Doug Brunk

By the time children of overweight mothers reach 6 years of age, they are 15 times more likely to be obese, compared with children of lean mothers, results from a novel study suggest.

“These are kids at extraordinary risk for developing obesity,” the study's lead author, Robert Berkowitz, M.D., said in an interview. “These are not kids who are going to get thin later.”

The finding suggests that children of overweight mothers could become a target group for obesity prevention efforts, said Dr. Berkowitz, chair of adolescent psychiatry and executive director of the behavioral health center at the Children's Hospital of Philadelphia.

“Common sense prevention approaches [for children] include regular activity that's healthy and safe, cutting down on TV watching and computer game usage, and eating a healthy, low-fat diet with fruits and vegetables and portion control,” he told this newspaper.

“But we don't know that for sure because we haven't done the obesity prevention treatment at such a young age.”

For the study, which is the largest of its kind, he and his associates followed 33 children at high risk of obesity and 37 children at low risk of obesity based on the mother's prepregnancy body mass index (Am. J. Clin. Nutr. 2005;81:140–6). Mothers of high-risk children had a mean prepregnancy BMI of 30.3 kg/m2 while mothers of low-risk children had a mean BMI of 19.5 kg/m2. The study was confined to white children because they have different growth patterns compared with nonwhite children.

Investigators examined the children from 3 months of age to 6 years, including measurements of height, weight, skin fold thickness, and fat mass and lean mass by dual-energy x-ray absorptiometry (DXA).

They defined childhood overweight as a BMI at or above the 85th percentile for age and gender according to the National Center for Health Statistics/Centers for Disease Control and Prevention growth charts.

By age 2, no clinical differences were observed between the high- and low-risk groups, but by age 4 years, weight, BMI, lean body mass, and waist circumference were significantly greater among high-risk children, compared with their low-risk counterparts. Dr. Berkowitz said these factors translated into an 11-fold risk of obesity developing in high-risk children.

By age 6 years, the weight, BMI, lean body mass, and waist circumference had increased even more among high-risk children compared with their low-risk counterparts. Skin fold thickness also increased. In addition, for the first time, fat mass was greater in high-risk children compared with their low-risk counterparts (6.7 kg vs. 3.8 kg, respectively). So was percentage of body fat (24.7% vs. 18.8%, respectively). Dr. Berkowitz said these factors translated into a 15-fold risk of obesity developing in high-risk children.

Harsohena Kaur, M.D., a pediatrician at the University of Kansas, Kansas City, called the study “another piece of the puzzle” in gaining a better understanding of the epidemic of childhood obesity.

“We have been seeing bigger and bigger babies who are becoming bigger and bigger toddlers,” said Dr. Kaur, whose research interests include childhood obesity. “They seem to be bigger across the board. I have no idea how that's going to impact everything 20 years from now. This study is scary in that sense.”

Dr. Berkowitz said he was surprised there were no clinical differences between the high- and low-risk groups of children in the first 2 years of life.

“The kids at 1 and 2 years were identical in measures of height and weight and skin fold and body composition,” he said. “Maybe one of the things that's happening is that certain genes are beginning to turn on, or environmental influences are strong at this age.” A limitation of the study, he said, was its relatively small sample size. The National Institutes of Health supported the study.

By the time children of overweight mothers reach 6 years of age, they are 15 times more likely to be obese, compared with children of lean mothers, results from a novel study suggest.

“These are kids at extraordinary risk for developing obesity,” the study's lead author, Robert Berkowitz, M.D., said in an interview. “These are not kids who are going to get thin later.”

The finding suggests that children of overweight mothers could become a target group for obesity prevention efforts, said Dr. Berkowitz, chair of adolescent psychiatry and executive director of the behavioral health center at the Children's Hospital of Philadelphia.

“Common sense prevention approaches [for children] include regular activity that's healthy and safe, cutting down on TV watching and computer game usage, and eating a healthy, low-fat diet with fruits and vegetables and portion control,” he told this newspaper.

“But we don't know that for sure because we haven't done the obesity prevention treatment at such a young age.”

For the study, which is the largest of its kind, he and his associates followed 33 children at high risk of obesity and 37 children at low risk of obesity based on the mother's prepregnancy body mass index (Am. J. Clin. Nutr. 2005;81:140–6). Mothers of high-risk children had a mean prepregnancy BMI of 30.3 kg/m2 while mothers of low-risk children had a mean BMI of 19.5 kg/m2. The study was confined to white children because they have different growth patterns compared with nonwhite children.

Investigators examined the children from 3 months of age to 6 years, including measurements of height, weight, skin fold thickness, and fat mass and lean mass by dual-energy x-ray absorptiometry (DXA).

They defined childhood overweight as a BMI at or above the 85th percentile for age and gender according to the National Center for Health Statistics/Centers for Disease Control and Prevention growth charts.

By age 2, no clinical differences were observed between the high- and low-risk groups, but by age 4 years, weight, BMI, lean body mass, and waist circumference were significantly greater among high-risk children, compared with their low-risk counterparts. Dr. Berkowitz said these factors translated into an 11-fold risk of obesity developing in high-risk children.

By age 6 years, the weight, BMI, lean body mass, and waist circumference had increased even more among high-risk children compared with their low-risk counterparts. Skin fold thickness also increased. In addition, for the first time, fat mass was greater in high-risk children compared with their low-risk counterparts (6.7 kg vs. 3.8 kg, respectively). So was percentage of body fat (24.7% vs. 18.8%, respectively). Dr. Berkowitz said these factors translated into a 15-fold risk of obesity developing in high-risk children.

Harsohena Kaur, M.D., a pediatrician at the University of Kansas, Kansas City, called the study “another piece of the puzzle” in gaining a better understanding of the epidemic of childhood obesity.

“We have been seeing bigger and bigger babies who are becoming bigger and bigger toddlers,” said Dr. Kaur, whose research interests include childhood obesity. “They seem to be bigger across the board. I have no idea how that's going to impact everything 20 years from now. This study is scary in that sense.”

Dr. Berkowitz said he was surprised there were no clinical differences between the high- and low-risk groups of children in the first 2 years of life.

“The kids at 1 and 2 years were identical in measures of height and weight and skin fold and body composition,” he said. “Maybe one of the things that's happening is that certain genes are beginning to turn on, or environmental influences are strong at this age.” A limitation of the study, he said, was its relatively small sample size. The National Institutes of Health supported the study.

By the time children of overweight mothers reach 6 years of age, they are 15 times more likely to be obese, compared with children of lean mothers, results from a novel study suggest.

“These are kids at extraordinary risk for developing obesity,” the study's lead author, Robert Berkowitz, M.D., said in an interview. “These are not kids who are going to get thin later.”

The finding suggests that children of overweight mothers could become a target group for obesity prevention efforts, said Dr. Berkowitz, chair of adolescent psychiatry and executive director of the behavioral health center at the Children's Hospital of Philadelphia.

“Common sense prevention approaches [for children] include regular activity that's healthy and safe, cutting down on TV watching and computer game usage, and eating a healthy, low-fat diet with fruits and vegetables and portion control,” he told this newspaper.

“But we don't know that for sure because we haven't done the obesity prevention treatment at such a young age.”

For the study, which is the largest of its kind, he and his associates followed 33 children at high risk of obesity and 37 children at low risk of obesity based on the mother's prepregnancy body mass index (Am. J. Clin. Nutr. 2005;81:140–6). Mothers of high-risk children had a mean prepregnancy BMI of 30.3 kg/m2 while mothers of low-risk children had a mean BMI of 19.5 kg/m2. The study was confined to white children because they have different growth patterns compared with nonwhite children.

Investigators examined the children from 3 months of age to 6 years, including measurements of height, weight, skin fold thickness, and fat mass and lean mass by dual-energy x-ray absorptiometry (DXA).

They defined childhood overweight as a BMI at or above the 85th percentile for age and gender according to the National Center for Health Statistics/Centers for Disease Control and Prevention growth charts.

By age 2, no clinical differences were observed between the high- and low-risk groups, but by age 4 years, weight, BMI, lean body mass, and waist circumference were significantly greater among high-risk children, compared with their low-risk counterparts. Dr. Berkowitz said these factors translated into an 11-fold risk of obesity developing in high-risk children.

By age 6 years, the weight, BMI, lean body mass, and waist circumference had increased even more among high-risk children compared with their low-risk counterparts. Skin fold thickness also increased. In addition, for the first time, fat mass was greater in high-risk children compared with their low-risk counterparts (6.7 kg vs. 3.8 kg, respectively). So was percentage of body fat (24.7% vs. 18.8%, respectively). Dr. Berkowitz said these factors translated into a 15-fold risk of obesity developing in high-risk children.

