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Two NOACs pose lower risk of ICH in real-world study
Photo courtesy of Pfizer
and Bristol-Myers Squibb
ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.
For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.
They found that patients had a similar risk of stroke regardless of which drug they received.
However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.
Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.
“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.
The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.
“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.
During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.
The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.
At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.
“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.
“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”
“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.” 
*Information in the abstract differs from that presented at the meeting.
Photo courtesy of Pfizer
and Bristol-Myers Squibb
ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.
For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.
They found that patients had a similar risk of stroke regardless of which drug they received.
However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.
Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.
“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.
The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.
“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.
During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.
The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.
At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.
“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.
“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”
“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.”
*Information in the abstract differs from that presented at the meeting.
Photo courtesy of Pfizer
and Bristol-Myers Squibb
ROME—Novel oral anticoagulants (NOACs) are as effective as warfarin for preventing stroke but may cause less intracranial hemorrhage (ICH) in patients with atrial fibrillation, according to research presented at ESC Congress 2016.
For this study, investigators compared 3 NOACs—dabigatran, rivaroxaban, and apixaban—to warfarin in a “real-world” setting.
They found that patients had a similar risk of stroke regardless of which drug they received.
However, the risk of ICH was lower with dabigatran and apixaban than with warfarin. There was no significant difference in ICH risk between warfarin and rivaroxaban.
Laila Staerk, PhD, of Gentofte Hospital Copenhagen University Hospital in Hellerup, Denmark, presented these results at the congress as abstract 1875.* The study was supported by Velux Foundations.
“There has been a need to investigate safety and effectiveness of NOACs versus warfarin in a ‘real-world’ population, and our Danish registries provide this opportunity,” Dr Staerk said.
The study included 43,299 atrial fibrillation patients from Danish nationwide administrative registries. Roughly 42% of the patients were taking warfarin, 29% were taking dabigatran, 16% were taking apixaban, and 13% were taking rivaroxaban.
“The inclusion and exclusion criteria in our study were broadly similar for patients initiating NOACs or warfarin, and this gave a straightforward opportunity to directly compare the treatment regimens, which is in contrast to the randomized trials,” Dr Staerk said.
During follow-up, stroke occurred in 1054 patients, and there were 261 intracranial bleeds.
The risk of having a stroke within 1 year was similar between the treatment groups. The absolute standardized risk was 2.01% for warfarin, 2.06% for rivaroxaban, 2.12% for dabigatran, and 2.46% for apixaban.
At 1 year, the standardized absolute risk of ICH was significantly lower in patients treated with dabigatran or apixaban—0.26% and 0.40%, respectively—than in those treated with warfarin—0.60% (P<0.05). The standardized absolute risk of ICH was 0.47% with rivaroxaban, which was not significantly different than the risk with warfarin.
“The results suggest that, although they have similar effects in preventing stroke, dabigatran and apixaban were associated with a safer use regarding the absolute 1-year risk of intracranial bleeding,” Dr Staerk said.
“Our results complement the large, randomized, phase 3 trials by providing ‘real-world’ data on stroke and intracranial bleeding with NOACs versus warfarin since fragile patients were not excluded from our nationwide cohort. For example, patients with increased risk of bleeding, liver disease, and chronic kidney disease are less represented in trials.”
“Registry studies have some limitations, such as the observational design, residual confounding, and confounding by drug indication. In the future, it would be exciting to see a head-to-head, randomized trial performed to compare the different NOAC treatments in patients with atrial fibrillation.”
*Information in the abstract differs from that presented at the meeting.
Shorter DAPT appears safe for pts with type of DES
ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.
Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.
The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.
“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.
However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.
Dr Nakamura presented the results at the congress as abstract 2218.
The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.
All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).
An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.
Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.
There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.
The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.
“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”
Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.
Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.
This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.
ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.
Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.
The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.
“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.
However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.
Dr Nakamura presented the results at the congress as abstract 2218.
The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.
All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).
An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.
Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.
There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.
The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.
“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”
Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.
Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.
This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.
ROME—A short-term course of dual antiplatelet therapy (DAPT) may be non-inferior to a longer course in patients who have a certain type of drug-eluting stent (DES), according to research presented at ESC Congress 2016.
Patients in this study, known as NIPPON, had the Nobori bioabsorbable abluminal-coated stent and received 6 months or 18 months of DAPT, which consisted of aspirin plus clopidogrel or ticlopidine.
The results showed similar rates of net adverse clinical and cerebrovascular events, as well as similar rates of bleeding complications, whether patients received DAPT for 6 months or 18 months.
“Based on these findings, a combination of short[-term] DAPT and a newer DES with bioabsorbable abluminal coating should be able to minimize the incidence of thrombotic events and bleeding complications simultaneously,” said Masato Nakamura, MD, PhD, of Toho University Ohashi Medical Center in Tokyo, Japan.
However, Dr Nakamura also noted that this study had limitations, so the results should be interpreted with caution.
Dr Nakamura presented the results at the congress as abstract 2218.
The study enrolled 3775 patients with coronary artery disease or acute myocardial infarction who had undergone percutaneous coronary intervention and stent placement at 130 Japanese institutions.
All patients had received the Nobori bioabsorbable abluminal-coated stent, with DAPT consisting of aspirin (81–162 mg/day) combined with clopidogrel (75 mg/day) or ticlopidine (200 mg/day).
An interim analysis of the study data showed slow enrolment and substantially lower events than expected, so the study was terminated early.
Dr Nakamura presented results from the first 2772 patients to be followed for at least 18 months.
There was no significant difference in the occurrence of the primary endpoint—net adverse clinical and cerebrovascular events—among patients randomized to either short-term or long-term DAPT—1.92% and 1.45%, respectively—confirming the non-inferiority of short-term therapy.
The rate of bleeding events was similar between the treatment arms as well—0.73% in the long-term arm and 0.96% in the short-term arm—as was the rate of stent thrombosis—0.07% in both arms.
“The results of the present study should be interpreted with caution before trying to draw firm conclusions,” Dr Nakamura said. “The interpretation of the NIPPON trial is complicated by the fact that the event rate was lower than the expected incidence of the primary endpoint in both groups. Therefore, the statistical power may not have been adequate to fully assess the risk of [the] primary endpoint.”
Dr Nakamura also noted that the follow-up period may not have been long enough to draw conclusions about the optimum duration of DAPT for patients with DES.
Furthermore, the early termination of the study, in conjunction with the enrollment of relatively low-risk subjects, suggests the study’s results may not be generalizable to high-risk patients. Similarly, as antiplatelet therapy was mainly limited to clopidogrel, the use of more potent antiplatelet agents may have led to different conclusions.
