Philadelphia, PA –The Society of Hospital Medicine (SHM)’s Physician in Training Committee recently announced the 2016 Student Hospitalist Scholar Grant recipients, who earned the scholarship based on their abilities and interest in hospital medicine, prior educational training and dedication to scholarly activity in the field.

SHM’s Physician in Training Committee launched the scholarship program for medical students in 2015 to inspire future hospitalists to play an active role in transforming healthcare and revolutionizing patient care. For more information on the Student Hospitalist Scholar Grant. All information for trainees interested in hospital medicine can be found at, SHM’s website dedicated to resources for those interested in a career as a hospitalist. To join SHM as a medical student member at no cost.

The four grant recipients, each of whom is a student member of SHM, will use their funding to complete scholarly work with an active SHM member as their mentor on a project related to patient safety or quality improvement. The 2016 Student Hospitalist Scholarship recipients are:

• Shane Ali, University of Texas School of Medicine at San Antonio

  Mentor: Nilam Soni, MD

  Project: Pleural Fluid Echogenicity by Ultrasound Imaging and Computer Based Pixilation to Determine Transudative vs. Exudative Effusions

  Project Site: University of Texas Health Science Center, San Antonio, Texas

• Joseph Moo-Young, University of North Carolina School of Medicine

  Mentor: Ria Dancel, MD, FHM

  Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

  Project Site: University of North Carolina Children's Hospital

• Aram Namavar, Loyola University Chicago – Stritch School of Medicine

  Mentor: Nasim Afsar, MD, SFHM

  Project: Evaluation of Decisional Conflict as a Simple Tool to assess Risk for Readmission

  Location of Project: Ronald Reagan UCLA Medical Center, Los Angeles, CA

• Haverly Snyder, Medical College of Wisconsin

  Mentor: Kathlyn Fletcher, MD, FHM

  Project: The Trauma of Hospitalization: Identifying Causes and Potential Solutions

  Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

Throughout their experiences, the student scholars will be blogging about their projects on SHM’s official blog, The Hospital Leader, and posting in the Future of Hospital Medicine community on the Hospital Medicine Exchange (HMX), SHM’s online member engagement platform. Upon completing their projects, the students will draft progress reports and submit their findings as abstracts for the Research, Innovations and Clinical Vignettes (RIV) competition at Hospital Medicine 2017, SHM’s annual meeting to be held in Las Vegas in May.

Philadelphia, PA –The Society of Hospital Medicine (SHM)’s Physician in Training Committee recently announced the 2016 Student Hospitalist Scholar Grant recipients, who earned the scholarship based on their abilities and interest in hospital medicine, prior educational training and dedication to scholarly activity in the field.

SHM’s Physician in Training Committee launched the scholarship program for medical students in 2015 to inspire future hospitalists to play an active role in transforming healthcare and revolutionizing patient care. For more information on the Student Hospitalist Scholar Grant. All information for trainees interested in hospital medicine can be found at, SHM’s website dedicated to resources for those interested in a career as a hospitalist. To join SHM as a medical student member at no cost.

The four grant recipients, each of whom is a student member of SHM, will use their funding to complete scholarly work with an active SHM member as their mentor on a project related to patient safety or quality improvement. The 2016 Student Hospitalist Scholarship recipients are:

• Shane Ali, University of Texas School of Medicine at San Antonio

  Mentor: Nilam Soni, MD

  Project: Pleural Fluid Echogenicity by Ultrasound Imaging and Computer Based Pixilation to Determine Transudative vs. Exudative Effusions

  Project Site: University of Texas Health Science Center, San Antonio, Texas

• Joseph Moo-Young, University of North Carolina School of Medicine

  Mentor: Ria Dancel, MD, FHM

  Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

  Project Site: University of North Carolina Children's Hospital

• Aram Namavar, Loyola University Chicago – Stritch School of Medicine

  Mentor: Nasim Afsar, MD, SFHM

  Project: Evaluation of Decisional Conflict as a Simple Tool to assess Risk for Readmission

  Location of Project: Ronald Reagan UCLA Medical Center, Los Angeles, CA

• Haverly Snyder, Medical College of Wisconsin

  Mentor: Kathlyn Fletcher, MD, FHM

  Project: The Trauma of Hospitalization: Identifying Causes and Potential Solutions

  Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

Throughout their experiences, the student scholars will be blogging about their projects on SHM’s official blog, The Hospital Leader, and posting in the Future of Hospital Medicine community on the Hospital Medicine Exchange (HMX), SHM’s online member engagement platform. Upon completing their projects, the students will draft progress reports and submit their findings as abstracts for the Research, Innovations and Clinical Vignettes (RIV) competition at Hospital Medicine 2017, SHM’s annual meeting to be held in Las Vegas in May.

Philadelphia, PA –The Society of Hospital Medicine (SHM)’s Physician in Training Committee recently announced the 2016 Student Hospitalist Scholar Grant recipients, who earned the scholarship based on their abilities and interest in hospital medicine, prior educational training and dedication to scholarly activity in the field.

SHM’s Physician in Training Committee launched the scholarship program for medical students in 2015 to inspire future hospitalists to play an active role in transforming healthcare and revolutionizing patient care. For more information on the Student Hospitalist Scholar Grant. All information for trainees interested in hospital medicine can be found at, SHM’s website dedicated to resources for those interested in a career as a hospitalist. To join SHM as a medical student member at no cost.

The four grant recipients, each of whom is a student member of SHM, will use their funding to complete scholarly work with an active SHM member as their mentor on a project related to patient safety or quality improvement. The 2016 Student Hospitalist Scholarship recipients are:

• Shane Ali, University of Texas School of Medicine at San Antonio

  Mentor: Nilam Soni, MD

  Project: Pleural Fluid Echogenicity by Ultrasound Imaging and Computer Based Pixilation to Determine Transudative vs. Exudative Effusions

  Project Site: University of Texas Health Science Center, San Antonio, Texas

• Joseph Moo-Young, University of North Carolina School of Medicine

  Mentor: Ria Dancel, MD, FHM

  Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

  Project Site: University of North Carolina Children's Hospital

• Aram Namavar, Loyola University Chicago – Stritch School of Medicine

  Mentor: Nasim Afsar, MD, SFHM

  Project: Evaluation of Decisional Conflict as a Simple Tool to assess Risk for Readmission

  Location of Project: Ronald Reagan UCLA Medical Center, Los Angeles, CA

• Haverly Snyder, Medical College of Wisconsin

  Mentor: Kathlyn Fletcher, MD, FHM

  Project: The Trauma of Hospitalization: Identifying Causes and Potential Solutions

  Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

Throughout their experiences, the student scholars will be blogging about their projects on SHM’s official blog, The Hospital Leader, and posting in the Future of Hospital Medicine community on the Hospital Medicine Exchange (HMX), SHM’s online member engagement platform. Upon completing their projects, the students will draft progress reports and submit their findings as abstracts for the Research, Innovations and Clinical Vignettes (RIV) competition at Hospital Medicine 2017, SHM’s annual meeting to be held in Las Vegas in May.

The novel uricosuric drug arhalofenate significantly reduced the incidence of gout flares, compared with allopurinol alone and placebo, and also modestly lowered serum urate levels in a phase IIb trial.

However, arhalofenate alone did not lower serum uric acid levels as much as did allopurinol plus colchicine, potentially making it “better suited for a combination regimen with a xanthine-oxidase inhibitor,” first author Dr. Jeffrey Poiley of Arthritis Associates in Orlando, and his coauthors at CymaBay Therapeutics in Newark, Calif.

The double-blind, randomized, placebo- and active-drug controlled trial of 239 gout patients showed that arhalofenate at a dose of 800 mg daily significantly reduced gout flares over 12 weeks by 46% versus allopurinol at a dose of 300 mg daily (0.66 flares vs. 1.24; P = .0056) and by 41% versus placebo (0.66 vs. 1.13; P = .049).

The 12-week incidence of flares with the 800-mg dose was no better than the combination of allopurinol 300 mg with 0.6 mg colchicine a day (0.40), but the study was not powered to detect this comparison. “The clinical utility of arhalofenate 800 mg will have to be judged in the context of the respective risk/benefit ratio of each flare treatment,” the study authors said (Arthritis Rheumatol. 2016 Mar 18. doi: 101002/art.39684).

The flare rate for arhalofenate at a lower daily dose of 600 mg was not significantly different from allopurinol 300 mg without flare prophylaxis (1.04 vs. 1.24, respectively).

Secondary outcomes of the study revealed that arhalofenate had modest effects on serum urate levels, compared with allopurinol on its own and in combination with colchicine. The average percentage change in serum uric acid levels from baseline to week 12 were –12.5% with 600 mg of arhalofenate; –16.5% with 800 mg; –28.8% with allopurinol 300 mg, and –24.9% for allopurinol plus colchicine, and –0.9% with placebo.

Arhalofenate lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney via inhibition of the urate transporter 1. In animal studies of urate crystal–induced inflammation, arhalofenate suppressed the release of proinflammatory cytokines and prevented the movement of neutrophils to the site of inflammation. Prior studies of arhalofenate in gout patients treated with colchicine suggested that the drug could prevent flares, but this was impossible to prove definitively because of the simultaneous use of colchicine, the authors wrote.

The study authors will now confirm their findings in a phase III trial with a treatment regimen that combines arhalofenate with febuxostat.

Patients involved in the study had more than three flares in the previous year, had discontinued urate-lowering therapy and colchicine, and had a serum urate level of 7.5-12 mg/dL.

They were randomized in a 2:2:2:2:1 fashion to one of five treatment groups: daily arhalofenate 600 mg or 800 mg, allopurinol 300 mg, allopurinol 300 mg together with 0.6 mg of colchicine, or placebo.

The researchers said there were no meaningful differences in adverse events between treatment groups. There were no significant changes in estimated creatinine clearance in any treatment group, including no declines in any group receiving arhalofenate.

The study was sponsored by CymaBay Therapeutics. Dr. Poiley was an investigator in the study, and five other authors are employees of CymaBay.

The novel uricosuric drug arhalofenate significantly reduced the incidence of gout flares, compared with allopurinol alone and placebo, and also modestly lowered serum urate levels in a phase IIb trial.

However, arhalofenate alone did not lower serum uric acid levels as much as did allopurinol plus colchicine, potentially making it “better suited for a combination regimen with a xanthine-oxidase inhibitor,” first author Dr. Jeffrey Poiley of Arthritis Associates in Orlando, and his coauthors at CymaBay Therapeutics in Newark, Calif.

The double-blind, randomized, placebo- and active-drug controlled trial of 239 gout patients showed that arhalofenate at a dose of 800 mg daily significantly reduced gout flares over 12 weeks by 46% versus allopurinol at a dose of 300 mg daily (0.66 flares vs. 1.24; P = .0056) and by 41% versus placebo (0.66 vs. 1.13; P = .049).

