Kate Johnson

Children diagnosed with celiac disease usually experience complete remission once they are started on a gluten-free diet, and thus early diagnosis can be beneficial. But early diagnosis may have adverse effects as well. A large British study has found that a diagnosis of celiac disease in childhood, as opposed to adulthood, is associated with threefold higher mortality–largely due to suicide, accidents, and violence.

The findings are “really surprising and unexpected,” according to Dr. Stefano Guandalini, chief of pediatric gastroenterology and director of the Celiac Disease Program at the University of Chicago. As one of the reviewers of the British study, he said he is confident that the increased mortality is more than a chance finding, but the reasons for it are open to interpretation. “One certainly cannot ignore this report; it's a well-done study,” he said in an interview.

The investigators analyzed data on a cohort of 625 celiac patients and found that those who were diagnosed in childhood (47%) had mortality rates three times higher than would be expected in the general, age-matched population, “with the main cause of the increase being deaths from accidents, suicide, and violence,” reported Dr. Masoud Solaymani-Dodoran and colleagues from the University of Nottingham (England). This increase was not seen in the cohort diagnosed in adulthood (Am. J. Gastroenterol. 2007;102:864-70).

“One explanation for this could be the psychological status of the children and possible changes in their risk-taking behaviors,” said Dr. Solaymani-Dodoran in an interview. The median age at diagnosis was 1.5 years in study subjects diagnosed in childhood (compared with 46 years in those diagnosed as adults), with the threefold increased mortality risk remaining through adolescence and beyond, to more than 25 years after diagnosis.

The Effect of Nonadherence

“Unfortunately [the researchers] had no available data to tell us what percentage of the subjects was on a gluten-free diet,” Dr. Guandalini said in an interview. Nonadherence with the diet has been reported, in other studies, in up to 60% of celiac patients during the rebellious teenage years.

This could explain the increased mortality, he suggested, because in some celiac patients, dietary lapses can have a dramatic effect on the brain. Gluten restriction is recommended, both to relieve the myriad and varied symptoms of celiac disease–ranging from dental to dermatologic to neurologic–and to reduce the potential long-term effects of prolonged exposure, including osteoporosis and malignancies.

“My speculation is that most of these deaths occurred in people who were not following the diet, and this caused the behavioral and psychiatric milieu that would lead to that kind of outcome,” he said.

Finnish authors have suggested that exposure to gluten in adolescents with celiac disease can impair the availability of tryptophan “and the possible consequent serotonergic dysfunction may play a role in vulnerability to depressive disorders” (BMC Psychiatry 2005;5:14-9). They noted that five of nine newly diagnosed, untreated adolescent celiac patients had depressive disorders and abnormal tryptophan levels, all of which improved after gluten was removed from their diets.

“I am personally convinced that eating gluten if you have celiac disease really induces serious changes in brain chemistry that would make you inclined to aggressive, depressive behavior and therefore expose you to this risk,” said Dr. Guandalini, who has seen such psychiatric effects in a celiac patient as young as 5 years old.

The Impact of Adherence

“We know adherence [to the diet] and depression and anxiety are related,” said Jessica Edwards George, Ph.D., psychologist and researcher at The Celiac Center at Beth Israel Deaconess Medical Center in Boston. But the relationship between adherence and psychological symptoms is not well understood, she said in an interview. Just as poor adherence is linked with psychiatric pathology, so too is good adherence–an aspect highlighted by the British authors.

“The actual process of labeling a child with celiac disease and requiring them to adhere to a gluten-free diet may be, in some way, detrimental,” they wrote. “As treatments go, taking a gluten-free diet must rank as one of the most intrusive for a child–more so than something like, for example, epilepsy or asthma,” coauthor Dr. Richard Logan said in an interview. “We wondered what were the psychological effects on a child of being brought up with a condition whose treatment has such a profound effect on daily life–something I suspect most adult gastroenterologists overlook.”

The psychological research on adults regarding this question leaves little open to debate: “There's a lot of anger and frustration about the rigidity of the diet, as well as the fact that it is chronic,” said Sharon Jedel, Psy.D., a clinical psychologist at Rush University's adult celiac disease program in Chicago. Furthermore, “a child doesn't necessarily have the developmental capacities to cope the way an adult might.”

As a former school psychologist, Dr. Edwards George agreed. “Children report feeling different and embarrassed, left out, and angry,” she wrote in a recent article for the National Association of School Psychologists (NASP Communiquè 2006 June;34:8). “It can be heart-breaking for a child to be unable to eat gluten-containing treats at special occasions, such as birthdays or holidays.”

However, both Dr. Edwards George and Dr. Jedel treat psychological issues in adult patients only, and there are very few studies examining the social burden of following a gluten-free diet in the vulnerable adolescent years. “The most important thing we think of with adolescents is the social network,” Dr. Jedel said. “If they are not able to eat what their friends eat, all of the shame, the embarrassment, the frustration associated with these ongoing social situations would I'm sure produce a lot of anger, and depression.”

One Italian study which included 39 adolescent patients pointed to the ages between 12 and 17 years as being the most problematic. “That is the period of life in which the individual tends to oppose the adult world in search of an individual personality,” wrote Dr. M. Cinquetti and colleagues from Verona (Italy) University (Pediatr. Med. Chir. 1999;21:279-83). “In this group, the search for an individual personality is disturbed.”

Even after adolescence, such experiences can have lasting effects. In one study of adult patients, a subset of patients who were diagnosed as children remembered situations from their childhood “with intense emotions, even if the events had occurred many years ago” (J. Hum. Nutr. Dietet. 2005;18:171-80).

In Search of Normalcy

Even in the absence of anger or depression about their condition, adolescents with chronic diseases are more likely to be “risk takers,” and this is another possible explanation for the increased deaths by accident and violence, the British authors noted.

“Adolescents in general don't have to prove they are 'normal', but adolescents with chronic conditions do,” explained Dr. Joan-Carles Suris, head of the research group on adolescent health at the Institute of Social and Preventive Medicine of the University of Lausanne (Switzerland).

One way to accomplish this is to behave the way they think their healthy peers are behaving, even though their assumption that “everyone” is drinking, or smoking, or doing drugs is often erroneous, he said in an interview. In his analysis of almost 7,000 adolescents, 665 (9.5%) had a variety of chronic conditions including diabetes, asthma, scoliosis, epilepsy, arthritis, and kidney disease. Dr. Suris found higher rates of risky sexual activity, history of pregnancy, history of sexually transmitted disease, smoking, drinking, and illegal drug use among those with the chronic conditions, compared with their healthy peers (Eur. J. Public Health 2005;15:484-8).

Although Dr. Suris' study did not include patients with celiac disease, he said any condition involving food restriction presents limitations to an adolescent's social life. “It is hard to go out for pizza with your friends and not be able to eat it,” he said. “It has been said that the best contribution for diabetic patients after insulin was the introduction of sugar-free beverages, because this allowed them to socialize with their peers without being seen as different. Maybe we should try to do that with other food problems, so that cafeterias or restaurants have options for them,” he said.

Such options are becoming more widely offered, but Dr. Edwards George said children with celiac disease also need the tools to cope in a gluten-filled world–lessons they might be taught with the help of more psychological research. “They need skills to advocate for themselves, and we can build in supports to help them be more organized and more conscientious.”

In the meantime, she also believes that vigilance is of utmost importance for physicians. “We need to be more aware of mood factors and more proactive about screening and treatment for depression, anxiety, and suicidal ideation.” Included in this careful follow-up should be targeted screening for eating disorders, she said–a practice soon to be adopted at her center–since her research suggests that these disorders may often be missed in this perhaps more vulnerable population.

“We see a lot of people fearful of eating anything at all” at diagnosis, she said. Patients may have a general fear of long-term consequences, such as cancer or osteoporosis, or may be afraid of short-term consequences, such as becoming violently ill after eating a food containing gluten. Patients also become “hyperfocused on food” as a result of constantly reading labels and asking about ingredients, she said.

