Jennie Smith

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

People who are admitted to the hospital with inflammatory bowel disease are six times more likely to die in the hospital, and nearly twice as likely to need emergency surgery, if they are also infected with diarrhea-causing Clostridium difficile, British researchers have found.

C. difficile has emerged in recent years as a significant cause of hospital morbidity and mortality, with elderly, immunocompromised, and frequently hospitalized people most at risk. People with IBD are already considered to be particularly vulnerable to C. difficile infection, and the use of immunosuppressant drugs may make them more vulnerable still. Some broad-spectrum antibiotics have also been implicated in facilitating C. difficile infection.

"Our findings reinforce the clinical importance of testing for C. difficile among IBD inpatients, and we further recommend [that] screening of all inpatients with diarrhea for C. difficile infection [be] ... part of mandatory surveillance," investigator Min-Hua Jen, Ph.D., of Imperial College London and colleagues wrote in Alimentary Pharmacology and Therapeutics (2011 April 24 [doi:10.1111/j.1365-2036.2011.04661.x]).

Photo credit: CDC/Dr. Gilda Jones

In the United Kingdom, the incidence of C. difficile infections about doubled between 2002 and 2008 among people with IBD. (The United States saw a similar rise between 1998 and 2004.) Because patients with IBD often present with diarrhea regardless of infection status, surveillance with toxin assays is needed to identify C. difficile as the cause, they noted.

The researchers examined records from 6 years’ worth of admissions at U.K. public hospitals, and found that people who were admitted with IBD and were determined to be infected with C. difficile between 2002 and 2008 had a higher risk of dying in the hospital (adjusted odds ratio, 6.32), than did those who were not infected.

The infected also stayed in the hospital a median 26 days (compared with 5 days for IBD patients who were not infected), and they were 1.87 times more likely to undergo emergency gastrointestinal surgery.

For their research, the investigators looked at National Health Service records from 241,478 hospital admissions for IBD from 2002 to 2008. Of these, 2,402 cases had documented C. difficile, established by in-hospital testing; some 91% of these infections were likely acquired in a hospital setting, as the patients had had recent hospitalizations.

The finding, the investigators wrote, "confirms a rising trend in coexistent C. difficile infection among patient admitted to hospital with IBD over the period 2002-2008," and among these coinfected patients, "there is an increased in-hospital mortality and morbidity."

However, the investigators noted, the trend was seen as flattening out in the last 2 years of the study. "This finding may reflect a growing clinical awareness of the higher risk of C. difficile infection in IBD patients and improvements in management once diagnosis is made," they wrote, acknowledging too that the earlier, rising trend could also have corresponded with better screening for C. difficile.

They also pointed out that a previously published study "indicates that IBD patients treated with corticosteroids in combination with an immunomodulator, such as azathioprine, may have an increased risk" of C. difficile infection (Aliment. Pharmacol. Ther. 2009;3:253-64).

The investigators acknowledged as weaknesses of the study the fact that the type of data they used to identify cases made possible no confirmation of C. difficile infection through corresponding medical or laboratory records. Also, the national records "do not contain information on disease severity, how C. difficile diagnosis was reached, or antibiotic and immunomodulator prescribing, all of which are potential confounders."

However, they wrote, despite its limitations, "our study provides important information quantifying the increased risk of morbidity and in-hospital mortality" among IBD patients infected with C. difficile.

The research was supported by the U.K.’s National Institute for Health Research. Dr. Jen disclosed ongoing support from HERON Evidence Development. Dr. Jen and her coauthors from Imperial College London also receive funding under a research grant from Dr. Foster Intelligence. Neither Dr. Jen nor any of her colleagues declared having any relevant conflicts of interest.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The U.S. Food and Drug Administration announced April 19 that it had approved rituximab, in combination with glucocorticoids, for the treatment of people with Wegener’s granulomatosis and microscopic polyangiitis.

Wegener’s granulomatosis and microscopic polyangiitis are related, rare, autoimmune diseases that cause vasculitis. The approval of rituximab (Roche’s Rixutan) offers clinicians an alternative to cyclophosphamide, a current standard treatment for these disorders.

