The FP diagnosed a varicella infection in this patient. The simultaneous appearance of papules, pustules, and crusted lesions on the patient’s trunk and face was highly suspicious for varicella, especially because there was no history of him receiving the varicella vaccine.

Varicella (chickenpox) is caused by a primary infection with the varicella zoster virus (VZV), which is a double-stranded, linear DNA herpes virus. Transmission occurs via contact with aerosolized droplets from nasopharyngeal secretions or by direct cutaneous contact with vesicle fluid from skin lesions. The incubation period for VZV is approximately 15 days, during which the virus undergoes replication in regional lymph nodes, followed by 2 viremic stages. In the first stage the virus spreads to internal organs, and in the second stage the virus spreads to the skin.

The vesicular rash appears in crops for several days and the lesions start as vesicles on a red base (classically described as a “dew drop on a rose petal”). The lesions gradually develop a pustular component followed by the evolution of crusted papules. The period of infectivity is generally considered to last from 48 hours prior to the onset of the rash until the skin lesions have fully crusted.

New varicella lesions stop forming in approximately 4 days, and most lesions become fully crusted by 7 days. Diagnosis is usually based on classic presentation. A culture of the lesions may provide a definitive diagnosis, but is positive in less than 40% of cases. Direct fluorescent antibody testing has good sensitivity and is more rapid than tissue culture. In this case, the diagnosis was made on clinical grounds.

Adults who get varicella should be assessed for neurologic and pulmonary disease; our patient showed no signs of either complication. Encephalitis is a serious potential complication of chickenpox that can develop toward the end of the first week of the exanthema. One form, acute cerebellar ataxia, occurs mostly in children and is generally followed by a complete recovery. In adults, a diffuse encephalitis can occur, and may produce delirium, seizures, and focal neurologic signs. It has significant rates of long-term neurologic sequelae and death.

Varicella pneumonia accounts for the majority of hospitalizations in adults with chickenpox, where it has up to a 30% mortality rate. It usually develops insidiously within a few days after the rash has appeared, with progressive tachypnea, dyspnea, and dry cough. Chest x-rays will reveal diffuse bilateral infiltrates. Varicella pneumonia requires prompt administration of intravenous acyclovir.

For adults with uncomplicated varicella, oral acyclovir 800 mg 5 times/d for 5 days may be used for treatment if started within the first 24 hours of the rash. The patient in this case denied risk factors for human immunodeficiency virus, and because he lacked health insurance, he did not want any blood tests or medications unless they were absolutely necessary. He wanted to return to work but was told that he needed to wait until all his lesions had crusted over.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Chickenpox. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:707-711.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed a varicella infection in this patient. The simultaneous appearance of papules, pustules, and crusted lesions on the patient’s trunk and face was highly suspicious for varicella, especially because there was no history of him receiving the varicella vaccine.

Varicella (chickenpox) is caused by a primary infection with the varicella zoster virus (VZV), which is a double-stranded, linear DNA herpes virus. Transmission occurs via contact with aerosolized droplets from nasopharyngeal secretions or by direct cutaneous contact with vesicle fluid from skin lesions. The incubation period for VZV is approximately 15 days, during which the virus undergoes replication in regional lymph nodes, followed by 2 viremic stages. In the first stage the virus spreads to internal organs, and in the second stage the virus spreads to the skin.

The vesicular rash appears in crops for several days and the lesions start as vesicles on a red base (classically described as a “dew drop on a rose petal”). The lesions gradually develop a pustular component followed by the evolution of crusted papules. The period of infectivity is generally considered to last from 48 hours prior to the onset of the rash until the skin lesions have fully crusted.

New varicella lesions stop forming in approximately 4 days, and most lesions become fully crusted by 7 days. Diagnosis is usually based on classic presentation. A culture of the lesions may provide a definitive diagnosis, but is positive in less than 40% of cases. Direct fluorescent antibody testing has good sensitivity and is more rapid than tissue culture. In this case, the diagnosis was made on clinical grounds.

Adults who get varicella should be assessed for neurologic and pulmonary disease; our patient showed no signs of either complication. Encephalitis is a serious potential complication of chickenpox that can develop toward the end of the first week of the exanthema. One form, acute cerebellar ataxia, occurs mostly in children and is generally followed by a complete recovery. In adults, a diffuse encephalitis can occur, and may produce delirium, seizures, and focal neurologic signs. It has significant rates of long-term neurologic sequelae and death.

Varicella pneumonia accounts for the majority of hospitalizations in adults with chickenpox, where it has up to a 30% mortality rate. It usually develops insidiously within a few days after the rash has appeared, with progressive tachypnea, dyspnea, and dry cough. Chest x-rays will reveal diffuse bilateral infiltrates. Varicella pneumonia requires prompt administration of intravenous acyclovir.

For adults with uncomplicated varicella, oral acyclovir 800 mg 5 times/d for 5 days may be used for treatment if started within the first 24 hours of the rash. The patient in this case denied risk factors for human immunodeficiency virus, and because he lacked health insurance, he did not want any blood tests or medications unless they were absolutely necessary. He wanted to return to work but was told that he needed to wait until all his lesions had crusted over.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Chickenpox. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:707-711.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

The FP diagnosed a varicella infection in this patient. The simultaneous appearance of papules, pustules, and crusted lesions on the patient’s trunk and face was highly suspicious for varicella, especially because there was no history of him receiving the varicella vaccine.

Varicella (chickenpox) is caused by a primary infection with the varicella zoster virus (VZV), which is a double-stranded, linear DNA herpes virus. Transmission occurs via contact with aerosolized droplets from nasopharyngeal secretions or by direct cutaneous contact with vesicle fluid from skin lesions. The incubation period for VZV is approximately 15 days, during which the virus undergoes replication in regional lymph nodes, followed by 2 viremic stages. In the first stage the virus spreads to internal organs, and in the second stage the virus spreads to the skin.

The vesicular rash appears in crops for several days and the lesions start as vesicles on a red base (classically described as a “dew drop on a rose petal”). The lesions gradually develop a pustular component followed by the evolution of crusted papules. The period of infectivity is generally considered to last from 48 hours prior to the onset of the rash until the skin lesions have fully crusted.

New varicella lesions stop forming in approximately 4 days, and most lesions become fully crusted by 7 days. Diagnosis is usually based on classic presentation. A culture of the lesions may provide a definitive diagnosis, but is positive in less than 40% of cases. Direct fluorescent antibody testing has good sensitivity and is more rapid than tissue culture. In this case, the diagnosis was made on clinical grounds.

Adults who get varicella should be assessed for neurologic and pulmonary disease; our patient showed no signs of either complication. Encephalitis is a serious potential complication of chickenpox that can develop toward the end of the first week of the exanthema. One form, acute cerebellar ataxia, occurs mostly in children and is generally followed by a complete recovery. In adults, a diffuse encephalitis can occur, and may produce delirium, seizures, and focal neurologic signs. It has significant rates of long-term neurologic sequelae and death.

Varicella pneumonia accounts for the majority of hospitalizations in adults with chickenpox, where it has up to a 30% mortality rate. It usually develops insidiously within a few days after the rash has appeared, with progressive tachypnea, dyspnea, and dry cough. Chest x-rays will reveal diffuse bilateral infiltrates. Varicella pneumonia requires prompt administration of intravenous acyclovir.

For adults with uncomplicated varicella, oral acyclovir 800 mg 5 times/d for 5 days may be used for treatment if started within the first 24 hours of the rash. The patient in this case denied risk factors for human immunodeficiency virus, and because he lacked health insurance, he did not want any blood tests or medications unless they were absolutely necessary. He wanted to return to work but was told that he needed to wait until all his lesions had crusted over.

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Mayeaux EJ. Chickenpox. In: Usatine R, Smith M, Mayeaux EJ, et al, eds. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:707-711.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com

Used to treat advanced melanoma, vemurafenib has been shown to increase serum creatinine; but neither the prevalence nor the mechanism for the increase is known, say researchers from Assistance-Publique-Hôpitaux de Paris. Their study suggests 2 mechanisms are at work.

In their retrospective study of 70 patients, the researchers found that 97% had an immediate—but stable—increase in their creatinine level after starting vemurafenib. At the first visit, 1 month after starting the drug, 68 patients had a significant increase in serum creatinine levels, with a median variation of 22.8%. However, in 44 of 52 patients who discontinued the drug, because the melanoma had progressed, creatinine levels returned to baseline.

Related: Promising Method to Evaluate Response to Treatment

Serum cystatin C levels also rose, although less than that of serum creatinine. Researchers say the increase showed that the creatinine increase was partly a result of renal function impairment. Moreover, renal explorations showed that vemurafenib led to inhibition of creatinine tubular secretion.

According to the researchers, the dual mechanism of both inhibition of creatinine tubular secretion and slight renal function impairment makes interpreting creatinine variations difficult. They offer a decision tree to help clinicians manage creatinine elevations due to the drug. The researchers suggest testing for serum creatinine and cystatin C before beginning the treatment and during monthly follow-ups.

