Pediatrics

Children’s and adolescents’ risk of blood pressure increases and hypertension rose as their body mass index increased, even over a short period of a few years, according to a recent study.

“Obesity, especially severe obesity, at a young age confers an increased risk of early onset of cardiometabolic diseases such as hypertension,” wrote Emily D. Parker, Ph.D., of the HealthPartners Institute for Education and Research in Minneapolis, and her associates online (Pediatrics. 2016 Feb 19. doi: 10.1542/peds.2015-1662). “The significant adverse effect of weight gain and obesity early in life, and over a short period of time, emphasizes the importance of developing early and effective clinical and public health strategies directed at the primary prevention of overweight and obesity.”

©Vishnu Kumar/Thinkstock

The researchers retrospectively analyzed the health care records of 100,606 children and adolescents, aged 3-17 years, who received care from HealthPartners Medical Group in Minnesota, Kaiser Permanente Colorado, or Kaiser Permanente Northern California. All the patients had not been hypertensive within the 6 months before baseline measurements and had at least three primary care visits with blood pressure measurements between January 2007 and December 2011.

At baseline, 16% of the patients were overweight, 2% were obese, and 4% were severely obese. The majority (92%) were below the 90th percentile for their systolic blood pressure at baseline, while 4% were prehypertensive and 4% were hypertensive (at or above 95th percentile). Over a median 3.1 years of follow-up per person, 0.3% of the patients became hypertensive, translating to an incidence rate of 0.15 new cases per year.

After accounting for demographics, baseline blood pressure percentiles, year, and site, both children (aged 3-11) and adolescents with obesity were about twice as likely as children and adolescents with low healthy weights to develop hypertension (hazard ratio, 2.02 and HR, 2.20, respectively). Children and adolescents with severe obesity had more than a four times greater risk of developing hypertension (HR, 4.42 and HR, 4.46, respectively), compared with those with a low healthy weight. These were significant differences. No association appeared between those with low-normal weights at baseline and either high-normal or overweight categories during follow-up.

Forty percent of the children and 24% of the adolescents dropped from severely obese to obese during follow-up, and 45% of the children and 55% of the adolescents who were obese at baseline remained so throughout follow-up. Among children overweight at baseline, 19% became obese, 0.7% became severely obese, and 44% became a healthy weight. Among initially overweight adolescents, 13% became obese, 0.1% became severely obese, and 34% became a healthy weight.

“There was a strong association between change in BMI [body mass index] category and change in blood pressure across BMI categories in both age groups and genders,” Dr. Parker and her associates wrote. “In girls and boys 3-11 years old, both systolic blood pressure and diastolic blood pressure percentiles increased significantly when BMI increased from normal to either overweight or obese and when it increased from overweight to obese.” Similar but greater changes were seen among the adolescents, particularly among girls aged 12-17 years.

Correspondingly, children and teens who dropped from a higher to a lower BMI category had statistically significant drops in both systolic and diastolic blood pressure.

Risk of hypertension tripled for those with obesity at baseline who remained obese through follow-up (HR, 3.71 for children; HR, 3.64 for teens).

The study was funded by the National Heart, Lung, and Blood Institute. Most of the investigators had no relevant financial disclosures. Dr. Joan C. Lo has received previous research funding from Sanofi unrelated to this study.

Children’s and adolescents’ risk of blood pressure increases and hypertension rose as their body mass index increased, even over a short period of a few years, according to a recent study.

“Obesity, especially severe obesity, at a young age confers an increased risk of early onset of cardiometabolic diseases such as hypertension,” wrote Emily D. Parker, Ph.D., of the HealthPartners Institute for Education and Research in Minneapolis, and her associates online (Pediatrics. 2016 Feb 19. doi: 10.1542/peds.2015-1662). “The significant adverse effect of weight gain and obesity early in life, and over a short period of time, emphasizes the importance of developing early and effective clinical and public health strategies directed at the primary prevention of overweight and obesity.”

©Vishnu Kumar/Thinkstock

The researchers retrospectively analyzed the health care records of 100,606 children and adolescents, aged 3-17 years, who received care from HealthPartners Medical Group in Minnesota, Kaiser Permanente Colorado, or Kaiser Permanente Northern California. All the patients had not been hypertensive within the 6 months before baseline measurements and had at least three primary care visits with blood pressure measurements between January 2007 and December 2011.

At baseline, 16% of the patients were overweight, 2% were obese, and 4% were severely obese. The majority (92%) were below the 90th percentile for their systolic blood pressure at baseline, while 4% were prehypertensive and 4% were hypertensive (at or above 95th percentile). Over a median 3.1 years of follow-up per person, 0.3% of the patients became hypertensive, translating to an incidence rate of 0.15 new cases per year.

After accounting for demographics, baseline blood pressure percentiles, year, and site, both children (aged 3-11) and adolescents with obesity were about twice as likely as children and adolescents with low healthy weights to develop hypertension (hazard ratio, 2.02 and HR, 2.20, respectively). Children and adolescents with severe obesity had more than a four times greater risk of developing hypertension (HR, 4.42 and HR, 4.46, respectively), compared with those with a low healthy weight. These were significant differences. No association appeared between those with low-normal weights at baseline and either high-normal or overweight categories during follow-up.

Forty percent of the children and 24% of the adolescents dropped from severely obese to obese during follow-up, and 45% of the children and 55% of the adolescents who were obese at baseline remained so throughout follow-up. Among children overweight at baseline, 19% became obese, 0.7% became severely obese, and 44% became a healthy weight. Among initially overweight adolescents, 13% became obese, 0.1% became severely obese, and 34% became a healthy weight.

“There was a strong association between change in BMI [body mass index] category and change in blood pressure across BMI categories in both age groups and genders,” Dr. Parker and her associates wrote. “In girls and boys 3-11 years old, both systolic blood pressure and diastolic blood pressure percentiles increased significantly when BMI increased from normal to either overweight or obese and when it increased from overweight to obese.” Similar but greater changes were seen among the adolescents, particularly among girls aged 12-17 years.

Correspondingly, children and teens who dropped from a higher to a lower BMI category had statistically significant drops in both systolic and diastolic blood pressure.

Risk of hypertension tripled for those with obesity at baseline who remained obese through follow-up (HR, 3.71 for children; HR, 3.64 for teens).

The study was funded by the National Heart, Lung, and Blood Institute. Most of the investigators had no relevant financial disclosures. Dr. Joan C. Lo has received previous research funding from Sanofi unrelated to this study.

Children’s and adolescents’ risk of blood pressure increases and hypertension rose as their body mass index increased, even over a short period of a few years, according to a recent study.

“Obesity, especially severe obesity, at a young age confers an increased risk of early onset of cardiometabolic diseases such as hypertension,” wrote Emily D. Parker, Ph.D., of the HealthPartners Institute for Education and Research in Minneapolis, and her associates online (Pediatrics. 2016 Feb 19. doi: 10.1542/peds.2015-1662). “The significant adverse effect of weight gain and obesity early in life, and over a short period of time, emphasizes the importance of developing early and effective clinical and public health strategies directed at the primary prevention of overweight and obesity.”

©Vishnu Kumar/Thinkstock

The researchers retrospectively analyzed the health care records of 100,606 children and adolescents, aged 3-17 years, who received care from HealthPartners Medical Group in Minnesota, Kaiser Permanente Colorado, or Kaiser Permanente Northern California. All the patients had not been hypertensive within the 6 months before baseline measurements and had at least three primary care visits with blood pressure measurements between January 2007 and December 2011.

At baseline, 16% of the patients were overweight, 2% were obese, and 4% were severely obese. The majority (92%) were below the 90th percentile for their systolic blood pressure at baseline, while 4% were prehypertensive and 4% were hypertensive (at or above 95th percentile). Over a median 3.1 years of follow-up per person, 0.3% of the patients became hypertensive, translating to an incidence rate of 0.15 new cases per year.

After accounting for demographics, baseline blood pressure percentiles, year, and site, both children (aged 3-11) and adolescents with obesity were about twice as likely as children and adolescents with low healthy weights to develop hypertension (hazard ratio, 2.02 and HR, 2.20, respectively). Children and adolescents with severe obesity had more than a four times greater risk of developing hypertension (HR, 4.42 and HR, 4.46, respectively), compared with those with a low healthy weight. These were significant differences. No association appeared between those with low-normal weights at baseline and either high-normal or overweight categories during follow-up.

Forty percent of the children and 24% of the adolescents dropped from severely obese to obese during follow-up, and 45% of the children and 55% of the adolescents who were obese at baseline remained so throughout follow-up. Among children overweight at baseline, 19% became obese, 0.7% became severely obese, and 44% became a healthy weight. Among initially overweight adolescents, 13% became obese, 0.1% became severely obese, and 34% became a healthy weight.

“There was a strong association between change in BMI [body mass index] category and change in blood pressure across BMI categories in both age groups and genders,” Dr. Parker and her associates wrote. “In girls and boys 3-11 years old, both systolic blood pressure and diastolic blood pressure percentiles increased significantly when BMI increased from normal to either overweight or obese and when it increased from overweight to obese.” Similar but greater changes were seen among the adolescents, particularly among girls aged 12-17 years.

Correspondingly, children and teens who dropped from a higher to a lower BMI category had statistically significant drops in both systolic and diastolic blood pressure.

Risk of hypertension tripled for those with obesity at baseline who remained obese through follow-up (HR, 3.71 for children; HR, 3.64 for teens).

The study was funded by the National Heart, Lung, and Blood Institute. Most of the investigators had no relevant financial disclosures. Dr. Joan C. Lo has received previous research funding from Sanofi unrelated to this study.

Lab mouse

The gene EZH2 is a driver of, and potential therapeutic target for, early T-cell precursor acute lymphoblastic leukemia (ETP-ALL), according to a new study.

A previous study, published in Nature in 2012, suggested that nearly half of ETP-ALLs have inactivating alterations in EZH2.

Loss of EZH2 function can inactivate Polycomb repressive complex 2 (PRC2), but it was not clear how PRC2 loss-of-function mutations would aid leukemia growth.

