Sherry Boschert

SAN FRANCISCO — Don't drop your suspicions about serious bacterial infection in infants up to 60 days old just because they're infected with respiratory syncytial virus, Dr. Laura M. Cerny cautioned at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

Recent reports implying that infants with respiratory syncytial virus (RSV) infection are less likely to have concurrent bacterial infection than are those without RSV may have moved some clinicians to stop screening for serious bacterial infection in these patients.

Therefore, Dr. Cerny and her associates retrospectively reviewed charts on 261 infants discharged from one hospital with a diagnosis of RSV from October 2003 to May 2005.

Serious bacterial infections were documented in 8% of the infants, the researchers reported in a poster presentation at the meeting, which was sponsored by the American Society for Microbiology.

Even if they have RSV, infants aged 60 days old or younger are still at risk for serious bacterial infection.

“Don't let your guard down” regarding possible other infections in RSV-infected infants, warned Dr. Cerny, a pediatric fellow at Children's Hospital of Orange County, Calif., and Harbor-University of California, Los Angeles, Medical Center.

The infections consisted of nine pneumonias, eight urinary tract infections, two cases of meningitis, one cellulitis, and one patient with both urinary tract infection and bacteremia (urosepsis), Dr. Cerny reported.

Be especially concerned about RSV-positive infants aged 60 days old or younger who look ill or have a fever higher than 39° C, because these factors may increase the risk for serious bacterial infection, the study suggested.

Don't simply attribute the ill appearance to RSV, she added.

The investigators retrospectively applied the Rochester criteria to screen for serious bacterial infection and found the criteria valuable for discerning patients with higher risk.

The criteria use historical, clinical, and laboratory data to predict risk.

Eighteen patients with serious bacterial infection met criteria for high risk, and three were low risk.

When Rochester criteria results excluded serious bacterial infection, they were correct 97% of the time (the negative predictive value).

High-risk patients by Rochester criteria were more likely to have serious bacterial infection whether or not they had fever.

All 12 afebrile patients with serious bacterial infection met Rochester criteria for high risk, including toxicity (5 patients), being “not previously healthy” (3), abnormal urinalysis (3), or high absolute band count (1).

SAN FRANCISCO — Don't drop your suspicions about serious bacterial infection in infants up to 60 days old just because they're infected with respiratory syncytial virus, Dr. Laura M. Cerny cautioned at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

Recent reports implying that infants with respiratory syncytial virus (RSV) infection are less likely to have concurrent bacterial infection than are those without RSV may have moved some clinicians to stop screening for serious bacterial infection in these patients.

Therefore, Dr. Cerny and her associates retrospectively reviewed charts on 261 infants discharged from one hospital with a diagnosis of RSV from October 2003 to May 2005.

Serious bacterial infections were documented in 8% of the infants, the researchers reported in a poster presentation at the meeting, which was sponsored by the American Society for Microbiology.

Even if they have RSV, infants aged 60 days old or younger are still at risk for serious bacterial infection.

“Don't let your guard down” regarding possible other infections in RSV-infected infants, warned Dr. Cerny, a pediatric fellow at Children's Hospital of Orange County, Calif., and Harbor-University of California, Los Angeles, Medical Center.

The infections consisted of nine pneumonias, eight urinary tract infections, two cases of meningitis, one cellulitis, and one patient with both urinary tract infection and bacteremia (urosepsis), Dr. Cerny reported.

Be especially concerned about RSV-positive infants aged 60 days old or younger who look ill or have a fever higher than 39° C, because these factors may increase the risk for serious bacterial infection, the study suggested.

Don't simply attribute the ill appearance to RSV, she added.

The investigators retrospectively applied the Rochester criteria to screen for serious bacterial infection and found the criteria valuable for discerning patients with higher risk.

The criteria use historical, clinical, and laboratory data to predict risk.

Eighteen patients with serious bacterial infection met criteria for high risk, and three were low risk.

When Rochester criteria results excluded serious bacterial infection, they were correct 97% of the time (the negative predictive value).

High-risk patients by Rochester criteria were more likely to have serious bacterial infection whether or not they had fever.

All 12 afebrile patients with serious bacterial infection met Rochester criteria for high risk, including toxicity (5 patients), being “not previously healthy” (3), abnormal urinalysis (3), or high absolute band count (1).

SAN FRANCISCO — Don't drop your suspicions about serious bacterial infection in infants up to 60 days old just because they're infected with respiratory syncytial virus, Dr. Laura M. Cerny cautioned at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

Recent reports implying that infants with respiratory syncytial virus (RSV) infection are less likely to have concurrent bacterial infection than are those without RSV may have moved some clinicians to stop screening for serious bacterial infection in these patients.

