Hematology Times

Cancer patient receives therapy

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.

Cancer patient receives therapy

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.

Cancer patient receives therapy

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.

Monoclonal antibodies

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.

Monoclonal antibodies

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.

Monoclonal antibodies

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.

Doctor with Syrian refugees

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.”

Doctor with Syrian refugees

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.”

Doctor with Syrian refugees

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.”

Doctor examines SCD patient

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.

Doctor examines SCD patient

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.

Doctor examines SCD patient

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.

Blood for transfusion

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.

Blood for transfusion

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.

Blood for transfusion

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.

CLL cells in the bone marrow

The US Food and Drug Administration (FDA) has granted orphan designation for MOR208, an anti-CD19 monoclonal antibody, for the treatment of chronic lymphocytic leukemia (CLL) or small lymphocytic leukemia (SLL).

The European Medicines Agency (EMA) also announced a positive opinion of the orphan medicinal product application for MOR208 to treat patients with CLL/SLL.

Researchers said MOR208 showed promise in a phase 1 study of CLL/SLL patients.

Orphan drug and orphan medicinal product status are granted by the FDA and EMA to promote the development of promising therapeutics for the treatment of rare diseases affecting fewer than 200,000 people in the US annually and no more than 5 in 10,000 people in the European Union (EU).

Orphan drug designation includes benefits such as a 7-year period of marketing exclusivity in the US and 10 years of market exclusivity in the EU after approval. Other potential advantages come in the form of protocol assistance, the ability to apply for research funding, tax credits for certain research expenses, and fee waivers for the regulatory procedures.

MOR208 development, results

MOR208 is a humanized monoclonal antibody that targets the antigen CD19 for treatment of B-cell malignancies and autoimmune diseases. The development program for MOR208 is currently in phase 2 development in CLL, B-cell acute lymphoblastic leukemia, and non-Hodgkin lymphoma.

The drug is being developed by MorphoSys AG. The development program was in-licensed from Xencor in 2010.

Researchers evaluated MOR208 (formerly known as XmAb5574) in a phase 1 study of patients with CLL/SLL and reported their results at the 2012 ASH Annual Meeting (abstract 2894). The study was sponsored by Xencor.

The study included 27 patients with relapsed or refractory CLL/SLL. The median patient age was 66 years (range, 40-84), and patients were generally high-risk. The median number of prior therapies was 4 (range, 1-14).

Patients received MOR208 at a range of doses—0.3 mg/kg, 1 mg/kg, 3 mg/kg, 6 mg/kg, 9 mg/kg, and 12 mg/kg. MOR208 was administered as an intravenous infusion on days 1, 4, 8, 15, and 22 of cycle 1, and on days 1, 8, 15, and 22 of cycle 2.

Dose escalation continued without dose-limiting toxicities until the highest dose level. At this dose, 1 patient experienced grade 4 neutropenia associated with febrile neutropenia, and the patient was taken off treatment.

All 27 patients experienced adverse events, but the majority of them were grade 1-2. The most common events were infusion reactions. These occurred in 67% (n=18) of patients and were all grade 1 or 2.

Nineteen percent of patients (n=5) experienced grade 3-4 treatment-related adverse events, including neutropenia (n=3), thrombocytopenia (n=2), increased aspartate aminotransferase (n=1), febrile neutropenia (n=1), and tumor lysis syndrome (n=1).  Four of these patients were on the 12 mg/kg dose, but 1 patient who experienced neutropenia was receiving 1 mg/kg.

Eleven percent of patients experienced a partial response according to IWCLL 2008 criteria. Responses occurred at the 6 mg/kg, 9 mg/kg, and 12 mg/kg dose levels.

All objective responses occurred in patients categorized as CLL as opposed to SLL, and none of the patients with lymph nodes greater than 5 cm responded. Two patients had progressed at the 8-week evaluation point.

CLL cells in the bone marrow

The US Food and Drug Administration (FDA) has granted orphan designation for MOR208, an anti-CD19 monoclonal antibody, for the treatment of chronic lymphocytic leukemia (CLL) or small lymphocytic leukemia (SLL).

The European Medicines Agency (EMA) also announced a positive opinion of the orphan medicinal product application for MOR208 to treat patients with CLL/SLL.

Researchers said MOR208 showed promise in a phase 1 study of CLL/SLL patients.