The new study, published in Cell Reports, provides some insight.

Tobias Neff, MD, of the University of Colorado Denver in Aurora, and his colleagues developed a mouse model of NRASQ61K-driven leukemia that recapitulates phenotypic and transcriptional features of ETP-ALL.

Experiments with this model revealed that inactivation of EZH2 helps accelerate leukemia development and enhances a stem-cell-related transcriptional program.

“We have 2 major features of [ETP-ALL]—stem-like cells and increased growth—and, now, we show an actor implicated in both—namely, EZH2/PRC2,” Dr Neff said.

“How exactly the stem-cell-like gene expression profile contributes to the aggressiveness of ETP-ALL is unknown, but we’ve known that these stem-like cells are associated with poor prognosis in acute leukemia.”

The researchers also found that EZH2 inactivation resulted in increased activation of STAT3 by tyrosine 705 phosphorylation. This led them to wonder whether the JAK/STAT pathway might be important in their ETP-ALL model.

The team tested the JAK1/2 inhibitor ruxolitinib in NRASQ61K cells with EZH2 deletion and observed inhibition of cell growth.

“Ruxolitinib is unlikely to treat the disease by itself, but this model will help us test possible drug combinations that could eventually benefit ETP-ALL patients,” Dr Neff said.

He and his colleagues also plan to test the activity of different drugs against other cell types with inactivated EZH2.

“In addition to our specific finding in this disease, we are excited to now have a model that allows us to explore consequences of EZH2 inactivation that may enrich our understanding of a number of other conditions with a similar set of genetic changes,” Dr Neff said.

He and his colleagues noted that EZH2 is known to be inactivated in myelodysplastic syndromes, myeloproliferative neoplasms, and other hematologic malignancies.

Lab mouse

The gene EZH2 is a driver of, and potential therapeutic target for, early T-cell precursor acute lymphoblastic leukemia (ETP-ALL), according to a new study.

A previous study, published in Nature in 2012, suggested that nearly half of ETP-ALLs have inactivating alterations in EZH2.

Loss of EZH2 function can inactivate Polycomb repressive complex 2 (PRC2), but it was not clear how PRC2 loss-of-function mutations would aid leukemia growth.

The new study, published in Cell Reports, provides some insight.

Tobias Neff, MD, of the University of Colorado Denver in Aurora, and his colleagues developed a mouse model of NRASQ61K-driven leukemia that recapitulates phenotypic and transcriptional features of ETP-ALL.

Experiments with this model revealed that inactivation of EZH2 helps accelerate leukemia development and enhances a stem-cell-related transcriptional program.

“We have 2 major features of [ETP-ALL]—stem-like cells and increased growth—and, now, we show an actor implicated in both—namely, EZH2/PRC2,” Dr Neff said.

“How exactly the stem-cell-like gene expression profile contributes to the aggressiveness of ETP-ALL is unknown, but we’ve known that these stem-like cells are associated with poor prognosis in acute leukemia.”

The researchers also found that EZH2 inactivation resulted in increased activation of STAT3 by tyrosine 705 phosphorylation. This led them to wonder whether the JAK/STAT pathway might be important in their ETP-ALL model.

The team tested the JAK1/2 inhibitor ruxolitinib in NRASQ61K cells with EZH2 deletion and observed inhibition of cell growth.

“Ruxolitinib is unlikely to treat the disease by itself, but this model will help us test possible drug combinations that could eventually benefit ETP-ALL patients,” Dr Neff said.

He and his colleagues also plan to test the activity of different drugs against other cell types with inactivated EZH2.

“In addition to our specific finding in this disease, we are excited to now have a model that allows us to explore consequences of EZH2 inactivation that may enrich our understanding of a number of other conditions with a similar set of genetic changes,” Dr Neff said.

He and his colleagues noted that EZH2 is known to be inactivated in myelodysplastic syndromes, myeloproliferative neoplasms, and other hematologic malignancies.

Lab mouse

The gene EZH2 is a driver of, and potential therapeutic target for, early T-cell precursor acute lymphoblastic leukemia (ETP-ALL), according to a new study.

A previous study, published in Nature in 2012, suggested that nearly half of ETP-ALLs have inactivating alterations in EZH2.

Loss of EZH2 function can inactivate Polycomb repressive complex 2 (PRC2), but it was not clear how PRC2 loss-of-function mutations would aid leukemia growth.

The new study, published in Cell Reports, provides some insight.

Tobias Neff, MD, of the University of Colorado Denver in Aurora, and his colleagues developed a mouse model of NRASQ61K-driven leukemia that recapitulates phenotypic and transcriptional features of ETP-ALL.

Experiments with this model revealed that inactivation of EZH2 helps accelerate leukemia development and enhances a stem-cell-related transcriptional program.

“We have 2 major features of [ETP-ALL]—stem-like cells and increased growth—and, now, we show an actor implicated in both—namely, EZH2/PRC2,” Dr Neff said.

“How exactly the stem-cell-like gene expression profile contributes to the aggressiveness of ETP-ALL is unknown, but we’ve known that these stem-like cells are associated with poor prognosis in acute leukemia.”

The researchers also found that EZH2 inactivation resulted in increased activation of STAT3 by tyrosine 705 phosphorylation. This led them to wonder whether the JAK/STAT pathway might be important in their ETP-ALL model.

The team tested the JAK1/2 inhibitor ruxolitinib in NRASQ61K cells with EZH2 deletion and observed inhibition of cell growth.

“Ruxolitinib is unlikely to treat the disease by itself, but this model will help us test possible drug combinations that could eventually benefit ETP-ALL patients,” Dr Neff said.

He and his colleagues also plan to test the activity of different drugs against other cell types with inactivated EZH2.

“In addition to our specific finding in this disease, we are excited to now have a model that allows us to explore consequences of EZH2 inactivation that may enrich our understanding of a number of other conditions with a similar set of genetic changes,” Dr Neff said.

He and his colleagues noted that EZH2 is known to be inactivated in myelodysplastic syndromes, myeloproliferative neoplasms, and other hematologic malignancies.

As the busy days of a long, gray winter drag on and an early season of Lent has begun, this column flows from reflections on life, death, and the promise of a new season of spring and green trees, hopefully coming soon – no matter what that groundhog saw.

Clinical ethics consultation often involves end of life (EOL) care. When I recall patients from my career, many memories are of patients who died. I trained with an intensivist who said he felt he was under less stress than the general pediatricians. While his patients were sicker, if one of his patients died, it was not unexpected. The presumption was that in the ICU everything possible had been done. General pediatricians rarely have a patient who dies. When they do, everyone, including the pediatrician, will ponder over whether something might have been caught earlier or something could have been done differently. But the most difficult problems in pediatric EOL care involve deciding when to stop aggressive care and let nature take its course.

I think the natural tendency for scholars is to approach difficult decisions by seeking more information. The delusion (which scholars can usually elucidate in great postmodern detail as long as it doesn’t apply to our own behavior) is that extensive information and deep reflection will lead to the best, most accurate, immutable, and nonambivalent declaration of goals, desires, values, and intents. To even make this delusion plausible, a sci-fi writer had to create a nonhuman species of Vulcans. But medical ethicists routinely apply this paradigm to existentially frightening EOL matters in a medical world full of prognostic uncertainty. Ethicists have recommended that this method of decision making be adopted by a population with low health literacy and a predilection to using Tinder.

For the internists, EOL care is mostly about specifying which modalities to use and which to limit. Over time, it became evident that a single check box, labeled Do Not Resuscitate yes/no, was insufficient to capture patient preferences. I recall once seeing a draft document with 49 boxes. It was clearly unwieldy. Most states that have adopted a POLST (Physician Orders for Life-Sustaining Treatment) paradigm have settled for forms with five to seven options. I think that if it were possible to capture advance directives better than that, eharmony.com, with its plethora of questions, would have already created an app for it. In adult medicine, we always can lament that the conversation about EOL care was too brief, but in my experience raising expectations of a more comprehensive discussion usually lowers the likelihood of people ever undertaking even an abbreviated conversation. In ethics, if you raise the bar high enough, people seem to walk under it.

Pediatrics at the EOL tends to focus discussion more on the goals of care, the likely outcomes, and the quality of life. These perspectives are then sometimes mapped, with poor reliability, onto the POLST paradigm designed for adults. Parents are usually at the bedside often enough to recognize their child’s suffering during aggressive care. Surrogate decision makers for adult EOL care occasionally lack that insight.

While advance directive documents are helpful, I don’t think there is a substitute for a physician motivated by empathy and a caring, involved surrogate decision maker at bedside. Providing information is not the key focus. The process should emphasize building trusting relationships, clear understanding, and reasonable expectations. I am reminded in those situations of an ancient quote: Medical care is “to cure sometimes, to relieve often, and to comfort always.”

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Dr. Powell said he had no relevant financial disclosures or conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.

As the busy days of a long, gray winter drag on and an early season of Lent has begun, this column flows from reflections on life, death, and the promise of a new season of spring and green trees, hopefully coming soon – no matter what that groundhog saw.

Clinical ethics consultation often involves end of life (EOL) care. When I recall patients from my career, many memories are of patients who died. I trained with an intensivist who said he felt he was under less stress than the general pediatricians. While his patients were sicker, if one of his patients died, it was not unexpected. The presumption was that in the ICU everything possible had been done. General pediatricians rarely have a patient who dies. When they do, everyone, including the pediatrician, will ponder over whether something might have been caught earlier or something could have been done differently. But the most difficult problems in pediatric EOL care involve deciding when to stop aggressive care and let nature take its course.

I think the natural tendency for scholars is to approach difficult decisions by seeking more information. The delusion (which scholars can usually elucidate in great postmodern detail as long as it doesn’t apply to our own behavior) is that extensive information and deep reflection will lead to the best, most accurate, immutable, and nonambivalent declaration of goals, desires, values, and intents. To even make this delusion plausible, a sci-fi writer had to create a nonhuman species of Vulcans. But medical ethicists routinely apply this paradigm to existentially frightening EOL matters in a medical world full of prognostic uncertainty. Ethicists have recommended that this method of decision making be adopted by a population with low health literacy and a predilection to using Tinder.

