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Bortezomib bolsters hematologic response in AL amyloidosis
SAN DIEGO – Adding bortezomib (B) to melphalan and dexamethasone (MDex) increased the frequency and depth of hematologic responses in a phase III trial of patients with previously untreated immunoglobulin light-chain (AL) amyloidosis.
Rates of hematologic response after three treatment cycles were 79% for BMDex and 52% for MDex (P = .002), Efstathios Kastritis, MD, said at the annual meeting of the American Society of Hematology. Very good partial responses accounted for most of this difference, with rates of 45% and 25%, respectively (P = .02). This first-in-kind trial establishes BMDex “as a novel standard of care in AL amyloidosis,” Dr. Kastritis concluded.
MDex is a standard regimen in intermediate-risk AL amyloidosis, while single-agent therapy with bortezomib yielded a median overall survival time of more than 5 years in one study, noted Dr. Kastritis of the University of Athens. In another matched case-control study, BMDex outperformed MDex based on overall response (69% vs. 51%; P = .01) and complete response (42% vs. 19%; P = .002).
Therefore, Dr. Kastritis and his associates in Europe and Australia randomly assigned 110 patients with newly diagnosed AL amyloidosis to receive either MDex (0.22 mg/kg melphalan plus 40 mg dexamethasone daily for 4 consecutive days every 28 days) or BMDex (MDex plus 1.3 mg/m2 bortezomib on days 1, 4, 8, and 11 during cycles one and two, and on days 1, 8, 15, and 22 during subsequent cycles). Treatment continued through nine cycles of MDex or eight cycles of BMDex, or through cycle six if patients had either a complete response or a partial response plus an organ response. Patients stopped treatment after three cycles if they did not have at least a partial response.
After a median of five treatment cycles, BMDex and MDex led to similar rates of complete response (23% vs. 20%), partial response (19% and 17%), cardiac response (38% vs. 29%), and renal response (44% vs. 44%). Twenty-eight patients died, with no significant difference in overall survival between treatment arms. However, overall survival did favor BMDex (P = .03) among the 77 patients who were in cardiac stage II. Also, median time to second-line therapy was not reached for BMDex but was only 12 months with MDex (P less than .001).
The BMDex regimen was associated with higher rates of peripheral neuropathy (19% vs. 4% for MDex; P less than .001). Furthermore, three patients (1%) developed severe peripheral neuropathy on BMDex, while none did so on MDex. Grade 3 or higher adverse events were more common with BMDex than with MDex, but the difference did not reach statistical significance (52% vs. 40%; P = .13). There were four cardiac deaths in the first 100 days of the trial, three in the BMDex arm and one in the MDex arm (P = .31).
The European Myeloma Network sponsored the trial. Dr. Kastritis disclosed ties to Genesis, Takeda, Janssen, and Amgen.
SAN DIEGO – Adding bortezomib (B) to melphalan and dexamethasone (MDex) increased the frequency and depth of hematologic responses in a phase III trial of patients with previously untreated immunoglobulin light-chain (AL) amyloidosis.
Rates of hematologic response after three treatment cycles were 79% for BMDex and 52% for MDex (P = .002), Efstathios Kastritis, MD, said at the annual meeting of the American Society of Hematology. Very good partial responses accounted for most of this difference, with rates of 45% and 25%, respectively (P = .02). This first-in-kind trial establishes BMDex “as a novel standard of care in AL amyloidosis,” Dr. Kastritis concluded.
MDex is a standard regimen in intermediate-risk AL amyloidosis, while single-agent therapy with bortezomib yielded a median overall survival time of more than 5 years in one study, noted Dr. Kastritis of the University of Athens. In another matched case-control study, BMDex outperformed MDex based on overall response (69% vs. 51%; P = .01) and complete response (42% vs. 19%; P = .002).
Therefore, Dr. Kastritis and his associates in Europe and Australia randomly assigned 110 patients with newly diagnosed AL amyloidosis to receive either MDex (0.22 mg/kg melphalan plus 40 mg dexamethasone daily for 4 consecutive days every 28 days) or BMDex (MDex plus 1.3 mg/m2 bortezomib on days 1, 4, 8, and 11 during cycles one and two, and on days 1, 8, 15, and 22 during subsequent cycles). Treatment continued through nine cycles of MDex or eight cycles of BMDex, or through cycle six if patients had either a complete response or a partial response plus an organ response. Patients stopped treatment after three cycles if they did not have at least a partial response.
After a median of five treatment cycles, BMDex and MDex led to similar rates of complete response (23% vs. 20%), partial response (19% and 17%), cardiac response (38% vs. 29%), and renal response (44% vs. 44%). Twenty-eight patients died, with no significant difference in overall survival between treatment arms. However, overall survival did favor BMDex (P = .03) among the 77 patients who were in cardiac stage II. Also, median time to second-line therapy was not reached for BMDex but was only 12 months with MDex (P less than .001).
The BMDex regimen was associated with higher rates of peripheral neuropathy (19% vs. 4% for MDex; P less than .001). Furthermore, three patients (1%) developed severe peripheral neuropathy on BMDex, while none did so on MDex. Grade 3 or higher adverse events were more common with BMDex than with MDex, but the difference did not reach statistical significance (52% vs. 40%; P = .13). There were four cardiac deaths in the first 100 days of the trial, three in the BMDex arm and one in the MDex arm (P = .31).
The European Myeloma Network sponsored the trial. Dr. Kastritis disclosed ties to Genesis, Takeda, Janssen, and Amgen.
SAN DIEGO – Adding bortezomib (B) to melphalan and dexamethasone (MDex) increased the frequency and depth of hematologic responses in a phase III trial of patients with previously untreated immunoglobulin light-chain (AL) amyloidosis.
Rates of hematologic response after three treatment cycles were 79% for BMDex and 52% for MDex (P = .002), Efstathios Kastritis, MD, said at the annual meeting of the American Society of Hematology. Very good partial responses accounted for most of this difference, with rates of 45% and 25%, respectively (P = .02). This first-in-kind trial establishes BMDex “as a novel standard of care in AL amyloidosis,” Dr. Kastritis concluded.
MDex is a standard regimen in intermediate-risk AL amyloidosis, while single-agent therapy with bortezomib yielded a median overall survival time of more than 5 years in one study, noted Dr. Kastritis of the University of Athens. In another matched case-control study, BMDex outperformed MDex based on overall response (69% vs. 51%; P = .01) and complete response (42% vs. 19%; P = .002).
Therefore, Dr. Kastritis and his associates in Europe and Australia randomly assigned 110 patients with newly diagnosed AL amyloidosis to receive either MDex (0.22 mg/kg melphalan plus 40 mg dexamethasone daily for 4 consecutive days every 28 days) or BMDex (MDex plus 1.3 mg/m2 bortezomib on days 1, 4, 8, and 11 during cycles one and two, and on days 1, 8, 15, and 22 during subsequent cycles). Treatment continued through nine cycles of MDex or eight cycles of BMDex, or through cycle six if patients had either a complete response or a partial response plus an organ response. Patients stopped treatment after three cycles if they did not have at least a partial response.
After a median of five treatment cycles, BMDex and MDex led to similar rates of complete response (23% vs. 20%), partial response (19% and 17%), cardiac response (38% vs. 29%), and renal response (44% vs. 44%). Twenty-eight patients died, with no significant difference in overall survival between treatment arms. However, overall survival did favor BMDex (P = .03) among the 77 patients who were in cardiac stage II. Also, median time to second-line therapy was not reached for BMDex but was only 12 months with MDex (P less than .001).
The BMDex regimen was associated with higher rates of peripheral neuropathy (19% vs. 4% for MDex; P less than .001). Furthermore, three patients (1%) developed severe peripheral neuropathy on BMDex, while none did so on MDex. Grade 3 or higher adverse events were more common with BMDex than with MDex, but the difference did not reach statistical significance (52% vs. 40%; P = .13). There were four cardiac deaths in the first 100 days of the trial, three in the BMDex arm and one in the MDex arm (P = .31).
The European Myeloma Network sponsored the trial. Dr. Kastritis disclosed ties to Genesis, Takeda, Janssen, and Amgen.
AT ASH 2016
Key clinical point: Adding bortezomib (B) to melphalan and dexamethasone (MDex) bolstered hematologic response in immunoglobulin light-chain (AL) amyloidosis.
Major finding: After three treatment cycles, rates of hematologic response were 79% in the BMDex arm and 52% for MDex (P = .002).
Data source: A multicenter randomized trial of 110 patients with newly diagnosed AL amyloidosis.
Disclosures: The European Myeloma Network sponsored the trial. Dr. Kastritis disclosed ties to Genesis, Takeda, Janssen, and Amgen.
FDG-PET/CT at maintenance predicts myeloma survival
SAN DIEGO – Having less than three focal lesions on FDG-PET/CT (fluorodeoxyglucose positron emission tomography integrated with computed tomography) when beginning lenalidomide maintenance therapy predicted significantly higher rates of progression-free and overall survival among patients with newly diagnosed multiple myeloma.
Survival in this prospective study of 102 patients also correlated with FDG uptake that did not exceed the level of the liver (Deauville score less than 3), reported Elena Zamagni, MD, PhD, of Bologna (Italy) University. The findings highlight FDG-PET/CT as “a powerful prognostic marker for survival, both in terms of number and score of focal lesions,” she said during an oral presentation at the annual meeting of the American Society of Hematology.
Although FDG-PET/CT is “well recognized” for staging and evaluating prognosis in multiple myeloma, a “major inconsistency in methodology between studies” inspired the current analysis, Dr. Zamagni said. “Different groups have used different interpretation criteria and arbitrary cutoffs with very variable results, especially in terms of posttreatment and borderline cases,” she noted.
Therefore, researchers from eight participating centers evaluated FDG-PET/CT scans from 103 patients with newly diagnosed multiple myeloma who were part of the randomized phase III EMN02 trial. Scans were performed at diagnosis, at the start of induction therapy, and just before patients started maintenance therapy with lenalidomide. Five nuclear medicine experts reviewed the scans in a blinded manner.