Related: FDA Approves Rescue Drug for Chemotherapy Overdose

The collected data are reassuring. Apart from rare cases of serious adverse events, such as severe acute renal failure, an increase in serum creatinine below 50% and/or moderate signs of tubular dysfunction should not lead to discontinuing treatment if it is otherwise effective.

Source:
Hurabielle C, Pillebout E, Stehlé T, et al. PLoS ONE. 2016;11(3):e0149873. doi:10.1371/journal.pone.0149873.

Used to treat advanced melanoma, vemurafenib has been shown to increase serum creatinine; but neither the prevalence nor the mechanism for the increase is known, say researchers from Assistance-Publique-Hôpitaux de Paris. Their study suggests 2 mechanisms are at work.

In their retrospective study of 70 patients, the researchers found that 97% had an immediate—but stable—increase in their creatinine level after starting vemurafenib. At the first visit, 1 month after starting the drug, 68 patients had a significant increase in serum creatinine levels, with a median variation of 22.8%. However, in 44 of 52 patients who discontinued the drug, because the melanoma had progressed, creatinine levels returned to baseline.

Related: Promising Method to Evaluate Response to Treatment

Serum cystatin C levels also rose, although less than that of serum creatinine. Researchers say the increase showed that the creatinine increase was partly a result of renal function impairment. Moreover, renal explorations showed that vemurafenib led to inhibition of creatinine tubular secretion.

According to the researchers, the dual mechanism of both inhibition of creatinine tubular secretion and slight renal function impairment makes interpreting creatinine variations difficult. They offer a decision tree to help clinicians manage creatinine elevations due to the drug. The researchers suggest testing for serum creatinine and cystatin C before beginning the treatment and during monthly follow-ups.

Related: FDA Approves Rescue Drug for Chemotherapy Overdose

The collected data are reassuring. Apart from rare cases of serious adverse events, such as severe acute renal failure, an increase in serum creatinine below 50% and/or moderate signs of tubular dysfunction should not lead to discontinuing treatment if it is otherwise effective.

Source:
Hurabielle C, Pillebout E, Stehlé T, et al. PLoS ONE. 2016;11(3):e0149873. doi:10.1371/journal.pone.0149873.

Used to treat advanced melanoma, vemurafenib has been shown to increase serum creatinine; but neither the prevalence nor the mechanism for the increase is known, say researchers from Assistance-Publique-Hôpitaux de Paris. Their study suggests 2 mechanisms are at work.

In their retrospective study of 70 patients, the researchers found that 97% had an immediate—but stable—increase in their creatinine level after starting vemurafenib. At the first visit, 1 month after starting the drug, 68 patients had a significant increase in serum creatinine levels, with a median variation of 22.8%. However, in 44 of 52 patients who discontinued the drug, because the melanoma had progressed, creatinine levels returned to baseline.

Related: Promising Method to Evaluate Response to Treatment

Serum cystatin C levels also rose, although less than that of serum creatinine. Researchers say the increase showed that the creatinine increase was partly a result of renal function impairment. Moreover, renal explorations showed that vemurafenib led to inhibition of creatinine tubular secretion.

According to the researchers, the dual mechanism of both inhibition of creatinine tubular secretion and slight renal function impairment makes interpreting creatinine variations difficult. They offer a decision tree to help clinicians manage creatinine elevations due to the drug. The researchers suggest testing for serum creatinine and cystatin C before beginning the treatment and during monthly follow-ups.

Related: FDA Approves Rescue Drug for Chemotherapy Overdose

The collected data are reassuring. Apart from rare cases of serious adverse events, such as severe acute renal failure, an increase in serum creatinine below 50% and/or moderate signs of tubular dysfunction should not lead to discontinuing treatment if it is otherwise effective.

Source:
Hurabielle C, Pillebout E, Stehlé T, et al. PLoS ONE. 2016;11(3):e0149873. doi:10.1371/journal.pone.0149873.

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Even though there was a steady rate of patients with critical limb ischemia (CLI) admitted to hospitals from 2003 to 2011, surgical revascularization decreased and endovascular treatment increased significantly, with concomitant decreases in in-hospital mortality and major amputation, according to the results of an analysis of the Nationwide Inpatient Sample of 642,433 patients hospitalized with CLI.

In addition, despite multiple adjustments, endovascular revascularization was associated with reduced in-hospital mortality, compared with surgical revascularization over the same period, according to a report online in the Journal of the American College of Cardiology.

©Ingram Publishing/Thinkstock

The annual in-hospital mortality rate decreased from 5.4% in 2003 to 3.4% in 2011 (P less than .001), and the major amputation rate dropped from 16.7% to 10.8%. There also was a significant decrease in length-of-stay (LOS) from 10 days to 8.4 days over the same period (P less than .001); however this did not translate to a significant difference in the cost of hospitalization, according to Dr. Shikhar Agarwal and colleagues at the Cleveland Clinic [doi:10.1016/j.jacc.2016.02.040].

Significant predictive factors of in-hospital mortality after multivariate regression analysis were female sex, older age, emergent admission, a primary indication of septicemia, heart failure, and respiratory disease, as well any stump complications present during admission. In contrast, any form of revascularization was associated with significantly reduced in-hospital mortality.

A comparison of revascularization methods showed that surgical revascularization significantly decreased from 13.9% in 2003 to 8.8% in 2011, while endovascular revascularization increased from 5.1% to 11%. Also, endovascular revascularization was associated with a significant decrease in in-hospital mortality compared with surgical revascularization over the study period (2.34% vs. 2.73%, respectively; odds ratio = .69). Major amputation rates were not significantly different between the two treatments (6.5% vs. 5.7%; OR = .99).

Length of stay was significantly lower with endovascular treatment compared with surgical (8.7 vs. 10.7 days) as were costs ($31,679 vs. $32,485, respectively).

Women had a higher rate of in-hospital mortality, but a lower rate of major amputation. Although race was not seen as a factor in predicting in-hospital mortality, blacks and other nonwhite races had significantly higher rates of amputation and lower rates of revascularization, compared with whites.

Approximately half of the patients assessed were admitted for primary CLI-related diagnoses. The other, non–CLI-related conditions – such as acute MI, cerebrovascular events, respiratory disease, heart failure, and acute kidney disease – have all been independently associated with increased in-hospital mortality and may be confounding, according to the authors. These are still relevant because CLI patients have an overall elevated cardiovascular risk in multiple vascular beds.

In terms of limitations, the authors noted the possibility of selection bias in the database, the rise of standalone outpatient centers in more recent years, which might funnel off select patients, and the lack of anatomical information in the NIS database, which precludes a determination of the appropriateness of treatment choice. Also, the type and invasiveness of the endovascular therapy cannot be determined. “It is possible that simple lesions were preferentially treated with endovascular therapy, whereas more complex lesions were treated by surgical techniques, leading to obvious differences in outcomes. Alternatively, it may be likely that the findings underestimate the impact of endovascular therapy, as sicker patients with higher comorbidities and poor targets were more likely to undergo endovascular revascularization,” the researchers pointed out.

“Despite similar rates of major amputation, endovascular revascularization was associated with reduced in-hospital mortality, mean LOS, and mean cost of hospitalization. Although the results are encouraging, there remain significant disparities and gaps that must be addressed,” Dr. Agarwal and his colleagues concluded.

The authors reported that they had no relevant disclosures.

[email protected]

Interested in a career in hospital medicine? Know someone who is? SHM hosts a series of special events for students and residents on campuses throughout the country. These catered networking receptions feature nationally recognized hospitalists speaking on their careers and the many options and opportunities within the hospital medicine specialty.

Don’t miss the opportunity to consider a career choice in medicine’s fastest growing specialty and network with the hospital medicine community. The tentative 2016 schedule includes stops in the following cities:

Spring: Baltimore, San Antonio, Seattle, Tempe, Ariz.

Fall: Atlanta, Chicago, Denver, New York City, Philadelphia, San Francisco, St. Louis

Visit www.futureofhospitalmedicine.org/events to learn more and see updated schedule details.

Interested in a career in hospital medicine? Know someone who is? SHM hosts a series of special events for students and residents on campuses throughout the country. These catered networking receptions feature nationally recognized hospitalists speaking on their careers and the many options and opportunities within the hospital medicine specialty.

Don’t miss the opportunity to consider a career choice in medicine’s fastest growing specialty and network with the hospital medicine community. The tentative 2016 schedule includes stops in the following cities:

Spring: Baltimore, San Antonio, Seattle, Tempe, Ariz.

Fall: Atlanta, Chicago, Denver, New York City, Philadelphia, San Francisco, St. Louis

Visit www.futureofhospitalmedicine.org/events to learn more and see updated schedule details.

Interested in a career in hospital medicine? Know someone who is? SHM hosts a series of special events for students and residents on campuses throughout the country. These catered networking receptions feature nationally recognized hospitalists speaking on their careers and the many options and opportunities within the hospital medicine specialty.

Don’t miss the opportunity to consider a career choice in medicine’s fastest growing specialty and network with the hospital medicine community. The tentative 2016 schedule includes stops in the following cities:

Spring: Baltimore, San Antonio, Seattle, Tempe, Ariz.