In one manufacturer-funded, randomized, controlled trial (n = 197) that enrolled people with Wegener’s granulomatosis and microscopic polyangiitis, 64% of subjects who were treated with rituximab plus glucocorticoids achieved remission in 6 months, compared with 53% of those treated with cyclophosphamide plus glucocorticoids (N. Engl. J. Med. 2010;363:221-32).

Patients in the study were not re-treated with rituximab after relapse, however, and more "data are needed to determine the safety of more than one course of Rituxan and long-term safety of use of Rituxan in patients with WG and MPA," the FDA said in a news release. "These questions will be further evaluated in a required post-marketing study."

Rituximab, a monoclonal antibody with indications for some types of lymphoma, leukemia, and some autoimmune disorders, works by reducing the number of B cells in the blood. In people with Wegener’s granulomatosis and microscopic polyangiitis, the percentage of activated peripheral-blood B lymphocytes correlates with disease activity.

The medication, which is administered by intravenous infusion, carries boxed warnings on its label for infusion reactions (which can occur during or after infusion), for rashes and sores in the skin and mouth, and for progressive multifocal leukoencephalopathy, which is usually fatal. Rituxan is not recommended for use in patients with severe, active infections, the FDA said.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

The first major overhaul in more than 25 years of diagnostic criteria for Alzheimer’s disease has resulted in a new, broader definition of Alzheimer’s that includes the disease’s mild and presymptomatic stages – yet it will be years before clinicians will be able to treat the disease in these early stages, authors of the new criteria say.

The criteria, developed through a joint workshops supported by the Alzheimer’s Association and the National Institutes of Health/National Institute on Aging, were published in four articles – collectively, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease – appearing online April 19 in the journal Alzheimer’s & Dementia (doi:10.1016/j.jalz.2011.03.008.)

The criteria divide the disease into three stages: preclinical Alzheimer’s, marked by no outward symptoms and only measurable changes in biomarkers such as spinal fluid chemistry; mild cognitive impairment, in which changes in memory and thinking appear but do not yet compromise everyday activities and functioning; and dementia, the defining trait of late-stage disease.

Currently, the criteria offer no way to diagnose Alzheimer’s in a preclinical state, as appropriate biomarkers are still being investigated and standardized, which means that "preclinical Alzheimer’s" remains mainly for future studies to define.

However, the publication of the new criteria makes it official that the middle stage, measurable mild cognitive impairment, can be considered part of the disease spectrum for Alzheimer’s. In other words, Alzheimer’s can now be defined by subtle brain changes rather than exclusively by dementia.

"The term we’re using is ‘MCI [mild cognitive impairment] due to Alzheimer’s disease,’ " said Marilyn Albert, Ph.D., of Johns Hopkins University, Baltimore, one of the papers’ lead authors, in an April 18 teleconference with the scientists who revised the criteria. Dr. Albert added that the term and the concept had been accepted in clinical practice for roughly a decade, if not formally defined.

In 1984, the last time comprehensive criteria for Alzheimer’s were published, "we thought of Alzheimer’s [primarily as] dementia," said Dr. Guy McKhann, also of Johns Hopkins, in the same teleconference. The biggest difference today, he said, "is that we now think of this process as a continuum" inclusive of MCI.

The authors cautioned that more work is needed to distinguish people with MCI who will go on to develop Alzheimer’s dementia from those who will not. Biomarkers such as beta-amyloid, they said, will likely play an important role in identifying these patients, whom the authors estimate to exist in numbers at least equal to the number of patients with current dementia.

The importance of viewing Alzheimer’s as a continuum or spectrum – making the early stages of Alzheimer’s officially Alzheimer’s – is that it aids research, particularly drug development, Dr. McKhann said, adding that there is little point in "looking for new medicines if you’re only going to try them in people with advanced dementia."

While there are currently no established clinical protocols for treating people with MCI, Dr. Reisa A. Sperling of Brigham and Women’s Hospital and Harvard Medical School, Boston, said in the teleconference that clinicians had the option of referring to research settings when possible. "There are ongoing clinical trials of drugs in people with MCI due to Alzheimer’s," Dr. Sperling said.