Therefore, Dr. Cerny and her associates retrospectively reviewed charts on 261 infants discharged from one hospital with a diagnosis of RSV from October 2003 to May 2005.

Serious bacterial infections were documented in 8% of the infants, the researchers reported in a poster presentation at the meeting, which was sponsored by the American Society for Microbiology.

Even if they have RSV, infants aged 60 days old or younger are still at risk for serious bacterial infection.

“Don't let your guard down” regarding possible other infections in RSV-infected infants, warned Dr. Cerny, a pediatric fellow at Children's Hospital of Orange County, Calif., and Harbor-University of California, Los Angeles, Medical Center.

The infections consisted of nine pneumonias, eight urinary tract infections, two cases of meningitis, one cellulitis, and one patient with both urinary tract infection and bacteremia (urosepsis), Dr. Cerny reported.

Be especially concerned about RSV-positive infants aged 60 days old or younger who look ill or have a fever higher than 39° C, because these factors may increase the risk for serious bacterial infection, the study suggested.

Don't simply attribute the ill appearance to RSV, she added.

The investigators retrospectively applied the Rochester criteria to screen for serious bacterial infection and found the criteria valuable for discerning patients with higher risk.

The criteria use historical, clinical, and laboratory data to predict risk.

Eighteen patients with serious bacterial infection met criteria for high risk, and three were low risk.

When Rochester criteria results excluded serious bacterial infection, they were correct 97% of the time (the negative predictive value).

High-risk patients by Rochester criteria were more likely to have serious bacterial infection whether or not they had fever.

All 12 afebrile patients with serious bacterial infection met Rochester criteria for high risk, including toxicity (5 patients), being “not previously healthy” (3), abnormal urinalysis (3), or high absolute band count (1).

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression. The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown.

Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression. The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown.

Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression. The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown.

Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression.

Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the very least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer and staff try to review the depression scale results during the visit. As a backup, her office works with a psychiatrist who reviews patients' results and flags those at risk for depression.

Postpartum depression is not the same as postpartum “blues,” which affect 30%–75% of new mothers but resolve spontaneously in 4–10 days after delivery. If the “blues” continue past 2 weeks postpartum, “we're dealing with something else,” she said.

The standard treatments for depression are used to treat postpartum depression.

Dr. Singer is on the speakers bureau of Pfizer, which makes an antidepressant drug.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression.

Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the very least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer and staff try to review the depression scale results during the visit. As a backup, her office works with a psychiatrist who reviews patients' results and flags those at risk for depression.

Postpartum depression is not the same as postpartum “blues,” which affect 30%–75% of new mothers but resolve spontaneously in 4–10 days after delivery. If the “blues” continue past 2 weeks postpartum, “we're dealing with something else,” she said.

The standard treatments for depression are used to treat postpartum depression.

Dr. Singer is on the speakers bureau of Pfizer, which makes an antidepressant drug.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at Perspectives in Women's Health sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression.

Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the very least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer and staff try to review the depression scale results during the visit. As a backup, her office works with a psychiatrist who reviews patients' results and flags those at risk for depression.

Postpartum depression is not the same as postpartum “blues,” which affect 30%–75% of new mothers but resolve spontaneously in 4–10 days after delivery. If the “blues” continue past 2 weeks postpartum, “we're dealing with something else,” she said.

The standard treatments for depression are used to treat postpartum depression.

Dr. Singer is on the speakers bureau of Pfizer, which makes an antidepressant drug.

SAN FRANCISCO—Routine thyroxine therapy for benign thyroid nodules is no longer recommended, Dr. Hossein Gharib said at Perspectives in Women's Health sponsored by Ob.Gyn. News.

Thyroxine does not shrink most benign thyroid nodules. In those that do shrink, size increases if the drug therapy is stopped. Long-term thyroxine therapy can be costly and may contribute to hyperthyroidism over time in some patients.

Fine-needle biopsy is a reliable diagnostic tool when done by an experienced clinician and can determine if a thyroid nodule is malignant or benign. Malignant lesions should be treated by surgery. Goiters that are benign but large and symptomatic should be treated by surgery or by radioactive iodine therapy, said Dr. Gharib, professor of medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

The vast majority of thyroid nodules deemed benign by fine-needle aspiration biopsy can be followed by observation, he said at the meeting. Ob.Gyn. News is published by the International Medical News Group, a division of Elsevier.

Thyroid nodules are very common, detectable by palpation in 5% of the U.S. population and by ultrasound in 50%. The nodules are benign in 95% of cases. More than 100 million U.S. residents have thyroid nodules, and 300,000 new nodules are detected each year, said Dr. Gharib, who has no association with the companies that make the treatments he discussed.