Fall: Atlanta, Chicago, Denver, New York City, Philadelphia, San Francisco, St. Louis

Visit www.futureofhospitalmedicine.org/events to learn more and see updated schedule details.

Editor’s note: Second in a three-part series.

This month continues my list of important issues that help position your hospitalist group for greatest success. SHM’s “Key Principles and Characteristics of an Effective Hospital Medicine Group” is the definitive list, and this is my much smaller list. Last month, I discussed a culture (or mindset) of practice ownership, a formal system of group decision-making, and the importance of hospitalists themselves playing an active role in recruitment.

Policy and Procedure Manual

New protocols and decisions are being implemented every day. It is impossible to keep track of them, especially the ones that come into play infrequently. For example, many adult hospitalist groups have reached decisions about whether to admit teenagers (e.g., admit only 16 and older or 18 and older, etc.) and whether a hospitalist or obstetrician serves as attending for pregnant women admitted for a medical problem like asthma or pneumonia. But ask everyone in your group to recite the policies, and I bet the answers will differ.

My experience is that only about 20% to 25% of hospitalist groups have written these things down in one place, but all should. It doesn’t need to be fancy and could just start as a Word document in which the lead hospitalist or other designated person writes down a handful of policies and then updates them on an ongoing basis. For example, if a group meeting results in adopting a new policy, it could be added to the document as soon as the meeting adjourns. In some cases, a policy is communicated by email; it would be fine to just copy the body of that email into the manual.

This “living” document could be maintained on a shared computer drive accessible from anywhere in or out of the hospital. That way, when the solo night doctor thinks, “Do we admit 17-year-olds or not?,” she has a place to find the answer right away. And the manual will be a real asset to orient new providers to your practice.

You could start the policy and procedure manual by listing categories, including human resource issues like sick-day policy, how to request days off or scheduling changes, clinical policies like which hip fractures are admitted by hospitalists versus orthopedics, billing and coding practices such as always turn in charges at end of each day, and so on.

I’ve seen useful manuals that are about 10 pages and others that run more than 50 pages.

An Effective Performance Dashboard

Every hospitalist group should have some sort of routine performance report (dashboard) provided in the same format at regular intervals, yet in my experience many, or even most, don’t. It is worth the sometimes considerable effort to develop a meaningful dashboard, and in 2006, SHM published a helpful guide. Even though it is getting old, most of the advice is still very relevant even if the metrics we care most about have changed.

I’m a big believer in providing unblinded performance data to all in the hospitalist group. For example, a report of individual work relative value unit (wRVU) productivity would show productivity for each doctor by name. I think it is healthy to be transparent and ensure all in the group know how others are performing. There is nothing like finding out you are a performance outlier to spark an interest in understanding why and what should be done about it.

Roles for NPs and PAs

Nurse practitioners (NPs) and physician assistants (PAs) can be valuable contributors to a successful hospitalist program, and according to the 2014 State of Hospital Medicine Report, 65% of hospitalist groups nationally had at least one such clinician—an increase over prior years.

While the idea of NP/PAs contributing to the practice is a sound one, my experience is that many groups execute the idea poorly and end up creating a role that can be both professionally unsatisfying and not serve as a platform to contribute effectively to the group. A common scenario is a hospitalist group has trouble with recruiting physicians, so it turns to NP/PAs because they are more readily available. But so often the group has thought little about the precise role NP/PAs will serve (nothing more than “they will help out the docs”). Too often the result is NP/PAs who will say many physician hospitalists simply repeat all the work on each patient, which certainly isn’t a rewarding or cost-effective role.

All should be convinced that the practice is better off in terms of increased overall productivity and/or other benefits by investing in NP/PAs than if those same dollars were instead invested in physician staffing. So one economic model to consider is to calculate the total cost (salary, benefits, malpractice, etc.) for an NP/PA and divide that by those costs for a physician. Let’s say that shows an NP/PA costs half as much as a physician (ranges 40% to 60% in my experience). That staffing cost could be considered in “physician FTE equivalents” so that, for example, a practice with four NP/PAs each costing 50% as much as a physician, or two physician equivalents, could be said to have a total of two physician-equivalent FTEs of staffing. Is the practice better off configured that way, or would it be better to have two physicians instead of the four NP/PAs? The answer will vary, but I think every practice should look at NP/PA staffing through this lens, as well as other considerations, to determine whether they’ve made the best choice.

Having NP/PAs and physicians share rounding duties can be tricky to do efficiently. In my experience, NP/PAs can be better positioned to contribute optimally and find greater professional satisfaction if responsible for a specific portion of the group’s work. For example, at a large hospital, NP/PAs might see all orthopedic consults or psych unit admissions reasonably independently, though with physician backup available. Or NP/PAs could serve as evening (“swing”) shift staffing and manage cross-cover and some admissions. In these roles, the division of labor between NP/PAs and physicians is clearer and allows NP/PAs to contribute most effectively. TH

Editor’s note: Second in a three-part series.

This month continues my list of important issues that help position your hospitalist group for greatest success. SHM’s “Key Principles and Characteristics of an Effective Hospital Medicine Group” is the definitive list, and this is my much smaller list. Last month, I discussed a culture (or mindset) of practice ownership, a formal system of group decision-making, and the importance of hospitalists themselves playing an active role in recruitment.

Policy and Procedure Manual

New protocols and decisions are being implemented every day. It is impossible to keep track of them, especially the ones that come into play infrequently. For example, many adult hospitalist groups have reached decisions about whether to admit teenagers (e.g., admit only 16 and older or 18 and older, etc.) and whether a hospitalist or obstetrician serves as attending for pregnant women admitted for a medical problem like asthma or pneumonia. But ask everyone in your group to recite the policies, and I bet the answers will differ.

My experience is that only about 20% to 25% of hospitalist groups have written these things down in one place, but all should. It doesn’t need to be fancy and could just start as a Word document in which the lead hospitalist or other designated person writes down a handful of policies and then updates them on an ongoing basis. For example, if a group meeting results in adopting a new policy, it could be added to the document as soon as the meeting adjourns. In some cases, a policy is communicated by email; it would be fine to just copy the body of that email into the manual.

This “living” document could be maintained on a shared computer drive accessible from anywhere in or out of the hospital. That way, when the solo night doctor thinks, “Do we admit 17-year-olds or not?,” she has a place to find the answer right away. And the manual will be a real asset to orient new providers to your practice.

You could start the policy and procedure manual by listing categories, including human resource issues like sick-day policy, how to request days off or scheduling changes, clinical policies like which hip fractures are admitted by hospitalists versus orthopedics, billing and coding practices such as always turn in charges at end of each day, and so on.

I’ve seen useful manuals that are about 10 pages and others that run more than 50 pages.

An Effective Performance Dashboard

Every hospitalist group should have some sort of routine performance report (dashboard) provided in the same format at regular intervals, yet in my experience many, or even most, don’t. It is worth the sometimes considerable effort to develop a meaningful dashboard, and in 2006, SHM published a helpful guide. Even though it is getting old, most of the advice is still very relevant even if the metrics we care most about have changed.

I’m a big believer in providing unblinded performance data to all in the hospitalist group. For example, a report of individual work relative value unit (wRVU) productivity would show productivity for each doctor by name. I think it is healthy to be transparent and ensure all in the group know how others are performing. There is nothing like finding out you are a performance outlier to spark an interest in understanding why and what should be done about it.

Roles for NPs and PAs

Nurse practitioners (NPs) and physician assistants (PAs) can be valuable contributors to a successful hospitalist program, and according to the 2014 State of Hospital Medicine Report, 65% of hospitalist groups nationally had at least one such clinician—an increase over prior years.

While the idea of NP/PAs contributing to the practice is a sound one, my experience is that many groups execute the idea poorly and end up creating a role that can be both professionally unsatisfying and not serve as a platform to contribute effectively to the group. A common scenario is a hospitalist group has trouble with recruiting physicians, so it turns to NP/PAs because they are more readily available. But so often the group has thought little about the precise role NP/PAs will serve (nothing more than “they will help out the docs”). Too often the result is NP/PAs who will say many physician hospitalists simply repeat all the work on each patient, which certainly isn’t a rewarding or cost-effective role.

All should be convinced that the practice is better off in terms of increased overall productivity and/or other benefits by investing in NP/PAs than if those same dollars were instead invested in physician staffing. So one economic model to consider is to calculate the total cost (salary, benefits, malpractice, etc.) for an NP/PA and divide that by those costs for a physician. Let’s say that shows an NP/PA costs half as much as a physician (ranges 40% to 60% in my experience). That staffing cost could be considered in “physician FTE equivalents” so that, for example, a practice with four NP/PAs each costing 50% as much as a physician, or two physician equivalents, could be said to have a total of two physician-equivalent FTEs of staffing. Is the practice better off configured that way, or would it be better to have two physicians instead of the four NP/PAs? The answer will vary, but I think every practice should look at NP/PA staffing through this lens, as well as other considerations, to determine whether they’ve made the best choice.

