Betsy Bates

Major Finding: Risk of breast cancer death was 24%–91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: None reported.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die of their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course) their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality (P = .0028).

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course (P = .0027).

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for a comment.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

Major Finding: Risk of breast cancer death was 24%–91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: None reported.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die of their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course) their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality (P = .0028).

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course (P = .0027).

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for a comment.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

Major Finding: Risk of breast cancer death was 24%–91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: None reported.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die of their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course) their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality (P = .0028).

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course (P = .0027).

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for a comment.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

Major Finding: Women with BMIs of 25–30 and greater than 30 were 26%–38% more likely than normal weight women to die of breast cancer 10 or more years after diagnosis.

Data Source: An analysis of a registry involving nearly 19,000 women with breast cancer.

Disclosures: Dr. Ewertz received a research grant from Novartis Pharmaceuticals Corp., and GlaxoSmithKline sponsored her trip to the meeting. The study, however, was conducted and analyzed without support from pharmaceutical companies.

SAN ANTONIO — Obese women are substantially more likely than women of normal weight to die of breast cancer, a large Danish registry study concluded.

Researchers from the Danish Breast Cancer Cooperative Group examined extensive health information from nearly 19,000 women with breast cancer, with follow-up data available for up to 30 years post diagnosis.

Breast cancer patients with body mass indexes (kg/m

The disparity showed up early in the course of their disease, Dr. Marianne Ewertz said at the annual meeting of the San Antonio Breast Cancer Symposium.

“For distant metastasis, the curves begin to separate after 3 years,” said Dr. Ewertz, professor of oncology at Odense (Denmark) University Hospital.

By 5 years, women with a BMI of 25–30 had an increased adjusted hazard ratio of developing distant metastasis of 1.42 (95% confidence interval, 1.17–1.73; P = .0005). For those with a BMI greater than 30, the adjusted odds of distant metastasis beginning at 5 years were 1.46 (95% confidence interval, 1.11–1.92; P = .007).

Women with BMIs of 25–30 and greater than 30, respectively, were 26%–38% (P = .002 and .003) more likely than normal-weight women to die of their disease 10 or more years after diagnosis, and more likely to die of other causes as well.

Heavier women in the study were older, were more likely to be postmenopausal, had larger tumors, had more positive lymph nodes, and had more tumor invasion into deep fascia than did those with a BMI less than 25 (all P values less than .0001). They also had more grade 3 tumors (P = 0.04).

However, all of these factors were statistically accounted for in the multivariate analyses of distant metastasis and overall survival.

Poorer outcomes over time may indicate that adjuvant therapy is less effective in obese women than in normal-weight women, Dr. Ewertz suggested.

Inadequate dosing or biological factors could account for the study's findings, said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston, who was the formal discussant of the presentation.

The impact of lifestyle factors on cancer can be “confounding” because they cannot be studied in prospective, randomized trials.

Therefore, prospective observational evidence is gathered from huge, well-controlled population databases such as the Danish health registries. “This is kind of as good as it gets, and it's pretty good,” Dr. Holmes said.

Major Finding: Women with BMIs of 25–30 and greater than 30 were 26%–38% more likely than normal weight women to die of breast cancer 10 or more years after diagnosis.

Data Source: An analysis of a registry involving nearly 19,000 women with breast cancer.

Disclosures: Dr. Ewertz received a research grant from Novartis Pharmaceuticals Corp., and GlaxoSmithKline sponsored her trip to the meeting. The study, however, was conducted and analyzed without support from pharmaceutical companies.

SAN ANTONIO — Obese women are substantially more likely than women of normal weight to die of breast cancer, a large Danish registry study concluded.

Researchers from the Danish Breast Cancer Cooperative Group examined extensive health information from nearly 19,000 women with breast cancer, with follow-up data available for up to 30 years post diagnosis.

Breast cancer patients with body mass indexes (kg/m

The disparity showed up early in the course of their disease, Dr. Marianne Ewertz said at the annual meeting of the San Antonio Breast Cancer Symposium.

“For distant metastasis, the curves begin to separate after 3 years,” said Dr. Ewertz, professor of oncology at Odense (Denmark) University Hospital.

By 5 years, women with a BMI of 25–30 had an increased adjusted hazard ratio of developing distant metastasis of 1.42 (95% confidence interval, 1.17–1.73; P = .0005). For those with a BMI greater than 30, the adjusted odds of distant metastasis beginning at 5 years were 1.46 (95% confidence interval, 1.11–1.92; P = .007).

Women with BMIs of 25–30 and greater than 30, respectively, were 26%–38% (P = .002 and .003) more likely than normal-weight women to die of their disease 10 or more years after diagnosis, and more likely to die of other causes as well.

Heavier women in the study were older, were more likely to be postmenopausal, had larger tumors, had more positive lymph nodes, and had more tumor invasion into deep fascia than did those with a BMI less than 25 (all P values less than .0001). They also had more grade 3 tumors (P = 0.04).

However, all of these factors were statistically accounted for in the multivariate analyses of distant metastasis and overall survival.

Poorer outcomes over time may indicate that adjuvant therapy is less effective in obese women than in normal-weight women, Dr. Ewertz suggested.

Inadequate dosing or biological factors could account for the study's findings, said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston, who was the formal discussant of the presentation.

The impact of lifestyle factors on cancer can be “confounding” because they cannot be studied in prospective, randomized trials.

Therefore, prospective observational evidence is gathered from huge, well-controlled population databases such as the Danish health registries. “This is kind of as good as it gets, and it's pretty good,” Dr. Holmes said.

Major Finding: Women with BMIs of 25–30 and greater than 30 were 26%–38% more likely than normal weight women to die of breast cancer 10 or more years after diagnosis.

Data Source: An analysis of a registry involving nearly 19,000 women with breast cancer.

Disclosures: Dr. Ewertz received a research grant from Novartis Pharmaceuticals Corp., and GlaxoSmithKline sponsored her trip to the meeting. The study, however, was conducted and analyzed without support from pharmaceutical companies.

SAN ANTONIO — Obese women are substantially more likely than women of normal weight to die of breast cancer, a large Danish registry study concluded.

Researchers from the Danish Breast Cancer Cooperative Group examined extensive health information from nearly 19,000 women with breast cancer, with follow-up data available for up to 30 years post diagnosis.

Breast cancer patients with body mass indexes (kg/m

The disparity showed up early in the course of their disease, Dr. Marianne Ewertz said at the annual meeting of the San Antonio Breast Cancer Symposium.

“For distant metastasis, the curves begin to separate after 3 years,” said Dr. Ewertz, professor of oncology at Odense (Denmark) University Hospital.

By 5 years, women with a BMI of 25–30 had an increased adjusted hazard ratio of developing distant metastasis of 1.42 (95% confidence interval, 1.17–1.73; P = .0005). For those with a BMI greater than 30, the adjusted odds of distant metastasis beginning at 5 years were 1.46 (95% confidence interval, 1.11–1.92; P = .007).

