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Group finds a way to target MDSCs
Researchers say they’ve found a way to target myeloid-derived suppressor cells (MDSCs) while sparing other immune cells.
In preclinical experiments, the team showed they could deplete MDSCs—and shrink tumors—using peptide antibodies.
These “peptibodies” wiped out MDSCs in the blood, spleen, and tumor cells of mice without binding to other white blood cells or dendritic cells.
The researchers described this work in Nature Medicine.
“We’ve known about [MDSCs] blocking immune response for a decade but haven’t been able to shut them down for lack of an identified target,” said the paper’s senior author, Larry Kwak, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston.
“This is the first demonstration of a molecule on these cells that allows us to make an antibody—in this case, a peptide—to bind to them and get rid of them. It’s a brand new immunotherapy target.”
Dr Kwak and his colleagues began this research by applying a peptide phage library to MDSCs, which allowed for a mass screening of candidate peptides that bind to the surface of MDSCs. This revealed 2 peptides, labeled G3 and H6, that bound only to MDSCs.
The researchers fused the 2 peptides to a portion of mouse immune globulin to generate experimental peptibodies called pep-G3 and pep-H6. Both peptibodies bound to both types of MDSCs—monocytic and granulocytic cells.
Dr Kwak and his colleagues then tested the peptibodies in 2 mouse models of thymic tumors, as well as models of melanoma and lymphoma. The team compared pep-G3 and pep-H6 to a control peptibody and an antibody against Gr-1.
Both pep-G3 and pep-H6 depleted monocytic and granulocytic MDSCs in the blood and spleens of all mice. But the Gr-1 antibody only worked against granulocytic MDSCs.
To see whether MDSC depletion would impede tumor growth, the researchers administered the peptibodies to mice with thymic tumors every other day for 2 weeks.
Mice treated with either pep-G3 or pep-H6 had tumors that were about half the size and weight of those in mice treated with the control peptibody or the Gr-1 antibody.
Lastly, the researchers analyzed surface proteins on the MDSCs and found that S100A9 and S100A8 are the likely binding targets for pep-G3 and pep-H6.
Dr Kwak and his colleagues said they are now working to extend these findings to human MDSCs. 
Researchers say they’ve found a way to target myeloid-derived suppressor cells (MDSCs) while sparing other immune cells.
In preclinical experiments, the team showed they could deplete MDSCs—and shrink tumors—using peptide antibodies.
These “peptibodies” wiped out MDSCs in the blood, spleen, and tumor cells of mice without binding to other white blood cells or dendritic cells.
The researchers described this work in Nature Medicine.
“We’ve known about [MDSCs] blocking immune response for a decade but haven’t been able to shut them down for lack of an identified target,” said the paper’s senior author, Larry Kwak, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston.
“This is the first demonstration of a molecule on these cells that allows us to make an antibody—in this case, a peptide—to bind to them and get rid of them. It’s a brand new immunotherapy target.”
Dr Kwak and his colleagues began this research by applying a peptide phage library to MDSCs, which allowed for a mass screening of candidate peptides that bind to the surface of MDSCs. This revealed 2 peptides, labeled G3 and H6, that bound only to MDSCs.
The researchers fused the 2 peptides to a portion of mouse immune globulin to generate experimental peptibodies called pep-G3 and pep-H6. Both peptibodies bound to both types of MDSCs—monocytic and granulocytic cells.
Dr Kwak and his colleagues then tested the peptibodies in 2 mouse models of thymic tumors, as well as models of melanoma and lymphoma. The team compared pep-G3 and pep-H6 to a control peptibody and an antibody against Gr-1.
Both pep-G3 and pep-H6 depleted monocytic and granulocytic MDSCs in the blood and spleens of all mice. But the Gr-1 antibody only worked against granulocytic MDSCs.
To see whether MDSC depletion would impede tumor growth, the researchers administered the peptibodies to mice with thymic tumors every other day for 2 weeks.
Mice treated with either pep-G3 or pep-H6 had tumors that were about half the size and weight of those in mice treated with the control peptibody or the Gr-1 antibody.
Lastly, the researchers analyzed surface proteins on the MDSCs and found that S100A9 and S100A8 are the likely binding targets for pep-G3 and pep-H6.
Dr Kwak and his colleagues said they are now working to extend these findings to human MDSCs.
Researchers say they’ve found a way to target myeloid-derived suppressor cells (MDSCs) while sparing other immune cells.
In preclinical experiments, the team showed they could deplete MDSCs—and shrink tumors—using peptide antibodies.
These “peptibodies” wiped out MDSCs in the blood, spleen, and tumor cells of mice without binding to other white blood cells or dendritic cells.
The researchers described this work in Nature Medicine.
“We’ve known about [MDSCs] blocking immune response for a decade but haven’t been able to shut them down for lack of an identified target,” said the paper’s senior author, Larry Kwak, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston.
“This is the first demonstration of a molecule on these cells that allows us to make an antibody—in this case, a peptide—to bind to them and get rid of them. It’s a brand new immunotherapy target.”
Dr Kwak and his colleagues began this research by applying a peptide phage library to MDSCs, which allowed for a mass screening of candidate peptides that bind to the surface of MDSCs. This revealed 2 peptides, labeled G3 and H6, that bound only to MDSCs.
The researchers fused the 2 peptides to a portion of mouse immune globulin to generate experimental peptibodies called pep-G3 and pep-H6. Both peptibodies bound to both types of MDSCs—monocytic and granulocytic cells.
Dr Kwak and his colleagues then tested the peptibodies in 2 mouse models of thymic tumors, as well as models of melanoma and lymphoma. The team compared pep-G3 and pep-H6 to a control peptibody and an antibody against Gr-1.
Both pep-G3 and pep-H6 depleted monocytic and granulocytic MDSCs in the blood and spleens of all mice. But the Gr-1 antibody only worked against granulocytic MDSCs.
To see whether MDSC depletion would impede tumor growth, the researchers administered the peptibodies to mice with thymic tumors every other day for 2 weeks.
Mice treated with either pep-G3 or pep-H6 had tumors that were about half the size and weight of those in mice treated with the control peptibody or the Gr-1 antibody.
Lastly, the researchers analyzed surface proteins on the MDSCs and found that S100A9 and S100A8 are the likely binding targets for pep-G3 and pep-H6.
Dr Kwak and his colleagues said they are now working to extend these findings to human MDSCs.
EMA’s transparency plans criticized
to be used in a clinical trial
Credit: Esther Dyson
Many in the research community have lauded the European Medicines Agency’s (EMA’s) plans to make clinical trial data available to the public.
But the agency has also drawn criticism for the way it plans to go about increasing transparency.
The EMA has said it plans to make trial data available online in a “read-only” mode. So readers will not be able to save or transfer the data, making scientific analysis difficult, if not impossible.
The EMA also plans to allow drug manufacturers to omit some trial data from its public posts.
In response to this news, the European Ombudsman, Emily O’Reilly, wrote a letter to the EMA expressing concern about their seemingly significant change in policy.
“We were pleased when EMA announced, in 2012, a new pro-active transparency policy, giving the broadest possible public access to clinical trial data,” O’Reilly said.
“I am now concerned about what appears to be a significant change in EMA’s policy, which could undermine the fundamental right of public access to documents established by EU law. European citizens, doctors, and researchers need maximum information about the medicines they take, prescribe, and analyze.”
Beate Wieseler, PhD, and her colleagues from the German Institute for Quality and Efficiency in Health Care, echoed this sentiment in a “rapid response” published in the British Medical Journal.
The authors said the proposed read-only mode of accessing data makes scientific analyses, such as risk-benefit assessments of drugs, impossible.
For these assessments, an enormous amount of data must be viewed, annotated and saved, pooled from different studies, analyzed statistically, and shared among researchers. But the read-only mode would not allow for that.
Dr Wieseler and other critics also take issue with EMA’s decision to allow drug manufacturers to omit some trial data from its public posts.
The EMA has said that, within the context of market approval, drug manufacturers will be able to submit 2 versions of a clinical study report to the EMA: a complete one, by means of which the agency will decide on approval, and an incomplete one for the public.
The EMA previously decided that individual patient data, which could allow patients to be identified, would be deleted from the study reports. Now, this step has been extended to cover study results.
For example, the EMA believes deleting information is acceptable in cases of results on exploratory outcomes that are not supportive for the approval decision. However, Dr Weiseler and her colleagues noted that such study results often contain analyses of patient-relevant outcomes such as health-related quality of life.
“We are talking about studies in people who participated in a clinical study because they hoped that, with the information gained, better treatments would be developed,” Dr Wieseler said. “This information can only be used to improve patient care if it is publicly available to all.”
About the policy change
In June 2013, the EMA released for public consultation a draft policy on “publication and access to clinical trial data.” In that draft, the agency proposed publishing data submitted in support of marketing-authorization applications (only for centrally approved medicines from 2014 onward).
The idea was that interested parties would no longer need to invoke the European Freedom of Information Regulation (Regulation [EC] N°1049/2001), when exercising their right to access documents held by the EMA.
However, according to documents the EMA shared during a stakeholder consultation earlier this month, the EMA now plans to allow systematic censorship by pharmaceutical companies and impose both strict confidentiality requirements and restrictions on the use of data.
