Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; [email protected]

Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; [email protected]

Luke, a 16-year-old basketball player, complains that he can’t finish a game without running out of breath. He says things are at their worst when the game is close and when it’s nearing the end. He doesn’t have the problem during practice, or when he is playing other sports. The team physician suggested using an albuterol inhaler half an hour before game time and when he has symptoms, but he gets only minimal relief. Now he has come to you.

His vital signs, lung exam, and cardiac exam are normal. Results of pulmonary function tests with pre- and post-albuterol challenge done a year ago were also normal. Does Luke have exercise-induced bronchoconstriction (EIB)? How can you be sure? And what can you do to help?

Symptoms like Luke’s are common among athletes of all abilities. They may add up to EIB, a condition with an estimated prevalence of 6% to 12% in the general population—or they may not.¹ One study showed that only a third of athletes with symptoms or prior diagnosis of EIB had positive objective testing for the condition, and current studies show that reported symptoms are not an accurate guide in athletes like Luke who do not have underlying asthma.^2,3 To treat him correctly, you will need to nail down the diagnosis with additional tests.^3,4

Shortness of breath that’s worse than expected

EIB can have many different presentations. The most common symptom is cough associated with exercise.³ Other common signs and symptoms include wheezing, chest tightness, and more severe than expected or worsening shortness of breath. More unusual symptoms include a decrease in performance or fatigue out of proportion to workload. Often patients with EIB have other associated medical conditions, such as allergic rhinitis.

Bronchoconstriction usually occurs with maximal or near maximal exertion. Generally, it takes 5 to 8 minutes of exercising at 80% of maximal heart rate to trigger EIB. Classically, the symptoms peak 5 to 10 minutes after exercise begins.⁵

Rule out cardiac problems. If EIB is the correct diagnosis, the physical exam is usually normal. The importance of the physical exam is to evaluate for other diagnoses with similar presentations. Conditions to rule out include cardiac problems, exercise-induced hyperventilation, upper and lower respiratory infections or abnormalities, exercise-induced laryngeal dysfunction, exercise-induced anaphylaxis, and gastroesophageal reflux disease (GERD). The differential diagnosis for EIB is summarized in TABLE 1.

Test for asthma. Once you have gone through the differential diagnosis and are comfortable that the symptoms are respiratory, the next step should be pulmonary function tests (PFT), pre- and post-albuterol challenge. Findings of obstruction, such as reduced forced expiratory volume in 1 second (FEV1) or increased lung volume, are consistent with a diagnosis of asthma. In that case, no further workup is needed—unless the patient is unresponsive to asthma treatment. In athletes like Luke who do not have asthma and have a normal nonprovocative spirometry, you can move on to either provocative spirometry or empiric treatment.

TABLE 1
Is it EIB, or something else?

Perform provocative spirometry

Direct spirometry is commonly done with a methacholine challenge. This test is less sensitive than indirect testing for EIB patients who do not have underlying asthma.

The gold standard for indirect testing is eucapnic voluntary hyperventilation (EVH). Because EVH requires special equipment, however, it may not be an option in your office. The more reasonable choice is exercise challenge testing, which can be done either in your office or in the milieu—the basketball court, for example—where the athlete’s symptoms usually occur. In an exercise challenge, you get a baseline spirometry measurement, have the athlete exercise to 80% to 90% of maximal heart rate, and then repeat spirometry at short intervals after exercise ends. If you do an exercise challenge in the office, you can reduce false-negative results by maintaining an ambient temperature between 68° and 77°F (20°-25°C) with a relative humidity of less than 50%.^6,7

Or try empiric treatment

Empiric treatment is a reasonable strategy for athletes with EIB symptoms, worth trying both for athletes who have underlying asthma and for those who do not. If the athlete with asthma responds to treatment, the problem is solved. For the athlete who does not have asthma, however, there are some exceptions to this approach—specifically, the elite athlete.

In the elite athlete, you will need to confirm the diagnosis because many of the substances used to treat EIB are restricted by governing bodies such as the International Olympic Committee (IOC) and require provocative testing to obtain a therapeutic use exemption.⁸ There is some debate as to whether nonelite athletes also need bronchoprovocative testing. Some recommendations advise testing all elite and competitive athletes and restricting empiric treatment to recreational athletes.¹ For more information on banned or restricted medications, see “Is that drug banned from competition?”.

