Michele G. Sullivan

WHITE SULPHUR SPRINGS, W.VA. — A treatment algorithm based on DNA identification of high-risk human papilloma virus subtypes could eliminate much unnecessary surgical intervention for women eventually found to have no cervical abnormality, William Irvin, M.D., reported.

“If the initial HPV DNA screening is negative, the likelihood that the patient harbors a high-grade squamous cervical lesion is very low, and rather than continue with diagnostic loop electrosurgical excision or conization, we would recommend conservative follow-up,” Dr. Irvin of the University of Virginia, Charlottesville, said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“It's hoped that by following this algorithm, we can reduce or avoid unnecessary conization and electrosurgical excision procedures in women who are truly at low risk for cervical or endocervical lesions.” (See box.)

Dr. Irvin based his suggestions on the results of two studies.

A 1999 Kaiser Permanente study of 137 women with cytologic atypical glandular cells (AGC) found that HPV DNA testing identified 94% of those with high-grade squamous intraepithelial lesions (HSIL) and 100% of those with endocervical adenocarcinoma in situ (Hum. Pathol. 1999;30:816-25).

And his own small study of 28 women with cytologic AGC found that the DNA testing had both a 100% sensitivity for detecting cervical intraepithelial neoplasia and a 100% negative predictive value for ruling out dysplasia.

“The take-home message of our study is that when a patient presents with cytologic AGC, and the HPV testing is negative [for high-risk strains], the likelihood of a high-grade endocervical lesion is exceedingly small, and you could consider that smear to be either reactive in nature or, if pathologic, most likely to be arising from lesions of the endometrium or adnexa,” he said.

Dr. Irvin prospectively analyzed 28 women who presented to a colposcopy clinic from 2002 to 2004. All women had a repeat ThinPrep System Pap smear for cytology and HPV testing, a colposcopy, and Fischer electrosurgical conization, followed by Pipelle endometrial biopsy.

A total of 58% of the group had significant pathologic abnormalities. Squamous intraepithelial lesions occurred in 50% of the group; 11 of those were HSIL, and three were low-grade squamous intraepithelial lesions. One woman had endocervical adenocarcinoma in situ, and one had endometrial hyperplasia. Normal cells were found in 42% of the group. No cancers were found.

Four of the HPV DNA samples were contaminated with blood, so results were available for 24 patients. Of those, 17 were positive for high-risk HPV, including all 13 dysplastic patients. Seven of the tests were negative for high-risk HPV, and none of the negative patients had dysplasia.

Tips on Managing These Patients

▸ For women older than 35 years, women younger than 35 years who have abnormal bleeding, and women with AGC that “favors endometrial cells”: Perform endometrial sampling.

▸ If AGC “favors endocervical adenocarcinoma in situ”: Perform cold-knife conization and subsequent cervical curettage.

▸ For AGC not otherwise specified: Perform HPV DNA testing.

If the patient is negative for high-risk HPV, repeat cytology at 6-month intervals until two consecutive normal results are obtained. If abnormal cytology persists, refer the patient to colposcopy.

If the patient is positive for high-risk HPV, the likelihood of a dysplastic cervical lesion—typically high-grade—is high. Perform colposcopy, biopsy as indicated, and obtain endocervical samplings. Base further management on the results of the evaluation.

Source: Dr. Irvin

WHITE SULPHUR SPRINGS, W.VA. — A treatment algorithm based on DNA identification of high-risk human papilloma virus subtypes could eliminate much unnecessary surgical intervention for women eventually found to have no cervical abnormality, William Irvin, M.D., reported.

“If the initial HPV DNA screening is negative, the likelihood that the patient harbors a high-grade squamous cervical lesion is very low, and rather than continue with diagnostic loop electrosurgical excision or conization, we would recommend conservative follow-up,” Dr. Irvin of the University of Virginia, Charlottesville, said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“It's hoped that by following this algorithm, we can reduce or avoid unnecessary conization and electrosurgical excision procedures in women who are truly at low risk for cervical or endocervical lesions.” (See box.)

Dr. Irvin based his suggestions on the results of two studies.

A 1999 Kaiser Permanente study of 137 women with cytologic atypical glandular cells (AGC) found that HPV DNA testing identified 94% of those with high-grade squamous intraepithelial lesions (HSIL) and 100% of those with endocervical adenocarcinoma in situ (Hum. Pathol. 1999;30:816-25).

And his own small study of 28 women with cytologic AGC found that the DNA testing had both a 100% sensitivity for detecting cervical intraepithelial neoplasia and a 100% negative predictive value for ruling out dysplasia.

“The take-home message of our study is that when a patient presents with cytologic AGC, and the HPV testing is negative [for high-risk strains], the likelihood of a high-grade endocervical lesion is exceedingly small, and you could consider that smear to be either reactive in nature or, if pathologic, most likely to be arising from lesions of the endometrium or adnexa,” he said.

Dr. Irvin prospectively analyzed 28 women who presented to a colposcopy clinic from 2002 to 2004. All women had a repeat ThinPrep System Pap smear for cytology and HPV testing, a colposcopy, and Fischer electrosurgical conization, followed by Pipelle endometrial biopsy.

A total of 58% of the group had significant pathologic abnormalities. Squamous intraepithelial lesions occurred in 50% of the group; 11 of those were HSIL, and three were low-grade squamous intraepithelial lesions. One woman had endocervical adenocarcinoma in situ, and one had endometrial hyperplasia. Normal cells were found in 42% of the group. No cancers were found.

Four of the HPV DNA samples were contaminated with blood, so results were available for 24 patients. Of those, 17 were positive for high-risk HPV, including all 13 dysplastic patients. Seven of the tests were negative for high-risk HPV, and none of the negative patients had dysplasia.

Tips on Managing These Patients

▸ For women older than 35 years, women younger than 35 years who have abnormal bleeding, and women with AGC that “favors endometrial cells”: Perform endometrial sampling.

▸ If AGC “favors endocervical adenocarcinoma in situ”: Perform cold-knife conization and subsequent cervical curettage.

▸ For AGC not otherwise specified: Perform HPV DNA testing.

If the patient is negative for high-risk HPV, repeat cytology at 6-month intervals until two consecutive normal results are obtained. If abnormal cytology persists, refer the patient to colposcopy.

If the patient is positive for high-risk HPV, the likelihood of a dysplastic cervical lesion—typically high-grade—is high. Perform colposcopy, biopsy as indicated, and obtain endocervical samplings. Base further management on the results of the evaluation.

Source: Dr. Irvin

WHITE SULPHUR SPRINGS, W.VA. — A treatment algorithm based on DNA identification of high-risk human papilloma virus subtypes could eliminate much unnecessary surgical intervention for women eventually found to have no cervical abnormality, William Irvin, M.D., reported.

“If the initial HPV DNA screening is negative, the likelihood that the patient harbors a high-grade squamous cervical lesion is very low, and rather than continue with diagnostic loop electrosurgical excision or conization, we would recommend conservative follow-up,” Dr. Irvin of the University of Virginia, Charlottesville, said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“It's hoped that by following this algorithm, we can reduce or avoid unnecessary conization and electrosurgical excision procedures in women who are truly at low risk for cervical or endocervical lesions.” (See box.)

Dr. Irvin based his suggestions on the results of two studies.

A 1999 Kaiser Permanente study of 137 women with cytologic atypical glandular cells (AGC) found that HPV DNA testing identified 94% of those with high-grade squamous intraepithelial lesions (HSIL) and 100% of those with endocervical adenocarcinoma in situ (Hum. Pathol. 1999;30:816-25).

And his own small study of 28 women with cytologic AGC found that the DNA testing had both a 100% sensitivity for detecting cervical intraepithelial neoplasia and a 100% negative predictive value for ruling out dysplasia.

“The take-home message of our study is that when a patient presents with cytologic AGC, and the HPV testing is negative [for high-risk strains], the likelihood of a high-grade endocervical lesion is exceedingly small, and you could consider that smear to be either reactive in nature or, if pathologic, most likely to be arising from lesions of the endometrium or adnexa,” he said.

Dr. Irvin prospectively analyzed 28 women who presented to a colposcopy clinic from 2002 to 2004. All women had a repeat ThinPrep System Pap smear for cytology and HPV testing, a colposcopy, and Fischer electrosurgical conization, followed by Pipelle endometrial biopsy.

A total of 58% of the group had significant pathologic abnormalities. Squamous intraepithelial lesions occurred in 50% of the group; 11 of those were HSIL, and three were low-grade squamous intraepithelial lesions. One woman had endocervical adenocarcinoma in situ, and one had endometrial hyperplasia. Normal cells were found in 42% of the group. No cancers were found.

Four of the HPV DNA samples were contaminated with blood, so results were available for 24 patients. Of those, 17 were positive for high-risk HPV, including all 13 dysplastic patients. Seven of the tests were negative for high-risk HPV, and none of the negative patients had dysplasia.

Tips on Managing These Patients

▸ For women older than 35 years, women younger than 35 years who have abnormal bleeding, and women with AGC that “favors endometrial cells”: Perform endometrial sampling.

▸ If AGC “favors endocervical adenocarcinoma in situ”: Perform cold-knife conization and subsequent cervical curettage.

▸ For AGC not otherwise specified: Perform HPV DNA testing.

If the patient is negative for high-risk HPV, repeat cytology at 6-month intervals until two consecutive normal results are obtained. If abnormal cytology persists, refer the patient to colposcopy.

If the patient is positive for high-risk HPV, the likelihood of a dysplastic cervical lesion—typically high-grade—is high. Perform colposcopy, biopsy as indicated, and obtain endocervical samplings. Base further management on the results of the evaluation.

Source: Dr. Irvin

The oral pathogen Actinomyces naeslundii appears to be associated with shorter gestation resulting in preterm low birth weight, while oral Lactobacillus casei is associated with longer gestation and higher birth weight.