This study was funded by Associations for Establishment of Evidence in Interventions Studies. Dr Nakamura has received research grant support and honoraria from Terumo Corporation, Sanofi, and Daiichi Sankyo.
ESC addresses cardiac toxicity of anticancer therapies
chemotherapy
Photo by Rhoda Baer
The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.
The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.
The paper was published in European Heart Journal and on the ESC website.
The document reviews the potential cardiovascular complications of anticancer therapies.
The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.
For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.
Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).
Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.
The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.
The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.
“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”
“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.
“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”
chemotherapy
Photo by Rhoda Baer
The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.
The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.
The paper was published in European Heart Journal and on the ESC website.
The document reviews the potential cardiovascular complications of anticancer therapies.
The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.
For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.
Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).
Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.
The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.
The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.
“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”
“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.
“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”
chemotherapy
Photo by Rhoda Baer
The European Society of Cardiology (ESC) has launched a novel position paper, under the auspices of its Committee for Practice Guidelines, on the cardiac toxicity of anticancer therapies.
The paper is a summary and evaluation of relevant scientific evidence that is intended to assist health professionals in selecting the best strategies for preventing and managing cardiac toxicity in patients with cancer, including leukemia, lymphoma, and multiple myeloma.
The paper was published in European Heart Journal and on the ESC website.
The document reviews the potential cardiovascular complications of anticancer therapies.
The complications are divided into 9 categories: myocardial dysfunction and heart failure, coronary artery disease, valvular disease, arrhythmias, arterial hypertension, thromboembolic disease, peripheral vascular disease and stroke, pulmonary hypertension, and pericardial complications.
For each type of complication, the authors outline which patients are at risk and how to detect and prevent the possible side effects. Recommendations are given on how to treat and follow patients who develop that type of cardiotoxicity.
Cardiotoxicity is detected using electrocardiogram, cardiac imaging, and biomarkers. Prevention and treatment may involve the use of cardioprotective drugs (such as angiotensin converting enzyme inhibitors or beta-blockers) and adopting a healthy lifestyle (eating a healthy diet, not smoking, exercising regularly, and controlling body weight).
Regarding long-term surveillance for cancer survivors, the paper says patients should be informed of their increased risk of cardiovascular disease at the outset of cancer treatment and supported to make lifestyle changes. They should be told to report early signs and symptoms of cardiovascular disease promptly.
The paper also emphasizes the importance of establishing multidisciplinary teams to provide the best care for cancer patients and survivors. These should include cardiologists, oncologists, nurses, and heart failure and imaging specialists. Ultimately, cardio-oncology centers with a structured service are needed.
The authors note that under- or over-diagnosis of cardiovascular disease sometimes results in failure to prevent adverse events or inappropriate interruption of a potentially life-saving anticancer treatment.
“We need to be clear when it’s a must to stop the treatment, when we should reduce the dose, or when we can continue with the therapy,” said author Jose Luis Zamorano, MD, of University Hospital Ramón in Madrid, Spain. “This position paper provides guidance in this area.”
“We hope the paper will increase awareness about heart disease in cancer patients and survivors and stimulate more research in this area,” added author Patrizio Lancellotti, MD, PhD, of University of Liège Hospital in Liège, Belgium.
“More information is needed on when to screen and monitor patients and on the cardiovascular effects of new anticancer therapies.”
FDA authorizes use of test to detect Zika virus
Photo by Graham Colm
The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.
The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.
The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.
The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.
About the EUA
The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.
The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.
This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of
in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.
About the test
The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.
Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.
The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.
The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.
Photo by Graham Colm
The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.
The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.
The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.
The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.
About the EUA
The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.
The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.
This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of
in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.
About the test
The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.
Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.
The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.
The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.
Photo by Graham Colm
The US Food and Drug Administration (FDA) has issued an emergency use authorization (EUA) for the LightMix® Zika rRT-PCR Test.
The test, distributed by Roche, is used to detect the Zika virus in EDTA plasma or serum samples.
The LightMix® Zika rRT-PCR Test is intended for use in patients meeting clinical criteria or epidemiological criteria for Zika virus testing according to the US Centers for Disease Control and Prevention.
The test can only be used by laboratories certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA), 42 U.S.C. § 263a, to perform high complexity tests, or by similarly qualified non-US laboratories.
About the EUA
The LightMix® Zika rRT-PCR Test has not been FDA-cleared or approved. An EUA allows for the use of unapproved medical products or unapproved uses of approved medical products in an emergency.
The products must be used to diagnose, treat, or prevent serious or life-threatening conditions caused by chemical, biological, radiological, or nuclear threat agents, when there are no adequate alternatives.
This means the LightMix® Zika rRT-PCR Test is only authorized for use as long as circumstances exist to justify the authorization of the emergency use of
in vitro diagnostics for the detection of Zika virus under section 564(b)(1) of the Federal Food, Drug & Cosmetic Act, 21 U.S.C.§360bbb-3(b)(1), unless the authorization is terminated or revoked sooner.
About the test
The LightMix® Zika rRT-PCR Test is designed to provide qualitative detection of Zika viral RNA in combination with a full process RNA control that monitors all steps from extraction to PCR result.
Nucleic acid extraction is authorized to be performed with Roche’s MagNA Pure Compact Instrument (and Isolation Kit I – Large Volume) or, for laboratories wanting to process a higher number of samples, the MagNA Pure 96 Instrument (and DNA and Viral NA Large Volume Kit) for high-throughput automated extraction.
The test was developed to run on Roche’s LightCycler® 480 Instrument II or cobas z 480 Analyzer. The end-to-end automated process from sample preparation to results for up to 96 samples can be performed in 2.5 hours.
The LightMix® Zika rRT-PCR Test is manufactured by TIB MOLBIOL GmbH and distributed by Roche.
Identifying and targeting malignant aging in sAML
Photo courtesy of the University
of California San Diego
Researchers say they have identified RNA-based biomarkers that distinguish normal, aged hematopoietic stem and progenitor cells (HSPCs) from leukemia stem cells (LSCs) associated with secondary acute myeloid leukemia (sAML).
The team believes their discovery may provide a new way to predict leukemic relapse and identify targets for drug development.
Catriona Jamieson, MD, PhD, of the University of California San Diego in La Jolla, and her colleagues described the discovery in Cell Stem Cell.