If you take the empiric approach and the athlete does not respond to treatment, consider further testing to rule out other, more serious problems. In Luke’s case, where empiric treatment with albuterol has failed, indirect testing would be the next step.

Medicate before exercise: SABAs and LABAs

Prophylaxis for EIB usually starts with an inhaled short-acting β2 agonist (SABA) such as albuterol or pirbuterol, taken 15 minutes before starting to exercise.^9,10 The effectiveness of both short- and long-acting β2 agonists decreases with frequent use, which may be Luke’s problem. For that reason, patients with mild EIB may choose to use pretreatment medication only for more demanding exercise sessions.¹¹ Advise EIB patients who need daily pretreatment to try adjunctive maintenance therapy (discussed at greater length, below.)

Longer-acting β2 agonists (LABAs) such as salmeterol or formoterol may be effective for prolonged or all-day exercise, but may lose their prophylactic effect with prolonged use.¹² Furthermore, the US Food and Drug Administration (FDA) has advised against using LABAs alone because of the possibility of severe asthma episodes or death. LABAs should be used only in conjunction with daily maintenance therapy with inhaled corticosteroids. The properties of these and other EIB medications are summarized in TABLE 2.

TABLE 2
EIB medications

Cromolyn, antileukotrienes are options, too

Mast cell stabilizers (cromolyn) can be used with β2 agonists as prophylactic therapy. When these agents are used together, they have an additive effect.¹³ The athlete may take them 10 minutes to an hour before exercise. Make sure your patient knows that mast cell stabilizers cannot be used as a rescue inhaler or bronchodilator.

Inhaled corticosteroids (flunisolide, fluticasone, others) may be needed for athletes with poorly controlled chronic asthma; they can also be used as adjunct preventive treatment for athletes who have EIB with no underlying chronic asthma.^14-16 Often, inhaled corticosteroids are used as combination therapy with a LABA or an antileukotriene agent (montelukast, zafirlukast; see below). Recent research shows that montelukast in combination with inhaled corticosteroids is more efficacious than LABA with inhaled corticosteroids.^14,17

Antileukotriene agents can be especially helpful for EIB in patients with mild, stable asthma.¹⁸ Patients who do respond to antileukotriene agents usually respond very favorably. Antileukotrienes offer a reasonable alternative to inhaled corticosteroids and LABAs. They have a low side-effect profile and should be considered as daily prophylaxis.^19,20 The effects of montelukast are evident as early as 2 hours after administration, and bronchoprotective effects can last as long as 24 hours.^21,22 For that reason, montelukast is especially useful in children whose exercise patterns are not always predictable.

Be prepared for acute exacerbations. Prophylactic medication does not always prevent acute exacerbations. When that happens, your EIB patient will need to use a β2 agonist as rescue therapy. Make sure your patient knows that none of the other medications are effective bronchodilators in acute exacerbations.

Remember, too, that EIB cannot be effectively treated if the athlete has poorly controlled chronic asthma. Underlying causes of asthma exacerbations like allergies or respiratory infections must be addressed and stabilized first, following guidelines of the National Asthma Education and Prevention Program (NAEPP).⁹ You can access the guidelines at www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.

These tips can help the athlete

Encourage athletes with EIB to keep up their exercise routines, because cardiovascular fitness has a beneficial effect on this condition. Fit individuals breathe more slowly, which reduces the likelihood of exacerbations. Of note, though: Certain sports are easier on patients with EIB. Patients may want to keep this in mind when deciding which team they want to go out for. Specifically, indoor sports, where air temperature, humidity, and exposure to allergens are controlled, and sports like baseball, sprinting, or football, which require less prolonged aerobic endurance, are good options.

Tell athletes whose sports require cold, dry conditions—ice skating, or skiing, for instance—to try breathing through a scarf or mask to keep inspired air warm and less irritating.

And tell all athletes with EIB to warm up properly before they start to compete.²³ That means a 15-minute warm-up at moderate exertion, followed by a 15- to 30-minute rest period. The rest period is the time to take their medication.

When therapy fails

When an EIB patient fails to respond despite multiple drug therapy, it’s time to reconsider other diagnoses, such as vocal cord dysfunction and severe GERD, which may mimic symptoms of EIB.

On the horizon. Other therapies for possible treatment of EIB are being studied. These include omega-3 fatty acid dietary supplementation and inhaled enoxaparin.^24,25 Data are currently insufficient to recommend use of these agents in clinical practice.

