BOSTON — Heightened activity of anti-double-stranded DNA antibodies may contribute to the poor cholesterol profiles of patients with active systemic lupus erythematosus, according to study findings.

Patients with SLE are often afflicted with a complex triad of risk factors involving high levels of serum triglycerides, high levels of VLDL cholesterol, and low levels of HDL cholesterol. These can hasten the development of premature atherosclerosis and coronary artery disease. Though researchers have posited several theories to explain this phenomenon, its etiology remains unknown.

Sara Kashef, M.D., and colleagues from the Shiraz University of Medical Sciences in Fars, Iran, compared serum lipoprotein levels and antibody activity in 30 patients with active lupus with that of 16 patients with inactive lupus, and 41 healthy controls matched for age and sex. Lupus activity was measured using the SLE disease activity index (SLEDAI). Dr. Kashef presented the study in a poster session at the annual meeting of the Federation of Clinical Immunology Societies.

Compared with healthy controls and people with inactive SLE, patients with active SLE had significantly higher levels of triglycerides and VLDL cholesterol, and lower levels of HDL cholesterol.

Moreover, poor cholesterol profiles were significantly more likely to appear in patients who tested positive for anti-dsDNA antibodies than in those who tested negative. There was no correlation between dyslipoproteinemia and anticardiolipin antibody activity, another suspect in the genesis of SLE atherosclerosis.

“The appearance of this pattern of dyslipoproteinemia—high triglycerides and VLDL cholesterol and low HDL cholesterol—in this selected group of patients seems to be a consequence of disease activity and SLE disease itself,” according to the authors. “Titers of anti-dsDNA correlated significantly with increased SLEDAI scores and low HDL cholesterol,” they noted.

Recent research suggests that the enzyme, lipoprotein lipase (LPL), may play a key role. LPL breaks down VLDL cholesterol. And when LPL is impaired, VLDL cholesterol proliferates, leading to an unhealthy duet of high triglycerides with low HDL cholesterol, the investigators explained.

Although antibodies to LPL were not measured, previous research suggests that increases in such antibodies are common in SLE patients (Arthritis Rheum. 2002;46:2957–63).

“These results reflect that one of the contributory causes of dyslipoproteinemia in active SLE is probably increased cross-reactivity of anti-dsDNA antibodies with LPL due to high production of these antibodies in the active phase of disease,” the investigators suggested.

Although these findings support an underlying autoimmune cause of dyslipoproteinemia in lupus patients with active disease, other factors likely contribute as well, the researchers said. These include inflammatory mediators (e.g., tumor necrosis factor, interleukin, interferon) that are known to suppress LPL activity and cause dyslipoproteinemia in SLE (Arthritis Rheum. 2003;48:2533–40), as well as physical inactivity.

BOSTON — Heightened activity of anti-double-stranded DNA antibodies may contribute to the poor cholesterol profiles of patients with active systemic lupus erythematosus, according to study findings.

Patients with SLE are often afflicted with a complex triad of risk factors involving high levels of serum triglycerides, high levels of VLDL cholesterol, and low levels of HDL cholesterol. These can hasten the development of premature atherosclerosis and coronary artery disease. Though researchers have posited several theories to explain this phenomenon, its etiology remains unknown.

Sara Kashef, M.D., and colleagues from the Shiraz University of Medical Sciences in Fars, Iran, compared serum lipoprotein levels and antibody activity in 30 patients with active lupus with that of 16 patients with inactive lupus, and 41 healthy controls matched for age and sex. Lupus activity was measured using the SLE disease activity index (SLEDAI). Dr. Kashef presented the study in a poster session at the annual meeting of the Federation of Clinical Immunology Societies.

Compared with healthy controls and people with inactive SLE, patients with active SLE had significantly higher levels of triglycerides and VLDL cholesterol, and lower levels of HDL cholesterol.

Moreover, poor cholesterol profiles were significantly more likely to appear in patients who tested positive for anti-dsDNA antibodies than in those who tested negative. There was no correlation between dyslipoproteinemia and anticardiolipin antibody activity, another suspect in the genesis of SLE atherosclerosis.

“The appearance of this pattern of dyslipoproteinemia—high triglycerides and VLDL cholesterol and low HDL cholesterol—in this selected group of patients seems to be a consequence of disease activity and SLE disease itself,” according to the authors. “Titers of anti-dsDNA correlated significantly with increased SLEDAI scores and low HDL cholesterol,” they noted.

Recent research suggests that the enzyme, lipoprotein lipase (LPL), may play a key role. LPL breaks down VLDL cholesterol. And when LPL is impaired, VLDL cholesterol proliferates, leading to an unhealthy duet of high triglycerides with low HDL cholesterol, the investigators explained.

Although antibodies to LPL were not measured, previous research suggests that increases in such antibodies are common in SLE patients (Arthritis Rheum. 2002;46:2957–63).

“These results reflect that one of the contributory causes of dyslipoproteinemia in active SLE is probably increased cross-reactivity of anti-dsDNA antibodies with LPL due to high production of these antibodies in the active phase of disease,” the investigators suggested.

Although these findings support an underlying autoimmune cause of dyslipoproteinemia in lupus patients with active disease, other factors likely contribute as well, the researchers said. These include inflammatory mediators (e.g., tumor necrosis factor, interleukin, interferon) that are known to suppress LPL activity and cause dyslipoproteinemia in SLE (Arthritis Rheum. 2003;48:2533–40), as well as physical inactivity.

BOSTON — Heightened activity of anti-double-stranded DNA antibodies may contribute to the poor cholesterol profiles of patients with active systemic lupus erythematosus, according to study findings.

Patients with SLE are often afflicted with a complex triad of risk factors involving high levels of serum triglycerides, high levels of VLDL cholesterol, and low levels of HDL cholesterol. These can hasten the development of premature atherosclerosis and coronary artery disease. Though researchers have posited several theories to explain this phenomenon, its etiology remains unknown.

Sara Kashef, M.D., and colleagues from the Shiraz University of Medical Sciences in Fars, Iran, compared serum lipoprotein levels and antibody activity in 30 patients with active lupus with that of 16 patients with inactive lupus, and 41 healthy controls matched for age and sex. Lupus activity was measured using the SLE disease activity index (SLEDAI). Dr. Kashef presented the study in a poster session at the annual meeting of the Federation of Clinical Immunology Societies.

Compared with healthy controls and people with inactive SLE, patients with active SLE had significantly higher levels of triglycerides and VLDL cholesterol, and lower levels of HDL cholesterol.