The researchers noted that age-related hematopoietic stem cell exhaustion and myeloid-lineage skewing promote the transformation of hematopoietic progenitors into therapy-resistant LSCs in sAML. However, the contribution of RNA processing alterations to HSPC aging and LSC generation remains unclear.
With this study, Dr Jamieson and her colleagues discovered RNA splice isoform expression patterns that distinguished normal, aged HSPCs from sAML LSCs.
The team said the aged HSPCs displayed pro-apoptotic BCL2 splice isoform switching, while sAML LSCs favored pro-survival expression of BCL2L1 (BCL-XL).
“These splicing signatures could potentially be used as clinical biomarkers to detect blood stem cells that show signs of early aging or leukemia and to monitor patient responses to treatment,” said study author Leslie Crews, PhD, of the University of California San Diego.
“By being able to distinguish benign from malignant aging based on distinctive RNA splicing patterns, we can develop therapeutic strategies that selectively target leukemia stem cells while sparing normal hematopoietic stem cells,” Dr Jamieson added.
In fact, she and her colleagues were able to show that treatment with a pharmacologic splicing modulator known as 17S-FD-895 could eradicate sAML LSCs while sparing normal HSPCs. The compound reversed pro-survival splice isoform switching and impaired LSC maintenance.
“Our findings show that RNA splicing is a unique therapeutic vulnerability for secondary AML,” Dr Jamieson said. “RNA-splicing-targeted therapies may be a potent and selective way to clear leukemia stem cells and prevent relapse.”
Photo courtesy of the University
of California San Diego
Researchers say they have identified RNA-based biomarkers that distinguish normal, aged hematopoietic stem and progenitor cells (HSPCs) from leukemia stem cells (LSCs) associated with secondary acute myeloid leukemia (sAML).
The team believes their discovery may provide a new way to predict leukemic relapse and identify targets for drug development.
Catriona Jamieson, MD, PhD, of the University of California San Diego in La Jolla, and her colleagues described the discovery in Cell Stem Cell.
The researchers noted that age-related hematopoietic stem cell exhaustion and myeloid-lineage skewing promote the transformation of hematopoietic progenitors into therapy-resistant LSCs in sAML. However, the contribution of RNA processing alterations to HSPC aging and LSC generation remains unclear.
With this study, Dr Jamieson and her colleagues discovered RNA splice isoform expression patterns that distinguished normal, aged HSPCs from sAML LSCs.
The team said the aged HSPCs displayed pro-apoptotic BCL2 splice isoform switching, while sAML LSCs favored pro-survival expression of BCL2L1 (BCL-XL).
“These splicing signatures could potentially be used as clinical biomarkers to detect blood stem cells that show signs of early aging or leukemia and to monitor patient responses to treatment,” said study author Leslie Crews, PhD, of the University of California San Diego.
“By being able to distinguish benign from malignant aging based on distinctive RNA splicing patterns, we can develop therapeutic strategies that selectively target leukemia stem cells while sparing normal hematopoietic stem cells,” Dr Jamieson added.
In fact, she and her colleagues were able to show that treatment with a pharmacologic splicing modulator known as 17S-FD-895 could eradicate sAML LSCs while sparing normal HSPCs. The compound reversed pro-survival splice isoform switching and impaired LSC maintenance.
“Our findings show that RNA splicing is a unique therapeutic vulnerability for secondary AML,” Dr Jamieson said. “RNA-splicing-targeted therapies may be a potent and selective way to clear leukemia stem cells and prevent relapse.”
Photo courtesy of the University
of California San Diego
Researchers say they have identified RNA-based biomarkers that distinguish normal, aged hematopoietic stem and progenitor cells (HSPCs) from leukemia stem cells (LSCs) associated with secondary acute myeloid leukemia (sAML).
The team believes their discovery may provide a new way to predict leukemic relapse and identify targets for drug development.
Catriona Jamieson, MD, PhD, of the University of California San Diego in La Jolla, and her colleagues described the discovery in Cell Stem Cell.
The researchers noted that age-related hematopoietic stem cell exhaustion and myeloid-lineage skewing promote the transformation of hematopoietic progenitors into therapy-resistant LSCs in sAML. However, the contribution of RNA processing alterations to HSPC aging and LSC generation remains unclear.
With this study, Dr Jamieson and her colleagues discovered RNA splice isoform expression patterns that distinguished normal, aged HSPCs from sAML LSCs.
The team said the aged HSPCs displayed pro-apoptotic BCL2 splice isoform switching, while sAML LSCs favored pro-survival expression of BCL2L1 (BCL-XL).
“These splicing signatures could potentially be used as clinical biomarkers to detect blood stem cells that show signs of early aging or leukemia and to monitor patient responses to treatment,” said study author Leslie Crews, PhD, of the University of California San Diego.
“By being able to distinguish benign from malignant aging based on distinctive RNA splicing patterns, we can develop therapeutic strategies that selectively target leukemia stem cells while sparing normal hematopoietic stem cells,” Dr Jamieson added.
In fact, she and her colleagues were able to show that treatment with a pharmacologic splicing modulator known as 17S-FD-895 could eradicate sAML LSCs while sparing normal HSPCs. The compound reversed pro-survival splice isoform switching and impaired LSC maintenance.
“Our findings show that RNA splicing is a unique therapeutic vulnerability for secondary AML,” Dr Jamieson said. “RNA-splicing-targeted therapies may be a potent and selective way to clear leukemia stem cells and prevent relapse.”
Combo extends PFS in previously treated MM
Photo courtesy of Janssen
Results of the phase 3 CASTOR trial suggest that adding daratumumab to treatment with bortezomib and dexamethasone can improve progression-free survival (PFS) in patients with previously treated multiple myeloma (MM).
Compared to patients who received only bortezomib and dexamethasone, those who received daratumumab as well had a higher response rate and longer PFS, but they also had a higher incidence of grade 3/4 adverse events (AEs).
These results were recently published in NEJM. They were previously presented at the 2016 ASCO Annual Meeting. The CASTOR trial was funded by Janssen Research & Development.
The trial enrolled 498 patients with relapsed or relapsed and refractory MM. Patients were randomized to receive bortezomib (1.3 mg/m2) and dexamethasone (20 mg) alone (control arm) or in combination with daratumumab (16 mg/kg).
Baseline characteristics were well balanced between the treatment arms. Across both groups, the median patient age was 64 (range, 30 to 88), the median time since MM diagnosis was 3.8 years, and the patients had received a median of 2 (range, 1 to 10) previous lines of therapy.
