LAKE TAHOE, CALIF. – Among children and adolescents, vitiligo appears to predominately affect nonwhite boys and girls between the ages of 10 and 17 years, results from a large cross-sectional analysis demonstrated.

Doug Brunk/MDedge News

During an interview at the annual meeting of the Society for Pediatric Dermatology, lead study author Jessica Haber, MD, said that, while it’s known vitiligo can have its onset in childhood, there have been no population-based analyses in the United States specific to children and adolescents with the condition.

“We wanted to examine disease burden in the U.S. specifically, because we have such a diverse population,” said Dr. Haber, a second-year resident in the department of dermatology at Northwell Health, New York.

For the study, she and her associates used IBM’s Explorys research analytics platform to conduct a cross-sectional analysis of more than 55 million unique patients across all census regions of the United States. There were 1,630 vitiligo cases identified from a total of 4,242,400 pediatric patients, for an overall standard prevalence of 0.04%, or 40.1 per 100,000 children and adolescents. The proportion of female and male patients with vitiligo was similar (49.1% and 50.9%, respectively), and nearly three-fourths (72.3%) were 10 years of age or older.

The researchers observed no significant difference in the prevalence of vitiligo between males and females (40.2 per 100,000 vs. 40 per 100,000, respectively). The standardized prevalence of vitiligo was greatest in pediatric patients who were of “other” races and ethnicities (including Asian, Hispanic, multiracial, and other; 69.1 per 100,000), followed by African Americans (51.5 per 100,000) and whites (37.9 per 100,000). There were too few vitiligo cases among biracial patients to determine standardized estimates, but the crude prevalence was greatest in this group (68.7 per 100,000).

Two factors could contribute to the increased prevalence of vitiligo observed in nonwhite children and adolescents, Dr. Haber said. One is selection bias.

“It has been reported that both children and adults with higher Fitzpatrick skin types tend to have increased morbidity of their vitiligo, so it may be a selection bias that these patients are seeking out treatment for their disease,” she said. “Also, according to recent research in the medical literature, increased melanin production may be a risk factor for the development of vitiligo (J Am Acad Dermatol. 2017;77[1]:1-13). That might explain some of our findings, as well.”

While the study findings “don’t necessarily change clinical practice, it is good for us to have a sense of the burden of disease in the pediatric patient population of vitiligo, and to be aware that this is a disease that predominately affects non-Caucasian children and adolescents,” Dr. Haber concluded.

She reported having no financial disclosures.

[email protected]

LAKE TAHOE, CALIF. – Among children and adolescents, vitiligo appears to predominately affect nonwhite boys and girls between the ages of 10 and 17 years, results from a large cross-sectional analysis demonstrated.

Doug Brunk/MDedge News

During an interview at the annual meeting of the Society for Pediatric Dermatology, lead study author Jessica Haber, MD, said that, while it’s known vitiligo can have its onset in childhood, there have been no population-based analyses in the United States specific to children and adolescents with the condition.

“We wanted to examine disease burden in the U.S. specifically, because we have such a diverse population,” said Dr. Haber, a second-year resident in the department of dermatology at Northwell Health, New York.

For the study, she and her associates used IBM’s Explorys research analytics platform to conduct a cross-sectional analysis of more than 55 million unique patients across all census regions of the United States. There were 1,630 vitiligo cases identified from a total of 4,242,400 pediatric patients, for an overall standard prevalence of 0.04%, or 40.1 per 100,000 children and adolescents. The proportion of female and male patients with vitiligo was similar (49.1% and 50.9%, respectively), and nearly three-fourths (72.3%) were 10 years of age or older.

The researchers observed no significant difference in the prevalence of vitiligo between males and females (40.2 per 100,000 vs. 40 per 100,000, respectively). The standardized prevalence of vitiligo was greatest in pediatric patients who were of “other” races and ethnicities (including Asian, Hispanic, multiracial, and other; 69.1 per 100,000), followed by African Americans (51.5 per 100,000) and whites (37.9 per 100,000). There were too few vitiligo cases among biracial patients to determine standardized estimates, but the crude prevalence was greatest in this group (68.7 per 100,000).

Two factors could contribute to the increased prevalence of vitiligo observed in nonwhite children and adolescents, Dr. Haber said. One is selection bias.

“It has been reported that both children and adults with higher Fitzpatrick skin types tend to have increased morbidity of their vitiligo, so it may be a selection bias that these patients are seeking out treatment for their disease,” she said. “Also, according to recent research in the medical literature, increased melanin production may be a risk factor for the development of vitiligo (J Am Acad Dermatol. 2017;77[1]:1-13). That might explain some of our findings, as well.”

While the study findings “don’t necessarily change clinical practice, it is good for us to have a sense of the burden of disease in the pediatric patient population of vitiligo, and to be aware that this is a disease that predominately affects non-Caucasian children and adolescents,” Dr. Haber concluded.

She reported having no financial disclosures.

[email protected]

LAKE TAHOE, CALIF. – Among children and adolescents, vitiligo appears to predominately affect nonwhite boys and girls between the ages of 10 and 17 years, results from a large cross-sectional analysis demonstrated.

Doug Brunk/MDedge News

During an interview at the annual meeting of the Society for Pediatric Dermatology, lead study author Jessica Haber, MD, said that, while it’s known vitiligo can have its onset in childhood, there have been no population-based analyses in the United States specific to children and adolescents with the condition.

“We wanted to examine disease burden in the U.S. specifically, because we have such a diverse population,” said Dr. Haber, a second-year resident in the department of dermatology at Northwell Health, New York.

For the study, she and her associates used IBM’s Explorys research analytics platform to conduct a cross-sectional analysis of more than 55 million unique patients across all census regions of the United States. There were 1,630 vitiligo cases identified from a total of 4,242,400 pediatric patients, for an overall standard prevalence of 0.04%, or 40.1 per 100,000 children and adolescents. The proportion of female and male patients with vitiligo was similar (49.1% and 50.9%, respectively), and nearly three-fourths (72.3%) were 10 years of age or older.

The researchers observed no significant difference in the prevalence of vitiligo between males and females (40.2 per 100,000 vs. 40 per 100,000, respectively). The standardized prevalence of vitiligo was greatest in pediatric patients who were of “other” races and ethnicities (including Asian, Hispanic, multiracial, and other; 69.1 per 100,000), followed by African Americans (51.5 per 100,000) and whites (37.9 per 100,000). There were too few vitiligo cases among biracial patients to determine standardized estimates, but the crude prevalence was greatest in this group (68.7 per 100,000).

Two factors could contribute to the increased prevalence of vitiligo observed in nonwhite children and adolescents, Dr. Haber said. One is selection bias.

“It has been reported that both children and adults with higher Fitzpatrick skin types tend to have increased morbidity of their vitiligo, so it may be a selection bias that these patients are seeking out treatment for their disease,” she said. “Also, according to recent research in the medical literature, increased melanin production may be a risk factor for the development of vitiligo (J Am Acad Dermatol. 2017;77[1]:1-13). That might explain some of our findings, as well.”

While the study findings “don’t necessarily change clinical practice, it is good for us to have a sense of the burden of disease in the pediatric patient population of vitiligo, and to be aware that this is a disease that predominately affects non-Caucasian children and adolescents,” Dr. Haber concluded.

She reported having no financial disclosures.

[email protected]

SAN DIEGO – Fatigue increases anterior cruciate ligament injury risk in adolescent athletes, results from a field-based drop-jump study demonstrate.

Doug Brunk/MDedge News

“The number of ACL reconstructions that occur annually are on the rise, particularly in high school and adolescent aged athletes,” lead study author Mohsin S. Fidai, MD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine. “About 70% of these are accounted for by noncontact injuries, the majority of which occur during jump landing. A number of risk factors that have previously been implicated in ACL injury include genetics and anatomy, but a modifiable risk factor is landing biomechanics.”

In 2005, researchers led by Timothy E. Hewett, PhD, determined biomechanical measures of neuromuscular control that might pose certain athletes to be at risk for ACL injury, particularly knee abduction and dynamic knee valgus during a drop-jump test (Am J Sports Med. 2005;33[4]:492-501). “Historically, these studies have required the use of sophisticated computer technology, which can be cumbersome from a time and cost perspective,” said Dr. Fidai, a third-year orthopedic surgery resident at Henry Ford Health System, Detroit.

In a more recent analysis, researchers validated a field-based drop vertical jump screening test for ACL injury (Phys Sportmed. 2016;44[1]:46-52). The sensitivity was 95%, the specificity was 46%, and it had a strong inter-rater reliability (k = 0.92; P less than .05).

The purpose of the current study was to evaluate the effect of fatigue on ACL injury risk using a field-based drop-jump test. “We hypothesized that fatigue would lead to greater dynamic knee valgus during a drop-jump test,” Dr. Fidai said. “We also wanted to identify individual characteristics which may place athletes at increased risk for ACL injury.”

The researchers recruited 85 athletes who competed in track and field, basketball, volleyball, and soccer. More than half (55%) were female, and the mean age was 15.4 years. They excluded athletes with any previous or current lower extremity injuries or neuromuscular deficits. Each athlete performed a maximum vertical jump, followed by a drop-jump test.

“We then fatigued all of our athletes with a standardized high-intensity fatigue protocol, and had each athlete perform another maximum vertical jump and drop-jump test,” Dr. Fidai said. “All drop-jumps were video recorded and sent to a number of orthopedic surgery residents, athletic trainers, and physical therapists for review.”

Of the 85 athletes, nearly half (45%) showed an increased risk for ACL injury after high-intensity aerobic activity. In addition, 68% of study participants were identified as having a medium or high risk for injury following the aerobic activity, compared with 44% at baseline. “When looking at fatigue, it seems to have a dose-dependent response,” Dr. Fidai noted. “In the group of athletes with higher levels of fatigue, there is a significantly increased risk, compared with their counterparts with lower levels of fatigue.”

Specifically, 14 of the 22 athletes who demonstrated over 20% fatigue showed an increased ACL injury risk. Subgroup analysis revealed that female athletes and those older than age 15 were more likely to demonstrate an increased injury risk.

“The findings of this study advocate for changes to current neuromuscular training programs to incorporate fatigue resistance, as well as to raise awareness amongst physical therapists, athletic trainers, coaches, and athletes about the effect of fatigue on ACL injury risk,” Dr. Fidai concluded. “We can target vulnerable athletes, particularly female athletes, in an effort to negate some of those effects.”

The study’s principal investigator was Eric C. Makhni, MD. Dr. Makhni, an orthopedic surgeon in West Bloomfield, Mich., disclosed that he is a paid consultant for Smith & Nephew and that he receives publishing royalties from Springer. Dr. Fidai reported having no financial disclosures.

[email protected]

SAN DIEGO – Fatigue increases anterior cruciate ligament injury risk in adolescent athletes, results from a field-based drop-jump study demonstrate.

Doug Brunk/MDedge News

“The number of ACL reconstructions that occur annually are on the rise, particularly in high school and adolescent aged athletes,” lead study author Mohsin S. Fidai, MD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine. “About 70% of these are accounted for by noncontact injuries, the majority of which occur during jump landing. A number of risk factors that have previously been implicated in ACL injury include genetics and anatomy, but a modifiable risk factor is landing biomechanics.”

In 2005, researchers led by Timothy E. Hewett, PhD, determined biomechanical measures of neuromuscular control that might pose certain athletes to be at risk for ACL injury, particularly knee abduction and dynamic knee valgus during a drop-jump test (Am J Sports Med. 2005;33[4]:492-501). “Historically, these studies have required the use of sophisticated computer technology, which can be cumbersome from a time and cost perspective,” said Dr. Fidai, a third-year orthopedic surgery resident at Henry Ford Health System, Detroit.

In a more recent analysis, researchers validated a field-based drop vertical jump screening test for ACL injury (Phys Sportmed. 2016;44[1]:46-52). The sensitivity was 95%, the specificity was 46%, and it had a strong inter-rater reliability (k = 0.92; P less than .05).

The purpose of the current study was to evaluate the effect of fatigue on ACL injury risk using a field-based drop-jump test. “We hypothesized that fatigue would lead to greater dynamic knee valgus during a drop-jump test,” Dr. Fidai said. “We also wanted to identify individual characteristics which may place athletes at increased risk for ACL injury.”

