Osteoporosis

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic. The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants, she noted.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up. It's likely that reduced mobility and increased risk of falling play an important role in the pathogenesis of fractures in obese postmenopausal women, although this is an issue that needs further study, she observed.

In a separate presentation, Helena Johansson presented an analysis of BMI and fracture risk in 281,637 women drawn from 27 prospective, population-based cohort studies that were conducted in more than two dozen countries. The women were aged 20–105 years (mean age, 63 years).

A total of 18,441 osteoporotic fractures occurred in the study population during a mean 4.8 years of follow-up. After adjustment for bone mineral density, obesity proved to be a risk factor for fracture. For example, women with a BMI of 34 had an adjusted 14% increased risk of osteoporotic fracture, compared with those having a BMI of 26, an elevation in risk that, while modest, was statistically significant. And women having a BMI of 34 had a more impressive adjusted 60% increased risk of humerus or elbow fracture, added Ms. Johansson, a statistician at the University of Gothenburg (Sweden).

Dr. Compston declared having no relevant financial disclosures. GLOW is supported by grants from Sanofi-Aventis and Warner Chilcott. Ms. Johansson declared having no relevant financial disclosures.

Only 27% of obese GLOW participants with incident fractures were placed on bone-protective medication.

Source DR. COMPSTON

Incident fractures of the ankle and tibia were significantly more common in obese women.

Source ©Living Art Enterprises, LLC / Photo Researchers, Inc

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic. The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants, she noted.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up. It's likely that reduced mobility and increased risk of falling play an important role in the pathogenesis of fractures in obese postmenopausal women, although this is an issue that needs further study, she observed.

In a separate presentation, Helena Johansson presented an analysis of BMI and fracture risk in 281,637 women drawn from 27 prospective, population-based cohort studies that were conducted in more than two dozen countries. The women were aged 20–105 years (mean age, 63 years).

A total of 18,441 osteoporotic fractures occurred in the study population during a mean 4.8 years of follow-up. After adjustment for bone mineral density, obesity proved to be a risk factor for fracture. For example, women with a BMI of 34 had an adjusted 14% increased risk of osteoporotic fracture, compared with those having a BMI of 26, an elevation in risk that, while modest, was statistically significant. And women having a BMI of 34 had a more impressive adjusted 60% increased risk of humerus or elbow fracture, added Ms. Johansson, a statistician at the University of Gothenburg (Sweden).

Dr. Compston declared having no relevant financial disclosures. GLOW is supported by grants from Sanofi-Aventis and Warner Chilcott. Ms. Johansson declared having no relevant financial disclosures.

Only 27% of obese GLOW participants with incident fractures were placed on bone-protective medication.

Source DR. COMPSTON

Incident fractures of the ankle and tibia were significantly more common in obese women.

Source ©Living Art Enterprises, LLC / Photo Researchers, Inc

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic. The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants, she noted.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up. It's likely that reduced mobility and increased risk of falling play an important role in the pathogenesis of fractures in obese postmenopausal women, although this is an issue that needs further study, she observed.

In a separate presentation, Helena Johansson presented an analysis of BMI and fracture risk in 281,637 women drawn from 27 prospective, population-based cohort studies that were conducted in more than two dozen countries. The women were aged 20–105 years (mean age, 63 years).

A total of 18,441 osteoporotic fractures occurred in the study population during a mean 4.8 years of follow-up. After adjustment for bone mineral density, obesity proved to be a risk factor for fracture. For example, women with a BMI of 34 had an adjusted 14% increased risk of osteoporotic fracture, compared with those having a BMI of 26, an elevation in risk that, while modest, was statistically significant. And women having a BMI of 34 had a more impressive adjusted 60% increased risk of humerus or elbow fracture, added Ms. Johansson, a statistician at the University of Gothenburg (Sweden).

Dr. Compston declared having no relevant financial disclosures. GLOW is supported by grants from Sanofi-Aventis and Warner Chilcott. Ms. Johansson declared having no relevant financial disclosures.

Only 27% of obese GLOW participants with incident fractures were placed on bone-protective medication.

Source DR. COMPSTON

Incident fractures of the ankle and tibia were significantly more common in obese women.

Source ©Living Art Enterprises, LLC / Photo Researchers, Inc

Major Finding: New osteoporotic fractures occurred in 1.6% of men on zoledronic acid and in 4.9% of those on placebo after 2 years of either active treatment or placebo.

Data Source: Multinational, randomized, phase III clinical trial of 1,199 men with primary or secondary osteoporosis.

Disclosures: Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

“This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis,” said Dr. Steven Boonen in presenting the study results at the meeting.

“These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year,” added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers.

At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up.

The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction.

The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction, Dr. Boonen reported.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls, he said.

“All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis,” the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events, Dr. Boonen reported.

At present, zoledronic acid's approved indications include treatment to increase bone mass in men with osteoporosis.

Bone mineral density was roughly 6% greater at the spine in the zoledronic acid group.

Source DR. BOONEN

Major Finding: New osteoporotic fractures occurred in 1.6% of men on zoledronic acid and in 4.9% of those on placebo after 2 years of either active treatment or placebo.

Data Source: Multinational, randomized, phase III clinical trial of 1,199 men with primary or secondary osteoporosis.

Disclosures: Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

“This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis,” said Dr. Steven Boonen in presenting the study results at the meeting.

“These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year,” added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers.

At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up.

The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction.

The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction, Dr. Boonen reported.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls, he said.

“All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis,” the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events, Dr. Boonen reported.

At present, zoledronic acid's approved indications include treatment to increase bone mass in men with osteoporosis.

Bone mineral density was roughly 6% greater at the spine in the zoledronic acid group.

Source DR. BOONEN

Major Finding: New osteoporotic fractures occurred in 1.6% of men on zoledronic acid and in 4.9% of those on placebo after 2 years of either active treatment or placebo.

Data Source: Multinational, randomized, phase III clinical trial of 1,199 men with primary or secondary osteoporosis.

Disclosures: Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

“This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis,” said Dr. Steven Boonen in presenting the study results at the meeting.

“These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year,” added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers.

At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up.

The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction.

The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction, Dr. Boonen reported.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls, he said.

“All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis,” the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events, Dr. Boonen reported.

At present, zoledronic acid's approved indications include treatment to increase bone mass in men with osteoporosis.

Bone mineral density was roughly 6% greater at the spine in the zoledronic acid group.

Source DR. BOONEN

Major Finding: The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese, compared with 7.3% in the underweight group.

Data Source: A study of 44,534 postmenopausal women in the United States and nine other countries who are participating in the ongoing prospective observational GLOW study.

Disclosures: The GLOW study is supported by grants from Sanofi-Aventis and Warner Chilcott. Dr. Compston declared having no relevant financial disclosures.

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic.

The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up.

Obese women with an incident fracture had much higher rates of diabetes, asthma, and emphysema.

Source DR. COMPSTON

Major Finding: The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese, compared with 7.3% in the underweight group.

Data Source: A study of 44,534 postmenopausal women in the United States and nine other countries who are participating in the ongoing prospective observational GLOW study.

Disclosures: The GLOW study is supported by grants from Sanofi-Aventis and Warner Chilcott. Dr. Compston declared having no relevant financial disclosures.

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic.

The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up.

Obese women with an incident fracture had much higher rates of diabetes, asthma, and emphysema.

Source DR. COMPSTON

Major Finding: The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese, compared with 7.3% in the underweight group.

Data Source: A study of 44,534 postmenopausal women in the United States and nine other countries who are participating in the ongoing prospective observational GLOW study.

Disclosures: The GLOW study is supported by grants from Sanofi-Aventis and Warner Chilcott. Dr. Compston declared having no relevant financial disclosures.

DENVER – New data indicate that obesity in postmenopausal women doesn't protect against fractures, contrary to the conventional wisdom.

Indeed, postmenopausal obesity actually appears to be a risk factor for fractures at selected sites, Dr. Juliet E. Compston reported at the meeting.

This is a finding with major public health implications because of the growing obesity epidemic.

The ramifications are especially pressing in light of new evidence that obese postmenopausal women who experience a fracture are far less likely than nonobese women to be placed on bone-protective medication, said Dr. Compston, professor of bone medicine at the University of Cambridge (England).

She reported on a study of 44,534 postmenopausal women (mean age, 67 years) in the United States and nine other countries who are participating in the ongoing, prospective, observational GLOW (Global Longitudinal Study of Osteoporosis in Women). At enrollment, 23.4% of the women had a body mass index of 30 kg/m

The prevalence of fracture at baseline was 23% in obese women, 24% in nonobese women, and 32% in the underweight study population. The incidence of one or more new fractures during 2 years of follow-up was 6.4% in the obese and similar at 6.8% in the nonobese women, compared with 7.3% in the underweight group.

Thus, nearly one in four postmenopausal women with a fracture is obese. As the obesity rate continues to climb in the developed world, fractures in the obese will increasingly contribute to the overall burden of fractures in the postmenopausal population, Dr. Compston observed.

The higher prevalence and incidence of fracture in underweight postmenopausal women comes as no surprise; low BMI is recognized as a major risk factor for fracture. What was surprising, though, was that only 27% of obese GLOW participants with an incident fracture were placed on bone-protective medication for secondary prevention.

In contrast, the treatment rate in nonobese women with an incident fracture was 41%, and in underweight women it was 57%. The likely explanation for the markedly lower treatment rate in the obese group is the widespread belief that obesity protects against fractures, according to Dr. Compston.

Incident fractures of the ankle and tibia were significantly more common and wrist fractures were less common in obese women, compared with nonobese study participants.

The obese subjects with an incident fracture had significantly higher rates of several comorbid conditions – asthma, emphysema, and type 1 diabetes – than did nonobese women. They also were more likely than nonobese participants with an incident fracture to have a baseline history of two or more falls within the past 2 years. They had more mobility issues as well, as reflected in their increased rate of self-reported need for arm assistance in standing up.

