Pulmonary Health Hub

Follow-up foul-up leads to metastatic disease

A PRECANCEROUS POLYP was found in the stomach of a 50-year-old man during diagnostic gastroscopy. The pathologist’s report noted that an adjacent or underlying malignant process could not be ruled out and recommended additional tissue sampling. Upon reading the report, the gastroenterologist who had performed the gastroscopy wrote that another biopsy should be done within a few months.

The patient was seen subsequently by his primary care physician, whose office note mentioned the precancerous biopsy findings and indicated that another biopsy was necessary; the physician also wrote that malignancy in the stomach would have to be ruled out eventually. The doctor’s plan called for a repeat gastroscopy to reevaluate the dysplastic polyp. However, neither the primary care physician nor the gastroenterologist took additional steps to order, perform, or refer the patient for a follow-up endoscopy and biopsy of the lesion.

Three years later, the patient developed difficulty swallowing and lost weight rapidly. Diagnostic testing revealed a malignant tumor, at the same location as the polyp, and malignant-appearing lymph nodes.

The patient received a feeding jejunostomy tube and underwent concomitant radiation and chemotherapy. Surgery was planned, but the disease metastasized and was deemed inoperable. Despite additional treatment, the patient died at age 54.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

DOCTORS’ DEFENSE The primary care physician argued that both he and the gastroenterologist were responsible for making sure the follow-up was done; the gastroenterologist claimed that the primary care physician was solely responsible for follow-up testing.

VERDICT $1.5 million Massachusetts settlement.

COMMENT Poor coordination of care and follow-up of results is a common source of malpractice actions. Keep a paper or electronic “tickler file” for important follow-up issues.

Unaddressed cardiovascular risks prove fatal

A 46-YEAR-OLD MAN went to the hospital, where he was seen by a family practitioner. The physician noted that the patient had a history of smoking, high cholesterol, and thyroid problems.

Early the following month, the patient died of cardiopulmonary arrest. Autopsy results showed arteriosclerotic disease, acute dissection of the coronary plaques, and left ventricular hypertrophy.

PLAINTIFF’S CLAIM The family practitioner failed to take a careful history and prescribe aspirin therapy and cholesterol-lowering medication. The patient should have been referred for a cardiac work-up.

DOCTOR’S DEFENSE The patient was advised of the importance of treatment to correct his condition.

VERDICT $575,000 Michigan settlement.

COMMENT I’m seeing a great increase in cases involving failure to address cardiovascular risk factors. Be sure to thoroughly document refusal of interventions or nonadherence.

Lack of surveillance delays lung cancer diagnosis

A 64-YEAR-OLD MAN was referred to a pulmonary specialist in January by his primary care physician after a computed tomography (CT) scan showed a spiculated density adjacent to the right main-stem bronchus and a prominent right hilar lymph node. The CT scan also revealed a noncalcified nodule in the right middle lobe.

Before examining the patient, the pulmonary specialist ordered a positron emission tomography (PET) scan, which he interpreted as showing no significant uptake and considered negative. He attributed the prominent lymph node to bronchitis and ordered surveillance at 3-month intervals.

A CT scan in May showed no change, but the radiologist noted that “the possibility of malignancy cannot be excluded.” When the patient saw the specialist in early June, the doctor recommended another CT scan in 3 months.

The patient did not return to the specialist until September of the following year. By that time, a CT scan taken a couple of months before (June) as part of preoperative clearance for knee surgery showed that the irregular mass had grown significantly since the CT scan in May of the previous year. A bronchoscopy done in September to evaluate the mass was negative. In November, however, a lymph node biopsy revealed that the patient had metastatic lung cancer. He died about a month later.

PLAINTIFF’S CLAIM Because the patient had a history of smoking and the CT scan revealed a density, the suspicion for cancer should have been high despite a negative PET scan. A specimen should have been obtained by thoracoscopy or thoracotomy to rule out cancer.

THE DEFENSE The pulmonary specialist followed the correct protocol; failure to diagnose cancer at the September visit didn’t affect the outcome because the cancer was already metastatic and incurable. The patient didn’t quit smoking or follow up regularly with his primary care physician. Moreover, the cancer was at least stage IIA when the primary care physician referred the patient to the specialist.

VERDICT Pennsylvania defense verdict.

COMMENT Although a defense verdict was ultimately returned, wouldn’t a “tickler file” or a reminder to the patient (and documentation if the patient failed to follow up as recommended) have been easier?

Follow-up foul-up leads to metastatic disease

A PRECANCEROUS POLYP was found in the stomach of a 50-year-old man during diagnostic gastroscopy. The pathologist’s report noted that an adjacent or underlying malignant process could not be ruled out and recommended additional tissue sampling. Upon reading the report, the gastroenterologist who had performed the gastroscopy wrote that another biopsy should be done within a few months.

The patient was seen subsequently by his primary care physician, whose office note mentioned the precancerous biopsy findings and indicated that another biopsy was necessary; the physician also wrote that malignancy in the stomach would have to be ruled out eventually. The doctor’s plan called for a repeat gastroscopy to reevaluate the dysplastic polyp. However, neither the primary care physician nor the gastroenterologist took additional steps to order, perform, or refer the patient for a follow-up endoscopy and biopsy of the lesion.

Three years later, the patient developed difficulty swallowing and lost weight rapidly. Diagnostic testing revealed a malignant tumor, at the same location as the polyp, and malignant-appearing lymph nodes.

The patient received a feeding jejunostomy tube and underwent concomitant radiation and chemotherapy. Surgery was planned, but the disease metastasized and was deemed inoperable. Despite additional treatment, the patient died at age 54.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

DOCTORS’ DEFENSE The primary care physician argued that both he and the gastroenterologist were responsible for making sure the follow-up was done; the gastroenterologist claimed that the primary care physician was solely responsible for follow-up testing.

VERDICT $1.5 million Massachusetts settlement.

COMMENT Poor coordination of care and follow-up of results is a common source of malpractice actions. Keep a paper or electronic “tickler file” for important follow-up issues.

Unaddressed cardiovascular risks prove fatal

A 46-YEAR-OLD MAN went to the hospital, where he was seen by a family practitioner. The physician noted that the patient had a history of smoking, high cholesterol, and thyroid problems.

Early the following month, the patient died of cardiopulmonary arrest. Autopsy results showed arteriosclerotic disease, acute dissection of the coronary plaques, and left ventricular hypertrophy.

PLAINTIFF’S CLAIM The family practitioner failed to take a careful history and prescribe aspirin therapy and cholesterol-lowering medication. The patient should have been referred for a cardiac work-up.

DOCTOR’S DEFENSE The patient was advised of the importance of treatment to correct his condition.

VERDICT $575,000 Michigan settlement.

COMMENT I’m seeing a great increase in cases involving failure to address cardiovascular risk factors. Be sure to thoroughly document refusal of interventions or nonadherence.

Lack of surveillance delays lung cancer diagnosis

A 64-YEAR-OLD MAN was referred to a pulmonary specialist in January by his primary care physician after a computed tomography (CT) scan showed a spiculated density adjacent to the right main-stem bronchus and a prominent right hilar lymph node. The CT scan also revealed a noncalcified nodule in the right middle lobe.

Before examining the patient, the pulmonary specialist ordered a positron emission tomography (PET) scan, which he interpreted as showing no significant uptake and considered negative. He attributed the prominent lymph node to bronchitis and ordered surveillance at 3-month intervals.

A CT scan in May showed no change, but the radiologist noted that “the possibility of malignancy cannot be excluded.” When the patient saw the specialist in early June, the doctor recommended another CT scan in 3 months.

The patient did not return to the specialist until September of the following year. By that time, a CT scan taken a couple of months before (June) as part of preoperative clearance for knee surgery showed that the irregular mass had grown significantly since the CT scan in May of the previous year. A bronchoscopy done in September to evaluate the mass was negative. In November, however, a lymph node biopsy revealed that the patient had metastatic lung cancer. He died about a month later.

PLAINTIFF’S CLAIM Because the patient had a history of smoking and the CT scan revealed a density, the suspicion for cancer should have been high despite a negative PET scan. A specimen should have been obtained by thoracoscopy or thoracotomy to rule out cancer.

THE DEFENSE The pulmonary specialist followed the correct protocol; failure to diagnose cancer at the September visit didn’t affect the outcome because the cancer was already metastatic and incurable. The patient didn’t quit smoking or follow up regularly with his primary care physician. Moreover, the cancer was at least stage IIA when the primary care physician referred the patient to the specialist.

VERDICT Pennsylvania defense verdict.

COMMENT Although a defense verdict was ultimately returned, wouldn’t a “tickler file” or a reminder to the patient (and documentation if the patient failed to follow up as recommended) have been easier?

Follow-up foul-up leads to metastatic disease

A PRECANCEROUS POLYP was found in the stomach of a 50-year-old man during diagnostic gastroscopy. The pathologist’s report noted that an adjacent or underlying malignant process could not be ruled out and recommended additional tissue sampling. Upon reading the report, the gastroenterologist who had performed the gastroscopy wrote that another biopsy should be done within a few months.

The patient was seen subsequently by his primary care physician, whose office note mentioned the precancerous biopsy findings and indicated that another biopsy was necessary; the physician also wrote that malignancy in the stomach would have to be ruled out eventually. The doctor’s plan called for a repeat gastroscopy to reevaluate the dysplastic polyp. However, neither the primary care physician nor the gastroenterologist took additional steps to order, perform, or refer the patient for a follow-up endoscopy and biopsy of the lesion.

Three years later, the patient developed difficulty swallowing and lost weight rapidly. Diagnostic testing revealed a malignant tumor, at the same location as the polyp, and malignant-appearing lymph nodes.

The patient received a feeding jejunostomy tube and underwent concomitant radiation and chemotherapy. Surgery was planned, but the disease metastasized and was deemed inoperable. Despite additional treatment, the patient died at age 54.

PLAINTIFF’S CLAIM No information about the plaintiff’s claim is available.

DOCTORS’ DEFENSE The primary care physician argued that both he and the gastroenterologist were responsible for making sure the follow-up was done; the gastroenterologist claimed that the primary care physician was solely responsible for follow-up testing.

VERDICT $1.5 million Massachusetts settlement.

COMMENT Poor coordination of care and follow-up of results is a common source of malpractice actions. Keep a paper or electronic “tickler file” for important follow-up issues.

Unaddressed cardiovascular risks prove fatal

A 46-YEAR-OLD MAN went to the hospital, where he was seen by a family practitioner. The physician noted that the patient had a history of smoking, high cholesterol, and thyroid problems.

Early the following month, the patient died of cardiopulmonary arrest. Autopsy results showed arteriosclerotic disease, acute dissection of the coronary plaques, and left ventricular hypertrophy.

PLAINTIFF’S CLAIM The family practitioner failed to take a careful history and prescribe aspirin therapy and cholesterol-lowering medication. The patient should have been referred for a cardiac work-up.

DOCTOR’S DEFENSE The patient was advised of the importance of treatment to correct his condition.

VERDICT $575,000 Michigan settlement.

COMMENT I’m seeing a great increase in cases involving failure to address cardiovascular risk factors. Be sure to thoroughly document refusal of interventions or nonadherence.

Lack of surveillance delays lung cancer diagnosis

A 64-YEAR-OLD MAN was referred to a pulmonary specialist in January by his primary care physician after a computed tomography (CT) scan showed a spiculated density adjacent to the right main-stem bronchus and a prominent right hilar lymph node. The CT scan also revealed a noncalcified nodule in the right middle lobe.

Before examining the patient, the pulmonary specialist ordered a positron emission tomography (PET) scan, which he interpreted as showing no significant uptake and considered negative. He attributed the prominent lymph node to bronchitis and ordered surveillance at 3-month intervals.