The incidence of thyroid cancer peaks in women at around 12 cases per 100,000 women, between ages 30 and 50 years. In men, incidence peaks at around 8 per 100,000 between ages 70 and 80 years. Detection differences may be due to women being seen more regularly for gynecologic care, with nodules detected as part of general physical exams, he speculated.

SAN FRANCISCO—Routine thyroxine therapy for benign thyroid nodules is no longer recommended, Dr. Hossein Gharib said at Perspectives in Women's Health sponsored by Ob.Gyn. News.

Thyroxine does not shrink most benign thyroid nodules. In those that do shrink, size increases if the drug therapy is stopped. Long-term thyroxine therapy can be costly and may contribute to hyperthyroidism over time in some patients.

Fine-needle biopsy is a reliable diagnostic tool when done by an experienced clinician and can determine if a thyroid nodule is malignant or benign. Malignant lesions should be treated by surgery. Goiters that are benign but large and symptomatic should be treated by surgery or by radioactive iodine therapy, said Dr. Gharib, professor of medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

The vast majority of thyroid nodules deemed benign by fine-needle aspiration biopsy can be followed by observation, he said at the meeting. Ob.Gyn. News is published by the International Medical News Group, a division of Elsevier.

Thyroid nodules are very common, detectable by palpation in 5% of the U.S. population and by ultrasound in 50%. The nodules are benign in 95% of cases. More than 100 million U.S. residents have thyroid nodules, and 300,000 new nodules are detected each year, said Dr. Gharib, who has no association with the companies that make the treatments he discussed.

The incidence of thyroid cancer peaks in women at around 12 cases per 100,000 women, between ages 30 and 50 years. In men, incidence peaks at around 8 per 100,000 between ages 70 and 80 years. Detection differences may be due to women being seen more regularly for gynecologic care, with nodules detected as part of general physical exams, he speculated.

SAN FRANCISCO—Routine thyroxine therapy for benign thyroid nodules is no longer recommended, Dr. Hossein Gharib said at Perspectives in Women's Health sponsored by Ob.Gyn. News.

Thyroxine does not shrink most benign thyroid nodules. In those that do shrink, size increases if the drug therapy is stopped. Long-term thyroxine therapy can be costly and may contribute to hyperthyroidism over time in some patients.

Fine-needle biopsy is a reliable diagnostic tool when done by an experienced clinician and can determine if a thyroid nodule is malignant or benign. Malignant lesions should be treated by surgery. Goiters that are benign but large and symptomatic should be treated by surgery or by radioactive iodine therapy, said Dr. Gharib, professor of medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

The vast majority of thyroid nodules deemed benign by fine-needle aspiration biopsy can be followed by observation, he said at the meeting. Ob.Gyn. News is published by the International Medical News Group, a division of Elsevier.

Thyroid nodules are very common, detectable by palpation in 5% of the U.S. population and by ultrasound in 50%. The nodules are benign in 95% of cases. More than 100 million U.S. residents have thyroid nodules, and 300,000 new nodules are detected each year, said Dr. Gharib, who has no association with the companies that make the treatments he discussed.

The incidence of thyroid cancer peaks in women at around 12 cases per 100,000 women, between ages 30 and 50 years. In men, incidence peaks at around 8 per 100,000 between ages 70 and 80 years. Detection differences may be due to women being seen more regularly for gynecologic care, with nodules detected as part of general physical exams, he speculated.

SAN DIEGO — People on very-low-carbohydrate diets who consumed three times as much daily saturated fat as people on high-carbohydrate, low-fat diets, lost more weight and had twice the reduction in saturated fat levels compared with the latter, according to a report on a small study at a symposium on obesity sponsored by the American Society of Bariatric Physicians.

“If you still believe that you are what you eat, [you are] wrong. You are what you save when you eat,” because the level of carbohydrate intake dictates how the body makes use of dietary fatty acids, Dr. Stephen D. Phinney said.

Total circulating saturated fats decreased by 57% over the 12-week study on the low-carbohydrate diet and by 24% on the low-fat diet, he reported.

The unpublished data came from a recent randomized study of 40 patients that was led by Jeff S. Volek, Ph.D., of the University of Connecticut, Storrs, with Dr. Phinney and associates. Two groups of 20 patients (10 men and 10 women in each) with triglyceride levels above 150 mg/dL and low HDL cholesterol levels (less than 40 mg/dL in men or less than 50 mg/dL in women) were put on either a low-carbohydrate, ketogenic diet or on a low-fat, high-carbohydrate diet.