Moreover, poor cholesterol profiles were significantly more likely to appear in patients who tested positive for anti-dsDNA antibodies than in those who tested negative. There was no correlation between dyslipoproteinemia and anticardiolipin antibody activity, another suspect in the genesis of SLE atherosclerosis.

“The appearance of this pattern of dyslipoproteinemia—high triglycerides and VLDL cholesterol and low HDL cholesterol—in this selected group of patients seems to be a consequence of disease activity and SLE disease itself,” according to the authors. “Titers of anti-dsDNA correlated significantly with increased SLEDAI scores and low HDL cholesterol,” they noted.

Recent research suggests that the enzyme, lipoprotein lipase (LPL), may play a key role. LPL breaks down VLDL cholesterol. And when LPL is impaired, VLDL cholesterol proliferates, leading to an unhealthy duet of high triglycerides with low HDL cholesterol, the investigators explained.

Although antibodies to LPL were not measured, previous research suggests that increases in such antibodies are common in SLE patients (Arthritis Rheum. 2002;46:2957–63).

“These results reflect that one of the contributory causes of dyslipoproteinemia in active SLE is probably increased cross-reactivity of anti-dsDNA antibodies with LPL due to high production of these antibodies in the active phase of disease,” the investigators suggested.

Although these findings support an underlying autoimmune cause of dyslipoproteinemia in lupus patients with active disease, other factors likely contribute as well, the researchers said. These include inflammatory mediators (e.g., tumor necrosis factor, interleukin, interferon) that are known to suppress LPL activity and cause dyslipoproteinemia in SLE (Arthritis Rheum. 2003;48:2533–40), as well as physical inactivity.

VIENNA — Prolonged intrauterine exposure to high-dose dexamethasone appears to be largely devoid of clinically significant adverse effects on normal T-cell development when evaluated up to a dozen years later, Paolo Airo, M.D., said at the annual European congress of rheumatology.

This has been a controversial issue. Some physicians are concerned that prolonged intrauterine exposure to corticosteroids might steer T-cell differentiation within the fetal thymus in a direction that predisposes to clinical immune dysfunction. They point to an increased rate of hospitalizations for infectious diseases during the first years of life in children with a history of prenatal steroid therapy for prematurity. But a corticosteroid effect is only one of a number of plausible explanations for such an association, said Dr. Airo of the University of Brescia (Italy).

To examine the effect of prenatal high-dose steroids on the T-cell component of the immune system, he and his coinvestigators studied eight children with a history of such therapy given after they were diagnosed in utero with neonatal lupus.

Neonatal lupus, he explained, is a serious condition occurring in children whose mothers have anti-Rho/SSA antibodies, which can cross the placenta. The most important clinical manifestation is congenital heart block; it is associated with significant mortality and permanent morbidity.

When affected fetuses are identified, they are typically treated with several weeks of a high-dose steroid given to the woman. Dexamethasone is the agent used most widely. Since it is a fluorinated corticosteroid, it is not inactivated by placental enzymes, so it can reach the fetus in its active form. The purpose of this therapy is to slow the inflammatory process to prevent progression of incomplete to complete congenital heart block, as well as to treat fetal hydrops and/or myocarditis.

The mean age of the children was 6.6 years, with a range of 2–12 years. All had a pacemaker. None had clinical or laboratory indications of autoimmune disease. A total of 31 age-matched healthy children served as controls, he said at the congress, sponsored by the European League Against Rheumatism.

The results showed that the children with a history of in utero steroid therapy had no abnormalities in the various measures of T-cell number or function having the most clear-cut potential clinical consequences. Thymic output—a key study end point—was normal in children with prolonged fetal exposure to steroids; this was shown by the number of T-cell receptor excision circles (TRECs) in their peripheral blood mononuclear cells, which were measured by real-time polymerase chain reaction. The total number of T cells circulating in peripheral blood was similar to that of controls, as was T-cell subset diversity. Nor did the patients' lymphocyte proliferative response to mitogens differ from that seen in control subjects. Peripheral blood mononuclear cell interferon-γ production and apoptotic response were also similar to that in controls.

The one abnormality seen in children with a history of fetal exposure to steroids involved evidence of oligoclonal T-cell expansion. Similar changes have been reported in animals with in utero exposure to high-dose steroids. However, such changes also can be readily observed in humans after a viral infection. And the clinical significance of this sort of alteration in T-cell repertoire remains unclear, Dr. Airo said.

“We don't know if there is a link between these kinds of changes in PCR repertoire and autoimmunity, but we know that this kind of restriction is frequently detected in patients with rheumatoid arthritis and other autoimmune disorders. And it has been reported that children with neonatal lupus are at increased risk of developing autoimmune disorders in their first years,” according to the rheumatologist.

Aside from the question of the effects on T cells of intrauterine steroid exposure, other adverse consequences have been reported by various investigators. These include increased rates of obstetric complications, adrenal insufficiency, hypertension, and neuropsychiatric impairment.

“We didn't observe any signs of neuropsychiatric impairment in a series of nine children treated with dexamethasone in utero for neonatal lupus,” he said.

VIENNA — Prolonged intrauterine exposure to high-dose dexamethasone appears to be largely devoid of clinically significant adverse effects on normal T-cell development when evaluated up to a dozen years later, Paolo Airo, M.D., said at the annual European congress of rheumatology.

This has been a controversial issue. Some physicians are concerned that prolonged intrauterine exposure to corticosteroids might steer T-cell differentiation within the fetal thymus in a direction that predisposes to clinical immune dysfunction. They point to an increased rate of hospitalizations for infectious diseases during the first years of life in children with a history of prenatal steroid therapy for prematurity. But a corticosteroid effect is only one of a number of plausible explanations for such an association, said Dr. Airo of the University of Brescia (Italy).

To examine the effect of prenatal high-dose steroids on the T-cell component of the immune system, he and his coinvestigators studied eight children with a history of such therapy given after they were diagnosed in utero with neonatal lupus.

Neonatal lupus, he explained, is a serious condition occurring in children whose mothers have anti-Rho/SSA antibodies, which can cross the placenta. The most important clinical manifestation is congenital heart block; it is associated with significant mortality and permanent morbidity.

When affected fetuses are identified, they are typically treated with several weeks of a high-dose steroid given to the woman. Dexamethasone is the agent used most widely. Since it is a fluorinated corticosteroid, it is not inactivated by placental enzymes, so it can reach the fetus in its active form. The purpose of this therapy is to slow the inflammatory process to prevent progression of incomplete to complete congenital heart block, as well as to treat fetal hydrops and/or myocarditis.