Harsohena Kaur, M.D., a pediatrician at the University of Kansas, Kansas City, called the study “another piece of the puzzle” in gaining a better understanding of the epidemic of childhood obesity.

“We have been seeing bigger and bigger babies who are becoming bigger and bigger toddlers,” said Dr. Kaur, whose research interests include childhood obesity. “They seem to be bigger across the board. I have no idea how that's going to impact everything 20 years from now. This study is scary in that sense.”

Dr. Berkowitz said he was surprised there were no clinical differences between the high- and low-risk groups of children in the first 2 years of life.

“The kids at 1 and 2 years were identical in measures of height and weight and skin fold and body composition,” he said. “Maybe one of the things that's happening is that certain genes are beginning to turn on, or environmental influences are strong at this age.” A limitation of the study, he said, was its relatively small sample size. The National Institutes of Health supported the study.

SAN DIEGO — Application of Spa MD Anti-Cellulite Cream effectively reduced cellulite of the thighs in 59% of patients who received the cream without occlusion and in 65% of patients who received it with occlusion, results from a small trial suggest.

The combination of topical agent plus occlusion intended to enhance penetration “offers a valuable treatment option for a condition that has few effective therapeutic choices,” Jaggi Rao, M.D., said in a poster session at the joint annual meeting of the American Society for Dermatologic Surgery and the American College of Mohs Micrographic Surgery and Cutaneous Oncology. Dr. Rao also said that the success of the results seen in this trial serves to confirm the theory that microcirculatory and lymphatic impairment causes cellulite development.

Available since 2003, Spa MD Anti-Cellulite Cream (La Jolla Spa MD, La Jolla, Calif.) contains the following active ingredients, which are thought to stimulate lymphatic and microvascular flow: black pepper seed extract, sweet orange peel, ginger root extract, green tea extract, cinnamon bark extract, capsicum annum resin, and caffeine (which is also thought to promote lipolysis of adipose tissue).

For the study, Dr. Rao and his associates enrolled 17 women aged 20–63 years with moderate to severe cellulite on the thighs and buttocks. They took digital photos of the posterior and lateral thighs with tangential lighting from the Verilux Happy Lite system. They also took baseline photos of each leg at 90 degrees, 45 degrees, and 180 degrees, and measured each leg's thigh circumference with a flexible measuring tape.

All study participants were fitted with bioceramic-coated neoprene shorts. Each pair of shorts was randomized to have either the right or left leg removed so as not to provide occlusion to the control leg.

Each patient received two 60-g tubes of the product and was instructed to apply the cream to the posterior and lateral aspects of both thighs on a daily basis for 4 weeks. The patients were also instructed to wear the modified shorts for at least 6 hours immediately after applying the cream.

After 4 weeks, they underwent repeat photography and thigh measurements and completed self-evaluation surveys. Four blinded, independent dermatologists reviewed all photographs.

Dr. Rao reported that more than half (65%) of the participants had a decrease in thigh circumference after 4 weeks.

The average decrease in thigh circumference was 1.2 cm. In addition, the physician evaluators observed that 65% of the occluded legs had improvement in cellulite, compared with 59% of the nonoccluded legs, said Dr. Rao, chief of dermatology at the University of Alberta, Edmonton.

In the self-report part of the study, 76% noticed an “overall improvement” in cellulite; 54% who noticed improvement in cellulite reported a greater improvement on the leg occluded with shorts, and 46% noticed the same amount of improvement in cellulite regardless of occlusal.

Dr. Rao concluded that the study results help increase the understanding of cellulite formation, which affects about 85% of women over age 20. “It is certain that with this and further studies to evaluate cellulite formation and maintenance, new modalities will continue to evolve,” he said.

La Jolla Spa MD provided the cream and supported the study.

SAN DIEGO — Application of Spa MD Anti-Cellulite Cream effectively reduced cellulite of the thighs in 59% of patients who received the cream without occlusion and in 65% of patients who received it with occlusion, results from a small trial suggest.

The combination of topical agent plus occlusion intended to enhance penetration “offers a valuable treatment option for a condition that has few effective therapeutic choices,” Jaggi Rao, M.D., said in a poster session at the joint annual meeting of the American Society for Dermatologic Surgery and the American College of Mohs Micrographic Surgery and Cutaneous Oncology. Dr. Rao also said that the success of the results seen in this trial serves to confirm the theory that microcirculatory and lymphatic impairment causes cellulite development.

Available since 2003, Spa MD Anti-Cellulite Cream (La Jolla Spa MD, La Jolla, Calif.) contains the following active ingredients, which are thought to stimulate lymphatic and microvascular flow: black pepper seed extract, sweet orange peel, ginger root extract, green tea extract, cinnamon bark extract, capsicum annum resin, and caffeine (which is also thought to promote lipolysis of adipose tissue).

For the study, Dr. Rao and his associates enrolled 17 women aged 20–63 years with moderate to severe cellulite on the thighs and buttocks. They took digital photos of the posterior and lateral thighs with tangential lighting from the Verilux Happy Lite system. They also took baseline photos of each leg at 90 degrees, 45 degrees, and 180 degrees, and measured each leg's thigh circumference with a flexible measuring tape.

All study participants were fitted with bioceramic-coated neoprene shorts. Each pair of shorts was randomized to have either the right or left leg removed so as not to provide occlusion to the control leg.

Each patient received two 60-g tubes of the product and was instructed to apply the cream to the posterior and lateral aspects of both thighs on a daily basis for 4 weeks. The patients were also instructed to wear the modified shorts for at least 6 hours immediately after applying the cream.

After 4 weeks, they underwent repeat photography and thigh measurements and completed self-evaluation surveys. Four blinded, independent dermatologists reviewed all photographs.

Dr. Rao reported that more than half (65%) of the participants had a decrease in thigh circumference after 4 weeks.

The average decrease in thigh circumference was 1.2 cm. In addition, the physician evaluators observed that 65% of the occluded legs had improvement in cellulite, compared with 59% of the nonoccluded legs, said Dr. Rao, chief of dermatology at the University of Alberta, Edmonton.

In the self-report part of the study, 76% noticed an “overall improvement” in cellulite; 54% who noticed improvement in cellulite reported a greater improvement on the leg occluded with shorts, and 46% noticed the same amount of improvement in cellulite regardless of occlusal.

Dr. Rao concluded that the study results help increase the understanding of cellulite formation, which affects about 85% of women over age 20. “It is certain that with this and further studies to evaluate cellulite formation and maintenance, new modalities will continue to evolve,” he said.

La Jolla Spa MD provided the cream and supported the study.

SAN DIEGO — Application of Spa MD Anti-Cellulite Cream effectively reduced cellulite of the thighs in 59% of patients who received the cream without occlusion and in 65% of patients who received it with occlusion, results from a small trial suggest.

The combination of topical agent plus occlusion intended to enhance penetration “offers a valuable treatment option for a condition that has few effective therapeutic choices,” Jaggi Rao, M.D., said in a poster session at the joint annual meeting of the American Society for Dermatologic Surgery and the American College of Mohs Micrographic Surgery and Cutaneous Oncology. Dr. Rao also said that the success of the results seen in this trial serves to confirm the theory that microcirculatory and lymphatic impairment causes cellulite development.

Available since 2003, Spa MD Anti-Cellulite Cream (La Jolla Spa MD, La Jolla, Calif.) contains the following active ingredients, which are thought to stimulate lymphatic and microvascular flow: black pepper seed extract, sweet orange peel, ginger root extract, green tea extract, cinnamon bark extract, capsicum annum resin, and caffeine (which is also thought to promote lipolysis of adipose tissue).

For the study, Dr. Rao and his associates enrolled 17 women aged 20–63 years with moderate to severe cellulite on the thighs and buttocks. They took digital photos of the posterior and lateral thighs with tangential lighting from the Verilux Happy Lite system. They also took baseline photos of each leg at 90 degrees, 45 degrees, and 180 degrees, and measured each leg's thigh circumference with a flexible measuring tape.

All study participants were fitted with bioceramic-coated neoprene shorts. Each pair of shorts was randomized to have either the right or left leg removed so as not to provide occlusion to the control leg.

Each patient received two 60-g tubes of the product and was instructed to apply the cream to the posterior and lateral aspects of both thighs on a daily basis for 4 weeks. The patients were also instructed to wear the modified shorts for at least 6 hours immediately after applying the cream.

After 4 weeks, they underwent repeat photography and thigh measurements and completed self-evaluation surveys. Four blinded, independent dermatologists reviewed all photographs.

