AML cells

Image by Lance Liotta

New research appears to explain how antibodies that target CD44 fight acute myeloid leukemia (AML).

Previous research showed that anti-CD44 antibodies inhibit proliferation and induce differentiation in AML, but it wasn’t clear how or why this happens.

The new study suggests anti-CD44 antibodies work by inhibiting 2 “major players” of the PI3K/Akt/mTOR pathway—mTORC1 and mTORC2.

Jasmeen Merzaban, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia, and her colleagues described this discovery in a letter to Leukemia.

The researchers tested an anti-CD44 antibody known as A3D8 in cell lines representing different AML subtypes (HL60, THP-1, and KG1a) as well as a mouse model of AML.

In these experiments, A3D8 inhibited proliferation and induced differentiation in AML cells. This was accompanied by a decrease in phosphorylation of the mTORC1 and mTORC2 complexes, which was strongly correlated with inhibition of the PI3K/Akt pathway.

The researchers said this finding is important because a complete shutdown of mTOR signaling is probably needed to disrupt the multiple feedback loops that can fuel AML growth, and drugs that only inhibit one of these complexes have, in the past, failed to demonstrate a therapeutic benefit for patients with AML.

“A growing body of evidence suggests that a broader inhibitor would result in a more potent therapeutic effect,” Dr Merzaban said.

She and her colleagues believe an anti-CD44 antibody like A3D8 might just be that type of inhibitor.

They also noted that A3D8 was able to induce differentiation in different subtypes of AML and did not seem to present any toxicity issues.

“We show that the anti-CD44 antibody used for our studies had no effect on normal blood cells,” said Samah Gadhoum, PhD, a research scientist in Dr Merzaban’s lab.

“However, more work is needed to carefully determine the effect of these antibodies on other cells and other cellular functions within the body.”

The researchers are now conducting follow-up experiments, but they believe their results support the use of anti-CD44 antibodies to treat different types of AML.

AML cells

Image by Lance Liotta

New research appears to explain how antibodies that target CD44 fight acute myeloid leukemia (AML).

Previous research showed that anti-CD44 antibodies inhibit proliferation and induce differentiation in AML, but it wasn’t clear how or why this happens.

The new study suggests anti-CD44 antibodies work by inhibiting 2 “major players” of the PI3K/Akt/mTOR pathway—mTORC1 and mTORC2.

Jasmeen Merzaban, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia, and her colleagues described this discovery in a letter to Leukemia.

The researchers tested an anti-CD44 antibody known as A3D8 in cell lines representing different AML subtypes (HL60, THP-1, and KG1a) as well as a mouse model of AML.

In these experiments, A3D8 inhibited proliferation and induced differentiation in AML cells. This was accompanied by a decrease in phosphorylation of the mTORC1 and mTORC2 complexes, which was strongly correlated with inhibition of the PI3K/Akt pathway.

The researchers said this finding is important because a complete shutdown of mTOR signaling is probably needed to disrupt the multiple feedback loops that can fuel AML growth, and drugs that only inhibit one of these complexes have, in the past, failed to demonstrate a therapeutic benefit for patients with AML.

“A growing body of evidence suggests that a broader inhibitor would result in a more potent therapeutic effect,” Dr Merzaban said.

She and her colleagues believe an anti-CD44 antibody like A3D8 might just be that type of inhibitor.

They also noted that A3D8 was able to induce differentiation in different subtypes of AML and did not seem to present any toxicity issues.

“We show that the anti-CD44 antibody used for our studies had no effect on normal blood cells,” said Samah Gadhoum, PhD, a research scientist in Dr Merzaban’s lab.

“However, more work is needed to carefully determine the effect of these antibodies on other cells and other cellular functions within the body.”

The researchers are now conducting follow-up experiments, but they believe their results support the use of anti-CD44 antibodies to treat different types of AML.

AML cells

Image by Lance Liotta

New research appears to explain how antibodies that target CD44 fight acute myeloid leukemia (AML).

Previous research showed that anti-CD44 antibodies inhibit proliferation and induce differentiation in AML, but it wasn’t clear how or why this happens.

The new study suggests anti-CD44 antibodies work by inhibiting 2 “major players” of the PI3K/Akt/mTOR pathway—mTORC1 and mTORC2.

Jasmeen Merzaban, PhD, of King Abdullah University of Science and Technology in Thuwal, Saudi Arabia, and her colleagues described this discovery in a letter to Leukemia.

The researchers tested an anti-CD44 antibody known as A3D8 in cell lines representing different AML subtypes (HL60, THP-1, and KG1a) as well as a mouse model of AML.

In these experiments, A3D8 inhibited proliferation and induced differentiation in AML cells. This was accompanied by a decrease in phosphorylation of the mTORC1 and mTORC2 complexes, which was strongly correlated with inhibition of the PI3K/Akt pathway.

The researchers said this finding is important because a complete shutdown of mTOR signaling is probably needed to disrupt the multiple feedback loops that can fuel AML growth, and drugs that only inhibit one of these complexes have, in the past, failed to demonstrate a therapeutic benefit for patients with AML.

“A growing body of evidence suggests that a broader inhibitor would result in a more potent therapeutic effect,” Dr Merzaban said.

She and her colleagues believe an anti-CD44 antibody like A3D8 might just be that type of inhibitor.

They also noted that A3D8 was able to induce differentiation in different subtypes of AML and did not seem to present any toxicity issues.

“We show that the anti-CD44 antibody used for our studies had no effect on normal blood cells,” said Samah Gadhoum, PhD, a research scientist in Dr Merzaban’s lab.

“However, more work is needed to carefully determine the effect of these antibodies on other cells and other cellular functions within the body.”

The researchers are now conducting follow-up experiments, but they believe their results support the use of anti-CD44 antibodies to treat different types of AML.

Clinician and cancer patient

Photo courtesy of NCI Clinical

Center/Mathews Media Group

Expectations may not correspond to reality for cancer patients considering enrollment in phase 1 trials, according to a study published in Cancer.

The study showed that, even after consulting with clinicians, nearly half of patients expected their tumors would shrink during the trial, and some patients expected to be cured.

In reality, the typical response rates of phase 1 cancer trials range from 4% to 20%, and patients survive for a median of 6 months.

Udai Banerji, MD, PhD, of The Institute of Cancer Research in London, England, and his colleagues conducted this study.