Obese women with an incident fracture had much higher rates of diabetes, asthma, and emphysema.

Source DR. COMPSTON

SAN DIEGO – Physicians overall are doing a less than stellar job of recognizing glucocorticoid-induced osteoporosis and prescribing bone-protective medications for affected or high-risk patients.

But some specialties are doing significantly better than others.

"While many rheumatologists and endocrinologists are doing a pretty good job, we know that collectively, internationally, this still continues to be a major therapeutic dilemma, and steroids still constitute the most common form of drug-induced osteoporosis," Dr. Kenneth G. Saag declared at the annual meeting of the American Society for Bone and Mineral Research.

He cited a recent as-yet-published study led by University of Alabama epidemiologist Ryan C. Outman, who, together with his coinvestigators, analyzed 106,310 patients in the Medco Pharmacy database who were at high risk for glucocorticoid-induced osteoporosis (GIOP) by virtue of having received more than 90 days of systemic corticosteroid therapy during the study years of 2004-2007.

The primary study outcome was prescription of any form of anti-GIOP medication within 12 months after patients reached the 90-day mark of steroid therapy. The 12-month mark is the point on the therapeutic time line when, according to American College of Rheumatology guidelines, physicians are supposed to initiate bone-protective therapy.

The steroids were prescribed by a total of 53,766 physicians. During the 12-month window, the physicians ordered bone mineral density tests in just 4.6% of the patients, and 23.5% of patients received a prescription for an anti- GIOP medication, according to Dr. Saag, professor of medicine and epidemiology at the University of Alabama, Birmingham.

The results varied by physician specialty. In a multivariate analysis adjusted for patient age, gender, and other potential confounders, endocrinologists were 61% more likely to prescribe anti-GIOP medication for patients having more than 90 days of exposure to systemic steroids than were internists, who served as the reference standard. Rheumatologists were 59% more likely than internists to prescribe therapy.

Nephrologists, pulmonologists, and gastroenterologists were 37%, 34%, and 15%, respectively, more likely to have prescribed bone-protective medications for their at-risk patients than were internists. Dermatologists and physicians in all other specialties who prescribed steroids for longer than 90 days were, collectively, 22% less likely to introduce anti-GIOP therapy than were internists.

Rates of prescription of anti-GIOP medications were particularly low in men of all ages and in premenopausal women. During the 12 months after more than 90 days of exposure to systemic steroids, 36.8% of affected women aged 50 years or older were prescribed bone-protective medication, compared with 11.4% of affected women under age 50 years and 14.7% of men of any age, said Dr. Saag, who was not involved in the study.

"We’ve got a lot of work to do in terms of initiating therapy, but adherence is a big problem, too. Less than half of patients who start on any bone-protective drug are still taking it a year later," he said.

Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Physicians overall are doing a less than stellar job of recognizing glucocorticoid-induced osteoporosis and prescribing bone-protective medications for affected or high-risk patients.

But some specialties are doing significantly better than others.

"While many rheumatologists and endocrinologists are doing a pretty good job, we know that collectively, internationally, this still continues to be a major therapeutic dilemma, and steroids still constitute the most common form of drug-induced osteoporosis," Dr. Kenneth G. Saag declared at the annual meeting of the American Society for Bone and Mineral Research.

He cited a recent as-yet-published study led by University of Alabama epidemiologist Ryan C. Outman, who, together with his coinvestigators, analyzed 106,310 patients in the Medco Pharmacy database who were at high risk for glucocorticoid-induced osteoporosis (GIOP) by virtue of having received more than 90 days of systemic corticosteroid therapy during the study years of 2004-2007.

The primary study outcome was prescription of any form of anti-GIOP medication within 12 months after patients reached the 90-day mark of steroid therapy. The 12-month mark is the point on the therapeutic time line when, according to American College of Rheumatology guidelines, physicians are supposed to initiate bone-protective therapy.

The steroids were prescribed by a total of 53,766 physicians. During the 12-month window, the physicians ordered bone mineral density tests in just 4.6% of the patients, and 23.5% of patients received a prescription for an anti- GIOP medication, according to Dr. Saag, professor of medicine and epidemiology at the University of Alabama, Birmingham.

The results varied by physician specialty. In a multivariate analysis adjusted for patient age, gender, and other potential confounders, endocrinologists were 61% more likely to prescribe anti-GIOP medication for patients having more than 90 days of exposure to systemic steroids than were internists, who served as the reference standard. Rheumatologists were 59% more likely than internists to prescribe therapy.

Nephrologists, pulmonologists, and gastroenterologists were 37%, 34%, and 15%, respectively, more likely to have prescribed bone-protective medications for their at-risk patients than were internists. Dermatologists and physicians in all other specialties who prescribed steroids for longer than 90 days were, collectively, 22% less likely to introduce anti-GIOP therapy than were internists.

Rates of prescription of anti-GIOP medications were particularly low in men of all ages and in premenopausal women. During the 12 months after more than 90 days of exposure to systemic steroids, 36.8% of affected women aged 50 years or older were prescribed bone-protective medication, compared with 11.4% of affected women under age 50 years and 14.7% of men of any age, said Dr. Saag, who was not involved in the study.

"We’ve got a lot of work to do in terms of initiating therapy, but adherence is a big problem, too. Less than half of patients who start on any bone-protective drug are still taking it a year later," he said.

Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Physicians overall are doing a less than stellar job of recognizing glucocorticoid-induced osteoporosis and prescribing bone-protective medications for affected or high-risk patients.

But some specialties are doing significantly better than others.

"While many rheumatologists and endocrinologists are doing a pretty good job, we know that collectively, internationally, this still continues to be a major therapeutic dilemma, and steroids still constitute the most common form of drug-induced osteoporosis," Dr. Kenneth G. Saag declared at the annual meeting of the American Society for Bone and Mineral Research.

He cited a recent as-yet-published study led by University of Alabama epidemiologist Ryan C. Outman, who, together with his coinvestigators, analyzed 106,310 patients in the Medco Pharmacy database who were at high risk for glucocorticoid-induced osteoporosis (GIOP) by virtue of having received more than 90 days of systemic corticosteroid therapy during the study years of 2004-2007.

The primary study outcome was prescription of any form of anti-GIOP medication within 12 months after patients reached the 90-day mark of steroid therapy. The 12-month mark is the point on the therapeutic time line when, according to American College of Rheumatology guidelines, physicians are supposed to initiate bone-protective therapy.

The steroids were prescribed by a total of 53,766 physicians. During the 12-month window, the physicians ordered bone mineral density tests in just 4.6% of the patients, and 23.5% of patients received a prescription for an anti- GIOP medication, according to Dr. Saag, professor of medicine and epidemiology at the University of Alabama, Birmingham.

The results varied by physician specialty. In a multivariate analysis adjusted for patient age, gender, and other potential confounders, endocrinologists were 61% more likely to prescribe anti-GIOP medication for patients having more than 90 days of exposure to systemic steroids than were internists, who served as the reference standard. Rheumatologists were 59% more likely than internists to prescribe therapy.

Nephrologists, pulmonologists, and gastroenterologists were 37%, 34%, and 15%, respectively, more likely to have prescribed bone-protective medications for their at-risk patients than were internists. Dermatologists and physicians in all other specialties who prescribed steroids for longer than 90 days were, collectively, 22% less likely to introduce anti-GIOP therapy than were internists.

Rates of prescription of anti-GIOP medications were particularly low in men of all ages and in premenopausal women. During the 12 months after more than 90 days of exposure to systemic steroids, 36.8% of affected women aged 50 years or older were prescribed bone-protective medication, compared with 11.4% of affected women under age 50 years and 14.7% of men of any age, said Dr. Saag, who was not involved in the study.

"We’ve got a lot of work to do in terms of initiating therapy, but adherence is a big problem, too. Less than half of patients who start on any bone-protective drug are still taking it a year later," he said.

Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Teriparatide has received a boost in status as a preferentially effective treatment for glucocorticoid-induced osteoporosis in the form of a second, confirmatory, randomized double-blind trial demonstrating the anabolic agent achieves substantially greater increases in bone mineral density compared to a bisphosphonate.

One of these studies also included fracture rates as a preplanned secondary endpoint; the trial demonstrated a significant reduction in vertebral fractures with teriparatide (Forteo) as compared to alendronate (Fosamax).

These positive study findings are bolstered by a biologically plausible mechanism of benefit, Dr. Kenneth G. Saag observed at the annual meeting of the American Society for Bone and Mineral Research.

"Based upon the pathogenesis of glucocorticoid-induced osteoporosis [(GIOP)], we think that an anabolic agent makes some sense. It may be beneficial to stimulate osteoblasts to promote new bone formation," said Dr. Saag, professor of medicine and epidemiology at the University of Alabama at Birmingham.

Steroids are known to have apoptosis-mediated deleterious effects on both osteocytes and osteoblasts that lead to decline in bone function and an abrupt increase in fracture risk independent of bone mineral density (BMD). Osteoclasts are also unfavorably impacted due to crosstalk and the indirect effects of sex steroids, insulin-like growth factor, and a modest effect of secondary hyperparathyroidism mediated through altered calcium absorption. In addition, higher-dose steroids have adverse effects upon muscle that can independently lead to a higher fracture rate, the rheumatologist explained.

The FDA has approved alendronate, zoledronic acid (Reclast), and risedronate (Actonel) for treatment GIOP. More recently, raloxifene (Evista) has joined the ranks of agents shown to increase BMD in patients on long-term steroids; this came in the form of a double-blind, placebo-controlled, 12-month study (Ann. Rheum. Dis. 2011;70:778-84).

Subcutaneous daily teriparatide for up to 2 years also has the approval of the Food and Drug Administration for use in adults at high fracture risk because they are on sustained systemic steroid therapy.