Having NP/PAs and physicians share rounding duties can be tricky to do efficiently. In my experience, NP/PAs can be better positioned to contribute optimally and find greater professional satisfaction if responsible for a specific portion of the group’s work. For example, at a large hospital, NP/PAs might see all orthopedic consults or psych unit admissions reasonably independently, though with physician backup available. Or NP/PAs could serve as evening (“swing”) shift staffing and manage cross-cover and some admissions. In these roles, the division of labor between NP/PAs and physicians is clearer and allows NP/PAs to contribute most effectively. TH

Editor’s note: Second in a three-part series.

This month continues my list of important issues that help position your hospitalist group for greatest success. SHM’s “Key Principles and Characteristics of an Effective Hospital Medicine Group” is the definitive list, and this is my much smaller list. Last month, I discussed a culture (or mindset) of practice ownership, a formal system of group decision-making, and the importance of hospitalists themselves playing an active role in recruitment.

Policy and Procedure Manual

New protocols and decisions are being implemented every day. It is impossible to keep track of them, especially the ones that come into play infrequently. For example, many adult hospitalist groups have reached decisions about whether to admit teenagers (e.g., admit only 16 and older or 18 and older, etc.) and whether a hospitalist or obstetrician serves as attending for pregnant women admitted for a medical problem like asthma or pneumonia. But ask everyone in your group to recite the policies, and I bet the answers will differ.

My experience is that only about 20% to 25% of hospitalist groups have written these things down in one place, but all should. It doesn’t need to be fancy and could just start as a Word document in which the lead hospitalist or other designated person writes down a handful of policies and then updates them on an ongoing basis. For example, if a group meeting results in adopting a new policy, it could be added to the document as soon as the meeting adjourns. In some cases, a policy is communicated by email; it would be fine to just copy the body of that email into the manual.

This “living” document could be maintained on a shared computer drive accessible from anywhere in or out of the hospital. That way, when the solo night doctor thinks, “Do we admit 17-year-olds or not?,” she has a place to find the answer right away. And the manual will be a real asset to orient new providers to your practice.

You could start the policy and procedure manual by listing categories, including human resource issues like sick-day policy, how to request days off or scheduling changes, clinical policies like which hip fractures are admitted by hospitalists versus orthopedics, billing and coding practices such as always turn in charges at end of each day, and so on.

I’ve seen useful manuals that are about 10 pages and others that run more than 50 pages.

An Effective Performance Dashboard

Every hospitalist group should have some sort of routine performance report (dashboard) provided in the same format at regular intervals, yet in my experience many, or even most, don’t. It is worth the sometimes considerable effort to develop a meaningful dashboard, and in 2006, SHM published a helpful guide. Even though it is getting old, most of the advice is still very relevant even if the metrics we care most about have changed.

I’m a big believer in providing unblinded performance data to all in the hospitalist group. For example, a report of individual work relative value unit (wRVU) productivity would show productivity for each doctor by name. I think it is healthy to be transparent and ensure all in the group know how others are performing. There is nothing like finding out you are a performance outlier to spark an interest in understanding why and what should be done about it.

Roles for NPs and PAs

Nurse practitioners (NPs) and physician assistants (PAs) can be valuable contributors to a successful hospitalist program, and according to the 2014 State of Hospital Medicine Report, 65% of hospitalist groups nationally had at least one such clinician—an increase over prior years.

While the idea of NP/PAs contributing to the practice is a sound one, my experience is that many groups execute the idea poorly and end up creating a role that can be both professionally unsatisfying and not serve as a platform to contribute effectively to the group. A common scenario is a hospitalist group has trouble with recruiting physicians, so it turns to NP/PAs because they are more readily available. But so often the group has thought little about the precise role NP/PAs will serve (nothing more than “they will help out the docs”). Too often the result is NP/PAs who will say many physician hospitalists simply repeat all the work on each patient, which certainly isn’t a rewarding or cost-effective role.

All should be convinced that the practice is better off in terms of increased overall productivity and/or other benefits by investing in NP/PAs than if those same dollars were instead invested in physician staffing. So one economic model to consider is to calculate the total cost (salary, benefits, malpractice, etc.) for an NP/PA and divide that by those costs for a physician. Let’s say that shows an NP/PA costs half as much as a physician (ranges 40% to 60% in my experience). That staffing cost could be considered in “physician FTE equivalents” so that, for example, a practice with four NP/PAs each costing 50% as much as a physician, or two physician equivalents, could be said to have a total of two physician-equivalent FTEs of staffing. Is the practice better off configured that way, or would it be better to have two physicians instead of the four NP/PAs? The answer will vary, but I think every practice should look at NP/PA staffing through this lens, as well as other considerations, to determine whether they’ve made the best choice.

Having NP/PAs and physicians share rounding duties can be tricky to do efficiently. In my experience, NP/PAs can be better positioned to contribute optimally and find greater professional satisfaction if responsible for a specific portion of the group’s work. For example, at a large hospital, NP/PAs might see all orthopedic consults or psych unit admissions reasonably independently, though with physician backup available. Or NP/PAs could serve as evening (“swing”) shift staffing and manage cross-cover and some admissions. In these roles, the division of labor between NP/PAs and physicians is clearer and allows NP/PAs to contribute most effectively. TH

(Reuters Health) - Over the last 40 years, heart disease rates have dropped in the U.S. overall, but the changes varied widely by region, with the highest rates of the disease shifting from the Northeast to the South, researchers say.

"The consistent progression southward over the past few decades suggests that the pattern is not random - and could be attributed to geographic differences in prevention and treatment opportunities," said lead author Michele Casper of the CDC's Division for Heart Disease and Stroke Prevention in Atlanta, Georgia.

"Identifying those counties and regions with the greatest burden of mortality is a necessary first step to target appropriate resources that will ultimately reduce death rates," Casper told Reuters Health by email.

The researchers used data on heart disease deaths among people age 35 and over in the U.S. collected in two year intervals, between 1973 and 2010, from more than 3,000 counties of the 48 contiguous states.

Every county saw a decline in heart disease deaths. The average decline across the U.S. was 61%, but some counties only saw a decline of 9% while others cut heart disease deaths by 83%.

At the beginning of the study, heart disease deaths were most common in the Northeast through Appalachia and into the Midwest. Coastal North Carolina, South Carolina and Georgia also had high rates.

Most counties with the lowest death rates were located in the West, with some low-rate counties also scattered in Alabama, Florida and Mississippi.

By 2010, most high-rate counties were still in the eastern half of the country, but in the South, rather than in the North, with some parts of New England becoming pockets with lower death rates.

Declines were slowest in counties in Alabama, Mississippi, Louisiana, Arkansas, Oklahoma and parts of Texas, the authors reported in a paper scheduled for publication in Circulation.

Since the 1970s, national attention on the dangers of cigarette smoking and uncontrolled high blood pressure has led to a significant decline in deaths from coronary heart disease and myocardial infarction, but "heart disease" includes other conditions, such as heart failure, which have not decreased as much, said Dr. Donald A. Barr of Stanford University School of Medicine in California, who wrote an editorial accompanying the new study.

Comparable data for heart failure (associated with diabetes, obesity and underlying hypertension) has not been coming down as fast, Barr told Reuters Health by phone. He noted that heart failure is projected to increase over the next couple of decades, while coronary heart disease is expected to decline.

Heart failure disproportionately affects low-income Americans and African Americans, he said. "These at-risk populations are found in a somewhat higher proportion in those southeastern states."

"Combining heart failure and coronary heart disease under the global term 'heart disease' combines good news with not so good news," Barr said.

There were still meaningful declines in heart disease deaths in the South, Casper noted.

"Heart disease-related deaths are largely preventable, and with targeted public health efforts, it's possible to alleviate much of the heavy burden of this disease and close the geographic gap in declining heart disease death rates," Casper said.

"With collaboration, government agencies, medical care organizations, community groups, businesses and other organizations can provide more local opportunities for physical activity, as well as access to smoke-free spaces, affordable healthy foods, quality healthcare and social and economic well-being," Casper said.

(Reuters Health) - Over the last 40 years, heart disease rates have dropped in the U.S. overall, but the changes varied widely by region, with the highest rates of the disease shifting from the Northeast to the South, researchers say.

"The consistent progression southward over the past few decades suggests that the pattern is not random - and could be attributed to geographic differences in prevention and treatment opportunities," said lead author Michele Casper of the CDC's Division for Heart Disease and Stroke Prevention in Atlanta, Georgia.

"Identifying those counties and regions with the greatest burden of mortality is a necessary first step to target appropriate resources that will ultimately reduce death rates," Casper told Reuters Health by email.

The researchers used data on heart disease deaths among people age 35 and over in the U.S. collected in two year intervals, between 1973 and 2010, from more than 3,000 counties of the 48 contiguous states.

Every county saw a decline in heart disease deaths. The average decline across the U.S. was 61%, but some counties only saw a decline of 9% while others cut heart disease deaths by 83%.