Efficacy
The overall response rate was significantly higher in the daratumumab arm than the control arm—82.9% and 63.2%, respectively (P<0.001). The rate of complete response or better was higher in the daratumumab arm as well—19.2% and 9.0%, respectively (P=0.001).
After a median follow-up of 7.4 months, the median PFS was not reached in the daratumumab arm and was 7.2 months in the control arm (hazard ratio=0.39, P<0.001). The estimated 12-month PFS was 60.7% and 26.9%, respectively.
Overall survival was not reached in either treatment arm.
This trial was unblinded after meeting its primary endpoint of improved PFS in this interim analysis. Based on the recommendation of an independent data monitoring committee, patients in the control arm were offered the option to receive daratumumab following confirmed disease progression.
Safety
AEs occurred in 98.8% of patients in the daratumumab arm and 95.4% of patients in the control arm. Grade 3/4 AEs occurred in 76.1% and 62.4%, respectively.
There was a higher incidence of the following AEs in the daratumumab arm than the control arm—thrombocytopenia (58.8% vs 43.9%), neutropenia (17.7% vs 9.3%), lymphopenia (13.2% vs 3.8%), peripheral sensory neuropathy (47.3% vs 37.6%), bleeding events (7.0% vs 3.8%), and secondary primary cancers (2.5% vs 0.4%).
Infusion-related reactions associated with daratumumab were reported in 45.3% of patients. These reactions were mostly grade 1 or 2.
The percentage of patients who discontinued treatment because of at least 1 AE was similar between the daratumumab and control arms (7.4% and 9.3%, respectively).
Photo courtesy of Janssen
Results of the phase 3 CASTOR trial suggest that adding daratumumab to treatment with bortezomib and dexamethasone can improve progression-free survival (PFS) in patients with previously treated multiple myeloma (MM).
Compared to patients who received only bortezomib and dexamethasone, those who received daratumumab as well had a higher response rate and longer PFS, but they also had a higher incidence of grade 3/4 adverse events (AEs).
These results were recently published in NEJM. They were previously presented at the 2016 ASCO Annual Meeting. The CASTOR trial was funded by Janssen Research & Development.
The trial enrolled 498 patients with relapsed or relapsed and refractory MM. Patients were randomized to receive bortezomib (1.3 mg/m2) and dexamethasone (20 mg) alone (control arm) or in combination with daratumumab (16 mg/kg).
Baseline characteristics were well balanced between the treatment arms. Across both groups, the median patient age was 64 (range, 30 to 88), the median time since MM diagnosis was 3.8 years, and the patients had received a median of 2 (range, 1 to 10) previous lines of therapy.
Efficacy
The overall response rate was significantly higher in the daratumumab arm than the control arm—82.9% and 63.2%, respectively (P<0.001). The rate of complete response or better was higher in the daratumumab arm as well—19.2% and 9.0%, respectively (P=0.001).
After a median follow-up of 7.4 months, the median PFS was not reached in the daratumumab arm and was 7.2 months in the control arm (hazard ratio=0.39, P<0.001). The estimated 12-month PFS was 60.7% and 26.9%, respectively.
Overall survival was not reached in either treatment arm.
This trial was unblinded after meeting its primary endpoint of improved PFS in this interim analysis. Based on the recommendation of an independent data monitoring committee, patients in the control arm were offered the option to receive daratumumab following confirmed disease progression.
Safety
AEs occurred in 98.8% of patients in the daratumumab arm and 95.4% of patients in the control arm. Grade 3/4 AEs occurred in 76.1% and 62.4%, respectively.
There was a higher incidence of the following AEs in the daratumumab arm than the control arm—thrombocytopenia (58.8% vs 43.9%), neutropenia (17.7% vs 9.3%), lymphopenia (13.2% vs 3.8%), peripheral sensory neuropathy (47.3% vs 37.6%), bleeding events (7.0% vs 3.8%), and secondary primary cancers (2.5% vs 0.4%).
Infusion-related reactions associated with daratumumab were reported in 45.3% of patients. These reactions were mostly grade 1 or 2.
The percentage of patients who discontinued treatment because of at least 1 AE was similar between the daratumumab and control arms (7.4% and 9.3%, respectively).
Photo courtesy of Janssen
Results of the phase 3 CASTOR trial suggest that adding daratumumab to treatment with bortezomib and dexamethasone can improve progression-free survival (PFS) in patients with previously treated multiple myeloma (MM).
Compared to patients who received only bortezomib and dexamethasone, those who received daratumumab as well had a higher response rate and longer PFS, but they also had a higher incidence of grade 3/4 adverse events (AEs).
These results were recently published in NEJM. They were previously presented at the 2016 ASCO Annual Meeting. The CASTOR trial was funded by Janssen Research & Development.
The trial enrolled 498 patients with relapsed or relapsed and refractory MM. Patients were randomized to receive bortezomib (1.3 mg/m2) and dexamethasone (20 mg) alone (control arm) or in combination with daratumumab (16 mg/kg).
Baseline characteristics were well balanced between the treatment arms. Across both groups, the median patient age was 64 (range, 30 to 88), the median time since MM diagnosis was 3.8 years, and the patients had received a median of 2 (range, 1 to 10) previous lines of therapy.
Efficacy
The overall response rate was significantly higher in the daratumumab arm than the control arm—82.9% and 63.2%, respectively (P<0.001). The rate of complete response or better was higher in the daratumumab arm as well—19.2% and 9.0%, respectively (P=0.001).
After a median follow-up of 7.4 months, the median PFS was not reached in the daratumumab arm and was 7.2 months in the control arm (hazard ratio=0.39, P<0.001). The estimated 12-month PFS was 60.7% and 26.9%, respectively.
Overall survival was not reached in either treatment arm.
This trial was unblinded after meeting its primary endpoint of improved PFS in this interim analysis. Based on the recommendation of an independent data monitoring committee, patients in the control arm were offered the option to receive daratumumab following confirmed disease progression.
Safety
AEs occurred in 98.8% of patients in the daratumumab arm and 95.4% of patients in the control arm. Grade 3/4 AEs occurred in 76.1% and 62.4%, respectively.
There was a higher incidence of the following AEs in the daratumumab arm than the control arm—thrombocytopenia (58.8% vs 43.9%), neutropenia (17.7% vs 9.3%), lymphopenia (13.2% vs 3.8%), peripheral sensory neuropathy (47.3% vs 37.6%), bleeding events (7.0% vs 3.8%), and secondary primary cancers (2.5% vs 0.4%).
Infusion-related reactions associated with daratumumab were reported in 45.3% of patients. These reactions were mostly grade 1 or 2.
