SCOTTSDALE, ARIZ. – Treatment with ustekinumab did not result in significant improvements in atopic dermatitis after 16 weeks, compared with placebo in a phase II study of adults with moderate to severe atopic dermatitis, Dr. Patrick Brunner reported at the annual meeting of the Society for Investigative Dermatology.

However, molecular studies revealed robust modulation of relevant transcriptomic genes after 1 month of ustekinumab, compared with placebo, said Dr. Brunner, who is with the Laboratory for Investigative Dermatology, Rockefeller University, New York. Since the crossover design of this trial and the use of topical corticosteroids by patients probably diluted the differences in clinical outcomes between the intervention and placebo groups, “another study with a different design and dosing is mandated,” he said in an oral presentation at the meeting.

© -aniaostudio-/ Thinkstockphotos.com

Ustekinumab (Stelara) is a long-acting injectable human interleukin-12 and interleukin-23 antagonist that suppresses Th1, Th17, and Th22 activation. It was approved in 2009 in the United States for moderate to severe plaque psoriasis, and in 2013 for active psoriatic arthritis.

To investigate ustekinumab as therapy for atopic dermatitis, Dr. Brunner and his associates randomly assigned 33 adults aged 18-75 years with refractory atopic dermatitis and baseline scores on the Scoring Atopic Dermatitis (SCORAD) severity scale above 15 to subcutaneous injections of either placebo (17 patients) or ustekinumab (16) at weeks 0, 4, and 16. Ustekinumab was dosed the same way as in psoriasis: 45 mg per injection for patients at or under 100 kg, and 90 mg per injection for heavier patients. At week 16, all patients crossed over to the other treatment for another 16 weeks.

The groups were similar in terms of baseline demographics, intrinsic versus extrinsic IgE status, mean SCORAD, and average levels of IgE and eosinophils. To increase enrollment and retention, both groups were given triamcinolone acetonide 0.025%.

The proportion of SCORAD50 responders (patients with at least a 50% drop from the baseline SCORAD) was greater for ustekinumab than placebo at weeks 12, 16, and 20, but the differences never reached statistical significance, Dr. Brunner reported. At week 16, five (31%) ustekinumab-treated patients had achieved SCORAD50 (the primary endpoint), compared with three (18%) of those on placebo. The ustekinumab SCORAD50 response reached 50% by week 20, but by then patients had crossed over and the two groups began to resemble each other, he said.

“The lessons learned for designing atopic dermatitis trials are to avoid a crossover design with a long-lasting drug, and to keep in mind that even mild background topical steroids can tremendously confound detection of drug effects,” Dr. Brunner commented.

Studies of the atopic dermatitis molecular profile, or transcriptome, revealed similar gene expression levels for both trial arms at baseline, but substantially more gene modulation after 4 weeks of ustekinumab, compared with placebo, he reported. This molecular response involved the Th1, Th17, Th22, but also Th2-related atopic dermatitis genes, and in all cases the differences from placebo were statistically significant (P less than .05). Furthermore, gene modulation became more pronounced through the end of the trial and correlated with clinical response, he added.

The most common adverse effect associated with ustekinumab was respiratory infection, which affected two patients. There were no serious adverse effects reported and none of the patients stopped treatment because of adverse effects.

“Ustekinumab had clear clinical and molecular effects, but clinical outcomes might have been obscured by a profound placebo effect, most likely due to background topical glucocorticosteroids and possibly insufficient dosing for atopic dermatitis,” Dr. Brunner and his associates concluded in a report of their findings, which was published online after the meeting in Experimental Dermatology (Exp Dermatol. 2016 Jun 15. doi: 10.1111/exd.13112).

The study was supported by Janssen, the manufacturer of ustekinumab, and by the National Institutes of Health. Dr. Brunner had no disclosures.

SCOTTSDALE, ARIZ. – Treatment with ustekinumab did not result in significant improvements in atopic dermatitis after 16 weeks, compared with placebo in a phase II study of adults with moderate to severe atopic dermatitis, Dr. Patrick Brunner reported at the annual meeting of the Society for Investigative Dermatology.