For more information on the policy, see the EMA website.
to be used in a clinical trial
Credit: Esther Dyson
Many in the research community have lauded the European Medicines Agency’s (EMA’s) plans to make clinical trial data available to the public.
But the agency has also drawn criticism for the way it plans to go about increasing transparency.
The EMA has said it plans to make trial data available online in a “read-only” mode. So readers will not be able to save or transfer the data, making scientific analysis difficult, if not impossible.
The EMA also plans to allow drug manufacturers to omit some trial data from its public posts.
In response to this news, the European Ombudsman, Emily O’Reilly, wrote a letter to the EMA expressing concern about their seemingly significant change in policy.
“We were pleased when EMA announced, in 2012, a new pro-active transparency policy, giving the broadest possible public access to clinical trial data,” O’Reilly said.
“I am now concerned about what appears to be a significant change in EMA’s policy, which could undermine the fundamental right of public access to documents established by EU law. European citizens, doctors, and researchers need maximum information about the medicines they take, prescribe, and analyze.”
Beate Wieseler, PhD, and her colleagues from the German Institute for Quality and Efficiency in Health Care, echoed this sentiment in a “rapid response” published in the British Medical Journal.
The authors said the proposed read-only mode of accessing data makes scientific analyses, such as risk-benefit assessments of drugs, impossible.
For these assessments, an enormous amount of data must be viewed, annotated and saved, pooled from different studies, analyzed statistically, and shared among researchers. But the read-only mode would not allow for that.
Dr Wieseler and other critics also take issue with EMA’s decision to allow drug manufacturers to omit some trial data from its public posts.
The EMA has said that, within the context of market approval, drug manufacturers will be able to submit 2 versions of a clinical study report to the EMA: a complete one, by means of which the agency will decide on approval, and an incomplete one for the public.
The EMA previously decided that individual patient data, which could allow patients to be identified, would be deleted from the study reports. Now, this step has been extended to cover study results.
For example, the EMA believes deleting information is acceptable in cases of results on exploratory outcomes that are not supportive for the approval decision. However, Dr Weiseler and her colleagues noted that such study results often contain analyses of patient-relevant outcomes such as health-related quality of life.
“We are talking about studies in people who participated in a clinical study because they hoped that, with the information gained, better treatments would be developed,” Dr Wieseler said. “This information can only be used to improve patient care if it is publicly available to all.”
About the policy change
In June 2013, the EMA released for public consultation a draft policy on “publication and access to clinical trial data.” In that draft, the agency proposed publishing data submitted in support of marketing-authorization applications (only for centrally approved medicines from 2014 onward).
The idea was that interested parties would no longer need to invoke the European Freedom of Information Regulation (Regulation [EC] N°1049/2001), when exercising their right to access documents held by the EMA.
However, according to documents the EMA shared during a stakeholder consultation earlier this month, the EMA now plans to allow systematic censorship by pharmaceutical companies and impose both strict confidentiality requirements and restrictions on the use of data.
For more information on the policy, see the EMA website.
to be used in a clinical trial
Credit: Esther Dyson
Many in the research community have lauded the European Medicines Agency’s (EMA’s) plans to make clinical trial data available to the public.
But the agency has also drawn criticism for the way it plans to go about increasing transparency.
The EMA has said it plans to make trial data available online in a “read-only” mode. So readers will not be able to save or transfer the data, making scientific analysis difficult, if not impossible.
The EMA also plans to allow drug manufacturers to omit some trial data from its public posts.
In response to this news, the European Ombudsman, Emily O’Reilly, wrote a letter to the EMA expressing concern about their seemingly significant change in policy.
“We were pleased when EMA announced, in 2012, a new pro-active transparency policy, giving the broadest possible public access to clinical trial data,” O’Reilly said.
“I am now concerned about what appears to be a significant change in EMA’s policy, which could undermine the fundamental right of public access to documents established by EU law. European citizens, doctors, and researchers need maximum information about the medicines they take, prescribe, and analyze.”
Beate Wieseler, PhD, and her colleagues from the German Institute for Quality and Efficiency in Health Care, echoed this sentiment in a “rapid response” published in the British Medical Journal.
The authors said the proposed read-only mode of accessing data makes scientific analyses, such as risk-benefit assessments of drugs, impossible.
For these assessments, an enormous amount of data must be viewed, annotated and saved, pooled from different studies, analyzed statistically, and shared among researchers. But the read-only mode would not allow for that.
Dr Wieseler and other critics also take issue with EMA’s decision to allow drug manufacturers to omit some trial data from its public posts.
The EMA has said that, within the context of market approval, drug manufacturers will be able to submit 2 versions of a clinical study report to the EMA: a complete one, by means of which the agency will decide on approval, and an incomplete one for the public.
The EMA previously decided that individual patient data, which could allow patients to be identified, would be deleted from the study reports. Now, this step has been extended to cover study results.
For example, the EMA believes deleting information is acceptable in cases of results on exploratory outcomes that are not supportive for the approval decision. However, Dr Weiseler and her colleagues noted that such study results often contain analyses of patient-relevant outcomes such as health-related quality of life.
“We are talking about studies in people who participated in a clinical study because they hoped that, with the information gained, better treatments would be developed,” Dr Wieseler said. “This information can only be used to improve patient care if it is publicly available to all.”
About the policy change
In June 2013, the EMA released for public consultation a draft policy on “publication and access to clinical trial data.” In that draft, the agency proposed publishing data submitted in support of marketing-authorization applications (only for centrally approved medicines from 2014 onward).
The idea was that interested parties would no longer need to invoke the European Freedom of Information Regulation (Regulation [EC] N°1049/2001), when exercising their right to access documents held by the EMA.
However, according to documents the EMA shared during a stakeholder consultation earlier this month, the EMA now plans to allow systematic censorship by pharmaceutical companies and impose both strict confidentiality requirements and restrictions on the use of data.
For more information on the policy, see the EMA website.
Mutation causes ibrutinib resistance in CLL
Credit: Rhoda Baer
Researchers say they have identified a source of drug resistance in chronic lymphocytic leukemia (CLL).
In a letter to The New England Journal of Medicine, the team described how a mutation in Bruton’s tyrosine kinase (BTK) triggers resistance to ibrutinib, a drug that treats CLL by inhibiting BTK.
The researchers discovered this point mutation in a CLL patient enrolled in a clinical trial. The patient initially responded well to ibrutinib but stopped responding after almost 20 months.
“In a way, we are repeating, at a faster pace, the story of Gleevec [imatinib],” said study author Y. Lynn Wang, MD, PhD, of the University of Chicago in Illinois.
“That story began with development of an effective drug with few side effects, but, in many patients, the leukemia eventually found a way around it after long-term use. So researchers developed second-line drugs to overcome resistance.”
The ibrutinib study began in 2010 at Weill Cornell Medical College in New York, one of several sites for a phase 1 trial of ibrutinib. The researchers recruited 16 patients with CLL whose disease had progressed or relapsed despite multiple treatments.
Dr Wang arranged to track the progress of each patient’s leukemic cells before and during treatment and to correlate any cellular or molecular changes with each patient’s disease activity.
One of the 16 patients in the trial seemed to be unusual. This 61-year-old woman was diagnosed in 2000 at age 49. She had unsuccessfully received several different treatments before entering the study.
Within 18 months of starting ibrutinib, she showed significant improvement. At about 20 months, however, she started to decline, developing a respiratory infection that did not improve with treatment. By 21 months, it was clear she was having a relapse. The clinical team increased her dose, with no discernable effect.
Dr Wang’s team quickly began analyzing her blood samples, looking for changes that occurred between the period when she was responding well to ibrutinib and after she began to relapse.
Because complete gene sequencing would be time consuming, Dr Wang asked a graduate student working on the project, Menu Setty from Memorial Sloan-Kettering in New York, to first focus on 3 proteins that were likely candidates. One of the candidates was BTK.
And sure enough, Setty discovered a tiny but consistent change in BTK in about 90% of post-relapse cells. It was a thymidine-to-adenine mutation at nucleotide 1634 of the BTK complementary DNA, leading to a substitution of serine for cysteine at residue 481 (C481S).
When the researchers later analyzed the entire set of the patient’s genes, they found no other genetic changes that correlated with the patient’s clinical course. BTK made perfect sense as the cause for drug resistance, the researchers noted, as it’s the primary target of ibrutinib binding, and it plays a central role in rapid cell proliferation.
Dr Wang and her colleagues used structural and biochemical measures to confirm that the C481S mutation made CLL cells resistant to ibrutinib. The studies indicated that ibrutinib was 500 times less likely to bind to mutant BTK.
In an attempt to save the patient, the researchers tested alternative kinase inhibitors against the patient’s leukemic cells in the lab.
They found some kinase inhibitors remained effective against ibrutinib-resistant cells. (These studies are described in a separate manuscript that has been submitted for publication.) Unfortunately, despite this effort, the patient passed away a few weeks later, due to sepsis.
The researchers noted that the C481S mutation is one of several mechanisms that underlie resistance to ibrutinib, but this research highlights the mutation’s role in disease development and drug resistance.
Understanding the molecular and cellular mechanisms of resistance is the first step toward monitoring, early detection, and development of novel strategies to overcome drug resistance.
Credit: Rhoda Baer
Researchers say they have identified a source of drug resistance in chronic lymphocytic leukemia (CLL).
