Mary Ann Moon

Plasma concentration of apolipoprotein B is a slightly better predictor of coronary heart disease than is non-HDL cholesterol and a much better predictor than is LDL cholesterol, reported Dr. Tobias Pischon of the Harvard School of Public Health, Boston, and his associates.

This finding is sure to add to the controversy over which lipid measurement is the best for assessing both coronary risk and treatment efficacy. Current National Cholesterol Education Program guidelines recommend LDL cholesterol as the primary target for lipid-lowering therapy. The guidelines consider HDL cholesterol a secondary treatment target and do not consider apolipoprotein B (apo B) a target at all, the investigators said.

Apo B concentration is a measure of the particle concentration of all atherogenic lipoproteins, whereas LDL and non-HDL cholesterol levels are measures of some of the cholesterol carried by these particles. Dr. Pischon and his associates conducted what they said was the first large prospective study to directly compare these three measures as predictors of coronary heart disease (CHD) risk.

Their results indicated that apo B is the best such predictor, and also that particle concentration of atherogenic lipoproteins is more crucial than is cholesterol content in the development of CHD (Circulation 2005;112:3375–83).

The researchers used a database of more than 51,000 male health professionals who had been followed every 2 years since 1986 to identify 243 subjects who had developed CHD during a 6-year study period and 496 matched control subjects who did not develop CHD. The baseline apo B level was the best predictor of CHD (relative risk 2.98). Non-HDL cholesterol also was strongly predictive (RR 2.75), with LDL cholesterol less so (RR 2.07).

In an editorial comment accompanying the report, Dr. Allan D. Sniderman of McGill University, Montreal, said that apo B should replace LDL and non-HDL cholesterol as the measurement of choice in assessing CHD risk, noting that it has now been more extensively validated in both epidemiologic studies and clinical trials. Measurement of apo B is already standardized, automated, and inexpensive, he said (Circulation 2005;112:3366–7).

In contrast, Dr. Margo A. Denke of the University of Texas Health Science Center at San Antonio said that abandoning cholesterol testing in favor of apo B testing would be too confusing for both physicians and the public. The cholesterol content of lipoprotein particles reliably predicted CHD in every major study, whereas apo B assessments have not consistently improved that prediction, she said (Circulation 2005;112:3368–70).

Plasma concentration of apolipoprotein B is a slightly better predictor of coronary heart disease than is non-HDL cholesterol and a much better predictor than is LDL cholesterol, reported Dr. Tobias Pischon of the Harvard School of Public Health, Boston, and his associates.

This finding is sure to add to the controversy over which lipid measurement is the best for assessing both coronary risk and treatment efficacy. Current National Cholesterol Education Program guidelines recommend LDL cholesterol as the primary target for lipid-lowering therapy. The guidelines consider HDL cholesterol a secondary treatment target and do not consider apolipoprotein B (apo B) a target at all, the investigators said.

Apo B concentration is a measure of the particle concentration of all atherogenic lipoproteins, whereas LDL and non-HDL cholesterol levels are measures of some of the cholesterol carried by these particles. Dr. Pischon and his associates conducted what they said was the first large prospective study to directly compare these three measures as predictors of coronary heart disease (CHD) risk.

Their results indicated that apo B is the best such predictor, and also that particle concentration of atherogenic lipoproteins is more crucial than is cholesterol content in the development of CHD (Circulation 2005;112:3375–83).

The researchers used a database of more than 51,000 male health professionals who had been followed every 2 years since 1986 to identify 243 subjects who had developed CHD during a 6-year study period and 496 matched control subjects who did not develop CHD. The baseline apo B level was the best predictor of CHD (relative risk 2.98). Non-HDL cholesterol also was strongly predictive (RR 2.75), with LDL cholesterol less so (RR 2.07).

In an editorial comment accompanying the report, Dr. Allan D. Sniderman of McGill University, Montreal, said that apo B should replace LDL and non-HDL cholesterol as the measurement of choice in assessing CHD risk, noting that it has now been more extensively validated in both epidemiologic studies and clinical trials. Measurement of apo B is already standardized, automated, and inexpensive, he said (Circulation 2005;112:3366–7).

In contrast, Dr. Margo A. Denke of the University of Texas Health Science Center at San Antonio said that abandoning cholesterol testing in favor of apo B testing would be too confusing for both physicians and the public. The cholesterol content of lipoprotein particles reliably predicted CHD in every major study, whereas apo B assessments have not consistently improved that prediction, she said (Circulation 2005;112:3368–70).

Plasma concentration of apolipoprotein B is a slightly better predictor of coronary heart disease than is non-HDL cholesterol and a much better predictor than is LDL cholesterol, reported Dr. Tobias Pischon of the Harvard School of Public Health, Boston, and his associates.

This finding is sure to add to the controversy over which lipid measurement is the best for assessing both coronary risk and treatment efficacy. Current National Cholesterol Education Program guidelines recommend LDL cholesterol as the primary target for lipid-lowering therapy. The guidelines consider HDL cholesterol a secondary treatment target and do not consider apolipoprotein B (apo B) a target at all, the investigators said.

Apo B concentration is a measure of the particle concentration of all atherogenic lipoproteins, whereas LDL and non-HDL cholesterol levels are measures of some of the cholesterol carried by these particles. Dr. Pischon and his associates conducted what they said was the first large prospective study to directly compare these three measures as predictors of coronary heart disease (CHD) risk.

Their results indicated that apo B is the best such predictor, and also that particle concentration of atherogenic lipoproteins is more crucial than is cholesterol content in the development of CHD (Circulation 2005;112:3375–83).

The researchers used a database of more than 51,000 male health professionals who had been followed every 2 years since 1986 to identify 243 subjects who had developed CHD during a 6-year study period and 496 matched control subjects who did not develop CHD. The baseline apo B level was the best predictor of CHD (relative risk 2.98). Non-HDL cholesterol also was strongly predictive (RR 2.75), with LDL cholesterol less so (RR 2.07).

In an editorial comment accompanying the report, Dr. Allan D. Sniderman of McGill University, Montreal, said that apo B should replace LDL and non-HDL cholesterol as the measurement of choice in assessing CHD risk, noting that it has now been more extensively validated in both epidemiologic studies and clinical trials. Measurement of apo B is already standardized, automated, and inexpensive, he said (Circulation 2005;112:3366–7).

In contrast, Dr. Margo A. Denke of the University of Texas Health Science Center at San Antonio said that abandoning cholesterol testing in favor of apo B testing would be too confusing for both physicians and the public. The cholesterol content of lipoprotein particles reliably predicted CHD in every major study, whereas apo B assessments have not consistently improved that prediction, she said (Circulation 2005;112:3368–70).

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as control subjects. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months. Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the AD placebo group and the control groups.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.

These results are encouraging, but they “do not warrant routine treatment” with testosterone until further studies with larger sample sizes verify the findings, the investigators noted.

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as control subjects. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months. Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the AD placebo group and the control groups.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.

These results are encouraging, but they “do not warrant routine treatment” with testosterone until further studies with larger sample sizes verify the findings, the investigators noted.

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as control subjects. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months. Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the AD placebo group and the control groups.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.

These results are encouraging, but they “do not warrant routine treatment” with testosterone until further studies with larger sample sizes verify the findings, the investigators noted.

The aromatase inhibitor letrozole compares favorably with tamoxifen as an adjuvant treatment for hormone receptor-positive breast cancer in postmenopausal women, reported Dr. Beat Thürlimann and associates in the Breast International Group 1–98 trial.