The mean age of the children was 6.6 years, with a range of 2–12 years. All had a pacemaker. None had clinical or laboratory indications of autoimmune disease. A total of 31 age-matched healthy children served as controls, he said at the congress, sponsored by the European League Against Rheumatism.

The results showed that the children with a history of in utero steroid therapy had no abnormalities in the various measures of T-cell number or function having the most clear-cut potential clinical consequences. Thymic output—a key study end point—was normal in children with prolonged fetal exposure to steroids; this was shown by the number of T-cell receptor excision circles (TRECs) in their peripheral blood mononuclear cells, which were measured by real-time polymerase chain reaction. The total number of T cells circulating in peripheral blood was similar to that of controls, as was T-cell subset diversity. Nor did the patients' lymphocyte proliferative response to mitogens differ from that seen in control subjects. Peripheral blood mononuclear cell interferon-γ production and apoptotic response were also similar to that in controls.

The one abnormality seen in children with a history of fetal exposure to steroids involved evidence of oligoclonal T-cell expansion. Similar changes have been reported in animals with in utero exposure to high-dose steroids. However, such changes also can be readily observed in humans after a viral infection. And the clinical significance of this sort of alteration in T-cell repertoire remains unclear, Dr. Airo said.

“We don't know if there is a link between these kinds of changes in PCR repertoire and autoimmunity, but we know that this kind of restriction is frequently detected in patients with rheumatoid arthritis and other autoimmune disorders. And it has been reported that children with neonatal lupus are at increased risk of developing autoimmune disorders in their first years,” according to the rheumatologist.

Aside from the question of the effects on T cells of intrauterine steroid exposure, other adverse consequences have been reported by various investigators. These include increased rates of obstetric complications, adrenal insufficiency, hypertension, and neuropsychiatric impairment.

“We didn't observe any signs of neuropsychiatric impairment in a series of nine children treated with dexamethasone in utero for neonatal lupus,” he said.

VIENNA — Prolonged intrauterine exposure to high-dose dexamethasone appears to be largely devoid of clinically significant adverse effects on normal T-cell development when evaluated up to a dozen years later, Paolo Airo, M.D., said at the annual European congress of rheumatology.

This has been a controversial issue. Some physicians are concerned that prolonged intrauterine exposure to corticosteroids might steer T-cell differentiation within the fetal thymus in a direction that predisposes to clinical immune dysfunction. They point to an increased rate of hospitalizations for infectious diseases during the first years of life in children with a history of prenatal steroid therapy for prematurity. But a corticosteroid effect is only one of a number of plausible explanations for such an association, said Dr. Airo of the University of Brescia (Italy).

To examine the effect of prenatal high-dose steroids on the T-cell component of the immune system, he and his coinvestigators studied eight children with a history of such therapy given after they were diagnosed in utero with neonatal lupus.

Neonatal lupus, he explained, is a serious condition occurring in children whose mothers have anti-Rho/SSA antibodies, which can cross the placenta. The most important clinical manifestation is congenital heart block; it is associated with significant mortality and permanent morbidity.

When affected fetuses are identified, they are typically treated with several weeks of a high-dose steroid given to the woman. Dexamethasone is the agent used most widely. Since it is a fluorinated corticosteroid, it is not inactivated by placental enzymes, so it can reach the fetus in its active form. The purpose of this therapy is to slow the inflammatory process to prevent progression of incomplete to complete congenital heart block, as well as to treat fetal hydrops and/or myocarditis.

The mean age of the children was 6.6 years, with a range of 2–12 years. All had a pacemaker. None had clinical or laboratory indications of autoimmune disease. A total of 31 age-matched healthy children served as controls, he said at the congress, sponsored by the European League Against Rheumatism.

The results showed that the children with a history of in utero steroid therapy had no abnormalities in the various measures of T-cell number or function having the most clear-cut potential clinical consequences. Thymic output—a key study end point—was normal in children with prolonged fetal exposure to steroids; this was shown by the number of T-cell receptor excision circles (TRECs) in their peripheral blood mononuclear cells, which were measured by real-time polymerase chain reaction. The total number of T cells circulating in peripheral blood was similar to that of controls, as was T-cell subset diversity. Nor did the patients' lymphocyte proliferative response to mitogens differ from that seen in control subjects. Peripheral blood mononuclear cell interferon-γ production and apoptotic response were also similar to that in controls.

The one abnormality seen in children with a history of fetal exposure to steroids involved evidence of oligoclonal T-cell expansion. Similar changes have been reported in animals with in utero exposure to high-dose steroids. However, such changes also can be readily observed in humans after a viral infection. And the clinical significance of this sort of alteration in T-cell repertoire remains unclear, Dr. Airo said.

“We don't know if there is a link between these kinds of changes in PCR repertoire and autoimmunity, but we know that this kind of restriction is frequently detected in patients with rheumatoid arthritis and other autoimmune disorders. And it has been reported that children with neonatal lupus are at increased risk of developing autoimmune disorders in their first years,” according to the rheumatologist.

Aside from the question of the effects on T cells of intrauterine steroid exposure, other adverse consequences have been reported by various investigators. These include increased rates of obstetric complications, adrenal insufficiency, hypertension, and neuropsychiatric impairment.

“We didn't observe any signs of neuropsychiatric impairment in a series of nine children treated with dexamethasone in utero for neonatal lupus,” he said.

SAN FRANCISCO — The risk for preeclampsia in pregnant women with lupus tripled if they had thrombocytopenia at conception, according to a review of data from a 10-year period at one institution.

This previously unreported finding was highly statistically significant, but prospective studies will be needed to confirm the association, study investigator Maurice L. Druzin, M.D., said at a meeting on antepartum and intrapartum management sponsored by the University of California, San Francisco.

“We certainly are going to be looking at patients with thrombocytopenia very closely,” said Dr. Druzin, professor of ob.gyn. and chief of maternal and fetal medicine at Stanford (Calif.) University.

The review of all pregnancies complicated by systemic lupus erythematosus seen at the university from 1991 to 2001 covered 63 pregnancies in 48 patients with a mean maternal age of 30 years. Lupus had been present for a mean of 4 years in these patients, and the disease was active at conception in 63% of pregnancies. As a group, these were sicker patients than those usually seen by an ob.gyn.