There is no definitive study demonstrating that any of these agents actually prevents fractures in patients with GIOP. Nor is it likely such a study will be undertaken. Such trials require large numbers of patients and lengthy follow-up, and pharmaceutical companies have little incentive to mount such a costly project given that the medications are already approved for use in patients on steroids, Dr. Saag noted.

However, data from a study in which Dr. Saag was lead investigator showed that teriparatide-treated patients had significantly fewer vertebral fractures than those assigned to alendronate. The study was a 36-month randomized, double-blind, clinical trial that assessed fracture rates as a preplanned secondary endpoint. The radiographic and clinical vertebral fracture rates in 169 alendronate-treated patients were 7.7% and 2.4%, respectively, compared to 1.7% and 0% in 173 teriparatide-treated patients (P = .007 and .037). No significant difference in nonvertebral fractures was found between the two treatment arms.

The primary study endpoint was the change in BMD from baseline. Here again teriparatide proved significantly more effective than the bisphosphonate, with a mean 11% increase at the lumbar spine, compared to 5.3% with alendronate. Teriparatide-treated patients also had a 5.2% increase in BMD at the total hip and a 6.3% boost at the femoral neck, compared to 2.7% and 3.4%, respectively, with alendronate (Arthritis Rheum. 2009;60:3346-55).

Confirmation of teriparatide’s superior BMD-building effect came from the EuroGIOPs trial presented by Dr. Claus C. Glüer at the ASBMR meeting.

EuroGIOPS was an 18-month, open-label, phase III clinical trial in which 92 men with GIOP were randomized to teriparatide or risedronate. At 6 months the mean increase in lumbar spine BMD was 5.7% in the teriparatide group, compared with 3.3% in the risedronate arm. At 18 months – the primary study endpoint – the teriparatide group averaged a 16.3% BMD increase over baseline, while the risedronate arm had a 3.8% rise.

Intriguingly, new clinical fractures occurred during 18 months of therapy in 5 patients on risedronate and none on teriparatide, a difference that came within a hair of statistical significance (P = .056).

Bone strength as formally measured in terms of anterior bending, axial compression, and axial torsion was also significantly greater in the teriparatide group, according to Dr. Glüer, who is professor of medical physics at the department of diagnostic radiology, University Hospital Schleswig-Holstein in Kiel, Germany.

The 2010 update of the American College of Rheumatology guidelines for the prevention and treatment of GIOP recommend bisphosphonates but not teriparatide for older adults at high risk of fracture who are taking less than 5 mg/day of prednisone for less than 1 month (Arthritis Care Res. 2010;62:1515-26). The ACR guidelines recommend reserving use of teriparatide for high-risk patients – that is, those with a prevalent fracture or a World Health Organization Fracture Risk Assessment Tool (FRAX) score indicative of a greater than 20% 10-year risk of a major osteoporotic fracture – who are on at least 6 mg/day of prednisone for less than 1 month or on any dose of glucocorticoids for longer than 1 month.

Although Dr. Saag was a coauthor of the ACR guidelines, he disagreed with this particular one in light of his own clinical trial findings as well as evidence that BMD loss and fracture risk increase early on after starting steroids, and at lower doses than previously thought problematic. So he was pleased to see a new commentary on the ACR guidelines published by the Professional Practice Committee of the ASBMR. The review recommends teriparatide or any of the bisphosphonates for high-risk patients, period.

Dr. Saag, who wasn’t involved in the ASBMR review, recommended it as useful reading both for its areas of agreement with the ACR guidelines as well as for raising several patient scenarios in which the ASBMR committee believes the ACR recommendations either don’t apply or might be improved upon.

The ASBMR commentary also lays out a research agenda, identifying key areas for future study. For example, what’s the best management strategy in lupus patients and others who may need to be on systemic steroids for a decade or more, given that teriparatide is only FDA approved for 2 years of daily use and the clinical trials of bisphosphonates for GIOPS were only 1 or 2 years long (J. Bone Miner. Res. 2011;26:1989-96).

Dr. Glüer declared having no financial conflicts regarding the Eli Lilly-funded EuroGIOPs trial. Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Teriparatide has received a boost in status as a preferentially effective treatment for glucocorticoid-induced osteoporosis in the form of a second, confirmatory, randomized double-blind trial demonstrating the anabolic agent achieves substantially greater increases in bone mineral density compared to a bisphosphonate.

One of these studies also included fracture rates as a preplanned secondary endpoint; the trial demonstrated a significant reduction in vertebral fractures with teriparatide (Forteo) as compared to alendronate (Fosamax).

These positive study findings are bolstered by a biologically plausible mechanism of benefit, Dr. Kenneth G. Saag observed at the annual meeting of the American Society for Bone and Mineral Research.

"Based upon the pathogenesis of glucocorticoid-induced osteoporosis [(GIOP)], we think that an anabolic agent makes some sense. It may be beneficial to stimulate osteoblasts to promote new bone formation," said Dr. Saag, professor of medicine and epidemiology at the University of Alabama at Birmingham.

Steroids are known to have apoptosis-mediated deleterious effects on both osteocytes and osteoblasts that lead to decline in bone function and an abrupt increase in fracture risk independent of bone mineral density (BMD). Osteoclasts are also unfavorably impacted due to crosstalk and the indirect effects of sex steroids, insulin-like growth factor, and a modest effect of secondary hyperparathyroidism mediated through altered calcium absorption. In addition, higher-dose steroids have adverse effects upon muscle that can independently lead to a higher fracture rate, the rheumatologist explained.

The FDA has approved alendronate, zoledronic acid (Reclast), and risedronate (Actonel) for treatment GIOP. More recently, raloxifene (Evista) has joined the ranks of agents shown to increase BMD in patients on long-term steroids; this came in the form of a double-blind, placebo-controlled, 12-month study (Ann. Rheum. Dis. 2011;70:778-84).

Subcutaneous daily teriparatide for up to 2 years also has the approval of the Food and Drug Administration for use in adults at high fracture risk because they are on sustained systemic steroid therapy.

There is no definitive study demonstrating that any of these agents actually prevents fractures in patients with GIOP. Nor is it likely such a study will be undertaken. Such trials require large numbers of patients and lengthy follow-up, and pharmaceutical companies have little incentive to mount such a costly project given that the medications are already approved for use in patients on steroids, Dr. Saag noted.

However, data from a study in which Dr. Saag was lead investigator showed that teriparatide-treated patients had significantly fewer vertebral fractures than those assigned to alendronate. The study was a 36-month randomized, double-blind, clinical trial that assessed fracture rates as a preplanned secondary endpoint. The radiographic and clinical vertebral fracture rates in 169 alendronate-treated patients were 7.7% and 2.4%, respectively, compared to 1.7% and 0% in 173 teriparatide-treated patients (P = .007 and .037). No significant difference in nonvertebral fractures was found between the two treatment arms.

The primary study endpoint was the change in BMD from baseline. Here again teriparatide proved significantly more effective than the bisphosphonate, with a mean 11% increase at the lumbar spine, compared to 5.3% with alendronate. Teriparatide-treated patients also had a 5.2% increase in BMD at the total hip and a 6.3% boost at the femoral neck, compared to 2.7% and 3.4%, respectively, with alendronate (Arthritis Rheum. 2009;60:3346-55).

Confirmation of teriparatide’s superior BMD-building effect came from the EuroGIOPs trial presented by Dr. Claus C. Glüer at the ASBMR meeting.

EuroGIOPS was an 18-month, open-label, phase III clinical trial in which 92 men with GIOP were randomized to teriparatide or risedronate. At 6 months the mean increase in lumbar spine BMD was 5.7% in the teriparatide group, compared with 3.3% in the risedronate arm. At 18 months – the primary study endpoint – the teriparatide group averaged a 16.3% BMD increase over baseline, while the risedronate arm had a 3.8% rise.

Intriguingly, new clinical fractures occurred during 18 months of therapy in 5 patients on risedronate and none on teriparatide, a difference that came within a hair of statistical significance (P = .056).

Bone strength as formally measured in terms of anterior bending, axial compression, and axial torsion was also significantly greater in the teriparatide group, according to Dr. Glüer, who is professor of medical physics at the department of diagnostic radiology, University Hospital Schleswig-Holstein in Kiel, Germany.

The 2010 update of the American College of Rheumatology guidelines for the prevention and treatment of GIOP recommend bisphosphonates but not teriparatide for older adults at high risk of fracture who are taking less than 5 mg/day of prednisone for less than 1 month (Arthritis Care Res. 2010;62:1515-26). The ACR guidelines recommend reserving use of teriparatide for high-risk patients – that is, those with a prevalent fracture or a World Health Organization Fracture Risk Assessment Tool (FRAX) score indicative of a greater than 20% 10-year risk of a major osteoporotic fracture – who are on at least 6 mg/day of prednisone for less than 1 month or on any dose of glucocorticoids for longer than 1 month.

Although Dr. Saag was a coauthor of the ACR guidelines, he disagreed with this particular one in light of his own clinical trial findings as well as evidence that BMD loss and fracture risk increase early on after starting steroids, and at lower doses than previously thought problematic. So he was pleased to see a new commentary on the ACR guidelines published by the Professional Practice Committee of the ASBMR. The review recommends teriparatide or any of the bisphosphonates for high-risk patients, period.

Dr. Saag, who wasn’t involved in the ASBMR review, recommended it as useful reading both for its areas of agreement with the ACR guidelines as well as for raising several patient scenarios in which the ASBMR committee believes the ACR recommendations either don’t apply or might be improved upon.

The ASBMR commentary also lays out a research agenda, identifying key areas for future study. For example, what’s the best management strategy in lupus patients and others who may need to be on systemic steroids for a decade or more, given that teriparatide is only FDA approved for 2 years of daily use and the clinical trials of bisphosphonates for GIOPS were only 1 or 2 years long (J. Bone Miner. Res. 2011;26:1989-96).