Interim results of this multinational phase III clinical trial at the 2-year mark “indicate that letrozole is an effective option for standard adjuvant therapy, with a relatively favorable safety profile,” compared with tamoxifen. Letrozole was superior to tamoxifen in decreasing the risk of distant metastases, said Dr. Thürlimann of the Swiss Group for Clinical Cancer Research and the Senology Center of Eastern Switzerland, Kantonsspital, St. Gallen, and associates.

Letrozole (Femara) was approved in December for adjuvant treatment of early hormone-sensitive breast cancer in postmenopausal women, based on the results of the BIG 1–98 trial. The trial involved 8,010 postmenopausal women with invasive breast cancer that was positive for estrogen receptors, progesterone receptors, or both. The women were randomly assigned to receive one of three regimens after surgery: monotherapy with either letrozole or tamoxifen for 5 years, letrozole for 2 years followed by tamoxifen for 3 years, or tamoxifen for 2 years followed by letrozole for 3 years.

This planned interim analysis compared outcomes after a median of 26 months for the 4,003 women assigned to letrozole initially with those of the 4,007 assigned to tamoxifen initially (New Engl. J. Med. 2005;353:2747–57).

Disease-free survival was significantly greater in the letrozole group, and the drug was particularly effective in reducing recurrences at distant sites. The 5-year estimates of disease-free survival were 84% in the letrozole group and 81.4% in the tamoxifen group.

Subgroup analysis showed that letrozole was superior to tamoxifen for the subset of patients who received chemotherapy, the subset who did not receive radiotherapy, and the subset with positive axillary nodes.

Letrozole significantly decreased the cumulative incidence of breast cancer relapse, compared with tamoxifen. “This difference became evident 1 year after randomization, and there was an absolute difference of 3.4 percentage points at 5 years,” they noted.

More patients in the letrozole group than in the tamoxifen group reported adverse events, but the incidence of life-threatening adverse events was 1.7% for both. Bone fractures were more frequent with letrozole (5.7% vs. 4.0%), and the interval before sustaining a fracture was significantly shorter.

Letrozole was associated with fewer thromboembolic events (1.5% vs. 3.5%), episodes of vaginal bleeding (3.3% vs. 6.6%), endometrial biopsies (2.3% vs. 9.1%), and invasive endometrial cancers (0.1% vs. 0.3%).

The overall incidence of adverse cardiovascular events was similar in the two groups (letrozole, 3.7%; tamoxifen, 4.2%), but more women on letrozole had severe cardiac events (2.1% vs. 1.1%).

This study was funded in part by Novartis Pharmaceuticals Corp., the manufacturer of letrozole (Femara).

The aromatase inhibitor letrozole compares favorably with tamoxifen as an adjuvant treatment for hormone receptor-positive breast cancer in postmenopausal women, reported Dr. Beat Thürlimann and associates in the Breast International Group 1–98 trial.

Interim results of this multinational phase III clinical trial at the 2-year mark “indicate that letrozole is an effective option for standard adjuvant therapy, with a relatively favorable safety profile,” compared with tamoxifen. Letrozole was superior to tamoxifen in decreasing the risk of distant metastases, said Dr. Thürlimann of the Swiss Group for Clinical Cancer Research and the Senology Center of Eastern Switzerland, Kantonsspital, St. Gallen, and associates.

Letrozole (Femara) was approved in December for adjuvant treatment of early hormone-sensitive breast cancer in postmenopausal women, based on the results of the BIG 1–98 trial. The trial involved 8,010 postmenopausal women with invasive breast cancer that was positive for estrogen receptors, progesterone receptors, or both. The women were randomly assigned to receive one of three regimens after surgery: monotherapy with either letrozole or tamoxifen for 5 years, letrozole for 2 years followed by tamoxifen for 3 years, or tamoxifen for 2 years followed by letrozole for 3 years.

This planned interim analysis compared outcomes after a median of 26 months for the 4,003 women assigned to letrozole initially with those of the 4,007 assigned to tamoxifen initially (New Engl. J. Med. 2005;353:2747–57).

Disease-free survival was significantly greater in the letrozole group, and the drug was particularly effective in reducing recurrences at distant sites. The 5-year estimates of disease-free survival were 84% in the letrozole group and 81.4% in the tamoxifen group.

Subgroup analysis showed that letrozole was superior to tamoxifen for the subset of patients who received chemotherapy, the subset who did not receive radiotherapy, and the subset with positive axillary nodes.

Letrozole significantly decreased the cumulative incidence of breast cancer relapse, compared with tamoxifen. “This difference became evident 1 year after randomization, and there was an absolute difference of 3.4 percentage points at 5 years,” they noted.

More patients in the letrozole group than in the tamoxifen group reported adverse events, but the incidence of life-threatening adverse events was 1.7% for both. Bone fractures were more frequent with letrozole (5.7% vs. 4.0%), and the interval before sustaining a fracture was significantly shorter.

Letrozole was associated with fewer thromboembolic events (1.5% vs. 3.5%), episodes of vaginal bleeding (3.3% vs. 6.6%), endometrial biopsies (2.3% vs. 9.1%), and invasive endometrial cancers (0.1% vs. 0.3%).

The overall incidence of adverse cardiovascular events was similar in the two groups (letrozole, 3.7%; tamoxifen, 4.2%), but more women on letrozole had severe cardiac events (2.1% vs. 1.1%).

This study was funded in part by Novartis Pharmaceuticals Corp., the manufacturer of letrozole (Femara).

The aromatase inhibitor letrozole compares favorably with tamoxifen as an adjuvant treatment for hormone receptor-positive breast cancer in postmenopausal women, reported Dr. Beat Thürlimann and associates in the Breast International Group 1–98 trial.

Interim results of this multinational phase III clinical trial at the 2-year mark “indicate that letrozole is an effective option for standard adjuvant therapy, with a relatively favorable safety profile,” compared with tamoxifen. Letrozole was superior to tamoxifen in decreasing the risk of distant metastases, said Dr. Thürlimann of the Swiss Group for Clinical Cancer Research and the Senology Center of Eastern Switzerland, Kantonsspital, St. Gallen, and associates.

Letrozole (Femara) was approved in December for adjuvant treatment of early hormone-sensitive breast cancer in postmenopausal women, based on the results of the BIG 1–98 trial. The trial involved 8,010 postmenopausal women with invasive breast cancer that was positive for estrogen receptors, progesterone receptors, or both. The women were randomly assigned to receive one of three regimens after surgery: monotherapy with either letrozole or tamoxifen for 5 years, letrozole for 2 years followed by tamoxifen for 3 years, or tamoxifen for 2 years followed by letrozole for 3 years.

This planned interim analysis compared outcomes after a median of 26 months for the 4,003 women assigned to letrozole initially with those of the 4,007 assigned to tamoxifen initially (New Engl. J. Med. 2005;353:2747–57).

Disease-free survival was significantly greater in the letrozole group, and the drug was particularly effective in reducing recurrences at distant sites. The 5-year estimates of disease-free survival were 84% in the letrozole group and 81.4% in the tamoxifen group.

Subgroup analysis showed that letrozole was superior to tamoxifen for the subset of patients who received chemotherapy, the subset who did not receive radiotherapy, and the subset with positive axillary nodes.

Letrozole significantly decreased the cumulative incidence of breast cancer relapse, compared with tamoxifen. “This difference became evident 1 year after randomization, and there was an absolute difference of 3.4 percentage points at 5 years,” they noted.

More patients in the letrozole group than in the tamoxifen group reported adverse events, but the incidence of life-threatening adverse events was 1.7% for both. Bone fractures were more frequent with letrozole (5.7% vs. 4.0%), and the interval before sustaining a fracture was significantly shorter.