Increased levels of A. naeslundii could account for as much as 4%-6% of preterm low-birth-weight babies, although more research is necessary to confirm causality, said Ananda P. Dasanayake, D.D.S., of the New York University College of Dentistry, and his colleagues (J. Periodontol. 2005;76:171-7).

The epidemiologic study offers one more tantalizing glimpse at the interrelationship between oral health and systemic disease, and points up the importance of dental care during pregnancy.

“It is advisable to tell patients to seek dental care during pregnancy,” Dr. Dasanayake said in an interview. “If they have chronic periodontal disease, that can be treated—usually mechanically, by scaling and root planing, but sometimes with combination therapy that includes antibiotics.”

Dr. Dasanayake and his colleagues compared the presence of oral bacteria during the third trimester and at delivery with pregnancy outcomes in 297 primigravidas. The women's mean age was 20 years; 93% were African American. About 85% had at least a high school education. Samples of saliva were obtained by expectoration after chewing on sterile paraffin wax.

Samples were tested for A. naeslundii, L. casei, Streptococcus mutans, Streptococcus sobrinus, Streptococcus sanguinus, and Lactobacillus acidophilus.

Most of the women (67%) had normal vaginal deliveries. The average infant birth weight was 3,200 g and average gestational age was 39 weeks. There were 26 low-birth-weight deliveries and 28 preterm deliveries. In a multivariate analysis, the only bacteria significantly associated with pregnancy outcomes were A. naeslundii and L. casei.

Increasing numbers of A. naeslundii were significantly associated with preterm low birth weight. For every one-unit increase in A. naeslundii levels, there was a 60-g decrease in birth weight and a 0.17-week decrease in gestational age.

L. casei was associated with increasing gestational age. Each unit increase in L. casei was associated with a 0.13-week increase in gestational age.

The connection between oral bacteria and preterm birth is biologically plausible, Dr. Dasanayake said. Infections trigger inflammation and increase cytokines, which in turn can increase prostaglandins and lead to cervical dilation and uterine contraction. Conversely, oral L. casei—which is associated with the incidence of dental caries—can have a protective effect by colonizing the vagina (migrating via elimination), where it suppresses the growth of pathogenic bacteria and inhibits bacterial vaginosis.

Because of the epidemiologic nature of the study, he said, it was not possible to separate the actual effect of either bacterial level from other contributing factors, such as drug and alcohol use or smoking. However, two ongoing randomized controlled trials, one in South America and one in the United States, may give more specific information.

“In these studies, pregnant women are randomized into two groups—one group has their periodontal disease treated during pregnancy and one group has it treated after pregnancy,” Dr. Dasanayake said.

He added that several studies, including one of his own, have failed to find any association between oral bacteria and pregnancy outcome. His study was performed in Sri Lanka with women who did not use tobacco, alcohol, or drugs because of cultural taboos and very low socioeconomic status. No association was seen in this group of women.

The oral pathogen Actinomyces naeslundii appears to be associated with shorter gestation resulting in preterm low birth weight, while oral Lactobacillus casei is associated with longer gestation and higher birth weight.

Increased levels of A. naeslundii could account for as much as 4%-6% of preterm low-birth-weight babies, although more research is necessary to confirm causality, said Ananda P. Dasanayake, D.D.S., of the New York University College of Dentistry, and his colleagues (J. Periodontol. 2005;76:171-7).

The epidemiologic study offers one more tantalizing glimpse at the interrelationship between oral health and systemic disease, and points up the importance of dental care during pregnancy.

“It is advisable to tell patients to seek dental care during pregnancy,” Dr. Dasanayake said in an interview. “If they have chronic periodontal disease, that can be treated—usually mechanically, by scaling and root planing, but sometimes with combination therapy that includes antibiotics.”

Dr. Dasanayake and his colleagues compared the presence of oral bacteria during the third trimester and at delivery with pregnancy outcomes in 297 primigravidas. The women's mean age was 20 years; 93% were African American. About 85% had at least a high school education. Samples of saliva were obtained by expectoration after chewing on sterile paraffin wax.

Samples were tested for A. naeslundii, L. casei, Streptococcus mutans, Streptococcus sobrinus, Streptococcus sanguinus, and Lactobacillus acidophilus.

Most of the women (67%) had normal vaginal deliveries. The average infant birth weight was 3,200 g and average gestational age was 39 weeks. There were 26 low-birth-weight deliveries and 28 preterm deliveries. In a multivariate analysis, the only bacteria significantly associated with pregnancy outcomes were A. naeslundii and L. casei.

Increasing numbers of A. naeslundii were significantly associated with preterm low birth weight. For every one-unit increase in A. naeslundii levels, there was a 60-g decrease in birth weight and a 0.17-week decrease in gestational age.

L. casei was associated with increasing gestational age. Each unit increase in L. casei was associated with a 0.13-week increase in gestational age.

The connection between oral bacteria and preterm birth is biologically plausible, Dr. Dasanayake said. Infections trigger inflammation and increase cytokines, which in turn can increase prostaglandins and lead to cervical dilation and uterine contraction. Conversely, oral L. casei—which is associated with the incidence of dental caries—can have a protective effect by colonizing the vagina (migrating via elimination), where it suppresses the growth of pathogenic bacteria and inhibits bacterial vaginosis.

Because of the epidemiologic nature of the study, he said, it was not possible to separate the actual effect of either bacterial level from other contributing factors, such as drug and alcohol use or smoking. However, two ongoing randomized controlled trials, one in South America and one in the United States, may give more specific information.

“In these studies, pregnant women are randomized into two groups—one group has their periodontal disease treated during pregnancy and one group has it treated after pregnancy,” Dr. Dasanayake said.

He added that several studies, including one of his own, have failed to find any association between oral bacteria and pregnancy outcome. His study was performed in Sri Lanka with women who did not use tobacco, alcohol, or drugs because of cultural taboos and very low socioeconomic status. No association was seen in this group of women.

The oral pathogen Actinomyces naeslundii appears to be associated with shorter gestation resulting in preterm low birth weight, while oral Lactobacillus casei is associated with longer gestation and higher birth weight.

Increased levels of A. naeslundii could account for as much as 4%-6% of preterm low-birth-weight babies, although more research is necessary to confirm causality, said Ananda P. Dasanayake, D.D.S., of the New York University College of Dentistry, and his colleagues (J. Periodontol. 2005;76:171-7).

The epidemiologic study offers one more tantalizing glimpse at the interrelationship between oral health and systemic disease, and points up the importance of dental care during pregnancy.

“It is advisable to tell patients to seek dental care during pregnancy,” Dr. Dasanayake said in an interview. “If they have chronic periodontal disease, that can be treated—usually mechanically, by scaling and root planing, but sometimes with combination therapy that includes antibiotics.”

Dr. Dasanayake and his colleagues compared the presence of oral bacteria during the third trimester and at delivery with pregnancy outcomes in 297 primigravidas. The women's mean age was 20 years; 93% were African American. About 85% had at least a high school education. Samples of saliva were obtained by expectoration after chewing on sterile paraffin wax.

Samples were tested for A. naeslundii, L. casei, Streptococcus mutans, Streptococcus sobrinus, Streptococcus sanguinus, and Lactobacillus acidophilus.

Most of the women (67%) had normal vaginal deliveries. The average infant birth weight was 3,200 g and average gestational age was 39 weeks. There were 26 low-birth-weight deliveries and 28 preterm deliveries. In a multivariate analysis, the only bacteria significantly associated with pregnancy outcomes were A. naeslundii and L. casei.

Increasing numbers of A. naeslundii were significantly associated with preterm low birth weight. For every one-unit increase in A. naeslundii levels, there was a 60-g decrease in birth weight and a 0.17-week decrease in gestational age.

L. casei was associated with increasing gestational age. Each unit increase in L. casei was associated with a 0.13-week increase in gestational age.

The connection between oral bacteria and preterm birth is biologically plausible, Dr. Dasanayake said. Infections trigger inflammation and increase cytokines, which in turn can increase prostaglandins and lead to cervical dilation and uterine contraction. Conversely, oral L. casei—which is associated with the incidence of dental caries—can have a protective effect by colonizing the vagina (migrating via elimination), where it suppresses the growth of pathogenic bacteria and inhibits bacterial vaginosis.

Because of the epidemiologic nature of the study, he said, it was not possible to separate the actual effect of either bacterial level from other contributing factors, such as drug and alcohol use or smoking. However, two ongoing randomized controlled trials, one in South America and one in the United States, may give more specific information.

“In these studies, pregnant women are randomized into two groups—one group has their periodontal disease treated during pregnancy and one group has it treated after pregnancy,” Dr. Dasanayake said.

He added that several studies, including one of his own, have failed to find any association between oral bacteria and pregnancy outcome. His study was performed in Sri Lanka with women who did not use tobacco, alcohol, or drugs because of cultural taboos and very low socioeconomic status. No association was seen in this group of women.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories—such as mental retardation or speech disorders—are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially among those born between 1987 and 1992. In those years, the prevalence of autism rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of either reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

They also pointed out that these administrative data can't explain why autism is increasing. Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers include an enormous array of children whose disabilities range from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta. “In this category of autism, you will certainly have kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention may further illuminate the issue since they will use uniform diagnostic criteria. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation or you don't. In autism and Asperger's, you can be dealing with vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories—such as mental retardation or speech disorders—are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially among those born between 1987 and 1992. In those years, the prevalence of autism rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of either reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

They also pointed out that these administrative data can't explain why autism is increasing. Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers include an enormous array of children whose disabilities range from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta. “In this category of autism, you will certainly have kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention may further illuminate the issue since they will use uniform diagnostic criteria. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation or you don't. In autism and Asperger's, you can be dealing with vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories—such as mental retardation or speech disorders—are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially among those born between 1987 and 1992. In those years, the prevalence of autism rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of either reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

They also pointed out that these administrative data can't explain why autism is increasing. Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers include an enormous array of children whose disabilities range from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta. “In this category of autism, you will certainly have kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention may further illuminate the issue since they will use uniform diagnostic criteria. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation or you don't. In autism and Asperger's, you can be dealing with vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

NEW ORLEANS — Sequential therapy is a great way to get quick, effective control of chronic psoriasis while keeping costs down and minimizing the patient's exposure to potentially toxic systemic agents, John Koo, M.D., said at the annual meeting of the American Academy of Dermatology.