The percentage of patients who discontinued treatment because of at least 1 AE was similar between the daratumumab and control arms (7.4% and 9.3%, respectively).
Discovery in mice may have implications for HSCT
Preclinical research has shown how a cell surface molecule, Lymphotoxin β receptor, controls the entry of T cells into the thymus.
Researchers believe this might represent a pathway that could be targeted to reboot the immune system after hematopoietic stem cell transplant (HSCT).
Graham Anderson, PhD, of the University of Birmingham in the UK, and his colleagues conducted this research and reported their findings in the Journal of Immunology.
“The thymus is often something of an ignored organ, but it plays a crucial role in maintaining an effective immune system,” Dr Anderson said.
“Post-transplantation, T-cell progenitors derived from the bone marrow transplant can struggle to enter the thymus, as if the doorway to the thymus is closed. Identifying molecular regulators that can ‘prop open’ the door and allow these cells to enter and mature could well be a means to help reboot the immune system.”
Conducting experiments in mice, Dr Anderson and his colleagues found that Lymphotoxin β receptor was required to allow the entry of T-cell progenitors to the thymus both in a healthy state and during immune recovery after HSCT.
When the researchers used an antibody to stimulate Lymphotoxin β receptor after HSCT, they observed enhanced thymus recovery and an increase in the number of transplant-derived T cells, which correlated with increased adhesion molecule expression by thymic stroma.
The team said this study has revealed a novel link between Lymphotoxin β receptor and thymic stromal cells in thymus colonization and highlights its potential as an immunotherapeutic target to boost T-cell reconstitution after HSCT.
“This is just one piece of the puzzle,” said study author Beth Lucas, PhD, also of the University of Birmingham.
“It may be that there are adverse effects to opening the door to the thymus, but identifying a pathway that regulates this process is a significant step.”
For their next step, the researchers plan to study in vitro samples of the human thymus to examine the role Lymphotoxin β receptor might play in regulating thymus function in humans.
Preclinical research has shown how a cell surface molecule, Lymphotoxin β receptor, controls the entry of T cells into the thymus.
Researchers believe this might represent a pathway that could be targeted to reboot the immune system after hematopoietic stem cell transplant (HSCT).
Graham Anderson, PhD, of the University of Birmingham in the UK, and his colleagues conducted this research and reported their findings in the Journal of Immunology.
“The thymus is often something of an ignored organ, but it plays a crucial role in maintaining an effective immune system,” Dr Anderson said.
“Post-transplantation, T-cell progenitors derived from the bone marrow transplant can struggle to enter the thymus, as if the doorway to the thymus is closed. Identifying molecular regulators that can ‘prop open’ the door and allow these cells to enter and mature could well be a means to help reboot the immune system.”
Conducting experiments in mice, Dr Anderson and his colleagues found that Lymphotoxin β receptor was required to allow the entry of T-cell progenitors to the thymus both in a healthy state and during immune recovery after HSCT.
When the researchers used an antibody to stimulate Lymphotoxin β receptor after HSCT, they observed enhanced thymus recovery and an increase in the number of transplant-derived T cells, which correlated with increased adhesion molecule expression by thymic stroma.
The team said this study has revealed a novel link between Lymphotoxin β receptor and thymic stromal cells in thymus colonization and highlights its potential as an immunotherapeutic target to boost T-cell reconstitution after HSCT.
“This is just one piece of the puzzle,” said study author Beth Lucas, PhD, also of the University of Birmingham.
“It may be that there are adverse effects to opening the door to the thymus, but identifying a pathway that regulates this process is a significant step.”
For their next step, the researchers plan to study in vitro samples of the human thymus to examine the role Lymphotoxin β receptor might play in regulating thymus function in humans.
Preclinical research has shown how a cell surface molecule, Lymphotoxin β receptor, controls the entry of T cells into the thymus.
Researchers believe this might represent a pathway that could be targeted to reboot the immune system after hematopoietic stem cell transplant (HSCT).
Graham Anderson, PhD, of the University of Birmingham in the UK, and his colleagues conducted this research and reported their findings in the Journal of Immunology.
“The thymus is often something of an ignored organ, but it plays a crucial role in maintaining an effective immune system,” Dr Anderson said.
“Post-transplantation, T-cell progenitors derived from the bone marrow transplant can struggle to enter the thymus, as if the doorway to the thymus is closed. Identifying molecular regulators that can ‘prop open’ the door and allow these cells to enter and mature could well be a means to help reboot the immune system.”
Conducting experiments in mice, Dr Anderson and his colleagues found that Lymphotoxin β receptor was required to allow the entry of T-cell progenitors to the thymus both in a healthy state and during immune recovery after HSCT.
When the researchers used an antibody to stimulate Lymphotoxin β receptor after HSCT, they observed enhanced thymus recovery and an increase in the number of transplant-derived T cells, which correlated with increased adhesion molecule expression by thymic stroma.
The team said this study has revealed a novel link between Lymphotoxin β receptor and thymic stromal cells in thymus colonization and highlights its potential as an immunotherapeutic target to boost T-cell reconstitution after HSCT.
“This is just one piece of the puzzle,” said study author Beth Lucas, PhD, also of the University of Birmingham.
“It may be that there are adverse effects to opening the door to the thymus, but identifying a pathway that regulates this process is a significant step.”
For their next step, the researchers plan to study in vitro samples of the human thymus to examine the role Lymphotoxin β receptor might play in regulating thymus function in humans.
FDA advises testing all donated blood for Zika virus
The US Food and Drug Administration (FDA) has issued a revised guidance intended to reduce the risk of Zika virus transmission via blood.
The guidance recommends that all states and US territories screen donated whole blood and blood components for the Zika virus with a test authorized under an investigational new drug application or a licensed test when available.
For plasma and certain platelet products, an FDA-approved pathogen-reduction device can be used instead of a screening test.
“There is still much uncertainty regarding the nature and extent of Zika virus transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.
“At this time, the recommendation for testing the entire blood supply will help ensure that safe blood is available for all individuals who might need transfusion.”
In February, the FDA issued a guidance recommending that areas with active Zika virus transmission screen donated whole blood and blood components for the Zika virus, use pathogen-reduction devices, or halt blood collection and obtain blood from areas of the US without active virus transmission.
The FDA decided to update its guidance after considering the available scientific evidence, consulting with other public health agencies, and taking into consideration the potential serious health consequences of Zika virus infection to pregnant women and children born to women exposed to Zika virus during pregnancy.