The researchers recruited 85 athletes who competed in track and field, basketball, volleyball, and soccer. More than half (55%) were female, and the mean age was 15.4 years. They excluded athletes with any previous or current lower extremity injuries or neuromuscular deficits. Each athlete performed a maximum vertical jump, followed by a drop-jump test.

“We then fatigued all of our athletes with a standardized high-intensity fatigue protocol, and had each athlete perform another maximum vertical jump and drop-jump test,” Dr. Fidai said. “All drop-jumps were video recorded and sent to a number of orthopedic surgery residents, athletic trainers, and physical therapists for review.”

Of the 85 athletes, nearly half (45%) showed an increased risk for ACL injury after high-intensity aerobic activity. In addition, 68% of study participants were identified as having a medium or high risk for injury following the aerobic activity, compared with 44% at baseline. “When looking at fatigue, it seems to have a dose-dependent response,” Dr. Fidai noted. “In the group of athletes with higher levels of fatigue, there is a significantly increased risk, compared with their counterparts with lower levels of fatigue.”

Specifically, 14 of the 22 athletes who demonstrated over 20% fatigue showed an increased ACL injury risk. Subgroup analysis revealed that female athletes and those older than age 15 were more likely to demonstrate an increased injury risk.

“The findings of this study advocate for changes to current neuromuscular training programs to incorporate fatigue resistance, as well as to raise awareness amongst physical therapists, athletic trainers, coaches, and athletes about the effect of fatigue on ACL injury risk,” Dr. Fidai concluded. “We can target vulnerable athletes, particularly female athletes, in an effort to negate some of those effects.”

The study’s principal investigator was Eric C. Makhni, MD. Dr. Makhni, an orthopedic surgeon in West Bloomfield, Mich., disclosed that he is a paid consultant for Smith & Nephew and that he receives publishing royalties from Springer. Dr. Fidai reported having no financial disclosures.

[email protected]

SAN DIEGO – Fatigue increases anterior cruciate ligament injury risk in adolescent athletes, results from a field-based drop-jump study demonstrate.

Doug Brunk/MDedge News

“The number of ACL reconstructions that occur annually are on the rise, particularly in high school and adolescent aged athletes,” lead study author Mohsin S. Fidai, MD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine. “About 70% of these are accounted for by noncontact injuries, the majority of which occur during jump landing. A number of risk factors that have previously been implicated in ACL injury include genetics and anatomy, but a modifiable risk factor is landing biomechanics.”

In 2005, researchers led by Timothy E. Hewett, PhD, determined biomechanical measures of neuromuscular control that might pose certain athletes to be at risk for ACL injury, particularly knee abduction and dynamic knee valgus during a drop-jump test (Am J Sports Med. 2005;33[4]:492-501). “Historically, these studies have required the use of sophisticated computer technology, which can be cumbersome from a time and cost perspective,” said Dr. Fidai, a third-year orthopedic surgery resident at Henry Ford Health System, Detroit.

In a more recent analysis, researchers validated a field-based drop vertical jump screening test for ACL injury (Phys Sportmed. 2016;44[1]:46-52). The sensitivity was 95%, the specificity was 46%, and it had a strong inter-rater reliability (k = 0.92; P less than .05).

The purpose of the current study was to evaluate the effect of fatigue on ACL injury risk using a field-based drop-jump test. “We hypothesized that fatigue would lead to greater dynamic knee valgus during a drop-jump test,” Dr. Fidai said. “We also wanted to identify individual characteristics which may place athletes at increased risk for ACL injury.”

The researchers recruited 85 athletes who competed in track and field, basketball, volleyball, and soccer. More than half (55%) were female, and the mean age was 15.4 years. They excluded athletes with any previous or current lower extremity injuries or neuromuscular deficits. Each athlete performed a maximum vertical jump, followed by a drop-jump test.

“We then fatigued all of our athletes with a standardized high-intensity fatigue protocol, and had each athlete perform another maximum vertical jump and drop-jump test,” Dr. Fidai said. “All drop-jumps were video recorded and sent to a number of orthopedic surgery residents, athletic trainers, and physical therapists for review.”

Of the 85 athletes, nearly half (45%) showed an increased risk for ACL injury after high-intensity aerobic activity. In addition, 68% of study participants were identified as having a medium or high risk for injury following the aerobic activity, compared with 44% at baseline. “When looking at fatigue, it seems to have a dose-dependent response,” Dr. Fidai noted. “In the group of athletes with higher levels of fatigue, there is a significantly increased risk, compared with their counterparts with lower levels of fatigue.”

Specifically, 14 of the 22 athletes who demonstrated over 20% fatigue showed an increased ACL injury risk. Subgroup analysis revealed that female athletes and those older than age 15 were more likely to demonstrate an increased injury risk.

“The findings of this study advocate for changes to current neuromuscular training programs to incorporate fatigue resistance, as well as to raise awareness amongst physical therapists, athletic trainers, coaches, and athletes about the effect of fatigue on ACL injury risk,” Dr. Fidai concluded. “We can target vulnerable athletes, particularly female athletes, in an effort to negate some of those effects.”

The study’s principal investigator was Eric C. Makhni, MD. Dr. Makhni, an orthopedic surgeon in West Bloomfield, Mich., disclosed that he is a paid consultant for Smith & Nephew and that he receives publishing royalties from Springer. Dr. Fidai reported having no financial disclosures.

[email protected]

SAN DIEGO – Patients who received a corticosteroid injection within 6 months prior to rotator cuff repair were more likely to undergo a revision rotator cuff surgery within the following 3 years, results from a large database study show.

“Corticosteroid injections are frequently utilized in the nonoperative management of rotator cuff tears,” researchers led by Sophia A. Traven, MD, wrote in an abstract presented during a poster session at the annual meeting of the American Orthopaedic Society for Sports Medicine. “However, recent literature suggests that injections may reduce biomechanical strengths of tendons and ligaments in animal models.”

In an effort to examine the effect of preoperative shoulder injections on the rate of revision cuff repair following arthroscopic rotator cuff repair, the researchers retrospectively reviewed MarketScan claims data between 2010 and 2014 to identify 4,959 patients with an ICD-9 diagnosis of a rotator cuff tear with subsequent arthroscopic rotator cuff repair (CPT 29827).

They used multivariable logistic regression to compare the odds of reoperation between groups, while controlling for certain demographic and comorbid variables, including age and gender, tobacco use, diabetes, and the Charlson comorbidity index score.

Dr. Traven, an orthopedic surgeon at the Medical University of South Carolina, Charleston, and her associates reported that 392 of the 4,959 patients required rotator cuff repair revision within the following 3 years. Compared with those who did not require revision, those who did were older (a mean age of 53 vs. 49 years, respectively), more likely to be smokers (7% vs. 4%), and more likely to receive any injection prior to rotator cuff repair (36% vs 25%; P less than .0001 for all associations).

The risk for revision rotator cuff repair was highest for patients who received an injection 3-6 months before the primary rotator cuff repair (odds ratio, 1.822), followed by those who received an injection 0-3 months before the primary repair (OR, 1.375), and those who received an injection 6-12 months before the primary repair (OR, 1.237).

“The risk of revision rotator cuff repair remains elevated for 6 months following a shoulder injection,” the researchers concluded in their poster. “Consideration should therefore be given to minimizing preoperative injections in patients who may require rotator cuff repair.”

They reported having no financial disclosures.

[email protected]

SAN DIEGO – Patients who received a corticosteroid injection within 6 months prior to rotator cuff repair were more likely to undergo a revision rotator cuff surgery within the following 3 years, results from a large database study show.

“Corticosteroid injections are frequently utilized in the nonoperative management of rotator cuff tears,” researchers led by Sophia A. Traven, MD, wrote in an abstract presented during a poster session at the annual meeting of the American Orthopaedic Society for Sports Medicine. “However, recent literature suggests that injections may reduce biomechanical strengths of tendons and ligaments in animal models.”

In an effort to examine the effect of preoperative shoulder injections on the rate of revision cuff repair following arthroscopic rotator cuff repair, the researchers retrospectively reviewed MarketScan claims data between 2010 and 2014 to identify 4,959 patients with an ICD-9 diagnosis of a rotator cuff tear with subsequent arthroscopic rotator cuff repair (CPT 29827).

They used multivariable logistic regression to compare the odds of reoperation between groups, while controlling for certain demographic and comorbid variables, including age and gender, tobacco use, diabetes, and the Charlson comorbidity index score.

Dr. Traven, an orthopedic surgeon at the Medical University of South Carolina, Charleston, and her associates reported that 392 of the 4,959 patients required rotator cuff repair revision within the following 3 years. Compared with those who did not require revision, those who did were older (a mean age of 53 vs. 49 years, respectively), more likely to be smokers (7% vs. 4%), and more likely to receive any injection prior to rotator cuff repair (36% vs 25%; P less than .0001 for all associations).

The risk for revision rotator cuff repair was highest for patients who received an injection 3-6 months before the primary rotator cuff repair (odds ratio, 1.822), followed by those who received an injection 0-3 months before the primary repair (OR, 1.375), and those who received an injection 6-12 months before the primary repair (OR, 1.237).

“The risk of revision rotator cuff repair remains elevated for 6 months following a shoulder injection,” the researchers concluded in their poster. “Consideration should therefore be given to minimizing preoperative injections in patients who may require rotator cuff repair.”

They reported having no financial disclosures.

[email protected]

SAN DIEGO – Patients who received a corticosteroid injection within 6 months prior to rotator cuff repair were more likely to undergo a revision rotator cuff surgery within the following 3 years, results from a large database study show.

“Corticosteroid injections are frequently utilized in the nonoperative management of rotator cuff tears,” researchers led by Sophia A. Traven, MD, wrote in an abstract presented during a poster session at the annual meeting of the American Orthopaedic Society for Sports Medicine. “However, recent literature suggests that injections may reduce biomechanical strengths of tendons and ligaments in animal models.”

In an effort to examine the effect of preoperative shoulder injections on the rate of revision cuff repair following arthroscopic rotator cuff repair, the researchers retrospectively reviewed MarketScan claims data between 2010 and 2014 to identify 4,959 patients with an ICD-9 diagnosis of a rotator cuff tear with subsequent arthroscopic rotator cuff repair (CPT 29827).

They used multivariable logistic regression to compare the odds of reoperation between groups, while controlling for certain demographic and comorbid variables, including age and gender, tobacco use, diabetes, and the Charlson comorbidity index score.

Dr. Traven, an orthopedic surgeon at the Medical University of South Carolina, Charleston, and her associates reported that 392 of the 4,959 patients required rotator cuff repair revision within the following 3 years. Compared with those who did not require revision, those who did were older (a mean age of 53 vs. 49 years, respectively), more likely to be smokers (7% vs. 4%), and more likely to receive any injection prior to rotator cuff repair (36% vs 25%; P less than .0001 for all associations).

The risk for revision rotator cuff repair was highest for patients who received an injection 3-6 months before the primary rotator cuff repair (odds ratio, 1.822), followed by those who received an injection 0-3 months before the primary repair (OR, 1.375), and those who received an injection 6-12 months before the primary repair (OR, 1.237).

“The risk of revision rotator cuff repair remains elevated for 6 months following a shoulder injection,” the researchers concluded in their poster. “Consideration should therefore be given to minimizing preoperative injections in patients who may require rotator cuff repair.”

They reported having no financial disclosures.

[email protected]

SAN DIEGO – When it comes to soft tissue recovery modalities for elite athletes beyond rest, recovery, and retaining movement efficiency, not all options are created equal.

In fact, the science for most supplemental recovery modalities stems from cohort studies examining physiologic response – not high-level randomized clinical trials, Chuck Thigpen, PhD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine.

“We should be very careful when we discuss overtraining and overload,” said Dr. Thigpen, senior director of practice innovation and analytics for ATI Physical Therapy, Greenville, S.C. “In fact, we need training load to create an anabolic response, so then the question is, how do we manage that load? I would suggest that it’s not overtraining, but underrecovery after a load that results in increasing fatigue, decreased performance, and potential increased injury risk.”