However, molecular studies revealed robust modulation of relevant transcriptomic genes after 1 month of ustekinumab, compared with placebo, said Dr. Brunner, who is with the Laboratory for Investigative Dermatology, Rockefeller University, New York. Since the crossover design of this trial and the use of topical corticosteroids by patients probably diluted the differences in clinical outcomes between the intervention and placebo groups, “another study with a different design and dosing is mandated,” he said in an oral presentation at the meeting.

© -aniaostudio-/ Thinkstockphotos.com

Ustekinumab (Stelara) is a long-acting injectable human interleukin-12 and interleukin-23 antagonist that suppresses Th1, Th17, and Th22 activation. It was approved in 2009 in the United States for moderate to severe plaque psoriasis, and in 2013 for active psoriatic arthritis.

To investigate ustekinumab as therapy for atopic dermatitis, Dr. Brunner and his associates randomly assigned 33 adults aged 18-75 years with refractory atopic dermatitis and baseline scores on the Scoring Atopic Dermatitis (SCORAD) severity scale above 15 to subcutaneous injections of either placebo (17 patients) or ustekinumab (16) at weeks 0, 4, and 16. Ustekinumab was dosed the same way as in psoriasis: 45 mg per injection for patients at or under 100 kg, and 90 mg per injection for heavier patients. At week 16, all patients crossed over to the other treatment for another 16 weeks.

The groups were similar in terms of baseline demographics, intrinsic versus extrinsic IgE status, mean SCORAD, and average levels of IgE and eosinophils. To increase enrollment and retention, both groups were given triamcinolone acetonide 0.025%.

The proportion of SCORAD50 responders (patients with at least a 50% drop from the baseline SCORAD) was greater for ustekinumab than placebo at weeks 12, 16, and 20, but the differences never reached statistical significance, Dr. Brunner reported. At week 16, five (31%) ustekinumab-treated patients had achieved SCORAD50 (the primary endpoint), compared with three (18%) of those on placebo. The ustekinumab SCORAD50 response reached 50% by week 20, but by then patients had crossed over and the two groups began to resemble each other, he said.

“The lessons learned for designing atopic dermatitis trials are to avoid a crossover design with a long-lasting drug, and to keep in mind that even mild background topical steroids can tremendously confound detection of drug effects,” Dr. Brunner commented.

Studies of the atopic dermatitis molecular profile, or transcriptome, revealed similar gene expression levels for both trial arms at baseline, but substantially more gene modulation after 4 weeks of ustekinumab, compared with placebo, he reported. This molecular response involved the Th1, Th17, Th22, but also Th2-related atopic dermatitis genes, and in all cases the differences from placebo were statistically significant (P less than .05). Furthermore, gene modulation became more pronounced through the end of the trial and correlated with clinical response, he added.

The most common adverse effect associated with ustekinumab was respiratory infection, which affected two patients. There were no serious adverse effects reported and none of the patients stopped treatment because of adverse effects.

“Ustekinumab had clear clinical and molecular effects, but clinical outcomes might have been obscured by a profound placebo effect, most likely due to background topical glucocorticosteroids and possibly insufficient dosing for atopic dermatitis,” Dr. Brunner and his associates concluded in a report of their findings, which was published online after the meeting in Experimental Dermatology (Exp Dermatol. 2016 Jun 15. doi: 10.1111/exd.13112).

The study was supported by Janssen, the manufacturer of ustekinumab, and by the National Institutes of Health. Dr. Brunner had no disclosures.

SCOTTSDALE, ARIZ. – Treatment with ustekinumab did not result in significant improvements in atopic dermatitis after 16 weeks, compared with placebo in a phase II study of adults with moderate to severe atopic dermatitis, Dr. Patrick Brunner reported at the annual meeting of the Society for Investigative Dermatology.

However, molecular studies revealed robust modulation of relevant transcriptomic genes after 1 month of ustekinumab, compared with placebo, said Dr. Brunner, who is with the Laboratory for Investigative Dermatology, Rockefeller University, New York. Since the crossover design of this trial and the use of topical corticosteroids by patients probably diluted the differences in clinical outcomes between the intervention and placebo groups, “another study with a different design and dosing is mandated,” he said in an oral presentation at the meeting.