The team explored patients’ motivations for considering participation in phase 1 trials and assessed their expectations both before and after they consulted with clinicians.

The study included 396 patients who were considering enrollment in a phase 1 trial. All of these patients completed questionnaires prior to a consultation with a clinician, and 301 completed an abbreviated follow-up questionnaire after their consultation.

A majority of the patients said they were willing to enroll in a trial—72% pre-consultation and 84% after.

Before their consultation, 84% of patients ranked the possibility of tumor shrinkage as the most important reason for considering a phase 1 trial.

Fifty-six percent of patients said the most important reason was a lack of alternative treatments, 44% said it was their physician’s recommendation, and 38% said it was the possibility that the research might benefit others. (Patients could give the same rank to multiple reasons.)

Before their consultation, 43% of patients predicted their tumors would shrink if they participated in a trial. After the consultation, this increased to 47%, and 14% of patients thought they would be cured by participating in the trial. (Patients were not asked about the possibility of cure in the pre-consultation questionnaire.)

Before their consultation, 71% of patients said they expected moderate side effects related to the treatment being tested. This increased to 77% after the consultation. Only 11% of patients expected severe side effects pre-consultation, a figure that decreased to 7% after consultation.

Before consultation, about half of patients did not expect that weekly hospital visits would be required for participation in the trial. After the consultation, 93% of patients expected weekly visits.

“There is a positive message in this [study], which is that 84% of patients are willing to participate in phase 1 oncology studies after a discussion with clinical and nursing staff who lay out the conservative estimates of benefit and requirements of hospital visits,” Dr Banerji said.

“This is good for current and future patients and cancer medicine in general. [However,] the high percentage of patients expecting their tumors to shrink was a sobering finding. This creates a challenge for healthcare professionals to manage expectations but to do so without being patronizing or dismissing human hope.”

Clinician and cancer patient

Photo courtesy of NCI Clinical

Center/Mathews Media Group

Expectations may not correspond to reality for cancer patients considering enrollment in phase 1 trials, according to a study published in Cancer.

The study showed that, even after consulting with clinicians, nearly half of patients expected their tumors would shrink during the trial, and some patients expected to be cured.

In reality, the typical response rates of phase 1 cancer trials range from 4% to 20%, and patients survive for a median of 6 months.

Udai Banerji, MD, PhD, of The Institute of Cancer Research in London, England, and his colleagues conducted this study.

The team explored patients’ motivations for considering participation in phase 1 trials and assessed their expectations both before and after they consulted with clinicians.

The study included 396 patients who were considering enrollment in a phase 1 trial. All of these patients completed questionnaires prior to a consultation with a clinician, and 301 completed an abbreviated follow-up questionnaire after their consultation.

A majority of the patients said they were willing to enroll in a trial—72% pre-consultation and 84% after.

Before their consultation, 84% of patients ranked the possibility of tumor shrinkage as the most important reason for considering a phase 1 trial.

Fifty-six percent of patients said the most important reason was a lack of alternative treatments, 44% said it was their physician’s recommendation, and 38% said it was the possibility that the research might benefit others. (Patients could give the same rank to multiple reasons.)

Before their consultation, 43% of patients predicted their tumors would shrink if they participated in a trial. After the consultation, this increased to 47%, and 14% of patients thought they would be cured by participating in the trial. (Patients were not asked about the possibility of cure in the pre-consultation questionnaire.)

Before their consultation, 71% of patients said they expected moderate side effects related to the treatment being tested. This increased to 77% after the consultation. Only 11% of patients expected severe side effects pre-consultation, a figure that decreased to 7% after consultation.

Before consultation, about half of patients did not expect that weekly hospital visits would be required for participation in the trial. After the consultation, 93% of patients expected weekly visits.

“There is a positive message in this [study], which is that 84% of patients are willing to participate in phase 1 oncology studies after a discussion with clinical and nursing staff who lay out the conservative estimates of benefit and requirements of hospital visits,” Dr Banerji said.

“This is good for current and future patients and cancer medicine in general. [However,] the high percentage of patients expecting their tumors to shrink was a sobering finding. This creates a challenge for healthcare professionals to manage expectations but to do so without being patronizing or dismissing human hope.”

Clinician and cancer patient

Photo courtesy of NCI Clinical

Center/Mathews Media Group

Expectations may not correspond to reality for cancer patients considering enrollment in phase 1 trials, according to a study published in Cancer.

The study showed that, even after consulting with clinicians, nearly half of patients expected their tumors would shrink during the trial, and some patients expected to be cured.

In reality, the typical response rates of phase 1 cancer trials range from 4% to 20%, and patients survive for a median of 6 months.

Udai Banerji, MD, PhD, of The Institute of Cancer Research in London, England, and his colleagues conducted this study.

The team explored patients’ motivations for considering participation in phase 1 trials and assessed their expectations both before and after they consulted with clinicians.

The study included 396 patients who were considering enrollment in a phase 1 trial. All of these patients completed questionnaires prior to a consultation with a clinician, and 301 completed an abbreviated follow-up questionnaire after their consultation.

A majority of the patients said they were willing to enroll in a trial—72% pre-consultation and 84% after.

Before their consultation, 84% of patients ranked the possibility of tumor shrinkage as the most important reason for considering a phase 1 trial.

Fifty-six percent of patients said the most important reason was a lack of alternative treatments, 44% said it was their physician’s recommendation, and 38% said it was the possibility that the research might benefit others. (Patients could give the same rank to multiple reasons.)

Before their consultation, 43% of patients predicted their tumors would shrink if they participated in a trial. After the consultation, this increased to 47%, and 14% of patients thought they would be cured by participating in the trial. (Patients were not asked about the possibility of cure in the pre-consultation questionnaire.)

Before their consultation, 71% of patients said they expected moderate side effects related to the treatment being tested. This increased to 77% after the consultation. Only 11% of patients expected severe side effects pre-consultation, a figure that decreased to 7% after consultation.

Before consultation, about half of patients did not expect that weekly hospital visits would be required for participation in the trial. After the consultation, 93% of patients expected weekly visits.

“There is a positive message in this [study], which is that 84% of patients are willing to participate in phase 1 oncology studies after a discussion with clinical and nursing staff who lay out the conservative estimates of benefit and requirements of hospital visits,” Dr Banerji said.

“This is good for current and future patients and cancer medicine in general. [However,] the high percentage of patients expecting their tumors to shrink was a sobering finding. This creates a challenge for healthcare professionals to manage expectations but to do so without being patronizing or dismissing human hope.”