Orphan drug and orphan medicinal product status are granted by the FDA and EMA to promote the development of promising therapeutics for the treatment of rare diseases affecting fewer than 200,000 people in the US annually and no more than 5 in 10,000 people in the European Union (EU).

Orphan drug designation includes benefits such as a 7-year period of marketing exclusivity in the US and 10 years of market exclusivity in the EU after approval. Other potential advantages come in the form of protocol assistance, the ability to apply for research funding, tax credits for certain research expenses, and fee waivers for the regulatory procedures.

MOR208 development, results

MOR208 is a humanized monoclonal antibody that targets the antigen CD19 for treatment of B-cell malignancies and autoimmune diseases. The development program for MOR208 is currently in phase 2 development in CLL, B-cell acute lymphoblastic leukemia, and non-Hodgkin lymphoma.

The drug is being developed by MorphoSys AG. The development program was in-licensed from Xencor in 2010.

Researchers evaluated MOR208 (formerly known as XmAb5574) in a phase 1 study of patients with CLL/SLL and reported their results at the 2012 ASH Annual Meeting (abstract 2894). The study was sponsored by Xencor.

The study included 27 patients with relapsed or refractory CLL/SLL. The median patient age was 66 years (range, 40-84), and patients were generally high-risk. The median number of prior therapies was 4 (range, 1-14).

Patients received MOR208 at a range of doses—0.3 mg/kg, 1 mg/kg, 3 mg/kg, 6 mg/kg, 9 mg/kg, and 12 mg/kg. MOR208 was administered as an intravenous infusion on days 1, 4, 8, 15, and 22 of cycle 1, and on days 1, 8, 15, and 22 of cycle 2.

Dose escalation continued without dose-limiting toxicities until the highest dose level. At this dose, 1 patient experienced grade 4 neutropenia associated with febrile neutropenia, and the patient was taken off treatment.

All 27 patients experienced adverse events, but the majority of them were grade 1-2. The most common events were infusion reactions. These occurred in 67% (n=18) of patients and were all grade 1 or 2.

Nineteen percent of patients (n=5) experienced grade 3-4 treatment-related adverse events, including neutropenia (n=3), thrombocytopenia (n=2), increased aspartate aminotransferase (n=1), febrile neutropenia (n=1), and tumor lysis syndrome (n=1).  Four of these patients were on the 12 mg/kg dose, but 1 patient who experienced neutropenia was receiving 1 mg/kg.

Eleven percent of patients experienced a partial response according to IWCLL 2008 criteria. Responses occurred at the 6 mg/kg, 9 mg/kg, and 12 mg/kg dose levels.

All objective responses occurred in patients categorized as CLL as opposed to SLL, and none of the patients with lymph nodes greater than 5 cm responded. Two patients had progressed at the 8-week evaluation point.

CLL cells in the bone marrow

The US Food and Drug Administration (FDA) has granted orphan designation for MOR208, an anti-CD19 monoclonal antibody, for the treatment of chronic lymphocytic leukemia (CLL) or small lymphocytic leukemia (SLL).

The European Medicines Agency (EMA) also announced a positive opinion of the orphan medicinal product application for MOR208 to treat patients with CLL/SLL.

Researchers said MOR208 showed promise in a phase 1 study of CLL/SLL patients.

Orphan drug and orphan medicinal product status are granted by the FDA and EMA to promote the development of promising therapeutics for the treatment of rare diseases affecting fewer than 200,000 people in the US annually and no more than 5 in 10,000 people in the European Union (EU).

Orphan drug designation includes benefits such as a 7-year period of marketing exclusivity in the US and 10 years of market exclusivity in the EU after approval. Other potential advantages come in the form of protocol assistance, the ability to apply for research funding, tax credits for certain research expenses, and fee waivers for the regulatory procedures.

MOR208 development, results

MOR208 is a humanized monoclonal antibody that targets the antigen CD19 for treatment of B-cell malignancies and autoimmune diseases. The development program for MOR208 is currently in phase 2 development in CLL, B-cell acute lymphoblastic leukemia, and non-Hodgkin lymphoma.

The drug is being developed by MorphoSys AG. The development program was in-licensed from Xencor in 2010.

Researchers evaluated MOR208 (formerly known as XmAb5574) in a phase 1 study of patients with CLL/SLL and reported their results at the 2012 ASH Annual Meeting (abstract 2894). The study was sponsored by Xencor.

The study included 27 patients with relapsed or refractory CLL/SLL. The median patient age was 66 years (range, 40-84), and patients were generally high-risk. The median number of prior therapies was 4 (range, 1-14).