© -aniaostudio-/ Thinkstockphotos.com

Ustekinumab (Stelara) is a long-acting injectable human interleukin-12 and interleukin-23 antagonist that suppresses Th1, Th17, and Th22 activation. It was approved in 2009 in the United States for moderate to severe plaque psoriasis, and in 2013 for active psoriatic arthritis.

To investigate ustekinumab as therapy for atopic dermatitis, Dr. Brunner and his associates randomly assigned 33 adults aged 18-75 years with refractory atopic dermatitis and baseline scores on the Scoring Atopic Dermatitis (SCORAD) severity scale above 15 to subcutaneous injections of either placebo (17 patients) or ustekinumab (16) at weeks 0, 4, and 16. Ustekinumab was dosed the same way as in psoriasis: 45 mg per injection for patients at or under 100 kg, and 90 mg per injection for heavier patients. At week 16, all patients crossed over to the other treatment for another 16 weeks.

The groups were similar in terms of baseline demographics, intrinsic versus extrinsic IgE status, mean SCORAD, and average levels of IgE and eosinophils. To increase enrollment and retention, both groups were given triamcinolone acetonide 0.025%.

The proportion of SCORAD50 responders (patients with at least a 50% drop from the baseline SCORAD) was greater for ustekinumab than placebo at weeks 12, 16, and 20, but the differences never reached statistical significance, Dr. Brunner reported. At week 16, five (31%) ustekinumab-treated patients had achieved SCORAD50 (the primary endpoint), compared with three (18%) of those on placebo. The ustekinumab SCORAD50 response reached 50% by week 20, but by then patients had crossed over and the two groups began to resemble each other, he said.

“The lessons learned for designing atopic dermatitis trials are to avoid a crossover design with a long-lasting drug, and to keep in mind that even mild background topical steroids can tremendously confound detection of drug effects,” Dr. Brunner commented.

Studies of the atopic dermatitis molecular profile, or transcriptome, revealed similar gene expression levels for both trial arms at baseline, but substantially more gene modulation after 4 weeks of ustekinumab, compared with placebo, he reported. This molecular response involved the Th1, Th17, Th22, but also Th2-related atopic dermatitis genes, and in all cases the differences from placebo were statistically significant (P less than .05). Furthermore, gene modulation became more pronounced through the end of the trial and correlated with clinical response, he added.

The most common adverse effect associated with ustekinumab was respiratory infection, which affected two patients. There were no serious adverse effects reported and none of the patients stopped treatment because of adverse effects.

“Ustekinumab had clear clinical and molecular effects, but clinical outcomes might have been obscured by a profound placebo effect, most likely due to background topical glucocorticosteroids and possibly insufficient dosing for atopic dermatitis,” Dr. Brunner and his associates concluded in a report of their findings, which was published online after the meeting in Experimental Dermatology (Exp Dermatol. 2016 Jun 15. doi: 10.1111/exd.13112).

The study was supported by Janssen, the manufacturer of ustekinumab, and by the National Institutes of Health. Dr. Brunner had no disclosures.

