“Drugs don’t work in patients who don’t take them.”

–C. Everett Koop, M.D.

While it would be hard to imagine accountable care organizations being able to get the data they need to manage care without electronic health records, and EHRs are critical as payment has evolved to emphasize the outcomes of treatment, one area remains the holy grail of disease management: how to get patients to take the medications that are prescribed.

Poor adherence to medications is a critical issue in the management of chronic disease. The causes for suboptimal adherence are numerous, including the cost of medications, patient-physician communication, patient education, motivation, and simple forgetfulness.

Approximately 1.5 billion prescriptions, at a cost of more than $250 billion, are dispensed each year in the United States. A large body of evidence supports the use of these medications. For patients with diabetes, for instance, correct medication use can lower blood sugar, blood pressure, and cholesterol, and by so doing, decrease morbidity and mortality from both microvascular and macrovascular disease.

The act of taking medications is influenced by many factors, and all of these factors come together at a point in time when patients are not directly engaged with the health care system. It is at that moment that patients remember and decide whether to take their medications.

Numerous studies show that individuals often do not take their medicines as prescribed. Adherence rates for medications for chronic disease show that patients on average take only about 50% of prescribed doses. For patients with diabetes, the average adherence rate is about 70%, with rates ranging in different studies from 31% to 87%.

When patients do not take their medications correctly, there can be severe consequences. Poor medication adherence can lead to poorer clinical outcomes, including increased hospitalizations. One large dataset of more than 56,000 individuals with type 2 diabetes covered by employer-sponsored health insurance showed that increased adherence to medications significantly reduced hospitalizations and emergency department visits. When adherence rates increased, the hospitalization rate fell 23%, and the rate of emergency department visits decreased 46%, resulting in significant cost savings for the health system.¹

In response to this issue, many strategies have emerged. We now regularly get correspondence from insurance companies alerting us to nonadherence of individual patients. This information tends to be of little benefit, because the information is received long after the decision to take or not take the medication is made. Our response in the office to our patients is generally to remind them to take their medications, which is not much different from the discussion we have with them without that information.

Recently, a new set of apps for smartphones and tablets has emerged to help patients organize their approach to taking medications. Examples of some of these apps include Care4Today, Dosecast, Medisafe, MedSimple, MyMedREc, MyMeds, and OnTimeRx. Most of these apps allow a patient to put in their medication schedule and are organized to provide reminders when it is time to take medications.

The problem with reminders, of course, is that they don’t always happen at a time when it is convenient for a person to take their medications. For example, if your app reminds you to take your medicines at 9 p.m. each night, and you are at the movies on a Saturday night, you may extinguish the reminder and not remember to take the medications when you get home.

Many of the apps also track adherence rates so that patients can see how well they are doing in taking their medications. The results are often startling to patients, and it is hoped that such information would encourage more effort in taking medications.

One problem with many of the apps currently available is that they essentially function as sophisticated alarm clocks. They do not get at some of the fundamental reasons that people do not take their medications, which would require more behavioral input.

In fact, a recent article in the American Journal of Preventive Medicine looked at 166 medication adherence apps and concluded that current apps contained little in the way of evidence-based behavioral change techniques that have been shown to help change behavior. In fact, only about one-third of apps contained any feedback on behavior at all.²

While adherence apps still have a way to go, they can be helpful, and many contain interesting, novel features. Some allow the patient to input the name of a medication by scanning the name from the medication’s pill bottle. Some have the ability not only to remind a patient to take a medication, but also to text that patient’s caregiver (or parent, in the case of a teenager) if the medication is not taken.

While not perfect, these adherence apps are worth learning more about. They may be helpful additions to our efforts to achieve the best outcomes for our patients by helping them to actually take the medications that we so carefully prescribe.

References

1. Encinosa, W.E.; Bernard, D.; Dor, A. Does prescription drug adherence reduce hospitalizations and costs? The case of diabetes. Advances in Health Economics and Health Services Research 22, pp. 151-73, 2010 (AHRQ Publication No. 11-R008).

2. Am J Prev Med. 2015 Nov 17. pii: S0749-3797(15)00637-6. doi: 10.1016/j.amepre.2015.09.034.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.

“Drugs don’t work in patients who don’t take them.”

–C. Everett Koop, M.D.

While it would be hard to imagine accountable care organizations being able to get the data they need to manage care without electronic health records, and EHRs are critical as payment has evolved to emphasize the outcomes of treatment, one area remains the holy grail of disease management: how to get patients to take the medications that are prescribed.

Poor adherence to medications is a critical issue in the management of chronic disease. The causes for suboptimal adherence are numerous, including the cost of medications, patient-physician communication, patient education, motivation, and simple forgetfulness.

Approximately 1.5 billion prescriptions, at a cost of more than $250 billion, are dispensed each year in the United States. A large body of evidence supports the use of these medications. For patients with diabetes, for instance, correct medication use can lower blood sugar, blood pressure, and cholesterol, and by so doing, decrease morbidity and mortality from both microvascular and macrovascular disease.

The act of taking medications is influenced by many factors, and all of these factors come together at a point in time when patients are not directly engaged with the health care system. It is at that moment that patients remember and decide whether to take their medications.

Numerous studies show that individuals often do not take their medicines as prescribed. Adherence rates for medications for chronic disease show that patients on average take only about 50% of prescribed doses. For patients with diabetes, the average adherence rate is about 70%, with rates ranging in different studies from 31% to 87%.

When patients do not take their medications correctly, there can be severe consequences. Poor medication adherence can lead to poorer clinical outcomes, including increased hospitalizations. One large dataset of more than 56,000 individuals with type 2 diabetes covered by employer-sponsored health insurance showed that increased adherence to medications significantly reduced hospitalizations and emergency department visits. When adherence rates increased, the hospitalization rate fell 23%, and the rate of emergency department visits decreased 46%, resulting in significant cost savings for the health system.¹

In response to this issue, many strategies have emerged. We now regularly get correspondence from insurance companies alerting us to nonadherence of individual patients. This information tends to be of little benefit, because the information is received long after the decision to take or not take the medication is made. Our response in the office to our patients is generally to remind them to take their medications, which is not much different from the discussion we have with them without that information.

Recently, a new set of apps for smartphones and tablets has emerged to help patients organize their approach to taking medications. Examples of some of these apps include Care4Today, Dosecast, Medisafe, MedSimple, MyMedREc, MyMeds, and OnTimeRx. Most of these apps allow a patient to put in their medication schedule and are organized to provide reminders when it is time to take medications.

The problem with reminders, of course, is that they don’t always happen at a time when it is convenient for a person to take their medications. For example, if your app reminds you to take your medicines at 9 p.m. each night, and you are at the movies on a Saturday night, you may extinguish the reminder and not remember to take the medications when you get home.

Many of the apps also track adherence rates so that patients can see how well they are doing in taking their medications. The results are often startling to patients, and it is hoped that such information would encourage more effort in taking medications.

One problem with many of the apps currently available is that they essentially function as sophisticated alarm clocks. They do not get at some of the fundamental reasons that people do not take their medications, which would require more behavioral input.

In fact, a recent article in the American Journal of Preventive Medicine looked at 166 medication adherence apps and concluded that current apps contained little in the way of evidence-based behavioral change techniques that have been shown to help change behavior. In fact, only about one-third of apps contained any feedback on behavior at all.²

While adherence apps still have a way to go, they can be helpful, and many contain interesting, novel features. Some allow the patient to input the name of a medication by scanning the name from the medication’s pill bottle. Some have the ability not only to remind a patient to take a medication, but also to text that patient’s caregiver (or parent, in the case of a teenager) if the medication is not taken.

While not perfect, these adherence apps are worth learning more about. They may be helpful additions to our efforts to achieve the best outcomes for our patients by helping them to actually take the medications that we so carefully prescribe.

References

1. Encinosa, W.E.; Bernard, D.; Dor, A. Does prescription drug adherence reduce hospitalizations and costs? The case of diabetes. Advances in Health Economics and Health Services Research 22, pp. 151-73, 2010 (AHRQ Publication No. 11-R008).

2. Am J Prev Med. 2015 Nov 17. pii: S0749-3797(15)00637-6. doi: 10.1016/j.amepre.2015.09.034.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.

“Drugs don’t work in patients who don’t take them.”

–C. Everett Koop, M.D.

While it would be hard to imagine accountable care organizations being able to get the data they need to manage care without electronic health records, and EHRs are critical as payment has evolved to emphasize the outcomes of treatment, one area remains the holy grail of disease management: how to get patients to take the medications that are prescribed.

Poor adherence to medications is a critical issue in the management of chronic disease. The causes for suboptimal adherence are numerous, including the cost of medications, patient-physician communication, patient education, motivation, and simple forgetfulness.

Approximately 1.5 billion prescriptions, at a cost of more than $250 billion, are dispensed each year in the United States. A large body of evidence supports the use of these medications. For patients with diabetes, for instance, correct medication use can lower blood sugar, blood pressure, and cholesterol, and by so doing, decrease morbidity and mortality from both microvascular and macrovascular disease.

The act of taking medications is influenced by many factors, and all of these factors come together at a point in time when patients are not directly engaged with the health care system. It is at that moment that patients remember and decide whether to take their medications.

Numerous studies show that individuals often do not take their medicines as prescribed. Adherence rates for medications for chronic disease show that patients on average take only about 50% of prescribed doses. For patients with diabetes, the average adherence rate is about 70%, with rates ranging in different studies from 31% to 87%.

When patients do not take their medications correctly, there can be severe consequences. Poor medication adherence can lead to poorer clinical outcomes, including increased hospitalizations. One large dataset of more than 56,000 individuals with type 2 diabetes covered by employer-sponsored health insurance showed that increased adherence to medications significantly reduced hospitalizations and emergency department visits. When adherence rates increased, the hospitalization rate fell 23%, and the rate of emergency department visits decreased 46%, resulting in significant cost savings for the health system.¹

In response to this issue, many strategies have emerged. We now regularly get correspondence from insurance companies alerting us to nonadherence of individual patients. This information tends to be of little benefit, because the information is received long after the decision to take or not take the medication is made. Our response in the office to our patients is generally to remind them to take their medications, which is not much different from the discussion we have with them without that information.