With regard to potential conflicts of interest, Dr. Albert serves as a consultant to Genentech and Eli Lilly and receives grants to her institution from GE Healthcare. Dr. McKhann serves on a Data Safety Monitoring Board for Merck; Dr. Sperling has served as a site investigator and/or consultant to several companies developing imaging biomarkers and pharmacologic treatments for early AD, including Avid, Bayer, Bristol-Myers Squibb, Elan, Eisai, Janssen, Pfizer, and Wyeth.

Triglyceride levels, which play a large role in both atherosclerotic risk and metabolic health, are highly responsive to decreases in dietary sugar intake and saturated and trans fat intake, along with increases in omega-3 acid intake and exercise, according to a scientific statement from the American Heart Association.

"What’s new is that we point out that triglycerides might be considered a marker for metabolic health," said Dr. Neil J. Stone of Northwestern University, Chicago, vice chair of the statement’s writing group, in an interview. "If you have a country where you’re seeing more obesity and more diabetes, it becomes important for people to start asking themselves ‘are there signs that I should be doing something different?’ and this is one," he said.

Photo credit: © Paul Johnson/iStock.com

The scientific advisory, published online April 18 in the journal Circulation and citing some 528 sources, was not presented as a clinical guideline so much as a distillation of 30 years worth of evidence on the complex relationship among lifestyle factors, triglycerides, and cardiovascular and metabolic health (Circulation 2011 [doi:10.1161/ CIR.0b013e3182160726]).

However, the statement’s authors, led by Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland, Baltimore, included a number of recommendations on diagnosing and treating hypertriglyceridemia, focusing on dietary and lifestyle changes.

The statement emphasizes the "increasingly crucial role" of triglycerides in the evaluation and management of cardiovascular disease, and the importance of diet – including consumption of sugars common in beverages – in contributing to unhealthy triglyceride levels.

Reductions of 50% or more are achievable without the use of medication – indeed medication is not a widely accepted strategy for reducing triglycerides except among people with extremely high values of greater than 500 mg/dL. "The subject of medication and triglycerides is still lacking crucial clinical trial evidence," Dr. Miller and colleagues wrote in their analysis, noting that certain medications, including hormonal treatments, can also contribute to elevated triglycerides.

About a third of American adults have elevated triglyceride levels, which are defined as fasting triglyceride of 150 mg/dL or higher. The authors recommended that optimal fasting triglyceride levels now be defined as 100 mg/dL – and that clinicians screen initially for nonfasting triglyceride, defining normal at below 200 mg/dL. People with higher nonfasting levels may then be further screened for fasting triglyceride.

The new dietary recommendations include restricting added dietary sugar to 5%-10% percent of calories consumed. In support of this, the authors cited a study of 6,113 U.S. adults showing that the lowest triglyceride levels were observed when added sugar represented less than 10% of total energy, and that higher triglyceride levels corresponded with added sugar accounting for a greater proportion of energy intake (JAMA 2010;303:1490-7).

The authors singled out fructose, a type of dietary sugar increasingly common in processed foods and soft drinks, as particularly problematic. Fructose in excess of 100 g/day, and possibly in excess of 50 g/day, has been associated with raised triglyceride levels. A typical can of cola or lemon-lime soda contains more than 20 grams of fructose, the authors noted.

Dr. Miller and his colleagues advocated weight loss of 5%-10% of body weight, which is associated with a 20% reduction in triglycerides, and regular aerobic exercise, to reduce triglyceride levels closer to optimal.

They also promoted increasing dietary fiber, keeping saturated fat below 7% of calories, eliminating trans fat from the diet, and increasing omega-3 polyunsaturated fatty acid consumption in the form of marine fish, though the authors said more research was needed to determine whether supplementing with fish-oil capsules provided equivalent benefits. Complete abstinence from alcohol was also recommended for people with very high triglycerides.

"Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%," they concluded.