In a letter to The New England Journal of Medicine, the team described how a mutation in Bruton’s tyrosine kinase (BTK) triggers resistance to ibrutinib, a drug that treats CLL by inhibiting BTK.
The researchers discovered this point mutation in a CLL patient enrolled in a clinical trial. The patient initially responded well to ibrutinib but stopped responding after almost 20 months.
“In a way, we are repeating, at a faster pace, the story of Gleevec [imatinib],” said study author Y. Lynn Wang, MD, PhD, of the University of Chicago in Illinois.
“That story began with development of an effective drug with few side effects, but, in many patients, the leukemia eventually found a way around it after long-term use. So researchers developed second-line drugs to overcome resistance.”
The ibrutinib study began in 2010 at Weill Cornell Medical College in New York, one of several sites for a phase 1 trial of ibrutinib. The researchers recruited 16 patients with CLL whose disease had progressed or relapsed despite multiple treatments.
Dr Wang arranged to track the progress of each patient’s leukemic cells before and during treatment and to correlate any cellular or molecular changes with each patient’s disease activity.
One of the 16 patients in the trial seemed to be unusual. This 61-year-old woman was diagnosed in 2000 at age 49. She had unsuccessfully received several different treatments before entering the study.
Within 18 months of starting ibrutinib, she showed significant improvement. At about 20 months, however, she started to decline, developing a respiratory infection that did not improve with treatment. By 21 months, it was clear she was having a relapse. The clinical team increased her dose, with no discernable effect.
Dr Wang’s team quickly began analyzing her blood samples, looking for changes that occurred between the period when she was responding well to ibrutinib and after she began to relapse.
Because complete gene sequencing would be time consuming, Dr Wang asked a graduate student working on the project, Menu Setty from Memorial Sloan-Kettering in New York, to first focus on 3 proteins that were likely candidates. One of the candidates was BTK.
And sure enough, Setty discovered a tiny but consistent change in BTK in about 90% of post-relapse cells. It was a thymidine-to-adenine mutation at nucleotide 1634 of the BTK complementary DNA, leading to a substitution of serine for cysteine at residue 481 (C481S).
When the researchers later analyzed the entire set of the patient’s genes, they found no other genetic changes that correlated with the patient’s clinical course. BTK made perfect sense as the cause for drug resistance, the researchers noted, as it’s the primary target of ibrutinib binding, and it plays a central role in rapid cell proliferation.
Dr Wang and her colleagues used structural and biochemical measures to confirm that the C481S mutation made CLL cells resistant to ibrutinib. The studies indicated that ibrutinib was 500 times less likely to bind to mutant BTK.
In an attempt to save the patient, the researchers tested alternative kinase inhibitors against the patient’s leukemic cells in the lab.
They found some kinase inhibitors remained effective against ibrutinib-resistant cells. (These studies are described in a separate manuscript that has been submitted for publication.) Unfortunately, despite this effort, the patient passed away a few weeks later, due to sepsis.
The researchers noted that the C481S mutation is one of several mechanisms that underlie resistance to ibrutinib, but this research highlights the mutation’s role in disease development and drug resistance.
Understanding the molecular and cellular mechanisms of resistance is the first step toward monitoring, early detection, and development of novel strategies to overcome drug resistance.
Credit: Rhoda Baer
Researchers say they have identified a source of drug resistance in chronic lymphocytic leukemia (CLL).
In a letter to The New England Journal of Medicine, the team described how a mutation in Bruton’s tyrosine kinase (BTK) triggers resistance to ibrutinib, a drug that treats CLL by inhibiting BTK.
The researchers discovered this point mutation in a CLL patient enrolled in a clinical trial. The patient initially responded well to ibrutinib but stopped responding after almost 20 months.
“In a way, we are repeating, at a faster pace, the story of Gleevec [imatinib],” said study author Y. Lynn Wang, MD, PhD, of the University of Chicago in Illinois.
“That story began with development of an effective drug with few side effects, but, in many patients, the leukemia eventually found a way around it after long-term use. So researchers developed second-line drugs to overcome resistance.”
The ibrutinib study began in 2010 at Weill Cornell Medical College in New York, one of several sites for a phase 1 trial of ibrutinib. The researchers recruited 16 patients with CLL whose disease had progressed or relapsed despite multiple treatments.
Dr Wang arranged to track the progress of each patient’s leukemic cells before and during treatment and to correlate any cellular or molecular changes with each patient’s disease activity.
One of the 16 patients in the trial seemed to be unusual. This 61-year-old woman was diagnosed in 2000 at age 49. She had unsuccessfully received several different treatments before entering the study.
Within 18 months of starting ibrutinib, she showed significant improvement. At about 20 months, however, she started to decline, developing a respiratory infection that did not improve with treatment. By 21 months, it was clear she was having a relapse. The clinical team increased her dose, with no discernable effect.
Dr Wang’s team quickly began analyzing her blood samples, looking for changes that occurred between the period when she was responding well to ibrutinib and after she began to relapse.
Because complete gene sequencing would be time consuming, Dr Wang asked a graduate student working on the project, Menu Setty from Memorial Sloan-Kettering in New York, to first focus on 3 proteins that were likely candidates. One of the candidates was BTK.
And sure enough, Setty discovered a tiny but consistent change in BTK in about 90% of post-relapse cells. It was a thymidine-to-adenine mutation at nucleotide 1634 of the BTK complementary DNA, leading to a substitution of serine for cysteine at residue 481 (C481S).
When the researchers later analyzed the entire set of the patient’s genes, they found no other genetic changes that correlated with the patient’s clinical course. BTK made perfect sense as the cause for drug resistance, the researchers noted, as it’s the primary target of ibrutinib binding, and it plays a central role in rapid cell proliferation.
Dr Wang and her colleagues used structural and biochemical measures to confirm that the C481S mutation made CLL cells resistant to ibrutinib. The studies indicated that ibrutinib was 500 times less likely to bind to mutant BTK.
In an attempt to save the patient, the researchers tested alternative kinase inhibitors against the patient’s leukemic cells in the lab.
They found some kinase inhibitors remained effective against ibrutinib-resistant cells. (These studies are described in a separate manuscript that has been submitted for publication.) Unfortunately, despite this effort, the patient passed away a few weeks later, due to sepsis.
The researchers noted that the C481S mutation is one of several mechanisms that underlie resistance to ibrutinib, but this research highlights the mutation’s role in disease development and drug resistance.
Understanding the molecular and cellular mechanisms of resistance is the first step toward monitoring, early detection, and development of novel strategies to overcome drug resistance.
FDA clears device to treat PE
Credit: Andre E.X. Brown
The US Food and Drug Administration has cleared for marketing a device that facilitates the treatment of pulmonary embolism (PE).
The EkoSonic Endovascular System is intended for controlled and selective infusion of physician-specified fluids, including thrombolytics, into the peripheral vasculature.
The device is designed to gently accelerate the penetration of thrombolytic agents into thrombi, thereby providing high levels of lysis.
The EkoSonic Endovascular System is the only minimally invasive endovascular therapy that is FDA-cleared for the treatment of PE. The device is manufactured by EKOS Corporation.
“The EKOS clinical data established that patients stricken with a life-threatening pulmonary embolism can be successfully and safely treated with the EkoSonic system,” said Samuel Z. Goldhaber, MD, of Brigham and Woman’s Hospital in Boston, Massachusetts.
The system produced favorable results in the ULTIMA and SEATTLE II trials.
Results of the ULTIMA trial were published in Circulation. The trial showed that, for PE patients at intermediate risk of adverse events, EKOS treatment was clinically superior to anticoagulation with heparin alone in reversing right ventricular dilation at 24 hours, without an increase in bleeding complications.
The results of SEATTLE II, the prospective, single-arm, multicenter trial of 150 patients, were released at the American College of Cardiology’s 63rd Annual Scientific Session & Expo.
SEATTLE II showed that ultrasound-facilitated catheter-directed low-dose fibrinolysis for acute PE minimizes the risk of intracranial hemorrhage, improves right ventricle function, and decreases pulmonary hypertension.
Credit: Andre E.X. Brown
The US Food and Drug Administration has cleared for marketing a device that facilitates the treatment of pulmonary embolism (PE).
The EkoSonic Endovascular System is intended for controlled and selective infusion of physician-specified fluids, including thrombolytics, into the peripheral vasculature.
The device is designed to gently accelerate the penetration of thrombolytic agents into thrombi, thereby providing high levels of lysis.
The EkoSonic Endovascular System is the only minimally invasive endovascular therapy that is FDA-cleared for the treatment of PE. The device is manufactured by EKOS Corporation.
“The EKOS clinical data established that patients stricken with a life-threatening pulmonary embolism can be successfully and safely treated with the EkoSonic system,” said Samuel Z. Goldhaber, MD, of Brigham and Woman’s Hospital in Boston, Massachusetts.
The system produced favorable results in the ULTIMA and SEATTLE II trials.
Results of the ULTIMA trial were published in Circulation. The trial showed that, for PE patients at intermediate risk of adverse events, EKOS treatment was clinically superior to anticoagulation with heparin alone in reversing right ventricular dilation at 24 hours, without an increase in bleeding complications.