Recently, a new set of apps for smartphones and tablets has emerged to help patients organize their approach to taking medications. Examples of some of these apps include Care4Today, Dosecast, Medisafe, MedSimple, MyMedREc, MyMeds, and OnTimeRx. Most of these apps allow a patient to put in their medication schedule and are organized to provide reminders when it is time to take medications.

The problem with reminders, of course, is that they don’t always happen at a time when it is convenient for a person to take their medications. For example, if your app reminds you to take your medicines at 9 p.m. each night, and you are at the movies on a Saturday night, you may extinguish the reminder and not remember to take the medications when you get home.

Many of the apps also track adherence rates so that patients can see how well they are doing in taking their medications. The results are often startling to patients, and it is hoped that such information would encourage more effort in taking medications.

One problem with many of the apps currently available is that they essentially function as sophisticated alarm clocks. They do not get at some of the fundamental reasons that people do not take their medications, which would require more behavioral input.

In fact, a recent article in the American Journal of Preventive Medicine looked at 166 medication adherence apps and concluded that current apps contained little in the way of evidence-based behavioral change techniques that have been shown to help change behavior. In fact, only about one-third of apps contained any feedback on behavior at all.²

While adherence apps still have a way to go, they can be helpful, and many contain interesting, novel features. Some allow the patient to input the name of a medication by scanning the name from the medication’s pill bottle. Some have the ability not only to remind a patient to take a medication, but also to text that patient’s caregiver (or parent, in the case of a teenager) if the medication is not taken.

While not perfect, these adherence apps are worth learning more about. They may be helpful additions to our efforts to achieve the best outcomes for our patients by helping them to actually take the medications that we so carefully prescribe.

References

1. Encinosa, W.E.; Bernard, D.; Dor, A. Does prescription drug adherence reduce hospitalizations and costs? The case of diabetes. Advances in Health Economics and Health Services Research 22, pp. 151-73, 2010 (AHRQ Publication No. 11-R008).

2. Am J Prev Med. 2015 Nov 17. pii: S0749-3797(15)00637-6. doi: 10.1016/j.amepre.2015.09.034.

Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.

In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

In a case study published online on March 2 in JAMA Dermatology, Geller et al examined the relationship between total nevi, atypical nevi, and melanoma thickness. The study included 566 patients with melanoma. They were administered written surveys and underwent skin examinations at academic centers in Michigan and California within 3 months of diagnosis, measuring current total nevus count and atypical nevus count in addition to cataloguing melanoma thickness, histologic subtype, patient age, sex, marital status, skin self-examination and physician skin examination tendency, other health care visits, and mode of melanoma discovery.

Many epidemiologic trends were noted, but in summary, most melanoma patients had 0 to 20 total nevi (66.4%) and no atypical nevi (73.3%), a trend most pronounced in older patients (≥60 years). In patients younger than 60 years, higher nevus count (>50) was associated with thinner melanomas (≤2.0 mm), and the presence of more than 5 atypical nevi was associated with thicker melanomas (>2.0 mm).

What’s the issue?Studies clarifying the overall clinical characteristics of patients with aggressive melanomas appear every month in reputable journals, touting that concurrent total nevus count is important; or nevus size is important; or atypia is important; or clinical stigmata, medical history, and family history are important. Who is correct? Is everyone correct? On the pathology arm of the argument, Rosendahl et al (J Am Acad Dermatol. 2015;73:507-512) highlighted the same dilemma in which clinicians do not agree on the histopathologic features of nevi that consistently put patients at risk for individual lesion or de novo melanoma.

For me, each clinic day involves performing many total-body skin examinations, and many of these patients have innumerable nevi and various scars from lesions removed over the years with “atypical mole,” “premelanoma,” “precancer,” and various other self-reported labels. Some lesions may have documented pathology reports, but many do not. Some reports refer to dysplasia as a gradient, some do not. Some reports include molecular testing or clinical markers to grade lesions, and each can vary between institutions and pathologists. On the macroscopic level, clinically atypical nevi do not have a widely agreed upon set of criteria or threshold for biopsy; some clinicians use dermoscopic markers, and others utilize some version of the ABCDE (a=asymmetry; b=border; c=color; d=diameter; e=evolving) features.

The Geller et al study supports that these melanoma patients did not necessarily have more total nevi, and younger patients with aggressive melanoma may have a tendency toward more clinically atypical nevi. Although the study establishes what those institutions and clinicians determined to be atypical, I’m not sure that this is something that most clinicians widely agree upon. Additionally, these features were not paired with histopathologic dysplasia because the lesions were not biopsied.

What I find in conversation with colleagues is that some agree with what Geller et al defined as atypical, but some clinicians do not even refer to nevi as clinically atypical in a medical record unless they have pathology evidence of atypia (or the term their pathologist may use), which may be to avoid controversy regarding legal implications of atypia or “open-note” misunderstanding that the patient may have about this term, likening it to Papanicolaou test premalignancy verbiage.

I am not aware of one dermatologist or dermatopathologist who does not find this quandary to be frustrating. How do any of us really know which patients to follow more often for melanoma surveillance? How does your practice or institution report atypia in the clinical and histopathologic setting, and what do you find are the most important markers for development of melanoma?

We want to know your views! Tell us what you think.

The Society of Hospital Medicine Center for Hospital Innovation is supporting the implementation of a second iteration of the Multi-Center Medication Reconciliation Quality Improvement Study, or MARQUIS2.  This is a mentored implementation program developed to assist hospitals and hospital clinicians with developing better ways for medications to be prescribed, recorded and reconciled accurately and safely at times of care transitions, e.g., when patients enter and leave the hospital.  The ultimate goal of the study is reduce medication errors, adverse drug events and patient harm during transitions of care. The program is funded through a grant provided by the Agency for Healthcare Research and Quality (AHRQ).

Unintentional medication discrepancies during transitions in care represent a major threat to patient safety. Medication reconciliation enables healthcare providers – and hospitalists in particular – to avoid medication errors such as omissions, duplications, dosing errors and adverse drug interactions and should be completed at every transition of care, including hospital admission and discharge. Beginning in April 2016, SHM will begin working with 18 selected hospital sites to identify, implement and sustain medication reconciliation interventions with guidance from expert physician mentors. Key examples of intervention components include educating providers on how to take a best possible medication history, improving access to preadmission medication sources, encouraging patient ownership of medication lists and identifying patients at higher risk for adverse drug events in need of more intensive efforts.

The Society of Hospital Medicine Center for Hospital Innovation is supporting the implementation of a second iteration of the Multi-Center Medication Reconciliation Quality Improvement Study, or MARQUIS2.  This is a mentored implementation program developed to assist hospitals and hospital clinicians with developing better ways for medications to be prescribed, recorded and reconciled accurately and safely at times of care transitions, e.g., when patients enter and leave the hospital.  The ultimate goal of the study is reduce medication errors, adverse drug events and patient harm during transitions of care. The program is funded through a grant provided by the Agency for Healthcare Research and Quality (AHRQ).

Unintentional medication discrepancies during transitions in care represent a major threat to patient safety. Medication reconciliation enables healthcare providers – and hospitalists in particular – to avoid medication errors such as omissions, duplications, dosing errors and adverse drug interactions and should be completed at every transition of care, including hospital admission and discharge. Beginning in April 2016, SHM will begin working with 18 selected hospital sites to identify, implement and sustain medication reconciliation interventions with guidance from expert physician mentors. Key examples of intervention components include educating providers on how to take a best possible medication history, improving access to preadmission medication sources, encouraging patient ownership of medication lists and identifying patients at higher risk for adverse drug events in need of more intensive efforts.

The Society of Hospital Medicine Center for Hospital Innovation is supporting the implementation of a second iteration of the Multi-Center Medication Reconciliation Quality Improvement Study, or MARQUIS2.  This is a mentored implementation program developed to assist hospitals and hospital clinicians with developing better ways for medications to be prescribed, recorded and reconciled accurately and safely at times of care transitions, e.g., when patients enter and leave the hospital.  The ultimate goal of the study is reduce medication errors, adverse drug events and patient harm during transitions of care. The program is funded through a grant provided by the Agency for Healthcare Research and Quality (AHRQ).

Unintentional medication discrepancies during transitions in care represent a major threat to patient safety. Medication reconciliation enables healthcare providers – and hospitalists in particular – to avoid medication errors such as omissions, duplications, dosing errors and adverse drug interactions and should be completed at every transition of care, including hospital admission and discharge. Beginning in April 2016, SHM will begin working with 18 selected hospital sites to identify, implement and sustain medication reconciliation interventions with guidance from expert physician mentors. Key examples of intervention components include educating providers on how to take a best possible medication history, improving access to preadmission medication sources, encouraging patient ownership of medication lists and identifying patients at higher risk for adverse drug events in need of more intensive efforts.

A few weeks ago, a young man, a child psychiatrist, called saying that he had read the first Weighty Issues column and that he agreed that psychiatrists should be actively involved in the weight loss arena.

He shared that he had several children in his practice whose body-mass indices were over 40 and that he was frustrated that the pediatricians he had spoken with seemed to be only watching and waiting for the children to grow taller. I told him what he already knew: Pediatricians have in place a very specific protocol to follow regarding the treatment of overweight and obesity in children.

I had the impression from him that he was not exactly sure that the protocol was being followed and that he was absolutely sure that the pediatricians had no appreciation of the emotional aspects of these children’s weights. He said he was so fired up about this that he was going to pursue American Board of Obesity Medicine diplomate status himself. In addition to his background in child psychiatry, he also had studied public health, and his parents had worked in the area of disease prevention.