“As new scientific and epidemiological information regarding Zika virus has become available, it’s clear that additional precautionary measures are necessary,” said Luciana Borio, MD, the FDA’s acting chief scientist.
“We are issuing revised guidance for immediate implementation in order to help maintain the safety of the US blood supply.”
Testing of donated blood is already underway in Florida, Puerto Rico, and other areas, and it has proven effective in identifying donations infected with Zika virus.
The FDA said nationwide testing will be in effect until the risk of Zika virus transmission via transfusion is reduced.
The US Food and Drug Administration (FDA) has issued a revised guidance intended to reduce the risk of Zika virus transmission via blood.
The guidance recommends that all states and US territories screen donated whole blood and blood components for the Zika virus with a test authorized under an investigational new drug application or a licensed test when available.
For plasma and certain platelet products, an FDA-approved pathogen-reduction device can be used instead of a screening test.
“There is still much uncertainty regarding the nature and extent of Zika virus transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.
“At this time, the recommendation for testing the entire blood supply will help ensure that safe blood is available for all individuals who might need transfusion.”
In February, the FDA issued a guidance recommending that areas with active Zika virus transmission screen donated whole blood and blood components for the Zika virus, use pathogen-reduction devices, or halt blood collection and obtain blood from areas of the US without active virus transmission.
The FDA decided to update its guidance after considering the available scientific evidence, consulting with other public health agencies, and taking into consideration the potential serious health consequences of Zika virus infection to pregnant women and children born to women exposed to Zika virus during pregnancy.
“As new scientific and epidemiological information regarding Zika virus has become available, it’s clear that additional precautionary measures are necessary,” said Luciana Borio, MD, the FDA’s acting chief scientist.
“We are issuing revised guidance for immediate implementation in order to help maintain the safety of the US blood supply.”
Testing of donated blood is already underway in Florida, Puerto Rico, and other areas, and it has proven effective in identifying donations infected with Zika virus.
The FDA said nationwide testing will be in effect until the risk of Zika virus transmission via transfusion is reduced.
The US Food and Drug Administration (FDA) has issued a revised guidance intended to reduce the risk of Zika virus transmission via blood.
The guidance recommends that all states and US territories screen donated whole blood and blood components for the Zika virus with a test authorized under an investigational new drug application or a licensed test when available.
For plasma and certain platelet products, an FDA-approved pathogen-reduction device can be used instead of a screening test.
“There is still much uncertainty regarding the nature and extent of Zika virus transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.
“At this time, the recommendation for testing the entire blood supply will help ensure that safe blood is available for all individuals who might need transfusion.”
In February, the FDA issued a guidance recommending that areas with active Zika virus transmission screen donated whole blood and blood components for the Zika virus, use pathogen-reduction devices, or halt blood collection and obtain blood from areas of the US without active virus transmission.
The FDA decided to update its guidance after considering the available scientific evidence, consulting with other public health agencies, and taking into consideration the potential serious health consequences of Zika virus infection to pregnant women and children born to women exposed to Zika virus during pregnancy.
“As new scientific and epidemiological information regarding Zika virus has become available, it’s clear that additional precautionary measures are necessary,” said Luciana Borio, MD, the FDA’s acting chief scientist.
“We are issuing revised guidance for immediate implementation in order to help maintain the safety of the US blood supply.”
Testing of donated blood is already underway in Florida, Puerto Rico, and other areas, and it has proven effective in identifying donations infected with Zika virus.
The FDA said nationwide testing will be in effect until the risk of Zika virus transmission via transfusion is reduced.
Native Israelis have higher risk of Hodgkin lymphoma
Photo from Hebrew
University of Jerusalem
A study of 2.3 million Jewish subjects suggests that being born in Israel increases a person’s risk of developing Hodgkin lymphoma (HL).
Native Israelis had a higher risk of HL than subjects who immigrated to Israel from Europe, Asia, or North Africa.
Researchers said this finding, published in Leukemia & Lymphoma, suggests that exposure to as-yet-unidentified elements of Israel’s environment increases the risk of HL.
“While we still need further studies to identify the specific causes of the high rates of Hodgkin lymphoma among native Israelis, our findings direct us to search for possible environmental causes in Israel and the neighboring countries,” said study author Hagai Levine, MD, of Hebrew University of Jerusalem in Israel.
“These causes could be not only environmental exposures but also diet, climate, social environment, and stress that may be related to chronic regional conflict.”
Dr Levine and his colleagues noted that the incidence of HL in Israel is among the highest in the world. Based on GLOBOCAN estimates for 2012, Israeli females have the highest age-standardized incidence rate of HL worldwide, and Israeli males have the second highest. From 1960 through 2005, Israel experienced a sharp rise in HL incidence among Israeli-born individuals of both sexes.
Despite evidence for an environmental etiology, very few risk factors have been identified. Studying immigrant populations provides a means of investigating the relative importance of genetic factors as compared to environmental factors in disease development.
With all that in mind, Dr Levine and his colleagues conducted the current study. They included Jewish men and women, ages 16 to 19 at examination, with no history of a cancer diagnosis.
Nationwide data on 2,285,009 adolescents, collected from 1967 through 2011, were linked to Israel’s Cancer Registry to obtain the incidence of HL until 2012.
During 47 million person-years of follow-up, there were 2093 cases of HL detected.
Multivariate analysis suggested native Israelis had a significantly higher risk of developing HL than individuals who immigrated to the country (hazard ratio=1.29, P<0.001). This increased risk was driven largely by an elevated risk for the nodular sclerosis subtype of HL (hazard ratio=1.59, P<0.001).
The researchers noted that the elevated risk appeared within one generation. The low incidence of HL observed for immigrants from Western Asia was no longer evident among Israeli-born individuals of Asian origin. Among immigrants, there was no difference by age at migration.
Therefore, the researchers suggested that immigration from a low-risk to a high-risk location, mostly to locales with a modern lifestyle and environment, is associated with an increase in HL incidence (mainly the nodular sclerosis subtype) within short periods, making genetic drift unlikely as a causal explanation.
On the other hand, the Israeli lifestyle and environment, either independently or by gene-environment interaction, may pose exceptional risks for HL.
“There is increasing evidence for developmental origins of health and disease, with different possible mechanisms, including epigenetic changes or endocrine disruption,” Dr Levine said.
“There is also increasing evidence on the role of prenatal stress in offspring development, including cancer development, especially for hematological malignancies. These data suggest that risk of HL (the nodular sclerosis subtype) is possibly increased due to preconception, prenatal, or early life exposures to a changing lifestyle and environment and its interaction with susceptibility genes.”