Women with BMIs of 25–30 and greater than 30, respectively, were 26%–38% (P = .002 and .003) more likely than normal-weight women to die of their disease 10 or more years after diagnosis, and more likely to die of other causes as well.

Heavier women in the study were older, were more likely to be postmenopausal, had larger tumors, had more positive lymph nodes, and had more tumor invasion into deep fascia than did those with a BMI less than 25 (all P values less than .0001). They also had more grade 3 tumors (P = 0.04).

However, all of these factors were statistically accounted for in the multivariate analyses of distant metastasis and overall survival.

Poorer outcomes over time may indicate that adjuvant therapy is less effective in obese women than in normal-weight women, Dr. Ewertz suggested.

Inadequate dosing or biological factors could account for the study's findings, said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston, who was the formal discussant of the presentation.

The impact of lifestyle factors on cancer can be “confounding” because they cannot be studied in prospective, randomized trials.

Therefore, prospective observational evidence is gathered from huge, well-controlled population databases such as the Danish health registries. “This is kind of as good as it gets, and it's pretty good,” Dr. Holmes said.

Major Finding: School-age children with ADHD are at increased risk of developing substance use in late adolescence, including drug use or dependence and cigarette smoking. The only significant independent risk factor for later substance use among children with ADHD was conduct disorder.

Data Source: Ten-year prospective, longitudinal case-control family study of ADHD youth (n = 361) and controls (n = 417) first assessed by comprehensive interview at about age 11 and, for most recent findings, at about age 20.

Disclosures: Dr. Wilens receives research support from numerous pharmaceutical companies that make medications used to treat ADHD. This study was funded exclusively by government grants, including from the National Institute of Mental Health.

LOS ANGELES — Early conduct disorder in children with attention-deficit/hyperactivity disorder (ADHD) predicts substance use disorders in adolescence and early adulthood, according to researchers who conducted a long-term prospective study on 778 children.

“I'm a child psychiatrist. I treat kids and work with families. I'd like to know in 10-year-olds, whom do I worry about?” said Dr. Timothy E. Wilens, a pediatric psychopharmacologist at Massachusetts General Hospital in Boston and lead investigator of a 10-year, prospective study of 361 children with ADHD and 417 matched controls.

Children aged 10-11 years and their families underwent extensive interviews, and at periodic intervals over the subsequent decade, culminating in a follow-up evaluation when subjects were in their early 20s.

His overall hypothesis—that ADHD in school-age children would confer an elevated risk of later substance use—was supported, with significant hazard ratios for any substance use of 2.15; alcohol use or dependence, 2.19; drug use or drug dependence, 4.12; and cigarette smoking, 3.21.

As expected, conduct disorder in a child with ADHD “solidly” and independently predicted substance use (hazard ratio, 5.26), including alcohol use or dependence (2.85), drug use or dependence (2.36), and cigarette smoking (2.74).

“We know conduct disorder is big,” he said at the annual meeting of the American Academy of Addiction Psychiatry.

“What you may not know is that you can identify it in a 10-year-old pretty clearly, and if you see it in a 10-year-old, you know you're going to have a problem in adolescence.”

What failed to materialize in the study was a hypothesized link to other independent risk factors for eventual substance use in children with ADHD.

Early difficulties with socialization, family environment, school performance, full-scale IQ or the digit span subtest, arithmetic skills, and a family history of ADHD or substance use all failed to significantly increase the risk of substance use over and above the baseline risk faced by children with ADHD.

Similarly, neither depression nor anxiety independently increased risk for substance use.

“Remember, we have a bit of a ceiling effect here,” cautioned Dr. Wilens, who nonetheless expressed surprise at the results.

One strong trend that failed to reach significance because of a small sample size was a possible link between bipolar disorder and later substance use in children with ADHD.

Previous studies conducted by Dr. Wilens and his group also have drawn associations between substance use among older children with ADHD when they have experienced parental substance use during certain vulnerable developmental stages, he said.

Overall, however, Dr. Wilens said the study suggests that children with ADHD who do not have conduct disorder or severe mood dysregulation face a baseline elevated risk of substance abuse that is not exacerbated by other comorbidities.

He drew attention to a large body of research showing that substance use initiation is delayed if children with ADHD are well managed with medication, although the protective effects of medication are lost in adulthood.

“Aggressively treating the ADHD is really critical,” he said.

He also advised careful assessment of potential conduct disorder in young children, which may present as a history of aggressiveness, bullying, a dearth of positive interactions with other children, harm to animals or younger children, a problematic response to parental discipline, and a lack of empathy.

Minor property damage such as breaking windows might be part of the picture in a 10-year-old, but conduct disorder is likely to look different in younger children, Dr. Wilens said.

“You're not going to see them stealing a car.”

Major Finding: School-age children with ADHD are at increased risk of developing substance use in late adolescence, including drug use or dependence and cigarette smoking. The only significant independent risk factor for later substance use among children with ADHD was conduct disorder.

Data Source: Ten-year prospective, longitudinal case-control family study of ADHD youth (n = 361) and controls (n = 417) first assessed by comprehensive interview at about age 11 and, for most recent findings, at about age 20.

Disclosures: Dr. Wilens receives research support from numerous pharmaceutical companies that make medications used to treat ADHD. This study was funded exclusively by government grants, including from the National Institute of Mental Health.

LOS ANGELES — Early conduct disorder in children with attention-deficit/hyperactivity disorder (ADHD) predicts substance use disorders in adolescence and early adulthood, according to researchers who conducted a long-term prospective study on 778 children.

“I'm a child psychiatrist. I treat kids and work with families. I'd like to know in 10-year-olds, whom do I worry about?” said Dr. Timothy E. Wilens, a pediatric psychopharmacologist at Massachusetts General Hospital in Boston and lead investigator of a 10-year, prospective study of 361 children with ADHD and 417 matched controls.

Children aged 10-11 years and their families underwent extensive interviews, and at periodic intervals over the subsequent decade, culminating in a follow-up evaluation when subjects were in their early 20s.

His overall hypothesis—that ADHD in school-age children would confer an elevated risk of later substance use—was supported, with significant hazard ratios for any substance use of 2.15; alcohol use or dependence, 2.19; drug use or drug dependence, 4.12; and cigarette smoking, 3.21.

As expected, conduct disorder in a child with ADHD “solidly” and independently predicted substance use (hazard ratio, 5.26), including alcohol use or dependence (2.85), drug use or dependence (2.36), and cigarette smoking (2.74).

“We know conduct disorder is big,” he said at the annual meeting of the American Academy of Addiction Psychiatry.

“What you may not know is that you can identify it in a 10-year-old pretty clearly, and if you see it in a 10-year-old, you know you're going to have a problem in adolescence.”

What failed to materialize in the study was a hypothesized link to other independent risk factors for eventual substance use in children with ADHD.

Early difficulties with socialization, family environment, school performance, full-scale IQ or the digit span subtest, arithmetic skills, and a family history of ADHD or substance use all failed to significantly increase the risk of substance use over and above the baseline risk faced by children with ADHD.

Similarly, neither depression nor anxiety independently increased risk for substance use.