Dr. Glüer declared having no financial conflicts regarding the Eli Lilly-funded EuroGIOPs trial. Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Teriparatide has received a boost in status as a preferentially effective treatment for glucocorticoid-induced osteoporosis in the form of a second, confirmatory, randomized double-blind trial demonstrating the anabolic agent achieves substantially greater increases in bone mineral density compared to a bisphosphonate.

One of these studies also included fracture rates as a preplanned secondary endpoint; the trial demonstrated a significant reduction in vertebral fractures with teriparatide (Forteo) as compared to alendronate (Fosamax).

These positive study findings are bolstered by a biologically plausible mechanism of benefit, Dr. Kenneth G. Saag observed at the annual meeting of the American Society for Bone and Mineral Research.

"Based upon the pathogenesis of glucocorticoid-induced osteoporosis [(GIOP)], we think that an anabolic agent makes some sense. It may be beneficial to stimulate osteoblasts to promote new bone formation," said Dr. Saag, professor of medicine and epidemiology at the University of Alabama at Birmingham.

Steroids are known to have apoptosis-mediated deleterious effects on both osteocytes and osteoblasts that lead to decline in bone function and an abrupt increase in fracture risk independent of bone mineral density (BMD). Osteoclasts are also unfavorably impacted due to crosstalk and the indirect effects of sex steroids, insulin-like growth factor, and a modest effect of secondary hyperparathyroidism mediated through altered calcium absorption. In addition, higher-dose steroids have adverse effects upon muscle that can independently lead to a higher fracture rate, the rheumatologist explained.

The FDA has approved alendronate, zoledronic acid (Reclast), and risedronate (Actonel) for treatment GIOP. More recently, raloxifene (Evista) has joined the ranks of agents shown to increase BMD in patients on long-term steroids; this came in the form of a double-blind, placebo-controlled, 12-month study (Ann. Rheum. Dis. 2011;70:778-84).

Subcutaneous daily teriparatide for up to 2 years also has the approval of the Food and Drug Administration for use in adults at high fracture risk because they are on sustained systemic steroid therapy.

There is no definitive study demonstrating that any of these agents actually prevents fractures in patients with GIOP. Nor is it likely such a study will be undertaken. Such trials require large numbers of patients and lengthy follow-up, and pharmaceutical companies have little incentive to mount such a costly project given that the medications are already approved for use in patients on steroids, Dr. Saag noted.

However, data from a study in which Dr. Saag was lead investigator showed that teriparatide-treated patients had significantly fewer vertebral fractures than those assigned to alendronate. The study was a 36-month randomized, double-blind, clinical trial that assessed fracture rates as a preplanned secondary endpoint. The radiographic and clinical vertebral fracture rates in 169 alendronate-treated patients were 7.7% and 2.4%, respectively, compared to 1.7% and 0% in 173 teriparatide-treated patients (P = .007 and .037). No significant difference in nonvertebral fractures was found between the two treatment arms.

The primary study endpoint was the change in BMD from baseline. Here again teriparatide proved significantly more effective than the bisphosphonate, with a mean 11% increase at the lumbar spine, compared to 5.3% with alendronate. Teriparatide-treated patients also had a 5.2% increase in BMD at the total hip and a 6.3% boost at the femoral neck, compared to 2.7% and 3.4%, respectively, with alendronate (Arthritis Rheum. 2009;60:3346-55).

Confirmation of teriparatide’s superior BMD-building effect came from the EuroGIOPs trial presented by Dr. Claus C. Glüer at the ASBMR meeting.

EuroGIOPS was an 18-month, open-label, phase III clinical trial in which 92 men with GIOP were randomized to teriparatide or risedronate. At 6 months the mean increase in lumbar spine BMD was 5.7% in the teriparatide group, compared with 3.3% in the risedronate arm. At 18 months – the primary study endpoint – the teriparatide group averaged a 16.3% BMD increase over baseline, while the risedronate arm had a 3.8% rise.

Intriguingly, new clinical fractures occurred during 18 months of therapy in 5 patients on risedronate and none on teriparatide, a difference that came within a hair of statistical significance (P = .056).

Bone strength as formally measured in terms of anterior bending, axial compression, and axial torsion was also significantly greater in the teriparatide group, according to Dr. Glüer, who is professor of medical physics at the department of diagnostic radiology, University Hospital Schleswig-Holstein in Kiel, Germany.

The 2010 update of the American College of Rheumatology guidelines for the prevention and treatment of GIOP recommend bisphosphonates but not teriparatide for older adults at high risk of fracture who are taking less than 5 mg/day of prednisone for less than 1 month (Arthritis Care Res. 2010;62:1515-26). The ACR guidelines recommend reserving use of teriparatide for high-risk patients – that is, those with a prevalent fracture or a World Health Organization Fracture Risk Assessment Tool (FRAX) score indicative of a greater than 20% 10-year risk of a major osteoporotic fracture – who are on at least 6 mg/day of prednisone for less than 1 month or on any dose of glucocorticoids for longer than 1 month.

Although Dr. Saag was a coauthor of the ACR guidelines, he disagreed with this particular one in light of his own clinical trial findings as well as evidence that BMD loss and fracture risk increase early on after starting steroids, and at lower doses than previously thought problematic. So he was pleased to see a new commentary on the ACR guidelines published by the Professional Practice Committee of the ASBMR. The review recommends teriparatide or any of the bisphosphonates for high-risk patients, period.

Dr. Saag, who wasn’t involved in the ASBMR review, recommended it as useful reading both for its areas of agreement with the ACR guidelines as well as for raising several patient scenarios in which the ASBMR committee believes the ACR recommendations either don’t apply or might be improved upon.

The ASBMR commentary also lays out a research agenda, identifying key areas for future study. For example, what’s the best management strategy in lupus patients and others who may need to be on systemic steroids for a decade or more, given that teriparatide is only FDA approved for 2 years of daily use and the clinical trials of bisphosphonates for GIOPS were only 1 or 2 years long (J. Bone Miner. Res. 2011;26:1989-96).

Dr. Glüer declared having no financial conflicts regarding the Eli Lilly-funded EuroGIOPs trial. Dr. Saag disclosed that he has received research grants from and serves as a paid consultant to Amgen, Eli Lilly, Merck, and Novartis.

SAN DIEGO – Heart failure constitutes a previously unrecognized independent risk factor for major osteoporotic fractures, according to a Canadian cohort study.

"Patients with heart failure have double the 5-year risk of fracture," compared with those without heart failure. And "patients with heart failure have lower bone mineral density at every skeletal site at the time of their first test," compared with those without heart failure. "Finally, neither differences in bone mass nor shared risk factors [are enough] to explain the increased risk," said Dr. Sumit Majumdar at the annual meeting of the American Society for Bone and Mineral Research.

He presented a population-based cohort study that included all Manitobans older than age 50 years who had their first bone mineral density test in 1998-2009. The study earned him the 2011 ASBMR Most Outstanding Clinical Abstract Award.

Overall, 4% of the nearly 46,000 Manitobans who had an initial bone minteral density (BMD) test during the study years were identified as having recent-onset heart failure (that is, heart failure diagnosed within the previous 2 years). There were 2,703 new fractures in the study population during a median 5 years of follow-up. The recent heart failure group had a 10% incidence of major nontraumatic fractures of the upper extremities, vertebrae, and hip during the 5 years following the first BMD test, compared with a 5% incidence in subjects without heart failure.

The median time to first fracture in the heart failure group was 3.6 years. The curves describing fracture incidence started to diverge soon after the first BMD test and continued to widen throughout the maximum 10 years of follow-up, reported Dr. Majumdar, professor of general internal medicine at the University of Alberta, Edmonton.

Patients with heart failure had more of all the standard risk factors for osteoporosis (except weight) than did subjects without heart failure. They were significantly older (mean age, 74 vs. 66 years) and 21% of them had a prior major osteoporotic fracture, compared with 13% of those without heart failure. Some 12% of heart failure patients had been on systemic corticosteroids for longer than 90 days, compared with 4% of those without heart failure.

Moreover, 40% of heart failure patients had osteoporosis at the time of their first BMD measurement (defined as a T score less than –2.5 at any skeletal site), compared with 29% of individuals without heart failure. T scores were significantly lower in the heart failure group at all measured sites.

"A diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture."

On the other hand, nearly every medication used in treating heart failure has previously been shown to increase BMD and to reduce fracture risk, with the exception of loop diuretics, which reduce BMD.

In addition, osteoporosis and heart failure are common, chronic conditions that share several etiologic risk factors, including older age, postmenopausal status, diabetes, and smoking, he continued.

The unadjusted risk of a major osteoporotic fracture was increased 2.45-fold in patients with heart failure. But upon adjustment in a multivariate analysis for nearly 30 potential confounders including age, sex, osteoporosis-related factors, medications, comorbidities, and total hip BMD, heart failure remained independently associated with a highly significant 28% increased risk of major osteoporotic fractures.

A disturbing finding of the study was that a mere 14% of heart failure patients who experienced an osteoporotic fracture were then placed on a bisphosphonate or other bone-protective therapy. Bisphosphonates had no association with mortality in the heart failure group.

"For clinicians, I think our study means we need to start understanding that a diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture, in our data. And we need to learn that patients with heart failure are easily diagnosed and need much more attention to their bone health," Dr. Majumdar observed.

This study also opens up research opportunities for bench scientists, as the Manitoba database contains no information on patients’ aldosterone, parathyroid hormone, or vitamin D levels, or indeed on any other variables that might provide a mechanistic explanation for the link between heart failure and osteoporotic fractures.

"Ours is an example of bedside-to-bench research," he said.

In that vein, one audience member noted that increased adrenergic drive is a hallmark of heart failure. He wondered if heart failure patients on beta-blocker therapy had a lower fracture risk. Dr. Majumdar replied that he and his coinvestigators had had the same thought. However, when they specifically compared the nearly 35% of heart failure patients who were on a beta-blocker vs. those who weren’t, they found that fracture rates in the two groups weren’t significantly different.