All of the patients consumed about 1,500 calories per day. The low-carbohydrate diet contained more protein than the low-fat diet (28% of calories vs. 20%, respectively), more total fat (59% vs. 24%), and more saturated fat (37 g/day vs. 12 g/day).

Although people tend to assume that the low-carbohydrate diet “would be dangerous with all that fat,” said Dr. Phinney of Elk Grove, Calif., and a professor of medicine, emeritus, University of California, Davis, patients in the low-carbohydrate group lost more weight than did those on the low-fat diet (10 kg vs. 5 kg) and more fat (6 kg vs. 4 kg).

In addition, those on the low-carbohydrate diet also lost more abdominal fat (828 g), compared with those in the low-fat diet group (526 g). Besides fat loss, water loss accounted for most of the weight loss, he said.

The study results suggested benefits in lipid levels, Dr. Phinney reported. Triglyceride levels decreased by 51% on the low-carbohydrate diet and by 19% on the low-fat diet. HDL-cholesterol levels increased by 13% on the low-carbohydrate diet and remained essentially unchanged on the low-fat diet.

There were no significant differences between groups in LDL cholesterol levels. LDL cholesterol particle size increased by 3% in the low-carbohydrate group and did not change in the low-fat group; this may be significant because smaller, denser LDL particles increase cardiovascular risk, he said.

Saturated fats as a percentage of triglycerides decreased by 12% in the low-carbohydrate group and by 5% in the low-fat group. Fatty acids esterified to cholesterol ester decreased by 10% in the low-carbohydrate group and by 5% in the low-fat group. “So it's a uniform decrease in both compartments of circulating lipids,” he said.

Dietary saturated fatty acids seem to be of much less concern when consumed during a carbohydrate-restricted diet, Dr. Phinney explained. “The human machinery [seems to be] well equipped to handle this kind of diet.”

He also reviewed separate data showing that serum cholesterol levels tend to decrease during weight loss of up to 10% of body weight in people on low-carbohydrate diets. Total cholesterol and LDL cholesterol levels then rise transiently as weight loss approaches 20% of baseline body weight, but lipid levels stabilize (with decreases in LDL cholesterol and increases in HDL) when the patient switches to a maintenance diet.

“If you look at cholesterol during weight loss, this can be alarming, but it's pre-owned” cholesterol that was stored in fat cells and is secreted into plasma during weight loss on low-carbohydrate diets, he explained. Return to a maintenance diet should stabilize lipid levels, he noted.

SAN DIEGO — People on very-low-carbohydrate diets who consumed three times as much daily saturated fat as people on high-carbohydrate, low-fat diets, lost more weight and had twice the reduction in saturated fat levels compared with the latter, according to a report on a small study at a symposium on obesity sponsored by the American Society of Bariatric Physicians.

“If you still believe that you are what you eat, [you are] wrong. You are what you save when you eat,” because the level of carbohydrate intake dictates how the body makes use of dietary fatty acids, Dr. Stephen D. Phinney said.

Total circulating saturated fats decreased by 57% over the 12-week study on the low-carbohydrate diet and by 24% on the low-fat diet, he reported.

The unpublished data came from a recent randomized study of 40 patients that was led by Jeff S. Volek, Ph.D., of the University of Connecticut, Storrs, with Dr. Phinney and associates. Two groups of 20 patients (10 men and 10 women in each) with triglyceride levels above 150 mg/dL and low HDL cholesterol levels (less than 40 mg/dL in men or less than 50 mg/dL in women) were put on either a low-carbohydrate, ketogenic diet or on a low-fat, high-carbohydrate diet.

All of the patients consumed about 1,500 calories per day. The low-carbohydrate diet contained more protein than the low-fat diet (28% of calories vs. 20%, respectively), more total fat (59% vs. 24%), and more saturated fat (37 g/day vs. 12 g/day).

Although people tend to assume that the low-carbohydrate diet “would be dangerous with all that fat,” said Dr. Phinney of Elk Grove, Calif., and a professor of medicine, emeritus, University of California, Davis, patients in the low-carbohydrate group lost more weight than did those on the low-fat diet (10 kg vs. 5 kg) and more fat (6 kg vs. 4 kg).

In addition, those on the low-carbohydrate diet also lost more abdominal fat (828 g), compared with those in the low-fat diet group (526 g). Besides fat loss, water loss accounted for most of the weight loss, he said.

The study results suggested benefits in lipid levels, Dr. Phinney reported. Triglyceride levels decreased by 51% on the low-carbohydrate diet and by 19% on the low-fat diet. HDL-cholesterol levels increased by 13% on the low-carbohydrate diet and remained essentially unchanged on the low-fat diet.