“Remember, we have a bit of a ceiling effect here,” cautioned Dr. Wilens, who nonetheless expressed surprise at the results.

One strong trend that failed to reach significance because of a small sample size was a possible link between bipolar disorder and later substance use in children with ADHD.

Previous studies conducted by Dr. Wilens and his group also have drawn associations between substance use among older children with ADHD when they have experienced parental substance use during certain vulnerable developmental stages, he said.

Overall, however, Dr. Wilens said the study suggests that children with ADHD who do not have conduct disorder or severe mood dysregulation face a baseline elevated risk of substance abuse that is not exacerbated by other comorbidities.

He drew attention to a large body of research showing that substance use initiation is delayed if children with ADHD are well managed with medication, although the protective effects of medication are lost in adulthood.

“Aggressively treating the ADHD is really critical,” he said.

He also advised careful assessment of potential conduct disorder in young children, which may present as a history of aggressiveness, bullying, a dearth of positive interactions with other children, harm to animals or younger children, a problematic response to parental discipline, and a lack of empathy.

Minor property damage such as breaking windows might be part of the picture in a 10-year-old, but conduct disorder is likely to look different in younger children, Dr. Wilens said.

“You're not going to see them stealing a car.”

Major Finding: School-age children with ADHD are at increased risk of developing substance use in late adolescence, including drug use or dependence and cigarette smoking. The only significant independent risk factor for later substance use among children with ADHD was conduct disorder.

Data Source: Ten-year prospective, longitudinal case-control family study of ADHD youth (n = 361) and controls (n = 417) first assessed by comprehensive interview at about age 11 and, for most recent findings, at about age 20.

Disclosures: Dr. Wilens receives research support from numerous pharmaceutical companies that make medications used to treat ADHD. This study was funded exclusively by government grants, including from the National Institute of Mental Health.

LOS ANGELES — Early conduct disorder in children with attention-deficit/hyperactivity disorder (ADHD) predicts substance use disorders in adolescence and early adulthood, according to researchers who conducted a long-term prospective study on 778 children.

“I'm a child psychiatrist. I treat kids and work with families. I'd like to know in 10-year-olds, whom do I worry about?” said Dr. Timothy E. Wilens, a pediatric psychopharmacologist at Massachusetts General Hospital in Boston and lead investigator of a 10-year, prospective study of 361 children with ADHD and 417 matched controls.

Children aged 10-11 years and their families underwent extensive interviews, and at periodic intervals over the subsequent decade, culminating in a follow-up evaluation when subjects were in their early 20s.

His overall hypothesis—that ADHD in school-age children would confer an elevated risk of later substance use—was supported, with significant hazard ratios for any substance use of 2.15; alcohol use or dependence, 2.19; drug use or drug dependence, 4.12; and cigarette smoking, 3.21.

As expected, conduct disorder in a child with ADHD “solidly” and independently predicted substance use (hazard ratio, 5.26), including alcohol use or dependence (2.85), drug use or dependence (2.36), and cigarette smoking (2.74).

“We know conduct disorder is big,” he said at the annual meeting of the American Academy of Addiction Psychiatry.

“What you may not know is that you can identify it in a 10-year-old pretty clearly, and if you see it in a 10-year-old, you know you're going to have a problem in adolescence.”

What failed to materialize in the study was a hypothesized link to other independent risk factors for eventual substance use in children with ADHD.

Early difficulties with socialization, family environment, school performance, full-scale IQ or the digit span subtest, arithmetic skills, and a family history of ADHD or substance use all failed to significantly increase the risk of substance use over and above the baseline risk faced by children with ADHD.

Similarly, neither depression nor anxiety independently increased risk for substance use.

“Remember, we have a bit of a ceiling effect here,” cautioned Dr. Wilens, who nonetheless expressed surprise at the results.

One strong trend that failed to reach significance because of a small sample size was a possible link between bipolar disorder and later substance use in children with ADHD.

Previous studies conducted by Dr. Wilens and his group also have drawn associations between substance use among older children with ADHD when they have experienced parental substance use during certain vulnerable developmental stages, he said.

Overall, however, Dr. Wilens said the study suggests that children with ADHD who do not have conduct disorder or severe mood dysregulation face a baseline elevated risk of substance abuse that is not exacerbated by other comorbidities.

He drew attention to a large body of research showing that substance use initiation is delayed if children with ADHD are well managed with medication, although the protective effects of medication are lost in adulthood.

“Aggressively treating the ADHD is really critical,” he said.

He also advised careful assessment of potential conduct disorder in young children, which may present as a history of aggressiveness, bullying, a dearth of positive interactions with other children, harm to animals or younger children, a problematic response to parental discipline, and a lack of empathy.

Minor property damage such as breaking windows might be part of the picture in a 10-year-old, but conduct disorder is likely to look different in younger children, Dr. Wilens said.

“You're not going to see them stealing a car.”

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: The National Longitudinal Study of Adolescent Health, involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 in the mid-1990s, when the first and second waves of interviews were conducted. About half the sample was white; 23% were African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

Median age at Wave 1 was 16 years, and at Wave 3 (2001-2002), 22. Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27, compared with nonusers. That risk increased to 1.33 among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, Dr. Ho reported.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and cannabis use at Wave 3, but found no significant temporal relationship. “Depression did not seem to increase risk of cannabis use at a later time,” he said.

The large sample size was a strength of the study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes. The association of early cannabis use with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

There are policy and practice implications, said Dr. Hon Ho.

Source Courtesy Mark Groth, University of Colorado Denver

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: The National Longitudinal Study of Adolescent Health, involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 in the mid-1990s, when the first and second waves of interviews were conducted. About half the sample was white; 23% were African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

Median age at Wave 1 was 16 years, and at Wave 3 (2001-2002), 22. Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27, compared with nonusers. That risk increased to 1.33 among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, Dr. Ho reported.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and cannabis use at Wave 3, but found no significant temporal relationship. “Depression did not seem to increase risk of cannabis use at a later time,” he said.

The large sample size was a strength of the study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes. The association of early cannabis use with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

There are policy and practice implications, said Dr. Hon Ho.

Source Courtesy Mark Groth, University of Colorado Denver

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: The National Longitudinal Study of Adolescent Health, involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 in the mid-1990s, when the first and second waves of interviews were conducted. About half the sample was white; 23% were African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

Median age at Wave 1 was 16 years, and at Wave 3 (2001-2002), 22. Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27, compared with nonusers. That risk increased to 1.33 among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, Dr. Ho reported.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and cannabis use at Wave 3, but found no significant temporal relationship. “Depression did not seem to increase risk of cannabis use at a later time,” he said.

The large sample size was a strength of the study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes. The association of early cannabis use with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

There are policy and practice implications, said Dr. Hon Ho.

Source Courtesy Mark Groth, University of Colorado Denver

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: National Longitudinal Study of Adolescent Health involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 years in the mid-1990s, when the first and second waves of interviews were conducted.

About half the sample was white; 23% was African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

The median age at Wave 1 was 16, and at Wave 3 (during 2001-2002) the median age was 22.

Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27 (95% confidence interval 1.07-1.49), compared with nonusers. That risk increased to 1.33 (1.07-1.64) among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, reported Dr. Ho in an oral presentation of his paper.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and subsequent cannabis use at Wave 3, but found no significant temporal relationship.

“Depression did not seem to increase risk of cannabis use at a later time,” he said.

Dr. Ho said that the large sample size was a strength of his study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes, he said.

The fact that early cannabis use is associated with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

Prior cannabis use proved to be a statistically significant predictor of later depression.

Source DR. HO

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: National Longitudinal Study of Adolescent Health involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 years in the mid-1990s, when the first and second waves of interviews were conducted.

About half the sample was white; 23% was African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

The median age at Wave 1 was 16, and at Wave 3 (during 2001-2002) the median age was 22.

Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27 (95% confidence interval 1.07-1.49), compared with nonusers. That risk increased to 1.33 (1.07-1.64) among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, reported Dr. Ho in an oral presentation of his paper.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and subsequent cannabis use at Wave 3, but found no significant temporal relationship.

“Depression did not seem to increase risk of cannabis use at a later time,” he said.

Dr. Ho said that the large sample size was a strength of his study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes, he said.

The fact that early cannabis use is associated with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

Prior cannabis use proved to be a statistically significant predictor of later depression.

Source DR. HO

Major Findings: The relative risk for depression after any cannabis use was 1.27, compared with nonusers, and 1.33 after use on 10 or more occasions.

Data Source: National Longitudinal Study of Adolescent Health involving more than 21,000 subjects.

Disclosures: The researchers received federal funding for the study. They reported no financial conflicts of interest.

LOS ANGELES — Cannabis use in adolescence was associated with the subsequent development of depression, but the reverse did not prove to be true in a large, longitudinal study presented at the annual meeting of the American Academy of Addiction Psychiatry.

Dr. Hon Ho and associates from the department of psychiatry at the University of Colorado, Denver, examined data from the National Longitudinal Study of Adolescent Health, a national probability sample of individuals who were surveyed several times over a 14-year period on social, economic, psychological, and medical topics.

The sample included 10,778 female and 10,519 male participants who were between the ages of 11 and 21 years in the mid-1990s, when the first and second waves of interviews were conducted.

About half the sample was white; 23% was African American; 13%, Hispanic, 8%, Asian, and 2%, Native American.

The median age at Wave 1 was 16, and at Wave 3 (during 2001-2002) the median age was 22.

Dr. Ho combined responses from Waves 1 and 2, which represented only a few years (1994-1996) and then tracked temporal patterns between first stated use of cannabis and the first indicator of depression based on the Center for Epidemiologic Studies–Depression (CES-D) scale.

Prior cannabis use proved to be a statistically significant predictor of later depression after adjustment for age, sex, race, socioeconomic status, and drug and alcohol use.

The relative risk for depression after any cannabis use was 1.27 (95% confidence interval 1.07-1.49), compared with nonusers. That risk increased to 1.33 (1.07-1.64) among people who reported using cannabis on 10 or more occasions.

Low socioeconomic status and black, Native American, or Asian race were also predictive of later depression; being male was a protective factor, reported Dr. Ho in an oral presentation of his paper.

The investigators then examined the reverse scenario: depression at Waves 1 or 2 and subsequent cannabis use at Wave 3, but found no significant temporal relationship.

“Depression did not seem to increase risk of cannabis use at a later time,” he said.

Dr. Ho said that the large sample size was a strength of his study, but reliance on self-reported behaviors and the lack of more precise dose information about cannabis use compromised the study's ability to determine causality, rather than a mere association.

Nonetheless, the findings do have some policy and practice implications, particularly as local governments consider easing restrictions on marijuana purchasing and use for medicinal purposes, he said.

The fact that early cannabis use is associated with later depression is “definitely something we want to consider,” both societally and in counseling of adolescents and families, he said.

Prior cannabis use proved to be a statistically significant predictor of later depression.

Source DR. HO

Major Finding: Risk of breast cancer death was 24%-91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: Dr. Kelly reported having no relevant financial disclosures.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die from their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course), their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality.

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course.

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for comment on the study.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

Major Finding: Risk of breast cancer death was 24%-91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: Dr. Kelly reported having no relevant financial disclosures.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die from their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course), their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality.

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course.

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for comment on the study.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

Major Finding: Risk of breast cancer death was 24%-91% higher when women took paroxetine while on tamoxifen.

Source of Data: Retrospective, population-based cohort study of 2,430 women.

Disclosures: Dr. Kelly reported having no relevant financial disclosures.

SAN ANTONIO — Breast cancer patients who took the antidepressant paroxetine during their course of tamoxifen therapy were up to 91% more likely to die from their disease than were those who did not take the two drugs together, according to a retrospective, population-based cohort study conducted in the Canadian province of Ontario.

Investigators used health card identification numbers to track women aged 66 years and older who were treated with tamoxifen for breast cancer between 1993 and 2005. Almost a third of patients were taking an antidepressant during their tamoxifen therapy, including 2,430 who were taking a selective serotonin reuptake inhibitor.

As a class, SSRIs are known to inhibit cytochrome P450 2D6 (CYP 2D6), an enzyme critical for the conversion of tamoxifen to endoxifen, its active metabolite, in the body. The ability of SSRIs to interfere with the efficacy of tamoxifen—at least in some women—has been theorized, but studies attempting to clarify the issue have reported conflicting results.

In the Canadian study reported at the annual meeting of the San Antonio Breast Cancer Symposium, 1,074 (44.2%) of the women taking an SSRI during tamoxifen therapy had died as of Dec. 31, 2007, when primary data analysis began. After statistical adjustment for age, socioeconomic status, comorbidity, use of other CYP 2D6 drugs, and timing and duration of tamoxifen therapy, investigators found that the breast cancer mortality risk was increased 24% among women who were coprescribed paroxetine during 25% of their tamoxifen treatment.

If patients took paroxetine longer (that is, for more than half of their tamoxifen course), their breast cancer mortality risk rose to 54%. Patients who took both drugs for 75% of the time they received tamoxifen had a 91% risk of breast cancer mortality.

Mortality from any cause was also sharply elevated among women who took paroxetine for 75% or more of their tamoxifen course.

The striking results were significant only for paroxetine, and not for other SSRIs—including fluoxetine, sertraline, fluvoxamine, or citalopram—that were taken concurrently with tamoxifen, reported Dr. Catherine M. Kelly at the meeting.

Dr. Kelly hypothesized that the explanation lies in the degree to which various SSRIs inhibit CYP 2D6. “Paroxetine is the only SSRI that is an irreversible—or 'suicide'—inhibitor of CYP 2D6,” she said in an interview.

The dose-response curve of the study, with escalating mortality risk paralleling time on paroxetine, adds significant weight to the findings with regard to paroxetine, marketed as Paxil by GlaxoSmithKline. (The company did not respond to a request for comment on the study.)