One option for soft tissue recovery is whole body vibration, for which the athlete stands, sits, or lies on a machine with a vibrating platform, while he or she performs static or isotonic exercise. “With this modality, you get a rapid co-contraction of muscle, which increases muscle preactivation,” said Dr. Thigpen, who is also directs the program in observational clinical research in orthopedics at the Greenville, S.C.–based Center for Effectiveness Research in Orthopaedics. “It has demonstrated increased blood flow as well as increased motor neuron excitability. There seems to be some physiologic benefit coming potentially from muscle waste removal (lactate) and nutrient delivery, as well as decreasing subsequent inhibition.”

In terms of parameters, benefits have been observed when athletes perform one or two sets of a static stretch or contact massage on a body vibration machine for a minute or so at a frequency of 30-50 Hz. “The application is what becomes challenging,” Dr. Thigpen said. “Where are you going to work this in? Is it a pre or post activity? Recent evidence implicates use during halftime may maintain strength and power. However, most of the work that has been done with vibration has been as an adjunct to exercise and not really in terms of recovery.”

Massage is another popular recovery tool, and most elite sports team have a masseuse on staff. Soft tissue manipulation creates release of oxytocin and other neurotransmitters, some central nervous system response, and increased blood flow to the treated area, but it also influences the athlete’s general disposition.

“There’s something about laying hands on somebody that seems to affect a person’s mood state,” Dr. Thigpen said. “Some studies have reported better perceived recovery status, even though the physiologic markers are about the same. Therefore, I would classify body vibration and massage in the same bucket. They seem to work; they seem to have some perceived benefit.”

Another soft tissue recovery option, compression therapy, has been shown to increase the local pressure gradient of the impacted area, thereby increasing progressive venous return and creating some muscle splinting (or protective muscle spasms). “Compression therapy seems to clear the system and get some waste removal, as well as increase nutrient delivery,” Dr. Thigpen said. “A couple of studies have looked at the ultrastructure of the muscle concurrently after using compression garments. The nice thing is that you can put them on right after the activity. They should be worn for 24 hours.”

Another way to get compression therapy is to use compression devices; it is recommended that they are worn for 15-minute intervals for up to 4 hours after intense physical activity, depending on the device. “You see some of the same benefits that you see with compression garments,” he said.

Dr. Thigpen went on to discuss cryotherapy such as cold-water immersion in a tub, which has a long history of use in muscle recovery. In fact, many basic science studies have demonstrated a reduction of inflammatory markers and other immunologic responses after its use. “Cryotherapy is thought to create an acute decrease in blood flow and a concurrent increase in blood flow after you remove it, which creates the release of these neurotransmitters and immunosuppressants that seem to be helpful in the healing process,” he explained.

“The thought is, because of the decreased pain reduction, the waste removal, and the change in oxidative stress, this would be beneficial.” For example, cold water immersion in a tub four times over a 72-hour period has been found to decrease soreness and increase athletic performance on the backside. “That seems to be helpful in recovery, as an adjunct to heavy resistance training or eccentric and plyometric training,” he said.

Neuromuscular electrical stimulation has been shown to provide some analgesic effect to sore muscles via afferent stimulation, but the primary mechanism is contractile via the motor unit. Typically, neuromuscular electrical stimulation consists of about a 20-minute application to affected muscles, “and you can do multiple applications per day interspersed with periods of high-intensity training to restore the neuromuscular profile during the recovery period,” Dr. Thigpen said.

He reported having no financial disclosures.

[email protected]

SAN DIEGO – When it comes to soft tissue recovery modalities for elite athletes beyond rest, recovery, and retaining movement efficiency, not all options are created equal.

In fact, the science for most supplemental recovery modalities stems from cohort studies examining physiologic response – not high-level randomized clinical trials, Chuck Thigpen, PhD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine.

“We should be very careful when we discuss overtraining and overload,” said Dr. Thigpen, senior director of practice innovation and analytics for ATI Physical Therapy, Greenville, S.C. “In fact, we need training load to create an anabolic response, so then the question is, how do we manage that load? I would suggest that it’s not overtraining, but underrecovery after a load that results in increasing fatigue, decreased performance, and potential increased injury risk.”

One option for soft tissue recovery is whole body vibration, for which the athlete stands, sits, or lies on a machine with a vibrating platform, while he or she performs static or isotonic exercise. “With this modality, you get a rapid co-contraction of muscle, which increases muscle preactivation,” said Dr. Thigpen, who is also directs the program in observational clinical research in orthopedics at the Greenville, S.C.–based Center for Effectiveness Research in Orthopaedics. “It has demonstrated increased blood flow as well as increased motor neuron excitability. There seems to be some physiologic benefit coming potentially from muscle waste removal (lactate) and nutrient delivery, as well as decreasing subsequent inhibition.”

In terms of parameters, benefits have been observed when athletes perform one or two sets of a static stretch or contact massage on a body vibration machine for a minute or so at a frequency of 30-50 Hz. “The application is what becomes challenging,” Dr. Thigpen said. “Where are you going to work this in? Is it a pre or post activity? Recent evidence implicates use during halftime may maintain strength and power. However, most of the work that has been done with vibration has been as an adjunct to exercise and not really in terms of recovery.”

Massage is another popular recovery tool, and most elite sports team have a masseuse on staff. Soft tissue manipulation creates release of oxytocin and other neurotransmitters, some central nervous system response, and increased blood flow to the treated area, but it also influences the athlete’s general disposition.

“There’s something about laying hands on somebody that seems to affect a person’s mood state,” Dr. Thigpen said. “Some studies have reported better perceived recovery status, even though the physiologic markers are about the same. Therefore, I would classify body vibration and massage in the same bucket. They seem to work; they seem to have some perceived benefit.”

Another soft tissue recovery option, compression therapy, has been shown to increase the local pressure gradient of the impacted area, thereby increasing progressive venous return and creating some muscle splinting (or protective muscle spasms). “Compression therapy seems to clear the system and get some waste removal, as well as increase nutrient delivery,” Dr. Thigpen said. “A couple of studies have looked at the ultrastructure of the muscle concurrently after using compression garments. The nice thing is that you can put them on right after the activity. They should be worn for 24 hours.”

Another way to get compression therapy is to use compression devices; it is recommended that they are worn for 15-minute intervals for up to 4 hours after intense physical activity, depending on the device. “You see some of the same benefits that you see with compression garments,” he said.

Dr. Thigpen went on to discuss cryotherapy such as cold-water immersion in a tub, which has a long history of use in muscle recovery. In fact, many basic science studies have demonstrated a reduction of inflammatory markers and other immunologic responses after its use. “Cryotherapy is thought to create an acute decrease in blood flow and a concurrent increase in blood flow after you remove it, which creates the release of these neurotransmitters and immunosuppressants that seem to be helpful in the healing process,” he explained.

“The thought is, because of the decreased pain reduction, the waste removal, and the change in oxidative stress, this would be beneficial.” For example, cold water immersion in a tub four times over a 72-hour period has been found to decrease soreness and increase athletic performance on the backside. “That seems to be helpful in recovery, as an adjunct to heavy resistance training or eccentric and plyometric training,” he said.

Neuromuscular electrical stimulation has been shown to provide some analgesic effect to sore muscles via afferent stimulation, but the primary mechanism is contractile via the motor unit. Typically, neuromuscular electrical stimulation consists of about a 20-minute application to affected muscles, “and you can do multiple applications per day interspersed with periods of high-intensity training to restore the neuromuscular profile during the recovery period,” Dr. Thigpen said.

He reported having no financial disclosures.

[email protected]

SAN DIEGO – When it comes to soft tissue recovery modalities for elite athletes beyond rest, recovery, and retaining movement efficiency, not all options are created equal.

In fact, the science for most supplemental recovery modalities stems from cohort studies examining physiologic response – not high-level randomized clinical trials, Chuck Thigpen, PhD, said at the annual meeting of the American Orthopaedic Society for Sports Medicine.

“We should be very careful when we discuss overtraining and overload,” said Dr. Thigpen, senior director of practice innovation and analytics for ATI Physical Therapy, Greenville, S.C. “In fact, we need training load to create an anabolic response, so then the question is, how do we manage that load? I would suggest that it’s not overtraining, but underrecovery after a load that results in increasing fatigue, decreased performance, and potential increased injury risk.”

One option for soft tissue recovery is whole body vibration, for which the athlete stands, sits, or lies on a machine with a vibrating platform, while he or she performs static or isotonic exercise. “With this modality, you get a rapid co-contraction of muscle, which increases muscle preactivation,” said Dr. Thigpen, who is also directs the program in observational clinical research in orthopedics at the Greenville, S.C.–based Center for Effectiveness Research in Orthopaedics. “It has demonstrated increased blood flow as well as increased motor neuron excitability. There seems to be some physiologic benefit coming potentially from muscle waste removal (lactate) and nutrient delivery, as well as decreasing subsequent inhibition.”

In terms of parameters, benefits have been observed when athletes perform one or two sets of a static stretch or contact massage on a body vibration machine for a minute or so at a frequency of 30-50 Hz. “The application is what becomes challenging,” Dr. Thigpen said. “Where are you going to work this in? Is it a pre or post activity? Recent evidence implicates use during halftime may maintain strength and power. However, most of the work that has been done with vibration has been as an adjunct to exercise and not really in terms of recovery.”

Massage is another popular recovery tool, and most elite sports team have a masseuse on staff. Soft tissue manipulation creates release of oxytocin and other neurotransmitters, some central nervous system response, and increased blood flow to the treated area, but it also influences the athlete’s general disposition.

“There’s something about laying hands on somebody that seems to affect a person’s mood state,” Dr. Thigpen said. “Some studies have reported better perceived recovery status, even though the physiologic markers are about the same. Therefore, I would classify body vibration and massage in the same bucket. They seem to work; they seem to have some perceived benefit.”

Another soft tissue recovery option, compression therapy, has been shown to increase the local pressure gradient of the impacted area, thereby increasing progressive venous return and creating some muscle splinting (or protective muscle spasms). “Compression therapy seems to clear the system and get some waste removal, as well as increase nutrient delivery,” Dr. Thigpen said. “A couple of studies have looked at the ultrastructure of the muscle concurrently after using compression garments. The nice thing is that you can put them on right after the activity. They should be worn for 24 hours.”

Another way to get compression therapy is to use compression devices; it is recommended that they are worn for 15-minute intervals for up to 4 hours after intense physical activity, depending on the device. “You see some of the same benefits that you see with compression garments,” he said.

Dr. Thigpen went on to discuss cryotherapy such as cold-water immersion in a tub, which has a long history of use in muscle recovery. In fact, many basic science studies have demonstrated a reduction of inflammatory markers and other immunologic responses after its use. “Cryotherapy is thought to create an acute decrease in blood flow and a concurrent increase in blood flow after you remove it, which creates the release of these neurotransmitters and immunosuppressants that seem to be helpful in the healing process,” he explained.

“The thought is, because of the decreased pain reduction, the waste removal, and the change in oxidative stress, this would be beneficial.” For example, cold water immersion in a tub four times over a 72-hour period has been found to decrease soreness and increase athletic performance on the backside. “That seems to be helpful in recovery, as an adjunct to heavy resistance training or eccentric and plyometric training,” he said.

Neuromuscular electrical stimulation has been shown to provide some analgesic effect to sore muscles via afferent stimulation, but the primary mechanism is contractile via the motor unit. Typically, neuromuscular electrical stimulation consists of about a 20-minute application to affected muscles, “and you can do multiple applications per day interspersed with periods of high-intensity training to restore the neuromuscular profile during the recovery period,” Dr. Thigpen said.

He reported having no financial disclosures.

[email protected]

Treatment with isavuconazole resolved or substantially improved invasive fungal disease among seven of eight patients receiving concomitant ibrutinib, according to the results of a small two-center study.

The combination “was well-tolerated overall,” wrote Kaelyn C. Cummins of Brigham and Women’s Hospital, together with her associates there and at the Dana-Farber Cancer Institute, Boston. Their letter to the editor was published in Leukemia & Lymphoma.

Although ibrutinib is considered less immunosuppressive than conventional chemotherapy, it has been tied to invasive fungal infections, even in seemingly low-risk patients. The preferred treatment, voriconazole, is a very strong inhibitor of cytochrome P450 systems, of which ibrutinib is a substrate. For this study, the researchers queried the pharmacy databases of their institutions to identify adults who received concomitant isavuconazole (200 mg per day) and ibrutinib between 2015 and 2018. Drug exposures were confirmed by medical record review.