A CT scan in May showed no change, but the radiologist noted that “the possibility of malignancy cannot be excluded.” When the patient saw the specialist in early June, the doctor recommended another CT scan in 3 months.

The patient did not return to the specialist until September of the following year. By that time, a CT scan taken a couple of months before (June) as part of preoperative clearance for knee surgery showed that the irregular mass had grown significantly since the CT scan in May of the previous year. A bronchoscopy done in September to evaluate the mass was negative. In November, however, a lymph node biopsy revealed that the patient had metastatic lung cancer. He died about a month later.

PLAINTIFF’S CLAIM Because the patient had a history of smoking and the CT scan revealed a density, the suspicion for cancer should have been high despite a negative PET scan. A specimen should have been obtained by thoracoscopy or thoracotomy to rule out cancer.

THE DEFENSE The pulmonary specialist followed the correct protocol; failure to diagnose cancer at the September visit didn’t affect the outcome because the cancer was already metastatic and incurable. The patient didn’t quit smoking or follow up regularly with his primary care physician. Moreover, the cancer was at least stage IIA when the primary care physician referred the patient to the specialist.

VERDICT Pennsylvania defense verdict.

COMMENT Although a defense verdict was ultimately returned, wouldn’t a “tickler file” or a reminder to the patient (and documentation if the patient failed to follow up as recommended) have been easier?

SAN DIEGO — Postoperative pneumonia is an uncommon complication with daunting morbidity and mortality—and a fair number of previously unrecognized modifiable preoperative risk factors, according to a large national study.

The analysis involved prospectively collected data on more than 200,000 inpatient and outpatient operations in 2007 at 183 representative U.S. hospitals that participated in the American College of Surgeons' National Surgical Quality Improvement Program (NSQIP).

The incidence of postoperative pneumonia was 2.0%, with a 30-day mortality of 17.0%, as compared with 1.5% in individuals who did not develop the pulmonary infection, Dr. Himani Gupta reported at the annual meeting of the American College of Chest Physicians.

Complications associated with postoperative pneumonia included failure to wean from mechanical ventilation in 51% of cases, reintubation in 33%, septic shock in 33%, renal failure in 8%, deep venous thrombosis in 7%, blood transfusion in 5%, and cardiac arrest in 5%. The rates of each of these complications in patients without postoperative pneumonia were 1% or less, added Dr. Gupta of Creighton University, Omaha.

The NSQIP collects data on well over 100 variables per case, making it possible to use detailed multivariate logistic regression analyses to identify independent preoperative predictors of postoperative pneumonia.

Some of these risk factors were not modifiable, including inpatient status, which was associated with a 5.9-fold risk, male gender (1.5), emergency surgery (1.4), hypertension requiring medication (1.2), and a bleeding disorder (1.2).

However, other significant risk factors identified in the study could be amenable to preoperative risk optimization. For example, preoperative sepsis was associated with a 1.3-fold risk of postoperative pneumonia, worsening functional status conferred a 1.6-fold risk, and weight loss greater than 10% was associated with a 1.3-fold risk, she said.

In terms of risk factors related to neurologic status, quadriplegia was associated with a 1.8-fold risk of postoperative pneumonia. However, neither a history of a cerebrovascular accident nor an altered sensorium was linked to increased risk.

Unexpectedly, a history of heart failure or ventilator dependence within 48 hours prior to surgery was associated with significant 20%-30% decreased risks of postoperative pneumonia, Dr. Gupta observed.

Risk factors for postoperative pneumonia identified in prior small single-center studies, and confirmed in this vastly larger experience, included smoking, dyspnea, chronic obstructive pulmonary disease, and increased alcohol intake, each associated with a 1.2- to 1.5-fold increased risk.

There is a common assumption that obesity increases the risk of postoperative pulmonary complications. Not so in the NSQIP database.

The incidence of postoperative pneumonia was 2.4% in patients with a body mass index less than 25 kg/m

Dr. Gupta indicated that she and her coworkers are now in the midst of additional analyses looking more specifically at patients with a BMI of 18 or less, along with a new comparator group composed of patients with a BMI of 25-30.

Age was an independent risk factor for postoperative pneumonia. The incidence was 0.5% in patients under age 40 years, 1.3% in those aged 40-60 years, 2.7% in patients aged 60-80 years, and 4.5% in those older than 80 years.

The multivariate adjusted risk was 1.3-fold greater in patients aged 40-60 years than in those younger than 40, 1.3-fold greater in those aged 60-80 years than in patients aged 40-60, and 1.3-fold more in those over age 80 than in 60- to 80-year-olds.

The incidence of postoperative pneumonia varied markedly according to the organ addressed in the surgery. Low-risk operations—each with less than a 1% incidence of postoperative pneumonia—included anorectal, appendix, adrenal, bariatric, breast, ob.gyn., hernia, spleen, ENT/neck, spine, vein, and urologic surgery.

The high-risk procedures included nonesophageal thoracic surgery, which had a 3.8-fold risk of postoperative pneumonia, compared with the low-risk operations, and aortic (2.6), intestinal (2.5), brain (2.9), foregut and hepatopancreatobiliary (4.1), and other abdominal operations (2.1).

Disclosures: Dr. Gupta reported having no financial conflicts that were relevant to her study.

Adjusted risk was 1.2 times as great in patients with a BMI below 25 as in those with a BMI of 25-40 or 40-60.

Source DR. GUPTA

SAN DIEGO — Postoperative pneumonia is an uncommon complication with daunting morbidity and mortality—and a fair number of previously unrecognized modifiable preoperative risk factors, according to a large national study.

The analysis involved prospectively collected data on more than 200,000 inpatient and outpatient operations in 2007 at 183 representative U.S. hospitals that participated in the American College of Surgeons' National Surgical Quality Improvement Program (NSQIP).

The incidence of postoperative pneumonia was 2.0%, with a 30-day mortality of 17.0%, as compared with 1.5% in individuals who did not develop the pulmonary infection, Dr. Himani Gupta reported at the annual meeting of the American College of Chest Physicians.

Complications associated with postoperative pneumonia included failure to wean from mechanical ventilation in 51% of cases, reintubation in 33%, septic shock in 33%, renal failure in 8%, deep venous thrombosis in 7%, blood transfusion in 5%, and cardiac arrest in 5%. The rates of each of these complications in patients without postoperative pneumonia were 1% or less, added Dr. Gupta of Creighton University, Omaha.

The NSQIP collects data on well over 100 variables per case, making it possible to use detailed multivariate logistic regression analyses to identify independent preoperative predictors of postoperative pneumonia.

Some of these risk factors were not modifiable, including inpatient status, which was associated with a 5.9-fold risk, male gender (1.5), emergency surgery (1.4), hypertension requiring medication (1.2), and a bleeding disorder (1.2).

However, other significant risk factors identified in the study could be amenable to preoperative risk optimization. For example, preoperative sepsis was associated with a 1.3-fold risk of postoperative pneumonia, worsening functional status conferred a 1.6-fold risk, and weight loss greater than 10% was associated with a 1.3-fold risk, she said.

In terms of risk factors related to neurologic status, quadriplegia was associated with a 1.8-fold risk of postoperative pneumonia. However, neither a history of a cerebrovascular accident nor an altered sensorium was linked to increased risk.

Unexpectedly, a history of heart failure or ventilator dependence within 48 hours prior to surgery was associated with significant 20%-30% decreased risks of postoperative pneumonia, Dr. Gupta observed.

Risk factors for postoperative pneumonia identified in prior small single-center studies, and confirmed in this vastly larger experience, included smoking, dyspnea, chronic obstructive pulmonary disease, and increased alcohol intake, each associated with a 1.2- to 1.5-fold increased risk.

There is a common assumption that obesity increases the risk of postoperative pulmonary complications. Not so in the NSQIP database.

The incidence of postoperative pneumonia was 2.4% in patients with a body mass index less than 25 kg/m

Dr. Gupta indicated that she and her coworkers are now in the midst of additional analyses looking more specifically at patients with a BMI of 18 or less, along with a new comparator group composed of patients with a BMI of 25-30.

Age was an independent risk factor for postoperative pneumonia. The incidence was 0.5% in patients under age 40 years, 1.3% in those aged 40-60 years, 2.7% in patients aged 60-80 years, and 4.5% in those older than 80 years.

The multivariate adjusted risk was 1.3-fold greater in patients aged 40-60 years than in those younger than 40, 1.3-fold greater in those aged 60-80 years than in patients aged 40-60, and 1.3-fold more in those over age 80 than in 60- to 80-year-olds.

The incidence of postoperative pneumonia varied markedly according to the organ addressed in the surgery. Low-risk operations—each with less than a 1% incidence of postoperative pneumonia—included anorectal, appendix, adrenal, bariatric, breast, ob.gyn., hernia, spleen, ENT/neck, spine, vein, and urologic surgery.

The high-risk procedures included nonesophageal thoracic surgery, which had a 3.8-fold risk of postoperative pneumonia, compared with the low-risk operations, and aortic (2.6), intestinal (2.5), brain (2.9), foregut and hepatopancreatobiliary (4.1), and other abdominal operations (2.1).

Disclosures: Dr. Gupta reported having no financial conflicts that were relevant to her study.

Adjusted risk was 1.2 times as great in patients with a BMI below 25 as in those with a BMI of 25-40 or 40-60.

Source DR. GUPTA

SAN DIEGO — Postoperative pneumonia is an uncommon complication with daunting morbidity and mortality—and a fair number of previously unrecognized modifiable preoperative risk factors, according to a large national study.

The analysis involved prospectively collected data on more than 200,000 inpatient and outpatient operations in 2007 at 183 representative U.S. hospitals that participated in the American College of Surgeons' National Surgical Quality Improvement Program (NSQIP).

The incidence of postoperative pneumonia was 2.0%, with a 30-day mortality of 17.0%, as compared with 1.5% in individuals who did not develop the pulmonary infection, Dr. Himani Gupta reported at the annual meeting of the American College of Chest Physicians.

Complications associated with postoperative pneumonia included failure to wean from mechanical ventilation in 51% of cases, reintubation in 33%, septic shock in 33%, renal failure in 8%, deep venous thrombosis in 7%, blood transfusion in 5%, and cardiac arrest in 5%. The rates of each of these complications in patients without postoperative pneumonia were 1% or less, added Dr. Gupta of Creighton University, Omaha.

The NSQIP collects data on well over 100 variables per case, making it possible to use detailed multivariate logistic regression analyses to identify independent preoperative predictors of postoperative pneumonia.

Some of these risk factors were not modifiable, including inpatient status, which was associated with a 5.9-fold risk, male gender (1.5), emergency surgery (1.4), hypertension requiring medication (1.2), and a bleeding disorder (1.2).

However, other significant risk factors identified in the study could be amenable to preoperative risk optimization. For example, preoperative sepsis was associated with a 1.3-fold risk of postoperative pneumonia, worsening functional status conferred a 1.6-fold risk, and weight loss greater than 10% was associated with a 1.3-fold risk, she said.

In terms of risk factors related to neurologic status, quadriplegia was associated with a 1.8-fold risk of postoperative pneumonia. However, neither a history of a cerebrovascular accident nor an altered sensorium was linked to increased risk.

Unexpectedly, a history of heart failure or ventilator dependence within 48 hours prior to surgery was associated with significant 20%-30% decreased risks of postoperative pneumonia, Dr. Gupta observed.

Risk factors for postoperative pneumonia identified in prior small single-center studies, and confirmed in this vastly larger experience, included smoking, dyspnea, chronic obstructive pulmonary disease, and increased alcohol intake, each associated with a 1.2- to 1.5-fold increased risk.

There is a common assumption that obesity increases the risk of postoperative pulmonary complications. Not so in the NSQIP database.