The results of SEATTLE II, the prospective, single-arm, multicenter trial of 150 patients, were released at the American College of Cardiology’s 63rd Annual Scientific Session & Expo.
SEATTLE II showed that ultrasound-facilitated catheter-directed low-dose fibrinolysis for acute PE minimizes the risk of intracranial hemorrhage, improves right ventricle function, and decreases pulmonary hypertension.
Credit: Andre E.X. Brown
The US Food and Drug Administration has cleared for marketing a device that facilitates the treatment of pulmonary embolism (PE).
The EkoSonic Endovascular System is intended for controlled and selective infusion of physician-specified fluids, including thrombolytics, into the peripheral vasculature.
The device is designed to gently accelerate the penetration of thrombolytic agents into thrombi, thereby providing high levels of lysis.
The EkoSonic Endovascular System is the only minimally invasive endovascular therapy that is FDA-cleared for the treatment of PE. The device is manufactured by EKOS Corporation.
“The EKOS clinical data established that patients stricken with a life-threatening pulmonary embolism can be successfully and safely treated with the EkoSonic system,” said Samuel Z. Goldhaber, MD, of Brigham and Woman’s Hospital in Boston, Massachusetts.
The system produced favorable results in the ULTIMA and SEATTLE II trials.
Results of the ULTIMA trial were published in Circulation. The trial showed that, for PE patients at intermediate risk of adverse events, EKOS treatment was clinically superior to anticoagulation with heparin alone in reversing right ventricular dilation at 24 hours, without an increase in bleeding complications.
The results of SEATTLE II, the prospective, single-arm, multicenter trial of 150 patients, were released at the American College of Cardiology’s 63rd Annual Scientific Session & Expo.
SEATTLE II showed that ultrasound-facilitated catheter-directed low-dose fibrinolysis for acute PE minimizes the risk of intracranial hemorrhage, improves right ventricle function, and decreases pulmonary hypertension.
Delaying clopidogrel can increase risk of MI, death
Credit: CDC
Patients who delay filling a prescription of clopidogrel after coronary stenting may increase their risk of recurrent myocardial infarction (MI) and death, according to a study published in the Journal of the American Heart Association.
Researchers analyzed records of more than 15,000 patients who received drug-eluting or bare metal stents.
Roughly 30% of patients in each group failed to fill their prescription of the anticoagulant clopidogrel within 3 days of hospital discharge.
And this roughly doubled the patients’ risk of death and recurrent MI, regardless of their stent type.
“It is very important that patients take clopidogrel after having a coronary stent implanted to prevent blood clots forming within the stent,” said study author Nicholas Cruden, MBChB, PhD, of the Royal Infirmary of Edinburgh in the UK.
He and his colleagues analyzed hospital administrative, community pharmacy, and cardiac revascularization data from all patients who received a coronary stent in British Columbia between 2004 and 2006, with follow-up out to 2 years.
Of the 15,629 patients, 3599 had received at least 1 drug-eluting stent (DES), and 12,030 had received a bare metal stent (BMS). Thirty percent (n=1064) of patients in the DES group, and 31% (n=3758) of patients in the BMS group failed to fill their prescription for clopidogrel within 3 days of hospital discharge.
And a delay of more than 3 days was predictive of mortality and recurrent MI, regardless of the stent type. The hazard ratios (HRs) for mortality were 2.4 for the DES group and 2.2 for the BMS group. The HRs for recurrent MI were 2.0 and 1.8, respectively.
The excess risk associated with a delay in filling the prescription was greatest in the immediate period after hospital discharge—up to 30 days. In all patients, the HRs were 5.5 for mortality and 3.1 for recurrent MI.
Delaying filling the prescription for more than 3 days remained an independent predictor of death and MI beyond 30 days from hospital discharge. The HRs were 2.1 and 2.0, respectively, for patients in the DES group and 2.0 and 1.8, respectively, for patients in the BMS group.
“This study highlights the importance of ensuring patients have access to medications as soon as they leave the hospital,” Dr Cruden said. “Even a delay of a day or 2 was associated with worse outcomes.”
Discharging patients from the hospital with enough medicine for the highest-risk period (the first month or so) could help, he added.
Credit: CDC
Patients who delay filling a prescription of clopidogrel after coronary stenting may increase their risk of recurrent myocardial infarction (MI) and death, according to a study published in the Journal of the American Heart Association.
Researchers analyzed records of more than 15,000 patients who received drug-eluting or bare metal stents.
Roughly 30% of patients in each group failed to fill their prescription of the anticoagulant clopidogrel within 3 days of hospital discharge.
And this roughly doubled the patients’ risk of death and recurrent MI, regardless of their stent type.
“It is very important that patients take clopidogrel after having a coronary stent implanted to prevent blood clots forming within the stent,” said study author Nicholas Cruden, MBChB, PhD, of the Royal Infirmary of Edinburgh in the UK.
He and his colleagues analyzed hospital administrative, community pharmacy, and cardiac revascularization data from all patients who received a coronary stent in British Columbia between 2004 and 2006, with follow-up out to 2 years.
Of the 15,629 patients, 3599 had received at least 1 drug-eluting stent (DES), and 12,030 had received a bare metal stent (BMS). Thirty percent (n=1064) of patients in the DES group, and 31% (n=3758) of patients in the BMS group failed to fill their prescription for clopidogrel within 3 days of hospital discharge.
And a delay of more than 3 days was predictive of mortality and recurrent MI, regardless of the stent type. The hazard ratios (HRs) for mortality were 2.4 for the DES group and 2.2 for the BMS group. The HRs for recurrent MI were 2.0 and 1.8, respectively.
The excess risk associated with a delay in filling the prescription was greatest in the immediate period after hospital discharge—up to 30 days. In all patients, the HRs were 5.5 for mortality and 3.1 for recurrent MI.
Delaying filling the prescription for more than 3 days remained an independent predictor of death and MI beyond 30 days from hospital discharge. The HRs were 2.1 and 2.0, respectively, for patients in the DES group and 2.0 and 1.8, respectively, for patients in the BMS group.
“This study highlights the importance of ensuring patients have access to medications as soon as they leave the hospital,” Dr Cruden said. “Even a delay of a day or 2 was associated with worse outcomes.”
Discharging patients from the hospital with enough medicine for the highest-risk period (the first month or so) could help, he added.
Credit: CDC
Patients who delay filling a prescription of clopidogrel after coronary stenting may increase their risk of recurrent myocardial infarction (MI) and death, according to a study published in the Journal of the American Heart Association.
Researchers analyzed records of more than 15,000 patients who received drug-eluting or bare metal stents.
Roughly 30% of patients in each group failed to fill their prescription of the anticoagulant clopidogrel within 3 days of hospital discharge.
And this roughly doubled the patients’ risk of death and recurrent MI, regardless of their stent type.
“It is very important that patients take clopidogrel after having a coronary stent implanted to prevent blood clots forming within the stent,” said study author Nicholas Cruden, MBChB, PhD, of the Royal Infirmary of Edinburgh in the UK.
He and his colleagues analyzed hospital administrative, community pharmacy, and cardiac revascularization data from all patients who received a coronary stent in British Columbia between 2004 and 2006, with follow-up out to 2 years.
Of the 15,629 patients, 3599 had received at least 1 drug-eluting stent (DES), and 12,030 had received a bare metal stent (BMS). Thirty percent (n=1064) of patients in the DES group, and 31% (n=3758) of patients in the BMS group failed to fill their prescription for clopidogrel within 3 days of hospital discharge.
And a delay of more than 3 days was predictive of mortality and recurrent MI, regardless of the stent type. The hazard ratios (HRs) for mortality were 2.4 for the DES group and 2.2 for the BMS group. The HRs for recurrent MI were 2.0 and 1.8, respectively.
The excess risk associated with a delay in filling the prescription was greatest in the immediate period after hospital discharge—up to 30 days. In all patients, the HRs were 5.5 for mortality and 3.1 for recurrent MI.
Delaying filling the prescription for more than 3 days remained an independent predictor of death and MI beyond 30 days from hospital discharge. The HRs were 2.1 and 2.0, respectively, for patients in the DES group and 2.0 and 1.8, respectively, for patients in the BMS group.
“This study highlights the importance of ensuring patients have access to medications as soon as they leave the hospital,” Dr Cruden said. “Even a delay of a day or 2 was associated with worse outcomes.”
Discharging patients from the hospital with enough medicine for the highest-risk period (the first month or so) could help, he added.
Wealth appears to affect distribution of cancer types
Credit: Rhoda Baer
Results of a large study suggest certain malignanices are more concentrated in areas with high levels of poverty, while other cancer types arise more often in wealthy regions.
The research, conducted using data from nearly 3 million US cancer cases, also indicated that areas with higher poverty levels tended to have a lower cancer incidence but higher mortality rate than areas with lower poverty levels.
Researchers reported these findings in the journal Cancer.
Francis Boscoe, PhD, of the New York State Cancer Registry in Albany, and his colleagues conducted this research to evaluate the role of socioeconomics in cancer incidence and mortality.
So the team compared individuals living in areas with the highest poverty levels to those living in areas with the lowest poverty levels.
The researchers collected information on nearly 3 million cancer cases diagnosed between 2005 and 2009 in16 states, plus Los Angeles (an area covering 42% of the US population). Cases were divided into 1 of 4 groupings based on the poverty rate of the residential census tract at the time of diagnosis.