For the internists, EOL care is mostly about specifying which modalities to use and which to limit. Over time, it became evident that a single check box, labeled Do Not Resuscitate yes/no, was insufficient to capture patient preferences. I recall once seeing a draft document with 49 boxes. It was clearly unwieldy. Most states that have adopted a POLST (Physician Orders for Life-Sustaining Treatment) paradigm have settled for forms with five to seven options. I think that if it were possible to capture advance directives better than that, eharmony.com, with its plethora of questions, would have already created an app for it. In adult medicine, we always can lament that the conversation about EOL care was too brief, but in my experience raising expectations of a more comprehensive discussion usually lowers the likelihood of people ever undertaking even an abbreviated conversation. In ethics, if you raise the bar high enough, people seem to walk under it.

Pediatrics at the EOL tends to focus discussion more on the goals of care, the likely outcomes, and the quality of life. These perspectives are then sometimes mapped, with poor reliability, onto the POLST paradigm designed for adults. Parents are usually at the bedside often enough to recognize their child’s suffering during aggressive care. Surrogate decision makers for adult EOL care occasionally lack that insight.

While advance directive documents are helpful, I don’t think there is a substitute for a physician motivated by empathy and a caring, involved surrogate decision maker at bedside. Providing information is not the key focus. The process should emphasize building trusting relationships, clear understanding, and reasonable expectations. I am reminded in those situations of an ancient quote: Medical care is “to cure sometimes, to relieve often, and to comfort always.”

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Dr. Powell said he had no relevant financial disclosures or conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.

As the busy days of a long, gray winter drag on and an early season of Lent has begun, this column flows from reflections on life, death, and the promise of a new season of spring and green trees, hopefully coming soon – no matter what that groundhog saw.

Clinical ethics consultation often involves end of life (EOL) care. When I recall patients from my career, many memories are of patients who died. I trained with an intensivist who said he felt he was under less stress than the general pediatricians. While his patients were sicker, if one of his patients died, it was not unexpected. The presumption was that in the ICU everything possible had been done. General pediatricians rarely have a patient who dies. When they do, everyone, including the pediatrician, will ponder over whether something might have been caught earlier or something could have been done differently. But the most difficult problems in pediatric EOL care involve deciding when to stop aggressive care and let nature take its course.

I think the natural tendency for scholars is to approach difficult decisions by seeking more information. The delusion (which scholars can usually elucidate in great postmodern detail as long as it doesn’t apply to our own behavior) is that extensive information and deep reflection will lead to the best, most accurate, immutable, and nonambivalent declaration of goals, desires, values, and intents. To even make this delusion plausible, a sci-fi writer had to create a nonhuman species of Vulcans. But medical ethicists routinely apply this paradigm to existentially frightening EOL matters in a medical world full of prognostic uncertainty. Ethicists have recommended that this method of decision making be adopted by a population with low health literacy and a predilection to using Tinder.

For the internists, EOL care is mostly about specifying which modalities to use and which to limit. Over time, it became evident that a single check box, labeled Do Not Resuscitate yes/no, was insufficient to capture patient preferences. I recall once seeing a draft document with 49 boxes. It was clearly unwieldy. Most states that have adopted a POLST (Physician Orders for Life-Sustaining Treatment) paradigm have settled for forms with five to seven options. I think that if it were possible to capture advance directives better than that, eharmony.com, with its plethora of questions, would have already created an app for it. In adult medicine, we always can lament that the conversation about EOL care was too brief, but in my experience raising expectations of a more comprehensive discussion usually lowers the likelihood of people ever undertaking even an abbreviated conversation. In ethics, if you raise the bar high enough, people seem to walk under it.

Pediatrics at the EOL tends to focus discussion more on the goals of care, the likely outcomes, and the quality of life. These perspectives are then sometimes mapped, with poor reliability, onto the POLST paradigm designed for adults. Parents are usually at the bedside often enough to recognize their child’s suffering during aggressive care. Surrogate decision makers for adult EOL care occasionally lack that insight.

While advance directive documents are helpful, I don’t think there is a substitute for a physician motivated by empathy and a caring, involved surrogate decision maker at bedside. Providing information is not the key focus. The process should emphasize building trusting relationships, clear understanding, and reasonable expectations. I am reminded in those situations of an ancient quote: Medical care is “to cure sometimes, to relieve often, and to comfort always.”

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis. Dr. Powell said he had no relevant financial disclosures or conflicts of interest. E-mail him at pdnews@frontlinemedcom.com.

Many lesbian, gay, bisexual, and transgender (LGBT) youth face misconceptions about their sexual or gender identity. This is especially true when it comes to sex and relationships. Unfortunately, many clinicians believe these myths, and they can have devastating consequences on the health of LGBT youth.

Here are some common myths about sex and relationships in LGBT youth, and how you, as a provider, can combat them with knowledge and compassion:

Myth No. 1: Bisexual youth are promiscuous. This is a stereotype that even plagues bisexual adults. There is a persistent misconception that just because bisexuals are attracted to both sexes, they are naturally promiscuous. In fact, most bisexuals describe themselves as monogamous.¹

Myth No. 2: Youth who are transgender are lesbian/gay/bisexual before transition and are straight after transition. According to the National Transgender Discrimination Survey, regardless of where they are in the transition process, 23% of transgender people identify as heterosexual, 23% identify as gay or lesbian, 25% identify as bisexual, 23% label themselves as queer, 4% describe themselves as asexual and 2% wrote in other answers.²

Myth No. 3: Gay and lesbian teens only have sex or romantic relationships with the same sex. According to the Youth Risk Behavior Survey, although 22% of lesbian and gay teens say they have sex with the same sex only, about 9% say that they have sex with both sexes.³ This shows that sexual identity does not predict sexual behavior and has important implications for the following myths.

Myth No. 4: Lesbian and bisexual girls don’t experience intimate partner violence. Because the majority of those who perpetrate intimate partner violence are men, it is tempting to assume that lesbian and bisexual teenage girls don’t experience abuse in their relationships.

Unfortunately, one study shows that 42% of lesbian and bisexual girls experienced intimate partner violence in the past, compared with 16% of heterosexual girls.⁴ However, this study and others do not tell us whether they have experienced abuse in their relationships with girls or with boys.

Myth No. 5: Lesbian girls can’t get gonorrhea or chlamydia or pelvic inflammatory disease (PID). About 2% of young lesbians report ever having any sexually transmitted infection (STI). A small percentage of young lesbians report having chlamydia, and this is associated with PID. It is true, however, that gonorrhea is rare among lesbians,⁵ but don’t forget that young lesbian women may have had sex with men.

Interestingly, the prevalence of bacterial vaginosis, a condition characterized by overgrowth of vaginal anaerobic bacteria, is higher in young women who have sex with women.⁶ Possible sources of transmission include digital-to-vaginal contact, oral sex, or sex toys.

Myth No. 6: Young women who have sex with women can’t get pregnant, so you don’t have to worry about birth control. Don’t forget that heterosexuals use birth control for other reasons than preventing pregnancy. Some women use birth control to help regulate periods, to ease cramping, or to treat acne. Lesbians and bisexual girls are at the same risk for these problems as are heterosexual girls, so don’t assume that they’re not interested in birth control just because they are not concerned about getting pregnant.

Also, as previously mentioned, lesbian girls may be having sex with boys, so conversations about birth control should be driven by who they are having sex with, not by how they identify.

Myth No. 7: Gay boys can’t get girls pregnant. Lesbian girls can’t get pregnant. A study by the Toronto Teen Sex Survey found that 28% of sexual minority youth report involvement in pregnancy, compared with 7% of heterosexual youth.⁷

Now many who are reading this may be scratching their heads. If someone finds the same sex attractive, then why are they engaging in heterosexual sex? Some studies suggest that engaging in heterosexual sex is a way to hide their true sexual orientation,⁸ because we live in a heterosexist and homophobic environment. After all, what better way to prove that you’re heterosexual? Another study suggests that intentionally getting pregnant or getting someone pregnant is the quickest way to parenthood, and becoming a parent can compensate for one’s identity as a sexual minority.⁹

So how do you overcome these persistent myths? The most important thing to do is not assume. Identity and behaviors are not the same. Always be specific when you’re asking questions about sex and relationships in LGBT youth.

The Centers for Disease Control and Prevention (CDC) recommends the following when obtaining a sexual history:

• Ask, “Are your sexual partner’s male, female, or both?”

• Ask, “When you do have sex with your partner, what do you do?” Here, you have to be very specific. Younger teenagers tend to be concrete thinkers, so don’t just ask “Are you sexually active?” Instead, try asking, “Have you ever had a penis in your mouth, vagina, or anus?” or “Do you use sex toys?”

• In terms of protection from STIs, you might ask, “Do you use condoms or a dental dam?”

• Ask, “Have you ever had an STI, and if so, how was it treated?”

• Ask, “What do you use for birth control?” either hormonal or barrier methods.

In addition to above questions, I would also ask about intimate partner violence. Often, health care providers may ask if their patient has been hit, punch, slapped, or kicked by their partners. But intimate partner violence can go beyond physical violence. It also involves emotional manipulation or birth control sabotage. Sometimes, it is better to ask if a patient has been forced to do something sexual with her partners when she didn’t want to. The patient may deny it, however, even though you highly suspect it. So it is better to remember to build a rapport, and when the patient is ready to get out of an abusive relationship, he or she will come to you for help.

Some clinicians have told me that they have a hard time asking sexual histories in LGBT youth because they’re afraid of offending them, especially when it comes to asking about sex with the opposite sex. This is a valid concern and an area of ongoing research, but I think that by making things normative, just like with any behavior, teens and young adults are more likely to disclose critical pieces of information. It is a good idea, then, to start off with “Because of homophobia, many LGBT youth may engage in heterosexual sex. Tell me, have you ever…”

By not assuming and asking specific questions, LGBT youth are more likely to tell their health care provider important information. With that information, health care providers can prevent many adverse health outcomes like teen pregnancy, STIs, and intimate partner violence. It also will give health care providers an opportunity to address the rampant stigma and discrimination that plagues this vulnerable population.