About 34% of patients had positive focal lesions on FDG-PET/CT at the start of maintenance, Dr. Zamagni said. After a median follow-up of 2 years, rates of progression-free survival were 84% in those with fewer than three focal lesions and 47% in those with three or more lesions (hazard ratio, 3.5; P = .01). Rates of overall survival followed the same trend at 98% and 68%, respectively (HR, 13.6; P = .0002).
Likewise, among patients whose FDG uptake did not exceed that of the liver, 2-year rates of progression-free and overall survival were 87% and 100%, compared with 69% and 45% in patients with new focal lesions or slightly, moderately, or markedly greater FDG uptake than the liver (Deauville scores of 4 and 5; P less than .001 for each comparison).
Normalization of FDG-PET/CT after induction also predicted improved survival, Dr. Zamagni said. Two-year progression-free survival rates were 85% among patients who had become PET-negative by the time they began maintenance, but were only 66% among patients who remained PET-positive (HR, 1.5; P less than .01). Rates of overall survival at 2 years were 98% among PET-negative patients and 87% among PET-positive patients (HR, 1.6; P = .03).
The study also confirmed the value of performing FDG-PET/CT at de novo myeloma diagnosis. Strikingly, only 20% of patients with baseline FDG-PET/CT evidence of extramedullary disease at this time point were alive and progression free 2 years later, compared with 81% of those without extramedullary disease (HR, 5.0; P = .001). Once again, the same trend emerged for Deauville scores – 99% of patients with scores of 3 or lower at diagnosis were alive 2 years later, compared with 83% of those who scored 4 or 5 (HR, 5.6; P = .03).
The EMN02 trial included 714 patients with newly diagnosed multiple myeloma who underwent induction with bortezomib-cyclophosphamide-dexamethasone (VCD), followed by either standard-dose intensification therapy with bortezomib-melphalan-prednisone (VMP) or high-dose intensification therapy with melphalan followed by single or double autologous stem cell transplantation. After that, patients either underwent consolidation therapy followed by lenalidomide maintenance therapy or proceeded directly to maintenance. Among the study subgroup of 103 patients, median age was 58 years, 25% of patients had high-risk cytogenetics, and 15% were ISS stage III.
“FDG-PET/CT is by now the preferred imaging technique for evaluating and monitoring response to therapy,” Dr. Zamagni concluded. She and her associates will use data from four other trials to further validate prognostic criteria and more precisely define cutoff points, she said.
Fondazione del Monte di Bologna e Ravenna partially supported the study. Dr. Zamagni had no relevant financial conflicts of interest.
SAN DIEGO – Having less than three focal lesions on FDG-PET/CT (fluorodeoxyglucose positron emission tomography integrated with computed tomography) when beginning lenalidomide maintenance therapy predicted significantly higher rates of progression-free and overall survival among patients with newly diagnosed multiple myeloma.
Survival in this prospective study of 102 patients also correlated with FDG uptake that did not exceed the level of the liver (Deauville score less than 3), reported Elena Zamagni, MD, PhD, of Bologna (Italy) University. The findings highlight FDG-PET/CT as “a powerful prognostic marker for survival, both in terms of number and score of focal lesions,” she said during an oral presentation at the annual meeting of the American Society of Hematology.
Although FDG-PET/CT is “well recognized” for staging and evaluating prognosis in multiple myeloma, a “major inconsistency in methodology between studies” inspired the current analysis, Dr. Zamagni said. “Different groups have used different interpretation criteria and arbitrary cutoffs with very variable results, especially in terms of posttreatment and borderline cases,” she noted.
Therefore, researchers from eight participating centers evaluated FDG-PET/CT scans from 103 patients with newly diagnosed multiple myeloma who were part of the randomized phase III EMN02 trial. Scans were performed at diagnosis, at the start of induction therapy, and just before patients started maintenance therapy with lenalidomide. Five nuclear medicine experts reviewed the scans in a blinded manner.
About 34% of patients had positive focal lesions on FDG-PET/CT at the start of maintenance, Dr. Zamagni said. After a median follow-up of 2 years, rates of progression-free survival were 84% in those with fewer than three focal lesions and 47% in those with three or more lesions (hazard ratio, 3.5; P = .01). Rates of overall survival followed the same trend at 98% and 68%, respectively (HR, 13.6; P = .0002).
Likewise, among patients whose FDG uptake did not exceed that of the liver, 2-year rates of progression-free and overall survival were 87% and 100%, compared with 69% and 45% in patients with new focal lesions or slightly, moderately, or markedly greater FDG uptake than the liver (Deauville scores of 4 and 5; P less than .001 for each comparison).
Normalization of FDG-PET/CT after induction also predicted improved survival, Dr. Zamagni said. Two-year progression-free survival rates were 85% among patients who had become PET-negative by the time they began maintenance, but were only 66% among patients who remained PET-positive (HR, 1.5; P less than .01). Rates of overall survival at 2 years were 98% among PET-negative patients and 87% among PET-positive patients (HR, 1.6; P = .03).
The study also confirmed the value of performing FDG-PET/CT at de novo myeloma diagnosis. Strikingly, only 20% of patients with baseline FDG-PET/CT evidence of extramedullary disease at this time point were alive and progression free 2 years later, compared with 81% of those without extramedullary disease (HR, 5.0; P = .001). Once again, the same trend emerged for Deauville scores – 99% of patients with scores of 3 or lower at diagnosis were alive 2 years later, compared with 83% of those who scored 4 or 5 (HR, 5.6; P = .03).
The EMN02 trial included 714 patients with newly diagnosed multiple myeloma who underwent induction with bortezomib-cyclophosphamide-dexamethasone (VCD), followed by either standard-dose intensification therapy with bortezomib-melphalan-prednisone (VMP) or high-dose intensification therapy with melphalan followed by single or double autologous stem cell transplantation. After that, patients either underwent consolidation therapy followed by lenalidomide maintenance therapy or proceeded directly to maintenance. Among the study subgroup of 103 patients, median age was 58 years, 25% of patients had high-risk cytogenetics, and 15% were ISS stage III.
“FDG-PET/CT is by now the preferred imaging technique for evaluating and monitoring response to therapy,” Dr. Zamagni concluded. She and her associates will use data from four other trials to further validate prognostic criteria and more precisely define cutoff points, she said.
Fondazione del Monte di Bologna e Ravenna partially supported the study. Dr. Zamagni had no relevant financial conflicts of interest.
SAN DIEGO – Having less than three focal lesions on FDG-PET/CT (fluorodeoxyglucose positron emission tomography integrated with computed tomography) when beginning lenalidomide maintenance therapy predicted significantly higher rates of progression-free and overall survival among patients with newly diagnosed multiple myeloma.
Survival in this prospective study of 102 patients also correlated with FDG uptake that did not exceed the level of the liver (Deauville score less than 3), reported Elena Zamagni, MD, PhD, of Bologna (Italy) University. The findings highlight FDG-PET/CT as “a powerful prognostic marker for survival, both in terms of number and score of focal lesions,” she said during an oral presentation at the annual meeting of the American Society of Hematology.
Although FDG-PET/CT is “well recognized” for staging and evaluating prognosis in multiple myeloma, a “major inconsistency in methodology between studies” inspired the current analysis, Dr. Zamagni said. “Different groups have used different interpretation criteria and arbitrary cutoffs with very variable results, especially in terms of posttreatment and borderline cases,” she noted.
Therefore, researchers from eight participating centers evaluated FDG-PET/CT scans from 103 patients with newly diagnosed multiple myeloma who were part of the randomized phase III EMN02 trial. Scans were performed at diagnosis, at the start of induction therapy, and just before patients started maintenance therapy with lenalidomide. Five nuclear medicine experts reviewed the scans in a blinded manner.
About 34% of patients had positive focal lesions on FDG-PET/CT at the start of maintenance, Dr. Zamagni said. After a median follow-up of 2 years, rates of progression-free survival were 84% in those with fewer than three focal lesions and 47% in those with three or more lesions (hazard ratio, 3.5; P = .01). Rates of overall survival followed the same trend at 98% and 68%, respectively (HR, 13.6; P = .0002).
Likewise, among patients whose FDG uptake did not exceed that of the liver, 2-year rates of progression-free and overall survival were 87% and 100%, compared with 69% and 45% in patients with new focal lesions or slightly, moderately, or markedly greater FDG uptake than the liver (Deauville scores of 4 and 5; P less than .001 for each comparison).
Normalization of FDG-PET/CT after induction also predicted improved survival, Dr. Zamagni said. Two-year progression-free survival rates were 85% among patients who had become PET-negative by the time they began maintenance, but were only 66% among patients who remained PET-positive (HR, 1.5; P less than .01). Rates of overall survival at 2 years were 98% among PET-negative patients and 87% among PET-positive patients (HR, 1.6; P = .03).
The study also confirmed the value of performing FDG-PET/CT at de novo myeloma diagnosis. Strikingly, only 20% of patients with baseline FDG-PET/CT evidence of extramedullary disease at this time point were alive and progression free 2 years later, compared with 81% of those without extramedullary disease (HR, 5.0; P = .001). Once again, the same trend emerged for Deauville scores – 99% of patients with scores of 3 or lower at diagnosis were alive 2 years later, compared with 83% of those who scored 4 or 5 (HR, 5.6; P = .03).
The EMN02 trial included 714 patients with newly diagnosed multiple myeloma who underwent induction with bortezomib-cyclophosphamide-dexamethasone (VCD), followed by either standard-dose intensification therapy with bortezomib-melphalan-prednisone (VMP) or high-dose intensification therapy with melphalan followed by single or double autologous stem cell transplantation. After that, patients either underwent consolidation therapy followed by lenalidomide maintenance therapy or proceeded directly to maintenance. Among the study subgroup of 103 patients, median age was 58 years, 25% of patients had high-risk cytogenetics, and 15% were ISS stage III.
“FDG-PET/CT is by now the preferred imaging technique for evaluating and monitoring response to therapy,” Dr. Zamagni concluded. She and her associates will use data from four other trials to further validate prognostic criteria and more precisely define cutoff points, she said.
Fondazione del Monte di Bologna e Ravenna partially supported the study. Dr. Zamagni had no relevant financial conflicts of interest.
AT ASH 2016
Key clinical point: FDG-PET/CT helped predict survival in newly diagnosed multiple myeloma, regardless of induction regimen.
Major finding: Progression-free survival at 2 years was 84% when patients had less than three focal lesions at the start of maintenance, vs. 47% when they had three or more lesions (hazard ratio, 3.5; P = .01).
Data source: A prospective study of 103 patients with newly diagnosed, transplant-eligible multiple myeloma from a randomized phase III trial.
Disclosures: Fondazione del Monte di Bologna e Ravenna partially supported the study. Dr. Zamagni had no conflicts of interest.
Low value
The fact that the United States spends more of its gross domestic product on health care (18%) than any other nation is old and depressing news (JAMA. 2012 Apr 11;307[14]:1513-6). There may be some debate about whether the quality of the product we are getting is worth this outsized investment. But it is safe to assume that there must be some wastage in the system. Exactly how much of our health care dollar is going down the drain is unknown. And the thorny question of who is responsible for the leaks has escaped close scrutiny, probably because the answer is guaranteed to result in an uncomfortable and ugly circle of finger pointing. Is it the insurance companies, hospitals, the superspecialists, the drug companies, impatient patients, or those dastardly lawyers? Pediatricians are such small players on the health care stage that our contribution to the wastage must be minimal. Our patients are little people who are generally healthy. Most of us drive midsized cars and live in modest homes. We try to be careful users of the expensive diagnostic and therapeutic tools at our disposal. We don’t deserve a place on the list of likely suspects, do we?
Using a claims-based measure of 20 services that according to evidenced-based guidelines do not improve health, the authors discovered that among the nearly four and half million commercially insured children they studied, 9.6% received at least one of these 20 “low-value” services in 1 year. The ticket for these worthless services was $27 million,of which more than $9 million was out of pocket expenses for families. If extrapolated to all of the commercially insured children in the United States, the total cost of low-value services would be $227 million for 1 year. Regardless of how wasteful cardiologists or plastic surgeons may be, this contribution to the national cost of health care for low-value services by pediatricians cannot be considered chump change.
I urge you to check out the online version of Dr. Chua’s article and then click on Table 1 so you can look at the 20 services that the authors have chosen to label low value. Although I am always leery of accepting a guideline simply because it is has been labeled “evidence-based,” I think you will find that it hard to argue with their choices, such as blood tests in children with a simple febrile seizure, oral antibiotics after tonsillectomy, or neuroimaging in children with headache. How does your practice’s behavior stack up against their list?
The list could be much longer. For example, the authors chose to exclude head imaging ordered for minor head trauma because their claims-based method didn’t provide enough clinical information. I suspect that with an expanded list of clearly low-value services, the annual cost for low-value pediatric services would be a half a billion dollars.
As concerning as the findings in this study may be, it doesn’t answer the question of what we should do to correct the problem. We can dance around the issue by saying that patients and parents are pressuring us to do something even if it’s a low-value service. We can complain that for decades we have been practicing under the dark cloud of a malpractice suit, and that if we don’t turn over every stone in our evaluation of a patient we’re going to trip on one of them and end up in court.
But the bottom line is that we are the ones who are making the choice to order a study or prescribe a medication that is not only of low value, but more than likely worthless and possibly damaging to the patient. With the help of the American Academy of Pediatrics, we need to swallow hard and begin cleaning house, throwing out those low-value services we have gotten in the habit of ordering and prescribing. Education helps, but sometimes we have to do some finger pointing even if the finger points to us.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
The fact that the United States spends more of its gross domestic product on health care (18%) than any other nation is old and depressing news (JAMA. 2012 Apr 11;307[14]:1513-6). There may be some debate about whether the quality of the product we are getting is worth this outsized investment. But it is safe to assume that there must be some wastage in the system. Exactly how much of our health care dollar is going down the drain is unknown. And the thorny question of who is responsible for the leaks has escaped close scrutiny, probably because the answer is guaranteed to result in an uncomfortable and ugly circle of finger pointing. Is it the insurance companies, hospitals, the superspecialists, the drug companies, impatient patients, or those dastardly lawyers? Pediatricians are such small players on the health care stage that our contribution to the wastage must be minimal. Our patients are little people who are generally healthy. Most of us drive midsized cars and live in modest homes. We try to be careful users of the expensive diagnostic and therapeutic tools at our disposal. We don’t deserve a place on the list of likely suspects, do we?
Using a claims-based measure of 20 services that according to evidenced-based guidelines do not improve health, the authors discovered that among the nearly four and half million commercially insured children they studied, 9.6% received at least one of these 20 “low-value” services in 1 year. The ticket for these worthless services was $27 million,of which more than $9 million was out of pocket expenses for families. If extrapolated to all of the commercially insured children in the United States, the total cost of low-value services would be $227 million for 1 year. Regardless of how wasteful cardiologists or plastic surgeons may be, this contribution to the national cost of health care for low-value services by pediatricians cannot be considered chump change.
I urge you to check out the online version of Dr. Chua’s article and then click on Table 1 so you can look at the 20 services that the authors have chosen to label low value. Although I am always leery of accepting a guideline simply because it is has been labeled “evidence-based,” I think you will find that it hard to argue with their choices, such as blood tests in children with a simple febrile seizure, oral antibiotics after tonsillectomy, or neuroimaging in children with headache. How does your practice’s behavior stack up against their list?
The list could be much longer. For example, the authors chose to exclude head imaging ordered for minor head trauma because their claims-based method didn’t provide enough clinical information. I suspect that with an expanded list of clearly low-value services, the annual cost for low-value pediatric services would be a half a billion dollars.
As concerning as the findings in this study may be, it doesn’t answer the question of what we should do to correct the problem. We can dance around the issue by saying that patients and parents are pressuring us to do something even if it’s a low-value service. We can complain that for decades we have been practicing under the dark cloud of a malpractice suit, and that if we don’t turn over every stone in our evaluation of a patient we’re going to trip on one of them and end up in court.
But the bottom line is that we are the ones who are making the choice to order a study or prescribe a medication that is not only of low value, but more than likely worthless and possibly damaging to the patient. With the help of the American Academy of Pediatrics, we need to swallow hard and begin cleaning house, throwing out those low-value services we have gotten in the habit of ordering and prescribing. Education helps, but sometimes we have to do some finger pointing even if the finger points to us.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
The fact that the United States spends more of its gross domestic product on health care (18%) than any other nation is old and depressing news (JAMA. 2012 Apr 11;307[14]:1513-6). There may be some debate about whether the quality of the product we are getting is worth this outsized investment. But it is safe to assume that there must be some wastage in the system. Exactly how much of our health care dollar is going down the drain is unknown. And the thorny question of who is responsible for the leaks has escaped close scrutiny, probably because the answer is guaranteed to result in an uncomfortable and ugly circle of finger pointing. Is it the insurance companies, hospitals, the superspecialists, the drug companies, impatient patients, or those dastardly lawyers? Pediatricians are such small players on the health care stage that our contribution to the wastage must be minimal. Our patients are little people who are generally healthy. Most of us drive midsized cars and live in modest homes. We try to be careful users of the expensive diagnostic and therapeutic tools at our disposal. We don’t deserve a place on the list of likely suspects, do we?
Using a claims-based measure of 20 services that according to evidenced-based guidelines do not improve health, the authors discovered that among the nearly four and half million commercially insured children they studied, 9.6% received at least one of these 20 “low-value” services in 1 year. The ticket for these worthless services was $27 million,of which more than $9 million was out of pocket expenses for families. If extrapolated to all of the commercially insured children in the United States, the total cost of low-value services would be $227 million for 1 year. Regardless of how wasteful cardiologists or plastic surgeons may be, this contribution to the national cost of health care for low-value services by pediatricians cannot be considered chump change.
I urge you to check out the online version of Dr. Chua’s article and then click on Table 1 so you can look at the 20 services that the authors have chosen to label low value. Although I am always leery of accepting a guideline simply because it is has been labeled “evidence-based,” I think you will find that it hard to argue with their choices, such as blood tests in children with a simple febrile seizure, oral antibiotics after tonsillectomy, or neuroimaging in children with headache. How does your practice’s behavior stack up against their list?
The list could be much longer. For example, the authors chose to exclude head imaging ordered for minor head trauma because their claims-based method didn’t provide enough clinical information. I suspect that with an expanded list of clearly low-value services, the annual cost for low-value pediatric services would be a half a billion dollars.
As concerning as the findings in this study may be, it doesn’t answer the question of what we should do to correct the problem. We can dance around the issue by saying that patients and parents are pressuring us to do something even if it’s a low-value service. We can complain that for decades we have been practicing under the dark cloud of a malpractice suit, and that if we don’t turn over every stone in our evaluation of a patient we’re going to trip on one of them and end up in court.
But the bottom line is that we are the ones who are making the choice to order a study or prescribe a medication that is not only of low value, but more than likely worthless and possibly damaging to the patient. With the help of the American Academy of Pediatrics, we need to swallow hard and begin cleaning house, throwing out those low-value services we have gotten in the habit of ordering and prescribing. Education helps, but sometimes we have to do some finger pointing even if the finger points to us.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
‘And a child shall lead them’
With a moistened index finger pointing skyward, I always have tried to remain alert to where the winds of change are blowing. But every now and then I miss a trend in child care, and that is the case with something known as “baby-led weaning.” Influenced by the questionable notion that there is a “natural” way of doing almost everything, the concept hinges on the belief that an infant will “tell” his mother when it is time to stop nursing and begin solids, aka complementary feeding.
At face value, the concept of allowing the baby to lead is a good one simply because of universality of biologic variation. Just as with the question of how much sleep a baby needs, I don’t think anyone (let alone clinicians) can give with assurance an answer that can easily be applied to all infants. There are just too many variables.
For most dyads, breastfeeding is more than just passing calories from one individual to another. Nursing can offer a sense of security and calming both for infants and their mothers. In many cases, the breast unfortunately has become a critical ingredient in the infant’s ritual for falling to sleep. For some mothers, success at breastfeeding becomes an important validation of her feelings of confidence and self-worth that in the past may have been battered by a male-dominated environment. If breastfeeding has been an unpleasant experience, a mother may be more likely to interpret her infant’s behavior as a message that it is time to wean. The bottom line is that a mother’s perception of her baby’s messages about weaning often reflects her own feelings about nursing.
Of course, we clinicians can influence a mother’s perception of her baby’s messages by introducing our own biases about what we believe is the safest, most nutritionally sound way to introduce complementary feeding. And let’s be honest and acknowledge that those are biases mostly unsupported by good scientific study. In many cases, they are more of a reflection of the cultures in which we have grown up.
When asked by parents how they will know when their infant is ready for complementary feeding, I suggest that it’s time when the infant is not only curious about what the adults around him are eating, but obviously is upset that he isn’t being offered a taste. I add that exactly what that food should be is a matter of debate and common sense.
I also encourage parents to allow the child to do as much self-feeding as possible and not worry about the mess. An old shower curtain floor and plenty of sponges and paper towels are a must.
In most cases, I think we can trust babies to take the lead in weaning. But I also believe that as clinicians we must remain alert to the few situations when extended nursing is not in the best interest for the baby who is not growing well or for the mother for whom the nursing is taking an unreasonable toll on her physical and mental health.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
With a moistened index finger pointing skyward, I always have tried to remain alert to where the winds of change are blowing. But every now and then I miss a trend in child care, and that is the case with something known as “baby-led weaning.” Influenced by the questionable notion that there is a “natural” way of doing almost everything, the concept hinges on the belief that an infant will “tell” his mother when it is time to stop nursing and begin solids, aka complementary feeding.
At face value, the concept of allowing the baby to lead is a good one simply because of universality of biologic variation. Just as with the question of how much sleep a baby needs, I don’t think anyone (let alone clinicians) can give with assurance an answer that can easily be applied to all infants. There are just too many variables.
For most dyads, breastfeeding is more than just passing calories from one individual to another. Nursing can offer a sense of security and calming both for infants and their mothers. In many cases, the breast unfortunately has become a critical ingredient in the infant’s ritual for falling to sleep. For some mothers, success at breastfeeding becomes an important validation of her feelings of confidence and self-worth that in the past may have been battered by a male-dominated environment. If breastfeeding has been an unpleasant experience, a mother may be more likely to interpret her infant’s behavior as a message that it is time to wean. The bottom line is that a mother’s perception of her baby’s messages about weaning often reflects her own feelings about nursing.
Of course, we clinicians can influence a mother’s perception of her baby’s messages by introducing our own biases about what we believe is the safest, most nutritionally sound way to introduce complementary feeding. And let’s be honest and acknowledge that those are biases mostly unsupported by good scientific study. In many cases, they are more of a reflection of the cultures in which we have grown up.
When asked by parents how they will know when their infant is ready for complementary feeding, I suggest that it’s time when the infant is not only curious about what the adults around him are eating, but obviously is upset that he isn’t being offered a taste. I add that exactly what that food should be is a matter of debate and common sense.
I also encourage parents to allow the child to do as much self-feeding as possible and not worry about the mess. An old shower curtain floor and plenty of sponges and paper towels are a must.
In most cases, I think we can trust babies to take the lead in weaning. But I also believe that as clinicians we must remain alert to the few situations when extended nursing is not in the best interest for the baby who is not growing well or for the mother for whom the nursing is taking an unreasonable toll on her physical and mental health.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
With a moistened index finger pointing skyward, I always have tried to remain alert to where the winds of change are blowing. But every now and then I miss a trend in child care, and that is the case with something known as “baby-led weaning.” Influenced by the questionable notion that there is a “natural” way of doing almost everything, the concept hinges on the belief that an infant will “tell” his mother when it is time to stop nursing and begin solids, aka complementary feeding.
At face value, the concept of allowing the baby to lead is a good one simply because of universality of biologic variation. Just as with the question of how much sleep a baby needs, I don’t think anyone (let alone clinicians) can give with assurance an answer that can easily be applied to all infants. There are just too many variables.
For most dyads, breastfeeding is more than just passing calories from one individual to another. Nursing can offer a sense of security and calming both for infants and their mothers. In many cases, the breast unfortunately has become a critical ingredient in the infant’s ritual for falling to sleep. For some mothers, success at breastfeeding becomes an important validation of her feelings of confidence and self-worth that in the past may have been battered by a male-dominated environment. If breastfeeding has been an unpleasant experience, a mother may be more likely to interpret her infant’s behavior as a message that it is time to wean. The bottom line is that a mother’s perception of her baby’s messages about weaning often reflects her own feelings about nursing.
Of course, we clinicians can influence a mother’s perception of her baby’s messages by introducing our own biases about what we believe is the safest, most nutritionally sound way to introduce complementary feeding. And let’s be honest and acknowledge that those are biases mostly unsupported by good scientific study. In many cases, they are more of a reflection of the cultures in which we have grown up.
When asked by parents how they will know when their infant is ready for complementary feeding, I suggest that it’s time when the infant is not only curious about what the adults around him are eating, but obviously is upset that he isn’t being offered a taste. I add that exactly what that food should be is a matter of debate and common sense.
I also encourage parents to allow the child to do as much self-feeding as possible and not worry about the mess. An old shower curtain floor and plenty of sponges and paper towels are a must.
In most cases, I think we can trust babies to take the lead in weaning. But I also believe that as clinicians we must remain alert to the few situations when extended nursing is not in the best interest for the baby who is not growing well or for the mother for whom the nursing is taking an unreasonable toll on her physical and mental health.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.” Email him at [email protected].
Chemo-free induction regimen shines in MCL
SAN DIEGO – A chemotherapy-free induction regimen of ibrutinib and rituximab was well tolerated and achieved an overall response rate of 100% among patients with newly diagnosed mantle cell lymphoma (MCL), according to results of a small single-center phase II trial.
A total of 72% of patients had complete responses to induction, while 28% had partial responses, and 100% had complete responses to consolidation, reported Michael Wang, MD, at the annual meeting of the American Society of Hematology. The findings highlight a “window of opportunity” to effectively treat de novo MCL in young, fit patients while potentially sparing them from repeated cycles of intensive chemoimmunotherapy, the investigators noted.
Established treatments for MCL include eight cycles of rituximab–hyper-CVAD (hyper-fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) alternating with rituximab–methotrexate–Ara-C (cytarabine). Median overall survival with this regimen exceeds 10 years, but during that decade, more than 6% of patients will develop myeloid neoplasms related to treatment, noted Dr. Wang of the University of Texas MD Anderson Cancer Center in Houston.
For the study, patients up to 65 years old with newly diagnosed, untreated MCL underwent induction with continuous daily ibrutinib (560 mg), plus rituximab (375 mg/m2) administered weekly for 4 weeks during cycle 1 and on day 1 of cycles 3-12. Consolidation consisted of rituximab plus hyper-CVAD, alternating every 28 days with rituximab plus high-dose methotrexate–Ara-C. Complete responders to induction received four cycles of chemoimmunotherapy, while progressors and partial responders received chemoimmunotherapy for two cycles beyond the point of complete remission.
Among 36 evaluable patients, 28% had a partial response and the rest had complete responses to induction. Moreover, all 19 patients who completed consolidation had a complete response. During induction, the most common toxicities were fatigue, diarrhea, rash, and myalgia, nearly all of which were mild or moderate in severity. During consolidation, two patients developed severe neutropenia, one patient developed severe febrile neutropenia, and one developed a severe increase in liver enzymes. There were no treatment-related deaths.
“The toxicity after intensive immune-chemotherapy in shortened cycles [is] much improved compared to historical controls, but longer follow-up is needed,” the researchers wrote. “This unprecedented efficacy and safety may provide a window of opportunity for less chemoimmunotherapy needed for consolidation.”
Dr. Wang disclosed ties to Janssen, Onyx, BeiGene, Kite Pharma, Asana Biosciences, Juno Therapeutics, Acerta Pharma, and Celgene.
SAN DIEGO – A chemotherapy-free induction regimen of ibrutinib and rituximab was well tolerated and achieved an overall response rate of 100% among patients with newly diagnosed mantle cell lymphoma (MCL), according to results of a small single-center phase II trial.
A total of 72% of patients had complete responses to induction, while 28% had partial responses, and 100% had complete responses to consolidation, reported Michael Wang, MD, at the annual meeting of the American Society of Hematology. The findings highlight a “window of opportunity” to effectively treat de novo MCL in young, fit patients while potentially sparing them from repeated cycles of intensive chemoimmunotherapy, the investigators noted.
Established treatments for MCL include eight cycles of rituximab–hyper-CVAD (hyper-fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) alternating with rituximab–methotrexate–Ara-C (cytarabine). Median overall survival with this regimen exceeds 10 years, but during that decade, more than 6% of patients will develop myeloid neoplasms related to treatment, noted Dr. Wang of the University of Texas MD Anderson Cancer Center in Houston.
For the study, patients up to 65 years old with newly diagnosed, untreated MCL underwent induction with continuous daily ibrutinib (560 mg), plus rituximab (375 mg/m2) administered weekly for 4 weeks during cycle 1 and on day 1 of cycles 3-12. Consolidation consisted of rituximab plus hyper-CVAD, alternating every 28 days with rituximab plus high-dose methotrexate–Ara-C. Complete responders to induction received four cycles of chemoimmunotherapy, while progressors and partial responders received chemoimmunotherapy for two cycles beyond the point of complete remission.
Among 36 evaluable patients, 28% had a partial response and the rest had complete responses to induction. Moreover, all 19 patients who completed consolidation had a complete response. During induction, the most common toxicities were fatigue, diarrhea, rash, and myalgia, nearly all of which were mild or moderate in severity. During consolidation, two patients developed severe neutropenia, one patient developed severe febrile neutropenia, and one developed a severe increase in liver enzymes. There were no treatment-related deaths.
“The toxicity after intensive immune-chemotherapy in shortened cycles [is] much improved compared to historical controls, but longer follow-up is needed,” the researchers wrote. “This unprecedented efficacy and safety may provide a window of opportunity for less chemoimmunotherapy needed for consolidation.”
Dr. Wang disclosed ties to Janssen, Onyx, BeiGene, Kite Pharma, Asana Biosciences, Juno Therapeutics, Acerta Pharma, and Celgene.
SAN DIEGO – A chemotherapy-free induction regimen of ibrutinib and rituximab was well tolerated and achieved an overall response rate of 100% among patients with newly diagnosed mantle cell lymphoma (MCL), according to results of a small single-center phase II trial.
A total of 72% of patients had complete responses to induction, while 28% had partial responses, and 100% had complete responses to consolidation, reported Michael Wang, MD, at the annual meeting of the American Society of Hematology. The findings highlight a “window of opportunity” to effectively treat de novo MCL in young, fit patients while potentially sparing them from repeated cycles of intensive chemoimmunotherapy, the investigators noted.
Established treatments for MCL include eight cycles of rituximab–hyper-CVAD (hyper-fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) alternating with rituximab–methotrexate–Ara-C (cytarabine). Median overall survival with this regimen exceeds 10 years, but during that decade, more than 6% of patients will develop myeloid neoplasms related to treatment, noted Dr. Wang of the University of Texas MD Anderson Cancer Center in Houston.
For the study, patients up to 65 years old with newly diagnosed, untreated MCL underwent induction with continuous daily ibrutinib (560 mg), plus rituximab (375 mg/m2) administered weekly for 4 weeks during cycle 1 and on day 1 of cycles 3-12. Consolidation consisted of rituximab plus hyper-CVAD, alternating every 28 days with rituximab plus high-dose methotrexate–Ara-C. Complete responders to induction received four cycles of chemoimmunotherapy, while progressors and partial responders received chemoimmunotherapy for two cycles beyond the point of complete remission.
Among 36 evaluable patients, 28% had a partial response and the rest had complete responses to induction. Moreover, all 19 patients who completed consolidation had a complete response. During induction, the most common toxicities were fatigue, diarrhea, rash, and myalgia, nearly all of which were mild or moderate in severity. During consolidation, two patients developed severe neutropenia, one patient developed severe febrile neutropenia, and one developed a severe increase in liver enzymes. There were no treatment-related deaths.
“The toxicity after intensive immune-chemotherapy in shortened cycles [is] much improved compared to historical controls, but longer follow-up is needed,” the researchers wrote. “This unprecedented efficacy and safety may provide a window of opportunity for less chemoimmunotherapy needed for consolidation.”
Dr. Wang disclosed ties to Janssen, Onyx, BeiGene, Kite Pharma, Asana Biosciences, Juno Therapeutics, Acerta Pharma, and Celgene.
AT ASH 2016
Key clinical point: Induction with ibrutinib and rituximab achieved a 100% response rate in newly diagnosed mantle cell lymphoma, enabling patients to receive less intensive consolidation.
Major finding: Rates of complete response were 72% for induction and 100% for induction plus consolidation.
Data source: A single-center phase II trial of 36 patients with newly diagnosed, untreated mantle cell lymphoma.
Disclosures: Dr. Wang disclosed ties to Janssen, Onyx, BeiGene, Kite Pharma, Asana Biosciences, Juno Therapeutics, Acerta Pharma, and Celgene.
Debunking Psoriasis Myths: Do Systemic Steroids Used in Psoriasis Patients Cause Pustular Psoriasis?
Myth: Systemic steroids cause pustular psoriasis
The advent of biologic therapy for psoriasis has changed the landscape of treatments offered to patients. Nevertheless, systemic therapies still play an important role, according to the American Academy of Dermatology psoriasis treatment guidelines, due to their oral route of administration and low cost compared to biologics. They are options for patients with moderate to severe psoriasis that is unresponsive to topical therapies or phototherapy. However, many dermatologists feel that it is inappropriate to prescribe oral steroids to psoriasis patients due to the risk for steroid-induced conversion to pustular psoriasis, the long-term side effects of steroids, and deterioration of psoriasis after withdrawal of steroids.
Pustular psoriasis appears clinically as white pustules (blisters of noninfectious pus) surrounded by red skin. The pus consists of white blood cells. There are a number of triggers in addition to systemic steroids, such as internal medications, irritating topical agents, overexposure to UV light, and pregnancy. Stopping an oral steroid abruptly can cause serious disease flares, fatigue, and joint pain.
Westphal et al described the case of a 70-year-old woman with palmoplantar psoriasis who was diagnosed with acute generalized exanthematous pustulosis that was treated with corticotherapy by injection and then oral prednisone. She experienced improvement, but her symptoms worsened when she was in the process of reducing the prednisone dose. The dose was increased again, and the same worsening of symptoms was experienced when the dose was reduced. After completely abandoning oral steroid therapy, she developed a severe case of generalized pustular psoriasis that was treated with acitretin. This case illustrates the dangerous consequences of abruptly discontinuing oral steroids.
However, dermatologists may be using oral steroids for psoriasis more often than treatment guidelines suggest. In 2014, Al-Dabagh et al evaluated how frequently systemic corticosteroids are prescribed for psoriasis in the United States. The researchers reported, "Despite the absence or discouragement of systemic corticosteroids in psoriasis management guidelines, systemic corticosteroids are among the most common systemic treatments used for psoriasis." They found that systemic corticosteroids were prescribed at 650,000 of 21,020,000 psoriasis visits, of which 93% were visits to dermatologists. Prednisone was the most commonly prescribed systemic corticosteroid, followed by methylprednisolone and dexamethasone. To prevent rebound flares, systemic corticosteroids were prescribed with a topical corticosteroid in 45% of the visits in patients with psoriasis as the sole diagnosis. They concluded, "The striking contrast between the guidelines for psoriasis management and actual practice suggests that there is an acute need to better understand the use of systemic corticosteroids for psoriasis."
The benefits of systemic corticosteroids versus the frequency of adverse reactions should be weighed by dermatologists and patients to make evidence-based decisions about treatment. Patients should take oral steroids exactly as prescribed by physicians.
References
Al-Dabagh A, Al-Dabagh R, Davis SA, et al. Systemic corticosteroids are frequently prescribed for psoriasis. J Cutan Med Surg. 2014;18:195-199.
Delzell E. What you need to know about steroids. National Psoriasis Foundation website. https://www.psoriasis.org/advance/what-you-need-to-know-about-steroids. Published September 2, 2015. Accessed January 13, 2017.
Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol. 2009;61:451-485.
Pustular psoriasis. National Psoriasis Foundation website. https://www.psoriasis.org/about-psoriasis/types/pustular. Accessed January 13, 2017.
Westphal DC, Schettini APM, de Souza PP, et al. Generalized pustular psoriasis induced by systemic steroid dose reduction. An Bras Dermatol. 2016;91:664-666.
Expert Commentaries on next page
Expert Commentaries
When I was a resident, I was trained not to use systemic steroids in psoriasis patients for the reasons noted above, and I have faithfully followed these instructions 9 years into practice. However, I see many patients with severe psoriasis who are given systemic steroids by other physicians (ie, rheumatologists for psoriatic arthritis, pulmonologists for asthma). I often tell patients afterwards of the dangers of systemic steroids and to have them tell their other doctors to be cautious when giving another course of systemic steroids. However, I have yet to see a generalized pustular psoriasis outbreak or flare in psoriasis vulgaris after a course of systemic steroids. While I do not recommend systemic steroids for psoriasis patients since we have so many other systemic agents, I wonder if the risks that we were all trained about are really that high.
—Jashin J. Wu, MD (Los Angeles, California)
How bad is it to give patients with psoriasis systemic steroids? Are psoriasis patients treated with systemic steroids likely to get a pustular flare? Are patients with psoriasis who suddenly stop their corticosteroids more likely to get a pustular flare than psoriasis patients who suddenly stop other systemic psoriasis treatments? I don't have the answers to these questions. My sense is that we have a lot of dogma and strong opinions but very little hard evidence to answer these questions.
I don't typically prescribe systemic steroids to psoriasis patients, but systemic steroids are widely used. Sometimes there are problems. I have seen patients who received systemic steroids for psoriasis and who went on to have a pustular flare, but it's possible the systemic steroid was given because those patients were headed toward the pustular flare already.
I once had a psoriasis patient who came to see me with a suddenly inflamed tender joint. Not knowing what to do, I called a rheumatologist to see the patient. The rheumatologist, too busy to work the patient in, told me to give the patient a 2-week prednisone taper. I did, and nothing untoward happened with the psoriasis. This one anecdote doesn't give me much confidence that systemic steroids are safe for psoriasis patients.
Clearly, long-term steroids cause a host of problems (eg, osteoporosis, diabetes). But I'm not sure that the dogma that systemic steroids should be avoided in patients with psoriasis is well supported. Systemic steroids are being widely used, and I don't see an epidemic of pustular flares.
Is it a mistake to give systemic steroids to psoriasis patients? I just don't know.
—Steven R. Feldman, MD, PhD (Winston-Salem, North Carolina)
Myth: Systemic steroids cause pustular psoriasis
The advent of biologic therapy for psoriasis has changed the landscape of treatments offered to patients. Nevertheless, systemic therapies still play an important role, according to the American Academy of Dermatology psoriasis treatment guidelines, due to their oral route of administration and low cost compared to biologics. They are options for patients with moderate to severe psoriasis that is unresponsive to topical therapies or phototherapy. However, many dermatologists feel that it is inappropriate to prescribe oral steroids to psoriasis patients due to the risk for steroid-induced conversion to pustular psoriasis, the long-term side effects of steroids, and deterioration of psoriasis after withdrawal of steroids.
Pustular psoriasis appears clinically as white pustules (blisters of noninfectious pus) surrounded by red skin. The pus consists of white blood cells. There are a number of triggers in addition to systemic steroids, such as internal medications, irritating topical agents, overexposure to UV light, and pregnancy. Stopping an oral steroid abruptly can cause serious disease flares, fatigue, and joint pain.
Westphal et al described the case of a 70-year-old woman with palmoplantar psoriasis who was diagnosed with acute generalized exanthematous pustulosis that was treated with corticotherapy by injection and then oral prednisone. She experienced improvement, but her symptoms worsened when she was in the process of reducing the prednisone dose. The dose was increased again, and the same worsening of symptoms was experienced when the dose was reduced. After completely abandoning oral steroid therapy, she developed a severe case of generalized pustular psoriasis that was treated with acitretin. This case illustrates the dangerous consequences of abruptly discontinuing oral steroids.
However, dermatologists may be using oral steroids for psoriasis more often than treatment guidelines suggest. In 2014, Al-Dabagh et al evaluated how frequently systemic corticosteroids are prescribed for psoriasis in the United States. The researchers reported, "Despite the absence or discouragement of systemic corticosteroids in psoriasis management guidelines, systemic corticosteroids are among the most common systemic treatments used for psoriasis." They found that systemic corticosteroids were prescribed at 650,000 of 21,020,000 psoriasis visits, of which 93% were visits to dermatologists. Prednisone was the most commonly prescribed systemic corticosteroid, followed by methylprednisolone and dexamethasone. To prevent rebound flares, systemic corticosteroids were prescribed with a topical corticosteroid in 45% of the visits in patients with psoriasis as the sole diagnosis. They concluded, "The striking contrast between the guidelines for psoriasis management and actual practice suggests that there is an acute need to better understand the use of systemic corticosteroids for psoriasis."
The benefits of systemic corticosteroids versus the frequency of adverse reactions should be weighed by dermatologists and patients to make evidence-based decisions about treatment. Patients should take oral steroids exactly as prescribed by physicians.
References
Al-Dabagh A, Al-Dabagh R, Davis SA, et al. Systemic corticosteroids are frequently prescribed for psoriasis. J Cutan Med Surg. 2014;18:195-199.
Delzell E. What you need to know about steroids. National Psoriasis Foundation website. https://www.psoriasis.org/advance/what-you-need-to-know-about-steroids. Published September 2, 2015. Accessed January 13, 2017.
Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol. 2009;61:451-485.
Pustular psoriasis. National Psoriasis Foundation website. https://www.psoriasis.org/about-psoriasis/types/pustular. Accessed January 13, 2017.
Westphal DC, Schettini APM, de Souza PP, et al. Generalized pustular psoriasis induced by systemic steroid dose reduction. An Bras Dermatol. 2016;91:664-666.
Expert Commentaries on next page
Expert Commentaries
When I was a resident, I was trained not to use systemic steroids in psoriasis patients for the reasons noted above, and I have faithfully followed these instructions 9 years into practice. However, I see many patients with severe psoriasis who are given systemic steroids by other physicians (ie, rheumatologists for psoriatic arthritis, pulmonologists for asthma). I often tell patients afterwards of the dangers of systemic steroids and to have them tell their other doctors to be cautious when giving another course of systemic steroids. However, I have yet to see a generalized pustular psoriasis outbreak or flare in psoriasis vulgaris after a course of systemic steroids. While I do not recommend systemic steroids for psoriasis patients since we have so many other systemic agents, I wonder if the risks that we were all trained about are really that high.
—Jashin J. Wu, MD (Los Angeles, California)
How bad is it to give patients with psoriasis systemic steroids? Are psoriasis patients treated with systemic steroids likely to get a pustular flare? Are patients with psoriasis who suddenly stop their corticosteroids more likely to get a pustular flare than psoriasis patients who suddenly stop other systemic psoriasis treatments? I don't have the answers to these questions. My sense is that we have a lot of dogma and strong opinions but very little hard evidence to answer these questions.
I don't typically prescribe systemic steroids to psoriasis patients, but systemic steroids are widely used. Sometimes there are problems. I have seen patients who received systemic steroids for psoriasis and who went on to have a pustular flare, but it's possible the systemic steroid was given because those patients were headed toward the pustular flare already.
I once had a psoriasis patient who came to see me with a suddenly inflamed tender joint. Not knowing what to do, I called a rheumatologist to see the patient. The rheumatologist, too busy to work the patient in, told me to give the patient a 2-week prednisone taper. I did, and nothing untoward happened with the psoriasis. This one anecdote doesn't give me much confidence that systemic steroids are safe for psoriasis patients.
Clearly, long-term steroids cause a host of problems (eg, osteoporosis, diabetes). But I'm not sure that the dogma that systemic steroids should be avoided in patients with psoriasis is well supported. Systemic steroids are being widely used, and I don't see an epidemic of pustular flares.
Is it a mistake to give systemic steroids to psoriasis patients? I just don't know.
—Steven R. Feldman, MD, PhD (Winston-Salem, North Carolina)
Myth: Systemic steroids cause pustular psoriasis
The advent of biologic therapy for psoriasis has changed the landscape of treatments offered to patients. Nevertheless, systemic therapies still play an important role, according to the American Academy of Dermatology psoriasis treatment guidelines, due to their oral route of administration and low cost compared to biologics. They are options for patients with moderate to severe psoriasis that is unresponsive to topical therapies or phototherapy. However, many dermatologists feel that it is inappropriate to prescribe oral steroids to psoriasis patients due to the risk for steroid-induced conversion to pustular psoriasis, the long-term side effects of steroids, and deterioration of psoriasis after withdrawal of steroids.
Pustular psoriasis appears clinically as white pustules (blisters of noninfectious pus) surrounded by red skin. The pus consists of white blood cells. There are a number of triggers in addition to systemic steroids, such as internal medications, irritating topical agents, overexposure to UV light, and pregnancy. Stopping an oral steroid abruptly can cause serious disease flares, fatigue, and joint pain.
Westphal et al described the case of a 70-year-old woman with palmoplantar psoriasis who was diagnosed with acute generalized exanthematous pustulosis that was treated with corticotherapy by injection and then oral prednisone. She experienced improvement, but her symptoms worsened when she was in the process of reducing the prednisone dose. The dose was increased again, and the same worsening of symptoms was experienced when the dose was reduced. After completely abandoning oral steroid therapy, she developed a severe case of generalized pustular psoriasis that was treated with acitretin. This case illustrates the dangerous consequences of abruptly discontinuing oral steroids.
However, dermatologists may be using oral steroids for psoriasis more often than treatment guidelines suggest. In 2014, Al-Dabagh et al evaluated how frequently systemic corticosteroids are prescribed for psoriasis in the United States. The researchers reported, "Despite the absence or discouragement of systemic corticosteroids in psoriasis management guidelines, systemic corticosteroids are among the most common systemic treatments used for psoriasis." They found that systemic corticosteroids were prescribed at 650,000 of 21,020,000 psoriasis visits, of which 93% were visits to dermatologists. Prednisone was the most commonly prescribed systemic corticosteroid, followed by methylprednisolone and dexamethasone. To prevent rebound flares, systemic corticosteroids were prescribed with a topical corticosteroid in 45% of the visits in patients with psoriasis as the sole diagnosis. They concluded, "The striking contrast between the guidelines for psoriasis management and actual practice suggests that there is an acute need to better understand the use of systemic corticosteroids for psoriasis."
The benefits of systemic corticosteroids versus the frequency of adverse reactions should be weighed by dermatologists and patients to make evidence-based decisions about treatment. Patients should take oral steroids exactly as prescribed by physicians.
References
Al-Dabagh A, Al-Dabagh R, Davis SA, et al. Systemic corticosteroids are frequently prescribed for psoriasis. J Cutan Med Surg. 2014;18:195-199.
Delzell E. What you need to know about steroids. National Psoriasis Foundation website. https://www.psoriasis.org/advance/what-you-need-to-know-about-steroids. Published September 2, 2015. Accessed January 13, 2017.
Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol. 2009;61:451-485.
Pustular psoriasis. National Psoriasis Foundation website. https://www.psoriasis.org/about-psoriasis/types/pustular. Accessed January 13, 2017.
Westphal DC, Schettini APM, de Souza PP, et al. Generalized pustular psoriasis induced by systemic steroid dose reduction. An Bras Dermatol. 2016;91:664-666.
Expert Commentaries on next page
Expert Commentaries
When I was a resident, I was trained not to use systemic steroids in psoriasis patients for the reasons noted above, and I have faithfully followed these instructions 9 years into practice. However, I see many patients with severe psoriasis who are given systemic steroids by other physicians (ie, rheumatologists for psoriatic arthritis, pulmonologists for asthma). I often tell patients afterwards of the dangers of systemic steroids and to have them tell their other doctors to be cautious when giving another course of systemic steroids. However, I have yet to see a generalized pustular psoriasis outbreak or flare in psoriasis vulgaris after a course of systemic steroids. While I do not recommend systemic steroids for psoriasis patients since we have so many other systemic agents, I wonder if the risks that we were all trained about are really that high.
—Jashin J. Wu, MD (Los Angeles, California)
How bad is it to give patients with psoriasis systemic steroids? Are psoriasis patients treated with systemic steroids likely to get a pustular flare? Are patients with psoriasis who suddenly stop their corticosteroids more likely to get a pustular flare than psoriasis patients who suddenly stop other systemic psoriasis treatments? I don't have the answers to these questions. My sense is that we have a lot of dogma and strong opinions but very little hard evidence to answer these questions.
I don't typically prescribe systemic steroids to psoriasis patients, but systemic steroids are widely used. Sometimes there are problems. I have seen patients who received systemic steroids for psoriasis and who went on to have a pustular flare, but it's possible the systemic steroid was given because those patients were headed toward the pustular flare already.
I once had a psoriasis patient who came to see me with a suddenly inflamed tender joint. Not knowing what to do, I called a rheumatologist to see the patient. The rheumatologist, too busy to work the patient in, told me to give the patient a 2-week prednisone taper. I did, and nothing untoward happened with the psoriasis. This one anecdote doesn't give me much confidence that systemic steroids are safe for psoriasis patients.
Clearly, long-term steroids cause a host of problems (eg, osteoporosis, diabetes). But I'm not sure that the dogma that systemic steroids should be avoided in patients with psoriasis is well supported. Systemic steroids are being widely used, and I don't see an epidemic of pustular flares.
Is it a mistake to give systemic steroids to psoriasis patients? I just don't know.
—Steven R. Feldman, MD, PhD (Winston-Salem, North Carolina)
VA MRSA Prevention Initiative reports continued health care–associated infection declines
The U.S. Department of Veterans Affairs MRSA Prevention Initiative, implemented in October 2007, has shown progress at limiting health care–associated infections of methicillin-resistant Staphylococcus aureus through 2011 and 2012.
A new report published in the January 2017 issue of the American Journal of Infection Control tracks continued declines in infection through September 2015.
Monthly rates of health care–associated infections fell significantly in all settings from October 2007 to September 2015: an 87% decrease in ICUs, 80.1% in non-ICUs, 80.9% in spinal cord injury units, and 49.4% in long-term care facilities (P for all less than .0001).
“The VA data suggest that active surveillance followed by contact precautions (with or without decolonization) may be most useful when MRSA [health care–associated infection] rates are unacceptably high (as they were in VA facilities during 2007) or to decrease infections in high-risk units such as ICUs,” Dr. Evans and his colleagues concluded.
Details about the implementation of the initiative were previously published in the New England Journal of Medicine in 2011, including the initiative’s goal to promote “a change in the institutional culture whereby infection control would become the responsibility of everyone who had contact with patients” (N Engl J Med. 2011;364:1419-30).
Dr. Evans and his colleagues had no relevant financial disclosures.
The U.S. Department of Veterans Affairs MRSA Prevention Initiative, implemented in October 2007, has shown progress at limiting health care–associated infections of methicillin-resistant Staphylococcus aureus through 2011 and 2012.
A new report published in the January 2017 issue of the American Journal of Infection Control tracks continued declines in infection through September 2015.
Monthly rates of health care–associated infections fell significantly in all settings from October 2007 to September 2015: an 87% decrease in ICUs, 80.1% in non-ICUs, 80.9% in spinal cord injury units, and 49.4% in long-term care facilities (P for all less than .0001).
“The VA data suggest that active surveillance followed by contact precautions (with or without decolonization) may be most useful when MRSA [health care–associated infection] rates are unacceptably high (as they were in VA facilities during 2007) or to decrease infections in high-risk units such as ICUs,” Dr. Evans and his colleagues concluded.
Details about the implementation of the initiative were previously published in the New England Journal of Medicine in 2011, including the initiative’s goal to promote “a change in the institutional culture whereby infection control would become the responsibility of everyone who had contact with patients” (N Engl J Med. 2011;364:1419-30).
Dr. Evans and his colleagues had no relevant financial disclosures.
The U.S. Department of Veterans Affairs MRSA Prevention Initiative, implemented in October 2007, has shown progress at limiting health care–associated infections of methicillin-resistant Staphylococcus aureus through 2011 and 2012.
A new report published in the January 2017 issue of the American Journal of Infection Control tracks continued declines in infection through September 2015.
Monthly rates of health care–associated infections fell significantly in all settings from October 2007 to September 2015: an 87% decrease in ICUs, 80.1% in non-ICUs, 80.9% in spinal cord injury units, and 49.4% in long-term care facilities (P for all less than .0001).
“The VA data suggest that active surveillance followed by contact precautions (with or without decolonization) may be most useful when MRSA [health care–associated infection] rates are unacceptably high (as they were in VA facilities during 2007) or to decrease infections in high-risk units such as ICUs,” Dr. Evans and his colleagues concluded.
Details about the implementation of the initiative were previously published in the New England Journal of Medicine in 2011, including the initiative’s goal to promote “a change in the institutional culture whereby infection control would become the responsibility of everyone who had contact with patients” (N Engl J Med. 2011;364:1419-30).
Dr. Evans and his colleagues had no relevant financial disclosures.
FROM THE AMERICAN JOURNAL OF INFECTION CONTROL
Do not overtreat febrile neutropenia
Clinical question: Does emergency department management of patients with febrile neutropenia (FN) follow current guidelines?
Background: Chemotherapy-related FN is an oncologic emergency frequently leading to hospitalization and intravenous antibiotics. Familiarity with FN guidelines allows risk stratification for inpatient versus outpatient therapy.
Study design: Single-center, retrospective, cohort study.
Setting: Large, urban, tertiary-care academic hospital.
Synopsis: Of 173 patient visits, 25% were risk stratified as eligible for outpatient treatment and 75% as inpatient care. All patient care was assessed for guideline concordance at the time of ED disposition and therapy.
Primary outcome analysis demonstrated management was guideline discordant in 98% of low-risk patients versus 7% of high-risk patients. Secondary 30-day clinical outcomes showed high-risk patients were more likely to have positive blood cultures (54%), sepsis-induced hypotension (9.3%), and death (5.4%). Seventeen percent of all patients who received IV antibiotics were prescribed vancomycin without guideline support.
Bottom line: Low-risk FN patients in the ED received more aggressive treatment than recommended. Further research is needed to strategize means of better aligning FN management with standards of care.
Citation: Baugh CW, Wang TJ, Caterino JM, et al. ED management of patients with febrile neutropenia: guideline concordant or overly aggressive [published online ahead of print Sept. 9, 2016]? Acad Emerg Med. doi: 10.1111/acem.13079.
Dr. Zuleta is an assistant professor and associate program director of the Jackson Memorial/University of Miami Internal Medicine residency training program and the site director of the program at University of Miami Hospital.
Clinical question: Does emergency department management of patients with febrile neutropenia (FN) follow current guidelines?
Background: Chemotherapy-related FN is an oncologic emergency frequently leading to hospitalization and intravenous antibiotics. Familiarity with FN guidelines allows risk stratification for inpatient versus outpatient therapy.
Study design: Single-center, retrospective, cohort study.
Setting: Large, urban, tertiary-care academic hospital.
Synopsis: Of 173 patient visits, 25% were risk stratified as eligible for outpatient treatment and 75% as inpatient care. All patient care was assessed for guideline concordance at the time of ED disposition and therapy.
Primary outcome analysis demonstrated management was guideline discordant in 98% of low-risk patients versus 7% of high-risk patients. Secondary 30-day clinical outcomes showed high-risk patients were more likely to have positive blood cultures (54%), sepsis-induced hypotension (9.3%), and death (5.4%). Seventeen percent of all patients who received IV antibiotics were prescribed vancomycin without guideline support.
Bottom line: Low-risk FN patients in the ED received more aggressive treatment than recommended. Further research is needed to strategize means of better aligning FN management with standards of care.
Citation: Baugh CW, Wang TJ, Caterino JM, et al. ED management of patients with febrile neutropenia: guideline concordant or overly aggressive [published online ahead of print Sept. 9, 2016]? Acad Emerg Med. doi: 10.1111/acem.13079.
Dr. Zuleta is an assistant professor and associate program director of the Jackson Memorial/University of Miami Internal Medicine residency training program and the site director of the program at University of Miami Hospital.
Clinical question: Does emergency department management of patients with febrile neutropenia (FN) follow current guidelines?
Background: Chemotherapy-related FN is an oncologic emergency frequently leading to hospitalization and intravenous antibiotics. Familiarity with FN guidelines allows risk stratification for inpatient versus outpatient therapy.
Study design: Single-center, retrospective, cohort study.
Setting: Large, urban, tertiary-care academic hospital.
Synopsis: Of 173 patient visits, 25% were risk stratified as eligible for outpatient treatment and 75% as inpatient care. All patient care was assessed for guideline concordance at the time of ED disposition and therapy.
Primary outcome analysis demonstrated management was guideline discordant in 98% of low-risk patients versus 7% of high-risk patients. Secondary 30-day clinical outcomes showed high-risk patients were more likely to have positive blood cultures (54%), sepsis-induced hypotension (9.3%), and death (5.4%). Seventeen percent of all patients who received IV antibiotics were prescribed vancomycin without guideline support.
Bottom line: Low-risk FN patients in the ED received more aggressive treatment than recommended. Further research is needed to strategize means of better aligning FN management with standards of care.
Citation: Baugh CW, Wang TJ, Caterino JM, et al. ED management of patients with febrile neutropenia: guideline concordant or overly aggressive [published online ahead of print Sept. 9, 2016]? Acad Emerg Med. doi: 10.1111/acem.13079.
Dr. Zuleta is an assistant professor and associate program director of the Jackson Memorial/University of Miami Internal Medicine residency training program and the site director of the program at University of Miami Hospital.
Cancer risk six times higher in children with congenital heart defects
NEW ORLEANS – Children with congenital heart defects have a five- to sixfold increased risk of developing pediatric cancer, Matthew Oster, MD, reported at the American Heart Association scientific sessions.
“The absolute risk is small, but it’s still a five- to sixfold risk compared to the general pediatric population, and it does warrant monitoring and a high index of suspicion in our children with congenital heart defects,” said Dr. Oster of Children’s Healthcare of Atlanta.
The increased cancer risk in adults with congenital heart defects has recently been the focus of research attention. However, little is known about the risk of cancer during the childhood of patients with congenital heart defects.
This was the impetus for Dr. Oster’s nationwide retrospective study of 6.1 million children and adolescents continuously enrolled in private, employer-sponsored health insurance plans during 2009-2015. The data came from the Truven Health MarketScan administrative database.
