Blood donation

Photo by Charles Haymond

Low-dose oral iron supplementation can reduce the time to hemoglobin recovery after blood donation, according to a study published in JAMA.

Researchers found that a daily dose of ferrous gluconate (37.5 mg of elemental iron) reduced blood donors’ time to 80% hemoglobin recovery, whether the donors were iron-depleted (with ferritin levels of 26 ng/mL or lower) or iron-replete (with ferritin levels higher than 26 ng/mL).

Joseph E. Kiss, MD, of the Institute for Transfusion Medicine in Pittsburgh, Pennsylvania, and his colleagues conducted this study at 4 regional blood centers in the US.

The researchers randomized 215 subjects (who had not donated whole blood or red blood cells within 4 months) to receive one tablet of ferrous gluconate daily or no iron for 24 weeks after donating a unit of whole blood (500 mL).

The study’s primary outcomes were time to recovery of 80% of the post-donation decrease in hemoglobin and recovery of baseline ferritin levels.

The researchers found that subjects who received iron supplementation achieved 80% hemoglobin recovery more quickly than subjects who did not receive iron, regardless of ferritin levels.

In the low-ferritin group, the mean time to 80% hemoglobin recovery was 32 days in subjects who received iron and 158 days in those who did not (P<0.001). In the higher-ferritin group, the mean time to 80% hemoglobin recovery was 31 days in subjects who received iron and 78 days in those who did not (P=0.02).

In the low-ferritin group, the median time to recovery of baseline ferritin levels was 21 days in subjects who received iron and more than 168 days in subjects who did not. In the higher-ferritin group, the median time to recovery of baseline ferritin levels was 107 days in subjects who received iron and more than 168 days in those who did not.

The median time to recovery of iron stores was 76 days in all subjects who received iron supplements and more than 168 days in those who did not (P<0.001). Sixty-seven percent of subjects who did not receive iron had failed to recover their iron stores by 168 days.

The researchers said these findings raise important considerations regarding the 8-week minimum waiting period between blood donations that is required in the US and Canada. This is a shorter period than those allowed in many other countries.

The study suggests that hemoglobin recovery differs according to a donor’s pre-donation ferritin level, but, even in iron-replete donors, the mean recovery was only 70% at 8 weeks.

Prolonging the minimum wait time between blood donations would allow for more thorough recovery, the researchers noted, but it could also compromise the blood supply. Furthermore, increasing the waiting period might not be adequate for donors who do not take iron supplements.

Blood donation

Photo by Charles Haymond

Low-dose oral iron supplementation can reduce the time to hemoglobin recovery after blood donation, according to a study published in JAMA.

Researchers found that a daily dose of ferrous gluconate (37.5 mg of elemental iron) reduced blood donors’ time to 80% hemoglobin recovery, whether the donors were iron-depleted (with ferritin levels of 26 ng/mL or lower) or iron-replete (with ferritin levels higher than 26 ng/mL).

Joseph E. Kiss, MD, of the Institute for Transfusion Medicine in Pittsburgh, Pennsylvania, and his colleagues conducted this study at 4 regional blood centers in the US.

The researchers randomized 215 subjects (who had not donated whole blood or red blood cells within 4 months) to receive one tablet of ferrous gluconate daily or no iron for 24 weeks after donating a unit of whole blood (500 mL).

The study’s primary outcomes were time to recovery of 80% of the post-donation decrease in hemoglobin and recovery of baseline ferritin levels.

The researchers found that subjects who received iron supplementation achieved 80% hemoglobin recovery more quickly than subjects who did not receive iron, regardless of ferritin levels.

In the low-ferritin group, the mean time to 80% hemoglobin recovery was 32 days in subjects who received iron and 158 days in those who did not (P<0.001). In the higher-ferritin group, the mean time to 80% hemoglobin recovery was 31 days in subjects who received iron and 78 days in those who did not (P=0.02).

In the low-ferritin group, the median time to recovery of baseline ferritin levels was 21 days in subjects who received iron and more than 168 days in subjects who did not. In the higher-ferritin group, the median time to recovery of baseline ferritin levels was 107 days in subjects who received iron and more than 168 days in those who did not.

The median time to recovery of iron stores was 76 days in all subjects who received iron supplements and more than 168 days in those who did not (P<0.001). Sixty-seven percent of subjects who did not receive iron had failed to recover their iron stores by 168 days.

The researchers said these findings raise important considerations regarding the 8-week minimum waiting period between blood donations that is required in the US and Canada. This is a shorter period than those allowed in many other countries.

The study suggests that hemoglobin recovery differs according to a donor’s pre-donation ferritin level, but, even in iron-replete donors, the mean recovery was only 70% at 8 weeks.

Prolonging the minimum wait time between blood donations would allow for more thorough recovery, the researchers noted, but it could also compromise the blood supply. Furthermore, increasing the waiting period might not be adequate for donors who do not take iron supplements.

Blood donation

Photo by Charles Haymond

Low-dose oral iron supplementation can reduce the time to hemoglobin recovery after blood donation, according to a study published in JAMA.

Researchers found that a daily dose of ferrous gluconate (37.5 mg of elemental iron) reduced blood donors’ time to 80% hemoglobin recovery, whether the donors were iron-depleted (with ferritin levels of 26 ng/mL or lower) or iron-replete (with ferritin levels higher than 26 ng/mL).

Joseph E. Kiss, MD, of the Institute for Transfusion Medicine in Pittsburgh, Pennsylvania, and his colleagues conducted this study at 4 regional blood centers in the US.

The researchers randomized 215 subjects (who had not donated whole blood or red blood cells within 4 months) to receive one tablet of ferrous gluconate daily or no iron for 24 weeks after donating a unit of whole blood (500 mL).

The study’s primary outcomes were time to recovery of 80% of the post-donation decrease in hemoglobin and recovery of baseline ferritin levels.

The researchers found that subjects who received iron supplementation achieved 80% hemoglobin recovery more quickly than subjects who did not receive iron, regardless of ferritin levels.

In the low-ferritin group, the mean time to 80% hemoglobin recovery was 32 days in subjects who received iron and 158 days in those who did not (P<0.001). In the higher-ferritin group, the mean time to 80% hemoglobin recovery was 31 days in subjects who received iron and 78 days in those who did not (P=0.02).

In the low-ferritin group, the median time to recovery of baseline ferritin levels was 21 days in subjects who received iron and more than 168 days in subjects who did not. In the higher-ferritin group, the median time to recovery of baseline ferritin levels was 107 days in subjects who received iron and more than 168 days in those who did not.

The median time to recovery of iron stores was 76 days in all subjects who received iron supplements and more than 168 days in those who did not (P<0.001). Sixty-seven percent of subjects who did not receive iron had failed to recover their iron stores by 168 days.

The researchers said these findings raise important considerations regarding the 8-week minimum waiting period between blood donations that is required in the US and Canada. This is a shorter period than those allowed in many other countries.

The study suggests that hemoglobin recovery differs according to a donor’s pre-donation ferritin level, but, even in iron-replete donors, the mean recovery was only 70% at 8 weeks.

Prolonging the minimum wait time between blood donations would allow for more thorough recovery, the researchers noted, but it could also compromise the blood supply. Furthermore, increasing the waiting period might not be adequate for donors who do not take iron supplements.