As for Luke, indirect testing via exercise challenge was positive for EIB. Adjunctive therapy with montelukast was added to his albuterol inhaler, and the combination has worked well for him. He’s still playing basketball, and enjoying it.

Acknowledgments

The authors thank Ken Rundell, PhD, for reviewing this article. Dr. Rundell is director of the Human Physiology Laboratory at the Keith J. O’Neill Center of Marywood University, Scranton, Pa.

CORRESPONDENCE
Michael A. Krafczyk, MD, FAAFP, St. Luke’s Sports Medicine, 153 Brodhead Rd, Bethlehem, PA 18017; [email protected]

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

Posttraumatic stress disorder (PTSD) is a confusing diagnostic category because it includes victims of trauma as well as individuals exposed to trauma. Also, PTSD encompasses exposure to different types of trauma, which can have significant implications for symptom development and treatment.

Consider the treatment history of a male combat veteran who exhibits multiple PTSD symptoms, including nightmares, flashbacks, social isolation, anger, and guilt related to his war experiences. Several psychiatrists saw the patient, which resulted in multiple medication changes but little benefit. On further assessment, the practitioners noted that the veteran’s war experiences were minimally problematic; the prominent nightmares, ruminations, flashbacks, and guilt were related to his witnessing a civilian female being sexually assaulted. The veteran’s guilt about not intervening was the basis of his PTSD. This led to a change in treatment from pharmacotherapy to a focus on supportive therapy.

Conceptualizing subtypes of PTSD—similar to many DSM-IV-TR diagnoses such as phobias or delusional disorders—might help better define the diagnosis. Each sub-type, as conceptualized below, might have its own prognosis and treatment. Our hope is that this strategy will benefit the patient by improving research and evidence-based practice.

PTSD subtypes

Victim-related trauma. Related to witnessing a criminal act or being a victim of a criminal act such as rape or assault. The patient is in a passive role.

Natural disasters, such as a tornado, earthquake, or hurricane.

Survivor guilt. The patient is not a perpetrator and might have been exposed to trauma, but symptoms are related to surviving while others close to the patient did not.

Perpetrator guilt. It is debatable whether this should be a PTSD subtype but our experience suggests that this pattern severely complicates PTSD diagnosis and treatment. It often is not initially disclosed by patients but surfaces when treatment is not working despite a strong therapeutic alliance.

PTSD not otherwise specified. This subtype is typical in patients who were not directly involved in a traumatic event but experienced symptoms related to it. Examples include picking up dead bodies, cleaning up a tornado site, or observing siblings being beaten. This category also may reflect an unclear picture if no primary subtype accounts for the majority of symptoms.

Qualifiers

Individuals who previously have been exposed to trauma are more vulnerable to subsequent trauma. Experiencing ongoing multiple traumatic events—such as in military combat—can have a cumulative effect. Thus, identifying episodes of trauma also should be part of the PTSD assessment.

Single event. The patient is exposed to a single traumatic episode, such as being the victim of a crime.

Multiple events/single episode. The patient is exposed to repeated, related traumatic events. Examples include ongoing military combat or child abuse.

Multiple events. The patient is exposed to ≥2 separate traumatic events. A combination such as this might include a serious motor vehicle accident followed by a natural disaster.

As the diagnosis of PTSD evolves, utilizing subtypes and qualifiers might clarify treatment strategies because some subtypes might be more amenable to certain psychopharmacologic or psychotherapeutic treatment regimens.

Diagnostic confusion

Some researchers question whether traumatic stress causes PTSD syndrome,¹ whereas others recommend “tightening” the diagnostic criteria.² Concerns regarding PTSD diagnosis are multiple and include:

• the importance of ruling out malingering³
• the effects of different diagnostic criteria resulting in disparate prevalence rates
• emphasizing the importance of dysfunction as a criterion for PTSD.⁴

Conceptual inconsistencies in DSM-IV-TR diagnostic criteria also can lead to confusion. Although there is a category of arousal symptoms, Criterion B4 (intense psychological distress) and Criterion B5 (physiological reactivity) are listed as re-experiencing symptoms rather than arousal symptoms. Finally, the criteria presented do not follow a logical progression. Research suggests that re-experiencing symptoms do not lead to avoidance but result in arousal symptoms, which in turn trigger avoidance.⁵

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Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

[email protected]

Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

[email protected]

Chest pain is extremely common in children and adolescents—as many as 70% of healthy children experience chest pain. In most instances, following a thorough history and physical examination, no intervention is required.