I was thrilled by his call because he got it! Overweight and obesity are a public health menace. Every day, psychiatrists see patients with these maladies, and we should be more knowledgeable about them or armed to get the treatment started ourselves. Although this child psychiatrist continues to intervene with his patients’ pediatricians and embarks on his own ABOM studies, he can, as he sees his patients and their families, write prescriptions for exercise and play time for the family, limited screen time (TV and computer) for the youngsters, no sweetened beverages, fewer simple carbohydrates, and more plain water. These interventions all are consistent with routine lifestyle recommendations for children (and adults), and they also can promote improved well-being for children and family members.

A recent report indicated that about a quarter of 2- to 5-year-olds and one-third of school-aged children (6-18 years) are overweight or obese in the United States (JAMA. 2014 Feb 26;311[8]:306-14). By convention, body-mass index, a measure of relative body fat, is used to indicate underweight, normal weight, overweight, and obesity. It is derived from a formula: weight in kilograms divided by height in meters squared. In adults, normal is 18.5-24.9, overweight is 25-29.9, and obese is greater than or equal to 30 (National Institutes of Health/World Health Organization guidelines for BMI). For children, one calculates the BMI and then plots this on a graph in comparison to other children of the same age and sex to derive a percentile scale number. Percentile scale numbers from 58-94 indicate overweight, and percentiles greater than or equal to 95 indicate obesity in children aged 2-18 years. For children aged 0-2, a weight for length above the 95th percentile indicates overweight.

Childhood obesity is a major risk factor for overweight and obesity in adulthood, and for depression and cardiovascular disease in childhood and adulthood. It also sets one up for potential trouble in the areas of self-esteem, body image, body protection, poor school performance, and relationship issues with peers. These are areas of importance for psychiatrists, child and adult, as we assess, plan for, and treat our patients day to day. Furthermore, childhood overweight puts children at risk for type 2 diabetes, metabolic syndrome, high cholesterol and high blood pressure, asthma, sleep disorders, early puberty or menstruation, Blount’s disease (progressive turning of the lower leg, resembling bowleg), and nonalcoholic fatty liver disease. Obesity in adulthood leads to high blood pressure, strokes, type 2 diabetes, dementia, osteoarthritis, sleep apnea, obesity hypoventilation syndrome, reproductive problems, gallstones, and some cancers (esophagus, pancreas, colon, rectum, breast-after menopause, endometrium, kidney, thyroid, and gallbladder).

The late Dr. Hilde Bruch, one of my mentors in the 1970s, was an early thought leader in childhood obesity. She did research in this area starting in 1937 while practicing pediatrics before she became a psychiatrist in 1943. She said that she was struck by the number of overweight and obese children she observed in the United States, compared with what she had observed in Germany and England. (She died in 1984 at the age of 80 and would be greatly saddened that childhood obesity is now a global issue.) In her 1973 book, “Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within,” she grappled with the taking in of calories, and, speaking of hunger, said that “it is not innate, but something that contains important elements of learning.”

As an analyst, she thought of feeding learning as coming primarily from early mother-child interactions, but we now know that this learning can come through any repeated interaction and that genetic, social, cultural and environmental, and biological factors also apply.

The psychiatrist or anyone else working with children and families must endeavor to reduce self-blame, explore influences, and instill hope in the process toward normal weight and/or adequate management of weight. The psychiatrist and anyone else working with the child and family will appreciate that, if energy intake and physical activity output are manipulated consistently, the tendency for the child will be increasing height and decreasing BMI. The Prevention and Management of Obesity for Children and Adolescents Guideline is very clear about when to refer to a tertiary special weight management program for children. The guideline also speaks to use of weight-loss medication (orlistat for children 12 years and older, sibutramine for children 16 years and older). Bariatric surgery is recommended for children who have finished growing up (by growth plate evidence) and face imminent serious health issues if their weight cannot be brought under control. These children, after surgery, will need to radically restrain their eating, take supplements, and be followed for the rest of their lives to forestall complications and return to overweight and obesity. I believe that child and adult psychiatrists can be of tremendous use here in helping sort out both the physical and course-of-life issues that could threaten successful continued weight loss, whether the weight loss comes through lifestyle change, lifestyle change and medications, or bariatric surgery and subsequent lifestyle change.

I would like to thank that young child psychiatrist who called, because he spurred me to continue our “Weighty Issues” journey by looking at childhood and overweight and obesity and how it can affect our work as physicians and psychiatrists. Parental physical condition at conception and gestation, and genetics may set the stage, and then interaction with the family, the culture, the society, and the environment all interplay in the child’s development to produce an outcome of an overweight or obese child. We still are trying to discover why some but not all children in the same family, neighborhood, socioeconomic strata, culture, etc., are burdened by overweight. The reasons may be found through biological inquiry, but it may just as well in found in psychiatric/psychological inquiry.

Dr. Harris, a diplomate of the American Board of Obesity Medicine, is in private practice in adult and geriatric psychiatry in Hartford, Conn. She also works as a psychiatric consultant to continuing care retirement organizations and professional groups. Dr. Harris, a former president of the Black Psychiatrists of America, is a Distinguished Fellow of the American Psychiatric Association. Besides psychotherapy, her major clinical interests include geriatrics, and the interface between general medicine and psychiatry.

A few weeks ago, a young man, a child psychiatrist, called saying that he had read the first Weighty Issues column and that he agreed that psychiatrists should be actively involved in the weight loss arena.

He shared that he had several children in his practice whose body-mass indices were over 40 and that he was frustrated that the pediatricians he had spoken with seemed to be only watching and waiting for the children to grow taller. I told him what he already knew: Pediatricians have in place a very specific protocol to follow regarding the treatment of overweight and obesity in children.

I had the impression from him that he was not exactly sure that the protocol was being followed and that he was absolutely sure that the pediatricians had no appreciation of the emotional aspects of these children’s weights. He said he was so fired up about this that he was going to pursue American Board of Obesity Medicine diplomate status himself. In addition to his background in child psychiatry, he also had studied public health, and his parents had worked in the area of disease prevention.

I was thrilled by his call because he got it! Overweight and obesity are a public health menace. Every day, psychiatrists see patients with these maladies, and we should be more knowledgeable about them or armed to get the treatment started ourselves. Although this child psychiatrist continues to intervene with his patients’ pediatricians and embarks on his own ABOM studies, he can, as he sees his patients and their families, write prescriptions for exercise and play time for the family, limited screen time (TV and computer) for the youngsters, no sweetened beverages, fewer simple carbohydrates, and more plain water. These interventions all are consistent with routine lifestyle recommendations for children (and adults), and they also can promote improved well-being for children and family members.

A recent report indicated that about a quarter of 2- to 5-year-olds and one-third of school-aged children (6-18 years) are overweight or obese in the United States (JAMA. 2014 Feb 26;311[8]:306-14). By convention, body-mass index, a measure of relative body fat, is used to indicate underweight, normal weight, overweight, and obesity. It is derived from a formula: weight in kilograms divided by height in meters squared. In adults, normal is 18.5-24.9, overweight is 25-29.9, and obese is greater than or equal to 30 (National Institutes of Health/World Health Organization guidelines for BMI). For children, one calculates the BMI and then plots this on a graph in comparison to other children of the same age and sex to derive a percentile scale number. Percentile scale numbers from 58-94 indicate overweight, and percentiles greater than or equal to 95 indicate obesity in children aged 2-18 years. For children aged 0-2, a weight for length above the 95th percentile indicates overweight.

Childhood obesity is a major risk factor for overweight and obesity in adulthood, and for depression and cardiovascular disease in childhood and adulthood. It also sets one up for potential trouble in the areas of self-esteem, body image, body protection, poor school performance, and relationship issues with peers. These are areas of importance for psychiatrists, child and adult, as we assess, plan for, and treat our patients day to day. Furthermore, childhood overweight puts children at risk for type 2 diabetes, metabolic syndrome, high cholesterol and high blood pressure, asthma, sleep disorders, early puberty or menstruation, Blount’s disease (progressive turning of the lower leg, resembling bowleg), and nonalcoholic fatty liver disease. Obesity in adulthood leads to high blood pressure, strokes, type 2 diabetes, dementia, osteoarthritis, sleep apnea, obesity hypoventilation syndrome, reproductive problems, gallstones, and some cancers (esophagus, pancreas, colon, rectum, breast-after menopause, endometrium, kidney, thyroid, and gallbladder).

The late Dr. Hilde Bruch, one of my mentors in the 1970s, was an early thought leader in childhood obesity. She did research in this area starting in 1937 while practicing pediatrics before she became a psychiatrist in 1943. She said that she was struck by the number of overweight and obese children she observed in the United States, compared with what she had observed in Germany and England. (She died in 1984 at the age of 80 and would be greatly saddened that childhood obesity is now a global issue.) In her 1973 book, “Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within,” she grappled with the taking in of calories, and, speaking of hunger, said that “it is not innate, but something that contains important elements of learning.”

As an analyst, she thought of feeding learning as coming primarily from early mother-child interactions, but we now know that this learning can come through any repeated interaction and that genetic, social, cultural and environmental, and biological factors also apply.

The psychiatrist or anyone else working with children and families must endeavor to reduce self-blame, explore influences, and instill hope in the process toward normal weight and/or adequate management of weight. The psychiatrist and anyone else working with the child and family will appreciate that, if energy intake and physical activity output are manipulated consistently, the tendency for the child will be increasing height and decreasing BMI. The Prevention and Management of Obesity for Children and Adolescents Guideline is very clear about when to refer to a tertiary special weight management program for children. The guideline also speaks to use of weight-loss medication (orlistat for children 12 years and older, sibutramine for children 16 years and older). Bariatric surgery is recommended for children who have finished growing up (by growth plate evidence) and face imminent serious health issues if their weight cannot be brought under control. These children, after surgery, will need to radically restrain their eating, take supplements, and be followed for the rest of their lives to forestall complications and return to overweight and obesity. I believe that child and adult psychiatrists can be of tremendous use here in helping sort out both the physical and course-of-life issues that could threaten successful continued weight loss, whether the weight loss comes through lifestyle change, lifestyle change and medications, or bariatric surgery and subsequent lifestyle change.