Fluoxetine is also a potent inhibitor of CYP 2D6, but was not shown to increase breast cancer mortality in the study. “I would like to see further data on that and would use caution in using any of the drugs that inhibit CYP 2D6 in women who are taking tamoxifen, said Dr. Kelly, who was with the University of Toronto Sunnybrook Health Sciences Centre while conducting the study and is currently a breast medical oncology fellow at the University of Texas M.D. Anderson Cancer Center in Houston.

“There are other options,” she noted, including non-SSRI antidepressants that do not inhibit CYP 2D6.

Women need to discuss their choices with a medical oncologist, psychiatrist, or family physician before undergoing tamoxifen therapy, she suggested.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal cancer survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years following their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol: 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, Dr. Kwan reported. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, the survivors who drank at least the equivalent of 3 to 4 drinks per week (about a half-drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, Dr. Kwan said.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption, particularly now that many women live for decades following a diagnosis.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations,” she added.

But based on the signals offered in the study, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

Disclosures: Dr. Kwan reported having no relevant conflicts of interest.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal cancer survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years following their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol: 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, Dr. Kwan reported. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, the survivors who drank at least the equivalent of 3 to 4 drinks per week (about a half-drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, Dr. Kwan said.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption, particularly now that many women live for decades following a diagnosis.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations,” she added.

But based on the signals offered in the study, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

Disclosures: Dr. Kwan reported having no relevant conflicts of interest.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal cancer survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years following their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol: 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, Dr. Kwan reported. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, the survivors who drank at least the equivalent of 3 to 4 drinks per week (about a half-drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, Dr. Kwan said.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption, particularly now that many women live for decades following a diagnosis.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations,” she added.

But based on the signals offered in the study, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

Disclosures: Dr. Kwan reported having no relevant conflicts of interest.

Major Finding: Moderate to heavy drinkers of alcohol were at significantly greater risk for breast cancer recurrence than were those who abstained or drank little alcohol.

Data Source: A prospective 8-year study of 1,897 women diagnosed with early-stage breast cancer.

Disclosures: None reported.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years after their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol; 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, reported Dr. Kwan. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, survivors who drank at least the equivalent of three or four drinks per week (about a half drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, said Dr. Kwan.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

Whether a survivor's breast cancer was estrogen-receptor positive or negative had no influence on her risk for recurrence if she drank alcohol.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said discussant Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations”

Based on this study, however, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

Major Finding: Moderate to heavy drinkers of alcohol were at significantly greater risk for breast cancer recurrence than were those who abstained or drank little alcohol.

Data Source: A prospective 8-year study of 1,897 women diagnosed with early-stage breast cancer.

Disclosures: None reported.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years after their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol; 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, reported Dr. Kwan. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, survivors who drank at least the equivalent of three or four drinks per week (about a half drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, said Dr. Kwan.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

Whether a survivor's breast cancer was estrogen-receptor positive or negative had no influence on her risk for recurrence if she drank alcohol.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said discussant Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations”

Based on this study, however, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

Major Finding: Moderate to heavy drinkers of alcohol were at significantly greater risk for breast cancer recurrence than were those who abstained or drank little alcohol.

Data Source: A prospective 8-year study of 1,897 women diagnosed with early-stage breast cancer.

Disclosures: None reported.

SAN ANTONIO — Women who were moderate to heavy drinkers had a 1.3-fold increase in breast cancer recurrence, compared with those who abstained or drank only minimally, according to a study presented at the San Antonio Breast Cancer Symposium.

The highest risk was seen among the heaviest drinkers and overweight and/or postmenopausal survivors.

Researchers from Kaiser Permanente in Oakland, Calif., prospectively followed 1,897 women for 8 years after their diagnoses with early-stage breast cancer, studying lifestyle factors that might be associated with recurrence or death, either from cancer or other causes.

About half the cohort reported drinking alcohol; 90% drank wine, 43% drank liquor, and 36% drank beer, said Marilyn L. Kwan, Ph.D., a research scientist with the large Northern California HMO.

In all, 18% of the cohort experienced a recurrence, and 17% of the cohort died, reported Dr. Kwan. Slightly more than half of the women who died succumbed to breast cancer, while 43% died from other causes.

Women who drank alcohol tended to be younger, thinner, better educated, and white, but statisticians accounted for these factors in their analysis.

After adjustment, survivors who drank at least the equivalent of three or four drinks per week (about a half drink per day) were 1.3 times more likely to have a recurrence of their cancer, compared with those who either did not drink or drank less than an average of 0.5 g of alcohol per day. The results followed a positive dose-response curve, indicating that the more women drank, the more likely they were to experience a recurrence.

Women who drank less than 6 g of alcohol per day (about a half-glass) had no increased recurrence risk, said Dr. Kwan.

When researchers examined subgroups of survivors, they found a 1.5-fold elevated risk among postmenopausal women, but no elevated risk among pre-menopausal women and a 1.58-fold increase in risk among overweight and obese women but no increase among normal-weight women.

Whether a survivor's breast cancer was estrogen-receptor positive or negative had no influence on her risk for recurrence if she drank alcohol.

The risk of death from breast cancer was elevated 1.5-fold among survivors who drank a mean of a half-glass of alcohol per day or more.

There was no association with death from all causes, and even a suggestion of survival protection among moderate to heavy drinkers, likely capturing the well-known cardiovascular benefits of modest alcohol consumption. Thus, the results leave unanswered the question of whether some women with breast cancer—like their counterparts without the disease—might ultimately benefit in terms of overall survival from modest alcohol consumption.

“Our message to women with breast cancer may need to be as nuanced as our message to women without breast cancer,” said discussant Dr. Michelle D. Holmes of the Dana-Farber/Harvard Cancer Center in Boston.

“Our results are consistent with alcohol's effect on increasing the risk of primary breast cancer,” Dr. Kwan said during her podium session. “We do need the confirmation of a large, prospective study in breast cancer survivors before we can make any [definitive] lifestyle recommendations”

Based on this study, however, women “should possibly consider limiting” their use of alcohol after a breast cancer diagnosis, realizing that the highest risk appears to be conferred on postmenopausal women and those who are overweight or obese, she said.

LAS VEGAS — Physician office overhead costs are up 15%; reimbursements and collections are down. To say the least, 2009 hasn't been a boom year for pediatricians.

But don't despair.

There are ways to save money and tilt your balance sheet back in the direction of a healthy bottom line, said Dr. Norman “Chip” Harbaugh, a primary care pediatrician and practice management specialist from Atlanta.

Here are some cost-saving tips from his talks at a seminar on practical pediatrics sponsored by the American Academy of Pediatrics:

▸ Maximize tax-free benefits for you and your partner(s). Don't forget to deduct payments for malpractice, major medical, disability, life, and liability insurance. Personal expense account charges are deductible as well, including the cost of attending CME meetings; dues and subscriptions; and up to $45,000 a year for retirement spending. Younger physicians may also want to self-fund their own buyouts over the long term by purchasing variable adjustable life insurance policies.

▸ Stretch your office services with mid-level providers. Salaries for nurse practitioners and physician assistants can quickly reach the “breakeven” point and begin increasing the profits of the practice once they perform 10-13 checkups a day. Such providers also can coordinate hugely popular “quick visit” clinics, such as a sore-throat/earache walk-in clinic each weekday morning from 8 a.m. to 10 a.m.