At the beginning of the study, heart disease deaths were most common in the Northeast through Appalachia and into the Midwest. Coastal North Carolina, South Carolina and Georgia also had high rates.

Most counties with the lowest death rates were located in the West, with some low-rate counties also scattered in Alabama, Florida and Mississippi.

By 2010, most high-rate counties were still in the eastern half of the country, but in the South, rather than in the North, with some parts of New England becoming pockets with lower death rates.

Declines were slowest in counties in Alabama, Mississippi, Louisiana, Arkansas, Oklahoma and parts of Texas, the authors reported in a paper scheduled for publication in Circulation.

Since the 1970s, national attention on the dangers of cigarette smoking and uncontrolled high blood pressure has led to a significant decline in deaths from coronary heart disease and myocardial infarction, but "heart disease" includes other conditions, such as heart failure, which have not decreased as much, said Dr. Donald A. Barr of Stanford University School of Medicine in California, who wrote an editorial accompanying the new study.

Comparable data for heart failure (associated with diabetes, obesity and underlying hypertension) has not been coming down as fast, Barr told Reuters Health by phone. He noted that heart failure is projected to increase over the next couple of decades, while coronary heart disease is expected to decline.

Heart failure disproportionately affects low-income Americans and African Americans, he said. "These at-risk populations are found in a somewhat higher proportion in those southeastern states."

"Combining heart failure and coronary heart disease under the global term 'heart disease' combines good news with not so good news," Barr said.

There were still meaningful declines in heart disease deaths in the South, Casper noted.

"Heart disease-related deaths are largely preventable, and with targeted public health efforts, it's possible to alleviate much of the heavy burden of this disease and close the geographic gap in declining heart disease death rates," Casper said.

"With collaboration, government agencies, medical care organizations, community groups, businesses and other organizations can provide more local opportunities for physical activity, as well as access to smoke-free spaces, affordable healthy foods, quality healthcare and social and economic well-being," Casper said.

(Reuters Health) - Over the last 40 years, heart disease rates have dropped in the U.S. overall, but the changes varied widely by region, with the highest rates of the disease shifting from the Northeast to the South, researchers say.

"The consistent progression southward over the past few decades suggests that the pattern is not random - and could be attributed to geographic differences in prevention and treatment opportunities," said lead author Michele Casper of the CDC's Division for Heart Disease and Stroke Prevention in Atlanta, Georgia.

"Identifying those counties and regions with the greatest burden of mortality is a necessary first step to target appropriate resources that will ultimately reduce death rates," Casper told Reuters Health by email.

The researchers used data on heart disease deaths among people age 35 and over in the U.S. collected in two year intervals, between 1973 and 2010, from more than 3,000 counties of the 48 contiguous states.

Every county saw a decline in heart disease deaths. The average decline across the U.S. was 61%, but some counties only saw a decline of 9% while others cut heart disease deaths by 83%.

At the beginning of the study, heart disease deaths were most common in the Northeast through Appalachia and into the Midwest. Coastal North Carolina, South Carolina and Georgia also had high rates.

Most counties with the lowest death rates were located in the West, with some low-rate counties also scattered in Alabama, Florida and Mississippi.

By 2010, most high-rate counties were still in the eastern half of the country, but in the South, rather than in the North, with some parts of New England becoming pockets with lower death rates.

Declines were slowest in counties in Alabama, Mississippi, Louisiana, Arkansas, Oklahoma and parts of Texas, the authors reported in a paper scheduled for publication in Circulation.

Since the 1970s, national attention on the dangers of cigarette smoking and uncontrolled high blood pressure has led to a significant decline in deaths from coronary heart disease and myocardial infarction, but "heart disease" includes other conditions, such as heart failure, which have not decreased as much, said Dr. Donald A. Barr of Stanford University School of Medicine in California, who wrote an editorial accompanying the new study.

Comparable data for heart failure (associated with diabetes, obesity and underlying hypertension) has not been coming down as fast, Barr told Reuters Health by phone. He noted that heart failure is projected to increase over the next couple of decades, while coronary heart disease is expected to decline.

Heart failure disproportionately affects low-income Americans and African Americans, he said. "These at-risk populations are found in a somewhat higher proportion in those southeastern states."

"Combining heart failure and coronary heart disease under the global term 'heart disease' combines good news with not so good news," Barr said.

There were still meaningful declines in heart disease deaths in the South, Casper noted.

"Heart disease-related deaths are largely preventable, and with targeted public health efforts, it's possible to alleviate much of the heavy burden of this disease and close the geographic gap in declining heart disease death rates," Casper said.

"With collaboration, government agencies, medical care organizations, community groups, businesses and other organizations can provide more local opportunities for physical activity, as well as access to smoke-free spaces, affordable healthy foods, quality healthcare and social and economic well-being," Casper said.

Ticagrelor tablets

Photo courtesy of AstraZeneca

The American College of Cardiology (ACC) and American Heart Association (AHA) have released updated guidelines for the use of dual antiplatelet therapy (DAPT) in patients with coronary artery disease.

DAPT, the combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), is used to reduce the risks of future heart attack and coronary stent thrombosis in this patient population.

Overall, the new guidelines, which update recommendations from 6 previous guidelines, recommend an individualized approach to DAPT.

The guidelines were published in the Journal of the American College of Cardiology.

The new recommendations are based on the current use of coronary stents that present a lower risk of thrombosis than some older stents.

The recommendations are also based on the findings of recent studies investigating the duration of DAPT in patients with coronary artery disease, specifically those with myocardial infarction and those undergoing coronary stent implantation.

Studies examining shorter duration (3 to 6 months) of DAPT compared with a standard 12 months of DAPT in select, generally lower-risk patients did not show an increased risk of stent thrombosis. And, in some cases, a shorter treatment duration was associated with less bleeding.

Other studies investigating extending DAPT for an additional 18 or 36 months (beyond a year) showed a decrease in the risk of heart attack and stent thrombosis at the expense of an increase in bleeding risk.

Overview of recommendations

In general, the recommendations regarding DAPT duration consist of a Class I recommendation of “should be given” for a minimum period of time (usually 6 to 12 months), and a Class IIb recommendation of “may be considered” for continuation beyond that time.

Shorter duration of DAPT is recommended for patients at lower ischemic risk with high bleeding risk, whereas longer duration of DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk.

These recommendations for duration of DAPT apply to newer-generation stents and, in general, only to those not treated with oral anticoagulant therapy.

An aspirin dose of 81 mg daily (range, 75-100 mg) is now recommended in patients treated with DAPT. Regardless of the duration of DAPT, aspirin is almost always continued indefinitely in patients with coronary artery disease.

The updated guidelines also address DAPT after coronary artery bypass grafting and issues regarding the timing of non-cardiac surgery in patients treated with coronary stent implantation and DAPT.

Decisions about the timing of surgery and whether to discontinue DAPT after coronary stent implantation involve weighing the particular surgical procedure and the risks of delaying the procedure, the risks of ischemia and stent thrombosis, and the risk and consequences of bleeding, and are therefore best individualized, according to the guidelines.

The new guidelines update recommendations on the duration of DAPT across 6 previously published guidelines:

• The 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention
• The 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery
• The 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease
• The 2013 ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction
• The 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes
• The 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.
  

Ticagrelor tablets

Photo courtesy of AstraZeneca

The American College of Cardiology (ACC) and American Heart Association (AHA) have released updated guidelines for the use of dual antiplatelet therapy (DAPT) in patients with coronary artery disease.

DAPT, the combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), is used to reduce the risks of future heart attack and coronary stent thrombosis in this patient population.

Overall, the new guidelines, which update recommendations from 6 previous guidelines, recommend an individualized approach to DAPT.

The guidelines were published in the Journal of the American College of Cardiology.

The new recommendations are based on the current use of coronary stents that present a lower risk of thrombosis than some older stents.

The recommendations are also based on the findings of recent studies investigating the duration of DAPT in patients with coronary artery disease, specifically those with myocardial infarction and those undergoing coronary stent implantation.

Studies examining shorter duration (3 to 6 months) of DAPT compared with a standard 12 months of DAPT in select, generally lower-risk patients did not show an increased risk of stent thrombosis. And, in some cases, a shorter treatment duration was associated with less bleeding.

Other studies investigating extending DAPT for an additional 18 or 36 months (beyond a year) showed a decrease in the risk of heart attack and stent thrombosis at the expense of an increase in bleeding risk.

Overview of recommendations

In general, the recommendations regarding DAPT duration consist of a Class I recommendation of “should be given” for a minimum period of time (usually 6 to 12 months), and a Class IIb recommendation of “may be considered” for continuation beyond that time.

Shorter duration of DAPT is recommended for patients at lower ischemic risk with high bleeding risk, whereas longer duration of DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk.

These recommendations for duration of DAPT apply to newer-generation stents and, in general, only to those not treated with oral anticoagulant therapy.

An aspirin dose of 81 mg daily (range, 75-100 mg) is now recommended in patients treated with DAPT. Regardless of the duration of DAPT, aspirin is almost always continued indefinitely in patients with coronary artery disease.