Letrozole was associated with fewer thromboembolic events (1.5% vs. 3.5%), episodes of vaginal bleeding (3.3% vs. 6.6%), endometrial biopsies (2.3% vs. 9.1%), and invasive endometrial cancers (0.1% vs. 0.3%).

The overall incidence of adverse cardiovascular events was similar in the two groups (letrozole, 3.7%; tamoxifen, 4.2%), but more women on letrozole had severe cardiac events (2.1% vs. 1.1%).

This study was funded in part by Novartis Pharmaceuticals Corp., the manufacturer of letrozole (Femara).

Cyclooxygenase-2 inhibitors were found to be no safer than nonselective NSAIDs in averting adverse gastrointestinal events in a large observational study conducted in the United Kingdom.

The finding is important “given that enhanced gastrointestinal safety has been one of the main justifications for these drugs,” wrote Dr. Julia Hippisley-Cox and her associates at the University of Nottingham (England). The COX-2 inhibitors were developed to relieve pain without inducing the GI side effects common with NSAIDs, but long-term safety data are lacking.

The researchers calculated the risk of GI events in patients who took these prescription pain relievers between 2000 and 2004. After reviewing the medical records in a database of more than 7 million patients treated at general practices throughout England, Scotland, and Wales, the investigators identified 9,407 who had an adverse GI event and matched them with more than 88,000 controls who had no such events (BMJ 2005;331:1310–6).

Patients with GI events were more likely to have taken either prescription NSAIDs (odds ratio 1.69) or prescription COX-2 inhibitors (odds ratio 1.89) than were control subjects.

The researchers also found that the concomitant use of ulcer-healing drugs reduces the GI risks of COX-2 inhibitors, which suggests “that there is some risk to protect against.” Taken together, these results indicate that COX-2 inhibitors “may not be as safe as originally thought,” the authors said.

Celecoxib was the only agent out of 27 pain relievers used by the study subjects to show no link with adverse GI events. However, the number of celecoxib users was very small, so this finding remains “difficult to interpret,” the researchers noted.

The use of ulcer-healing drugs such as proton pump inhibitors reduced the risk for GI events in users of both COX-2 inhibitors and NSAIDs, again suggesting that the GI risks of the two types of pain relievers are similar, they added.

Cyclooxygenase-2 inhibitors were found to be no safer than nonselective NSAIDs in averting adverse gastrointestinal events in a large observational study conducted in the United Kingdom.

The finding is important “given that enhanced gastrointestinal safety has been one of the main justifications for these drugs,” wrote Dr. Julia Hippisley-Cox and her associates at the University of Nottingham (England). The COX-2 inhibitors were developed to relieve pain without inducing the GI side effects common with NSAIDs, but long-term safety data are lacking.

The researchers calculated the risk of GI events in patients who took these prescription pain relievers between 2000 and 2004. After reviewing the medical records in a database of more than 7 million patients treated at general practices throughout England, Scotland, and Wales, the investigators identified 9,407 who had an adverse GI event and matched them with more than 88,000 controls who had no such events (BMJ 2005;331:1310–6).

Patients with GI events were more likely to have taken either prescription NSAIDs (odds ratio 1.69) or prescription COX-2 inhibitors (odds ratio 1.89) than were control subjects.

The researchers also found that the concomitant use of ulcer-healing drugs reduces the GI risks of COX-2 inhibitors, which suggests “that there is some risk to protect against.” Taken together, these results indicate that COX-2 inhibitors “may not be as safe as originally thought,” the authors said.

Celecoxib was the only agent out of 27 pain relievers used by the study subjects to show no link with adverse GI events. However, the number of celecoxib users was very small, so this finding remains “difficult to interpret,” the researchers noted.

The use of ulcer-healing drugs such as proton pump inhibitors reduced the risk for GI events in users of both COX-2 inhibitors and NSAIDs, again suggesting that the GI risks of the two types of pain relievers are similar, they added.

Cyclooxygenase-2 inhibitors were found to be no safer than nonselective NSAIDs in averting adverse gastrointestinal events in a large observational study conducted in the United Kingdom.

The finding is important “given that enhanced gastrointestinal safety has been one of the main justifications for these drugs,” wrote Dr. Julia Hippisley-Cox and her associates at the University of Nottingham (England). The COX-2 inhibitors were developed to relieve pain without inducing the GI side effects common with NSAIDs, but long-term safety data are lacking.

The researchers calculated the risk of GI events in patients who took these prescription pain relievers between 2000 and 2004. After reviewing the medical records in a database of more than 7 million patients treated at general practices throughout England, Scotland, and Wales, the investigators identified 9,407 who had an adverse GI event and matched them with more than 88,000 controls who had no such events (BMJ 2005;331:1310–6).

Patients with GI events were more likely to have taken either prescription NSAIDs (odds ratio 1.69) or prescription COX-2 inhibitors (odds ratio 1.89) than were control subjects.

The researchers also found that the concomitant use of ulcer-healing drugs reduces the GI risks of COX-2 inhibitors, which suggests “that there is some risk to protect against.” Taken together, these results indicate that COX-2 inhibitors “may not be as safe as originally thought,” the authors said.

Celecoxib was the only agent out of 27 pain relievers used by the study subjects to show no link with adverse GI events. However, the number of celecoxib users was very small, so this finding remains “difficult to interpret,” the researchers noted.

The use of ulcer-healing drugs such as proton pump inhibitors reduced the risk for GI events in users of both COX-2 inhibitors and NSAIDs, again suggesting that the GI risks of the two types of pain relievers are similar, they added.

A short stay in the ICU is safe and cost effective for low-risk patients who have undergone coronary artery bypass grafting, according to Ghislaine van Mastrigt of Maastricht (the Netherlands) University Hospital and associates.

A “fast-track” ICU stay of 8 hours or less “can be considered as an alternative to conventional postoperative ICU treatment for low-risk CABG patients,” the researchers said.

They assessed the safety of early ICU discharge in a study of 600 CABG patients after noting that “fast-track treatment after cardiac surgery is becoming very popular, although evidence-based research on safety and cost effectiveness is limited.”

A total of 300 subjects were randomly assigned to a short ICU stay and 300 to a conventional overnight stay in the ICU after CABG surgery at the university hospital between 2001 and 2003. Mean patient age was 62 years, and 80% of the patients were men. The rate of readmission to the ICU was 2.7% (eight patients) in the short-stay group and 1.3% (four patients) in the control group, a difference that was not statistically significant. There also were no significant differences between the two groups in postoperative morbidity, 30-day mortality, or total hospital stay, the investigators said (Crit. Care Med. 2006:34:65–75)

There was a small but significant advantage in quality of life measures for the short-stay group, “However, it is questionable whether [quality of life] improvement is clinically relevant,” Ms. Mastrigt and associates noted.

Hospital costs were significantly lower for the fast-track patients, mainly because their stays in the high-cost ICU were a mean of 11 hours shorter than those in the conventional-care group. The short-stay group also had fewer of the laboratory tests that are usually done in the ICU. Costs of other routine hospital care and outpatient procedures were comparable for the two groups.

A short stay in the ICU is safe and cost effective for low-risk patients who have undergone coronary artery bypass grafting, according to Ghislaine van Mastrigt of Maastricht (the Netherlands) University Hospital and associates.

A “fast-track” ICU stay of 8 hours or less “can be considered as an alternative to conventional postoperative ICU treatment for low-risk CABG patients,” the researchers said.

They assessed the safety of early ICU discharge in a study of 600 CABG patients after noting that “fast-track treatment after cardiac surgery is becoming very popular, although evidence-based research on safety and cost effectiveness is limited.”

