Sharon Worcester

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Survey.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Survey (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see box), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratio 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations of selenium in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidative stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Survey.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Survey (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see box), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratio 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations of selenium in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidative stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Survey.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Survey (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see box), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratio 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations of selenium in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidative stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

DESTIN, FLA. — Ethnicity appears to play an important role in the incidence and clinical manifestations of pediatric systemic lupus erythematosus, data from a recent study suggest.

Findings from the study of 87 white and 154 nonwhite children showed that whites accounted for more than 60% of age-matched controls without pediatric systemic lupus erythematosus (SLE) but fewer than 40% of the children with pediatric SLE. Specifically, Black, Asian, and South Asian patients are overrepresented in the pediatric SLE population, Dr. Earl Silverman reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

Mucocutaneous manifestations—usually malar rash and photosensitivity—were more common in white children and organ involvement—usually renal—was more common in nonwhite children, reported Dr. Silverman, professor of pediatrics and immunology at the University of Toronto.

Although anti-DNA, anticardiolipin, lupus anticoagulant, and anti-La antibodies were similar in white and nonwhite children, anti-Sm, anti-RNP, and anti-Ro were expressed more in the nonwhite patients (34% vs. 56%; 30% vs. 42%; and 28% vs. 45%, respectively). The differences in course and incidence of SLE, based on ethnicity, are likely a result of interactions between genes and environment, he said.

Rates of arthritis, serositis, renal disease, central nervous system disease, and hematologic complications have been shown by other researchers not to differ between groups, nor did median SLE disease activity index, he noted.

However, findings from one study show intensive care unit admissions and deaths occurred more often in those younger than age 11 years, compared with those 11 years and older (32% vs. 21% and 11% vs. 0%, respectively), which suggests that SLE may be more severe in younger patients, Dr. Silverman said. Neuropsychiatric manifestations also can occur in pediatric SLE. Studies suggest that, among patients with neurologic involvement (about 25% of SLE patients), headache occurs in 68%, psychosis occurs in 36%, cognitive dysfunction occurs in 27%, cardiovascular disease occurs in 24%, seizures occur in 18%, mood disorders occur in 15%, and chorea occurs in 11%, noted Dr. Silverman.

DESTIN, FLA. — Ethnicity appears to play an important role in the incidence and clinical manifestations of pediatric systemic lupus erythematosus, data from a recent study suggest.

Findings from the study of 87 white and 154 nonwhite children showed that whites accounted for more than 60% of age-matched controls without pediatric systemic lupus erythematosus (SLE) but fewer than 40% of the children with pediatric SLE. Specifically, Black, Asian, and South Asian patients are overrepresented in the pediatric SLE population, Dr. Earl Silverman reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

Mucocutaneous manifestations—usually malar rash and photosensitivity—were more common in white children and organ involvement—usually renal—was more common in nonwhite children, reported Dr. Silverman, professor of pediatrics and immunology at the University of Toronto.

Although anti-DNA, anticardiolipin, lupus anticoagulant, and anti-La antibodies were similar in white and nonwhite children, anti-Sm, anti-RNP, and anti-Ro were expressed more in the nonwhite patients (34% vs. 56%; 30% vs. 42%; and 28% vs. 45%, respectively). The differences in course and incidence of SLE, based on ethnicity, are likely a result of interactions between genes and environment, he said.

Rates of arthritis, serositis, renal disease, central nervous system disease, and hematologic complications have been shown by other researchers not to differ between groups, nor did median SLE disease activity index, he noted.

However, findings from one study show intensive care unit admissions and deaths occurred more often in those younger than age 11 years, compared with those 11 years and older (32% vs. 21% and 11% vs. 0%, respectively), which suggests that SLE may be more severe in younger patients, Dr. Silverman said. Neuropsychiatric manifestations also can occur in pediatric SLE. Studies suggest that, among patients with neurologic involvement (about 25% of SLE patients), headache occurs in 68%, psychosis occurs in 36%, cognitive dysfunction occurs in 27%, cardiovascular disease occurs in 24%, seizures occur in 18%, mood disorders occur in 15%, and chorea occurs in 11%, noted Dr. Silverman.

DESTIN, FLA. — Ethnicity appears to play an important role in the incidence and clinical manifestations of pediatric systemic lupus erythematosus, data from a recent study suggest.

Findings from the study of 87 white and 154 nonwhite children showed that whites accounted for more than 60% of age-matched controls without pediatric systemic lupus erythematosus (SLE) but fewer than 40% of the children with pediatric SLE. Specifically, Black, Asian, and South Asian patients are overrepresented in the pediatric SLE population, Dr. Earl Silverman reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

Mucocutaneous manifestations—usually malar rash and photosensitivity—were more common in white children and organ involvement—usually renal—was more common in nonwhite children, reported Dr. Silverman, professor of pediatrics and immunology at the University of Toronto.

Although anti-DNA, anticardiolipin, lupus anticoagulant, and anti-La antibodies were similar in white and nonwhite children, anti-Sm, anti-RNP, and anti-Ro were expressed more in the nonwhite patients (34% vs. 56%; 30% vs. 42%; and 28% vs. 45%, respectively). The differences in course and incidence of SLE, based on ethnicity, are likely a result of interactions between genes and environment, he said.

Rates of arthritis, serositis, renal disease, central nervous system disease, and hematologic complications have been shown by other researchers not to differ between groups, nor did median SLE disease activity index, he noted.