Follow a case and the associated discussion, to learn the latest evidence on fetal heart rate monitoring and the appropriate approaches to monitoring in labor and delivery units via an exercise sponsored by the Agency for Healthcare Research and Quality.

Click here to learn more at the AHRQ Web M&M site.

Follow a case and the associated discussion, to learn the latest evidence on fetal heart rate monitoring and the appropriate approaches to monitoring in labor and delivery units via an exercise sponsored by the Agency for Healthcare Research and Quality.

Click here to learn more at the AHRQ Web M&M site.

Follow a case and the associated discussion, to learn the latest evidence on fetal heart rate monitoring and the appropriate approaches to monitoring in labor and delivery units via an exercise sponsored by the Agency for Healthcare Research and Quality.

Click here to learn more at the AHRQ Web M&M site.

During transitions in care, unintentional medication discrepancies commonly occur and can threaten patient safety. To improve medication reconciliation, and in response to Joint Commission requirements, most hospitals have developed medication reconciliation processes.

The successes of such programs have been varied, but there is now collective experience about effective approaches to medication reconciliation.

MARQUIS identifies best practices and offers a framework for assembling a team and adaptable implementation strategy.

To download a copy of the implementation strategy developed by the Society of Hospital Medicine, click here.

During transitions in care, unintentional medication discrepancies commonly occur and can threaten patient safety. To improve medication reconciliation, and in response to Joint Commission requirements, most hospitals have developed medication reconciliation processes.

The successes of such programs have been varied, but there is now collective experience about effective approaches to medication reconciliation.

MARQUIS identifies best practices and offers a framework for assembling a team and adaptable implementation strategy.

To download a copy of the implementation strategy developed by the Society of Hospital Medicine, click here.

During transitions in care, unintentional medication discrepancies commonly occur and can threaten patient safety. To improve medication reconciliation, and in response to Joint Commission requirements, most hospitals have developed medication reconciliation processes.

The successes of such programs have been varied, but there is now collective experience about effective approaches to medication reconciliation.

MARQUIS identifies best practices and offers a framework for assembling a team and adaptable implementation strategy.

To download a copy of the implementation strategy developed by the Society of Hospital Medicine, click here.

Hospitalists should not only lead efforts to control potential Ebola outbreaks in the U.S. but should also play a role in improving global healthcare, say the authors of a recent article in the Journal of Hospital Medicine.

Author Phuoc Le, MD, MPH, assistant professor of medicine and pediatrics at the University of California San Francisco where he co-directs the Global Health-Hospital Medicine Fellowship, is also cofounder of the HEAL Initiative, a global healthcare campaign designed to improve the health of vulnerable populations worldwide. HEAL, short for Health, Equity, Action, and Leadership, recently won the 2015 SHM Award for Excellence in Humanitarian Service.

Dr. Le recently spoke with TH about why hospitalists are well-equipped to handle global health problems.

Question: In your paper, you call on hospitalists to join the ranks of global health hospitalists. Can you explain?

Answer: Whether it’s Navajo Nation in Arizona or rural Haiti, the healthcare needs of the poor are very similar. Global health hospitalists play an important role in building capacity, running a health system, improving quality while reducing costs, working in teams to provide holistic care for the inpatient, and improving transitions to the outpatient setting.

Q: How do the skills learned in resource-poor settings apply back home?

A: Let's say you have a patient with tuberculosis, which is very common in places like Liberia, and you suspect fluid in the lungs. [In Liberia], you would insert a needle and remove the fluid. In the U.S., a lot of providers would not be able to remove the fluid without getting an ultrasound and multiple other studies. Those costs add up. Global health hospitalists are very well-versed in the skills of ultrasonography because there are no ultrasonographers in the field working with us.

Q: You've spent time in Haiti and said that is where you began to notice volunteers arriving with good intentions but without needed skills. What exactly did you learn?

A: I spent a lot of time there, responding to the earthquake and also the cholera epidemic in 2010. I came across dozens of healthcare volunteers who had passion and commitment but really came ill-prepared, not through any fault of their own but because they never had an opportunity to learn the skills needed to be effective in the field. For example, take a nurse from an ivory-tower hospital and suddenly put her where she doesn’t have IVs to work with or the right type of fluids or tubing. Well, suddenly she feels like her efficacy has gone way down. That could easily lead to a lot of frustration and potential burnout. That’s why we started the HEAL Initiative, which is a two-year program for healthcare workers who want to learn the skills needed to work in poor settings.

Q: How can hospitalists get involved in global health?

A: Come to the Society of Hospital Medicine annual meeting in March where we’ll be hosting a special-interest session called Global Health and Human Rights.

Visit our website for more information about global health hospitalists.

Hospitalists should not only lead efforts to control potential Ebola outbreaks in the U.S. but should also play a role in improving global healthcare, say the authors of a recent article in the Journal of Hospital Medicine.

Author Phuoc Le, MD, MPH, assistant professor of medicine and pediatrics at the University of California San Francisco where he co-directs the Global Health-Hospital Medicine Fellowship, is also cofounder of the HEAL Initiative, a global healthcare campaign designed to improve the health of vulnerable populations worldwide. HEAL, short for Health, Equity, Action, and Leadership, recently won the 2015 SHM Award for Excellence in Humanitarian Service.

Dr. Le recently spoke with TH about why hospitalists are well-equipped to handle global health problems.

Question: In your paper, you call on hospitalists to join the ranks of global health hospitalists. Can you explain?

Answer: Whether it’s Navajo Nation in Arizona or rural Haiti, the healthcare needs of the poor are very similar. Global health hospitalists play an important role in building capacity, running a health system, improving quality while reducing costs, working in teams to provide holistic care for the inpatient, and improving transitions to the outpatient setting.

Q: How do the skills learned in resource-poor settings apply back home?

A: Let's say you have a patient with tuberculosis, which is very common in places like Liberia, and you suspect fluid in the lungs. [In Liberia], you would insert a needle and remove the fluid. In the U.S., a lot of providers would not be able to remove the fluid without getting an ultrasound and multiple other studies. Those costs add up. Global health hospitalists are very well-versed in the skills of ultrasonography because there are no ultrasonographers in the field working with us.

Q: You've spent time in Haiti and said that is where you began to notice volunteers arriving with good intentions but without needed skills. What exactly did you learn?

A: I spent a lot of time there, responding to the earthquake and also the cholera epidemic in 2010. I came across dozens of healthcare volunteers who had passion and commitment but really came ill-prepared, not through any fault of their own but because they never had an opportunity to learn the skills needed to be effective in the field. For example, take a nurse from an ivory-tower hospital and suddenly put her where she doesn’t have IVs to work with or the right type of fluids or tubing. Well, suddenly she feels like her efficacy has gone way down. That could easily lead to a lot of frustration and potential burnout. That’s why we started the HEAL Initiative, which is a two-year program for healthcare workers who want to learn the skills needed to work in poor settings.

Q: How can hospitalists get involved in global health?

A: Come to the Society of Hospital Medicine annual meeting in March where we’ll be hosting a special-interest session called Global Health and Human Rights.

Visit our website for more information about global health hospitalists.