I would like to thank that young child psychiatrist who called, because he spurred me to continue our “Weighty Issues” journey by looking at childhood and overweight and obesity and how it can affect our work as physicians and psychiatrists. Parental physical condition at conception and gestation, and genetics may set the stage, and then interaction with the family, the culture, the society, and the environment all interplay in the child’s development to produce an outcome of an overweight or obese child. We still are trying to discover why some but not all children in the same family, neighborhood, socioeconomic strata, culture, etc., are burdened by overweight. The reasons may be found through biological inquiry, but it may just as well in found in psychiatric/psychological inquiry.

Dr. Harris, a diplomate of the American Board of Obesity Medicine, is in private practice in adult and geriatric psychiatry in Hartford, Conn. She also works as a psychiatric consultant to continuing care retirement organizations and professional groups. Dr. Harris, a former president of the Black Psychiatrists of America, is a Distinguished Fellow of the American Psychiatric Association. Besides psychotherapy, her major clinical interests include geriatrics, and the interface between general medicine and psychiatry.

A few weeks ago, a young man, a child psychiatrist, called saying that he had read the first Weighty Issues column and that he agreed that psychiatrists should be actively involved in the weight loss arena.

He shared that he had several children in his practice whose body-mass indices were over 40 and that he was frustrated that the pediatricians he had spoken with seemed to be only watching and waiting for the children to grow taller. I told him what he already knew: Pediatricians have in place a very specific protocol to follow regarding the treatment of overweight and obesity in children.

I had the impression from him that he was not exactly sure that the protocol was being followed and that he was absolutely sure that the pediatricians had no appreciation of the emotional aspects of these children’s weights. He said he was so fired up about this that he was going to pursue American Board of Obesity Medicine diplomate status himself. In addition to his background in child psychiatry, he also had studied public health, and his parents had worked in the area of disease prevention.

I was thrilled by his call because he got it! Overweight and obesity are a public health menace. Every day, psychiatrists see patients with these maladies, and we should be more knowledgeable about them or armed to get the treatment started ourselves. Although this child psychiatrist continues to intervene with his patients’ pediatricians and embarks on his own ABOM studies, he can, as he sees his patients and their families, write prescriptions for exercise and play time for the family, limited screen time (TV and computer) for the youngsters, no sweetened beverages, fewer simple carbohydrates, and more plain water. These interventions all are consistent with routine lifestyle recommendations for children (and adults), and they also can promote improved well-being for children and family members.

A recent report indicated that about a quarter of 2- to 5-year-olds and one-third of school-aged children (6-18 years) are overweight or obese in the United States (JAMA. 2014 Feb 26;311[8]:306-14). By convention, body-mass index, a measure of relative body fat, is used to indicate underweight, normal weight, overweight, and obesity. It is derived from a formula: weight in kilograms divided by height in meters squared. In adults, normal is 18.5-24.9, overweight is 25-29.9, and obese is greater than or equal to 30 (National Institutes of Health/World Health Organization guidelines for BMI). For children, one calculates the BMI and then plots this on a graph in comparison to other children of the same age and sex to derive a percentile scale number. Percentile scale numbers from 58-94 indicate overweight, and percentiles greater than or equal to 95 indicate obesity in children aged 2-18 years. For children aged 0-2, a weight for length above the 95th percentile indicates overweight.

Childhood obesity is a major risk factor for overweight and obesity in adulthood, and for depression and cardiovascular disease in childhood and adulthood. It also sets one up for potential trouble in the areas of self-esteem, body image, body protection, poor school performance, and relationship issues with peers. These are areas of importance for psychiatrists, child and adult, as we assess, plan for, and treat our patients day to day. Furthermore, childhood overweight puts children at risk for type 2 diabetes, metabolic syndrome, high cholesterol and high blood pressure, asthma, sleep disorders, early puberty or menstruation, Blount’s disease (progressive turning of the lower leg, resembling bowleg), and nonalcoholic fatty liver disease. Obesity in adulthood leads to high blood pressure, strokes, type 2 diabetes, dementia, osteoarthritis, sleep apnea, obesity hypoventilation syndrome, reproductive problems, gallstones, and some cancers (esophagus, pancreas, colon, rectum, breast-after menopause, endometrium, kidney, thyroid, and gallbladder).

The late Dr. Hilde Bruch, one of my mentors in the 1970s, was an early thought leader in childhood obesity. She did research in this area starting in 1937 while practicing pediatrics before she became a psychiatrist in 1943. She said that she was struck by the number of overweight and obese children she observed in the United States, compared with what she had observed in Germany and England. (She died in 1984 at the age of 80 and would be greatly saddened that childhood obesity is now a global issue.) In her 1973 book, “Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within,” she grappled with the taking in of calories, and, speaking of hunger, said that “it is not innate, but something that contains important elements of learning.”

As an analyst, she thought of feeding learning as coming primarily from early mother-child interactions, but we now know that this learning can come through any repeated interaction and that genetic, social, cultural and environmental, and biological factors also apply.

The psychiatrist or anyone else working with children and families must endeavor to reduce self-blame, explore influences, and instill hope in the process toward normal weight and/or adequate management of weight. The psychiatrist and anyone else working with the child and family will appreciate that, if energy intake and physical activity output are manipulated consistently, the tendency for the child will be increasing height and decreasing BMI. The Prevention and Management of Obesity for Children and Adolescents Guideline is very clear about when to refer to a tertiary special weight management program for children. The guideline also speaks to use of weight-loss medication (orlistat for children 12 years and older, sibutramine for children 16 years and older). Bariatric surgery is recommended for children who have finished growing up (by growth plate evidence) and face imminent serious health issues if their weight cannot be brought under control. These children, after surgery, will need to radically restrain their eating, take supplements, and be followed for the rest of their lives to forestall complications and return to overweight and obesity. I believe that child and adult psychiatrists can be of tremendous use here in helping sort out both the physical and course-of-life issues that could threaten successful continued weight loss, whether the weight loss comes through lifestyle change, lifestyle change and medications, or bariatric surgery and subsequent lifestyle change.

I would like to thank that young child psychiatrist who called, because he spurred me to continue our “Weighty Issues” journey by looking at childhood and overweight and obesity and how it can affect our work as physicians and psychiatrists. Parental physical condition at conception and gestation, and genetics may set the stage, and then interaction with the family, the culture, the society, and the environment all interplay in the child’s development to produce an outcome of an overweight or obese child. We still are trying to discover why some but not all children in the same family, neighborhood, socioeconomic strata, culture, etc., are burdened by overweight. The reasons may be found through biological inquiry, but it may just as well in found in psychiatric/psychological inquiry.

Dr. Harris, a diplomate of the American Board of Obesity Medicine, is in private practice in adult and geriatric psychiatry in Hartford, Conn. She also works as a psychiatric consultant to continuing care retirement organizations and professional groups. Dr. Harris, a former president of the Black Psychiatrists of America, is a Distinguished Fellow of the American Psychiatric Association. Besides psychotherapy, her major clinical interests include geriatrics, and the interface between general medicine and psychiatry.

To improve patient care and outcomes, leading dermatologists offered their recommendations on scar treatments. Consideration must be given to:

• bioCorneum+

• Mederma Scar Cream Plus SPF 30

• Organic vitamin E oil

• ScarAway Silicone Scar Sheets

• Scar Recovery Gel with Centelline

Cutis invites readers to send us their recommendations. Body scrubs, OTC acne treatments, self-tanners, and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on scar treatments. Consideration must be given to:

• bioCorneum+

• Mederma Scar Cream Plus SPF 30

• Organic vitamin E oil

• ScarAway Silicone Scar Sheets

• Scar Recovery Gel with Centelline

Cutis invites readers to send us their recommendations. Body scrubs, OTC acne treatments, self-tanners, and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

To improve patient care and outcomes, leading dermatologists offered their recommendations on scar treatments. Consideration must be given to:

• bioCorneum+

• Mederma Scar Cream Plus SPF 30

• Organic vitamin E oil

• ScarAway Silicone Scar Sheets

• Scar Recovery Gel with Centelline

Cutis invites readers to send us their recommendations. Body scrubs, OTC acne treatments, self-tanners, and cleansing devices will be featured in upcoming editions of Cosmetic Corner. Please e-mail your recommendation(s) to the Editorial Office.

Disclaimer: Opinions expressed herein do not necessarily reflect those of Cutis or Frontline Medical Communications Inc. and shall not be used for product endorsement purposes. Any reference made to a specific commercial product does not indicate or imply that Cutis or Frontline Medical Communications Inc. endorses, recommends, or favors the product mentioned. No guarantee is given to the effects of recommended products.

A phase 2 study findings suggest that AV7909, a new vaccine for postexposure prophylaxis of anthrax disease, may work faster and require fewer vaccinations with fewer antigens when compared with BioThrax. The authors also speculate that AV7909 might require shorter stints with antimicrobial drugs than the 60-day regimen currently recommended along with the 3-dose series of BioThrax vaccine, which could lead to increased patients adherence.

Related: Clinical Trials Begin for Another Anthrax Vaccine

The drug AV7909 combines BioThrax with CPG7909, a synthetic immunostimulatory oligonucleotide. Earlier trials identified a formulation that enhanced immune response without increasing adverse events (AEs). In a multicenter phase 2 trial that evaluated this formulation, researchers tested 3 vaccine schedules and 2 doses in 168 healthy volunteers. Serum samples were collected before the vaccination and on days 35, 42, 49, 63, and 84. Safety was assessed through Day 84.