A total of 300 subjects were randomly assigned to a short ICU stay and 300 to a conventional overnight stay in the ICU after CABG surgery at the university hospital between 2001 and 2003. Mean patient age was 62 years, and 80% of the patients were men. The rate of readmission to the ICU was 2.7% (eight patients) in the short-stay group and 1.3% (four patients) in the control group, a difference that was not statistically significant. There also were no significant differences between the two groups in postoperative morbidity, 30-day mortality, or total hospital stay, the investigators said (Crit. Care Med. 2006:34:65–75)

There was a small but significant advantage in quality of life measures for the short-stay group, “However, it is questionable whether [quality of life] improvement is clinically relevant,” Ms. Mastrigt and associates noted.

Hospital costs were significantly lower for the fast-track patients, mainly because their stays in the high-cost ICU were a mean of 11 hours shorter than those in the conventional-care group. The short-stay group also had fewer of the laboratory tests that are usually done in the ICU. Costs of other routine hospital care and outpatient procedures were comparable for the two groups.

A short stay in the ICU is safe and cost effective for low-risk patients who have undergone coronary artery bypass grafting, according to Ghislaine van Mastrigt of Maastricht (the Netherlands) University Hospital and associates.

A “fast-track” ICU stay of 8 hours or less “can be considered as an alternative to conventional postoperative ICU treatment for low-risk CABG patients,” the researchers said.

They assessed the safety of early ICU discharge in a study of 600 CABG patients after noting that “fast-track treatment after cardiac surgery is becoming very popular, although evidence-based research on safety and cost effectiveness is limited.”

A total of 300 subjects were randomly assigned to a short ICU stay and 300 to a conventional overnight stay in the ICU after CABG surgery at the university hospital between 2001 and 2003. Mean patient age was 62 years, and 80% of the patients were men. The rate of readmission to the ICU was 2.7% (eight patients) in the short-stay group and 1.3% (four patients) in the control group, a difference that was not statistically significant. There also were no significant differences between the two groups in postoperative morbidity, 30-day mortality, or total hospital stay, the investigators said (Crit. Care Med. 2006:34:65–75)

There was a small but significant advantage in quality of life measures for the short-stay group, “However, it is questionable whether [quality of life] improvement is clinically relevant,” Ms. Mastrigt and associates noted.

Hospital costs were significantly lower for the fast-track patients, mainly because their stays in the high-cost ICU were a mean of 11 hours shorter than those in the conventional-care group. The short-stay group also had fewer of the laboratory tests that are usually done in the ICU. Costs of other routine hospital care and outpatient procedures were comparable for the two groups.

Vapotherm respiratory gas administration devices are being voluntarily recalled, following federal government reports that 29 hospitals in 16 states found Ralstonia organisms colonizing the devices, and cultures from approximately 40 pediatric patients also yielded the bacteria.

The Centers for Disease Control and Prevention and the Food and Drug Administration late last year had advised clinicians to use alternative devices to provide humidified oxygen therapy until the source of contamination has been identified and removed. They also recommended that any patients who have been exposed to the Vapotherm system be monitored for signs and symptoms suggesting infection, including fever, poor feeding, irritability, and changes in hematologic indices.

In addition, “clinicians may want to consider Ralstonia species infection in the differential diagnosis of symptomatic patients even if the organism has not been isolated,” the FDA said in a public health notification (www.fda.gov/cdrh/safety/122005-vapotherm.html

In response, the device manufacturer, Vapotherm, announced last month that it would recall and disinfect Vapotherm 2000i and 2000h devices. Units will then be returned to the owners with updated disinfection and usage recommendations.

Contamination of the Vapotherm system was first reported by the CDC and the FDA in October 2005, after a Pennsylvania hospital isolated Ralstonia in several patients who had used the device. The Vapotherm system is used “to add moisture to and to warm breathing gases for administration to patients,” according to its manufacturer, Vapotherm Inc. (Stevensville, Md.).

Since the October reports, the CDC and FDA have found additional cases of Ralstonia contamination. Cultures of unused Vapotherm cartridges at two hospitals yielded Ralstonia, but cultures of other unused cartridges from the same lot did not grow the organism.

After the procedures for disinfecting the device that were listed in its original instructions were found to be inadequate, the manufacturer issued new instructions for chloride dioxide disinfection.

However, this method also “may not achieve sustained bacterial control,” according to the FDA.

Several alternative devices are listed on the FDA Web site cited above.

Ralstonia, gram-negative bacteria usually found in water and soil and on plants, formerly were included in Pseudomonas or Burkholderia species and still can be misidentified as such. “Infections caused by Ralstonia should be treated on the basis of results of susceptibility testing of the patient's isolate,” according to the CDC (MMWR 2005;54:1–2).

“Clinicians who elect to use Vapotherm are encouraged to weigh the risk of potential bacterial contamination of the device against the benefits Vapotherm might provide patients who require humidified oxygen therapy,” the CDC said.

For more information about the recall, visit www.vtherm.com/recallwww.fda.gov/Medwatch

Vapotherm respiratory gas administration devices are being voluntarily recalled, following federal government reports that 29 hospitals in 16 states found Ralstonia organisms colonizing the devices, and cultures from approximately 40 pediatric patients also yielded the bacteria.

The Centers for Disease Control and Prevention and the Food and Drug Administration late last year had advised clinicians to use alternative devices to provide humidified oxygen therapy until the source of contamination has been identified and removed. They also recommended that any patients who have been exposed to the Vapotherm system be monitored for signs and symptoms suggesting infection, including fever, poor feeding, irritability, and changes in hematologic indices.

In addition, “clinicians may want to consider Ralstonia species infection in the differential diagnosis of symptomatic patients even if the organism has not been isolated,” the FDA said in a public health notification (www.fda.gov/cdrh/safety/122005-vapotherm.html

In response, the device manufacturer, Vapotherm, announced last month that it would recall and disinfect Vapotherm 2000i and 2000h devices. Units will then be returned to the owners with updated disinfection and usage recommendations.

Contamination of the Vapotherm system was first reported by the CDC and the FDA in October 2005, after a Pennsylvania hospital isolated Ralstonia in several patients who had used the device. The Vapotherm system is used “to add moisture to and to warm breathing gases for administration to patients,” according to its manufacturer, Vapotherm Inc. (Stevensville, Md.).

Since the October reports, the CDC and FDA have found additional cases of Ralstonia contamination. Cultures of unused Vapotherm cartridges at two hospitals yielded Ralstonia, but cultures of other unused cartridges from the same lot did not grow the organism.

After the procedures for disinfecting the device that were listed in its original instructions were found to be inadequate, the manufacturer issued new instructions for chloride dioxide disinfection.

However, this method also “may not achieve sustained bacterial control,” according to the FDA.

Several alternative devices are listed on the FDA Web site cited above.

Ralstonia, gram-negative bacteria usually found in water and soil and on plants, formerly were included in Pseudomonas or Burkholderia species and still can be misidentified as such. “Infections caused by Ralstonia should be treated on the basis of results of susceptibility testing of the patient's isolate,” according to the CDC (MMWR 2005;54:1–2).

“Clinicians who elect to use Vapotherm are encouraged to weigh the risk of potential bacterial contamination of the device against the benefits Vapotherm might provide patients who require humidified oxygen therapy,” the CDC said.

For more information about the recall, visit www.vtherm.com/recallwww.fda.gov/Medwatch

Vapotherm respiratory gas administration devices are being voluntarily recalled, following federal government reports that 29 hospitals in 16 states found Ralstonia organisms colonizing the devices, and cultures from approximately 40 pediatric patients also yielded the bacteria.