▸ Reevaluate your ratio of front office to clinical personnel. A “good” ratio is 1 front office person to 3.5 clinical staff. “Better” is 1:3.4 if your office has a lab and 1:3.2 if your office has no lab. A ratio that's “too low” is 1:2.8 or 1:2.3, said Dr. Harbaugh.

▸ Charge patients for simple but time-consuming tasks. For example, consider charging a fee for filling out forms for camp.

▸ Save on supplies. Become part of a Physician Buying Group (PBG) for office supplies, medical supplies, and lab supplies, and especially, vaccines. Such groups have the potential for saving a practice 10%-25% on “big ticket” items and thousands of dollars a year on vaccines. Three PBGs are the National Discount Vaccine Alliance, 785-273-4165, http://nationaldiscountvaccinealliance.comwww.atlantichealthpartners.comwww.physall.com

▸ Renegotiate your rent. “Commercial real estate? They're hurting,” said Dr. Harbaugh. He suggested that any physician or group whose lease is expiring within 2 years should “renegotiate now.” Some landlords are offering 3-6 months of free rent in exchange for a renewal of an office space lease. Another option, especially in light of the dismal commercial real estate market, is to consider buying your own building while prices are low.

▸ Stretch the use of your office space. Could you accommodate another provider and expand your business hours from early morning to late evening, with physicians staggering their hours? Could you sublease space during off-hours to a lactation consultant; physical, occupational, or speech therapist; or registered dietitian who could provide nutrition counseling and diabetes education?

▸ Target missed appointments. Automated dialing systems can be set to make reminder calls and reduce expensive no-shows, if this is a problem in your practice.

▸ Cede out-of-office care. Dr. Harbaugh admitted that this idea could “run me out of town,” but he suggested that practices tally up the cost of delivery/newborn hospital visits, pediatric hospital rounds, and courtesy emergency department visits. The office, he said, “is where we provide the most service. It's our cost center.” Some practices may want to poll families to see whether they would be willing to trade a visit to the hospital to see their newborn for an expanded level of office care, including early morning and evening walk-in visits.

▸ Consider participating in clinical trials. “It's a lot of work,” but adding research to a pediatric practice can be rewarding and intellectually invigorating, as well as profitable, infusing up to $100,000 a year into a practice's bottom line. The concept works only as long as a dedicated physician wants to take on the role of principal investigator and at least one office staff member can devote the bulk of his or her time to coordinating the trial(s).

Disclosures: Dr. Harbaugh disclosed that he is on the national advisory boards, is on the speakers bureaus, and/or serves as a consultant for several pharmaceutical companies. He recently served as CEO and chairman of the board for Kids First Pediatric Alliance, a metropolitan Atlanta IPA.

LAS VEGAS — Physician office overhead costs are up 15%; reimbursements and collections are down. To say the least, 2009 hasn't been a boom year for pediatricians.

But don't despair.

There are ways to save money and tilt your balance sheet back in the direction of a healthy bottom line, said Dr. Norman “Chip” Harbaugh, a primary care pediatrician and practice management specialist from Atlanta.

Here are some cost-saving tips from his talks at a seminar on practical pediatrics sponsored by the American Academy of Pediatrics:

▸ Maximize tax-free benefits for you and your partner(s). Don't forget to deduct payments for malpractice, major medical, disability, life, and liability insurance. Personal expense account charges are deductible as well, including the cost of attending CME meetings; dues and subscriptions; and up to $45,000 a year for retirement spending. Younger physicians may also want to self-fund their own buyouts over the long term by purchasing variable adjustable life insurance policies.

▸ Stretch your office services with mid-level providers. Salaries for nurse practitioners and physician assistants can quickly reach the “breakeven” point and begin increasing the profits of the practice once they perform 10-13 checkups a day. Such providers also can coordinate hugely popular “quick visit” clinics, such as a sore-throat/earache walk-in clinic each weekday morning from 8 a.m. to 10 a.m.

▸ Reevaluate your ratio of front office to clinical personnel. A “good” ratio is 1 front office person to 3.5 clinical staff. “Better” is 1:3.4 if your office has a lab and 1:3.2 if your office has no lab. A ratio that's “too low” is 1:2.8 or 1:2.3, said Dr. Harbaugh.

▸ Charge patients for simple but time-consuming tasks. For example, consider charging a fee for filling out forms for camp.

▸ Save on supplies. Become part of a Physician Buying Group (PBG) for office supplies, medical supplies, and lab supplies, and especially, vaccines. Such groups have the potential for saving a practice 10%-25% on “big ticket” items and thousands of dollars a year on vaccines. Three PBGs are the National Discount Vaccine Alliance, 785-273-4165, http://nationaldiscountvaccinealliance.comwww.atlantichealthpartners.comwww.physall.com

▸ Renegotiate your rent. “Commercial real estate? They're hurting,” said Dr. Harbaugh. He suggested that any physician or group whose lease is expiring within 2 years should “renegotiate now.” Some landlords are offering 3-6 months of free rent in exchange for a renewal of an office space lease. Another option, especially in light of the dismal commercial real estate market, is to consider buying your own building while prices are low.

▸ Stretch the use of your office space. Could you accommodate another provider and expand your business hours from early morning to late evening, with physicians staggering their hours? Could you sublease space during off-hours to a lactation consultant; physical, occupational, or speech therapist; or registered dietitian who could provide nutrition counseling and diabetes education?

▸ Target missed appointments. Automated dialing systems can be set to make reminder calls and reduce expensive no-shows, if this is a problem in your practice.

▸ Cede out-of-office care. Dr. Harbaugh admitted that this idea could “run me out of town,” but he suggested that practices tally up the cost of delivery/newborn hospital visits, pediatric hospital rounds, and courtesy emergency department visits. The office, he said, “is where we provide the most service. It's our cost center.” Some practices may want to poll families to see whether they would be willing to trade a visit to the hospital to see their newborn for an expanded level of office care, including early morning and evening walk-in visits.

▸ Consider participating in clinical trials. “It's a lot of work,” but adding research to a pediatric practice can be rewarding and intellectually invigorating, as well as profitable, infusing up to $100,000 a year into a practice's bottom line. The concept works only as long as a dedicated physician wants to take on the role of principal investigator and at least one office staff member can devote the bulk of his or her time to coordinating the trial(s).

Disclosures: Dr. Harbaugh disclosed that he is on the national advisory boards, is on the speakers bureaus, and/or serves as a consultant for several pharmaceutical companies. He recently served as CEO and chairman of the board for Kids First Pediatric Alliance, a metropolitan Atlanta IPA.

LAS VEGAS — Physician office overhead costs are up 15%; reimbursements and collections are down. To say the least, 2009 hasn't been a boom year for pediatricians.

But don't despair.

There are ways to save money and tilt your balance sheet back in the direction of a healthy bottom line, said Dr. Norman “Chip” Harbaugh, a primary care pediatrician and practice management specialist from Atlanta.