However, findings from one study show intensive care unit admissions and deaths occurred more often in those younger than age 11 years, compared with those 11 years and older (32% vs. 21% and 11% vs. 0%, respectively), which suggests that SLE may be more severe in younger patients, Dr. Silverman said. Neuropsychiatric manifestations also can occur in pediatric SLE. Studies suggest that, among patients with neurologic involvement (about 25% of SLE patients), headache occurs in 68%, psychosis occurs in 36%, cognitive dysfunction occurs in 27%, cardiovascular disease occurs in 24%, seizures occur in 18%, mood disorders occur in 15%, and chorea occurs in 11%, noted Dr. Silverman.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients, and can pose particular challenges to clinicians caring for these patients.

Not only can such manifestations be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk in some studies (RHEUMATOLOGY NEWS, August 2008, p. 8), and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8%; and psychosis, which occurs in up to 5%. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1%, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within one year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

Possible neuropathological/pathophysiological explanations for neuropsychiatric manifestations in lupus patients include microangiopathy, the presence of autoantibodies, intrathecal production of proinflammatory cytokines, atherosclerosis, complement activation in brain blood vessels, loss of integrity of the blood-brain barrier, Dr. Brey said.

As with the many other clinical manifestations of lupus, there are numerous possible causes. Given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging (see box on prior page), and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered; lupus is not always to blame.

Treatments are the same as those used to treat other serious lupus manifestations—corticosteroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments may also be useful, such as for headaches, seizures, and stroke, and these appear to work as well in lupus patients as in those without lupus. Nonpharmacologic treatments may also be useful, such as stress management, lifestyle changes, psychotherapy, and cognitive rehabilitation.

fMRI May Prove Useful for Lupus

Magnetic resonance imaging and resting 18fluorodeoxyglucose-positron emission tomography both show a high frequency of anatomic brain abnormalities in newly diagnosed lupus patients, Dr. Brey said.

The finding suggests that damage to the brain is apparent early in the course of disease, but the findings using these modalities are nonspecific. Functional MRI and other newer imaging modalities might prove to be better approaches to evaluating and following lupus patients with neuropsychiatric manifestations, she said.

For example, functional imaging is being used in an ongoing pilot study to help identify which networks are involved in the neuropsychiatric manifestations in lupus. Functional MRI is used to identify areas of increased oxygen metabolism after controls, patients with lupus and impaired cognition, and patients with lupus and normal cognition participate in a cognitive test involving spatial working memory.

“It's like a stress test for the brain,” Dr. Brey said, noting that functional MRI appears to be a useful tool in this setting.

The findings could eventually help to identify sources of pathology and surrogate end points for trials of treatments for neuropsychiatric manifestations of lupus, she said.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients, and can pose particular challenges to clinicians caring for these patients.

Not only can such manifestations be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk in some studies (RHEUMATOLOGY NEWS, August 2008, p. 8), and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8%; and psychosis, which occurs in up to 5%. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1%, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within one year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

Possible neuropathological/pathophysiological explanations for neuropsychiatric manifestations in lupus patients include microangiopathy, the presence of autoantibodies, intrathecal production of proinflammatory cytokines, atherosclerosis, complement activation in brain blood vessels, loss of integrity of the blood-brain barrier, Dr. Brey said.

As with the many other clinical manifestations of lupus, there are numerous possible causes. Given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging (see box on prior page), and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered; lupus is not always to blame.

Treatments are the same as those used to treat other serious lupus manifestations—corticosteroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments may also be useful, such as for headaches, seizures, and stroke, and these appear to work as well in lupus patients as in those without lupus. Nonpharmacologic treatments may also be useful, such as stress management, lifestyle changes, psychotherapy, and cognitive rehabilitation.

fMRI May Prove Useful for Lupus

Magnetic resonance imaging and resting 18fluorodeoxyglucose-positron emission tomography both show a high frequency of anatomic brain abnormalities in newly diagnosed lupus patients, Dr. Brey said.

The finding suggests that damage to the brain is apparent early in the course of disease, but the findings using these modalities are nonspecific. Functional MRI and other newer imaging modalities might prove to be better approaches to evaluating and following lupus patients with neuropsychiatric manifestations, she said.

For example, functional imaging is being used in an ongoing pilot study to help identify which networks are involved in the neuropsychiatric manifestations in lupus. Functional MRI is used to identify areas of increased oxygen metabolism after controls, patients with lupus and impaired cognition, and patients with lupus and normal cognition participate in a cognitive test involving spatial working memory.

“It's like a stress test for the brain,” Dr. Brey said, noting that functional MRI appears to be a useful tool in this setting.

The findings could eventually help to identify sources of pathology and surrogate end points for trials of treatments for neuropsychiatric manifestations of lupus, she said.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients, and can pose particular challenges to clinicians caring for these patients.

Not only can such manifestations be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk in some studies (RHEUMATOLOGY NEWS, August 2008, p. 8), and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8%; and psychosis, which occurs in up to 5%. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1%, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within one year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

Possible neuropathological/pathophysiological explanations for neuropsychiatric manifestations in lupus patients include microangiopathy, the presence of autoantibodies, intrathecal production of proinflammatory cytokines, atherosclerosis, complement activation in brain blood vessels, loss of integrity of the blood-brain barrier, Dr. Brey said.

As with the many other clinical manifestations of lupus, there are numerous possible causes. Given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging (see box on prior page), and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered; lupus is not always to blame.

Treatments are the same as those used to treat other serious lupus manifestations—corticosteroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments may also be useful, such as for headaches, seizures, and stroke, and these appear to work as well in lupus patients as in those without lupus. Nonpharmacologic treatments may also be useful, such as stress management, lifestyle changes, psychotherapy, and cognitive rehabilitation.

fMRI May Prove Useful for Lupus

Magnetic resonance imaging and resting 18fluorodeoxyglucose-positron emission tomography both show a high frequency of anatomic brain abnormalities in newly diagnosed lupus patients, Dr. Brey said.