S. Godfrey, Alabama

A. Velayati, MD, Alabama

M. Neyman, MD, Arizona

S. StimsonRiahi, FACP, Arizona

D. Testa, Arizona

S. Thomas, MD, Arizona

A. Babaki, California

K. Blanton, BSN, California

K. Chan, DO, California

J. Cipa-Tatum, MD, California

M. Essig, California

R. Garcia, MPH, PA-C, California

C. Ho, California

J. Hoppe, California

M. Hudock, PA-C, California

V. Huynh, California

N. Lakhera, California

P. Lin, California

G. Martinez, California

R. Mistry, PA-C, California

A. Murphy, California

V. Reddy, California

S. Sharif, DO, California

J. Smith Jonas, RN, MSN, California

A. Williams, DO, California

H. Crossman, Colorado

L. Donigan, Colorado

F. Merritt, MD, Colorado

B. Clark, Connecticut

A. Kimowicz Ely, Delaware

V. Ramdoss, Delaware

B. Bhimji, MD, Florida

J. Dyer, Florida

S. Hussain, MD, Florida

J. Rodemeyer, Florida

R. A. Adene-Peter, MD, Georgia

M. Burnett, PA-C, Georgia

C. Gordon, MD, FACP, Georgia

M. Morris, Georgia

A. Roberson, PA-C, Georgia

A. Gorham, Idaho

M. Ashraf, Illinois

A. Kovalsky, DO, MPH, Illinois

G. Patel, USA, Illinois

A. Brown, ACNP, Indiana

A. Brown, ANP-BC, Indiana

R. De Los Santos, MD, Indiana

C. Frame, ACNP, Indiana

J. Myers, FNP, Indiana

A. Greif, MD, Iowa

M. Jones, DO, Kansas

S. Suman, MD, MPH, Kentucky

S. Davuluri, MD, Louisiana

A. LaComb, FAAFP, Louisiana

E. Von Felten, FAAFP, Maine

K. Anwar, Maryland

R. Sedighi Manesh, MD, Maryland

K. Islam, Massachusetts

V. Kandimalla, MD, Massachusetts

K. Ntiforo, Massachusetts

S. Paudel, MD, Massachusetts

O. Enaohwo, MD, Michigan

N. Wisniewski, MEd, MPAS, PA-C, Michigan

M. Buchner-Mehling, Minnesota

T. Mukonje, Minnesota

T. Perttula, Minnesota

C. Plooster, MPAS, PA-C, Minnesota

S. Reichl, Minnesota

J. Sundberg, MD, Minnesota

D. Wolbrink, MD, Minnesota

D. Haddad, MD, Mississippi

K. Bleisch, AGNP, Missouri

V. Kenguva, MD, Missouri

R. Kroeger, MD, Missouri

H. McKeever, ACAGNP, Missouri

A. Pickrell, MD, Missouri

P. Podaralla, MD, Missouri

C. Robertson, FNP, Missouri

E. Robinson-Mitchell, MD, Missouri

K. Schaefermeier, AGNP, Missouri

A. Shah, MD, Missouri

S. V. Yew, MBBS, Missouri

T. Hylland, FNP, Montana

R. Goodwin, Nebraska

M. Hofreiter, FACP, New Hampshire

G. Looser, PA-C, New Hampshire

V. Verma, MD, New Jersey

M. Behl, MD, New Mexico

P. Boehringer, MD, FACP, New Mexico

L. Fatemi, DO, New Mexico

L. Flores, New Mexico

B. Khan, MD, New Mexico

M. Knof, New Mexico

H. McKnight, MD, New Mexico

B. Murguia, MD, New Mexico

R. Pierce, MD, New Mexico

A. Belman, MD, New York

W. Dissanayake, MD, New York

M. Fabisevich, MD, New York

S. Madderla, MD, New York

M. Maynard, DO, New York

P. Park, MD, New York

V. Subramanian, MD, New York

M. Wolfe, New York

A. Chatterjee, MD, North Carolina

G. Gilson, MHA, North Carolina

C. Nashatizadeh, MD, North Carolina

J. Perez Coste, North Carolina

K. Gupta, North Dakota

M. Sampson, CCFP, MD, Nova Scotia

M. J. Belderol, MD, Ohio

K. Crouser, MD, Ohio