Such disturbed eating patterns and hypervigilance, coupled with a common increase in weight after a malnourished patient is diagnosed and treated, can be a cause for concern. In one of her studies “we did find some people who actually ate gluten in order to lose weight,” just as diabetic patients have been known to withhold insulin for the same reason, she said (Eur. J. Gastroenterol. Hepatol. 2007;19:251-5).

As awareness about celiac disease continues to grow, experts agree that the current average 11-year gap between symptom onset and diagnosis will shrink, resulting in more diagnoses in childhood and adolescence.

There was also a consensus among all the experts interviewed that, given the recent findings of an increased mortality rate associated with this earlier diagnosis, any attempts to reduce this higher mortality must begin with a better understanding of the unique burdens that childhood diagnosis and treatment may bring.

Get Help With Celiac Disease

Dr. Edwards George recommends these organizations as good resources for patients and families dealing with celiac disease:

PICeliac Disease Foundation

Phone: 213-654-4085

Web site:

www.celiac.org

PICeliac Sprue Association of the United States of America

Phone: 402-558-0600

Web site:

www.csaceliacs.org

PIGluten Intolerance Group

Phone: 253-833-6655

Web site:

www.gluten.net

PINational Foundation for Celiac Awareness

Phone: 215-325-1306

Web site:

www.celiaccentral.org

Children diagnosed with celiac disease usually experience complete remission once they are started on a gluten-free diet, and thus early diagnosis can be beneficial. But early diagnosis may have adverse effects as well. A large British study has found that a diagnosis of celiac disease in childhood, as opposed to adulthood, is associated with threefold higher mortality–largely due to suicide, accidents, and violence.

The findings are “really surprising and unexpected,” according to Dr. Stefano Guandalini, chief of pediatric gastroenterology and director of the Celiac Disease Program at the University of Chicago. As one of the reviewers of the British study, he said he is confident that the increased mortality is more than a chance finding, but the reasons for it are open to interpretation. “One certainly cannot ignore this report; it's a well-done study,” he said in an interview.

The investigators analyzed data on a cohort of 625 celiac patients and found that those who were diagnosed in childhood (47%) had mortality rates three times higher than would be expected in the general, age-matched population, “with the main cause of the increase being deaths from accidents, suicide, and violence,” reported Dr. Masoud Solaymani-Dodoran and colleagues from the University of Nottingham (England). This increase was not seen in the cohort diagnosed in adulthood (Am. J. Gastroenterol. 2007;102:864-70).

“One explanation for this could be the psychological status of the children and possible changes in their risk-taking behaviors,” said Dr. Solaymani-Dodoran in an interview. The median age at diagnosis was 1.5 years in study subjects diagnosed in childhood (compared with 46 years in those diagnosed as adults), with the threefold increased mortality risk remaining through adolescence and beyond, to more than 25 years after diagnosis.

The Effect of Nonadherence

“Unfortunately [the researchers] had no available data to tell us what percentage of the subjects was on a gluten-free diet,” Dr. Guandalini said in an interview. Nonadherence with the diet has been reported, in other studies, in up to 60% of celiac patients during the rebellious teenage years.

This could explain the increased mortality, he suggested, because in some celiac patients, dietary lapses can have a dramatic effect on the brain. Gluten restriction is recommended, both to relieve the myriad and varied symptoms of celiac disease–ranging from dental to dermatologic to neurologic–and to reduce the potential long-term effects of prolonged exposure, including osteoporosis and malignancies.

“My speculation is that most of these deaths occurred in people who were not following the diet, and this caused the behavioral and psychiatric milieu that would lead to that kind of outcome,” he said.

Finnish authors have suggested that exposure to gluten in adolescents with celiac disease can impair the availability of tryptophan “and the possible consequent serotonergic dysfunction may play a role in vulnerability to depressive disorders” (BMC Psychiatry 2005;5:14-9). They noted that five of nine newly diagnosed, untreated adolescent celiac patients had depressive disorders and abnormal tryptophan levels, all of which improved after gluten was removed from their diets.

“I am personally convinced that eating gluten if you have celiac disease really induces serious changes in brain chemistry that would make you inclined to aggressive, depressive behavior and therefore expose you to this risk,” said Dr. Guandalini, who has seen such psychiatric effects in a celiac patient as young as 5 years old.

The Impact of Adherence

“We know adherence [to the diet] and depression and anxiety are related,” said Jessica Edwards George, Ph.D., psychologist and researcher at The Celiac Center at Beth Israel Deaconess Medical Center in Boston. But the relationship between adherence and psychological symptoms is not well understood, she said in an interview. Just as poor adherence is linked with psychiatric pathology, so too is good adherence–an aspect highlighted by the British authors.

“The actual process of labeling a child with celiac disease and requiring them to adhere to a gluten-free diet may be, in some way, detrimental,” they wrote. “As treatments go, taking a gluten-free diet must rank as one of the most intrusive for a child–more so than something like, for example, epilepsy or asthma,” coauthor Dr. Richard Logan said in an interview. “We wondered what were the psychological effects on a child of being brought up with a condition whose treatment has such a profound effect on daily life–something I suspect most adult gastroenterologists overlook.”

The psychological research on adults regarding this question leaves little open to debate: “There's a lot of anger and frustration about the rigidity of the diet, as well as the fact that it is chronic,” said Sharon Jedel, Psy.D., a clinical psychologist at Rush University's adult celiac disease program in Chicago. Furthermore, “a child doesn't necessarily have the developmental capacities to cope the way an adult might.”

As a former school psychologist, Dr. Edwards George agreed. “Children report feeling different and embarrassed, left out, and angry,” she wrote in a recent article for the National Association of School Psychologists (NASP Communiquè 2006 June;34:8). “It can be heart-breaking for a child to be unable to eat gluten-containing treats at special occasions, such as birthdays or holidays.”

However, both Dr. Edwards George and Dr. Jedel treat psychological issues in adult patients only, and there are very few studies examining the social burden of following a gluten-free diet in the vulnerable adolescent years. “The most important thing we think of with adolescents is the social network,” Dr. Jedel said. “If they are not able to eat what their friends eat, all of the shame, the embarrassment, the frustration associated with these ongoing social situations would I'm sure produce a lot of anger, and depression.”

One Italian study which included 39 adolescent patients pointed to the ages between 12 and 17 years as being the most problematic. “That is the period of life in which the individual tends to oppose the adult world in search of an individual personality,” wrote Dr. M. Cinquetti and colleagues from Verona (Italy) University (Pediatr. Med. Chir. 1999;21:279-83). “In this group, the search for an individual personality is disturbed.”

Even after adolescence, such experiences can have lasting effects. In one study of adult patients, a subset of patients who were diagnosed as children remembered situations from their childhood “with intense emotions, even if the events had occurred many years ago” (J. Hum. Nutr. Dietet. 2005;18:171-80).

In Search of Normalcy

Even in the absence of anger or depression about their condition, adolescents with chronic diseases are more likely to be “risk takers,” and this is another possible explanation for the increased deaths by accident and violence, the British authors noted.

“Adolescents in general don't have to prove they are 'normal', but adolescents with chronic conditions do,” explained Dr. Joan-Carles Suris, head of the research group on adolescent health at the Institute of Social and Preventive Medicine of the University of Lausanne (Switzerland).

One way to accomplish this is to behave the way they think their healthy peers are behaving, even though their assumption that “everyone” is drinking, or smoking, or doing drugs is often erroneous, he said in an interview. In his analysis of almost 7,000 adolescents, 665 (9.5%) had a variety of chronic conditions including diabetes, asthma, scoliosis, epilepsy, arthritis, and kidney disease. Dr. Suris found higher rates of risky sexual activity, history of pregnancy, history of sexually transmitted disease, smoking, drinking, and illegal drug use among those with the chronic conditions, compared with their healthy peers (Eur. J. Public Health 2005;15:484-8).

Although Dr. Suris' study did not include patients with celiac disease, he said any condition involving food restriction presents limitations to an adolescent's social life. “It is hard to go out for pizza with your friends and not be able to eat it,” he said. “It has been said that the best contribution for diabetic patients after insulin was the introduction of sugar-free beverages, because this allowed them to socialize with their peers without being seen as different. Maybe we should try to do that with other food problems, so that cafeterias or restaurants have options for them,” he said.