Dr. Rao reported that more than half (65%) of the participants had a decrease in thigh circumference after 4 weeks.

The average decrease in thigh circumference was 1.2 cm. In addition, the physician evaluators observed that 65% of the occluded legs had improvement in cellulite, compared with 59% of the nonoccluded legs, said Dr. Rao, chief of dermatology at the University of Alberta, Edmonton.

In the self-report part of the study, 76% noticed an “overall improvement” in cellulite; 54% who noticed improvement in cellulite reported a greater improvement on the leg occluded with shorts, and 46% noticed the same amount of improvement in cellulite regardless of occlusal.

Dr. Rao concluded that the study results help increase the understanding of cellulite formation, which affects about 85% of women over age 20. “It is certain that with this and further studies to evaluate cellulite formation and maintenance, new modalities will continue to evolve,” he said.

La Jolla Spa MD provided the cream and supported the study.

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212–6 and Nat. Med. 2004;10:368–73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven. “Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality.”

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492–8). They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay. In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children. Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

The most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-month-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499–502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212–6 and Nat. Med. 2004;10:368–73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven. “Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality.”

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492–8). They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay. In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children. Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

The most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-month-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499–502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212–6 and Nat. Med. 2004;10:368–73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven. “Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality.”

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492–8). They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay. In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children. Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

The most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-month-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499–502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.

LA JOLLA, CALIF. — Several natural supplements are useful for lowering blood lipids, Erminia M. Guarneri, M.D., said at a meeting on natural supplements in evidence-based practice sponsored by the Scripps Clinic. They include:

▸ Soluble fiber. Ingesting 2–10 g/day of soluble fiber has been found to lower total cholesterol levels by 15%-18% (Am. J. Clin. Nutr. 1999;69:30–42). Common sources include oats, psyllium, pectin, and guar gum. GI complaints from ingesting soluble fiber are frequent.

▸ Phytosterols. Produced by plants, these substances impair intestinal absorption of cholesterol. Studies have found that 2–3 g/day of phytosterols can reduce LDL-cholesterol levels by 10%-15%. In one study of 167 patients on stable statin therapy, the 83 patients who received three servings per day of a plant stanol-ester spread showed reduction in LDL cholesterol of more than 16% at 8 weeks, compared with a nearly 7% reduction in the 84 patients who received a placebo spread. The stanol spread provided the equivalent of 2–3 g/day of phytosterols (Am. J. Cardiol. 2000;86:46–52).

In an unpublished study of 14 Scripps patients who were “maxed out on nutrition and cholesterol-lowering medicines,” adding 2 g/day of phytosterols led to a 14% reduction in total cholesterol, a 16% reduction in LDL cholesterol, an 11% reduction in triglycerides, and a 2% increase in HDL cholesterol.

Phytosterols are found in certain margarines that can be purchased at the grocery store, but “I'd avoiding doing that, especially when I look at some of these [food] labels, and I see partially hydrogenated oils,” said Dr. Guarneri, founder and medical director of the Scripps Center for Integrative Medicine. She recommends getting phytosterols from two products: CholestePure (Emerson Ecologics) and UltraMeal Plus (Metagenics).

▸ B vitamins. Deficiencies of vitamin B6, vitamin B12, and folic acid have been linked to elevated plasma homocysteine levels, which are a strong predictor of mortality in coronary artery disease patients.

In fact, one study of 587 coronary artery disease patients found that the risk of mortality for those with plasma homocysteine levels of less than 9.0 μmol/L was 3.8% while the risk of mortality in those with levels of 15 μmol/L or greater was 24.7%.

Dr. Guarneri recommends Cardio B (Ortho Molecular Products), a mix of folic acid and vitamins B6 and B12, “in one pill, instead of popping a bunch of pills,” she said at the meeting, which was cosponsored by the University of California, San Diego.

▸ Niacin. Regular use of niacin has been found to lower LDL cholesterol by 5%-25%, lower triglycerides by 20%-50%, and raise HDL cholesterol by 15%-35%.

“The first treatment [for low HDL] is to get the weight off the midline,” she said. “But if I have to reach for a supplement to fix this, I fix it with niacin. Niacin doesn't affect the LDL as much as it affects the LDL subtype. Frequently people will see me and say, 'I'm drinking all this wine to raise my HDL.' A lot of times all that wine gives you more weight on the midline, so that's not necessarily the solution.”

Side effects may include flushing, hyperglycemia, hyperuricemia, upper GI distress, and hepatotoxicity.

Niacin is contraindicated in patients with liver disease, severe gout, or peptic ulcer.

“I like short-acting niacin so people can take it with each meal if they need to, as opposed to the long-acting prescription niacin, which you're really only supposed to take once a day,” she added. “When I use short-acting niacins, I can also use them at higher doses. Start low and go up slowly, [but] you do have to monitor liver function.”

▸ Magnesium. For patients with arrhythmia, Dr. Guarneri called it one of her favorite supplements. Magnesium is a front-line treatment for torsades de pointes, and some studies have found it beneficial for mitral valve prolapse patients who have low magnesium levels.

“At least one study demonstrated a decrease in blood pressure with a 1,000-mg dose [of magnesium],” she said. “If someone has normal renal function, and they have arrhythmia or skipped heartbeats, and I get them off caffeine and sugar, I will use chelated magnesium and titrate it and warn them about the potential for soft stool.”

The cardiac benefits of the following supplements are less clear, Dr. Guarneri noted: L-arginine, coenzyme Q10, hawthorn, gingko biloba, red yeast rice, policosanol, and horse chestnut. She said that she has no financial interest in any of the products she recommended.

LA JOLLA, CALIF. — Several natural supplements are useful for lowering blood lipids, Erminia M. Guarneri, M.D., said at a meeting on natural supplements in evidence-based practice sponsored by the Scripps Clinic. They include:

▸ Soluble fiber. Ingesting 2–10 g/day of soluble fiber has been found to lower total cholesterol levels by 15%-18% (Am. J. Clin. Nutr. 1999;69:30–42). Common sources include oats, psyllium, pectin, and guar gum. GI complaints from ingesting soluble fiber are frequent.

▸ Phytosterols. Produced by plants, these substances impair intestinal absorption of cholesterol. Studies have found that 2–3 g/day of phytosterols can reduce LDL-cholesterol levels by 10%-15%. In one study of 167 patients on stable statin therapy, the 83 patients who received three servings per day of a plant stanol-ester spread showed reduction in LDL cholesterol of more than 16% at 8 weeks, compared with a nearly 7% reduction in the 84 patients who received a placebo spread. The stanol spread provided the equivalent of 2–3 g/day of phytosterols (Am. J. Cardiol. 2000;86:46–52).

In an unpublished study of 14 Scripps patients who were “maxed out on nutrition and cholesterol-lowering medicines,” adding 2 g/day of phytosterols led to a 14% reduction in total cholesterol, a 16% reduction in LDL cholesterol, an 11% reduction in triglycerides, and a 2% increase in HDL cholesterol.

Phytosterols are found in certain margarines that can be purchased at the grocery store, but “I'd avoiding doing that, especially when I look at some of these [food] labels, and I see partially hydrogenated oils,” said Dr. Guarneri, founder and medical director of the Scripps Center for Integrative Medicine. She recommends getting phytosterols from two products: CholestePure (Emerson Ecologics) and UltraMeal Plus (Metagenics).

▸ B vitamins. Deficiencies of vitamin B6, vitamin B12, and folic acid have been linked to elevated plasma homocysteine levels, which are a strong predictor of mortality in coronary artery disease patients.

In fact, one study of 587 coronary artery disease patients found that the risk of mortality for those with plasma homocysteine levels of less than 9.0 μmol/L was 3.8% while the risk of mortality in those with levels of 15 μmol/L or greater was 24.7%.

Dr. Guarneri recommends Cardio B (Ortho Molecular Products), a mix of folic acid and vitamins B6 and B12, “in one pill, instead of popping a bunch of pills,” she said at the meeting, which was cosponsored by the University of California, San Diego.

▸ Niacin. Regular use of niacin has been found to lower LDL cholesterol by 5%-25%, lower triglycerides by 20%-50%, and raise HDL cholesterol by 15%-35%.

“The first treatment [for low HDL] is to get the weight off the midline,” she said. “But if I have to reach for a supplement to fix this, I fix it with niacin. Niacin doesn't affect the LDL as much as it affects the LDL subtype. Frequently people will see me and say, 'I'm drinking all this wine to raise my HDL.' A lot of times all that wine gives you more weight on the midline, so that's not necessarily the solution.”

Side effects may include flushing, hyperglycemia, hyperuricemia, upper GI distress, and hepatotoxicity.