Hospitalists should not only lead efforts to control potential Ebola outbreaks in the U.S. but should also play a role in improving global healthcare, say the authors of a recent article in the Journal of Hospital Medicine.

Author Phuoc Le, MD, MPH, assistant professor of medicine and pediatrics at the University of California San Francisco where he co-directs the Global Health-Hospital Medicine Fellowship, is also cofounder of the HEAL Initiative, a global healthcare campaign designed to improve the health of vulnerable populations worldwide. HEAL, short for Health, Equity, Action, and Leadership, recently won the 2015 SHM Award for Excellence in Humanitarian Service.

Dr. Le recently spoke with TH about why hospitalists are well-equipped to handle global health problems.

Question: In your paper, you call on hospitalists to join the ranks of global health hospitalists. Can you explain?

Answer: Whether it’s Navajo Nation in Arizona or rural Haiti, the healthcare needs of the poor are very similar. Global health hospitalists play an important role in building capacity, running a health system, improving quality while reducing costs, working in teams to provide holistic care for the inpatient, and improving transitions to the outpatient setting.

Q: How do the skills learned in resource-poor settings apply back home?

A: Let's say you have a patient with tuberculosis, which is very common in places like Liberia, and you suspect fluid in the lungs. [In Liberia], you would insert a needle and remove the fluid. In the U.S., a lot of providers would not be able to remove the fluid without getting an ultrasound and multiple other studies. Those costs add up. Global health hospitalists are very well-versed in the skills of ultrasonography because there are no ultrasonographers in the field working with us.

Q: You've spent time in Haiti and said that is where you began to notice volunteers arriving with good intentions but without needed skills. What exactly did you learn?

A: I spent a lot of time there, responding to the earthquake and also the cholera epidemic in 2010. I came across dozens of healthcare volunteers who had passion and commitment but really came ill-prepared, not through any fault of their own but because they never had an opportunity to learn the skills needed to be effective in the field. For example, take a nurse from an ivory-tower hospital and suddenly put her where she doesn’t have IVs to work with or the right type of fluids or tubing. Well, suddenly she feels like her efficacy has gone way down. That could easily lead to a lot of frustration and potential burnout. That’s why we started the HEAL Initiative, which is a two-year program for healthcare workers who want to learn the skills needed to work in poor settings.

Q: How can hospitalists get involved in global health?

A: Come to the Society of Hospital Medicine annual meeting in March where we’ll be hosting a special-interest session called Global Health and Human Rights.

Visit our website for more information about global health hospitalists.

News that the American Board of Internal Medicine (ABIM) will reboot its controversial Maintenance of Certification (MOC) program is an opportunity for hospitalists to help shape their own professional development, according to former ABIM chair and hospital medicine pioneer Robert Wachter, MD, MHM.

A year ago, ABIM moved from an MOC every 10 years to a more continuous certification process. The goal was to keep physicians more current, but the change sparked backlash over education costs, the applicability and usefulness of exam questions, and bureaucratic burdens of the new process.

In a public statement last week, ABIM president and CEO Richard Baron, MD, acknowledged that "ABIM clearly got it wrong. We launched programs that weren't ready and we didn't deliver an MOC program that physicians found meaningful."

Dr. Wachter, who was ABIM's chair when Dr. Baron was hired, says that ABIM's new plan to reach out to specialty societies means SHM can lobby for an MOC process that is more current, more applicable, and more meaningful to practitioners. Given that HM as a specialty was launched as a novel idea on what would make a good care model for hospitalized patients, Dr. Wachter is confident that SHM can be helpful in guiding the creation of a better MOC process.

Hospital medicine "was built on out-of-the-box thinking, on accepting certain parts of the old model of what a good doctor was but throwing other parts out and saying, 'We want to rethink this,'" Dr. Wachter says. "I can't think of a specialty that’s better positioned to help."

Meanwhile, hospitalist and ABIM Council member Jeff Wiese, MD, MHM, sees an opportunity to make sure the overall process for "knowledge improvement" is enhanced so that disconnects between practitioners and ABIM do not continue.

"We have to ensure that what happened over the past 20 years doesn't happen again," Dr. Wiese says. "Namely, that the world of medicine doesn't move so fast that the ABIM MOC requirements don't keep up. If we engage as physicians and specialty organizations in meaningful dialogues…then we have a much better chance of making MOC sufficiently dynamic to meet the changing times."

SHM President Burke Kealey, MD, SFHM, says that hospitalists were less impacted than some other specialists by the MOC change because they could use the Focused Practice in Hospital Medicine (FPHM) exam. The FPHM test was crafted by "real practicing hospitalists [writing] the questions for hospitalists from the point of view of what a hospitalist needs to know to do their job," he says.

Dr. Kealey adds that SHM plans to help hospitalists prepare for exams through courses featured at next month’s annual meeting and with the publication of a study guide due out this fall focused on the test's nonclinical aspects. Since it was posted last week, Dr. Kealey's blog on "The Hospital Leader" has attracted the interest of thousands of hospitalists and has been shared more than 70 times.

Visit our website for more information on Maintenance of Certification issues.

News that the American Board of Internal Medicine (ABIM) will reboot its controversial Maintenance of Certification (MOC) program is an opportunity for hospitalists to help shape their own professional development, according to former ABIM chair and hospital medicine pioneer Robert Wachter, MD, MHM.

A year ago, ABIM moved from an MOC every 10 years to a more continuous certification process. The goal was to keep physicians more current, but the change sparked backlash over education costs, the applicability and usefulness of exam questions, and bureaucratic burdens of the new process.

In a public statement last week, ABIM president and CEO Richard Baron, MD, acknowledged that "ABIM clearly got it wrong. We launched programs that weren't ready and we didn't deliver an MOC program that physicians found meaningful."

Dr. Wachter, who was ABIM's chair when Dr. Baron was hired, says that ABIM's new plan to reach out to specialty societies means SHM can lobby for an MOC process that is more current, more applicable, and more meaningful to practitioners. Given that HM as a specialty was launched as a novel idea on what would make a good care model for hospitalized patients, Dr. Wachter is confident that SHM can be helpful in guiding the creation of a better MOC process.

Hospital medicine "was built on out-of-the-box thinking, on accepting certain parts of the old model of what a good doctor was but throwing other parts out and saying, 'We want to rethink this,'" Dr. Wachter says. "I can't think of a specialty that’s better positioned to help."

Meanwhile, hospitalist and ABIM Council member Jeff Wiese, MD, MHM, sees an opportunity to make sure the overall process for "knowledge improvement" is enhanced so that disconnects between practitioners and ABIM do not continue.

"We have to ensure that what happened over the past 20 years doesn't happen again," Dr. Wiese says. "Namely, that the world of medicine doesn't move so fast that the ABIM MOC requirements don't keep up. If we engage as physicians and specialty organizations in meaningful dialogues…then we have a much better chance of making MOC sufficiently dynamic to meet the changing times."

SHM President Burke Kealey, MD, SFHM, says that hospitalists were less impacted than some other specialists by the MOC change because they could use the Focused Practice in Hospital Medicine (FPHM) exam. The FPHM test was crafted by "real practicing hospitalists [writing] the questions for hospitalists from the point of view of what a hospitalist needs to know to do their job," he says.