Preeclampsia occurred in 22% of all pregnancies. Thrombocytopenia at conception predicted the development of preeclampsia, according to multivariate analyses to identify clinical predictors of prematurity and preeclampsia.

Gestational diabetes occurred in 5% of pregnancies, and 4% of the cohort developed hemolysis, elevated liver, low platelet (HELLP) syndrome.

Among the pregnancies with active maternal lupus at conception, treatments included prednisone in 48%, hydroxychloroquine in 21%, and antihypertensives in 13%.

Maternal antiphospholipid antibodies were detected in about half of all pregnancies. The cohort had a higher likelihood of having anti-Ro/SSA or anti-La/SSB antibodies than generally is seen in patients with lupus—38% vs. 25%—again emphasizing the select nature of this referral population. Maternal renal disease was present in 35% of pregnancies, and maternal CNS disease affected 10% of pregnancies.

Despite this, birth outcomes were “very good,” with 54 live births, Dr. Druzin said. “When a woman with lupus comes to you, you can tell her that she has a very good chance of having a live birth, which was not true 25 years ago.” The remaining pregnancies ended in first-trimester losses or therapeutic abortions.

As in other studies of pregnancy and lupus, premature delivery was the main fetal problem, occurring n 54% of pregnancies. However, 46% of these were delivered at 32–37 weeks' gestation. “In modern intensive care units, those babies tend to do very well,” he said. An additional 4% were born at 28–32 weeks, and 4% were delivered earlier than 28 weeks.

Lupus flares occurred in 68% of pregnancies. Of these, 71% were mild to moderate flares and were treated with 4–20 mg of additional prednisone. The risk for flare nearly doubled if lupus was active at conception. Prednisone use at conception predicted a 57% increased risk of flare, and a higher disease activity index score predicted a 56% increased risk for flare.

A severe flare was associated with nearly a doubling in risk for premature delivery. Maternal use of antihypertensives or prednisone at conception was associated with an 83% or 77% increase, respectively, in risk for premature birth.

Among 13 women on hydroxychloroquine at conception, severe flares occurred in 2 of 11 women who stopped taking the medication after conception but not in women who continued treatment or stopped before conception, he noted. This difference was not significant, but the finding plus other data suggest that hydroxychloroquine is safe to use in pregnancy.

The review will be published in the American Journal of Obstetrics and Gynecology. The lead author of the paper is Eliza F. Chakravarty, M.D., a rheumatology fellow at Stanford University.

SAN FRANCISCO — The risk for preeclampsia in pregnant women with lupus tripled if they had thrombocytopenia at conception, according to a review of data from a 10-year period at one institution.

This previously unreported finding was highly statistically significant, but prospective studies will be needed to confirm the association, study investigator Maurice L. Druzin, M.D., said at a meeting on antepartum and intrapartum management sponsored by the University of California, San Francisco.

“We certainly are going to be looking at patients with thrombocytopenia very closely,” said Dr. Druzin, professor of ob.gyn. and chief of maternal and fetal medicine at Stanford (Calif.) University.

The review of all pregnancies complicated by systemic lupus erythematosus seen at the university from 1991 to 2001 covered 63 pregnancies in 48 patients with a mean maternal age of 30 years. Lupus had been present for a mean of 4 years in these patients, and the disease was active at conception in 63% of pregnancies. As a group, these were sicker patients than those usually seen by an ob.gyn.

Preeclampsia occurred in 22% of all pregnancies. Thrombocytopenia at conception predicted the development of preeclampsia, according to multivariate analyses to identify clinical predictors of prematurity and preeclampsia.

Gestational diabetes occurred in 5% of pregnancies, and 4% of the cohort developed hemolysis, elevated liver, low platelet (HELLP) syndrome.

Among the pregnancies with active maternal lupus at conception, treatments included prednisone in 48%, hydroxychloroquine in 21%, and antihypertensives in 13%.

Maternal antiphospholipid antibodies were detected in about half of all pregnancies. The cohort had a higher likelihood of having anti-Ro/SSA or anti-La/SSB antibodies than generally is seen in patients with lupus—38% vs. 25%—again emphasizing the select nature of this referral population. Maternal renal disease was present in 35% of pregnancies, and maternal CNS disease affected 10% of pregnancies.

Despite this, birth outcomes were “very good,” with 54 live births, Dr. Druzin said. “When a woman with lupus comes to you, you can tell her that she has a very good chance of having a live birth, which was not true 25 years ago.” The remaining pregnancies ended in first-trimester losses or therapeutic abortions.

As in other studies of pregnancy and lupus, premature delivery was the main fetal problem, occurring n 54% of pregnancies. However, 46% of these were delivered at 32–37 weeks' gestation. “In modern intensive care units, those babies tend to do very well,” he said. An additional 4% were born at 28–32 weeks, and 4% were delivered earlier than 28 weeks.

Lupus flares occurred in 68% of pregnancies. Of these, 71% were mild to moderate flares and were treated with 4–20 mg of additional prednisone. The risk for flare nearly doubled if lupus was active at conception. Prednisone use at conception predicted a 57% increased risk of flare, and a higher disease activity index score predicted a 56% increased risk for flare.

A severe flare was associated with nearly a doubling in risk for premature delivery. Maternal use of antihypertensives or prednisone at conception was associated with an 83% or 77% increase, respectively, in risk for premature birth.

Among 13 women on hydroxychloroquine at conception, severe flares occurred in 2 of 11 women who stopped taking the medication after conception but not in women who continued treatment or stopped before conception, he noted. This difference was not significant, but the finding plus other data suggest that hydroxychloroquine is safe to use in pregnancy.

The review will be published in the American Journal of Obstetrics and Gynecology. The lead author of the paper is Eliza F. Chakravarty, M.D., a rheumatology fellow at Stanford University.

SAN FRANCISCO — The risk for preeclampsia in pregnant women with lupus tripled if they had thrombocytopenia at conception, according to a review of data from a 10-year period at one institution.

This previously unreported finding was highly statistically significant, but prospective studies will be needed to confirm the association, study investigator Maurice L. Druzin, M.D., said at a meeting on antepartum and intrapartum management sponsored by the University of California, San Francisco.

“We certainly are going to be looking at patients with thrombocytopenia very closely,” said Dr. Druzin, professor of ob.gyn. and chief of maternal and fetal medicine at Stanford (Calif.) University.