The 12-week incidence of flares with the 800-mg dose was no better than the combination of allopurinol 300 mg with 0.6 mg colchicine a day (0.40), but the study was not powered to detect this comparison. “The clinical utility of arhalofenate 800 mg will have to be judged in the context of the respective risk/benefit ratio of each flare treatment,” the study authors said (Arthritis Rheumatol. 2016 Mar 18. doi: 101002/art.39684).

The flare rate for arhalofenate at a lower daily dose of 600 mg was not significantly different from allopurinol 300 mg without flare prophylaxis (1.04 vs. 1.24, respectively).

Secondary outcomes of the study revealed that arhalofenate had modest effects on serum urate levels, compared with allopurinol on its own and in combination with colchicine. The average percentage change in serum uric acid levels from baseline to week 12 were –12.5% with 600 mg of arhalofenate; –16.5% with 800 mg; –28.8% with allopurinol 300 mg, and –24.9% for allopurinol plus colchicine, and –0.9% with placebo.

Arhalofenate lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney via inhibition of the urate transporter 1. In animal studies of urate crystal–induced inflammation, arhalofenate suppressed the release of proinflammatory cytokines and prevented the movement of neutrophils to the site of inflammation. Prior studies of arhalofenate in gout patients treated with colchicine suggested that the drug could prevent flares, but this was impossible to prove definitively because of the simultaneous use of colchicine, the authors wrote.

The study authors will now confirm their findings in a phase III trial with a treatment regimen that combines arhalofenate with febuxostat.

Patients involved in the study had more than three flares in the previous year, had discontinued urate-lowering therapy and colchicine, and had a serum urate level of 7.5-12 mg/dL.

They were randomized in a 2:2:2:2:1 fashion to one of five treatment groups: daily arhalofenate 600 mg or 800 mg, allopurinol 300 mg, allopurinol 300 mg together with 0.6 mg of colchicine, or placebo.

The researchers said there were no meaningful differences in adverse events between treatment groups. There were no significant changes in estimated creatinine clearance in any treatment group, including no declines in any group receiving arhalofenate.

The study was sponsored by CymaBay Therapeutics. Dr. Poiley was an investigator in the study, and five other authors are employees of CymaBay.

The novel uricosuric drug arhalofenate significantly reduced the incidence of gout flares, compared with allopurinol alone and placebo, and also modestly lowered serum urate levels in a phase IIb trial.

However, arhalofenate alone did not lower serum uric acid levels as much as did allopurinol plus colchicine, potentially making it “better suited for a combination regimen with a xanthine-oxidase inhibitor,” first author Dr. Jeffrey Poiley of Arthritis Associates in Orlando, and his coauthors at CymaBay Therapeutics in Newark, Calif.

The double-blind, randomized, placebo- and active-drug controlled trial of 239 gout patients showed that arhalofenate at a dose of 800 mg daily significantly reduced gout flares over 12 weeks by 46% versus allopurinol at a dose of 300 mg daily (0.66 flares vs. 1.24; P = .0056) and by 41% versus placebo (0.66 vs. 1.13; P = .049).

The 12-week incidence of flares with the 800-mg dose was no better than the combination of allopurinol 300 mg with 0.6 mg colchicine a day (0.40), but the study was not powered to detect this comparison. “The clinical utility of arhalofenate 800 mg will have to be judged in the context of the respective risk/benefit ratio of each flare treatment,” the study authors said (Arthritis Rheumatol. 2016 Mar 18. doi: 101002/art.39684).

The flare rate for arhalofenate at a lower daily dose of 600 mg was not significantly different from allopurinol 300 mg without flare prophylaxis (1.04 vs. 1.24, respectively).

Secondary outcomes of the study revealed that arhalofenate had modest effects on serum urate levels, compared with allopurinol on its own and in combination with colchicine. The average percentage change in serum uric acid levels from baseline to week 12 were –12.5% with 600 mg of arhalofenate; –16.5% with 800 mg; –28.8% with allopurinol 300 mg, and –24.9% for allopurinol plus colchicine, and –0.9% with placebo.

Arhalofenate lowers serum urate by blocking its reabsorption by the proximal tubules of the kidney via inhibition of the urate transporter 1. In animal studies of urate crystal–induced inflammation, arhalofenate suppressed the release of proinflammatory cytokines and prevented the movement of neutrophils to the site of inflammation. Prior studies of arhalofenate in gout patients treated with colchicine suggested that the drug could prevent flares, but this was impossible to prove definitively because of the simultaneous use of colchicine, the authors wrote.

The study authors will now confirm their findings in a phase III trial with a treatment regimen that combines arhalofenate with febuxostat.

Patients involved in the study had more than three flares in the previous year, had discontinued urate-lowering therapy and colchicine, and had a serum urate level of 7.5-12 mg/dL.

They were randomized in a 2:2:2:2:1 fashion to one of five treatment groups: daily arhalofenate 600 mg or 800 mg, allopurinol 300 mg, allopurinol 300 mg together with 0.6 mg of colchicine, or placebo.

The researchers said there were no meaningful differences in adverse events between treatment groups. There were no significant changes in estimated creatinine clearance in any treatment group, including no declines in any group receiving arhalofenate.

The study was sponsored by CymaBay Therapeutics. Dr. Poiley was an investigator in the study, and five other authors are employees of CymaBay.

Progression to structural damage occurs slowly among patients with early axial spondyloarthritis and more often takes place in current smokers, HLAB27 carriers, and those with signs of inflammation on MRI, according to new observations from the French DESIR cohort study.

The findings help to establish risk factors for early progression of nonradiographic axial spondyloarthritis (nr-axSpA) to radiographic disease, said Dr. Maxime Dougados of the department of rheumatology at Cochin Hospital, Paris, and his colleagues (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39666).

The study involved 449 patients with recent-onset inflammatory back pain who were participating in the multicenter, longitudinal DESIR study and had x-rays available at baseline and 2-year follow-up.

A total of 16 (4.9%) out of 326 patients who did not fulfill the modified New York criteria (mNY) at baseline progressed from nonradiographic to radiographic axSpA over the 2-year study period.

Of the 123 patients who met the mNY criteria at baseline, 7 (5.7%) no longer met the criteria at follow-up.

Independent factors found to influence the odds of progressing to radiographic axSpA were smoking status (odds ratio, 3.3; 95% confidence interval, 1.0-11.5), HLAB27 positivity (OR, 12.6; 95% CI, 2.3-274), and the presence of inflammation at MRI in the sacroiliac joints (SIJs) at baseline (OR, 48.8; 95% CI, 9.3-904), a multivariate analysis showed.

However, when the authors defined radiographic progression as “a worsening of at least one grade in at least one SIJ,” HLAB27 positivity (OR, 1.68; 95% CI, 0.8-3.71, P = .02), MRI positivity (OR, 5.85; 95% CI, 2.38-15.37, P less than .001), and baseline structural damage at SIJs on pelvic x-rays (OR, 6.35; 95% CI, 2.14-18.88; P less than .001) were predictors of radiographic disease progression. Another analysis confirmed those as risk factors even when the definition of progression also required a final absolute grade of at least 2 in the worsened SIJs.

When the authors considered the change in total score (based on the mean of two readers), only HLAB27 positivity and baseline MRI positivity were highlighted as independent predictors of disease progression. In this analysis, HLAB27 positivity and inflammation on MRI had grading score increases of 0.41 (P = .014) and 1.03 (P less than .001), respectively.

Unlike other studies, the researchers did not see a clear relationship between abnormal C-reactive protein at baseline and radiographic progression.

The findings suggest that, in early SpA, “structural progression does exist but is quite small and observed in a small number of patients,” the study authors wrote.

The authors noted that their findings should be “interpreted with caution” because they were based on a small number of patients, and additional studies with a longer-follow-up period are needed to confirm the findings.

The DESIR cohort was sponsored by the Department de la recherché Clinique et du Development de l’Assistance Publique-Hopitaux de Paris. An unrestricted grant from Pfizer was allocated for the 10 years of follow-up.

Progression to structural damage occurs slowly among patients with early axial spondyloarthritis and more often takes place in current smokers, HLAB27 carriers, and those with signs of inflammation on MRI, according to new observations from the French DESIR cohort study.

The findings help to establish risk factors for early progression of nonradiographic axial spondyloarthritis (nr-axSpA) to radiographic disease, said Dr. Maxime Dougados of the department of rheumatology at Cochin Hospital, Paris, and his colleagues (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39666).

The study involved 449 patients with recent-onset inflammatory back pain who were participating in the multicenter, longitudinal DESIR study and had x-rays available at baseline and 2-year follow-up.

A total of 16 (4.9%) out of 326 patients who did not fulfill the modified New York criteria (mNY) at baseline progressed from nonradiographic to radiographic axSpA over the 2-year study period.

Of the 123 patients who met the mNY criteria at baseline, 7 (5.7%) no longer met the criteria at follow-up.

Independent factors found to influence the odds of progressing to radiographic axSpA were smoking status (odds ratio, 3.3; 95% confidence interval, 1.0-11.5), HLAB27 positivity (OR, 12.6; 95% CI, 2.3-274), and the presence of inflammation at MRI in the sacroiliac joints (SIJs) at baseline (OR, 48.8; 95% CI, 9.3-904), a multivariate analysis showed.

However, when the authors defined radiographic progression as “a worsening of at least one grade in at least one SIJ,” HLAB27 positivity (OR, 1.68; 95% CI, 0.8-3.71, P = .02), MRI positivity (OR, 5.85; 95% CI, 2.38-15.37, P less than .001), and baseline structural damage at SIJs on pelvic x-rays (OR, 6.35; 95% CI, 2.14-18.88; P less than .001) were predictors of radiographic disease progression. Another analysis confirmed those as risk factors even when the definition of progression also required a final absolute grade of at least 2 in the worsened SIJs.

When the authors considered the change in total score (based on the mean of two readers), only HLAB27 positivity and baseline MRI positivity were highlighted as independent predictors of disease progression. In this analysis, HLAB27 positivity and inflammation on MRI had grading score increases of 0.41 (P = .014) and 1.03 (P less than .001), respectively.

Unlike other studies, the researchers did not see a clear relationship between abnormal C-reactive protein at baseline and radiographic progression.

The findings suggest that, in early SpA, “structural progression does exist but is quite small and observed in a small number of patients,” the study authors wrote.

The authors noted that their findings should be “interpreted with caution” because they were based on a small number of patients, and additional studies with a longer-follow-up period are needed to confirm the findings.