Funding for the scientific advisory statement was provided by the American Heart Association. Dr. Miller declared no conflicts of interest affecting the drafting of the statement. However, Dr. Stone and the report’s third author, Dr. Christie Ballantyne of Baylor College of Medicine in Houston, disclosed support from pharmaceutical industry sources. Other coauthors and some reviewers disclosed additional support from pharmaceutical and agricultural firms.

Triglyceride levels, which play a large role in both atherosclerotic risk and metabolic health, are highly responsive to decreases in dietary sugar intake and saturated and trans fat intake, along with increases in omega-3 acid intake and exercise, according to a scientific statement from the American Heart Association.

"What’s new is that we point out that triglycerides might be considered a marker for metabolic health," said Dr. Neil J. Stone of Northwestern University, Chicago, vice chair of the statement’s writing group, in an interview. "If you have a country where you’re seeing more obesity and more diabetes, it becomes important for people to start asking themselves ‘are there signs that I should be doing something different?’ and this is one," he said.

Photo credit: © Paul Johnson/iStock.com

The scientific advisory, published online April 18 in the journal Circulation and citing some 528 sources, was not presented as a clinical guideline so much as a distillation of 30 years worth of evidence on the complex relationship among lifestyle factors, triglycerides, and cardiovascular and metabolic health (Circulation 2011 [doi:10.1161/ CIR.0b013e3182160726]).

However, the statement’s authors, led by Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland, Baltimore, included a number of recommendations on diagnosing and treating hypertriglyceridemia, focusing on dietary and lifestyle changes.

The statement emphasizes the "increasingly crucial role" of triglycerides in the evaluation and management of cardiovascular disease, and the importance of diet – including consumption of sugars common in beverages – in contributing to unhealthy triglyceride levels.

Reductions of 50% or more are achievable without the use of medication – indeed medication is not a widely accepted strategy for reducing triglycerides except among people with extremely high values of greater than 500 mg/dL. "The subject of medication and triglycerides is still lacking crucial clinical trial evidence," Dr. Miller and colleagues wrote in their analysis, noting that certain medications, including hormonal treatments, can also contribute to elevated triglycerides.

About a third of American adults have elevated triglyceride levels, which are defined as fasting triglyceride of 150 mg/dL or higher. The authors recommended that optimal fasting triglyceride levels now be defined as 100 mg/dL – and that clinicians screen initially for nonfasting triglyceride, defining normal at below 200 mg/dL. People with higher nonfasting levels may then be further screened for fasting triglyceride.

The new dietary recommendations include restricting added dietary sugar to 5%-10% percent of calories consumed. In support of this, the authors cited a study of 6,113 U.S. adults showing that the lowest triglyceride levels were observed when added sugar represented less than 10% of total energy, and that higher triglyceride levels corresponded with added sugar accounting for a greater proportion of energy intake (JAMA 2010;303:1490-7).

The authors singled out fructose, a type of dietary sugar increasingly common in processed foods and soft drinks, as particularly problematic. Fructose in excess of 100 g/day, and possibly in excess of 50 g/day, has been associated with raised triglyceride levels. A typical can of cola or lemon-lime soda contains more than 20 grams of fructose, the authors noted.

Dr. Miller and his colleagues advocated weight loss of 5%-10% of body weight, which is associated with a 20% reduction in triglycerides, and regular aerobic exercise, to reduce triglyceride levels closer to optimal.

They also promoted increasing dietary fiber, keeping saturated fat below 7% of calories, eliminating trans fat from the diet, and increasing omega-3 polyunsaturated fatty acid consumption in the form of marine fish, though the authors said more research was needed to determine whether supplementing with fish-oil capsules provided equivalent benefits. Complete abstinence from alcohol was also recommended for people with very high triglycerides.

"Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%," they concluded.

Funding for the scientific advisory statement was provided by the American Heart Association. Dr. Miller declared no conflicts of interest affecting the drafting of the statement. However, Dr. Stone and the report’s third author, Dr. Christie Ballantyne of Baylor College of Medicine in Houston, disclosed support from pharmaceutical industry sources. Other coauthors and some reviewers disclosed additional support from pharmaceutical and agricultural firms.