Patients received MOR208 at a range of doses—0.3 mg/kg, 1 mg/kg, 3 mg/kg, 6 mg/kg, 9 mg/kg, and 12 mg/kg. MOR208 was administered as an intravenous infusion on days 1, 4, 8, 15, and 22 of cycle 1, and on days 1, 8, 15, and 22 of cycle 2.

Dose escalation continued without dose-limiting toxicities until the highest dose level. At this dose, 1 patient experienced grade 4 neutropenia associated with febrile neutropenia, and the patient was taken off treatment.

All 27 patients experienced adverse events, but the majority of them were grade 1-2. The most common events were infusion reactions. These occurred in 67% (n=18) of patients and were all grade 1 or 2.

Nineteen percent of patients (n=5) experienced grade 3-4 treatment-related adverse events, including neutropenia (n=3), thrombocytopenia (n=2), increased aspartate aminotransferase (n=1), febrile neutropenia (n=1), and tumor lysis syndrome (n=1).  Four of these patients were on the 12 mg/kg dose, but 1 patient who experienced neutropenia was receiving 1 mg/kg.

Eleven percent of patients experienced a partial response according to IWCLL 2008 criteria. Responses occurred at the 6 mg/kg, 9 mg/kg, and 12 mg/kg dose levels.

All objective responses occurred in patients categorized as CLL as opposed to SLL, and none of the patients with lymph nodes greater than 5 cm responded. Two patients had progressed at the 8-week evaluation point.

Blood sample collection

Credit: Juan D. Alfonso

The US Food and Drug Administration (FDA) has approved the first molecular assay for determining blood compatibility prior to transfusion.

The Immucor PreciseType Human Erythrocyte Antigen (HEA) Molecular BeadChip Test can be used to determine donor and patient non-ABO/non-RhD red blood cell types.

The test provides an alternative to serological typing and may enhance patient care in certain situations, according to Karen Midthun, MD, director of the FDA’s Center for Biologics Evaluation and Research.

The Immucor PreciseType HEA Molecular BeadChip Test works by detecting genes that govern the expression of 36 antigens that can appear on the surface of red blood cells.

The test uses thousands of coded beads that bind with the genes coding for non-ABO red blood cell antigens that are present in a blood sample.

A light signal is generated from each bead that has captured a specific gene. Accompanying computer software decodes the light signals and reports which antigens are predicted to be present on the red cells, based on the genes detected.

Researchers conducted a study to compare the typing results of the PreciseType HEA Molecular BeadChip Test with licensed serological reagents and DNA sequencing. And the results demonstrated comparable performance between the methods.

The product was brought before the FDA’s Blood Products Advisory Committee on March 18, 2014. After reviewing the relevant information, the committee said the data provided reasonable assurance that the Immucor PreciseType HEA Molecular BeadChip Test is safe and effective for its intended use.

The test is manufactured by BioArray Solutions Ltd. of Warren, New Jersey.

Blood sample collection

Credit: Juan D. Alfonso

The US Food and Drug Administration (FDA) has approved the first molecular assay for determining blood compatibility prior to transfusion.

The Immucor PreciseType Human Erythrocyte Antigen (HEA) Molecular BeadChip Test can be used to determine donor and patient non-ABO/non-RhD red blood cell types.

The test provides an alternative to serological typing and may enhance patient care in certain situations, according to Karen Midthun, MD, director of the FDA’s Center for Biologics Evaluation and Research.

The Immucor PreciseType HEA Molecular BeadChip Test works by detecting genes that govern the expression of 36 antigens that can appear on the surface of red blood cells.

The test uses thousands of coded beads that bind with the genes coding for non-ABO red blood cell antigens that are present in a blood sample.

A light signal is generated from each bead that has captured a specific gene. Accompanying computer software decodes the light signals and reports which antigens are predicted to be present on the red cells, based on the genes detected.

Researchers conducted a study to compare the typing results of the PreciseType HEA Molecular BeadChip Test with licensed serological reagents and DNA sequencing. And the results demonstrated comparable performance between the methods.

The product was brought before the FDA’s Blood Products Advisory Committee on March 18, 2014. After reviewing the relevant information, the committee said the data provided reasonable assurance that the Immucor PreciseType HEA Molecular BeadChip Test is safe and effective for its intended use.

The test is manufactured by BioArray Solutions Ltd. of Warren, New Jersey.