The DESIR cohort was sponsored by the Department de la recherché Clinique et du Development de l’Assistance Publique-Hopitaux de Paris. An unrestricted grant from Pfizer was allocated for the 10 years of follow-up.

Progression to structural damage occurs slowly among patients with early axial spondyloarthritis and more often takes place in current smokers, HLAB27 carriers, and those with signs of inflammation on MRI, according to new observations from the French DESIR cohort study.

The findings help to establish risk factors for early progression of nonradiographic axial spondyloarthritis (nr-axSpA) to radiographic disease, said Dr. Maxime Dougados of the department of rheumatology at Cochin Hospital, Paris, and his colleagues (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39666).

The study involved 449 patients with recent-onset inflammatory back pain who were participating in the multicenter, longitudinal DESIR study and had x-rays available at baseline and 2-year follow-up.

A total of 16 (4.9%) out of 326 patients who did not fulfill the modified New York criteria (mNY) at baseline progressed from nonradiographic to radiographic axSpA over the 2-year study period.

Of the 123 patients who met the mNY criteria at baseline, 7 (5.7%) no longer met the criteria at follow-up.

Independent factors found to influence the odds of progressing to radiographic axSpA were smoking status (odds ratio, 3.3; 95% confidence interval, 1.0-11.5), HLAB27 positivity (OR, 12.6; 95% CI, 2.3-274), and the presence of inflammation at MRI in the sacroiliac joints (SIJs) at baseline (OR, 48.8; 95% CI, 9.3-904), a multivariate analysis showed.

However, when the authors defined radiographic progression as “a worsening of at least one grade in at least one SIJ,” HLAB27 positivity (OR, 1.68; 95% CI, 0.8-3.71, P = .02), MRI positivity (OR, 5.85; 95% CI, 2.38-15.37, P less than .001), and baseline structural damage at SIJs on pelvic x-rays (OR, 6.35; 95% CI, 2.14-18.88; P less than .001) were predictors of radiographic disease progression. Another analysis confirmed those as risk factors even when the definition of progression also required a final absolute grade of at least 2 in the worsened SIJs.

When the authors considered the change in total score (based on the mean of two readers), only HLAB27 positivity and baseline MRI positivity were highlighted as independent predictors of disease progression. In this analysis, HLAB27 positivity and inflammation on MRI had grading score increases of 0.41 (P = .014) and 1.03 (P less than .001), respectively.

Unlike other studies, the researchers did not see a clear relationship between abnormal C-reactive protein at baseline and radiographic progression.

The findings suggest that, in early SpA, “structural progression does exist but is quite small and observed in a small number of patients,” the study authors wrote.

The authors noted that their findings should be “interpreted with caution” because they were based on a small number of patients, and additional studies with a longer-follow-up period are needed to confirm the findings.

The DESIR cohort was sponsored by the Department de la recherché Clinique et du Development de l’Assistance Publique-Hopitaux de Paris. An unrestricted grant from Pfizer was allocated for the 10 years of follow-up.

NEW YORK (Reuters Health) - In the absence of a congenital anomaly, the main cause of inferior vena cava (IVC) thrombosis is the presence of an unretrieved IVC filter, researchers report.

"Since IVC filter thrombosis is the main etiology for IVC thrombosis, physicians may want to ensure the absolute need for the filter before its placement," Dr. Mohamad Alkhouli from University of Rochester Medical Center, New York told Reuters Health by email. "A tracking system should be instituted to follow up with these patients, and the implanted IVC filter should be pulled out as soon as is safe and reasonable."

IVC thrombosis accompanies lower extremity deep vein thrombosis (DVT) in 4% or more of patients, leading to post-thrombotic syndrome (PTS) in up to 90% of patients, disabling venous claudication in 45%, pulmonary embolism in 30%, and venous ulceration in 15%, according to Dr. Alkhouli and colleagues, who reviewed the diagnosis and management of IVC thrombosis in a report online March 9th in JACC: Cardiovascular Interventions.

IVC filter placement rates are 25 times higher in the U.S. than in Europe, and late filter thrombosis has been reported in up to a third of patients, yet retrieval rates are consistently low.

Presenting symptoms of IVC thrombosis include leg heaviness, pain, swelling, and cramping, often preceded by nonspecific back and abdominal/pelvic pain. Because of the ambiguous symptoms and insidious onset, IVC thrombosis often goes undiagnosed until clot migration or embolization into the lungs and renal veins results in dyspnea and oliguria.

Lower extremity duplex ultrasound can be used to screen for IVC thrombosis, but appropriately timed CT and MRI are essential for diagnosis and assessment of the extent of thrombosis.

Once IVC thrombosis is diagnosed, the mainstay of treatment is anticoagulation, although specific guidelines are lacking.

In observational studies, thrombus removal with pharmacomechanical catheter directed thrombolysis (PMCT) has reduced the incidence of PTS and improved quality of life, but whether this is as safe as standard anticoagulation remains unclear.

While acute thrombosis may be amenable to PMCT and catheter-directed thrombolysis (CDT), the presence of a fibrotic component in patients who present late may require balloon venoplasty with or without stenting.

The available treatments work best when IVC thrombosis is recognized early, Dr. Alkhouli said.

Dr. Michael Jaff from Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, who wrote an editorial related to this report, told Reuters Health by email, "Limit placement of IVC filters to only absolute indications, and retrieve them as soon as possible."

Dr. Jaff explained, "There are three basic questions I ask myself when considering catheter-based intervention for IVC thrombosis: (1) How long has the patient had symptoms/signs suggestive of this, and how severe are they? (2) What is my estimation of bleeding risk? (3) Do I have an interventionist with skill and experience available to perform the intervention?"

He continued, "Regarding question 1, shorter duration of symptoms and more severe symptoms and signs prompt me to aggressively consider catheter-based intervention. Regarding question 2, if there is significant bleeding risk (for example, inflammatory bowel disease as the underlying culprit for the IVC thrombosis), I am reluctant to consider catheter-based intervention.Regarding question 3, don't consider this if your colleague has little experience performing this procedure or managing the complications of the procedure."

Dr. Xiao-Qiang Li from Second Affiliated Hospital of Soochow University in Suzhou, China, who recently described the experience with CDT combined with manual aspiration thrombectomy for acute inferior vena cava filter thrombosis, told Reuters Health by email, "As you see, no consensuses have been reached."

 

"For a new patient with acute DVT, if he or she has no contraindications for thrombolysis, especially with a life expectancy more than one year, we prefer to perform catheter-based interventions, including catheter-directed thrombolysis, pharmacomechanical thrombolysis, ultrasound-assisted catheter-directed thrombolysis and subsequent percutaneous transluminal angioplasty and stenting,"Dr. Li said."But, of note, anticoagulation is the basic treatment whatever catheter-based interventions are adopted."

 

 

 

 

NEW YORK (Reuters Health) - In the absence of a congenital anomaly, the main cause of inferior vena cava (IVC) thrombosis is the presence of an unretrieved IVC filter, researchers report.

"Since IVC filter thrombosis is the main etiology for IVC thrombosis, physicians may want to ensure the absolute need for the filter before its placement," Dr. Mohamad Alkhouli from University of Rochester Medical Center, New York told Reuters Health by email. "A tracking system should be instituted to follow up with these patients, and the implanted IVC filter should be pulled out as soon as is safe and reasonable."

IVC thrombosis accompanies lower extremity deep vein thrombosis (DVT) in 4% or more of patients, leading to post-thrombotic syndrome (PTS) in up to 90% of patients, disabling venous claudication in 45%, pulmonary embolism in 30%, and venous ulceration in 15%, according to Dr. Alkhouli and colleagues, who reviewed the diagnosis and management of IVC thrombosis in a report online March 9th in JACC: Cardiovascular Interventions.

IVC filter placement rates are 25 times higher in the U.S. than in Europe, and late filter thrombosis has been reported in up to a third of patients, yet retrieval rates are consistently low.

Presenting symptoms of IVC thrombosis include leg heaviness, pain, swelling, and cramping, often preceded by nonspecific back and abdominal/pelvic pain. Because of the ambiguous symptoms and insidious onset, IVC thrombosis often goes undiagnosed until clot migration or embolization into the lungs and renal veins results in dyspnea and oliguria.

Lower extremity duplex ultrasound can be used to screen for IVC thrombosis, but appropriately timed CT and MRI are essential for diagnosis and assessment of the extent of thrombosis.

Once IVC thrombosis is diagnosed, the mainstay of treatment is anticoagulation, although specific guidelines are lacking.

In observational studies, thrombus removal with pharmacomechanical catheter directed thrombolysis (PMCT) has reduced the incidence of PTS and improved quality of life, but whether this is as safe as standard anticoagulation remains unclear.

While acute thrombosis may be amenable to PMCT and catheter-directed thrombolysis (CDT), the presence of a fibrotic component in patients who present late may require balloon venoplasty with or without stenting.

The available treatments work best when IVC thrombosis is recognized early, Dr. Alkhouli said.

Dr. Michael Jaff from Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, who wrote an editorial related to this report, told Reuters Health by email, "Limit placement of IVC filters to only absolute indications, and retrieve them as soon as possible."

Dr. Jaff explained, "There are three basic questions I ask myself when considering catheter-based intervention for IVC thrombosis: (1) How long has the patient had symptoms/signs suggestive of this, and how severe are they? (2) What is my estimation of bleeding risk? (3) Do I have an interventionist with skill and experience available to perform the intervention?"

He continued, "Regarding question 1, shorter duration of symptoms and more severe symptoms and signs prompt me to aggressively consider catheter-based intervention. Regarding question 2, if there is significant bleeding risk (for example, inflammatory bowel disease as the underlying culprit for the IVC thrombosis), I am reluctant to consider catheter-based intervention.Regarding question 3, don't consider this if your colleague has little experience performing this procedure or managing the complications of the procedure."

Dr. Xiao-Qiang Li from Second Affiliated Hospital of Soochow University in Suzhou, China, who recently described the experience with CDT combined with manual aspiration thrombectomy for acute inferior vena cava filter thrombosis, told Reuters Health by email, "As you see, no consensuses have been reached."

 

"For a new patient with acute DVT, if he or she has no contraindications for thrombolysis, especially with a life expectancy more than one year, we prefer to perform catheter-based interventions, including catheter-directed thrombolysis, pharmacomechanical thrombolysis, ultrasound-assisted catheter-directed thrombolysis and subsequent percutaneous transluminal angioplasty and stenting,"Dr. Li said."But, of note, anticoagulation is the basic treatment whatever catheter-based interventions are adopted."

 

 

 

 

NEW YORK (Reuters Health) - In the absence of a congenital anomaly, the main cause of inferior vena cava (IVC) thrombosis is the presence of an unretrieved IVC filter, researchers report.