Related: Better Anthrax Vaccine on the Horizon

The schedule of 2 full doses of AV7909, given 2 weeks apart, showed a comparable immune response to a 0/14/28-day BioThrax schedule but had a higher and earlier peak. The AV7909 vaccine was safe and well tolerated. Although the AV7909 group reported more AEs (79% for AV7909 vs 65% for BioThrax), no serious AEs were assessed as potentially vaccine related, and none were deemed of potential autoimmune etiology.

Source:Hopkin RJ, Kalsi G, Montalvo-Lugo VM, et al. Vaccine. 2016;34(18):2096-2105.doi: 10.1016/j.vaccine.2016.03.006. 

A phase 2 study findings suggest that AV7909, a new vaccine for postexposure prophylaxis of anthrax disease, may work faster and require fewer vaccinations with fewer antigens when compared with BioThrax. The authors also speculate that AV7909 might require shorter stints with antimicrobial drugs than the 60-day regimen currently recommended along with the 3-dose series of BioThrax vaccine, which could lead to increased patients adherence.

Related: Clinical Trials Begin for Another Anthrax Vaccine

The drug AV7909 combines BioThrax with CPG7909, a synthetic immunostimulatory oligonucleotide. Earlier trials identified a formulation that enhanced immune response without increasing adverse events (AEs). In a multicenter phase 2 trial that evaluated this formulation, researchers tested 3 vaccine schedules and 2 doses in 168 healthy volunteers. Serum samples were collected before the vaccination and on days 35, 42, 49, 63, and 84. Safety was assessed through Day 84.

Related: Better Anthrax Vaccine on the Horizon

The schedule of 2 full doses of AV7909, given 2 weeks apart, showed a comparable immune response to a 0/14/28-day BioThrax schedule but had a higher and earlier peak. The AV7909 vaccine was safe and well tolerated. Although the AV7909 group reported more AEs (79% for AV7909 vs 65% for BioThrax), no serious AEs were assessed as potentially vaccine related, and none were deemed of potential autoimmune etiology.

Source:Hopkin RJ, Kalsi G, Montalvo-Lugo VM, et al. Vaccine. 2016;34(18):2096-2105.doi: 10.1016/j.vaccine.2016.03.006. 

A phase 2 study findings suggest that AV7909, a new vaccine for postexposure prophylaxis of anthrax disease, may work faster and require fewer vaccinations with fewer antigens when compared with BioThrax. The authors also speculate that AV7909 might require shorter stints with antimicrobial drugs than the 60-day regimen currently recommended along with the 3-dose series of BioThrax vaccine, which could lead to increased patients adherence.

Related: Clinical Trials Begin for Another Anthrax Vaccine

The drug AV7909 combines BioThrax with CPG7909, a synthetic immunostimulatory oligonucleotide. Earlier trials identified a formulation that enhanced immune response without increasing adverse events (AEs). In a multicenter phase 2 trial that evaluated this formulation, researchers tested 3 vaccine schedules and 2 doses in 168 healthy volunteers. Serum samples were collected before the vaccination and on days 35, 42, 49, 63, and 84. Safety was assessed through Day 84.

Related: Better Anthrax Vaccine on the Horizon

The schedule of 2 full doses of AV7909, given 2 weeks apart, showed a comparable immune response to a 0/14/28-day BioThrax schedule but had a higher and earlier peak. The AV7909 vaccine was safe and well tolerated. Although the AV7909 group reported more AEs (79% for AV7909 vs 65% for BioThrax), no serious AEs were assessed as potentially vaccine related, and none were deemed of potential autoimmune etiology.

Source:Hopkin RJ, Kalsi G, Montalvo-Lugo VM, et al. Vaccine. 2016;34(18):2096-2105.doi: 10.1016/j.vaccine.2016.03.006. 

Federal officials took the next step in their moonshot to end cancer by announcing on April 4 a blue ribbon panel to guide the effort.

A total of 28 leading researchers, clinicians, and patient advocates have been named to the panel charged with informing the scientific direction and goals of the National Cancer Moonshot Initiative, led by Vice President Joe Biden.

“This Blue Ribbon Panel will ensure that, as [the National Institutes of Health] allocates new resources through the Moonshot, decisions will be grounded in the best science,” Vice President Biden said in a statement. “I look forward to working with this panel and many others involved with the Moonshot to make unprecedented improvements in prevention, diagnosis, and treatment of cancer.”

The key goals of the initiative were set out simultaneously in a perspective from Dr. Francis S. Collins, NIH director, and Dr. Douglas R. Lowy, director of the National Cancer Institute. The editorial was published in the New England Journal of Medicine.

“Fueled by an additional $680 million in the proposed fiscal year 2017 budget for the NIH, plus additional resources for the Food and Drug Administration, the initiative will aim to accelerate progress toward the next generation of interventions that we hope will substantially reduce cancer incidence and dramatically improve patient outcomes,” Dr. Collins and Dr. Lowy wrote. “The NIH’s most compelling opportunities for progress will be set forth by late summer 2016 in a research plan informed by the deliberations of a blue-ribbon panel of experts, which will provide scientific input to the National Cancer Advisory Board. Some possible opportunities include vaccine development, early-detection technology, single-cell genomic analysis, immunotherapy, a focus on pediatric cancer, and enhanced data sharing.”

To read the full editorial, click here.

[email protected]

On Twitter @denisefulton

Federal officials took the next step in their moonshot to end cancer by announcing on April 4 a blue ribbon panel to guide the effort.

A total of 28 leading researchers, clinicians, and patient advocates have been named to the panel charged with informing the scientific direction and goals of the National Cancer Moonshot Initiative, led by Vice President Joe Biden.

“This Blue Ribbon Panel will ensure that, as [the National Institutes of Health] allocates new resources through the Moonshot, decisions will be grounded in the best science,” Vice President Biden said in a statement. “I look forward to working with this panel and many others involved with the Moonshot to make unprecedented improvements in prevention, diagnosis, and treatment of cancer.”

The key goals of the initiative were set out simultaneously in a perspective from Dr. Francis S. Collins, NIH director, and Dr. Douglas R. Lowy, director of the National Cancer Institute. The editorial was published in the New England Journal of Medicine.

“Fueled by an additional $680 million in the proposed fiscal year 2017 budget for the NIH, plus additional resources for the Food and Drug Administration, the initiative will aim to accelerate progress toward the next generation of interventions that we hope will substantially reduce cancer incidence and dramatically improve patient outcomes,” Dr. Collins and Dr. Lowy wrote. “The NIH’s most compelling opportunities for progress will be set forth by late summer 2016 in a research plan informed by the deliberations of a blue-ribbon panel of experts, which will provide scientific input to the National Cancer Advisory Board. Some possible opportunities include vaccine development, early-detection technology, single-cell genomic analysis, immunotherapy, a focus on pediatric cancer, and enhanced data sharing.”

To read the full editorial, click here.

[email protected]

On Twitter @denisefulton

Federal officials took the next step in their moonshot to end cancer by announcing on April 4 a blue ribbon panel to guide the effort.

A total of 28 leading researchers, clinicians, and patient advocates have been named to the panel charged with informing the scientific direction and goals of the National Cancer Moonshot Initiative, led by Vice President Joe Biden.

“This Blue Ribbon Panel will ensure that, as [the National Institutes of Health] allocates new resources through the Moonshot, decisions will be grounded in the best science,” Vice President Biden said in a statement. “I look forward to working with this panel and many others involved with the Moonshot to make unprecedented improvements in prevention, diagnosis, and treatment of cancer.”

The key goals of the initiative were set out simultaneously in a perspective from Dr. Francis S. Collins, NIH director, and Dr. Douglas R. Lowy, director of the National Cancer Institute. The editorial was published in the New England Journal of Medicine.

“Fueled by an additional $680 million in the proposed fiscal year 2017 budget for the NIH, plus additional resources for the Food and Drug Administration, the initiative will aim to accelerate progress toward the next generation of interventions that we hope will substantially reduce cancer incidence and dramatically improve patient outcomes,” Dr. Collins and Dr. Lowy wrote. “The NIH’s most compelling opportunities for progress will be set forth by late summer 2016 in a research plan informed by the deliberations of a blue-ribbon panel of experts, which will provide scientific input to the National Cancer Advisory Board. Some possible opportunities include vaccine development, early-detection technology, single-cell genomic analysis, immunotherapy, a focus on pediatric cancer, and enhanced data sharing.”

To read the full editorial, click here.

[email protected]

On Twitter @denisefulton

Renal status should be evaluated at diagnosis and follow-up in all myeloma patients, according to new guidance from the International Myeloma Working Group published online in the Journal of Clinical Oncology.

Renal impairment (RI) affects up to half of patients with multiple myeloma, and severe RI predicts early death, noted Dr. Meletios Dimopoulos of National and Kapodistrian University of Athens and his associates. Novel therapies have substantially increased survival for myeloma with less severe kidney disease, underscoring the importance of early treatment. To develop the guidelines, the authors reviewed all evidence from randomized trials, systematic reviews, meta-analyses, and prospective and observational studies published through December 2015 (J Clin Oncol. 2016 Mar 14. doi: 10.1200/JCO.2015.65.0044).

Grade A recommendations (evidence obtained from meta-analysis of multiple well-designed, randomized controlled trials) include the following:

Evaluate serum creatinine, estimated glomerular filtration rate, and electrolytes at initial diagnosis and follow-up assessments. Also perform the serum free light chain test, if available, and electrophoresis of a 24-hour urine specimen.

In patients with stabilized serum creatinine, evaluate GFR using the Chronic Kidney Disease Epidemiology Collaboration (preferred) or the Modification of Diet in Renal Disease formulas.

Based on GFR, determine stage of chronic kidney disease (ranging from 1, kidney damage with normal or elevated GFR, to 5, renal failure).