Such options are becoming more widely offered, but Dr. Edwards George said children with celiac disease also need the tools to cope in a gluten-filled world–lessons they might be taught with the help of more psychological research. “They need skills to advocate for themselves, and we can build in supports to help them be more organized and more conscientious.”

In the meantime, she also believes that vigilance is of utmost importance for physicians. “We need to be more aware of mood factors and more proactive about screening and treatment for depression, anxiety, and suicidal ideation.” Included in this careful follow-up should be targeted screening for eating disorders, she said–a practice soon to be adopted at her center–since her research suggests that these disorders may often be missed in this perhaps more vulnerable population.

“We see a lot of people fearful of eating anything at all” at diagnosis, she said. Patients may have a general fear of long-term consequences, such as cancer or osteoporosis, or may be afraid of short-term consequences, such as becoming violently ill after eating a food containing gluten. Patients also become “hyperfocused on food” as a result of constantly reading labels and asking about ingredients, she said.

Such disturbed eating patterns and hypervigilance, coupled with a common increase in weight after a malnourished patient is diagnosed and treated, can be a cause for concern. In one of her studies “we did find some people who actually ate gluten in order to lose weight,” just as diabetic patients have been known to withhold insulin for the same reason, she said (Eur. J. Gastroenterol. Hepatol. 2007;19:251-5).

As awareness about celiac disease continues to grow, experts agree that the current average 11-year gap between symptom onset and diagnosis will shrink, resulting in more diagnoses in childhood and adolescence.

There was also a consensus among all the experts interviewed that, given the recent findings of an increased mortality rate associated with this earlier diagnosis, any attempts to reduce this higher mortality must begin with a better understanding of the unique burdens that childhood diagnosis and treatment may bring.

Get Help With Celiac Disease

Dr. Edwards George recommends these organizations as good resources for patients and families dealing with celiac disease:

PICeliac Disease Foundation

Phone: 213-654-4085

Web site:

www.celiac.org

PICeliac Sprue Association of the United States of America

Phone: 402-558-0600

Web site:

www.csaceliacs.org

PIGluten Intolerance Group

Phone: 253-833-6655

Web site:

www.gluten.net

PINational Foundation for Celiac Awareness

Phone: 215-325-1306

Web site:

www.celiaccentral.org

Children diagnosed with celiac disease usually experience complete remission once they are started on a gluten-free diet, and thus early diagnosis can be beneficial. But early diagnosis may have adverse effects as well. A large British study has found that a diagnosis of celiac disease in childhood, as opposed to adulthood, is associated with threefold higher mortality–largely due to suicide, accidents, and violence.

The findings are “really surprising and unexpected,” according to Dr. Stefano Guandalini, chief of pediatric gastroenterology and director of the Celiac Disease Program at the University of Chicago. As one of the reviewers of the British study, he said he is confident that the increased mortality is more than a chance finding, but the reasons for it are open to interpretation. “One certainly cannot ignore this report; it's a well-done study,” he said in an interview.

The investigators analyzed data on a cohort of 625 celiac patients and found that those who were diagnosed in childhood (47%) had mortality rates three times higher than would be expected in the general, age-matched population, “with the main cause of the increase being deaths from accidents, suicide, and violence,” reported Dr. Masoud Solaymani-Dodoran and colleagues from the University of Nottingham (England). This increase was not seen in the cohort diagnosed in adulthood (Am. J. Gastroenterol. 2007;102:864-70).

“One explanation for this could be the psychological status of the children and possible changes in their risk-taking behaviors,” said Dr. Solaymani-Dodoran in an interview. The median age at diagnosis was 1.5 years in study subjects diagnosed in childhood (compared with 46 years in those diagnosed as adults), with the threefold increased mortality risk remaining through adolescence and beyond, to more than 25 years after diagnosis.

The Effect of Nonadherence

“Unfortunately [the researchers] had no available data to tell us what percentage of the subjects was on a gluten-free diet,” Dr. Guandalini said in an interview. Nonadherence with the diet has been reported, in other studies, in up to 60% of celiac patients during the rebellious teenage years.

This could explain the increased mortality, he suggested, because in some celiac patients, dietary lapses can have a dramatic effect on the brain. Gluten restriction is recommended, both to relieve the myriad and varied symptoms of celiac disease–ranging from dental to dermatologic to neurologic–and to reduce the potential long-term effects of prolonged exposure, including osteoporosis and malignancies.

“My speculation is that most of these deaths occurred in people who were not following the diet, and this caused the behavioral and psychiatric milieu that would lead to that kind of outcome,” he said.

Finnish authors have suggested that exposure to gluten in adolescents with celiac disease can impair the availability of tryptophan “and the possible consequent serotonergic dysfunction may play a role in vulnerability to depressive disorders” (BMC Psychiatry 2005;5:14-9). They noted that five of nine newly diagnosed, untreated adolescent celiac patients had depressive disorders and abnormal tryptophan levels, all of which improved after gluten was removed from their diets.

“I am personally convinced that eating gluten if you have celiac disease really induces serious changes in brain chemistry that would make you inclined to aggressive, depressive behavior and therefore expose you to this risk,” said Dr. Guandalini, who has seen such psychiatric effects in a celiac patient as young as 5 years old.

The Impact of Adherence

“We know adherence [to the diet] and depression and anxiety are related,” said Jessica Edwards George, Ph.D., psychologist and researcher at The Celiac Center at Beth Israel Deaconess Medical Center in Boston. But the relationship between adherence and psychological symptoms is not well understood, she said in an interview. Just as poor adherence is linked with psychiatric pathology, so too is good adherence–an aspect highlighted by the British authors.

“The actual process of labeling a child with celiac disease and requiring them to adhere to a gluten-free diet may be, in some way, detrimental,” they wrote. “As treatments go, taking a gluten-free diet must rank as one of the most intrusive for a child–more so than something like, for example, epilepsy or asthma,” coauthor Dr. Richard Logan said in an interview. “We wondered what were the psychological effects on a child of being brought up with a condition whose treatment has such a profound effect on daily life–something I suspect most adult gastroenterologists overlook.”

The psychological research on adults regarding this question leaves little open to debate: “There's a lot of anger and frustration about the rigidity of the diet, as well as the fact that it is chronic,” said Sharon Jedel, Psy.D., a clinical psychologist at Rush University's adult celiac disease program in Chicago. Furthermore, “a child doesn't necessarily have the developmental capacities to cope the way an adult might.”

As a former school psychologist, Dr. Edwards George agreed. “Children report feeling different and embarrassed, left out, and angry,” she wrote in a recent article for the National Association of School Psychologists (NASP Communiquè 2006 June;34:8). “It can be heart-breaking for a child to be unable to eat gluten-containing treats at special occasions, such as birthdays or holidays.”

However, both Dr. Edwards George and Dr. Jedel treat psychological issues in adult patients only, and there are very few studies examining the social burden of following a gluten-free diet in the vulnerable adolescent years. “The most important thing we think of with adolescents is the social network,” Dr. Jedel said. “If they are not able to eat what their friends eat, all of the shame, the embarrassment, the frustration associated with these ongoing social situations would I'm sure produce a lot of anger, and depression.”

One Italian study which included 39 adolescent patients pointed to the ages between 12 and 17 years as being the most problematic. “That is the period of life in which the individual tends to oppose the adult world in search of an individual personality,” wrote Dr. M. Cinquetti and colleagues from Verona (Italy) University (Pediatr. Med. Chir. 1999;21:279-83). “In this group, the search for an individual personality is disturbed.”

Even after adolescence, such experiences can have lasting effects. In one study of adult patients, a subset of patients who were diagnosed as children remembered situations from their childhood “with intense emotions, even if the events had occurred many years ago” (J. Hum. Nutr. Dietet. 2005;18:171-80).

In Search of Normalcy

Even in the absence of anger or depression about their condition, adolescents with chronic diseases are more likely to be “risk takers,” and this is another possible explanation for the increased deaths by accident and violence, the British authors noted.

“Adolescents in general don't have to prove they are 'normal', but adolescents with chronic conditions do,” explained Dr. Joan-Carles Suris, head of the research group on adolescent health at the Institute of Social and Preventive Medicine of the University of Lausanne (Switzerland).