"Since IVC filter thrombosis is the main etiology for IVC thrombosis, physicians may want to ensure the absolute need for the filter before its placement," Dr. Mohamad Alkhouli from University of Rochester Medical Center, New York told Reuters Health by email. "A tracking system should be instituted to follow up with these patients, and the implanted IVC filter should be pulled out as soon as is safe and reasonable."

IVC thrombosis accompanies lower extremity deep vein thrombosis (DVT) in 4% or more of patients, leading to post-thrombotic syndrome (PTS) in up to 90% of patients, disabling venous claudication in 45%, pulmonary embolism in 30%, and venous ulceration in 15%, according to Dr. Alkhouli and colleagues, who reviewed the diagnosis and management of IVC thrombosis in a report online March 9th in JACC: Cardiovascular Interventions.

IVC filter placement rates are 25 times higher in the U.S. than in Europe, and late filter thrombosis has been reported in up to a third of patients, yet retrieval rates are consistently low.

Presenting symptoms of IVC thrombosis include leg heaviness, pain, swelling, and cramping, often preceded by nonspecific back and abdominal/pelvic pain. Because of the ambiguous symptoms and insidious onset, IVC thrombosis often goes undiagnosed until clot migration or embolization into the lungs and renal veins results in dyspnea and oliguria.

Lower extremity duplex ultrasound can be used to screen for IVC thrombosis, but appropriately timed CT and MRI are essential for diagnosis and assessment of the extent of thrombosis.

Once IVC thrombosis is diagnosed, the mainstay of treatment is anticoagulation, although specific guidelines are lacking.

In observational studies, thrombus removal with pharmacomechanical catheter directed thrombolysis (PMCT) has reduced the incidence of PTS and improved quality of life, but whether this is as safe as standard anticoagulation remains unclear.

While acute thrombosis may be amenable to PMCT and catheter-directed thrombolysis (CDT), the presence of a fibrotic component in patients who present late may require balloon venoplasty with or without stenting.

The available treatments work best when IVC thrombosis is recognized early, Dr. Alkhouli said.

Dr. Michael Jaff from Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, who wrote an editorial related to this report, told Reuters Health by email, "Limit placement of IVC filters to only absolute indications, and retrieve them as soon as possible."

Dr. Jaff explained, "There are three basic questions I ask myself when considering catheter-based intervention for IVC thrombosis: (1) How long has the patient had symptoms/signs suggestive of this, and how severe are they? (2) What is my estimation of bleeding risk? (3) Do I have an interventionist with skill and experience available to perform the intervention?"

He continued, "Regarding question 1, shorter duration of symptoms and more severe symptoms and signs prompt me to aggressively consider catheter-based intervention. Regarding question 2, if there is significant bleeding risk (for example, inflammatory bowel disease as the underlying culprit for the IVC thrombosis), I am reluctant to consider catheter-based intervention.Regarding question 3, don't consider this if your colleague has little experience performing this procedure or managing the complications of the procedure."

Dr. Xiao-Qiang Li from Second Affiliated Hospital of Soochow University in Suzhou, China, who recently described the experience with CDT combined with manual aspiration thrombectomy for acute inferior vena cava filter thrombosis, told Reuters Health by email, "As you see, no consensuses have been reached."

 

"For a new patient with acute DVT, if he or she has no contraindications for thrombolysis, especially with a life expectancy more than one year, we prefer to perform catheter-based interventions, including catheter-directed thrombolysis, pharmacomechanical thrombolysis, ultrasound-assisted catheter-directed thrombolysis and subsequent percutaneous transluminal angioplasty and stenting,"Dr. Li said."But, of note, anticoagulation is the basic treatment whatever catheter-based interventions are adopted."

 

 

 

 

Thanks to everyone who showed their commitment to fighting antibiotic resistance at HM16 in San Diego by signing our “Fight the Resistance” posters at the SHM booth. Wear your “Fight the Resistance” pin with pride, and don’t forget to hang the campaign posters in your hospital.

If you missed HM16 but still want to show your support, visit www.FightTheResistance.org to review SHM’s recommendations for promoting antibiotic stewardship, download copies of our three posters, and submit your case study about how you’re fighting antibiotic resistance in your hospital.

Continue to check www.FightTheResistance.org and follow the #FightTheResistance hashtag on Twitter to learn about new SHM resources to help you continue the fight.

Thanks to everyone who showed their commitment to fighting antibiotic resistance at HM16 in San Diego by signing our “Fight the Resistance” posters at the SHM booth. Wear your “Fight the Resistance” pin with pride, and don’t forget to hang the campaign posters in your hospital.

If you missed HM16 but still want to show your support, visit www.FightTheResistance.org to review SHM’s recommendations for promoting antibiotic stewardship, download copies of our three posters, and submit your case study about how you’re fighting antibiotic resistance in your hospital.

Continue to check www.FightTheResistance.org and follow the #FightTheResistance hashtag on Twitter to learn about new SHM resources to help you continue the fight.

Thanks to everyone who showed their commitment to fighting antibiotic resistance at HM16 in San Diego by signing our “Fight the Resistance” posters at the SHM booth. Wear your “Fight the Resistance” pin with pride, and don’t forget to hang the campaign posters in your hospital.

If you missed HM16 but still want to show your support, visit www.FightTheResistance.org to review SHM’s recommendations for promoting antibiotic stewardship, download copies of our three posters, and submit your case study about how you’re fighting antibiotic resistance in your hospital.

Continue to check www.FightTheResistance.org and follow the #FightTheResistance hashtag on Twitter to learn about new SHM resources to help you continue the fight.

Editor’s note: As SHM celebrates the “Year of the Hospitalist,” we’re putting the spotlight on some of our most active members who are making substantial contributions to hospital medicine. You can get involved, too! Log on to www.hospitalmedicine.org/yoth for more information on how you can join the yearlong celebration and help SHM improve the care of hospitalized patients.

Hospitalist Jerome C. Siy, MD, SFHM, CHIE, is head of the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul, Minn., and chair of SHM’s Practice Management Committee. As a member of SHM for more than 15 years and recipient of SHM’s prestigious Award of Excellence for Clinical Excellence in 2009, Dr. Siy has been a driving force in advancing hospitalist practice and improving patient care in the U.S. and beyond.

Question: What led you to a career in hospital medicine?

Answer: After graduating from the Mayo Graduate School of Medical Education, I started in the med-peds residency program at the University of Minnesota and then transitioned to an internal medicine residency program. It was at the University of Minnesota that I recognized my intense passion for the care of acutely ill hospitalized patients. During my residency, I had the good fortune of finding exceptional hospitalist role models in my program. As I worked with them, my passion for working with hospitalized patients continued to grow; I realized that my ideal job was to work with this group of doctors that I so greatly admired. In 2000, I joined the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul and now proudly lead the department.

Q: When did you first get involved with SHM? What value does it bring to your daily practice?

A: When I first joined HealthPartners, Dr. Rusty Holman was our director. He was extremely active in the early days of SHM, when it was known as the National Association of Inpatient Physicians (NAIP). Our team at HealthPartners was fairly small, between 15 and 18 hospitalists, and identified early on with the hospital medicine specialty and NAIP. Many of them are still engaged with SHM 16 years later. As a team, we continue to encourage our entire group of over 90 practitioners, including our PAs and NPs, to get involved with SHM.

At SHM, chances to connect with people exist everywhere. So many hospitalists tell stories about how they went to an SHM meeting and ran into an old friend or medical school colleague that they didn’t realize was a hospitalist. That’s exactly why the SHM community is a fertile ground to build and expand upon ideas for your own program. For example, at HealthPartners, we are embarking on early work with telemedicine. With the network of hospitalists at SHM, I immediately knew colleagues who were working in hospital medicine and was able to visit some of them at their telemedicine specialty center.

Whether you join committees, give a joint lecture, or attend a session at an annual meeting with someone, you are opening yourself up to collaboration that will ultimately lead to better care for patients.

Q: What is one of the most unique or rewarding experiences you have had while practicing hospital medicine?

A: After 10 years at HealthPartners, I took a personal sabbatical to study Chinese in Taiwan for eight months. Even though I was away from my hospital, hospital medicine followed me overseas. While in Asia, I visited contacts in Taiwan and Japan. With the U.S. government just rolling out the Affordable Care Act, I wanted to gain a better understanding of how nationalized healthcare programs impacted care providers and care delivery.

 

While visiting the University of Osaka and one of the earliest hospital medicine groups at National Taiwan University Hospital, I had the opportunity to explore how a nation’s healthcare system impacted physicians and patients outside the U.S. A major takeaway for me was how important it is for physicians and care providers to be an active part of the healthcare system to create change that can influence the way they practice—and ultimately improve patient care.

In East Asia, whenever there was concern about evolving their healthcare models and the way providers take care of patients, physicians often felt limited in their potential impact. Culturally, senior physicians are the ones more apt to network and influence policy changes. The more physicians felt empowered to influence these senior leaders to address these issues with government officials, the better the chances of driving positive change.

As luck would have it, a hospitalist colleague invited me back to National Taiwan University Hospital in December 2015 to share my knowledge of how the specialty can continue to evolve, taking into consideration the challenges of navigating healthcare systems, physician engagement, and burnout. Even though many of their programs are relatively new, I stressed the fact that the more interactive you are with your healthcare system, the better your chances of engaging the right stakeholders and effectively influencing healthcare policy.

While their definition of burnout may differ slightly from ours in the U.S., they wanted to hear about what we experience in the U.S. and how we address it. I was able to share some techniques we are implementing at HealthPartners to minimize burnout and maximize engagement, including regular department meetings, during which there is an open forum for hot topics. This provides the care team with an avenue to express concerns or address important topics affecting their daily practice. We also have an internal website, where our team can access a repository of resources and a discussion board to share challenges, concerns, and best practices. I also emphasized the importance of professional development and investing in staff to improve their professional career and their patient care.

Q: What are some initiatives you are currently working on that you see having a substantial impact in hospital medicine?

A: As part of the Practice Management Committee at SHM, we are exploring opportunities in telemedicine, especially as it relates to rural care. Telemedicine could be the next big step to provide support for rural hospitalists and rural communities. Geographically speaking, the vast majority of the U.S. is rural, and SHM is poised to have a great impact on the clinicians serving these communities.

Another initiative the committee is working on is developing an update to co-management best practices. As hospital medicine has matured, its scope has changed dramatically, and so has the idea of co-management. We must truly embrace opportunities to improve care across specialties. This is especially important as we welcome younger physicians to the specialty who have not had the benefit of witnessing the evolution of the practice. They need to have a firm hold on the varied daily interactions of a hospitalist and their ultimate impact on outcomes.