Niacin is contraindicated in patients with liver disease, severe gout, or peptic ulcer.

“I like short-acting niacin so people can take it with each meal if they need to, as opposed to the long-acting prescription niacin, which you're really only supposed to take once a day,” she added. “When I use short-acting niacins, I can also use them at higher doses. Start low and go up slowly, [but] you do have to monitor liver function.”

▸ Magnesium. For patients with arrhythmia, Dr. Guarneri called it one of her favorite supplements. Magnesium is a front-line treatment for torsades de pointes, and some studies have found it beneficial for mitral valve prolapse patients who have low magnesium levels.

“At least one study demonstrated a decrease in blood pressure with a 1,000-mg dose [of magnesium],” she said. “If someone has normal renal function, and they have arrhythmia or skipped heartbeats, and I get them off caffeine and sugar, I will use chelated magnesium and titrate it and warn them about the potential for soft stool.”

The cardiac benefits of the following supplements are less clear, Dr. Guarneri noted: L-arginine, coenzyme Q10, hawthorn, gingko biloba, red yeast rice, policosanol, and horse chestnut. She said that she has no financial interest in any of the products she recommended.

LA JOLLA, CALIF. — Several natural supplements are useful for lowering blood lipids, Erminia M. Guarneri, M.D., said at a meeting on natural supplements in evidence-based practice sponsored by the Scripps Clinic. They include:

▸ Soluble fiber. Ingesting 2–10 g/day of soluble fiber has been found to lower total cholesterol levels by 15%-18% (Am. J. Clin. Nutr. 1999;69:30–42). Common sources include oats, psyllium, pectin, and guar gum. GI complaints from ingesting soluble fiber are frequent.

▸ Phytosterols. Produced by plants, these substances impair intestinal absorption of cholesterol. Studies have found that 2–3 g/day of phytosterols can reduce LDL-cholesterol levels by 10%-15%. In one study of 167 patients on stable statin therapy, the 83 patients who received three servings per day of a plant stanol-ester spread showed reduction in LDL cholesterol of more than 16% at 8 weeks, compared with a nearly 7% reduction in the 84 patients who received a placebo spread. The stanol spread provided the equivalent of 2–3 g/day of phytosterols (Am. J. Cardiol. 2000;86:46–52).

In an unpublished study of 14 Scripps patients who were “maxed out on nutrition and cholesterol-lowering medicines,” adding 2 g/day of phytosterols led to a 14% reduction in total cholesterol, a 16% reduction in LDL cholesterol, an 11% reduction in triglycerides, and a 2% increase in HDL cholesterol.

Phytosterols are found in certain margarines that can be purchased at the grocery store, but “I'd avoiding doing that, especially when I look at some of these [food] labels, and I see partially hydrogenated oils,” said Dr. Guarneri, founder and medical director of the Scripps Center for Integrative Medicine. She recommends getting phytosterols from two products: CholestePure (Emerson Ecologics) and UltraMeal Plus (Metagenics).

▸ B vitamins. Deficiencies of vitamin B6, vitamin B12, and folic acid have been linked to elevated plasma homocysteine levels, which are a strong predictor of mortality in coronary artery disease patients.

In fact, one study of 587 coronary artery disease patients found that the risk of mortality for those with plasma homocysteine levels of less than 9.0 μmol/L was 3.8% while the risk of mortality in those with levels of 15 μmol/L or greater was 24.7%.

Dr. Guarneri recommends Cardio B (Ortho Molecular Products), a mix of folic acid and vitamins B6 and B12, “in one pill, instead of popping a bunch of pills,” she said at the meeting, which was cosponsored by the University of California, San Diego.

▸ Niacin. Regular use of niacin has been found to lower LDL cholesterol by 5%-25%, lower triglycerides by 20%-50%, and raise HDL cholesterol by 15%-35%.

“The first treatment [for low HDL] is to get the weight off the midline,” she said. “But if I have to reach for a supplement to fix this, I fix it with niacin. Niacin doesn't affect the LDL as much as it affects the LDL subtype. Frequently people will see me and say, 'I'm drinking all this wine to raise my HDL.' A lot of times all that wine gives you more weight on the midline, so that's not necessarily the solution.”

Side effects may include flushing, hyperglycemia, hyperuricemia, upper GI distress, and hepatotoxicity.

Niacin is contraindicated in patients with liver disease, severe gout, or peptic ulcer.

“I like short-acting niacin so people can take it with each meal if they need to, as opposed to the long-acting prescription niacin, which you're really only supposed to take once a day,” she added. “When I use short-acting niacins, I can also use them at higher doses. Start low and go up slowly, [but] you do have to monitor liver function.”

▸ Magnesium. For patients with arrhythmia, Dr. Guarneri called it one of her favorite supplements. Magnesium is a front-line treatment for torsades de pointes, and some studies have found it beneficial for mitral valve prolapse patients who have low magnesium levels.

“At least one study demonstrated a decrease in blood pressure with a 1,000-mg dose [of magnesium],” she said. “If someone has normal renal function, and they have arrhythmia or skipped heartbeats, and I get them off caffeine and sugar, I will use chelated magnesium and titrate it and warn them about the potential for soft stool.”

The cardiac benefits of the following supplements are less clear, Dr. Guarneri noted: L-arginine, coenzyme Q10, hawthorn, gingko biloba, red yeast rice, policosanol, and horse chestnut. She said that she has no financial interest in any of the products she recommended.

Well before rheumatoid arthritis patients receive their diagnosis, they are three to six times more likely than are those without the disease to suffer acute myocardial infarction, results from a large retrospective study have shown.

The results support the idea that the heart disease associated with rheumatoid arthritis (RA) is not an issue for the back burner.

Physicians and their patients need to recognize that heart disease may not only be present, but well underway and quite serious at the time of RA diagnosis, the study's lead author, Hilal Maradit-Kremers, M.D., said in an interview.

Furthermore, the findings “certainly fit with the sense that a period of systemic inflammation antedates the clinical diagnosis of RA, and this systemic inflammatory burden increases cardiovascular risk,” said Mary Chester Wasko, M.D., of the division of rheumatology and clinical immunology at the University of Pittsburgh, who was not affiliated with the study.

Dr. Maradit-Kremers and her associates at the Mayo Clinic, Rochester, Minn., conducted the population-based cohort study, which involved 603 Rochester residents who fulfilled American College of Rheumatology (ACR) criteria for RA between January 1955 and January 1995, and 603 age- and gender-matched controls from the area (Arthritis Rheum. 2005;52:402-11).

They collected data on coronary heart disease (CHD) events and risk factors such as diabetes, hypertension, dyslipidemia, body mass index, and tobacco smoking.

CHD events included hospitalization for MI, unrecognized MI, coronary revascularization procedures, and sudden CHD deaths.

The investigators used conditional logistic regression and Cox regression to estimate the risk of CHD associated with RA before and after the RA diagnosis.

The mean age of study participants in both cohorts was 58 years, and nearly three-fourths (73%) were female.

The investigators observed that 2 years prior to being diagnosed with RA, patients with the disease were 3.17 times more likely than were their non-RA counterparts to have been hospitalized for acute MI and 5.86 times more likely to have experienced unrecognized MIs.

After receiving their diagnosis of rheumatoid arthritis, those patients were 1.09 times more likely than their non-RA counterparts to be hospitalized with MI, 2.13 times more likely to have unrecognized MI, and 1.94 times more likely to experience sudden cardiac death.

The risk estimates did not change significantly when the investigators adjusted for the CHD risk factors.

In an interview, Dr. Maradit-Kremers called the findings “another piece of evidence that inflammation is related to atherosclerosis and coronary heart disease.” The findings support the use of RA as a model to study the effects of chronic inflammation on the cardiovascular system.

“We haven't studied whether a more vigilant approach [to monitoring RA patients for heart disease] would be more beneficial, but our findings imply that it would be beneficial,” Dr. Maradit-Kremers added.

At baseline, 30% of the RA patients were current smokers and 26% were former smokers, compared with 24% and 20% of the non-RA patients, respectively. “When we think about interventions that a physician might implement to reduce cardiovascular risk, smoking is one that really stands out,” Dr. Wasko said. “Physicians need to be proactive about trying to minimize modifiable risk factors such as tobacco use.”

Limitations of the study, the investigators noted, include the fact that more than 95% of the study population was white and that only 57% of the RA patients received a disease-modifying antirheumatic drug.

Dr. Wasko pointed out that RA is more effectively controlled with disease modifying agents today than it was when the study ended in 1995. “One wonders if the study cohort were larger, or if the study were extended through the current era, perhaps the findings would be different,” Dr. Wasko said.