The incidence of chest pain with a cardiac etiology is extraordinarily low, less than 1%. Patient and family histories and physical examination dictate when management by a general pediatrician is appropriate. First, determine through history if the child has exercise-induced pain. Patients with noncardiac chest pain often have sharp stabbing pain that lasts a few seconds to 1-2 minutes, and the pain is not associated with exercise.

Exercise-induced chest pain is concerning, but the most common cause is exercise-induced bronchospasm. Ask the child or adolescent to describe the painful episodes. If the patient says: “I run, and then I feel like there is an elephant sitting on my chest,” that should prompt referral to a cardiologist. In contrast, if the patient says: “I run, and I feel like I cannot breathe and/or I cough,” that is more likely exercise-induced asthma.

There are red flags in the history and physical examination that prompt referral of the child to a specialist. But keep in mind that overreferral is a concern. Many general pediatricians understandably are scared when a patient presents with chest pain, but most communities do not have the resources to support widespread referral nor is it warranted in most cases.

Anticipatory guidance is critical for pediatricians managing most children and adolescents with chest pain. Inform the typical patient with sharp, stabbing pain and the family members that such episodes are likely to continue in the future. The patient does not necessarily need to return or go to the emergency department every time the pain recurs.

In contrast, a patient with a history of exercise-induced chest pain or who reports passing out during exercise is more of a concern. Ask patients about any extreme fatigue associated with exercise that is different from what their peers experience. Also, children with an unexplained seizure disorder or a history of passing out after an emotional startle (from a loud noise) might have long QT syndrome. Referral to a specialist is warranted. Although Kawasaki disease is rare, consider it in your differential diagnosis; keep in mind that some patients might experience chest pain associated with Marfan syndrome.

In terms of family history, ask if any relatives were diagnosed with long QT syndrome or hypertrophic cardiomyopathy. Family history also is relevant if there were any unexpected or unexplained deaths before age 50 years. A family member who died of cardiac causes before age 50, especially in the absence of typical risk factors, is also a concern. Listen for a murmur, especially a murmur that gets louder when the patient stands. This feature could be consistent with hypertrophic cardiomyopathy.

I do not recommend an electrocardiogram for most patients with a history of sedentary chest pain because there is a high false-positive rate with this test. Also, I generally do not recommend exercise stress tests because they are not helpful in the setting of routine chest pain. For the minority of patients with true exercise-induced chest pain, however, these tests can be useful, but they should be ordered by a cardiologist.

Children's Healthcare of Atlanta provides a Pediatric Sudden Cardiac Death Risk Assessment Form online for any health care provider. This tool can be accessed at www.choa.org/default.aspx?id=7317

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

Results of the PLATO trial suggest the antiplatelet therapy ticagrelor is superior to clopidogrel in patients with acute coronary syndromes, with or without ST-segment elevation.

Ticagrelor significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in major bleeding.

Investigators published the results of the study in The New England Journal of Medicine.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12. It has a faster onset and greater platelet inhibition than clopidogrel, which also blocks the adenosine diphosphate receptor P2Y12, but irreversibly.

Lars Wallentin, MD, PhD, of Uppsala Clinical Research Center in Sweden, and his colleagues set out to ascertain whether ticagrelor is superior to clopidogrel for the prevention of vascular events and death.

They enrolled 18,624 patients from 862 centers in 43 countries from October 2006 through July 2008. They randomized the patients to receive 90 mg of ticagrelor twice daily after a loading dose of 180 mg, or 75 mg of clopidogrel after a 300 mg loading dose. Patients in both cohorts took 75-100 mg aspirin daily.

Baseline patient characteristics were similar in the 2 groups.

After a 12-month follow-up, investigators determined that patients in the ticagrelor group experienced significantly fewer deaths from vascular causes, myocardial infarction, or stroke (9.8%) than those in the clopidogrel group (11.7%; P<0.001). And the treatment effect was noticeable within the first 30 days.

Investigators also observed that ticagrelor significantly reduced myocardial infarction alone (5.8% vs 6.9%; P=0.005), death from vascular causes (4.0% vs 5.1%; P=0.001), and death from any cause (4.5% vs 5.9%; P<0.001).

However, ticagrelor did not reduce stroke alone compared to clopidogrel (P=0.22). And patients on tricagrelor experienced more hemorrhagic strokes than those on clopidogrel.