Dr Levine and his colleagues also found a higher risk of HL for women, subjects born in more recent years, those with a higher body mass index, and subjects of taller stature.
Photo from Hebrew
University of Jerusalem
A study of 2.3 million Jewish subjects suggests that being born in Israel increases a person’s risk of developing Hodgkin lymphoma (HL).
Native Israelis had a higher risk of HL than subjects who immigrated to Israel from Europe, Asia, or North Africa.
Researchers said this finding, published in Leukemia & Lymphoma, suggests that exposure to as-yet-unidentified elements of Israel’s environment increases the risk of HL.
“While we still need further studies to identify the specific causes of the high rates of Hodgkin lymphoma among native Israelis, our findings direct us to search for possible environmental causes in Israel and the neighboring countries,” said study author Hagai Levine, MD, of Hebrew University of Jerusalem in Israel.
“These causes could be not only environmental exposures but also diet, climate, social environment, and stress that may be related to chronic regional conflict.”
Dr Levine and his colleagues noted that the incidence of HL in Israel is among the highest in the world. Based on GLOBOCAN estimates for 2012, Israeli females have the highest age-standardized incidence rate of HL worldwide, and Israeli males have the second highest. From 1960 through 2005, Israel experienced a sharp rise in HL incidence among Israeli-born individuals of both sexes.
Despite evidence for an environmental etiology, very few risk factors have been identified. Studying immigrant populations provides a means of investigating the relative importance of genetic factors as compared to environmental factors in disease development.
With all that in mind, Dr Levine and his colleagues conducted the current study. They included Jewish men and women, ages 16 to 19 at examination, with no history of a cancer diagnosis.
Nationwide data on 2,285,009 adolescents, collected from 1967 through 2011, were linked to Israel’s Cancer Registry to obtain the incidence of HL until 2012.
During 47 million person-years of follow-up, there were 2093 cases of HL detected.
Multivariate analysis suggested native Israelis had a significantly higher risk of developing HL than individuals who immigrated to the country (hazard ratio=1.29, P<0.001). This increased risk was driven largely by an elevated risk for the nodular sclerosis subtype of HL (hazard ratio=1.59, P<0.001).
The researchers noted that the elevated risk appeared within one generation. The low incidence of HL observed for immigrants from Western Asia was no longer evident among Israeli-born individuals of Asian origin. Among immigrants, there was no difference by age at migration.
Therefore, the researchers suggested that immigration from a low-risk to a high-risk location, mostly to locales with a modern lifestyle and environment, is associated with an increase in HL incidence (mainly the nodular sclerosis subtype) within short periods, making genetic drift unlikely as a causal explanation.
On the other hand, the Israeli lifestyle and environment, either independently or by gene-environment interaction, may pose exceptional risks for HL.
“There is increasing evidence for developmental origins of health and disease, with different possible mechanisms, including epigenetic changes or endocrine disruption,” Dr Levine said.
“There is also increasing evidence on the role of prenatal stress in offspring development, including cancer development, especially for hematological malignancies. These data suggest that risk of HL (the nodular sclerosis subtype) is possibly increased due to preconception, prenatal, or early life exposures to a changing lifestyle and environment and its interaction with susceptibility genes.”
Dr Levine and his colleagues also found a higher risk of HL for women, subjects born in more recent years, those with a higher body mass index, and subjects of taller stature.
Photo from Hebrew
University of Jerusalem
A study of 2.3 million Jewish subjects suggests that being born in Israel increases a person’s risk of developing Hodgkin lymphoma (HL).
Native Israelis had a higher risk of HL than subjects who immigrated to Israel from Europe, Asia, or North Africa.
Researchers said this finding, published in Leukemia & Lymphoma, suggests that exposure to as-yet-unidentified elements of Israel’s environment increases the risk of HL.
“While we still need further studies to identify the specific causes of the high rates of Hodgkin lymphoma among native Israelis, our findings direct us to search for possible environmental causes in Israel and the neighboring countries,” said study author Hagai Levine, MD, of Hebrew University of Jerusalem in Israel.
“These causes could be not only environmental exposures but also diet, climate, social environment, and stress that may be related to chronic regional conflict.”
Dr Levine and his colleagues noted that the incidence of HL in Israel is among the highest in the world. Based on GLOBOCAN estimates for 2012, Israeli females have the highest age-standardized incidence rate of HL worldwide, and Israeli males have the second highest. From 1960 through 2005, Israel experienced a sharp rise in HL incidence among Israeli-born individuals of both sexes.
Despite evidence for an environmental etiology, very few risk factors have been identified. Studying immigrant populations provides a means of investigating the relative importance of genetic factors as compared to environmental factors in disease development.
With all that in mind, Dr Levine and his colleagues conducted the current study. They included Jewish men and women, ages 16 to 19 at examination, with no history of a cancer diagnosis.
Nationwide data on 2,285,009 adolescents, collected from 1967 through 2011, were linked to Israel’s Cancer Registry to obtain the incidence of HL until 2012.
During 47 million person-years of follow-up, there were 2093 cases of HL detected.
Multivariate analysis suggested native Israelis had a significantly higher risk of developing HL than individuals who immigrated to the country (hazard ratio=1.29, P<0.001). This increased risk was driven largely by an elevated risk for the nodular sclerosis subtype of HL (hazard ratio=1.59, P<0.001).
The researchers noted that the elevated risk appeared within one generation. The low incidence of HL observed for immigrants from Western Asia was no longer evident among Israeli-born individuals of Asian origin. Among immigrants, there was no difference by age at migration.
Therefore, the researchers suggested that immigration from a low-risk to a high-risk location, mostly to locales with a modern lifestyle and environment, is associated with an increase in HL incidence (mainly the nodular sclerosis subtype) within short periods, making genetic drift unlikely as a causal explanation.
On the other hand, the Israeli lifestyle and environment, either independently or by gene-environment interaction, may pose exceptional risks for HL.
“There is increasing evidence for developmental origins of health and disease, with different possible mechanisms, including epigenetic changes or endocrine disruption,” Dr Levine said.
“There is also increasing evidence on the role of prenatal stress in offspring development, including cancer development, especially for hematological malignancies. These data suggest that risk of HL (the nodular sclerosis subtype) is possibly increased due to preconception, prenatal, or early life exposures to a changing lifestyle and environment and its interaction with susceptibility genes.”
Dr Levine and his colleagues also found a higher risk of HL for women, subjects born in more recent years, those with a higher body mass index, and subjects of taller stature.