At HealthPartners, we are actively addressing hospitalist engagement and burnout. We are mindful of how much our health systems have evolved and how much extra work they have asked us to accommodate. To be proactive, we are trying to be much more creative and innovative with our staffing model and our use of scarce resources in order to provide the best patient care possible. Over the last 16 years, we have worked hard to continue to develop our program but, more important, develop our patient care through the development of our physicians, NPs, and PAs. This includes developing a pathway for residents who wish to become hospitalists, introducing vigorous training for PAs during their student and post-graduate years, and providing staff with the professional development resources they need to expand their skills and knowledge base and stay up-to-date on the latest advances in medicine—whether that is through leadership development or skill straining like point-of-care ultrasound.

 

Hospital medicine has matured and grown, and our scope has changed dramatically to include observation care, research and academic medicine, telemedicine, palliative care, perioperative medicine, and more. At HealthPartners, we are embracing the opportunity to grow in scope and improve care across specialties.

Q: Given your experience in the U.S. and abroad, what words of advice would you give to medical students and residents considering a career in hospital medicine?

A: As you enter this career out of training, recognize that your potential impact is greater than you ever imagined in medical school. As you continue to grow in your career and make it your own, you will make lasting impacts on your patients and also be extremely creative in what you do. Just as the specialty continues to evolve, so will you. Keep an open mind and embrace the many opportunities that come your way. TH

---

Brett Radler is SHM’s communications coordinator.

Editor’s note: As SHM celebrates the “Year of the Hospitalist,” we’re putting the spotlight on some of our most active members who are making substantial contributions to hospital medicine. You can get involved, too! Log on to www.hospitalmedicine.org/yoth for more information on how you can join the yearlong celebration and help SHM improve the care of hospitalized patients.

Hospitalist Jerome C. Siy, MD, SFHM, CHIE, is head of the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul, Minn., and chair of SHM’s Practice Management Committee. As a member of SHM for more than 15 years and recipient of SHM’s prestigious Award of Excellence for Clinical Excellence in 2009, Dr. Siy has been a driving force in advancing hospitalist practice and improving patient care in the U.S. and beyond.

Question: What led you to a career in hospital medicine?

Answer: After graduating from the Mayo Graduate School of Medical Education, I started in the med-peds residency program at the University of Minnesota and then transitioned to an internal medicine residency program. It was at the University of Minnesota that I recognized my intense passion for the care of acutely ill hospitalized patients. During my residency, I had the good fortune of finding exceptional hospitalist role models in my program. As I worked with them, my passion for working with hospitalized patients continued to grow; I realized that my ideal job was to work with this group of doctors that I so greatly admired. In 2000, I joined the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul and now proudly lead the department.

Q: When did you first get involved with SHM? What value does it bring to your daily practice?

A: When I first joined HealthPartners, Dr. Rusty Holman was our director. He was extremely active in the early days of SHM, when it was known as the National Association of Inpatient Physicians (NAIP). Our team at HealthPartners was fairly small, between 15 and 18 hospitalists, and identified early on with the hospital medicine specialty and NAIP. Many of them are still engaged with SHM 16 years later. As a team, we continue to encourage our entire group of over 90 practitioners, including our PAs and NPs, to get involved with SHM.

At SHM, chances to connect with people exist everywhere. So many hospitalists tell stories about how they went to an SHM meeting and ran into an old friend or medical school colleague that they didn’t realize was a hospitalist. That’s exactly why the SHM community is a fertile ground to build and expand upon ideas for your own program. For example, at HealthPartners, we are embarking on early work with telemedicine. With the network of hospitalists at SHM, I immediately knew colleagues who were working in hospital medicine and was able to visit some of them at their telemedicine specialty center.

Whether you join committees, give a joint lecture, or attend a session at an annual meeting with someone, you are opening yourself up to collaboration that will ultimately lead to better care for patients.

Q: What is one of the most unique or rewarding experiences you have had while practicing hospital medicine?

A: After 10 years at HealthPartners, I took a personal sabbatical to study Chinese in Taiwan for eight months. Even though I was away from my hospital, hospital medicine followed me overseas. While in Asia, I visited contacts in Taiwan and Japan. With the U.S. government just rolling out the Affordable Care Act, I wanted to gain a better understanding of how nationalized healthcare programs impacted care providers and care delivery.

 

While visiting the University of Osaka and one of the earliest hospital medicine groups at National Taiwan University Hospital, I had the opportunity to explore how a nation’s healthcare system impacted physicians and patients outside the U.S. A major takeaway for me was how important it is for physicians and care providers to be an active part of the healthcare system to create change that can influence the way they practice—and ultimately improve patient care.

In East Asia, whenever there was concern about evolving their healthcare models and the way providers take care of patients, physicians often felt limited in their potential impact. Culturally, senior physicians are the ones more apt to network and influence policy changes. The more physicians felt empowered to influence these senior leaders to address these issues with government officials, the better the chances of driving positive change.

As luck would have it, a hospitalist colleague invited me back to National Taiwan University Hospital in December 2015 to share my knowledge of how the specialty can continue to evolve, taking into consideration the challenges of navigating healthcare systems, physician engagement, and burnout. Even though many of their programs are relatively new, I stressed the fact that the more interactive you are with your healthcare system, the better your chances of engaging the right stakeholders and effectively influencing healthcare policy.

While their definition of burnout may differ slightly from ours in the U.S., they wanted to hear about what we experience in the U.S. and how we address it. I was able to share some techniques we are implementing at HealthPartners to minimize burnout and maximize engagement, including regular department meetings, during which there is an open forum for hot topics. This provides the care team with an avenue to express concerns or address important topics affecting their daily practice. We also have an internal website, where our team can access a repository of resources and a discussion board to share challenges, concerns, and best practices. I also emphasized the importance of professional development and investing in staff to improve their professional career and their patient care.

Q: What are some initiatives you are currently working on that you see having a substantial impact in hospital medicine?

A: As part of the Practice Management Committee at SHM, we are exploring opportunities in telemedicine, especially as it relates to rural care. Telemedicine could be the next big step to provide support for rural hospitalists and rural communities. Geographically speaking, the vast majority of the U.S. is rural, and SHM is poised to have a great impact on the clinicians serving these communities.

Another initiative the committee is working on is developing an update to co-management best practices. As hospital medicine has matured, its scope has changed dramatically, and so has the idea of co-management. We must truly embrace opportunities to improve care across specialties. This is especially important as we welcome younger physicians to the specialty who have not had the benefit of witnessing the evolution of the practice. They need to have a firm hold on the varied daily interactions of a hospitalist and their ultimate impact on outcomes.

At HealthPartners, we are actively addressing hospitalist engagement and burnout. We are mindful of how much our health systems have evolved and how much extra work they have asked us to accommodate. To be proactive, we are trying to be much more creative and innovative with our staffing model and our use of scarce resources in order to provide the best patient care possible. Over the last 16 years, we have worked hard to continue to develop our program but, more important, develop our patient care through the development of our physicians, NPs, and PAs. This includes developing a pathway for residents who wish to become hospitalists, introducing vigorous training for PAs during their student and post-graduate years, and providing staff with the professional development resources they need to expand their skills and knowledge base and stay up-to-date on the latest advances in medicine—whether that is through leadership development or skill straining like point-of-care ultrasound.

 

Hospital medicine has matured and grown, and our scope has changed dramatically to include observation care, research and academic medicine, telemedicine, palliative care, perioperative medicine, and more. At HealthPartners, we are embracing the opportunity to grow in scope and improve care across specialties.

Q: Given your experience in the U.S. and abroad, what words of advice would you give to medical students and residents considering a career in hospital medicine?

A: As you enter this career out of training, recognize that your potential impact is greater than you ever imagined in medical school. As you continue to grow in your career and make it your own, you will make lasting impacts on your patients and also be extremely creative in what you do. Just as the specialty continues to evolve, so will you. Keep an open mind and embrace the many opportunities that come your way. TH

---

Brett Radler is SHM’s communications coordinator.

Editor’s note: As SHM celebrates the “Year of the Hospitalist,” we’re putting the spotlight on some of our most active members who are making substantial contributions to hospital medicine. You can get involved, too! Log on to www.hospitalmedicine.org/yoth for more information on how you can join the yearlong celebration and help SHM improve the care of hospitalized patients.

Hospitalist Jerome C. Siy, MD, SFHM, CHIE, is head of the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul, Minn., and chair of SHM’s Practice Management Committee. As a member of SHM for more than 15 years and recipient of SHM’s prestigious Award of Excellence for Clinical Excellence in 2009, Dr. Siy has been a driving force in advancing hospitalist practice and improving patient care in the U.S. and beyond.

Question: What led you to a career in hospital medicine?

Answer: After graduating from the Mayo Graduate School of Medical Education, I started in the med-peds residency program at the University of Minnesota and then transitioned to an internal medicine residency program. It was at the University of Minnesota that I recognized my intense passion for the care of acutely ill hospitalized patients. During my residency, I had the good fortune of finding exceptional hospitalist role models in my program. As I worked with them, my passion for working with hospitalized patients continued to grow; I realized that my ideal job was to work with this group of doctors that I so greatly admired. In 2000, I joined the Department of Hospital Medicine at HealthPartners in Minneapolis-St. Paul and now proudly lead the department.

Q: When did you first get involved with SHM? What value does it bring to your daily practice?

A: When I first joined HealthPartners, Dr. Rusty Holman was our director. He was extremely active in the early days of SHM, when it was known as the National Association of Inpatient Physicians (NAIP). Our team at HealthPartners was fairly small, between 15 and 18 hospitalists, and identified early on with the hospital medicine specialty and NAIP. Many of them are still engaged with SHM 16 years later. As a team, we continue to encourage our entire group of over 90 practitioners, including our PAs and NPs, to get involved with SHM.

At SHM, chances to connect with people exist everywhere. So many hospitalists tell stories about how they went to an SHM meeting and ran into an old friend or medical school colleague that they didn’t realize was a hospitalist. That’s exactly why the SHM community is a fertile ground to build and expand upon ideas for your own program. For example, at HealthPartners, we are embarking on early work with telemedicine. With the network of hospitalists at SHM, I immediately knew colleagues who were working in hospital medicine and was able to visit some of them at their telemedicine specialty center.

Whether you join committees, give a joint lecture, or attend a session at an annual meeting with someone, you are opening yourself up to collaboration that will ultimately lead to better care for patients.

Q: What is one of the most unique or rewarding experiences you have had while practicing hospital medicine?