The incidence of postoperative pneumonia was 2.4% in patients with a body mass index less than 25 kg/m

Dr. Gupta indicated that she and her coworkers are now in the midst of additional analyses looking more specifically at patients with a BMI of 18 or less, along with a new comparator group composed of patients with a BMI of 25-30.

Age was an independent risk factor for postoperative pneumonia. The incidence was 0.5% in patients under age 40 years, 1.3% in those aged 40-60 years, 2.7% in patients aged 60-80 years, and 4.5% in those older than 80 years.

The multivariate adjusted risk was 1.3-fold greater in patients aged 40-60 years than in those younger than 40, 1.3-fold greater in those aged 60-80 years than in patients aged 40-60, and 1.3-fold more in those over age 80 than in 60- to 80-year-olds.

The incidence of postoperative pneumonia varied markedly according to the organ addressed in the surgery. Low-risk operations—each with less than a 1% incidence of postoperative pneumonia—included anorectal, appendix, adrenal, bariatric, breast, ob.gyn., hernia, spleen, ENT/neck, spine, vein, and urologic surgery.

The high-risk procedures included nonesophageal thoracic surgery, which had a 3.8-fold risk of postoperative pneumonia, compared with the low-risk operations, and aortic (2.6), intestinal (2.5), brain (2.9), foregut and hepatopancreatobiliary (4.1), and other abdominal operations (2.1).

Disclosures: Dr. Gupta reported having no financial conflicts that were relevant to her study.

Adjusted risk was 1.2 times as great in patients with a BMI below 25 as in those with a BMI of 25-40 or 40-60.

Source DR. GUPTA

ORLANDO — Both the indication and the incidence of adenotonsillar procedures in children have changed, according to Dr. Laura Orvidas.

“We seem to do more adenotonsillectomies for sleep-disordered breathing than we have in the past,” she said at the combined sections meeting of the Triological Society.

To evaluate changes in the incidence and indications for tonsillectomy and adenotonsillectomy, Dr. Orvidas of the Mayo Clinic in Rochester, Minn., reviewed data from the Mayo Clinic's database for a 35-year period between 1970 and 2005. The study population included 8,106 tonsillectomy and/or adenotonsillectomy patients aged 6 months to 29 years (mean age, 10.5 years).

The most interesting finding was the change in surgical indications for all procedures, said Dr. Orvidas: “Early on we were treating mostly for infection, and now it seems to be mostly for upper airway obstruction.” In 1970, treatment of infection accounted for approximately 90% of either adenotonsillectomies or tonsillectomies, while upper airway obstruction accounted for about 10%. In 2005, upper airway obstruction accounted for more than half of the indications for both procedures, while infection accounted for about 25% and a combination of both upper airway obstruction and infection accounted for approximately 20%.

The incidence of tonsillectomy or adenotonsillectomy was 369/100,000 person-years during the period from 1970 to 1974, compared with 642/100,000 person-years from 2001 to 2005, Dr. Orvidas said. Sixty-five percent of the tonsillectomy patients, 48% of the adenotonsillectomy patients, and 55% of the patients for both conditions were female.

“Neither the indication nor the incidence for adenotonsillar surgery has been static,” Dr. Orvidas noted at the meeting, jointly sponsored by the Triological Society and the American College of Surgeons.

Adenotonsillectomy incidence increased more than tonsillectomy incidence overall, although there was a high density of tonsillectomies in adolescent females, she said. For tonsillectomy alone, the mean age across the entire study period was 16 years vs. a mean of 7 years for adenotonsillectomy.

Dr. Orvidas also noted an increase in both adenotonsillectomy and tonsillectomy procedures for younger males. The possible reasons for these two trends were not addressed in the Mayo Clinic study.

Disclosures: Dr. Orvidas said she had no financial conflicts to disclose.

ORLANDO — Both the indication and the incidence of adenotonsillar procedures in children have changed, according to Dr. Laura Orvidas.

“We seem to do more adenotonsillectomies for sleep-disordered breathing than we have in the past,” she said at the combined sections meeting of the Triological Society.

To evaluate changes in the incidence and indications for tonsillectomy and adenotonsillectomy, Dr. Orvidas of the Mayo Clinic in Rochester, Minn., reviewed data from the Mayo Clinic's database for a 35-year period between 1970 and 2005. The study population included 8,106 tonsillectomy and/or adenotonsillectomy patients aged 6 months to 29 years (mean age, 10.5 years).

The most interesting finding was the change in surgical indications for all procedures, said Dr. Orvidas: “Early on we were treating mostly for infection, and now it seems to be mostly for upper airway obstruction.” In 1970, treatment of infection accounted for approximately 90% of either adenotonsillectomies or tonsillectomies, while upper airway obstruction accounted for about 10%. In 2005, upper airway obstruction accounted for more than half of the indications for both procedures, while infection accounted for about 25% and a combination of both upper airway obstruction and infection accounted for approximately 20%.

The incidence of tonsillectomy or adenotonsillectomy was 369/100,000 person-years during the period from 1970 to 1974, compared with 642/100,000 person-years from 2001 to 2005, Dr. Orvidas said. Sixty-five percent of the tonsillectomy patients, 48% of the adenotonsillectomy patients, and 55% of the patients for both conditions were female.

“Neither the indication nor the incidence for adenotonsillar surgery has been static,” Dr. Orvidas noted at the meeting, jointly sponsored by the Triological Society and the American College of Surgeons.

Adenotonsillectomy incidence increased more than tonsillectomy incidence overall, although there was a high density of tonsillectomies in adolescent females, she said. For tonsillectomy alone, the mean age across the entire study period was 16 years vs. a mean of 7 years for adenotonsillectomy.

Dr. Orvidas also noted an increase in both adenotonsillectomy and tonsillectomy procedures for younger males. The possible reasons for these two trends were not addressed in the Mayo Clinic study.

Disclosures: Dr. Orvidas said she had no financial conflicts to disclose.

ORLANDO — Both the indication and the incidence of adenotonsillar procedures in children have changed, according to Dr. Laura Orvidas.

“We seem to do more adenotonsillectomies for sleep-disordered breathing than we have in the past,” she said at the combined sections meeting of the Triological Society.

To evaluate changes in the incidence and indications for tonsillectomy and adenotonsillectomy, Dr. Orvidas of the Mayo Clinic in Rochester, Minn., reviewed data from the Mayo Clinic's database for a 35-year period between 1970 and 2005. The study population included 8,106 tonsillectomy and/or adenotonsillectomy patients aged 6 months to 29 years (mean age, 10.5 years).

The most interesting finding was the change in surgical indications for all procedures, said Dr. Orvidas: “Early on we were treating mostly for infection, and now it seems to be mostly for upper airway obstruction.” In 1970, treatment of infection accounted for approximately 90% of either adenotonsillectomies or tonsillectomies, while upper airway obstruction accounted for about 10%. In 2005, upper airway obstruction accounted for more than half of the indications for both procedures, while infection accounted for about 25% and a combination of both upper airway obstruction and infection accounted for approximately 20%.

The incidence of tonsillectomy or adenotonsillectomy was 369/100,000 person-years during the period from 1970 to 1974, compared with 642/100,000 person-years from 2001 to 2005, Dr. Orvidas said. Sixty-five percent of the tonsillectomy patients, 48% of the adenotonsillectomy patients, and 55% of the patients for both conditions were female.

“Neither the indication nor the incidence for adenotonsillar surgery has been static,” Dr. Orvidas noted at the meeting, jointly sponsored by the Triological Society and the American College of Surgeons.

Adenotonsillectomy incidence increased more than tonsillectomy incidence overall, although there was a high density of tonsillectomies in adolescent females, she said. For tonsillectomy alone, the mean age across the entire study period was 16 years vs. a mean of 7 years for adenotonsillectomy.

Dr. Orvidas also noted an increase in both adenotonsillectomy and tonsillectomy procedures for younger males. The possible reasons for these two trends were not addressed in the Mayo Clinic study.

Disclosures: Dr. Orvidas said she had no financial conflicts to disclose.

Estrogen-only hormone therapy has been shown to increase the risk of developing asthma after menopause by 54% among postmenopausal women compared with those never treated with HT, according to a new analysis.

Researchers at the National Instituto of Public Health, Cuernavaca, Mexico, and INSERM and the Université Paris-Sud, France, used data from the E3N cohort, a health survey of nearly 100,000 French women born between 1925 and 1950. The women, mostly teachers, responded to biannual questionnaires between 1990 and 2002 (Thorax 2010 Feb. 8 [doi:10.1136/thx.2009.116079]).

Of the 57,664 women free of asthma at menopause, just under two-thirds used some sort of HT, and 569 were later diagnosed with asthma. The study, led by Dr. Isabelle Romieu of the Mexican institute, found that “the increased risk of asthma onset among women using [HT] was present only in users of estrogen alone [hazard ratio 1.54]. The effect was observed only in recent users including current users and women for whom time since last use was <1.5 years.”

Moreover, the authors wrote, “Fifty-eight percent of women reporting the use of estrogen alone at the time of asthma onset or as last treatment before asthma onset had previously used another [HT]. This supports our finding that the increased risk of asthma onset is linked to estrogen use.”

The authors found the risk of developing asthma increased to 80% and 86% (hazard ratios of 1.80 and 1.86), respectively, among postmenopausal women treated with estrogen-only HT who never smoked or had a history of allergies before menopause, compared with untreated women. The authors cautioned, however, that the allergy histories were self-reported and that potential misclassifications of allergic disease could have occurred.

The apparently lower susceptibility of HT-treated women who smoke or have smoked to postmenopausal asthma, the authors said, had been noted in earlier studies. “This might be due to the antioestrogenic effect of smoking or to the difficulty of isolating the additional effect of [HT] among smokers,” they wrote.

Female hormones have long been suspected to play a role in the development of asthma, and the connection between HT and postmenopausal asthma had been investigated in a large-scale U.S. study published in 2004 (Arch. Int. Med. 2004;164:379-86). That study determined that recent HT treatment was linked to an increased risk of postmenopausal patients developing asthma. But it found the risk to be similar whether patients were treated with estrogen only, or a combination therapy.

Dr. Romieu and colleagues offered as a possible explanation for the disparity the fact that French and American physicians generally use different ratios of estrogen and progestin, as well as different types of progestin, in HT treatment regimens.

Also in contrast to the earlier U.S. study, Dr. Romieu's team did not observe interactions between body mass index and risk of asthma among HT and non-HT patients following menopause, but stated that this may have been because the French cohort presented leaner body mass as a whole.

Disclosures: The study investigators reported no financial conflicts of interest.

Estrogen-only hormone therapy has been shown to increase the risk of developing asthma after menopause by 54% among postmenopausal women compared with those never treated with HT, according to a new analysis.

Researchers at the National Instituto of Public Health, Cuernavaca, Mexico, and INSERM and the Université Paris-Sud, France, used data from the E3N cohort, a health survey of nearly 100,000 French women born between 1925 and 1950. The women, mostly teachers, responded to biannual questionnaires between 1990 and 2002 (Thorax 2010 Feb. 8 [doi:10.1136/thx.2009.116079]).

Of the 57,664 women free of asthma at menopause, just under two-thirds used some sort of HT, and 569 were later diagnosed with asthma. The study, led by Dr. Isabelle Romieu of the Mexican institute, found that “the increased risk of asthma onset among women using [HT] was present only in users of estrogen alone [hazard ratio 1.54]. The effect was observed only in recent users including current users and women for whom time since last use was <1.5 years.”

Moreover, the authors wrote, “Fifty-eight percent of women reporting the use of estrogen alone at the time of asthma onset or as last treatment before asthma onset had previously used another [HT]. This supports our finding that the increased risk of asthma onset is linked to estrogen use.”