Four patients experienced clinical and radiologic resolution of invasive aspergillosis, fusariosis, mucormycosis, or phaeohyphomycosis. Another three had clinical and radiologic improvement of confirmed or probable aspergillosis or histoplasmosis. One of these patients underwent five debridements for central nervous system invasive aspergillosis but had 8 months of clinical improvement between debridements. This patient’s fungal isolate remained susceptible to isavuconazole throughout treatment. The patient who did not respond at all to isavuconazole had invasive aspergillosis with recurrent brain abscesses. The fungal isolate remained susceptible to isavuconazole, and the patient switched to long-term voriconazole therapy after stopping ibrutinib.

Several adverse events occurred while patients were on concomitant therapy. One patient developed paroxysmal atrial fibrillation that persisted after stopping ibrutinib. Another had worsening of preexisting thrombocytopenia. Among four patients with electrocardiogram data, two had transient QTc prolongation. No patient died within 12 weeks of starting concomitant therapy. Two patients eventually died after their cancer progressed.

The median age of the patients was 60 years (range, 38-76 years). Five were men. Six had chronic lymphocytic leukemia (CLL) and two had marginal zone lymphoma. Two CLL patients were on ibrutinib monotherapy, two also received rituximab, one also received umbralisib, and one also received obinutuzumab. One patient with marginal zone lymphoma was on ibrutinib monotherapy, and the other received concomitant rituximab, gemcitabine, dexamethasone, and cisplatin.

Researchers should study the mechanisms by which [Bruton’s tyrosine kinase] inhibitors might increase susceptibility to fungal infections among patients with lymphoma or CLL, said Ms. Cummins and her associates. Because the CYP3A enzyme system also metabolizes PI3K and BCL-2 inhibitors, their results “could be more broadly applicable.”

Ms. Cummins had no disclosures.

SOURCE: Cummins KC et al. Leuk. Lymphoma 2018 Jul 24. doi: 10.1080/10428194.2018.1485913.

Treatment with isavuconazole resolved or substantially improved invasive fungal disease among seven of eight patients receiving concomitant ibrutinib, according to the results of a small two-center study.

The combination “was well-tolerated overall,” wrote Kaelyn C. Cummins of Brigham and Women’s Hospital, together with her associates there and at the Dana-Farber Cancer Institute, Boston. Their letter to the editor was published in Leukemia & Lymphoma.

Although ibrutinib is considered less immunosuppressive than conventional chemotherapy, it has been tied to invasive fungal infections, even in seemingly low-risk patients. The preferred treatment, voriconazole, is a very strong inhibitor of cytochrome P450 systems, of which ibrutinib is a substrate. For this study, the researchers queried the pharmacy databases of their institutions to identify adults who received concomitant isavuconazole (200 mg per day) and ibrutinib between 2015 and 2018. Drug exposures were confirmed by medical record review.

Four patients experienced clinical and radiologic resolution of invasive aspergillosis, fusariosis, mucormycosis, or phaeohyphomycosis. Another three had clinical and radiologic improvement of confirmed or probable aspergillosis or histoplasmosis. One of these patients underwent five debridements for central nervous system invasive aspergillosis but had 8 months of clinical improvement between debridements. This patient’s fungal isolate remained susceptible to isavuconazole throughout treatment. The patient who did not respond at all to isavuconazole had invasive aspergillosis with recurrent brain abscesses. The fungal isolate remained susceptible to isavuconazole, and the patient switched to long-term voriconazole therapy after stopping ibrutinib.

Several adverse events occurred while patients were on concomitant therapy. One patient developed paroxysmal atrial fibrillation that persisted after stopping ibrutinib. Another had worsening of preexisting thrombocytopenia. Among four patients with electrocardiogram data, two had transient QTc prolongation. No patient died within 12 weeks of starting concomitant therapy. Two patients eventually died after their cancer progressed.

The median age of the patients was 60 years (range, 38-76 years). Five were men. Six had chronic lymphocytic leukemia (CLL) and two had marginal zone lymphoma. Two CLL patients were on ibrutinib monotherapy, two also received rituximab, one also received umbralisib, and one also received obinutuzumab. One patient with marginal zone lymphoma was on ibrutinib monotherapy, and the other received concomitant rituximab, gemcitabine, dexamethasone, and cisplatin.

Researchers should study the mechanisms by which [Bruton’s tyrosine kinase] inhibitors might increase susceptibility to fungal infections among patients with lymphoma or CLL, said Ms. Cummins and her associates. Because the CYP3A enzyme system also metabolizes PI3K and BCL-2 inhibitors, their results “could be more broadly applicable.”

Ms. Cummins had no disclosures.

SOURCE: Cummins KC et al. Leuk. Lymphoma 2018 Jul 24. doi: 10.1080/10428194.2018.1485913.

Treatment with isavuconazole resolved or substantially improved invasive fungal disease among seven of eight patients receiving concomitant ibrutinib, according to the results of a small two-center study.

The combination “was well-tolerated overall,” wrote Kaelyn C. Cummins of Brigham and Women’s Hospital, together with her associates there and at the Dana-Farber Cancer Institute, Boston. Their letter to the editor was published in Leukemia & Lymphoma.

Although ibrutinib is considered less immunosuppressive than conventional chemotherapy, it has been tied to invasive fungal infections, even in seemingly low-risk patients. The preferred treatment, voriconazole, is a very strong inhibitor of cytochrome P450 systems, of which ibrutinib is a substrate. For this study, the researchers queried the pharmacy databases of their institutions to identify adults who received concomitant isavuconazole (200 mg per day) and ibrutinib between 2015 and 2018. Drug exposures were confirmed by medical record review.

Four patients experienced clinical and radiologic resolution of invasive aspergillosis, fusariosis, mucormycosis, or phaeohyphomycosis. Another three had clinical and radiologic improvement of confirmed or probable aspergillosis or histoplasmosis. One of these patients underwent five debridements for central nervous system invasive aspergillosis but had 8 months of clinical improvement between debridements. This patient’s fungal isolate remained susceptible to isavuconazole throughout treatment. The patient who did not respond at all to isavuconazole had invasive aspergillosis with recurrent brain abscesses. The fungal isolate remained susceptible to isavuconazole, and the patient switched to long-term voriconazole therapy after stopping ibrutinib.

Several adverse events occurred while patients were on concomitant therapy. One patient developed paroxysmal atrial fibrillation that persisted after stopping ibrutinib. Another had worsening of preexisting thrombocytopenia. Among four patients with electrocardiogram data, two had transient QTc prolongation. No patient died within 12 weeks of starting concomitant therapy. Two patients eventually died after their cancer progressed.

The median age of the patients was 60 years (range, 38-76 years). Five were men. Six had chronic lymphocytic leukemia (CLL) and two had marginal zone lymphoma. Two CLL patients were on ibrutinib monotherapy, two also received rituximab, one also received umbralisib, and one also received obinutuzumab. One patient with marginal zone lymphoma was on ibrutinib monotherapy, and the other received concomitant rituximab, gemcitabine, dexamethasone, and cisplatin.

Researchers should study the mechanisms by which [Bruton’s tyrosine kinase] inhibitors might increase susceptibility to fungal infections among patients with lymphoma or CLL, said Ms. Cummins and her associates. Because the CYP3A enzyme system also metabolizes PI3K and BCL-2 inhibitors, their results “could be more broadly applicable.”

Ms. Cummins had no disclosures.

SOURCE: Cummins KC et al. Leuk. Lymphoma 2018 Jul 24. doi: 10.1080/10428194.2018.1485913.

CHICAGO – Among the many difficult decisions dermatologists have to make, some of the more challenging involve caring for patients with atypical melanocytic lesions. A session at the summer meeting of the American Academy of Dermatology provided some guidance for surveillance of these patients.

Caroline C. Kim, MD, directs the pigmented lesion clinic at Beth Israel Deaconess Medical Center, Boston, and shared the evidence base for her management schema, along with some clinical pearls. No dermatologist ever wants to miss a melanoma, she acknowledged. “We want to avoid those scenarios but not make people feel like Swiss cheese” from multiple biopsies, she said during her presentation.

One key concept that can help physicians find the balance, she said, is that although the presence of atypical or dysplastic nevi increases the risk for melanoma in a given patient, the actual transformation rate of dysplastic nevi to melanomas is not known. In fact, she said, between 50% and 75% of melanomas may arise de novo.

From a dermatopathologic perspective, nevi exist along a continuum of mild to moderate to severe dysplasia, and some lesions are melanomas. But mildly dysplastic nevi are not fated to continue a transformation to increasingly severely dysplastic ones, or to melanomas.

Bringing these ideas to the patient discussion means that one should avoid ever calling a dysplastic nevus “precancerous,” said Dr. Kim; not only is this inaccurate, but it is unnecessarily anxiety provoking, she said.

Within this framework, the initial exam can begin with a search for signature patterns – and ugly ducklings. Each patient will have a pattern, or several patterns, that typify their nevi. Though the markings may be “atypical,” they’ll have some consistency; if the nevus has several neighbors that look just like it, it’s much less likely to be melanoma. “If they are matching partners, it’s more likely that it’s your typical nevus pattern,” said Dr. Kim, also an assistant professor of dermatology at Harvard Medical School, Boston.

By contrast, some lesions stand out from the patient’s other atypical nevi. They may be larger, darker, more elevated, but sometimes, “Even from the doorway, they just stand out,” Dr. Kim said. And these dual concepts of signature patterns and ugly ducklings are useful to talk over with patients, she said. “It’s so easy for patients to grab on to – they totally get it.”

“Use dermoscopy” when you get to the detailed skin exam, she said. “Data have shown that as clinicians, we are pretty good at picking up melanomas ... But with dermoscopy, our detection rate goes up to 70%-95%,” Dr. Kim said. The caveat is that dermoscopy without proper training is a dangerous tool: Several studies have shown that melanoma detection rates drop compared to the naked eye when dermoscopy is performed by untrained users, she said. “Training matters.”

A further tool to help train the eye and mind to recognize benign and malignant patterns when performing dermoscopy of atypical nevi is a now-classic paper that maps these patterns out, she said (Dermatol Surg. 2007;33[11]:1388-91).

“Beware of de novo and changing lesions,” Dr. Kim said. “A picture truly is worth a thousand words” for tracking these, she said.

Total body digital photography, if it’s available, is the best way to track subtle changes, and to spot new lesions as they crop up, said Dr. Kim. In head-to-head studies with dermoscopy and visual exam alone, digital photography can reduce the number of lesions excised, detect early melanoma, and reduce patient anxiety. One study found a 3.8-fold reduction in the mean rate of nevus biopsies when total body digital photography was used, she said (J Am Acad Dermatol. 2016 Mar. doi: 10.1016/j.jaad.2016.02.1152).

A patient care pearl Dr. Kim shared is that she’ll ask patients for their smartphones and take a photograph of the patients’ backs with those phones. This lets them have a handy reference image for monitoring their own skin in the intervals between visits. But make sure, she said, that patients know that “all change is not bad change – you can get new nevi through your 50s.

“Consider sharing care with a local pigmented lesion clinic” if digital photography is not available at your site, said Dr. Kim. She does this for several of her patients, alternating visits with the primary dermatologist.

When should you perform a biopsy?

“You don’t need to biopsy an atypical nevus to call it atypical. You biopsy lesions if you’re suspicious for calling it melanoma,” Dr. Kim said. Removal also can be considered if, for example, a patient lives alone and the nevi of concern are on her back so home monitoring is a challenge, she said.

Once you’ve decided to biopsy, a narrow excisional biopsy with saucerization and 1- to 3-mm margins is preferred when there’s a high suspicion for melanoma, said Dr. Kim, citing a study that found that 2-mm margins using this method yielded an 87% rate of clear pathologic specimen margins in dysplastic nevi (J Am Acad Dermatol. 2017 Dec;77[6]:1096-9). There is some leeway in the guidelines, but “the preferred technique is a narrow excisional biopsy when you are worried,” she said.

There may be times when a partial or incisional biopsy is a rational choice, as when lesions are very large, located on the face or acral areas, or when suspicion for melanoma is low. “If you do partial biopsies, you really have to be aware of the limitations” of the technique since it may miss the nidus of melanoma within an otherwise bland lesion, Dr. Kim pointed out.