Blood sample collection

Credit: Juan D. Alfonso

The US Food and Drug Administration (FDA) has approved the first molecular assay for determining blood compatibility prior to transfusion.

The Immucor PreciseType Human Erythrocyte Antigen (HEA) Molecular BeadChip Test can be used to determine donor and patient non-ABO/non-RhD red blood cell types.

The test provides an alternative to serological typing and may enhance patient care in certain situations, according to Karen Midthun, MD, director of the FDA’s Center for Biologics Evaluation and Research.

The Immucor PreciseType HEA Molecular BeadChip Test works by detecting genes that govern the expression of 36 antigens that can appear on the surface of red blood cells.

The test uses thousands of coded beads that bind with the genes coding for non-ABO red blood cell antigens that are present in a blood sample.

A light signal is generated from each bead that has captured a specific gene. Accompanying computer software decodes the light signals and reports which antigens are predicted to be present on the red cells, based on the genes detected.

Researchers conducted a study to compare the typing results of the PreciseType HEA Molecular BeadChip Test with licensed serological reagents and DNA sequencing. And the results demonstrated comparable performance between the methods.

The product was brought before the FDA’s Blood Products Advisory Committee on March 18, 2014. After reviewing the relevant information, the committee said the data provided reasonable assurance that the Immucor PreciseType HEA Molecular BeadChip Test is safe and effective for its intended use.

The test is manufactured by BioArray Solutions Ltd. of Warren, New Jersey.

Malaria parasite in a cell

Credit: St Jude Children’s

Research Hospital

Investigators have identified antibodies that prevent malaria-causing parasites at the schizont stage from rupturing and spilling into the bloodstream.

These antibodies reduced loads of the parasite significantly in mice and humans, and they might one day be exploited to create a malaria vaccine, according to the researchers.

Jonathan Kurtis, MD, PhD, of Rhode Island Hospital in Providence, and his colleagues described the antibodies and their effects in Science.

The investigators studied the plasma of malaria-resistant 2-year-olds in Tanzania, where the disease is endemic. The team thought the naturally acquired immunity in these chronically exposed individuals provided a good model through which to identify vaccine antigens.

The analysis revealed that a particular Plasmodium falciparum antigen, known as P falciparum schizont egress antigen-1 (PfSEA-1), triggered antibodies in the children that, in turn, blocked replication of the parasite.

When the researchers vaccinated malaria-infected mice with the antigen or passively transferred PfSEA-1 antibodies to the rodents, they observed a 4-fold reduction of malaria parasites in the animals’ blood.

“When my post-doctoral fellow, Dipak Raj, discovered that antibodies to this protein, PfSEA-1, effectively trapped the malaria-causing parasite within the red blood cells, it was truly a moment of discovery,” Dr Kurtis said.

“Many researchers are trying to find ways to develop a malaria vaccine by preventing the parasite from entering the red blood cell, and, here, we found a way to block it from leaving the cell once it has entered. If it’s trapped in the red blood cell, it can’t go anywhere. It can’t do any further damage.”

The presence of PfSEA-1 antibodies also appeared to protect the Tanzanian study participants from severe cases of malaria. The investigators measured antibodies to PfSEA-1 in the entire cohort of 785 children and found that, among those with antibodies to PfSEA-1, there were no cases of severe malaria.

To generalize their results, the researchers then went back to serum samples they had collected from 140 children in Kenya in 1997. Analyses revealed that individuals with antibodies to PfSEA-1 had 50% lower parasitemia than individuals without these antibodies during a high-transmission season.

The investigators believe these findings could bring researchers a step closer to an effective malaria vaccine that targets parasites at multiple life stages.

“We still have additional trials ahead of us, first in another animal model, but we hope to begin phase 1 trials in humans very soon,” Dr Kurtis said.

“Our findings support PfSEA-1 as a potential vaccine candidate. And we are confident that, by partnering with our colleagues at the National Institutes of Health and other researchers focused on vaccines to prevent the parasites from entering red blood cells, we can approach the parasite from all angles, which could help us develop a truly effective vaccine to prevent this infectious disease that kills millions of children every year.”

Malaria parasite in a cell

Credit: St Jude Children’s

Research Hospital

Investigators have identified antibodies that prevent malaria-causing parasites at the schizont stage from rupturing and spilling into the bloodstream.

These antibodies reduced loads of the parasite significantly in mice and humans, and they might one day be exploited to create a malaria vaccine, according to the researchers.