The investigators also determined that ticagrelor did not increase the rate of overall bleeding. However, it did increase the rate of non-procedure-related bleeding.

The investigators noted more dyspnea in the ticagrelor group than the clopidogrel group (14.2% vs 9.2%; P<0.001). The investigators pointed out that few patients dropped out of the study, however, because of dyspnea.

In an accompanying editorial, Albert Schömig, MD, of the Deutsches Herzzentrum München in Germany, emphasized that the absence of increased bleeding with ticagrelor “highlights the important advantage of reversibility in the mechanism of action of ticagrelor.”

Dr Schömig felt that the study would have been stronger, however, if ticagrelor had been administered for at least a year, if the clopidogrel loading dose had been used for all patients in that arm irrespective of whether they had previously been treated with clopidogrel, and if patients had used proton-pump inhibitors less frequently after randomization.

Nevertheless, Dr Schömig concluded that “efforts to develop new effective and safe antithrombotic drug regimens should not be discouraged by the perception that an increase in antithrombotic efficacy is necessarily associated with a higher risk of bleeding.”

The study was supported by AstraZeneca, the company developing ticagrelor. The drug is not yet on the market.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A 2-year noninferiority trial has shown dabigatran to be not inferior to warfarin in preventing stroke and systemic embolism in patients with atrial fibrillation. And the higher, 150 mg dose of dabigatran was shown to be superior to warfarin in preventing these outcomes.

Stuart J. Connolly, MD, at the Population Health Research Institute in Hamilton, Ontario, Canada, and colleagues report the results on behalf of the RE-LY Study Group in the August 30 edition of The New England Journal of Medicine.

The investigators enrolled 18,113 patients with atrial fibrillation from 951 clinical centers in 44 countries between December 2005 and December 2007. Patients were a mean age of 71 years, and 63.6% were men.

The investigators randomly assigned the patients to receive 110 mg or 150 mg of dabigatran twice daily, or to receive 1, 3, or 5 mg of warfarin to an INR of 2 to 3.

The investigators administered dabigatran in a blinded fashion and warfarin in an unblinded fashion.

After a median follow-up of 2 years, 182 patients on 110 mg dabigatran, 134 patients on 150 mg dabigatran, and 199 patients on warfarin had a stroke or embolism.

The investigators determined that both doses of dabigatran were noninferior to warfarin (P<0.001). And the 150 mg dose was superior to warfarin (P<0.001). However, the lower dose of dabigatran was not superior to warfarin.

Warfarin, however, produced a lower rate of myocardial infarction than dabigatran: 0.53% per year, compared to 0.72% per year in the 110 mg dabigatran group (P=0.07) and 0.74% in the 150 mg group (P=0.048). The investigators attribute this to the superior protection warfarin provides against coronary ischemic events.

The rate of major bleeding was lower with the 150 mg dose of dabigatran and significantly lower with the 110 mg dose compared to warfarin.

And rates of life-threatening bleeding, intracranial bleeding, and major or minor bleeding were all significantly lower with either dose of dabigatran than warfarin. However, the 150 mg dose of dabigatran produced a significantly higher rate of gastrointestinal bleeding than warfarin.

The investigators also compared the 2 doses of dabigatran and found the 150 mg dose significantly reduced the risk of stroke or systemic embolism compared to the 110 mg dose (P=0.005).

The investigators correlated the higher dose of dabigatran with a trend toward an increased risk of major, gastrointestinal, minor, and any bleeding. They calculated that “the net clinical benefit was almost identical for the two doses.”

Dyspepsia was the only adverse event that was significantly more common with dabigatran than with warfarin.

The investigators concluded that because dabigatran achieved a rate of intracranial hemorrhage a third less than the rate with warfarin without a reduction in stroke protection, this “suggests an important advantage of dabigatran.”

Dabigatran is a new oral direct thrombin inhibitor. It was approved in 2008 by the European Medicines Agency, the National Health Service in Britain, and Health Canada for hip and knee surgery patients.

RE-LY stands for Randomized Evaluation of Long-Term Anticoagulation Therapy.

The study was funded by Boehringer Ingelheim and was coordinated by the Population Health Research Institute in Hamilton, Ontario, Canada.

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”

A new report on how hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) spreads after patients are discharged has at least one hospitalist wondering whether HM could, or should, take a leading role in reducing MRSA transfers.