Colony of iPSCs

Image from Salk Institute

A study published in Cell Reports indicates that BET inhibitors can improve the reprogramming of human fibroblasts to create induced pluripotent stem cells (iPSCs).

According to researchers, this improvement in reprogramming can increase the yield of iPSCs from fibroblasts and enhance the quality of the iPSCs by ensuring that more somatic genes are efficiently turned down or turned off during reprogramming.

Study author Kejin Hu, PhD, of the University of Alabama at Birmingham, said the factors that are commonly used to create iPSCs from fibroblasts face a reprogramming barrier.

“If we can lower the barrier, we can enhance the reprogramming efficiency,” he explained. “My strategy is to use chemicals to erase the transcriptional program specific to the starting cells.”

Dr Hu and his colleagues found that BET-specific chemical inhibitors were effective in this regard.

For example, a low concentration of the BET inhibitor JQ1:

• Downregulated 390 fibroblast-specific genes when applied to naïve human fibroblasts
• Downregulated 651 fibroblast-specific genes when applied to human fibroblasts during reprogramming
• Increased the efficiency of successful reprogramming of human fibroblasts to iPSCs by 20-fold.

The researchers also found that fibroblasts change shape when treated with JQ1.

The cells transform from a long spindle shape to polygonal or rounded cells, which shows loss of fibroblast identity and transition to pluripotent stem cells. Presumably, genes that are needed to maintain the spindle shape are downregulated by JQ1.

Dr Hu proposed the following model to explain his team’s findings.

During normal cell division, active fibroblast genes are “bookmarked” by the attachment of BET proteins to acetylated chromatin during the mitotic phases, while RNA Polymerase II drops off of the chromatin.

At the start of interphase, these bookmarks guide the polymerase back to the genes, and they are transcribed by RNA Polymerase II.

In contrast, when JQ1 is added, the active fibroblast genes are de-bookmarked by the interaction of JQ1 with the BET proteins during the mitotic phases of cell division.

This “erases” the epigenetic memory of fibroblast gene expression, which, in turn, results in loss of fibroblast gene transcription when interphase returns.

This also increases the success of reprogramming into iPSCs.

Colony of iPSCs

Image from Salk Institute

A study published in Cell Reports indicates that BET inhibitors can improve the reprogramming of human fibroblasts to create induced pluripotent stem cells (iPSCs).

According to researchers, this improvement in reprogramming can increase the yield of iPSCs from fibroblasts and enhance the quality of the iPSCs by ensuring that more somatic genes are efficiently turned down or turned off during reprogramming.

Study author Kejin Hu, PhD, of the University of Alabama at Birmingham, said the factors that are commonly used to create iPSCs from fibroblasts face a reprogramming barrier.

“If we can lower the barrier, we can enhance the reprogramming efficiency,” he explained. “My strategy is to use chemicals to erase the transcriptional program specific to the starting cells.”

Dr Hu and his colleagues found that BET-specific chemical inhibitors were effective in this regard.

For example, a low concentration of the BET inhibitor JQ1:

• Downregulated 390 fibroblast-specific genes when applied to naïve human fibroblasts
• Downregulated 651 fibroblast-specific genes when applied to human fibroblasts during reprogramming
• Increased the efficiency of successful reprogramming of human fibroblasts to iPSCs by 20-fold.

The researchers also found that fibroblasts change shape when treated with JQ1.

The cells transform from a long spindle shape to polygonal or rounded cells, which shows loss of fibroblast identity and transition to pluripotent stem cells. Presumably, genes that are needed to maintain the spindle shape are downregulated by JQ1.

Dr Hu proposed the following model to explain his team’s findings.

During normal cell division, active fibroblast genes are “bookmarked” by the attachment of BET proteins to acetylated chromatin during the mitotic phases, while RNA Polymerase II drops off of the chromatin.

At the start of interphase, these bookmarks guide the polymerase back to the genes, and they are transcribed by RNA Polymerase II.

In contrast, when JQ1 is added, the active fibroblast genes are de-bookmarked by the interaction of JQ1 with the BET proteins during the mitotic phases of cell division.

This “erases” the epigenetic memory of fibroblast gene expression, which, in turn, results in loss of fibroblast gene transcription when interphase returns.

This also increases the success of reprogramming into iPSCs.

Colony of iPSCs

Image from Salk Institute

A study published in Cell Reports indicates that BET inhibitors can improve the reprogramming of human fibroblasts to create induced pluripotent stem cells (iPSCs).

According to researchers, this improvement in reprogramming can increase the yield of iPSCs from fibroblasts and enhance the quality of the iPSCs by ensuring that more somatic genes are efficiently turned down or turned off during reprogramming.

Study author Kejin Hu, PhD, of the University of Alabama at Birmingham, said the factors that are commonly used to create iPSCs from fibroblasts face a reprogramming barrier.

“If we can lower the barrier, we can enhance the reprogramming efficiency,” he explained. “My strategy is to use chemicals to erase the transcriptional program specific to the starting cells.”

Dr Hu and his colleagues found that BET-specific chemical inhibitors were effective in this regard.

For example, a low concentration of the BET inhibitor JQ1:

• Downregulated 390 fibroblast-specific genes when applied to naïve human fibroblasts
• Downregulated 651 fibroblast-specific genes when applied to human fibroblasts during reprogramming
• Increased the efficiency of successful reprogramming of human fibroblasts to iPSCs by 20-fold.

The researchers also found that fibroblasts change shape when treated with JQ1.

The cells transform from a long spindle shape to polygonal or rounded cells, which shows loss of fibroblast identity and transition to pluripotent stem cells. Presumably, genes that are needed to maintain the spindle shape are downregulated by JQ1.

Dr Hu proposed the following model to explain his team’s findings.

During normal cell division, active fibroblast genes are “bookmarked” by the attachment of BET proteins to acetylated chromatin during the mitotic phases, while RNA Polymerase II drops off of the chromatin.

At the start of interphase, these bookmarks guide the polymerase back to the genes, and they are transcribed by RNA Polymerase II.

In contrast, when JQ1 is added, the active fibroblast genes are de-bookmarked by the interaction of JQ1 with the BET proteins during the mitotic phases of cell division.

This “erases” the epigenetic memory of fibroblast gene expression, which, in turn, results in loss of fibroblast gene transcription when interphase returns.