One way to accomplish this is to behave the way they think their healthy peers are behaving, even though their assumption that “everyone” is drinking, or smoking, or doing drugs is often erroneous, he said in an interview. In his analysis of almost 7,000 adolescents, 665 (9.5%) had a variety of chronic conditions including diabetes, asthma, scoliosis, epilepsy, arthritis, and kidney disease. Dr. Suris found higher rates of risky sexual activity, history of pregnancy, history of sexually transmitted disease, smoking, drinking, and illegal drug use among those with the chronic conditions, compared with their healthy peers (Eur. J. Public Health 2005;15:484-8).

Although Dr. Suris' study did not include patients with celiac disease, he said any condition involving food restriction presents limitations to an adolescent's social life. “It is hard to go out for pizza with your friends and not be able to eat it,” he said. “It has been said that the best contribution for diabetic patients after insulin was the introduction of sugar-free beverages, because this allowed them to socialize with their peers without being seen as different. Maybe we should try to do that with other food problems, so that cafeterias or restaurants have options for them,” he said.

Such options are becoming more widely offered, but Dr. Edwards George said children with celiac disease also need the tools to cope in a gluten-filled world–lessons they might be taught with the help of more psychological research. “They need skills to advocate for themselves, and we can build in supports to help them be more organized and more conscientious.”

In the meantime, she also believes that vigilance is of utmost importance for physicians. “We need to be more aware of mood factors and more proactive about screening and treatment for depression, anxiety, and suicidal ideation.” Included in this careful follow-up should be targeted screening for eating disorders, she said–a practice soon to be adopted at her center–since her research suggests that these disorders may often be missed in this perhaps more vulnerable population.

“We see a lot of people fearful of eating anything at all” at diagnosis, she said. Patients may have a general fear of long-term consequences, such as cancer or osteoporosis, or may be afraid of short-term consequences, such as becoming violently ill after eating a food containing gluten. Patients also become “hyperfocused on food” as a result of constantly reading labels and asking about ingredients, she said.

Such disturbed eating patterns and hypervigilance, coupled with a common increase in weight after a malnourished patient is diagnosed and treated, can be a cause for concern. In one of her studies “we did find some people who actually ate gluten in order to lose weight,” just as diabetic patients have been known to withhold insulin for the same reason, she said (Eur. J. Gastroenterol. Hepatol. 2007;19:251-5).

As awareness about celiac disease continues to grow, experts agree that the current average 11-year gap between symptom onset and diagnosis will shrink, resulting in more diagnoses in childhood and adolescence.

There was also a consensus among all the experts interviewed that, given the recent findings of an increased mortality rate associated with this earlier diagnosis, any attempts to reduce this higher mortality must begin with a better understanding of the unique burdens that childhood diagnosis and treatment may bring.

Get Help With Celiac Disease

Dr. Edwards George recommends these organizations as good resources for patients and families dealing with celiac disease:

PICeliac Disease Foundation

Phone: 213-654-4085

Web site:

www.celiac.org

PICeliac Sprue Association of the United States of America

Phone: 402-558-0600

Web site:

www.csaceliacs.org

PIGluten Intolerance Group

Phone: 253-833-6655

Web site:

www.gluten.net

PINational Foundation for Celiac Awareness

Phone: 215-325-1306

Web site:

www.celiaccentral.org

For performance on inhibition tasks, not much evidence suggests that marijuana accounts for brain abnormalities among teens.

MONTREAL – Teens who report heavy alcohol use have reduced hippocampal volume, compared with their nondrinking peers, but those who combine marijuana with heavy drinking do not show these abnormalities, Susan Tapert, Ph.D., reported at the annual conference of the EEG and Clinical Neuroscience Society.

“It's possible there could be some neuroprotective effect of marijuana against the effects of alcohol,” said Dr. Tapert of the University of California, San Diego, noting that simultaneous marijuana and alcohol use has been shown to reduce blood alcohol levels.

However, another potential explanation is that “there may be competing pathologies that cancel each other out,” she said in an interview. “Microstructural hippocampal changes related to marijuana use may include increased glial proliferation and white matter density, as well as reduced gray matter density,” which might result in “relatively normal hippocampal volumes … despite functional pathology,” she wrote in a recent study (Neurotoxicol. Teratol. 2007;29:141-52). “This is speculative, and spectroscopic, diffusion, and segmentation studies will be needed to verify these impressions,” she stressed.

In the study, which she presented at the meeting, her group used magnetic resonance imaging to compare hippocampal volumes in 16 adolescent alcohol users, 26 marijuana and alcohol users, and 21 abstainers. The subjects were aged 15-18 years, and MRI was performed after at least 2 days of abstinence from all substances.

The smaller hippocampal volume seen in the alcohol users resulted in an abnormal pattern of right-to-left hippocampal asymmetry, compared with both controls and users of marijuana plus alcohol–and this abnormal asymmetry was related to memory function.

“In the nonusing control group, right-to-left hippocampal ratios were linearly related to best performance on verbal learning tasks, with right greater than left ratios linked to the best performances,” Dr. Tapert said. “In contrast, adolescent drinkers and adolescent users of marijuana plus alcohol did not show any relationship between hippocampal asymmetry and learning performance. This could indicate underlying pathology in the substance-using teens, in which hippocampal ratios no longer index encoding ability.”

She went on to speculate that the pathological lack of correspondence between performance and volumes might be attributable to a combination of simultaneous microstructural factors, such as edema, atrophy, altered myelination, and altered synaptic pruning.

Brain volume studies may show little effect of marijuana use, but brain function tests tell another story, Dr. Tapert said. In another recent study by her group, although marijuana-using adolescents who had abstained for 28 days performed similarly to nonusers on an inhibition task, functional MRI showed evidence of more brain processing effort to achieve adequate performance levels in the users (Psychopharmacology [Berl] 2007;194:173-83).

And in another study by her group, 31 marijuana-using adolescents were compared with 34 controls on neuropsychological functioning. Users had slower psychomotor speed and poorer complex attention, verbal learning and memory, and planning and sequencing ability, even after more than 23 days of abstinence (J. Int. Neuropsychol. Soc. 2007;13:807-20).

Dr. Tapert suggested that some brain function abnormalities noted in adolescent marijuana users may not be caused by substance use but could possibly predate it.

“For performance on inhibition tasks, there is not much evidence to suggest that marijuana is accounting for the abnormalities, and there is a suggestion of premorbid differences,” she said. “In contrast, abnormalities in verbal learning and memory do not appear linked to premorbid functioning and may possibly relate specifically to heavy marijuana use during adolescence.”

For performance on inhibition tasks, not much evidence suggests that marijuana accounts for brain abnormalities among teens.

MONTREAL – Teens who report heavy alcohol use have reduced hippocampal volume, compared with their nondrinking peers, but those who combine marijuana with heavy drinking do not show these abnormalities, Susan Tapert, Ph.D., reported at the annual conference of the EEG and Clinical Neuroscience Society.

“It's possible there could be some neuroprotective effect of marijuana against the effects of alcohol,” said Dr. Tapert of the University of California, San Diego, noting that simultaneous marijuana and alcohol use has been shown to reduce blood alcohol levels.

However, another potential explanation is that “there may be competing pathologies that cancel each other out,” she said in an interview. “Microstructural hippocampal changes related to marijuana use may include increased glial proliferation and white matter density, as well as reduced gray matter density,” which might result in “relatively normal hippocampal volumes … despite functional pathology,” she wrote in a recent study (Neurotoxicol. Teratol. 2007;29:141-52). “This is speculative, and spectroscopic, diffusion, and segmentation studies will be needed to verify these impressions,” she stressed.

In the study, which she presented at the meeting, her group used magnetic resonance imaging to compare hippocampal volumes in 16 adolescent alcohol users, 26 marijuana and alcohol users, and 21 abstainers. The subjects were aged 15-18 years, and MRI was performed after at least 2 days of abstinence from all substances.

The smaller hippocampal volume seen in the alcohol users resulted in an abnormal pattern of right-to-left hippocampal asymmetry, compared with both controls and users of marijuana plus alcohol–and this abnormal asymmetry was related to memory function.