Children with Down syndrome were excluded from the study because their condition is known to be associated with increased rates of both congenital heart defects and pediatric cancers.
Among 88,493 individuals under age 18 with a diagnosed congenital heart defect, the incidence of any neoplasm diagnosed at least 30 days after diagnosis of the heart defect was 3.91/1,000, compared with 0.79/1,000 in more than 6 million children and adolescents without congenital heart disease.
Thus, children with a congenital heart defect were at a 4.9-fold increased risk for developing a childhood cancer. The risk for bone tumors was 11.2-fold greater than in the general pediatric population, and their neuroblastoma risk was 9.8-fold greater. Their risks of lymphoma and leukemia were increased 5.2- and 2.8-fold, respectively. Of note, they had no increased risk of brain tumors.
To confirm their results, Dr. Oster and his coinvestigators also conducted a sensitivity analysis limited to the 55,079 children and adolescents with at least two outpatient or one inpatient ICD-9 diagnostic code for congenital heart disease. Here the incidence of childhood malignancies was 5.1/1,000 patients, for an overall 6.4-fold increased relative risk.
“Bedside-to-bench work is now needed to determine potential mechanisms,” he said. “We believe the increased risk is related more to a common genetic pathway than to an exposure or treatment pathway because it occurs so early. But there may be some impact of exposures or treatment as well. We think that radiation exposure is more of a longer-term risk.”
He and his coinvestigators next plan to look at the impact on pediatric cancer risk of specific types of congenital heart defects.
Dr. Oster reported having no financial conflicts of interest regarding this study, which received Centers for Disease Control and Prevention funding.
NEW ORLEANS – Children with congenital heart defects have a five- to sixfold increased risk of developing pediatric cancer, Matthew Oster, MD, reported at the American Heart Association scientific sessions.
“The absolute risk is small, but it’s still a five- to sixfold risk compared to the general pediatric population, and it does warrant monitoring and a high index of suspicion in our children with congenital heart defects,” said Dr. Oster of Children’s Healthcare of Atlanta.
The increased cancer risk in adults with congenital heart defects has recently been the focus of research attention. However, little is known about the risk of cancer during the childhood of patients with congenital heart defects.
This was the impetus for Dr. Oster’s nationwide retrospective study of 6.1 million children and adolescents continuously enrolled in private, employer-sponsored health insurance plans during 2009-2015. The data came from the Truven Health MarketScan administrative database.
Children with Down syndrome were excluded from the study because their condition is known to be associated with increased rates of both congenital heart defects and pediatric cancers.
Among 88,493 individuals under age 18 with a diagnosed congenital heart defect, the incidence of any neoplasm diagnosed at least 30 days after diagnosis of the heart defect was 3.91/1,000, compared with 0.79/1,000 in more than 6 million children and adolescents without congenital heart disease.
Thus, children with a congenital heart defect were at a 4.9-fold increased risk for developing a childhood cancer. The risk for bone tumors was 11.2-fold greater than in the general pediatric population, and their neuroblastoma risk was 9.8-fold greater. Their risks of lymphoma and leukemia were increased 5.2- and 2.8-fold, respectively. Of note, they had no increased risk of brain tumors.
To confirm their results, Dr. Oster and his coinvestigators also conducted a sensitivity analysis limited to the 55,079 children and adolescents with at least two outpatient or one inpatient ICD-9 diagnostic code for congenital heart disease. Here the incidence of childhood malignancies was 5.1/1,000 patients, for an overall 6.4-fold increased relative risk.
“Bedside-to-bench work is now needed to determine potential mechanisms,” he said. “We believe the increased risk is related more to a common genetic pathway than to an exposure or treatment pathway because it occurs so early. But there may be some impact of exposures or treatment as well. We think that radiation exposure is more of a longer-term risk.”
He and his coinvestigators next plan to look at the impact on pediatric cancer risk of specific types of congenital heart defects.
Dr. Oster reported having no financial conflicts of interest regarding this study, which received Centers for Disease Control and Prevention funding.
NEW ORLEANS – Children with congenital heart defects have a five- to sixfold increased risk of developing pediatric cancer, Matthew Oster, MD, reported at the American Heart Association scientific sessions.
“The absolute risk is small, but it’s still a five- to sixfold risk compared to the general pediatric population, and it does warrant monitoring and a high index of suspicion in our children with congenital heart defects,” said Dr. Oster of Children’s Healthcare of Atlanta.
The increased cancer risk in adults with congenital heart defects has recently been the focus of research attention. However, little is known about the risk of cancer during the childhood of patients with congenital heart defects.
This was the impetus for Dr. Oster’s nationwide retrospective study of 6.1 million children and adolescents continuously enrolled in private, employer-sponsored health insurance plans during 2009-2015. The data came from the Truven Health MarketScan administrative database.
Children with Down syndrome were excluded from the study because their condition is known to be associated with increased rates of both congenital heart defects and pediatric cancers.
Among 88,493 individuals under age 18 with a diagnosed congenital heart defect, the incidence of any neoplasm diagnosed at least 30 days after diagnosis of the heart defect was 3.91/1,000, compared with 0.79/1,000 in more than 6 million children and adolescents without congenital heart disease.
Thus, children with a congenital heart defect were at a 4.9-fold increased risk for developing a childhood cancer. The risk for bone tumors was 11.2-fold greater than in the general pediatric population, and their neuroblastoma risk was 9.8-fold greater. Their risks of lymphoma and leukemia were increased 5.2- and 2.8-fold, respectively. Of note, they had no increased risk of brain tumors.
To confirm their results, Dr. Oster and his coinvestigators also conducted a sensitivity analysis limited to the 55,079 children and adolescents with at least two outpatient or one inpatient ICD-9 diagnostic code for congenital heart disease. Here the incidence of childhood malignancies was 5.1/1,000 patients, for an overall 6.4-fold increased relative risk.
“Bedside-to-bench work is now needed to determine potential mechanisms,” he said. “We believe the increased risk is related more to a common genetic pathway than to an exposure or treatment pathway because it occurs so early. But there may be some impact of exposures or treatment as well. We think that radiation exposure is more of a longer-term risk.”
He and his coinvestigators next plan to look at the impact on pediatric cancer risk of specific types of congenital heart defects.
Dr. Oster reported having no financial conflicts of interest regarding this study, which received Centers for Disease Control and Prevention funding.
AT THE AHA SCIENTIFIC SESSIONS
Key clinical point:
Major finding: Children with congenital heart defects are at a roughly sixfold increased risk of developing a pediatric cancer.
Data source: A retrospective analysis of administrative health insurance plan data on 6.1 million U.S. subjects under age 18 years, more than 88,000 of whom had congenital heart defects.
Disclosures: The presenter reported having no financial conflicts of interest regarding this study, which received Centers for Disease Control and Prevention funding.
VA Program Rewards Innovators and Best Practices
In December 2016, Federal Practitioner sat down with Shereef M. Elnahal, MD, MBA, VHA chief quality & safety officer, to discuss the VA Diffusion of Excellence (VADOE) program, which seeks to change VA culture and reward employees who have developed innovative programs that increase patient satisfaction, access to care, and clinical results, among other VA priorities. A recent JAMA article by Dr. Elnahal, VA Secretary Nominee David Shulkin, MD, and Deputy Under Secretary for Health for Organizational Excellence Carolyn Clancy, MD, highlights how VADOE can be a model for excellence at other large-scale health care systems.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
According to Dr. Elnahal, in 1 year, more than 400 VADOE programs have been submitted, more than 20 have been replicated at multiple sites, and 8 are targeted nationally, including a virtual tumor board and clinical pharmacy best practices. “We really empower and recognize the frontline employees who not only contribute the best practices but who replicate them,” Dr. Elnahal told Federal Practitioner. “Essentially, we give them a systemwide leadership role… This is part of many different initiatives that are trying to recognize and elevate the great work that physicians do and really improve their morale and reduce burnout.”
In December 2016, Federal Practitioner sat down with Shereef M. Elnahal, MD, MBA, VHA chief quality & safety officer, to discuss the VA Diffusion of Excellence (VADOE) program, which seeks to change VA culture and reward employees who have developed innovative programs that increase patient satisfaction, access to care, and clinical results, among other VA priorities. A recent JAMA article by Dr. Elnahal, VA Secretary Nominee David Shulkin, MD, and Deputy Under Secretary for Health for Organizational Excellence Carolyn Clancy, MD, highlights how VADOE can be a model for excellence at other large-scale health care systems.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
According to Dr. Elnahal, in 1 year, more than 400 VADOE programs have been submitted, more than 20 have been replicated at multiple sites, and 8 are targeted nationally, including a virtual tumor board and clinical pharmacy best practices. “We really empower and recognize the frontline employees who not only contribute the best practices but who replicate them,” Dr. Elnahal told Federal Practitioner. “Essentially, we give them a systemwide leadership role… This is part of many different initiatives that are trying to recognize and elevate the great work that physicians do and really improve their morale and reduce burnout.”
In December 2016, Federal Practitioner sat down with Shereef M. Elnahal, MD, MBA, VHA chief quality & safety officer, to discuss the VA Diffusion of Excellence (VADOE) program, which seeks to change VA culture and reward employees who have developed innovative programs that increase patient satisfaction, access to care, and clinical results, among other VA priorities. A recent JAMA article by Dr. Elnahal, VA Secretary Nominee David Shulkin, MD, and Deputy Under Secretary for Health for Organizational Excellence Carolyn Clancy, MD, highlights how VADOE can be a model for excellence at other large-scale health care systems.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
According to Dr. Elnahal, in 1 year, more than 400 VADOE programs have been submitted, more than 20 have been replicated at multiple sites, and 8 are targeted nationally, including a virtual tumor board and clinical pharmacy best practices. “We really empower and recognize the frontline employees who not only contribute the best practices but who replicate them,” Dr. Elnahal told Federal Practitioner. “Essentially, we give them a systemwide leadership role… This is part of many different initiatives that are trying to recognize and elevate the great work that physicians do and really improve their morale and reduce burnout.”