There were no significant differences between groups in LDL cholesterol levels. LDL cholesterol particle size increased by 3% in the low-carbohydrate group and did not change in the low-fat group; this may be significant because smaller, denser LDL particles increase cardiovascular risk, he said.

Saturated fats as a percentage of triglycerides decreased by 12% in the low-carbohydrate group and by 5% in the low-fat group. Fatty acids esterified to cholesterol ester decreased by 10% in the low-carbohydrate group and by 5% in the low-fat group. “So it's a uniform decrease in both compartments of circulating lipids,” he said.

Dietary saturated fatty acids seem to be of much less concern when consumed during a carbohydrate-restricted diet, Dr. Phinney explained. “The human machinery [seems to be] well equipped to handle this kind of diet.”

He also reviewed separate data showing that serum cholesterol levels tend to decrease during weight loss of up to 10% of body weight in people on low-carbohydrate diets. Total cholesterol and LDL cholesterol levels then rise transiently as weight loss approaches 20% of baseline body weight, but lipid levels stabilize (with decreases in LDL cholesterol and increases in HDL) when the patient switches to a maintenance diet.

“If you look at cholesterol during weight loss, this can be alarming, but it's pre-owned” cholesterol that was stored in fat cells and is secreted into plasma during weight loss on low-carbohydrate diets, he explained. Return to a maintenance diet should stabilize lipid levels, he noted.

SAN DIEGO — People on very-low-carbohydrate diets who consumed three times as much daily saturated fat as people on high-carbohydrate, low-fat diets, lost more weight and had twice the reduction in saturated fat levels compared with the latter, according to a report on a small study at a symposium on obesity sponsored by the American Society of Bariatric Physicians.

“If you still believe that you are what you eat, [you are] wrong. You are what you save when you eat,” because the level of carbohydrate intake dictates how the body makes use of dietary fatty acids, Dr. Stephen D. Phinney said.

Total circulating saturated fats decreased by 57% over the 12-week study on the low-carbohydrate diet and by 24% on the low-fat diet, he reported.

The unpublished data came from a recent randomized study of 40 patients that was led by Jeff S. Volek, Ph.D., of the University of Connecticut, Storrs, with Dr. Phinney and associates. Two groups of 20 patients (10 men and 10 women in each) with triglyceride levels above 150 mg/dL and low HDL cholesterol levels (less than 40 mg/dL in men or less than 50 mg/dL in women) were put on either a low-carbohydrate, ketogenic diet or on a low-fat, high-carbohydrate diet.

All of the patients consumed about 1,500 calories per day. The low-carbohydrate diet contained more protein than the low-fat diet (28% of calories vs. 20%, respectively), more total fat (59% vs. 24%), and more saturated fat (37 g/day vs. 12 g/day).

Although people tend to assume that the low-carbohydrate diet “would be dangerous with all that fat,” said Dr. Phinney of Elk Grove, Calif., and a professor of medicine, emeritus, University of California, Davis, patients in the low-carbohydrate group lost more weight than did those on the low-fat diet (10 kg vs. 5 kg) and more fat (6 kg vs. 4 kg).

In addition, those on the low-carbohydrate diet also lost more abdominal fat (828 g), compared with those in the low-fat diet group (526 g). Besides fat loss, water loss accounted for most of the weight loss, he said.

The study results suggested benefits in lipid levels, Dr. Phinney reported. Triglyceride levels decreased by 51% on the low-carbohydrate diet and by 19% on the low-fat diet. HDL-cholesterol levels increased by 13% on the low-carbohydrate diet and remained essentially unchanged on the low-fat diet.

There were no significant differences between groups in LDL cholesterol levels. LDL cholesterol particle size increased by 3% in the low-carbohydrate group and did not change in the low-fat group; this may be significant because smaller, denser LDL particles increase cardiovascular risk, he said.

Saturated fats as a percentage of triglycerides decreased by 12% in the low-carbohydrate group and by 5% in the low-fat group. Fatty acids esterified to cholesterol ester decreased by 10% in the low-carbohydrate group and by 5% in the low-fat group. “So it's a uniform decrease in both compartments of circulating lipids,” he said.

Dietary saturated fatty acids seem to be of much less concern when consumed during a carbohydrate-restricted diet, Dr. Phinney explained. “The human machinery [seems to be] well equipped to handle this kind of diet.”