“In the nonusing control group, right-to-left hippocampal ratios were linearly related to best performance on verbal learning tasks, with right greater than left ratios linked to the best performances,” Dr. Tapert said. “In contrast, adolescent drinkers and adolescent users of marijuana plus alcohol did not show any relationship between hippocampal asymmetry and learning performance. This could indicate underlying pathology in the substance-using teens, in which hippocampal ratios no longer index encoding ability.”

She went on to speculate that the pathological lack of correspondence between performance and volumes might be attributable to a combination of simultaneous microstructural factors, such as edema, atrophy, altered myelination, and altered synaptic pruning.

Brain volume studies may show little effect of marijuana use, but brain function tests tell another story, Dr. Tapert said. In another recent study by her group, although marijuana-using adolescents who had abstained for 28 days performed similarly to nonusers on an inhibition task, functional MRI showed evidence of more brain processing effort to achieve adequate performance levels in the users (Psychopharmacology [Berl] 2007;194:173-83).

And in another study by her group, 31 marijuana-using adolescents were compared with 34 controls on neuropsychological functioning. Users had slower psychomotor speed and poorer complex attention, verbal learning and memory, and planning and sequencing ability, even after more than 23 days of abstinence (J. Int. Neuropsychol. Soc. 2007;13:807-20).

Dr. Tapert suggested that some brain function abnormalities noted in adolescent marijuana users may not be caused by substance use but could possibly predate it.

“For performance on inhibition tasks, there is not much evidence to suggest that marijuana is accounting for the abnormalities, and there is a suggestion of premorbid differences,” she said. “In contrast, abnormalities in verbal learning and memory do not appear linked to premorbid functioning and may possibly relate specifically to heavy marijuana use during adolescence.”

For performance on inhibition tasks, not much evidence suggests that marijuana accounts for brain abnormalities among teens.

MONTREAL – Teens who report heavy alcohol use have reduced hippocampal volume, compared with their nondrinking peers, but those who combine marijuana with heavy drinking do not show these abnormalities, Susan Tapert, Ph.D., reported at the annual conference of the EEG and Clinical Neuroscience Society.

“It's possible there could be some neuroprotective effect of marijuana against the effects of alcohol,” said Dr. Tapert of the University of California, San Diego, noting that simultaneous marijuana and alcohol use has been shown to reduce blood alcohol levels.

However, another potential explanation is that “there may be competing pathologies that cancel each other out,” she said in an interview. “Microstructural hippocampal changes related to marijuana use may include increased glial proliferation and white matter density, as well as reduced gray matter density,” which might result in “relatively normal hippocampal volumes … despite functional pathology,” she wrote in a recent study (Neurotoxicol. Teratol. 2007;29:141-52). “This is speculative, and spectroscopic, diffusion, and segmentation studies will be needed to verify these impressions,” she stressed.

In the study, which she presented at the meeting, her group used magnetic resonance imaging to compare hippocampal volumes in 16 adolescent alcohol users, 26 marijuana and alcohol users, and 21 abstainers. The subjects were aged 15-18 years, and MRI was performed after at least 2 days of abstinence from all substances.

The smaller hippocampal volume seen in the alcohol users resulted in an abnormal pattern of right-to-left hippocampal asymmetry, compared with both controls and users of marijuana plus alcohol–and this abnormal asymmetry was related to memory function.

“In the nonusing control group, right-to-left hippocampal ratios were linearly related to best performance on verbal learning tasks, with right greater than left ratios linked to the best performances,” Dr. Tapert said. “In contrast, adolescent drinkers and adolescent users of marijuana plus alcohol did not show any relationship between hippocampal asymmetry and learning performance. This could indicate underlying pathology in the substance-using teens, in which hippocampal ratios no longer index encoding ability.”

She went on to speculate that the pathological lack of correspondence between performance and volumes might be attributable to a combination of simultaneous microstructural factors, such as edema, atrophy, altered myelination, and altered synaptic pruning.

Brain volume studies may show little effect of marijuana use, but brain function tests tell another story, Dr. Tapert said. In another recent study by her group, although marijuana-using adolescents who had abstained for 28 days performed similarly to nonusers on an inhibition task, functional MRI showed evidence of more brain processing effort to achieve adequate performance levels in the users (Psychopharmacology [Berl] 2007;194:173-83).

And in another study by her group, 31 marijuana-using adolescents were compared with 34 controls on neuropsychological functioning. Users had slower psychomotor speed and poorer complex attention, verbal learning and memory, and planning and sequencing ability, even after more than 23 days of abstinence (J. Int. Neuropsychol. Soc. 2007;13:807-20).

Dr. Tapert suggested that some brain function abnormalities noted in adolescent marijuana users may not be caused by substance use but could possibly predate it.

“For performance on inhibition tasks, there is not much evidence to suggest that marijuana is accounting for the abnormalities, and there is a suggestion of premorbid differences,” she said. “In contrast, abnormalities in verbal learning and memory do not appear linked to premorbid functioning and may possibly relate specifically to heavy marijuana use during adolescence.”

MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.

“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.

The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”

In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).

Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.

Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.

Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.

But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.

In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.

MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.

“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.

The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”

In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).

Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.

Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.

Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.

But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.

In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.

MONTREAL — Comorbid antisocial personality disorder blunts the brain dysfunction associated with HIV/AIDS but also blunts the brain benefits associated with antiretroviral therapy, reported Lance Bauer, Ph.D., professor of psychiatry at the University of Connecticut, Farmington.

“There is good evidence that both ASPD [antisocial personality disorder] and HIV affect the same regions of the brain,” he said at the annual conference of the EEG and Clinical Neuroscience Society.

The prevalence of ASPD is disproportionately high in the HIV/AIDS population, with one study estimating it as high as 74%, making it important to screen for this psychiatric disorder, he said in an interview. The diagnosis of ASPD “may provide a context for the treatment plan. Such patients may require more frequent follow-ups to deal with compliance issues or may require a more structured approach for their treatment—for example, greater involvement of the spouse or family member, or simplifying the treatment regimen.”

In his published study, which he presented at the meeting, Dr. Bauer compared the effect of ASPD on brain function in 26 treated and 71 untreated HIV patients, compared with 68 seronegative controls using the P300 event-related potential (ERP) test (Neuropsychobiology 2006;53:17–25).

Using ERP, previous studies have shown increased P300 latency and decreased P300 amplitude associated with untreated HIV. These changes in P300 suggest a subtle underlying dysfunction in the brain that sometimes is accompanied by slowing of motor skills and information processing, as well as impaired attention or memory skills, according to Dr. Bauer. These abnormalities have been shown to be reversible with antiretroviral therapy.

Similarly, in ASPD patients, previous P300 ERP studies have revealed decrements in frontal brain structure and function.

Dr. Bauer's study confirmed previous findings in that ASPD was associated with frontal brain dysfunction, both in HIV-negative and HIV-positive patients on antiretroviral therapy.

But among untreated HIV patients, ASPD appeared to have no deleterious effect on brain function. “ASPD may initially compromise the function of this region to such a degree that the additional effects of untreated HIV/AIDS are blunted,” he suggested.

In addition, among HIV-positive patients, ASPD blunted the ability of antiretroviral therapy to reverse brain dysfunction. This is probably related to the effect of ASPD in diminishing the capacity of the nervous system “to respond to the presence of medications that would normally improve frontal brain function,” Dr. Bauer said.

LYON, FRANCE — The increased risk of cancer seen in patients with endometriosis is unrelated to parity, according to a large study—the first to examine this association.

“We found that contrary to what one might expect, endometriosis and nulliparity did not combine to give a higher cancer risk,” said Dr. Anna-Sofia Mellin, who presented the results at the annual meeting of the European Society for Human Reproduction and Embryology. “We could not show a difference in risk between parous and nonparous women.”

Her study identified 63,630 women, using the National Swedish Inpatient Register, who were discharged from hospital with a diagnosis of endometriosis between 1969 and 2002. From this cohort, 3,822 cancer cases were subsequently identified, using the National Swedish Cancer Register.