The authors found the risk of developing asthma increased to 80% and 86% (hazard ratios of 1.80 and 1.86), respectively, among postmenopausal women treated with estrogen-only HT who never smoked or had a history of allergies before menopause, compared with untreated women. The authors cautioned, however, that the allergy histories were self-reported and that potential misclassifications of allergic disease could have occurred.

The apparently lower susceptibility of HT-treated women who smoke or have smoked to postmenopausal asthma, the authors said, had been noted in earlier studies. “This might be due to the antioestrogenic effect of smoking or to the difficulty of isolating the additional effect of [HT] among smokers,” they wrote.

Female hormones have long been suspected to play a role in the development of asthma, and the connection between HT and postmenopausal asthma had been investigated in a large-scale U.S. study published in 2004 (Arch. Int. Med. 2004;164:379-86). That study determined that recent HT treatment was linked to an increased risk of postmenopausal patients developing asthma. But it found the risk to be similar whether patients were treated with estrogen only, or a combination therapy.

Dr. Romieu and colleagues offered as a possible explanation for the disparity the fact that French and American physicians generally use different ratios of estrogen and progestin, as well as different types of progestin, in HT treatment regimens.

Also in contrast to the earlier U.S. study, Dr. Romieu's team did not observe interactions between body mass index and risk of asthma among HT and non-HT patients following menopause, but stated that this may have been because the French cohort presented leaner body mass as a whole.

Disclosures: The study investigators reported no financial conflicts of interest.

Estrogen-only hormone therapy has been shown to increase the risk of developing asthma after menopause by 54% among postmenopausal women compared with those never treated with HT, according to a new analysis.

Researchers at the National Instituto of Public Health, Cuernavaca, Mexico, and INSERM and the Université Paris-Sud, France, used data from the E3N cohort, a health survey of nearly 100,000 French women born between 1925 and 1950. The women, mostly teachers, responded to biannual questionnaires between 1990 and 2002 (Thorax 2010 Feb. 8 [doi:10.1136/thx.2009.116079]).

Of the 57,664 women free of asthma at menopause, just under two-thirds used some sort of HT, and 569 were later diagnosed with asthma. The study, led by Dr. Isabelle Romieu of the Mexican institute, found that “the increased risk of asthma onset among women using [HT] was present only in users of estrogen alone [hazard ratio 1.54]. The effect was observed only in recent users including current users and women for whom time since last use was <1.5 years.”

Moreover, the authors wrote, “Fifty-eight percent of women reporting the use of estrogen alone at the time of asthma onset or as last treatment before asthma onset had previously used another [HT]. This supports our finding that the increased risk of asthma onset is linked to estrogen use.”

The authors found the risk of developing asthma increased to 80% and 86% (hazard ratios of 1.80 and 1.86), respectively, among postmenopausal women treated with estrogen-only HT who never smoked or had a history of allergies before menopause, compared with untreated women. The authors cautioned, however, that the allergy histories were self-reported and that potential misclassifications of allergic disease could have occurred.

The apparently lower susceptibility of HT-treated women who smoke or have smoked to postmenopausal asthma, the authors said, had been noted in earlier studies. “This might be due to the antioestrogenic effect of smoking or to the difficulty of isolating the additional effect of [HT] among smokers,” they wrote.

Female hormones have long been suspected to play a role in the development of asthma, and the connection between HT and postmenopausal asthma had been investigated in a large-scale U.S. study published in 2004 (Arch. Int. Med. 2004;164:379-86). That study determined that recent HT treatment was linked to an increased risk of postmenopausal patients developing asthma. But it found the risk to be similar whether patients were treated with estrogen only, or a combination therapy.

Dr. Romieu and colleagues offered as a possible explanation for the disparity the fact that French and American physicians generally use different ratios of estrogen and progestin, as well as different types of progestin, in HT treatment regimens.

Also in contrast to the earlier U.S. study, Dr. Romieu's team did not observe interactions between body mass index and risk of asthma among HT and non-HT patients following menopause, but stated that this may have been because the French cohort presented leaner body mass as a whole.

Disclosures: The study investigators reported no financial conflicts of interest.

Major Finding: Children with asthma who underwent adenotonsillectomies required significantly less asthma medication and had fewer hospitalizations, compared with presurgical utilization.

Data Source: A retrospective review of 465 consecutive children with and without asthma who underwent adenotonsillectomy at a single institution. Symptoms of asthma were compared 12 months pre- and post surgery.

Disclosures: Dr. Busino had no financial conflicts to disclose.

ORLANDO — Children with asthma who underwent adenotonsillectomies showed significant improvement in their asthma symptoms, compared with presurgical levels, according to findings from a retrospective review of 93 children with asthma.

Children with asthma are at greater risk for sleep-disordered breathing than their peers without asthma, said Dr. Rowley S. Busino of the University of Medicine and Dentistry of New Jersey, Newark. Consequently, asthma is a common comorbidity in children undergoing adenotonsillectomy.

Parents of children with asthma often report that their children's asthmatic symptoms improve after an adenotonsillectomy, but that observation has not been well studied, Dr. Busino observed.

Dr. Busino and her colleagues reviewed data from all children who underwent adenotonsillectomy at a single institution between 2002 and 2007. The study population included 93 children with asthma and 372 children without asthma. The children were aged 3-14 years, with an average age of 6 years. Children younger than 3 years and those with comorbid medical conditions including Down syndrome, heart disease, subglottic stenosis, prematurity, and neurological disorders were excluded.

Both groups were similar in terms of age and gender distribution, and the most common reason for surgery in both groups was obstructive sleep apnea/adenotonsillar hypertrophy. Asthma symptoms were assessed 12 months before and 12 months after surgery, according to a poster presented at the Triological Society's Combined Sections Meeting.

After surgery, the children with asthma had significantly fewer hospital visits (1.6 vs. 0.1), and used significantly fewer daily medications (2.6 vs. 2.3) and systemic steroids (2.0 vs. 0.5), compared with presurgery levels.

Scores on the Asthma Control Test also improved significantly after surgery, compared with presurgery scores, from 18.5 to 20.5.

Because of the small number of respiratory complications in each group, the researchers were not able to assess whether children with asthma had a higher postoperative respiratory complication rate, compared with children without asthma. The average length of postoperative hospital stay was not significantly different between the asthma and control groups.

“This study suggests that adenotonsillectomy, which provides improvement in the upper airways of children, may in turn lead to improvement of their lower airways,” Dr. Busino said at the meeting, which was jointly sponsored by the Triological Society and the American College of Surgeons.

Prospective studies to clarify the relationship between asthma, adenotonsillectomy, and obstructive sleep apnea are needed to improve clinical care, she said.

Major Finding: Children with asthma who underwent adenotonsillectomies required significantly less asthma medication and had fewer hospitalizations, compared with presurgical utilization.

Data Source: A retrospective review of 465 consecutive children with and without asthma who underwent adenotonsillectomy at a single institution. Symptoms of asthma were compared 12 months pre- and post surgery.

Disclosures: Dr. Busino had no financial conflicts to disclose.

ORLANDO — Children with asthma who underwent adenotonsillectomies showed significant improvement in their asthma symptoms, compared with presurgical levels, according to findings from a retrospective review of 93 children with asthma.

Children with asthma are at greater risk for sleep-disordered breathing than their peers without asthma, said Dr. Rowley S. Busino of the University of Medicine and Dentistry of New Jersey, Newark. Consequently, asthma is a common comorbidity in children undergoing adenotonsillectomy.

Parents of children with asthma often report that their children's asthmatic symptoms improve after an adenotonsillectomy, but that observation has not been well studied, Dr. Busino observed.

Dr. Busino and her colleagues reviewed data from all children who underwent adenotonsillectomy at a single institution between 2002 and 2007. The study population included 93 children with asthma and 372 children without asthma. The children were aged 3-14 years, with an average age of 6 years. Children younger than 3 years and those with comorbid medical conditions including Down syndrome, heart disease, subglottic stenosis, prematurity, and neurological disorders were excluded.

Both groups were similar in terms of age and gender distribution, and the most common reason for surgery in both groups was obstructive sleep apnea/adenotonsillar hypertrophy. Asthma symptoms were assessed 12 months before and 12 months after surgery, according to a poster presented at the Triological Society's Combined Sections Meeting.

After surgery, the children with asthma had significantly fewer hospital visits (1.6 vs. 0.1), and used significantly fewer daily medications (2.6 vs. 2.3) and systemic steroids (2.0 vs. 0.5), compared with presurgery levels.

Scores on the Asthma Control Test also improved significantly after surgery, compared with presurgery scores, from 18.5 to 20.5.

Because of the small number of respiratory complications in each group, the researchers were not able to assess whether children with asthma had a higher postoperative respiratory complication rate, compared with children without asthma. The average length of postoperative hospital stay was not significantly different between the asthma and control groups.

“This study suggests that adenotonsillectomy, which provides improvement in the upper airways of children, may in turn lead to improvement of their lower airways,” Dr. Busino said at the meeting, which was jointly sponsored by the Triological Society and the American College of Surgeons.

Prospective studies to clarify the relationship between asthma, adenotonsillectomy, and obstructive sleep apnea are needed to improve clinical care, she said.

Major Finding: Children with asthma who underwent adenotonsillectomies required significantly less asthma medication and had fewer hospitalizations, compared with presurgical utilization.

Data Source: A retrospective review of 465 consecutive children with and without asthma who underwent adenotonsillectomy at a single institution. Symptoms of asthma were compared 12 months pre- and post surgery.

Disclosures: Dr. Busino had no financial conflicts to disclose.

ORLANDO — Children with asthma who underwent adenotonsillectomies showed significant improvement in their asthma symptoms, compared with presurgical levels, according to findings from a retrospective review of 93 children with asthma.

Children with asthma are at greater risk for sleep-disordered breathing than their peers without asthma, said Dr. Rowley S. Busino of the University of Medicine and Dentistry of New Jersey, Newark. Consequently, asthma is a common comorbidity in children undergoing adenotonsillectomy.

Parents of children with asthma often report that their children's asthmatic symptoms improve after an adenotonsillectomy, but that observation has not been well studied, Dr. Busino observed.

Dr. Busino and her colleagues reviewed data from all children who underwent adenotonsillectomy at a single institution between 2002 and 2007. The study population included 93 children with asthma and 372 children without asthma. The children were aged 3-14 years, with an average age of 6 years. Children younger than 3 years and those with comorbid medical conditions including Down syndrome, heart disease, subglottic stenosis, prematurity, and neurological disorders were excluded.

Both groups were similar in terms of age and gender distribution, and the most common reason for surgery in both groups was obstructive sleep apnea/adenotonsillar hypertrophy. Asthma symptoms were assessed 12 months before and 12 months after surgery, according to a poster presented at the Triological Society's Combined Sections Meeting.

After surgery, the children with asthma had significantly fewer hospital visits (1.6 vs. 0.1), and used significantly fewer daily medications (2.6 vs. 2.3) and systemic steroids (2.0 vs. 0.5), compared with presurgery levels.

Scores on the Asthma Control Test also improved significantly after surgery, compared with presurgery scores, from 18.5 to 20.5.

Because of the small number of respiratory complications in each group, the researchers were not able to assess whether children with asthma had a higher postoperative respiratory complication rate, compared with children without asthma. The average length of postoperative hospital stay was not significantly different between the asthma and control groups.

“This study suggests that adenotonsillectomy, which provides improvement in the upper airways of children, may in turn lead to improvement of their lower airways,” Dr. Busino said at the meeting, which was jointly sponsored by the Triological Society and the American College of Surgeons.

Prospective studies to clarify the relationship between asthma, adenotonsillectomy, and obstructive sleep apnea are needed to improve clinical care, she said.