The finding suggests that damage to the brain is apparent early in the course of disease, but the findings using these modalities are nonspecific. Functional MRI and other newer imaging modalities might prove to be better approaches to evaluating and following lupus patients with neuropsychiatric manifestations, she said.

For example, functional imaging is being used in an ongoing pilot study to help identify which networks are involved in the neuropsychiatric manifestations in lupus. Functional MRI is used to identify areas of increased oxygen metabolism after controls, patients with lupus and impaired cognition, and patients with lupus and normal cognition participate in a cognitive test involving spatial working memory.

“It's like a stress test for the brain,” Dr. Brey said, noting that functional MRI appears to be a useful tool in this setting.

The findings could eventually help to identify sources of pathology and surrogate end points for trials of treatments for neuropsychiatric manifestations of lupus, she said.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% nightly during sleep, compared with waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two groups.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% nightly during sleep, compared with waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two groups.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% nightly during sleep, compared with waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two groups.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Surveys.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Surveys (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see graphic), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratios 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidate stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Surveys.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Surveys (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see graphic), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratios 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidate stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Reduced serum selenium is an independent predictor of hypertension, according to an analysis of data from the third National Health and Nutrition Examination Surveys.

The findings from this and other studies, that serum selenium concentrations are reduced in African Americans, compared with whites, may in part explain the increased incidence of hypertension in African Americans, Dr. Chizobam Ani reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

Serum selenium is an essential component in substances shown to mediate the incidence of cardiovascular disease, such as glutathione peroxidase and homocysteine. In 9,881 nonpregnant adults aged 40 years and older who participated in the third National Health and Nutrition Examination Surveys (NHANES III), significant differences in the concentrations of serum selenium were noted between African Americans and whites at the highest and lowest quartile concentrations (see graphic), reported Dr. Ani of Charles Drew University of Medicine and Science, Los Angeles.

On bivariate analysis, there was a significant association between serum selenium concentration and the prevalence of hypertension and other cardiovascular disease, including peripheral vascular disease, myocardial infarction, and congestive heart failure. An analysis that controlled for known predictors of cardiovascular disease, including family history, diabetes, renal disease, and sociodemographic variables, showed a significant relationship between serum selenium and the prevalence of hypertension (odds ratios 1.30), as well as a significant interaction effect between ethnicity and serum selenium among individuals with hypertension (odds ratio 1.10).

These findings are important because African Americans have higher rates of hypertension and mortality from heart disease and stroke than do whites and Hispanics in the United States, and because African American men have three times the risk of sudden death as do white men.

“Inquiry into biomarkers [that may be] predictors of differential risk and incidence, particularly at the population level, may provide useful explanatory insight regarding the differential burden on cardiovascular disease among African Americans,” Dr. Ani wrote.

Based on the emerging understanding of the role of serum selenium in hypertension and cardiovascular disease, and the differing concentrations in African Americans and whites, Dr. Ani and his colleagues theorized that high serum concentrations of selenium might predict reduced levels of oxidate stress and vascular injury in certain ethnic groups that correlates with the incidence of cardiovascular diseases.

The current findings of a statistically significant interaction between serum selenium concentration and ethnicity in individuals with hypertension appear to support this theory of “differential oxidative protection for cardiovascular injury” in African Americans, compared with whites, he said in an interview, adding that the findings are of particular interest because low serum selenium concentration is a modifiable risk factor.

ELSEVIER GLOBAL MEDICAL NEWS

DESTIN, FLA. — The prevalence of metabolic syndrome is increased in patients with rheumatoid arthritis, compared with the general population, as is the prevalence of insulin resistance, data from numerous studies show.

Likewise, insulin resistance is increased in those with systemic lupus erythematosus, and the increased risks are independent of age, sex, race, body mass index, and corticosteroid use. These findings suggest that inflammation plays a role in the development of insulin resistance and other components of metabolic syndrome, although the mechanisms in the two diseases differ, Dr. C. Michael Stein reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

For example, in a study in press at the time of Dr. Stein's presentation, the prevalence of insulin resistance was nearly 60% in patients with long-standing rheumatoid arthritis, and about 50% in those with early rheumatoid arthritis, compared with about 20% in controls. In a published study of lupus patients, more than 30% had insulin resistance, compared with about 11% of controls (Ann. Rheum. Dis. 2007;66:208-14).

However, interleukin-6 levels have been shown to be significantly associated with insulin resistance in rheumatoid arthritis, (rho 0.63; P less than.001), but not in lupus (rho 0.16; P = .18), and the same has been shown to be true for tumor necrosis factor-α (rho 0.50; P less than .001and rho 0.11; P = .24, respectively), said Dr. Stein of Vanderbilt University, Nashville, Tenn.

Body mass index traditionally is an important factor in the metabolic syndrome pathway to coronary heart disease, and was significantly associated with insulin resistance in lupus in the study (rho 0.54; P less than .001), but it appears that inflammation also can lead to the same pathway, he explained.

In addition, atherosclerosis is accelerated in both diseases. This also may be a factor of inflammation, as well as of insulin resistance and metabolic syndrome. It does not appear, in these diseases, to be associated with traditional cholesterol/lipid concentration-related mechanisms, Dr. Stein noted.

“The good news is that the features of metabolic syndrome can be reversed,” he said.

The same lifestyle interventions recommended for other patients with metabolic syndrome are recommended for those with rheumatoid arthritis or lupus. As for the potential for treatments that target the inflammatory mediators of these diseases to have a beneficial effect on insulin resistance and metabolic syndrome, he said, research is underway.