The Centers for Disease Control and Prevention and the Food and Drug Administration late last year had advised clinicians to use alternative devices to provide humidified oxygen therapy until the source of contamination has been identified and removed. They also recommended that any patients who have been exposed to the Vapotherm system be monitored for signs and symptoms suggesting infection, including fever, poor feeding, irritability, and changes in hematologic indices.

In addition, “clinicians may want to consider Ralstonia species infection in the differential diagnosis of symptomatic patients even if the organism has not been isolated,” the FDA said in a public health notification (www.fda.gov/cdrh/safety/122005-vapotherm.html

In response, the device manufacturer, Vapotherm, announced last month that it would recall and disinfect Vapotherm 2000i and 2000h devices. Units will then be returned to the owners with updated disinfection and usage recommendations.

Contamination of the Vapotherm system was first reported by the CDC and the FDA in October 2005, after a Pennsylvania hospital isolated Ralstonia in several patients who had used the device. The Vapotherm system is used “to add moisture to and to warm breathing gases for administration to patients,” according to its manufacturer, Vapotherm Inc. (Stevensville, Md.).

Since the October reports, the CDC and FDA have found additional cases of Ralstonia contamination. Cultures of unused Vapotherm cartridges at two hospitals yielded Ralstonia, but cultures of other unused cartridges from the same lot did not grow the organism.

After the procedures for disinfecting the device that were listed in its original instructions were found to be inadequate, the manufacturer issued new instructions for chloride dioxide disinfection.

However, this method also “may not achieve sustained bacterial control,” according to the FDA.

Several alternative devices are listed on the FDA Web site cited above.

Ralstonia, gram-negative bacteria usually found in water and soil and on plants, formerly were included in Pseudomonas or Burkholderia species and still can be misidentified as such. “Infections caused by Ralstonia should be treated on the basis of results of susceptibility testing of the patient's isolate,” according to the CDC (MMWR 2005;54:1–2).

“Clinicians who elect to use Vapotherm are encouraged to weigh the risk of potential bacterial contamination of the device against the benefits Vapotherm might provide patients who require humidified oxygen therapy,” the CDC said.

For more information about the recall, visit www.vtherm.com/recallwww.fda.gov/Medwatch

Tooth Loss Linked to CHD

Loss of permanent teeth may raise the risk for coronary heart disease, and the risk could increase as the extent of tooth loss worsens, reported Catherine A. Okoro and her associates at the Centers for Disease Control and Prevention, Atlanta.

Epidemiologic studies have shown a link between coronary heart disease (CHD) and tooth loss due to periodontal or other oral disease, but other studies have cast doubt on this association. Ms. Okoro and her colleagues assessed tooth loss and CHD prevalence using data from a surveillance study involving 41,891 people aged 40–79 years in the general U.S. population.

The rate of CHD was 4.7% in subjects who had all their natural teeth but was 5.7% in those who were missing 1–5 teeth, 7.5% in those missing 6–31 teeth, and 8.5% in those missing all of their teeth due to tooth decay or gum disease.

In addition, patients with CHD were more likely to be missing several teeth (29.4%) or all of their teeth (23.6%) than were people who didn't have CHD (17.6% and 10.1%, respectively). Like other local infections, periodontal infections are thought to raise systemic levels of inflammatory mediators and thus promote inflammation-associated atherosclerotic processes, the investigators said (Am. J. Preventive Med. doi:10.1016/j.amepre.2005.07.006).

This study was not designed to identify any possible causal links between tooth loss and CHD. It is possible that the findings simply indicate that people who are more health conscious have better oral health and lower CHD risk, they noted.

Diesel Fumes Harm Vascular Function

Inhaling diesel exhaust impairs two complementary aspects of vascular function: the regulation of vascular tone and the performance of endogenous fibrinolysis.

This may be the mechanism by which air pollution exerts its well-known adverse effects on the cardiovascular system, reported Dr. Nicholas L. Mills of Edinburgh University and his associates.

Noting that transient exposure to road traffic appears to raise the risk of MI and that long-term residence near major highways increases cardiopulmonary mortality, Dr. Mills and his associates assessed the effects of diluted diesel exhaust inhalation on endothelial function in a study involving 30 healthy male nonsmokers aged 20–38 years.

Half of the subjects were randomly assigned to breathe diesel exhaust in a specially designed chamber while performing moderate exercise and resting. The other 15 subjects breathed normal room air and performed the same activities in the chamber. In a second session 2 weeks later, all subjects were crossed over to the other group. The exhaust was produced by an idling diesel engine. Over 90% of it was shunted away, and the remainder was diluted with room air and fed into the testing chamber, the researchers said (Circulation 2005;112:3930–6).

Breathing diesel fumes was found to impair the vasomotor responses in the forearm vascular bed to both endothelium-dependent and endothelium-independent vasodilators, but it had no effect on the vasomotor response to a calcium channel antagonist. This suggests that the mechanism of vascular dysfunction involved increased consumption of nitrogen oxides, the investigators said.

Binge Drinking Imperils MI Survivors

Binge drinking doubles short-term mortality in patients who have survived an MI, regardless of their usual level of drinking and the type of alcohol they consume, reported Dr. Kenneth J. Mukamal of Beth Israel Deaconess Medical Center, Boston, and his associates.

The researchers assessed mortality in a subset of patients who had participated in a multicenter cohort study on the causes of MI. The 1,919 patients had been interviewed about their drinking habits and other factors while they were hospitalized for an initial MI between 1989 and 1994.

A total of 318 of the patients died during a median of 3.8 years of follow-up. As expected, light and moderate drinking were found to protect against cardiovascular mortality and total mortality, as has been reported in previous studies, the investigators said (Circulation 2005:112:3839–45).

In contrast, binge drinking (consuming 3 or more drinks in 1–2 hours) was linked to a twofold increase in cardiovascular mortality and total mortality. This association held true for subjects who binged on beer, wine, liquor, or any combination of these drinks. It also persisted after the data were adjusted to account for differences in infarct size and severity; smoking status; and intake of coffee, tea, marijuana, and cocaine.

There also appeared to be a dose-response relationship, with mortality risk rising as the frequency of binge drinking episodes increased.

Binge drinking raised mortality among people who customarily were light drinkers as well as those who drank more heavily. This suggests that “any potential benefits of moderate drinking must be weighed against the risks of even occasional binge drinking,” Dr. Mukamal and associates said. “In our analyses, the apparent benefit associated with otherwise light drinking among patients with acute MI was completely eliminated by episodes of binge drinking.”

Tooth Loss Linked to CHD

Loss of permanent teeth may raise the risk for coronary heart disease, and the risk could increase as the extent of tooth loss worsens, reported Catherine A. Okoro and her associates at the Centers for Disease Control and Prevention, Atlanta.

Epidemiologic studies have shown a link between coronary heart disease (CHD) and tooth loss due to periodontal or other oral disease, but other studies have cast doubt on this association. Ms. Okoro and her colleagues assessed tooth loss and CHD prevalence using data from a surveillance study involving 41,891 people aged 40–79 years in the general U.S. population.

The rate of CHD was 4.7% in subjects who had all their natural teeth but was 5.7% in those who were missing 1–5 teeth, 7.5% in those missing 6–31 teeth, and 8.5% in those missing all of their teeth due to tooth decay or gum disease.

In addition, patients with CHD were more likely to be missing several teeth (29.4%) or all of their teeth (23.6%) than were people who didn't have CHD (17.6% and 10.1%, respectively). Like other local infections, periodontal infections are thought to raise systemic levels of inflammatory mediators and thus promote inflammation-associated atherosclerotic processes, the investigators said (Am. J. Preventive Med. doi:10.1016/j.amepre.2005.07.006).

