Kate Johnson

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.

TORONTO — A designated care coordinator can significantly improve the management of children and youth with special health care needs, Mary Krauthoefer said at the annual meeting of the Pediatric Academic Societies.

“Complex, medically fragile children with special health care needs require thorough communication and coordination among providers, which are best directed through the primary care setting,” said Ms. Krauthoefer, case manager at Children's Hospital of Wisconsin in Milwaukee. “But this [service] is time consuming and poorly reimbursed, making it difficult for primary care physicians alone to provide medical homes for this population.”

Care coordination provided by a pediatric nurse manager at the Children's Hospital of Wisconsin resulted in more efficient and effective use of resources among these complex patients, according to study results Ms. Krauthoefer presented at the meeting.

She described a Special Needs Program, set up by the hospital, which was established to partner with families and primary care physicians to ensure care coordination. A pediatric nurse manager served as the tertiary center care coordinator for 219 patients with special health care needs enrolled in the program. All patients met complexity and fragility criteria—the presence of five or more specialists, uncertain or multiple diagnoses, use of multiple community services, and frequent visits to a hospital and clinic.

In examining resource utilization among the patients during equal time periods both before and after the implementation of care coordination, the investigators found care coordination resulted in a decreased number of hospital days and an increased number of clinic visits, indicating a shift from inpatient to outpatient care. Hospital length of stay for all patients combined declined by a total of 2,790 days; outpatient clinic visits increased by a total of 1,878 days. There were approximately the same number of hospital admissions as before. Hospital charges and payments decreased by $2.8 million and $2.7 million, respectively.

Surveys of families and patients' primary care physicians indicated a high level of satisfaction with the care coordination initiative, Ms. Krauthoefer said.

TORONTO — A designated care coordinator can significantly improve the management of children and youth with special health care needs, Mary Krauthoefer said at the annual meeting of the Pediatric Academic Societies.

“Complex, medically fragile children with special health care needs require thorough communication and coordination among providers, which are best directed through the primary care setting,” said Ms. Krauthoefer, case manager at Children's Hospital of Wisconsin in Milwaukee. “But this [service] is time consuming and poorly reimbursed, making it difficult for primary care physicians alone to provide medical homes for this population.”

Care coordination provided by a pediatric nurse manager at the Children's Hospital of Wisconsin resulted in more efficient and effective use of resources among these complex patients, according to study results Ms. Krauthoefer presented at the meeting.

She described a Special Needs Program, set up by the hospital, which was established to partner with families and primary care physicians to ensure care coordination. A pediatric nurse manager served as the tertiary center care coordinator for 219 patients with special health care needs enrolled in the program. All patients met complexity and fragility criteria—the presence of five or more specialists, uncertain or multiple diagnoses, use of multiple community services, and frequent visits to a hospital and clinic.

In examining resource utilization among the patients during equal time periods both before and after the implementation of care coordination, the investigators found care coordination resulted in a decreased number of hospital days and an increased number of clinic visits, indicating a shift from inpatient to outpatient care. Hospital length of stay for all patients combined declined by a total of 2,790 days; outpatient clinic visits increased by a total of 1,878 days. There were approximately the same number of hospital admissions as before. Hospital charges and payments decreased by $2.8 million and $2.7 million, respectively.

Surveys of families and patients' primary care physicians indicated a high level of satisfaction with the care coordination initiative, Ms. Krauthoefer said.

TORONTO — A designated care coordinator can significantly improve the management of children and youth with special health care needs, Mary Krauthoefer said at the annual meeting of the Pediatric Academic Societies.

“Complex, medically fragile children with special health care needs require thorough communication and coordination among providers, which are best directed through the primary care setting,” said Ms. Krauthoefer, case manager at Children's Hospital of Wisconsin in Milwaukee. “But this [service] is time consuming and poorly reimbursed, making it difficult for primary care physicians alone to provide medical homes for this population.”

Care coordination provided by a pediatric nurse manager at the Children's Hospital of Wisconsin resulted in more efficient and effective use of resources among these complex patients, according to study results Ms. Krauthoefer presented at the meeting.

She described a Special Needs Program, set up by the hospital, which was established to partner with families and primary care physicians to ensure care coordination. A pediatric nurse manager served as the tertiary center care coordinator for 219 patients with special health care needs enrolled in the program. All patients met complexity and fragility criteria—the presence of five or more specialists, uncertain or multiple diagnoses, use of multiple community services, and frequent visits to a hospital and clinic.