A: After 10 years at HealthPartners, I took a personal sabbatical to study Chinese in Taiwan for eight months. Even though I was away from my hospital, hospital medicine followed me overseas. While in Asia, I visited contacts in Taiwan and Japan. With the U.S. government just rolling out the Affordable Care Act, I wanted to gain a better understanding of how nationalized healthcare programs impacted care providers and care delivery.

 

While visiting the University of Osaka and one of the earliest hospital medicine groups at National Taiwan University Hospital, I had the opportunity to explore how a nation’s healthcare system impacted physicians and patients outside the U.S. A major takeaway for me was how important it is for physicians and care providers to be an active part of the healthcare system to create change that can influence the way they practice—and ultimately improve patient care.

In East Asia, whenever there was concern about evolving their healthcare models and the way providers take care of patients, physicians often felt limited in their potential impact. Culturally, senior physicians are the ones more apt to network and influence policy changes. The more physicians felt empowered to influence these senior leaders to address these issues with government officials, the better the chances of driving positive change.

As luck would have it, a hospitalist colleague invited me back to National Taiwan University Hospital in December 2015 to share my knowledge of how the specialty can continue to evolve, taking into consideration the challenges of navigating healthcare systems, physician engagement, and burnout. Even though many of their programs are relatively new, I stressed the fact that the more interactive you are with your healthcare system, the better your chances of engaging the right stakeholders and effectively influencing healthcare policy.

While their definition of burnout may differ slightly from ours in the U.S., they wanted to hear about what we experience in the U.S. and how we address it. I was able to share some techniques we are implementing at HealthPartners to minimize burnout and maximize engagement, including regular department meetings, during which there is an open forum for hot topics. This provides the care team with an avenue to express concerns or address important topics affecting their daily practice. We also have an internal website, where our team can access a repository of resources and a discussion board to share challenges, concerns, and best practices. I also emphasized the importance of professional development and investing in staff to improve their professional career and their patient care.

Q: What are some initiatives you are currently working on that you see having a substantial impact in hospital medicine?

A: As part of the Practice Management Committee at SHM, we are exploring opportunities in telemedicine, especially as it relates to rural care. Telemedicine could be the next big step to provide support for rural hospitalists and rural communities. Geographically speaking, the vast majority of the U.S. is rural, and SHM is poised to have a great impact on the clinicians serving these communities.

Another initiative the committee is working on is developing an update to co-management best practices. As hospital medicine has matured, its scope has changed dramatically, and so has the idea of co-management. We must truly embrace opportunities to improve care across specialties. This is especially important as we welcome younger physicians to the specialty who have not had the benefit of witnessing the evolution of the practice. They need to have a firm hold on the varied daily interactions of a hospitalist and their ultimate impact on outcomes.

At HealthPartners, we are actively addressing hospitalist engagement and burnout. We are mindful of how much our health systems have evolved and how much extra work they have asked us to accommodate. To be proactive, we are trying to be much more creative and innovative with our staffing model and our use of scarce resources in order to provide the best patient care possible. Over the last 16 years, we have worked hard to continue to develop our program but, more important, develop our patient care through the development of our physicians, NPs, and PAs. This includes developing a pathway for residents who wish to become hospitalists, introducing vigorous training for PAs during their student and post-graduate years, and providing staff with the professional development resources they need to expand their skills and knowledge base and stay up-to-date on the latest advances in medicine—whether that is through leadership development or skill straining like point-of-care ultrasound.

 

Hospital medicine has matured and grown, and our scope has changed dramatically to include observation care, research and academic medicine, telemedicine, palliative care, perioperative medicine, and more. At HealthPartners, we are embracing the opportunity to grow in scope and improve care across specialties.

Q: Given your experience in the U.S. and abroad, what words of advice would you give to medical students and residents considering a career in hospital medicine?

A: As you enter this career out of training, recognize that your potential impact is greater than you ever imagined in medical school. As you continue to grow in your career and make it your own, you will make lasting impacts on your patients and also be extremely creative in what you do. Just as the specialty continues to evolve, so will you. Keep an open mind and embrace the many opportunities that come your way. TH

---

Brett Radler is SHM’s communications coordinator.

A new study suggests that cost-sharing policies in the US create a barrier to the treatment of chronic myeloid leukemia (CML).

Researchers examined Medicare claims data and found that “Part D” (prescription drug plan) co-insurance policies for “specialty drugs” seem to be reducing or delaying the use of tyrosine kinase inhibitors (TKIs) in patients with CML.

The team reported these findings in the American Journal of Managed Care.

“High out-of-pocket costs for specialty drugs appear to pose a very real barrier to treatment,” said study author Jalpa A. Doshi, PhD, of the Perelman School of Medicine at the University of Pennsylvania in Philadelphia.

While there is no standard definition for specialty drugs, the term typically refers to medications requiring special handling, administration, or monitoring. Most are aimed at treating chronic or life-threatening diseases.

Although specialty drugs typically tend to offer significant medical advances over non-specialty drugs, they are correspondingly more expensive. In 2014, such drugs accounted for less than 1% of prescriptions in the US but nearly a third of total prescription spending.

While insurers have been imposing higher cost-sharing requirements as part of their efforts to manage specialty drug spending, there has been limited information about the corresponding impact on patients.

“[I]t was particularly important to examine the extent to which the aggressive cost-sharing policies for specialty drugs seen under Medicare Part D, which are increasingly making their way into the private insurance market, adversely impact access to these treatments even for a condition like cancer,” Dr Doshi said.

So she and her colleagues examined the impact of specialty drug cost-sharing under the Medicare Part D prescription drug benefit on patients with CML. The team analyzed Medicare data on patients who were newly diagnosed with CML to examine whether and how quickly they initiated TKI treatment.

The researchers compared patients who were eligible for low-income subsidies and therefore faced nominal out-of-pocket costs to patients who faced average out-of-pocket costs of $2600 or more for their first 30-day TKI prescription fill.

Results showed that patients in the high-cost group were significantly less likely than the low-cost group to have a Part D claim for a TKI prescription within 6 months of their CML diagnosis. The rates were 45.3% and 66.9%, respectively (P<0.001).

Patients in the high cost-sharing group also took twice as long, on average, to initiate TKI treatment. The mean time to fill a TKI prescription was 50.9 days in the high-cost group and 23.7 days in the low-cost group (P<0.001).

“Medicare Part D was created to increase access to prescription drug treatment among beneficiaries, but our data suggest that current policies are interfering with that goal when it comes to specialty drugs,” Dr Doshi said.

She added that making Part D out-of-pocket costs more consistent and limiting them to more reasonable sums would help mitigate this negative impact.

Dr Doshi and her colleagues are now pursuing further studies of the impact of Part D cost-sharing policies in different disease areas. They hope to gain a better understanding of changes in drug access and of the long-range clinical outcomes and costs associated with any delays or interruptions in treatment.

“We need to know if the current aggressive cost-sharing arrangements have adverse long-term impacts on health and perhaps, paradoxically, increase overall spending due to complications of poorly controlled disease,” Dr Doshi said.

A new study suggests that cost-sharing policies in the US create a barrier to the treatment of chronic myeloid leukemia (CML).

Researchers examined Medicare claims data and found that “Part D” (prescription drug plan) co-insurance policies for “specialty drugs” seem to be reducing or delaying the use of tyrosine kinase inhibitors (TKIs) in patients with CML.

The team reported these findings in the American Journal of Managed Care.

“High out-of-pocket costs for specialty drugs appear to pose a very real barrier to treatment,” said study author Jalpa A. Doshi, PhD, of the Perelman School of Medicine at the University of Pennsylvania in Philadelphia.

While there is no standard definition for specialty drugs, the term typically refers to medications requiring special handling, administration, or monitoring. Most are aimed at treating chronic or life-threatening diseases.

Although specialty drugs typically tend to offer significant medical advances over non-specialty drugs, they are correspondingly more expensive. In 2014, such drugs accounted for less than 1% of prescriptions in the US but nearly a third of total prescription spending.

While insurers have been imposing higher cost-sharing requirements as part of their efforts to manage specialty drug spending, there has been limited information about the corresponding impact on patients.

“[I]t was particularly important to examine the extent to which the aggressive cost-sharing policies for specialty drugs seen under Medicare Part D, which are increasingly making their way into the private insurance market, adversely impact access to these treatments even for a condition like cancer,” Dr Doshi said.

So she and her colleagues examined the impact of specialty drug cost-sharing under the Medicare Part D prescription drug benefit on patients with CML. The team analyzed Medicare data on patients who were newly diagnosed with CML to examine whether and how quickly they initiated TKI treatment.

The researchers compared patients who were eligible for low-income subsidies and therefore faced nominal out-of-pocket costs to patients who faced average out-of-pocket costs of $2600 or more for their first 30-day TKI prescription fill.

Results showed that patients in the high-cost group were significantly less likely than the low-cost group to have a Part D claim for a TKI prescription within 6 months of their CML diagnosis. The rates were 45.3% and 66.9%, respectively (P<0.001).

Patients in the high cost-sharing group also took twice as long, on average, to initiate TKI treatment. The mean time to fill a TKI prescription was 50.9 days in the high-cost group and 23.7 days in the low-cost group (P<0.001).

“Medicare Part D was created to increase access to prescription drug treatment among beneficiaries, but our data suggest that current policies are interfering with that goal when it comes to specialty drugs,” Dr Doshi said.

She added that making Part D out-of-pocket costs more consistent and limiting them to more reasonable sums would help mitigate this negative impact.

Dr Doshi and her colleagues are now pursuing further studies of the impact of Part D cost-sharing policies in different disease areas. They hope to gain a better understanding of changes in drug access and of the long-range clinical outcomes and costs associated with any delays or interruptions in treatment.

“We need to know if the current aggressive cost-sharing arrangements have adverse long-term impacts on health and perhaps, paradoxically, increase overall spending due to complications of poorly controlled disease,” Dr Doshi said.

A new study suggests that cost-sharing policies in the US create a barrier to the treatment of chronic myeloid leukemia (CML).

Researchers examined Medicare claims data and found that “Part D” (prescription drug plan) co-insurance policies for “specialty drugs” seem to be reducing or delaying the use of tyrosine kinase inhibitors (TKIs) in patients with CML.

The team reported these findings in the American Journal of Managed Care.

“High out-of-pocket costs for specialty drugs appear to pose a very real barrier to treatment,” said study author Jalpa A. Doshi, PhD, of the Perelman School of Medicine at the University of Pennsylvania in Philadelphia.

While there is no standard definition for specialty drugs, the term typically refers to medications requiring special handling, administration, or monitoring. Most are aimed at treating chronic or life-threatening diseases.

Although specialty drugs typically tend to offer significant medical advances over non-specialty drugs, they are correspondingly more expensive. In 2014, such drugs accounted for less than 1% of prescriptions in the US but nearly a third of total prescription spending.