And don’t forget to plan your closure with future follow-up in mind: Dr. Kim related that she’d seen a patient for melanoma who’d had the large excisional biopsy performed elsewhere; the patient’s site was closed with an advancement flap, which made sentinel node biopsy impossible.

When the results come back, then what?

Studies have found that atypical nevi are characterized differently at different sites and that management strategies vary geographically, Dr. Kim said. “There’s a need for large-scale data to further investigate the role of observation versus re-excision of dysplastic nevi,” and a multicenter study is underway to do just that, she said, under the auspices of the Pigmented Lesion Subcommittee of the Melanoma Prevention Working Group (ECOG/SWOG).

That same subcommittee has issued a consensus statement for dealing with histologically positive excisional biopsy margins. For mildly dysplastic lesions without clinically observable residual pigment, observation is preferred. Severely dysplastic lesions with unpigmented margins should be re-excised, says the statement (JAMA Dermatol. 2015;151[2]:212-18).

For the intermediate lesions, the group recommended that a reasonable option is to observe a moderately dysplastic nevus site that’s been excisionally biopsied with a finding of positive margins, while acknowledging that more data are needed.

All biopsy sites should be followed for regrowth, though recurrence of pigment alone doesn’t necessarily mean another excision is in the patient’s future, Dr. Kim said.

She reported no conflicts of interest.

[email protected]

SOURCE: Kim C. Summer AAD 2018, Presentation F014.

CHICAGO – Among the many difficult decisions dermatologists have to make, some of the more challenging involve caring for patients with atypical melanocytic lesions. A session at the summer meeting of the American Academy of Dermatology provided some guidance for surveillance of these patients.

Caroline C. Kim, MD, directs the pigmented lesion clinic at Beth Israel Deaconess Medical Center, Boston, and shared the evidence base for her management schema, along with some clinical pearls. No dermatologist ever wants to miss a melanoma, she acknowledged. “We want to avoid those scenarios but not make people feel like Swiss cheese” from multiple biopsies, she said during her presentation.

One key concept that can help physicians find the balance, she said, is that although the presence of atypical or dysplastic nevi increases the risk for melanoma in a given patient, the actual transformation rate of dysplastic nevi to melanomas is not known. In fact, she said, between 50% and 75% of melanomas may arise de novo.

From a dermatopathologic perspective, nevi exist along a continuum of mild to moderate to severe dysplasia, and some lesions are melanomas. But mildly dysplastic nevi are not fated to continue a transformation to increasingly severely dysplastic ones, or to melanomas.

Bringing these ideas to the patient discussion means that one should avoid ever calling a dysplastic nevus “precancerous,” said Dr. Kim; not only is this inaccurate, but it is unnecessarily anxiety provoking, she said.

Within this framework, the initial exam can begin with a search for signature patterns – and ugly ducklings. Each patient will have a pattern, or several patterns, that typify their nevi. Though the markings may be “atypical,” they’ll have some consistency; if the nevus has several neighbors that look just like it, it’s much less likely to be melanoma. “If they are matching partners, it’s more likely that it’s your typical nevus pattern,” said Dr. Kim, also an assistant professor of dermatology at Harvard Medical School, Boston.

By contrast, some lesions stand out from the patient’s other atypical nevi. They may be larger, darker, more elevated, but sometimes, “Even from the doorway, they just stand out,” Dr. Kim said. And these dual concepts of signature patterns and ugly ducklings are useful to talk over with patients, she said. “It’s so easy for patients to grab on to – they totally get it.”

“Use dermoscopy” when you get to the detailed skin exam, she said. “Data have shown that as clinicians, we are pretty good at picking up melanomas ... But with dermoscopy, our detection rate goes up to 70%-95%,” Dr. Kim said. The caveat is that dermoscopy without proper training is a dangerous tool: Several studies have shown that melanoma detection rates drop compared to the naked eye when dermoscopy is performed by untrained users, she said. “Training matters.”

A further tool to help train the eye and mind to recognize benign and malignant patterns when performing dermoscopy of atypical nevi is a now-classic paper that maps these patterns out, she said (Dermatol Surg. 2007;33[11]:1388-91).

“Beware of de novo and changing lesions,” Dr. Kim said. “A picture truly is worth a thousand words” for tracking these, she said.

Total body digital photography, if it’s available, is the best way to track subtle changes, and to spot new lesions as they crop up, said Dr. Kim. In head-to-head studies with dermoscopy and visual exam alone, digital photography can reduce the number of lesions excised, detect early melanoma, and reduce patient anxiety. One study found a 3.8-fold reduction in the mean rate of nevus biopsies when total body digital photography was used, she said (J Am Acad Dermatol. 2016 Mar. doi: 10.1016/j.jaad.2016.02.1152).

A patient care pearl Dr. Kim shared is that she’ll ask patients for their smartphones and take a photograph of the patients’ backs with those phones. This lets them have a handy reference image for monitoring their own skin in the intervals between visits. But make sure, she said, that patients know that “all change is not bad change – you can get new nevi through your 50s.

“Consider sharing care with a local pigmented lesion clinic” if digital photography is not available at your site, said Dr. Kim. She does this for several of her patients, alternating visits with the primary dermatologist.

When should you perform a biopsy?

“You don’t need to biopsy an atypical nevus to call it atypical. You biopsy lesions if you’re suspicious for calling it melanoma,” Dr. Kim said. Removal also can be considered if, for example, a patient lives alone and the nevi of concern are on her back so home monitoring is a challenge, she said.

Once you’ve decided to biopsy, a narrow excisional biopsy with saucerization and 1- to 3-mm margins is preferred when there’s a high suspicion for melanoma, said Dr. Kim, citing a study that found that 2-mm margins using this method yielded an 87% rate of clear pathologic specimen margins in dysplastic nevi (J Am Acad Dermatol. 2017 Dec;77[6]:1096-9). There is some leeway in the guidelines, but “the preferred technique is a narrow excisional biopsy when you are worried,” she said.

There may be times when a partial or incisional biopsy is a rational choice, as when lesions are very large, located on the face or acral areas, or when suspicion for melanoma is low. “If you do partial biopsies, you really have to be aware of the limitations” of the technique since it may miss the nidus of melanoma within an otherwise bland lesion, Dr. Kim pointed out.

And don’t forget to plan your closure with future follow-up in mind: Dr. Kim related that she’d seen a patient for melanoma who’d had the large excisional biopsy performed elsewhere; the patient’s site was closed with an advancement flap, which made sentinel node biopsy impossible.

When the results come back, then what?

Studies have found that atypical nevi are characterized differently at different sites and that management strategies vary geographically, Dr. Kim said. “There’s a need for large-scale data to further investigate the role of observation versus re-excision of dysplastic nevi,” and a multicenter study is underway to do just that, she said, under the auspices of the Pigmented Lesion Subcommittee of the Melanoma Prevention Working Group (ECOG/SWOG).

That same subcommittee has issued a consensus statement for dealing with histologically positive excisional biopsy margins. For mildly dysplastic lesions without clinically observable residual pigment, observation is preferred. Severely dysplastic lesions with unpigmented margins should be re-excised, says the statement (JAMA Dermatol. 2015;151[2]:212-18).

For the intermediate lesions, the group recommended that a reasonable option is to observe a moderately dysplastic nevus site that’s been excisionally biopsied with a finding of positive margins, while acknowledging that more data are needed.

All biopsy sites should be followed for regrowth, though recurrence of pigment alone doesn’t necessarily mean another excision is in the patient’s future, Dr. Kim said.

She reported no conflicts of interest.

[email protected]

SOURCE: Kim C. Summer AAD 2018, Presentation F014.

CHICAGO – Among the many difficult decisions dermatologists have to make, some of the more challenging involve caring for patients with atypical melanocytic lesions. A session at the summer meeting of the American Academy of Dermatology provided some guidance for surveillance of these patients.

Caroline C. Kim, MD, directs the pigmented lesion clinic at Beth Israel Deaconess Medical Center, Boston, and shared the evidence base for her management schema, along with some clinical pearls. No dermatologist ever wants to miss a melanoma, she acknowledged. “We want to avoid those scenarios but not make people feel like Swiss cheese” from multiple biopsies, she said during her presentation.

One key concept that can help physicians find the balance, she said, is that although the presence of atypical or dysplastic nevi increases the risk for melanoma in a given patient, the actual transformation rate of dysplastic nevi to melanomas is not known. In fact, she said, between 50% and 75% of melanomas may arise de novo.

From a dermatopathologic perspective, nevi exist along a continuum of mild to moderate to severe dysplasia, and some lesions are melanomas. But mildly dysplastic nevi are not fated to continue a transformation to increasingly severely dysplastic ones, or to melanomas.

Bringing these ideas to the patient discussion means that one should avoid ever calling a dysplastic nevus “precancerous,” said Dr. Kim; not only is this inaccurate, but it is unnecessarily anxiety provoking, she said.

Within this framework, the initial exam can begin with a search for signature patterns – and ugly ducklings. Each patient will have a pattern, or several patterns, that typify their nevi. Though the markings may be “atypical,” they’ll have some consistency; if the nevus has several neighbors that look just like it, it’s much less likely to be melanoma. “If they are matching partners, it’s more likely that it’s your typical nevus pattern,” said Dr. Kim, also an assistant professor of dermatology at Harvard Medical School, Boston.

By contrast, some lesions stand out from the patient’s other atypical nevi. They may be larger, darker, more elevated, but sometimes, “Even from the doorway, they just stand out,” Dr. Kim said. And these dual concepts of signature patterns and ugly ducklings are useful to talk over with patients, she said. “It’s so easy for patients to grab on to – they totally get it.”

“Use dermoscopy” when you get to the detailed skin exam, she said. “Data have shown that as clinicians, we are pretty good at picking up melanomas ... But with dermoscopy, our detection rate goes up to 70%-95%,” Dr. Kim said. The caveat is that dermoscopy without proper training is a dangerous tool: Several studies have shown that melanoma detection rates drop compared to the naked eye when dermoscopy is performed by untrained users, she said. “Training matters.”

A further tool to help train the eye and mind to recognize benign and malignant patterns when performing dermoscopy of atypical nevi is a now-classic paper that maps these patterns out, she said (Dermatol Surg. 2007;33[11]:1388-91).

“Beware of de novo and changing lesions,” Dr. Kim said. “A picture truly is worth a thousand words” for tracking these, she said.

Total body digital photography, if it’s available, is the best way to track subtle changes, and to spot new lesions as they crop up, said Dr. Kim. In head-to-head studies with dermoscopy and visual exam alone, digital photography can reduce the number of lesions excised, detect early melanoma, and reduce patient anxiety. One study found a 3.8-fold reduction in the mean rate of nevus biopsies when total body digital photography was used, she said (J Am Acad Dermatol. 2016 Mar. doi: 10.1016/j.jaad.2016.02.1152).

A patient care pearl Dr. Kim shared is that she’ll ask patients for their smartphones and take a photograph of the patients’ backs with those phones. This lets them have a handy reference image for monitoring their own skin in the intervals between visits. But make sure, she said, that patients know that “all change is not bad change – you can get new nevi through your 50s.

“Consider sharing care with a local pigmented lesion clinic” if digital photography is not available at your site, said Dr. Kim. She does this for several of her patients, alternating visits with the primary dermatologist.

When should you perform a biopsy?

“You don’t need to biopsy an atypical nevus to call it atypical. You biopsy lesions if you’re suspicious for calling it melanoma,” Dr. Kim said. Removal also can be considered if, for example, a patient lives alone and the nevi of concern are on her back so home monitoring is a challenge, she said.

Once you’ve decided to biopsy, a narrow excisional biopsy with saucerization and 1- to 3-mm margins is preferred when there’s a high suspicion for melanoma, said Dr. Kim, citing a study that found that 2-mm margins using this method yielded an 87% rate of clear pathologic specimen margins in dysplastic nevi (J Am Acad Dermatol. 2017 Dec;77[6]:1096-9). There is some leeway in the guidelines, but “the preferred technique is a narrow excisional biopsy when you are worried,” she said.