In examining resource utilization among the patients during equal time periods both before and after the implementation of care coordination, the investigators found care coordination resulted in a decreased number of hospital days and an increased number of clinic visits, indicating a shift from inpatient to outpatient care. Hospital length of stay for all patients combined declined by a total of 2,790 days; outpatient clinic visits increased by a total of 1,878 days. There were approximately the same number of hospital admissions as before. Hospital charges and payments decreased by $2.8 million and $2.7 million, respectively.

Surveys of families and patients' primary care physicians indicated a high level of satisfaction with the care coordination initiative, Ms. Krauthoefer said.

TORONTO — Cognitive impairment in patients who have childhood-onset systemic lupus erythematosus can be identified with functional magnetic resonance imaging, reported Svetlana Lvovich, D.O., in a poster presentation at the annual meeting of the Pediatric Academic Societies.

The pilot study, which was done by Dr. Lvovich and her associates, included 10 patients who had systemic lupus erythematosus (SLE). Five of the patients had cognitive impairment (CI), and five of them did not have CI.

Functional magnetic resonance imaging (fMRI) showed differences between the patients with CI and those without.

“They [those with CI] need to recruit more neurons to do the task,” she said in an interview. The three tasks that patients were required to perform during fMRI were specially designed to evaluate attention, working memory, and language processing.

Neuropsychiatric testing is the preferred method for diagnosing CI in SLE patients. However, it is time consuming and it requires extensive training to be able to administer it, said Dr. Lvovich of the Cincinnati Children's Hospital Medical Center.

In contrast, fMRI is quick and easy to perform.

There also were subtle fMRI differences seen between SLE patients with normal cognition, compared with healthy controls, which suggested that it is SLE-specific processes that contribute to CI rather than the long-term use of steroids,” she noted.

“However, to determine this, we will need to look at patients who are on steroids but don't have SLE,” she said.

“We think that fMRI may be useful to investigate and identify cortical roots of cognitive impairment in children with SLE,” she concluded.

TORONTO — Cognitive impairment in patients who have childhood-onset systemic lupus erythematosus can be identified with functional magnetic resonance imaging, reported Svetlana Lvovich, D.O., in a poster presentation at the annual meeting of the Pediatric Academic Societies.

The pilot study, which was done by Dr. Lvovich and her associates, included 10 patients who had systemic lupus erythematosus (SLE). Five of the patients had cognitive impairment (CI), and five of them did not have CI.

Functional magnetic resonance imaging (fMRI) showed differences between the patients with CI and those without.

“They [those with CI] need to recruit more neurons to do the task,” she said in an interview. The three tasks that patients were required to perform during fMRI were specially designed to evaluate attention, working memory, and language processing.

Neuropsychiatric testing is the preferred method for diagnosing CI in SLE patients. However, it is time consuming and it requires extensive training to be able to administer it, said Dr. Lvovich of the Cincinnati Children's Hospital Medical Center.

In contrast, fMRI is quick and easy to perform.

There also were subtle fMRI differences seen between SLE patients with normal cognition, compared with healthy controls, which suggested that it is SLE-specific processes that contribute to CI rather than the long-term use of steroids,” she noted.

“However, to determine this, we will need to look at patients who are on steroids but don't have SLE,” she said.

“We think that fMRI may be useful to investigate and identify cortical roots of cognitive impairment in children with SLE,” she concluded.

TORONTO — Cognitive impairment in patients who have childhood-onset systemic lupus erythematosus can be identified with functional magnetic resonance imaging, reported Svetlana Lvovich, D.O., in a poster presentation at the annual meeting of the Pediatric Academic Societies.

The pilot study, which was done by Dr. Lvovich and her associates, included 10 patients who had systemic lupus erythematosus (SLE). Five of the patients had cognitive impairment (CI), and five of them did not have CI.

Functional magnetic resonance imaging (fMRI) showed differences between the patients with CI and those without.

“They [those with CI] need to recruit more neurons to do the task,” she said in an interview. The three tasks that patients were required to perform during fMRI were specially designed to evaluate attention, working memory, and language processing.

Neuropsychiatric testing is the preferred method for diagnosing CI in SLE patients. However, it is time consuming and it requires extensive training to be able to administer it, said Dr. Lvovich of the Cincinnati Children's Hospital Medical Center.

In contrast, fMRI is quick and easy to perform.

There also were subtle fMRI differences seen between SLE patients with normal cognition, compared with healthy controls, which suggested that it is SLE-specific processes that contribute to CI rather than the long-term use of steroids,” she noted.

“However, to determine this, we will need to look at patients who are on steroids but don't have SLE,” she said.

“We think that fMRI may be useful to investigate and identify cortical roots of cognitive impairment in children with SLE,” she concluded.