Jonathan Kurtis, MD, PhD, of Rhode Island Hospital in Providence, and his colleagues described the antibodies and their effects in Science.

The investigators studied the plasma of malaria-resistant 2-year-olds in Tanzania, where the disease is endemic. The team thought the naturally acquired immunity in these chronically exposed individuals provided a good model through which to identify vaccine antigens.

The analysis revealed that a particular Plasmodium falciparum antigen, known as P falciparum schizont egress antigen-1 (PfSEA-1), triggered antibodies in the children that, in turn, blocked replication of the parasite.

When the researchers vaccinated malaria-infected mice with the antigen or passively transferred PfSEA-1 antibodies to the rodents, they observed a 4-fold reduction of malaria parasites in the animals’ blood.

“When my post-doctoral fellow, Dipak Raj, discovered that antibodies to this protein, PfSEA-1, effectively trapped the malaria-causing parasite within the red blood cells, it was truly a moment of discovery,” Dr Kurtis said.

“Many researchers are trying to find ways to develop a malaria vaccine by preventing the parasite from entering the red blood cell, and, here, we found a way to block it from leaving the cell once it has entered. If it’s trapped in the red blood cell, it can’t go anywhere. It can’t do any further damage.”

The presence of PfSEA-1 antibodies also appeared to protect the Tanzanian study participants from severe cases of malaria. The investigators measured antibodies to PfSEA-1 in the entire cohort of 785 children and found that, among those with antibodies to PfSEA-1, there were no cases of severe malaria.

To generalize their results, the researchers then went back to serum samples they had collected from 140 children in Kenya in 1997. Analyses revealed that individuals with antibodies to PfSEA-1 had 50% lower parasitemia than individuals without these antibodies during a high-transmission season.

The investigators believe these findings could bring researchers a step closer to an effective malaria vaccine that targets parasites at multiple life stages.

“We still have additional trials ahead of us, first in another animal model, but we hope to begin phase 1 trials in humans very soon,” Dr Kurtis said.

“Our findings support PfSEA-1 as a potential vaccine candidate. And we are confident that, by partnering with our colleagues at the National Institutes of Health and other researchers focused on vaccines to prevent the parasites from entering red blood cells, we can approach the parasite from all angles, which could help us develop a truly effective vaccine to prevent this infectious disease that kills millions of children every year.”

Malaria parasite in a cell

Credit: St Jude Children’s

Research Hospital

Investigators have identified antibodies that prevent malaria-causing parasites at the schizont stage from rupturing and spilling into the bloodstream.

These antibodies reduced loads of the parasite significantly in mice and humans, and they might one day be exploited to create a malaria vaccine, according to the researchers.

Jonathan Kurtis, MD, PhD, of Rhode Island Hospital in Providence, and his colleagues described the antibodies and their effects in Science.

The investigators studied the plasma of malaria-resistant 2-year-olds in Tanzania, where the disease is endemic. The team thought the naturally acquired immunity in these chronically exposed individuals provided a good model through which to identify vaccine antigens.

The analysis revealed that a particular Plasmodium falciparum antigen, known as P falciparum schizont egress antigen-1 (PfSEA-1), triggered antibodies in the children that, in turn, blocked replication of the parasite.

When the researchers vaccinated malaria-infected mice with the antigen or passively transferred PfSEA-1 antibodies to the rodents, they observed a 4-fold reduction of malaria parasites in the animals’ blood.

“When my post-doctoral fellow, Dipak Raj, discovered that antibodies to this protein, PfSEA-1, effectively trapped the malaria-causing parasite within the red blood cells, it was truly a moment of discovery,” Dr Kurtis said.

“Many researchers are trying to find ways to develop a malaria vaccine by preventing the parasite from entering the red blood cell, and, here, we found a way to block it from leaving the cell once it has entered. If it’s trapped in the red blood cell, it can’t go anywhere. It can’t do any further damage.”

The presence of PfSEA-1 antibodies also appeared to protect the Tanzanian study participants from severe cases of malaria. The investigators measured antibodies to PfSEA-1 in the entire cohort of 785 children and found that, among those with antibodies to PfSEA-1, there were no cases of severe malaria.

To generalize their results, the researchers then went back to serum samples they had collected from 140 children in Kenya in 1997. Analyses revealed that individuals with antibodies to PfSEA-1 had 50% lower parasitemia than individuals without these antibodies during a high-transmission season.