Here are some resources on sex and relationships in LGBT youth:

• The CDC 2015 STI Guidelines have a special section on STIs in men who have sex with men, women who have sex with women, and transgender men and women.

• Bedsider.org is an excellent website about birth control options and STI prevention for all sexual orientations and gender identities.

• Futures Without Violence provides resources for health care professionals to manage and prevent intimate partner violence.

References

1. J Bisex. 2000;1(1):31-68.

2. National Transgender Discrimination Survey: Full Report. 2012.

3. MMWR Surveill Summ. 2011 Jun 10;60(7):1-133.

4. J Youth Adolesc. 2015 Jan;44(1):211-24.

5. Perspect Sex Reprod Health. 2008 Dec;40(4):212-7.

6. Sex Transm Dis. 2010 May;37(5):335-9.

7. Sexpress: The Toronto teen survey report. 2009.

8. Fletcher RC. Social context and social support: Exploring the lived experiences of LGBTQ youth who have been pregnant. [Master’s Project]: School of Public Health, University of Minnesota; 2011.

9. Can J Hum Sex. 2008;17(3):123-139.

Dr. Montano is an adolescent medicine fellow at Children’s Hospital of Pittsburgh of UPMC and a postdoctoral fellow in the department of pediatrics at the University of Pittsburgh. He has no relevant financial disclosures.

Many lesbian, gay, bisexual, and transgender (LGBT) youth face misconceptions about their sexual or gender identity. This is especially true when it comes to sex and relationships. Unfortunately, many clinicians believe these myths, and they can have devastating consequences on the health of LGBT youth.

Here are some common myths about sex and relationships in LGBT youth, and how you, as a provider, can combat them with knowledge and compassion:

Myth No. 1: Bisexual youth are promiscuous. This is a stereotype that even plagues bisexual adults. There is a persistent misconception that just because bisexuals are attracted to both sexes, they are naturally promiscuous. In fact, most bisexuals describe themselves as monogamous.¹

Myth No. 2: Youth who are transgender are lesbian/gay/bisexual before transition and are straight after transition. According to the National Transgender Discrimination Survey, regardless of where they are in the transition process, 23% of transgender people identify as heterosexual, 23% identify as gay or lesbian, 25% identify as bisexual, 23% label themselves as queer, 4% describe themselves as asexual and 2% wrote in other answers.²

Myth No. 3: Gay and lesbian teens only have sex or romantic relationships with the same sex. According to the Youth Risk Behavior Survey, although 22% of lesbian and gay teens say they have sex with the same sex only, about 9% say that they have sex with both sexes.³ This shows that sexual identity does not predict sexual behavior and has important implications for the following myths.

Myth No. 4: Lesbian and bisexual girls don’t experience intimate partner violence. Because the majority of those who perpetrate intimate partner violence are men, it is tempting to assume that lesbian and bisexual teenage girls don’t experience abuse in their relationships.

Unfortunately, one study shows that 42% of lesbian and bisexual girls experienced intimate partner violence in the past, compared with 16% of heterosexual girls.⁴ However, this study and others do not tell us whether they have experienced abuse in their relationships with girls or with boys.

Myth No. 5: Lesbian girls can’t get gonorrhea or chlamydia or pelvic inflammatory disease (PID). About 2% of young lesbians report ever having any sexually transmitted infection (STI). A small percentage of young lesbians report having chlamydia, and this is associated with PID. It is true, however, that gonorrhea is rare among lesbians,⁵ but don’t forget that young lesbian women may have had sex with men.

Interestingly, the prevalence of bacterial vaginosis, a condition characterized by overgrowth of vaginal anaerobic bacteria, is higher in young women who have sex with women.⁶ Possible sources of transmission include digital-to-vaginal contact, oral sex, or sex toys.

Myth No. 6: Young women who have sex with women can’t get pregnant, so you don’t have to worry about birth control. Don’t forget that heterosexuals use birth control for other reasons than preventing pregnancy. Some women use birth control to help regulate periods, to ease cramping, or to treat acne. Lesbians and bisexual girls are at the same risk for these problems as are heterosexual girls, so don’t assume that they’re not interested in birth control just because they are not concerned about getting pregnant.

Also, as previously mentioned, lesbian girls may be having sex with boys, so conversations about birth control should be driven by who they are having sex with, not by how they identify.

Myth No. 7: Gay boys can’t get girls pregnant. Lesbian girls can’t get pregnant. A study by the Toronto Teen Sex Survey found that 28% of sexual minority youth report involvement in pregnancy, compared with 7% of heterosexual youth.⁷

Now many who are reading this may be scratching their heads. If someone finds the same sex attractive, then why are they engaging in heterosexual sex? Some studies suggest that engaging in heterosexual sex is a way to hide their true sexual orientation,⁸ because we live in a heterosexist and homophobic environment. After all, what better way to prove that you’re heterosexual? Another study suggests that intentionally getting pregnant or getting someone pregnant is the quickest way to parenthood, and becoming a parent can compensate for one’s identity as a sexual minority.⁹

So how do you overcome these persistent myths? The most important thing to do is not assume. Identity and behaviors are not the same. Always be specific when you’re asking questions about sex and relationships in LGBT youth.

The Centers for Disease Control and Prevention (CDC) recommends the following when obtaining a sexual history:

• Ask, “Are your sexual partner’s male, female, or both?”

• Ask, “When you do have sex with your partner, what do you do?” Here, you have to be very specific. Younger teenagers tend to be concrete thinkers, so don’t just ask “Are you sexually active?” Instead, try asking, “Have you ever had a penis in your mouth, vagina, or anus?” or “Do you use sex toys?”

• In terms of protection from STIs, you might ask, “Do you use condoms or a dental dam?”

• Ask, “Have you ever had an STI, and if so, how was it treated?”

• Ask, “What do you use for birth control?” either hormonal or barrier methods.

In addition to above questions, I would also ask about intimate partner violence. Often, health care providers may ask if their patient has been hit, punch, slapped, or kicked by their partners. But intimate partner violence can go beyond physical violence. It also involves emotional manipulation or birth control sabotage. Sometimes, it is better to ask if a patient has been forced to do something sexual with her partners when she didn’t want to. The patient may deny it, however, even though you highly suspect it. So it is better to remember to build a rapport, and when the patient is ready to get out of an abusive relationship, he or she will come to you for help.

Some clinicians have told me that they have a hard time asking sexual histories in LGBT youth because they’re afraid of offending them, especially when it comes to asking about sex with the opposite sex. This is a valid concern and an area of ongoing research, but I think that by making things normative, just like with any behavior, teens and young adults are more likely to disclose critical pieces of information. It is a good idea, then, to start off with “Because of homophobia, many LGBT youth may engage in heterosexual sex. Tell me, have you ever…”

By not assuming and asking specific questions, LGBT youth are more likely to tell their health care provider important information. With that information, health care providers can prevent many adverse health outcomes like teen pregnancy, STIs, and intimate partner violence. It also will give health care providers an opportunity to address the rampant stigma and discrimination that plagues this vulnerable population.

Here are some resources on sex and relationships in LGBT youth:

• The CDC 2015 STI Guidelines have a special section on STIs in men who have sex with men, women who have sex with women, and transgender men and women.

• Bedsider.org is an excellent website about birth control options and STI prevention for all sexual orientations and gender identities.

• Futures Without Violence provides resources for health care professionals to manage and prevent intimate partner violence.

References

1. J Bisex. 2000;1(1):31-68.

2. National Transgender Discrimination Survey: Full Report. 2012.

3. MMWR Surveill Summ. 2011 Jun 10;60(7):1-133.

4. J Youth Adolesc. 2015 Jan;44(1):211-24.

5. Perspect Sex Reprod Health. 2008 Dec;40(4):212-7.

6. Sex Transm Dis. 2010 May;37(5):335-9.

7. Sexpress: The Toronto teen survey report. 2009.

8. Fletcher RC. Social context and social support: Exploring the lived experiences of LGBTQ youth who have been pregnant. [Master’s Project]: School of Public Health, University of Minnesota; 2011.

9. Can J Hum Sex. 2008;17(3):123-139.

Dr. Montano is an adolescent medicine fellow at Children’s Hospital of Pittsburgh of UPMC and a postdoctoral fellow in the department of pediatrics at the University of Pittsburgh. He has no relevant financial disclosures.

Many lesbian, gay, bisexual, and transgender (LGBT) youth face misconceptions about their sexual or gender identity. This is especially true when it comes to sex and relationships. Unfortunately, many clinicians believe these myths, and they can have devastating consequences on the health of LGBT youth.

Here are some common myths about sex and relationships in LGBT youth, and how you, as a provider, can combat them with knowledge and compassion:

Myth No. 1: Bisexual youth are promiscuous. This is a stereotype that even plagues bisexual adults. There is a persistent misconception that just because bisexuals are attracted to both sexes, they are naturally promiscuous. In fact, most bisexuals describe themselves as monogamous.¹

Myth No. 2: Youth who are transgender are lesbian/gay/bisexual before transition and are straight after transition. According to the National Transgender Discrimination Survey, regardless of where they are in the transition process, 23% of transgender people identify as heterosexual, 23% identify as gay or lesbian, 25% identify as bisexual, 23% label themselves as queer, 4% describe themselves as asexual and 2% wrote in other answers.²

Myth No. 3: Gay and lesbian teens only have sex or romantic relationships with the same sex. According to the Youth Risk Behavior Survey, although 22% of lesbian and gay teens say they have sex with the same sex only, about 9% say that they have sex with both sexes.³ This shows that sexual identity does not predict sexual behavior and has important implications for the following myths.

Myth No. 4: Lesbian and bisexual girls don’t experience intimate partner violence. Because the majority of those who perpetrate intimate partner violence are men, it is tempting to assume that lesbian and bisexual teenage girls don’t experience abuse in their relationships.

Unfortunately, one study shows that 42% of lesbian and bisexual girls experienced intimate partner violence in the past, compared with 16% of heterosexual girls.⁴ However, this study and others do not tell us whether they have experienced abuse in their relationships with girls or with boys.