This also increases the success of reprogramming into iPSCs.

The prevalence of amyotrophic lateral sclerosis (ALS) seems to have gone up—from 4.7 cases per 100,000 in 2012 to 5.0 cases per 100,000 in 2013. But “seems” is the operative word, according to researchers writing in the August 5, 2016, Morbidity and Mortality Weekly Report. It is more likely that the increase is attributable to better detection methods, remarked Paul Mehta, MD, medical epidemiologist and principal investigator of the National ALS Registry and lead author of the report.

Related: A Combined Treatment Protocol for Patients With Diabetic Peripheral Neuropathy

He also credits greater public awareness of the registry, which is the only available data source that can be used to estimate the prevalence of ALS in the U.S. Because ALS is not a nationally notifiable disease, the registry uses administrative data from Medicare, Medicaid, and the VHA to determine “definite” cases. It also uses a secure web portal (https://wwwn.cdc.gov/als/) to identify cases not included in the national administrative databases.

Related: Amyotrophic Lateral Sclerosis, Nutrition, and Feeding Tube Placement

This fall, the registry will launch the National ALS Biorepository, which will store samples (eg, blood, hair, or saliva) from home visits and postmortem collection (eg, brain, bone, spinal cord). Currently, the few existing ALS biorepositories largely rely on samples from specific clinics or medical practices or clinical trials. The specimens for National ALS Biorepository will be collected from a geographically representative sample of people with ALS. The specimens will be used for research, such as genetic analysis, identification of biomarkers, and exposure to environmental toxic substances.

The full report is available at www.cdc.gov/mmwr/index2016.html.

The prevalence of amyotrophic lateral sclerosis (ALS) seems to have gone up—from 4.7 cases per 100,000 in 2012 to 5.0 cases per 100,000 in 2013. But “seems” is the operative word, according to researchers writing in the August 5, 2016, Morbidity and Mortality Weekly Report. It is more likely that the increase is attributable to better detection methods, remarked Paul Mehta, MD, medical epidemiologist and principal investigator of the National ALS Registry and lead author of the report.

Related: A Combined Treatment Protocol for Patients With Diabetic Peripheral Neuropathy

He also credits greater public awareness of the registry, which is the only available data source that can be used to estimate the prevalence of ALS in the U.S. Because ALS is not a nationally notifiable disease, the registry uses administrative data from Medicare, Medicaid, and the VHA to determine “definite” cases. It also uses a secure web portal (https://wwwn.cdc.gov/als/) to identify cases not included in the national administrative databases.

Related: Amyotrophic Lateral Sclerosis, Nutrition, and Feeding Tube Placement

This fall, the registry will launch the National ALS Biorepository, which will store samples (eg, blood, hair, or saliva) from home visits and postmortem collection (eg, brain, bone, spinal cord). Currently, the few existing ALS biorepositories largely rely on samples from specific clinics or medical practices or clinical trials. The specimens for National ALS Biorepository will be collected from a geographically representative sample of people with ALS. The specimens will be used for research, such as genetic analysis, identification of biomarkers, and exposure to environmental toxic substances.

The full report is available at www.cdc.gov/mmwr/index2016.html.

The prevalence of amyotrophic lateral sclerosis (ALS) seems to have gone up—from 4.7 cases per 100,000 in 2012 to 5.0 cases per 100,000 in 2013. But “seems” is the operative word, according to researchers writing in the August 5, 2016, Morbidity and Mortality Weekly Report. It is more likely that the increase is attributable to better detection methods, remarked Paul Mehta, MD, medical epidemiologist and principal investigator of the National ALS Registry and lead author of the report.

Related: A Combined Treatment Protocol for Patients With Diabetic Peripheral Neuropathy

He also credits greater public awareness of the registry, which is the only available data source that can be used to estimate the prevalence of ALS in the U.S. Because ALS is not a nationally notifiable disease, the registry uses administrative data from Medicare, Medicaid, and the VHA to determine “definite” cases. It also uses a secure web portal (https://wwwn.cdc.gov/als/) to identify cases not included in the national administrative databases.

Related: Amyotrophic Lateral Sclerosis, Nutrition, and Feeding Tube Placement

This fall, the registry will launch the National ALS Biorepository, which will store samples (eg, blood, hair, or saliva) from home visits and postmortem collection (eg, brain, bone, spinal cord). Currently, the few existing ALS biorepositories largely rely on samples from specific clinics or medical practices or clinical trials. The specimens for National ALS Biorepository will be collected from a geographically representative sample of people with ALS. The specimens will be used for research, such as genetic analysis, identification of biomarkers, and exposure to environmental toxic substances.

The full report is available at www.cdc.gov/mmwr/index2016.html.

Pregnant woman

Photo by Nina Matthews

Research has shown that women have an increased risk of venous thromboembolism (VTE) after giving birth, but it’s believed that a cesarean section (CS) leaves a woman more vulnerable to VTE than a vaginal delivery (VD).

A meta-analysis published in CHEST supports this idea. The data showed that CS carried a greater risk of VTE than VD, and emergency CS was associated with a greater risk than elective CS.

“We found that CS is an important, independent risk factor for the development of VTE in the postpartum period and that approximately 3 VTE will occur for every 1000 CS performed, with greater risks for nonscheduled, emergency CS,” said study investigator Marc Blondon, MD, of Geneva University Hospitals in Geneva, Switzerland.

Analysis results

Dr Blondon and his colleagues evaluated 28 studies (most of them retrospective) comparing the risk of VTE after CS and VD (>53,000 VTEs) and 32 prospective studies reporting the risk of VTE after CS (218 VTEs).

In unadjusted analyses of the individual studies, the risk of VTE was 1 to 22 times higher after CS than after VD. The pooled random effect odds ratio (OR) was 3.7 (95% CI, 3.0-4.6).

The investigators said adjusting analyses for at least maternal age had a marginal effect in the 7 studies that included both univariate and multivariate analyses. The OR comparing CS with VD was 3.3 (95% CI, 2.5-4.5) in univariate analyses and 2.8 (95% CI, 2.1-3.8) in adjusted analyses.

Similarly, adjusting analyses for both maternal age and body mass index had a slight effect in the 4 studies in which researchers adjusted for at least these 2 factors. The pooled OR was 2.8 (95% CI, 2.1-3.7) in crude analyses and 2.5 (95% CI, 1.8-3.1) in adjusted analyses.