For all malignancies combined, there was a negligible association between cancer incidence and poverty. However, 32 of 39 cancer types showed a significant association with poverty.
Fourteen cancers were positively associated with poverty, and 18 were negatively associated. Myeloma, Hodgkin lymphoma, and non-Hodgkin lymphoma (NHL) were among the negatively associated malignancies.
The cancers most significantly associated with higher poverty levels were Kaposi sarcoma and cancers of the larynx, cervix, penis, and liver. The cancers most significantly associated with lower poverty levels were melanoma, thyroid cancer, other non-epithelial skin cancers, and testis cancer.
Overall, male malignancy rates were more sensitive to poverty level than female rates. And, in general, the race-specific cancer incidence rates differed, but the poverty gradients were similar.
For example, there was a roughly 20-fold difference in rates of melanoma between white and black individuals, but the relationship between poverty and incidence remained regardless of race.
This was not true for NHL, however. Among black individuals, the incidence of NHL increased as the poverty level increased. But among white individuals, the incidence of NHL decreased as the poverty level increased.
The researchers pointed out that—for all cancer sites, races, and sexes combined—the difference in risk between the greatest and lowest poverty category was less than 2%.
“At first glance, the effects seem to cancel one another out,” Dr Boscoe said. “But the cancers more associated with poverty have lower incidence and higher mortality, and those associated with wealth have higher incidence and lower mortality. When it comes to cancer, the poor are more likely to die of the disease, while the affluent are more likely to die with the disease.”
Dr Boscoe noted that recent gains in technology have made it much easier to link patient addresses with neighborhood characteristics, therefore making it possible to incorporate socioeconomic status into cancer surveillance.
“Our hope is that our paper will illustrate the value and necessity of doing this routinely in the future,” he concluded.
Credit: Rhoda Baer
Results of a large study suggest certain malignanices are more concentrated in areas with high levels of poverty, while other cancer types arise more often in wealthy regions.
The research, conducted using data from nearly 3 million US cancer cases, also indicated that areas with higher poverty levels tended to have a lower cancer incidence but higher mortality rate than areas with lower poverty levels.
Researchers reported these findings in the journal Cancer.
Francis Boscoe, PhD, of the New York State Cancer Registry in Albany, and his colleagues conducted this research to evaluate the role of socioeconomics in cancer incidence and mortality.
So the team compared individuals living in areas with the highest poverty levels to those living in areas with the lowest poverty levels.
The researchers collected information on nearly 3 million cancer cases diagnosed between 2005 and 2009 in16 states, plus Los Angeles (an area covering 42% of the US population). Cases were divided into 1 of 4 groupings based on the poverty rate of the residential census tract at the time of diagnosis.
For all malignancies combined, there was a negligible association between cancer incidence and poverty. However, 32 of 39 cancer types showed a significant association with poverty.
Fourteen cancers were positively associated with poverty, and 18 were negatively associated. Myeloma, Hodgkin lymphoma, and non-Hodgkin lymphoma (NHL) were among the negatively associated malignancies.
The cancers most significantly associated with higher poverty levels were Kaposi sarcoma and cancers of the larynx, cervix, penis, and liver. The cancers most significantly associated with lower poverty levels were melanoma, thyroid cancer, other non-epithelial skin cancers, and testis cancer.
Overall, male malignancy rates were more sensitive to poverty level than female rates. And, in general, the race-specific cancer incidence rates differed, but the poverty gradients were similar.
For example, there was a roughly 20-fold difference in rates of melanoma between white and black individuals, but the relationship between poverty and incidence remained regardless of race.
This was not true for NHL, however. Among black individuals, the incidence of NHL increased as the poverty level increased. But among white individuals, the incidence of NHL decreased as the poverty level increased.
The researchers pointed out that—for all cancer sites, races, and sexes combined—the difference in risk between the greatest and lowest poverty category was less than 2%.
“At first glance, the effects seem to cancel one another out,” Dr Boscoe said. “But the cancers more associated with poverty have lower incidence and higher mortality, and those associated with wealth have higher incidence and lower mortality. When it comes to cancer, the poor are more likely to die of the disease, while the affluent are more likely to die with the disease.”
Dr Boscoe noted that recent gains in technology have made it much easier to link patient addresses with neighborhood characteristics, therefore making it possible to incorporate socioeconomic status into cancer surveillance.
“Our hope is that our paper will illustrate the value and necessity of doing this routinely in the future,” he concluded.
Credit: Rhoda Baer
Results of a large study suggest certain malignanices are more concentrated in areas with high levels of poverty, while other cancer types arise more often in wealthy regions.
The research, conducted using data from nearly 3 million US cancer cases, also indicated that areas with higher poverty levels tended to have a lower cancer incidence but higher mortality rate than areas with lower poverty levels.
Researchers reported these findings in the journal Cancer.
Francis Boscoe, PhD, of the New York State Cancer Registry in Albany, and his colleagues conducted this research to evaluate the role of socioeconomics in cancer incidence and mortality.
So the team compared individuals living in areas with the highest poverty levels to those living in areas with the lowest poverty levels.
The researchers collected information on nearly 3 million cancer cases diagnosed between 2005 and 2009 in16 states, plus Los Angeles (an area covering 42% of the US population). Cases were divided into 1 of 4 groupings based on the poverty rate of the residential census tract at the time of diagnosis.
For all malignancies combined, there was a negligible association between cancer incidence and poverty. However, 32 of 39 cancer types showed a significant association with poverty.
Fourteen cancers were positively associated with poverty, and 18 were negatively associated. Myeloma, Hodgkin lymphoma, and non-Hodgkin lymphoma (NHL) were among the negatively associated malignancies.
The cancers most significantly associated with higher poverty levels were Kaposi sarcoma and cancers of the larynx, cervix, penis, and liver. The cancers most significantly associated with lower poverty levels were melanoma, thyroid cancer, other non-epithelial skin cancers, and testis cancer.
Overall, male malignancy rates were more sensitive to poverty level than female rates. And, in general, the race-specific cancer incidence rates differed, but the poverty gradients were similar.
For example, there was a roughly 20-fold difference in rates of melanoma between white and black individuals, but the relationship between poverty and incidence remained regardless of race.
This was not true for NHL, however. Among black individuals, the incidence of NHL increased as the poverty level increased. But among white individuals, the incidence of NHL decreased as the poverty level increased.
The researchers pointed out that—for all cancer sites, races, and sexes combined—the difference in risk between the greatest and lowest poverty category was less than 2%.
“At first glance, the effects seem to cancel one another out,” Dr Boscoe said. “But the cancers more associated with poverty have lower incidence and higher mortality, and those associated with wealth have higher incidence and lower mortality. When it comes to cancer, the poor are more likely to die of the disease, while the affluent are more likely to die with the disease.”
Dr Boscoe noted that recent gains in technology have made it much easier to link patient addresses with neighborhood characteristics, therefore making it possible to incorporate socioeconomic status into cancer surveillance.
“Our hope is that our paper will illustrate the value and necessity of doing this routinely in the future,” he concluded.
CHMP recommends ofatumumab for CLL
Credit: Linda Bartlett
The European Medicine Agency’s Committee for Medicinal Products for Human Use (CHMP) has issued a positive opinion for ofatumumab (Arzerra), a monoclonal antibody targeting CD20.
The CHMP is recommending that ofatumumab receive conditional approval for use in combination with chlorambucil or bendamustine to treat patients with chronic lymphocytic leukemia (CLL) who have not received prior therapy and are not eligible for fludarabine-based therapy.
The European Commission (EC) will take the CHMP’s opinion into account when deciding whether to approve ofatumumab for this indication.
Ofatumumab already has conditional approval in the Europe Union to treat CLL patients who are refractory to fludarabine and alemtuzumab.
Ofatumumab received conditional approval because the drug’s benefits appear to outweigh the risks it poses. The drug will not receive full
approval until the companies developing ofatumumab, GlaxoSmithKline and Genmab, submit results of additional research to the EC.
The CHMP’s recommendation for expanded approval is based on results from 2 trials in patients with CLL who were ineligible for fludarabine-based treatment.
The first is a phase 2 study (OMB115991) in which researchers evaluated the efficacy of ofatumumab in combination with bendamustine. The second is the phase 3 COMPLEMENT 1 study (OMB110911), a randomized trial in which researchers compared ofatumumab and chlorambucil in combination to chlorambucil alone.
Phase 2 study
Results from this single-arm study were presented at the 2013 International Workshop on CLL. Researchers enrolled 97 patients with CLL, 44 of whom were previously untreated and 53 who had relapsed. The median ages were 62.5 and 68 years, respectively.
Treatment began with acetaminophen, an antihistamine, and a glucocorticoid. Patients then received ofatumumab at 300 mg on day 1 and 1000 mg on day 8 of cycle 1. For cycles 2 through 6, they received 1000 mg on day 1 every 28 days.
Patients received bendamustine on days 1 and 2, every 28 days for up to 6 cycles. The initial dose was 90 mg/m2 for the untreated patients and 70 mg/m2 for relapsed patients.
However, patients required a dose reduction due to toxicity. The previously untreated patients were reduced to 60 mg/m2, and the relapsed patients were reduced to 50 mg/m2.