There may be times when a partial or incisional biopsy is a rational choice, as when lesions are very large, located on the face or acral areas, or when suspicion for melanoma is low. “If you do partial biopsies, you really have to be aware of the limitations” of the technique since it may miss the nidus of melanoma within an otherwise bland lesion, Dr. Kim pointed out.

And don’t forget to plan your closure with future follow-up in mind: Dr. Kim related that she’d seen a patient for melanoma who’d had the large excisional biopsy performed elsewhere; the patient’s site was closed with an advancement flap, which made sentinel node biopsy impossible.

When the results come back, then what?

Studies have found that atypical nevi are characterized differently at different sites and that management strategies vary geographically, Dr. Kim said. “There’s a need for large-scale data to further investigate the role of observation versus re-excision of dysplastic nevi,” and a multicenter study is underway to do just that, she said, under the auspices of the Pigmented Lesion Subcommittee of the Melanoma Prevention Working Group (ECOG/SWOG).

That same subcommittee has issued a consensus statement for dealing with histologically positive excisional biopsy margins. For mildly dysplastic lesions without clinically observable residual pigment, observation is preferred. Severely dysplastic lesions with unpigmented margins should be re-excised, says the statement (JAMA Dermatol. 2015;151[2]:212-18).

For the intermediate lesions, the group recommended that a reasonable option is to observe a moderately dysplastic nevus site that’s been excisionally biopsied with a finding of positive margins, while acknowledging that more data are needed.

All biopsy sites should be followed for regrowth, though recurrence of pigment alone doesn’t necessarily mean another excision is in the patient’s future, Dr. Kim said.

She reported no conflicts of interest.

[email protected]

SOURCE: Kim C. Summer AAD 2018, Presentation F014.

ORLANDO – Among children with genetic risks for type 1 diabetes and autoantibodies against pancreatic islet cells, a hemoglobin A_1c at or above 5.6% strongly predicts the onset of type 1 diabetes within a year, according to investigators from The Environmental Determinants of Diabetes in the Young (TEDDY) study.

M. Alexander Otto/MDedge News

The risk is even greater if other factors – age at A_1c test, month of A_1c test, continent of residence, and the z-score for one antibody in particular, IA2A, a tyrosine phosphatase antigen protein – are taken into account, with an area under the curve (AUC) of about 0.97. The study team is developing an online risk calculator for clinicians so they can simply plug in the numbers.

But the 5.6% cutpoint works well even by itself, with an AUC of about 0.86. Among the children with genetic risk factors and islet cell autoantibodies who hit that mark in the study, the median time to diagnosis of type 1 diabetes mellitus (T1DM) was 7.1 months.

The point of the work is to catch disease onset early to prevent children from going into diabetic ketoacidosis.

The ultimate goal of TEDDY is to identify infectious agents, dietary factors, and other environmental agents that either trigger or protect against T1DM in genetically susceptible children, to develop strategies to prevent, delay, or even reverse T1DM. For more than a decade, the consortium has been following more than 8,000 children who screened positive at birth for genetic anomalies in the human leukocyte antigen region on their 6th chromosome, a major risk factor for T1DM. The team is following them to find out what puts them over the edge; A_1c seems to be key.

Catching the disease early is a goal. Until now, the TEDDY team has used the development of pancreatic islet cell autoantibodies to trigger oral glucose tolerance tests (OGTTs) every 6 months.

The problem is that islet antibodies “are great at saying that you are going to get diabetes but not when. We have kids who have been multiple antibody positive now for 6, 7, 8 years” but who still haven’t developed T1DM. In the meantime, their parents have been dragging them in for OGTTs every 6 months for years, said lead investigator and TEDDY study coordinator Michael Killian, of the Pacific Northwest Research Institute, Seattle.

With the A_1c cutpoint, it should be safe to hold off on direct glycemic surveillance until A_1c levels reach 5.6%, and even safer when the full risk prediction model with 1A2A z-scores and other factors are available. Once children hit the parameters, it’s near certain they will develop T1DM within a year, so the findings should reduce the number of OGTT tests to just two or three. In the end, “we’ll get better compliance” with testing and still “catch these kids early,” Mr. Killian said at the annual scientific sessions of the American Diabetes Association.

Rare is the newborn who is screened for diabetes risk at birth, and even rarer is the child who is followed for autoantibodies. If the findings hold out, however, such early action could be the future.

“We envision a time” when newborns are screened for T1DM risk and followed for autoantibodies. Glycemic surveillance will kick in if they hit A_1c levels of 5.6%, said William Hagopian, MD, PhD, clinical associate professor at the University of Washington, Seattle, and a TEDDY principal investigator.

Among the 8,000-plus children followed, 456 had persistent islet autoantibodies and at least three A_1c tests in the prior 12 months; 104 progressed to T1DM and 352 did not. The mean age to islet autoantibody seroconversion was 43 months, and mean age to T1DM diagnosis was 73 months. The team ran a receiver operating curve analysis to identify the optimum A_1c cutpoint, 5.6%.

The month of testing mattered, because “glycemia is higher in the winter, lower in the summer, and insulin sensitivity is lower in the winter, and higher in the summer,” Dr. Hagopian said. It probably has something to do with what the stresses of early human evolution bred into the genes.

The IA2A autoantibody z-score is the only number that will be cumbersome to plug into the upcoming online risk calculator. It’s the number of standard deviations off your reference lab’s mean. “You have to talk to the lab that does your IA2As to know what the standard deviation is,” Dr. Hagopian said.

The investigators had no disclosures. TEDDY is supported by the National Institutes of Health, among other entities.

[email protected]

SOURCE: Killian M et al. ADA 2018, Abstract 162-LB

ORLANDO – Among children with genetic risks for type 1 diabetes and autoantibodies against pancreatic islet cells, a hemoglobin A_1c at or above 5.6% strongly predicts the onset of type 1 diabetes within a year, according to investigators from The Environmental Determinants of Diabetes in the Young (TEDDY) study.

M. Alexander Otto/MDedge News

The risk is even greater if other factors – age at A_1c test, month of A_1c test, continent of residence, and the z-score for one antibody in particular, IA2A, a tyrosine phosphatase antigen protein – are taken into account, with an area under the curve (AUC) of about 0.97. The study team is developing an online risk calculator for clinicians so they can simply plug in the numbers.

But the 5.6% cutpoint works well even by itself, with an AUC of about 0.86. Among the children with genetic risk factors and islet cell autoantibodies who hit that mark in the study, the median time to diagnosis of type 1 diabetes mellitus (T1DM) was 7.1 months.

The point of the work is to catch disease onset early to prevent children from going into diabetic ketoacidosis.

The ultimate goal of TEDDY is to identify infectious agents, dietary factors, and other environmental agents that either trigger or protect against T1DM in genetically susceptible children, to develop strategies to prevent, delay, or even reverse T1DM. For more than a decade, the consortium has been following more than 8,000 children who screened positive at birth for genetic anomalies in the human leukocyte antigen region on their 6th chromosome, a major risk factor for T1DM. The team is following them to find out what puts them over the edge; A_1c seems to be key.

Catching the disease early is a goal. Until now, the TEDDY team has used the development of pancreatic islet cell autoantibodies to trigger oral glucose tolerance tests (OGTTs) every 6 months.

The problem is that islet antibodies “are great at saying that you are going to get diabetes but not when. We have kids who have been multiple antibody positive now for 6, 7, 8 years” but who still haven’t developed T1DM. In the meantime, their parents have been dragging them in for OGTTs every 6 months for years, said lead investigator and TEDDY study coordinator Michael Killian, of the Pacific Northwest Research Institute, Seattle.

With the A_1c cutpoint, it should be safe to hold off on direct glycemic surveillance until A_1c levels reach 5.6%, and even safer when the full risk prediction model with 1A2A z-scores and other factors are available. Once children hit the parameters, it’s near certain they will develop T1DM within a year, so the findings should reduce the number of OGTT tests to just two or three. In the end, “we’ll get better compliance” with testing and still “catch these kids early,” Mr. Killian said at the annual scientific sessions of the American Diabetes Association.

Rare is the newborn who is screened for diabetes risk at birth, and even rarer is the child who is followed for autoantibodies. If the findings hold out, however, such early action could be the future.

“We envision a time” when newborns are screened for T1DM risk and followed for autoantibodies. Glycemic surveillance will kick in if they hit A_1c levels of 5.6%, said William Hagopian, MD, PhD, clinical associate professor at the University of Washington, Seattle, and a TEDDY principal investigator.

Among the 8,000-plus children followed, 456 had persistent islet autoantibodies and at least three A_1c tests in the prior 12 months; 104 progressed to T1DM and 352 did not. The mean age to islet autoantibody seroconversion was 43 months, and mean age to T1DM diagnosis was 73 months. The team ran a receiver operating curve analysis to identify the optimum A_1c cutpoint, 5.6%.

The month of testing mattered, because “glycemia is higher in the winter, lower in the summer, and insulin sensitivity is lower in the winter, and higher in the summer,” Dr. Hagopian said. It probably has something to do with what the stresses of early human evolution bred into the genes.

The IA2A autoantibody z-score is the only number that will be cumbersome to plug into the upcoming online risk calculator. It’s the number of standard deviations off your reference lab’s mean. “You have to talk to the lab that does your IA2As to know what the standard deviation is,” Dr. Hagopian said.

The investigators had no disclosures. TEDDY is supported by the National Institutes of Health, among other entities.

[email protected]

SOURCE: Killian M et al. ADA 2018, Abstract 162-LB

ORLANDO – Among children with genetic risks for type 1 diabetes and autoantibodies against pancreatic islet cells, a hemoglobin A_1c at or above 5.6% strongly predicts the onset of type 1 diabetes within a year, according to investigators from The Environmental Determinants of Diabetes in the Young (TEDDY) study.

M. Alexander Otto/MDedge News

The risk is even greater if other factors – age at A_1c test, month of A_1c test, continent of residence, and the z-score for one antibody in particular, IA2A, a tyrosine phosphatase antigen protein – are taken into account, with an area under the curve (AUC) of about 0.97. The study team is developing an online risk calculator for clinicians so they can simply plug in the numbers.

But the 5.6% cutpoint works well even by itself, with an AUC of about 0.86. Among the children with genetic risk factors and islet cell autoantibodies who hit that mark in the study, the median time to diagnosis of type 1 diabetes mellitus (T1DM) was 7.1 months.

The point of the work is to catch disease onset early to prevent children from going into diabetic ketoacidosis.

The ultimate goal of TEDDY is to identify infectious agents, dietary factors, and other environmental agents that either trigger or protect against T1DM in genetically susceptible children, to develop strategies to prevent, delay, or even reverse T1DM. For more than a decade, the consortium has been following more than 8,000 children who screened positive at birth for genetic anomalies in the human leukocyte antigen region on their 6th chromosome, a major risk factor for T1DM. The team is following them to find out what puts them over the edge; A_1c seems to be key.

Catching the disease early is a goal. Until now, the TEDDY team has used the development of pancreatic islet cell autoantibodies to trigger oral glucose tolerance tests (OGTTs) every 6 months.

The problem is that islet antibodies “are great at saying that you are going to get diabetes but not when. We have kids who have been multiple antibody positive now for 6, 7, 8 years” but who still haven’t developed T1DM. In the meantime, their parents have been dragging them in for OGTTs every 6 months for years, said lead investigator and TEDDY study coordinator Michael Killian, of the Pacific Northwest Research Institute, Seattle.

With the A_1c cutpoint, it should be safe to hold off on direct glycemic surveillance until A_1c levels reach 5.6%, and even safer when the full risk prediction model with 1A2A z-scores and other factors are available. Once children hit the parameters, it’s near certain they will develop T1DM within a year, so the findings should reduce the number of OGTT tests to just two or three. In the end, “we’ll get better compliance” with testing and still “catch these kids early,” Mr. Killian said at the annual scientific sessions of the American Diabetes Association.

Rare is the newborn who is screened for diabetes risk at birth, and even rarer is the child who is followed for autoantibodies. If the findings hold out, however, such early action could be the future.

“We envision a time” when newborns are screened for T1DM risk and followed for autoantibodies. Glycemic surveillance will kick in if they hit A_1c levels of 5.6%, said William Hagopian, MD, PhD, clinical associate professor at the University of Washington, Seattle, and a TEDDY principal investigator.