This study was not designed to identify any possible causal links between tooth loss and CHD. It is possible that the findings simply indicate that people who are more health conscious have better oral health and lower CHD risk, they noted.

Diesel Fumes Harm Vascular Function

Inhaling diesel exhaust impairs two complementary aspects of vascular function: the regulation of vascular tone and the performance of endogenous fibrinolysis.

This may be the mechanism by which air pollution exerts its well-known adverse effects on the cardiovascular system, reported Dr. Nicholas L. Mills of Edinburgh University and his associates.

Noting that transient exposure to road traffic appears to raise the risk of MI and that long-term residence near major highways increases cardiopulmonary mortality, Dr. Mills and his associates assessed the effects of diluted diesel exhaust inhalation on endothelial function in a study involving 30 healthy male nonsmokers aged 20–38 years.

Half of the subjects were randomly assigned to breathe diesel exhaust in a specially designed chamber while performing moderate exercise and resting. The other 15 subjects breathed normal room air and performed the same activities in the chamber. In a second session 2 weeks later, all subjects were crossed over to the other group. The exhaust was produced by an idling diesel engine. Over 90% of it was shunted away, and the remainder was diluted with room air and fed into the testing chamber, the researchers said (Circulation 2005;112:3930–6).

Breathing diesel fumes was found to impair the vasomotor responses in the forearm vascular bed to both endothelium-dependent and endothelium-independent vasodilators, but it had no effect on the vasomotor response to a calcium channel antagonist. This suggests that the mechanism of vascular dysfunction involved increased consumption of nitrogen oxides, the investigators said.

Binge Drinking Imperils MI Survivors

Binge drinking doubles short-term mortality in patients who have survived an MI, regardless of their usual level of drinking and the type of alcohol they consume, reported Dr. Kenneth J. Mukamal of Beth Israel Deaconess Medical Center, Boston, and his associates.

The researchers assessed mortality in a subset of patients who had participated in a multicenter cohort study on the causes of MI. The 1,919 patients had been interviewed about their drinking habits and other factors while they were hospitalized for an initial MI between 1989 and 1994.

A total of 318 of the patients died during a median of 3.8 years of follow-up. As expected, light and moderate drinking were found to protect against cardiovascular mortality and total mortality, as has been reported in previous studies, the investigators said (Circulation 2005:112:3839–45).

In contrast, binge drinking (consuming 3 or more drinks in 1–2 hours) was linked to a twofold increase in cardiovascular mortality and total mortality. This association held true for subjects who binged on beer, wine, liquor, or any combination of these drinks. It also persisted after the data were adjusted to account for differences in infarct size and severity; smoking status; and intake of coffee, tea, marijuana, and cocaine.

There also appeared to be a dose-response relationship, with mortality risk rising as the frequency of binge drinking episodes increased.

Binge drinking raised mortality among people who customarily were light drinkers as well as those who drank more heavily. This suggests that “any potential benefits of moderate drinking must be weighed against the risks of even occasional binge drinking,” Dr. Mukamal and associates said. “In our analyses, the apparent benefit associated with otherwise light drinking among patients with acute MI was completely eliminated by episodes of binge drinking.”

Tooth Loss Linked to CHD

Loss of permanent teeth may raise the risk for coronary heart disease, and the risk could increase as the extent of tooth loss worsens, reported Catherine A. Okoro and her associates at the Centers for Disease Control and Prevention, Atlanta.

Epidemiologic studies have shown a link between coronary heart disease (CHD) and tooth loss due to periodontal or other oral disease, but other studies have cast doubt on this association. Ms. Okoro and her colleagues assessed tooth loss and CHD prevalence using data from a surveillance study involving 41,891 people aged 40–79 years in the general U.S. population.

The rate of CHD was 4.7% in subjects who had all their natural teeth but was 5.7% in those who were missing 1–5 teeth, 7.5% in those missing 6–31 teeth, and 8.5% in those missing all of their teeth due to tooth decay or gum disease.

In addition, patients with CHD were more likely to be missing several teeth (29.4%) or all of their teeth (23.6%) than were people who didn't have CHD (17.6% and 10.1%, respectively). Like other local infections, periodontal infections are thought to raise systemic levels of inflammatory mediators and thus promote inflammation-associated atherosclerotic processes, the investigators said (Am. J. Preventive Med. doi:10.1016/j.amepre.2005.07.006).

This study was not designed to identify any possible causal links between tooth loss and CHD. It is possible that the findings simply indicate that people who are more health conscious have better oral health and lower CHD risk, they noted.

Diesel Fumes Harm Vascular Function

Inhaling diesel exhaust impairs two complementary aspects of vascular function: the regulation of vascular tone and the performance of endogenous fibrinolysis.

This may be the mechanism by which air pollution exerts its well-known adverse effects on the cardiovascular system, reported Dr. Nicholas L. Mills of Edinburgh University and his associates.

Noting that transient exposure to road traffic appears to raise the risk of MI and that long-term residence near major highways increases cardiopulmonary mortality, Dr. Mills and his associates assessed the effects of diluted diesel exhaust inhalation on endothelial function in a study involving 30 healthy male nonsmokers aged 20–38 years.

Half of the subjects were randomly assigned to breathe diesel exhaust in a specially designed chamber while performing moderate exercise and resting. The other 15 subjects breathed normal room air and performed the same activities in the chamber. In a second session 2 weeks later, all subjects were crossed over to the other group. The exhaust was produced by an idling diesel engine. Over 90% of it was shunted away, and the remainder was diluted with room air and fed into the testing chamber, the researchers said (Circulation 2005;112:3930–6).

Breathing diesel fumes was found to impair the vasomotor responses in the forearm vascular bed to both endothelium-dependent and endothelium-independent vasodilators, but it had no effect on the vasomotor response to a calcium channel antagonist. This suggests that the mechanism of vascular dysfunction involved increased consumption of nitrogen oxides, the investigators said.

Binge Drinking Imperils MI Survivors

Binge drinking doubles short-term mortality in patients who have survived an MI, regardless of their usual level of drinking and the type of alcohol they consume, reported Dr. Kenneth J. Mukamal of Beth Israel Deaconess Medical Center, Boston, and his associates.

The researchers assessed mortality in a subset of patients who had participated in a multicenter cohort study on the causes of MI. The 1,919 patients had been interviewed about their drinking habits and other factors while they were hospitalized for an initial MI between 1989 and 1994.

A total of 318 of the patients died during a median of 3.8 years of follow-up. As expected, light and moderate drinking were found to protect against cardiovascular mortality and total mortality, as has been reported in previous studies, the investigators said (Circulation 2005:112:3839–45).

In contrast, binge drinking (consuming 3 or more drinks in 1–2 hours) was linked to a twofold increase in cardiovascular mortality and total mortality. This association held true for subjects who binged on beer, wine, liquor, or any combination of these drinks. It also persisted after the data were adjusted to account for differences in infarct size and severity; smoking status; and intake of coffee, tea, marijuana, and cocaine.

There also appeared to be a dose-response relationship, with mortality risk rising as the frequency of binge drinking episodes increased.

Binge drinking raised mortality among people who customarily were light drinkers as well as those who drank more heavily. This suggests that “any potential benefits of moderate drinking must be weighed against the risks of even occasional binge drinking,” Dr. Mukamal and associates said. “In our analyses, the apparent benefit associated with otherwise light drinking among patients with acute MI was completely eliminated by episodes of binge drinking.”