C. Lambert, MD, Ohio

J. Muriithi, MD, Ohio

Y. Omran, USA, Ohio

T. Scheufler, DO, Ohio

J. Springer, Ohio

H. Szugye, DO, Ohio

J. Zang, MS, Ohio

J. Zimmerman, FACEP, Ohio

D. Beeson, MD, Oklahoma

E. Mathias, LPN, Oklahoma

M. Salehidobakhshari, Ontario

J. Hull, DO, Oregon

R. Asaad, Pennsylvania

N. Desai, MD, Pennsylvania

N. Ezeife, MD, Pennsylvania

M. Mazich, PA, Pennsylvania

K. Mezue, MSC, Pennsylvania

V. Shah, MD, MBBS, Pennsylvania

W. Sherman, DO, MBA, MS, Pennsylvania

S. Tripp, Pennsylvania

M. Weidner, CRNP, Pennsylvania

B. Weinbaum, MD, Pennsylvania

A. Gupta, MD, Rhode Island

S. El-Ibiary, South Carolina

C. Obi, South Carolina

J. Reed, MD, South Dakota

R. Mahboob, MD, Tennessee

L. Ackerman, MD, Texas

K. Chung, Texas

N. Jayaswal, MBBS, Texas

R. Kessel, MD, Texas

A. Khatoon, Texas

C. Renner, Texas

H. Smith, PA-C, Texas

R. Trien, Texas

J. Anderson, ACNP, Utah

C. Mitchell, MD, Vermont

L. Lawson, Virginia

S. Glass, MD, Washington

J. Joy, MHA, Washington

D. Farmer, BS, DO, MS, West Virginia

D. Nunev, MD, West Virginia

S. Godfrey, Alabama

A. Velayati, MD, Alabama

M. Neyman, MD, Arizona

S. StimsonRiahi, FACP, Arizona

D. Testa, Arizona

S. Thomas, MD, Arizona

A. Babaki, California

K. Blanton, BSN, California

K. Chan, DO, California

J. Cipa-Tatum, MD, California

M. Essig, California

R. Garcia, MPH, PA-C, California

C. Ho, California

J. Hoppe, California

M. Hudock, PA-C, California

V. Huynh, California

N. Lakhera, California

P. Lin, California

G. Martinez, California

R. Mistry, PA-C, California

A. Murphy, California

V. Reddy, California

S. Sharif, DO, California

J. Smith Jonas, RN, MSN, California

A. Williams, DO, California

H. Crossman, Colorado

L. Donigan, Colorado

F. Merritt, MD, Colorado

B. Clark, Connecticut

A. Kimowicz Ely, Delaware

V. Ramdoss, Delaware

B. Bhimji, MD, Florida

J. Dyer, Florida

S. Hussain, MD, Florida

J. Rodemeyer, Florida

R. A. Adene-Peter, MD, Georgia

M. Burnett, PA-C, Georgia

C. Gordon, MD, FACP, Georgia

M. Morris, Georgia

A. Roberson, PA-C, Georgia

A. Gorham, Idaho

M. Ashraf, Illinois

A. Kovalsky, DO, MPH, Illinois

G. Patel, USA, Illinois

A. Brown, ACNP, Indiana

A. Brown, ANP-BC, Indiana

R. De Los Santos, MD, Indiana

C. Frame, ACNP, Indiana

J. Myers, FNP, Indiana

A. Greif, MD, Iowa

M. Jones, DO, Kansas

S. Suman, MD, MPH, Kentucky

S. Davuluri, MD, Louisiana

A. LaComb, FAAFP, Louisiana

E. Von Felten, FAAFP, Maine

K. Anwar, Maryland

R. Sedighi Manesh, MD, Maryland

K. Islam, Massachusetts

V. Kandimalla, MD, Massachusetts

K. Ntiforo, Massachusetts

S. Paudel, MD, Massachusetts

O. Enaohwo, MD, Michigan

N. Wisniewski, MEd, MPAS, PA-C, Michigan

M. Buchner-Mehling, Minnesota

T. Mukonje, Minnesota

T. Perttula, Minnesota

C. Plooster, MPAS, PA-C, Minnesota

S. Reichl, Minnesota

J. Sundberg, MD, Minnesota

D. Wolbrink, MD, Minnesota

D. Haddad, MD, Mississippi

K. Bleisch, AGNP, Missouri

V. Kenguva, MD, Missouri

R. Kroeger, MD, Missouri