Dr. Kealey adds that SHM plans to help hospitalists prepare for exams through courses featured at next month’s annual meeting and with the publication of a study guide due out this fall focused on the test's nonclinical aspects. Since it was posted last week, Dr. Kealey's blog on "The Hospital Leader" has attracted the interest of thousands of hospitalists and has been shared more than 70 times.

Visit our website for more information on Maintenance of Certification issues.

News that the American Board of Internal Medicine (ABIM) will reboot its controversial Maintenance of Certification (MOC) program is an opportunity for hospitalists to help shape their own professional development, according to former ABIM chair and hospital medicine pioneer Robert Wachter, MD, MHM.

A year ago, ABIM moved from an MOC every 10 years to a more continuous certification process. The goal was to keep physicians more current, but the change sparked backlash over education costs, the applicability and usefulness of exam questions, and bureaucratic burdens of the new process.

In a public statement last week, ABIM president and CEO Richard Baron, MD, acknowledged that "ABIM clearly got it wrong. We launched programs that weren't ready and we didn't deliver an MOC program that physicians found meaningful."

Dr. Wachter, who was ABIM's chair when Dr. Baron was hired, says that ABIM's new plan to reach out to specialty societies means SHM can lobby for an MOC process that is more current, more applicable, and more meaningful to practitioners. Given that HM as a specialty was launched as a novel idea on what would make a good care model for hospitalized patients, Dr. Wachter is confident that SHM can be helpful in guiding the creation of a better MOC process.

Hospital medicine "was built on out-of-the-box thinking, on accepting certain parts of the old model of what a good doctor was but throwing other parts out and saying, 'We want to rethink this,'" Dr. Wachter says. "I can't think of a specialty that’s better positioned to help."

Meanwhile, hospitalist and ABIM Council member Jeff Wiese, MD, MHM, sees an opportunity to make sure the overall process for "knowledge improvement" is enhanced so that disconnects between practitioners and ABIM do not continue.

"We have to ensure that what happened over the past 20 years doesn't happen again," Dr. Wiese says. "Namely, that the world of medicine doesn't move so fast that the ABIM MOC requirements don't keep up. If we engage as physicians and specialty organizations in meaningful dialogues…then we have a much better chance of making MOC sufficiently dynamic to meet the changing times."

SHM President Burke Kealey, MD, SFHM, says that hospitalists were less impacted than some other specialists by the MOC change because they could use the Focused Practice in Hospital Medicine (FPHM) exam. The FPHM test was crafted by "real practicing hospitalists [writing] the questions for hospitalists from the point of view of what a hospitalist needs to know to do their job," he says.

Dr. Kealey adds that SHM plans to help hospitalists prepare for exams through courses featured at next month’s annual meeting and with the publication of a study guide due out this fall focused on the test's nonclinical aspects. Since it was posted last week, Dr. Kealey's blog on "The Hospital Leader" has attracted the interest of thousands of hospitalists and has been shared more than 70 times.

Visit our website for more information on Maintenance of Certification issues.

No association between an increased risk of acute pancreatitis and treatment with incretin therapy for type 2 diabetes was found in a large case control-study.

To evaluate whether the risk of acute pancreatitis was increased among patients treated with incretin-based drugs – glucagonlike peptide–1 (GLP-1) receptor agonists and dipeptidyl peptidase–4 (DPP-4) inhibitors – the investigators compared the risks of acute pancreatitis associated with different antihyperglycemic drugs in 12,868 people hospitalized for the first time for acute pancreatitis, and in 12,680 controls matched for birth year, sex, and region of residence in Denmark.

The study addressed evidence indicating that incretins may cause pancreatitis and pancreatic cancer in humans, which includes adverse event reports suggesting a signal of pancreatitis, but the association between incretins and acute pancreatitis is controversial and is an issue that “remains under debate,” they noted.

The data used were from three Danish databases, including one of reimbursed prescriptions. After adjustment for comorbidities and drugs associated with pancreatitis, including alcoholism and obesity, the risk of acute pancreatitis was not increased among those who had ever used an incretin, with an odds ratio of 0.95, according to Dr. Reimar Thomsen of the department of clinical epidemiology, Institute of Clinical Medicine, Aarhus (Denmark) University Hospital, and his associates (Diabetes Care 2015 [doi:10.2337/dc13-2983])

Risk was also not increased among those who had been ever treated with a DPP-4 inhibitor (OR, 1.04), which included an OR of 1.06 for sitagliptin, or among those who had been treated with a GLP-1 receptor agonist (OR, 0.82), which included an OR of 0.75 for liraglutide. Nor was risk elevated among those treated with nonincretin antihyperglycemic drugs (OR, 1.05).

In addition, the adjusted odds ratio comparing the risk of acute pancreatitis associated with incretin treatments and other antihyperglycemics was not increased, approaching 1.

The crude odds ratios, before adjustment for confounding factors, was 1.36 in patients who had been treated with incretins and 1.44 among those who had been treated with other antihyperglycemic drugs. “The fact that crude ORs were increased to very similar levels for all antihyperglycemic drugs – given their different modes of action – points to a general underlying diabetes effect on pancreatitis risk, rather than a specific drug effect,” they commented. In the crude analyses, they determined that obesity, gallstones, and other diabetes-related risk factors “may explain much of the apparent risk increase,” the investigators added.

Other findings included an increased risk of acute pancreatitis among those who had recently started treatment with a DPP-4 inhibitor and in those who had recently started treatment with several other antihyperglycemic drugs, including sulfonylureas and insulin. “This lack of specificity suggests that either the increased pancreatitis risk is related to newly diagnosed and drug-treated type 2 diabetes per se, with a possibility of reverse causality due to pancreatogenic diabetes,” or that starting therapy with sulfonylureas and insulin “also causes acute pancreatitis, which should be further investigated,” they said.

Incretin-based drugs include injectable incretin mimetic agents (GLP-1 receptor agonists) such as liraglutide; and incretin enhancers (DPP-4) inhibitors, such as sitagliptin.

The study was supported by the Clinical Epidemiological Research Foundation in Denmark. One of the authors, from the Danish Center for Strategic Research in Type 2 Diabetes, at Odense University Hospital, disclosed having received research grants form Novo-Nordisk. Of the six authors, four are from the Aarhus University Hospital clinical epidemiology department, a member of the center, which receives funding that includes an unrestricted donation from Novo-Nordisk.

emechcatie@frontlinemedcom.com

No association between an increased risk of acute pancreatitis and treatment with incretin therapy for type 2 diabetes was found in a large case control-study.

To evaluate whether the risk of acute pancreatitis was increased among patients treated with incretin-based drugs – glucagonlike peptide–1 (GLP-1) receptor agonists and dipeptidyl peptidase–4 (DPP-4) inhibitors – the investigators compared the risks of acute pancreatitis associated with different antihyperglycemic drugs in 12,868 people hospitalized for the first time for acute pancreatitis, and in 12,680 controls matched for birth year, sex, and region of residence in Denmark.

The study addressed evidence indicating that incretins may cause pancreatitis and pancreatic cancer in humans, which includes adverse event reports suggesting a signal of pancreatitis, but the association between incretins and acute pancreatitis is controversial and is an issue that “remains under debate,” they noted.