The review of all pregnancies complicated by systemic lupus erythematosus seen at the university from 1991 to 2001 covered 63 pregnancies in 48 patients with a mean maternal age of 30 years. Lupus had been present for a mean of 4 years in these patients, and the disease was active at conception in 63% of pregnancies. As a group, these were sicker patients than those usually seen by an ob.gyn.

Preeclampsia occurred in 22% of all pregnancies. Thrombocytopenia at conception predicted the development of preeclampsia, according to multivariate analyses to identify clinical predictors of prematurity and preeclampsia.

Gestational diabetes occurred in 5% of pregnancies, and 4% of the cohort developed hemolysis, elevated liver, low platelet (HELLP) syndrome.

Among the pregnancies with active maternal lupus at conception, treatments included prednisone in 48%, hydroxychloroquine in 21%, and antihypertensives in 13%.

Maternal antiphospholipid antibodies were detected in about half of all pregnancies. The cohort had a higher likelihood of having anti-Ro/SSA or anti-La/SSB antibodies than generally is seen in patients with lupus—38% vs. 25%—again emphasizing the select nature of this referral population. Maternal renal disease was present in 35% of pregnancies, and maternal CNS disease affected 10% of pregnancies.

Despite this, birth outcomes were “very good,” with 54 live births, Dr. Druzin said. “When a woman with lupus comes to you, you can tell her that she has a very good chance of having a live birth, which was not true 25 years ago.” The remaining pregnancies ended in first-trimester losses or therapeutic abortions.

As in other studies of pregnancy and lupus, premature delivery was the main fetal problem, occurring n 54% of pregnancies. However, 46% of these were delivered at 32–37 weeks' gestation. “In modern intensive care units, those babies tend to do very well,” he said. An additional 4% were born at 28–32 weeks, and 4% were delivered earlier than 28 weeks.

Lupus flares occurred in 68% of pregnancies. Of these, 71% were mild to moderate flares and were treated with 4–20 mg of additional prednisone. The risk for flare nearly doubled if lupus was active at conception. Prednisone use at conception predicted a 57% increased risk of flare, and a higher disease activity index score predicted a 56% increased risk for flare.

A severe flare was associated with nearly a doubling in risk for premature delivery. Maternal use of antihypertensives or prednisone at conception was associated with an 83% or 77% increase, respectively, in risk for premature birth.

Among 13 women on hydroxychloroquine at conception, severe flares occurred in 2 of 11 women who stopped taking the medication after conception but not in women who continued treatment or stopped before conception, he noted. This difference was not significant, but the finding plus other data suggest that hydroxychloroquine is safe to use in pregnancy.

The review will be published in the American Journal of Obstetrics and Gynecology. The lead author of the paper is Eliza F. Chakravarty, M.D., a rheumatology fellow at Stanford University.

MIAMI BEACH — Neurologists are less likely than cardiologists to favor closure of patent foramen ovale in an attempt to prevent stroke, according to survey results presented at the annual meeting of the American Academy of Neurology.

Although there is a higher prevalence of patent foramen ovale (PFO) among patients who experience a stroke when no other cause is identified, studies have yet to prove that percutaneous closure makes a difference in outcomes. “It is not yet proven that closing the PFO through cardiac catheterization is better than medication,” Steven R. Messe, M.D., told this newspaper during an interview at his poster presentation.

To compare how different specialists manage these patients, Dr. Messe and his colleagues surveyed 129 cardiologists and 108 neurologists. All the physicians were investigators in the CLOSURE-I trial, a study comparing percutaneous closure with medical therapy.

The response rate was 39.5%, with 36% of cardiologists and 44% of neurologists answering the survey. The 17-item questionnaire assessed practice regarding PFO diagnosis, high-risk characteristics, treatment choices, and alternative indications for PFO closure.

According to the survey, 78% of the cardiologists and 65% of the neurologists believe that PFO is relevant to future stroke risk regardless of age.

Despite insufficient outcome data, cardiologists said they recommend percutaneous closure for 55% of patients with a PFO, compared with neurologists, who recommend it for only 20%.

“Closure in general is being used frequently without data at this point, for one in five neurology patients,” said Dr. Messe, attending neurologist, Hospital of the University of Pennsylvania, Philadelphia.

“Interventional cardiologists do the procedure, and they are eager to do it. Neurologists are more conservative,” Dr. Messe said.

A minority, 9% of cardiologists and 2% of neurologists, have recommended closure for asymptomatic PFO patients. A total of 24% of cardiologists and 6% of neurologists would close a patent foramen ovale in a patient who scuba dives, according to the survey. In addition, 14% of cardiologists but no neurologists said they have recommended PFO closure for migraine treatment.

Neurologists prescribe antiplatelet therapy, such as warfarin, for 49% of patients with a PFO. Cardiologists prescribe the same medications for 26% of patients.

Most neurologists may be waiting for more evidence of improved outcomes, Dr. Messe said. “I think neurologists will be excited to refer PFO patients for closure once it's proven to make a difference in prevention of stroke.”

MIAMI BEACH — Neurologists are less likely than cardiologists to favor closure of patent foramen ovale in an attempt to prevent stroke, according to survey results presented at the annual meeting of the American Academy of Neurology.

Although there is a higher prevalence of patent foramen ovale (PFO) among patients who experience a stroke when no other cause is identified, studies have yet to prove that percutaneous closure makes a difference in outcomes. “It is not yet proven that closing the PFO through cardiac catheterization is better than medication,” Steven R. Messe, M.D., told this newspaper during an interview at his poster presentation.

To compare how different specialists manage these patients, Dr. Messe and his colleagues surveyed 129 cardiologists and 108 neurologists. All the physicians were investigators in the CLOSURE-I trial, a study comparing percutaneous closure with medical therapy.

The response rate was 39.5%, with 36% of cardiologists and 44% of neurologists answering the survey. The 17-item questionnaire assessed practice regarding PFO diagnosis, high-risk characteristics, treatment choices, and alternative indications for PFO closure.

According to the survey, 78% of the cardiologists and 65% of the neurologists believe that PFO is relevant to future stroke risk regardless of age.

Despite insufficient outcome data, cardiologists said they recommend percutaneous closure for 55% of patients with a PFO, compared with neurologists, who recommend it for only 20%.

“Closure in general is being used frequently without data at this point, for one in five neurology patients,” said Dr. Messe, attending neurologist, Hospital of the University of Pennsylvania, Philadelphia.

“Interventional cardiologists do the procedure, and they are eager to do it. Neurologists are more conservative,” Dr. Messe said.