Triglyceride levels, which play a large role in both atherosclerotic risk and metabolic health, are highly responsive to decreases in dietary sugar intake and saturated and trans fat intake, along with increases in omega-3 acid intake and exercise, according to a scientific statement from the American Heart Association.

"What’s new is that we point out that triglycerides might be considered a marker for metabolic health," said Dr. Neil J. Stone of Northwestern University, Chicago, vice chair of the statement’s writing group, in an interview. "If you have a country where you’re seeing more obesity and more diabetes, it becomes important for people to start asking themselves ‘are there signs that I should be doing something different?’ and this is one," he said.

Photo credit: © Paul Johnson/iStock.com

The scientific advisory, published online April 18 in the journal Circulation and citing some 528 sources, was not presented as a clinical guideline so much as a distillation of 30 years worth of evidence on the complex relationship among lifestyle factors, triglycerides, and cardiovascular and metabolic health (Circulation 2011 [doi:10.1161/ CIR.0b013e3182160726]).

However, the statement’s authors, led by Dr. Michael Miller, director of the Center for Preventive Cardiology at the University of Maryland, Baltimore, included a number of recommendations on diagnosing and treating hypertriglyceridemia, focusing on dietary and lifestyle changes.

The statement emphasizes the "increasingly crucial role" of triglycerides in the evaluation and management of cardiovascular disease, and the importance of diet – including consumption of sugars common in beverages – in contributing to unhealthy triglyceride levels.

Reductions of 50% or more are achievable without the use of medication – indeed medication is not a widely accepted strategy for reducing triglycerides except among people with extremely high values of greater than 500 mg/dL. "The subject of medication and triglycerides is still lacking crucial clinical trial evidence," Dr. Miller and colleagues wrote in their analysis, noting that certain medications, including hormonal treatments, can also contribute to elevated triglycerides.

About a third of American adults have elevated triglyceride levels, which are defined as fasting triglyceride of 150 mg/dL or higher. The authors recommended that optimal fasting triglyceride levels now be defined as 100 mg/dL – and that clinicians screen initially for nonfasting triglyceride, defining normal at below 200 mg/dL. People with higher nonfasting levels may then be further screened for fasting triglyceride.

The new dietary recommendations include restricting added dietary sugar to 5%-10% percent of calories consumed. In support of this, the authors cited a study of 6,113 U.S. adults showing that the lowest triglyceride levels were observed when added sugar represented less than 10% of total energy, and that higher triglyceride levels corresponded with added sugar accounting for a greater proportion of energy intake (JAMA 2010;303:1490-7).

The authors singled out fructose, a type of dietary sugar increasingly common in processed foods and soft drinks, as particularly problematic. Fructose in excess of 100 g/day, and possibly in excess of 50 g/day, has been associated with raised triglyceride levels. A typical can of cola or lemon-lime soda contains more than 20 grams of fructose, the authors noted.

Dr. Miller and his colleagues advocated weight loss of 5%-10% of body weight, which is associated with a 20% reduction in triglycerides, and regular aerobic exercise, to reduce triglyceride levels closer to optimal.

They also promoted increasing dietary fiber, keeping saturated fat below 7% of calories, eliminating trans fat from the diet, and increasing omega-3 polyunsaturated fatty acid consumption in the form of marine fish, though the authors said more research was needed to determine whether supplementing with fish-oil capsules provided equivalent benefits. Complete abstinence from alcohol was also recommended for people with very high triglycerides.

"Overall, optimization of nutrition-related practices can result in a marked triglyceride-lowering effect that ranges between 20% and 50%," they concluded.

Funding for the scientific advisory statement was provided by the American Heart Association. Dr. Miller declared no conflicts of interest affecting the drafting of the statement. However, Dr. Stone and the report’s third author, Dr. Christie Ballantyne of Baylor College of Medicine in Houston, disclosed support from pharmaceutical industry sources. Other coauthors and some reviewers disclosed additional support from pharmaceutical and agricultural firms.