The study found no overall increased risk of cancer associated with endometriosis (standardized incidence ratio [SIR] 1.01); however, significantly elevated risks were found for specific cancers such as endocrine tumors (SIR 1.38), ovarian cancer (SIR 1.37), kidney cancer (SIR 1.36), thyroid cancer (SIR 1.33), brain tumors (SIR 1.27), melanoma (SIR 1.23), and breast cancer (SIR 1.08), said Dr. Mellin of the Karolinska Institute in Stockholm.

Endometriosis was associated with a reduced risk of cervical cancer (SIR 0.71).

When parity was considered, no significant differences were noted between parous and nonparous women, although a nonsignificant decrease in ovarian cancer was noted with parity (from SIR 1.48 in nonparous women to SIR 1.3 in parous women).

Most of the increased cancer risk was seen in women with ovarian endometriosis, with only a small but significant increase seen in those with peritoneal endometriosis and no increased risk associated with adenomyosis, she said.

Although the findings are cause for concern, Dr. Mellin said it is too early to recommend that all endometriosis patients receive cancer screening.

“We don't even have any screening for ovarian cancer, so we don't know how to follow these patients. We know that even if you get an ultrasound every year you still get ovarian cancer and it still may have grown too far,” she said in an interview.

LYON, FRANCE — The increased risk of cancer seen in patients with endometriosis is unrelated to parity, according to a large study—the first to examine this association.

“We found that contrary to what one might expect, endometriosis and nulliparity did not combine to give a higher cancer risk,” said Dr. Anna-Sofia Mellin, who presented the results at the annual meeting of the European Society for Human Reproduction and Embryology. “We could not show a difference in risk between parous and nonparous women.”

Her study identified 63,630 women, using the National Swedish Inpatient Register, who were discharged from hospital with a diagnosis of endometriosis between 1969 and 2002. From this cohort, 3,822 cancer cases were subsequently identified, using the National Swedish Cancer Register.

The study found no overall increased risk of cancer associated with endometriosis (standardized incidence ratio [SIR] 1.01); however, significantly elevated risks were found for specific cancers such as endocrine tumors (SIR 1.38), ovarian cancer (SIR 1.37), kidney cancer (SIR 1.36), thyroid cancer (SIR 1.33), brain tumors (SIR 1.27), melanoma (SIR 1.23), and breast cancer (SIR 1.08), said Dr. Mellin of the Karolinska Institute in Stockholm.

Endometriosis was associated with a reduced risk of cervical cancer (SIR 0.71).

When parity was considered, no significant differences were noted between parous and nonparous women, although a nonsignificant decrease in ovarian cancer was noted with parity (from SIR 1.48 in nonparous women to SIR 1.3 in parous women).

Most of the increased cancer risk was seen in women with ovarian endometriosis, with only a small but significant increase seen in those with peritoneal endometriosis and no increased risk associated with adenomyosis, she said.

Although the findings are cause for concern, Dr. Mellin said it is too early to recommend that all endometriosis patients receive cancer screening.

“We don't even have any screening for ovarian cancer, so we don't know how to follow these patients. We know that even if you get an ultrasound every year you still get ovarian cancer and it still may have grown too far,” she said in an interview.

LYON, FRANCE — The increased risk of cancer seen in patients with endometriosis is unrelated to parity, according to a large study—the first to examine this association.

“We found that contrary to what one might expect, endometriosis and nulliparity did not combine to give a higher cancer risk,” said Dr. Anna-Sofia Mellin, who presented the results at the annual meeting of the European Society for Human Reproduction and Embryology. “We could not show a difference in risk between parous and nonparous women.”

Her study identified 63,630 women, using the National Swedish Inpatient Register, who were discharged from hospital with a diagnosis of endometriosis between 1969 and 2002. From this cohort, 3,822 cancer cases were subsequently identified, using the National Swedish Cancer Register.

The study found no overall increased risk of cancer associated with endometriosis (standardized incidence ratio [SIR] 1.01); however, significantly elevated risks were found for specific cancers such as endocrine tumors (SIR 1.38), ovarian cancer (SIR 1.37), kidney cancer (SIR 1.36), thyroid cancer (SIR 1.33), brain tumors (SIR 1.27), melanoma (SIR 1.23), and breast cancer (SIR 1.08), said Dr. Mellin of the Karolinska Institute in Stockholm.

Endometriosis was associated with a reduced risk of cervical cancer (SIR 0.71).

When parity was considered, no significant differences were noted between parous and nonparous women, although a nonsignificant decrease in ovarian cancer was noted with parity (from SIR 1.48 in nonparous women to SIR 1.3 in parous women).

Most of the increased cancer risk was seen in women with ovarian endometriosis, with only a small but significant increase seen in those with peritoneal endometriosis and no increased risk associated with adenomyosis, she said.

Although the findings are cause for concern, Dr. Mellin said it is too early to recommend that all endometriosis patients receive cancer screening.

“We don't even have any screening for ovarian cancer, so we don't know how to follow these patients. We know that even if you get an ultrasound every year you still get ovarian cancer and it still may have grown too far,” she said in an interview.

Low serum magnesium levels are associated with depressive symptoms in elderly diabetic patients, a finding that has potentially therapeutic implications, investigators reported.

“Whether hypomagnesemia is a risk factor for depression or merely an associated epiphenomenon in older people with diabetes cannot be ascertained. Interventional studies with magnesium supplementation are needed in order to convincingly demonstrate a cause-effect relationship,” wrote Lázaro Barragan-Rodríguez and colleagues from the Mexican Social Security Institute's Medical Research Unit in Clinical Epidemiology, and the Research Group on Diabetes and Chronic Illnesses, both in Durango, Mexico.

The authors studied 110 type 2 diabetic subjects, aged 65 years or older, who had no previous diagnosis of either depression or hypomagnesemia. A total of 55 subjects (40 women and 15 men) screened positive for depressive symptoms (a score of 11 points or more on the Yesavage Geriatric Depression Scale) and were included as cases, whereas the other 55 subjects (43 women and 12 men) with no depressive symptoms served as the control group. The mean depression score was 17 for subjects in the case group, compared with 6 for controls.

Venous whole blood samples were collected under fasting conditions to identify hypomagnesemia, which was defined as a serum magnesium level of less than 0.74 mmol/L. Serum magnesium levels were significantly lower in the case group, compared with controls. In the case group, 44% of subjects exhibited hypomagnesemia, compared with 13% in the control group.

After adjusting for age, gender, duration of diabetes, hemoglobin A_1c, concomitant physical illness, serum triglycerides, albumin, and creatinine levels, the odds ratio (OR) between hypomagnesemia and depressive symptoms was calculated as 1.79. After lowering the cut-off point of serum magnesium to 0.66 mmol/L or less, hypomagnesemia still remained significantly associated with depressive symptoms (OR 1.74), noted the authors (Arch. Med. Res. 2007;38:752–6).

Low serum magnesium levels are associated with depressive symptoms in elderly diabetic patients, a finding that has potentially therapeutic implications, investigators reported.

“Whether hypomagnesemia is a risk factor for depression or merely an associated epiphenomenon in older people with diabetes cannot be ascertained. Interventional studies with magnesium supplementation are needed in order to convincingly demonstrate a cause-effect relationship,” wrote Lázaro Barragan-Rodríguez and colleagues from the Mexican Social Security Institute's Medical Research Unit in Clinical Epidemiology, and the Research Group on Diabetes and Chronic Illnesses, both in Durango, Mexico.

The authors studied 110 type 2 diabetic subjects, aged 65 years or older, who had no previous diagnosis of either depression or hypomagnesemia. A total of 55 subjects (40 women and 15 men) screened positive for depressive symptoms (a score of 11 points or more on the Yesavage Geriatric Depression Scale) and were included as cases, whereas the other 55 subjects (43 women and 12 men) with no depressive symptoms served as the control group. The mean depression score was 17 for subjects in the case group, compared with 6 for controls.

Venous whole blood samples were collected under fasting conditions to identify hypomagnesemia, which was defined as a serum magnesium level of less than 0.74 mmol/L. Serum magnesium levels were significantly lower in the case group, compared with controls. In the case group, 44% of subjects exhibited hypomagnesemia, compared with 13% in the control group.