“Earlier diagnosis of RA and prompt initiation of effective disease-modifying agents such as methotrexate and anti-TNF [tumor necrosis factor] therapies may favorably impact CHD risk in patients with this disease,” Dr. Wasko said.

“This research is unique and is an interesting contribution to our understanding of both coronary heart disease and increased risk of CHD in RA,” she added.

Well before rheumatoid arthritis patients receive their diagnosis, they are three to six times more likely than are those without the disease to suffer acute myocardial infarction, results from a large retrospective study have shown.

The results support the idea that the heart disease associated with rheumatoid arthritis (RA) is not an issue for the back burner.

Physicians and their patients need to recognize that heart disease may not only be present, but well underway and quite serious at the time of RA diagnosis, the study's lead author, Hilal Maradit-Kremers, M.D., said in an interview.

Furthermore, the findings “certainly fit with the sense that a period of systemic inflammation antedates the clinical diagnosis of RA, and this systemic inflammatory burden increases cardiovascular risk,” said Mary Chester Wasko, M.D., of the division of rheumatology and clinical immunology at the University of Pittsburgh, who was not affiliated with the study.

Dr. Maradit-Kremers and her associates at the Mayo Clinic, Rochester, Minn., conducted the population-based cohort study, which involved 603 Rochester residents who fulfilled American College of Rheumatology (ACR) criteria for RA between January 1955 and January 1995, and 603 age- and gender-matched controls from the area (Arthritis Rheum. 2005;52:402-11).

They collected data on coronary heart disease (CHD) events and risk factors such as diabetes, hypertension, dyslipidemia, body mass index, and tobacco smoking.

CHD events included hospitalization for MI, unrecognized MI, coronary revascularization procedures, and sudden CHD deaths.

The investigators used conditional logistic regression and Cox regression to estimate the risk of CHD associated with RA before and after the RA diagnosis.

The mean age of study participants in both cohorts was 58 years, and nearly three-fourths (73%) were female.

The investigators observed that 2 years prior to being diagnosed with RA, patients with the disease were 3.17 times more likely than were their non-RA counterparts to have been hospitalized for acute MI and 5.86 times more likely to have experienced unrecognized MIs.

After receiving their diagnosis of rheumatoid arthritis, those patients were 1.09 times more likely than their non-RA counterparts to be hospitalized with MI, 2.13 times more likely to have unrecognized MI, and 1.94 times more likely to experience sudden cardiac death.

The risk estimates did not change significantly when the investigators adjusted for the CHD risk factors.

In an interview, Dr. Maradit-Kremers called the findings “another piece of evidence that inflammation is related to atherosclerosis and coronary heart disease.” The findings support the use of RA as a model to study the effects of chronic inflammation on the cardiovascular system.

“We haven't studied whether a more vigilant approach [to monitoring RA patients for heart disease] would be more beneficial, but our findings imply that it would be beneficial,” Dr. Maradit-Kremers added.

At baseline, 30% of the RA patients were current smokers and 26% were former smokers, compared with 24% and 20% of the non-RA patients, respectively. “When we think about interventions that a physician might implement to reduce cardiovascular risk, smoking is one that really stands out,” Dr. Wasko said. “Physicians need to be proactive about trying to minimize modifiable risk factors such as tobacco use.”

Limitations of the study, the investigators noted, include the fact that more than 95% of the study population was white and that only 57% of the RA patients received a disease-modifying antirheumatic drug.

Dr. Wasko pointed out that RA is more effectively controlled with disease modifying agents today than it was when the study ended in 1995. “One wonders if the study cohort were larger, or if the study were extended through the current era, perhaps the findings would be different,” Dr. Wasko said.

“Earlier diagnosis of RA and prompt initiation of effective disease-modifying agents such as methotrexate and anti-TNF [tumor necrosis factor] therapies may favorably impact CHD risk in patients with this disease,” Dr. Wasko said.

“This research is unique and is an interesting contribution to our understanding of both coronary heart disease and increased risk of CHD in RA,” she added.

Well before rheumatoid arthritis patients receive their diagnosis, they are three to six times more likely than are those without the disease to suffer acute myocardial infarction, results from a large retrospective study have shown.

The results support the idea that the heart disease associated with rheumatoid arthritis (RA) is not an issue for the back burner.

Physicians and their patients need to recognize that heart disease may not only be present, but well underway and quite serious at the time of RA diagnosis, the study's lead author, Hilal Maradit-Kremers, M.D., said in an interview.

Furthermore, the findings “certainly fit with the sense that a period of systemic inflammation antedates the clinical diagnosis of RA, and this systemic inflammatory burden increases cardiovascular risk,” said Mary Chester Wasko, M.D., of the division of rheumatology and clinical immunology at the University of Pittsburgh, who was not affiliated with the study.

Dr. Maradit-Kremers and her associates at the Mayo Clinic, Rochester, Minn., conducted the population-based cohort study, which involved 603 Rochester residents who fulfilled American College of Rheumatology (ACR) criteria for RA between January 1955 and January 1995, and 603 age- and gender-matched controls from the area (Arthritis Rheum. 2005;52:402-11).

They collected data on coronary heart disease (CHD) events and risk factors such as diabetes, hypertension, dyslipidemia, body mass index, and tobacco smoking.

CHD events included hospitalization for MI, unrecognized MI, coronary revascularization procedures, and sudden CHD deaths.

The investigators used conditional logistic regression and Cox regression to estimate the risk of CHD associated with RA before and after the RA diagnosis.

The mean age of study participants in both cohorts was 58 years, and nearly three-fourths (73%) were female.

The investigators observed that 2 years prior to being diagnosed with RA, patients with the disease were 3.17 times more likely than were their non-RA counterparts to have been hospitalized for acute MI and 5.86 times more likely to have experienced unrecognized MIs.

After receiving their diagnosis of rheumatoid arthritis, those patients were 1.09 times more likely than their non-RA counterparts to be hospitalized with MI, 2.13 times more likely to have unrecognized MI, and 1.94 times more likely to experience sudden cardiac death.

The risk estimates did not change significantly when the investigators adjusted for the CHD risk factors.

In an interview, Dr. Maradit-Kremers called the findings “another piece of evidence that inflammation is related to atherosclerosis and coronary heart disease.” The findings support the use of RA as a model to study the effects of chronic inflammation on the cardiovascular system.

“We haven't studied whether a more vigilant approach [to monitoring RA patients for heart disease] would be more beneficial, but our findings imply that it would be beneficial,” Dr. Maradit-Kremers added.

At baseline, 30% of the RA patients were current smokers and 26% were former smokers, compared with 24% and 20% of the non-RA patients, respectively. “When we think about interventions that a physician might implement to reduce cardiovascular risk, smoking is one that really stands out,” Dr. Wasko said. “Physicians need to be proactive about trying to minimize modifiable risk factors such as tobacco use.”

Limitations of the study, the investigators noted, include the fact that more than 95% of the study population was white and that only 57% of the RA patients received a disease-modifying antirheumatic drug.

Dr. Wasko pointed out that RA is more effectively controlled with disease modifying agents today than it was when the study ended in 1995. “One wonders if the study cohort were larger, or if the study were extended through the current era, perhaps the findings would be different,” Dr. Wasko said.

“Earlier diagnosis of RA and prompt initiation of effective disease-modifying agents such as methotrexate and anti-TNF [tumor necrosis factor] therapies may favorably impact CHD risk in patients with this disease,” Dr. Wasko said.

“This research is unique and is an interesting contribution to our understanding of both coronary heart disease and increased risk of CHD in RA,” she added.

SAN DIEGO—Prophylaxis for deep vein thrombosis in hospitalized, acutely ill patients is clearly underused in the United States and Europe, results from a large international trial suggest.

“Despite the [American College of Chest Physicians] consensus guideline recommendations of 2001 and 2002 and evidence from clinical studies showing the benefits of DVT prophylaxis in acutely ill medical patients, only 44% received in-hospital prophylaxis,” Victor F. Tapson, M.D., reported in a poster session at the annual meeting of the American Society of Hematology. “I was a bit surprised at how low the rates actually were.”

The findings are part of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).

Funded by an unrestricted grant from Aventis Pharmaceuticals Inc., the purpose of the multicenter registry is to assess routine clinical practices for providing hospitalized, acutely ill patients with venous thromboembolism prophylaxis and to test predictive models of the relationship between patient characteristics, prophylaxis use, and key clinical end points.

For the trial, patients aged 18 years and older who were hospitalized for at least 3 days were enrolled consecutively. Data were recorded at discharge and 3 months after discharge.