The investigators believe these findings could bring researchers a step closer to an effective malaria vaccine that targets parasites at multiple life stages.

“We still have additional trials ahead of us, first in another animal model, but we hope to begin phase 1 trials in humans very soon,” Dr Kurtis said.

“Our findings support PfSEA-1 as a potential vaccine candidate. And we are confident that, by partnering with our colleagues at the National Institutes of Health and other researchers focused on vaccines to prevent the parasites from entering red blood cells, we can approach the parasite from all angles, which could help us develop a truly effective vaccine to prevent this infectious disease that kills millions of children every year.”

Doctor and patient

Credit: CDC

The medical technology company CareFusion has announced a Class I recall of its Alaris Pump model 8100, software version 9.1.18.

This large-volume infusion pump is used for the delivery of fluids, medicines, blood, and blood products.

Version 9.1.18 of the Alaris Pump model 8100 is being recalled due to the possibility of a software failure in which the pump module will not properly delay an infusion when the “Delay Until” option or “Multidose” feature is used.

There have been no reports of adverse events or deaths related to this malfunction, but it does pose risks. CareFusion has received 1 report where the device malfunctioned when the “Delay Until” option was selected.

The software failure also prevents the pump from properly delivering a multidose infusion under the following conditions:

• When the first dose is programmed to infuse when the system time is earlier than 7 pm and a subsequent dose is intended to infuse between 7 pm and 11:59 pm
• When the first dose is programmed to infuse when the system time is between 7 pm and 11:59 pm and a subsequent dose is intended to infuse between 12 am and 6:59 pm the next day.

If the infusion starts earlier or later than intended and is not immediately detected and stopped, serious injury or death could result. Therefore, healthcare professionals should not use the Alaris Pump module “Delay Until” option or the “Multidose” option.

However, CareFusion said it has identified the root cause of the issue and recommends that the previous Alaris Pump module software version 9.1.17 be installed to address this recall. The company said it will contact all affected customers to schedule the installation of software version 9.1.17.

As an interim guidance, customers may update their dataset to disable both “Delay” options (“Delay Until” and “Delay For”) and/or the “Multidose” option across all profiles to prevent the use of these features. These are shared configurations with the Alaris Syringe module and, if disabled, would prevent use of these features with the Alaris Syringe module as well.

For more information on this recall, see CareFusion’s recall notice, or contact the CareFusion Support Center at 888-562-6018 or SupportCenter@carefusion.com.

To report adverse reactions or quality problems associated with this product, visit the Food and Drug Administration’s MedWatch website.

Doctor and patient

Credit: CDC

The medical technology company CareFusion has announced a Class I recall of its Alaris Pump model 8100, software version 9.1.18.

This large-volume infusion pump is used for the delivery of fluids, medicines, blood, and blood products.

Version 9.1.18 of the Alaris Pump model 8100 is being recalled due to the possibility of a software failure in which the pump module will not properly delay an infusion when the “Delay Until” option or “Multidose” feature is used.

There have been no reports of adverse events or deaths related to this malfunction, but it does pose risks. CareFusion has received 1 report where the device malfunctioned when the “Delay Until” option was selected.

The software failure also prevents the pump from properly delivering a multidose infusion under the following conditions:

• When the first dose is programmed to infuse when the system time is earlier than 7 pm and a subsequent dose is intended to infuse between 7 pm and 11:59 pm
• When the first dose is programmed to infuse when the system time is between 7 pm and 11:59 pm and a subsequent dose is intended to infuse between 12 am and 6:59 pm the next day.

If the infusion starts earlier or later than intended and is not immediately detected and stopped, serious injury or death could result. Therefore, healthcare professionals should not use the Alaris Pump module “Delay Until” option or the “Multidose” option.

However, CareFusion said it has identified the root cause of the issue and recommends that the previous Alaris Pump module software version 9.1.17 be installed to address this recall. The company said it will contact all affected customers to schedule the installation of software version 9.1.17.

As an interim guidance, customers may update their dataset to disable both “Delay” options (“Delay Until” and “Delay For”) and/or the “Multidose” option across all profiles to prevent the use of these features. These are shared configurations with the Alaris Syringe module and, if disabled, would prevent use of these features with the Alaris Syringe module as well.

For more information on this recall, see CareFusion’s recall notice, or contact the CareFusion Support Center at 888-562-6018 or SupportCenter@carefusion.com.