He also reviewed separate data showing that serum cholesterol levels tend to decrease during weight loss of up to 10% of body weight in people on low-carbohydrate diets. Total cholesterol and LDL cholesterol levels then rise transiently as weight loss approaches 20% of baseline body weight, but lipid levels stabilize (with decreases in LDL cholesterol and increases in HDL) when the patient switches to a maintenance diet.

“If you look at cholesterol during weight loss, this can be alarming, but it's pre-owned” cholesterol that was stored in fat cells and is secreted into plasma during weight loss on low-carbohydrate diets, he explained. Return to a maintenance diet should stabilize lipid levels, he noted.

SAN FRANCISCO — Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue said at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease. Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications.

There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” Dr. Huse said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO — Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue said at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease. Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications.

There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” Dr. Huse said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO — Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue said at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease. Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications.

There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” Dr. Huse said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO—Clinical signs and symptoms of acute bacterial exacerbation of chronic bronchitis improved in patients treated with 5 days of an experimental ketolide antibiotic, cethromycin, or 7 days of levofloxacin, David A. Eiznhamer, Ph.D., reported.

The phase III, double-blind, multicenter trial randomized 509 outpatients aged 40 years or older to oral therapy with 150 mg of cethromycin per day or 500 mg of levofloxacin per day. Improvements at 14–19 days after enrollment were not significantly different between groups, but the investigators could not rule out the possibility, based on statistical analyses, that cethromycin might be inferior to levofloxacin at those doses, Dr. Eiznhamer said in a poster presentation at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The lead investigator was S. Bukofzer of Abbott Laboratories, which is an investor in Advanced Life Sciences, and all of the investigators came from the two companies.

The 150-mg dose of cethromycin was chosen to minimize adverse events. A new study comparing a 300-mg daily dose of cethromycin with levofloxacin therapy is warranted, said Dr. Eiznhamer of Advanced Life Sciences, the company that is developing cethromycin.

The drug is also being studied in phase III trials for the treatment of community-acquired pneumonia. Advanced Life Sciences plans to submit a new drug application in 2007 with a goal of obtaining Food and Drug Administration approval in 2008, he said in an interview. The conference was sponsored by the American Society for Microbiology.

In an intent-to-treat analysis of 450 patients in the current study, clinical cure was seen in 81% of patients on cethromycin and 84% of those on levofloxacin. Clinical cure was defined as the resolution of at least one clinical symptom (dyspnea, sputum volume, purulence, cough, or fever) and improvement in at least half of the other symptoms.

An intent-to-treat analysis of overall pathogen eradication rates in 231 patients found eradication in 85% of the cethromycin group and 87% of the levofloxacin group.

For Streptococcus pneumoniae, however, cethromycin eradicated the organism in 14 (78%) of 18 patients, compared with 23 (92%) of 25 patients given levofloxacin.

SAN FRANCISCO—Clinical signs and symptoms of acute bacterial exacerbation of chronic bronchitis improved in patients treated with 5 days of an experimental ketolide antibiotic, cethromycin, or 7 days of levofloxacin, David A. Eiznhamer, Ph.D., reported.

The phase III, double-blind, multicenter trial randomized 509 outpatients aged 40 years or older to oral therapy with 150 mg of cethromycin per day or 500 mg of levofloxacin per day. Improvements at 14–19 days after enrollment were not significantly different between groups, but the investigators could not rule out the possibility, based on statistical analyses, that cethromycin might be inferior to levofloxacin at those doses, Dr. Eiznhamer said in a poster presentation at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The lead investigator was S. Bukofzer of Abbott Laboratories, which is an investor in Advanced Life Sciences, and all of the investigators came from the two companies.

The 150-mg dose of cethromycin was chosen to minimize adverse events. A new study comparing a 300-mg daily dose of cethromycin with levofloxacin therapy is warranted, said Dr. Eiznhamer of Advanced Life Sciences, the company that is developing cethromycin.

The drug is also being studied in phase III trials for the treatment of community-acquired pneumonia. Advanced Life Sciences plans to submit a new drug application in 2007 with a goal of obtaining Food and Drug Administration approval in 2008, he said in an interview. The conference was sponsored by the American Society for Microbiology.

In an intent-to-treat analysis of 450 patients in the current study, clinical cure was seen in 81% of patients on cethromycin and 84% of those on levofloxacin. Clinical cure was defined as the resolution of at least one clinical symptom (dyspnea, sputum volume, purulence, cough, or fever) and improvement in at least half of the other symptoms.

An intent-to-treat analysis of overall pathogen eradication rates in 231 patients found eradication in 85% of the cethromycin group and 87% of the levofloxacin group.

For Streptococcus pneumoniae, however, cethromycin eradicated the organism in 14 (78%) of 18 patients, compared with 23 (92%) of 25 patients given levofloxacin.