“You can start with a fast-acting agent like cyclosporine, then add a biologic and try to taper the cyclosporine,” said Dr. Koo of the University of California, San Francisco. It's important to maintain the initial systemic treatment for at least 3 months, he stressed, because any biologic will take that long to kick in.

“It's not a good idea to stop the prebiologic agent when starting the biologic because the biologic takes at least 3 months to build efficacy and the prebiologic's efficacy will fade within 1 month,” setting the stage for a flare, Dr. Koo said.

After the combination achieves good control, the plan should downshift, eliminating the more toxic systemic agent in favor of some form of maintenance therapy. This could be the biologic alone (with the temporary addition of a systemic if flare occurs), a biologic plus UVB or oral retinoid, or another safe and effective long-term regimen.

Unfortunately, some older therapies are falling by the wayside as the heavily promoted biologics take center stage. But focusing so heavily on these new drugs shortchanges patients who need access to the entire arsenal of treatment. “For optimal care, these patients need the full range, whether it's being promoted or not. PUVA isn't heavily promoted anymore, but it still works,” he said.

When one looks at overall efficacy, “biologics are in the less effective range. They aren't always adequate as monotherapy, even with optimized topical therapy, especially if the patient is large or if it's during the winter,” Dr. Koo said.

As a rough comparison of effectiveness, he said, retinoid plus psoralen and UVA will effect an improvement of 75% in the Psoriasis Area and Severity Index (PASI 75) in 100% of patients by 3 months. This is slightly better than the best biologic, infliximab (PASI 75 in about 90% by 3 months), but it's a lot cheaper and doesn't carry infliximab's risk of infection. The other biologics fall far behind this efficacy level: PASI 75 improvement by 3 months in 21% for alefacept, 28% for efalizumab, 34% for etanercept 25 mg biweekly, and 49% for etanercept 50 mg biweekly.

In contrast, PASI 75 by 3 months is seen in about 90% of patients on PUVA plus calcipotriene; 80% of those on moderate-dose cyclosporine; 71% of those on PUVA alone; 60% of those on methotrexate; and 55% of those on narrowband UVB phototherapy. The downside of these older treatments is that they're not as convenient as simply taking a pill, Dr. Koo said. They involve multiple office visits, which can be a problem in areas of limited medical access, or with noncompliant patients. And some carry a risk of organ damage.

This risk is one reason why some have shunned older systemic agents and embraced the biologics, Dr. Koo noted. “A third of U.S. dermatologists don't feel comfortable prescribing methotrexate or cyclosporine. Another third will only use them when 'pushed to the wall.' The remaining third account for more than 95% of all prebiologic systemic therapy prescribed in the United States.”

Cost should be another consideration, Dr. Koo said. The biologics are considerably more expensive than prebiologic treatments. Approximate annual cost of alefacept approaches $20,000; infliximab, $18,000; and etanercept, $17,000. In contrast, a year of cyclosporine runs about $10,000; acitretin, $5,000; PUVA and UVB, about $2,500; and methotrexate, about $1,500.

NEW ORLEANS — Sequential therapy is a great way to get quick, effective control of chronic psoriasis while keeping costs down and minimizing the patient's exposure to potentially toxic systemic agents, John Koo, M.D., said at the annual meeting of the American Academy of Dermatology.

“You can start with a fast-acting agent like cyclosporine, then add a biologic and try to taper the cyclosporine,” said Dr. Koo of the University of California, San Francisco. It's important to maintain the initial systemic treatment for at least 3 months, he stressed, because any biologic will take that long to kick in.

“It's not a good idea to stop the prebiologic agent when starting the biologic because the biologic takes at least 3 months to build efficacy and the prebiologic's efficacy will fade within 1 month,” setting the stage for a flare, Dr. Koo said.

After the combination achieves good control, the plan should downshift, eliminating the more toxic systemic agent in favor of some form of maintenance therapy. This could be the biologic alone (with the temporary addition of a systemic if flare occurs), a biologic plus UVB or oral retinoid, or another safe and effective long-term regimen.

Unfortunately, some older therapies are falling by the wayside as the heavily promoted biologics take center stage. But focusing so heavily on these new drugs shortchanges patients who need access to the entire arsenal of treatment. “For optimal care, these patients need the full range, whether it's being promoted or not. PUVA isn't heavily promoted anymore, but it still works,” he said.

When one looks at overall efficacy, “biologics are in the less effective range. They aren't always adequate as monotherapy, even with optimized topical therapy, especially if the patient is large or if it's during the winter,” Dr. Koo said.

As a rough comparison of effectiveness, he said, retinoid plus psoralen and UVA will effect an improvement of 75% in the Psoriasis Area and Severity Index (PASI 75) in 100% of patients by 3 months. This is slightly better than the best biologic, infliximab (PASI 75 in about 90% by 3 months), but it's a lot cheaper and doesn't carry infliximab's risk of infection. The other biologics fall far behind this efficacy level: PASI 75 improvement by 3 months in 21% for alefacept, 28% for efalizumab, 34% for etanercept 25 mg biweekly, and 49% for etanercept 50 mg biweekly.

In contrast, PASI 75 by 3 months is seen in about 90% of patients on PUVA plus calcipotriene; 80% of those on moderate-dose cyclosporine; 71% of those on PUVA alone; 60% of those on methotrexate; and 55% of those on narrowband UVB phototherapy. The downside of these older treatments is that they're not as convenient as simply taking a pill, Dr. Koo said. They involve multiple office visits, which can be a problem in areas of limited medical access, or with noncompliant patients. And some carry a risk of organ damage.

This risk is one reason why some have shunned older systemic agents and embraced the biologics, Dr. Koo noted. “A third of U.S. dermatologists don't feel comfortable prescribing methotrexate or cyclosporine. Another third will only use them when 'pushed to the wall.' The remaining third account for more than 95% of all prebiologic systemic therapy prescribed in the United States.”

Cost should be another consideration, Dr. Koo said. The biologics are considerably more expensive than prebiologic treatments. Approximate annual cost of alefacept approaches $20,000; infliximab, $18,000; and etanercept, $17,000. In contrast, a year of cyclosporine runs about $10,000; acitretin, $5,000; PUVA and UVB, about $2,500; and methotrexate, about $1,500.

NEW ORLEANS — Sequential therapy is a great way to get quick, effective control of chronic psoriasis while keeping costs down and minimizing the patient's exposure to potentially toxic systemic agents, John Koo, M.D., said at the annual meeting of the American Academy of Dermatology.

“You can start with a fast-acting agent like cyclosporine, then add a biologic and try to taper the cyclosporine,” said Dr. Koo of the University of California, San Francisco. It's important to maintain the initial systemic treatment for at least 3 months, he stressed, because any biologic will take that long to kick in.

“It's not a good idea to stop the prebiologic agent when starting the biologic because the biologic takes at least 3 months to build efficacy and the prebiologic's efficacy will fade within 1 month,” setting the stage for a flare, Dr. Koo said.

After the combination achieves good control, the plan should downshift, eliminating the more toxic systemic agent in favor of some form of maintenance therapy. This could be the biologic alone (with the temporary addition of a systemic if flare occurs), a biologic plus UVB or oral retinoid, or another safe and effective long-term regimen.

Unfortunately, some older therapies are falling by the wayside as the heavily promoted biologics take center stage. But focusing so heavily on these new drugs shortchanges patients who need access to the entire arsenal of treatment. “For optimal care, these patients need the full range, whether it's being promoted or not. PUVA isn't heavily promoted anymore, but it still works,” he said.

When one looks at overall efficacy, “biologics are in the less effective range. They aren't always adequate as monotherapy, even with optimized topical therapy, especially if the patient is large or if it's during the winter,” Dr. Koo said.

As a rough comparison of effectiveness, he said, retinoid plus psoralen and UVA will effect an improvement of 75% in the Psoriasis Area and Severity Index (PASI 75) in 100% of patients by 3 months. This is slightly better than the best biologic, infliximab (PASI 75 in about 90% by 3 months), but it's a lot cheaper and doesn't carry infliximab's risk of infection. The other biologics fall far behind this efficacy level: PASI 75 improvement by 3 months in 21% for alefacept, 28% for efalizumab, 34% for etanercept 25 mg biweekly, and 49% for etanercept 50 mg biweekly.

In contrast, PASI 75 by 3 months is seen in about 90% of patients on PUVA plus calcipotriene; 80% of those on moderate-dose cyclosporine; 71% of those on PUVA alone; 60% of those on methotrexate; and 55% of those on narrowband UVB phototherapy. The downside of these older treatments is that they're not as convenient as simply taking a pill, Dr. Koo said. They involve multiple office visits, which can be a problem in areas of limited medical access, or with noncompliant patients. And some carry a risk of organ damage.

This risk is one reason why some have shunned older systemic agents and embraced the biologics, Dr. Koo noted. “A third of U.S. dermatologists don't feel comfortable prescribing methotrexate or cyclosporine. Another third will only use them when 'pushed to the wall.' The remaining third account for more than 95% of all prebiologic systemic therapy prescribed in the United States.”

Cost should be another consideration, Dr. Koo said. The biologics are considerably more expensive than prebiologic treatments. Approximate annual cost of alefacept approaches $20,000; infliximab, $18,000; and etanercept, $17,000. In contrast, a year of cyclosporine runs about $10,000; acitretin, $5,000; PUVA and UVB, about $2,500; and methotrexate, about $1,500.