Bortezomib remains the foundational treatment for myeloma-related renal impairment, the authors emphasized. This 26S proteasome inhibitor should be started at the standard dose of 1.3 mg/m² on days 1, 4, 8, and 11 of a 3-week cycle.

Another option for patients with creatinine clearance above 15 mL/min is carfilzomib, which needs no dose modification and yields similar results regardless of RI status. However, more data are needed on its renal safety, the authors said.

Patients with creatinine clearance above 30 mL/min can safely receive ixazomib in combination with lenalidomide and dexamethasone.

Those with creatinine clearance above 45 mL/min should receive pomalidomide at a dose of 4 mg/day; it is not yet clear whether the dose should be cut for more severe renal impairment.

Hypercalcemia can be treated with bisphosphonates, but patients with creatinine clearance below 30 mL/min should not receive pamidronate or zoledronic acid.

Avoid nephrotoxic agents, such as as aminoglycosides, furosemide, and contrast agents, in all patients with multiple myeloma and RI.

Dr. Dimopoulos reported receiving honoraria or financial support related to travel, accommodations, or expenses from Amgen, Celgene, Onyx Pharmaceuticals, Janssen-Cilag, Bristol-Myers Squibb, Novartis, and Genesis Pharmaceuticals. Seventeen coauthors also reported financial relationships with a number of pharmaceutical companies. The remaining three coauthors had no disclosures.

Renal status should be evaluated at diagnosis and follow-up in all myeloma patients, according to new guidance from the International Myeloma Working Group published online in the Journal of Clinical Oncology.

Renal impairment (RI) affects up to half of patients with multiple myeloma, and severe RI predicts early death, noted Dr. Meletios Dimopoulos of National and Kapodistrian University of Athens and his associates. Novel therapies have substantially increased survival for myeloma with less severe kidney disease, underscoring the importance of early treatment. To develop the guidelines, the authors reviewed all evidence from randomized trials, systematic reviews, meta-analyses, and prospective and observational studies published through December 2015 (J Clin Oncol. 2016 Mar 14. doi: 10.1200/JCO.2015.65.0044).

Grade A recommendations (evidence obtained from meta-analysis of multiple well-designed, randomized controlled trials) include the following:

Evaluate serum creatinine, estimated glomerular filtration rate, and electrolytes at initial diagnosis and follow-up assessments. Also perform the serum free light chain test, if available, and electrophoresis of a 24-hour urine specimen.

In patients with stabilized serum creatinine, evaluate GFR using the Chronic Kidney Disease Epidemiology Collaboration (preferred) or the Modification of Diet in Renal Disease formulas.

Based on GFR, determine stage of chronic kidney disease (ranging from 1, kidney damage with normal or elevated GFR, to 5, renal failure).

Bortezomib remains the foundational treatment for myeloma-related renal impairment, the authors emphasized. This 26S proteasome inhibitor should be started at the standard dose of 1.3 mg/m² on days 1, 4, 8, and 11 of a 3-week cycle.

Another option for patients with creatinine clearance above 15 mL/min is carfilzomib, which needs no dose modification and yields similar results regardless of RI status. However, more data are needed on its renal safety, the authors said.

Patients with creatinine clearance above 30 mL/min can safely receive ixazomib in combination with lenalidomide and dexamethasone.

Those with creatinine clearance above 45 mL/min should receive pomalidomide at a dose of 4 mg/day; it is not yet clear whether the dose should be cut for more severe renal impairment.

Hypercalcemia can be treated with bisphosphonates, but patients with creatinine clearance below 30 mL/min should not receive pamidronate or zoledronic acid.

Avoid nephrotoxic agents, such as as aminoglycosides, furosemide, and contrast agents, in all patients with multiple myeloma and RI.

Dr. Dimopoulos reported receiving honoraria or financial support related to travel, accommodations, or expenses from Amgen, Celgene, Onyx Pharmaceuticals, Janssen-Cilag, Bristol-Myers Squibb, Novartis, and Genesis Pharmaceuticals. Seventeen coauthors also reported financial relationships with a number of pharmaceutical companies. The remaining three coauthors had no disclosures.

Renal status should be evaluated at diagnosis and follow-up in all myeloma patients, according to new guidance from the International Myeloma Working Group published online in the Journal of Clinical Oncology.

Renal impairment (RI) affects up to half of patients with multiple myeloma, and severe RI predicts early death, noted Dr. Meletios Dimopoulos of National and Kapodistrian University of Athens and his associates. Novel therapies have substantially increased survival for myeloma with less severe kidney disease, underscoring the importance of early treatment. To develop the guidelines, the authors reviewed all evidence from randomized trials, systematic reviews, meta-analyses, and prospective and observational studies published through December 2015 (J Clin Oncol. 2016 Mar 14. doi: 10.1200/JCO.2015.65.0044).

Grade A recommendations (evidence obtained from meta-analysis of multiple well-designed, randomized controlled trials) include the following:

Evaluate serum creatinine, estimated glomerular filtration rate, and electrolytes at initial diagnosis and follow-up assessments. Also perform the serum free light chain test, if available, and electrophoresis of a 24-hour urine specimen.

In patients with stabilized serum creatinine, evaluate GFR using the Chronic Kidney Disease Epidemiology Collaboration (preferred) or the Modification of Diet in Renal Disease formulas.

Based on GFR, determine stage of chronic kidney disease (ranging from 1, kidney damage with normal or elevated GFR, to 5, renal failure).

Bortezomib remains the foundational treatment for myeloma-related renal impairment, the authors emphasized. This 26S proteasome inhibitor should be started at the standard dose of 1.3 mg/m² on days 1, 4, 8, and 11 of a 3-week cycle.

Another option for patients with creatinine clearance above 15 mL/min is carfilzomib, which needs no dose modification and yields similar results regardless of RI status. However, more data are needed on its renal safety, the authors said.

Patients with creatinine clearance above 30 mL/min can safely receive ixazomib in combination with lenalidomide and dexamethasone.

Those with creatinine clearance above 45 mL/min should receive pomalidomide at a dose of 4 mg/day; it is not yet clear whether the dose should be cut for more severe renal impairment.

Hypercalcemia can be treated with bisphosphonates, but patients with creatinine clearance below 30 mL/min should not receive pamidronate or zoledronic acid.

Avoid nephrotoxic agents, such as as aminoglycosides, furosemide, and contrast agents, in all patients with multiple myeloma and RI.

Dr. Dimopoulos reported receiving honoraria or financial support related to travel, accommodations, or expenses from Amgen, Celgene, Onyx Pharmaceuticals, Janssen-Cilag, Bristol-Myers Squibb, Novartis, and Genesis Pharmaceuticals. Seventeen coauthors also reported financial relationships with a number of pharmaceutical companies. The remaining three coauthors had no disclosures.

WAIKOLOA, HAWAII – Intralesional injection of interferon alfa-2b is an excellent option for the treatment of large problematic basal cell carcinomas in patients who aren’t interested in the higher-morbidity options, Dr. David L. Swanson said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“This is a really effective way to treat basal cell carcinomas. These things just melt away before your eyes. It’s really quite amazing,” observed Dr. Swanson of Mayo Clinic Scottsdale (Ariz.).

He finds this therapy particularly useful in frail elderly patients who have a large BCC on the head or neck. A good example would be an 89-year-old with multiple comorbid conditions who has a 2-cm BCC on the tip of the nose and doesn’t want anything done about it. The patient declines the options of Mohs micrographic surgery or radiotherapy.

“This is the patient who just wants to be left alone. That’s fine if they’re going to be dead within a year, but if they’re going to be around for several years, that basal cell carcinoma could become a major issue for them,” the dermatologist continued.

He and his colleagues at the Mayo Clinic follow a treatment regimen similar to one laid out by Turkish investigators more than a decade ago in one of the few long-term outcome studies of intralesional interferon for treatment of BCCs.

Although interferon alfa-2b is approved for the intralesional treatment of genital warts and subcutaneously for Kaposi’s sarcoma and malignant melanoma, among other conditions, it’s off-label therapy for BCCs. The treatment entails thrice-weekly intralesional injections for 3 weeks. The dosing is 1.5 million units per injection for BCCs smaller than 2 cm and 3 million units per injection for BCCs that are 2 cm or larger. The injections are given without anesthesia, but premedication with 500-1,000 mg of acetaminophen is advisable to minimize aches and fever.

Interferon alfa-2b (Intron A) comes in a vial containing 10 million units with 1 mL of diluent. It’s important to reconstitute it carefully, similar to onabotulinumtoxin. Don’t shake it, Dr. Swanson advised.

The Turkish report included 20 patients with histopathologically proven BCCs on the head or neck. At clinical and dermatopathologic follow-up 8 weeks after the last interferon injection, 11 BCCs showed complete clinical and histopathologic cure, six showed partial remission, two showed no response, and one actually increased in size during treatment.

The 11 patients with an initial complete cure were followed for 7 years. During that period, only one of the 11 skin cancers recurred, at the fifth year (Clin Drug Investig. 2005;25[10]:661-7).

Dr. Swanson reported having no financial conflicts regarding his presentation. SDEF and this news organization are owned by the same parent company.

[email protected]

WAIKOLOA, HAWAII – Intralesional injection of interferon alfa-2b is an excellent option for the treatment of large problematic basal cell carcinomas in patients who aren’t interested in the higher-morbidity options, Dr. David L. Swanson said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“This is a really effective way to treat basal cell carcinomas. These things just melt away before your eyes. It’s really quite amazing,” observed Dr. Swanson of Mayo Clinic Scottsdale (Ariz.).

He finds this therapy particularly useful in frail elderly patients who have a large BCC on the head or neck. A good example would be an 89-year-old with multiple comorbid conditions who has a 2-cm BCC on the tip of the nose and doesn’t want anything done about it. The patient declines the options of Mohs micrographic surgery or radiotherapy.