Myth No. 5: Lesbian girls can’t get gonorrhea or chlamydia or pelvic inflammatory disease (PID). About 2% of young lesbians report ever having any sexually transmitted infection (STI). A small percentage of young lesbians report having chlamydia, and this is associated with PID. It is true, however, that gonorrhea is rare among lesbians,⁵ but don’t forget that young lesbian women may have had sex with men.

Interestingly, the prevalence of bacterial vaginosis, a condition characterized by overgrowth of vaginal anaerobic bacteria, is higher in young women who have sex with women.⁶ Possible sources of transmission include digital-to-vaginal contact, oral sex, or sex toys.

Myth No. 6: Young women who have sex with women can’t get pregnant, so you don’t have to worry about birth control. Don’t forget that heterosexuals use birth control for other reasons than preventing pregnancy. Some women use birth control to help regulate periods, to ease cramping, or to treat acne. Lesbians and bisexual girls are at the same risk for these problems as are heterosexual girls, so don’t assume that they’re not interested in birth control just because they are not concerned about getting pregnant.

Also, as previously mentioned, lesbian girls may be having sex with boys, so conversations about birth control should be driven by who they are having sex with, not by how they identify.

Myth No. 7: Gay boys can’t get girls pregnant. Lesbian girls can’t get pregnant. A study by the Toronto Teen Sex Survey found that 28% of sexual minority youth report involvement in pregnancy, compared with 7% of heterosexual youth.⁷

Now many who are reading this may be scratching their heads. If someone finds the same sex attractive, then why are they engaging in heterosexual sex? Some studies suggest that engaging in heterosexual sex is a way to hide their true sexual orientation,⁸ because we live in a heterosexist and homophobic environment. After all, what better way to prove that you’re heterosexual? Another study suggests that intentionally getting pregnant or getting someone pregnant is the quickest way to parenthood, and becoming a parent can compensate for one’s identity as a sexual minority.⁹

So how do you overcome these persistent myths? The most important thing to do is not assume. Identity and behaviors are not the same. Always be specific when you’re asking questions about sex and relationships in LGBT youth.

The Centers for Disease Control and Prevention (CDC) recommends the following when obtaining a sexual history:

• Ask, “Are your sexual partner’s male, female, or both?”

• Ask, “When you do have sex with your partner, what do you do?” Here, you have to be very specific. Younger teenagers tend to be concrete thinkers, so don’t just ask “Are you sexually active?” Instead, try asking, “Have you ever had a penis in your mouth, vagina, or anus?” or “Do you use sex toys?”

• In terms of protection from STIs, you might ask, “Do you use condoms or a dental dam?”

• Ask, “Have you ever had an STI, and if so, how was it treated?”

• Ask, “What do you use for birth control?” either hormonal or barrier methods.

In addition to above questions, I would also ask about intimate partner violence. Often, health care providers may ask if their patient has been hit, punch, slapped, or kicked by their partners. But intimate partner violence can go beyond physical violence. It also involves emotional manipulation or birth control sabotage. Sometimes, it is better to ask if a patient has been forced to do something sexual with her partners when she didn’t want to. The patient may deny it, however, even though you highly suspect it. So it is better to remember to build a rapport, and when the patient is ready to get out of an abusive relationship, he or she will come to you for help.

Some clinicians have told me that they have a hard time asking sexual histories in LGBT youth because they’re afraid of offending them, especially when it comes to asking about sex with the opposite sex. This is a valid concern and an area of ongoing research, but I think that by making things normative, just like with any behavior, teens and young adults are more likely to disclose critical pieces of information. It is a good idea, then, to start off with “Because of homophobia, many LGBT youth may engage in heterosexual sex. Tell me, have you ever…”

By not assuming and asking specific questions, LGBT youth are more likely to tell their health care provider important information. With that information, health care providers can prevent many adverse health outcomes like teen pregnancy, STIs, and intimate partner violence. It also will give health care providers an opportunity to address the rampant stigma and discrimination that plagues this vulnerable population.

Here are some resources on sex and relationships in LGBT youth:

• The CDC 2015 STI Guidelines have a special section on STIs in men who have sex with men, women who have sex with women, and transgender men and women.

• Bedsider.org is an excellent website about birth control options and STI prevention for all sexual orientations and gender identities.

• Futures Without Violence provides resources for health care professionals to manage and prevent intimate partner violence.

References

1. J Bisex. 2000;1(1):31-68.

2. National Transgender Discrimination Survey: Full Report. 2012.

3. MMWR Surveill Summ. 2011 Jun 10;60(7):1-133.

4. J Youth Adolesc. 2015 Jan;44(1):211-24.

5. Perspect Sex Reprod Health. 2008 Dec;40(4):212-7.

6. Sex Transm Dis. 2010 May;37(5):335-9.

7. Sexpress: The Toronto teen survey report. 2009.

8. Fletcher RC. Social context and social support: Exploring the lived experiences of LGBTQ youth who have been pregnant. [Master’s Project]: School of Public Health, University of Minnesota; 2011.

9. Can J Hum Sex. 2008;17(3):123-139.

Dr. Montano is an adolescent medicine fellow at Children’s Hospital of Pittsburgh of UPMC and a postdoctoral fellow in the department of pediatrics at the University of Pittsburgh. He has no relevant financial disclosures.

Lead poisoning is a well-established cause of serious and permanent neurological, cognitive, and behavioral problems, particularly in exposed children.

Children can be exposed to lead from ingesting paint chips in their homes, when old paint is scrapped from the exterior of houses or bridges, and through the water they drink. The damage caused by lead poisoning was first recognized in the United States in the early 20th century, although lead was added to gasoline and paint until the 1970’s. Since then, regulations for lead in consumer products have become increasingly strict, and the Centers for Disease Control and Prevention’s definition of a toxic lead level has shifted from 60 micrograms/deciliter (mcg/dL) in 1970 to 5 mcg/dL in 2012. In many communities, removing lead paint up to the height of a young child is a requirement whenever an older home is sold.

Unfortunately, these regulations did not protect the families in Flint, Michigan from being exposed to high levels of lead when a change in water supply and inadequate water treatment allowed lead to enter the system from decaying water pipes. It is worth reviewing what is known about the short- and long-term consequences of lead exposure, and what lies ahead for the children of Flint.

Lead is a naturally occurring element that is not metabolized, but rather absorbed, distributed to tissues, and excreted. Lead can be inhaled (with 100% absorption) and introduced through the GI tract (with about 70% absorption in children and 20% absorption in adults). GI absorption is enhanced by calcium or iron deficiency, both conditions that are relatively common, especially in poor children and can lead to pica (or eating of non-nutritious materials), further increasing the chances of lead exposure. Absorbed lead is distributed to blood (for 28-36 days), soft tissue, including the nervous system (40 days), and to bone (where it lasts for over 25 years). Blood that is retained in growing bones can be mobilized during periods of physiologic stress (such as illness, injury, or pregnancy), meaning children exposed to lead during a period of rapid bone growth are at long-term risk for acute lead poisoning from their endogenous reservoir without a new exposure. What lead is not retained by tissues is excreted by the kidneys, with adults retaining about 1% of absorbed lead, while children younger than 2 years retain over 30% of absorbed lead. So children, especially toddlers, have a greater likelihood to absorb lead from the GI tract and to retain lead in their tissues, both due to active mineralization of bone and the permeability of the blood brain barrier, primarily in children under 3 years old. This is why we are addressing what will happen to the children of Flint and not to all the residents of Flint.

Lead competitively inhibits interactions between cations and sulfhydryl groups, which are present in most human biochemical reactions. This leads to irreversible cell damage and often cell death, especially within the central nervous system. Lead exposure is associated with particular dysfunction within dopaminergic pathways within the brain, and has been associated in a dose-dependent fashion with decreased prefrontal gray matter volume. Lead poisoning also has hematologic consequences (anemia), renal consequences (interstitial nephritis), gastrointestinal symptoms (vomiting, constipation), and endocrine consequences (reversible inhibition of Vitamin D metabolism and permanently short stature). But the CNS consequences of lead exposure are particularly devastating, as they appear to have no threshold and are permanent. Their incidence is the driving force for the CDC’s lowering of the official toxic lead level and the public health efforts to screen children and educate parents about the risk of lead exposure.

So what do these serious consequences look like? People with severe lead intoxication (blood lead levels greater than 70 mcg/dL) typically present with signs of acute encephalopathy (headache, vomiting, seizures, or coma) and require intensive medical management including chelation therapy. More typically, exposed children have low but accumulating levels of lead and present with nonspecific symptoms, including lost appetite, fatigue, irritability, and insomnia, which gradually worsen.

Behavior

High levels of impulsivity, aggression, and impaired attention are the prototypical sequelae of lead poisoning (following recovery from the acute intoxication). Multiple studies have demonstrated these high levels of aggressive and impulsive behaviors in preschoolers who were exposed to lead, and these behaviors appear to continue into adolescence and adulthood. Indeed, one study found that compared with children with the lowest measurable blood lead levels (0.2-0.7 mcg/dL), those children who were in the next two quartiles had seven and twelve times the odds of meeting diagnostic criteria for conduct disorder.¹ There have even been studies which correlated atmospheric lead levels (when leaded gasoline was common) with crime rates 20 years later, which supported an association between childhood lead exposure and adult criminal activity.^2-4.

Multiple studies have demonstrated higher rates of inattention, distractibility, and impulsivity in lead-exposed children than would be expected given the prevalence of attention-deficit/hyperactivity disorder (ADHD) in the general population. The incidence of these symptoms goes up in a dose-dependent fashion and appears to have no threshold (so they occur at even the lowest measurable blood lead levels). In a 2006 study of nearly 5,000 children between ages 4-15 years, those with blood lead levels greater than 2 mcg/dL (still below the level the CDC deems toxic) were four times more likely to be carrying a diagnosis of ADHD and be on stimulant medication than their peers with blood lead levels less than 0.8mcg/dL.