Here are some cost-saving tips from his talks at a seminar on practical pediatrics sponsored by the American Academy of Pediatrics:

▸ Maximize tax-free benefits for you and your partner(s). Don't forget to deduct payments for malpractice, major medical, disability, life, and liability insurance. Personal expense account charges are deductible as well, including the cost of attending CME meetings; dues and subscriptions; and up to $45,000 a year for retirement spending. Younger physicians may also want to self-fund their own buyouts over the long term by purchasing variable adjustable life insurance policies.

▸ Stretch your office services with mid-level providers. Salaries for nurse practitioners and physician assistants can quickly reach the “breakeven” point and begin increasing the profits of the practice once they perform 10-13 checkups a day. Such providers also can coordinate hugely popular “quick visit” clinics, such as a sore-throat/earache walk-in clinic each weekday morning from 8 a.m. to 10 a.m.

▸ Reevaluate your ratio of front office to clinical personnel. A “good” ratio is 1 front office person to 3.5 clinical staff. “Better” is 1:3.4 if your office has a lab and 1:3.2 if your office has no lab. A ratio that's “too low” is 1:2.8 or 1:2.3, said Dr. Harbaugh.

▸ Charge patients for simple but time-consuming tasks. For example, consider charging a fee for filling out forms for camp.

▸ Save on supplies. Become part of a Physician Buying Group (PBG) for office supplies, medical supplies, and lab supplies, and especially, vaccines. Such groups have the potential for saving a practice 10%-25% on “big ticket” items and thousands of dollars a year on vaccines. Three PBGs are the National Discount Vaccine Alliance, 785-273-4165, http://nationaldiscountvaccinealliance.comwww.atlantichealthpartners.comwww.physall.com

▸ Renegotiate your rent. “Commercial real estate? They're hurting,” said Dr. Harbaugh. He suggested that any physician or group whose lease is expiring within 2 years should “renegotiate now.” Some landlords are offering 3-6 months of free rent in exchange for a renewal of an office space lease. Another option, especially in light of the dismal commercial real estate market, is to consider buying your own building while prices are low.

▸ Stretch the use of your office space. Could you accommodate another provider and expand your business hours from early morning to late evening, with physicians staggering their hours? Could you sublease space during off-hours to a lactation consultant; physical, occupational, or speech therapist; or registered dietitian who could provide nutrition counseling and diabetes education?

▸ Target missed appointments. Automated dialing systems can be set to make reminder calls and reduce expensive no-shows, if this is a problem in your practice.

▸ Cede out-of-office care. Dr. Harbaugh admitted that this idea could “run me out of town,” but he suggested that practices tally up the cost of delivery/newborn hospital visits, pediatric hospital rounds, and courtesy emergency department visits. The office, he said, “is where we provide the most service. It's our cost center.” Some practices may want to poll families to see whether they would be willing to trade a visit to the hospital to see their newborn for an expanded level of office care, including early morning and evening walk-in visits.

▸ Consider participating in clinical trials. “It's a lot of work,” but adding research to a pediatric practice can be rewarding and intellectually invigorating, as well as profitable, infusing up to $100,000 a year into a practice's bottom line. The concept works only as long as a dedicated physician wants to take on the role of principal investigator and at least one office staff member can devote the bulk of his or her time to coordinating the trial(s).

Disclosures: Dr. Harbaugh disclosed that he is on the national advisory boards, is on the speakers bureaus, and/or serves as a consultant for several pharmaceutical companies. He recently served as CEO and chairman of the board for Kids First Pediatric Alliance, a metropolitan Atlanta IPA.

LAS VEGAS — Amid the alphabet soup of hepatitis virus types, the one that should most concern physicians these days is hepatitis C.

“This is going to be the big virus in the next 20 years in the U.S.,” Dr. Marsha H. Kay predicted at a meeting sponsored by the American Academy of Pediatrics.

Hepatitis C virus already infects 1.6% of the general U.S. population—4 million people—but “the vast majority of people who are infected do not know it,” said Dr. Kay, a pediatric gastroenterologist and director of pediatric endoscopy at the Cleveland Clinic Children's Hospital.

Known to be at risk are infants born to mothers with hepatitis C; young adult survivors of leukemia, childhood malignancies, and childhood cardiac surgery; hemophiliacs; dialysis patients; intravenous drug users; sexual partners of a person with hepatitis C; recipients of blood transfusions prior to 1989; first responders; and health care workers.

However, 32% of the current cases involve no known risk factor.

“We don't know exactly how this virus is transmitted,” said Dr. Kay.

There is no way to prevent hepatitis C (except for universal body fluid precautions) and there is no vaccine.

Among those infected, 80%-85% will develop chronic hepatitis, and of those, half will develop cirrhosis, putting them at highly elevated risk for hepatocellular carcinoma. Hepatitis C is already the leading cause of liver transplantation in the nation.

All things considered, the perfect storm of hepatitis C constitutes “a really terrible outcome compared to hepatitis B infection,” she said, adding, “I lose a lot of sleep about this.”

Among children, the leading cause of hepatitis C transmission is perinatal exposure, with transmission risk correlated to the mother's viral load at delivery.

Unfortunately, drugs used to treat acute hepatitis C are teratogenic and cannot be used during pregnancy. Some experts recommend avoiding fetal scalp monitoring and prolonging labor beyond 6 hours after the rupture of membranes to reduce the risk of transmission.

Breastfeeding, Dr. Kay said, is controversial. Hepatitis C acquired via perinatal transmission has an increased likelihood of becoming chronic.

Anti-HCV testing is ideally performed between 15 and 18 months of age. Although HCV RNA testing may be positive at 2 months and 6 months, positive anti-HCV at that time may reflect the mother's HCV status rather than the infant's HCV status.

Other patients who should be considered at risk in a primary care practice include young people who overcame serious illnesses early in life and those who received blood products before 1989.

That means the cardiac babies who are “doing great, and they're now 20 years old,” said Dr. Kay.

Individuals who received Gammagard (immune globulin) from a particular manufacturer during 1993 and 1994 may also be at risk.

Health care providers, especially those who work in emergency departments, surgery, or procedurally related specialties, have an estimated 1% prevalence rate that is rising, she said.

“I have to say, the majority of the kids I see in my practice with hepatitis C are the children, typically, of a nurse—a health care provider who likely got it occupationally,” she noted.

New data suggest that prompt treatment with interferon and ribavirin may produce a sustained virologic response in up to 80% of patients with acute hepatitis C. “If you're sure of [acute infection], you want to treat them early,” she said.

Antibody testing has been available for nearly 20 years, but the antibody just signals exposure to the virus, not immunity. By 1994, Japanese researchers had characterized the virus particle, a single-stranded RNA molecule. At least 9 genotypes and 90 subtypes have been identified to date, with genotype 1, unfortunately, most prevalent in the U.S. population. Patients with this genotype are less responsive to treatment, she said.

Disclosures: None was reported.

Of those infected with hepatitis C virus, 80%-85% develop chronic hepatitis.

Source 2009 Cavallini/Custom Medical Stock Photo, All Rights Reserved

LAS VEGAS — Amid the alphabet soup of hepatitis virus types, the one that should most concern physicians these days is hepatitis C.