NEW ORLEANS — Because of its myriad presentations on black skin, sarcoidosis can be called “the great imitator,” Rebat Halder, M.D., said at the annual meeting of the American Academy of Dermatology.

“The appearance on the skin can have many different morphologies,” said Dr. Halder, chair of the department of dermatology at Howard University, Washington. “It can really fool you: The lesions can be macular, papular, ichthyosiform, nodular, ulcerative, vesicular, annular, or it can simply present as areas of hypopigmentation with no apparent inflammation.”

Sarcoidosis, characterized by noncaseating epithelioid granulomas that may affect any organ system, is uncommon in any group of patients. However, it is about 16 times more common in blacks than in whites, with an incidence of 35-65/100,000 among blacks. Black women in their fourth decade are most commonly affected, with an incidence of about 100/100,000, Dr. Halder said in an interview.

The etiology of sarcoidosis is unknown, although familial clustering has been observed. For unknown reasons, sarcoidosis is often more aggressive and difficult to treat in blacks.

They have a higher rate of relapse, are more likely to experience multiorgan involvement, and have a slightly higher mortality rate than whites.

About 90% of patients have lung involvement, usually fibrosis due to granulomatous lesions.

Skin lesions appear in about 35% of patients. Other affected organs are the eyes, liver, heart, central nervous system, and spleen.

Any suspicious lesions should be biopsied. Typically, histology will show characteristic noncaseating granulomas. Since so many patients have lung involvement, a chest x-ray is imperative, Dr. Halder said.

“If you suspect a skin lesion is sarcoidosis, you must search for the disease elsewhere in the body.”

Papular sarcoidosis consists of red-brown papules usually occurring on the face, around the eyes, nose, mouth, and nape of neck. The papules can be larger, or quite fine, with the skin assuming a sandpaperlike texture.

Lupus pernio lesions are red or purple indurated plaques usually occurring around the nose.

These lesions can affect the nasal cartilage or bone and upper respiratory system as well.

Plaquelike sarcoidosis can occur anywhere on the skin, but is most common on the back of the neck and on the arms and legs.

This condition is characterized by round or oval, red-brown to purple, infiltrated plaques.

Ulcerative sarcoidosis can be especially debilitating, especially when it occurs on the palms of the hands or soles of the feet. These lesions are small but can become quite deep, Dr. Halder said.

Vesicular sarcoidosis can occur anywhere on the skin and can easily be confused with other blistering diseases or with skin infections.

Hypopigmented sarcoidosis is especially difficult to recognize, he said. “This presents only as areas of the skin without pigment. You would have to consider sarcoidosis along with hypopigmented cutaneous T-cell lymphoma, vitiligo, or tinea versicolor. Again, biopsy is crucial to diagnosis.”

Treatment for skin lesions usually consists of topical or intralesional steroids. Extensive or recalcitrant disease requires more aggressive treatment: oral steroids, methotrexate, allopurinol, thalidomide, or oral retinoids. There has been some success with infliximab as well, Dr. Halder said.

Adjunctive phototherapy is useful for hypopigmented sarcoidosis.

NEW ORLEANS — Because of its myriad presentations on black skin, sarcoidosis can be called “the great imitator,” Rebat Halder, M.D., said at the annual meeting of the American Academy of Dermatology.

“The appearance on the skin can have many different morphologies,” said Dr. Halder, chair of the department of dermatology at Howard University, Washington. “It can really fool you: The lesions can be macular, papular, ichthyosiform, nodular, ulcerative, vesicular, annular, or it can simply present as areas of hypopigmentation with no apparent inflammation.”

Sarcoidosis, characterized by noncaseating epithelioid granulomas that may affect any organ system, is uncommon in any group of patients. However, it is about 16 times more common in blacks than in whites, with an incidence of 35-65/100,000 among blacks. Black women in their fourth decade are most commonly affected, with an incidence of about 100/100,000, Dr. Halder said in an interview.

The etiology of sarcoidosis is unknown, although familial clustering has been observed. For unknown reasons, sarcoidosis is often more aggressive and difficult to treat in blacks.

They have a higher rate of relapse, are more likely to experience multiorgan involvement, and have a slightly higher mortality rate than whites.

About 90% of patients have lung involvement, usually fibrosis due to granulomatous lesions.

Skin lesions appear in about 35% of patients. Other affected organs are the eyes, liver, heart, central nervous system, and spleen.

Any suspicious lesions should be biopsied. Typically, histology will show characteristic noncaseating granulomas. Since so many patients have lung involvement, a chest x-ray is imperative, Dr. Halder said.

“If you suspect a skin lesion is sarcoidosis, you must search for the disease elsewhere in the body.”

Papular sarcoidosis consists of red-brown papules usually occurring on the face, around the eyes, nose, mouth, and nape of neck. The papules can be larger, or quite fine, with the skin assuming a sandpaperlike texture.

Lupus pernio lesions are red or purple indurated plaques usually occurring around the nose.

These lesions can affect the nasal cartilage or bone and upper respiratory system as well.

Plaquelike sarcoidosis can occur anywhere on the skin, but is most common on the back of the neck and on the arms and legs.

This condition is characterized by round or oval, red-brown to purple, infiltrated plaques.

Ulcerative sarcoidosis can be especially debilitating, especially when it occurs on the palms of the hands or soles of the feet. These lesions are small but can become quite deep, Dr. Halder said.

Vesicular sarcoidosis can occur anywhere on the skin and can easily be confused with other blistering diseases or with skin infections.

Hypopigmented sarcoidosis is especially difficult to recognize, he said. “This presents only as areas of the skin without pigment. You would have to consider sarcoidosis along with hypopigmented cutaneous T-cell lymphoma, vitiligo, or tinea versicolor. Again, biopsy is crucial to diagnosis.”

Treatment for skin lesions usually consists of topical or intralesional steroids. Extensive or recalcitrant disease requires more aggressive treatment: oral steroids, methotrexate, allopurinol, thalidomide, or oral retinoids. There has been some success with infliximab as well, Dr. Halder said.

Adjunctive phototherapy is useful for hypopigmented sarcoidosis.

NEW ORLEANS — Because of its myriad presentations on black skin, sarcoidosis can be called “the great imitator,” Rebat Halder, M.D., said at the annual meeting of the American Academy of Dermatology.

“The appearance on the skin can have many different morphologies,” said Dr. Halder, chair of the department of dermatology at Howard University, Washington. “It can really fool you: The lesions can be macular, papular, ichthyosiform, nodular, ulcerative, vesicular, annular, or it can simply present as areas of hypopigmentation with no apparent inflammation.”

Sarcoidosis, characterized by noncaseating epithelioid granulomas that may affect any organ system, is uncommon in any group of patients. However, it is about 16 times more common in blacks than in whites, with an incidence of 35-65/100,000 among blacks. Black women in their fourth decade are most commonly affected, with an incidence of about 100/100,000, Dr. Halder said in an interview.

The etiology of sarcoidosis is unknown, although familial clustering has been observed. For unknown reasons, sarcoidosis is often more aggressive and difficult to treat in blacks.

They have a higher rate of relapse, are more likely to experience multiorgan involvement, and have a slightly higher mortality rate than whites.

About 90% of patients have lung involvement, usually fibrosis due to granulomatous lesions.

Skin lesions appear in about 35% of patients. Other affected organs are the eyes, liver, heart, central nervous system, and spleen.

Any suspicious lesions should be biopsied. Typically, histology will show characteristic noncaseating granulomas. Since so many patients have lung involvement, a chest x-ray is imperative, Dr. Halder said.

“If you suspect a skin lesion is sarcoidosis, you must search for the disease elsewhere in the body.”

Papular sarcoidosis consists of red-brown papules usually occurring on the face, around the eyes, nose, mouth, and nape of neck. The papules can be larger, or quite fine, with the skin assuming a sandpaperlike texture.

Lupus pernio lesions are red or purple indurated plaques usually occurring around the nose.

These lesions can affect the nasal cartilage or bone and upper respiratory system as well.

Plaquelike sarcoidosis can occur anywhere on the skin, but is most common on the back of the neck and on the arms and legs.

This condition is characterized by round or oval, red-brown to purple, infiltrated plaques.

Ulcerative sarcoidosis can be especially debilitating, especially when it occurs on the palms of the hands or soles of the feet. These lesions are small but can become quite deep, Dr. Halder said.

Vesicular sarcoidosis can occur anywhere on the skin and can easily be confused with other blistering diseases or with skin infections.

Hypopigmented sarcoidosis is especially difficult to recognize, he said. “This presents only as areas of the skin without pigment. You would have to consider sarcoidosis along with hypopigmented cutaneous T-cell lymphoma, vitiligo, or tinea versicolor. Again, biopsy is crucial to diagnosis.”

Treatment for skin lesions usually consists of topical or intralesional steroids. Extensive or recalcitrant disease requires more aggressive treatment: oral steroids, methotrexate, allopurinol, thalidomide, or oral retinoids. There has been some success with infliximab as well, Dr. Halder said.

Adjunctive phototherapy is useful for hypopigmented sarcoidosis.

NEW ORLEANS — Melanoma and other skin cancers in blacks and Hispanics are likely to be discovered at a more advanced stage and are associated with significantly poorer survival rates, researchers said at the annual meeting of the American Academy of Dermatology.

Blacks and Hispanics—and their primary care physicians—may believe that darker skin protects against these cancers, said Susan Taylor, M.D. As a result, these patients don't perform frequent skin self-exams, aren't taught the warning signs of skin cancers, and don't see pigmented lesions as a concern. These problems, coupled with the fact that skin cancers often occur in atypical or sun-protected areas, contribute to their poorer prognosis.

“Develop a high index of suspicion for melanoma in the black population and fully evaluate any suspected lesion,” advised Dr. Taylor, director of the Skin of Color Center at St. Luke's-Roosevelt Hospital Center, New York. “The standard of care must include the performance of a complete cutaneous examination emphasizing the palms, soles, fingers, all web spaces, subungual regions, and mucosal surfaces.”