Cognition

Closely related to impulse control and attention, the cognitive domains of intelligence and executive function are clearly damaged by lead exposure. Poor performance on tasks requiring focus, cognitive flexibility, and inhibition of automatic responses was directly associated with higher blood lead levels in a group of preschoolers with levels between 0 and 13 mcg/dL.⁵

IQ has been found to be so consistently diminished by increasing blood lead levels that it is used as an overall index of neurodevelopmental morbidity of lead exposure, leading to the CDC’s adoption of a lower standard definition of toxic lead levels. Even very low blood lead levels are associated with decrements in IQ: children with blood lead levels less than 7.5 mcg/dL lost an average of 3 IQ points for every 1 mcg/dL increase in blood lead levels.⁶ In a study of 57,000 elementary school students in 2009, Miranda et al. found that those who had a blood lead level of 4 mcg/dL at 3 years old were significantly more likely to be diagnosed with a learning disability in elementary school. Another study of 48,000 children who had a blood lead level of 5 mcg/dL were 30% more likely to fail third grade reading and math tests than their peers without measurable lead levels.

Speech and language

More recent studies have demonstrated that children with higher bone lead concentrations had poorer performance on several language-processing measures, suggesting that childhood lead exposure damages language processing and function as the young people grow. These deficits in language processing can make social development and self-regulation much more challenging in adolescence, and make school and work settings much more challenging. These findings also have implications for the utility of psychotherapy, a language-based treatment, for the other behavioral problems of lead exposure.

Motor skills

Several recent studies have assessed both fine and gross motor skills in lead-exposed children. Findings have demonstrated that balance, coordination, gross motor and fine motor skills all appear to be compromised in a dose-dependent fashion by childhood lead exposure. These findings suggest that not only are children at greater risk for accident and injury through childhood and into adulthood, a risk already increased by their compromised attention and impulse control. But they also are likely to be physically clumsy, compromising an opportunity to cultivate strengths or experience mastery when cognitive tasks may prove frustrating for them.

With deficits in such fundamental cognitive, motor, and behavioral processes, exposed children are clearly vulnerable to more than ADHD, conduct disorder, and learning disabilities. These struggles may lead to secondary vulnerabilities to anxiety or mood symptoms or substance abuse as these children grow into teenagers who face frustration at every turn. In addition to treatment for their deficits in attention and executive function, these children will ideally receive specialized supports in school and at home, to be able to master cognitive tasks, manage new social circumstances and make friends, discover their interests and talents, and generally stay on their best developmental trajectories. Lastly, the specific consequences of lead exposure will vary for any individual child, so parents will have to deal with the uncertainty of their child’s behavior and development over many years. Clearly, the children of Flint face a long road that has been substantially impacted by their lead exposure. The only good that can come from the exposure in Flint is to heighten efforts to ensure that it never happens again.

1. Environ Health Perspect. 2008 Jul;116(7):956-62.

2. Environ Res. 2000 May;83(1):1-22.

3. Environ Res. 2007 Jul;104(3):315-36.

4. Arch Pediatr Adolesc Med. 2001 May;155(5):579-82.

5. Dev Neuropsychol. 2004;26(1):513-40.

6. Environ Health Perspect. 2005 Jul;113(7):894-9.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton (Mass.) Wellesley Hospital. Dr. Jellinek is professor of psychiatry and of pediatrics at Harvard Medical School, Boston.

Lead poisoning is a well-established cause of serious and permanent neurological, cognitive, and behavioral problems, particularly in exposed children.

Children can be exposed to lead from ingesting paint chips in their homes, when old paint is scrapped from the exterior of houses or bridges, and through the water they drink. The damage caused by lead poisoning was first recognized in the United States in the early 20th century, although lead was added to gasoline and paint until the 1970’s. Since then, regulations for lead in consumer products have become increasingly strict, and the Centers for Disease Control and Prevention’s definition of a toxic lead level has shifted from 60 micrograms/deciliter (mcg/dL) in 1970 to 5 mcg/dL in 2012. In many communities, removing lead paint up to the height of a young child is a requirement whenever an older home is sold.

Unfortunately, these regulations did not protect the families in Flint, Michigan from being exposed to high levels of lead when a change in water supply and inadequate water treatment allowed lead to enter the system from decaying water pipes. It is worth reviewing what is known about the short- and long-term consequences of lead exposure, and what lies ahead for the children of Flint.

Lead is a naturally occurring element that is not metabolized, but rather absorbed, distributed to tissues, and excreted. Lead can be inhaled (with 100% absorption) and introduced through the GI tract (with about 70% absorption in children and 20% absorption in adults). GI absorption is enhanced by calcium or iron deficiency, both conditions that are relatively common, especially in poor children and can lead to pica (or eating of non-nutritious materials), further increasing the chances of lead exposure. Absorbed lead is distributed to blood (for 28-36 days), soft tissue, including the nervous system (40 days), and to bone (where it lasts for over 25 years). Blood that is retained in growing bones can be mobilized during periods of physiologic stress (such as illness, injury, or pregnancy), meaning children exposed to lead during a period of rapid bone growth are at long-term risk for acute lead poisoning from their endogenous reservoir without a new exposure. What lead is not retained by tissues is excreted by the kidneys, with adults retaining about 1% of absorbed lead, while children younger than 2 years retain over 30% of absorbed lead. So children, especially toddlers, have a greater likelihood to absorb lead from the GI tract and to retain lead in their tissues, both due to active mineralization of bone and the permeability of the blood brain barrier, primarily in children under 3 years old. This is why we are addressing what will happen to the children of Flint and not to all the residents of Flint.

Lead competitively inhibits interactions between cations and sulfhydryl groups, which are present in most human biochemical reactions. This leads to irreversible cell damage and often cell death, especially within the central nervous system. Lead exposure is associated with particular dysfunction within dopaminergic pathways within the brain, and has been associated in a dose-dependent fashion with decreased prefrontal gray matter volume. Lead poisoning also has hematologic consequences (anemia), renal consequences (interstitial nephritis), gastrointestinal symptoms (vomiting, constipation), and endocrine consequences (reversible inhibition of Vitamin D metabolism and permanently short stature). But the CNS consequences of lead exposure are particularly devastating, as they appear to have no threshold and are permanent. Their incidence is the driving force for the CDC’s lowering of the official toxic lead level and the public health efforts to screen children and educate parents about the risk of lead exposure.

So what do these serious consequences look like? People with severe lead intoxication (blood lead levels greater than 70 mcg/dL) typically present with signs of acute encephalopathy (headache, vomiting, seizures, or coma) and require intensive medical management including chelation therapy. More typically, exposed children have low but accumulating levels of lead and present with nonspecific symptoms, including lost appetite, fatigue, irritability, and insomnia, which gradually worsen.

Behavior

High levels of impulsivity, aggression, and impaired attention are the prototypical sequelae of lead poisoning (following recovery from the acute intoxication). Multiple studies have demonstrated these high levels of aggressive and impulsive behaviors in preschoolers who were exposed to lead, and these behaviors appear to continue into adolescence and adulthood. Indeed, one study found that compared with children with the lowest measurable blood lead levels (0.2-0.7 mcg/dL), those children who were in the next two quartiles had seven and twelve times the odds of meeting diagnostic criteria for conduct disorder.¹ There have even been studies which correlated atmospheric lead levels (when leaded gasoline was common) with crime rates 20 years later, which supported an association between childhood lead exposure and adult criminal activity.^2-4.

Multiple studies have demonstrated higher rates of inattention, distractibility, and impulsivity in lead-exposed children than would be expected given the prevalence of attention-deficit/hyperactivity disorder (ADHD) in the general population. The incidence of these symptoms goes up in a dose-dependent fashion and appears to have no threshold (so they occur at even the lowest measurable blood lead levels). In a 2006 study of nearly 5,000 children between ages 4-15 years, those with blood lead levels greater than 2 mcg/dL (still below the level the CDC deems toxic) were four times more likely to be carrying a diagnosis of ADHD and be on stimulant medication than their peers with blood lead levels less than 0.8mcg/dL.

Cognition

Closely related to impulse control and attention, the cognitive domains of intelligence and executive function are clearly damaged by lead exposure. Poor performance on tasks requiring focus, cognitive flexibility, and inhibition of automatic responses was directly associated with higher blood lead levels in a group of preschoolers with levels between 0 and 13 mcg/dL.⁵

IQ has been found to be so consistently diminished by increasing blood lead levels that it is used as an overall index of neurodevelopmental morbidity of lead exposure, leading to the CDC’s adoption of a lower standard definition of toxic lead levels. Even very low blood lead levels are associated with decrements in IQ: children with blood lead levels less than 7.5 mcg/dL lost an average of 3 IQ points for every 1 mcg/dL increase in blood lead levels.⁶ In a study of 57,000 elementary school students in 2009, Miranda et al. found that those who had a blood lead level of 4 mcg/dL at 3 years old were significantly more likely to be diagnosed with a learning disability in elementary school. Another study of 48,000 children who had a blood lead level of 5 mcg/dL were 30% more likely to fail third grade reading and math tests than their peers without measurable lead levels.

Speech and language

More recent studies have demonstrated that children with higher bone lead concentrations had poorer performance on several language-processing measures, suggesting that childhood lead exposure damages language processing and function as the young people grow. These deficits in language processing can make social development and self-regulation much more challenging in adolescence, and make school and work settings much more challenging. These findings also have implications for the utility of psychotherapy, a language-based treatment, for the other behavioral problems of lead exposure.

Motor skills

Several recent studies have assessed both fine and gross motor skills in lead-exposed children. Findings have demonstrated that balance, coordination, gross motor and fine motor skills all appear to be compromised in a dose-dependent fashion by childhood lead exposure. These findings suggest that not only are children at greater risk for accident and injury through childhood and into adulthood, a risk already increased by their compromised attention and impulse control. But they also are likely to be physically clumsy, compromising an opportunity to cultivate strengths or experience mastery when cognitive tasks may prove frustrating for them.