“This is going to be the big virus in the next 20 years in the U.S.,” Dr. Marsha H. Kay predicted at a meeting sponsored by the American Academy of Pediatrics.

Hepatitis C virus already infects 1.6% of the general U.S. population—4 million people—but “the vast majority of people who are infected do not know it,” said Dr. Kay, a pediatric gastroenterologist and director of pediatric endoscopy at the Cleveland Clinic Children's Hospital.

Known to be at risk are infants born to mothers with hepatitis C; young adult survivors of leukemia, childhood malignancies, and childhood cardiac surgery; hemophiliacs; dialysis patients; intravenous drug users; sexual partners of a person with hepatitis C; recipients of blood transfusions prior to 1989; first responders; and health care workers.

However, 32% of the current cases involve no known risk factor.

“We don't know exactly how this virus is transmitted,” said Dr. Kay.

There is no way to prevent hepatitis C (except for universal body fluid precautions) and there is no vaccine.

Among those infected, 80%-85% will develop chronic hepatitis, and of those, half will develop cirrhosis, putting them at highly elevated risk for hepatocellular carcinoma. Hepatitis C is already the leading cause of liver transplantation in the nation.

All things considered, the perfect storm of hepatitis C constitutes “a really terrible outcome compared to hepatitis B infection,” she said, adding, “I lose a lot of sleep about this.”

Among children, the leading cause of hepatitis C transmission is perinatal exposure, with transmission risk correlated to the mother's viral load at delivery.

Unfortunately, drugs used to treat acute hepatitis C are teratogenic and cannot be used during pregnancy. Some experts recommend avoiding fetal scalp monitoring and prolonging labor beyond 6 hours after the rupture of membranes to reduce the risk of transmission.

Breastfeeding, Dr. Kay said, is controversial. Hepatitis C acquired via perinatal transmission has an increased likelihood of becoming chronic.

Anti-HCV testing is ideally performed between 15 and 18 months of age. Although HCV RNA testing may be positive at 2 months and 6 months, positive anti-HCV at that time may reflect the mother's HCV status rather than the infant's HCV status.

Other patients who should be considered at risk in a primary care practice include young people who overcame serious illnesses early in life and those who received blood products before 1989.

That means the cardiac babies who are “doing great, and they're now 20 years old,” said Dr. Kay.

Individuals who received Gammagard (immune globulin) from a particular manufacturer during 1993 and 1994 may also be at risk.

Health care providers, especially those who work in emergency departments, surgery, or procedurally related specialties, have an estimated 1% prevalence rate that is rising, she said.

“I have to say, the majority of the kids I see in my practice with hepatitis C are the children, typically, of a nurse—a health care provider who likely got it occupationally,” she noted.

New data suggest that prompt treatment with interferon and ribavirin may produce a sustained virologic response in up to 80% of patients with acute hepatitis C. “If you're sure of [acute infection], you want to treat them early,” she said.

Antibody testing has been available for nearly 20 years, but the antibody just signals exposure to the virus, not immunity. By 1994, Japanese researchers had characterized the virus particle, a single-stranded RNA molecule. At least 9 genotypes and 90 subtypes have been identified to date, with genotype 1, unfortunately, most prevalent in the U.S. population. Patients with this genotype are less responsive to treatment, she said.

Disclosures: None was reported.

Of those infected with hepatitis C virus, 80%-85% develop chronic hepatitis.

Source 2009 Cavallini/Custom Medical Stock Photo, All Rights Reserved

LAS VEGAS — Amid the alphabet soup of hepatitis virus types, the one that should most concern physicians these days is hepatitis C.

“This is going to be the big virus in the next 20 years in the U.S.,” Dr. Marsha H. Kay predicted at a meeting sponsored by the American Academy of Pediatrics.

Hepatitis C virus already infects 1.6% of the general U.S. population—4 million people—but “the vast majority of people who are infected do not know it,” said Dr. Kay, a pediatric gastroenterologist and director of pediatric endoscopy at the Cleveland Clinic Children's Hospital.

Known to be at risk are infants born to mothers with hepatitis C; young adult survivors of leukemia, childhood malignancies, and childhood cardiac surgery; hemophiliacs; dialysis patients; intravenous drug users; sexual partners of a person with hepatitis C; recipients of blood transfusions prior to 1989; first responders; and health care workers.

However, 32% of the current cases involve no known risk factor.

“We don't know exactly how this virus is transmitted,” said Dr. Kay.

There is no way to prevent hepatitis C (except for universal body fluid precautions) and there is no vaccine.

Among those infected, 80%-85% will develop chronic hepatitis, and of those, half will develop cirrhosis, putting them at highly elevated risk for hepatocellular carcinoma. Hepatitis C is already the leading cause of liver transplantation in the nation.

All things considered, the perfect storm of hepatitis C constitutes “a really terrible outcome compared to hepatitis B infection,” she said, adding, “I lose a lot of sleep about this.”

Among children, the leading cause of hepatitis C transmission is perinatal exposure, with transmission risk correlated to the mother's viral load at delivery.

Unfortunately, drugs used to treat acute hepatitis C are teratogenic and cannot be used during pregnancy. Some experts recommend avoiding fetal scalp monitoring and prolonging labor beyond 6 hours after the rupture of membranes to reduce the risk of transmission.

Breastfeeding, Dr. Kay said, is controversial. Hepatitis C acquired via perinatal transmission has an increased likelihood of becoming chronic.

Anti-HCV testing is ideally performed between 15 and 18 months of age. Although HCV RNA testing may be positive at 2 months and 6 months, positive anti-HCV at that time may reflect the mother's HCV status rather than the infant's HCV status.

Other patients who should be considered at risk in a primary care practice include young people who overcame serious illnesses early in life and those who received blood products before 1989.

That means the cardiac babies who are “doing great, and they're now 20 years old,” said Dr. Kay.

Individuals who received Gammagard (immune globulin) from a particular manufacturer during 1993 and 1994 may also be at risk.

Health care providers, especially those who work in emergency departments, surgery, or procedurally related specialties, have an estimated 1% prevalence rate that is rising, she said.

“I have to say, the majority of the kids I see in my practice with hepatitis C are the children, typically, of a nurse—a health care provider who likely got it occupationally,” she noted.

New data suggest that prompt treatment with interferon and ribavirin may produce a sustained virologic response in up to 80% of patients with acute hepatitis C. “If you're sure of [acute infection], you want to treat them early,” she said.

Antibody testing has been available for nearly 20 years, but the antibody just signals exposure to the virus, not immunity. By 1994, Japanese researchers had characterized the virus particle, a single-stranded RNA molecule. At least 9 genotypes and 90 subtypes have been identified to date, with genotype 1, unfortunately, most prevalent in the U.S. population. Patients with this genotype are less responsive to treatment, she said.

Disclosures: None was reported.

Of those infected with hepatitis C virus, 80%-85% develop chronic hepatitis.

Source 2009 Cavallini/Custom Medical Stock Photo, All Rights Reserved