The updated guidelines also address DAPT after coronary artery bypass grafting and issues regarding the timing of non-cardiac surgery in patients treated with coronary stent implantation and DAPT.

Decisions about the timing of surgery and whether to discontinue DAPT after coronary stent implantation involve weighing the particular surgical procedure and the risks of delaying the procedure, the risks of ischemia and stent thrombosis, and the risk and consequences of bleeding, and are therefore best individualized, according to the guidelines.

The new guidelines update recommendations on the duration of DAPT across 6 previously published guidelines:

• The 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention
• The 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery
• The 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease
• The 2013 ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction
• The 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes
• The 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.
  

Ticagrelor tablets

Photo courtesy of AstraZeneca

The American College of Cardiology (ACC) and American Heart Association (AHA) have released updated guidelines for the use of dual antiplatelet therapy (DAPT) in patients with coronary artery disease.

DAPT, the combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), is used to reduce the risks of future heart attack and coronary stent thrombosis in this patient population.

Overall, the new guidelines, which update recommendations from 6 previous guidelines, recommend an individualized approach to DAPT.

The guidelines were published in the Journal of the American College of Cardiology.

The new recommendations are based on the current use of coronary stents that present a lower risk of thrombosis than some older stents.

The recommendations are also based on the findings of recent studies investigating the duration of DAPT in patients with coronary artery disease, specifically those with myocardial infarction and those undergoing coronary stent implantation.

Studies examining shorter duration (3 to 6 months) of DAPT compared with a standard 12 months of DAPT in select, generally lower-risk patients did not show an increased risk of stent thrombosis. And, in some cases, a shorter treatment duration was associated with less bleeding.

Other studies investigating extending DAPT for an additional 18 or 36 months (beyond a year) showed a decrease in the risk of heart attack and stent thrombosis at the expense of an increase in bleeding risk.

Overview of recommendations

In general, the recommendations regarding DAPT duration consist of a Class I recommendation of “should be given” for a minimum period of time (usually 6 to 12 months), and a Class IIb recommendation of “may be considered” for continuation beyond that time.

Shorter duration of DAPT is recommended for patients at lower ischemic risk with high bleeding risk, whereas longer duration of DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk.

These recommendations for duration of DAPT apply to newer-generation stents and, in general, only to those not treated with oral anticoagulant therapy.

An aspirin dose of 81 mg daily (range, 75-100 mg) is now recommended in patients treated with DAPT. Regardless of the duration of DAPT, aspirin is almost always continued indefinitely in patients with coronary artery disease.

The updated guidelines also address DAPT after coronary artery bypass grafting and issues regarding the timing of non-cardiac surgery in patients treated with coronary stent implantation and DAPT.

Decisions about the timing of surgery and whether to discontinue DAPT after coronary stent implantation involve weighing the particular surgical procedure and the risks of delaying the procedure, the risks of ischemia and stent thrombosis, and the risk and consequences of bleeding, and are therefore best individualized, according to the guidelines.

The new guidelines update recommendations on the duration of DAPT across 6 previously published guidelines:

• The 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention
• The 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery
• The 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease
• The 2013 ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction
• The 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes
• The 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.
  

HSCT preparation

Photo by Chad McNeeley

The US Food and Drug Administration (FDA) has approved the use of defibrotide sodium (Defitelio).

The product can now be used to treat adult and pediatric patients who develop hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome, with renal or pulmonary dysfunction after receiving a hematopoietic stem cell transplant (HSCT).

Defibrotide sodium is the first FDA-approved therapy for patients with this rare, potentially fatal complication.

Defibrotide sodium is a product of Jazz Pharmaceuticals, Inc. The company said shipments of the drug to distribution channels will begin within a week.

The recommended dose and schedule for defibrotide sodium is 6.25 mg/kg every 6 hours, given as a 2-hour intravenous infusion, for at least 21 days, and continued until VOD resolution or up to 60 days of treatment.

In vitro defibrotide sodium has profibrinolytic activity. The use of defibrotide sodium is contraindicated in patients receiving concurrent anticoagulants or fibrinolytic therapies. Hemorrhage and hypersensitivity reactions are the major potential adverse reactions.

The FDA previously granted the defibrotide sodium application priority review status, and the drug received orphan drug designation from the FDA for the treatment of hepatic VOD.

Full prescribing information for defibrotide sodium can be found on the FDA website.

Trial results

The FDA’s approval of defibrotide sodium is supported by data in 528 patients treated on 3 studies: a phase 2 trial, a phase 3 trial, and an expanded access study. Data from the expanded access study were presented at the 2015 BMT Tandem Meetings, and data from the phase 3 trial were published in Blood earlier this year.

The 528 patients all had hepatic VOD with multi-organ dysfunction after HSCT. They received defibrotide sodium at 6.25 mg/kg intravenously every 6 hours until resolution of VOD.

The approval was based on survival at day +100 after HSCT. The day +100 survival rates for Study 1 (phase 3, n=102), Study 2 (phase 2, n=75), and Study 3 (expanded access, n=351) were 38%, 44%, and 45%, respectively.

Based on published reports and analyses of patient-level data, the day +100 survival rates were 21% to 31% for patients with hepatic VOD with renal or pulmonary dysfunction who received supportive care or interventions other than defibrotide sodium.

The safety of defibrotide sodium to support approval is based on data from 176 patients in the clinical development program for the treatment of VOD with renal and/or pulmonary dysfunction following HSCT.

The most common adverse events (incidence ≥10% and independent of causality) were hypotension, diarrhea, vomiting, nausea, and epistaxis. The most common serious adverse events (incidence ≥5% and independent of causality) were hypotension (11%) and pulmonary alveolar hemorrhage (7%).

HSCT preparation

Photo by Chad McNeeley

The US Food and Drug Administration (FDA) has approved the use of defibrotide sodium (Defitelio).

The product can now be used to treat adult and pediatric patients who develop hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome, with renal or pulmonary dysfunction after receiving a hematopoietic stem cell transplant (HSCT).

Defibrotide sodium is the first FDA-approved therapy for patients with this rare, potentially fatal complication.

Defibrotide sodium is a product of Jazz Pharmaceuticals, Inc. The company said shipments of the drug to distribution channels will begin within a week.

The recommended dose and schedule for defibrotide sodium is 6.25 mg/kg every 6 hours, given as a 2-hour intravenous infusion, for at least 21 days, and continued until VOD resolution or up to 60 days of treatment.

In vitro defibrotide sodium has profibrinolytic activity. The use of defibrotide sodium is contraindicated in patients receiving concurrent anticoagulants or fibrinolytic therapies. Hemorrhage and hypersensitivity reactions are the major potential adverse reactions.

The FDA previously granted the defibrotide sodium application priority review status, and the drug received orphan drug designation from the FDA for the treatment of hepatic VOD.

Full prescribing information for defibrotide sodium can be found on the FDA website.

Trial results

The FDA’s approval of defibrotide sodium is supported by data in 528 patients treated on 3 studies: a phase 2 trial, a phase 3 trial, and an expanded access study. Data from the expanded access study were presented at the 2015 BMT Tandem Meetings, and data from the phase 3 trial were published in Blood earlier this year.

The 528 patients all had hepatic VOD with multi-organ dysfunction after HSCT. They received defibrotide sodium at 6.25 mg/kg intravenously every 6 hours until resolution of VOD.

The approval was based on survival at day +100 after HSCT. The day +100 survival rates for Study 1 (phase 3, n=102), Study 2 (phase 2, n=75), and Study 3 (expanded access, n=351) were 38%, 44%, and 45%, respectively.

Based on published reports and analyses of patient-level data, the day +100 survival rates were 21% to 31% for patients with hepatic VOD with renal or pulmonary dysfunction who received supportive care or interventions other than defibrotide sodium.

The safety of defibrotide sodium to support approval is based on data from 176 patients in the clinical development program for the treatment of VOD with renal and/or pulmonary dysfunction following HSCT.

The most common adverse events (incidence ≥10% and independent of causality) were hypotension, diarrhea, vomiting, nausea, and epistaxis. The most common serious adverse events (incidence ≥5% and independent of causality) were hypotension (11%) and pulmonary alveolar hemorrhage (7%).

HSCT preparation

Photo by Chad McNeeley

The US Food and Drug Administration (FDA) has approved the use of defibrotide sodium (Defitelio).

The product can now be used to treat adult and pediatric patients who develop hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome, with renal or pulmonary dysfunction after receiving a hematopoietic stem cell transplant (HSCT).

Defibrotide sodium is the first FDA-approved therapy for patients with this rare, potentially fatal complication.

Defibrotide sodium is a product of Jazz Pharmaceuticals, Inc. The company said shipments of the drug to distribution channels will begin within a week.

The recommended dose and schedule for defibrotide sodium is 6.25 mg/kg every 6 hours, given as a 2-hour intravenous infusion, for at least 21 days, and continued until VOD resolution or up to 60 days of treatment.