Additionally, she said, physicians should tell dark-skinned patients that they are at risk for melanoma, must wear sunscreen, and should perform monthly skin exams.

Malignant melanoma is about 10 times more common in whites than in blacks. Dark skin transmits only about 7.4% of ultraviolet B and 17.5% of ultraviolet A, while white skin transmits more than 55% of UVB and 29% of UVA, said Rebat Halder, M.D., of Howard University, Washington. “As a result of this additional filtering, black skin has a natural SPF of about 13.4,” he added.

But this natural protection isn't enough, noted Shasa Hu, M.D., of the University of Miami. Dr. Hu presented the results of a population-based study of skin cancer registries in six states: California, Texas, Florida, New Jersey, Illinois, and New York. Her results showed that increasing ultraviolet index and decreasing latitude were both significantly associated with invasive melanoma in blacks and Hispanics, especially among women.

Both Dr. Halder and Dr. Taylor advised physicians to look for suspicious lesions in unexpected areas of the body. A chart review of 649 melanoma patients at Washington Hospital Center found that while 90% of melanomas in whites occurred on sun-exposed skin, only 33% of those in blacks occurred on sun-exposed skin. The most common site of melanoma for black patients was the foot. Almost 40% of melanomas on blacks occurred there, vs. 2.4% of the melanomas on whites.

This same study found significant differences in stage and survival rates between the groups (J. Am. Acad. Dermatol. 2004;50:21-4). Stage I occurred in 60% of whites and 39% of blacks. Stage III or IV occurred in 33% of blacks but only 13% of whites. Five-year survival rates were about 59% for blacks and 85% for whites.

Other skin cancers have similar characteristics when they occur in blacks, Dr. Rebat said.

Squamous cell carcinoma is the most frequently seen skin cancer in blacks, but 65% of cases occur on sun-protected skin, frequently in the anus (15% of SCC overall, and 25% of SCC in black females). SCC also is associated with a later diagnosis and a more aggressive form of the disease. “SCC on covered skin has a greater potential for metastasis,” Dr. Halder said.

SCC is more common in blacks with light or albino skin and on skin that has been damaged by burns, chronic ulcers or inflammation, chemical exposure, or lupus.

NEW ORLEANS — Melanoma and other skin cancers in blacks and Hispanics are likely to be discovered at a more advanced stage and are associated with significantly poorer survival rates, researchers said at the annual meeting of the American Academy of Dermatology.

Blacks and Hispanics—and their primary care physicians—may believe that darker skin protects against these cancers, said Susan Taylor, M.D. As a result, these patients don't perform frequent skin self-exams, aren't taught the warning signs of skin cancers, and don't see pigmented lesions as a concern. These problems, coupled with the fact that skin cancers often occur in atypical or sun-protected areas, contribute to their poorer prognosis.

“Develop a high index of suspicion for melanoma in the black population and fully evaluate any suspected lesion,” advised Dr. Taylor, director of the Skin of Color Center at St. Luke's-Roosevelt Hospital Center, New York. “The standard of care must include the performance of a complete cutaneous examination emphasizing the palms, soles, fingers, all web spaces, subungual regions, and mucosal surfaces.”

Additionally, she said, physicians should tell dark-skinned patients that they are at risk for melanoma, must wear sunscreen, and should perform monthly skin exams.

Malignant melanoma is about 10 times more common in whites than in blacks. Dark skin transmits only about 7.4% of ultraviolet B and 17.5% of ultraviolet A, while white skin transmits more than 55% of UVB and 29% of UVA, said Rebat Halder, M.D., of Howard University, Washington. “As a result of this additional filtering, black skin has a natural SPF of about 13.4,” he added.

But this natural protection isn't enough, noted Shasa Hu, M.D., of the University of Miami. Dr. Hu presented the results of a population-based study of skin cancer registries in six states: California, Texas, Florida, New Jersey, Illinois, and New York. Her results showed that increasing ultraviolet index and decreasing latitude were both significantly associated with invasive melanoma in blacks and Hispanics, especially among women.

Both Dr. Halder and Dr. Taylor advised physicians to look for suspicious lesions in unexpected areas of the body. A chart review of 649 melanoma patients at Washington Hospital Center found that while 90% of melanomas in whites occurred on sun-exposed skin, only 33% of those in blacks occurred on sun-exposed skin. The most common site of melanoma for black patients was the foot. Almost 40% of melanomas on blacks occurred there, vs. 2.4% of the melanomas on whites.

This same study found significant differences in stage and survival rates between the groups (J. Am. Acad. Dermatol. 2004;50:21-4). Stage I occurred in 60% of whites and 39% of blacks. Stage III or IV occurred in 33% of blacks but only 13% of whites. Five-year survival rates were about 59% for blacks and 85% for whites.

Other skin cancers have similar characteristics when they occur in blacks, Dr. Rebat said.

Squamous cell carcinoma is the most frequently seen skin cancer in blacks, but 65% of cases occur on sun-protected skin, frequently in the anus (15% of SCC overall, and 25% of SCC in black females). SCC also is associated with a later diagnosis and a more aggressive form of the disease. “SCC on covered skin has a greater potential for metastasis,” Dr. Halder said.

SCC is more common in blacks with light or albino skin and on skin that has been damaged by burns, chronic ulcers or inflammation, chemical exposure, or lupus.

NEW ORLEANS — Melanoma and other skin cancers in blacks and Hispanics are likely to be discovered at a more advanced stage and are associated with significantly poorer survival rates, researchers said at the annual meeting of the American Academy of Dermatology.

Blacks and Hispanics—and their primary care physicians—may believe that darker skin protects against these cancers, said Susan Taylor, M.D. As a result, these patients don't perform frequent skin self-exams, aren't taught the warning signs of skin cancers, and don't see pigmented lesions as a concern. These problems, coupled with the fact that skin cancers often occur in atypical or sun-protected areas, contribute to their poorer prognosis.

“Develop a high index of suspicion for melanoma in the black population and fully evaluate any suspected lesion,” advised Dr. Taylor, director of the Skin of Color Center at St. Luke's-Roosevelt Hospital Center, New York. “The standard of care must include the performance of a complete cutaneous examination emphasizing the palms, soles, fingers, all web spaces, subungual regions, and mucosal surfaces.”

Additionally, she said, physicians should tell dark-skinned patients that they are at risk for melanoma, must wear sunscreen, and should perform monthly skin exams.

Malignant melanoma is about 10 times more common in whites than in blacks. Dark skin transmits only about 7.4% of ultraviolet B and 17.5% of ultraviolet A, while white skin transmits more than 55% of UVB and 29% of UVA, said Rebat Halder, M.D., of Howard University, Washington. “As a result of this additional filtering, black skin has a natural SPF of about 13.4,” he added.

But this natural protection isn't enough, noted Shasa Hu, M.D., of the University of Miami. Dr. Hu presented the results of a population-based study of skin cancer registries in six states: California, Texas, Florida, New Jersey, Illinois, and New York. Her results showed that increasing ultraviolet index and decreasing latitude were both significantly associated with invasive melanoma in blacks and Hispanics, especially among women.

Both Dr. Halder and Dr. Taylor advised physicians to look for suspicious lesions in unexpected areas of the body. A chart review of 649 melanoma patients at Washington Hospital Center found that while 90% of melanomas in whites occurred on sun-exposed skin, only 33% of those in blacks occurred on sun-exposed skin. The most common site of melanoma for black patients was the foot. Almost 40% of melanomas on blacks occurred there, vs. 2.4% of the melanomas on whites.

This same study found significant differences in stage and survival rates between the groups (J. Am. Acad. Dermatol. 2004;50:21-4). Stage I occurred in 60% of whites and 39% of blacks. Stage III or IV occurred in 33% of blacks but only 13% of whites. Five-year survival rates were about 59% for blacks and 85% for whites.

Other skin cancers have similar characteristics when they occur in blacks, Dr. Rebat said.

Squamous cell carcinoma is the most frequently seen skin cancer in blacks, but 65% of cases occur on sun-protected skin, frequently in the anus (15% of SCC overall, and 25% of SCC in black females). SCC also is associated with a later diagnosis and a more aggressive form of the disease. “SCC on covered skin has a greater potential for metastasis,” Dr. Halder said.

SCC is more common in blacks with light or albino skin and on skin that has been damaged by burns, chronic ulcers or inflammation, chemical exposure, or lupus.

SAVANNAH, GA. — Any patient who presents with the neurologic symptoms of acute-onset weakness or paralysis during mosquito season should be evaluated for West Nile virus infection, regardless of whether there was a viral prodrome.

Only about 1% of West Nile patients develop symptoms, but about 21% of that group will develop a neurologic complication. Recovery is highly variable and almost impossible to predict, two researchers said at the annual meeting of the American Association of Electrodiagnostic Medicine.

An early and virulent season for West Nile virus infection has already been predicted for California and the southwestern United States by the Centers for Disease Control and Prevention's division of vector-borne infectious diseases (FAMILY PRACTICE NEWS, March 15, 2005, p. 10). The culprit is the area's wetter than normal winter.

The International Society for Infectious Diseases has issued a statement predicting a tough year for Oregon in terms of cases of West Nile virus infection. The state saw 88 deaths from West Nile virus infection last year, according to CDC data. State public health officials are meeting to develop control strategies (www.promedmail.org/pls/pm/pm?an=20050305.0670

“These paralytic illnesses are seen a lot in patients who are elderly, immunocompromised, or otherwise sick, but every once in a while you'll see them in a young, healthy patient,” said Bjorn Oskarsson, M.D.

“And the severity of illness at onset isn't a good predictor of recovery,” noted Dr. Oskarsson, a fellow at the University of Colorado, Denver.