“This is the patient who just wants to be left alone. That’s fine if they’re going to be dead within a year, but if they’re going to be around for several years, that basal cell carcinoma could become a major issue for them,” the dermatologist continued.

He and his colleagues at the Mayo Clinic follow a treatment regimen similar to one laid out by Turkish investigators more than a decade ago in one of the few long-term outcome studies of intralesional interferon for treatment of BCCs.

Although interferon alfa-2b is approved for the intralesional treatment of genital warts and subcutaneously for Kaposi’s sarcoma and malignant melanoma, among other conditions, it’s off-label therapy for BCCs. The treatment entails thrice-weekly intralesional injections for 3 weeks. The dosing is 1.5 million units per injection for BCCs smaller than 2 cm and 3 million units per injection for BCCs that are 2 cm or larger. The injections are given without anesthesia, but premedication with 500-1,000 mg of acetaminophen is advisable to minimize aches and fever.

Interferon alfa-2b (Intron A) comes in a vial containing 10 million units with 1 mL of diluent. It’s important to reconstitute it carefully, similar to onabotulinumtoxin. Don’t shake it, Dr. Swanson advised.

The Turkish report included 20 patients with histopathologically proven BCCs on the head or neck. At clinical and dermatopathologic follow-up 8 weeks after the last interferon injection, 11 BCCs showed complete clinical and histopathologic cure, six showed partial remission, two showed no response, and one actually increased in size during treatment.

The 11 patients with an initial complete cure were followed for 7 years. During that period, only one of the 11 skin cancers recurred, at the fifth year (Clin Drug Investig. 2005;25[10]:661-7).

Dr. Swanson reported having no financial conflicts regarding his presentation. SDEF and this news organization are owned by the same parent company.

[email protected]

WAIKOLOA, HAWAII – Intralesional injection of interferon alfa-2b is an excellent option for the treatment of large problematic basal cell carcinomas in patients who aren’t interested in the higher-morbidity options, Dr. David L. Swanson said at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.

“This is a really effective way to treat basal cell carcinomas. These things just melt away before your eyes. It’s really quite amazing,” observed Dr. Swanson of Mayo Clinic Scottsdale (Ariz.).

He finds this therapy particularly useful in frail elderly patients who have a large BCC on the head or neck. A good example would be an 89-year-old with multiple comorbid conditions who has a 2-cm BCC on the tip of the nose and doesn’t want anything done about it. The patient declines the options of Mohs micrographic surgery or radiotherapy.

“This is the patient who just wants to be left alone. That’s fine if they’re going to be dead within a year, but if they’re going to be around for several years, that basal cell carcinoma could become a major issue for them,” the dermatologist continued.

He and his colleagues at the Mayo Clinic follow a treatment regimen similar to one laid out by Turkish investigators more than a decade ago in one of the few long-term outcome studies of intralesional interferon for treatment of BCCs.

Although interferon alfa-2b is approved for the intralesional treatment of genital warts and subcutaneously for Kaposi’s sarcoma and malignant melanoma, among other conditions, it’s off-label therapy for BCCs. The treatment entails thrice-weekly intralesional injections for 3 weeks. The dosing is 1.5 million units per injection for BCCs smaller than 2 cm and 3 million units per injection for BCCs that are 2 cm or larger. The injections are given without anesthesia, but premedication with 500-1,000 mg of acetaminophen is advisable to minimize aches and fever.

Interferon alfa-2b (Intron A) comes in a vial containing 10 million units with 1 mL of diluent. It’s important to reconstitute it carefully, similar to onabotulinumtoxin. Don’t shake it, Dr. Swanson advised.

The Turkish report included 20 patients with histopathologically proven BCCs on the head or neck. At clinical and dermatopathologic follow-up 8 weeks after the last interferon injection, 11 BCCs showed complete clinical and histopathologic cure, six showed partial remission, two showed no response, and one actually increased in size during treatment.

The 11 patients with an initial complete cure were followed for 7 years. During that period, only one of the 11 skin cancers recurred, at the fifth year (Clin Drug Investig. 2005;25[10]:661-7).

Dr. Swanson reported having no financial conflicts regarding his presentation. SDEF and this news organization are owned by the same parent company.

[email protected]

VALENCIA, SPAIN—Results of a phase 2 trial suggest a personalized T-cell immunotherapy may improve outcomes in patients undergoing T-cell-depleted haploidentical hematopoietic stem cell transplant (HSCT).

Patients who received the therapy, ATIR101, after HSCT had significant improvements in transplant-related mortality (TRM) and overall survival (OS) when compared to historical controls who received a T-cell-depleted haploidentical HSCT without ATIR101.

None of the patients who received ATIR101 developed grade 3-4 graft-versus-host disease (GVHD), despite the fact that they had not received any prophylactic immunosuppressants. Still, there were a few cases of grade 2 GVHD reported.

Denis-Claude Roy, MD, of the University of Montreal in Québec, Canada, presented the results of this trial at the 42nd Annual Meeting of the European Society of Blood and Marrow Transplantation (abstract O042*). The trial was sponsored by Kiadis Pharma, the company developing ATIR101.

Patients and treatment

The trial included 23 leukemia patients with a median age of 41 (range, 21-64). They were eligible for an allogeneic HSCT but could not find a matching donor in time. Sixteen patients had acute myeloid leukemia, and 7 had acute lymphoblastic leukemia.

All patients were in complete remission (CR) at the time of the HSCT. Fifteen were in CR1, and 8 were in CR2/3. The majority of patients (57%) had a poor prognosis based on their disease risk index and cytogenetic profile.

A myeloablative conditioning regimen was used, which consisted of total body irradiation (1200 cGy; n=11) or melphalan (120 mg/m²; n=12), along with thiotepa (10 mg/kg), fludarabine (30 mg/m² x 5d), and anti-thymocyte globulin (2.5 mg/kg x 4d).

Patients then received a CD34⁺ selected graft from a haploidentical donor, containing 11 x 10⁶ CD34⁺ cells/kg (range, 4.7-24.4) and 0.29 x 10⁴ CD3⁺ cells/kg (range, 0-1.8).

The patients achieved neutrophil and platelet engraftment at a median of 12 days post-HSCT (range, 8-34 and 9-35, respectively). They did not receive any post-transplant GVHD prophylaxis.

At a median of 28 days post-transplant (range, 28-73), ATIR101 was infused, at a fixed dose of 2 x 10⁶ CD3⁺ cells/kg.

ATIR101 is a personalized T-cell immunotherapy based on a donor lymphocyte preparation selectively depleted of host-alloreactive T cells through the use of photo-dynamic therapy.

Recipient-reactive T cells from the donor are activated in a unidirectional mixed-lymphocyte reaction. The cells are then treated with a compound known as TH9402, which is selectively retained in activated T cells. Subsequent light exposure eliminates the activated recipient-reactive T cells but preserves the other T cells.

Primary endpoint: TRM

The median follow-up, on March 24, 2016, was 414 days (range, 110-742) post-HSCT. At that point, all patients were beyond 6 months post-HSCT. This allowed for assessment of the primary endpoint, which is TRM at 6 months.

Three cases of TRM were reported, for a rate of 13%. In all cases, the cause of death was an infection.

The researchers compared these results to those in a historic control group. It consisted of 35 patients who matched the inclusion and exclusion criteria of this trial and underwent a similar HSCT procedure from haploidentical family members but without the addition of ATIR101.

TRM was significantly lower (P=0.005) in patients who received ATIR101 after a T-cell-depleted haploidentical transplant than in the historical controls. The 6-month TRM for HSCT + ATIR101 was 13%, compared to 37% for HSCT only.

Relapse and survival

Two patients experienced disease relapse within the first 12 months after HSCT—at days 61 and 90. And 1 patient died from disease relapse within the first 6 months.

The researchers said the low rates of relapse and TRM translated into significantly improved OS for patients undergoing HSCT + ATIR101 compared to the historical controls.

Based on Kaplan-Meier estimates, the 1-year OS was 64% in the HSCT + ATIR101 group and 20% in the historical control group (P=0.0026).

GVHD

None of the patients in this trial (0/23) developed grade 3-4 GVHD upon infusion of ATIR101.

However, 3 cases of grade 2 acute GVHD were reported. One case occurred before ATIR101 infusion, and the other 2 cases had a delayed onset, at day 173 and day 247 post-HSCT (145 and 219 days post-ATIR101 infusion).

In the patient who developed GVHD before ATIR101 infusion, GVHD resolved quickly. The patient then received ATIR101 and did not experience any further GVHD.

“With this latest data, we can confirm the safety of ATIR101, without any incidents of grade 3-4 GVHD, significant reduction in transplant-related mortality, low relapse rates, and very good event-free survival, which we believe confirms the efficiency of photodepletion-based elimination of allo-reactive T cells,” Dr Roy said.

“Indeed, the data of patients receiving transplants with a haploidentical donor and an ATIR101 infusion are very similar to those from patients with a matched donor. As a doctor, I am very excited about this development and its potential to change patient fates.”

Dr Roy and his colleagues will continue to follow patients in this trial to collect further long-term outcome data.

Kiadis Pharma is planning to proceed with the development of ATIR101 as an adjunctive immuno-therapeutic treatment to a haploidentical HSCT for patients with acute leukemia, initiating a randomized phase 3 trial in the second half of 2016.

*Information in the abstract differs from that presented at the meeting.

VALENCIA, SPAIN—Results of a phase 2 trial suggest a personalized T-cell immunotherapy may improve outcomes in patients undergoing T-cell-depleted haploidentical hematopoietic stem cell transplant (HSCT).

Patients who received the therapy, ATIR101, after HSCT had significant improvements in transplant-related mortality (TRM) and overall survival (OS) when compared to historical controls who received a T-cell-depleted haploidentical HSCT without ATIR101.

None of the patients who received ATIR101 developed grade 3-4 graft-versus-host disease (GVHD), despite the fact that they had not received any prophylactic immunosuppressants. Still, there were a few cases of grade 2 GVHD reported.