Statins neither raise nor lower the risk of cancer or cancer mortality, according to a metaanalysis of 26 randomized clinical trials.

Several retrospective studies have suggested that statins reduce the risk of developing cancer by as much as 50%. Some researchers have proposed that the drugs may inhibit carcinogenesis by decreasing systemic inflammation, interfering with neovascular formation, and inhibiting cell proliferation.

However, three metaanalyses have failed to confirm that statins exert a protective effect against cancer, and some investigators have noted that statins have properties that could actually enhance cancer risk, such as inhibiting selenoprotein synthesis and impairing the function of natural killer cells.

To shed light on the issue, Krista M. Dale, Pharm.D., of the University of Connecticut School of Pharmacy, Hartford, and her associates conducted a much larger metaanalysis of 26 randomized clinical trials involving 86,936 subjects. The participants were followed up for 2–10 years for the development of cancer.

The trials included only placebo-controlled or standard-treatment-controlled studies enrolling a minimum of 100 subjects each. Most of these trials assessed the ability of statins to prevent coronary artery disease, but all examined cancer diagnosis or cancer death as a primary or secondary end point.

Statins did not reduce the risk of cancer or of cancer death, Dr. Dale and her associates said (JAMA 2006;295:74–80).

When six major subtypes of cancer—breast, colon, gastrointestinal, prostate, respiratory tract, and skin cancers—were considered individually, statins did not reduce the risk of any of these types.

Similarly, when pravastatin, simvastatin, atorvastatin, cerivastatin, fluvastatin, and lovastatin were considered individually, none of the agents reduced the risk of cancer or cancer death.

And when the metaanalysis was narrowed to assess natural versus synthetic statins and low-lipophilic versus high-lipophilic statins, the results did not change.

“We thought that hydrophilic statins, with their impaired ability to penetrate biological membranes, might provide different effects than lipophilic statins, which readily enter cells, but this was not evident in our study. Similarly, naturally derived statins have a markedly different structure than synthetic statins, but neither type affected the results,” the investigators noted.

“Our results are in agreement with three previous case-control studies that found that statins did not reduce the incidence of cancer,” Dr. Dale and her associates said.

Statins neither raise nor lower the risk of cancer or cancer mortality, according to a metaanalysis of 26 randomized clinical trials.

Several retrospective studies have suggested that statins reduce the risk of developing cancer by as much as 50%. Some researchers have proposed that the drugs may inhibit carcinogenesis by decreasing systemic inflammation, interfering with neovascular formation, and inhibiting cell proliferation.

However, three metaanalyses have failed to confirm that statins exert a protective effect against cancer, and some investigators have noted that statins have properties that could actually enhance cancer risk, such as inhibiting selenoprotein synthesis and impairing the function of natural killer cells.

To shed light on the issue, Krista M. Dale, Pharm.D., of the University of Connecticut School of Pharmacy, Hartford, and her associates conducted a much larger metaanalysis of 26 randomized clinical trials involving 86,936 subjects. The participants were followed up for 2–10 years for the development of cancer.

The trials included only placebo-controlled or standard-treatment-controlled studies enrolling a minimum of 100 subjects each. Most of these trials assessed the ability of statins to prevent coronary artery disease, but all examined cancer diagnosis or cancer death as a primary or secondary end point.

Statins did not reduce the risk of cancer or of cancer death, Dr. Dale and her associates said (JAMA 2006;295:74–80).

When six major subtypes of cancer—breast, colon, gastrointestinal, prostate, respiratory tract, and skin cancers—were considered individually, statins did not reduce the risk of any of these types.

Similarly, when pravastatin, simvastatin, atorvastatin, cerivastatin, fluvastatin, and lovastatin were considered individually, none of the agents reduced the risk of cancer or cancer death.

And when the metaanalysis was narrowed to assess natural versus synthetic statins and low-lipophilic versus high-lipophilic statins, the results did not change.

“We thought that hydrophilic statins, with their impaired ability to penetrate biological membranes, might provide different effects than lipophilic statins, which readily enter cells, but this was not evident in our study. Similarly, naturally derived statins have a markedly different structure than synthetic statins, but neither type affected the results,” the investigators noted.

“Our results are in agreement with three previous case-control studies that found that statins did not reduce the incidence of cancer,” Dr. Dale and her associates said.

Statins neither raise nor lower the risk of cancer or cancer mortality, according to a metaanalysis of 26 randomized clinical trials.

Several retrospective studies have suggested that statins reduce the risk of developing cancer by as much as 50%. Some researchers have proposed that the drugs may inhibit carcinogenesis by decreasing systemic inflammation, interfering with neovascular formation, and inhibiting cell proliferation.

However, three metaanalyses have failed to confirm that statins exert a protective effect against cancer, and some investigators have noted that statins have properties that could actually enhance cancer risk, such as inhibiting selenoprotein synthesis and impairing the function of natural killer cells.

To shed light on the issue, Krista M. Dale, Pharm.D., of the University of Connecticut School of Pharmacy, Hartford, and her associates conducted a much larger metaanalysis of 26 randomized clinical trials involving 86,936 subjects. The participants were followed up for 2–10 years for the development of cancer.

The trials included only placebo-controlled or standard-treatment-controlled studies enrolling a minimum of 100 subjects each. Most of these trials assessed the ability of statins to prevent coronary artery disease, but all examined cancer diagnosis or cancer death as a primary or secondary end point.

Statins did not reduce the risk of cancer or of cancer death, Dr. Dale and her associates said (JAMA 2006;295:74–80).

When six major subtypes of cancer—breast, colon, gastrointestinal, prostate, respiratory tract, and skin cancers—were considered individually, statins did not reduce the risk of any of these types.

Similarly, when pravastatin, simvastatin, atorvastatin, cerivastatin, fluvastatin, and lovastatin were considered individually, none of the agents reduced the risk of cancer or cancer death.

And when the metaanalysis was narrowed to assess natural versus synthetic statins and low-lipophilic versus high-lipophilic statins, the results did not change.

“We thought that hydrophilic statins, with their impaired ability to penetrate biological membranes, might provide different effects than lipophilic statins, which readily enter cells, but this was not evident in our study. Similarly, naturally derived statins have a markedly different structure than synthetic statins, but neither type affected the results,” the investigators noted.

“Our results are in agreement with three previous case-control studies that found that statins did not reduce the incidence of cancer,” Dr. Dale and her associates said.

Regular administration of acetaminophen raises levels of general activity, social interaction, engagement with media, and worklike activity in elderly patients with moderate to severe dementia, reported John T. Chibnall, Ph.D., of St. Louis University School of Medicine, and his associates.

Regular dosing with the analgesic presumably addresses untreated pain in these patients, who often cannot report pain and who have a high prevalence of comorbidities, which can generate significant pain, the researchers said.

Their study findings imply that untreated pain inhibits dementia patients' active engagement with the environment and promotes their withdrawal, Dr. Chibnall, a professor of psychiatry at the university, and his associates added (J. Am. Geriatr. Soc. 2005;53:1921–9).

Behavioral changes in 25 elderly (mean age 85.9 years) nursing home residents with moderate to severe dementia during an 8-week study were evaluated. The subjects had degenerative dementia, Alzheimer's disease, or multi-infarct dementia and had resided in nursing homes for a mean of 35 months. All had moderate to severe cognitive decline and impairment in daily living activities.

The subjects were given either two 500-mg tablets of acetaminophen or two placebo tablets at mealtimes every day for 4 weeks, then switched to the other treatment for 4 weeks, following a 1-week washout period between the two phases. Their behavior was evaluated under both conditions using the Dementia Care Mapping (DCM) tool, in which trained “mappers” observed patients for 5 hours between 9 a.m. and 2 p.m., when subjects were likely to be most active. At 5-minute intervals, the observers quantified a wide range of behaviors across 24 domains such as direct or passive social involvement, creative activities, exercise, listening to music, sleeping, and eating.