In vitro defibrotide sodium has profibrinolytic activity. The use of defibrotide sodium is contraindicated in patients receiving concurrent anticoagulants or fibrinolytic therapies. Hemorrhage and hypersensitivity reactions are the major potential adverse reactions.

The FDA previously granted the defibrotide sodium application priority review status, and the drug received orphan drug designation from the FDA for the treatment of hepatic VOD.

Full prescribing information for defibrotide sodium can be found on the FDA website.

Trial results

The FDA’s approval of defibrotide sodium is supported by data in 528 patients treated on 3 studies: a phase 2 trial, a phase 3 trial, and an expanded access study. Data from the expanded access study were presented at the 2015 BMT Tandem Meetings, and data from the phase 3 trial were published in Blood earlier this year.

The 528 patients all had hepatic VOD with multi-organ dysfunction after HSCT. They received defibrotide sodium at 6.25 mg/kg intravenously every 6 hours until resolution of VOD.

The approval was based on survival at day +100 after HSCT. The day +100 survival rates for Study 1 (phase 3, n=102), Study 2 (phase 2, n=75), and Study 3 (expanded access, n=351) were 38%, 44%, and 45%, respectively.

Based on published reports and analyses of patient-level data, the day +100 survival rates were 21% to 31% for patients with hepatic VOD with renal or pulmonary dysfunction who received supportive care or interventions other than defibrotide sodium.

The safety of defibrotide sodium to support approval is based on data from 176 patients in the clinical development program for the treatment of VOD with renal and/or pulmonary dysfunction following HSCT.

The most common adverse events (incidence ≥10% and independent of causality) were hypotension, diarrhea, vomiting, nausea, and epistaxis. The most common serious adverse events (incidence ≥5% and independent of causality) were hypotension (11%) and pulmonary alveolar hemorrhage (7%).

Lab mouse

Researchers have developed a mouse model of an aggressive type of acute myeloid leukemia (AML) that, they believe, accurately replicates the human form of the disease.

The model replicates AML with co-occurring mutations in FLT3 and DNMT3A.

The researchers said they found that mice with Flt3-ITD and inducible deletion of Dnmt3a developed a rapidly lethal, completely penetrant, and transplantable AML of normal karyotype.

The team described this work in Cancer Discovery.

“Our goal was to create a model that was faithful to the human form of the disease that can be used for preclinical testing of potential cures,” said study author H. Leighton Grimes, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“Previous models were slow, difficult to analyze, and did not accurately represent the human disease. This model is rapid, fully penetrant, and completely spontaneous. We hope that it will open the way for other researchers to join us in attacking this particularly lethal AML subtype.”

Dr Grimes and his colleagues said they were able to look at the disease in a new way with the help of a powerful new core facility utilizing analytical tools related to single-cell RNA sequencing. The team used complementary single-cell analyses to identify the core leukemia-causing stem cells of the tumor.

“Before, researchers were comparing the gene expression patterns of one AML subtype to either normal cells or other AML subtypes,” said study author Sara Meyer, PhD, a fellow in the Grimes lab.

“That approach made it difficult to tease out the specific impact of Dnmt3a mutation. Instead, we isolated the variables and studied only human and murine AML with Flt3 mutation. Comparing Flt3-mutant AML with and without Dnmt3a mutation allowed us to more finely identify those patterns that were specific to the Dnmt3a mutation.”

With that more detailed understanding, the researchers gained new insights into the contributions of the Dnmt3a mutation to the disease.

First, their work confirms suspicions that low-level Dnmt3a activity is cancer-causing. Moreover, they discovered that reduced Dnmt3a function allows genes that are normally expressed only at early development stages of blood cell formation to continue expression at later stages, leading to the development of AML.

The researchers also found that, in mouse tumor cells, rescuing expression of Dnmt3a reversed the leukemia phenotypes and gene expression. But they said more research is warranted to determine if rescuing normal levels of DNMT3A function is a viable method for treating human AML.

The team also identified several potential treatment targets that are unique to this type of AML. In future studies, they plan to proceed with testing potential therapies.

Lab mouse

Researchers have developed a mouse model of an aggressive type of acute myeloid leukemia (AML) that, they believe, accurately replicates the human form of the disease.

The model replicates AML with co-occurring mutations in FLT3 and DNMT3A.

The researchers said they found that mice with Flt3-ITD and inducible deletion of Dnmt3a developed a rapidly lethal, completely penetrant, and transplantable AML of normal karyotype.

The team described this work in Cancer Discovery.

“Our goal was to create a model that was faithful to the human form of the disease that can be used for preclinical testing of potential cures,” said study author H. Leighton Grimes, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“Previous models were slow, difficult to analyze, and did not accurately represent the human disease. This model is rapid, fully penetrant, and completely spontaneous. We hope that it will open the way for other researchers to join us in attacking this particularly lethal AML subtype.”

Dr Grimes and his colleagues said they were able to look at the disease in a new way with the help of a powerful new core facility utilizing analytical tools related to single-cell RNA sequencing. The team used complementary single-cell analyses to identify the core leukemia-causing stem cells of the tumor.

“Before, researchers were comparing the gene expression patterns of one AML subtype to either normal cells or other AML subtypes,” said study author Sara Meyer, PhD, a fellow in the Grimes lab.

“That approach made it difficult to tease out the specific impact of Dnmt3a mutation. Instead, we isolated the variables and studied only human and murine AML with Flt3 mutation. Comparing Flt3-mutant AML with and without Dnmt3a mutation allowed us to more finely identify those patterns that were specific to the Dnmt3a mutation.”

With that more detailed understanding, the researchers gained new insights into the contributions of the Dnmt3a mutation to the disease.

First, their work confirms suspicions that low-level Dnmt3a activity is cancer-causing. Moreover, they discovered that reduced Dnmt3a function allows genes that are normally expressed only at early development stages of blood cell formation to continue expression at later stages, leading to the development of AML.

The researchers also found that, in mouse tumor cells, rescuing expression of Dnmt3a reversed the leukemia phenotypes and gene expression. But they said more research is warranted to determine if rescuing normal levels of DNMT3A function is a viable method for treating human AML.

The team also identified several potential treatment targets that are unique to this type of AML. In future studies, they plan to proceed with testing potential therapies.

Lab mouse

Researchers have developed a mouse model of an aggressive type of acute myeloid leukemia (AML) that, they believe, accurately replicates the human form of the disease.

The model replicates AML with co-occurring mutations in FLT3 and DNMT3A.

The researchers said they found that mice with Flt3-ITD and inducible deletion of Dnmt3a developed a rapidly lethal, completely penetrant, and transplantable AML of normal karyotype.

The team described this work in Cancer Discovery.

“Our goal was to create a model that was faithful to the human form of the disease that can be used for preclinical testing of potential cures,” said study author H. Leighton Grimes, PhD, of Cincinnati Children’s Hospital Medical Center in Ohio.

“Previous models were slow, difficult to analyze, and did not accurately represent the human disease. This model is rapid, fully penetrant, and completely spontaneous. We hope that it will open the way for other researchers to join us in attacking this particularly lethal AML subtype.”

Dr Grimes and his colleagues said they were able to look at the disease in a new way with the help of a powerful new core facility utilizing analytical tools related to single-cell RNA sequencing. The team used complementary single-cell analyses to identify the core leukemia-causing stem cells of the tumor.

“Before, researchers were comparing the gene expression patterns of one AML subtype to either normal cells or other AML subtypes,” said study author Sara Meyer, PhD, a fellow in the Grimes lab.

“That approach made it difficult to tease out the specific impact of Dnmt3a mutation. Instead, we isolated the variables and studied only human and murine AML with Flt3 mutation. Comparing Flt3-mutant AML with and without Dnmt3a mutation allowed us to more finely identify those patterns that were specific to the Dnmt3a mutation.”

With that more detailed understanding, the researchers gained new insights into the contributions of the Dnmt3a mutation to the disease.

First, their work confirms suspicions that low-level Dnmt3a activity is cancer-causing. Moreover, they discovered that reduced Dnmt3a function allows genes that are normally expressed only at early development stages of blood cell formation to continue expression at later stages, leading to the development of AML.

The researchers also found that, in mouse tumor cells, rescuing expression of Dnmt3a reversed the leukemia phenotypes and gene expression. But they said more research is warranted to determine if rescuing normal levels of DNMT3A function is a viable method for treating human AML.

The team also identified several potential treatment targets that are unique to this type of AML. In future studies, they plan to proceed with testing potential therapies.

The US Food and Drug Administration (FDA) is allowing the use of an investigational test to screen blood donations for Zika virus.

The test, known as the cobas® Zika test, has not been granted FDA clearance or approval, but it may be used under an investigational new drug application protocol for screening donated blood in areas with active, mosquito-borne transmission of Zika virus.

This means the test can be used by US blood screening laboratories, but the laboratories will need to be enrolled in and contracted into a clinical trial for the test, as specified and agreed with the FDA’s Center for Biologics Evaluation and Research.

By authorizing use of the cobas® Zika test, the FDA is allowing blood establishments in Puerto Rico—a US territory with local, mosquito-borne transmission of the Zika virus—to resume collecting donations of whole blood and blood components.