DESTIN, FLA. — The prevalence of metabolic syndrome is increased in patients with rheumatoid arthritis, compared with the general population, as is the prevalence of insulin resistance, data from numerous studies show.

Likewise, insulin resistance is increased in those with systemic lupus erythematosus, and the increased risks are independent of age, sex, race, body mass index, and corticosteroid use. These findings suggest that inflammation plays a role in the development of insulin resistance and other components of metabolic syndrome, although the mechanisms in the two diseases differ, Dr. C. Michael Stein reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

For example, in a study in press at the time of Dr. Stein's presentation, the prevalence of insulin resistance was nearly 60% in patients with long-standing rheumatoid arthritis, and about 50% in those with early rheumatoid arthritis, compared with about 20% in controls. In a published study of lupus patients, more than 30% had insulin resistance, compared with about 11% of controls (Ann. Rheum. Dis. 2007;66:208-14).

However, interleukin-6 levels have been shown to be significantly associated with insulin resistance in rheumatoid arthritis, (rho 0.63; P less than.001), but not in lupus (rho 0.16; P = .18), and the same has been shown to be true for tumor necrosis factor-α (rho 0.50; P less than .001and rho 0.11; P = .24, respectively), said Dr. Stein of Vanderbilt University, Nashville, Tenn.

Body mass index traditionally is an important factor in the metabolic syndrome pathway to coronary heart disease, and was significantly associated with insulin resistance in lupus in the study (rho 0.54; P less than .001), but it appears that inflammation also can lead to the same pathway, he explained.

In addition, atherosclerosis is accelerated in both diseases. This also may be a factor of inflammation, as well as of insulin resistance and metabolic syndrome. It does not appear, in these diseases, to be associated with traditional cholesterol/lipid concentration-related mechanisms, Dr. Stein noted.

“The good news is that the features of metabolic syndrome can be reversed,” he said.

The same lifestyle interventions recommended for other patients with metabolic syndrome are recommended for those with rheumatoid arthritis or lupus. As for the potential for treatments that target the inflammatory mediators of these diseases to have a beneficial effect on insulin resistance and metabolic syndrome, he said, research is underway.

DESTIN, FLA. — The prevalence of metabolic syndrome is increased in patients with rheumatoid arthritis, compared with the general population, as is the prevalence of insulin resistance, data from numerous studies show.

Likewise, insulin resistance is increased in those with systemic lupus erythematosus, and the increased risks are independent of age, sex, race, body mass index, and corticosteroid use. These findings suggest that inflammation plays a role in the development of insulin resistance and other components of metabolic syndrome, although the mechanisms in the two diseases differ, Dr. C. Michael Stein reported at a rheumatology conference sponsored by Virginia Commonwealth University, Richmond.

For example, in a study in press at the time of Dr. Stein's presentation, the prevalence of insulin resistance was nearly 60% in patients with long-standing rheumatoid arthritis, and about 50% in those with early rheumatoid arthritis, compared with about 20% in controls. In a published study of lupus patients, more than 30% had insulin resistance, compared with about 11% of controls (Ann. Rheum. Dis. 2007;66:208-14).

However, interleukin-6 levels have been shown to be significantly associated with insulin resistance in rheumatoid arthritis, (rho 0.63; P less than.001), but not in lupus (rho 0.16; P = .18), and the same has been shown to be true for tumor necrosis factor-α (rho 0.50; P less than .001and rho 0.11; P = .24, respectively), said Dr. Stein of Vanderbilt University, Nashville, Tenn.

Body mass index traditionally is an important factor in the metabolic syndrome pathway to coronary heart disease, and was significantly associated with insulin resistance in lupus in the study (rho 0.54; P less than .001), but it appears that inflammation also can lead to the same pathway, he explained.

In addition, atherosclerosis is accelerated in both diseases. This also may be a factor of inflammation, as well as of insulin resistance and metabolic syndrome. It does not appear, in these diseases, to be associated with traditional cholesterol/lipid concentration-related mechanisms, Dr. Stein noted.

“The good news is that the features of metabolic syndrome can be reversed,” he said.

The same lifestyle interventions recommended for other patients with metabolic syndrome are recommended for those with rheumatoid arthritis or lupus. As for the potential for treatments that target the inflammatory mediators of these diseases to have a beneficial effect on insulin resistance and metabolic syndrome, he said, research is underway.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients during the course of disease, and can pose challenges in caring for these patients.

Not only can such manifestations of lupus be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest that migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk seen in some studies, and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR case definition, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8% of adult patients; and psychosis, which occurs in up to 5% of adult patients. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1% of adult patients, respectively, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within 1 year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

As with the many other clinical manifestations of lupus, there are numerous possible causes. And given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations, she added.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging, and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered as a possible cause of the symptoms; lupus is not always to blame, she added.

Treatments are the same as those used to treat other serious lupus manifestations, and may include cortico-steroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments—depending on the manifestation—may also be useful, such as for headaches, seizures, and stroke.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients during the course of disease, and can pose challenges in caring for these patients.

Not only can such manifestations of lupus be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest that migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk seen in some studies, and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR case definition, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8% of adult patients; and psychosis, which occurs in up to 5% of adult patients. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1% of adult patients, respectively, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within 1 year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

As with the many other clinical manifestations of lupus, there are numerous possible causes. And given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations, she added.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging, and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered as a possible cause of the symptoms; lupus is not always to blame, she added.

Treatments are the same as those used to treat other serious lupus manifestations, and may include cortico-steroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments—depending on the manifestation—may also be useful, such as for headaches, seizures, and stroke.

DESTIN, FLA. — Neuropsychiatric manifestations of systemic lupus erythematosus occur in more than 80% of patients during the course of disease, and can pose challenges in caring for these patients.