SAN DIEGO — Only 1 in 20 individuals with idiopathic pulmonary arterial hypertension can be successfully managed long term with oral calcium channel blockers, but even a slim chance of using this simple, inexpensive therapy is so attractive that acute vasoreactivity testing to identify suitable candidates is warranted in all patients with the disorder.

The best agent to use for this testing, which is done during right heart catheterization, is inhaled nitric oxide, Dr. Lewis J. Rubin said at the annual meeting of the American College of Chest Physicians.

“It's very potent, it's short acting, it's a very good identifier of patients who have vasoreactivity—and when you see it, there's no question about it. Within a few breaths of nitric oxide in a responder, you will see the pulmonary artery pressure come down. It's not subtle at all,” said Dr. Rubin, professor of pulmonary and critical care medicine at the University of California, San Diego.

Roughly 10% of patients with idiopathic pulmonary arterial hypertension (IPAH) will demonstrate a dominant vasoreactive response on testing and therefore are suitable for a therapeutic trial using an oral calcium channel blocker. Earlier studies had put that figure as high as 20%-25%. Moreover, only about half of acute responders will maintain that response long term on calcium channel blocker therapy, as defined by New York Heart Association class I or II status and sustained hemodynamic improvement without additional PAH-specific agents.

Reasonable alternatives to inhaled nitric oxide for acute vasoreactivity testing are intravenous epoprostenol (Flolan) and intravenous adenosine. Calcium channel blockers should never be used for the testing, a point emphasized in the latest American College of Cardiology/American Heart Association expert consensus document on pulmonary hypertension, coauthored by Dr. Rubin (J. Am. Coll. Cardiol. 2009;53:1573-1619).

“They're nontitratable and nonselective, and it's exceedingly dangerous. So you either test for vasoreactivity with something that's available and safe or you don't do it and you let somebody who does this for a living do it for you,” Dr. Rubin said.

Only a tiny percentage of patients with PAH associated with connective tissue disease, portal hypertension, HIV infection, or other nonidiopathic forms of PAH have pulmonary vasoconstriction as the dominant cause of their pulmonary hypertension are thus candidates for calcium channel blocker therapy.

“Some people say there's no use in testing for acute vasoreactivity in anything other than IPAH. But if you're set up to do it and you can do it relatively efficiently, safely, and quickly, I think it's worth doing for all patients with PAH,” the physician continued.

Dr. Rubin made a plea for physicians in the community to have no hesitation in referring their patients with PAH to experts at centers of excellence.

“This is a highly complex and rapidly evolving condition in terms of management. As treatments have diffused into the community, I think there are concerns about delays in referring patients for more complex management. This is a shared responsibility. We can't see these patients as frequently as you can because they often come from a distance. We serve as a resource for you. We need to see these patients at intervals,” he said.

Disclosures: Dr. Rubin is a consultant and/or on the speakers bureaus for Gilead Sciences Inc., Actelion Pharmaceuticals Ltd., Pfizer Inc., United Therapeutics Corp., Aires Pharmaceuticals Inc., Solvay Pharmaceuticals Inc., and other pharmaceutical companies.

Calcium channel blockers should never be used for vasoreactivity testing.

Source DR. RUBIN

SAN DIEGO — Only 1 in 20 individuals with idiopathic pulmonary arterial hypertension can be successfully managed long term with oral calcium channel blockers, but even a slim chance of using this simple, inexpensive therapy is so attractive that acute vasoreactivity testing to identify suitable candidates is warranted in all patients with the disorder.

The best agent to use for this testing, which is done during right heart catheterization, is inhaled nitric oxide, Dr. Lewis J. Rubin said at the annual meeting of the American College of Chest Physicians.

“It's very potent, it's short acting, it's a very good identifier of patients who have vasoreactivity—and when you see it, there's no question about it. Within a few breaths of nitric oxide in a responder, you will see the pulmonary artery pressure come down. It's not subtle at all,” said Dr. Rubin, professor of pulmonary and critical care medicine at the University of California, San Diego.

Roughly 10% of patients with idiopathic pulmonary arterial hypertension (IPAH) will demonstrate a dominant vasoreactive response on testing and therefore are suitable for a therapeutic trial using an oral calcium channel blocker. Earlier studies had put that figure as high as 20%-25%. Moreover, only about half of acute responders will maintain that response long term on calcium channel blocker therapy, as defined by New York Heart Association class I or II status and sustained hemodynamic improvement without additional PAH-specific agents.

Reasonable alternatives to inhaled nitric oxide for acute vasoreactivity testing are intravenous epoprostenol (Flolan) and intravenous adenosine. Calcium channel blockers should never be used for the testing, a point emphasized in the latest American College of Cardiology/American Heart Association expert consensus document on pulmonary hypertension, coauthored by Dr. Rubin (J. Am. Coll. Cardiol. 2009;53:1573-1619).

“They're nontitratable and nonselective, and it's exceedingly dangerous. So you either test for vasoreactivity with something that's available and safe or you don't do it and you let somebody who does this for a living do it for you,” Dr. Rubin said.

Only a tiny percentage of patients with PAH associated with connective tissue disease, portal hypertension, HIV infection, or other nonidiopathic forms of PAH have pulmonary vasoconstriction as the dominant cause of their pulmonary hypertension are thus candidates for calcium channel blocker therapy.

“Some people say there's no use in testing for acute vasoreactivity in anything other than IPAH. But if you're set up to do it and you can do it relatively efficiently, safely, and quickly, I think it's worth doing for all patients with PAH,” the physician continued.

Dr. Rubin made a plea for physicians in the community to have no hesitation in referring their patients with PAH to experts at centers of excellence.

“This is a highly complex and rapidly evolving condition in terms of management. As treatments have diffused into the community, I think there are concerns about delays in referring patients for more complex management. This is a shared responsibility. We can't see these patients as frequently as you can because they often come from a distance. We serve as a resource for you. We need to see these patients at intervals,” he said.

Disclosures: Dr. Rubin is a consultant and/or on the speakers bureaus for Gilead Sciences Inc., Actelion Pharmaceuticals Ltd., Pfizer Inc., United Therapeutics Corp., Aires Pharmaceuticals Inc., Solvay Pharmaceuticals Inc., and other pharmaceutical companies.

Calcium channel blockers should never be used for vasoreactivity testing.

Source DR. RUBIN

SAN DIEGO — Only 1 in 20 individuals with idiopathic pulmonary arterial hypertension can be successfully managed long term with oral calcium channel blockers, but even a slim chance of using this simple, inexpensive therapy is so attractive that acute vasoreactivity testing to identify suitable candidates is warranted in all patients with the disorder.

The best agent to use for this testing, which is done during right heart catheterization, is inhaled nitric oxide, Dr. Lewis J. Rubin said at the annual meeting of the American College of Chest Physicians.

“It's very potent, it's short acting, it's a very good identifier of patients who have vasoreactivity—and when you see it, there's no question about it. Within a few breaths of nitric oxide in a responder, you will see the pulmonary artery pressure come down. It's not subtle at all,” said Dr. Rubin, professor of pulmonary and critical care medicine at the University of California, San Diego.

Roughly 10% of patients with idiopathic pulmonary arterial hypertension (IPAH) will demonstrate a dominant vasoreactive response on testing and therefore are suitable for a therapeutic trial using an oral calcium channel blocker. Earlier studies had put that figure as high as 20%-25%. Moreover, only about half of acute responders will maintain that response long term on calcium channel blocker therapy, as defined by New York Heart Association class I or II status and sustained hemodynamic improvement without additional PAH-specific agents.

Reasonable alternatives to inhaled nitric oxide for acute vasoreactivity testing are intravenous epoprostenol (Flolan) and intravenous adenosine. Calcium channel blockers should never be used for the testing, a point emphasized in the latest American College of Cardiology/American Heart Association expert consensus document on pulmonary hypertension, coauthored by Dr. Rubin (J. Am. Coll. Cardiol. 2009;53:1573-1619).

“They're nontitratable and nonselective, and it's exceedingly dangerous. So you either test for vasoreactivity with something that's available and safe or you don't do it and you let somebody who does this for a living do it for you,” Dr. Rubin said.

Only a tiny percentage of patients with PAH associated with connective tissue disease, portal hypertension, HIV infection, or other nonidiopathic forms of PAH have pulmonary vasoconstriction as the dominant cause of their pulmonary hypertension are thus candidates for calcium channel blocker therapy.

“Some people say there's no use in testing for acute vasoreactivity in anything other than IPAH. But if you're set up to do it and you can do it relatively efficiently, safely, and quickly, I think it's worth doing for all patients with PAH,” the physician continued.

Dr. Rubin made a plea for physicians in the community to have no hesitation in referring their patients with PAH to experts at centers of excellence.

“This is a highly complex and rapidly evolving condition in terms of management. As treatments have diffused into the community, I think there are concerns about delays in referring patients for more complex management. This is a shared responsibility. We can't see these patients as frequently as you can because they often come from a distance. We serve as a resource for you. We need to see these patients at intervals,” he said.

Disclosures: Dr. Rubin is a consultant and/or on the speakers bureaus for Gilead Sciences Inc., Actelion Pharmaceuticals Ltd., Pfizer Inc., United Therapeutics Corp., Aires Pharmaceuticals Inc., Solvay Pharmaceuticals Inc., and other pharmaceutical companies.

Calcium channel blockers should never be used for vasoreactivity testing.

Source DR. RUBIN

CORONADO, CALIF. — A variety of lung cancer–associated biomarkers are being tested in assays that may improve diagnosis and treatment of this disease, according to three studies reported at a joint conference of the American Association for Cancer Research and the International Association for the Study of Lung Cancer.

Blood-Based Biomarker Profile

A blood-based biomarker profile discriminates well between patients who have early-stage lung cancer and those individuals who are cancer free but at high risk, reported Dr. Gina Lee, a pulmonary and critical care physician at the University of California, Los Angeles.

She and her colleagues hypothesized that molecular changes in the developing tumor environment would be reflected in changes in levels of inflammatory, angiogenic, and tumorigenic proteins that can be detected in peripheral blood.

They used a bead-based multiplex immunoassay to assess levels of 40 biomarkers in serum samples from 90 patients who had lung cancer of any stage and from 56 cancer-free controls who were at high risk because of lengthy former smoking status and older age.

Levels of 21 biomarkers differed significantly between the 28 patients with stage I lung cancer and the cancer-free controls.

In a logistic regression model that focused on selected biomarkers, participants were more likely to have stage I cancer if they had higher levels of interleukin 2 (odds ratio, 51.4), interleukin 3 (OR, 11.0), and macrophage-derived chemokine (OR, 10.9).

“Our results suggest that we can find tumor-associated biomarkers that are differentially expressed in stage I vs. at-risk controls,” Dr. Lee said. “However, we are also interested in the clinical scenario where individuals present to clinicians with a lung nodule seen on chest x-ray or a CT scan of indeterminate significance.”

Therefore, she and her colleagues will evaluate the 40 biomarkers in pre- and postresection serum samples from patients in the ACOSOG (American College of Surgeons Oncology Group) Z4031 trial. Roughly one-fifth of patients undergoing resection for lung nodules in that trial were found to have benign lung disease.

High-Throughput Protein Assay

A protein signature identified by a high-throughput assay correctly classifies the large majority of patients with and without lung cancer, reported Dr. Rachel Ostroff, clinical research director at SomaLogic Inc., a diagnostic development company in Boulder, Colo.

The SOMAmer technology used in the study relies on aptamers (oligonucleotides that bind to specific proteins with high affinity) to measure 825 proteins in serum simultaneously with subpicomolar sensitivity, she explained.