Among the 8,000-plus children followed, 456 had persistent islet autoantibodies and at least three A_1c tests in the prior 12 months; 104 progressed to T1DM and 352 did not. The mean age to islet autoantibody seroconversion was 43 months, and mean age to T1DM diagnosis was 73 months. The team ran a receiver operating curve analysis to identify the optimum A_1c cutpoint, 5.6%.

The month of testing mattered, because “glycemia is higher in the winter, lower in the summer, and insulin sensitivity is lower in the winter, and higher in the summer,” Dr. Hagopian said. It probably has something to do with what the stresses of early human evolution bred into the genes.

The IA2A autoantibody z-score is the only number that will be cumbersome to plug into the upcoming online risk calculator. It’s the number of standard deviations off your reference lab’s mean. “You have to talk to the lab that does your IA2As to know what the standard deviation is,” Dr. Hagopian said.

The investigators had no disclosures. TEDDY is supported by the National Institutes of Health, among other entities.

[email protected]

SOURCE: Killian M et al. ADA 2018, Abstract 162-LB

AMSTERDAM – Middle-aged and elderly people infected with HIV were more likely to meet an established definition of frailty than were uninfected people of the same age, and during 4 years of follow-up frailty significantly linked with an increased incidence of both mortality and development of new comorbidities, based on a Dutch prospective study of 1,146 people.

Mitchel L. Zoler/MDedge News

People living with HIV also showed, despite antiretroviral treatment, a significantly increased rate of progression to frailty over the course of 4 years, compared with uninfected people, after adjustment for demographic differences. This progression to frailty appeared mediated by a high waist-to-hip ratio, a higher number of preexisting comorbidities, and symptoms of depression, Eveline Verheij, MD, said at the 22nd International AIDS Conference.

At entry into the study, people living with HIV had a 10% prevalence of frailty, compared with 3% among those who were uninfected, said Dr. Verheij, a researcher with the Amsterdam Institute for Global Health & Development. She defined frailty using criteria first introduced by researchers in 2001, which established five characteristics as markers of frailty: slow gait, low grip strength, a low level of physical activity, self-reported exhaustion, and unintentional weight loss of at least 10 pounds during the preceding year (J Gerontol A Biol Sci Med. 2001 Mar 1;56[3]:M146-57).

People with three or more of these conditions were identified as frail, those with one or two were tagged as prefrail, and people with none of these five characteristics were considered robust.

In the study reported by Dr. Verheij, the prevalence of people identified as robust at the time they entered the study was about 60% of those without an HIV infection and about 40% of those infected with HIV. During the 4 years she and her associates followed these people, their rates of progression from a robust state to frailty occurred more than twice as often among the people living with HIV, compared with those who were uninfected, after adjustment for age, ethnicity, and education.

Dr. Verheij admitted that she and her associates have not identified interventions that are effective for reversing frailty. “People who are already frail are likely to remain frail,” she noted. A better strategy is to take steps to defer frailty and help people who are robust retain that status. This could involve measures such as smoking cessation, exercise, and maintaining or expanding social networks, she suggested.

The AGEhiV Cohort Study enrolled 596 people living with HIV and 550 uninfected people who were all at least 45 years old. The average age was 52 years, with about 10% in each group older than 65 years. About 90% of the enrollees were Dutch, nearly three-quarters of those in both groups were men who have sex with men, and 14% of those who were uninfected and 20% of those living with HIV had symptoms of depression.

At baseline, 61% of those without HIV and 48% of people with HIV had no comorbidities, and while the percentage in both groups with one comorbidity at entry was nearly the same, 28% and 31%, respectively, the percentage with two or more comorbidities was more divergent. Among those without HIV infection, 8% had two comorbidities and 3% had three or more, while among those with HIV, 14% had two comorbidities and 6% had three or more.

The people living with HIV had been infected for an average of 12 years. At enrollment, 96% were on antiretroviral therapy, and those on treatment had received it for an average of 10 years. At enrollment, their average CD4 cell count was 565 cells/mm³. Their average nadir cell count had been 170 cells/mm³, and 32% had a history of being diagnosed with AIDS.

Dr. Verheij and her associates examined each participant at baseline and twice more, 2 and 4 years after enrollment. During the 4 years of follow-up, 17 people died. After adjustment for age, baseline comorbidities, and HIV infection, the mortality was more than 10-fold higher among people who had been frail at entry, compared with those who were robust.

During follow-up, 276 of all enrollees developed 329 comorbidities. The four most common incident comorbidities were hypertension, followed by chronic obstructive lung disease, renal insufficiency, and osteoporosis. These four conditions accounted for three-quarters of all incident comorbidities. After adjustment for demographics, baseline comorbidities, and HIV status, people who entered the study as frail or who became frail during the study had about a 90% increased rate of developing a new comorbidity compared with those who were not frail.

[email protected]

SOURCE: Verheij E et al. AIDS 2018, Abstract 9303, THAB01015.

AMSTERDAM – Middle-aged and elderly people infected with HIV were more likely to meet an established definition of frailty than were uninfected people of the same age, and during 4 years of follow-up frailty significantly linked with an increased incidence of both mortality and development of new comorbidities, based on a Dutch prospective study of 1,146 people.

Mitchel L. Zoler/MDedge News

People living with HIV also showed, despite antiretroviral treatment, a significantly increased rate of progression to frailty over the course of 4 years, compared with uninfected people, after adjustment for demographic differences. This progression to frailty appeared mediated by a high waist-to-hip ratio, a higher number of preexisting comorbidities, and symptoms of depression, Eveline Verheij, MD, said at the 22nd International AIDS Conference.

At entry into the study, people living with HIV had a 10% prevalence of frailty, compared with 3% among those who were uninfected, said Dr. Verheij, a researcher with the Amsterdam Institute for Global Health & Development. She defined frailty using criteria first introduced by researchers in 2001, which established five characteristics as markers of frailty: slow gait, low grip strength, a low level of physical activity, self-reported exhaustion, and unintentional weight loss of at least 10 pounds during the preceding year (J Gerontol A Biol Sci Med. 2001 Mar 1;56[3]:M146-57).

People with three or more of these conditions were identified as frail, those with one or two were tagged as prefrail, and people with none of these five characteristics were considered robust.

In the study reported by Dr. Verheij, the prevalence of people identified as robust at the time they entered the study was about 60% of those without an HIV infection and about 40% of those infected with HIV. During the 4 years she and her associates followed these people, their rates of progression from a robust state to frailty occurred more than twice as often among the people living with HIV, compared with those who were uninfected, after adjustment for age, ethnicity, and education.

Dr. Verheij admitted that she and her associates have not identified interventions that are effective for reversing frailty. “People who are already frail are likely to remain frail,” she noted. A better strategy is to take steps to defer frailty and help people who are robust retain that status. This could involve measures such as smoking cessation, exercise, and maintaining or expanding social networks, she suggested.

The AGEhiV Cohort Study enrolled 596 people living with HIV and 550 uninfected people who were all at least 45 years old. The average age was 52 years, with about 10% in each group older than 65 years. About 90% of the enrollees were Dutch, nearly three-quarters of those in both groups were men who have sex with men, and 14% of those who were uninfected and 20% of those living with HIV had symptoms of depression.

At baseline, 61% of those without HIV and 48% of people with HIV had no comorbidities, and while the percentage in both groups with one comorbidity at entry was nearly the same, 28% and 31%, respectively, the percentage with two or more comorbidities was more divergent. Among those without HIV infection, 8% had two comorbidities and 3% had three or more, while among those with HIV, 14% had two comorbidities and 6% had three or more.

The people living with HIV had been infected for an average of 12 years. At enrollment, 96% were on antiretroviral therapy, and those on treatment had received it for an average of 10 years. At enrollment, their average CD4 cell count was 565 cells/mm³. Their average nadir cell count had been 170 cells/mm³, and 32% had a history of being diagnosed with AIDS.

Dr. Verheij and her associates examined each participant at baseline and twice more, 2 and 4 years after enrollment. During the 4 years of follow-up, 17 people died. After adjustment for age, baseline comorbidities, and HIV infection, the mortality was more than 10-fold higher among people who had been frail at entry, compared with those who were robust.

During follow-up, 276 of all enrollees developed 329 comorbidities. The four most common incident comorbidities were hypertension, followed by chronic obstructive lung disease, renal insufficiency, and osteoporosis. These four conditions accounted for three-quarters of all incident comorbidities. After adjustment for demographics, baseline comorbidities, and HIV status, people who entered the study as frail or who became frail during the study had about a 90% increased rate of developing a new comorbidity compared with those who were not frail.

[email protected]

SOURCE: Verheij E et al. AIDS 2018, Abstract 9303, THAB01015.

AMSTERDAM – Middle-aged and elderly people infected with HIV were more likely to meet an established definition of frailty than were uninfected people of the same age, and during 4 years of follow-up frailty significantly linked with an increased incidence of both mortality and development of new comorbidities, based on a Dutch prospective study of 1,146 people.

Mitchel L. Zoler/MDedge News

People living with HIV also showed, despite antiretroviral treatment, a significantly increased rate of progression to frailty over the course of 4 years, compared with uninfected people, after adjustment for demographic differences. This progression to frailty appeared mediated by a high waist-to-hip ratio, a higher number of preexisting comorbidities, and symptoms of depression, Eveline Verheij, MD, said at the 22nd International AIDS Conference.

At entry into the study, people living with HIV had a 10% prevalence of frailty, compared with 3% among those who were uninfected, said Dr. Verheij, a researcher with the Amsterdam Institute for Global Health & Development. She defined frailty using criteria first introduced by researchers in 2001, which established five characteristics as markers of frailty: slow gait, low grip strength, a low level of physical activity, self-reported exhaustion, and unintentional weight loss of at least 10 pounds during the preceding year (J Gerontol A Biol Sci Med. 2001 Mar 1;56[3]:M146-57).

People with three or more of these conditions were identified as frail, those with one or two were tagged as prefrail, and people with none of these five characteristics were considered robust.

In the study reported by Dr. Verheij, the prevalence of people identified as robust at the time they entered the study was about 60% of those without an HIV infection and about 40% of those infected with HIV. During the 4 years she and her associates followed these people, their rates of progression from a robust state to frailty occurred more than twice as often among the people living with HIV, compared with those who were uninfected, after adjustment for age, ethnicity, and education.

Dr. Verheij admitted that she and her associates have not identified interventions that are effective for reversing frailty. “People who are already frail are likely to remain frail,” she noted. A better strategy is to take steps to defer frailty and help people who are robust retain that status. This could involve measures such as smoking cessation, exercise, and maintaining or expanding social networks, she suggested.

The AGEhiV Cohort Study enrolled 596 people living with HIV and 550 uninfected people who were all at least 45 years old. The average age was 52 years, with about 10% in each group older than 65 years. About 90% of the enrollees were Dutch, nearly three-quarters of those in both groups were men who have sex with men, and 14% of those who were uninfected and 20% of those living with HIV had symptoms of depression.

At baseline, 61% of those without HIV and 48% of people with HIV had no comorbidities, and while the percentage in both groups with one comorbidity at entry was nearly the same, 28% and 31%, respectively, the percentage with two or more comorbidities was more divergent. Among those without HIV infection, 8% had two comorbidities and 3% had three or more, while among those with HIV, 14% had two comorbidities and 6% had three or more.

The people living with HIV had been infected for an average of 12 years. At enrollment, 96% were on antiretroviral therapy, and those on treatment had received it for an average of 10 years. At enrollment, their average CD4 cell count was 565 cells/mm³. Their average nadir cell count had been 170 cells/mm³, and 32% had a history of being diagnosed with AIDS.

Dr. Verheij and her associates examined each participant at baseline and twice more, 2 and 4 years after enrollment. During the 4 years of follow-up, 17 people died. After adjustment for age, baseline comorbidities, and HIV infection, the mortality was more than 10-fold higher among people who had been frail at entry, compared with those who were robust.

During follow-up, 276 of all enrollees developed 329 comorbidities. The four most common incident comorbidities were hypertension, followed by chronic obstructive lung disease, renal insufficiency, and osteoporosis. These four conditions accounted for three-quarters of all incident comorbidities. After adjustment for demographics, baseline comorbidities, and HIV status, people who entered the study as frail or who became frail during the study had about a 90% increased rate of developing a new comorbidity compared with those who were not frail.