Not only can such manifestations of lupus be difficult to distinguish from infectious or other nonimmunologically mediated processes, they can occur in the absence of serologic disease activity or other systemic manifestations, Dr. Robin L. Brey said at a rheumatology conference sponsored by Virginia Commonwealth University.

“The challenge to us in caring for patients complaining of some kind of neuropsychiatric manifestation … is really, first and foremost, determining if it is related to lupus,” said Dr. Brey, professor of medicine and associate dean for research at the University of Texas Health Science Center, San Antonio.

The American College of Rheumatology has developed case definitions of several neuropsychiatric manifestations of lupus, including cerebrovascular disease, cognitive disorders, headaches, and movement disorders, among many others. Based on these case definitions, the prevalence of the manifestations in adults has been shown to be between 14% and 80%. Headaches, for example, occur in up to 61% of patients.

There is some controversy over whether headaches should be included in this list, as they are common both in lupus and nonlupus patients, but studies suggest that migraine with aura is especially likely to be a neuropsychiatric manifestation of lupus—a particular concern given the association between migraine with aura and increased stroke risk seen in some studies, and an important factor to evaluate for in general practice when treating lupus patients, Dr. Brey said.

Other lupus-related manifestations, according to the ACR case definition, include seizures, which occur in up to 18% of adults with lupus; cardiovascular disease, which occurs in up to 8% of adult patients; and psychosis, which occurs in up to 5% of adult patients. Cranial neuropathy and movement disorders occur only rarely—in about 2% and 1% of adult patients, respectively, Dr. Brey said.

Children with lupus have also been found to exhibit neuropsychiatric manifestations, and both children and adults tend to exhibit the manifestations early, she noted.

Studies show that between 28% and 40% of adults, and 11% of children, exhibit such manifestations at the time of lupus diagnosis, with up to 26% of children experiencing neuropsychiatric manifestations within 1 year of diagnosis.

Among the most common complaints are those associated with cognitive dysfunction. A subcortical pattern of complaints involving impairments in complex attention, cognitive processing speed, and memory retrieval is known as cognitive inefficiency, which can be very bothersome for patients and vexing for physicians to treat, she said.

This pattern is similar to that seen in HIV dementia, with a great deal more energy than normal required to perform cognitive functions. Some researchers believe this contributes to the fatigue experienced by many lupus patients, she noted.

Risk factors for the development of lupus-related cognitive dysfunction include Hispanic ethnicity, higher depression scores, higher damage scores and acute disease activity scores, consistent prednisone use, and persistently positive antiphospholipid and antiribosomal antibodies. Effects of neuropsychiatric manifestations may include decreased quality of life and increased lupus-related organ damage—both of which have been linked with these manifestations in adults.

Mortality may also be increased in those with these manifestations. In one study, the mortality rate over 20 years in children with lupus who experienced neuropsychiatric manifestations was 45%, compared with 17% in those without such manifestations.

As with the many other clinical manifestations of lupus, there are numerous possible causes. And given the varying manifestations, no single diagnostic test is sensitive or specific for identifying lupus-related neuropsychiatric manifestations, she added.

“Essentially, it takes an individualized approach, and it really, truly does depend on the complaint that the patient comes in with,” she said.

Appropriate assessment for clinical care might include immunoserologic testing, brain imaging, and neurophysiological, psychiatric, and neuropsychological assessments, she said. However, infection must always be considered as a possible cause of the symptoms; lupus is not always to blame, she added.

Treatments are the same as those used to treat other serious lupus manifestations, and may include cortico-steroids, azathioprine, cyclophosphamide, and mycophenolate mofetil. Symptomatic treatments—depending on the manifestation—may also be useful, such as for headaches, seizures, and stroke.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% at night during sleep, compared with blood pressure during waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

In the study, hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The researchers found that as BMI increased, so did the rates of nocturnal nondipping. The rates of nondipping were 26%, 41%, and 76% for the three BMI categories, respectively. Additionally, 36% of the patients were “reverse dippers,” meaning their blood pressure actually increased at night, reported Dr. Randall, professor of medicine and cardiology at Howard University, Washington.

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two BMI groups. Daytime blood pressure for this study was defined as the average of hourly readings between 8 a.m. and 10 p.m., and nighttime blood pressure was defined as the average of hourly readings from 10 p.m. to 6 a.m.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% at night during sleep, compared with blood pressure during waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

In the study, hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The researchers found that as BMI increased, so did the rates of nocturnal nondipping. The rates of nondipping were 26%, 41%, and 76% for the three BMI categories, respectively. Additionally, 36% of the patients were “reverse dippers,” meaning their blood pressure actually increased at night, reported Dr. Randall, professor of medicine and cardiology at Howard University, Washington.

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two BMI groups. Daytime blood pressure for this study was defined as the average of hourly readings between 8 a.m. and 10 p.m., and nighttime blood pressure was defined as the average of hourly readings from 10 p.m. to 6 a.m.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

NEW ORLEANS — Obesity blunts the normal pattern of nocturnal blood pressure dipping, and this might be one mechanism through which obesity contributes to adverse cardiovascular outcomes, findings from a recent study suggest.

Blood pressure normally drops by 10%–20% at night during sleep, compared with blood pressure during waking hours during the day, and studies have shown that nondipping (defined as less than a 10% decrease in blood pressure at night) is associated with increased cardiovascular morbidity and mortality, Dr. Otelio Randall reported in a poster at a meeting sponsored by the International Society on Hypertension in Blacks.