The data used were from three Danish databases, including one of reimbursed prescriptions. After adjustment for comorbidities and drugs associated with pancreatitis, including alcoholism and obesity, the risk of acute pancreatitis was not increased among those who had ever used an incretin, with an odds ratio of 0.95, according to Dr. Reimar Thomsen of the department of clinical epidemiology, Institute of Clinical Medicine, Aarhus (Denmark) University Hospital, and his associates (Diabetes Care 2015 [doi:10.2337/dc13-2983])

Risk was also not increased among those who had been ever treated with a DPP-4 inhibitor (OR, 1.04), which included an OR of 1.06 for sitagliptin, or among those who had been treated with a GLP-1 receptor agonist (OR, 0.82), which included an OR of 0.75 for liraglutide. Nor was risk elevated among those treated with nonincretin antihyperglycemic drugs (OR, 1.05).

In addition, the adjusted odds ratio comparing the risk of acute pancreatitis associated with incretin treatments and other antihyperglycemics was not increased, approaching 1.

The crude odds ratios, before adjustment for confounding factors, was 1.36 in patients who had been treated with incretins and 1.44 among those who had been treated with other antihyperglycemic drugs. “The fact that crude ORs were increased to very similar levels for all antihyperglycemic drugs – given their different modes of action – points to a general underlying diabetes effect on pancreatitis risk, rather than a specific drug effect,” they commented. In the crude analyses, they determined that obesity, gallstones, and other diabetes-related risk factors “may explain much of the apparent risk increase,” the investigators added.

Other findings included an increased risk of acute pancreatitis among those who had recently started treatment with a DPP-4 inhibitor and in those who had recently started treatment with several other antihyperglycemic drugs, including sulfonylureas and insulin. “This lack of specificity suggests that either the increased pancreatitis risk is related to newly diagnosed and drug-treated type 2 diabetes per se, with a possibility of reverse causality due to pancreatogenic diabetes,” or that starting therapy with sulfonylureas and insulin “also causes acute pancreatitis, which should be further investigated,” they said.

Incretin-based drugs include injectable incretin mimetic agents (GLP-1 receptor agonists) such as liraglutide; and incretin enhancers (DPP-4) inhibitors, such as sitagliptin.

The study was supported by the Clinical Epidemiological Research Foundation in Denmark. One of the authors, from the Danish Center for Strategic Research in Type 2 Diabetes, at Odense University Hospital, disclosed having received research grants form Novo-Nordisk. Of the six authors, four are from the Aarhus University Hospital clinical epidemiology department, a member of the center, which receives funding that includes an unrestricted donation from Novo-Nordisk.

emechcatie@frontlinemedcom.com

No association between an increased risk of acute pancreatitis and treatment with incretin therapy for type 2 diabetes was found in a large case control-study.

To evaluate whether the risk of acute pancreatitis was increased among patients treated with incretin-based drugs – glucagonlike peptide–1 (GLP-1) receptor agonists and dipeptidyl peptidase–4 (DPP-4) inhibitors – the investigators compared the risks of acute pancreatitis associated with different antihyperglycemic drugs in 12,868 people hospitalized for the first time for acute pancreatitis, and in 12,680 controls matched for birth year, sex, and region of residence in Denmark.

The study addressed evidence indicating that incretins may cause pancreatitis and pancreatic cancer in humans, which includes adverse event reports suggesting a signal of pancreatitis, but the association between incretins and acute pancreatitis is controversial and is an issue that “remains under debate,” they noted.

The data used were from three Danish databases, including one of reimbursed prescriptions. After adjustment for comorbidities and drugs associated with pancreatitis, including alcoholism and obesity, the risk of acute pancreatitis was not increased among those who had ever used an incretin, with an odds ratio of 0.95, according to Dr. Reimar Thomsen of the department of clinical epidemiology, Institute of Clinical Medicine, Aarhus (Denmark) University Hospital, and his associates (Diabetes Care 2015 [doi:10.2337/dc13-2983])

Risk was also not increased among those who had been ever treated with a DPP-4 inhibitor (OR, 1.04), which included an OR of 1.06 for sitagliptin, or among those who had been treated with a GLP-1 receptor agonist (OR, 0.82), which included an OR of 0.75 for liraglutide. Nor was risk elevated among those treated with nonincretin antihyperglycemic drugs (OR, 1.05).

In addition, the adjusted odds ratio comparing the risk of acute pancreatitis associated with incretin treatments and other antihyperglycemics was not increased, approaching 1.

The crude odds ratios, before adjustment for confounding factors, was 1.36 in patients who had been treated with incretins and 1.44 among those who had been treated with other antihyperglycemic drugs. “The fact that crude ORs were increased to very similar levels for all antihyperglycemic drugs – given their different modes of action – points to a general underlying diabetes effect on pancreatitis risk, rather than a specific drug effect,” they commented. In the crude analyses, they determined that obesity, gallstones, and other diabetes-related risk factors “may explain much of the apparent risk increase,” the investigators added.

Other findings included an increased risk of acute pancreatitis among those who had recently started treatment with a DPP-4 inhibitor and in those who had recently started treatment with several other antihyperglycemic drugs, including sulfonylureas and insulin. “This lack of specificity suggests that either the increased pancreatitis risk is related to newly diagnosed and drug-treated type 2 diabetes per se, with a possibility of reverse causality due to pancreatogenic diabetes,” or that starting therapy with sulfonylureas and insulin “also causes acute pancreatitis, which should be further investigated,” they said.

Incretin-based drugs include injectable incretin mimetic agents (GLP-1 receptor agonists) such as liraglutide; and incretin enhancers (DPP-4) inhibitors, such as sitagliptin.

The study was supported by the Clinical Epidemiological Research Foundation in Denmark. One of the authors, from the Danish Center for Strategic Research in Type 2 Diabetes, at Odense University Hospital, disclosed having received research grants form Novo-Nordisk. Of the six authors, four are from the Aarhus University Hospital clinical epidemiology department, a member of the center, which receives funding that includes an unrestricted donation from Novo-Nordisk.

emechcatie@frontlinemedcom.com

Clinical question

Can a procalcitonin-based algorithm reduce antibiotic use in critically ill patients?

Bottom line

A procalcitonin-based algorithm using a 0.1 ng/mL cutoff does not significantly decrease the duration of antibiotic treatment in critically ill patients nor does it reduce length of stay or number of deaths. The rate of decline in the procalcitonin level over the first 72 hours, however, does serve as an independent predictor of short-term and long-term all-cause mortality. (LOE = 1b-)

Reference

Shehabi Y, Sterba M, Garrett PM, et al, for the ProGUARD Study Investigators and the ANZICS Clinical Trials Group. Procalcitonin algorithm in critically ill adults with undifferentiated infection or suspected sepsis. Am J Respir Crit Care Med 2014;190(10):1102-1110.