Denis-Claude Roy, MD, of the University of Montreal in Québec, Canada, presented the results of this trial at the 42nd Annual Meeting of the European Society of Blood and Marrow Transplantation (abstract O042*). The trial was sponsored by Kiadis Pharma, the company developing ATIR101.

Patients and treatment

The trial included 23 leukemia patients with a median age of 41 (range, 21-64). They were eligible for an allogeneic HSCT but could not find a matching donor in time. Sixteen patients had acute myeloid leukemia, and 7 had acute lymphoblastic leukemia.

All patients were in complete remission (CR) at the time of the HSCT. Fifteen were in CR1, and 8 were in CR2/3. The majority of patients (57%) had a poor prognosis based on their disease risk index and cytogenetic profile.

A myeloablative conditioning regimen was used, which consisted of total body irradiation (1200 cGy; n=11) or melphalan (120 mg/m²; n=12), along with thiotepa (10 mg/kg), fludarabine (30 mg/m² x 5d), and anti-thymocyte globulin (2.5 mg/kg x 4d).

Patients then received a CD34⁺ selected graft from a haploidentical donor, containing 11 x 10⁶ CD34⁺ cells/kg (range, 4.7-24.4) and 0.29 x 10⁴ CD3⁺ cells/kg (range, 0-1.8).

The patients achieved neutrophil and platelet engraftment at a median of 12 days post-HSCT (range, 8-34 and 9-35, respectively). They did not receive any post-transplant GVHD prophylaxis.

At a median of 28 days post-transplant (range, 28-73), ATIR101 was infused, at a fixed dose of 2 x 10⁶ CD3⁺ cells/kg.

ATIR101 is a personalized T-cell immunotherapy based on a donor lymphocyte preparation selectively depleted of host-alloreactive T cells through the use of photo-dynamic therapy.

Recipient-reactive T cells from the donor are activated in a unidirectional mixed-lymphocyte reaction. The cells are then treated with a compound known as TH9402, which is selectively retained in activated T cells. Subsequent light exposure eliminates the activated recipient-reactive T cells but preserves the other T cells.

Primary endpoint: TRM

The median follow-up, on March 24, 2016, was 414 days (range, 110-742) post-HSCT. At that point, all patients were beyond 6 months post-HSCT. This allowed for assessment of the primary endpoint, which is TRM at 6 months.

Three cases of TRM were reported, for a rate of 13%. In all cases, the cause of death was an infection.

The researchers compared these results to those in a historic control group. It consisted of 35 patients who matched the inclusion and exclusion criteria of this trial and underwent a similar HSCT procedure from haploidentical family members but without the addition of ATIR101.

TRM was significantly lower (P=0.005) in patients who received ATIR101 after a T-cell-depleted haploidentical transplant than in the historical controls. The 6-month TRM for HSCT + ATIR101 was 13%, compared to 37% for HSCT only.

Relapse and survival

Two patients experienced disease relapse within the first 12 months after HSCT—at days 61 and 90. And 1 patient died from disease relapse within the first 6 months.

The researchers said the low rates of relapse and TRM translated into significantly improved OS for patients undergoing HSCT + ATIR101 compared to the historical controls.

Based on Kaplan-Meier estimates, the 1-year OS was 64% in the HSCT + ATIR101 group and 20% in the historical control group (P=0.0026).

GVHD

None of the patients in this trial (0/23) developed grade 3-4 GVHD upon infusion of ATIR101.

However, 3 cases of grade 2 acute GVHD were reported. One case occurred before ATIR101 infusion, and the other 2 cases had a delayed onset, at day 173 and day 247 post-HSCT (145 and 219 days post-ATIR101 infusion).

In the patient who developed GVHD before ATIR101 infusion, GVHD resolved quickly. The patient then received ATIR101 and did not experience any further GVHD.

“With this latest data, we can confirm the safety of ATIR101, without any incidents of grade 3-4 GVHD, significant reduction in transplant-related mortality, low relapse rates, and very good event-free survival, which we believe confirms the efficiency of photodepletion-based elimination of allo-reactive T cells,” Dr Roy said.

“Indeed, the data of patients receiving transplants with a haploidentical donor and an ATIR101 infusion are very similar to those from patients with a matched donor. As a doctor, I am very excited about this development and its potential to change patient fates.”

Dr Roy and his colleagues will continue to follow patients in this trial to collect further long-term outcome data.

Kiadis Pharma is planning to proceed with the development of ATIR101 as an adjunctive immuno-therapeutic treatment to a haploidentical HSCT for patients with acute leukemia, initiating a randomized phase 3 trial in the second half of 2016.

*Information in the abstract differs from that presented at the meeting.

VALENCIA, SPAIN—Results of a phase 2 trial suggest a personalized T-cell immunotherapy may improve outcomes in patients undergoing T-cell-depleted haploidentical hematopoietic stem cell transplant (HSCT).

Patients who received the therapy, ATIR101, after HSCT had significant improvements in transplant-related mortality (TRM) and overall survival (OS) when compared to historical controls who received a T-cell-depleted haploidentical HSCT without ATIR101.

None of the patients who received ATIR101 developed grade 3-4 graft-versus-host disease (GVHD), despite the fact that they had not received any prophylactic immunosuppressants. Still, there were a few cases of grade 2 GVHD reported.

Denis-Claude Roy, MD, of the University of Montreal in Québec, Canada, presented the results of this trial at the 42nd Annual Meeting of the European Society of Blood and Marrow Transplantation (abstract O042*). The trial was sponsored by Kiadis Pharma, the company developing ATIR101.

Patients and treatment

The trial included 23 leukemia patients with a median age of 41 (range, 21-64). They were eligible for an allogeneic HSCT but could not find a matching donor in time. Sixteen patients had acute myeloid leukemia, and 7 had acute lymphoblastic leukemia.

All patients were in complete remission (CR) at the time of the HSCT. Fifteen were in CR1, and 8 were in CR2/3. The majority of patients (57%) had a poor prognosis based on their disease risk index and cytogenetic profile.

A myeloablative conditioning regimen was used, which consisted of total body irradiation (1200 cGy; n=11) or melphalan (120 mg/m²; n=12), along with thiotepa (10 mg/kg), fludarabine (30 mg/m² x 5d), and anti-thymocyte globulin (2.5 mg/kg x 4d).

Patients then received a CD34⁺ selected graft from a haploidentical donor, containing 11 x 10⁶ CD34⁺ cells/kg (range, 4.7-24.4) and 0.29 x 10⁴ CD3⁺ cells/kg (range, 0-1.8).

The patients achieved neutrophil and platelet engraftment at a median of 12 days post-HSCT (range, 8-34 and 9-35, respectively). They did not receive any post-transplant GVHD prophylaxis.

At a median of 28 days post-transplant (range, 28-73), ATIR101 was infused, at a fixed dose of 2 x 10⁶ CD3⁺ cells/kg.

ATIR101 is a personalized T-cell immunotherapy based on a donor lymphocyte preparation selectively depleted of host-alloreactive T cells through the use of photo-dynamic therapy.

Recipient-reactive T cells from the donor are activated in a unidirectional mixed-lymphocyte reaction. The cells are then treated with a compound known as TH9402, which is selectively retained in activated T cells. Subsequent light exposure eliminates the activated recipient-reactive T cells but preserves the other T cells.

Primary endpoint: TRM

The median follow-up, on March 24, 2016, was 414 days (range, 110-742) post-HSCT. At that point, all patients were beyond 6 months post-HSCT. This allowed for assessment of the primary endpoint, which is TRM at 6 months.

Three cases of TRM were reported, for a rate of 13%. In all cases, the cause of death was an infection.

The researchers compared these results to those in a historic control group. It consisted of 35 patients who matched the inclusion and exclusion criteria of this trial and underwent a similar HSCT procedure from haploidentical family members but without the addition of ATIR101.

TRM was significantly lower (P=0.005) in patients who received ATIR101 after a T-cell-depleted haploidentical transplant than in the historical controls. The 6-month TRM for HSCT + ATIR101 was 13%, compared to 37% for HSCT only.

Relapse and survival

Two patients experienced disease relapse within the first 12 months after HSCT—at days 61 and 90. And 1 patient died from disease relapse within the first 6 months.

The researchers said the low rates of relapse and TRM translated into significantly improved OS for patients undergoing HSCT + ATIR101 compared to the historical controls.

Based on Kaplan-Meier estimates, the 1-year OS was 64% in the HSCT + ATIR101 group and 20% in the historical control group (P=0.0026).

GVHD

None of the patients in this trial (0/23) developed grade 3-4 GVHD upon infusion of ATIR101.

However, 3 cases of grade 2 acute GVHD were reported. One case occurred before ATIR101 infusion, and the other 2 cases had a delayed onset, at day 173 and day 247 post-HSCT (145 and 219 days post-ATIR101 infusion).

In the patient who developed GVHD before ATIR101 infusion, GVHD resolved quickly. The patient then received ATIR101 and did not experience any further GVHD.

“With this latest data, we can confirm the safety of ATIR101, without any incidents of grade 3-4 GVHD, significant reduction in transplant-related mortality, low relapse rates, and very good event-free survival, which we believe confirms the efficiency of photodepletion-based elimination of allo-reactive T cells,” Dr Roy said.

“Indeed, the data of patients receiving transplants with a haploidentical donor and an ATIR101 infusion are very similar to those from patients with a matched donor. As a doctor, I am very excited about this development and its potential to change patient fates.”

Dr Roy and his colleagues will continue to follow patients in this trial to collect further long-term outcome data.

Kiadis Pharma is planning to proceed with the development of ATIR101 as an adjunctive immuno-therapeutic treatment to a haploidentical HSCT for patients with acute leukemia, initiating a randomized phase 3 trial in the second half of 2016.

*Information in the abstract differs from that presented at the meeting.