Ties to industry among NCCN guideline authors
A study published in JAMA Oncology has quantified financial ties to the pharmaceutical industry among authors of National Comprehensive Cancer Network (NCCN) guidelines.
In 2014, the authors studied received more money in research payments than “general” payments (for things like consulting, meals, and lodging)—$29 million vs $1.25 million.
But more of the authors received general payments than research payments—84% vs 47%.
Study investigators said this finding may mean that some of the guideline authors are receiving general payments unconnected to research. However, because the study only included 1 year of data, these results may not tell the full story.
“Understanding the extent to which guideline authors have financial relationships with the pharmaceutical industry—and the types of financial arrangements that they have—is useful for the NCCN and for the public,” said investigator Stacie Dusetzina, PhD, of the University of North Carolina at Chapel Hill.
“As we learn more about the role of industry payments in shaping prescribing and practice, it is best to proceed with caution and continue to encourage transparency.”
For this study, Dr Dusetzina and her colleagues analyzed financial conflicts of interest (FCOIs) for 125 panelists who worked on setting the NCCN guidelines for lung, breast, prostate, and colorectal cancer (the cancers with the highest incidence in the US).
Eighty-six percent (n=108) of the guideline authors reported at least 1 FCOI in 2014. The total value of FCOIs was $30,287,549, which included $29,036,127 in research payments and $1,251,422 in general payments.
Eighty-four percent of the authors (n=105) received general payments, and 47% (n=59) received research payments.
The authors received an average of $10,011 in general payments and an average of $236,066 in research payments.
The majority of the payments received were within the limits set by the NCCN, but 8 authors (6%) exceeded them. The NCCN says guideline authors cannot receive $20,000 or more from a single company or $50,000 or more in total.
Dr Dusetzina and her colleagues noted that this study was not designed to explore whether the payments influenced the guideline authors’ clinical practice or the recommendations they made in the guidelines.
However, finding a high prevalence of financial relationships with industry among guideline authors lays the foundation for future studies to investigate the impact of such relationships.
“It is not a given that industry funding leads to undue influence,” Dr Dusetzina said, “but it is important to analyze these relationships and the potential impact they have on care guidelines because they do influence patient care decisions and the cost of providing patient care.”
A study published in JAMA Oncology has quantified financial ties to the pharmaceutical industry among authors of National Comprehensive Cancer Network (NCCN) guidelines.
In 2014, the authors studied received more money in research payments than “general” payments (for things like consulting, meals, and lodging)—$29 million vs $1.25 million.
But more of the authors received general payments than research payments—84% vs 47%.
Study investigators said this finding may mean that some of the guideline authors are receiving general payments unconnected to research. However, because the study only included 1 year of data, these results may not tell the full story.
“Understanding the extent to which guideline authors have financial relationships with the pharmaceutical industry—and the types of financial arrangements that they have—is useful for the NCCN and for the public,” said investigator Stacie Dusetzina, PhD, of the University of North Carolina at Chapel Hill.
“As we learn more about the role of industry payments in shaping prescribing and practice, it is best to proceed with caution and continue to encourage transparency.”
For this study, Dr Dusetzina and her colleagues analyzed financial conflicts of interest (FCOIs) for 125 panelists who worked on setting the NCCN guidelines for lung, breast, prostate, and colorectal cancer (the cancers with the highest incidence in the US).
Eighty-six percent (n=108) of the guideline authors reported at least 1 FCOI in 2014. The total value of FCOIs was $30,287,549, which included $29,036,127 in research payments and $1,251,422 in general payments.
Eighty-four percent of the authors (n=105) received general payments, and 47% (n=59) received research payments.
The authors received an average of $10,011 in general payments and an average of $236,066 in research payments.
The majority of the payments received were within the limits set by the NCCN, but 8 authors (6%) exceeded them. The NCCN says guideline authors cannot receive $20,000 or more from a single company or $50,000 or more in total.
Dr Dusetzina and her colleagues noted that this study was not designed to explore whether the payments influenced the guideline authors’ clinical practice or the recommendations they made in the guidelines.
However, finding a high prevalence of financial relationships with industry among guideline authors lays the foundation for future studies to investigate the impact of such relationships.
“It is not a given that industry funding leads to undue influence,” Dr Dusetzina said, “but it is important to analyze these relationships and the potential impact they have on care guidelines because they do influence patient care decisions and the cost of providing patient care.”
A study published in JAMA Oncology has quantified financial ties to the pharmaceutical industry among authors of National Comprehensive Cancer Network (NCCN) guidelines.
In 2014, the authors studied received more money in research payments than “general” payments (for things like consulting, meals, and lodging)—$29 million vs $1.25 million.
But more of the authors received general payments than research payments—84% vs 47%.
Study investigators said this finding may mean that some of the guideline authors are receiving general payments unconnected to research. However, because the study only included 1 year of data, these results may not tell the full story.
“Understanding the extent to which guideline authors have financial relationships with the pharmaceutical industry—and the types of financial arrangements that they have—is useful for the NCCN and for the public,” said investigator Stacie Dusetzina, PhD, of the University of North Carolina at Chapel Hill.
“As we learn more about the role of industry payments in shaping prescribing and practice, it is best to proceed with caution and continue to encourage transparency.”
For this study, Dr Dusetzina and her colleagues analyzed financial conflicts of interest (FCOIs) for 125 panelists who worked on setting the NCCN guidelines for lung, breast, prostate, and colorectal cancer (the cancers with the highest incidence in the US).
Eighty-six percent (n=108) of the guideline authors reported at least 1 FCOI in 2014. The total value of FCOIs was $30,287,549, which included $29,036,127 in research payments and $1,251,422 in general payments.
Eighty-four percent of the authors (n=105) received general payments, and 47% (n=59) received research payments.
The authors received an average of $10,011 in general payments and an average of $236,066 in research payments.
The majority of the payments received were within the limits set by the NCCN, but 8 authors (6%) exceeded them. The NCCN says guideline authors cannot receive $20,000 or more from a single company or $50,000 or more in total.
Dr Dusetzina and her colleagues noted that this study was not designed to explore whether the payments influenced the guideline authors’ clinical practice or the recommendations they made in the guidelines.
However, finding a high prevalence of financial relationships with industry among guideline authors lays the foundation for future studies to investigate the impact of such relationships.
“It is not a given that industry funding leads to undue influence,” Dr Dusetzina said, “but it is important to analyze these relationships and the potential impact they have on care guidelines because they do influence patient care decisions and the cost of providing patient care.”