Dr. Tapson reported on 4,315 patients from 37 hospitals in 11 countries who were enrolled between January 1, 2002 and June 30, 2004. Half were female and the mean age was 69 years.

Less than half of the patients (44%) received in-hospital DVT prophylaxis, said Dr. Tapson, of Duke University Medical Center, Durham, N.C.

Low-molecular-weight heparin and unfractionated heparin were used most often. Low-molecular-weight heparin regimens were usually given once daily.

Unfractionated heparin regimens varied. Outside of the United States, most regimens (85%) were given every 12 hours. In the United States, a similar number of patients received unfractionated heparin every 12 hours (55%) or every 8 hours (40%).

Aspirin was given as DVT prophylaxis to 7% of patients in the United States and to 3% of patients in other countries.

“Unfractionated heparin is used more for medical patient prophylaxis than low-molecular-weight heparin in the United States, while the reverse is true in Europe and certain other parts of the world,” Dr. Tapson said in an interview.

“Low-molecular-weight heparin has considerable advantages, including once-daily injection and, for example, a lower risk of heparin-induced thrombocytopenia. This is very relevant to the primary care physician, particularly those that do inpatient work. They need to consider prophylaxis for every medical patient admitted, as most need it,” he added.

As for mechanical methods of DVT prophylaxis, clinicians in the United States used pneumatic compression more often, compared with clinicians in other countries (19% vs. 0.3%). In contrast, clinicians in other countries used elastic stockings more often, compared with those in the United States (8% vs. 2%).

SAN DIEGO—Prophylaxis for deep vein thrombosis in hospitalized, acutely ill patients is clearly underused in the United States and Europe, results from a large international trial suggest.

“Despite the [American College of Chest Physicians] consensus guideline recommendations of 2001 and 2002 and evidence from clinical studies showing the benefits of DVT prophylaxis in acutely ill medical patients, only 44% received in-hospital prophylaxis,” Victor F. Tapson, M.D., reported in a poster session at the annual meeting of the American Society of Hematology. “I was a bit surprised at how low the rates actually were.”

The findings are part of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).

Funded by an unrestricted grant from Aventis Pharmaceuticals Inc., the purpose of the multicenter registry is to assess routine clinical practices for providing hospitalized, acutely ill patients with venous thromboembolism prophylaxis and to test predictive models of the relationship between patient characteristics, prophylaxis use, and key clinical end points.

For the trial, patients aged 18 years and older who were hospitalized for at least 3 days were enrolled consecutively. Data were recorded at discharge and 3 months after discharge.

Dr. Tapson reported on 4,315 patients from 37 hospitals in 11 countries who were enrolled between January 1, 2002 and June 30, 2004. Half were female and the mean age was 69 years.

Less than half of the patients (44%) received in-hospital DVT prophylaxis, said Dr. Tapson, of Duke University Medical Center, Durham, N.C.

Low-molecular-weight heparin and unfractionated heparin were used most often. Low-molecular-weight heparin regimens were usually given once daily.

Unfractionated heparin regimens varied. Outside of the United States, most regimens (85%) were given every 12 hours. In the United States, a similar number of patients received unfractionated heparin every 12 hours (55%) or every 8 hours (40%).

Aspirin was given as DVT prophylaxis to 7% of patients in the United States and to 3% of patients in other countries.

“Unfractionated heparin is used more for medical patient prophylaxis than low-molecular-weight heparin in the United States, while the reverse is true in Europe and certain other parts of the world,” Dr. Tapson said in an interview.

“Low-molecular-weight heparin has considerable advantages, including once-daily injection and, for example, a lower risk of heparin-induced thrombocytopenia. This is very relevant to the primary care physician, particularly those that do inpatient work. They need to consider prophylaxis for every medical patient admitted, as most need it,” he added.

As for mechanical methods of DVT prophylaxis, clinicians in the United States used pneumatic compression more often, compared with clinicians in other countries (19% vs. 0.3%). In contrast, clinicians in other countries used elastic stockings more often, compared with those in the United States (8% vs. 2%).

SAN DIEGO—Prophylaxis for deep vein thrombosis in hospitalized, acutely ill patients is clearly underused in the United States and Europe, results from a large international trial suggest.

“Despite the [American College of Chest Physicians] consensus guideline recommendations of 2001 and 2002 and evidence from clinical studies showing the benefits of DVT prophylaxis in acutely ill medical patients, only 44% received in-hospital prophylaxis,” Victor F. Tapson, M.D., reported in a poster session at the annual meeting of the American Society of Hematology. “I was a bit surprised at how low the rates actually were.”

The findings are part of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).

Funded by an unrestricted grant from Aventis Pharmaceuticals Inc., the purpose of the multicenter registry is to assess routine clinical practices for providing hospitalized, acutely ill patients with venous thromboembolism prophylaxis and to test predictive models of the relationship between patient characteristics, prophylaxis use, and key clinical end points.

For the trial, patients aged 18 years and older who were hospitalized for at least 3 days were enrolled consecutively. Data were recorded at discharge and 3 months after discharge.

Dr. Tapson reported on 4,315 patients from 37 hospitals in 11 countries who were enrolled between January 1, 2002 and June 30, 2004. Half were female and the mean age was 69 years.

Less than half of the patients (44%) received in-hospital DVT prophylaxis, said Dr. Tapson, of Duke University Medical Center, Durham, N.C.

Low-molecular-weight heparin and unfractionated heparin were used most often. Low-molecular-weight heparin regimens were usually given once daily.

Unfractionated heparin regimens varied. Outside of the United States, most regimens (85%) were given every 12 hours. In the United States, a similar number of patients received unfractionated heparin every 12 hours (55%) or every 8 hours (40%).

Aspirin was given as DVT prophylaxis to 7% of patients in the United States and to 3% of patients in other countries.

“Unfractionated heparin is used more for medical patient prophylaxis than low-molecular-weight heparin in the United States, while the reverse is true in Europe and certain other parts of the world,” Dr. Tapson said in an interview.

“Low-molecular-weight heparin has considerable advantages, including once-daily injection and, for example, a lower risk of heparin-induced thrombocytopenia. This is very relevant to the primary care physician, particularly those that do inpatient work. They need to consider prophylaxis for every medical patient admitted, as most need it,” he added.

As for mechanical methods of DVT prophylaxis, clinicians in the United States used pneumatic compression more often, compared with clinicians in other countries (19% vs. 0.3%). In contrast, clinicians in other countries used elastic stockings more often, compared with those in the United States (8% vs. 2%).

SAN DIEGO—Thrombotic events occur frequently in critically ill patients yet may often go unrecognized, Wendy Lim, M.D., reported during a poster session at the annual meeting of the American Society of Hematology.

“We're doing a poor job in actually recognizing these diseases,” said Dr. Lim, a clinical research scholar in the department of medicine at McMaster University, Hamilton, Ont. “Because a lot of critically ill patients are endotracheally intubated or sedated, they can't complain of pain in their leg if they have a blood clot, or they can't complain of chest pain if they have a heart attack. We're dependent on patients to express symptoms, and in the case of critically ill patients, we don't have that luxury. We're limited in our abilities.”

She and her associates conducted a retrospective chart review of 198 critically ill patients admitted to the medical-surgical intensive care unit at St. Joseph's Hospital in Hamilton, Ont. The patients were part of a prospective cohort study in which twice-daily ultrasound was used to screen for deep vein thrombosis (DVT). Other thrombotic events were diagnosed based on clinical suspicion and confirmed by conventional diagnostic tests.

On admission to the ICU, ultrasound screening revealed DVT in 6 of the 198 patients (3%), but only 3 of the 6 cases (50%) were clinically suspected.

During the ICU stay, 15 patients (7.6%) developed DVT but only 3 of 15 (20%) were clinically suspected.

On admission to the ICU, pulmonary embolism was clinically recognized in 4 patients (2%), while no cases of PE transpired during the ICU stay.

As for arterial events, 4 patients (2%) were admitted with ischemic stroke and 8 (4%) had a stroke in the ICU.

Levels of cardiac troponin I were measured at least once in the first 24 hours of admission in nearly every patient (90%).

On admission to the ICU, 72 patients (36%) had elevated troponin levels and 38 patients (19%) were diagnosed with myocardial infarction. Dr. Lim reported that 29 patients (15%) had elevated troponin levels without typical ischemic ECG changes while 3 patients (1.5%) had elevated troponin levels with a normal ECG.

During the ICU stay, 12 patients (6%) developed elevated troponin levels with associated ischemic ECG changes. Of these patients, only 5 (42%) were diagnosed with MI on admission.