In the study, hourly blood pressure measurements were taken in 200 obese African American patients who were classified into three groups on the basis of their body mass index, in kg/m

The researchers found that as BMI increased, so did the rates of nocturnal nondipping. The rates of nondipping were 26%, 41%, and 76% for the three BMI categories, respectively. Additionally, 36% of the patients were “reverse dippers,” meaning their blood pressure actually increased at night, reported Dr. Randall, professor of medicine and cardiology at Howard University, Washington.

The mean percentage of dipping was 8.6% in those with a BMI of less than 40, 8.4% in those with a BMI of 40–49, and 3.9% in those with a BMI of 50 or greater. Those with a BMI of at least 50 had a significantly smaller decrease in nocturnal blood pressure than the other two BMI groups. Daytime blood pressure for this study was defined as the average of hourly readings between 8 a.m. and 10 p.m., and nighttime blood pressure was defined as the average of hourly readings from 10 p.m. to 6 a.m.

“Nondipping and reverse dipping are known to be associated with the potential risk for target organ damage. The high rates of nondipping and reverse dipping in this obese population reinforces the need to reduce BMI and improve hemodynamic and lipid profiles through lifestyle changes,” Dr. Randall said.

CHICAGO — The incidence of multicentric Castleman's disease is increasing among patients with human immunodeficiency virus, including those who have access to highly active antiretroviral therapy, Mark Bower, Ph.D., reported in a poster at the annual meeting of the American Society of Clinical Oncology.

Also called angiofollicular or giant lymph node hyperplasia, multicentric Castleman's disease is an atypical lymphoproliferative disorder characterized by the growth of tumors in lymph node tissue. It is causally related to infection with human herpesvirus-8 (HHV-8), and patients are at increased risk of developing a malignancy, such as non-Hodgkin's lymphoma.

In a prospective cohort of nearly 10,997 HIV-positive patients with more than 56,000 patient years of follow-up, Dr. Bower and his coauthors calculated that the overall event rate for multicentric Castleman's disease was 4.3 per 10,000 years of patient follow-up. They reported:

▸ From 1983 to 1996 (the era before highly active antiretroviral therapy [HAART]) the incidence was 2.3 per 10,000 years of patient follow-up.

▸ From 1997 to 2001 (the initial HAART era) the incidence was 2.8 per 10,000 years of patient follow-up.

▸ From 2002 to 2007 (the HAART era) the incidence was 8.3 per 10,000 years of patient follow-up.

The increase over time was significant, but was not associated with gender or prior AIDS, noted Dr. Bower of Chelsea and Westminster Hospital, London. In contrast, the incidence of Kaposi's sarcoma (also causally related to infection with HHV-8) is greater in men, and has decreased with improved immune function and HAART availability.

For the study, plasma HHV-8 DNA levels were measured in 24 HIV-positive patients with newly diagnosed multicentric Castleman's disease, 72 with newly diagnosed Kaposi's sarcoma, 74 with newly diagnosed lymphoma, and in 53 HIV-positive controls with none of these diagnoses.

On multivariate analysis, increased risk of multicentric Castleman's disease was associated with nadir CD4 cell count above 200/mm

A higher proportion of patients with multicentric Castleman's disease had detectable plasma HHV-8 DNA levels at diagnosis, compared with Kaposi's sarcoma patients and lymphoma patients (83% vs. 35% and 3%, respectively). The levels also were higher in patients with newly diagnosed multicentric Castleman's disease (41,000 copies/mL), compared with Kaposi's sarcoma patients (3,500 copies/mL).

In an additional analysis involving the three main HAART drug classes, only nucleoside reverse transcriptase inhibitors were associated with decreased incidence of multicentric Castleman's disease.

The incidence of multicentric Castleman's disease is increasing despite the availability of HAART, and it appears that comparatively well-preserved immune function, increased age, nonwhite race, a short known duration of HIV infection, and no HAART use predispose HIV patients to development of the disease, according to the investigators.

Multicentric Castleman's disease appears to occur more often in older HIV-positive patients with well-preserved immune function, Dr. Bower noted, adding that the role of HHV-8 appears to be different in this disease and Kaposi's sarcoma.

Additional investigation is required to explore the cause of the increased incidence of this disease, he said.

CHICAGO — The incidence of multicentric Castleman's disease is increasing among patients with human immunodeficiency virus, including those who have access to highly active antiretroviral therapy, Mark Bower, Ph.D., reported in a poster at the annual meeting of the American Society of Clinical Oncology.

Also called angiofollicular or giant lymph node hyperplasia, multicentric Castleman's disease is an atypical lymphoproliferative disorder characterized by the growth of tumors in lymph node tissue. It is causally related to infection with human herpesvirus-8 (HHV-8), and patients are at increased risk of developing a malignancy, such as non-Hodgkin's lymphoma.

In a prospective cohort of nearly 10,997 HIV-positive patients with more than 56,000 patient years of follow-up, Dr. Bower and his coauthors calculated that the overall event rate for multicentric Castleman's disease was 4.3 per 10,000 years of patient follow-up. They reported:

▸ From 1983 to 1996 (the era before highly active antiretroviral therapy [HAART]) the incidence was 2.3 per 10,000 years of patient follow-up.

▸ From 1997 to 2001 (the initial HAART era) the incidence was 2.8 per 10,000 years of patient follow-up.

▸ From 2002 to 2007 (the HAART era) the incidence was 8.3 per 10,000 years of patient follow-up.

The increase over time was significant, but was not associated with gender or prior AIDS, noted Dr. Bower of Chelsea and Westminster Hospital, London. In contrast, the incidence of Kaposi's sarcoma (also causally related to infection with HHV-8) is greater in men, and has decreased with improved immune function and HAART availability.

For the study, plasma HHV-8 DNA levels were measured in 24 HIV-positive patients with newly diagnosed multicentric Castleman's disease, 72 with newly diagnosed Kaposi's sarcoma, 74 with newly diagnosed lymphoma, and in 53 HIV-positive controls with none of these diagnoses.