Study design: Randomized controlled trial (nonblinded)

Funding source: Foundation

Allocation: Concealed

Setting: Inpatient (ICU only)

Synopsis

Procalcitonin (PCT) is a sepsis biomarker that has been utilized to guide antibiotic use in different patient populations. In this study, the authors tested a PCT-algorithm using a 0.1 ng/mL cut-off to reduce antibiotic exposure in critically ill patients. Patients newly admitted to intensive care units (ICUs) who were receiving antibiotics for suspected infections were randomized, using concealed allocation, to receive PCT-guided care (n = 196) or standard care (n = 198). All patients had PCT levels drawn daily until discharge from the ICU or up to a maximum of 7 days. In the PCT group, antibiotics were stopped if PCT levels were negative (< 0.1 ng/mL), if PCT levels were borderline (0.1 - 0.25 ng/mL) and infection was unlikely, or if PCT levels decreased more than 90% from baseline values. In the standard care group, the treating clinician determined antibiotic use without knowledge of the PCT results. Baseline characteristics of the 2 groups were similar with regard to severity-of-disease scores and baseline PCT values. There was high compliance with the PCT algorithm, with less than 3% of study days when the algorithm was not followed. There was no significant difference detected between the 2 groups for the primary outcome of time to antibiotic cessation. However, duration of antibiotic use was longer than expected in the control group (11 days actual vs 9 days expected), so the study may have been underpowered to detect an expected 25% reduction. Nevertheless, the 2 groups were similar with regard to ICU and hospital lengths of stay, as well as ICU, hospital, and 90-day mortality rates. Of note, the rate of decline in PCT level over the first 72 hours was an independent predictor of hospital mortality and 90-day mortality, with a slower decline corresponding to a higher mortality.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

Clinical question

Can a procalcitonin-based algorithm reduce antibiotic use in critically ill patients?

Bottom line

A procalcitonin-based algorithm using a 0.1 ng/mL cutoff does not significantly decrease the duration of antibiotic treatment in critically ill patients nor does it reduce length of stay or number of deaths. The rate of decline in the procalcitonin level over the first 72 hours, however, does serve as an independent predictor of short-term and long-term all-cause mortality. (LOE = 1b-)

Reference

Shehabi Y, Sterba M, Garrett PM, et al, for the ProGUARD Study Investigators and the ANZICS Clinical Trials Group. Procalcitonin algorithm in critically ill adults with undifferentiated infection or suspected sepsis. Am J Respir Crit Care Med 2014;190(10):1102-1110.

Study design: Randomized controlled trial (nonblinded)

Funding source: Foundation

Allocation: Concealed

Setting: Inpatient (ICU only)

Synopsis

Procalcitonin (PCT) is a sepsis biomarker that has been utilized to guide antibiotic use in different patient populations. In this study, the authors tested a PCT-algorithm using a 0.1 ng/mL cut-off to reduce antibiotic exposure in critically ill patients. Patients newly admitted to intensive care units (ICUs) who were receiving antibiotics for suspected infections were randomized, using concealed allocation, to receive PCT-guided care (n = 196) or standard care (n = 198). All patients had PCT levels drawn daily until discharge from the ICU or up to a maximum of 7 days. In the PCT group, antibiotics were stopped if PCT levels were negative (< 0.1 ng/mL), if PCT levels were borderline (0.1 - 0.25 ng/mL) and infection was unlikely, or if PCT levels decreased more than 90% from baseline values. In the standard care group, the treating clinician determined antibiotic use without knowledge of the PCT results. Baseline characteristics of the 2 groups were similar with regard to severity-of-disease scores and baseline PCT values. There was high compliance with the PCT algorithm, with less than 3% of study days when the algorithm was not followed. There was no significant difference detected between the 2 groups for the primary outcome of time to antibiotic cessation. However, duration of antibiotic use was longer than expected in the control group (11 days actual vs 9 days expected), so the study may have been underpowered to detect an expected 25% reduction. Nevertheless, the 2 groups were similar with regard to ICU and hospital lengths of stay, as well as ICU, hospital, and 90-day mortality rates. Of note, the rate of decline in PCT level over the first 72 hours was an independent predictor of hospital mortality and 90-day mortality, with a slower decline corresponding to a higher mortality.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

Clinical question

Can a procalcitonin-based algorithm reduce antibiotic use in critically ill patients?

Bottom line

A procalcitonin-based algorithm using a 0.1 ng/mL cutoff does not significantly decrease the duration of antibiotic treatment in critically ill patients nor does it reduce length of stay or number of deaths. The rate of decline in the procalcitonin level over the first 72 hours, however, does serve as an independent predictor of short-term and long-term all-cause mortality. (LOE = 1b-)

Reference

Shehabi Y, Sterba M, Garrett PM, et al, for the ProGUARD Study Investigators and the ANZICS Clinical Trials Group. Procalcitonin algorithm in critically ill adults with undifferentiated infection or suspected sepsis. Am J Respir Crit Care Med 2014;190(10):1102-1110.

Study design: Randomized controlled trial (nonblinded)

Funding source: Foundation

Allocation: Concealed

Setting: Inpatient (ICU only)

Synopsis

Procalcitonin (PCT) is a sepsis biomarker that has been utilized to guide antibiotic use in different patient populations. In this study, the authors tested a PCT-algorithm using a 0.1 ng/mL cut-off to reduce antibiotic exposure in critically ill patients. Patients newly admitted to intensive care units (ICUs) who were receiving antibiotics for suspected infections were randomized, using concealed allocation, to receive PCT-guided care (n = 196) or standard care (n = 198). All patients had PCT levels drawn daily until discharge from the ICU or up to a maximum of 7 days. In the PCT group, antibiotics were stopped if PCT levels were negative (< 0.1 ng/mL), if PCT levels were borderline (0.1 - 0.25 ng/mL) and infection was unlikely, or if PCT levels decreased more than 90% from baseline values. In the standard care group, the treating clinician determined antibiotic use without knowledge of the PCT results. Baseline characteristics of the 2 groups were similar with regard to severity-of-disease scores and baseline PCT values. There was high compliance with the PCT algorithm, with less than 3% of study days when the algorithm was not followed. There was no significant difference detected between the 2 groups for the primary outcome of time to antibiotic cessation. However, duration of antibiotic use was longer than expected in the control group (11 days actual vs 9 days expected), so the study may have been underpowered to detect an expected 25% reduction. Nevertheless, the 2 groups were similar with regard to ICU and hospital lengths of stay, as well as ICU, hospital, and 90-day mortality rates. Of note, the rate of decline in PCT level over the first 72 hours was an independent predictor of hospital mortality and 90-day mortality, with a slower decline corresponding to a higher mortality.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

Clinical question

Does early nasoenteric feeding decrease the rate of infections or death in patients hospitalized with severe acute pancreatitis?

Bottom line

In patients with severe acute pancreatitis, early nasoenteric feeding initiated within 24 hours of presentation, as compared with oral feeding after 72 hours, does not improve mortality or reduce the rate of major infections. (LOE = 1b-)

Reference

Bakker OJ, van Brunschot S, van Santvoort HC, et al, for the Dutch Pancreatitis Study Group. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med 2014;371(21):1983-1993.