“I think we need to learn a lot more about how to interpret this high frequency of elevated troponin levels in critically ill patients,” Dr. Lim commented. “Are all of these patients actually having injuries that are being missed and not being treated appropriately? What does this represent?”

A prospective study is underway to help answer these questions, she said.

SAN DIEGO—Thrombotic events occur frequently in critically ill patients yet may often go unrecognized, Wendy Lim, M.D., reported during a poster session at the annual meeting of the American Society of Hematology.

“We're doing a poor job in actually recognizing these diseases,” said Dr. Lim, a clinical research scholar in the department of medicine at McMaster University, Hamilton, Ont. “Because a lot of critically ill patients are endotracheally intubated or sedated, they can't complain of pain in their leg if they have a blood clot, or they can't complain of chest pain if they have a heart attack. We're dependent on patients to express symptoms, and in the case of critically ill patients, we don't have that luxury. We're limited in our abilities.”

She and her associates conducted a retrospective chart review of 198 critically ill patients admitted to the medical-surgical intensive care unit at St. Joseph's Hospital in Hamilton, Ont. The patients were part of a prospective cohort study in which twice-daily ultrasound was used to screen for deep vein thrombosis (DVT). Other thrombotic events were diagnosed based on clinical suspicion and confirmed by conventional diagnostic tests.

On admission to the ICU, ultrasound screening revealed DVT in 6 of the 198 patients (3%), but only 3 of the 6 cases (50%) were clinically suspected.

During the ICU stay, 15 patients (7.6%) developed DVT but only 3 of 15 (20%) were clinically suspected.

On admission to the ICU, pulmonary embolism was clinically recognized in 4 patients (2%), while no cases of PE transpired during the ICU stay.

As for arterial events, 4 patients (2%) were admitted with ischemic stroke and 8 (4%) had a stroke in the ICU.

Levels of cardiac troponin I were measured at least once in the first 24 hours of admission in nearly every patient (90%).

On admission to the ICU, 72 patients (36%) had elevated troponin levels and 38 patients (19%) were diagnosed with myocardial infarction. Dr. Lim reported that 29 patients (15%) had elevated troponin levels without typical ischemic ECG changes while 3 patients (1.5%) had elevated troponin levels with a normal ECG.

During the ICU stay, 12 patients (6%) developed elevated troponin levels with associated ischemic ECG changes. Of these patients, only 5 (42%) were diagnosed with MI on admission.

“I think we need to learn a lot more about how to interpret this high frequency of elevated troponin levels in critically ill patients,” Dr. Lim commented. “Are all of these patients actually having injuries that are being missed and not being treated appropriately? What does this represent?”

A prospective study is underway to help answer these questions, she said.

SAN DIEGO—Thrombotic events occur frequently in critically ill patients yet may often go unrecognized, Wendy Lim, M.D., reported during a poster session at the annual meeting of the American Society of Hematology.

“We're doing a poor job in actually recognizing these diseases,” said Dr. Lim, a clinical research scholar in the department of medicine at McMaster University, Hamilton, Ont. “Because a lot of critically ill patients are endotracheally intubated or sedated, they can't complain of pain in their leg if they have a blood clot, or they can't complain of chest pain if they have a heart attack. We're dependent on patients to express symptoms, and in the case of critically ill patients, we don't have that luxury. We're limited in our abilities.”

She and her associates conducted a retrospective chart review of 198 critically ill patients admitted to the medical-surgical intensive care unit at St. Joseph's Hospital in Hamilton, Ont. The patients were part of a prospective cohort study in which twice-daily ultrasound was used to screen for deep vein thrombosis (DVT). Other thrombotic events were diagnosed based on clinical suspicion and confirmed by conventional diagnostic tests.

On admission to the ICU, ultrasound screening revealed DVT in 6 of the 198 patients (3%), but only 3 of the 6 cases (50%) were clinically suspected.

During the ICU stay, 15 patients (7.6%) developed DVT but only 3 of 15 (20%) were clinically suspected.

On admission to the ICU, pulmonary embolism was clinically recognized in 4 patients (2%), while no cases of PE transpired during the ICU stay.

As for arterial events, 4 patients (2%) were admitted with ischemic stroke and 8 (4%) had a stroke in the ICU.

Levels of cardiac troponin I were measured at least once in the first 24 hours of admission in nearly every patient (90%).

On admission to the ICU, 72 patients (36%) had elevated troponin levels and 38 patients (19%) were diagnosed with myocardial infarction. Dr. Lim reported that 29 patients (15%) had elevated troponin levels without typical ischemic ECG changes while 3 patients (1.5%) had elevated troponin levels with a normal ECG.

During the ICU stay, 12 patients (6%) developed elevated troponin levels with associated ischemic ECG changes. Of these patients, only 5 (42%) were diagnosed with MI on admission.

“I think we need to learn a lot more about how to interpret this high frequency of elevated troponin levels in critically ill patients,” Dr. Lim commented. “Are all of these patients actually having injuries that are being missed and not being treated appropriately? What does this represent?”

A prospective study is underway to help answer these questions, she said.

SAN DIEGO — There is no one technique or strategy that will protect you from the risk of physical attacks in your workplace by patients or coworkers, Donna Pence declared at a conference sponsored by the Chadwick Center for Children and Families at Children's Hospital and Health Center, San Diego.

“There is nothing about who and what you are that makes you immune from people intent on doing bad things,” said Ms. Pence, training coordinator for San Diego State University's Public Child Welfare Training Academy. “Not looks, not money, not profession, not uniform, not where you live, not how religious you are, or how good you are.”

The best self-protection involves a combination of factors, including being aware of your capabilities, your environment, your habits, realistic hazards, and your options should a violent episode occur.

She offered the following tips:

▸Do some self-reflection. What is your history of violence and anger and your response to it? Have you been in situations where you felt threatened, and now you feel hypervigilant? Your personal history of violence “will affect your response to situations,” said Ms. Pence, who spent 25 years as a special agent with the Tennessee Bureau of Investigation. “It will impact the lens through which you view [someone's] behavior. That can be good, but it also could lead you to jump the gun and have a perception of violence and danger when it doesn't really exist.”

▸Make an effort to understand your colleague's attitudes about personal safety and anger in the workplace. Are you allowed to talk about it? Are you encouraged to talk about it? “Is there a forum where you can ventilate about any anxieties you have about a client, or any anger you may have toward the client?” Ms. Pence asked. “Because if you're angry and they're angry, that's not a real healthy combination.”

Also, ask yourself, are there people in the office who can hear you if you yell for help? Is there an emergency buzzer nearby? If somebody enters the office and a buzzer goes off, do we have a plan on what to do?

▸Think twice before visiting a patient in his or her home. Look at prior referrals. Consult with social workers or other physicians to see if the patient has a history of violent behavior. “If I have somebody who's been arrested for drugs, weapons, domestic violence, or child abuse, I'm going to think twice before going out to their turf by myself,” she said.

To protect against workplace violence and abuse, Ms. Pence recommended working on “target hardening.” Target hardening is a military term that refers to the notion that you are the person you are trying to make most safe.

“Until you recognize your personal, physical, mental, and environmental culpabilities and the possibility of victimization and do what you can realistically to reduce these, you're not a hard target,” she explained.

This means:

▸You must be aware.

▸You must think in a different way. For example, “Don't walk down a sidewalk that has doors on one side and bushes on the other,” she advised. Also, when you approach a parking lot, don't skirt the edge of it. Rather, “walk toward the middle of the parking lot and look to the left and right.”

▸You must act in a different way. “The way you walk, look, and carry yourself makes a difference in the degree of vulnerability that is ascribed to you by someone looking to attack,” Ms. Pence said. “Look confident, look aware, and be in the present.”

▸You must recognize your personal vulnerabilities. Ask yourself, how could I defend myself in the event of a personal attack? “For example, I'm not a long distance runner,” Ms. Pence said. “I don't aspire to be a runner. That's a realistic assessment of my physical abilities. If there are areas where you have a deficit, ask, what can I do to enhance my abilities? Maybe it's learning some form of self-protection or learning verbal de-escalation techniques.”

SAN DIEGO — There is no one technique or strategy that will protect you from the risk of physical attacks in your workplace by patients or coworkers, Donna Pence declared at a conference sponsored by the Chadwick Center for Children and Families at Children's Hospital and Health Center, San Diego.

“There is nothing about who and what you are that makes you immune from people intent on doing bad things,” said Ms. Pence, training coordinator for San Diego State University's Public Child Welfare Training Academy. “Not looks, not money, not profession, not uniform, not where you live, not how religious you are, or how good you are.”