Weakness or paralysis associated with West Nile infection apparently occurs when the virus destroys motor neurons in the anterior horn of the spinal cord. Although magnetic resonance imaging is generally unhelpful in patients with symptomatic West Nile virus infection, those with paralytic illness often will show abnormal signal intensity in the anterior horn, Dr. Oskarsson said in a poster presentation.

In a separate presentation, Jun Li, M.D., said that needle electromyography will show severe denervation in the muscles of the weak limbs and their corresponding paraspinal muscles. These findings confirm the localization of the lesion to the anterior horn motor neurons or their ventral nerve roots, he said.

“The cardinal clinical feature of these patients is acute asymmetric flaccid paralysis that reaches a plateau within hours in most patients,” said Dr. Li of the department of neurology at Wayne State University, Detroit.

The paralysis is slightly more frequent in the lower extremities than in the upper, and there is minimal or no sensory disturbance.

Many patients will report a flu-like illness preceding onset of weakness by days or weeks, but this is not a certainty, he said. Paralysis can occur in previously healthy individuals as well as those who are immunocompromised or those who have chronic health problems.

Because West Nile virus has become endemic in most states, the presence of IgM antibodies in serum is no longer an acceptable way of confirming diagnosis, Dr. Li noted. “Many people in the United States have been exposed and carry antibodies in their serum,” he said.

Instead, the antibodies must be detected in cerebrospinal fluid by enzyme-linked immunosorbent assay. Patients with a paralytic complication may also show increased serum creatine kinase, ranging from several hundred up to 20,000 mg/dL. “This elevated CK may have originated from necrotized muscle fibers,” Dr. Li said.

There is no current treatment for this condition, Dr. Li noted. Intravenous immunoglobulin has been found ineffective.

Both Dr. Li and Dr. Oskarsson presented case studies illustrating the unpredictable nature of this illness.

Dr. Li presented two cases. A previously healthy 36-year-old woman developed a mild flu-like illness followed by low back pain. She then awoke to find her left leg paralyzed. She was unresponsive to a short course of intravenous immunoglobulin.

The second case was a previously healthy 44-year-old man who first noticed a tingling sensation in his back followed by a flu-like illness. Four days later, his legs suddenly became paralyzed. Ten days after that, his right arm was paralyzed and within another 24 hours, the left arm was also paralyzed. He also developed bilateral facial muscle weakness.

These two patients vividly illustrate the unpredictable outcomes of this illness, Dr. Li noted. The man had more systemic symptoms and severe four-limb paralysis. His condition appeared much worse than that of the woman. Yet his strength recovered completely, while the paralysis of the woman's leg improved only minimally after 20 months, he said.

Dr. Oskarsson presented five cases: Three of them were immunocompromised patients. One patient died. She was a 46-year-old woman with a history of bone marrow transplant for large cell lymphoma. She presented with generalized weakness after a flu-like illness. She rapidly became comatose. Her brain MRI showed severe panencephalitic changes with multifocal necrosis in the cerebral deep gray nuclei, brainstem, and spinal cord.

The other patients survived, but only one regained baseline strength: a 48-year old woman with a prior kidney transplant. A month after developing gastroenteritis she became confused and developed proximal bilateral arm weakness.

The other three patients survived but with neurologic deficit: a previously healthy 54-year-old woman who developed paraplegia after a flu-like illness; a previously healthy 32-year-old woman who developed left arm, face, and leg weakness after 3 days of severe headache and truncal rash; and a 50-year-old man with a liver transplant who developed rapidly progressive quadriplegia after experiencing severe abdominal pain and encephalopathy.

SAVANNAH, GA. — Any patient who presents with the neurologic symptoms of acute-onset weakness or paralysis during mosquito season should be evaluated for West Nile virus infection, regardless of whether there was a viral prodrome.

Only about 1% of West Nile patients develop symptoms, but about 21% of that group will develop a neurologic complication. Recovery is highly variable and almost impossible to predict, two researchers said at the annual meeting of the American Association of Electrodiagnostic Medicine.

An early and virulent season for West Nile virus infection has already been predicted for California and the southwestern United States by the Centers for Disease Control and Prevention's division of vector-borne infectious diseases (FAMILY PRACTICE NEWS, March 15, 2005, p. 10). The culprit is the area's wetter than normal winter.

The International Society for Infectious Diseases has issued a statement predicting a tough year for Oregon in terms of cases of West Nile virus infection. The state saw 88 deaths from West Nile virus infection last year, according to CDC data. State public health officials are meeting to develop control strategies (www.promedmail.org/pls/pm/pm?an=20050305.0670

“These paralytic illnesses are seen a lot in patients who are elderly, immunocompromised, or otherwise sick, but every once in a while you'll see them in a young, healthy patient,” said Bjorn Oskarsson, M.D.

“And the severity of illness at onset isn't a good predictor of recovery,” noted Dr. Oskarsson, a fellow at the University of Colorado, Denver.

Weakness or paralysis associated with West Nile infection apparently occurs when the virus destroys motor neurons in the anterior horn of the spinal cord. Although magnetic resonance imaging is generally unhelpful in patients with symptomatic West Nile virus infection, those with paralytic illness often will show abnormal signal intensity in the anterior horn, Dr. Oskarsson said in a poster presentation.

In a separate presentation, Jun Li, M.D., said that needle electromyography will show severe denervation in the muscles of the weak limbs and their corresponding paraspinal muscles. These findings confirm the localization of the lesion to the anterior horn motor neurons or their ventral nerve roots, he said.

“The cardinal clinical feature of these patients is acute asymmetric flaccid paralysis that reaches a plateau within hours in most patients,” said Dr. Li of the department of neurology at Wayne State University, Detroit.

The paralysis is slightly more frequent in the lower extremities than in the upper, and there is minimal or no sensory disturbance.

Many patients will report a flu-like illness preceding onset of weakness by days or weeks, but this is not a certainty, he said. Paralysis can occur in previously healthy individuals as well as those who are immunocompromised or those who have chronic health problems.

Because West Nile virus has become endemic in most states, the presence of IgM antibodies in serum is no longer an acceptable way of confirming diagnosis, Dr. Li noted. “Many people in the United States have been exposed and carry antibodies in their serum,” he said.

Instead, the antibodies must be detected in cerebrospinal fluid by enzyme-linked immunosorbent assay. Patients with a paralytic complication may also show increased serum creatine kinase, ranging from several hundred up to 20,000 mg/dL. “This elevated CK may have originated from necrotized muscle fibers,” Dr. Li said.

There is no current treatment for this condition, Dr. Li noted. Intravenous immunoglobulin has been found ineffective.

Both Dr. Li and Dr. Oskarsson presented case studies illustrating the unpredictable nature of this illness.

Dr. Li presented two cases. A previously healthy 36-year-old woman developed a mild flu-like illness followed by low back pain. She then awoke to find her left leg paralyzed. She was unresponsive to a short course of intravenous immunoglobulin.

The second case was a previously healthy 44-year-old man who first noticed a tingling sensation in his back followed by a flu-like illness. Four days later, his legs suddenly became paralyzed. Ten days after that, his right arm was paralyzed and within another 24 hours, the left arm was also paralyzed. He also developed bilateral facial muscle weakness.

These two patients vividly illustrate the unpredictable outcomes of this illness, Dr. Li noted. The man had more systemic symptoms and severe four-limb paralysis. His condition appeared much worse than that of the woman. Yet his strength recovered completely, while the paralysis of the woman's leg improved only minimally after 20 months, he said.

Dr. Oskarsson presented five cases: Three of them were immunocompromised patients. One patient died. She was a 46-year-old woman with a history of bone marrow transplant for large cell lymphoma. She presented with generalized weakness after a flu-like illness. She rapidly became comatose. Her brain MRI showed severe panencephalitic changes with multifocal necrosis in the cerebral deep gray nuclei, brainstem, and spinal cord.

The other patients survived, but only one regained baseline strength: a 48-year old woman with a prior kidney transplant. A month after developing gastroenteritis she became confused and developed proximal bilateral arm weakness.

The other three patients survived but with neurologic deficit: a previously healthy 54-year-old woman who developed paraplegia after a flu-like illness; a previously healthy 32-year-old woman who developed left arm, face, and leg weakness after 3 days of severe headache and truncal rash; and a 50-year-old man with a liver transplant who developed rapidly progressive quadriplegia after experiencing severe abdominal pain and encephalopathy.

SAVANNAH, GA. — Any patient who presents with the neurologic symptoms of acute-onset weakness or paralysis during mosquito season should be evaluated for West Nile virus infection, regardless of whether there was a viral prodrome.

Only about 1% of West Nile patients develop symptoms, but about 21% of that group will develop a neurologic complication. Recovery is highly variable and almost impossible to predict, two researchers said at the annual meeting of the American Association of Electrodiagnostic Medicine.

An early and virulent season for West Nile virus infection has already been predicted for California and the southwestern United States by the Centers for Disease Control and Prevention's division of vector-borne infectious diseases (FAMILY PRACTICE NEWS, March 15, 2005, p. 10). The culprit is the area's wetter than normal winter.

The International Society for Infectious Diseases has issued a statement predicting a tough year for Oregon in terms of cases of West Nile virus infection. The state saw 88 deaths from West Nile virus infection last year, according to CDC data. State public health officials are meeting to develop control strategies (www.promedmail.org/pls/pm/pm?an=20050305.0670

“These paralytic illnesses are seen a lot in patients who are elderly, immunocompromised, or otherwise sick, but every once in a while you'll see them in a young, healthy patient,” said Bjorn Oskarsson, M.D.

“And the severity of illness at onset isn't a good predictor of recovery,” noted Dr. Oskarsson, a fellow at the University of Colorado, Denver.

Weakness or paralysis associated with West Nile infection apparently occurs when the virus destroys motor neurons in the anterior horn of the spinal cord. Although magnetic resonance imaging is generally unhelpful in patients with symptomatic West Nile virus infection, those with paralytic illness often will show abnormal signal intensity in the anterior horn, Dr. Oskarsson said in a poster presentation.