Study design: Randomized controlled trial (nonblinded)

Funding source: Government

Allocation: Concealed

Setting: Inpatient (ward only)

Synopsis

Previous observational studies suggest that early nasoenteric feeding in patients with acute pancreatitis may reduce the rate of major infections by stimulating intestinal motility, reducing bacterial overgrowth, and increasing splanchnic blood flow. Using concealed allocation, these authors randomized patients presenting to the emergency department with severe acute pancreatitis to receive either early nasoenteric tube feeding initiated within 24 hours (n = 102) or oral feeding started at 72 hours (n = 106). If the oral diet was not tolerated, tube feeding was initiated after 96 hours. The 2 groups were similar at baseline: the mean age was 65 years and 60% of the patients had evidence of systemic inflammatory response syndrome (SIRS). Analysis was by intention to treat. One third of patients in the oral group eventually required tube feeding. For the primary composite end point of death or major infection (infected pancreatic necrosis, bacteremia, or pneumonia), there was no significant difference detected between the 2 groups. When the outcomes of major infection and death were examined separately, the 2 groups again had comparable results. Finally, patients in both groups had similar rates of admission to the intensive care unit and similar need for mechanical ventilation. Given fewer-than-expected events in the control group, it is possible that the study was too small to detect a difference in the primary outcome, if such a difference exists.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

Clinical question

Does early nasoenteric feeding decrease the rate of infections or death in patients hospitalized with severe acute pancreatitis?

Bottom line

In patients with severe acute pancreatitis, early nasoenteric feeding initiated within 24 hours of presentation, as compared with oral feeding after 72 hours, does not improve mortality or reduce the rate of major infections. (LOE = 1b-)

Reference

Bakker OJ, van Brunschot S, van Santvoort HC, et al, for the Dutch Pancreatitis Study Group. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med 2014;371(21):1983-1993.

Study design: Randomized controlled trial (nonblinded)

Funding source: Government

Allocation: Concealed

Setting: Inpatient (ward only)

Synopsis

Previous observational studies suggest that early nasoenteric feeding in patients with acute pancreatitis may reduce the rate of major infections by stimulating intestinal motility, reducing bacterial overgrowth, and increasing splanchnic blood flow. Using concealed allocation, these authors randomized patients presenting to the emergency department with severe acute pancreatitis to receive either early nasoenteric tube feeding initiated within 24 hours (n = 102) or oral feeding started at 72 hours (n = 106). If the oral diet was not tolerated, tube feeding was initiated after 96 hours. The 2 groups were similar at baseline: the mean age was 65 years and 60% of the patients had evidence of systemic inflammatory response syndrome (SIRS). Analysis was by intention to treat. One third of patients in the oral group eventually required tube feeding. For the primary composite end point of death or major infection (infected pancreatic necrosis, bacteremia, or pneumonia), there was no significant difference detected between the 2 groups. When the outcomes of major infection and death were examined separately, the 2 groups again had comparable results. Finally, patients in both groups had similar rates of admission to the intensive care unit and similar need for mechanical ventilation. Given fewer-than-expected events in the control group, it is possible that the study was too small to detect a difference in the primary outcome, if such a difference exists.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

Clinical question

Does early nasoenteric feeding decrease the rate of infections or death in patients hospitalized with severe acute pancreatitis?

Bottom line

In patients with severe acute pancreatitis, early nasoenteric feeding initiated within 24 hours of presentation, as compared with oral feeding after 72 hours, does not improve mortality or reduce the rate of major infections. (LOE = 1b-)

Reference

Bakker OJ, van Brunschot S, van Santvoort HC, et al, for the Dutch Pancreatitis Study Group. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med 2014;371(21):1983-1993.

Study design: Randomized controlled trial (nonblinded)

Funding source: Government

Allocation: Concealed

Setting: Inpatient (ward only)

Synopsis

Previous observational studies suggest that early nasoenteric feeding in patients with acute pancreatitis may reduce the rate of major infections by stimulating intestinal motility, reducing bacterial overgrowth, and increasing splanchnic blood flow. Using concealed allocation, these authors randomized patients presenting to the emergency department with severe acute pancreatitis to receive either early nasoenteric tube feeding initiated within 24 hours (n = 102) or oral feeding started at 72 hours (n = 106). If the oral diet was not tolerated, tube feeding was initiated after 96 hours. The 2 groups were similar at baseline: the mean age was 65 years and 60% of the patients had evidence of systemic inflammatory response syndrome (SIRS). Analysis was by intention to treat. One third of patients in the oral group eventually required tube feeding. For the primary composite end point of death or major infection (infected pancreatic necrosis, bacteremia, or pneumonia), there was no significant difference detected between the 2 groups. When the outcomes of major infection and death were examined separately, the 2 groups again had comparable results. Finally, patients in both groups had similar rates of admission to the intensive care unit and similar need for mechanical ventilation. Given fewer-than-expected events in the control group, it is possible that the study was too small to detect a difference in the primary outcome, if such a difference exists.

Dr. Kulkarni is an assistant professor of hospital medicine at Northwestern University in Chicago.

I say “Thank you” a lot to patients. And I mean it.

I like being a doctor. It’s something I always wanted to do. For all the difficulties that go along with it, I still enjoy the actual job of caring for those who come to me. They’re the reason I’m here, and they keep my practice afloat and let me do what I want in life.

Like any other business, I have competitors. In my area, people have a choice of neurologists, and I appreciate that they picked me. So I always try to thank them when walking up to checkout.

A big part of what makes the job rewarding are those who feel the same way about me. It’s always nice when they thank me for helping, or trying to help, or just listening. I try to be a good doctor, so I’m glad to have someone recognize that. In this field, you can’t make everyone happy, but if I can have a solid majority who understand that I’m doing my best for them, I’ll take it.

I’m not fishing for compliments, or gifts, or a parade. Experience has taught me that patients who are overly flattering are most likely not to mean it. If someone calls me too many wonderful things, I immediately worry about their ulterior motives. Are they looking for narcotics? Disability? A legal action?

But a simple, sincere, “Thank you” from a patient can make it all worthwhile. Even on a bad day, it’s still a bright spot. It’s nice to know I’m making a difference. When I get a small note or appreciative Christmas card from a patient, I save it. They go in a drawer to be taken out and read after a particularly rough time, to remind myself that I must be doing something right.

Being appreciated reminds me why I’m here, and that this was the right choice for me. It lets me know that I’m doing what I set out to do many years ago: to help people.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I say “Thank you” a lot to patients. And I mean it.

I like being a doctor. It’s something I always wanted to do. For all the difficulties that go along with it, I still enjoy the actual job of caring for those who come to me. They’re the reason I’m here, and they keep my practice afloat and let me do what I want in life.

Like any other business, I have competitors. In my area, people have a choice of neurologists, and I appreciate that they picked me. So I always try to thank them when walking up to checkout.

A big part of what makes the job rewarding are those who feel the same way about me. It’s always nice when they thank me for helping, or trying to help, or just listening. I try to be a good doctor, so I’m glad to have someone recognize that. In this field, you can’t make everyone happy, but if I can have a solid majority who understand that I’m doing my best for them, I’ll take it.

I’m not fishing for compliments, or gifts, or a parade. Experience has taught me that patients who are overly flattering are most likely not to mean it. If someone calls me too many wonderful things, I immediately worry about their ulterior motives. Are they looking for narcotics? Disability? A legal action?