They also were evaluated using the Cohen-Mansfield Agitation Inventory (CMAI), a 29-item scale in which personnel assessed how often the patients displayed a variety of agitated behaviors during the preceding 2 weeks.

With acetaminophen, subjects clearly showed higher levels of general activity, spent more time in direct social interactions and in engagement with media, and participated more in worklike activity. They also spent significantly less time alone in their rooms.

However, subjects also spent more time in passive social involvement, and slightly more time experiencing unattended distress.

Agitation did not decrease, and the use of psychotropic medications did not decrease, while patients were taking acetaminophen. However, the levels of agitation and the frequency of agitated behaviors were quite low in this study, which may have confounded the results. Similarly, the use of psychotropic drugs was quite low overall, leaving little room for the intervention to show an effect, the researchers noted.

Regular administration of acetaminophen raises levels of general activity, social interaction, engagement with media, and worklike activity in elderly patients with moderate to severe dementia, reported John T. Chibnall, Ph.D., of St. Louis University School of Medicine, and his associates.

Regular dosing with the analgesic presumably addresses untreated pain in these patients, who often cannot report pain and who have a high prevalence of comorbidities, which can generate significant pain, the researchers said.

Their study findings imply that untreated pain inhibits dementia patients' active engagement with the environment and promotes their withdrawal, Dr. Chibnall, a professor of psychiatry at the university, and his associates added (J. Am. Geriatr. Soc. 2005;53:1921–9).

Behavioral changes in 25 elderly (mean age 85.9 years) nursing home residents with moderate to severe dementia during an 8-week study were evaluated. The subjects had degenerative dementia, Alzheimer's disease, or multi-infarct dementia and had resided in nursing homes for a mean of 35 months. All had moderate to severe cognitive decline and impairment in daily living activities.

The subjects were given either two 500-mg tablets of acetaminophen or two placebo tablets at mealtimes every day for 4 weeks, then switched to the other treatment for 4 weeks, following a 1-week washout period between the two phases. Their behavior was evaluated under both conditions using the Dementia Care Mapping (DCM) tool, in which trained “mappers” observed patients for 5 hours between 9 a.m. and 2 p.m., when subjects were likely to be most active. At 5-minute intervals, the observers quantified a wide range of behaviors across 24 domains such as direct or passive social involvement, creative activities, exercise, listening to music, sleeping, and eating.

They also were evaluated using the Cohen-Mansfield Agitation Inventory (CMAI), a 29-item scale in which personnel assessed how often the patients displayed a variety of agitated behaviors during the preceding 2 weeks.

With acetaminophen, subjects clearly showed higher levels of general activity, spent more time in direct social interactions and in engagement with media, and participated more in worklike activity. They also spent significantly less time alone in their rooms.

However, subjects also spent more time in passive social involvement, and slightly more time experiencing unattended distress.

Agitation did not decrease, and the use of psychotropic medications did not decrease, while patients were taking acetaminophen. However, the levels of agitation and the frequency of agitated behaviors were quite low in this study, which may have confounded the results. Similarly, the use of psychotropic drugs was quite low overall, leaving little room for the intervention to show an effect, the researchers noted.

Regular administration of acetaminophen raises levels of general activity, social interaction, engagement with media, and worklike activity in elderly patients with moderate to severe dementia, reported John T. Chibnall, Ph.D., of St. Louis University School of Medicine, and his associates.

Regular dosing with the analgesic presumably addresses untreated pain in these patients, who often cannot report pain and who have a high prevalence of comorbidities, which can generate significant pain, the researchers said.

Their study findings imply that untreated pain inhibits dementia patients' active engagement with the environment and promotes their withdrawal, Dr. Chibnall, a professor of psychiatry at the university, and his associates added (J. Am. Geriatr. Soc. 2005;53:1921–9).

Behavioral changes in 25 elderly (mean age 85.9 years) nursing home residents with moderate to severe dementia during an 8-week study were evaluated. The subjects had degenerative dementia, Alzheimer's disease, or multi-infarct dementia and had resided in nursing homes for a mean of 35 months. All had moderate to severe cognitive decline and impairment in daily living activities.

The subjects were given either two 500-mg tablets of acetaminophen or two placebo tablets at mealtimes every day for 4 weeks, then switched to the other treatment for 4 weeks, following a 1-week washout period between the two phases. Their behavior was evaluated under both conditions using the Dementia Care Mapping (DCM) tool, in which trained “mappers” observed patients for 5 hours between 9 a.m. and 2 p.m., when subjects were likely to be most active. At 5-minute intervals, the observers quantified a wide range of behaviors across 24 domains such as direct or passive social involvement, creative activities, exercise, listening to music, sleeping, and eating.

They also were evaluated using the Cohen-Mansfield Agitation Inventory (CMAI), a 29-item scale in which personnel assessed how often the patients displayed a variety of agitated behaviors during the preceding 2 weeks.

With acetaminophen, subjects clearly showed higher levels of general activity, spent more time in direct social interactions and in engagement with media, and participated more in worklike activity. They also spent significantly less time alone in their rooms.

However, subjects also spent more time in passive social involvement, and slightly more time experiencing unattended distress.

Agitation did not decrease, and the use of psychotropic medications did not decrease, while patients were taking acetaminophen. However, the levels of agitation and the frequency of agitated behaviors were quite low in this study, which may have confounded the results. Similarly, the use of psychotropic drugs was quite low overall, leaving little room for the intervention to show an effect, the researchers noted.

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as controls. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months.

Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the placebo group and the control groups.

Both the improved QOL and the improved cognitive functioning were correlated with increased serum testosterone levels.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as controls. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months.

Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the placebo group and the control groups.

Both the improved QOL and the improved cognitive functioning were correlated with increased serum testosterone levels.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.

Testosterone replacement improved the quality of life for men with Alzheimer's disease and low serum testosterone levels in a small preliminary study, reported Po H. Lu, Psy.D., and associates at the University of California, Los Angeles, David Geffen School of Medicine.

Testosterone therapy has been shown to improve mood, muscle mass, strength, bone density, libido, and certain cognitive functions in hypogonadal men who are otherwise healthy, but this is the first study to report that testosterone may exert positive effects in Alzheimer's disease (AD), the researchers said (Arch. Neurol. 2006;63:1–9).

They assessed testosterone's effects on a variety of cognitive, behavioral, mood, and quality of life (QOL) measures in 16 men with mild to moderate AD and 22 healthy elderly men who served as controls. The study subjects were randomly assigned to apply either testosterone patches (7 patients and 10 controls) or placebo patches (9 patients and 12 controls) every day for 6 months.

Five of the AD patients and six of the control subjects were hypogonadal at baseline, with serum testosterone levels below 298 ng/dL.

As a group, the AD patients who received testosterone showed a significantly better QOL, as assessed by their caregivers using the 13-item Quality of Life-Alzheimer's Disease scale, than AD patients who received placebo. This effect occurred because the testosterone recipients showed a nonsignificant trend toward improved QOL over the 6-month study period, while the placebo group showed significant declines.

Similarly, the AD patients who received testosterone showed either greater improvement or less decline in three measures of visual-spatial cognitive functioning, compared with the placebo group and the control groups.

Both the improved QOL and the improved cognitive functioning were correlated with increased serum testosterone levels.

Two AD patients and four control subjects withdrew from the study because of adverse effects, including skin rash at the testosterone patch application site.