Dr. Majumdar declared having no relevant financial interests.

SAN DIEGO – Heart failure constitutes a previously unrecognized independent risk factor for major osteoporotic fractures, according to a Canadian cohort study.

"Patients with heart failure have double the 5-year risk of fracture," compared with those without heart failure. And "patients with heart failure have lower bone mineral density at every skeletal site at the time of their first test," compared with those without heart failure. "Finally, neither differences in bone mass nor shared risk factors [are enough] to explain the increased risk," said Dr. Sumit Majumdar at the annual meeting of the American Society for Bone and Mineral Research.

He presented a population-based cohort study that included all Manitobans older than age 50 years who had their first bone mineral density test in 1998-2009. The study earned him the 2011 ASBMR Most Outstanding Clinical Abstract Award.

Overall, 4% of the nearly 46,000 Manitobans who had an initial bone minteral density (BMD) test during the study years were identified as having recent-onset heart failure (that is, heart failure diagnosed within the previous 2 years). There were 2,703 new fractures in the study population during a median 5 years of follow-up. The recent heart failure group had a 10% incidence of major nontraumatic fractures of the upper extremities, vertebrae, and hip during the 5 years following the first BMD test, compared with a 5% incidence in subjects without heart failure.

The median time to first fracture in the heart failure group was 3.6 years. The curves describing fracture incidence started to diverge soon after the first BMD test and continued to widen throughout the maximum 10 years of follow-up, reported Dr. Majumdar, professor of general internal medicine at the University of Alberta, Edmonton.

Patients with heart failure had more of all the standard risk factors for osteoporosis (except weight) than did subjects without heart failure. They were significantly older (mean age, 74 vs. 66 years) and 21% of them had a prior major osteoporotic fracture, compared with 13% of those without heart failure. Some 12% of heart failure patients had been on systemic corticosteroids for longer than 90 days, compared with 4% of those without heart failure.

Moreover, 40% of heart failure patients had osteoporosis at the time of their first BMD measurement (defined as a T score less than –2.5 at any skeletal site), compared with 29% of individuals without heart failure. T scores were significantly lower in the heart failure group at all measured sites.

"A diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture."

On the other hand, nearly every medication used in treating heart failure has previously been shown to increase BMD and to reduce fracture risk, with the exception of loop diuretics, which reduce BMD.

In addition, osteoporosis and heart failure are common, chronic conditions that share several etiologic risk factors, including older age, postmenopausal status, diabetes, and smoking, he continued.

The unadjusted risk of a major osteoporotic fracture was increased 2.45-fold in patients with heart failure. But upon adjustment in a multivariate analysis for nearly 30 potential confounders including age, sex, osteoporosis-related factors, medications, comorbidities, and total hip BMD, heart failure remained independently associated with a highly significant 28% increased risk of major osteoporotic fractures.

A disturbing finding of the study was that a mere 14% of heart failure patients who experienced an osteoporotic fracture were then placed on a bisphosphonate or other bone-protective therapy. Bisphosphonates had no association with mortality in the heart failure group.

"For clinicians, I think our study means we need to start understanding that a diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture, in our data. And we need to learn that patients with heart failure are easily diagnosed and need much more attention to their bone health," Dr. Majumdar observed.

This study also opens up research opportunities for bench scientists, as the Manitoba database contains no information on patients’ aldosterone, parathyroid hormone, or vitamin D levels, or indeed on any other variables that might provide a mechanistic explanation for the link between heart failure and osteoporotic fractures.

"Ours is an example of bedside-to-bench research," he said.

In that vein, one audience member noted that increased adrenergic drive is a hallmark of heart failure. He wondered if heart failure patients on beta-blocker therapy had a lower fracture risk. Dr. Majumdar replied that he and his coinvestigators had had the same thought. However, when they specifically compared the nearly 35% of heart failure patients who were on a beta-blocker vs. those who weren’t, they found that fracture rates in the two groups weren’t significantly different.

Dr. Majumdar declared having no relevant financial interests.

SAN DIEGO – Heart failure constitutes a previously unrecognized independent risk factor for major osteoporotic fractures, according to a Canadian cohort study.

"Patients with heart failure have double the 5-year risk of fracture," compared with those without heart failure. And "patients with heart failure have lower bone mineral density at every skeletal site at the time of their first test," compared with those without heart failure. "Finally, neither differences in bone mass nor shared risk factors [are enough] to explain the increased risk," said Dr. Sumit Majumdar at the annual meeting of the American Society for Bone and Mineral Research.

He presented a population-based cohort study that included all Manitobans older than age 50 years who had their first bone mineral density test in 1998-2009. The study earned him the 2011 ASBMR Most Outstanding Clinical Abstract Award.

Overall, 4% of the nearly 46,000 Manitobans who had an initial bone minteral density (BMD) test during the study years were identified as having recent-onset heart failure (that is, heart failure diagnosed within the previous 2 years). There were 2,703 new fractures in the study population during a median 5 years of follow-up. The recent heart failure group had a 10% incidence of major nontraumatic fractures of the upper extremities, vertebrae, and hip during the 5 years following the first BMD test, compared with a 5% incidence in subjects without heart failure.

The median time to first fracture in the heart failure group was 3.6 years. The curves describing fracture incidence started to diverge soon after the first BMD test and continued to widen throughout the maximum 10 years of follow-up, reported Dr. Majumdar, professor of general internal medicine at the University of Alberta, Edmonton.

Patients with heart failure had more of all the standard risk factors for osteoporosis (except weight) than did subjects without heart failure. They were significantly older (mean age, 74 vs. 66 years) and 21% of them had a prior major osteoporotic fracture, compared with 13% of those without heart failure. Some 12% of heart failure patients had been on systemic corticosteroids for longer than 90 days, compared with 4% of those without heart failure.

Moreover, 40% of heart failure patients had osteoporosis at the time of their first BMD measurement (defined as a T score less than –2.5 at any skeletal site), compared with 29% of individuals without heart failure. T scores were significantly lower in the heart failure group at all measured sites.

"A diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture."

On the other hand, nearly every medication used in treating heart failure has previously been shown to increase BMD and to reduce fracture risk, with the exception of loop diuretics, which reduce BMD.

In addition, osteoporosis and heart failure are common, chronic conditions that share several etiologic risk factors, including older age, postmenopausal status, diabetes, and smoking, he continued.

The unadjusted risk of a major osteoporotic fracture was increased 2.45-fold in patients with heart failure. But upon adjustment in a multivariate analysis for nearly 30 potential confounders including age, sex, osteoporosis-related factors, medications, comorbidities, and total hip BMD, heart failure remained independently associated with a highly significant 28% increased risk of major osteoporotic fractures.

A disturbing finding of the study was that a mere 14% of heart failure patients who experienced an osteoporotic fracture were then placed on a bisphosphonate or other bone-protective therapy. Bisphosphonates had no association with mortality in the heart failure group.

"For clinicians, I think our study means we need to start understanding that a diagnosis of heart failure portends an increased risk of fracture greater than rheumatoid arthritis or prior fracture, in our data. And we need to learn that patients with heart failure are easily diagnosed and need much more attention to their bone health," Dr. Majumdar observed.

This study also opens up research opportunities for bench scientists, as the Manitoba database contains no information on patients’ aldosterone, parathyroid hormone, or vitamin D levels, or indeed on any other variables that might provide a mechanistic explanation for the link between heart failure and osteoporotic fractures.

"Ours is an example of bedside-to-bench research," he said.

In that vein, one audience member noted that increased adrenergic drive is a hallmark of heart failure. He wondered if heart failure patients on beta-blocker therapy had a lower fracture risk. Dr. Majumdar replied that he and his coinvestigators had had the same thought. However, when they specifically compared the nearly 35% of heart failure patients who were on a beta-blocker vs. those who weren’t, they found that fracture rates in the two groups weren’t significantly different.

Dr. Majumdar declared having no relevant financial interests.

Mortality risk doubles during the year after hip fracture among women aged 65 years and older, then returns to baseline in many women; but this pattern doesn’t apply in all cases, according to a report published online Sept. 26 in Archives of Internal Medicine.

Mortality risk after sustaining a hip fracture differs by patient age, underlying health, and the interval since the injury occurred in this population, said Dr. Erin S. LeBlanc of the center for health research at Kaiser Permanente Northwest Region, Portland, Ore., and her associates.

Previous studies of this issue have had methodological limitations and have yielded inconsistent results. Most have shown increased short-term mortality, but have had mixed findings on long-term mortality. "Our data suggest that previous mixed results ... may have been the result of differences in the underlying age and health status of the population being studied," Dr. LeBlanc and her colleagues said (Arch. Intern. Med. 2011 Sept. 26 [doi:10.1001/archinternmed.2011.447]).

They used data from the SOF (Study of Osteoporotic Fractures) to address these methodological limitations. The subjects were identified before hip fractures occurred, the study design was prospective, and extensive data on comorbidities allowed adjustment for potentially confounding factors.

The SOF subjects were 5,580 community-dwelling women aged 65 and older who resided in Maryland, Minnesota, Oregon, and Pennsylvania at baseline in 1986-1988. This population included 1,116 women who sustained incident hip fractures during a mean follow-up of 14 years, and 4,464 age-matched control subjects without hip fracture.

Mortality risk was highest in the first year after hip fracture. The rate was 16.9% among cases, compared with only 8.4% among controls. This doubling of risk persisted when the analysis was adjusted to account for factors such as total hip bone mineral density.

Moreover, deaths in the control group were evenly spread throughout the year, whereas those in the case group were concentrated within the first 6 months of the year. "In addition, more than half the deaths (99 of 189 [52.4%]) in the first year following hip fracture occurred within the first 3 months for the cases," the investigators said.