The investigators analyzed more than 1,300 serum samples from patients with stage I-III non–small cell lung cancer (20%) and two control groups: individuals with benign calcified pulmonary nodules (40%) and long-term smokers with no evidence of cancer (40%). They were divided into training and verification sets.

Analyses identified a signature of 12 proteins that were differentially expressed between the groups with and without lung cancer, including cell adhesion molecules, cytokines, angiogenesis markers, and tyrosine kinases, among others.

The signature had an area under the curve of 0.91 in the training set and 0.90 in the verification set, Dr. Ostroff reported. In the training set, sensitivity was 91% for cancer of all stages (90% for stage I) and specificity was 84%. In the verification set, sensitivity was 89% for cancer of all stages (87% for stage I) and specificity was 84%.

The signature has also been tested in breast, prostate, and other cancers. “Certainly, some of the markers are also differentially expressed in those cancers, as you would expect,” Dr. Ostroff said. “But … when you combine all of those 12 markers together, it is much more specific for lung cancer than those others.”

Tumor MicroRNA Analysis

A trio of tumor microRNAs predict de novo resistance to first-line chemotherapy among patients with small cell lung cancer, reported Dr. Glenn J. Weiss, a pulmonary oncologist with Scottsdale (Ariz.) Healthcare and the Translational Genomics Research Institute (TGen) in Phoenix.

“Small cell lung cancer patients have not had key breakthroughs for improved therapy in years, in part, because a one-size-fits-all approach for treatment is the current standard,” he commented in an interview.

In the study, which was funded in part by the TGen Foundation, he and his colleagues extracted RNA from formalin-fixed, paraffin-embedded tumor specimens obtained from 34 patients with small cell lung cancer before they started chemotherapy, which was a platinum-based regimen in most cases.

Study results, reported in a poster, showed that of 21 evaluable patients, 4 (19%) had chemoresistance (defined as progression despite chemotherapy).

MicroRNA array analyses identified 16 microRNA biomarkers as possible predictors of progression.

Polymerase chain reaction analyses validated that three of them—miR-92a-2&ast;, miR-147, and miR-574-5p—were indeed associated with progression, Dr. Weiss said.

The investigators are currently assessing how the identified microRNAs may reduce a tumor's sensitivity to chemotherapy, according to Dr. Weiss.

“If we can independently validate our findings in other tumor sample sets collected from small cell lung cancer patients, we can begin to explore [by] using these microRNAs to design better clinical trials and perhaps find new therapies that help patients at higher risk for resistance to current standard chemotherapy treatment,” he concluded.

Disclosures: Dr. Lee reported that she had no conflicts of interest related to the study. Dr. Ostroff's employer is the manufacturer of the study assay. Dr. Weiss has filed patents for the use of microRNAs as theranostics, and has received funding from the Sylvia-Chase Foundation, the American Cancer Society, the IBIS Foundation of Arizona, the TGen Foundation, and Scottsdale Healthcare to conduct this work.

CORONADO, CALIF. — A variety of lung cancer–associated biomarkers are being tested in assays that may improve diagnosis and treatment of this disease, according to three studies reported at a joint conference of the American Association for Cancer Research and the International Association for the Study of Lung Cancer.

Blood-Based Biomarker Profile

A blood-based biomarker profile discriminates well between patients who have early-stage lung cancer and those individuals who are cancer free but at high risk, reported Dr. Gina Lee, a pulmonary and critical care physician at the University of California, Los Angeles.

She and her colleagues hypothesized that molecular changes in the developing tumor environment would be reflected in changes in levels of inflammatory, angiogenic, and tumorigenic proteins that can be detected in peripheral blood.

They used a bead-based multiplex immunoassay to assess levels of 40 biomarkers in serum samples from 90 patients who had lung cancer of any stage and from 56 cancer-free controls who were at high risk because of lengthy former smoking status and older age.

Levels of 21 biomarkers differed significantly between the 28 patients with stage I lung cancer and the cancer-free controls.

In a logistic regression model that focused on selected biomarkers, participants were more likely to have stage I cancer if they had higher levels of interleukin 2 (odds ratio, 51.4), interleukin 3 (OR, 11.0), and macrophage-derived chemokine (OR, 10.9).

“Our results suggest that we can find tumor-associated biomarkers that are differentially expressed in stage I vs. at-risk controls,” Dr. Lee said. “However, we are also interested in the clinical scenario where individuals present to clinicians with a lung nodule seen on chest x-ray or a CT scan of indeterminate significance.”

Therefore, she and her colleagues will evaluate the 40 biomarkers in pre- and postresection serum samples from patients in the ACOSOG (American College of Surgeons Oncology Group) Z4031 trial. Roughly one-fifth of patients undergoing resection for lung nodules in that trial were found to have benign lung disease.

High-Throughput Protein Assay

A protein signature identified by a high-throughput assay correctly classifies the large majority of patients with and without lung cancer, reported Dr. Rachel Ostroff, clinical research director at SomaLogic Inc., a diagnostic development company in Boulder, Colo.

The SOMAmer technology used in the study relies on aptamers (oligonucleotides that bind to specific proteins with high affinity) to measure 825 proteins in serum simultaneously with subpicomolar sensitivity, she explained.

The investigators analyzed more than 1,300 serum samples from patients with stage I-III non–small cell lung cancer (20%) and two control groups: individuals with benign calcified pulmonary nodules (40%) and long-term smokers with no evidence of cancer (40%). They were divided into training and verification sets.

Analyses identified a signature of 12 proteins that were differentially expressed between the groups with and without lung cancer, including cell adhesion molecules, cytokines, angiogenesis markers, and tyrosine kinases, among others.

The signature had an area under the curve of 0.91 in the training set and 0.90 in the verification set, Dr. Ostroff reported. In the training set, sensitivity was 91% for cancer of all stages (90% for stage I) and specificity was 84%. In the verification set, sensitivity was 89% for cancer of all stages (87% for stage I) and specificity was 84%.

The signature has also been tested in breast, prostate, and other cancers. “Certainly, some of the markers are also differentially expressed in those cancers, as you would expect,” Dr. Ostroff said. “But … when you combine all of those 12 markers together, it is much more specific for lung cancer than those others.”

Tumor MicroRNA Analysis

A trio of tumor microRNAs predict de novo resistance to first-line chemotherapy among patients with small cell lung cancer, reported Dr. Glenn J. Weiss, a pulmonary oncologist with Scottsdale (Ariz.) Healthcare and the Translational Genomics Research Institute (TGen) in Phoenix.

“Small cell lung cancer patients have not had key breakthroughs for improved therapy in years, in part, because a one-size-fits-all approach for treatment is the current standard,” he commented in an interview.

In the study, which was funded in part by the TGen Foundation, he and his colleagues extracted RNA from formalin-fixed, paraffin-embedded tumor specimens obtained from 34 patients with small cell lung cancer before they started chemotherapy, which was a platinum-based regimen in most cases.

Study results, reported in a poster, showed that of 21 evaluable patients, 4 (19%) had chemoresistance (defined as progression despite chemotherapy).

MicroRNA array analyses identified 16 microRNA biomarkers as possible predictors of progression.

Polymerase chain reaction analyses validated that three of them—miR-92a-2&ast;, miR-147, and miR-574-5p—were indeed associated with progression, Dr. Weiss said.

The investigators are currently assessing how the identified microRNAs may reduce a tumor's sensitivity to chemotherapy, according to Dr. Weiss.

“If we can independently validate our findings in other tumor sample sets collected from small cell lung cancer patients, we can begin to explore [by] using these microRNAs to design better clinical trials and perhaps find new therapies that help patients at higher risk for resistance to current standard chemotherapy treatment,” he concluded.

Disclosures: Dr. Lee reported that she had no conflicts of interest related to the study. Dr. Ostroff's employer is the manufacturer of the study assay. Dr. Weiss has filed patents for the use of microRNAs as theranostics, and has received funding from the Sylvia-Chase Foundation, the American Cancer Society, the IBIS Foundation of Arizona, the TGen Foundation, and Scottsdale Healthcare to conduct this work.

CORONADO, CALIF. — A variety of lung cancer–associated biomarkers are being tested in assays that may improve diagnosis and treatment of this disease, according to three studies reported at a joint conference of the American Association for Cancer Research and the International Association for the Study of Lung Cancer.

Blood-Based Biomarker Profile

A blood-based biomarker profile discriminates well between patients who have early-stage lung cancer and those individuals who are cancer free but at high risk, reported Dr. Gina Lee, a pulmonary and critical care physician at the University of California, Los Angeles.

She and her colleagues hypothesized that molecular changes in the developing tumor environment would be reflected in changes in levels of inflammatory, angiogenic, and tumorigenic proteins that can be detected in peripheral blood.

They used a bead-based multiplex immunoassay to assess levels of 40 biomarkers in serum samples from 90 patients who had lung cancer of any stage and from 56 cancer-free controls who were at high risk because of lengthy former smoking status and older age.

Levels of 21 biomarkers differed significantly between the 28 patients with stage I lung cancer and the cancer-free controls.

In a logistic regression model that focused on selected biomarkers, participants were more likely to have stage I cancer if they had higher levels of interleukin 2 (odds ratio, 51.4), interleukin 3 (OR, 11.0), and macrophage-derived chemokine (OR, 10.9).

“Our results suggest that we can find tumor-associated biomarkers that are differentially expressed in stage I vs. at-risk controls,” Dr. Lee said. “However, we are also interested in the clinical scenario where individuals present to clinicians with a lung nodule seen on chest x-ray or a CT scan of indeterminate significance.”

Therefore, she and her colleagues will evaluate the 40 biomarkers in pre- and postresection serum samples from patients in the ACOSOG (American College of Surgeons Oncology Group) Z4031 trial. Roughly one-fifth of patients undergoing resection for lung nodules in that trial were found to have benign lung disease.

High-Throughput Protein Assay

A protein signature identified by a high-throughput assay correctly classifies the large majority of patients with and without lung cancer, reported Dr. Rachel Ostroff, clinical research director at SomaLogic Inc., a diagnostic development company in Boulder, Colo.

The SOMAmer technology used in the study relies on aptamers (oligonucleotides that bind to specific proteins with high affinity) to measure 825 proteins in serum simultaneously with subpicomolar sensitivity, she explained.

The investigators analyzed more than 1,300 serum samples from patients with stage I-III non–small cell lung cancer (20%) and two control groups: individuals with benign calcified pulmonary nodules (40%) and long-term smokers with no evidence of cancer (40%). They were divided into training and verification sets.

Analyses identified a signature of 12 proteins that were differentially expressed between the groups with and without lung cancer, including cell adhesion molecules, cytokines, angiogenesis markers, and tyrosine kinases, among others.

The signature had an area under the curve of 0.91 in the training set and 0.90 in the verification set, Dr. Ostroff reported. In the training set, sensitivity was 91% for cancer of all stages (90% for stage I) and specificity was 84%. In the verification set, sensitivity was 89% for cancer of all stages (87% for stage I) and specificity was 84%.

The signature has also been tested in breast, prostate, and other cancers. “Certainly, some of the markers are also differentially expressed in those cancers, as you would expect,” Dr. Ostroff said. “But … when you combine all of those 12 markers together, it is much more specific for lung cancer than those others.”

Tumor MicroRNA Analysis

A trio of tumor microRNAs predict de novo resistance to first-line chemotherapy among patients with small cell lung cancer, reported Dr. Glenn J. Weiss, a pulmonary oncologist with Scottsdale (Ariz.) Healthcare and the Translational Genomics Research Institute (TGen) in Phoenix.

“Small cell lung cancer patients have not had key breakthroughs for improved therapy in years, in part, because a one-size-fits-all approach for treatment is the current standard,” he commented in an interview.