After adjusting for age, gender, duration of diabetes, hemoglobin A_1c, concomitant physical illness, serum triglycerides, albumin, and creatinine levels, the odds ratio (OR) between hypomagnesemia and depressive symptoms was calculated as 1.79. After lowering the cut-off point of serum magnesium to 0.66 mmol/L or less, hypomagnesemia still remained significantly associated with depressive symptoms (OR 1.74), noted the authors (Arch. Med. Res. 2007;38:752–6).

Low serum magnesium levels are associated with depressive symptoms in elderly diabetic patients, a finding that has potentially therapeutic implications, investigators reported.

“Whether hypomagnesemia is a risk factor for depression or merely an associated epiphenomenon in older people with diabetes cannot be ascertained. Interventional studies with magnesium supplementation are needed in order to convincingly demonstrate a cause-effect relationship,” wrote Lázaro Barragan-Rodríguez and colleagues from the Mexican Social Security Institute's Medical Research Unit in Clinical Epidemiology, and the Research Group on Diabetes and Chronic Illnesses, both in Durango, Mexico.

The authors studied 110 type 2 diabetic subjects, aged 65 years or older, who had no previous diagnosis of either depression or hypomagnesemia. A total of 55 subjects (40 women and 15 men) screened positive for depressive symptoms (a score of 11 points or more on the Yesavage Geriatric Depression Scale) and were included as cases, whereas the other 55 subjects (43 women and 12 men) with no depressive symptoms served as the control group. The mean depression score was 17 for subjects in the case group, compared with 6 for controls.

Venous whole blood samples were collected under fasting conditions to identify hypomagnesemia, which was defined as a serum magnesium level of less than 0.74 mmol/L. Serum magnesium levels were significantly lower in the case group, compared with controls. In the case group, 44% of subjects exhibited hypomagnesemia, compared with 13% in the control group.

After adjusting for age, gender, duration of diabetes, hemoglobin A_1c, concomitant physical illness, serum triglycerides, albumin, and creatinine levels, the odds ratio (OR) between hypomagnesemia and depressive symptoms was calculated as 1.79. After lowering the cut-off point of serum magnesium to 0.66 mmol/L or less, hypomagnesemia still remained significantly associated with depressive symptoms (OR 1.74), noted the authors (Arch. Med. Res. 2007;38:752–6).

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.

TORONTO — As few as 12 pediatric influenza immunizations and probably even fewer in each practice could prevent an outpatient visit for influenza later in the season, according to a poster presented at the annual meeting of the Pediatric Academic Societies.

“Most physicians already know the benefits of influenza immunization, but when you have such a simple number it's just easier to stick inside your head,” said the study's author Elizabeth Lewis, a medical student at Vanderbilt University, Nashville, Tenn. “Our goal was to provide a clinically relevant number for primary care providers.”

The study used published literature to ascertain rates of influenza infection in children aged between 6 and 59 months, and assumed various rates of vaccine efficacy, also published in the literature. “The published range of efficacy is anywhere from 46% to 80% or 90%,” she said in an interview. “Assuming only half of 6- to 59-month-old children are vaccinated—at a conservative 50% vaccine efficacy—that eliminates 2,250 hospitalizations and upwards of 650,000 outpatient visits.”

Translating that down to the individual physician, Ms. Lewis and her colleagues estimated that, depending on season severity and children's ages, between 12 and 42 would need to be vaccinated to prevent one outpatient visit for influenza. The corresponding range for preventing one influenza-attributable hospitalization was about 1,000–3,000 for children aged 6–23 months, and twice that for those aged 24–59 months.

“We also conservatively assumed no herd immunity, but we know there is a basis in the literature for herd immunity. Influenza is highly contagious, and vaccination of schoolchildren decreases influenza in the entire population. So, accounting for herd immunity, the number needed to treat would be less,” she said.

TORONTO — As few as 12 pediatric influenza immunizations and probably even fewer in each practice could prevent an outpatient visit for influenza later in the season, according to a poster presented at the annual meeting of the Pediatric Academic Societies.

“Most physicians already know the benefits of influenza immunization, but when you have such a simple number it's just easier to stick inside your head,” said the study's author Elizabeth Lewis, a medical student at Vanderbilt University, Nashville, Tenn. “Our goal was to provide a clinically relevant number for primary care providers.”

The study used published literature to ascertain rates of influenza infection in children aged between 6 and 59 months, and assumed various rates of vaccine efficacy, also published in the literature. “The published range of efficacy is anywhere from 46% to 80% or 90%,” she said in an interview. “Assuming only half of 6- to 59-month-old children are vaccinated—at a conservative 50% vaccine efficacy—that eliminates 2,250 hospitalizations and upwards of 650,000 outpatient visits.”

Translating that down to the individual physician, Ms. Lewis and her colleagues estimated that, depending on season severity and children's ages, between 12 and 42 would need to be vaccinated to prevent one outpatient visit for influenza. The corresponding range for preventing one influenza-attributable hospitalization was about 1,000–3,000 for children aged 6–23 months, and twice that for those aged 24–59 months.

“We also conservatively assumed no herd immunity, but we know there is a basis in the literature for herd immunity. Influenza is highly contagious, and vaccination of schoolchildren decreases influenza in the entire population. So, accounting for herd immunity, the number needed to treat would be less,” she said.

TORONTO — As few as 12 pediatric influenza immunizations and probably even fewer in each practice could prevent an outpatient visit for influenza later in the season, according to a poster presented at the annual meeting of the Pediatric Academic Societies.

“Most physicians already know the benefits of influenza immunization, but when you have such a simple number it's just easier to stick inside your head,” said the study's author Elizabeth Lewis, a medical student at Vanderbilt University, Nashville, Tenn. “Our goal was to provide a clinically relevant number for primary care providers.”

The study used published literature to ascertain rates of influenza infection in children aged between 6 and 59 months, and assumed various rates of vaccine efficacy, also published in the literature. “The published range of efficacy is anywhere from 46% to 80% or 90%,” she said in an interview. “Assuming only half of 6- to 59-month-old children are vaccinated—at a conservative 50% vaccine efficacy—that eliminates 2,250 hospitalizations and upwards of 650,000 outpatient visits.”

Translating that down to the individual physician, Ms. Lewis and her colleagues estimated that, depending on season severity and children's ages, between 12 and 42 would need to be vaccinated to prevent one outpatient visit for influenza. The corresponding range for preventing one influenza-attributable hospitalization was about 1,000–3,000 for children aged 6–23 months, and twice that for those aged 24–59 months.

“We also conservatively assumed no herd immunity, but we know there is a basis in the literature for herd immunity. Influenza is highly contagious, and vaccination of schoolchildren decreases influenza in the entire population. So, accounting for herd immunity, the number needed to treat would be less,” she said.

BANFF, ALTA. — Initial conservative treatment of post-dural puncture headache, with delayed placement of a blood patch, may increase the likelihood of early treatment success, Dr. Paul Tan suggested at the annual meeting of the Society of Obstetric Anesthesia and Perinatology.

“One of the explanations for this is that local anesthetics are still residual in the epidural space and can inhibit the coagulation of the blood that's given in the blood patch,” said Dr. Tan of the Cleveland Clinic in an interview.

The study he presented reviewed 130 patients who received therapeutic epidural blood patches (EPB) for post-dural puncture headache. Forty-seven (36%) of the patients required a repeat EPB. In exploring factors that might be associated with the need for a repeat EPB, including body mass index, parity, needle type, amount of blood injected in the first EPB, time from dural puncture to headache onset, and time from headache onset to first EPB, the authors found that the time measurements were the only independent predictors of first EPB success.

“To my knowledge this is the first time that both the time from puncture to headache onset, and the time from headache onset to first blood patch, have been looked at separately,” he said, adding that although the time from puncture to headache onset is not modifiable, information about it can help in counseling patients. “If the patient develops a headache quickly after the puncture, they should be counseled it is likely the first blood patch will fail, and they may need more than one,” he said.

These patients can also be encouraged to undertake a trial of conservative treatment measures such as intravenous hydration, caffeine, and oral pain medications in an effort to delay placement of the first blood patch, he added.