When the study subjects were categorized by age (younger than 70 years, 70-79 years, or 80 years and older), the youngest group showed a fivefold rise in mortality risk during the first year after hip fracture (16.3%), compared with women younger than 70 who did not sustain a hip fracture (3.7%).

In contrast, the oldest women showed no increased mortality risk in the year following hip fracture, and the women in the middle group showed an intermediate risk.

In addition, mortality risk remained elevated for years 1-10 among women in the youngest age group, but it was somewhat lower than the mortality risk in the first year. In contrast, mortality risk declined to baseline for the next 10 years among women in the two older age groups.

"We hypothesize that age influences the risk of death after hip fracture by affecting the baseline death rate in the population. Those who are younger ... have a low risk of dying from other causes. Therefore, experiencing a hip fracture may increase their mortality risk compared with nonfracture controls.

"In contrast, octogenarians generally have a relatively high risk of dying from other causes; therefore, experiencing a hip fracture does not result in an increased risk of death during the next year compared with other women their age," the researchers said.

Because women aged 65-70 years remain at increased risk of death for an additional 5-10 years following hip fracture, prevention of the injury should be a high priority in this age group, they added.

The leading causes of death – coronary heart disease, cancer, and stroke – were the same between cases and controls. Rates of death from sepsis also were the same between the two groups. However, more women who sustained hip fractures, compared with control women, died from pneumonia (10.5% vs. 5.6%), cognitive disorders (9.2% vs. 6.7%), and osteoporotic fracture (2% vs. 0%). More control women died from cancer (11% vs. 18.2%).

"Although, in our study, [fewer than] 15% of the deaths were due to infection or osteoporosis (the most likely causes of death to be directly attributed to the fracture itself), hip fracture could have been a contributing cause in many of the remaining deaths, including those attributed to coronary heart disease and stroke," Dr. LeBlanc and her associates noted.

This study was limited in that 99% of the subjects were non-Hispanic white women aged 65 and older, so the results may not be generalizable to men, other ethnic groups, or younger women, they added.

This study was supported by the U.S. Public Health Service, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute on Aging, and the National Center for Research Resources. No financial conflicts of interest were reported.

Mortality risk doubles during the year after hip fracture among women aged 65 years and older, then returns to baseline in many women; but this pattern doesn’t apply in all cases, according to a report published online Sept. 26 in Archives of Internal Medicine.

Mortality risk after sustaining a hip fracture differs by patient age, underlying health, and the interval since the injury occurred in this population, said Dr. Erin S. LeBlanc of the center for health research at Kaiser Permanente Northwest Region, Portland, Ore., and her associates.

Previous studies of this issue have had methodological limitations and have yielded inconsistent results. Most have shown increased short-term mortality, but have had mixed findings on long-term mortality. "Our data suggest that previous mixed results ... may have been the result of differences in the underlying age and health status of the population being studied," Dr. LeBlanc and her colleagues said (Arch. Intern. Med. 2011 Sept. 26 [doi:10.1001/archinternmed.2011.447]).

They used data from the SOF (Study of Osteoporotic Fractures) to address these methodological limitations. The subjects were identified before hip fractures occurred, the study design was prospective, and extensive data on comorbidities allowed adjustment for potentially confounding factors.

The SOF subjects were 5,580 community-dwelling women aged 65 and older who resided in Maryland, Minnesota, Oregon, and Pennsylvania at baseline in 1986-1988. This population included 1,116 women who sustained incident hip fractures during a mean follow-up of 14 years, and 4,464 age-matched control subjects without hip fracture.

Mortality risk was highest in the first year after hip fracture. The rate was 16.9% among cases, compared with only 8.4% among controls. This doubling of risk persisted when the analysis was adjusted to account for factors such as total hip bone mineral density.

Moreover, deaths in the control group were evenly spread throughout the year, whereas those in the case group were concentrated within the first 6 months of the year. "In addition, more than half the deaths (99 of 189 [52.4%]) in the first year following hip fracture occurred within the first 3 months for the cases," the investigators said.

When the study subjects were categorized by age (younger than 70 years, 70-79 years, or 80 years and older), the youngest group showed a fivefold rise in mortality risk during the first year after hip fracture (16.3%), compared with women younger than 70 who did not sustain a hip fracture (3.7%).

In contrast, the oldest women showed no increased mortality risk in the year following hip fracture, and the women in the middle group showed an intermediate risk.

In addition, mortality risk remained elevated for years 1-10 among women in the youngest age group, but it was somewhat lower than the mortality risk in the first year. In contrast, mortality risk declined to baseline for the next 10 years among women in the two older age groups.

"We hypothesize that age influences the risk of death after hip fracture by affecting the baseline death rate in the population. Those who are younger ... have a low risk of dying from other causes. Therefore, experiencing a hip fracture may increase their mortality risk compared with nonfracture controls.

"In contrast, octogenarians generally have a relatively high risk of dying from other causes; therefore, experiencing a hip fracture does not result in an increased risk of death during the next year compared with other women their age," the researchers said.

Because women aged 65-70 years remain at increased risk of death for an additional 5-10 years following hip fracture, prevention of the injury should be a high priority in this age group, they added.

The leading causes of death – coronary heart disease, cancer, and stroke – were the same between cases and controls. Rates of death from sepsis also were the same between the two groups. However, more women who sustained hip fractures, compared with control women, died from pneumonia (10.5% vs. 5.6%), cognitive disorders (9.2% vs. 6.7%), and osteoporotic fracture (2% vs. 0%). More control women died from cancer (11% vs. 18.2%).

"Although, in our study, [fewer than] 15% of the deaths were due to infection or osteoporosis (the most likely causes of death to be directly attributed to the fracture itself), hip fracture could have been a contributing cause in many of the remaining deaths, including those attributed to coronary heart disease and stroke," Dr. LeBlanc and her associates noted.

This study was limited in that 99% of the subjects were non-Hispanic white women aged 65 and older, so the results may not be generalizable to men, other ethnic groups, or younger women, they added.

This study was supported by the U.S. Public Health Service, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute on Aging, and the National Center for Research Resources. No financial conflicts of interest were reported.

Mortality risk doubles during the year after hip fracture among women aged 65 years and older, then returns to baseline in many women; but this pattern doesn’t apply in all cases, according to a report published online Sept. 26 in Archives of Internal Medicine.

Mortality risk after sustaining a hip fracture differs by patient age, underlying health, and the interval since the injury occurred in this population, said Dr. Erin S. LeBlanc of the center for health research at Kaiser Permanente Northwest Region, Portland, Ore., and her associates.

Previous studies of this issue have had methodological limitations and have yielded inconsistent results. Most have shown increased short-term mortality, but have had mixed findings on long-term mortality. "Our data suggest that previous mixed results ... may have been the result of differences in the underlying age and health status of the population being studied," Dr. LeBlanc and her colleagues said (Arch. Intern. Med. 2011 Sept. 26 [doi:10.1001/archinternmed.2011.447]).

They used data from the SOF (Study of Osteoporotic Fractures) to address these methodological limitations. The subjects were identified before hip fractures occurred, the study design was prospective, and extensive data on comorbidities allowed adjustment for potentially confounding factors.

The SOF subjects were 5,580 community-dwelling women aged 65 and older who resided in Maryland, Minnesota, Oregon, and Pennsylvania at baseline in 1986-1988. This population included 1,116 women who sustained incident hip fractures during a mean follow-up of 14 years, and 4,464 age-matched control subjects without hip fracture.

Mortality risk was highest in the first year after hip fracture. The rate was 16.9% among cases, compared with only 8.4% among controls. This doubling of risk persisted when the analysis was adjusted to account for factors such as total hip bone mineral density.

Moreover, deaths in the control group were evenly spread throughout the year, whereas those in the case group were concentrated within the first 6 months of the year. "In addition, more than half the deaths (99 of 189 [52.4%]) in the first year following hip fracture occurred within the first 3 months for the cases," the investigators said.

When the study subjects were categorized by age (younger than 70 years, 70-79 years, or 80 years and older), the youngest group showed a fivefold rise in mortality risk during the first year after hip fracture (16.3%), compared with women younger than 70 who did not sustain a hip fracture (3.7%).

In contrast, the oldest women showed no increased mortality risk in the year following hip fracture, and the women in the middle group showed an intermediate risk.

In addition, mortality risk remained elevated for years 1-10 among women in the youngest age group, but it was somewhat lower than the mortality risk in the first year. In contrast, mortality risk declined to baseline for the next 10 years among women in the two older age groups.

"We hypothesize that age influences the risk of death after hip fracture by affecting the baseline death rate in the population. Those who are younger ... have a low risk of dying from other causes. Therefore, experiencing a hip fracture may increase their mortality risk compared with nonfracture controls.

"In contrast, octogenarians generally have a relatively high risk of dying from other causes; therefore, experiencing a hip fracture does not result in an increased risk of death during the next year compared with other women their age," the researchers said.

Because women aged 65-70 years remain at increased risk of death for an additional 5-10 years following hip fracture, prevention of the injury should be a high priority in this age group, they added.

The leading causes of death – coronary heart disease, cancer, and stroke – were the same between cases and controls. Rates of death from sepsis also were the same between the two groups. However, more women who sustained hip fractures, compared with control women, died from pneumonia (10.5% vs. 5.6%), cognitive disorders (9.2% vs. 6.7%), and osteoporotic fracture (2% vs. 0%). More control women died from cancer (11% vs. 18.2%).

"Although, in our study, [fewer than] 15% of the deaths were due to infection or osteoporosis (the most likely causes of death to be directly attributed to the fracture itself), hip fracture could have been a contributing cause in many of the remaining deaths, including those attributed to coronary heart disease and stroke," Dr. LeBlanc and her associates noted.

This study was limited in that 99% of the subjects were non-Hispanic white women aged 65 and older, so the results may not be generalizable to men, other ethnic groups, or younger women, they added.