In the study, which was funded in part by the TGen Foundation, he and his colleagues extracted RNA from formalin-fixed, paraffin-embedded tumor specimens obtained from 34 patients with small cell lung cancer before they started chemotherapy, which was a platinum-based regimen in most cases.

Study results, reported in a poster, showed that of 21 evaluable patients, 4 (19%) had chemoresistance (defined as progression despite chemotherapy).

MicroRNA array analyses identified 16 microRNA biomarkers as possible predictors of progression.

Polymerase chain reaction analyses validated that three of them—miR-92a-2&ast;, miR-147, and miR-574-5p—were indeed associated with progression, Dr. Weiss said.

The investigators are currently assessing how the identified microRNAs may reduce a tumor's sensitivity to chemotherapy, according to Dr. Weiss.

“If we can independently validate our findings in other tumor sample sets collected from small cell lung cancer patients, we can begin to explore [by] using these microRNAs to design better clinical trials and perhaps find new therapies that help patients at higher risk for resistance to current standard chemotherapy treatment,” he concluded.

Disclosures: Dr. Lee reported that she had no conflicts of interest related to the study. Dr. Ostroff's employer is the manufacturer of the study assay. Dr. Weiss has filed patents for the use of microRNAs as theranostics, and has received funding from the Sylvia-Chase Foundation, the American Cancer Society, the IBIS Foundation of Arizona, the TGen Foundation, and Scottsdale Healthcare to conduct this work.

SAN DIEGO — Golfers with obstructive sleep apnea can anticipate knocking strokes off their game by adhering to treatment with continuous positive airway pressure.

What's more, the better the player at baseline, the bigger the improvement in golf handicap resulting from CPAP, as demonstrated in a small prospective controlled study presented at the annual meeting of the American College of Chest Physicians.

Compliance with CPAP is notoriously challenging. Many patients with OSA, put off by CPAP's noise, inconvenience, and expense, remained unswayed by physician warnings of the medical risks they face in not being treated. For the avid golfer, however, the prospect of playing a better game appears to be a powerful and previously untapped motivator to seek and adhere to treatment for OSA.

“The adherence in this study was absolutely off the charts,” said Dr. Marc L. Benton, who has a sleep disorders and pulmonary medicine practice in Madison, N.J.

He came up with the idea of studying the impact of OSA therapy on golf performance after two physician friends, both golfers, that he treated for OSA told him their handicaps had improved and they felt better able to manage their game.

“More so than almost any other sport, golf has a strong intellectual component, with on-course strategizing, focus, and endurance being integral components to achieving good play,” he noted. “Through treatment with nasal positive airway pressure [NPAP], we can improve many cognitive metrics, including attention span, memory, decision-making abilities, and frustration management, which may in turn positively affect a person's golf game.”

Dr. Benton's study involved 12 golfers with moderate to severe OSA and 12 control subjects matched by age and golf handicap. None of the golfers with OSA had previously been interested in treatment for their disorder—but the prospect of potentially lowering their handicap lured them into study participation.

After 3-5 months of NPAP, during which the patients played 20 rounds of golf, their handicap dropped from an average of 12.4 to 11.0. All of them felt that they were able to perform better on the course.

Their mean score on the Epworth Sleepiness Scale decreased from 11.8 to 5.5, and their score on a sleep questionnaire improved from 14.3 to 3.1, placing them in the normal range.

Meanwhile, the control subjects showed no change from baseline in golf handicap, the Epworth Scale, or sleep questionnaire score.

The study participants didn't take golf lessons or get new clubs during the study period.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game, as defined by a baseline handicap below 12. Their average handicap dropped from 9.2 to 6.3, nearly a 3-stroke improvement, about which they were exultant.

Sleep specialists typically consider the use of CPAP for 4 hours or more per night on 75% of nights to be acceptable compliance. The golfers took their treatment far more seriously, using their CPAP machines for 5.5 to 7 hours per night on 92% of nights, as measured by the equipment's data cards.

Dr. Benton estimated 1-3 million American golfers have OSA, in most cases undiagnosed or untreated.

Disclosures: Dr. Benton reported having no financial conflicts of interest in connection with his study.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game.

Source DR. BENTON

SAN DIEGO — Golfers with obstructive sleep apnea can anticipate knocking strokes off their game by adhering to treatment with continuous positive airway pressure.

What's more, the better the player at baseline, the bigger the improvement in golf handicap resulting from CPAP, as demonstrated in a small prospective controlled study presented at the annual meeting of the American College of Chest Physicians.

Compliance with CPAP is notoriously challenging. Many patients with OSA, put off by CPAP's noise, inconvenience, and expense, remained unswayed by physician warnings of the medical risks they face in not being treated. For the avid golfer, however, the prospect of playing a better game appears to be a powerful and previously untapped motivator to seek and adhere to treatment for OSA.

“The adherence in this study was absolutely off the charts,” said Dr. Marc L. Benton, who has a sleep disorders and pulmonary medicine practice in Madison, N.J.

He came up with the idea of studying the impact of OSA therapy on golf performance after two physician friends, both golfers, that he treated for OSA told him their handicaps had improved and they felt better able to manage their game.

“More so than almost any other sport, golf has a strong intellectual component, with on-course strategizing, focus, and endurance being integral components to achieving good play,” he noted. “Through treatment with nasal positive airway pressure [NPAP], we can improve many cognitive metrics, including attention span, memory, decision-making abilities, and frustration management, which may in turn positively affect a person's golf game.”

Dr. Benton's study involved 12 golfers with moderate to severe OSA and 12 control subjects matched by age and golf handicap. None of the golfers with OSA had previously been interested in treatment for their disorder—but the prospect of potentially lowering their handicap lured them into study participation.

After 3-5 months of NPAP, during which the patients played 20 rounds of golf, their handicap dropped from an average of 12.4 to 11.0. All of them felt that they were able to perform better on the course.

Their mean score on the Epworth Sleepiness Scale decreased from 11.8 to 5.5, and their score on a sleep questionnaire improved from 14.3 to 3.1, placing them in the normal range.

Meanwhile, the control subjects showed no change from baseline in golf handicap, the Epworth Scale, or sleep questionnaire score.

The study participants didn't take golf lessons or get new clubs during the study period.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game, as defined by a baseline handicap below 12. Their average handicap dropped from 9.2 to 6.3, nearly a 3-stroke improvement, about which they were exultant.

Sleep specialists typically consider the use of CPAP for 4 hours or more per night on 75% of nights to be acceptable compliance. The golfers took their treatment far more seriously, using their CPAP machines for 5.5 to 7 hours per night on 92% of nights, as measured by the equipment's data cards.

Dr. Benton estimated 1-3 million American golfers have OSA, in most cases undiagnosed or untreated.

Disclosures: Dr. Benton reported having no financial conflicts of interest in connection with his study.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game.

Source DR. BENTON

SAN DIEGO — Golfers with obstructive sleep apnea can anticipate knocking strokes off their game by adhering to treatment with continuous positive airway pressure.

What's more, the better the player at baseline, the bigger the improvement in golf handicap resulting from CPAP, as demonstrated in a small prospective controlled study presented at the annual meeting of the American College of Chest Physicians.

Compliance with CPAP is notoriously challenging. Many patients with OSA, put off by CPAP's noise, inconvenience, and expense, remained unswayed by physician warnings of the medical risks they face in not being treated. For the avid golfer, however, the prospect of playing a better game appears to be a powerful and previously untapped motivator to seek and adhere to treatment for OSA.

“The adherence in this study was absolutely off the charts,” said Dr. Marc L. Benton, who has a sleep disorders and pulmonary medicine practice in Madison, N.J.

He came up with the idea of studying the impact of OSA therapy on golf performance after two physician friends, both golfers, that he treated for OSA told him their handicaps had improved and they felt better able to manage their game.

“More so than almost any other sport, golf has a strong intellectual component, with on-course strategizing, focus, and endurance being integral components to achieving good play,” he noted. “Through treatment with nasal positive airway pressure [NPAP], we can improve many cognitive metrics, including attention span, memory, decision-making abilities, and frustration management, which may in turn positively affect a person's golf game.”

Dr. Benton's study involved 12 golfers with moderate to severe OSA and 12 control subjects matched by age and golf handicap. None of the golfers with OSA had previously been interested in treatment for their disorder—but the prospect of potentially lowering their handicap lured them into study participation.

After 3-5 months of NPAP, during which the patients played 20 rounds of golf, their handicap dropped from an average of 12.4 to 11.0. All of them felt that they were able to perform better on the course.

Their mean score on the Epworth Sleepiness Scale decreased from 11.8 to 5.5, and their score on a sleep questionnaire improved from 14.3 to 3.1, placing them in the normal range.

Meanwhile, the control subjects showed no change from baseline in golf handicap, the Epworth Scale, or sleep questionnaire score.

The study participants didn't take golf lessons or get new clubs during the study period.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game, as defined by a baseline handicap below 12. Their average handicap dropped from 9.2 to 6.3, nearly a 3-stroke improvement, about which they were exultant.

Sleep specialists typically consider the use of CPAP for 4 hours or more per night on 75% of nights to be acceptable compliance. The golfers took their treatment far more seriously, using their CPAP machines for 5.5 to 7 hours per night on 92% of nights, as measured by the equipment's data cards.

Dr. Benton estimated 1-3 million American golfers have OSA, in most cases undiagnosed or untreated.

Disclosures: Dr. Benton reported having no financial conflicts of interest in connection with his study.

The outcomes were particularly striking in the five golfers with OSA who were already quite skilled at the game.

Source DR. BENTON

SAN FRANCISCO — Sleep apnea can cause metabolic dysfunction, some of which can be reversed by treating the disorder with continuous positive airway pressure, a small 8-week study of 29 patients suggests.

Nine women with polycystic ovarian syndrome (PCOS) and 20 women without PCOS, all of whom had obstructive sleep apnea, were treated with continuous positive airway pressure (CPAP) at home for 8 weeks. Investigators monitored the use of CPAP to ensure good compliance, and took metabolic measurements at the start and end of the study.

Measures of sleep quality improved for the cohort as a whole after treatment. This was accompanied by both nighttime and daytime reductions in catecholamine levels, Dr. David A. Ehrmann said at the Sixth Annual World Congress on Insulin Resistance Syndrome.

“This has important implications in terms of both the metabolic and cardiovascular effects of obstructive sleep apnea in this population,” said Dr. Ehrmann, professor of medicine at the University of Chicago.

Sophisticated spectral analysis of heart rate variability as a measure of autonomic function showed that lowered catecholamine levels were reflected functionally in a slowing of heart rate, a lower autonomic function, and a lesser degree of epinephrine-induced variability in heart rate after treatment with CPAP, he added.

In lean subjects, greater compliance with CPAP therapy was associated with increased insulin sensitivity. Obese subjects showed a lesser improvement in insulin sensitivity—but an improvement nonetheless—that also was associated with greater use of CPAP, Dr. Ehrmann said. “There's sort of a dose-response relationship between the use of CPAP and changes in metabolic measurements,” he noted.

Among the measures of sleep quality that improved significantly with CPAP therapy, the apnea-hypopnea index score decreased from 24 to 2 per hour of sleep. The oxygen desaturation index score decreased from 12 to 1 per hour of sleep. The arousal index score decreased from 27 to 23 per hour of sleep.

Sleep apnea is recognized as a reversible risk factor for hypertension and for a number of abnormalities associated with insulin resistance syndromes. Women with PCOS are predisposed to develop obstructive sleep apnea at a rate sevenfold higher than women without PCOS, previous studies suggest. Although obesity plays a role, it does not by itself fully account for the higher risk for sleep apnea in women with PCOS.

Nor does androgen excess explain the higher prevalence of sleep apnea with PCOS, he added. In the nine women with PCOS in his study, 24-hour cortisol levels did not change significantly after CPAP treatment, compared with baseline.