In a separate presentation, Jun Li, M.D., said that needle electromyography will show severe denervation in the muscles of the weak limbs and their corresponding paraspinal muscles. These findings confirm the localization of the lesion to the anterior horn motor neurons or their ventral nerve roots, he said.

“The cardinal clinical feature of these patients is acute asymmetric flaccid paralysis that reaches a plateau within hours in most patients,” said Dr. Li of the department of neurology at Wayne State University, Detroit.

The paralysis is slightly more frequent in the lower extremities than in the upper, and there is minimal or no sensory disturbance.

Many patients will report a flu-like illness preceding onset of weakness by days or weeks, but this is not a certainty, he said. Paralysis can occur in previously healthy individuals as well as those who are immunocompromised or those who have chronic health problems.

Because West Nile virus has become endemic in most states, the presence of IgM antibodies in serum is no longer an acceptable way of confirming diagnosis, Dr. Li noted. “Many people in the United States have been exposed and carry antibodies in their serum,” he said.

Instead, the antibodies must be detected in cerebrospinal fluid by enzyme-linked immunosorbent assay. Patients with a paralytic complication may also show increased serum creatine kinase, ranging from several hundred up to 20,000 mg/dL. “This elevated CK may have originated from necrotized muscle fibers,” Dr. Li said.

There is no current treatment for this condition, Dr. Li noted. Intravenous immunoglobulin has been found ineffective.

Both Dr. Li and Dr. Oskarsson presented case studies illustrating the unpredictable nature of this illness.

Dr. Li presented two cases. A previously healthy 36-year-old woman developed a mild flu-like illness followed by low back pain. She then awoke to find her left leg paralyzed. She was unresponsive to a short course of intravenous immunoglobulin.

The second case was a previously healthy 44-year-old man who first noticed a tingling sensation in his back followed by a flu-like illness. Four days later, his legs suddenly became paralyzed. Ten days after that, his right arm was paralyzed and within another 24 hours, the left arm was also paralyzed. He also developed bilateral facial muscle weakness.

These two patients vividly illustrate the unpredictable outcomes of this illness, Dr. Li noted. The man had more systemic symptoms and severe four-limb paralysis. His condition appeared much worse than that of the woman. Yet his strength recovered completely, while the paralysis of the woman's leg improved only minimally after 20 months, he said.

Dr. Oskarsson presented five cases: Three of them were immunocompromised patients. One patient died. She was a 46-year-old woman with a history of bone marrow transplant for large cell lymphoma. She presented with generalized weakness after a flu-like illness. She rapidly became comatose. Her brain MRI showed severe panencephalitic changes with multifocal necrosis in the cerebral deep gray nuclei, brainstem, and spinal cord.

The other patients survived, but only one regained baseline strength: a 48-year old woman with a prior kidney transplant. A month after developing gastroenteritis she became confused and developed proximal bilateral arm weakness.

The other three patients survived but with neurologic deficit: a previously healthy 54-year-old woman who developed paraplegia after a flu-like illness; a previously healthy 32-year-old woman who developed left arm, face, and leg weakness after 3 days of severe headache and truncal rash; and a 50-year-old man with a liver transplant who developed rapidly progressive quadriplegia after experiencing severe abdominal pain and encephalopathy.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories–such as mental retardation or speech disorders–are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially those born between 1987 and 1992. During those years, autism prevalence rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers included an array of children whose disabilities ranged from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta, because it included “kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention, which use uniform diagnostic criteria, may further illuminate the issue. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation, or you don't. With autism and Asperger's, you can be dealing with very vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories–such as mental retardation or speech disorders–are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially those born between 1987 and 1992. During those years, autism prevalence rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers included an array of children whose disabilities ranged from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta, because it included “kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention, which use uniform diagnostic criteria, may further illuminate the issue. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation, or you don't. With autism and Asperger's, you can be dealing with very vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

The apparent increase in autism disorders reflects an actual increase in prevalence, rather than a reclassification of other developmental disorders as autism, reported Craig Newschaffer, Ph.D., of Johns Hopkins University, Baltimore, and his colleagues.

Some researchers have suggested that children who would once have been classified in other categories–such as mental retardation or speech disorders–are now being diagnosed as autistic and that this “diagnostic shifting” accounts for the increase in autism. This is not the case, the investigators maintained, because although autism diagnoses have risen, there has been no corresponding decrease in other diagnostic categories (Pediatrics 2005;115:e277-82).

Dr. Newschaffer and his associates examined data from the U.S. Department of Education's office of special education programs for 1992-2001. These records reflect state counts of children who received free public education services. The children were classified into 13 primary disability categories defined under the Individuals with Disabilities Education Act.

The researchers calculated the prevalence of autism, traumatic brain injury, mental retardation, speech/language impairment, and other health impairments in children aged 6-17 years during each of these years. They then superimposed those data onto birth cohorts extending as far back as 1975.

There were clear, significant increases in the prevalence of autism among younger birth cohorts, especially those born between 1987 and 1992. During those years, autism prevalence rose by about 50% every 2 years; the prevalence was 5.3/10,000 in 1984, 7.8/10,000 in 1986, 11.8/10,000 in 1988, and 18.3/10,000 in 1990.

There were no changes, however, in the prevalence of mental retardation, speech/language impairment, or traumatic brain injury, which suggests that the increase in autism is real and not the result of reclassification of diagnoses or across-the-board increases in special education classification.

The yearly increases seemed to begin leveling off after 1992. It's impossible to know if that observation represents a true decrease in prevalence, however. Since 1997, federal law has allowed state and local education agencies to classify as “developmentally delayed” children as old as 9 years, Dr. Newschaffer and his associates noted.

“It is possible that increasing proportions of children in younger cohorts who would have been classified previously as having autism as they transitioned out of preschool special education retain developmental delay classifications,” the investigators said. This may mean that children are now simply being diagnosed with autism at later ages.

Additionally, Thomas Burns, Psy.D., said in an interview, the numbers paint the spectrum of autism diagnoses with the broadest brush possible.

The Department of Education uses only one autism classification, which includes all students receiving services who have been diagnosed with any one of the autism spectrum disorders. Thus, the study's prevalence numbers included an array of children whose disabilities ranged from severe to mild, Dr. Burns said.

“The study makes it a little hard to compare apples to apples,” said Dr. Burns, director of neuropsychology at Children's Healthcare of Atlanta, because it included “kids who are severely mentally handicapped as well as kids with IQs of 130 who are delayed socially.”

Upcoming studies by the Centers for Disease Control and Prevention, which use uniform diagnostic criteria, may further illuminate the issue. “Some of these other disorders are really objective and easy to identify. You either have traumatic brain injury or you don't. You either have a low IQ and mental retardation, or you don't. With autism and Asperger's, you can be dealing with very vague symptoms and diagnostic criteria that vary from physician to physician and from study to study,” he said.

NEW ORLEANS — Nonablative laser therapy for acne doesn't kill Propionibacterium acnes or decrease sebum production but instead appears to work by inducing a rapid and dramatic increase in transforming growth factor beta, Edward Seaton, M.D., and colleagues said in a poster presented at the annual meeting of the American Academy of Dermatology.

"TGF-β is very important anti-inflammatory cytokine that plays a pivotal role in decreasing inflammation and is the first stimulus of neocollagenesis," Dr. Seaton of Hammersmith Hospital, London, said in an interview. "This is the first time a biologic explanation of lasers' effect on acne has been proposed."

Dr. Seaton used nonablative laser therapy on the foreheads of 19 subjects with mild to moderate acne who had received no previous treatment. He took before and after measurements of P. acnes colony count, sebum production, and several cytokines and receptors: interleukin-1 (comedogenic), interleukin-1 receptor antagonist (anticomedogenic), interleukin-10 (anti-inflammatory), tumor necrosis factor (proinflammatory), TGF-βanti-inflammatory), and melanocortin-1 receptor (expressed in healthy sebaceous glands).

Each subject received one session of nonablative laser therapy (wavelength 585 nm, pulse duration 350 msec, 2 J/cm2, spot diameter 7 mm). Cytokine levels were obtained from 4-mm punch biopsies from the buttocks before laser treatment and 3 and 24 hours post treatment.

After 24 hours, there was no decrease in the number of P. acnes colonies on the treated area; in fact, there was a non-statistically significant increase in the number of colonies. There was no significant decrease in the sebum excretion rate at 2, 4, 8, or 24 weeks post treatment.

After 24 hours, there was a fivefold increase in TGF-β but no significant changes in any other cytokine or receptor levels. The TGF-β levels had increased slightly, but nonsignificantly, by 3 hours post therapy.

In addition to inhibiting the inflammatory response, Dr. Seaton said, TGF-βstimulates collagen, proteoglycan, fibronectin, and integrin production and inhibits matrix metalloproteinase-induced collagen degradation. Thus, the benefits of nonablative laser therapy in acne seem similar to those it exerts for photorejuvenation.

"They induce collagen remodeling at the ultrastructural level and increase collagen production," he said. "The molecular mechanism of this is unclear, but it is thought to be secondary to nonlethal dermal wounding."

NEW ORLEANS — Nonablative laser therapy for acne doesn't kill Propionibacterium acnes or decrease sebum production but instead appears to work by inducing a rapid and dramatic increase in transforming growth factor beta, Edward Seaton, M.D., and colleagues said in a poster presented at the annual meeting of the American Academy of Dermatology.

"TGF-β is very important anti-inflammatory cytokine that plays a pivotal role in decreasing inflammation and is the first stimulus of neocollagenesis," Dr. Seaton of Hammersmith Hospital, London, said in an interview. "This is the first time a biologic explanation of lasers' effect on acne has been proposed."