This study was supported by the U.S. Public Health Service, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute on Aging, and the National Center for Research Resources. No financial conflicts of interest were reported.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

"This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis," said Dr. Steven Boonen in presenting the study results at the annual meeting of the American Society for Bone and Mineral Research.

"These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year," added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers. At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up. The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction. The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls.

"All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis," the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events.

At present, zoledronic acid’s approved indications include treatment to increase bone mass in men with osteoporosis.

Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

"This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis," said Dr. Steven Boonen in presenting the study results at the annual meeting of the American Society for Bone and Mineral Research.

"These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year," added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers. At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up. The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction. The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls.

"All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis," the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events.

At present, zoledronic acid’s approved indications include treatment to increase bone mass in men with osteoporosis.

Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

DENVER – Once-yearly intravenous zoledronic acid in men with osteoporosis reduced their risk of vertebral fractures by 67% over 2 years, compared with placebo, in a large, multinational, phase III, randomized clinical trial.

"This is the first clear demonstration of antifracture efficacy for an osteoporosis agent in male osteoporosis," said Dr. Steven Boonen in presenting the study results at the annual meeting of the American Society for Bone and Mineral Research.

"These findings suggest the use of zoledronic acid as a treatment option in male patients, particularly because annual infusions ensure that patients will have the full effect of treatment for at least the next year," added Dr. Boonen, professor of geriatric medicine and head of the gerontology and geriatrics section at Catholic University of Leuven (Belgium).

He reported on 1,199 men (mean age, 66 years) with primary osteoporosis or osteoporosis secondary to hypogonadism who were randomized in a double-blind fashion to a once-yearly 15-minute infusion of 5 mg of zoledronic acid (Reclast) or placebo at 134 centers. At enrollment, 32% of the men had one or more vertebral fractures.

The primary study end point was the proportion of subjects with one or more new vertebral fractures during 2 years of follow-up. The rate was 1.6% in men assigned to zoledronic acid and 4.9% in placebo-treated controls, which translated to a highly significant 67% relative risk reduction. The 12-month rate was 0.9% in the zoledronic acid group vs. 2.8% in controls, for a 68% relative risk reduction.

The incidence of moderate to severe vertebral fractures was similarly reduced by 63% in zoledronic acid recipients, compared with controls.

Men on zoledronic acid had a stable 60% reduction in levels of the bone turnover biomarker CTx, compared with the placebo group, throughout the study.

At 2 years, bone mineral density was roughly 6% greater at the spine and 2% greater at the total hip in the zoledronic acid group, compared with controls.

"All of these findings are remarkably similar in magnitude to the risk reductions that have been documented with zoledronic acid in the pivotal fracture trial in postmenopausal osteoporosis," the geriatrician observed.

Men on zoledronic acid also experienced a smaller height loss, compared with controls (mean, 2.34 vs. 4.49 mm).

No major safety issues arose in the study. Similar numbers of patients in both study arms dropped out of the trial because of adverse events.

At present, zoledronic acid’s approved indications include treatment to increase bone mass in men with osteoporosis.

Dr. Boonen disclosed that he has received research grants from and serves as a consultant to Novartis.

SAN DIEGO – A novel once-daily oral calcitonin tablet hit all of its efficacy and safety end points in a phase III clinical trial for treatment of postmenopausal osteoporosis.

The oral formulation of recombinant salmon calcitonin, known as Ostora, proved significantly more effective at building bone mineral density than conventional nasal calcitonin in the 18-site, multinational, double-blind, double-placebo ORACAL trial, Dr. Neil Binkley reported at the annual meeting of the American Society for Bone and Mineral Research.

ORACAL involved 565 postmenopausal women with osteoporosis and a mean age of 66 years. They were randomized 4:3:2 to once-daily bedtime therapy with oral calcitonin at 200 mcg, conventional nasal calcitonin at 200 IU, or placebo.

The absolute change in lumbar spine bone mineral density at 48 weeks – the primary study end point – showed a relatively modest 1.5% increase in the oral calcitonin group. But this was significantly greater than the 0.8% increase with the commercially available nasal calcitonin, which in turn was significantly better than the placebo response.

Potential safety issues with the bisphosphonates and other currently available medications have led many osteoporosis patients to decline therapy, while other women stop treatment due to side effects. Calcitonin, in contrast, has a 30-year history of safe prescription use via the intranasal and injectable routes. An oral formulation "might improve convenience and compliance with calcitonin therapy," observed Dr. Binkley, an endocrinologist at the University of Wisconsin, Madison.

Salmon calcitonin is an analog of human calcitonin that’s 30- to 50-fold more potent in suppressing osteoclast resorption.

In the ORACAL trial, levels of CTx (C-terminal telopeptide), a biomarker of bone resorption, dropped by 30% in the oral calcitonin group at 48 weeks, compared with 11% reductions in the nasal calcitonin and placebo arms.

Only 6.5% of women assigned to oral calcitonin developed anticalcitonin antibodies, compared with 32.5% of those on nasal calcitonin. This suggests delivery of the agent via the gastrointestinal tract is less immunogenic than the nasal mucosa. In any case, the production of antibodies had no apparent impacts on safety or efficacy, the endocrinologist continued.

The side effect picture in the oral and nasal calcitonin groups mirrored that in placebo-treated controls.

Tarsa Therapeutics, which is developing oral calcitonin, estimates at least 2 million American women have discontinued osteoporosis treatment. The company plans to file with the Food and Drug Administration for marketing approval later this year and with the European regulatory agency next year.

In addition, the company is developing oral calcitonin for the prevention of osteoporosis in postmenopausal women with osteopenia. A double-blind phase II trial is underway.

Dr. Binkley disclosed he has received a research grant from Tarsa, which sponsored the phase III trial.

SAN DIEGO – A novel once-daily oral calcitonin tablet hit all of its efficacy and safety end points in a phase III clinical trial for treatment of postmenopausal osteoporosis.

The oral formulation of recombinant salmon calcitonin, known as Ostora, proved significantly more effective at building bone mineral density than conventional nasal calcitonin in the 18-site, multinational, double-blind, double-placebo ORACAL trial, Dr. Neil Binkley reported at the annual meeting of the American Society for Bone and Mineral Research.

ORACAL involved 565 postmenopausal women with osteoporosis and a mean age of 66 years. They were randomized 4:3:2 to once-daily bedtime therapy with oral calcitonin at 200 mcg, conventional nasal calcitonin at 200 IU, or placebo.

The absolute change in lumbar spine bone mineral density at 48 weeks – the primary study end point – showed a relatively modest 1.5% increase in the oral calcitonin group. But this was significantly greater than the 0.8% increase with the commercially available nasal calcitonin, which in turn was significantly better than the placebo response.

Potential safety issues with the bisphosphonates and other currently available medications have led many osteoporosis patients to decline therapy, while other women stop treatment due to side effects. Calcitonin, in contrast, has a 30-year history of safe prescription use via the intranasal and injectable routes. An oral formulation "might improve convenience and compliance with calcitonin therapy," observed Dr. Binkley, an endocrinologist at the University of Wisconsin, Madison.

Salmon calcitonin is an analog of human calcitonin that’s 30- to 50-fold more potent in suppressing osteoclast resorption.

In the ORACAL trial, levels of CTx (C-terminal telopeptide), a biomarker of bone resorption, dropped by 30% in the oral calcitonin group at 48 weeks, compared with 11% reductions in the nasal calcitonin and placebo arms.

Only 6.5% of women assigned to oral calcitonin developed anticalcitonin antibodies, compared with 32.5% of those on nasal calcitonin. This suggests delivery of the agent via the gastrointestinal tract is less immunogenic than the nasal mucosa. In any case, the production of antibodies had no apparent impacts on safety or efficacy, the endocrinologist continued.

The side effect picture in the oral and nasal calcitonin groups mirrored that in placebo-treated controls.

Tarsa Therapeutics, which is developing oral calcitonin, estimates at least 2 million American women have discontinued osteoporosis treatment. The company plans to file with the Food and Drug Administration for marketing approval later this year and with the European regulatory agency next year.

In addition, the company is developing oral calcitonin for the prevention of osteoporosis in postmenopausal women with osteopenia. A double-blind phase II trial is underway.

Dr. Binkley disclosed he has received a research grant from Tarsa, which sponsored the phase III trial.

SAN DIEGO – A novel once-daily oral calcitonin tablet hit all of its efficacy and safety end points in a phase III clinical trial for treatment of postmenopausal osteoporosis.

The oral formulation of recombinant salmon calcitonin, known as Ostora, proved significantly more effective at building bone mineral density than conventional nasal calcitonin in the 18-site, multinational, double-blind, double-placebo ORACAL trial, Dr. Neil Binkley reported at the annual meeting of the American Society for Bone and Mineral Research.

ORACAL involved 565 postmenopausal women with osteoporosis and a mean age of 66 years. They were randomized 4:3:2 to once-daily bedtime therapy with oral calcitonin at 200 mcg, conventional nasal calcitonin at 200 IU, or placebo.

The absolute change in lumbar spine bone mineral density at 48 weeks – the primary study end point – showed a relatively modest 1.5% increase in the oral calcitonin group. But this was significantly greater than the 0.8% increase with the commercially available nasal calcitonin, which in turn was significantly better than the placebo response.

Potential safety issues with the bisphosphonates and other currently available medications have led many osteoporosis patients to decline therapy, while other women stop treatment due to side effects. Calcitonin, in contrast, has a 30-year history of safe prescription use via the intranasal and injectable routes. An oral formulation "might improve convenience and compliance with calcitonin therapy," observed Dr. Binkley, an endocrinologist at the University of Wisconsin, Madison.

Salmon calcitonin is an analog of human calcitonin that’s 30- to 50-fold more potent in suppressing osteoclast resorption.

In the ORACAL trial, levels of CTx (C-terminal telopeptide), a biomarker of bone resorption, dropped by 30% in the oral calcitonin group at 48 weeks, compared with 11% reductions in the nasal calcitonin and placebo arms.