The study, "Carriage of Methicillin-Resistant Staphylococcus aureus in Home Care Settings," identified MRSA in 191 of the 1,501 patients (12.7%) who were screened before discharge from French hospitals in 2003 and 2004. Researchers reported that 19% of relatives and caretakers who came into contact with the patients identified with MRSA also acquired the bacteria (Arch Intern Med. 2009;169(15)1372-1378).

Hospitalist and infectious-disease specialist James Pile, MD, FACP, FHM, interim director of the Division of Hospital Medicine at CWRU/MetroHealth Medical Center in Cleveland, says the study might be most important for the questions it raises regarding the degree to which community-acquired MRSA (CA-MRSA) is colonizing household contacts of discharged patients, as the burden of clinical disease in those individuals is likely to be greater than in those colonized with traditional, healthcare-associated MRSA (HA-MRSA). CA-MRSA appears to be supplanting HA-MRSA in many hospitals, Dr. Pile says, and the simple intervention of more rigorous hand washing by caregivers and other household contacts of patients discharged with MRSA infections could help limit the associated fallout.

“This is a chance for healthcare professionals, and hospitalists specifically, to recognize that and to counsel that as patients leave the hospital,” Dr. Pile says.

The authors note that “because none of the household contacts who acquired MRSA developed an infection, it is unclear whether this transmission represents a serious health problem.”

To that end, Dr. Pile says HM should wait for more definitive studies before committing to potentially time-consuming QI projects focused on MRSA transmissions to the home. “Before hospitalists galvanize their resources to try to tackle this problem,” Dr. Pile says, “we want to make sure there is enough bang for the buck.”

Published research on hospitalist quality, cost-effectiveness, and other outcomes, such as a recent study in Archives of Internal Medicine (2009;169(15):1389-1394) that shows hospitalists achieve higher scores on three quality-of-care measures, can provide ammunition for HM leaders trying to justify their programs’ worth to hospital administrators, says one HM group leader.

In the study, Lenny Lopez, MD, MPH, and colleagues at Massachusetts General Hospital examined Hospital Quality Alliance data from 3,619 hospitals, 40% of which had hospitalists. They compared composite measures of quality of care for acute myocardial infarction, congestive heart failure, and pneumonia, and found that scores were higher for the hospitals with hospitalist programs.

Such studies help shed light on the central questions of hospitalists’ value, says Julia Wright, MD, FHM, head of the hospital medicine section at the University of Wisconsin in Madison. Initially, the question was whether the hospitalist model was even viable, which Dr. Wright believes has been laid to rest. The next questions involved efficiency and bottom-line issues—such as length of stay—and a strong case has been made overall for HM’s cost-effectiveness, she says. Quality of care has been harder to demonstrate, but newer quality measures make it easier to report, Dr. Wright adds.

Dr. Wright says the Lopez study, which highlights hospitalists’ ability to conform to guidelines, will be valuable to hospitalist groups. “We do talk with our administration about these questions, although we focus more on alignment of goals and mission, occasionally citing articles like this,” she says. “More important is to be aware of the core quality issues and have metrics of our own.”

Then again, programs just starting out might find the research essential, she says.

“Hospitalists participate in any number of quality initiatives,” Dr. Wright adds. “A lot of their data could be published and added to the small library of research on hospital medicine’s contributions to quality.”

Published research on hospitalist quality, cost-effectiveness, and other outcomes, such as a recent study in Archives of Internal Medicine (2009;169(15):1389-1394) that shows hospitalists achieve higher scores on three quality-of-care measures, can provide ammunition for HM leaders trying to justify their programs’ worth to hospital administrators, says one HM group leader.

In the study, Lenny Lopez, MD, MPH, and colleagues at Massachusetts General Hospital examined Hospital Quality Alliance data from 3,619 hospitals, 40% of which had hospitalists. They compared composite measures of quality of care for acute myocardial infarction, congestive heart failure, and pneumonia, and found that scores were higher for the hospitals with hospitalist programs.

Such studies help shed light on the central questions of hospitalists’ value, says Julia Wright, MD, FHM, head of the hospital medicine section at the University of Wisconsin in Madison. Initially, the question was whether the hospitalist model was even viable, which Dr. Wright believes has been laid to rest. The next questions involved efficiency and bottom-line issues—such as length of stay—and a strong case has been made overall for HM’s cost-effectiveness, she says. Quality of care has been harder to demonstrate, but newer quality measures make it easier to report, Dr. Wright adds.