With deficits in such fundamental cognitive, motor, and behavioral processes, exposed children are clearly vulnerable to more than ADHD, conduct disorder, and learning disabilities. These struggles may lead to secondary vulnerabilities to anxiety or mood symptoms or substance abuse as these children grow into teenagers who face frustration at every turn. In addition to treatment for their deficits in attention and executive function, these children will ideally receive specialized supports in school and at home, to be able to master cognitive tasks, manage new social circumstances and make friends, discover their interests and talents, and generally stay on their best developmental trajectories. Lastly, the specific consequences of lead exposure will vary for any individual child, so parents will have to deal with the uncertainty of their child’s behavior and development over many years. Clearly, the children of Flint face a long road that has been substantially impacted by their lead exposure. The only good that can come from the exposure in Flint is to heighten efforts to ensure that it never happens again.

1. Environ Health Perspect. 2008 Jul;116(7):956-62.

2. Environ Res. 2000 May;83(1):1-22.

3. Environ Res. 2007 Jul;104(3):315-36.

4. Arch Pediatr Adolesc Med. 2001 May;155(5):579-82.

5. Dev Neuropsychol. 2004;26(1):513-40.

6. Environ Health Perspect. 2005 Jul;113(7):894-9.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton (Mass.) Wellesley Hospital. Dr. Jellinek is professor of psychiatry and of pediatrics at Harvard Medical School, Boston.

Lead poisoning is a well-established cause of serious and permanent neurological, cognitive, and behavioral problems, particularly in exposed children.

Children can be exposed to lead from ingesting paint chips in their homes, when old paint is scrapped from the exterior of houses or bridges, and through the water they drink. The damage caused by lead poisoning was first recognized in the United States in the early 20th century, although lead was added to gasoline and paint until the 1970’s. Since then, regulations for lead in consumer products have become increasingly strict, and the Centers for Disease Control and Prevention’s definition of a toxic lead level has shifted from 60 micrograms/deciliter (mcg/dL) in 1970 to 5 mcg/dL in 2012. In many communities, removing lead paint up to the height of a young child is a requirement whenever an older home is sold.

Unfortunately, these regulations did not protect the families in Flint, Michigan from being exposed to high levels of lead when a change in water supply and inadequate water treatment allowed lead to enter the system from decaying water pipes. It is worth reviewing what is known about the short- and long-term consequences of lead exposure, and what lies ahead for the children of Flint.

Lead is a naturally occurring element that is not metabolized, but rather absorbed, distributed to tissues, and excreted. Lead can be inhaled (with 100% absorption) and introduced through the GI tract (with about 70% absorption in children and 20% absorption in adults). GI absorption is enhanced by calcium or iron deficiency, both conditions that are relatively common, especially in poor children and can lead to pica (or eating of non-nutritious materials), further increasing the chances of lead exposure. Absorbed lead is distributed to blood (for 28-36 days), soft tissue, including the nervous system (40 days), and to bone (where it lasts for over 25 years). Blood that is retained in growing bones can be mobilized during periods of physiologic stress (such as illness, injury, or pregnancy), meaning children exposed to lead during a period of rapid bone growth are at long-term risk for acute lead poisoning from their endogenous reservoir without a new exposure. What lead is not retained by tissues is excreted by the kidneys, with adults retaining about 1% of absorbed lead, while children younger than 2 years retain over 30% of absorbed lead. So children, especially toddlers, have a greater likelihood to absorb lead from the GI tract and to retain lead in their tissues, both due to active mineralization of bone and the permeability of the blood brain barrier, primarily in children under 3 years old. This is why we are addressing what will happen to the children of Flint and not to all the residents of Flint.

Lead competitively inhibits interactions between cations and sulfhydryl groups, which are present in most human biochemical reactions. This leads to irreversible cell damage and often cell death, especially within the central nervous system. Lead exposure is associated with particular dysfunction within dopaminergic pathways within the brain, and has been associated in a dose-dependent fashion with decreased prefrontal gray matter volume. Lead poisoning also has hematologic consequences (anemia), renal consequences (interstitial nephritis), gastrointestinal symptoms (vomiting, constipation), and endocrine consequences (reversible inhibition of Vitamin D metabolism and permanently short stature). But the CNS consequences of lead exposure are particularly devastating, as they appear to have no threshold and are permanent. Their incidence is the driving force for the CDC’s lowering of the official toxic lead level and the public health efforts to screen children and educate parents about the risk of lead exposure.

So what do these serious consequences look like? People with severe lead intoxication (blood lead levels greater than 70 mcg/dL) typically present with signs of acute encephalopathy (headache, vomiting, seizures, or coma) and require intensive medical management including chelation therapy. More typically, exposed children have low but accumulating levels of lead and present with nonspecific symptoms, including lost appetite, fatigue, irritability, and insomnia, which gradually worsen.

Behavior

High levels of impulsivity, aggression, and impaired attention are the prototypical sequelae of lead poisoning (following recovery from the acute intoxication). Multiple studies have demonstrated these high levels of aggressive and impulsive behaviors in preschoolers who were exposed to lead, and these behaviors appear to continue into adolescence and adulthood. Indeed, one study found that compared with children with the lowest measurable blood lead levels (0.2-0.7 mcg/dL), those children who were in the next two quartiles had seven and twelve times the odds of meeting diagnostic criteria for conduct disorder.¹ There have even been studies which correlated atmospheric lead levels (when leaded gasoline was common) with crime rates 20 years later, which supported an association between childhood lead exposure and adult criminal activity.^2-4.

Multiple studies have demonstrated higher rates of inattention, distractibility, and impulsivity in lead-exposed children than would be expected given the prevalence of attention-deficit/hyperactivity disorder (ADHD) in the general population. The incidence of these symptoms goes up in a dose-dependent fashion and appears to have no threshold (so they occur at even the lowest measurable blood lead levels). In a 2006 study of nearly 5,000 children between ages 4-15 years, those with blood lead levels greater than 2 mcg/dL (still below the level the CDC deems toxic) were four times more likely to be carrying a diagnosis of ADHD and be on stimulant medication than their peers with blood lead levels less than 0.8mcg/dL.

Cognition

Closely related to impulse control and attention, the cognitive domains of intelligence and executive function are clearly damaged by lead exposure. Poor performance on tasks requiring focus, cognitive flexibility, and inhibition of automatic responses was directly associated with higher blood lead levels in a group of preschoolers with levels between 0 and 13 mcg/dL.⁵

IQ has been found to be so consistently diminished by increasing blood lead levels that it is used as an overall index of neurodevelopmental morbidity of lead exposure, leading to the CDC’s adoption of a lower standard definition of toxic lead levels. Even very low blood lead levels are associated with decrements in IQ: children with blood lead levels less than 7.5 mcg/dL lost an average of 3 IQ points for every 1 mcg/dL increase in blood lead levels.⁶ In a study of 57,000 elementary school students in 2009, Miranda et al. found that those who had a blood lead level of 4 mcg/dL at 3 years old were significantly more likely to be diagnosed with a learning disability in elementary school. Another study of 48,000 children who had a blood lead level of 5 mcg/dL were 30% more likely to fail third grade reading and math tests than their peers without measurable lead levels.

Speech and language

More recent studies have demonstrated that children with higher bone lead concentrations had poorer performance on several language-processing measures, suggesting that childhood lead exposure damages language processing and function as the young people grow. These deficits in language processing can make social development and self-regulation much more challenging in adolescence, and make school and work settings much more challenging. These findings also have implications for the utility of psychotherapy, a language-based treatment, for the other behavioral problems of lead exposure.

Motor skills

Several recent studies have assessed both fine and gross motor skills in lead-exposed children. Findings have demonstrated that balance, coordination, gross motor and fine motor skills all appear to be compromised in a dose-dependent fashion by childhood lead exposure. These findings suggest that not only are children at greater risk for accident and injury through childhood and into adulthood, a risk already increased by their compromised attention and impulse control. But they also are likely to be physically clumsy, compromising an opportunity to cultivate strengths or experience mastery when cognitive tasks may prove frustrating for them.

With deficits in such fundamental cognitive, motor, and behavioral processes, exposed children are clearly vulnerable to more than ADHD, conduct disorder, and learning disabilities. These struggles may lead to secondary vulnerabilities to anxiety or mood symptoms or substance abuse as these children grow into teenagers who face frustration at every turn. In addition to treatment for their deficits in attention and executive function, these children will ideally receive specialized supports in school and at home, to be able to master cognitive tasks, manage new social circumstances and make friends, discover their interests and talents, and generally stay on their best developmental trajectories. Lastly, the specific consequences of lead exposure will vary for any individual child, so parents will have to deal with the uncertainty of their child’s behavior and development over many years. Clearly, the children of Flint face a long road that has been substantially impacted by their lead exposure. The only good that can come from the exposure in Flint is to heighten efforts to ensure that it never happens again.

1. Environ Health Perspect. 2008 Jul;116(7):956-62.

2. Environ Res. 2000 May;83(1):1-22.

3. Environ Res. 2007 Jul;104(3):315-36.

4. Arch Pediatr Adolesc Med. 2001 May;155(5):579-82.

5. Dev Neuropsychol. 2004;26(1):513-40.

6. Environ Health Perspect. 2005 Jul;113(7):894-9.

Dr. Swick is an attending psychiatrist in the division of child psychiatry at Massachusetts General Hospital, Boston, and director of the Parenting at a Challenging Time (PACT) Program at the Vernon Cancer Center at Newton (Mass.) Wellesley Hospital. Dr. Jellinek is professor of psychiatry and of pediatrics at Harvard Medical School, Boston.

PHOENIX – A prosthetic conduit that contains a porcine valve showed excellent intermediate-term durability for repairing the right ventricular outflow tract in 100 teenagers and young adults at a single U.S. center.

“The Carpentier-Edwards xenograft for right ventricular outflow tract [RVOT] reconstruction provides excellent freedom from reoperation and valve dysfunction, as well as sustained improvement in right-ventricular chamber size at intermediate-term follow-up,” Dr. Heidi B. Schubmehl said at the Society of Thoracic Surgeons annual meeting.