While insurers have been imposing higher cost-sharing requirements as part of their efforts to manage specialty drug spending, there has been limited information about the corresponding impact on patients.

“[I]t was particularly important to examine the extent to which the aggressive cost-sharing policies for specialty drugs seen under Medicare Part D, which are increasingly making their way into the private insurance market, adversely impact access to these treatments even for a condition like cancer,” Dr Doshi said.

So she and her colleagues examined the impact of specialty drug cost-sharing under the Medicare Part D prescription drug benefit on patients with CML. The team analyzed Medicare data on patients who were newly diagnosed with CML to examine whether and how quickly they initiated TKI treatment.

The researchers compared patients who were eligible for low-income subsidies and therefore faced nominal out-of-pocket costs to patients who faced average out-of-pocket costs of $2600 or more for their first 30-day TKI prescription fill.

Results showed that patients in the high-cost group were significantly less likely than the low-cost group to have a Part D claim for a TKI prescription within 6 months of their CML diagnosis. The rates were 45.3% and 66.9%, respectively (P<0.001).

Patients in the high cost-sharing group also took twice as long, on average, to initiate TKI treatment. The mean time to fill a TKI prescription was 50.9 days in the high-cost group and 23.7 days in the low-cost group (P<0.001).

“Medicare Part D was created to increase access to prescription drug treatment among beneficiaries, but our data suggest that current policies are interfering with that goal when it comes to specialty drugs,” Dr Doshi said.

She added that making Part D out-of-pocket costs more consistent and limiting them to more reasonable sums would help mitigate this negative impact.

Dr Doshi and her colleagues are now pursuing further studies of the impact of Part D cost-sharing policies in different disease areas. They hope to gain a better understanding of changes in drug access and of the long-range clinical outcomes and costs associated with any delays or interruptions in treatment.

“We need to know if the current aggressive cost-sharing arrangements have adverse long-term impacts on health and perhaps, paradoxically, increase overall spending due to complications of poorly controlled disease,” Dr Doshi said.

Researchers say they have generated induced pluripotent stem cells (iPSCs) that can differentiate into multiple lineages of functional lymphocytes.

The team noted that lymphohematopoietic stem cells (L-HSCs) generated from self-somatic cell-derived iPSCs could potentially be used to treat hematologic disorders, but no one has generated “truly functional” L-HSCs from iPSCs.

So the researchers set out to determine whether iPSCs have the inherent potential to generate multiple lineages of functional, terminally differentiated lymphocytes.

They described this work in Stem Cells and Development.

The researchers said they used tetraploid embryo complementation to provide a normal environment for the differentiation of L-HSCs from iPSCs and embryonic stem cells (ESCs). The team then compared lymphocytes derived from iPSCs, ESCs, and naïve isogenic C57BL/6 mice.

The researchers found that iPSC-derived lymphocytes expressed normal levels of major histocompatibility complex-I. Levels were comparable in iPSC-derived lymphocytes, ESC-derived lymphocytes, and lymphocytes from the control mice.

In addition, iPSC-derived lymphocytes were able to differentiate into multiple cell types—CD4+ T cells, CD8+ T cells, regulatory T cells, B cells, and natural killer cells.

Lymphocytes generated from iPSCs and lymphocytes generated from ESCs had the same capacity as lymphocytes from the control mice to proliferate and secrete chemical signals, such as cytokines.

All 3 types of lymphocytes proliferated under allogeneic stimulation but not under syngeneic stimulation. And the researchers found similar levels of IL-2, IL-4, IL-6, IL-10, IL-17, TNF, and IFN-γ in iPSC, ESC, and C57BL/6 lymphocyte culture supernatants.

The team also found that lymphocytes generated by iPSC-derived bone marrow cells could repopulate the hematopoietic systems of lethally irradiated recipient mice.

The iPSC bone marrow cells proved as effective as ESC-derived bone marrow cells and wild-type bone marrow cells. All 3 types of cells negated lymphocyte storage exhaustion in the spleen and peripheral blood.

In addition, there were no major phenotypic or behavioral abnormalities in any of the mice more than 1 month after cell transplantation.

The researchers said this work shows that truly functional lymphocytes can be generated from iPSCs, and it supports the clinical application of iPSC technology to develop treatments for hematologic disorders.

Researchers say they have generated induced pluripotent stem cells (iPSCs) that can differentiate into multiple lineages of functional lymphocytes.

The team noted that lymphohematopoietic stem cells (L-HSCs) generated from self-somatic cell-derived iPSCs could potentially be used to treat hematologic disorders, but no one has generated “truly functional” L-HSCs from iPSCs.

So the researchers set out to determine whether iPSCs have the inherent potential to generate multiple lineages of functional, terminally differentiated lymphocytes.

They described this work in Stem Cells and Development.

The researchers said they used tetraploid embryo complementation to provide a normal environment for the differentiation of L-HSCs from iPSCs and embryonic stem cells (ESCs). The team then compared lymphocytes derived from iPSCs, ESCs, and naïve isogenic C57BL/6 mice.

The researchers found that iPSC-derived lymphocytes expressed normal levels of major histocompatibility complex-I. Levels were comparable in iPSC-derived lymphocytes, ESC-derived lymphocytes, and lymphocytes from the control mice.

In addition, iPSC-derived lymphocytes were able to differentiate into multiple cell types—CD4+ T cells, CD8+ T cells, regulatory T cells, B cells, and natural killer cells.

Lymphocytes generated from iPSCs and lymphocytes generated from ESCs had the same capacity as lymphocytes from the control mice to proliferate and secrete chemical signals, such as cytokines.

All 3 types of lymphocytes proliferated under allogeneic stimulation but not under syngeneic stimulation. And the researchers found similar levels of IL-2, IL-4, IL-6, IL-10, IL-17, TNF, and IFN-γ in iPSC, ESC, and C57BL/6 lymphocyte culture supernatants.

The team also found that lymphocytes generated by iPSC-derived bone marrow cells could repopulate the hematopoietic systems of lethally irradiated recipient mice.

The iPSC bone marrow cells proved as effective as ESC-derived bone marrow cells and wild-type bone marrow cells. All 3 types of cells negated lymphocyte storage exhaustion in the spleen and peripheral blood.

In addition, there were no major phenotypic or behavioral abnormalities in any of the mice more than 1 month after cell transplantation.

The researchers said this work shows that truly functional lymphocytes can be generated from iPSCs, and it supports the clinical application of iPSC technology to develop treatments for hematologic disorders.

Researchers say they have generated induced pluripotent stem cells (iPSCs) that can differentiate into multiple lineages of functional lymphocytes.

The team noted that lymphohematopoietic stem cells (L-HSCs) generated from self-somatic cell-derived iPSCs could potentially be used to treat hematologic disorders, but no one has generated “truly functional” L-HSCs from iPSCs.

So the researchers set out to determine whether iPSCs have the inherent potential to generate multiple lineages of functional, terminally differentiated lymphocytes.

They described this work in Stem Cells and Development.

The researchers said they used tetraploid embryo complementation to provide a normal environment for the differentiation of L-HSCs from iPSCs and embryonic stem cells (ESCs). The team then compared lymphocytes derived from iPSCs, ESCs, and naïve isogenic C57BL/6 mice.

The researchers found that iPSC-derived lymphocytes expressed normal levels of major histocompatibility complex-I. Levels were comparable in iPSC-derived lymphocytes, ESC-derived lymphocytes, and lymphocytes from the control mice.

In addition, iPSC-derived lymphocytes were able to differentiate into multiple cell types—CD4+ T cells, CD8+ T cells, regulatory T cells, B cells, and natural killer cells.

Lymphocytes generated from iPSCs and lymphocytes generated from ESCs had the same capacity as lymphocytes from the control mice to proliferate and secrete chemical signals, such as cytokines.

All 3 types of lymphocytes proliferated under allogeneic stimulation but not under syngeneic stimulation. And the researchers found similar levels of IL-2, IL-4, IL-6, IL-10, IL-17, TNF, and IFN-γ in iPSC, ESC, and C57BL/6 lymphocyte culture supernatants.

The team also found that lymphocytes generated by iPSC-derived bone marrow cells could repopulate the hematopoietic systems of lethally irradiated recipient mice.

The iPSC bone marrow cells proved as effective as ESC-derived bone marrow cells and wild-type bone marrow cells. All 3 types of cells negated lymphocyte storage exhaustion in the spleen and peripheral blood.

In addition, there were no major phenotypic or behavioral abnormalities in any of the mice more than 1 month after cell transplantation.

The researchers said this work shows that truly functional lymphocytes can be generated from iPSCs, and it supports the clinical application of iPSC technology to develop treatments for hematologic disorders.

A novel molecular probe can detect amyloidosis at least as well as—and perhaps even better than—traditional methods, according to research published in Amyloid: The Journal of Protein Folding Disorders.

Investigators found that a luminescent conjugated oligothiophene, h-FTAA, allowed them to correctly identify amyloidosis in every sample tested.

But results also suggested h-FTAA may be more sensitive than traditional methods used to diagnose amyloidosis, as h-FTAA detected small amyloid deposits in samples that were previously determined to be amyloid-free.

The investigators said this suggests h-FTAA could be used to detect amyloidosis before symptoms present, leading to faster treatment.

“Given the sensitivity of the probe, we think this would make an excellent complement to traditional methods and could eventually be a replacement,” said study author Per Hammarström, PhD, of Linköping University in Sweden.

Dr Hammarström and his colleagues screened amyloid-containing tissues from 107 patients who had their amyloidosis verified by Congo red staining and/or immunohistochemistry, as well as tissues from 32 negative control cases.

The results showed that h-FTAA could detect amyloidosis with 100% sensitivity, identifying amyloid deposits in all 107 patients.

However, h-FTAA also detected microdeposits of amyloid-like protein aggregates in 5 of the control samples that were negative according to Congo red.

The investigators said they don’t know the clinical significance of these “false-positive” lesions. However, because h-FTAA fluorescence is 1 magnitude brighter than Congo red and because the staining is performed 4 magnitudes lower than the concentration of dye, the team believes these 5 cases may have been beyond detection by Congo red and h-FTAA may be a more sensitive technique.

They therefore concluded that h-FTAA could potentially be used as a complementary technique for accurate detection of amyloid in routine surgical pathology settings, for the detection of prodromal amyloidosis, and for the discovery of new amyloid-like protein aggregates.

A novel molecular probe can detect amyloidosis at least as well as—and perhaps even better than—traditional methods, according to research published in Amyloid: The Journal of Protein Folding Disorders.

Investigators found that a luminescent conjugated oligothiophene, h-FTAA, allowed them to correctly identify amyloidosis in every sample tested.