Dr. Wright says the Lopez study, which highlights hospitalists’ ability to conform to guidelines, will be valuable to hospitalist groups. “We do talk with our administration about these questions, although we focus more on alignment of goals and mission, occasionally citing articles like this,” she says. “More important is to be aware of the core quality issues and have metrics of our own.”

Then again, programs just starting out might find the research essential, she says.

“Hospitalists participate in any number of quality initiatives,” Dr. Wright adds. “A lot of their data could be published and added to the small library of research on hospital medicine’s contributions to quality.”

Published research on hospitalist quality, cost-effectiveness, and other outcomes, such as a recent study in Archives of Internal Medicine (2009;169(15):1389-1394) that shows hospitalists achieve higher scores on three quality-of-care measures, can provide ammunition for HM leaders trying to justify their programs’ worth to hospital administrators, says one HM group leader.

In the study, Lenny Lopez, MD, MPH, and colleagues at Massachusetts General Hospital examined Hospital Quality Alliance data from 3,619 hospitals, 40% of which had hospitalists. They compared composite measures of quality of care for acute myocardial infarction, congestive heart failure, and pneumonia, and found that scores were higher for the hospitals with hospitalist programs.

Such studies help shed light on the central questions of hospitalists’ value, says Julia Wright, MD, FHM, head of the hospital medicine section at the University of Wisconsin in Madison. Initially, the question was whether the hospitalist model was even viable, which Dr. Wright believes has been laid to rest. The next questions involved efficiency and bottom-line issues—such as length of stay—and a strong case has been made overall for HM’s cost-effectiveness, she says. Quality of care has been harder to demonstrate, but newer quality measures make it easier to report, Dr. Wright adds.

Dr. Wright says the Lopez study, which highlights hospitalists’ ability to conform to guidelines, will be valuable to hospitalist groups. “We do talk with our administration about these questions, although we focus more on alignment of goals and mission, occasionally citing articles like this,” she says. “More important is to be aware of the core quality issues and have metrics of our own.”

Then again, programs just starting out might find the research essential, she says.

“Hospitalists participate in any number of quality initiatives,” Dr. Wright adds. “A lot of their data could be published and added to the small library of research on hospital medicine’s contributions to quality.”

New research suggests adolescents and young adults (AYAs) with leukemias and lymphomas are living longer than such patients did 2 decades ago.

However, their survival still lags behind survival in children. It even lags behind survival in older adults in the case of acute myeloblastic leukemia (AML).

Investigators reported these findings online August 24 ahead of the November 1 print edition of Cancer.

Dianne Pulte, MD, of the University of Medicine and Dentistry of New Jersey, and colleagues analyzed data from the Surveillance, Epidemiology and End Results (SEER) database to determine survival rates of young people with Hodgkin lymphoma, non-Hodgkin lymphoma (NHL), acute lymphoblastic leukemia (ALL), AML, and chronic myelocytic leukemia (CML).

They compared data from 1981–1985 with data from 2001–2005.

The investigators found that survival had improved significantly in each of the 5 malignancies. For AYAs with Hodgkin’s lymphoma, 10-year survival increased from 80.4% to 93.4%. For those with NHL, it increased from 55.6% to 76.2%; for those with ALL, from 30.5% to 52.1%; for those with AML, from 15.2% to 45.1%; and for those with CML, from 0% to 74.5%.

They analyzed the data further and found that the survival rate for young people with the lymphomas or CML had improved steadily over the 2 decades. And the survival rate was stable for patients with the acute leukemias during the late 1990s and early 21st century.

However, they found that survival in AYAs is still not as good as the survival rate for children with these hematologic malignancies, with the exception of patients with Hodgkin lymphoma. And survival in AYAs with AML lags behind survival in older adults.

The investigators acknowledge that improving survival rates for the AYA population is a major challenge. Dr Pulte suggests that “more research into how to treat these diseases and how to make sure that all patients have access to the best treatment is needed.”

New research suggests adolescents and young adults (AYAs) with leukemias and lymphomas are living longer than such patients did 2 decades ago.

However, their survival still lags behind survival in children. It even lags behind survival in older adults in the case of acute myeloblastic leukemia (AML).

Investigators reported these findings online August 24 ahead of the November 1 print edition of Cancer.