[email protected]

SOURCE: Verheij E et al. AIDS 2018, Abstract 9303, THAB01015.

Photo by Rhoda Baer

Research has shown an increase in the global incidence of leukemia and non-Hodgkin lymphoma (NHL) in recent years.

The Global Burden of Disease (GBD) study showed that, from 2006 to 2016, the incidence of NHL increased 45%, and the incidence of leukemia increased 26%.

These increases were largely due to population growth and aging.

Results from the GDB study were published in JAMA Oncology.

The study indicated that, in 2016, there were 17.2 million cases of cancer worldwide and 8.9 million cancer deaths.

One in 3 men were likely to get cancer during their lifetime, as were 1 in 5 women. Cancer was associated with 213.2 million disability-adjusted life years (DALYs).

The following table lists the 2016 global incidence and mortality figures for all cancers combined and for individual hematologic malignancies.

Leukemia

In 2016, there were 467,000 new cases of leukemia and 310,000 leukemia deaths. Leukemia was responsible for 10.2 million DALYs. Leukemia developed in 1 in 118 men and 1 in 194 women worldwide.

Between 2006 and 2016, the global leukemia incidence increased by 26%—from 370,482 to 466,802 cases.

The researchers said the factors contributing to this increase were population growth (12%), population aging (10%), and an increase in age-specific incidence rates (3%).

NHL

In 2016, there were 461,000 new cases of NHL and 240,000 NHL deaths. NHL was responsible for 6.8 million DALYs. NHL developed in 1 in 110 men and 1 in 161 women worldwide.

Between 2006 and 2016, NHL increased by 45%, from 319,078 to 461,164 cases.

The factors contributing to this increase were increasing age-specific incidence rates (17%), changing population age structure (15%), and population growth (12%).

“A large proportion of the increase in cancer incidence can be explained by improving life expectancy and population growth—a development that can at least partially be attributed to a reduced burden from other common diseases,” the study authors wrote.

The authors also pointed out that prevention efforts are less effective for hematologic malignancies than for other cancers.

Photo by Rhoda Baer

Research has shown an increase in the global incidence of leukemia and non-Hodgkin lymphoma (NHL) in recent years.

The Global Burden of Disease (GBD) study showed that, from 2006 to 2016, the incidence of NHL increased 45%, and the incidence of leukemia increased 26%.

These increases were largely due to population growth and aging.

Results from the GDB study were published in JAMA Oncology.

The study indicated that, in 2016, there were 17.2 million cases of cancer worldwide and 8.9 million cancer deaths.

One in 3 men were likely to get cancer during their lifetime, as were 1 in 5 women. Cancer was associated with 213.2 million disability-adjusted life years (DALYs).

The following table lists the 2016 global incidence and mortality figures for all cancers combined and for individual hematologic malignancies.

Leukemia

In 2016, there were 467,000 new cases of leukemia and 310,000 leukemia deaths. Leukemia was responsible for 10.2 million DALYs. Leukemia developed in 1 in 118 men and 1 in 194 women worldwide.

Between 2006 and 2016, the global leukemia incidence increased by 26%—from 370,482 to 466,802 cases.

The researchers said the factors contributing to this increase were population growth (12%), population aging (10%), and an increase in age-specific incidence rates (3%).

NHL

In 2016, there were 461,000 new cases of NHL and 240,000 NHL deaths. NHL was responsible for 6.8 million DALYs. NHL developed in 1 in 110 men and 1 in 161 women worldwide.

Between 2006 and 2016, NHL increased by 45%, from 319,078 to 461,164 cases.

The factors contributing to this increase were increasing age-specific incidence rates (17%), changing population age structure (15%), and population growth (12%).

“A large proportion of the increase in cancer incidence can be explained by improving life expectancy and population growth—a development that can at least partially be attributed to a reduced burden from other common diseases,” the study authors wrote.

The authors also pointed out that prevention efforts are less effective for hematologic malignancies than for other cancers.

Photo by Rhoda Baer

Research has shown an increase in the global incidence of leukemia and non-Hodgkin lymphoma (NHL) in recent years.

The Global Burden of Disease (GBD) study showed that, from 2006 to 2016, the incidence of NHL increased 45%, and the incidence of leukemia increased 26%.

These increases were largely due to population growth and aging.

Results from the GDB study were published in JAMA Oncology.

The study indicated that, in 2016, there were 17.2 million cases of cancer worldwide and 8.9 million cancer deaths.

One in 3 men were likely to get cancer during their lifetime, as were 1 in 5 women. Cancer was associated with 213.2 million disability-adjusted life years (DALYs).

The following table lists the 2016 global incidence and mortality figures for all cancers combined and for individual hematologic malignancies.

Leukemia

In 2016, there were 467,000 new cases of leukemia and 310,000 leukemia deaths. Leukemia was responsible for 10.2 million DALYs. Leukemia developed in 1 in 118 men and 1 in 194 women worldwide.

Between 2006 and 2016, the global leukemia incidence increased by 26%—from 370,482 to 466,802 cases.

The researchers said the factors contributing to this increase were population growth (12%), population aging (10%), and an increase in age-specific incidence rates (3%).

NHL

In 2016, there were 461,000 new cases of NHL and 240,000 NHL deaths. NHL was responsible for 6.8 million DALYs. NHL developed in 1 in 110 men and 1 in 161 women worldwide.

Between 2006 and 2016, NHL increased by 45%, from 319,078 to 461,164 cases.

The factors contributing to this increase were increasing age-specific incidence rates (17%), changing population age structure (15%), and population growth (12%).

“A large proportion of the increase in cancer incidence can be explained by improving life expectancy and population growth—a development that can at least partially be attributed to a reduced burden from other common diseases,” the study authors wrote.

The authors also pointed out that prevention efforts are less effective for hematologic malignancies than for other cancers.

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.

The horrors faced by migrant families forced to separate under the new U.S. “zero tolerance” policy continue to unfold. Tragic emblems of this policy include tapes of crying children and the reported suicide of a father who had been separated from his children.

A federal judge had issued an injunction requiring the reunification of thousands of families by July 26. Despite that deadline, hundreds of adults are no longer in the United States, and hundreds of children are scattered in shelters across the country.

In response to those events, mental health and medical organizations have released powerful statements. The American Psychological Association stated: “The administration’s policy ... is not only needless and cruel, it threatens the mental and physical health of both the children and their caregivers.” The American Medical Association issued a call asserting that separating children from their parents “will do great harm” and “create negative health impacts that will last an individual’s entire lifespan.” Meanwhile, the American Psychiatric Association’s president, Altha J. Stewart, MD, released a statement affirming that “any forced separation is highly stressful for children and can cause lifelong trauma, as well as an increased risk of other mental illnesses, such as depression, anxiety, and posttraumatic stress disorder.”

As forensic experts who testify about the mental well-being of immigration detainees, we applaud those powerful and unambiguous messages from the leaders in our fields. Yet, their statements also underscore the limitations of our diagnostic models: Our field is caught in the difficult position of either applying ill-fitting diagnostic labels or overpathologizing a normal reaction to horrific circumstances. While not applying diagnoses potentially minimizes the enormous psychological burden of separation, diagnosing depression or PTSD as catchalls for suffering incorrectly defines the experience of many survivors of ongoing trauma.

Currently, most providers, in trying to communicate the effects of ongoing trauma, rely on the diagnoses of depression or PTSD. Both of these diagnoses, however, are problematic. The diagnosis of major depressive disorder, for example, is useful in communicating a loss of hope, and the inability to enjoy pleasurable things. However, depression is an episodic illness, often part of a larger chronic disorder.¹ Depression often has a genetic-hereditary component. On the other hand, children suffering from childhood traumas often present lifelong and wide-ranging problems, which may be triggered by reminders but are not episodic. For example, children experiencing parental separation have difficulty forming attachments, which, in turn, leads to subsequent difficulty forming meaningful interpersonal relationships.

The diagnosis of PTSD is useful in communicating a myriad of possible symptoms, which may accompany the trauma. However, PTSD implies a traumatic event as described in criteria A of the DSM-5: “exposure to actual or threatened death, serious injury, or sexual violence.” As such, PTSD poorly encompasses the wide array of smaller yet repetitive traumas experienced by victims of ongoing trauma, such as those youth separated from their parents at the U.S. border. Furthermore, PTSD is a disorder with specific symptoms that, based on a vast body of research,^2,3 inadequately describes the multitude of interpersonal, psychological, and physical consequences associated with the type of trauma caused by family separations.

Our understanding of the long-term sequelae of childhood trauma has been greatly influenced by the adverse childhood experiences (ACE) study. The ACE study, one of the largest investigations ever conducted to assess associations between childhood maltreatment and later-life health and well-being, collected the life histories of more than 17,000 patients in a collaborative effort between the Centers for Disease Control and Prevention and Kaiser Permanente’s Health Appraisal Clinic.

The ACE study identified 10 forms of childhood trauma, including: abuse, neglect, abandonment, household dysfunction, and exposure to violence, that were strongly associated with negative psychological outcomes such as depression, suicide attempts, and engagement in high-risk behaviors, as well as significant medical consequences, including higher incidence of heart disease, diabetes, and stroke. Ultimately, having four or more ACEs was associated with early death.

In response to the emerging body of research on childhood trauma, various terms, including complex trauma, type-II trauma, and complex PTSD, have entered our professional lexicon as a means of communicating the wide-ranging consequences of developmental trauma. On the one hand, the less defined and rigid nature of these terms permits mental health providers to develop a rich narrative of a patient’s background, encompassing the patient’s behavior, character, and symptoms. However, the absence of formal terminology also has its drawbacks: Courts and juries have grown accustomed to diagnoses, labels, and syndromes. Most forensic mental health providers who testify about developmental trauma in court can predict the question: “So doctor, you are saying that the individual’s presentation is not severe enough to be considered PTSD, am I correct?” Disorders justify treatment, can explain disability, and warrant empathy; concomitantly, “complex trauma” runs the risk of being considered an academic explanation for trauma victims’ lifelong problems, rather than a societal failure that merits care.

Recognizing the limitations of our current diagnoses, the forthcoming update to the International Classification of Diseases (ICD-11) will add a new category: complex PTSD. The ICD-11 will attempt to widen the concept of trauma to include “conditions of prolonged adversity, in the form of sustained, repeated, or multiple forms of traumatic exposure.” Trauma exposure examples include genocide campaigns, childhood sexual abuse, child soldiering, severe domestic violence, torture, or slavery. The ICD-11 also expands our understanding of the consequences of trauma to include “affective dysregulation,” “negative self-concept,” and “disturbances in relationships” as part of a concept called “disturbances in self-organization.” Those are important steps in acknowledging the consequences of different forms of trauma as well as noticing a richer array of damages from those incidents.⁴

While the World Health Organization’s latest iteration of the ICD takes an important step in widening the scope of our diagnostic tools, we are cognizant that our field’s obsessional search for diagnoses, labels, and nomenclature reinforces a detrimental focus on symptoms over stories. However, as forensic mental health providers, we also are keenly aware that a failure to adopt common definitions impedes forensic evaluations, patient advocacy, public policy, and most importantly, patient care.

In the end, we have trained society to understand pathology through narrow lenses, and therefore, in the face of tragic events such as family separations, we need the appropriate language to clearly define and communicate the experiences of our patients. So, despite the limitations of labels, let’s be encouraged by the World Health Organization’s efforts and continue in that direction.

 Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Lehman is a licensed clinical and forensic psychologist in San Diego. Her practice consists of conducting forensic psychological evaluations for the courts with children, adolescents, and adults. Dr. Lehman has been qualified as an expert witness in California as well as in the federal courts. She previously was a supervisor at Sharper Future, a forensic rehabilitation program, and previously served as an adjunct faculty member at Alliant International University, San Diego. Dr. Lehman can be reached at [email protected].

References

1. Am J Psychiatry. 2000 Sep;157(9):1501-4.

2. Psychiatr Ann. 2005;35(5):390-8.

3. Psychiatr Ann. 2005;35(5):401-8.

4. Eur J Psychotraumatol. 2018 Jan 15. doi: 10.1080/20008198.2017.1418103.