When the investigators combined all 7 studies reporting adjusted risk estimates, the OR was 2.7 (95% CI, 2.2-3.3).

The data also showed an increased risk of VTE for both elective and emergency CS when compared to VD. The pooled ORs were 2.3 (95% CI, 1.7-3.1) for elective CS and 3.6 (95% CI, 2.8-4.7) for emergency CS.

After adjustment (in 6 studies), the pooled ORs were 2.1 for elective CS and 2.8 for emergency CS.

Explanations and implications

The investigators noted that pregnant women become more susceptible to VTE due to a variety of factors, including venous stasis and trauma associated with delivery. In addition, hemostatic changes drive increases in some coagulation factors while decreasing bleeding inhibitors.

For some reason, these changes seem to be worse for women who deliver via CS.

“In the postpartum period specifically, women following CS exhibit greater activation of coagulation than women following VD, as reflected by greater D-dimer levels,” Dr Blondon explained.

“This outcome may be a result of the conditions leading to the CS or to the procedure itself, similar to the increased VTE risk following non-obstetric surgery. Furthermore, physical activity is reduced following CS compared with following VD, with delayed recovery of mobility occurring in the first 2 days following delivery.”

Dr Blondon and his colleagues said this study helps shed some light on VTE risks associated with CS. Practitioners should be aware of the risks, and further research is needed to plot the best course of action and inform future guidelines concerning thromboprophylaxis.

“Thromboprophylaxis [after CS] seems widely underutilized in the United States,” Dr Blondon said. “It is estimated that 75% of women following CS do not receive any prophylaxis in the postpartum period. This scenario may arise from a lack of recognition by care providers of the risk of VTE following CS.”

“Preventing postpartum VTE following CS may lead to an important reduction of its associated morbidity and mortality from a public health perspective. In this setting, further observational studies and randomized trials are needed to better appreciate the risks of VTE in specific groups following CS and to define the efficacy and safety of thromboprophylaxis.”

Pregnant woman

Photo by Nina Matthews

Research has shown that women have an increased risk of venous thromboembolism (VTE) after giving birth, but it’s believed that a cesarean section (CS) leaves a woman more vulnerable to VTE than a vaginal delivery (VD).

A meta-analysis published in CHEST supports this idea. The data showed that CS carried a greater risk of VTE than VD, and emergency CS was associated with a greater risk than elective CS.

“We found that CS is an important, independent risk factor for the development of VTE in the postpartum period and that approximately 3 VTE will occur for every 1000 CS performed, with greater risks for nonscheduled, emergency CS,” said study investigator Marc Blondon, MD, of Geneva University Hospitals in Geneva, Switzerland.

Analysis results

Dr Blondon and his colleagues evaluated 28 studies (most of them retrospective) comparing the risk of VTE after CS and VD (>53,000 VTEs) and 32 prospective studies reporting the risk of VTE after CS (218 VTEs).

In unadjusted analyses of the individual studies, the risk of VTE was 1 to 22 times higher after CS than after VD. The pooled random effect odds ratio (OR) was 3.7 (95% CI, 3.0-4.6).

The investigators said adjusting analyses for at least maternal age had a marginal effect in the 7 studies that included both univariate and multivariate analyses. The OR comparing CS with VD was 3.3 (95% CI, 2.5-4.5) in univariate analyses and 2.8 (95% CI, 2.1-3.8) in adjusted analyses.

Similarly, adjusting analyses for both maternal age and body mass index had a slight effect in the 4 studies in which researchers adjusted for at least these 2 factors. The pooled OR was 2.8 (95% CI, 2.1-3.7) in crude analyses and 2.5 (95% CI, 1.8-3.1) in adjusted analyses.

When the investigators combined all 7 studies reporting adjusted risk estimates, the OR was 2.7 (95% CI, 2.2-3.3).

The data also showed an increased risk of VTE for both elective and emergency CS when compared to VD. The pooled ORs were 2.3 (95% CI, 1.7-3.1) for elective CS and 3.6 (95% CI, 2.8-4.7) for emergency CS.

After adjustment (in 6 studies), the pooled ORs were 2.1 for elective CS and 2.8 for emergency CS.

Explanations and implications

The investigators noted that pregnant women become more susceptible to VTE due to a variety of factors, including venous stasis and trauma associated with delivery. In addition, hemostatic changes drive increases in some coagulation factors while decreasing bleeding inhibitors.

For some reason, these changes seem to be worse for women who deliver via CS.

“In the postpartum period specifically, women following CS exhibit greater activation of coagulation than women following VD, as reflected by greater D-dimer levels,” Dr Blondon explained.

“This outcome may be a result of the conditions leading to the CS or to the procedure itself, similar to the increased VTE risk following non-obstetric surgery. Furthermore, physical activity is reduced following CS compared with following VD, with delayed recovery of mobility occurring in the first 2 days following delivery.”

Dr Blondon and his colleagues said this study helps shed some light on VTE risks associated with CS. Practitioners should be aware of the risks, and further research is needed to plot the best course of action and inform future guidelines concerning thromboprophylaxis.

“Thromboprophylaxis [after CS] seems widely underutilized in the United States,” Dr Blondon said. “It is estimated that 75% of women following CS do not receive any prophylaxis in the postpartum period. This scenario may arise from a lack of recognition by care providers of the risk of VTE following CS.”

“Preventing postpartum VTE following CS may lead to an important reduction of its associated morbidity and mortality from a public health perspective. In this setting, further observational studies and randomized trials are needed to better appreciate the risks of VTE in specific groups following CS and to define the efficacy and safety of thromboprophylaxis.”

Pregnant woman

Photo by Nina Matthews

Research has shown that women have an increased risk of venous thromboembolism (VTE) after giving birth, but it’s believed that a cesarean section (CS) leaves a woman more vulnerable to VTE than a vaginal delivery (VD).

A meta-analysis published in CHEST supports this idea. The data showed that CS carried a greater risk of VTE than VD, and emergency CS was associated with a greater risk than elective CS.

“We found that CS is an important, independent risk factor for the development of VTE in the postpartum period and that approximately 3 VTE will occur for every 1000 CS performed, with greater risks for nonscheduled, emergency CS,” said study investigator Marc Blondon, MD, of Geneva University Hospitals in Geneva, Switzerland.

Analysis results

Dr Blondon and his colleagues evaluated 28 studies (most of them retrospective) comparing the risk of VTE after CS and VD (>53,000 VTEs) and 32 prospective studies reporting the risk of VTE after CS (218 VTEs).