On multivariate analysis, increased risk of multicentric Castleman's disease was associated with nadir CD4 cell count above 200/mm

A higher proportion of patients with multicentric Castleman's disease had detectable plasma HHV-8 DNA levels at diagnosis, compared with Kaposi's sarcoma patients and lymphoma patients (83% vs. 35% and 3%, respectively). The levels also were higher in patients with newly diagnosed multicentric Castleman's disease (41,000 copies/mL), compared with Kaposi's sarcoma patients (3,500 copies/mL).

In an additional analysis involving the three main HAART drug classes, only nucleoside reverse transcriptase inhibitors were associated with decreased incidence of multicentric Castleman's disease.

The incidence of multicentric Castleman's disease is increasing despite the availability of HAART, and it appears that comparatively well-preserved immune function, increased age, nonwhite race, a short known duration of HIV infection, and no HAART use predispose HIV patients to development of the disease, according to the investigators.

Multicentric Castleman's disease appears to occur more often in older HIV-positive patients with well-preserved immune function, Dr. Bower noted, adding that the role of HHV-8 appears to be different in this disease and Kaposi's sarcoma.

Additional investigation is required to explore the cause of the increased incidence of this disease, he said.

CHICAGO — The incidence of multicentric Castleman's disease is increasing among patients with human immunodeficiency virus, including those who have access to highly active antiretroviral therapy, Mark Bower, Ph.D., reported in a poster at the annual meeting of the American Society of Clinical Oncology.

Also called angiofollicular or giant lymph node hyperplasia, multicentric Castleman's disease is an atypical lymphoproliferative disorder characterized by the growth of tumors in lymph node tissue. It is causally related to infection with human herpesvirus-8 (HHV-8), and patients are at increased risk of developing a malignancy, such as non-Hodgkin's lymphoma.

In a prospective cohort of nearly 10,997 HIV-positive patients with more than 56,000 patient years of follow-up, Dr. Bower and his coauthors calculated that the overall event rate for multicentric Castleman's disease was 4.3 per 10,000 years of patient follow-up. They reported:

▸ From 1983 to 1996 (the era before highly active antiretroviral therapy [HAART]) the incidence was 2.3 per 10,000 years of patient follow-up.

▸ From 1997 to 2001 (the initial HAART era) the incidence was 2.8 per 10,000 years of patient follow-up.

▸ From 2002 to 2007 (the HAART era) the incidence was 8.3 per 10,000 years of patient follow-up.

The increase over time was significant, but was not associated with gender or prior AIDS, noted Dr. Bower of Chelsea and Westminster Hospital, London. In contrast, the incidence of Kaposi's sarcoma (also causally related to infection with HHV-8) is greater in men, and has decreased with improved immune function and HAART availability.

For the study, plasma HHV-8 DNA levels were measured in 24 HIV-positive patients with newly diagnosed multicentric Castleman's disease, 72 with newly diagnosed Kaposi's sarcoma, 74 with newly diagnosed lymphoma, and in 53 HIV-positive controls with none of these diagnoses.

On multivariate analysis, increased risk of multicentric Castleman's disease was associated with nadir CD4 cell count above 200/mm

A higher proportion of patients with multicentric Castleman's disease had detectable plasma HHV-8 DNA levels at diagnosis, compared with Kaposi's sarcoma patients and lymphoma patients (83% vs. 35% and 3%, respectively). The levels also were higher in patients with newly diagnosed multicentric Castleman's disease (41,000 copies/mL), compared with Kaposi's sarcoma patients (3,500 copies/mL).

In an additional analysis involving the three main HAART drug classes, only nucleoside reverse transcriptase inhibitors were associated with decreased incidence of multicentric Castleman's disease.

The incidence of multicentric Castleman's disease is increasing despite the availability of HAART, and it appears that comparatively well-preserved immune function, increased age, nonwhite race, a short known duration of HIV infection, and no HAART use predispose HIV patients to development of the disease, according to the investigators.

Multicentric Castleman's disease appears to occur more often in older HIV-positive patients with well-preserved immune function, Dr. Bower noted, adding that the role of HHV-8 appears to be different in this disease and Kaposi's sarcoma.

Additional investigation is required to explore the cause of the increased incidence of this disease, he said.

DESTIN, FLA. — A soft, fluctuant lesion near the midline of the forehead or on the scalp might look like a port wine stain, but it could be a serious, potentially fatal condition known as sinus pericranii.

Maintain a high index of suspicion for such lesions, Dr. Bari Cunningham advised at a meeting sponsored by the Alabama Dermatology Society.

Dr. Cunningham, of the University of California, San Diego, described a case involving an adolescent boy who presented with a complaint about comedomal acne of the forehead. During examination of the patient, an astute colleague noticed what appeared to be a vascular stain on his glabella.

The patient noted that the stain had been present since birth, and that it was not a concern for him. However, when the physician had him lie down, the lesion became puffy, swollen and blood filled—a sign that this was not the "run-of-the-mill port wine stain," Dr. Cunningham said.

On magnetic resonance imaging, the lesion was found to be sinus pericranii—a rare disorder described in the literature as being "characterized by a congenital or acquired epicranial blood-filled nodule of the scalp that is in communication with an intracranial dural sinus through dilated diploic veins of the skull" (J. Am. Acad. Dermatol. 2002;46:934–41).

Sinus pericranii can be congenital, spontaneous, or traumatic in origin, Dr. Cunningham noted, explaining that the condition can result from incidental increased intracranial pressure from something as innocuous as a sneeze or cough in a predisposed individual, or from traumatic delivery. One recent report involved a child with PHACES (posterior fossa anomalies; facial hemangioma; arterial, cardiac, and eye anomalies; and sternal cleft anomalies), suggesting that the condition does not necessarily occur in isolation.