Dr. Seaton used nonablative laser therapy on the foreheads of 19 subjects with mild to moderate acne who had received no previous treatment. He took before and after measurements of P. acnes colony count, sebum production, and several cytokines and receptors: interleukin-1 (comedogenic), interleukin-1 receptor antagonist (anticomedogenic), interleukin-10 (anti-inflammatory), tumor necrosis factor (proinflammatory), TGF-βanti-inflammatory), and melanocortin-1 receptor (expressed in healthy sebaceous glands).

Each subject received one session of nonablative laser therapy (wavelength 585 nm, pulse duration 350 msec, 2 J/cm2, spot diameter 7 mm). Cytokine levels were obtained from 4-mm punch biopsies from the buttocks before laser treatment and 3 and 24 hours post treatment.

After 24 hours, there was no decrease in the number of P. acnes colonies on the treated area; in fact, there was a non-statistically significant increase in the number of colonies. There was no significant decrease in the sebum excretion rate at 2, 4, 8, or 24 weeks post treatment.

After 24 hours, there was a fivefold increase in TGF-β but no significant changes in any other cytokine or receptor levels. The TGF-β levels had increased slightly, but nonsignificantly, by 3 hours post therapy.

In addition to inhibiting the inflammatory response, Dr. Seaton said, TGF-βstimulates collagen, proteoglycan, fibronectin, and integrin production and inhibits matrix metalloproteinase-induced collagen degradation. Thus, the benefits of nonablative laser therapy in acne seem similar to those it exerts for photorejuvenation.

"They induce collagen remodeling at the ultrastructural level and increase collagen production," he said. "The molecular mechanism of this is unclear, but it is thought to be secondary to nonlethal dermal wounding."

NEW ORLEANS — Nonablative laser therapy for acne doesn't kill Propionibacterium acnes or decrease sebum production but instead appears to work by inducing a rapid and dramatic increase in transforming growth factor beta, Edward Seaton, M.D., and colleagues said in a poster presented at the annual meeting of the American Academy of Dermatology.

"TGF-β is very important anti-inflammatory cytokine that plays a pivotal role in decreasing inflammation and is the first stimulus of neocollagenesis," Dr. Seaton of Hammersmith Hospital, London, said in an interview. "This is the first time a biologic explanation of lasers' effect on acne has been proposed."

Dr. Seaton used nonablative laser therapy on the foreheads of 19 subjects with mild to moderate acne who had received no previous treatment. He took before and after measurements of P. acnes colony count, sebum production, and several cytokines and receptors: interleukin-1 (comedogenic), interleukin-1 receptor antagonist (anticomedogenic), interleukin-10 (anti-inflammatory), tumor necrosis factor (proinflammatory), TGF-βanti-inflammatory), and melanocortin-1 receptor (expressed in healthy sebaceous glands).

Each subject received one session of nonablative laser therapy (wavelength 585 nm, pulse duration 350 msec, 2 J/cm2, spot diameter 7 mm). Cytokine levels were obtained from 4-mm punch biopsies from the buttocks before laser treatment and 3 and 24 hours post treatment.

After 24 hours, there was no decrease in the number of P. acnes colonies on the treated area; in fact, there was a non-statistically significant increase in the number of colonies. There was no significant decrease in the sebum excretion rate at 2, 4, 8, or 24 weeks post treatment.

After 24 hours, there was a fivefold increase in TGF-β but no significant changes in any other cytokine or receptor levels. The TGF-β levels had increased slightly, but nonsignificantly, by 3 hours post therapy.

In addition to inhibiting the inflammatory response, Dr. Seaton said, TGF-βstimulates collagen, proteoglycan, fibronectin, and integrin production and inhibits matrix metalloproteinase-induced collagen degradation. Thus, the benefits of nonablative laser therapy in acne seem similar to those it exerts for photorejuvenation.

"They induce collagen remodeling at the ultrastructural level and increase collagen production," he said. "The molecular mechanism of this is unclear, but it is thought to be secondary to nonlethal dermal wounding."

NEW ORLEANS — The pulsed dye lasers 585 nm and 595 nm are equally effective in surgical-scar ablation, Maria P. Rivas, M.D., reported at the annual meeting of the American Academy of Dermatology.

Although there were no significant histologic or clinical differences between the treated sites, the sites treated with the lower-fluence laser showed slightly more elastic fibers and slight advantages in pliability, vascularity, and scar height, said Dr. Rivas of the department of dermatology and cutaneous surgery at the University of Miami.

She and her colleagues examined outcomes on 19 linear postsurgical scars greater than 3 cm; the scars occurred on 14 patients aged 18-85 years. Their skin types were I-IV. A blinded examiner evaluated the scars on suture-removal day and after treatment using the Vancouver Scar Scale, which assesses pigmentation, vascularity, pliability, and height. The investigators also rated the scars for cosmetic appearance using a cosmetic visual-analog scale.

Each scar was divided into three equal segments. The center segment was left untreated, and the outer segments were randomized to treatment with either pulsed dye laser (PDL) 585 nm or 595 nm (10-mm spot size, 3.5 J/cm2).

Each scar was treated once a month for 3 months, and final assessment was made 1 month after series completion.

At that time, sites treated with the 585-nm PDL showed slightly more elastic fibers on histology than did sites treated with the 595-nm PDL.

All treated sites showed a greater improvement than control sites on the Vancouver Scar Scale. The control sites showed an average 32% improvement, the 595-nm sites showed an average 55% improvement, and the 585-nm sites showed and average 67% improvement. The difference between the treated sites was not statistically significant.

All the Vancouver Scar Scale parameters were more improved on the treated sites than on the control sites, with vascularity and pliability showing the greatest improvements. All treated sites scored significantly higher than the untreated sites on the cosmetic visual-analog scale. Again, the 585-nm sites score slightly higher than the 595-nm sites, but not significantly so.

Comparison of efficacy of 585-nm vs. 595-nm pulsed dye laser on treating surgical scars is shown on suture removal day. Courtesy Dr. Maria P. Rivas

NEW ORLEANS — The pulsed dye lasers 585 nm and 595 nm are equally effective in surgical-scar ablation, Maria P. Rivas, M.D., reported at the annual meeting of the American Academy of Dermatology.

Although there were no significant histologic or clinical differences between the treated sites, the sites treated with the lower-fluence laser showed slightly more elastic fibers and slight advantages in pliability, vascularity, and scar height, said Dr. Rivas of the department of dermatology and cutaneous surgery at the University of Miami.

She and her colleagues examined outcomes on 19 linear postsurgical scars greater than 3 cm; the scars occurred on 14 patients aged 18-85 years. Their skin types were I-IV. A blinded examiner evaluated the scars on suture-removal day and after treatment using the Vancouver Scar Scale, which assesses pigmentation, vascularity, pliability, and height. The investigators also rated the scars for cosmetic appearance using a cosmetic visual-analog scale.

Each scar was divided into three equal segments. The center segment was left untreated, and the outer segments were randomized to treatment with either pulsed dye laser (PDL) 585 nm or 595 nm (10-mm spot size, 3.5 J/cm2).

Each scar was treated once a month for 3 months, and final assessment was made 1 month after series completion.

At that time, sites treated with the 585-nm PDL showed slightly more elastic fibers on histology than did sites treated with the 595-nm PDL.

All treated sites showed a greater improvement than control sites on the Vancouver Scar Scale. The control sites showed an average 32% improvement, the 595-nm sites showed an average 55% improvement, and the 585-nm sites showed and average 67% improvement. The difference between the treated sites was not statistically significant.

All the Vancouver Scar Scale parameters were more improved on the treated sites than on the control sites, with vascularity and pliability showing the greatest improvements. All treated sites scored significantly higher than the untreated sites on the cosmetic visual-analog scale. Again, the 585-nm sites score slightly higher than the 595-nm sites, but not significantly so.

Comparison of efficacy of 585-nm vs. 595-nm pulsed dye laser on treating surgical scars is shown on suture removal day. Courtesy Dr. Maria P. Rivas

NEW ORLEANS — The pulsed dye lasers 585 nm and 595 nm are equally effective in surgical-scar ablation, Maria P. Rivas, M.D., reported at the annual meeting of the American Academy of Dermatology.

Although there were no significant histologic or clinical differences between the treated sites, the sites treated with the lower-fluence laser showed slightly more elastic fibers and slight advantages in pliability, vascularity, and scar height, said Dr. Rivas of the department of dermatology and cutaneous surgery at the University of Miami.

She and her colleagues examined outcomes on 19 linear postsurgical scars greater than 3 cm; the scars occurred on 14 patients aged 18-85 years. Their skin types were I-IV. A blinded examiner evaluated the scars on suture-removal day and after treatment using the Vancouver Scar Scale, which assesses pigmentation, vascularity, pliability, and height. The investigators also rated the scars for cosmetic appearance using a cosmetic visual-analog scale.

Each scar was divided into three equal segments. The center segment was left untreated, and the outer segments were randomized to treatment with either pulsed dye laser (PDL) 585 nm or 595 nm (10-mm spot size, 3.5 J/cm2).

Each scar was treated once a month for 3 months, and final assessment was made 1 month after series completion.

At that time, sites treated with the 585-nm PDL showed slightly more elastic fibers on histology than did sites treated with the 595-nm PDL.

All treated sites showed a greater improvement than control sites on the Vancouver Scar Scale. The control sites showed an average 32% improvement, the 595-nm sites showed an average 55% improvement, and the 585-nm sites showed and average 67% improvement. The difference between the treated sites was not statistically significant.

All the Vancouver Scar Scale parameters were more improved on the treated sites than on the control sites, with vascularity and pliability showing the greatest improvements. All treated sites scored significantly higher than the untreated sites on the cosmetic visual-analog scale. Again, the 585-nm sites score slightly higher than the 595-nm sites, but not significantly so.

Comparison of efficacy of 585-nm vs. 595-nm pulsed dye laser on treating surgical scars is shown on suture removal day. Courtesy Dr. Maria P. Rivas