In unadjusted analyses of the individual studies, the risk of VTE was 1 to 22 times higher after CS than after VD. The pooled random effect odds ratio (OR) was 3.7 (95% CI, 3.0-4.6).

The investigators said adjusting analyses for at least maternal age had a marginal effect in the 7 studies that included both univariate and multivariate analyses. The OR comparing CS with VD was 3.3 (95% CI, 2.5-4.5) in univariate analyses and 2.8 (95% CI, 2.1-3.8) in adjusted analyses.

Similarly, adjusting analyses for both maternal age and body mass index had a slight effect in the 4 studies in which researchers adjusted for at least these 2 factors. The pooled OR was 2.8 (95% CI, 2.1-3.7) in crude analyses and 2.5 (95% CI, 1.8-3.1) in adjusted analyses.

When the investigators combined all 7 studies reporting adjusted risk estimates, the OR was 2.7 (95% CI, 2.2-3.3).

The data also showed an increased risk of VTE for both elective and emergency CS when compared to VD. The pooled ORs were 2.3 (95% CI, 1.7-3.1) for elective CS and 3.6 (95% CI, 2.8-4.7) for emergency CS.

After adjustment (in 6 studies), the pooled ORs were 2.1 for elective CS and 2.8 for emergency CS.

Explanations and implications

The investigators noted that pregnant women become more susceptible to VTE due to a variety of factors, including venous stasis and trauma associated with delivery. In addition, hemostatic changes drive increases in some coagulation factors while decreasing bleeding inhibitors.

For some reason, these changes seem to be worse for women who deliver via CS.

“In the postpartum period specifically, women following CS exhibit greater activation of coagulation than women following VD, as reflected by greater D-dimer levels,” Dr Blondon explained.

“This outcome may be a result of the conditions leading to the CS or to the procedure itself, similar to the increased VTE risk following non-obstetric surgery. Furthermore, physical activity is reduced following CS compared with following VD, with delayed recovery of mobility occurring in the first 2 days following delivery.”

Dr Blondon and his colleagues said this study helps shed some light on VTE risks associated with CS. Practitioners should be aware of the risks, and further research is needed to plot the best course of action and inform future guidelines concerning thromboprophylaxis.

“Thromboprophylaxis [after CS] seems widely underutilized in the United States,” Dr Blondon said. “It is estimated that 75% of women following CS do not receive any prophylaxis in the postpartum period. This scenario may arise from a lack of recognition by care providers of the risk of VTE following CS.”

“Preventing postpartum VTE following CS may lead to an important reduction of its associated morbidity and mortality from a public health perspective. In this setting, further observational studies and randomized trials are needed to better appreciate the risks of VTE in specific groups following CS and to define the efficacy and safety of thromboprophylaxis.”

In 2012, a survey found that 1 in 4 American adults had > 1 chronic health condition. In 2014, the National Health Interview Survey of 36,697 adults found the same thing. The stable prevalence of multiple chronic conditions (MCC) indicates a continuing public health issue, according to an article in the July 29, 2016 Morbidity and Mortality Weekly Report.

The prevalence varied across the country, from 19% in Colorado to 38% in Kentucky. Prevalence was higher than the national average percentage in Alabama, West Virginia, Mississippi, Montana, New Mexico, Maine, Michigan, Ohio, and Pennsylvania.

Several states with higher prevalence of MCC overlapped the so-called stroke belt, which includes much of the southern U.S. Similarly, MCC prevalence also overlapped the diabetes belt—again taking in much of the South and parts of the Midwest and West.

The survey covered 10 conditions: arthritis, asthma, cancer, chronic obstructive pulmonary disease, coronary artery disease, diabetes, hepatitis, hypertension, stroke, and weak or failing kidneys. But those are only 10 of the 20 conditions HHS has identified for inclusion in studies of MCC. Moreover, no data on mental health conditions, undiagnosed conditions, or adults in long-term care or congregant facilities were included, so the findings are limited in generalizability. Nonetheless, the MMWR report authors say the findings further HHS research and surveillance objectives. Geographic disparities in MCC prevalence can inform state-level surveillance programs and groups targeting service delivery or allocating resources.

In 2012, a survey found that 1 in 4 American adults had > 1 chronic health condition. In 2014, the National Health Interview Survey of 36,697 adults found the same thing. The stable prevalence of multiple chronic conditions (MCC) indicates a continuing public health issue, according to an article in the July 29, 2016 Morbidity and Mortality Weekly Report.

The prevalence varied across the country, from 19% in Colorado to 38% in Kentucky. Prevalence was higher than the national average percentage in Alabama, West Virginia, Mississippi, Montana, New Mexico, Maine, Michigan, Ohio, and Pennsylvania.

Several states with higher prevalence of MCC overlapped the so-called stroke belt, which includes much of the southern U.S. Similarly, MCC prevalence also overlapped the diabetes belt—again taking in much of the South and parts of the Midwest and West.

The survey covered 10 conditions: arthritis, asthma, cancer, chronic obstructive pulmonary disease, coronary artery disease, diabetes, hepatitis, hypertension, stroke, and weak or failing kidneys. But those are only 10 of the 20 conditions HHS has identified for inclusion in studies of MCC. Moreover, no data on mental health conditions, undiagnosed conditions, or adults in long-term care or congregant facilities were included, so the findings are limited in generalizability. Nonetheless, the MMWR report authors say the findings further HHS research and surveillance objectives. Geographic disparities in MCC prevalence can inform state-level surveillance programs and groups targeting service delivery or allocating resources.

In 2012, a survey found that 1 in 4 American adults had > 1 chronic health condition. In 2014, the National Health Interview Survey of 36,697 adults found the same thing. The stable prevalence of multiple chronic conditions (MCC) indicates a continuing public health issue, according to an article in the July 29, 2016 Morbidity and Mortality Weekly Report.

The prevalence varied across the country, from 19% in Colorado to 38% in Kentucky. Prevalence was higher than the national average percentage in Alabama, West Virginia, Mississippi, Montana, New Mexico, Maine, Michigan, Ohio, and Pennsylvania.

Several states with higher prevalence of MCC overlapped the so-called stroke belt, which includes much of the southern U.S. Similarly, MCC prevalence also overlapped the diabetes belt—again taking in much of the South and parts of the Midwest and West.