The nodules associated with sinus pericranii can connect from anywhere on the skull or scalp—including in the midline of the forehead—through the intracranial dural sinus (usually the saggital sinus). Some patients complain of vertigo, headache, and localized pain in association with the condition, but others—such as the adolescent she described—remain asymptomatic.

It is essential to be alert for such lesions because they can be associated with catastrophic outcomes, including hemorrhage, infection, and air emboli, particularly when surgery is performed for the misdiagnosis. In some cases, several liters of blood have been encountered intraoperatively, with fatal outcomes from sinus pericranii that was misdiagnosed.

"Just be aware," Dr. Cunningham said.

If sinus pericranii is suspected, imaging and appropriate referral to a neurosurgeon is necessary to avoid misdiagnosis and subsequent, potentially fatal, surgery, she said.

DESTIN, FLA. — A soft, fluctuant lesion near the midline of the forehead or on the scalp might look like a port wine stain, but it could be a serious, potentially fatal condition known as sinus pericranii.

Maintain a high index of suspicion for such lesions, Dr. Bari Cunningham advised at a meeting sponsored by the Alabama Dermatology Society.

Dr. Cunningham, of the University of California, San Diego, described a case involving an adolescent boy who presented with a complaint about comedomal acne of the forehead. During examination of the patient, an astute colleague noticed what appeared to be a vascular stain on his glabella.

The patient noted that the stain had been present since birth, and that it was not a concern for him. However, when the physician had him lie down, the lesion became puffy, swollen and blood filled—a sign that this was not the "run-of-the-mill port wine stain," Dr. Cunningham said.

On magnetic resonance imaging, the lesion was found to be sinus pericranii—a rare disorder described in the literature as being "characterized by a congenital or acquired epicranial blood-filled nodule of the scalp that is in communication with an intracranial dural sinus through dilated diploic veins of the skull" (J. Am. Acad. Dermatol. 2002;46:934–41).

Sinus pericranii can be congenital, spontaneous, or traumatic in origin, Dr. Cunningham noted, explaining that the condition can result from incidental increased intracranial pressure from something as innocuous as a sneeze or cough in a predisposed individual, or from traumatic delivery. One recent report involved a child with PHACES (posterior fossa anomalies; facial hemangioma; arterial, cardiac, and eye anomalies; and sternal cleft anomalies), suggesting that the condition does not necessarily occur in isolation.

The nodules associated with sinus pericranii can connect from anywhere on the skull or scalp—including in the midline of the forehead—through the intracranial dural sinus (usually the saggital sinus). Some patients complain of vertigo, headache, and localized pain in association with the condition, but others—such as the adolescent she described—remain asymptomatic.

It is essential to be alert for such lesions because they can be associated with catastrophic outcomes, including hemorrhage, infection, and air emboli, particularly when surgery is performed for the misdiagnosis. In some cases, several liters of blood have been encountered intraoperatively, with fatal outcomes from sinus pericranii that was misdiagnosed.

"Just be aware," Dr. Cunningham said.

If sinus pericranii is suspected, imaging and appropriate referral to a neurosurgeon is necessary to avoid misdiagnosis and subsequent, potentially fatal, surgery, she said.

DESTIN, FLA. — A soft, fluctuant lesion near the midline of the forehead or on the scalp might look like a port wine stain, but it could be a serious, potentially fatal condition known as sinus pericranii.

Maintain a high index of suspicion for such lesions, Dr. Bari Cunningham advised at a meeting sponsored by the Alabama Dermatology Society.

Dr. Cunningham, of the University of California, San Diego, described a case involving an adolescent boy who presented with a complaint about comedomal acne of the forehead. During examination of the patient, an astute colleague noticed what appeared to be a vascular stain on his glabella.

The patient noted that the stain had been present since birth, and that it was not a concern for him. However, when the physician had him lie down, the lesion became puffy, swollen and blood filled—a sign that this was not the "run-of-the-mill port wine stain," Dr. Cunningham said.

On magnetic resonance imaging, the lesion was found to be sinus pericranii—a rare disorder described in the literature as being "characterized by a congenital or acquired epicranial blood-filled nodule of the scalp that is in communication with an intracranial dural sinus through dilated diploic veins of the skull" (J. Am. Acad. Dermatol. 2002;46:934–41).

Sinus pericranii can be congenital, spontaneous, or traumatic in origin, Dr. Cunningham noted, explaining that the condition can result from incidental increased intracranial pressure from something as innocuous as a sneeze or cough in a predisposed individual, or from traumatic delivery. One recent report involved a child with PHACES (posterior fossa anomalies; facial hemangioma; arterial, cardiac, and eye anomalies; and sternal cleft anomalies), suggesting that the condition does not necessarily occur in isolation.

The nodules associated with sinus pericranii can connect from anywhere on the skull or scalp—including in the midline of the forehead—through the intracranial dural sinus (usually the saggital sinus). Some patients complain of vertigo, headache, and localized pain in association with the condition, but others—such as the adolescent she described—remain asymptomatic.

It is essential to be alert for such lesions because they can be associated with catastrophic outcomes, including hemorrhage, infection, and air emboli, particularly when surgery is performed for the misdiagnosis. In some cases, several liters of blood have been encountered intraoperatively, with fatal outcomes from sinus pericranii that was misdiagnosed.

"Just be aware," Dr. Cunningham said.

If sinus pericranii is suspected, imaging and appropriate referral to a neurosurgeon is necessary to avoid misdiagnosis and subsequent, potentially fatal, surgery, she said.