H. McKeever, ACAGNP, Missouri

A. Pickrell, MD, Missouri

P. Podaralla, MD, Missouri

C. Robertson, FNP, Missouri

E. Robinson-Mitchell, MD, Missouri

K. Schaefermeier, AGNP, Missouri

A. Shah, MD, Missouri

S. V. Yew, MBBS, Missouri

T. Hylland, FNP, Montana

R. Goodwin, Nebraska

M. Hofreiter, FACP, New Hampshire

G. Looser, PA-C, New Hampshire

V. Verma, MD, New Jersey

M. Behl, MD, New Mexico

P. Boehringer, MD, FACP, New Mexico

L. Fatemi, DO, New Mexico

L. Flores, New Mexico

B. Khan, MD, New Mexico

M. Knof, New Mexico

H. McKnight, MD, New Mexico

B. Murguia, MD, New Mexico

R. Pierce, MD, New Mexico

A. Belman, MD, New York

W. Dissanayake, MD, New York

M. Fabisevich, MD, New York

S. Madderla, MD, New York

M. Maynard, DO, New York

P. Park, MD, New York

V. Subramanian, MD, New York

M. Wolfe, New York

A. Chatterjee, MD, North Carolina

G. Gilson, MHA, North Carolina

C. Nashatizadeh, MD, North Carolina

J. Perez Coste, North Carolina

K. Gupta, North Dakota

M. Sampson, CCFP, MD, Nova Scotia

M. J. Belderol, MD, Ohio

K. Crouser, MD, Ohio

C. Lambert, MD, Ohio

J. Muriithi, MD, Ohio

Y. Omran, USA, Ohio

T. Scheufler, DO, Ohio

J. Springer, Ohio

H. Szugye, DO, Ohio

J. Zang, MS, Ohio

J. Zimmerman, FACEP, Ohio

D. Beeson, MD, Oklahoma

E. Mathias, LPN, Oklahoma

M. Salehidobakhshari, Ontario

J. Hull, DO, Oregon

R. Asaad, Pennsylvania

N. Desai, MD, Pennsylvania

N. Ezeife, MD, Pennsylvania

M. Mazich, PA, Pennsylvania

K. Mezue, MSC, Pennsylvania

V. Shah, MD, MBBS, Pennsylvania

W. Sherman, DO, MBA, MS, Pennsylvania

S. Tripp, Pennsylvania

M. Weidner, CRNP, Pennsylvania

B. Weinbaum, MD, Pennsylvania

A. Gupta, MD, Rhode Island

S. El-Ibiary, South Carolina

C. Obi, South Carolina

J. Reed, MD, South Dakota

R. Mahboob, MD, Tennessee

L. Ackerman, MD, Texas

K. Chung, Texas

N. Jayaswal, MBBS, Texas

R. Kessel, MD, Texas

A. Khatoon, Texas

C. Renner, Texas

H. Smith, PA-C, Texas

R. Trien, Texas

J. Anderson, ACNP, Utah

C. Mitchell, MD, Vermont

L. Lawson, Virginia

S. Glass, MD, Washington

J. Joy, MHA, Washington

D. Farmer, BS, DO, MS, West Virginia

D. Nunev, MD, West Virginia

S. Godfrey, Alabama

A. Velayati, MD, Alabama

M. Neyman, MD, Arizona

S. StimsonRiahi, FACP, Arizona

D. Testa, Arizona

S. Thomas, MD, Arizona

A. Babaki, California

K. Blanton, BSN, California

K. Chan, DO, California

J. Cipa-Tatum, MD, California

M. Essig, California

R. Garcia, MPH, PA-C, California

C. Ho, California

J. Hoppe, California

M. Hudock, PA-C, California

V. Huynh, California

N. Lakhera, California

P. Lin, California

G. Martinez, California

R. Mistry, PA-C, California

A. Murphy, California

V. Reddy, California

S. Sharif, DO, California

J. Smith Jonas, RN, MSN, California

A. Williams, DO, California

H. Crossman, Colorado

L. Donigan, Colorado

F. Merritt, MD, Colorado

B. Clark, Connecticut

A. Kimowicz Ely, Delaware

V. Ramdoss, Delaware

B. Bhimji, MD, Florida

J. Dyer, Florida

S. Hussain, MD, Florida