In a previous study of 53 women with PCOS and 452 controls, the PCOS group was 30 times more likely to have sleep-disordered breathing and nine times more likely to have daytime sleepiness after researchers controlled for body mass index. Insulin resistance was a stronger predictor of sleep-disordered breathing than was age, BMI, or testosterone levels (J. Clin. Endocrinol. Metab. 2001;86:517-20).

A separate study found that in 29 women with PCOS and 4 controls with obstructive sleep apnea, the risk for apnea was seven times higher in the PCOS group (J. Clin. Endocrinol. Metab. 2006;91:36-42). In that study, the likelihood of impaired glucose correlated with the severity of sleep apnea.

Another study by Dr. Ehrmann and his associates showed that 29 women with PCOS and sleep apnea were significantly more insulin resistant than were 23 women with PCOS but not apnea (J. Clin. Endocrinol. Metab. 2008;93:3878-84).

Disclosures: Dr. Ehrmann reported having no relevant conflicts of interest.

SAN FRANCISCO — Sleep apnea can cause metabolic dysfunction, some of which can be reversed by treating the disorder with continuous positive airway pressure, a small 8-week study of 29 patients suggests.

Nine women with polycystic ovarian syndrome (PCOS) and 20 women without PCOS, all of whom had obstructive sleep apnea, were treated with continuous positive airway pressure (CPAP) at home for 8 weeks. Investigators monitored the use of CPAP to ensure good compliance, and took metabolic measurements at the start and end of the study.

Measures of sleep quality improved for the cohort as a whole after treatment. This was accompanied by both nighttime and daytime reductions in catecholamine levels, Dr. David A. Ehrmann said at the Sixth Annual World Congress on Insulin Resistance Syndrome.

“This has important implications in terms of both the metabolic and cardiovascular effects of obstructive sleep apnea in this population,” said Dr. Ehrmann, professor of medicine at the University of Chicago.

Sophisticated spectral analysis of heart rate variability as a measure of autonomic function showed that lowered catecholamine levels were reflected functionally in a slowing of heart rate, a lower autonomic function, and a lesser degree of epinephrine-induced variability in heart rate after treatment with CPAP, he added.

In lean subjects, greater compliance with CPAP therapy was associated with increased insulin sensitivity. Obese subjects showed a lesser improvement in insulin sensitivity—but an improvement nonetheless—that also was associated with greater use of CPAP, Dr. Ehrmann said. “There's sort of a dose-response relationship between the use of CPAP and changes in metabolic measurements,” he noted.

Among the measures of sleep quality that improved significantly with CPAP therapy, the apnea-hypopnea index score decreased from 24 to 2 per hour of sleep. The oxygen desaturation index score decreased from 12 to 1 per hour of sleep. The arousal index score decreased from 27 to 23 per hour of sleep.

Sleep apnea is recognized as a reversible risk factor for hypertension and for a number of abnormalities associated with insulin resistance syndromes. Women with PCOS are predisposed to develop obstructive sleep apnea at a rate sevenfold higher than women without PCOS, previous studies suggest. Although obesity plays a role, it does not by itself fully account for the higher risk for sleep apnea in women with PCOS.

Nor does androgen excess explain the higher prevalence of sleep apnea with PCOS, he added. In the nine women with PCOS in his study, 24-hour cortisol levels did not change significantly after CPAP treatment, compared with baseline.

In a previous study of 53 women with PCOS and 452 controls, the PCOS group was 30 times more likely to have sleep-disordered breathing and nine times more likely to have daytime sleepiness after researchers controlled for body mass index. Insulin resistance was a stronger predictor of sleep-disordered breathing than was age, BMI, or testosterone levels (J. Clin. Endocrinol. Metab. 2001;86:517-20).

A separate study found that in 29 women with PCOS and 4 controls with obstructive sleep apnea, the risk for apnea was seven times higher in the PCOS group (J. Clin. Endocrinol. Metab. 2006;91:36-42). In that study, the likelihood of impaired glucose correlated with the severity of sleep apnea.

Another study by Dr. Ehrmann and his associates showed that 29 women with PCOS and sleep apnea were significantly more insulin resistant than were 23 women with PCOS but not apnea (J. Clin. Endocrinol. Metab. 2008;93:3878-84).

Disclosures: Dr. Ehrmann reported having no relevant conflicts of interest.

SAN FRANCISCO — Sleep apnea can cause metabolic dysfunction, some of which can be reversed by treating the disorder with continuous positive airway pressure, a small 8-week study of 29 patients suggests.

Nine women with polycystic ovarian syndrome (PCOS) and 20 women without PCOS, all of whom had obstructive sleep apnea, were treated with continuous positive airway pressure (CPAP) at home for 8 weeks. Investigators monitored the use of CPAP to ensure good compliance, and took metabolic measurements at the start and end of the study.

Measures of sleep quality improved for the cohort as a whole after treatment. This was accompanied by both nighttime and daytime reductions in catecholamine levels, Dr. David A. Ehrmann said at the Sixth Annual World Congress on Insulin Resistance Syndrome.

“This has important implications in terms of both the metabolic and cardiovascular effects of obstructive sleep apnea in this population,” said Dr. Ehrmann, professor of medicine at the University of Chicago.

Sophisticated spectral analysis of heart rate variability as a measure of autonomic function showed that lowered catecholamine levels were reflected functionally in a slowing of heart rate, a lower autonomic function, and a lesser degree of epinephrine-induced variability in heart rate after treatment with CPAP, he added.

In lean subjects, greater compliance with CPAP therapy was associated with increased insulin sensitivity. Obese subjects showed a lesser improvement in insulin sensitivity—but an improvement nonetheless—that also was associated with greater use of CPAP, Dr. Ehrmann said. “There's sort of a dose-response relationship between the use of CPAP and changes in metabolic measurements,” he noted.

Among the measures of sleep quality that improved significantly with CPAP therapy, the apnea-hypopnea index score decreased from 24 to 2 per hour of sleep. The oxygen desaturation index score decreased from 12 to 1 per hour of sleep. The arousal index score decreased from 27 to 23 per hour of sleep.

Sleep apnea is recognized as a reversible risk factor for hypertension and for a number of abnormalities associated with insulin resistance syndromes. Women with PCOS are predisposed to develop obstructive sleep apnea at a rate sevenfold higher than women without PCOS, previous studies suggest. Although obesity plays a role, it does not by itself fully account for the higher risk for sleep apnea in women with PCOS.

Nor does androgen excess explain the higher prevalence of sleep apnea with PCOS, he added. In the nine women with PCOS in his study, 24-hour cortisol levels did not change significantly after CPAP treatment, compared with baseline.

In a previous study of 53 women with PCOS and 452 controls, the PCOS group was 30 times more likely to have sleep-disordered breathing and nine times more likely to have daytime sleepiness after researchers controlled for body mass index. Insulin resistance was a stronger predictor of sleep-disordered breathing than was age, BMI, or testosterone levels (J. Clin. Endocrinol. Metab. 2001;86:517-20).

A separate study found that in 29 women with PCOS and 4 controls with obstructive sleep apnea, the risk for apnea was seven times higher in the PCOS group (J. Clin. Endocrinol. Metab. 2006;91:36-42). In that study, the likelihood of impaired glucose correlated with the severity of sleep apnea.

Another study by Dr. Ehrmann and his associates showed that 29 women with PCOS and sleep apnea were significantly more insulin resistant than were 23 women with PCOS but not apnea (J. Clin. Endocrinol. Metab. 2008;93:3878-84).

Disclosures: Dr. Ehrmann reported having no relevant conflicts of interest.

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.

SANTA MONICA, CALIF. — Management of pulmonary hypertension in systemic sclerosis is inching its way toward a new age of prevention.

The change is coming from the appreciation that the finding of exercise-induced pulmonary hypertension (PH) likely represents abnormal hemodynamic manifestation in patients with systemic sclerosis (SSc) who have normal resting mean pulmonary artery pressure. And that this finding may flag those patients who are most likely to benefit from early, aggressive treatment.

Currently, by the time most cases of resting PH in SSc are diagnosed, the underlying hemodynamic disease process has become irreversible. “We are able to treat it. However, we are not able to cure it,” said Dr. Rajeev Saggar. As a result, the prognosis is grim.

PH-SSc tends to have a poorer prognosis, compared with other WHO Group I diagnoses. Recently, isolated PH-SSc survival, while receiving pulmonary vasodilator therapy, was reported at 78% at 1 year and 47% at 3 years. Furthermore, survival in PH-SSc associated with interstitial lung disease is even worse, said Dr. Saggar, a pulmonologist in the lung transplant and pulmonary hypertension division of the University of California, Los Angeles.

In an investigational program at his institution, treatment is being started in patients who have exercise-induced PH.

The exercise stress regimen involves patients, with a right heart catheter in place, riding a stationary supine bicycle for 3-9 minutes.

Those with an exercise mean pulmonary artery pressure greater than or equal to 30 mm Hg and a pulmonary wedge pressure less than or equal to 18 mm Hg receive treatment with an endothelin antagonist. All of these patients have normal resting mean pulmonary artery pressures.

Recent data from a U.K. study of 42 SSc patients with exercise-induced PH showed that 8 progressed to resting PH within 2-3 years, and 4 died from complications of pulmonary vascular disease within 3 years. “By waiting to diagnose this disease until it is present in the resting state, we are losing our opportunity to treat it,” he said.

These findings support the observation that “patients with SSc should be evaluated for exercise-induced PH. It's abnormal and should be treated in the context of a clinical study,” said Dr. Saggar said at a meeting sponsored by

For now, until the concept of screening for exercise-induced PH catches on, “before you ever treat a patient with PH, you have to get a right heart catheterization. Right heart catheterization is not that invasive in the right hands. The risk of associated mortality is less than 0.05%,” he said. Prognosis can be based on the findings from this test, he added.

Not all physicians are comfortable going straight to right heart catheterization. For them, yearly echocardiography and spirometry can be used to screen for PH. Certain clinical findings in scleroderma patients can identify which patients are likely to have PH. Early screening with noninvasive studies such as an echocardiogram and pulmonary function tests may detect these patients earlier.

Typical symptoms of any patient with scleroderma who has unexplained shortness of breath should also raise the physician's concern. Likewise PH should be on the short list of the differential diagnosis in any young scleroderma patient who has syncope. “These patients tell their physicians: 'I coughed and passed out.' Or 'I stood up and passed out,'” Dr. Saggar said at the meeting.

However, once a patient develops unexplained breathlessness, it is necessary to do right heart catheterization, he said. Breathlessness in any patients with PH associated with SSc is a sign that the disease is progressing. Aggressive management is the best hope for survival in SSc patients with PH.

The available treatments for PH remain of “arguable” efficacy, especially when they are initiated late in the course of the disease, when it has become incurable, according to Dr. Saggar.

In this progressive disease, increased pulmonary pressure is only part of the pathology. The benefit of serial right heart catheterization is that it enables the physician to assess the degree of right ventricular impairment. “What you are really worried about is the right ventricle. Failure of the right heart drives death,” he said.

As long as vascular resistance continues to increase, the patient remains in jeopardy. The right ventricle begins to fail in response to the increased vascular resistance.

PH is very rare. It is estimated to occur in 2.3-10 cases per 1 million population. Patients with SSc make up about 20% of all newly diagnosed PH patients. A recent French study that screened for PH in SSc using echocardiography and right heart catheterization showed a prevalence of 7.9%. However, findings from an autopsy study show that 60% of patients with SSc have findings typical of PH.

“This disease goes undiagnosed a lot of the time,” said Dr. Saggar.

Disclosures: Dr. Saggar reported no financial relationships that are relevant to this presentation. This newspaper and Skin Disease Education Foundation are owned by Elsevier.