A minority, 9% of cardiologists and 2% of neurologists, have recommended closure for asymptomatic PFO patients. A total of 24% of cardiologists and 6% of neurologists would close a patent foramen ovale in a patient who scuba dives, according to the survey. In addition, 14% of cardiologists but no neurologists said they have recommended PFO closure for migraine treatment.

Neurologists prescribe antiplatelet therapy, such as warfarin, for 49% of patients with a PFO. Cardiologists prescribe the same medications for 26% of patients.

Most neurologists may be waiting for more evidence of improved outcomes, Dr. Messe said. “I think neurologists will be excited to refer PFO patients for closure once it's proven to make a difference in prevention of stroke.”

MIAMI BEACH — Neurologists are less likely than cardiologists to favor closure of patent foramen ovale in an attempt to prevent stroke, according to survey results presented at the annual meeting of the American Academy of Neurology.

Although there is a higher prevalence of patent foramen ovale (PFO) among patients who experience a stroke when no other cause is identified, studies have yet to prove that percutaneous closure makes a difference in outcomes. “It is not yet proven that closing the PFO through cardiac catheterization is better than medication,” Steven R. Messe, M.D., told this newspaper during an interview at his poster presentation.

To compare how different specialists manage these patients, Dr. Messe and his colleagues surveyed 129 cardiologists and 108 neurologists. All the physicians were investigators in the CLOSURE-I trial, a study comparing percutaneous closure with medical therapy.

The response rate was 39.5%, with 36% of cardiologists and 44% of neurologists answering the survey. The 17-item questionnaire assessed practice regarding PFO diagnosis, high-risk characteristics, treatment choices, and alternative indications for PFO closure.

According to the survey, 78% of the cardiologists and 65% of the neurologists believe that PFO is relevant to future stroke risk regardless of age.

Despite insufficient outcome data, cardiologists said they recommend percutaneous closure for 55% of patients with a PFO, compared with neurologists, who recommend it for only 20%.

“Closure in general is being used frequently without data at this point, for one in five neurology patients,” said Dr. Messe, attending neurologist, Hospital of the University of Pennsylvania, Philadelphia.

“Interventional cardiologists do the procedure, and they are eager to do it. Neurologists are more conservative,” Dr. Messe said.

A minority, 9% of cardiologists and 2% of neurologists, have recommended closure for asymptomatic PFO patients. A total of 24% of cardiologists and 6% of neurologists would close a patent foramen ovale in a patient who scuba dives, according to the survey. In addition, 14% of cardiologists but no neurologists said they have recommended PFO closure for migraine treatment.

Neurologists prescribe antiplatelet therapy, such as warfarin, for 49% of patients with a PFO. Cardiologists prescribe the same medications for 26% of patients.

Most neurologists may be waiting for more evidence of improved outcomes, Dr. Messe said. “I think neurologists will be excited to refer PFO patients for closure once it's proven to make a difference in prevention of stroke.”

MIAMI BEACH — The triple combination of antiplatelet therapy, statins, and ACE inhibitors reduces primary stroke severity and improves outcome compared with antiplatelet monotherapy or dual drug therapy, according to preliminary findings presented by Magdy Selim, M.D., at the annual meeting of the American Academy of Neurology.

Antiplatelet therapy, statins, or ACE inhibitors can each reduce incidence and recurrence of ischemic stroke when used as monotherapy, according to findings from numerous published studies.

In addition, these agents have been shown to have independent neuroprotective effects, and data from animal studies suggest there is additional protection when the three agents are combined.

Dr. Selim and his associates retrospectively studied data that had been prospectively collected on 210 consecutive stroke patients who presented within 24 hours of stroke onset to the emergency department at Beth Israel Deaconess Medical Center in Boston, where he is an attending physician in neurology.

A total of 110 patients were taking antiplatelet therapy before presentation and were assessed further. The investigators used magnetic resonance perfusion/diffusion imaging to confirm the diagnosis of ischemic stroke and assess stroke lesion volumes in 80 of the 110 patients.

A stroke team measured clinical severity in the emergency department. The 49 participants taking antiplatelet therapy alone (45 [92%] of whom took aspirin) had a mean National Institutes of Health Stroke Scale score of 11.5. The 43 participants taking an antiplatelet agent plus a statin or ACE inhibitor (dual therapy) had a score of 8.7. The 18 participants in the triple therapy group had a mean score of 4.1.

“Triple therapy resulted in an additive reduction in clinical severity of ischemic stroke and better outcomes upon discharge,” Dr. Selim explained.

Outcome was measured indirectly—for example, a higher percentage of triple therapy patients were discharged home.

There were no significant differences between groups in age (mean 72-74 years), time-to-imaging, risk factor profile, blood pressure, or lesion volume as assessed by diffusion-weighted imaging (DWI). “The only significant difference was patients with hyperlipidemia were more likely to be taking a statin,” Dr. Selim said.

Magnetic resonance imaging showed that patients on triple therapy had significantly smaller stroke lesions, with a mean volume based on perfusion-weighted imaging (PWI) of 49.1 cc, compared with 74.6 cc with single therapy and 78.5 cc with dual therapy.

Similarly, the volume of tissue at risk, based on assessment of the PWI-DWI mismatch (the difference in lesion volume as measured by PWI and DWI) was significantly smaller in patients on triple therapy (27.4 cc), compared with 46.8 cc with single therapy and 60 cc with dual therapy.

“I want to stress these findings are preliminary and require validation in larger studies,” said Dr. Selim, who received research support from the Harvard Center for Neurodegeneration and Repair in Boston.

The mismatch between DWI assessment of volume of tissue at risk (white area in image at left) and PWI (right) was smaller in patients on triple therapy. Photos courtesy Dr. Magdy Selim

MIAMI BEACH — The triple combination of antiplatelet therapy, statins, and ACE inhibitors reduces primary stroke severity and improves outcome compared with antiplatelet monotherapy or dual drug therapy, according to preliminary findings presented by Magdy Selim, M.D., at the annual meeting of the American Academy of Neurology.

Antiplatelet therapy, statins, or ACE inhibitors can each reduce incidence and recurrence of ischemic stroke when used as monotherapy, according to findings from numerous published studies.

In addition, these agents have been shown to have independent neuroprotective effects, and data from animal studies suggest there is additional protection when the three agents are combined.

Dr. Selim and his associates retrospectively studied data that had been prospectively collected on 210 consecutive stroke patients who presented within 24 hours of stroke onset to the emergency department at Beth Israel Deaconess Medical Center in Boston, where he is an attending physician in neurology.

A total of 110 patients were taking antiplatelet therapy before presentation and were assessed further. The investigators used magnetic resonance perfusion/diffusion imaging to confirm the diagnosis of ischemic stroke and assess stroke lesion volumes in 80 of the 110 patients.

A stroke team measured clinical severity in the emergency department. The 49 participants taking antiplatelet therapy alone (45 [92%] of whom took aspirin) had a mean National Institutes of Health Stroke Scale score of 11.5. The 43 participants taking an antiplatelet agent plus a statin or ACE inhibitor (dual therapy) had a score of 8.7. The 18 participants in the triple therapy group had a mean score of 4.1.

“Triple therapy resulted in an additive reduction in clinical severity of ischemic stroke and better outcomes upon discharge,” Dr. Selim explained.

Outcome was measured indirectly—for example, a higher percentage of triple therapy patients were discharged home.

There were no significant differences between groups in age (mean 72-74 years), time-to-imaging, risk factor profile, blood pressure, or lesion volume as assessed by diffusion-weighted imaging (DWI). “The only significant difference was patients with hyperlipidemia were more likely to be taking a statin,” Dr. Selim said.

Magnetic resonance imaging showed that patients on triple therapy had significantly smaller stroke lesions, with a mean volume based on perfusion-weighted imaging (PWI) of 49.1 cc, compared with 74.6 cc with single therapy and 78.5 cc with dual therapy.

Similarly, the volume of tissue at risk, based on assessment of the PWI-DWI mismatch (the difference in lesion volume as measured by PWI and DWI) was significantly smaller in patients on triple therapy (27.4 cc), compared with 46.8 cc with single therapy and 60 cc with dual therapy.

“I want to stress these findings are preliminary and require validation in larger studies,” said Dr. Selim, who received research support from the Harvard Center for Neurodegeneration and Repair in Boston.

The mismatch between DWI assessment of volume of tissue at risk (white area in image at left) and PWI (right) was smaller in patients on triple therapy. Photos courtesy Dr. Magdy Selim

MIAMI BEACH — The triple combination of antiplatelet therapy, statins, and ACE inhibitors reduces primary stroke severity and improves outcome compared with antiplatelet monotherapy or dual drug therapy, according to preliminary findings presented by Magdy Selim, M.D., at the annual meeting of the American Academy of Neurology.

Antiplatelet therapy, statins, or ACE inhibitors can each reduce incidence and recurrence of ischemic stroke when used as monotherapy, according to findings from numerous published studies.

In addition, these agents have been shown to have independent neuroprotective effects, and data from animal studies suggest there is additional protection when the three agents are combined.

Dr. Selim and his associates retrospectively studied data that had been prospectively collected on 210 consecutive stroke patients who presented within 24 hours of stroke onset to the emergency department at Beth Israel Deaconess Medical Center in Boston, where he is an attending physician in neurology.

A total of 110 patients were taking antiplatelet therapy before presentation and were assessed further. The investigators used magnetic resonance perfusion/diffusion imaging to confirm the diagnosis of ischemic stroke and assess stroke lesion volumes in 80 of the 110 patients.

A stroke team measured clinical severity in the emergency department. The 49 participants taking antiplatelet therapy alone (45 [92%] of whom took aspirin) had a mean National Institutes of Health Stroke Scale score of 11.5. The 43 participants taking an antiplatelet agent plus a statin or ACE inhibitor (dual therapy) had a score of 8.7. The 18 participants in the triple therapy group had a mean score of 4.1.

“Triple therapy resulted in an additive reduction in clinical severity of ischemic stroke and better outcomes upon discharge,” Dr. Selim explained.

Outcome was measured indirectly—for example, a higher percentage of triple therapy patients were discharged home.

There were no significant differences between groups in age (mean 72-74 years), time-to-imaging, risk factor profile, blood pressure, or lesion volume as assessed by diffusion-weighted imaging (DWI). “The only significant difference was patients with hyperlipidemia were more likely to be taking a statin,” Dr. Selim said.

Magnetic resonance imaging showed that patients on triple therapy had significantly smaller stroke lesions, with a mean volume based on perfusion-weighted imaging (PWI) of 49.1 cc, compared with 74.6 cc with single therapy and 78.5 cc with dual therapy.

Similarly, the volume of tissue at risk, based on assessment of the PWI-DWI mismatch (the difference in lesion volume as measured by PWI and DWI) was significantly smaller in patients on triple therapy (27.4 cc), compared with 46.8 cc with single therapy and 60 cc with dual therapy.

“I want to stress these findings are preliminary and require validation in larger studies,” said Dr. Selim, who received research support from the Harvard Center for Neurodegeneration and Repair in Boston.

The mismatch between DWI assessment of volume of tissue at risk (white area in image at left) and PWI (right) was smaller in patients on triple therapy. Photos courtesy Dr. Magdy Selim

One of SHM’s missions is to advocate policies and positions that support hospital medicine, hospitalists, and our patients. SHM also engages broader issues impacting the delivery, quality, and safety of medical care and lobbies for policies that ensure public health and safety. Legislators, payers, and healthcare administrators use SHM’s policy statements to guide their understanding of and expectations for hospital medicine and its practitioners.

The Public Policy Committee (PPC) is SHM’s primary resource for researching and recommending policy and advocacy positions to the Board of Directors. We respond to issues raised by SHM members, federal and state healthcare legislation, and hospital and health plan policies that affect hospital medicine, hospitalists, and patients.

• In 1999, SHM stood firmly against health plans mandating PCP referral to hospitalists. Our stance defused concerns about hospital medicine raised by primary care physicians and helped to fuel the rapid growth of hospital medicine.
• In 2001, some hospitalists were having hospital privileges withheld because of their designation as hospitalists. The SHM condemned this practice and insisted that hospitalists should be subject to the same privileging and credentialing process as other physicians practicing inpatient medicine.

Recently, SHM members raised concerns over hospitals’ mandating that hospitalists maintain responsibility for patient follow-up after discharge. Based upon the PPC’s research and recommendation, the SHM Board approved a policy clarifying the role of the hospitalist in the continuum of care. (“The Hospitalist,” May/June 2005) This policy will clarify expectations for hospital medicine practices as they develop care management arrangements with hospitals, physicians, and payers.