Dianne Pulte, MD, of the University of Medicine and Dentistry of New Jersey, and colleagues analyzed data from the Surveillance, Epidemiology and End Results (SEER) database to determine survival rates of young people with Hodgkin lymphoma, non-Hodgkin lymphoma (NHL), acute lymphoblastic leukemia (ALL), AML, and chronic myelocytic leukemia (CML).

They compared data from 1981–1985 with data from 2001–2005.

The investigators found that survival had improved significantly in each of the 5 malignancies. For AYAs with Hodgkin’s lymphoma, 10-year survival increased from 80.4% to 93.4%. For those with NHL, it increased from 55.6% to 76.2%; for those with ALL, from 30.5% to 52.1%; for those with AML, from 15.2% to 45.1%; and for those with CML, from 0% to 74.5%.

They analyzed the data further and found that the survival rate for young people with the lymphomas or CML had improved steadily over the 2 decades. And the survival rate was stable for patients with the acute leukemias during the late 1990s and early 21st century.

However, they found that survival in AYAs is still not as good as the survival rate for children with these hematologic malignancies, with the exception of patients with Hodgkin lymphoma. And survival in AYAs with AML lags behind survival in older adults.

The investigators acknowledge that improving survival rates for the AYA population is a major challenge. Dr Pulte suggests that “more research into how to treat these diseases and how to make sure that all patients have access to the best treatment is needed.”

New research suggests adolescents and young adults (AYAs) with leukemias and lymphomas are living longer than such patients did 2 decades ago.

However, their survival still lags behind survival in children. It even lags behind survival in older adults in the case of acute myeloblastic leukemia (AML).

Investigators reported these findings online August 24 ahead of the November 1 print edition of Cancer.

Dianne Pulte, MD, of the University of Medicine and Dentistry of New Jersey, and colleagues analyzed data from the Surveillance, Epidemiology and End Results (SEER) database to determine survival rates of young people with Hodgkin lymphoma, non-Hodgkin lymphoma (NHL), acute lymphoblastic leukemia (ALL), AML, and chronic myelocytic leukemia (CML).

They compared data from 1981–1985 with data from 2001–2005.

The investigators found that survival had improved significantly in each of the 5 malignancies. For AYAs with Hodgkin’s lymphoma, 10-year survival increased from 80.4% to 93.4%. For those with NHL, it increased from 55.6% to 76.2%; for those with ALL, from 30.5% to 52.1%; for those with AML, from 15.2% to 45.1%; and for those with CML, from 0% to 74.5%.

They analyzed the data further and found that the survival rate for young people with the lymphomas or CML had improved steadily over the 2 decades. And the survival rate was stable for patients with the acute leukemias during the late 1990s and early 21st century.

However, they found that survival in AYAs is still not as good as the survival rate for children with these hematologic malignancies, with the exception of patients with Hodgkin lymphoma. And survival in AYAs with AML lags behind survival in older adults.

The investigators acknowledge that improving survival rates for the AYA population is a major challenge. Dr Pulte suggests that “more research into how to treat these diseases and how to make sure that all patients have access to the best treatment is needed.”

Dr. Joel Gelfand discusses research concerning the use of biologics and lymphoma risk. Kerri Wachter of the Global Medical News Network (GMNN) reports from the American Academy of Dermatology's Academy 2009 meeting in Boston.

Dr. Joel Gelfand discusses research concerning the use of biologics and lymphoma risk. Kerri Wachter of the Global Medical News Network (GMNN) reports from the American Academy of Dermatology's Academy 2009 meeting in Boston.

Dr. Joel Gelfand discusses research concerning the use of biologics and lymphoma risk. Kerri Wachter of the Global Medical News Network (GMNN) reports from the American Academy of Dermatology's Academy 2009 meeting in Boston.

Endobronchial dysplasia significantly improved in former smokees who received oral iloprost during a phase II trial, says study investigator Dr. Robert Keith. Bob Finn of the Global Medical News Network (GMNN) reports from the World Conference on Lung Cancer in San Francisco.

Endobronchial dysplasia significantly improved in former smokees who received oral iloprost during a phase II trial, says study investigator Dr. Robert Keith. Bob Finn of the Global Medical News Network (GMNN) reports from the World Conference on Lung Cancer in San Francisco.

Endobronchial dysplasia significantly improved in former smokees who received oral iloprost during a phase II trial, says study investigator Dr. Robert Keith. Bob Finn of the Global Medical News Network (GMNN) reports from the World Conference on Lung Cancer in San Francisco.