The best self-protection involves a combination of factors, including being aware of your capabilities, your environment, your habits, realistic hazards, and your options should a violent episode occur.

She offered the following tips:

▸Do some self-reflection. What is your history of violence and anger and your response to it? Have you been in situations where you felt threatened, and now you feel hypervigilant? Your personal history of violence “will affect your response to situations,” said Ms. Pence, who spent 25 years as a special agent with the Tennessee Bureau of Investigation. “It will impact the lens through which you view [someone's] behavior. That can be good, but it also could lead you to jump the gun and have a perception of violence and danger when it doesn't really exist.”

▸Make an effort to understand your colleague's attitudes about personal safety and anger in the workplace. Are you allowed to talk about it? Are you encouraged to talk about it? “Is there a forum where you can ventilate about any anxieties you have about a client, or any anger you may have toward the client?” Ms. Pence asked. “Because if you're angry and they're angry, that's not a real healthy combination.”

Also, ask yourself, are there people in the office who can hear you if you yell for help? Is there an emergency buzzer nearby? If somebody enters the office and a buzzer goes off, do we have a plan on what to do?

▸Think twice before visiting a patient in his or her home. Look at prior referrals. Consult with social workers or other physicians to see if the patient has a history of violent behavior. “If I have somebody who's been arrested for drugs, weapons, domestic violence, or child abuse, I'm going to think twice before going out to their turf by myself,” she said.

To protect against workplace violence and abuse, Ms. Pence recommended working on “target hardening.” Target hardening is a military term that refers to the notion that you are the person you are trying to make most safe.

“Until you recognize your personal, physical, mental, and environmental culpabilities and the possibility of victimization and do what you can realistically to reduce these, you're not a hard target,” she explained.

This means:

▸You must be aware.

▸You must think in a different way. For example, “Don't walk down a sidewalk that has doors on one side and bushes on the other,” she advised. Also, when you approach a parking lot, don't skirt the edge of it. Rather, “walk toward the middle of the parking lot and look to the left and right.”

▸You must act in a different way. “The way you walk, look, and carry yourself makes a difference in the degree of vulnerability that is ascribed to you by someone looking to attack,” Ms. Pence said. “Look confident, look aware, and be in the present.”

▸You must recognize your personal vulnerabilities. Ask yourself, how could I defend myself in the event of a personal attack? “For example, I'm not a long distance runner,” Ms. Pence said. “I don't aspire to be a runner. That's a realistic assessment of my physical abilities. If there are areas where you have a deficit, ask, what can I do to enhance my abilities? Maybe it's learning some form of self-protection or learning verbal de-escalation techniques.”

SAN DIEGO — There is no one technique or strategy that will protect you from the risk of physical attacks in your workplace by patients or coworkers, Donna Pence declared at a conference sponsored by the Chadwick Center for Children and Families at Children's Hospital and Health Center, San Diego.

“There is nothing about who and what you are that makes you immune from people intent on doing bad things,” said Ms. Pence, training coordinator for San Diego State University's Public Child Welfare Training Academy. “Not looks, not money, not profession, not uniform, not where you live, not how religious you are, or how good you are.”

The best self-protection involves a combination of factors, including being aware of your capabilities, your environment, your habits, realistic hazards, and your options should a violent episode occur.

She offered the following tips:

▸Do some self-reflection. What is your history of violence and anger and your response to it? Have you been in situations where you felt threatened, and now you feel hypervigilant? Your personal history of violence “will affect your response to situations,” said Ms. Pence, who spent 25 years as a special agent with the Tennessee Bureau of Investigation. “It will impact the lens through which you view [someone's] behavior. That can be good, but it also could lead you to jump the gun and have a perception of violence and danger when it doesn't really exist.”

▸Make an effort to understand your colleague's attitudes about personal safety and anger in the workplace. Are you allowed to talk about it? Are you encouraged to talk about it? “Is there a forum where you can ventilate about any anxieties you have about a client, or any anger you may have toward the client?” Ms. Pence asked. “Because if you're angry and they're angry, that's not a real healthy combination.”

Also, ask yourself, are there people in the office who can hear you if you yell for help? Is there an emergency buzzer nearby? If somebody enters the office and a buzzer goes off, do we have a plan on what to do?

▸Think twice before visiting a patient in his or her home. Look at prior referrals. Consult with social workers or other physicians to see if the patient has a history of violent behavior. “If I have somebody who's been arrested for drugs, weapons, domestic violence, or child abuse, I'm going to think twice before going out to their turf by myself,” she said.

To protect against workplace violence and abuse, Ms. Pence recommended working on “target hardening.” Target hardening is a military term that refers to the notion that you are the person you are trying to make most safe.

“Until you recognize your personal, physical, mental, and environmental culpabilities and the possibility of victimization and do what you can realistically to reduce these, you're not a hard target,” she explained.

This means:

▸You must be aware.

▸You must think in a different way. For example, “Don't walk down a sidewalk that has doors on one side and bushes on the other,” she advised. Also, when you approach a parking lot, don't skirt the edge of it. Rather, “walk toward the middle of the parking lot and look to the left and right.”

▸You must act in a different way. “The way you walk, look, and carry yourself makes a difference in the degree of vulnerability that is ascribed to you by someone looking to attack,” Ms. Pence said. “Look confident, look aware, and be in the present.”

▸You must recognize your personal vulnerabilities. Ask yourself, how could I defend myself in the event of a personal attack? “For example, I'm not a long distance runner,” Ms. Pence said. “I don't aspire to be a runner. That's a realistic assessment of my physical abilities. If there are areas where you have a deficit, ask, what can I do to enhance my abilities? Maybe it's learning some form of self-protection or learning verbal de-escalation techniques.”

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212-6 and Nat. Med. 2004;10:368-73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven.

“Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality,” they said.

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492-8).

They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay.

In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children.

Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

According to the investigators, the most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-year-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499-502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212-6 and Nat. Med. 2004;10:368-73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven.

“Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality,” they said.

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492-8).

They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay.

In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children.

Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

According to the investigators, the most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-year-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499-502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.

A novel human coronavirus discovered by molecular testing in Connecticut may account for about 9% of respiratory tract infections in infants and young children.

The initial discovery is similar to that of a coronavirus identified by investigators in the Netherlands in 2004 (Proc. Natl. Acad. Sci. USA 2004;101:6212-6 and Nat. Med. 2004;10:368-73).

“Whether this virus is associated with other clinical syndromes remains to be determined,” wrote the investigators, led by Frank Esper, M.D., of the department of pediatrics at Yale University, New Haven.

“Population-based studies are required to define the burden of disease caused by this novel HCoV, and such studies could provide information on causality,” they said.

For the study, he and his associates developed PCR probes to target regions of the replicase 1a gene that are conserved among genetically diverse animal and human coronaviruses (J. Infect. Dis. 2005;191:492-8).

They obtained specimens from the respiratory tracts of 895 children in the New Haven area who were less than 5 years old and who tested negative for common respiratory infections via direct fluorescent antibody assay.

In the process, the investigators identified genomic sequences of a novel HCoV they called the New Haven coronavirus (HCoV-NH).

Of the 895 children 79 (8.8%) tested positive for HCoV-NH. Clinical data were available for 76 of the 79 children.

Of these, 9 (11.8%) had evidence of a recent infection with another respiratory virus.

According to the investigators, the most common clinical findings among the 67 children infected only with HCoV-NH were cough (64.2%), rhinorrhea (61.2%), tachypnea (58.2%), fever (47.8%), abnormal breathing sounds (44.8%), and hypoxia (37.3%).

A comparison of the HCoV-NH with the HCoV identified in the studies from the Netherlands “revealed that these viruses are closely related and likely represent the same species,” the investigators observed.

They went on to conclude that the present study demonstrates “the power of the tools of molecular biology to define and characterize potential infectious agents associated with human disease.”

In a related analysis, Dr. Esper and his associates conducted a case-control trial after one of the study participants—a 6-year-old infant with Kawasaki disease—tested positive for HCoV-NH. They studied respiratory specimens from 11 children with Kawasaki disease and 22 age-matched controls (J. Infect. Dis. 2005;191:499-502).

Of the 11 children with Kawasaki disease, nearly three-fourths (72.7%) tested positive for HCoV-NH compared with 1 child (4.5%) in the control group. That translated into a 16-fold risk of HCoV-NH infection among children with Kawasaki disease.

“Further studies—such as prospective cohort studies, seroepidemiological investigations, and investigations of inflamed tissue for the presence of the virus—are required to determine the precise role played by HCoV-NH in the pathogenesis of Kawasaki disease and to determine whether other infectious agents can also trigger this syndrome,” the investigators concluded.