The survey covered 10 conditions: arthritis, asthma, cancer, chronic obstructive pulmonary disease, coronary artery disease, diabetes, hepatitis, hypertension, stroke, and weak or failing kidneys. But those are only 10 of the 20 conditions HHS has identified for inclusion in studies of MCC. Moreover, no data on mental health conditions, undiagnosed conditions, or adults in long-term care or congregant facilities were included, so the findings are limited in generalizability. Nonetheless, the MMWR report authors say the findings further HHS research and surveillance objectives. Geographic disparities in MCC prevalence can inform state-level surveillance programs and groups targeting service delivery or allocating resources.

Did you know that you can honor a family member, friend, or colleague through a gift to the AGA Research Foundation? A simple, flexible, and versatile way to ensure the AGA Research Foundation can continue our work for years to come is a gift in your will or living trust, known as a charitable bequest. To make a charitable gift in a will, you need a current will or living trust.

You can include a gift in your will or living trust stating that a specific asset, certain dollar amount, or – more commonly – a percentage of your estate will pass to the AGA following your death in honor of your loved one. A gift of $50,000 or more in your will qualifies for membership in the AGA Legacy Society.

We hope you’ll consider including a gift to the AGA Research Foundation in your will or living trust. It’s simple – just a few sentences in your will or trust are all that is needed. The official bequest language for the AGA Research Foundation is: “I, [name], of [city, state, ZIP], give, devise and bequeath to the AGA Research Foundation [written amount or percentage of the estate or description of property] for its unrestricted use and purpose.”

For more information on how to give and recognize your loved one, contact Harmony Excellent at 301-272-1602 or [email protected] or visit http://gastro.planmylegacy.org/.

[email protected]

Did you know that you can honor a family member, friend, or colleague through a gift to the AGA Research Foundation? A simple, flexible, and versatile way to ensure the AGA Research Foundation can continue our work for years to come is a gift in your will or living trust, known as a charitable bequest. To make a charitable gift in a will, you need a current will or living trust.

You can include a gift in your will or living trust stating that a specific asset, certain dollar amount, or – more commonly – a percentage of your estate will pass to the AGA following your death in honor of your loved one. A gift of $50,000 or more in your will qualifies for membership in the AGA Legacy Society.

We hope you’ll consider including a gift to the AGA Research Foundation in your will or living trust. It’s simple – just a few sentences in your will or trust are all that is needed. The official bequest language for the AGA Research Foundation is: “I, [name], of [city, state, ZIP], give, devise and bequeath to the AGA Research Foundation [written amount or percentage of the estate or description of property] for its unrestricted use and purpose.”

For more information on how to give and recognize your loved one, contact Harmony Excellent at 301-272-1602 or [email protected] or visit http://gastro.planmylegacy.org/.

[email protected]

Did you know that you can honor a family member, friend, or colleague through a gift to the AGA Research Foundation? A simple, flexible, and versatile way to ensure the AGA Research Foundation can continue our work for years to come is a gift in your will or living trust, known as a charitable bequest. To make a charitable gift in a will, you need a current will or living trust.

You can include a gift in your will or living trust stating that a specific asset, certain dollar amount, or – more commonly – a percentage of your estate will pass to the AGA following your death in honor of your loved one. A gift of $50,000 or more in your will qualifies for membership in the AGA Legacy Society.

We hope you’ll consider including a gift to the AGA Research Foundation in your will or living trust. It’s simple – just a few sentences in your will or trust are all that is needed. The official bequest language for the AGA Research Foundation is: “I, [name], of [city, state, ZIP], give, devise and bequeath to the AGA Research Foundation [written amount or percentage of the estate or description of property] for its unrestricted use and purpose.”

For more information on how to give and recognize your loved one, contact Harmony Excellent at 301-272-1602 or [email protected] or visit http://gastro.planmylegacy.org/.

[email protected]

Cellular and Molecular Gastroenterology and Hepatology (CMGH) – AGA’s newest scientific journal, which launched in January 2015 – has been accepted to PubMed Central. This means that all CMGH articles, beginning with the very first issue of the journal, will now be available when you search in the PubMed database. Articles should be available by the end of September.

Being searchable in PubMed will increase the visibility of the high-quality digestive biology research published in CMGH, and will also allow easier access to journal content.

Visit the journal at www.cmghjournal.org.

[email protected]

Cellular and Molecular Gastroenterology and Hepatology (CMGH) – AGA’s newest scientific journal, which launched in January 2015 – has been accepted to PubMed Central. This means that all CMGH articles, beginning with the very first issue of the journal, will now be available when you search in the PubMed database. Articles should be available by the end of September.

Being searchable in PubMed will increase the visibility of the high-quality digestive biology research published in CMGH, and will also allow easier access to journal content.

Visit the journal at www.cmghjournal.org.

[email protected]

Cellular and Molecular Gastroenterology and Hepatology (CMGH) – AGA’s newest scientific journal, which launched in January 2015 – has been accepted to PubMed Central. This means that all CMGH articles, beginning with the very first issue of the journal, will now be available when you search in the PubMed database. Articles should be available by the end of September.

Being searchable in PubMed will increase the visibility of the high-quality digestive biology research published in CMGH, and will also allow easier access to journal content.

Visit the journal at www.cmghjournal.org.

[email protected]

Progress toward value-based care by Medicare and commercial payors will continue regardless of the election outcome in November. The health care market will continue to move away from fee-for-service and toward reimbursement systems that reward physicians for improving the quality of patient care and controlling costs. AGA is shaping the future of practice. We continue to be at the forefront of the value-based movement, creating the tools gastroenterologists need for success in new reimbursement environments and preparing our members for a successful future.

Did you know?

• AGA has created bundle and episode payment models for GI issues, including colonoscopy screening and surveillance and GERD, with obesity to launch in 2016 and more to come. These alternative payment models reward providers for identifying efficiency gains, effectively coordinating patient care and improving quality. By the time the Medicare Access and CHIP Reauthorization Act (MACRA) was enacted in 2015, AGA was ready with fully developed, practical alternative payment model solutions for GI.

• AGA is the only GI society to advocate for Medicare to recognize established GI payment models as advanced alternative payment models (APMs) so that gastroenterologists will have a pathway to greater earnings than under the Merit-based Incentive Payment System (MIPS). Not sure what MACRA, MIPS, and APMs are? AGA can help.