SAN FRANCISCO—Clinical signs and symptoms of acute bacterial exacerbation of chronic bronchitis improved in patients treated with 5 days of an experimental ketolide antibiotic, cethromycin, or 7 days of levofloxacin, David A. Eiznhamer, Ph.D., reported.

The phase III, double-blind, multicenter trial randomized 509 outpatients aged 40 years or older to oral therapy with 150 mg of cethromycin per day or 500 mg of levofloxacin per day. Improvements at 14–19 days after enrollment were not significantly different between groups, but the investigators could not rule out the possibility, based on statistical analyses, that cethromycin might be inferior to levofloxacin at those doses, Dr. Eiznhamer said in a poster presentation at the annual Interscience Conference on Antimicrobial Agents and Chemotherapy.

The lead investigator was S. Bukofzer of Abbott Laboratories, which is an investor in Advanced Life Sciences, and all of the investigators came from the two companies.

The 150-mg dose of cethromycin was chosen to minimize adverse events. A new study comparing a 300-mg daily dose of cethromycin with levofloxacin therapy is warranted, said Dr. Eiznhamer of Advanced Life Sciences, the company that is developing cethromycin.

The drug is also being studied in phase III trials for the treatment of community-acquired pneumonia. Advanced Life Sciences plans to submit a new drug application in 2007 with a goal of obtaining Food and Drug Administration approval in 2008, he said in an interview. The conference was sponsored by the American Society for Microbiology.

In an intent-to-treat analysis of 450 patients in the current study, clinical cure was seen in 81% of patients on cethromycin and 84% of those on levofloxacin. Clinical cure was defined as the resolution of at least one clinical symptom (dyspnea, sputum volume, purulence, cough, or fever) and improvement in at least half of the other symptoms.

An intent-to-treat analysis of overall pathogen eradication rates in 231 patients found eradication in 85% of the cethromycin group and 87% of the levofloxacin group.

For Streptococcus pneumoniae, however, cethromycin eradicated the organism in 14 (78%) of 18 patients, compared with 23 (92%) of 25 patients given levofloxacin.

SAN FRANCISCO—Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue advised at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain who are seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease.

Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications. There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” she said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO—Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue advised at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain who are seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease.

Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications. There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” she said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO—Consider cocaine use as a cause of chest pain, especially in young patients, Dr. Priscilla Hsue advised at a meeting sponsored by the California chapter of the American College of Cardiology.

In 2004, 2 million Americans were cocaine users, and cocaine was the most frequently used illicit drug among patients seeking care in emergency departments. About 6% of patients with cocaine-associated chest pain who are seen in emergency departments develop MI, one study suggests.

“I was covering the cardiology service a couple of weeks ago, and almost every day 50% of our admissions were for some kind of side effect from cocaine,” said Dr. Hsue of San Francisco General Hospital. “This is something we see so often.”

Patients with cocaine-related chest pain, unstable angina, or MI tend to be younger than 40 years old, male, and cigarette smokers who have no other risk factors for coronary artery disease.

Chronic and first-time cocaine users have the same risk for MI. Symptoms can appear within minutes or hours after exposure to any dose of cocaine via any route—smoking, snorting, or ingesting.

Cocaine increases the risk of MI 24-fold within 1 hour of use, with the risk decreasing over time after that. The overall likelihood of MI is seven times higher in chronic cocaine users, compared with nonusers. Combining cocaine with alcohol use increases the risk of sudden death by more than 20 times, compared with nonusers, studies suggest.

Cocaine use increases the risk for MI in three ways: by increasing the heart rate and blood pressure in a setting of limited oxygen supply; by vasoconstriction (which is a danger especially in patients who smoke cigarettes or who have preexisting cardiovascular disease), and by promoting inflammation (possibly due to increases in C-reactive protein and platelet levels), she said at the meeting, also sponsored by the University of California, San Francisco.

Ischemic chest discomfort from cocaine use can be indistinguishable from unstable angina or non-ST-segment elevation MI due to coronary atherosclerosis. Only 13% of the patients who presented with chest pain to an emergency department were assessed for cocaine use, one study found.

If cocaine use is suspected or known in a patient with chest pain who has ECG changes, treat with oral nitroglycerin and a calcium antagonist, in accordance with 2002 guidelines from the ACC and American Heart Association. If ST-segment elevations persist, perform coronary arteriography immediately. Give thrombolytic therapy if a thrombus is detected, and consider it if catheterization is not available, the guidelines state.