To report adverse reactions or quality problems associated with this product, visit the Food and Drug Administration’s MedWatch website.

Doctor and patient

Credit: CDC

The medical technology company CareFusion has announced a Class I recall of its Alaris Pump model 8100, software version 9.1.18.

This large-volume infusion pump is used for the delivery of fluids, medicines, blood, and blood products.

Version 9.1.18 of the Alaris Pump model 8100 is being recalled due to the possibility of a software failure in which the pump module will not properly delay an infusion when the “Delay Until” option or “Multidose” feature is used.

There have been no reports of adverse events or deaths related to this malfunction, but it does pose risks. CareFusion has received 1 report where the device malfunctioned when the “Delay Until” option was selected.

The software failure also prevents the pump from properly delivering a multidose infusion under the following conditions:

• When the first dose is programmed to infuse when the system time is earlier than 7 pm and a subsequent dose is intended to infuse between 7 pm and 11:59 pm
• When the first dose is programmed to infuse when the system time is between 7 pm and 11:59 pm and a subsequent dose is intended to infuse between 12 am and 6:59 pm the next day.

If the infusion starts earlier or later than intended and is not immediately detected and stopped, serious injury or death could result. Therefore, healthcare professionals should not use the Alaris Pump module “Delay Until” option or the “Multidose” option.

However, CareFusion said it has identified the root cause of the issue and recommends that the previous Alaris Pump module software version 9.1.17 be installed to address this recall. The company said it will contact all affected customers to schedule the installation of software version 9.1.17.

As an interim guidance, customers may update their dataset to disable both “Delay” options (“Delay Until” and “Delay For”) and/or the “Multidose” option across all profiles to prevent the use of these features. These are shared configurations with the Alaris Syringe module and, if disabled, would prevent use of these features with the Alaris Syringe module as well.

For more information on this recall, see CareFusion’s recall notice, or contact the CareFusion Support Center at 888-562-6018 or SupportCenter@carefusion.com.

To report adverse reactions or quality problems associated with this product, visit the Food and Drug Administration’s MedWatch website.

TPN components

The US Food and Drug Administration (FDA) has announced a Class I recall of Baxter Corporation Englewood’s ABACUS Total Parenteral Nutrition (TPN) Calculation Software, versions 3.1, 3.0, 2.1, and 2.0.

Baxter has received 2 reports of malfunctioning software and said errors with this software may cause adverse effects.

ABACUS TPN Calculation Software is a Windows-based software application used by pharmacists to calculate or order TPN formulas.

The errors explained

Due to software failures, the following errors may occur:

• ABACUS v3.1 may calculate quantities of electrolytes that are double the expected values during the creation of TPN orders.
• ABACUS v3.1 may automatically add additional sterile water to a formula equal to the volume of a premix, resulting in an over-dilution.
• All software versions of ABACUS software display the calcium phosphate curve points for Premasol incorrectly.
• All software versions of ABACUS may display an inaccurate estimation for calcium and phosphate precipitation in certain circumstances where multiple ingredients provide calcium.

If any of these failures occur, patients may be at risk of developing overdose symptoms. The symptoms are varied and depend on the type of software failure and composition of the fluid being compounded.

Symptoms may be non-specific and include nausea, vomiting, dizziness, or fatigue. Some more severe symptoms include cardiac arrhythmia, pulmonary edema, congestive heart failure, and seizures. A fatal outcome is possible, especially in the high-risk population.

Actions to take

Baxter is recommending that customers contact the company to ensure the ABACUS software is configured correctly.

Customers with a software version earlier than 3.1 will have software version 3.1 installed, which addresses the issues that prompted the recall. In addition, Baxter Support Services will schedule upgrades and assist customers with establishing the proper ABACUS configuration in the customers’ facilities.

Baxter has also requested that customers follow safe compounding practices. Namely, use the “Summary” button to verify the order against the calculated amounts prior to completing the order.

In addition, verify that the ordered ingredients and quantities displayed in the software and printed on the Bag label and the Solution Formula label match the PN prescription prior to preparation. And use a filter for administration of a PN bag.

For more information on the recall, see the FDA’s recall notice, or contact Baxter at 303-617-2242. For technical support, call 1-800-678-2292 or email COtechsupport@baxter.com.

To report adverse reactions or quality problems related to this product, visit the FDA’s MedWatch website.

TPN components

The US Food and Drug Administration (FDA) has announced a Class I recall of Baxter Corporation Englewood’s ABACUS Total Parenteral Nutrition (TPN) Calculation Software, versions 3.1, 3.0, 2.1, and 2.0.