Mitchel L. Zoler/Frontline Medical News

Dr. Schubmehl reported a 92% rate of freedom from valve dysfunction with follow-up out to about 10 years, and significant reductions in right ventricular size at follow-up, compared with baseline, as measured by both echocardiography and by MRI.

The Carpentier-Edwards porcine valve and conduit “seemed to hold up better than a lot of other [prosthetic] valves,” said Dr. George M. Alfieris, director of pediatric cardiac surgery at the University of Rochester (N.Y.), and senior author for the study. In addition to the valve’s durability over approximately the first 10 years following placement, the results also showed the positive impact the valve had on right ventricular size, an important result of the repair’s efficacy, Dr. Alfieris said.

“It’s a mistake to allow the right ventricle to be under high pressure or to reach a large volume. We now focus on preserving the right ventricle,” he said in an interview. “I’ve become very concerned about preventing right ventricular dilation and preserving right ventricular function.”

Dr. Alfieris noted that his prior experience using other types of valves in the pulmonary valve and RVOT position showed those valves “did great for the first 10 years and then failed. What’s different in this series is that after 10 years, we have not seen the same dysfunction as with the prior generation of valves. I will be very interested to see what happens to them” as follow-up continues beyond 10 years. He also expressed dismay that recently the company that had been marketing the valve and conduit used in the current study, the Carpentier-Edwards, stopped selling them. He expects that as his supply of conduits runs out he’ll have to start using a different commercial valve and conduit that he believes will not perform as well or create his own conduits with a porcine valve from a different supplier.

The series of 100 patients comprised individuals aged 17 or older who received a pulmonary artery and had RVOT reconstruction at the University of Rochester during 2000-2010, Dr. Schubmehl reported. The series included 78 patients with a history of tetralogy of Fallot, 8 patients born with transposition of their great arteries, 8 patients with truncus arteriosus, and 6 patients with other congenital heart diseases. Their median age at the time they received the RVOT conduit was 24 years, 59% were men, and 99 had undergone a prior sternotomy. At the time they received the conduit, 55 had pulmonary valve insufficiency, 30 had valve stenosis, and 15 had both. Follow-up occurred an average of 7 years after conduit placement.

Two recipients died: One death occurred perioperatively in a 41-year old who had a massive cerebrovascular event, and the second death was in a 39-year old who died 2.6 years after conduit placement from respiratory failure. Two additional patients required a reintervention during follow-up, said Dr. Schubmehl, a general surgeon at the University of Rochester. One reintervention occurred after 11 years to treat endocarditis, and the second after 11 years to perform balloon valvuloplasty because of valve stenosis.

The results reported by Dr. Schubmehl for echocardiography examinations showed that the patients had a statistically significant reduction in their RVOT pressure gradient from baseline to 1-year follow-up that was sustained through their intermediate-term follow-up. Seventy-seven patients had pulmonary valve insufficiency at baseline that resolved in all patients at 1-year follow-up and remained resolved in all but one patient at extended follow-up. Nineteen patients underwent additional imaging with MRI at an average follow-up of 7 years, and these findings confirmed the echo results.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler

PHOENIX – A prosthetic conduit that contains a porcine valve showed excellent intermediate-term durability for repairing the right ventricular outflow tract in 100 teenagers and young adults at a single U.S. center.

“The Carpentier-Edwards xenograft for right ventricular outflow tract [RVOT] reconstruction provides excellent freedom from reoperation and valve dysfunction, as well as sustained improvement in right-ventricular chamber size at intermediate-term follow-up,” Dr. Heidi B. Schubmehl said at the Society of Thoracic Surgeons annual meeting.

Mitchel L. Zoler/Frontline Medical News

Dr. Schubmehl reported a 92% rate of freedom from valve dysfunction with follow-up out to about 10 years, and significant reductions in right ventricular size at follow-up, compared with baseline, as measured by both echocardiography and by MRI.

The Carpentier-Edwards porcine valve and conduit “seemed to hold up better than a lot of other [prosthetic] valves,” said Dr. George M. Alfieris, director of pediatric cardiac surgery at the University of Rochester (N.Y.), and senior author for the study. In addition to the valve’s durability over approximately the first 10 years following placement, the results also showed the positive impact the valve had on right ventricular size, an important result of the repair’s efficacy, Dr. Alfieris said.

“It’s a mistake to allow the right ventricle to be under high pressure or to reach a large volume. We now focus on preserving the right ventricle,” he said in an interview. “I’ve become very concerned about preventing right ventricular dilation and preserving right ventricular function.”

Dr. Alfieris noted that his prior experience using other types of valves in the pulmonary valve and RVOT position showed those valves “did great for the first 10 years and then failed. What’s different in this series is that after 10 years, we have not seen the same dysfunction as with the prior generation of valves. I will be very interested to see what happens to them” as follow-up continues beyond 10 years. He also expressed dismay that recently the company that had been marketing the valve and conduit used in the current study, the Carpentier-Edwards, stopped selling them. He expects that as his supply of conduits runs out he’ll have to start using a different commercial valve and conduit that he believes will not perform as well or create his own conduits with a porcine valve from a different supplier.

The series of 100 patients comprised individuals aged 17 or older who received a pulmonary artery and had RVOT reconstruction at the University of Rochester during 2000-2010, Dr. Schubmehl reported. The series included 78 patients with a history of tetralogy of Fallot, 8 patients born with transposition of their great arteries, 8 patients with truncus arteriosus, and 6 patients with other congenital heart diseases. Their median age at the time they received the RVOT conduit was 24 years, 59% were men, and 99 had undergone a prior sternotomy. At the time they received the conduit, 55 had pulmonary valve insufficiency, 30 had valve stenosis, and 15 had both. Follow-up occurred an average of 7 years after conduit placement.

Two recipients died: One death occurred perioperatively in a 41-year old who had a massive cerebrovascular event, and the second death was in a 39-year old who died 2.6 years after conduit placement from respiratory failure. Two additional patients required a reintervention during follow-up, said Dr. Schubmehl, a general surgeon at the University of Rochester. One reintervention occurred after 11 years to treat endocarditis, and the second after 11 years to perform balloon valvuloplasty because of valve stenosis.

The results reported by Dr. Schubmehl for echocardiography examinations showed that the patients had a statistically significant reduction in their RVOT pressure gradient from baseline to 1-year follow-up that was sustained through their intermediate-term follow-up. Seventy-seven patients had pulmonary valve insufficiency at baseline that resolved in all patients at 1-year follow-up and remained resolved in all but one patient at extended follow-up. Nineteen patients underwent additional imaging with MRI at an average follow-up of 7 years, and these findings confirmed the echo results.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler

PHOENIX – A prosthetic conduit that contains a porcine valve showed excellent intermediate-term durability for repairing the right ventricular outflow tract in 100 teenagers and young adults at a single U.S. center.

“The Carpentier-Edwards xenograft for right ventricular outflow tract [RVOT] reconstruction provides excellent freedom from reoperation and valve dysfunction, as well as sustained improvement in right-ventricular chamber size at intermediate-term follow-up,” Dr. Heidi B. Schubmehl said at the Society of Thoracic Surgeons annual meeting.

Mitchel L. Zoler/Frontline Medical News

Dr. Schubmehl reported a 92% rate of freedom from valve dysfunction with follow-up out to about 10 years, and significant reductions in right ventricular size at follow-up, compared with baseline, as measured by both echocardiography and by MRI.

The Carpentier-Edwards porcine valve and conduit “seemed to hold up better than a lot of other [prosthetic] valves,” said Dr. George M. Alfieris, director of pediatric cardiac surgery at the University of Rochester (N.Y.), and senior author for the study. In addition to the valve’s durability over approximately the first 10 years following placement, the results also showed the positive impact the valve had on right ventricular size, an important result of the repair’s efficacy, Dr. Alfieris said.

“It’s a mistake to allow the right ventricle to be under high pressure or to reach a large volume. We now focus on preserving the right ventricle,” he said in an interview. “I’ve become very concerned about preventing right ventricular dilation and preserving right ventricular function.”

Dr. Alfieris noted that his prior experience using other types of valves in the pulmonary valve and RVOT position showed those valves “did great for the first 10 years and then failed. What’s different in this series is that after 10 years, we have not seen the same dysfunction as with the prior generation of valves. I will be very interested to see what happens to them” as follow-up continues beyond 10 years. He also expressed dismay that recently the company that had been marketing the valve and conduit used in the current study, the Carpentier-Edwards, stopped selling them. He expects that as his supply of conduits runs out he’ll have to start using a different commercial valve and conduit that he believes will not perform as well or create his own conduits with a porcine valve from a different supplier.

The series of 100 patients comprised individuals aged 17 or older who received a pulmonary artery and had RVOT reconstruction at the University of Rochester during 2000-2010, Dr. Schubmehl reported. The series included 78 patients with a history of tetralogy of Fallot, 8 patients born with transposition of their great arteries, 8 patients with truncus arteriosus, and 6 patients with other congenital heart diseases. Their median age at the time they received the RVOT conduit was 24 years, 59% were men, and 99 had undergone a prior sternotomy. At the time they received the conduit, 55 had pulmonary valve insufficiency, 30 had valve stenosis, and 15 had both. Follow-up occurred an average of 7 years after conduit placement.

Two recipients died: One death occurred perioperatively in a 41-year old who had a massive cerebrovascular event, and the second death was in a 39-year old who died 2.6 years after conduit placement from respiratory failure. Two additional patients required a reintervention during follow-up, said Dr. Schubmehl, a general surgeon at the University of Rochester. One reintervention occurred after 11 years to treat endocarditis, and the second after 11 years to perform balloon valvuloplasty because of valve stenosis.

The results reported by Dr. Schubmehl for echocardiography examinations showed that the patients had a statistically significant reduction in their RVOT pressure gradient from baseline to 1-year follow-up that was sustained through their intermediate-term follow-up. Seventy-seven patients had pulmonary valve insufficiency at baseline that resolved in all patients at 1-year follow-up and remained resolved in all but one patient at extended follow-up. Nineteen patients underwent additional imaging with MRI at an average follow-up of 7 years, and these findings confirmed the echo results.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler