total 320/9 mcg) or BUD pMDI (160 mcg × 2 inhalations, total 320 mcg) twice daily. Twelve-lead electrocardiograms were obtained before the morning dose of study medication in all patients at visits two through nine.

All patients were on a consistent daily medium to high dose of ICS either taken alone or as combination therapy with a LABA for 30 days or longer before screening.

Changes from baseline to treatment maximum for BUD/FM vs. BUD were similar for heart rate (9.87 vs. 9.04 beats/minute) and QT interval corrected for heart rate, with QTc 18.46 vs. 18.18 msec (Bazett’s correction) and QTc 13.47 vs. 14.73 msec (Fridericia’s correction), but lower for the uncorrected QT interval, 15.59 vs. 19.12 msec (unadjusted P = .002).

The proportion of patients with a heart rate greater than 100 beats/min or an increase of 20 or more beats per minute were 11.4% for BUD/FM and 8.5% for BUD, which is consistent with known effects of beta₂-adrenergic agonists, Dr. Lampl and her associates said.

Cardiac events were infrequent, and all were considered nonserious. Cardiac adverse events occurred in six patients (1.6%) in the BUD/FM pMDI group, including cardiac conduction disorders (one patient, 0.3%), ischemic coronary artery disorders (one patient, 0.3%), rate and rhythm disorders (two patients, 0.5%), supraventricular arrhythmias (two patients, 0.5%), and ventricular arrhythmias and cardiac arrest (one patient, 0.3%). Four patients (1.1%) in the BUD pMDI group experienced a cardiac adverse event, including cardiac conduction disorders (two patients, 0.5%), cardiac signs and symptoms (one patient, 0.3%), and noninfectious pericarditis (one patient, 0.3%).

"Overall, the results of this study further support the long-term tolerability of BUD/FM pMDI in African-American adolescents and adults with moderate to severe asthma not adequately controlled on an ICS alone," Dr. Lampl and her associates concluded.

Dr. Lampl is a paid employee of AstraZeneca, which funded the study.

ORLANDO – Budesonide/formoterol pressurized metered-dose inhaler demonstrated similar cardiovascular safety to that of budesonide treatment alone in a study of 742 black adolescents and adults with moderate to severe asthma.

There has been concern that regular long-acting beta₂-adrenergic agonist (LABA) therapy may increase the risk of mortality, including that from cardiac adverse events. An analysis of asthma trials suggested that formoterol does not increase cardiac-related serious adverse events or cardiac-related deaths (Eur. Respir. J. 2009;33:21-32).

And a recent study showed that budesonide/formoterol pressurized metered-dose inhaler (BUD/FM pMDI) was well tolerated and more effective for preventing exacerbations, compared with monotherapy BUD pMDI, in a black patient population (Am. J. Respir. Crit. Care Med. 2011;183:A1294).

However, data have been limited on the cardiovascular safety of combination inhaled corticosteroids (ICSs) and LABAs in specific racial/ethnic patient populations with asthma, Dr. Kathy L. Lampl of AstraZeneca and her associates reported in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

In a randomized, double-blind, parallel-group, multicenter, 52-week study, 742 patients with moderate to severe persistent asthma who self-reported their race as black were randomized 1:1 to receive BUD/FM pMDI (160/4.5 mcg × 2 inhalations, total 320/9 mcg) or BUD pMDI (160 mcg × 2 inhalations, total 320 mcg) twice daily. Twelve-lead electrocardiograms were obtained before the morning dose of study medication in all patients at visits two through nine.

All patients were on a consistent daily medium to high dose of ICS either taken alone or as combination therapy with a LABA for 30 days or longer before screening.

Changes from baseline to treatment maximum for BUD/FM vs. BUD were similar for heart rate (9.87 vs. 9.04 beats/minute) and QT interval corrected for heart rate, with QTc 18.46 vs. 18.18 msec (Bazett’s correction) and QTc 13.47 vs. 14.73 msec (Fridericia’s correction), but lower for the uncorrected QT interval, 15.59 vs. 19.12 msec (unadjusted P = .002).

The proportion of patients with a heart rate greater than 100 beats/min or an increase of 20 or more beats per minute were 11.4% for BUD/FM and 8.5% for BUD, which is consistent with known effects of beta₂-adrenergic agonists, Dr. Lampl and her associates said.

Cardiac events were infrequent, and all were considered nonserious. Cardiac adverse events occurred in six patients (1.6%) in the BUD/FM pMDI group, including cardiac conduction disorders (one patient, 0.3%), ischemic coronary artery disorders (one patient, 0.3%), rate and rhythm disorders (two patients, 0.5%), supraventricular arrhythmias (two patients, 0.5%), and ventricular arrhythmias and cardiac arrest (one patient, 0.3%). Four patients (1.1%) in the BUD pMDI group experienced a cardiac adverse event, including cardiac conduction disorders (two patients, 0.5%), cardiac signs and symptoms (one patient, 0.3%), and noninfectious pericarditis (one patient, 0.3%).

"Overall, the results of this study further support the long-term tolerability of BUD/FM pMDI in African-American adolescents and adults with moderate to severe asthma not adequately controlled on an ICS alone," Dr. Lampl and her associates concluded.

Dr. Lampl is a paid employee of AstraZeneca, which funded the study.

ORLANDO – Budesonide/formoterol pressurized metered-dose inhaler demonstrated similar cardiovascular safety to that of budesonide treatment alone in a study of 742 black adolescents and adults with moderate to severe asthma.

There has been concern that regular long-acting beta₂-adrenergic agonist (LABA) therapy may increase the risk of mortality, including that from cardiac adverse events. An analysis of asthma trials suggested that formoterol does not increase cardiac-related serious adverse events or cardiac-related deaths (Eur. Respir. J. 2009;33:21-32).

And a recent study showed that budesonide/formoterol pressurized metered-dose inhaler (BUD/FM pMDI) was well tolerated and more effective for preventing exacerbations, compared with monotherapy BUD pMDI, in a black patient population (Am. J. Respir. Crit. Care Med. 2011;183:A1294).

However, data have been limited on the cardiovascular safety of combination inhaled corticosteroids (ICSs) and LABAs in specific racial/ethnic patient populations with asthma, Dr. Kathy L. Lampl of AstraZeneca and her associates reported in a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

In a randomized, double-blind, parallel-group, multicenter, 52-week study, 742 patients with moderate to severe persistent asthma who self-reported their race as black were randomized 1:1 to receive BUD/FM pMDI (160/4.5 mcg × 2 inhalations, total 320/9 mcg) or BUD pMDI (160 mcg × 2 inhalations, total 320 mcg) twice daily. Twelve-lead electrocardiograms were obtained before the morning dose of study medication in all patients at visits two through nine.

All patients were on a consistent daily medium to high dose of ICS either taken alone or as combination therapy with a LABA for 30 days or longer before screening.

Changes from baseline to treatment maximum for BUD/FM vs. BUD were similar for heart rate (9.87 vs. 9.04 beats/minute) and QT interval corrected for heart rate, with QTc 18.46 vs. 18.18 msec (Bazett’s correction) and QTc 13.47 vs. 14.73 msec (Fridericia’s correction), but lower for the uncorrected QT interval, 15.59 vs. 19.12 msec (unadjusted P = .002).

The proportion of patients with a heart rate greater than 100 beats/min or an increase of 20 or more beats per minute were 11.4% for BUD/FM and 8.5% for BUD, which is consistent with known effects of beta₂-adrenergic agonists, Dr. Lampl and her associates said.

Cardiac events were infrequent, and all were considered nonserious. Cardiac adverse events occurred in six patients (1.6%) in the BUD/FM pMDI group, including cardiac conduction disorders (one patient, 0.3%), ischemic coronary artery disorders (one patient, 0.3%), rate and rhythm disorders (two patients, 0.5%), supraventricular arrhythmias (two patients, 0.5%), and ventricular arrhythmias and cardiac arrest (one patient, 0.3%). Four patients (1.1%) in the BUD pMDI group experienced a cardiac adverse event, including cardiac conduction disorders (two patients, 0.5%), cardiac signs and symptoms (one patient, 0.3%), and noninfectious pericarditis (one patient, 0.3%).

"Overall, the results of this study further support the long-term tolerability of BUD/FM pMDI in African-American adolescents and adults with moderate to severe asthma not adequately controlled on an ICS alone," Dr. Lampl and her associates concluded.

Dr. Lampl is a paid employee of AstraZeneca, which funded the study.

ORLANDO – Children with severe asthma may have their already serious symptoms further worsened by sensitization to common household fungi in the genus Alternaria, suggested investigators at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Among 187 children with asthma enrolled in the National Heart, Lung and Blood Institutes’ Severe Asthma Research Program (SARP), 28% had a positive skin prick test reaction to Alternaria, reported Dr. Jennifer Shih, an allergy and immunology fellow in the department of pediatrics at Emory University in Atlanta.

Photo courtesy CDC/Dr. Lucille K. Georg

Sensitization to Alternaria was significantly more prevalent among children with severe vs. mild to moderate asthma (P less than .01), and children with severe presentation were significantly more likely to exhibit increased airway hyperresponsiveness (P less than .01) and to report a history of acute or chronic sinusitis requiring antibiotics (P less than .05).

"In the future, routine evaluation of Alternaria sensitization may be useful in the clinical management of children with severe asthma. Future studies are needed to evaluate the mechanistic underpinning of Alternaria sensitization in children with severe asthma," she said.

Sensitization to Alternaria has been associated in other studies with asthma persistence into early adulthood, Dr, Shih said. One study showed that Alternaria sensitization was associated with an odds ratio (OR) of 3.6 for chronic asthma at age 22 years (Lancet 2008;372:1058-64).

Increased airway hyperresponsiveness, a hallmark of severe asthma in children, was associated with Alternaria sensitization in the Childhood Asthma Management Research Program, she noted.

To see whether there were differences in Alternaria sensitization between school-age children with mild to moderate or severe asthma, and whether sensitization was associated with clinical features of asthma severity, Dr. Shih and her colleague Dr. Anne Fitzpatrick took a retrospective look at 187 children enrolled in SARP at their institution. The children ranged in age from 6 to 18 years, and all had skin prick test data available. In all, 90 had severe asthma, and 97 mild to moderate asthma.

Asthma severity was determined according to American Thoracic Society 2000 criteria, which require daily use of systemic or high-dose inhaled corticosteroids, plus at least two of the following: additional controller medication, beta-agonist use on at least 5 of 7 days, a baseline forced expiratory volume in 1 second (FEV₁)less than 80% of predicted, 1 or more emergency department visits within the past year, 3 or more oral steroid burst within the past year, prompt deterioration with steroid reduction, and/or a history of intubation(Am. J. Respir. Crit. Care Med. 2000;162:2341-51).

The investigators also reviewed asthma questionnaires, lung function–testing results, allergy evaluations, and biomarker evaluations.

In an analysis adjusted for race and socioeconomic status, they found that 37% of the children with severe asthma tested positive for Alternaria sensitization, compared with 21% of children with mild-to-moderate disease (adjusted OR 2.13, P = .015).

Among children with severe asthma, Alternaria sensitization was not significantly associated with differences in either blood eosinophil or total serum immunoglobulin E (IgE) levels, or in FEV₁, airflow limitation, air trapping, medication requirements, or health care use.

However, exhaled nitric oxide levels were significantly higher among those with severe asthma and sensitivity to Alternaria (P = .029), as was airway hyperresponsiveness to methacholine challenge (P = .012).

Additionally, in an analysis adjusted for socioeconomic status, children with severe asthma and a positive skin prick test to Alternaria had an adjusted OR for sinusitis of 2.43 (P = .046).

"These findings support previous observations from the Childhood Asthma Management Research Program," Dr. Shih said.

In the question and answer portion of her presentation, several clinicians commented that Alternaria might be a general marker for atopy rather than for airway hyperresponsiveness and sinusitis as seen in her study, and that other allergens such as cockroach and mites might account for exacerbations of severe asthma. Dr. Shih agreed that further studies would help to resolve this question.

The study was supported by the NHLBI and Emory University. Dr. Shih reported that she had no relevant disclosures.

ORLANDO – Children with severe asthma may have their already serious symptoms further worsened by sensitization to common household fungi in the genus Alternaria, suggested investigators at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Among 187 children with asthma enrolled in the National Heart, Lung and Blood Institutes’ Severe Asthma Research Program (SARP), 28% had a positive skin prick test reaction to Alternaria, reported Dr. Jennifer Shih, an allergy and immunology fellow in the department of pediatrics at Emory University in Atlanta.

Photo courtesy CDC/Dr. Lucille K. Georg

Sensitization to Alternaria was significantly more prevalent among children with severe vs. mild to moderate asthma (P less than .01), and children with severe presentation were significantly more likely to exhibit increased airway hyperresponsiveness (P less than .01) and to report a history of acute or chronic sinusitis requiring antibiotics (P less than .05).

"In the future, routine evaluation of Alternaria sensitization may be useful in the clinical management of children with severe asthma. Future studies are needed to evaluate the mechanistic underpinning of Alternaria sensitization in children with severe asthma," she said.

Sensitization to Alternaria has been associated in other studies with asthma persistence into early adulthood, Dr, Shih said. One study showed that Alternaria sensitization was associated with an odds ratio (OR) of 3.6 for chronic asthma at age 22 years (Lancet 2008;372:1058-64).

Increased airway hyperresponsiveness, a hallmark of severe asthma in children, was associated with Alternaria sensitization in the Childhood Asthma Management Research Program, she noted.

To see whether there were differences in Alternaria sensitization between school-age children with mild to moderate or severe asthma, and whether sensitization was associated with clinical features of asthma severity, Dr. Shih and her colleague Dr. Anne Fitzpatrick took a retrospective look at 187 children enrolled in SARP at their institution. The children ranged in age from 6 to 18 years, and all had skin prick test data available. In all, 90 had severe asthma, and 97 mild to moderate asthma.

Asthma severity was determined according to American Thoracic Society 2000 criteria, which require daily use of systemic or high-dose inhaled corticosteroids, plus at least two of the following: additional controller medication, beta-agonist use on at least 5 of 7 days, a baseline forced expiratory volume in 1 second (FEV₁)less than 80% of predicted, 1 or more emergency department visits within the past year, 3 or more oral steroid burst within the past year, prompt deterioration with steroid reduction, and/or a history of intubation(Am. J. Respir. Crit. Care Med. 2000;162:2341-51).

The investigators also reviewed asthma questionnaires, lung function–testing results, allergy evaluations, and biomarker evaluations.

In an analysis adjusted for race and socioeconomic status, they found that 37% of the children with severe asthma tested positive for Alternaria sensitization, compared with 21% of children with mild-to-moderate disease (adjusted OR 2.13, P = .015).

Among children with severe asthma, Alternaria sensitization was not significantly associated with differences in either blood eosinophil or total serum immunoglobulin E (IgE) levels, or in FEV₁, airflow limitation, air trapping, medication requirements, or health care use.

However, exhaled nitric oxide levels were significantly higher among those with severe asthma and sensitivity to Alternaria (P = .029), as was airway hyperresponsiveness to methacholine challenge (P = .012).

Additionally, in an analysis adjusted for socioeconomic status, children with severe asthma and a positive skin prick test to Alternaria had an adjusted OR for sinusitis of 2.43 (P = .046).

"These findings support previous observations from the Childhood Asthma Management Research Program," Dr. Shih said.

In the question and answer portion of her presentation, several clinicians commented that Alternaria might be a general marker for atopy rather than for airway hyperresponsiveness and sinusitis as seen in her study, and that other allergens such as cockroach and mites might account for exacerbations of severe asthma. Dr. Shih agreed that further studies would help to resolve this question.

The study was supported by the NHLBI and Emory University. Dr. Shih reported that she had no relevant disclosures.

ORLANDO – Children with severe asthma may have their already serious symptoms further worsened by sensitization to common household fungi in the genus Alternaria, suggested investigators at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Among 187 children with asthma enrolled in the National Heart, Lung and Blood Institutes’ Severe Asthma Research Program (SARP), 28% had a positive skin prick test reaction to Alternaria, reported Dr. Jennifer Shih, an allergy and immunology fellow in the department of pediatrics at Emory University in Atlanta.

Photo courtesy CDC/Dr. Lucille K. Georg

Sensitization to Alternaria was significantly more prevalent among children with severe vs. mild to moderate asthma (P less than .01), and children with severe presentation were significantly more likely to exhibit increased airway hyperresponsiveness (P less than .01) and to report a history of acute or chronic sinusitis requiring antibiotics (P less than .05).

"In the future, routine evaluation of Alternaria sensitization may be useful in the clinical management of children with severe asthma. Future studies are needed to evaluate the mechanistic underpinning of Alternaria sensitization in children with severe asthma," she said.

Sensitization to Alternaria has been associated in other studies with asthma persistence into early adulthood, Dr, Shih said. One study showed that Alternaria sensitization was associated with an odds ratio (OR) of 3.6 for chronic asthma at age 22 years (Lancet 2008;372:1058-64).

Increased airway hyperresponsiveness, a hallmark of severe asthma in children, was associated with Alternaria sensitization in the Childhood Asthma Management Research Program, she noted.

To see whether there were differences in Alternaria sensitization between school-age children with mild to moderate or severe asthma, and whether sensitization was associated with clinical features of asthma severity, Dr. Shih and her colleague Dr. Anne Fitzpatrick took a retrospective look at 187 children enrolled in SARP at their institution. The children ranged in age from 6 to 18 years, and all had skin prick test data available. In all, 90 had severe asthma, and 97 mild to moderate asthma.

Asthma severity was determined according to American Thoracic Society 2000 criteria, which require daily use of systemic or high-dose inhaled corticosteroids, plus at least two of the following: additional controller medication, beta-agonist use on at least 5 of 7 days, a baseline forced expiratory volume in 1 second (FEV₁)less than 80% of predicted, 1 or more emergency department visits within the past year, 3 or more oral steroid burst within the past year, prompt deterioration with steroid reduction, and/or a history of intubation(Am. J. Respir. Crit. Care Med. 2000;162:2341-51).

The investigators also reviewed asthma questionnaires, lung function–testing results, allergy evaluations, and biomarker evaluations.

In an analysis adjusted for race and socioeconomic status, they found that 37% of the children with severe asthma tested positive for Alternaria sensitization, compared with 21% of children with mild-to-moderate disease (adjusted OR 2.13, P = .015).

Among children with severe asthma, Alternaria sensitization was not significantly associated with differences in either blood eosinophil or total serum immunoglobulin E (IgE) levels, or in FEV₁, airflow limitation, air trapping, medication requirements, or health care use.

However, exhaled nitric oxide levels were significantly higher among those with severe asthma and sensitivity to Alternaria (P = .029), as was airway hyperresponsiveness to methacholine challenge (P = .012).

Additionally, in an analysis adjusted for socioeconomic status, children with severe asthma and a positive skin prick test to Alternaria had an adjusted OR for sinusitis of 2.43 (P = .046).

"These findings support previous observations from the Childhood Asthma Management Research Program," Dr. Shih said.

In the question and answer portion of her presentation, several clinicians commented that Alternaria might be a general marker for atopy rather than for airway hyperresponsiveness and sinusitis as seen in her study, and that other allergens such as cockroach and mites might account for exacerbations of severe asthma. Dr. Shih agreed that further studies would help to resolve this question.

The study was supported by the NHLBI and Emory University. Dr. Shih reported that she had no relevant disclosures.

ORLANDO – Reports of U.S. children with a food allergy jumped by a third between 2003-2004 and 2007-2008.

The finding is based on survey responses collected by the Centers for Disease Control and Prevention from more than 90,000 patients during each of the two time periods. An analysis of other data collected by the surveys implicated younger age, lack of health insurance, and eczema as three factors associated with the increased prevalence of food allergies in children, Dr. Karen A. DeMuth said during a poster presentation at the meeting (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.147]).

Other possible factors not accounted for in the survey results might also have played a role in the sharp rise, such as an increased level of awareness about food allergies among parents, and an increased rate of testing children for food allergies, she acknowledged in an interview. The telephone surveys conducted by the CDC relied exclusively on parents’ reports of allergies in their children, and so the rates do not reflect allergy rates documented by physician examinations or food-challenge tests. But the fact that these limitations applied in both survey periods – 2003-2004 and 2007-2008 – makes it less likely that they played a major role in explaining the increased food allergy prevalence.

"These data show us how many parents think their kids have a food allergy," Dr. DeMuth said.

She and her associate used data collected in the first two National Surveys of Children’s Health. During 2003-2004, the CDC completed telephone surveys with 102,353 U.S. households, and during 2007-2008, the agency obtained responses from 91,642 families. During each survey, the CDC collected data for a single child aged 0-17 years from each responding family.

During the first survey, parents reported a food allergy in their child at a rate of 3,566 cases/100,000 children, a prevalence rate of 3.6%. By the second survey, the prevalence rose to 4,848 cases/100,000 children, a rate of 4.8%, a 33% relative increase that was statistically significant, reported Dr. DeMuth, an allergist and immunologist at Emory University in Atlanta.

The prevalence rates increased by an absolute rate of more than 2% in eight states: Arkansas, Delaware, Georgia, Hawaii, Maryland, Ohio, Oklahoma, and New Hampshire. The greatest absolute rise in percent terms was in Oklahoma, where the prevalence rate jumped by 3.2 percentage points. During 2007-2008, the highest overall reported prevalence rate for pediatric food allergies was in New Hampshire, where 6.7% of families reported having a child with a food allergy. The lowest prevalence rate during 2007-2008 was in Wisconsin, with a 3.3% rate. Between 2003-2004 and 2007-2008, a statistically significant increase in the prevalence of pediatric food allergies occurred in 17 states.

Three factors were linked on a statistically significant level with the increased rate of food allergies: Age of 0-5 years boosted the food allergies rate by 33%, compared with older children; having no health insurance was linked with a 48% higher rate of food allergy increase; and having eczema or atopic dermatitis was linked with a 4.7-fold higher rate of food-allergy increase, compared with children without skin atopy.

Results from two other studies reported in posters at the meeting further documented recent prevalence rates of pediatric food allergies in U.S. populations.

A survey of randomly-selected U.S. families was conducted during June 2009-February 2010 and collected information on 38,480 children aged 0-17. The results found that 3,218 parents (8%) said they had a child with a food allergy, reported Dr. Ruchi S. Gupta and her associates from Northwestern University in Chicago (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.145]).

The parents said that 70% of these children had been identified as having a food allergy by a physician, and that 20% of the children had their food allergy documented by an oral food-challenge test. The allergens that the responding parents reported were peanut, milk, tree nut, shellfish, egg, fin fish, wheat, soy, and sesame. The most common presenting symptom was urticaria, reported for roughly half of the children with a food allergy.

The second report included data from a retrospective chart review done at a single, hospital-based Medicaid clinic in the East Harlem section of New York City. During July 1, 2008-July 1, 2010, the clinic saw 9,314 children, of whom 331 (3.6%) had a physician-diagnosed food allergy, reported Dr. Sarah A. Taylor-Black and her associate from Mount Sinai Medical Center in New York (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.148]). The patients’ average age at diagnosis was 1.7 years, with a range of 4 months to 10 years old. The most common allergy was to peanut, followed by shellfish, egg, tree nut, milk, fruit, fish, soy, vegetable, seed, and wheat. Allergy prevalence was 5.6% among black children, compared with 3.0% among Hispanic children, a statistically significant difference. Skin symptoms were the most common presentation in children with allergies to peanut, shellfish, egg, milk, and fish.

Dr. DeMuth, Dr. Gupta, and Dr. Taylor-Black all said that they had no disclosures.

Mitchel L. Zoler/IMNG Medical Media

ORLANDO – Reports of U.S. children with a food allergy jumped by a third between 2003-2004 and 2007-2008.

The finding is based on survey responses collected by the Centers for Disease Control and Prevention from more than 90,000 patients during each of the two time periods. An analysis of other data collected by the surveys implicated younger age, lack of health insurance, and eczema as three factors associated with the increased prevalence of food allergies in children, Dr. Karen A. DeMuth said during a poster presentation at the meeting (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.147]).

Other possible factors not accounted for in the survey results might also have played a role in the sharp rise, such as an increased level of awareness about food allergies among parents, and an increased rate of testing children for food allergies, she acknowledged in an interview. The telephone surveys conducted by the CDC relied exclusively on parents’ reports of allergies in their children, and so the rates do not reflect allergy rates documented by physician examinations or food-challenge tests. But the fact that these limitations applied in both survey periods – 2003-2004 and 2007-2008 – makes it less likely that they played a major role in explaining the increased food allergy prevalence.

"These data show us how many parents think their kids have a food allergy," Dr. DeMuth said.

She and her associate used data collected in the first two National Surveys of Children’s Health. During 2003-2004, the CDC completed telephone surveys with 102,353 U.S. households, and during 2007-2008, the agency obtained responses from 91,642 families. During each survey, the CDC collected data for a single child aged 0-17 years from each responding family.

During the first survey, parents reported a food allergy in their child at a rate of 3,566 cases/100,000 children, a prevalence rate of 3.6%. By the second survey, the prevalence rose to 4,848 cases/100,000 children, a rate of 4.8%, a 33% relative increase that was statistically significant, reported Dr. DeMuth, an allergist and immunologist at Emory University in Atlanta.

The prevalence rates increased by an absolute rate of more than 2% in eight states: Arkansas, Delaware, Georgia, Hawaii, Maryland, Ohio, Oklahoma, and New Hampshire. The greatest absolute rise in percent terms was in Oklahoma, where the prevalence rate jumped by 3.2 percentage points. During 2007-2008, the highest overall reported prevalence rate for pediatric food allergies was in New Hampshire, where 6.7% of families reported having a child with a food allergy. The lowest prevalence rate during 2007-2008 was in Wisconsin, with a 3.3% rate. Between 2003-2004 and 2007-2008, a statistically significant increase in the prevalence of pediatric food allergies occurred in 17 states.

Three factors were linked on a statistically significant level with the increased rate of food allergies: Age of 0-5 years boosted the food allergies rate by 33%, compared with older children; having no health insurance was linked with a 48% higher rate of food allergy increase; and having eczema or atopic dermatitis was linked with a 4.7-fold higher rate of food-allergy increase, compared with children without skin atopy.

Results from two other studies reported in posters at the meeting further documented recent prevalence rates of pediatric food allergies in U.S. populations.

A survey of randomly-selected U.S. families was conducted during June 2009-February 2010 and collected information on 38,480 children aged 0-17. The results found that 3,218 parents (8%) said they had a child with a food allergy, reported Dr. Ruchi S. Gupta and her associates from Northwestern University in Chicago (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.145]).

The parents said that 70% of these children had been identified as having a food allergy by a physician, and that 20% of the children had their food allergy documented by an oral food-challenge test. The allergens that the responding parents reported were peanut, milk, tree nut, shellfish, egg, fin fish, wheat, soy, and sesame. The most common presenting symptom was urticaria, reported for roughly half of the children with a food allergy.

The second report included data from a retrospective chart review done at a single, hospital-based Medicaid clinic in the East Harlem section of New York City. During July 1, 2008-July 1, 2010, the clinic saw 9,314 children, of whom 331 (3.6%) had a physician-diagnosed food allergy, reported Dr. Sarah A. Taylor-Black and her associate from Mount Sinai Medical Center in New York (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.148]). The patients’ average age at diagnosis was 1.7 years, with a range of 4 months to 10 years old. The most common allergy was to peanut, followed by shellfish, egg, tree nut, milk, fruit, fish, soy, vegetable, seed, and wheat. Allergy prevalence was 5.6% among black children, compared with 3.0% among Hispanic children, a statistically significant difference. Skin symptoms were the most common presentation in children with allergies to peanut, shellfish, egg, milk, and fish.

Dr. DeMuth, Dr. Gupta, and Dr. Taylor-Black all said that they had no disclosures.

Mitchel L. Zoler/IMNG Medical Media

ORLANDO – Reports of U.S. children with a food allergy jumped by a third between 2003-2004 and 2007-2008.

The finding is based on survey responses collected by the Centers for Disease Control and Prevention from more than 90,000 patients during each of the two time periods. An analysis of other data collected by the surveys implicated younger age, lack of health insurance, and eczema as three factors associated with the increased prevalence of food allergies in children, Dr. Karen A. DeMuth said during a poster presentation at the meeting (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.147]).

Other possible factors not accounted for in the survey results might also have played a role in the sharp rise, such as an increased level of awareness about food allergies among parents, and an increased rate of testing children for food allergies, she acknowledged in an interview. The telephone surveys conducted by the CDC relied exclusively on parents’ reports of allergies in their children, and so the rates do not reflect allergy rates documented by physician examinations or food-challenge tests. But the fact that these limitations applied in both survey periods – 2003-2004 and 2007-2008 – makes it less likely that they played a major role in explaining the increased food allergy prevalence.

"These data show us how many parents think their kids have a food allergy," Dr. DeMuth said.

She and her associate used data collected in the first two National Surveys of Children’s Health. During 2003-2004, the CDC completed telephone surveys with 102,353 U.S. households, and during 2007-2008, the agency obtained responses from 91,642 families. During each survey, the CDC collected data for a single child aged 0-17 years from each responding family.

During the first survey, parents reported a food allergy in their child at a rate of 3,566 cases/100,000 children, a prevalence rate of 3.6%. By the second survey, the prevalence rose to 4,848 cases/100,000 children, a rate of 4.8%, a 33% relative increase that was statistically significant, reported Dr. DeMuth, an allergist and immunologist at Emory University in Atlanta.

The prevalence rates increased by an absolute rate of more than 2% in eight states: Arkansas, Delaware, Georgia, Hawaii, Maryland, Ohio, Oklahoma, and New Hampshire. The greatest absolute rise in percent terms was in Oklahoma, where the prevalence rate jumped by 3.2 percentage points. During 2007-2008, the highest overall reported prevalence rate for pediatric food allergies was in New Hampshire, where 6.7% of families reported having a child with a food allergy. The lowest prevalence rate during 2007-2008 was in Wisconsin, with a 3.3% rate. Between 2003-2004 and 2007-2008, a statistically significant increase in the prevalence of pediatric food allergies occurred in 17 states.

Three factors were linked on a statistically significant level with the increased rate of food allergies: Age of 0-5 years boosted the food allergies rate by 33%, compared with older children; having no health insurance was linked with a 48% higher rate of food allergy increase; and having eczema or atopic dermatitis was linked with a 4.7-fold higher rate of food-allergy increase, compared with children without skin atopy.

Results from two other studies reported in posters at the meeting further documented recent prevalence rates of pediatric food allergies in U.S. populations.

A survey of randomly-selected U.S. families was conducted during June 2009-February 2010 and collected information on 38,480 children aged 0-17. The results found that 3,218 parents (8%) said they had a child with a food allergy, reported Dr. Ruchi S. Gupta and her associates from Northwestern University in Chicago (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.145]).

The parents said that 70% of these children had been identified as having a food allergy by a physician, and that 20% of the children had their food allergy documented by an oral food-challenge test. The allergens that the responding parents reported were peanut, milk, tree nut, shellfish, egg, fin fish, wheat, soy, and sesame. The most common presenting symptom was urticaria, reported for roughly half of the children with a food allergy.

The second report included data from a retrospective chart review done at a single, hospital-based Medicaid clinic in the East Harlem section of New York City. During July 1, 2008-July 1, 2010, the clinic saw 9,314 children, of whom 331 (3.6%) had a physician-diagnosed food allergy, reported Dr. Sarah A. Taylor-Black and her associate from Mount Sinai Medical Center in New York (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.148]). The patients’ average age at diagnosis was 1.7 years, with a range of 4 months to 10 years old. The most common allergy was to peanut, followed by shellfish, egg, tree nut, milk, fruit, fish, soy, vegetable, seed, and wheat. Allergy prevalence was 5.6% among black children, compared with 3.0% among Hispanic children, a statistically significant difference. Skin symptoms were the most common presentation in children with allergies to peanut, shellfish, egg, milk, and fish.

Dr. DeMuth, Dr. Gupta, and Dr. Taylor-Black all said that they had no disclosures.

Mitchel L. Zoler/IMNG Medical Media

ORLANDO – The rate of U.S. hospitalizations for angioedema doubled among African Americans during 2000-2009 based on a national sampling of inpatients, and the rise appears largely driven by adverse drug reactions to angiotensin-converting enzyme inhibitors.

"The rate of angioedema due to an adverse drug reaction rose from about 40% in 2000 to about 60% in 2009," said Dr. Robert Y. Lin while presenting a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. Adverse drug reactions "are not the only reason [that angioedema occurs], but I think it’s driving the increase."

Angiotensin-converting enzyme (ACE) inhibitors are the drugs most responsible for causing angioedema, and it seems this drug class is especially responsible for the rapid increase in the number of angioedema cases among African Americans, he said.

Among African Americans, hospitalizations for angioedema jumped from 9 cases per 100,000 in 2000 to 18 cases per 100,000 in 2009. In contrast, among non–African American residents of the United States, hospitalizations for angioedema rose from 2.7 cases per 100,000 in 2000 to 3.6 cases per 100,000 in 2009(see table).

African Americans seem particularly susceptible to developing angioedema triggered by ACE inhibitors, noted Dr. Lin. In addition, diseases that often lead to treatment with an ACE inhibitor, such as hypertension, chronic kidney disease, and heart failure, are especially prevalent among African Americans.

Angiotensin-receptor blockers, which are not linked to causing angioedema, might be a better alternative for African American patients, said Dr. Lin, a professor of medicine at New York Medical College and chief of the division of allergy and immunology at New York Downtown Hospital.

The angioedema danger from ACE inhibitors is especially insidious because it appears to be a class effect that is not dose or duration related. The side effect can occur suddenly at any time during the course of treatment. "The lag period between when you start treatment and when you see a reaction can be so variable. It can be 2 weeks, or it can be 2 years. A patient can be fine on an ACE inhibitor for months or years and then suddenly have an angioedema reaction. We don’t know why," he said in an interview.

Although angioedema is rarely fatal—the mortality rate was 0.4% in the more than 128,000 hospitalized cases that Dr. Lin tallied in his analysis—it led to an intubation rate of 8% and average hospitalization charges of about $10,000 per case. With nearly 13,000 Americans hospitalized for angioedema annually during 2000-2009, that means the annual cost was roughly $130 million.

Dr. Lin identified angioedema cases in U.S. hospitalization records collected by the Nationwide Inpatient Sample, a database maintained by the U.S. Agency for Healthcare Research and Quality. He identified angioedema cases by their ICD code. During the study period, patients hospitalized with angioedema averaged 61 years old, 61% were women, and 37% were African American. The percent of all patients with angioedema who were African American rose from 32% of cases in 2000 to 41% in 2009.

Throughout the decade studied, 56% of the angioedema cases appeared secondary to an adverse drug reaction; 61% of the angioedema patients had hypertension. Adverse drug reactions linked to hypertension or cardiovascular disease occurred in 29% of the angioedema patients overall throughout the decade studied, rising from 22% of cases in 2000 to 36% of cases in 2009. Adverse drug reactions linked to drugs used to treat hypertension or cardiovascular disease occurred overall in 38% of African American patients hospitalized for angioedema, and hit a high of 44% of African Americans hospitalized for angioedema in 2009.

Dr. Lin said that he had no disclosures.

ORLANDO – The rate of U.S. hospitalizations for angioedema doubled among African Americans during 2000-2009 based on a national sampling of inpatients, and the rise appears largely driven by adverse drug reactions to angiotensin-converting enzyme inhibitors.

"The rate of angioedema due to an adverse drug reaction rose from about 40% in 2000 to about 60% in 2009," said Dr. Robert Y. Lin while presenting a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. Adverse drug reactions "are not the only reason [that angioedema occurs], but I think it’s driving the increase."

Angiotensin-converting enzyme (ACE) inhibitors are the drugs most responsible for causing angioedema, and it seems this drug class is especially responsible for the rapid increase in the number of angioedema cases among African Americans, he said.

Among African Americans, hospitalizations for angioedema jumped from 9 cases per 100,000 in 2000 to 18 cases per 100,000 in 2009. In contrast, among non–African American residents of the United States, hospitalizations for angioedema rose from 2.7 cases per 100,000 in 2000 to 3.6 cases per 100,000 in 2009(see table).

African Americans seem particularly susceptible to developing angioedema triggered by ACE inhibitors, noted Dr. Lin. In addition, diseases that often lead to treatment with an ACE inhibitor, such as hypertension, chronic kidney disease, and heart failure, are especially prevalent among African Americans.

Angiotensin-receptor blockers, which are not linked to causing angioedema, might be a better alternative for African American patients, said Dr. Lin, a professor of medicine at New York Medical College and chief of the division of allergy and immunology at New York Downtown Hospital.

The angioedema danger from ACE inhibitors is especially insidious because it appears to be a class effect that is not dose or duration related. The side effect can occur suddenly at any time during the course of treatment. "The lag period between when you start treatment and when you see a reaction can be so variable. It can be 2 weeks, or it can be 2 years. A patient can be fine on an ACE inhibitor for months or years and then suddenly have an angioedema reaction. We don’t know why," he said in an interview.

Although angioedema is rarely fatal—the mortality rate was 0.4% in the more than 128,000 hospitalized cases that Dr. Lin tallied in his analysis—it led to an intubation rate of 8% and average hospitalization charges of about $10,000 per case. With nearly 13,000 Americans hospitalized for angioedema annually during 2000-2009, that means the annual cost was roughly $130 million.

Dr. Lin identified angioedema cases in U.S. hospitalization records collected by the Nationwide Inpatient Sample, a database maintained by the U.S. Agency for Healthcare Research and Quality. He identified angioedema cases by their ICD code. During the study period, patients hospitalized with angioedema averaged 61 years old, 61% were women, and 37% were African American. The percent of all patients with angioedema who were African American rose from 32% of cases in 2000 to 41% in 2009.

Throughout the decade studied, 56% of the angioedema cases appeared secondary to an adverse drug reaction; 61% of the angioedema patients had hypertension. Adverse drug reactions linked to hypertension or cardiovascular disease occurred in 29% of the angioedema patients overall throughout the decade studied, rising from 22% of cases in 2000 to 36% of cases in 2009. Adverse drug reactions linked to drugs used to treat hypertension or cardiovascular disease occurred overall in 38% of African American patients hospitalized for angioedema, and hit a high of 44% of African Americans hospitalized for angioedema in 2009.

Dr. Lin said that he had no disclosures.

ORLANDO – The rate of U.S. hospitalizations for angioedema doubled among African Americans during 2000-2009 based on a national sampling of inpatients, and the rise appears largely driven by adverse drug reactions to angiotensin-converting enzyme inhibitors.

"The rate of angioedema due to an adverse drug reaction rose from about 40% in 2000 to about 60% in 2009," said Dr. Robert Y. Lin while presenting a poster at the annual meeting of the American Academy of Allergy, Asthma, and Immunology. Adverse drug reactions "are not the only reason [that angioedema occurs], but I think it’s driving the increase."

Angiotensin-converting enzyme (ACE) inhibitors are the drugs most responsible for causing angioedema, and it seems this drug class is especially responsible for the rapid increase in the number of angioedema cases among African Americans, he said.

Among African Americans, hospitalizations for angioedema jumped from 9 cases per 100,000 in 2000 to 18 cases per 100,000 in 2009. In contrast, among non–African American residents of the United States, hospitalizations for angioedema rose from 2.7 cases per 100,000 in 2000 to 3.6 cases per 100,000 in 2009(see table).

African Americans seem particularly susceptible to developing angioedema triggered by ACE inhibitors, noted Dr. Lin. In addition, diseases that often lead to treatment with an ACE inhibitor, such as hypertension, chronic kidney disease, and heart failure, are especially prevalent among African Americans.

Angiotensin-receptor blockers, which are not linked to causing angioedema, might be a better alternative for African American patients, said Dr. Lin, a professor of medicine at New York Medical College and chief of the division of allergy and immunology at New York Downtown Hospital.

The angioedema danger from ACE inhibitors is especially insidious because it appears to be a class effect that is not dose or duration related. The side effect can occur suddenly at any time during the course of treatment. "The lag period between when you start treatment and when you see a reaction can be so variable. It can be 2 weeks, or it can be 2 years. A patient can be fine on an ACE inhibitor for months or years and then suddenly have an angioedema reaction. We don’t know why," he said in an interview.

Although angioedema is rarely fatal—the mortality rate was 0.4% in the more than 128,000 hospitalized cases that Dr. Lin tallied in his analysis—it led to an intubation rate of 8% and average hospitalization charges of about $10,000 per case. With nearly 13,000 Americans hospitalized for angioedema annually during 2000-2009, that means the annual cost was roughly $130 million.

Dr. Lin identified angioedema cases in U.S. hospitalization records collected by the Nationwide Inpatient Sample, a database maintained by the U.S. Agency for Healthcare Research and Quality. He identified angioedema cases by their ICD code. During the study period, patients hospitalized with angioedema averaged 61 years old, 61% were women, and 37% were African American. The percent of all patients with angioedema who were African American rose from 32% of cases in 2000 to 41% in 2009.

Throughout the decade studied, 56% of the angioedema cases appeared secondary to an adverse drug reaction; 61% of the angioedema patients had hypertension. Adverse drug reactions linked to hypertension or cardiovascular disease occurred in 29% of the angioedema patients overall throughout the decade studied, rising from 22% of cases in 2000 to 36% of cases in 2009. Adverse drug reactions linked to drugs used to treat hypertension or cardiovascular disease occurred overall in 38% of African American patients hospitalized for angioedema, and hit a high of 44% of African Americans hospitalized for angioedema in 2009.

Dr. Lin said that he had no disclosures.

ORLANDO – Immunotherapy with a pill formulated from ragweed pollen safely and effectively reduced symptoms and the need for therapy to manage symptoms in patients with ragweed allergy.

The findings were noted in two pivotal, placebo-controlled trials that together enrolled 1,349 patients in North America and Europe. The company that is developing the oral formulation, Merck, plans to use the results as the basis for a licensing application to the Food and Drug Administration next year, Dr. Hendrick Nolte, the company’s senior director for research in Kenilworth, N.J., said at the meeting.

Mitchel L. Zoler/IMNG Medical Media

But the studies only assessed the pill’s efficacy for ragweed desensitization while patients were on treatment, and only during the first year of treatment. Thus, both studies failed to address the ability of the new formulation to modify disease, a hallmark effect of standard pollen desensitization by serial injections.

"Immunotherapy based on injections is disease modifying when used for 3-5 years. You can stop [the injections] and see continued benefit," said Dr. Peter S. Creticos, lead investigator for one of the two Merck studies (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.481]). Both ragweed pollen trials "were only single-season studies, so they can’t answer" whether disease was modified, he said in an interview during a poster presentation at the meeting.

However, a European study that used the same formulation examined the impact of 3 consecutive years of oral desensitization to ragweed followed by 2 years when patients received no immunotherapy. The results showed long-lasting tolerance that persisted during both follow-up years, said Dr. Creticos, an allergy and immunology physician at Johns Hopkins Hospital in Baltimore.

Reductions in symptoms and the need for symptom-controlling medications during ragweed-pollen season ranged from 21%-27%, compared with placebo, depending on the dosage. These differences were "clinically meaningful" and similar in efficacy to conventional, injection-based desensitization against ragweed, added Dr. Creticos. Unlike injections, the oral formulation did not cause any systemic reactions.

If the oral ragweed pill eventually receives U.S. marketing approval, it is likely to appeal to some patients, but may also have some downsides.

"A small percentage of patients won’t get injections because they are afraid of injections, they are afraid of systemic reactions, or they don’t want to have to regularly go to a doctor’s office," he said. "A daily pill is more convenient and easier, and it may be safer and just as effective." The main drawback is less reliable compliance. "A patient must be willing to take the pill daily, starting 16 weeks before the (allergy) season starts."

The study he presented randomized 565 North American adults with allergic rhinoconjunctivitis to ragweed to treatment with a pill containing 6 Amb a 1-U ragweed pollen, 12 Amb a 1-U, or placebo. Treatment began approximately 16 weeks before the start of each patient’s local ragweed pollen season, and continued for 52 weeks. Patients in all three arms could freely use symptom-controlling medications as needed: an oral antihistamine, antihistamine eyedrops, a nasal steroid, and an oral steroid.

The study’s primary efficacy end point was the patient’s total combined score – their rhinoconjunctivitis daily symptom score and daily medication-use score – during the peak of the ragweed season. For this measure, patients receiving the higher-dose ragweed pill had an average 27% reduction in their combined score, compared with the average among the placebo patients, and patients who received the lower-dose pill had an average 21% reduction, compared with placebo, both statistically significant differences. Both treatment groups showed similar improvements, compared with placebo, for secondary end points of total score throughout the entire ragweed season, symptom score during both the season’s peak and the entire season, and medication-use score during the season’s peak and the entire season.

The daily, oral pill was well tolerated at both dosages, with no deaths, systemic allergic reactions, or life-threatening events. The most common, treatment-related adverse events occurred early, and were transient and self-limited. Throat irritation occurred in 26%-29% of the active pill recipients, depending on the dosage. Other side effects included oral pruritus, in 19%; a swollen tongue, in 12%-19%; ear pruritus; tongue pruritus; oral paresthesia; and several other effects that occurred in less than 10% of treated patients. The majority of the adverse effects were mild or moderate, and none were serious. Two patients received epinephrine during the study. One patient had to a concomitant food-allergy reaction and the second was treated for local swelling and nervousness, so epinephrine treatment was not really needed.

"In routine practice, desensitization injections produce systemic reactions in 2%-6% of patients. I think we didn’t see that with the pill because the uptake is slower," Dr. Creticos said.

Results from the second trial, reported in a poster by Dr. Nolte, came from a study with a similar design that randomized 784 patients at sites in both North America and Europe (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.482]). This 52-week treatment study added a third active-treatment arm in which patients receive a daily pill containing 1.5 Amb a 1-U ragweed pollen. This low-dose pill did not produce a statistically-significant improvement in efficacy, compared with placebo. The 6 Amb a 1-U and 12 Amb a 1-U dosages resulted in a 19% and 24% average reduction in the total combined score during the peak ragweed season, statistically significant benefits for the study’s primary end point. The safety profile of the two highest doses also mimicked the first study, with no serious adverse effects and no systemic allergic reactions, anaphylaxis, or life-threatening effects. The type and severity of the treatment-related adverse effects were very similar to the first study. One patient in the second study received epinephrine, for a concomitant food-allergy reaction.

Both trials were sponsored by Merck, which is developing the oral ragweed-pollen desensitization pill. Dr. Creticos said that he has received research support from and has been a consultant to Merck as well as to several other drug companies. Dr. Nolte is an employee of Merck.

ORLANDO – Immunotherapy with a pill formulated from ragweed pollen safely and effectively reduced symptoms and the need for therapy to manage symptoms in patients with ragweed allergy.

The findings were noted in two pivotal, placebo-controlled trials that together enrolled 1,349 patients in North America and Europe. The company that is developing the oral formulation, Merck, plans to use the results as the basis for a licensing application to the Food and Drug Administration next year, Dr. Hendrick Nolte, the company’s senior director for research in Kenilworth, N.J., said at the meeting.

Mitchel L. Zoler/IMNG Medical Media

But the studies only assessed the pill’s efficacy for ragweed desensitization while patients were on treatment, and only during the first year of treatment. Thus, both studies failed to address the ability of the new formulation to modify disease, a hallmark effect of standard pollen desensitization by serial injections.

"Immunotherapy based on injections is disease modifying when used for 3-5 years. You can stop [the injections] and see continued benefit," said Dr. Peter S. Creticos, lead investigator for one of the two Merck studies (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.481]). Both ragweed pollen trials "were only single-season studies, so they can’t answer" whether disease was modified, he said in an interview during a poster presentation at the meeting.

However, a European study that used the same formulation examined the impact of 3 consecutive years of oral desensitization to ragweed followed by 2 years when patients received no immunotherapy. The results showed long-lasting tolerance that persisted during both follow-up years, said Dr. Creticos, an allergy and immunology physician at Johns Hopkins Hospital in Baltimore.

Reductions in symptoms and the need for symptom-controlling medications during ragweed-pollen season ranged from 21%-27%, compared with placebo, depending on the dosage. These differences were "clinically meaningful" and similar in efficacy to conventional, injection-based desensitization against ragweed, added Dr. Creticos. Unlike injections, the oral formulation did not cause any systemic reactions.

If the oral ragweed pill eventually receives U.S. marketing approval, it is likely to appeal to some patients, but may also have some downsides.

"A small percentage of patients won’t get injections because they are afraid of injections, they are afraid of systemic reactions, or they don’t want to have to regularly go to a doctor’s office," he said. "A daily pill is more convenient and easier, and it may be safer and just as effective." The main drawback is less reliable compliance. "A patient must be willing to take the pill daily, starting 16 weeks before the (allergy) season starts."

The study he presented randomized 565 North American adults with allergic rhinoconjunctivitis to ragweed to treatment with a pill containing 6 Amb a 1-U ragweed pollen, 12 Amb a 1-U, or placebo. Treatment began approximately 16 weeks before the start of each patient’s local ragweed pollen season, and continued for 52 weeks. Patients in all three arms could freely use symptom-controlling medications as needed: an oral antihistamine, antihistamine eyedrops, a nasal steroid, and an oral steroid.

The study’s primary efficacy end point was the patient’s total combined score – their rhinoconjunctivitis daily symptom score and daily medication-use score – during the peak of the ragweed season. For this measure, patients receiving the higher-dose ragweed pill had an average 27% reduction in their combined score, compared with the average among the placebo patients, and patients who received the lower-dose pill had an average 21% reduction, compared with placebo, both statistically significant differences. Both treatment groups showed similar improvements, compared with placebo, for secondary end points of total score throughout the entire ragweed season, symptom score during both the season’s peak and the entire season, and medication-use score during the season’s peak and the entire season.

The daily, oral pill was well tolerated at both dosages, with no deaths, systemic allergic reactions, or life-threatening events. The most common, treatment-related adverse events occurred early, and were transient and self-limited. Throat irritation occurred in 26%-29% of the active pill recipients, depending on the dosage. Other side effects included oral pruritus, in 19%; a swollen tongue, in 12%-19%; ear pruritus; tongue pruritus; oral paresthesia; and several other effects that occurred in less than 10% of treated patients. The majority of the adverse effects were mild or moderate, and none were serious. Two patients received epinephrine during the study. One patient had to a concomitant food-allergy reaction and the second was treated for local swelling and nervousness, so epinephrine treatment was not really needed.

"In routine practice, desensitization injections produce systemic reactions in 2%-6% of patients. I think we didn’t see that with the pill because the uptake is slower," Dr. Creticos said.

Results from the second trial, reported in a poster by Dr. Nolte, came from a study with a similar design that randomized 784 patients at sites in both North America and Europe (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.482]). This 52-week treatment study added a third active-treatment arm in which patients receive a daily pill containing 1.5 Amb a 1-U ragweed pollen. This low-dose pill did not produce a statistically-significant improvement in efficacy, compared with placebo. The 6 Amb a 1-U and 12 Amb a 1-U dosages resulted in a 19% and 24% average reduction in the total combined score during the peak ragweed season, statistically significant benefits for the study’s primary end point. The safety profile of the two highest doses also mimicked the first study, with no serious adverse effects and no systemic allergic reactions, anaphylaxis, or life-threatening effects. The type and severity of the treatment-related adverse effects were very similar to the first study. One patient in the second study received epinephrine, for a concomitant food-allergy reaction.

Both trials were sponsored by Merck, which is developing the oral ragweed-pollen desensitization pill. Dr. Creticos said that he has received research support from and has been a consultant to Merck as well as to several other drug companies. Dr. Nolte is an employee of Merck.

ORLANDO – Immunotherapy with a pill formulated from ragweed pollen safely and effectively reduced symptoms and the need for therapy to manage symptoms in patients with ragweed allergy.

The findings were noted in two pivotal, placebo-controlled trials that together enrolled 1,349 patients in North America and Europe. The company that is developing the oral formulation, Merck, plans to use the results as the basis for a licensing application to the Food and Drug Administration next year, Dr. Hendrick Nolte, the company’s senior director for research in Kenilworth, N.J., said at the meeting.

Mitchel L. Zoler/IMNG Medical Media

But the studies only assessed the pill’s efficacy for ragweed desensitization while patients were on treatment, and only during the first year of treatment. Thus, both studies failed to address the ability of the new formulation to modify disease, a hallmark effect of standard pollen desensitization by serial injections.

"Immunotherapy based on injections is disease modifying when used for 3-5 years. You can stop [the injections] and see continued benefit," said Dr. Peter S. Creticos, lead investigator for one of the two Merck studies (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.481]). Both ragweed pollen trials "were only single-season studies, so they can’t answer" whether disease was modified, he said in an interview during a poster presentation at the meeting.

However, a European study that used the same formulation examined the impact of 3 consecutive years of oral desensitization to ragweed followed by 2 years when patients received no immunotherapy. The results showed long-lasting tolerance that persisted during both follow-up years, said Dr. Creticos, an allergy and immunology physician at Johns Hopkins Hospital in Baltimore.

Reductions in symptoms and the need for symptom-controlling medications during ragweed-pollen season ranged from 21%-27%, compared with placebo, depending on the dosage. These differences were "clinically meaningful" and similar in efficacy to conventional, injection-based desensitization against ragweed, added Dr. Creticos. Unlike injections, the oral formulation did not cause any systemic reactions.

If the oral ragweed pill eventually receives U.S. marketing approval, it is likely to appeal to some patients, but may also have some downsides.

"A small percentage of patients won’t get injections because they are afraid of injections, they are afraid of systemic reactions, or they don’t want to have to regularly go to a doctor’s office," he said. "A daily pill is more convenient and easier, and it may be safer and just as effective." The main drawback is less reliable compliance. "A patient must be willing to take the pill daily, starting 16 weeks before the (allergy) season starts."

The study he presented randomized 565 North American adults with allergic rhinoconjunctivitis to ragweed to treatment with a pill containing 6 Amb a 1-U ragweed pollen, 12 Amb a 1-U, or placebo. Treatment began approximately 16 weeks before the start of each patient’s local ragweed pollen season, and continued for 52 weeks. Patients in all three arms could freely use symptom-controlling medications as needed: an oral antihistamine, antihistamine eyedrops, a nasal steroid, and an oral steroid.

The study’s primary efficacy end point was the patient’s total combined score – their rhinoconjunctivitis daily symptom score and daily medication-use score – during the peak of the ragweed season. For this measure, patients receiving the higher-dose ragweed pill had an average 27% reduction in their combined score, compared with the average among the placebo patients, and patients who received the lower-dose pill had an average 21% reduction, compared with placebo, both statistically significant differences. Both treatment groups showed similar improvements, compared with placebo, for secondary end points of total score throughout the entire ragweed season, symptom score during both the season’s peak and the entire season, and medication-use score during the season’s peak and the entire season.

The daily, oral pill was well tolerated at both dosages, with no deaths, systemic allergic reactions, or life-threatening events. The most common, treatment-related adverse events occurred early, and were transient and self-limited. Throat irritation occurred in 26%-29% of the active pill recipients, depending on the dosage. Other side effects included oral pruritus, in 19%; a swollen tongue, in 12%-19%; ear pruritus; tongue pruritus; oral paresthesia; and several other effects that occurred in less than 10% of treated patients. The majority of the adverse effects were mild or moderate, and none were serious. Two patients received epinephrine during the study. One patient had to a concomitant food-allergy reaction and the second was treated for local swelling and nervousness, so epinephrine treatment was not really needed.

"In routine practice, desensitization injections produce systemic reactions in 2%-6% of patients. I think we didn’t see that with the pill because the uptake is slower," Dr. Creticos said.

Results from the second trial, reported in a poster by Dr. Nolte, came from a study with a similar design that randomized 784 patients at sites in both North America and Europe (J. Allergy Clin. Immunol. 2012 [doi:10.1016/j.jaci.2011.12.482]). This 52-week treatment study added a third active-treatment arm in which patients receive a daily pill containing 1.5 Amb a 1-U ragweed pollen. This low-dose pill did not produce a statistically-significant improvement in efficacy, compared with placebo. The 6 Amb a 1-U and 12 Amb a 1-U dosages resulted in a 19% and 24% average reduction in the total combined score during the peak ragweed season, statistically significant benefits for the study’s primary end point. The safety profile of the two highest doses also mimicked the first study, with no serious adverse effects and no systemic allergic reactions, anaphylaxis, or life-threatening effects. The type and severity of the treatment-related adverse effects were very similar to the first study. One patient in the second study received epinephrine, for a concomitant food-allergy reaction.

Both trials were sponsored by Merck, which is developing the oral ragweed-pollen desensitization pill. Dr. Creticos said that he has received research support from and has been a consultant to Merck as well as to several other drug companies. Dr. Nolte is an employee of Merck.

ORLANDO – Aspirin sensitivity can be a real headache for patients and clinicians, but a safe and effective aspirin desensitization protocol can bring the analgesic and anti-inflammatory benefits of aspirin therapy to patients with aspirin-exacerbated respiratory disease, reported a clinician at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Patients with AERD who undergo aspirin desensitization have fewer bouts of sinusitis, show improvement in both asthma symptoms and sense of smell, and use less corticosteroid, compared with patients who don’t undergo desensitization, said Dr. Katharine M. Woessner, program director in the division of allergy, asthma, and immunology at the Scripps Clinic in San Diego.

©jimdeli/Fotolia.com

Aspirin desensitization also blunts the response to other NSAIDS like ibuprofen and naproxen, which – like aspirin – inhibit the cyclooxygenase-1 (COX-1) enzyme, Dr. Woessner said. Aspirin and other NSAIDs induce rhinitis and asthma attacks in patients with AERD, and the disease is progressive even when patients are careful to avoid all NSAIDs.

Only 3 of 1,400 consecutive patients with AERD that was treated with aspirin desensitization at Scripps experienced systemic reactions, and all of those responded to a single dose of intramuscular epinephrine, she said.

"I don’t know why aspirin desensitization works, but we clearly have a therapy that’s easy to use and is quite effective in managing these patients," Dr. Woessner said.

Aspirin Challenge

AERD usually begins in patients in their 30s or 40s who have a prior history of tolerance to aspirin and other NSAIDs. It is more than twice as likely to occur in women, and tends to be more severe in women than in men. Patients develop chronic congestion, rhinitis, anosmia, and nasal polyps, often followed by asthma 1-5 years after the onset of rhinitis.

The disease is characterized by chronic eosinophilic rhinosinusitis and nasal polyposis that are initially intermittent but evolve into chronic, hyperplasic eosinophilic sinusitis that often requires surgical intervention, Dr. Woessner said.

The asthma that develops in patients with AERD is persistent, usually moderate to severe, and related to the severity of sinus disease. However, "asthma is not necessarily a prerequisite to make a diagnosis of aspirin-exacerbated respiratory disease," she noted.

The clinical standard for AERD diagnosis is an oral aspirin challenge. Patients typically can experience a 20% or greater decline in FEV₁ (forced expiratory volume in 1 second) and a naso-ocular reaction, but purely upper airway or lower airway reactions can also occur. Patients may also have a partial asthma reaction, with a change in FEV₁ from baseline of –15% to –20% and a naso-ocular reaction or laryngospasm. Patients are considered to be negative for AERD if they have no reactions following a 325-mg oral aspirin challenge.

In those who test positive, treatment consists of avoiding all COX-1–inhibiting NSAIDS. Highly selective COX-2 inhibitors such as celecoxib (Celebrex) are generally well tolerated in patients with AERD, Dr. Woesnner said, noting that more than 200 AERD-proven patients at Scripps who were challenged with a highly selective COX-2 inhibitor had no reaction. However, cross reactivity is possible with higher doses of less-selective COX-2 inhibitors such as nimesulide (Sulide) or meloxicam (Mobic). Acetaminophen at doses up to 1,000 mg are also typically well tolerated in these patients.

"There are several drugs that don’t cross-react with aspirin in patients with AERD. The problem is that they’re not very good analgesics, so if we need something that’s analgesic or anti-inflammatory, patients are not going to get much benefit from these medications," Dr. Woessner said.

Outpatient Precautions

Aspirin challenge and desensitization in the outpatient setting can be safely performed with a few caveats. The patient should have stable asthma within 10% of the best prior value and an FEV₁ of at least 60%-80% of predicted, or an output of at least 1.5 L. The patient should be on inhaled steroids and a long-acting beta-agonist, and 2-4 weeks before desensitization should be started on montelukast or another leukotriene modifier.

The advent of leukotriene inhibitors has made aspirin desensitization a routine outpatient procedure, session moderator Dr. Mariana C. Castells noted in an interview.

"We used to do aspirin desensitization in the intensive care unit, just because the reactions were scary and we didn’t know how to control them. In the last 10 years, since we started to use montelukast [Singulair] and Zyflo [zileuton], less than 1% have been done in an intensive care unit," said Dr. Castells of the division of rheumatology, immunology, and allergy at Brigham and Women’s Hospital in Boston.

Patients are asked to not use antihistamines for 72 hours before the procedure so that their naso-ocular responses can be observed. Patients with nasal polyps may require debulking surgery prior to desensitization.

"We had recommended in the past that intravenous access be available, but we have data now that it may not be necessary," Dr. Woessner said.

On day 1 of sensitization, patients take 20-40 mg of aspirin at 8 a.m., 40-60 mg at 11 a.m., and 60-100 mg at 2 p.m. On day 2, the respective doses at the same times of day are 100-160 mg, 160-325 mg, and 325 mg.

During desensitization, FEV₁ should be measured every hour, and should be at least 1.5 L and greater than 60% of predicted. When a patient has a reaction and that reaction is resolved, the provoking dose should be repeated, and if there is no reaction, the escalating doses can be continued every 3 hours as scheduled. Patients are considered to be densensitized or aspirin tolerant if they can take a 325-mg dose with no reaction. The patient should be instructed to start on 650-mg aspirin that night as the first daily dose, and to continue with up to 650 mg twice daily. About half of all patients can decrease to 325 mg b.i.d. at 1-6 months after the densensitization protocol is completed.

Combining a nasal ketorolac challenge with the oral aspirin challenge can make the desensitization even safer, Dr. Woessner said. The patient is given ketorolac spray at increasing doses every half-hour over 2 hours, followed 1 hour after the last spray with 60-mg aspirin in two doses 1.5 hours apart. The patient is discharged and returns the next day to receive 150-mg aspirin, followed 3 hours later by 325 mg.

No funding source was reported. Dr. Woessner disclosed that she is on the speakers bureaus of Merck and Teva, and has been a speaker for GlaxoSmithKline.

ORLANDO – Aspirin sensitivity can be a real headache for patients and clinicians, but a safe and effective aspirin desensitization protocol can bring the analgesic and anti-inflammatory benefits of aspirin therapy to patients with aspirin-exacerbated respiratory disease, reported a clinician at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Patients with AERD who undergo aspirin desensitization have fewer bouts of sinusitis, show improvement in both asthma symptoms and sense of smell, and use less corticosteroid, compared with patients who don’t undergo desensitization, said Dr. Katharine M. Woessner, program director in the division of allergy, asthma, and immunology at the Scripps Clinic in San Diego.

©jimdeli/Fotolia.com

Aspirin desensitization also blunts the response to other NSAIDS like ibuprofen and naproxen, which – like aspirin – inhibit the cyclooxygenase-1 (COX-1) enzyme, Dr. Woessner said. Aspirin and other NSAIDs induce rhinitis and asthma attacks in patients with AERD, and the disease is progressive even when patients are careful to avoid all NSAIDs.

Only 3 of 1,400 consecutive patients with AERD that was treated with aspirin desensitization at Scripps experienced systemic reactions, and all of those responded to a single dose of intramuscular epinephrine, she said.

"I don’t know why aspirin desensitization works, but we clearly have a therapy that’s easy to use and is quite effective in managing these patients," Dr. Woessner said.

Aspirin Challenge

AERD usually begins in patients in their 30s or 40s who have a prior history of tolerance to aspirin and other NSAIDs. It is more than twice as likely to occur in women, and tends to be more severe in women than in men. Patients develop chronic congestion, rhinitis, anosmia, and nasal polyps, often followed by asthma 1-5 years after the onset of rhinitis.

The disease is characterized by chronic eosinophilic rhinosinusitis and nasal polyposis that are initially intermittent but evolve into chronic, hyperplasic eosinophilic sinusitis that often requires surgical intervention, Dr. Woessner said.

The asthma that develops in patients with AERD is persistent, usually moderate to severe, and related to the severity of sinus disease. However, "asthma is not necessarily a prerequisite to make a diagnosis of aspirin-exacerbated respiratory disease," she noted.

The clinical standard for AERD diagnosis is an oral aspirin challenge. Patients typically can experience a 20% or greater decline in FEV₁ (forced expiratory volume in 1 second) and a naso-ocular reaction, but purely upper airway or lower airway reactions can also occur. Patients may also have a partial asthma reaction, with a change in FEV₁ from baseline of –15% to –20% and a naso-ocular reaction or laryngospasm. Patients are considered to be negative for AERD if they have no reactions following a 325-mg oral aspirin challenge.

In those who test positive, treatment consists of avoiding all COX-1–inhibiting NSAIDS. Highly selective COX-2 inhibitors such as celecoxib (Celebrex) are generally well tolerated in patients with AERD, Dr. Woesnner said, noting that more than 200 AERD-proven patients at Scripps who were challenged with a highly selective COX-2 inhibitor had no reaction. However, cross reactivity is possible with higher doses of less-selective COX-2 inhibitors such as nimesulide (Sulide) or meloxicam (Mobic). Acetaminophen at doses up to 1,000 mg are also typically well tolerated in these patients.

"There are several drugs that don’t cross-react with aspirin in patients with AERD. The problem is that they’re not very good analgesics, so if we need something that’s analgesic or anti-inflammatory, patients are not going to get much benefit from these medications," Dr. Woessner said.

Outpatient Precautions

Aspirin challenge and desensitization in the outpatient setting can be safely performed with a few caveats. The patient should have stable asthma within 10% of the best prior value and an FEV₁ of at least 60%-80% of predicted, or an output of at least 1.5 L. The patient should be on inhaled steroids and a long-acting beta-agonist, and 2-4 weeks before desensitization should be started on montelukast or another leukotriene modifier.

The advent of leukotriene inhibitors has made aspirin desensitization a routine outpatient procedure, session moderator Dr. Mariana C. Castells noted in an interview.

"We used to do aspirin desensitization in the intensive care unit, just because the reactions were scary and we didn’t know how to control them. In the last 10 years, since we started to use montelukast [Singulair] and Zyflo [zileuton], less than 1% have been done in an intensive care unit," said Dr. Castells of the division of rheumatology, immunology, and allergy at Brigham and Women’s Hospital in Boston.

Patients are asked to not use antihistamines for 72 hours before the procedure so that their naso-ocular responses can be observed. Patients with nasal polyps may require debulking surgery prior to desensitization.

"We had recommended in the past that intravenous access be available, but we have data now that it may not be necessary," Dr. Woessner said.

On day 1 of sensitization, patients take 20-40 mg of aspirin at 8 a.m., 40-60 mg at 11 a.m., and 60-100 mg at 2 p.m. On day 2, the respective doses at the same times of day are 100-160 mg, 160-325 mg, and 325 mg.

During desensitization, FEV₁ should be measured every hour, and should be at least 1.5 L and greater than 60% of predicted. When a patient has a reaction and that reaction is resolved, the provoking dose should be repeated, and if there is no reaction, the escalating doses can be continued every 3 hours as scheduled. Patients are considered to be densensitized or aspirin tolerant if they can take a 325-mg dose with no reaction. The patient should be instructed to start on 650-mg aspirin that night as the first daily dose, and to continue with up to 650 mg twice daily. About half of all patients can decrease to 325 mg b.i.d. at 1-6 months after the densensitization protocol is completed.

Combining a nasal ketorolac challenge with the oral aspirin challenge can make the desensitization even safer, Dr. Woessner said. The patient is given ketorolac spray at increasing doses every half-hour over 2 hours, followed 1 hour after the last spray with 60-mg aspirin in two doses 1.5 hours apart. The patient is discharged and returns the next day to receive 150-mg aspirin, followed 3 hours later by 325 mg.

No funding source was reported. Dr. Woessner disclosed that she is on the speakers bureaus of Merck and Teva, and has been a speaker for GlaxoSmithKline.

ORLANDO – Aspirin sensitivity can be a real headache for patients and clinicians, but a safe and effective aspirin desensitization protocol can bring the analgesic and anti-inflammatory benefits of aspirin therapy to patients with aspirin-exacerbated respiratory disease, reported a clinician at the annual meeting of the American Academy of Allergy, Asthma, and Immunology.

Patients with AERD who undergo aspirin desensitization have fewer bouts of sinusitis, show improvement in both asthma symptoms and sense of smell, and use less corticosteroid, compared with patients who don’t undergo desensitization, said Dr. Katharine M. Woessner, program director in the division of allergy, asthma, and immunology at the Scripps Clinic in San Diego.

©jimdeli/Fotolia.com

Aspirin desensitization also blunts the response to other NSAIDS like ibuprofen and naproxen, which – like aspirin – inhibit the cyclooxygenase-1 (COX-1) enzyme, Dr. Woessner said. Aspirin and other NSAIDs induce rhinitis and asthma attacks in patients with AERD, and the disease is progressive even when patients are careful to avoid all NSAIDs.

Only 3 of 1,400 consecutive patients with AERD that was treated with aspirin desensitization at Scripps experienced systemic reactions, and all of those responded to a single dose of intramuscular epinephrine, she said.

"I don’t know why aspirin desensitization works, but we clearly have a therapy that’s easy to use and is quite effective in managing these patients," Dr. Woessner said.

Aspirin Challenge

AERD usually begins in patients in their 30s or 40s who have a prior history of tolerance to aspirin and other NSAIDs. It is more than twice as likely to occur in women, and tends to be more severe in women than in men. Patients develop chronic congestion, rhinitis, anosmia, and nasal polyps, often followed by asthma 1-5 years after the onset of rhinitis.

The disease is characterized by chronic eosinophilic rhinosinusitis and nasal polyposis that are initially intermittent but evolve into chronic, hyperplasic eosinophilic sinusitis that often requires surgical intervention, Dr. Woessner said.

The asthma that develops in patients with AERD is persistent, usually moderate to severe, and related to the severity of sinus disease. However, "asthma is not necessarily a prerequisite to make a diagnosis of aspirin-exacerbated respiratory disease," she noted.

The clinical standard for AERD diagnosis is an oral aspirin challenge. Patients typically can experience a 20% or greater decline in FEV₁ (forced expiratory volume in 1 second) and a naso-ocular reaction, but purely upper airway or lower airway reactions can also occur. Patients may also have a partial asthma reaction, with a change in FEV₁ from baseline of –15% to –20% and a naso-ocular reaction or laryngospasm. Patients are considered to be negative for AERD if they have no reactions following a 325-mg oral aspirin challenge.

In those who test positive, treatment consists of avoiding all COX-1–inhibiting NSAIDS. Highly selective COX-2 inhibitors such as celecoxib (Celebrex) are generally well tolerated in patients with AERD, Dr. Woesnner said, noting that more than 200 AERD-proven patients at Scripps who were challenged with a highly selective COX-2 inhibitor had no reaction. However, cross reactivity is possible with higher doses of less-selective COX-2 inhibitors such as nimesulide (Sulide) or meloxicam (Mobic). Acetaminophen at doses up to 1,000 mg are also typically well tolerated in these patients.

"There are several drugs that don’t cross-react with aspirin in patients with AERD. The problem is that they’re not very good analgesics, so if we need something that’s analgesic or anti-inflammatory, patients are not going to get much benefit from these medications," Dr. Woessner said.

Outpatient Precautions

Aspirin challenge and desensitization in the outpatient setting can be safely performed with a few caveats. The patient should have stable asthma within 10% of the best prior value and an FEV₁ of at least 60%-80% of predicted, or an output of at least 1.5 L. The patient should be on inhaled steroids and a long-acting beta-agonist, and 2-4 weeks before desensitization should be started on montelukast or another leukotriene modifier.

The advent of leukotriene inhibitors has made aspirin desensitization a routine outpatient procedure, session moderator Dr. Mariana C. Castells noted in an interview.

"We used to do aspirin desensitization in the intensive care unit, just because the reactions were scary and we didn’t know how to control them. In the last 10 years, since we started to use montelukast [Singulair] and Zyflo [zileuton], less than 1% have been done in an intensive care unit," said Dr. Castells of the division of rheumatology, immunology, and allergy at Brigham and Women’s Hospital in Boston.

Patients are asked to not use antihistamines for 72 hours before the procedure so that their naso-ocular responses can be observed. Patients with nasal polyps may require debulking surgery prior to desensitization.

"We had recommended in the past that intravenous access be available, but we have data now that it may not be necessary," Dr. Woessner said.

On day 1 of sensitization, patients take 20-40 mg of aspirin at 8 a.m., 40-60 mg at 11 a.m., and 60-100 mg at 2 p.m. On day 2, the respective doses at the same times of day are 100-160 mg, 160-325 mg, and 325 mg.

During desensitization, FEV₁ should be measured every hour, and should be at least 1.5 L and greater than 60% of predicted. When a patient has a reaction and that reaction is resolved, the provoking dose should be repeated, and if there is no reaction, the escalating doses can be continued every 3 hours as scheduled. Patients are considered to be densensitized or aspirin tolerant if they can take a 325-mg dose with no reaction. The patient should be instructed to start on 650-mg aspirin that night as the first daily dose, and to continue with up to 650 mg twice daily. About half of all patients can decrease to 325 mg b.i.d. at 1-6 months after the densensitization protocol is completed.

Combining a nasal ketorolac challenge with the oral aspirin challenge can make the desensitization even safer, Dr. Woessner said. The patient is given ketorolac spray at increasing doses every half-hour over 2 hours, followed 1 hour after the last spray with 60-mg aspirin in two doses 1.5 hours apart. The patient is discharged and returns the next day to receive 150-mg aspirin, followed 3 hours later by 325 mg.

No funding source was reported. Dr. Woessner disclosed that she is on the speakers bureaus of Merck and Teva, and has been a speaker for GlaxoSmithKline.

ORLANDO – Parents were able to identify patterns of nonrespiratory symptoms in their children that preceded loss of asthma control, a small study showed.

The findings, if replicated, suggest that parents could recognize these early patterns and potentially intervene to prevent loss of control, as well as asthma exacerbations. Currently, guidelines from the National Asthma Education Program recommend starting treatment once an asthma exacerbation has begun, and current asthma action plans focus mainly on respiratory tract symptoms. The guidelines do not provide specific information about what signs and symptoms might present before lower respiratory tract symptoms appear, said Dr. Lisanne Newton of the Cleveland Clinic.

Caregivers of children aged 2-11 years with persistent asthma completed daily diaries for 16 weeks, in which they categorized each of 41 signs and symptoms as usual, less than usual, or more than usual. The signs and symptoms were derived from a prior study in which caregivers had identified them as potential early warnings (J. Pediatr. 2009;154:877-81).

Of 33 caregivers (32 parents and 1 grandparent) enrolled, 27 completed at least some of the questionnaire, and 19 completed all 16 weeks. Nearly all of the parents were female, and two-thirds of the children were male. The parents had a mean age of 38 years, and the children had a mean age of 7 years. Two-thirds of the parents had a history of atopic disease themselves, Dr. Newton noted.

The caregivers completed diary entries for 82% of days overall. At least one episode of loss of control, defined as 2 or more consecutive days of increased lower respiratory symptoms, occurred in 78% of the children. A total of 41% had at least one course of oral corticosteroids, 22% had at least one emergency department visit, and 41% had at least one unexpected medical provider visit.

Overall there was a significant change from baseline in all symptom types during an episode, compared with a controlled period, which was defined as the days excluding the episodes and the 5 days prior and 2 days after an episode. The odds of a child having unusual nonrespiratory signs or symptoms were significant at 3 days, 2 days, and 1 day prior to an episode, compared with controlled periods, with odds ratios of 1.6, 2.1, and 2.3, respectively. The change from baseline in upper and lower respiratory symptoms in the 3 days prior to an episode was not significant, she said.

Specific nonrespiratory signs and symptoms included irritability, low activity levels, tiredness, and sunken eyes. Parents reported an unusual amount of irritability in their children starting 5 days before an episode, with odds ratios of 2.2 at 5 days ahead and 4.1 at 1 day ahead. Unusually low activity levels were significant starting at 3 days before an episode, with odds ratios of 2.7 at 3 days and 4.4 at 1 day prior to the episode. Tiredness was also significantly more common, with an odds ratio of 2.8 at 3 days and 7.6 at 1 day. Sunken eyes were reported starting at 2 days prior, with an odds ratio of 2.5. All of these signs and symptoms were even more common during an episode.

Surprisingly, the overall odds of a child having an unusual amount of an upper respiratory sign or symptom, compared with controlled periods, was not significant in the 5 days before an episode, though they were significant during an episode. An itchy throat was the only upper respiratory symptom that was significant, and only at 3 days (OR, 2.9) and 2 days (4.3) prior to and during an episode but not the day prior, she noted.

Though limited by a small sample size, some consistent symptom patterns were seen in 5 of the 12 children who had at least three episodes during the 16-week period. One child had an unusual amount of crying and irritability the day prior to two of his three episodes. Another child had an unusual amount of talking, activity, and energy in the 2 days before half of her episodes. A third child had sleeping problems in the 2 days prior to three-quarters of his episodes and watery eyes in the 2 days prior to half of his episodes.

There were no differences between episodes occurring during weeks when oral corticosteroids were prescribed versus episodes occurring during weeks when no oral corticosteroids were prescribed, Dr. Newton said.

Further investigation is needed to determine whether parents would treat their children when these symptoms occurred, and if treatment modification could prevent loss of asthma control and exacerbations, she said.

Dr. Newton stated that she had no relevant financial disclosures.

ORLANDO – Parents were able to identify patterns of nonrespiratory symptoms in their children that preceded loss of asthma control, a small study showed.

The findings, if replicated, suggest that parents could recognize these early patterns and potentially intervene to prevent loss of control, as well as asthma exacerbations. Currently, guidelines from the National Asthma Education Program recommend starting treatment once an asthma exacerbation has begun, and current asthma action plans focus mainly on respiratory tract symptoms. The guidelines do not provide specific information about what signs and symptoms might present before lower respiratory tract symptoms appear, said Dr. Lisanne Newton of the Cleveland Clinic.

Caregivers of children aged 2-11 years with persistent asthma completed daily diaries for 16 weeks, in which they categorized each of 41 signs and symptoms as usual, less than usual, or more than usual. The signs and symptoms were derived from a prior study in which caregivers had identified them as potential early warnings (J. Pediatr. 2009;154:877-81).

Of 33 caregivers (32 parents and 1 grandparent) enrolled, 27 completed at least some of the questionnaire, and 19 completed all 16 weeks. Nearly all of the parents were female, and two-thirds of the children were male. The parents had a mean age of 38 years, and the children had a mean age of 7 years. Two-thirds of the parents had a history of atopic disease themselves, Dr. Newton noted.

The caregivers completed diary entries for 82% of days overall. At least one episode of loss of control, defined as 2 or more consecutive days of increased lower respiratory symptoms, occurred in 78% of the children. A total of 41% had at least one course of oral corticosteroids, 22% had at least one emergency department visit, and 41% had at least one unexpected medical provider visit.

Overall there was a significant change from baseline in all symptom types during an episode, compared with a controlled period, which was defined as the days excluding the episodes and the 5 days prior and 2 days after an episode. The odds of a child having unusual nonrespiratory signs or symptoms were significant at 3 days, 2 days, and 1 day prior to an episode, compared with controlled periods, with odds ratios of 1.6, 2.1, and 2.3, respectively. The change from baseline in upper and lower respiratory symptoms in the 3 days prior to an episode was not significant, she said.

Specific nonrespiratory signs and symptoms included irritability, low activity levels, tiredness, and sunken eyes. Parents reported an unusual amount of irritability in their children starting 5 days before an episode, with odds ratios of 2.2 at 5 days ahead and 4.1 at 1 day ahead. Unusually low activity levels were significant starting at 3 days before an episode, with odds ratios of 2.7 at 3 days and 4.4 at 1 day prior to the episode. Tiredness was also significantly more common, with an odds ratio of 2.8 at 3 days and 7.6 at 1 day. Sunken eyes were reported starting at 2 days prior, with an odds ratio of 2.5. All of these signs and symptoms were even more common during an episode.

Surprisingly, the overall odds of a child having an unusual amount of an upper respiratory sign or symptom, compared with controlled periods, was not significant in the 5 days before an episode, though they were significant during an episode. An itchy throat was the only upper respiratory symptom that was significant, and only at 3 days (OR, 2.9) and 2 days (4.3) prior to and during an episode but not the day prior, she noted.

Though limited by a small sample size, some consistent symptom patterns were seen in 5 of the 12 children who had at least three episodes during the 16-week period. One child had an unusual amount of crying and irritability the day prior to two of his three episodes. Another child had an unusual amount of talking, activity, and energy in the 2 days before half of her episodes. A third child had sleeping problems in the 2 days prior to three-quarters of his episodes and watery eyes in the 2 days prior to half of his episodes.

There were no differences between episodes occurring during weeks when oral corticosteroids were prescribed versus episodes occurring during weeks when no oral corticosteroids were prescribed, Dr. Newton said.

Further investigation is needed to determine whether parents would treat their children when these symptoms occurred, and if treatment modification could prevent loss of asthma control and exacerbations, she said.

Dr. Newton stated that she had no relevant financial disclosures.

ORLANDO – Parents were able to identify patterns of nonrespiratory symptoms in their children that preceded loss of asthma control, a small study showed.

The findings, if replicated, suggest that parents could recognize these early patterns and potentially intervene to prevent loss of control, as well as asthma exacerbations. Currently, guidelines from the National Asthma Education Program recommend starting treatment once an asthma exacerbation has begun, and current asthma action plans focus mainly on respiratory tract symptoms. The guidelines do not provide specific information about what signs and symptoms might present before lower respiratory tract symptoms appear, said Dr. Lisanne Newton of the Cleveland Clinic.

Caregivers of children aged 2-11 years with persistent asthma completed daily diaries for 16 weeks, in which they categorized each of 41 signs and symptoms as usual, less than usual, or more than usual. The signs and symptoms were derived from a prior study in which caregivers had identified them as potential early warnings (J. Pediatr. 2009;154:877-81).

Of 33 caregivers (32 parents and 1 grandparent) enrolled, 27 completed at least some of the questionnaire, and 19 completed all 16 weeks. Nearly all of the parents were female, and two-thirds of the children were male. The parents had a mean age of 38 years, and the children had a mean age of 7 years. Two-thirds of the parents had a history of atopic disease themselves, Dr. Newton noted.

The caregivers completed diary entries for 82% of days overall. At least one episode of loss of control, defined as 2 or more consecutive days of increased lower respiratory symptoms, occurred in 78% of the children. A total of 41% had at least one course of oral corticosteroids, 22% had at least one emergency department visit, and 41% had at least one unexpected medical provider visit.

Overall there was a significant change from baseline in all symptom types during an episode, compared with a controlled period, which was defined as the days excluding the episodes and the 5 days prior and 2 days after an episode. The odds of a child having unusual nonrespiratory signs or symptoms were significant at 3 days, 2 days, and 1 day prior to an episode, compared with controlled periods, with odds ratios of 1.6, 2.1, and 2.3, respectively. The change from baseline in upper and lower respiratory symptoms in the 3 days prior to an episode was not significant, she said.

Specific nonrespiratory signs and symptoms included irritability, low activity levels, tiredness, and sunken eyes. Parents reported an unusual amount of irritability in their children starting 5 days before an episode, with odds ratios of 2.2 at 5 days ahead and 4.1 at 1 day ahead. Unusually low activity levels were significant starting at 3 days before an episode, with odds ratios of 2.7 at 3 days and 4.4 at 1 day prior to the episode. Tiredness was also significantly more common, with an odds ratio of 2.8 at 3 days and 7.6 at 1 day. Sunken eyes were reported starting at 2 days prior, with an odds ratio of 2.5. All of these signs and symptoms were even more common during an episode.

Surprisingly, the overall odds of a child having an unusual amount of an upper respiratory sign or symptom, compared with controlled periods, was not significant in the 5 days before an episode, though they were significant during an episode. An itchy throat was the only upper respiratory symptom that was significant, and only at 3 days (OR, 2.9) and 2 days (4.3) prior to and during an episode but not the day prior, she noted.

Though limited by a small sample size, some consistent symptom patterns were seen in 5 of the 12 children who had at least three episodes during the 16-week period. One child had an unusual amount of crying and irritability the day prior to two of his three episodes. Another child had an unusual amount of talking, activity, and energy in the 2 days before half of her episodes. A third child had sleeping problems in the 2 days prior to three-quarters of his episodes and watery eyes in the 2 days prior to half of his episodes.

There were no differences between episodes occurring during weeks when oral corticosteroids were prescribed versus episodes occurring during weeks when no oral corticosteroids were prescribed, Dr. Newton said.

Further investigation is needed to determine whether parents would treat their children when these symptoms occurred, and if treatment modification could prevent loss of asthma control and exacerbations, she said.

Dr. Newton stated that she had no relevant financial disclosures.