Only 6.5% of women assigned to oral calcitonin developed anticalcitonin antibodies, compared with 32.5% of those on nasal calcitonin. This suggests delivery of the agent via the gastrointestinal tract is less immunogenic than the nasal mucosa. In any case, the production of antibodies had no apparent impacts on safety or efficacy, the endocrinologist continued.

The side effect picture in the oral and nasal calcitonin groups mirrored that in placebo-treated controls.

Tarsa Therapeutics, which is developing oral calcitonin, estimates at least 2 million American women have discontinued osteoporosis treatment. The company plans to file with the Food and Drug Administration for marketing approval later this year and with the European regulatory agency next year.

In addition, the company is developing oral calcitonin for the prevention of osteoporosis in postmenopausal women with osteopenia. A double-blind phase II trial is underway.

Dr. Binkley disclosed he has received a research grant from Tarsa, which sponsored the phase III trial.

SAN DIEGO – People who are overweight or younger than 75 years when they have a total hip replacement face an increased risk for revision within 12 years; the risk is also increased if cement was used to hold the femoral stem of the implant in place.

"Patients and physicians may wish to weave some of these findings into their decisions about whether to undergo primary [total hip replacement] because they inform the subsequent risk of revision," said the study’s lead author, Dr. Jeffrey Katz, professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

Using hospital records and Medicare claims data, Dr. Katz and his associates examined the presurgery characteristics of 836 people who had initial total hip replacements (THRs) from July 1995 to June 1996 and subsequent revisions sometime before 2009. The researchers then compared those patients to 836 matched controls who also had THRs in the mid-1990s but whose prosthetic hip had not been revised by the time their case had a revision.

Patients who had a prior contralateral hip replacement, a prior history of other orthopedic surgery, and those who lived with others, instead of alone, also had a higher revision risk. Odds ratios were modest but statistically significant, ranging from 1.3 to 1.7.

"Age and weight were not surprising. We thought we might see an effect of sex [since] there is a literature of males being at higher risk, but we did not. There is also literature on comorbidity being associated with revision, which we did not see," Dr. Katz said at the World Congress on Osteoarthritis.

The cement finding adds "to what is a rather conflicted literature on the durability of cemented versus uncemented designs," he said. The odds ratio for the finding was 1.4.

Cement techniques – including techniques for reaming out the femur and applying the pressure to the cement – have improved since the mid-1990s, so "you have to be careful interpreting the [cement] data. They may not apply to the way cement is used now," Dr. Katz said.

Based on the findings, "when you talk to somebody who is in their mid to late 70s about hip replacement, I think you can say revision is not particularly likely. For a younger person, they should recognize that we may have to go back again. At that point, they’ll be older and have greater surgical risk," he said.

The manufacturer of the implants, the initial surgeon’s level of experience with the procedure, and the reasons for the revisions were not captured by the study.

The researchers also found a higher risk of revision if, at the time of their initial surgery, patients had a body mass index (BMI) greater than 30 kg/m² (OR, 1.5) or were in the highest tertile for weight (OR, 1.7) or height (OR, 1.4).

Dr. Katz offered several interpretations. Height, weight, and BMI are likely related to the biomechanical load on the implant. Regarding the greater risk below age 75 years (OR, 1.5), younger, more active patients may be more likely to have a faulty THR fixed. Increased risk for prior contralateral hip replacements (OR, 1.4) or orthopedic surgery (OR, 1.5) may indicated a willingness and ability to undergo surgery.

The added risk from living with others (OR, 1.3) "may represent having the social support in place to deal with rehab and a temporary dependency," which facilitates elective surgery, he said.

There are about 280,000 primary THRs in the United States annually, and about 50,000 revisions. The revision rate is about 1% a year, "so 100 people who go out 20 years, you might expect 20 of them to be revised," Dr. Katz said at the congress, which was sponsored by the Osteoarthritis Research Society International.

The work was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Katz said he has no disclosures.

SAN DIEGO – People who are overweight or younger than 75 years when they have a total hip replacement face an increased risk for revision within 12 years; the risk is also increased if cement was used to hold the femoral stem of the implant in place.

"Patients and physicians may wish to weave some of these findings into their decisions about whether to undergo primary [total hip replacement] because they inform the subsequent risk of revision," said the study’s lead author, Dr. Jeffrey Katz, professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

Using hospital records and Medicare claims data, Dr. Katz and his associates examined the presurgery characteristics of 836 people who had initial total hip replacements (THRs) from July 1995 to June 1996 and subsequent revisions sometime before 2009. The researchers then compared those patients to 836 matched controls who also had THRs in the mid-1990s but whose prosthetic hip had not been revised by the time their case had a revision.

Patients who had a prior contralateral hip replacement, a prior history of other orthopedic surgery, and those who lived with others, instead of alone, also had a higher revision risk. Odds ratios were modest but statistically significant, ranging from 1.3 to 1.7.

"Age and weight were not surprising. We thought we might see an effect of sex [since] there is a literature of males being at higher risk, but we did not. There is also literature on comorbidity being associated with revision, which we did not see," Dr. Katz said at the World Congress on Osteoarthritis.

The cement finding adds "to what is a rather conflicted literature on the durability of cemented versus uncemented designs," he said. The odds ratio for the finding was 1.4.

Cement techniques – including techniques for reaming out the femur and applying the pressure to the cement – have improved since the mid-1990s, so "you have to be careful interpreting the [cement] data. They may not apply to the way cement is used now," Dr. Katz said.

Based on the findings, "when you talk to somebody who is in their mid to late 70s about hip replacement, I think you can say revision is not particularly likely. For a younger person, they should recognize that we may have to go back again. At that point, they’ll be older and have greater surgical risk," he said.

The manufacturer of the implants, the initial surgeon’s level of experience with the procedure, and the reasons for the revisions were not captured by the study.

The researchers also found a higher risk of revision if, at the time of their initial surgery, patients had a body mass index (BMI) greater than 30 kg/m² (OR, 1.5) or were in the highest tertile for weight (OR, 1.7) or height (OR, 1.4).

Dr. Katz offered several interpretations. Height, weight, and BMI are likely related to the biomechanical load on the implant. Regarding the greater risk below age 75 years (OR, 1.5), younger, more active patients may be more likely to have a faulty THR fixed. Increased risk for prior contralateral hip replacements (OR, 1.4) or orthopedic surgery (OR, 1.5) may indicated a willingness and ability to undergo surgery.

The added risk from living with others (OR, 1.3) "may represent having the social support in place to deal with rehab and a temporary dependency," which facilitates elective surgery, he said.

There are about 280,000 primary THRs in the United States annually, and about 50,000 revisions. The revision rate is about 1% a year, "so 100 people who go out 20 years, you might expect 20 of them to be revised," Dr. Katz said at the congress, which was sponsored by the Osteoarthritis Research Society International.

The work was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Katz said he has no disclosures.

SAN DIEGO – People who are overweight or younger than 75 years when they have a total hip replacement face an increased risk for revision within 12 years; the risk is also increased if cement was used to hold the femoral stem of the implant in place.

"Patients and physicians may wish to weave some of these findings into their decisions about whether to undergo primary [total hip replacement] because they inform the subsequent risk of revision," said the study’s lead author, Dr. Jeffrey Katz, professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

Using hospital records and Medicare claims data, Dr. Katz and his associates examined the presurgery characteristics of 836 people who had initial total hip replacements (THRs) from July 1995 to June 1996 and subsequent revisions sometime before 2009. The researchers then compared those patients to 836 matched controls who also had THRs in the mid-1990s but whose prosthetic hip had not been revised by the time their case had a revision.

Patients who had a prior contralateral hip replacement, a prior history of other orthopedic surgery, and those who lived with others, instead of alone, also had a higher revision risk. Odds ratios were modest but statistically significant, ranging from 1.3 to 1.7.

"Age and weight were not surprising. We thought we might see an effect of sex [since] there is a literature of males being at higher risk, but we did not. There is also literature on comorbidity being associated with revision, which we did not see," Dr. Katz said at the World Congress on Osteoarthritis.

The cement finding adds "to what is a rather conflicted literature on the durability of cemented versus uncemented designs," he said. The odds ratio for the finding was 1.4.

Cement techniques – including techniques for reaming out the femur and applying the pressure to the cement – have improved since the mid-1990s, so "you have to be careful interpreting the [cement] data. They may not apply to the way cement is used now," Dr. Katz said.

Based on the findings, "when you talk to somebody who is in their mid to late 70s about hip replacement, I think you can say revision is not particularly likely. For a younger person, they should recognize that we may have to go back again. At that point, they’ll be older and have greater surgical risk," he said.

The manufacturer of the implants, the initial surgeon’s level of experience with the procedure, and the reasons for the revisions were not captured by the study.

The researchers also found a higher risk of revision if, at the time of their initial surgery, patients had a body mass index (BMI) greater than 30 kg/m² (OR, 1.5) or were in the highest tertile for weight (OR, 1.7) or height (OR, 1.4).

Dr. Katz offered several interpretations. Height, weight, and BMI are likely related to the biomechanical load on the implant. Regarding the greater risk below age 75 years (OR, 1.5), younger, more active patients may be more likely to have a faulty THR fixed. Increased risk for prior contralateral hip replacements (OR, 1.4) or orthopedic surgery (OR, 1.5) may indicated a willingness and ability to undergo surgery.

The added risk from living with others (OR, 1.3) "may represent having the social support in place to deal with rehab and a temporary dependency," which facilitates elective surgery, he said.

There are about 280,000 primary THRs in the United States annually, and about 50,000 revisions. The revision rate is about 1% a year, "so 100 people who go out 20 years, you might expect 20 of them to be revised," Dr. Katz said at the congress, which was sponsored by the Osteoarthritis Research Society International.

The work was funded by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Dr. Katz said he has no disclosures.