The overall response rate was 95% in the previously untreated group and 74% in the relapsed group. Complete responses occurred in 43% and 11%, respectively.
CT results showed the overall response rate was 82% in the previously untreated group and 70% in the relapsed group. Complete responses occurred in 27% and 9%, respectively. The median time to response was 0.95 months for both groups.
Grade 3 or higher adverse events occurred in 25% of patients in the previously untreated group and 38% of those in the relapsed group.
This included infusion reactions (11% and 8%, respectively), neutropenia (16% and 29%, respectively), infections (11% and 15%, respectively), rash (2% of previously untreated patients), febrile neutropenia (4% of relapsed patients), and thrombocytopenia (4% of relapsed patients).
There were no deaths in the previously untreated group, but 4 patients died in the relapsed group. Two of these deaths may have been related to study treatment. One patient died of pneumonia and hemolytic anemia 15 days after the last dose of treatment, and 1 patient died of sepsis 4 days after the last dose of treatment.
Phase 3 study
Data from the COMPLEMENT 1 study were presented at ASH 2013. Researchers compared ofatumumab plus chlorambucil to chlorambucil alone in 447 previously untreated patients with CLL who were ineligible for fludarabine-based therapy.
Patients had a median age of 69 years (range, 35 to 92). Seventy-two percent had 2 or more comorbidities, and 48% had a creatinine clearance of less than 70 mL/min.
Patients in the ofatumumab arm received the drug at 300 mg in cycle 1 on day 1, 1000 mg in cycle 1 on day 8, and 1000 mg administered on day 1 of all subsequent 28-day cycles.
In both arms, patients received chlorambucil at a dose of 10 mg/m2 orally on days 1 to 7, every 28 days. Prior to each infusion of ofatumumab, patients received acetaminophen, an antihistamine, and a glucocorticoid.
The overall response rate was 82% in the ofatumumab-chlorambucil group and 69% in the chlorambucil-alone group (P=0.001). Complete response rates were 12% and 1%, respectively.
At a median follow-up of 29 months, the median overall survival was not reached for either treatment arm. However, ofatumumab-treated patients had longer progression-free survival than patients who received chlorambucil alone—22.4 months and 13.1 months, respectively (P<0.001).
Grade 3 or higher adverse events occurred in 50% of ofatumumab-treated patients and 43% of patients who received chlorambucil alone. The most common event was neutropenia, which occurred in 26% and 14% of patients, respectively.
Grade 3 or higher infections occurred in 15% of ofatumumab-treated patients and 14% of patients who received chlorambucil alone. The most common was pneumonia, which occurred in 4% and 3%, respectively.
In the entire cohort, grade 3 or higher infusion-related events occurred in 10% of patients, but there were no fatal infusion reactions. Two percent of subjects in both arms died during treatment.
Credit: Linda Bartlett
The European Medicine Agency’s Committee for Medicinal Products for Human Use (CHMP) has issued a positive opinion for ofatumumab (Arzerra), a monoclonal antibody targeting CD20.
The CHMP is recommending that ofatumumab receive conditional approval for use in combination with chlorambucil or bendamustine to treat patients with chronic lymphocytic leukemia (CLL) who have not received prior therapy and are not eligible for fludarabine-based therapy.
The European Commission (EC) will take the CHMP’s opinion into account when deciding whether to approve ofatumumab for this indication.
Ofatumumab already has conditional approval in the Europe Union to treat CLL patients who are refractory to fludarabine and alemtuzumab.
Ofatumumab received conditional approval because the drug’s benefits appear to outweigh the risks it poses. The drug will not receive full
approval until the companies developing ofatumumab, GlaxoSmithKline and Genmab, submit results of additional research to the EC.
The CHMP’s recommendation for expanded approval is based on results from 2 trials in patients with CLL who were ineligible for fludarabine-based treatment.
The first is a phase 2 study (OMB115991) in which researchers evaluated the efficacy of ofatumumab in combination with bendamustine. The second is the phase 3 COMPLEMENT 1 study (OMB110911), a randomized trial in which researchers compared ofatumumab and chlorambucil in combination to chlorambucil alone.
Phase 2 study
Results from this single-arm study were presented at the 2013 International Workshop on CLL. Researchers enrolled 97 patients with CLL, 44 of whom were previously untreated and 53 who had relapsed. The median ages were 62.5 and 68 years, respectively.
Treatment began with acetaminophen, an antihistamine, and a glucocorticoid. Patients then received ofatumumab at 300 mg on day 1 and 1000 mg on day 8 of cycle 1. For cycles 2 through 6, they received 1000 mg on day 1 every 28 days.
Patients received bendamustine on days 1 and 2, every 28 days for up to 6 cycles. The initial dose was 90 mg/m2 for the untreated patients and 70 mg/m2 for relapsed patients.
However, patients required a dose reduction due to toxicity. The previously untreated patients were reduced to 60 mg/m2, and the relapsed patients were reduced to 50 mg/m2.
The overall response rate was 95% in the previously untreated group and 74% in the relapsed group. Complete responses occurred in 43% and 11%, respectively.
CT results showed the overall response rate was 82% in the previously untreated group and 70% in the relapsed group. Complete responses occurred in 27% and 9%, respectively. The median time to response was 0.95 months for both groups.
Grade 3 or higher adverse events occurred in 25% of patients in the previously untreated group and 38% of those in the relapsed group.
This included infusion reactions (11% and 8%, respectively), neutropenia (16% and 29%, respectively), infections (11% and 15%, respectively), rash (2% of previously untreated patients), febrile neutropenia (4% of relapsed patients), and thrombocytopenia (4% of relapsed patients).
There were no deaths in the previously untreated group, but 4 patients died in the relapsed group. Two of these deaths may have been related to study treatment. One patient died of pneumonia and hemolytic anemia 15 days after the last dose of treatment, and 1 patient died of sepsis 4 days after the last dose of treatment.
Phase 3 study
Data from the COMPLEMENT 1 study were presented at ASH 2013. Researchers compared ofatumumab plus chlorambucil to chlorambucil alone in 447 previously untreated patients with CLL who were ineligible for fludarabine-based therapy.
Patients had a median age of 69 years (range, 35 to 92). Seventy-two percent had 2 or more comorbidities, and 48% had a creatinine clearance of less than 70 mL/min.
Patients in the ofatumumab arm received the drug at 300 mg in cycle 1 on day 1, 1000 mg in cycle 1 on day 8, and 1000 mg administered on day 1 of all subsequent 28-day cycles.
In both arms, patients received chlorambucil at a dose of 10 mg/m2 orally on days 1 to 7, every 28 days. Prior to each infusion of ofatumumab, patients received acetaminophen, an antihistamine, and a glucocorticoid.
The overall response rate was 82% in the ofatumumab-chlorambucil group and 69% in the chlorambucil-alone group (P=0.001). Complete response rates were 12% and 1%, respectively.
At a median follow-up of 29 months, the median overall survival was not reached for either treatment arm. However, ofatumumab-treated patients had longer progression-free survival than patients who received chlorambucil alone—22.4 months and 13.1 months, respectively (P<0.001).
Grade 3 or higher adverse events occurred in 50% of ofatumumab-treated patients and 43% of patients who received chlorambucil alone. The most common event was neutropenia, which occurred in 26% and 14% of patients, respectively.
Grade 3 or higher infections occurred in 15% of ofatumumab-treated patients and 14% of patients who received chlorambucil alone. The most common was pneumonia, which occurred in 4% and 3%, respectively.
In the entire cohort, grade 3 or higher infusion-related events occurred in 10% of patients, but there were no fatal infusion reactions. Two percent of subjects in both arms died during treatment.
Credit: Linda Bartlett
The European Medicine Agency’s Committee for Medicinal Products for Human Use (CHMP) has issued a positive opinion for ofatumumab (Arzerra), a monoclonal antibody targeting CD20.
The CHMP is recommending that ofatumumab receive conditional approval for use in combination with chlorambucil or bendamustine to treat patients with chronic lymphocytic leukemia (CLL) who have not received prior therapy and are not eligible for fludarabine-based therapy.
The European Commission (EC) will take the CHMP’s opinion into account when deciding whether to approve ofatumumab for this indication.
Ofatumumab already has conditional approval in the Europe Union to treat CLL patients who are refractory to fludarabine and alemtuzumab.
Ofatumumab received conditional approval because the drug’s benefits appear to outweigh the risks it poses. The drug will not receive full
approval until the companies developing ofatumumab, GlaxoSmithKline and Genmab, submit results of additional research to the EC.
The CHMP’s recommendation for expanded approval is based on results from 2 trials in patients with CLL who were ineligible for fludarabine-based treatment.
The first is a phase 2 study (OMB115991) in which researchers evaluated the efficacy of ofatumumab in combination with bendamustine. The second is the phase 3 COMPLEMENT 1 study (OMB110911), a randomized trial in which researchers compared ofatumumab and chlorambucil in combination to chlorambucil alone.
Phase 2 study
Results from this single-arm study were presented at the 2013 International Workshop on CLL. Researchers enrolled 97 patients with CLL, 44 of whom were previously untreated and 53 who had relapsed. The median ages were 62.5 and 68 years, respectively.