• AGA is also the only GI society to develop a MACRA education tool that explains, in plain language, MACRA’s impact on GIs and offers a customized plan for how to prepare based on your practice situation.

• AGA has established relationships with Medicare and commercial payors that allow us to provide input on coverage decisions. We recognize that payor coverage of procedures and technology plays a vital role in reimbursement success and we take every opportunity to provide payors with input from AGA member experts.

• In addition to AGA’s rigorous, evidence-based clinical practice guidelines, we provide expert reviews and other clinical practice guidance documents to provide best practice advice for physicians in areas in which there is not yet enough literature to produce a clinical guideline. Additionally, Technology Coverage Statements provide support when working with payors on coverage and reimbursement for proven procedures, diagnostics, and therapies that advance the science and practice of gastroenterology and improve care for the patients you treat.

AGA works hard for the gastroenterology field to ensure that you are poised for success under new reimbursement models and will continue to do so. Learn more at http://www.gastro.org/practice-management.

Progress toward value-based care by Medicare and commercial payors will continue regardless of the election outcome in November. The health care market will continue to move away from fee-for-service and toward reimbursement systems that reward physicians for improving the quality of patient care and controlling costs. AGA is shaping the future of practice. We continue to be at the forefront of the value-based movement, creating the tools gastroenterologists need for success in new reimbursement environments and preparing our members for a successful future.

Did you know?

• AGA has created bundle and episode payment models for GI issues, including colonoscopy screening and surveillance and GERD, with obesity to launch in 2016 and more to come. These alternative payment models reward providers for identifying efficiency gains, effectively coordinating patient care and improving quality. By the time the Medicare Access and CHIP Reauthorization Act (MACRA) was enacted in 2015, AGA was ready with fully developed, practical alternative payment model solutions for GI.

• AGA is the only GI society to advocate for Medicare to recognize established GI payment models as advanced alternative payment models (APMs) so that gastroenterologists will have a pathway to greater earnings than under the Merit-based Incentive Payment System (MIPS). Not sure what MACRA, MIPS, and APMs are? AGA can help.

• AGA is also the only GI society to develop a MACRA education tool that explains, in plain language, MACRA’s impact on GIs and offers a customized plan for how to prepare based on your practice situation.

• AGA has established relationships with Medicare and commercial payors that allow us to provide input on coverage decisions. We recognize that payor coverage of procedures and technology plays a vital role in reimbursement success and we take every opportunity to provide payors with input from AGA member experts.

• In addition to AGA’s rigorous, evidence-based clinical practice guidelines, we provide expert reviews and other clinical practice guidance documents to provide best practice advice for physicians in areas in which there is not yet enough literature to produce a clinical guideline. Additionally, Technology Coverage Statements provide support when working with payors on coverage and reimbursement for proven procedures, diagnostics, and therapies that advance the science and practice of gastroenterology and improve care for the patients you treat.

AGA works hard for the gastroenterology field to ensure that you are poised for success under new reimbursement models and will continue to do so. Learn more at http://www.gastro.org/practice-management.

Progress toward value-based care by Medicare and commercial payors will continue regardless of the election outcome in November. The health care market will continue to move away from fee-for-service and toward reimbursement systems that reward physicians for improving the quality of patient care and controlling costs. AGA is shaping the future of practice. We continue to be at the forefront of the value-based movement, creating the tools gastroenterologists need for success in new reimbursement environments and preparing our members for a successful future.

Did you know?

• AGA has created bundle and episode payment models for GI issues, including colonoscopy screening and surveillance and GERD, with obesity to launch in 2016 and more to come. These alternative payment models reward providers for identifying efficiency gains, effectively coordinating patient care and improving quality. By the time the Medicare Access and CHIP Reauthorization Act (MACRA) was enacted in 2015, AGA was ready with fully developed, practical alternative payment model solutions for GI.

• AGA is the only GI society to advocate for Medicare to recognize established GI payment models as advanced alternative payment models (APMs) so that gastroenterologists will have a pathway to greater earnings than under the Merit-based Incentive Payment System (MIPS). Not sure what MACRA, MIPS, and APMs are? AGA can help.

• AGA is also the only GI society to develop a MACRA education tool that explains, in plain language, MACRA’s impact on GIs and offers a customized plan for how to prepare based on your practice situation.

• AGA has established relationships with Medicare and commercial payors that allow us to provide input on coverage decisions. We recognize that payor coverage of procedures and technology plays a vital role in reimbursement success and we take every opportunity to provide payors with input from AGA member experts.

• In addition to AGA’s rigorous, evidence-based clinical practice guidelines, we provide expert reviews and other clinical practice guidance documents to provide best practice advice for physicians in areas in which there is not yet enough literature to produce a clinical guideline. Additionally, Technology Coverage Statements provide support when working with payors on coverage and reimbursement for proven procedures, diagnostics, and therapies that advance the science and practice of gastroenterology and improve care for the patients you treat.

AGA works hard for the gastroenterology field to ensure that you are poised for success under new reimbursement models and will continue to do so. Learn more at http://www.gastro.org/practice-management.

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes

LAS VEGAS – When rheumatologists consider a differential diagnosis that includes seronegative rheumatoid arthritis, they should also consider chikungunya, according to Len Calabrese, DO.

The patient who presents with weeks to months of unexplained arthralgia and perhaps arthritis and a negative autoimmune panel deserves consideration of chikungunya or another arbovirus, said Dr. Calabrese, speaking at the annual Perspectives in Rheumatic Diseases held by the Global Academy for Medical Education.

Among the mosquito-borne arboviruses now in play in the Western Hemisphere, chikungunya is particularly likely to cause long-lasting and sometimes debilitating joint pain weeks and even months after initial infection.

An alphavirus, chikungunya virus makes most affected individuals quite ill, and serum IgG and IgM titers persist long after infection. Testing is straightforward, as long as the virus is a candidate diagnosis, Dr. Calabrese said.

In addition to obtaining an accurate travel history, said Dr. Calabrese, physicians should consider the possibility of autochthonous transmission, which occurs when an infected individual who returns from an endemic area is bitten by mosquitoes once home. Flares of autochthonous transmission can result in pockets of locally heavy transmission far from the zones where chikungunya usually resides.

Dr. Calabrese is chair of clinical immunology and chair of osteopathic research and education at the Cleveland Clinic, and he reported no relevant financial disclosures.

Global Academy for Medical Education and this news organization are owned by the same parent company.

[email protected]

On Twitter @karioakes