But a simple, sincere, “Thank you” from a patient can make it all worthwhile. Even on a bad day, it’s still a bright spot. It’s nice to know I’m making a difference. When I get a small note or appreciative Christmas card from a patient, I save it. They go in a drawer to be taken out and read after a particularly rough time, to remind myself that I must be doing something right.

Being appreciated reminds me why I’m here, and that this was the right choice for me. It lets me know that I’m doing what I set out to do many years ago: to help people.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I say “Thank you” a lot to patients. And I mean it.

I like being a doctor. It’s something I always wanted to do. For all the difficulties that go along with it, I still enjoy the actual job of caring for those who come to me. They’re the reason I’m here, and they keep my practice afloat and let me do what I want in life.

Like any other business, I have competitors. In my area, people have a choice of neurologists, and I appreciate that they picked me. So I always try to thank them when walking up to checkout.

A big part of what makes the job rewarding are those who feel the same way about me. It’s always nice when they thank me for helping, or trying to help, or just listening. I try to be a good doctor, so I’m glad to have someone recognize that. In this field, you can’t make everyone happy, but if I can have a solid majority who understand that I’m doing my best for them, I’ll take it.

I’m not fishing for compliments, or gifts, or a parade. Experience has taught me that patients who are overly flattering are most likely not to mean it. If someone calls me too many wonderful things, I immediately worry about their ulterior motives. Are they looking for narcotics? Disability? A legal action?

But a simple, sincere, “Thank you” from a patient can make it all worthwhile. Even on a bad day, it’s still a bright spot. It’s nice to know I’m making a difference. When I get a small note or appreciative Christmas card from a patient, I save it. They go in a drawer to be taken out and read after a particularly rough time, to remind myself that I must be doing something right.

Being appreciated reminds me why I’m here, and that this was the right choice for me. It lets me know that I’m doing what I set out to do many years ago: to help people.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Bertie Gottgens, PhD

Photo courtesy of

University of Cambridge

A new computer model that simulates blood cell development could aid the discovery of novel treatments for hematologic malignancies, according to researchers.

“With this new computer model, we can carry out simulated experiments in seconds that would take many weeks to perform in the laboratory, dramatically speeding up research into blood development and the genetic mutations that cause leukemia,” said Bertie Gottgens, PhD, of the University of Cambridge in the UK.

Dr Gottgens and his colleagues explained this research in Nature Biotechnology.

To start, the researchers measured the activity of 48 genes in 3934 hematopoietic progenitor cells. They used the resulting dataset to construct the computer model of blood cell development, using computational approaches originally developed at Microsoft Research for the synthesis of computer code.

Subsequent lab experiments validated the accuracy of the model.

The researchers noted that the model can be used to simulate the activity of key genes implicated in hematologic malignancies. For example, around 1 in 5 children who develop leukemia have a faulty version of the RUNX1 gene, as do a similar proportion of adults with acute myeloid leukemia.

The computer model shows how RUNX1 interacts with other genes to control blood cell development. The gene produces the RUNX1 protein, which, in healthy patients, activates a network of key genes. In leukemia patients, an altered form of the protein is thought to suppress the network.

If the researchers change the “rules” in the network model, they can simulate the formation of abnormal leukemia cells. By tweaking the leukemia model until the behavior of the network reverts back to normal, the team can identify pathways that, potentially, could be targeted with drugs.

“Because the computer simulations are very fast, we can quickly screen through lots of possibilities to pick the most promising ones as pathways for drug development,” Dr Gottgens said.

“The cost of developing a new drug is enormous, and much of this cost comes from new candidate drugs failing late in the drug development process. Our model could significantly reduce the risk of failure, with the potential to make drug discovery faster and cheaper.”

Bertie Gottgens, PhD

Photo courtesy of

University of Cambridge

A new computer model that simulates blood cell development could aid the discovery of novel treatments for hematologic malignancies, according to researchers.

“With this new computer model, we can carry out simulated experiments in seconds that would take many weeks to perform in the laboratory, dramatically speeding up research into blood development and the genetic mutations that cause leukemia,” said Bertie Gottgens, PhD, of the University of Cambridge in the UK.

Dr Gottgens and his colleagues explained this research in Nature Biotechnology.

To start, the researchers measured the activity of 48 genes in 3934 hematopoietic progenitor cells. They used the resulting dataset to construct the computer model of blood cell development, using computational approaches originally developed at Microsoft Research for the synthesis of computer code.

Subsequent lab experiments validated the accuracy of the model.

The researchers noted that the model can be used to simulate the activity of key genes implicated in hematologic malignancies. For example, around 1 in 5 children who develop leukemia have a faulty version of the RUNX1 gene, as do a similar proportion of adults with acute myeloid leukemia.

The computer model shows how RUNX1 interacts with other genes to control blood cell development. The gene produces the RUNX1 protein, which, in healthy patients, activates a network of key genes. In leukemia patients, an altered form of the protein is thought to suppress the network.

If the researchers change the “rules” in the network model, they can simulate the formation of abnormal leukemia cells. By tweaking the leukemia model until the behavior of the network reverts back to normal, the team can identify pathways that, potentially, could be targeted with drugs.

“Because the computer simulations are very fast, we can quickly screen through lots of possibilities to pick the most promising ones as pathways for drug development,” Dr Gottgens said.

“The cost of developing a new drug is enormous, and much of this cost comes from new candidate drugs failing late in the drug development process. Our model could significantly reduce the risk of failure, with the potential to make drug discovery faster and cheaper.”

Bertie Gottgens, PhD

Photo courtesy of

University of Cambridge

A new computer model that simulates blood cell development could aid the discovery of novel treatments for hematologic malignancies, according to researchers.

“With this new computer model, we can carry out simulated experiments in seconds that would take many weeks to perform in the laboratory, dramatically speeding up research into blood development and the genetic mutations that cause leukemia,” said Bertie Gottgens, PhD, of the University of Cambridge in the UK.

Dr Gottgens and his colleagues explained this research in Nature Biotechnology.

To start, the researchers measured the activity of 48 genes in 3934 hematopoietic progenitor cells. They used the resulting dataset to construct the computer model of blood cell development, using computational approaches originally developed at Microsoft Research for the synthesis of computer code.

Subsequent lab experiments validated the accuracy of the model.

The researchers noted that the model can be used to simulate the activity of key genes implicated in hematologic malignancies. For example, around 1 in 5 children who develop leukemia have a faulty version of the RUNX1 gene, as do a similar proportion of adults with acute myeloid leukemia.

The computer model shows how RUNX1 interacts with other genes to control blood cell development. The gene produces the RUNX1 protein, which, in healthy patients, activates a network of key genes. In leukemia patients, an altered form of the protein is thought to suppress the network.

If the researchers change the “rules” in the network model, they can simulate the formation of abnormal leukemia cells. By tweaking the leukemia model until the behavior of the network reverts back to normal, the team can identify pathways that, potentially, could be targeted with drugs.

“Because the computer simulations are very fast, we can quickly screen through lots of possibilities to pick the most promising ones as pathways for drug development,” Dr Gottgens said.

“The cost of developing a new drug is enormous, and much of this cost comes from new candidate drugs failing late in the drug development process. Our model could significantly reduce the risk of failure, with the potential to make drug discovery faster and cheaper.”