But results also suggested h-FTAA may be more sensitive than traditional methods used to diagnose amyloidosis, as h-FTAA detected small amyloid deposits in samples that were previously determined to be amyloid-free.

The investigators said this suggests h-FTAA could be used to detect amyloidosis before symptoms present, leading to faster treatment.

“Given the sensitivity of the probe, we think this would make an excellent complement to traditional methods and could eventually be a replacement,” said study author Per Hammarström, PhD, of Linköping University in Sweden.

Dr Hammarström and his colleagues screened amyloid-containing tissues from 107 patients who had their amyloidosis verified by Congo red staining and/or immunohistochemistry, as well as tissues from 32 negative control cases.

The results showed that h-FTAA could detect amyloidosis with 100% sensitivity, identifying amyloid deposits in all 107 patients.

However, h-FTAA also detected microdeposits of amyloid-like protein aggregates in 5 of the control samples that were negative according to Congo red.

The investigators said they don’t know the clinical significance of these “false-positive” lesions. However, because h-FTAA fluorescence is 1 magnitude brighter than Congo red and because the staining is performed 4 magnitudes lower than the concentration of dye, the team believes these 5 cases may have been beyond detection by Congo red and h-FTAA may be a more sensitive technique.

They therefore concluded that h-FTAA could potentially be used as a complementary technique for accurate detection of amyloid in routine surgical pathology settings, for the detection of prodromal amyloidosis, and for the discovery of new amyloid-like protein aggregates.

A novel molecular probe can detect amyloidosis at least as well as—and perhaps even better than—traditional methods, according to research published in Amyloid: The Journal of Protein Folding Disorders.

Investigators found that a luminescent conjugated oligothiophene, h-FTAA, allowed them to correctly identify amyloidosis in every sample tested.

But results also suggested h-FTAA may be more sensitive than traditional methods used to diagnose amyloidosis, as h-FTAA detected small amyloid deposits in samples that were previously determined to be amyloid-free.

The investigators said this suggests h-FTAA could be used to detect amyloidosis before symptoms present, leading to faster treatment.

“Given the sensitivity of the probe, we think this would make an excellent complement to traditional methods and could eventually be a replacement,” said study author Per Hammarström, PhD, of Linköping University in Sweden.

Dr Hammarström and his colleagues screened amyloid-containing tissues from 107 patients who had their amyloidosis verified by Congo red staining and/or immunohistochemistry, as well as tissues from 32 negative control cases.

The results showed that h-FTAA could detect amyloidosis with 100% sensitivity, identifying amyloid deposits in all 107 patients.

However, h-FTAA also detected microdeposits of amyloid-like protein aggregates in 5 of the control samples that were negative according to Congo red.

The investigators said they don’t know the clinical significance of these “false-positive” lesions. However, because h-FTAA fluorescence is 1 magnitude brighter than Congo red and because the staining is performed 4 magnitudes lower than the concentration of dye, the team believes these 5 cases may have been beyond detection by Congo red and h-FTAA may be a more sensitive technique.

They therefore concluded that h-FTAA could potentially be used as a complementary technique for accurate detection of amyloid in routine surgical pathology settings, for the detection of prodromal amyloidosis, and for the discovery of new amyloid-like protein aggregates.

Results of a phase 2 trial suggest the drug APO866 is not suitable for the treatment of relapsed or refractory cutaneous T-cell lymphoma (CTCL).

Researchers said APO866 had “a reasonable toxic effect,” but it was “not powerful enough,” so the trial was stopped early.

Two of the 14 patients studied achieved a partial response during the trial, but there were no complete responses, and most patients withdrew from the study early.

The researchers described these results in a letter to JAMA Dermatology. The study was initially sponsored by Apoxis SA and later by TopoTarget A/S, which is now known as Onxeo after merging with BioAlliance Pharma.

According to Onxeo, APO866 is an injectable molecule that induces apoptosis by inhibiting the biosynthesis of NAD+ from niacinamide, which is essential for the cellular metabolism, protein modification, and calcium-dependent messenger synthesis.

In the phase 2 trial, researchers tested APO866 in 14 patients with relapsed or refractory CTCL. The patients were 19 to 83 years of age, and half were female.

Eight patients had mycosis fungoides, 3 had Sézary syndrome, 1 had CD30+ anaplastic large-cell lymphoma, 1 had poikilodermic mycosis fungoides, and 1 had CD30- nonepidermotropic CTCL. One patient had stage IB disease, 2 had stage IIA, 3 had stage IIB, and 8 had stage IVA.

The patients received a continuous intravenous infusion, via pump, of APO866 at 0.126 mg/m²/h over the course of 96 hours. Patients received this treatment every 28 days for a total of 3 cycles.

Five patients completed all 3 treatment cycles and had no major protocol violations. Nine patients discontinued treatment early due to consent withdrawal (n=2), early disease progression (n=5), or adverse events (AEs, n=2).

At week 8, 1 patient had achieved a partial response to treatment, 4 patients had stable disease, 5 had progressed, and 4 patients were not evaluable because they had withdrawn from the study.

At week 16, 1 patient had a partial response (not the same patient as at week 8), 4 patients had stable disease, and 9 patients were not evaluable due to withdrawal.

There were a total of 141 AEs, and 77 of these were considered related to APO866. Most patients (n=12) had mild to moderate AEs, but there were 7 serious AEs thought to be treatment-related. These included pyrexia, lymphopenia (n=2), spondylitis, Staphylococcal sepsis, rhabdomyolysis, and thrombocytopenia.

There were 4 deaths, but they were not considered drug-related.

The researchers said these results suggest APO866 should not be pursued as a treatment for CTCL. However, as the drug induces immunosuppression and has insulin-mimicking effects, it might prove useful for treating other conditions.

Results of a phase 2 trial suggest the drug APO866 is not suitable for the treatment of relapsed or refractory cutaneous T-cell lymphoma (CTCL).

Researchers said APO866 had “a reasonable toxic effect,” but it was “not powerful enough,” so the trial was stopped early.

Two of the 14 patients studied achieved a partial response during the trial, but there were no complete responses, and most patients withdrew from the study early.

The researchers described these results in a letter to JAMA Dermatology. The study was initially sponsored by Apoxis SA and later by TopoTarget A/S, which is now known as Onxeo after merging with BioAlliance Pharma.

According to Onxeo, APO866 is an injectable molecule that induces apoptosis by inhibiting the biosynthesis of NAD+ from niacinamide, which is essential for the cellular metabolism, protein modification, and calcium-dependent messenger synthesis.

In the phase 2 trial, researchers tested APO866 in 14 patients with relapsed or refractory CTCL. The patients were 19 to 83 years of age, and half were female.

Eight patients had mycosis fungoides, 3 had Sézary syndrome, 1 had CD30+ anaplastic large-cell lymphoma, 1 had poikilodermic mycosis fungoides, and 1 had CD30- nonepidermotropic CTCL. One patient had stage IB disease, 2 had stage IIA, 3 had stage IIB, and 8 had stage IVA.

The patients received a continuous intravenous infusion, via pump, of APO866 at 0.126 mg/m²/h over the course of 96 hours. Patients received this treatment every 28 days for a total of 3 cycles.

Five patients completed all 3 treatment cycles and had no major protocol violations. Nine patients discontinued treatment early due to consent withdrawal (n=2), early disease progression (n=5), or adverse events (AEs, n=2).

At week 8, 1 patient had achieved a partial response to treatment, 4 patients had stable disease, 5 had progressed, and 4 patients were not evaluable because they had withdrawn from the study.

At week 16, 1 patient had a partial response (not the same patient as at week 8), 4 patients had stable disease, and 9 patients were not evaluable due to withdrawal.

There were a total of 141 AEs, and 77 of these were considered related to APO866. Most patients (n=12) had mild to moderate AEs, but there were 7 serious AEs thought to be treatment-related. These included pyrexia, lymphopenia (n=2), spondylitis, Staphylococcal sepsis, rhabdomyolysis, and thrombocytopenia.

There were 4 deaths, but they were not considered drug-related.

The researchers said these results suggest APO866 should not be pursued as a treatment for CTCL. However, as the drug induces immunosuppression and has insulin-mimicking effects, it might prove useful for treating other conditions.

Results of a phase 2 trial suggest the drug APO866 is not suitable for the treatment of relapsed or refractory cutaneous T-cell lymphoma (CTCL).

Researchers said APO866 had “a reasonable toxic effect,” but it was “not powerful enough,” so the trial was stopped early.

Two of the 14 patients studied achieved a partial response during the trial, but there were no complete responses, and most patients withdrew from the study early.

The researchers described these results in a letter to JAMA Dermatology. The study was initially sponsored by Apoxis SA and later by TopoTarget A/S, which is now known as Onxeo after merging with BioAlliance Pharma.

According to Onxeo, APO866 is an injectable molecule that induces apoptosis by inhibiting the biosynthesis of NAD+ from niacinamide, which is essential for the cellular metabolism, protein modification, and calcium-dependent messenger synthesis.

In the phase 2 trial, researchers tested APO866 in 14 patients with relapsed or refractory CTCL. The patients were 19 to 83 years of age, and half were female.

Eight patients had mycosis fungoides, 3 had Sézary syndrome, 1 had CD30+ anaplastic large-cell lymphoma, 1 had poikilodermic mycosis fungoides, and 1 had CD30- nonepidermotropic CTCL. One patient had stage IB disease, 2 had stage IIA, 3 had stage IIB, and 8 had stage IVA.

The patients received a continuous intravenous infusion, via pump, of APO866 at 0.126 mg/m²/h over the course of 96 hours. Patients received this treatment every 28 days for a total of 3 cycles.

Five patients completed all 3 treatment cycles and had no major protocol violations. Nine patients discontinued treatment early due to consent withdrawal (n=2), early disease progression (n=5), or adverse events (AEs, n=2).

At week 8, 1 patient had achieved a partial response to treatment, 4 patients had stable disease, 5 had progressed, and 4 patients were not evaluable because they had withdrawn from the study.

At week 16, 1 patient had a partial response (not the same patient as at week 8), 4 patients had stable disease, and 9 patients were not evaluable due to withdrawal.

There were a total of 141 AEs, and 77 of these were considered related to APO866. Most patients (n=12) had mild to moderate AEs, but there were 7 serious AEs thought to be treatment-related. These included pyrexia, lymphopenia (n=2), spondylitis, Staphylococcal sepsis, rhabdomyolysis, and thrombocytopenia.

There were 4 deaths, but they were not considered drug-related.

The researchers said these results suggest APO866 should not be pursued as a treatment for CTCL. However, as the drug induces immunosuppression and has insulin-mimicking effects, it might prove useful for treating other conditions.