Study patients needing a second EPB had a mean time from puncture to headache onset of 10 hours, and a mean of 16 hours from headache onset to placement of the first patch, compared with 17 hours and 29 hours, respectively, in those not needing a second patch.

“A doubling of the time from puncture to headache onset resulted in a 46% reduction in the odds of the patient needing a repeat patch, and a doubling of the time from headache onset to first blood patch resulted in a 41% reduction in the odds of needing a repeat patch,” he said.

Dr. Tan suggested that the shorter times associated with needing a repeat patch could also be a marker for the severity of the dural puncture, and that the self-limiting nature of post-dural puncture headache could explain why the longer time interval resulted in less requirement for a repeat blood patch.

BANFF, ALTA. — Initial conservative treatment of post-dural puncture headache, with delayed placement of a blood patch, may increase the likelihood of early treatment success, Dr. Paul Tan suggested at the annual meeting of the Society of Obstetric Anesthesia and Perinatology.

“One of the explanations for this is that local anesthetics are still residual in the epidural space and can inhibit the coagulation of the blood that's given in the blood patch,” said Dr. Tan of the Cleveland Clinic in an interview.

The study he presented reviewed 130 patients who received therapeutic epidural blood patches (EPB) for post-dural puncture headache. Forty-seven (36%) of the patients required a repeat EPB. In exploring factors that might be associated with the need for a repeat EPB, including body mass index, parity, needle type, amount of blood injected in the first EPB, time from dural puncture to headache onset, and time from headache onset to first EPB, the authors found that the time measurements were the only independent predictors of first EPB success.

“To my knowledge this is the first time that both the time from puncture to headache onset, and the time from headache onset to first blood patch, have been looked at separately,” he said, adding that although the time from puncture to headache onset is not modifiable, information about it can help in counseling patients. “If the patient develops a headache quickly after the puncture, they should be counseled it is likely the first blood patch will fail, and they may need more than one,” he said.

These patients can also be encouraged to undertake a trial of conservative treatment measures such as intravenous hydration, caffeine, and oral pain medications in an effort to delay placement of the first blood patch, he added.

Study patients needing a second EPB had a mean time from puncture to headache onset of 10 hours, and a mean of 16 hours from headache onset to placement of the first patch, compared with 17 hours and 29 hours, respectively, in those not needing a second patch.

“A doubling of the time from puncture to headache onset resulted in a 46% reduction in the odds of the patient needing a repeat patch, and a doubling of the time from headache onset to first blood patch resulted in a 41% reduction in the odds of needing a repeat patch,” he said.

Dr. Tan suggested that the shorter times associated with needing a repeat patch could also be a marker for the severity of the dural puncture, and that the self-limiting nature of post-dural puncture headache could explain why the longer time interval resulted in less requirement for a repeat blood patch.

BANFF, ALTA. — Initial conservative treatment of post-dural puncture headache, with delayed placement of a blood patch, may increase the likelihood of early treatment success, Dr. Paul Tan suggested at the annual meeting of the Society of Obstetric Anesthesia and Perinatology.

“One of the explanations for this is that local anesthetics are still residual in the epidural space and can inhibit the coagulation of the blood that's given in the blood patch,” said Dr. Tan of the Cleveland Clinic in an interview.

The study he presented reviewed 130 patients who received therapeutic epidural blood patches (EPB) for post-dural puncture headache. Forty-seven (36%) of the patients required a repeat EPB. In exploring factors that might be associated with the need for a repeat EPB, including body mass index, parity, needle type, amount of blood injected in the first EPB, time from dural puncture to headache onset, and time from headache onset to first EPB, the authors found that the time measurements were the only independent predictors of first EPB success.

“To my knowledge this is the first time that both the time from puncture to headache onset, and the time from headache onset to first blood patch, have been looked at separately,” he said, adding that although the time from puncture to headache onset is not modifiable, information about it can help in counseling patients. “If the patient develops a headache quickly after the puncture, they should be counseled it is likely the first blood patch will fail, and they may need more than one,” he said.

These patients can also be encouraged to undertake a trial of conservative treatment measures such as intravenous hydration, caffeine, and oral pain medications in an effort to delay placement of the first blood patch, he added.

Study patients needing a second EPB had a mean time from puncture to headache onset of 10 hours, and a mean of 16 hours from headache onset to placement of the first patch, compared with 17 hours and 29 hours, respectively, in those not needing a second patch.

“A doubling of the time from puncture to headache onset resulted in a 46% reduction in the odds of the patient needing a repeat patch, and a doubling of the time from headache onset to first blood patch resulted in a 41% reduction in the odds of needing a repeat patch,” he said.

Dr. Tan suggested that the shorter times associated with needing a repeat patch could also be a marker for the severity of the dural puncture, and that the self-limiting nature of post-dural puncture headache could explain why the longer time interval resulted in less requirement for a repeat blood patch.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively.

The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with UA/NSTEMI. A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Several limitations to the study were noted by the authors, including the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Noting “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors pointed to “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population.” They recommended that “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS,” suggesting that, “more stringent targets for patients with diabetes may be better all around.

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they concluded.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively.

The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with UA/NSTEMI. A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Several limitations to the study were noted by the authors, including the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Noting “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors pointed to “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population.” They recommended that “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS,” suggesting that, “more stringent targets for patients with diabetes may be better all around.

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they concluded.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively.

The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with UA/NSTEMI. A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Several limitations to the study were noted by the authors, including the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Noting “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors pointed to “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population.” They recommended that “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS,” suggesting that, “more stringent targets for patients with diabetes may be better all around.

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they concluded.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment-elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively. The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with unstable angina/non-STEMI (UA/NSTEMI). A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Limitations to the study included the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Given “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors noted “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population” and wrote “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS.”

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they wrote.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment-elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively. The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with unstable angina/non-STEMI (UA/NSTEMI). A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Limitations to the study included the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Given “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors noted “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population” and wrote “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS.”

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they wrote.

Patients with diabetes have increased 30-day and 1-year mortality following acute coronary syndromes, compared with patients without diabetes, according to an analysis of more than 60,000 patients.

At 30 days after acute coronary syndrome (ACS), diabetes was a significant independent factor associated with all-cause mortality for patients presenting with ST-segment-elevation myocardial infarction (STEMI) and for those with unstable angina/non-STEMI (UA/NSTEMI), with adjusted odds ratios of 1.40 and 1.78, respectively. At 12 months, diabetes remained a significant independent predictor of mortality for both patient groups, with adjusted hazard ratios of 1.22 and 1.65, respectively. The data were adjusted for baseline characteristics, as well as features and management of the index ACS event.

Also at 12 months, “patients with diabetes and presenting with UA/NSTEMI had a mortality that approached patients without diabetes and presenting with STEMI (7.2% vs. 8.1%),” the researchers reported (JAMA 2007;298:765–75).

The analysis pooled 62,036 ACS patients from 11 independent Thrombolysis in Myocardial Infarction (TIMI) Study Group clinical trials. A total of 46,577 patients presented with STEMI, and the remaining 15,459 patients presented with unstable angina/non-STEMI (UA/NSTEMI). A total of 10,613 patients had diabetes by self-report, wrote lead author Dr. Sean M. Donahoe of Cornell University Medical Center, New York, and colleagues.

“The burden of cardiovascular risk inherent among the patients presenting with UA/NSTEMI marked the index ACS presentation as a sentinel event in a chronic, progressive course that was more accelerated among patients with diabetes,” they wrote. “The UA/NSTEMI population is enriched with this high-risk diabetic population.”

Limitations to the study included the possibility of intertrial variability in ACS management, and the self-reporting of diabetes status.

Given “the increasing burden of cardiovascular disease attributable to diabetes worldwide,” the authors noted “the need for a major research effort to identify aggressive new strategies to manage unstable ischemic heart disease among this high-risk population” and wrote “long-term, targeted, intensive use of proven therapies for the traditional coronary risk factors must be widely promoted for patients with diabetes, particularly following ACS.”

“Collaboration between medical societies, national health care organizations, and industry will be vital to halt the epidemic of diabetes-related cardiovascular disease,” they wrote.