Treatment began with acetaminophen, an antihistamine, and a glucocorticoid. Patients then received ofatumumab at 300 mg on day 1 and 1000 mg on day 8 of cycle 1. For cycles 2 through 6, they received 1000 mg on day 1 every 28 days.
Patients received bendamustine on days 1 and 2, every 28 days for up to 6 cycles. The initial dose was 90 mg/m2 for the untreated patients and 70 mg/m2 for relapsed patients.
However, patients required a dose reduction due to toxicity. The previously untreated patients were reduced to 60 mg/m2, and the relapsed patients were reduced to 50 mg/m2.
The overall response rate was 95% in the previously untreated group and 74% in the relapsed group. Complete responses occurred in 43% and 11%, respectively.
CT results showed the overall response rate was 82% in the previously untreated group and 70% in the relapsed group. Complete responses occurred in 27% and 9%, respectively. The median time to response was 0.95 months for both groups.
Grade 3 or higher adverse events occurred in 25% of patients in the previously untreated group and 38% of those in the relapsed group.
This included infusion reactions (11% and 8%, respectively), neutropenia (16% and 29%, respectively), infections (11% and 15%, respectively), rash (2% of previously untreated patients), febrile neutropenia (4% of relapsed patients), and thrombocytopenia (4% of relapsed patients).
There were no deaths in the previously untreated group, but 4 patients died in the relapsed group. Two of these deaths may have been related to study treatment. One patient died of pneumonia and hemolytic anemia 15 days after the last dose of treatment, and 1 patient died of sepsis 4 days after the last dose of treatment.
Phase 3 study
Data from the COMPLEMENT 1 study were presented at ASH 2013. Researchers compared ofatumumab plus chlorambucil to chlorambucil alone in 447 previously untreated patients with CLL who were ineligible for fludarabine-based therapy.
Patients had a median age of 69 years (range, 35 to 92). Seventy-two percent had 2 or more comorbidities, and 48% had a creatinine clearance of less than 70 mL/min.
Patients in the ofatumumab arm received the drug at 300 mg in cycle 1 on day 1, 1000 mg in cycle 1 on day 8, and 1000 mg administered on day 1 of all subsequent 28-day cycles.
In both arms, patients received chlorambucil at a dose of 10 mg/m2 orally on days 1 to 7, every 28 days. Prior to each infusion of ofatumumab, patients received acetaminophen, an antihistamine, and a glucocorticoid.
The overall response rate was 82% in the ofatumumab-chlorambucil group and 69% in the chlorambucil-alone group (P=0.001). Complete response rates were 12% and 1%, respectively.
At a median follow-up of 29 months, the median overall survival was not reached for either treatment arm. However, ofatumumab-treated patients had longer progression-free survival than patients who received chlorambucil alone—22.4 months and 13.1 months, respectively (P<0.001).
Grade 3 or higher adverse events occurred in 50% of ofatumumab-treated patients and 43% of patients who received chlorambucil alone. The most common event was neutropenia, which occurred in 26% and 14% of patients, respectively.
Grade 3 or higher infections occurred in 15% of ofatumumab-treated patients and 14% of patients who received chlorambucil alone. The most common was pneumonia, which occurred in 4% and 3%, respectively.
In the entire cohort, grade 3 or higher infusion-related events occurred in 10% of patients, but there were no fatal infusion reactions. Two percent of subjects in both arms died during treatment.
Refugees struggle to access cancer treatment
Credit: UK Department
for International Development
A new study published in The Lancet Oncology reveals a high demand for costly cancer treatment among refugees from the recent conflicts in Iraq and Syria, with host countries struggling to find the money and medicine to treat their new patients.
The findings prompted a call from study author Paul Spiegel, MD, the United Nations High Commissioner for Refugees (UNHCR) Chief Medical Expert, for schemes to improve access to affordable cancer care for refugees.
In the first study of its kind, Dr Spiegel and his colleagues examined data from funding applications made to the UNHCR Exceptional Care Committee (ECC) from refugees in Jordan and Syria whose cancer treatment costs were likely to exceed US$2000 a year.
The results indicate that cancer is an important public health problem in refugee settings, the researchers said. The study also highlights the challenges and costs national health systems and humanitarian organizations face when overwhelmed by massive influxes of refugees.
For example, in Jordan, the ECC assessed 1989 applications for treatment between 2010 and 2012. Roughly a quarter of these (511) were for cancer, with breast cancer and colorectal cancer being the most common. Around half (48%) of these cases were approved and funded.
Funding was often denied because the patient had a poor prognosis (43% of cases in 2011 and 31% in 2012) or the treatment was too costly (25% in 2011). The average amount requested from the ECC for cancer treatment was $11,540 in 2011 and $5151 in 2012. However, the amounts approved were substantially lower—$4626 in 2011 and $3501 in 2012.
“The countries in the Middle East have welcomed millions of refugees, first from Iraq and then Syria,” Dr Spiegel said. “This massive influx has strained health systems at all levels. Despite help from international organizations and donors to expand health facilities and pay for additional personnel and drugs, it has been insufficient.”
“The burden has fallen disproportionately on the host countries to absorb the costs. For example, the Jordanian Ministry of Health footed an estimated $53 million bill for medical care for refugees in the first 4 months of 2013.”
Dr Spiegel and his colleagues are therefore calling for improved cancer prevention and treatment in refugee settings through the use of innovative financing schemes; better primary care, including screening for common cancers (eg, colonoscopies and mammograms); and the development of web-based cancer registries to prevent the interruption of treatment.
“Until now, the responses to humanitarian crises have been primarily based on experiences from refugee camps in sub-Saharan Africa where infectious diseases and malnutrition have been the priority,” Dr Spiegel said. “In the 21st century, refugee situations are substantially longer and increasingly occur in middle-income countries where the levels of chronic diseases, including cancer, are higher.”
“Cancer diagnosis and care in humanitarian emergencies typifies a growing trend towards more costly chronic disease care, something that seems to have been overlooked but is of increasing importance because the number of refugees is growing.”
Credit: UK Department
for International Development
A new study published in The Lancet Oncology reveals a high demand for costly cancer treatment among refugees from the recent conflicts in Iraq and Syria, with host countries struggling to find the money and medicine to treat their new patients.
The findings prompted a call from study author Paul Spiegel, MD, the United Nations High Commissioner for Refugees (UNHCR) Chief Medical Expert, for schemes to improve access to affordable cancer care for refugees.
In the first study of its kind, Dr Spiegel and his colleagues examined data from funding applications made to the UNHCR Exceptional Care Committee (ECC) from refugees in Jordan and Syria whose cancer treatment costs were likely to exceed US$2000 a year.
The results indicate that cancer is an important public health problem in refugee settings, the researchers said. The study also highlights the challenges and costs national health systems and humanitarian organizations face when overwhelmed by massive influxes of refugees.
For example, in Jordan, the ECC assessed 1989 applications for treatment between 2010 and 2012. Roughly a quarter of these (511) were for cancer, with breast cancer and colorectal cancer being the most common. Around half (48%) of these cases were approved and funded.
Funding was often denied because the patient had a poor prognosis (43% of cases in 2011 and 31% in 2012) or the treatment was too costly (25% in 2011). The average amount requested from the ECC for cancer treatment was $11,540 in 2011 and $5151 in 2012. However, the amounts approved were substantially lower—$4626 in 2011 and $3501 in 2012.
“The countries in the Middle East have welcomed millions of refugees, first from Iraq and then Syria,” Dr Spiegel said. “This massive influx has strained health systems at all levels. Despite help from international organizations and donors to expand health facilities and pay for additional personnel and drugs, it has been insufficient.”
“The burden has fallen disproportionately on the host countries to absorb the costs. For example, the Jordanian Ministry of Health footed an estimated $53 million bill for medical care for refugees in the first 4 months of 2013.”
Dr Spiegel and his colleagues are therefore calling for improved cancer prevention and treatment in refugee settings through the use of innovative financing schemes; better primary care, including screening for common cancers (eg, colonoscopies and mammograms); and the development of web-based cancer registries to prevent the interruption of treatment.
“Until now, the responses to humanitarian crises have been primarily based on experiences from refugee camps in sub-Saharan Africa where infectious diseases and malnutrition have been the priority,” Dr Spiegel said. “In the 21st century, refugee situations are substantially longer and increasingly occur in middle-income countries where the levels of chronic diseases, including cancer, are higher.”
“Cancer diagnosis and care in humanitarian emergencies typifies a growing trend towards more costly chronic disease care, something that seems to have been overlooked but is of increasing importance because the number of refugees is growing.”
Credit: UK Department
for International Development
A new study published in The Lancet Oncology reveals a high demand for costly cancer treatment among refugees from the recent conflicts in Iraq and Syria, with host countries struggling to find the money and medicine to treat their new patients.
The findings prompted a call from study author Paul Spiegel, MD, the United Nations High Commissioner for Refugees (UNHCR) Chief Medical Expert, for schemes to improve access to affordable cancer care for refugees.
In the first study of its kind, Dr Spiegel and his colleagues examined data from funding applications made to the UNHCR Exceptional Care Committee (ECC) from refugees in Jordan and Syria whose cancer treatment costs were likely to exceed US$2000 a year.
The results indicate that cancer is an important public health problem in refugee settings, the researchers said. The study also highlights the challenges and costs national health systems and humanitarian organizations face when overwhelmed by massive influxes of refugees.