Currently, the PPC is spearheading several initiatives:

• We are coordinating SHM’s participation in CMS’s 5-year review of valuation of E&M codes.
• In conjunction with a respected health policy analysis firm, we are developing a “hospital medicine White Paper,” which will serve as the definitive description of what hospital medicine is and document its potential to change health care. It will serve as our primary tool to communicate with legislators, policy makers, third-party payers, and healthcare leaders to further the mission and values of hospital medicine as a specialty.
• Finally, the PPC is leveraging our Washington, DC, venue for the 2006 Annual Meeting to organize a “hospital medicine Legislative Day.” At this event, hospitalists will visit legislators to discuss issues of importance to hospital medicine, such as patient safety and allocation of healthcare resources. We hope that this event will further raise awareness of hospital medicine and spur hospitalists to become politically active on behalf of our specialty.

Finally, on behalf of the members of the PPC, I want to thank Mary Jo Gorman for her 2-year stewardship of the Public Policy Committee. Her drive, vision, and enthusiasm were key to many of the successes described above.

More Information

1. Visit www.hospitalmedicine.org > Click on “About SHM” > Click on “Committees > Scroll down to view “Public Policy Committee”
2. Visit www.hospitalmedicine.org > Click on “Advocacy & Policy”

One of SHM’s missions is to advocate policies and positions that support hospital medicine, hospitalists, and our patients. SHM also engages broader issues impacting the delivery, quality, and safety of medical care and lobbies for policies that ensure public health and safety. Legislators, payers, and healthcare administrators use SHM’s policy statements to guide their understanding of and expectations for hospital medicine and its practitioners.

The Public Policy Committee (PPC) is SHM’s primary resource for researching and recommending policy and advocacy positions to the Board of Directors. We respond to issues raised by SHM members, federal and state healthcare legislation, and hospital and health plan policies that affect hospital medicine, hospitalists, and patients.

• In 1999, SHM stood firmly against health plans mandating PCP referral to hospitalists. Our stance defused concerns about hospital medicine raised by primary care physicians and helped to fuel the rapid growth of hospital medicine.
• In 2001, some hospitalists were having hospital privileges withheld because of their designation as hospitalists. The SHM condemned this practice and insisted that hospitalists should be subject to the same privileging and credentialing process as other physicians practicing inpatient medicine.

Recently, SHM members raised concerns over hospitals’ mandating that hospitalists maintain responsibility for patient follow-up after discharge. Based upon the PPC’s research and recommendation, the SHM Board approved a policy clarifying the role of the hospitalist in the continuum of care. (“The Hospitalist,” May/June 2005) This policy will clarify expectations for hospital medicine practices as they develop care management arrangements with hospitals, physicians, and payers.

Currently, the PPC is spearheading several initiatives:

• We are coordinating SHM’s participation in CMS’s 5-year review of valuation of E&M codes.
• In conjunction with a respected health policy analysis firm, we are developing a “hospital medicine White Paper,” which will serve as the definitive description of what hospital medicine is and document its potential to change health care. It will serve as our primary tool to communicate with legislators, policy makers, third-party payers, and healthcare leaders to further the mission and values of hospital medicine as a specialty.
• Finally, the PPC is leveraging our Washington, DC, venue for the 2006 Annual Meeting to organize a “hospital medicine Legislative Day.” At this event, hospitalists will visit legislators to discuss issues of importance to hospital medicine, such as patient safety and allocation of healthcare resources. We hope that this event will further raise awareness of hospital medicine and spur hospitalists to become politically active on behalf of our specialty.

Finally, on behalf of the members of the PPC, I want to thank Mary Jo Gorman for her 2-year stewardship of the Public Policy Committee. Her drive, vision, and enthusiasm were key to many of the successes described above.

More Information

1. Visit www.hospitalmedicine.org > Click on “About SHM” > Click on “Committees > Scroll down to view “Public Policy Committee”
2. Visit www.hospitalmedicine.org > Click on “Advocacy & Policy”

One of SHM’s missions is to advocate policies and positions that support hospital medicine, hospitalists, and our patients. SHM also engages broader issues impacting the delivery, quality, and safety of medical care and lobbies for policies that ensure public health and safety. Legislators, payers, and healthcare administrators use SHM’s policy statements to guide their understanding of and expectations for hospital medicine and its practitioners.

The Public Policy Committee (PPC) is SHM’s primary resource for researching and recommending policy and advocacy positions to the Board of Directors. We respond to issues raised by SHM members, federal and state healthcare legislation, and hospital and health plan policies that affect hospital medicine, hospitalists, and patients.

• In 1999, SHM stood firmly against health plans mandating PCP referral to hospitalists. Our stance defused concerns about hospital medicine raised by primary care physicians and helped to fuel the rapid growth of hospital medicine.
• In 2001, some hospitalists were having hospital privileges withheld because of their designation as hospitalists. The SHM condemned this practice and insisted that hospitalists should be subject to the same privileging and credentialing process as other physicians practicing inpatient medicine.

Recently, SHM members raised concerns over hospitals’ mandating that hospitalists maintain responsibility for patient follow-up after discharge. Based upon the PPC’s research and recommendation, the SHM Board approved a policy clarifying the role of the hospitalist in the continuum of care. (“The Hospitalist,” May/June 2005) This policy will clarify expectations for hospital medicine practices as they develop care management arrangements with hospitals, physicians, and payers.

Currently, the PPC is spearheading several initiatives:

• We are coordinating SHM’s participation in CMS’s 5-year review of valuation of E&M codes.
• In conjunction with a respected health policy analysis firm, we are developing a “hospital medicine White Paper,” which will serve as the definitive description of what hospital medicine is and document its potential to change health care. It will serve as our primary tool to communicate with legislators, policy makers, third-party payers, and healthcare leaders to further the mission and values of hospital medicine as a specialty.
• Finally, the PPC is leveraging our Washington, DC, venue for the 2006 Annual Meeting to organize a “hospital medicine Legislative Day.” At this event, hospitalists will visit legislators to discuss issues of importance to hospital medicine, such as patient safety and allocation of healthcare resources. We hope that this event will further raise awareness of hospital medicine and spur hospitalists to become politically active on behalf of our specialty.

Finally, on behalf of the members of the PPC, I want to thank Mary Jo Gorman for her 2-year stewardship of the Public Policy Committee. Her drive, vision, and enthusiasm were key to many of the successes described above.

More Information

1. Visit www.hospitalmedicine.org > Click on “About SHM” > Click on “Committees > Scroll down to view “Public Policy Committee”
2. Visit www.hospitalmedicine.org > Click on “Advocacy & Policy”

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