“The availability of an investigational test to screen donated blood for Zika virus is an important step forward in maintaining the safety of the nation’s blood supply, especially for those US territories already experiencing active transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.

“In the future, should Zika virus transmission occur in other areas, blood collection establishments will be able to continue to collect blood and use the investigational screening test, minimizing disruption to the blood supply.”

About the test

The cobas® Zika test is a qualitative in vitro nucleic acid screening test for the direct detection of Zika virus RNA in plasma specimens from individual human

blood donors.

The test is based on fully automated sample preparation (nucleic acid extraction and purification), followed by PCR amplification and detection.

The cobas® Zika test is manufactured by Roche and is intended for use with Roche’s cobas® 6800/8800 Systems.

The cobas® 6800/8800 Systems consist of the sample supply module, the transfer module, the processing module, and the analytic module. Automated data management is performed by the cobas® 6800/8800 software, which assigns test results for all tests as non-reactive, reactive, or invalid.

“The cobas® Zika test has been specifically designed utilizing the generic cobas® omni Utility Channel on the cobas® 6800/8800 Systems,” said Roland Diggelmann, chief operating officer of Roche Diagnostics.

“These fully automated, high-volume systems provide solutions for blood services to detect the virus and ensure that potentially infected blood units are not made available for transfusion.”

Test availability

Initially, the cobas® Zika test will be deployed to screen blood donations collected locally in Puerto Rico. It is expected that this testing will enable the

reinstatement of the blood services in Puerto Rico and reduce the reliance of blood importation from other areas in the US.

The second stage of deployment for the cobas® Zika test will be to prepare for screening of blood donations collected by blood services in the southern US.

In addition, Roche said it is working with regulators around the world to determine the path forward to implement the cobas® Zika test for blood screening.

Implications for Puerto Rico

On February 16, the FDA issued a guidance for US blood establishments to reduce the risk of transfusion-transmitted Zika virus. In the guidance, the FDA recommended that areas with active transmission of Zika virus obtain whole blood and blood components from areas without active transmission of the virus.

As a result, local blood collection in Puerto Rico was suspended. On March 7, the Department of Health and Human Services announced that it arranged for shipments of blood products from the continental US to Puerto Rico.

The FDA guidance also states that establishments in areas with active Zika transmission may collect locally if a licensed or investigational test for screening donated blood is available.

Once screening of blood donations for Zika virus using the cobas® Zika test begins, blood establishments in Puerto Rico may resume collecting donations of whole blood and blood components. However, the FDA’s recommendations for Zika blood donor deferrals remain in place.

The US Food and Drug Administration (FDA) is allowing the use of an investigational test to screen blood donations for Zika virus.

The test, known as the cobas® Zika test, has not been granted FDA clearance or approval, but it may be used under an investigational new drug application protocol for screening donated blood in areas with active, mosquito-borne transmission of Zika virus.

This means the test can be used by US blood screening laboratories, but the laboratories will need to be enrolled in and contracted into a clinical trial for the test, as specified and agreed with the FDA’s Center for Biologics Evaluation and Research.

By authorizing use of the cobas® Zika test, the FDA is allowing blood establishments in Puerto Rico—a US territory with local, mosquito-borne transmission of the Zika virus—to resume collecting donations of whole blood and blood components.

“The availability of an investigational test to screen donated blood for Zika virus is an important step forward in maintaining the safety of the nation’s blood supply, especially for those US territories already experiencing active transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.

“In the future, should Zika virus transmission occur in other areas, blood collection establishments will be able to continue to collect blood and use the investigational screening test, minimizing disruption to the blood supply.”

About the test

The cobas® Zika test is a qualitative in vitro nucleic acid screening test for the direct detection of Zika virus RNA in plasma specimens from individual human

blood donors.

The test is based on fully automated sample preparation (nucleic acid extraction and purification), followed by PCR amplification and detection.

The cobas® Zika test is manufactured by Roche and is intended for use with Roche’s cobas® 6800/8800 Systems.

The cobas® 6800/8800 Systems consist of the sample supply module, the transfer module, the processing module, and the analytic module. Automated data management is performed by the cobas® 6800/8800 software, which assigns test results for all tests as non-reactive, reactive, or invalid.

“The cobas® Zika test has been specifically designed utilizing the generic cobas® omni Utility Channel on the cobas® 6800/8800 Systems,” said Roland Diggelmann, chief operating officer of Roche Diagnostics.

“These fully automated, high-volume systems provide solutions for blood services to detect the virus and ensure that potentially infected blood units are not made available for transfusion.”

Test availability

Initially, the cobas® Zika test will be deployed to screen blood donations collected locally in Puerto Rico. It is expected that this testing will enable the

reinstatement of the blood services in Puerto Rico and reduce the reliance of blood importation from other areas in the US.

The second stage of deployment for the cobas® Zika test will be to prepare for screening of blood donations collected by blood services in the southern US.

In addition, Roche said it is working with regulators around the world to determine the path forward to implement the cobas® Zika test for blood screening.

Implications for Puerto Rico

On February 16, the FDA issued a guidance for US blood establishments to reduce the risk of transfusion-transmitted Zika virus. In the guidance, the FDA recommended that areas with active transmission of Zika virus obtain whole blood and blood components from areas without active transmission of the virus.

As a result, local blood collection in Puerto Rico was suspended. On March 7, the Department of Health and Human Services announced that it arranged for shipments of blood products from the continental US to Puerto Rico.

The FDA guidance also states that establishments in areas with active Zika transmission may collect locally if a licensed or investigational test for screening donated blood is available.

Once screening of blood donations for Zika virus using the cobas® Zika test begins, blood establishments in Puerto Rico may resume collecting donations of whole blood and blood components. However, the FDA’s recommendations for Zika blood donor deferrals remain in place.

The US Food and Drug Administration (FDA) is allowing the use of an investigational test to screen blood donations for Zika virus.

The test, known as the cobas® Zika test, has not been granted FDA clearance or approval, but it may be used under an investigational new drug application protocol for screening donated blood in areas with active, mosquito-borne transmission of Zika virus.

This means the test can be used by US blood screening laboratories, but the laboratories will need to be enrolled in and contracted into a clinical trial for the test, as specified and agreed with the FDA’s Center for Biologics Evaluation and Research.

By authorizing use of the cobas® Zika test, the FDA is allowing blood establishments in Puerto Rico—a US territory with local, mosquito-borne transmission of the Zika virus—to resume collecting donations of whole blood and blood components.

“The availability of an investigational test to screen donated blood for Zika virus is an important step forward in maintaining the safety of the nation’s blood supply, especially for those US territories already experiencing active transmission,” said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research.

“In the future, should Zika virus transmission occur in other areas, blood collection establishments will be able to continue to collect blood and use the investigational screening test, minimizing disruption to the blood supply.”

About the test

The cobas® Zika test is a qualitative in vitro nucleic acid screening test for the direct detection of Zika virus RNA in plasma specimens from individual human

blood donors.

The test is based on fully automated sample preparation (nucleic acid extraction and purification), followed by PCR amplification and detection.

The cobas® Zika test is manufactured by Roche and is intended for use with Roche’s cobas® 6800/8800 Systems.

The cobas® 6800/8800 Systems consist of the sample supply module, the transfer module, the processing module, and the analytic module. Automated data management is performed by the cobas® 6800/8800 software, which assigns test results for all tests as non-reactive, reactive, or invalid.

“The cobas® Zika test has been specifically designed utilizing the generic cobas® omni Utility Channel on the cobas® 6800/8800 Systems,” said Roland Diggelmann, chief operating officer of Roche Diagnostics.

“These fully automated, high-volume systems provide solutions for blood services to detect the virus and ensure that potentially infected blood units are not made available for transfusion.”

Test availability

Initially, the cobas® Zika test will be deployed to screen blood donations collected locally in Puerto Rico. It is expected that this testing will enable the

reinstatement of the blood services in Puerto Rico and reduce the reliance of blood importation from other areas in the US.

The second stage of deployment for the cobas® Zika test will be to prepare for screening of blood donations collected by blood services in the southern US.

In addition, Roche said it is working with regulators around the world to determine the path forward to implement the cobas® Zika test for blood screening.

Implications for Puerto Rico

On February 16, the FDA issued a guidance for US blood establishments to reduce the risk of transfusion-transmitted Zika virus. In the guidance, the FDA recommended that areas with active transmission of Zika virus obtain whole blood and blood components from areas without active transmission of the virus.

As a result, local blood collection in Puerto Rico was suspended. On March 7, the Department of Health and Human Services announced that it arranged for shipments of blood products from the continental US to Puerto Rico.

The FDA guidance also states that establishments in areas with active Zika transmission may collect locally if a licensed or investigational test for screening donated blood is available.

Once screening of blood donations for Zika virus using the cobas® Zika test begins, blood establishments in Puerto Rico may resume collecting donations of whole blood and blood components. However, the FDA’s recommendations for Zika blood donor deferrals remain in place.