Baxter has received 2 reports of malfunctioning software and said errors with this software may cause adverse effects.

ABACUS TPN Calculation Software is a Windows-based software application used by pharmacists to calculate or order TPN formulas.

The errors explained

Due to software failures, the following errors may occur:

• ABACUS v3.1 may calculate quantities of electrolytes that are double the expected values during the creation of TPN orders.
• ABACUS v3.1 may automatically add additional sterile water to a formula equal to the volume of a premix, resulting in an over-dilution.
• All software versions of ABACUS software display the calcium phosphate curve points for Premasol incorrectly.
• All software versions of ABACUS may display an inaccurate estimation for calcium and phosphate precipitation in certain circumstances where multiple ingredients provide calcium.

If any of these failures occur, patients may be at risk of developing overdose symptoms. The symptoms are varied and depend on the type of software failure and composition of the fluid being compounded.

Symptoms may be non-specific and include nausea, vomiting, dizziness, or fatigue. Some more severe symptoms include cardiac arrhythmia, pulmonary edema, congestive heart failure, and seizures. A fatal outcome is possible, especially in the high-risk population.

Actions to take

Baxter is recommending that customers contact the company to ensure the ABACUS software is configured correctly.

Customers with a software version earlier than 3.1 will have software version 3.1 installed, which addresses the issues that prompted the recall. In addition, Baxter Support Services will schedule upgrades and assist customers with establishing the proper ABACUS configuration in the customers’ facilities.

Baxter has also requested that customers follow safe compounding practices. Namely, use the “Summary” button to verify the order against the calculated amounts prior to completing the order.

In addition, verify that the ordered ingredients and quantities displayed in the software and printed on the Bag label and the Solution Formula label match the PN prescription prior to preparation. And use a filter for administration of a PN bag.

For more information on the recall, see the FDA’s recall notice, or contact Baxter at 303-617-2242. For technical support, call 1-800-678-2292 or email COtechsupport@baxter.com.

To report adverse reactions or quality problems related to this product, visit the FDA’s MedWatch website.

TPN components

The US Food and Drug Administration (FDA) has announced a Class I recall of Baxter Corporation Englewood’s ABACUS Total Parenteral Nutrition (TPN) Calculation Software, versions 3.1, 3.0, 2.1, and 2.0.

Baxter has received 2 reports of malfunctioning software and said errors with this software may cause adverse effects.

ABACUS TPN Calculation Software is a Windows-based software application used by pharmacists to calculate or order TPN formulas.

The errors explained

Due to software failures, the following errors may occur:

• ABACUS v3.1 may calculate quantities of electrolytes that are double the expected values during the creation of TPN orders.
• ABACUS v3.1 may automatically add additional sterile water to a formula equal to the volume of a premix, resulting in an over-dilution.
• All software versions of ABACUS software display the calcium phosphate curve points for Premasol incorrectly.
• All software versions of ABACUS may display an inaccurate estimation for calcium and phosphate precipitation in certain circumstances where multiple ingredients provide calcium.

If any of these failures occur, patients may be at risk of developing overdose symptoms. The symptoms are varied and depend on the type of software failure and composition of the fluid being compounded.

Symptoms may be non-specific and include nausea, vomiting, dizziness, or fatigue. Some more severe symptoms include cardiac arrhythmia, pulmonary edema, congestive heart failure, and seizures. A fatal outcome is possible, especially in the high-risk population.

Actions to take

Baxter is recommending that customers contact the company to ensure the ABACUS software is configured correctly.

Customers with a software version earlier than 3.1 will have software version 3.1 installed, which addresses the issues that prompted the recall. In addition, Baxter Support Services will schedule upgrades and assist customers with establishing the proper ABACUS configuration in the customers’ facilities.

Baxter has also requested that customers follow safe compounding practices. Namely, use the “Summary” button to verify the order against the calculated amounts prior to completing the order.

In addition, verify that the ordered ingredients and quantities displayed in the software and printed on the Bag label and the Solution Formula label match the PN prescription prior to preparation. And use a filter for administration of a PN bag.

For more information on the recall, see the FDA’s recall notice, or contact Baxter at 303-617-2242. For technical support, call 1-800-678-2292 or email COtechsupport@baxter.com.

To report adverse reactions or quality problems related to this product, visit the FDA’s MedWatch website.