Those class I recommendations are backed by evidence for or general agreement about their effectiveness and usefulness. The guidelines include several class IIa recommendations based on conflicting evidence or opinions that tend to favor efficacy. These include giving β-blockers for patients with hypertension or sinus tachycardia, and giving intravenous calcium antagonists if the ECG changes suggest ischemia (J. Am. Coll. Cardiol. 2002;40:366–74).

Controversy over some of these treatment recommendations will be addressed in new guidelines for the management of patients with unstable angina and non-ST-segment elevation MI to be released in 2007, said Dr. Hsue, who helped draft the document.

Thrombolytic therapy is controversial in these patients because of case reports of complications. There is no way clinically to differentiate cocaine-related MI from non-cocaine-related MI, and 50%–80% of cocaine users with chest pain have abnormal ECG results that can persist for weeks, complicating the diagnosis.

“We tend not to recommend [thrombolytic therapy] in our cocaine users,” she said.

Many clinicians believe that β-blockers should not be given to patients with cocaine-induced chest pain, but this view is based on one small study of normotensive patients with no prior cocaine use, she noted. The evidence for use of calcium channel blockers likewise comes from a few small studies of patients not representative of cocaine users.

“These studies were small, and it's hard to base conclusions on them,” she said.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression. Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the antidepressant drug sertraline.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression. Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the antidepressant drug sertraline.

SAN FRANCISCO — Screen pregnant women to identify those who are at increased risk for postpartum depression, and plan home visits by a nurse with the at-risk group 10–14 days after delivery, Dr. Andrea J. Singer said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

“Don't wait for the 6-week postpartum visit” in this at-risk group, advised Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

Approximately one in every eight pregnant women will develop postpartum depression, which generally appears within 3–4 months after delivery and affects roughly 560,000 U.S. women per year. Check a patient's history for clues to postpartum depression risk, she said.

Half of pregnant women with a history of postpartum depression will develop it again, she noted. Consider prophylactic therapy in this group, starting at the end of the third trimester or immediately following delivery.

One-third of women with major depression during pregnancy develop postpartum depression, as do one-fourth of women with a history of major depression before pregnancy.

Stressful events during pregnancy or the postpartum period, a history of mood disorder in a first-degree relative, or conflicts with the baby's father or the woman's primary partner increase risk for postpartum depression. Women with shorter time intervals between pregnancies (who have other young children at home) or who deliver low-birth-weight infants or infants with frequent health problems also are at higher risk.

At the least, ask each mother to complete the Edinburgh Postnatal Depression Scale at the first postpartum visit, she urged. Any woman whose total score is greater than 10 or who indicates that “the thought of harming myself has occurred to me” on the questionnaire is likely to be depressed and needs an assessment.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the antidepressant drug sertraline.

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression.

The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown. Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression.

The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown. Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.

SAN FRANCISCO — All psychotropic medications are excreted into breast milk, but the benefits of breast-feeding generally outweigh the relatively small risks to the baby from antidepressants, Dr. Andrea J. Singer said.

The nutritional advantages and the bonding that occurs between mother and child during breast-feeding outweigh concerns about antidepressant effects on the infant, she said at the Perspectives in Women's Health conference sponsored by OB.GYN. NEWS.

The dose of antidepressant that the infant receives from the mother during breast-feeding is much lower than the dose received in utero because the drug crosses the placenta. If a mother and fetus have done well on an antidepressant during pregnancy, stick with that therapy after delivery. “The decision is easy—just continue,” said Dr. Singer, director of women's primary care at Georgetown University Medical Center, Washington.

SSRIs are first-line therapy for lactating women with depression because they have the most data supporting safe use during breast-feeding and efficacy in treating postpartum depression.

The aminoketone drug bupropion is a “not unreasonable alternative,” but the amount of data on it is far more limited, she said.

Combining an SSRI with other supportive services is recommended for severe postpartum depression. There is no consensus for treatment of mild postpartum depression, Dr. Singer added. Consider psychotherapy either alone or with an SSRI for mild depression in lactating women.

Dr. Singer is on the speakers' bureau of Pfizer, which makes the SSRI sertraline.

Generally, sertraline is the treatment of choice for depressed lactating women because of the amount of data available on its use. The SSRIs paroxetine or fluvoxamine are first-line alternatives. Second-line treatment choices include citalopram and fluoxetine. Start with monotherapy when possible, she advised.

The long-term impact of trace levels of antidepressants in infants is unknown. Most SSRIs and bupropion are rated Pregnancy Category C by the Food and Drug Administration. Tricyclic antidepressants fall in Category C or D.

“Most of my psychiatric colleagues don't look at labels so much as the amount of clinical trial data. There is far more experience with the SSRIs, particularly sertraline,” she said.