For example, in Jordan, the ECC assessed 1989 applications for treatment between 2010 and 2012. Roughly a quarter of these (511) were for cancer, with breast cancer and colorectal cancer being the most common. Around half (48%) of these cases were approved and funded.
Funding was often denied because the patient had a poor prognosis (43% of cases in 2011 and 31% in 2012) or the treatment was too costly (25% in 2011). The average amount requested from the ECC for cancer treatment was $11,540 in 2011 and $5151 in 2012. However, the amounts approved were substantially lower—$4626 in 2011 and $3501 in 2012.
“The countries in the Middle East have welcomed millions of refugees, first from Iraq and then Syria,” Dr Spiegel said. “This massive influx has strained health systems at all levels. Despite help from international organizations and donors to expand health facilities and pay for additional personnel and drugs, it has been insufficient.”
“The burden has fallen disproportionately on the host countries to absorb the costs. For example, the Jordanian Ministry of Health footed an estimated $53 million bill for medical care for refugees in the first 4 months of 2013.”
Dr Spiegel and his colleagues are therefore calling for improved cancer prevention and treatment in refugee settings through the use of innovative financing schemes; better primary care, including screening for common cancers (eg, colonoscopies and mammograms); and the development of web-based cancer registries to prevent the interruption of treatment.
“Until now, the responses to humanitarian crises have been primarily based on experiences from refugee camps in sub-Saharan Africa where infectious diseases and malnutrition have been the priority,” Dr Spiegel said. “In the 21st century, refugee situations are substantially longer and increasingly occur in middle-income countries where the levels of chronic diseases, including cancer, are higher.”
“Cancer diagnosis and care in humanitarian emergencies typifies a growing trend towards more costly chronic disease care, something that seems to have been overlooked but is of increasing importance because the number of refugees is growing.”
Study explains why pneumococcal vaccines fall short in SCD
Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems.
Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems.
Credit: St Jude Children’s
Research Hospital
A new study reveals differences in the pneumococcal genome that explain why current vaccines do not sufficiently protect children with sickle cell disease (SCD) from pneumococcal infections.
Researchers performed whole-genome sequencing of hundreds of pneumococcal bacteria collected from healthy subjects and patients with SCD.
The team found that disease-causing strains of the bacteria differed between the 2 groups.
And the pneumococcal strains from the SCD patients differed from the 13 pneumococcal strains included in the current vaccine recommended for children age 5 and younger.
“The results help explain why current vaccines haven’t been as successful at protecting children with sickle cell disease from pneumococcal infections as they have in protecting other children,” said Joshua Wolf, MD, of St Jude Children’s Research Hospital.
Dr Wolf and his colleagues detailed these results in Cell Host & Microbe.
The researchers had compared the genomes of 322 pneumococcal bacteria collected from SCD patients between 1994 and 2011 to DNA from 327 strains obtained from individuals without SCD.
The analysis revealed that, over time, the genomes of bacteria isolated from SCD patients shrank, as genes and the corresponding DNA were discarded or combined. The changes reflected bacterial adaptation to the SCD host and contributed to the bacteria’s ability to persist despite advances in preventive care.
The researchers then used transposon sequencing to compare the bacterial fitness of pneumococcal genes in mice with and without SCD. This revealed 60 genes whose transposon disruption resulted in fitness differences between the 2 types of mice.
So the bacteria faced different conditions in animals with and without SCD. The bloodstream of normal mice was a more hostile environment for pneumococcal bacteria than the bloodstream of mice with SCD.
When the researchers evaluated the aforementioned 60 genes in bacteria isolated from SCD patients, they found 6 that were missing or altered in a significant percentage of samples (P<0.05). This included SP0511, SP0946, SP1032, SP1449, SP1483, and SP1835.
These genes are involved in transporting iron into bacteria, bacterial metabolism, and other processes that are likely altered in patients with SCD.
“We demonstrated that genes necessary to cause disease in the general public are expendable in patients with sickle cell disease,” said study author Jason Rosch, PhD, also of St Jude.
The researchers believe these findings will aid efforts to improve vaccine effectiveness and inform research into new ways to protect young SCD patients from life-threatening pneumococcal infections that can lead to pneumonia, meningitis, bloodstream infections, and other problems.
South Africa changes blood donation policy
Photo courtesy of UAB Hospital
The South African National Blood Service (SANBS) has lessened restrictions on blood donation for men who have sex with men (MSM) but placed a new restriction on heterosexual donors.
Now, all South Africans are prohibited from donating blood unless they have been celibate or in a monogamous sexual relationship for at least 6 months.
So any individual with a new sexual partner or multiple partners will not be allowed to donate blood, regardless of sexual orientation.
South Africa’s former policy was that MSM could only donate blood if they had been celibate for 6 months or longer. But heterosexual individuals who engaged in risky or casual sex were still allowed to donate.
This was because MSM were considered at high risk of contracting HIV. However, the South African HIV epidemic is primarily a heterosexual one, so the SANBS’s policy was thought by many to be discriminatory.
With the new policy, the question intended to identify MSM has been removed from the blood donor questionnaire. The new questionnaire addresses sexual risk in general, and any sexual act or contact with a new partner or partners during the preceding 6 months will be deemed a risk to the safety of the blood supply.
“It took us a while [to make this decision] because we didn’t have local facts that warranted changing our policy, although we knew South Africa was different from other countries in terms of risk of HIV,” said Vanessa Raju, SANBS Communications Manager.
“The policy wasn’t meant to be discriminatory, but it was seen as such. We then worked closely with the Department of Health and other organizations to reassess the situation.”
Blood donation policies perceived as discriminatory against MSM are in place in many countries.
In the US and Northern Ireland, for example, MSM are banned from donating blood for life. Canada lifted its lifetime ban last year but still requires that MSM be celibate for 5 years before donating.
Other countries have recently adopted similar policies. In England, Scotland, and Wales, MSM must be celibate for 12 months prior to donating blood. 
Photo courtesy of UAB Hospital
The South African National Blood Service (SANBS) has lessened restrictions on blood donation for men who have sex with men (MSM) but placed a new restriction on heterosexual donors.
Now, all South Africans are prohibited from donating blood unless they have been celibate or in a monogamous sexual relationship for at least 6 months.
So any individual with a new sexual partner or multiple partners will not be allowed to donate blood, regardless of sexual orientation.
South Africa’s former policy was that MSM could only donate blood if they had been celibate for 6 months or longer. But heterosexual individuals who engaged in risky or casual sex were still allowed to donate.
This was because MSM were considered at high risk of contracting HIV. However, the South African HIV epidemic is primarily a heterosexual one, so the SANBS’s policy was thought by many to be discriminatory.
With the new policy, the question intended to identify MSM has been removed from the blood donor questionnaire. The new questionnaire addresses sexual risk in general, and any sexual act or contact with a new partner or partners during the preceding 6 months will be deemed a risk to the safety of the blood supply.
“It took us a while [to make this decision] because we didn’t have local facts that warranted changing our policy, although we knew South Africa was different from other countries in terms of risk of HIV,” said Vanessa Raju, SANBS Communications Manager.
“The policy wasn’t meant to be discriminatory, but it was seen as such. We then worked closely with the Department of Health and other organizations to reassess the situation.”
Blood donation policies perceived as discriminatory against MSM are in place in many countries.
In the US and Northern Ireland, for example, MSM are banned from donating blood for life. Canada lifted its lifetime ban last year but still requires that MSM be celibate for 5 years before donating.
Other countries have recently adopted similar policies. In England, Scotland, and Wales, MSM must be celibate for 12 months prior to donating blood.
Photo courtesy of UAB Hospital
The South African National Blood Service (SANBS) has lessened restrictions on blood donation for men who have sex with men (MSM) but placed a new restriction on heterosexual donors.
Now, all South Africans are prohibited from donating blood unless they have been celibate or in a monogamous sexual relationship for at least 6 months.
So any individual with a new sexual partner or multiple partners will not be allowed to donate blood, regardless of sexual orientation.
South Africa’s former policy was that MSM could only donate blood if they had been celibate for 6 months or longer. But heterosexual individuals who engaged in risky or casual sex were still allowed to donate.
This was because MSM were considered at high risk of contracting HIV. However, the South African HIV epidemic is primarily a heterosexual one, so the SANBS’s policy was thought by many to be discriminatory.
With the new policy, the question intended to identify MSM has been removed from the blood donor questionnaire. The new questionnaire addresses sexual risk in general, and any sexual act or contact with a new partner or partners during the preceding 6 months will be deemed a risk to the safety of the blood supply.
“It took us a while [to make this decision] because we didn’t have local facts that warranted changing our policy, although we knew South Africa was different from other countries in terms of risk of HIV,” said Vanessa Raju, SANBS Communications Manager.
“The policy wasn’t meant to be discriminatory, but it was seen as such. We then worked closely with the Department of Health and other organizations to reassess the situation.”
Blood donation policies perceived as discriminatory against MSM are in place in many countries.
In the US and Northern Ireland, for example, MSM are banned from donating blood for life. Canada lifted its lifetime ban last year but still requires that MSM be celibate for 5 years before donating.
Other countries have recently adopted similar policies. In England, Scotland, and Wales, MSM must be celibate for 12 months prior to donating blood.