J. Rodemeyer, Florida

R. A. Adene-Peter, MD, Georgia

M. Burnett, PA-C, Georgia

C. Gordon, MD, FACP, Georgia

M. Morris, Georgia

A. Roberson, PA-C, Georgia

A. Gorham, Idaho

M. Ashraf, Illinois

A. Kovalsky, DO, MPH, Illinois

G. Patel, USA, Illinois

A. Brown, ACNP, Indiana

A. Brown, ANP-BC, Indiana

R. De Los Santos, MD, Indiana

C. Frame, ACNP, Indiana

J. Myers, FNP, Indiana

A. Greif, MD, Iowa

M. Jones, DO, Kansas

S. Suman, MD, MPH, Kentucky

S. Davuluri, MD, Louisiana

A. LaComb, FAAFP, Louisiana

E. Von Felten, FAAFP, Maine

K. Anwar, Maryland

R. Sedighi Manesh, MD, Maryland

K. Islam, Massachusetts

V. Kandimalla, MD, Massachusetts

K. Ntiforo, Massachusetts

S. Paudel, MD, Massachusetts

O. Enaohwo, MD, Michigan

N. Wisniewski, MEd, MPAS, PA-C, Michigan

M. Buchner-Mehling, Minnesota

T. Mukonje, Minnesota

T. Perttula, Minnesota

C. Plooster, MPAS, PA-C, Minnesota

S. Reichl, Minnesota

J. Sundberg, MD, Minnesota

D. Wolbrink, MD, Minnesota

D. Haddad, MD, Mississippi

K. Bleisch, AGNP, Missouri

V. Kenguva, MD, Missouri

R. Kroeger, MD, Missouri

H. McKeever, ACAGNP, Missouri

A. Pickrell, MD, Missouri

P. Podaralla, MD, Missouri

C. Robertson, FNP, Missouri

E. Robinson-Mitchell, MD, Missouri

K. Schaefermeier, AGNP, Missouri

A. Shah, MD, Missouri

S. V. Yew, MBBS, Missouri

T. Hylland, FNP, Montana

R. Goodwin, Nebraska

M. Hofreiter, FACP, New Hampshire

G. Looser, PA-C, New Hampshire

V. Verma, MD, New Jersey

M. Behl, MD, New Mexico

P. Boehringer, MD, FACP, New Mexico

L. Fatemi, DO, New Mexico

L. Flores, New Mexico

B. Khan, MD, New Mexico

M. Knof, New Mexico

H. McKnight, MD, New Mexico

B. Murguia, MD, New Mexico

R. Pierce, MD, New Mexico

A. Belman, MD, New York

W. Dissanayake, MD, New York

M. Fabisevich, MD, New York

S. Madderla, MD, New York

M. Maynard, DO, New York

P. Park, MD, New York

V. Subramanian, MD, New York

M. Wolfe, New York

A. Chatterjee, MD, North Carolina

G. Gilson, MHA, North Carolina

C. Nashatizadeh, MD, North Carolina

J. Perez Coste, North Carolina

K. Gupta, North Dakota

M. Sampson, CCFP, MD, Nova Scotia

M. J. Belderol, MD, Ohio

K. Crouser, MD, Ohio

C. Lambert, MD, Ohio

J. Muriithi, MD, Ohio

Y. Omran, USA, Ohio

T. Scheufler, DO, Ohio

J. Springer, Ohio

H. Szugye, DO, Ohio

J. Zang, MS, Ohio

J. Zimmerman, FACEP, Ohio

D. Beeson, MD, Oklahoma

E. Mathias, LPN, Oklahoma

M. Salehidobakhshari, Ontario

J. Hull, DO, Oregon

R. Asaad, Pennsylvania

N. Desai, MD, Pennsylvania

N. Ezeife, MD, Pennsylvania

M. Mazich, PA, Pennsylvania

K. Mezue, MSC, Pennsylvania

V. Shah, MD, MBBS, Pennsylvania

W. Sherman, DO, MBA, MS, Pennsylvania

S. Tripp, Pennsylvania

M. Weidner, CRNP, Pennsylvania

B. Weinbaum, MD, Pennsylvania

A. Gupta, MD, Rhode Island

S. El-Ibiary, South Carolina

C. Obi, South Carolina

J. Reed, MD, South Dakota

R. Mahboob, MD, Tennessee

L. Ackerman, MD, Texas

K. Chung, Texas

N. Jayaswal, MBBS, Texas

R. Kessel, MD, Texas

A. Khatoon, Texas

C. Renner, Texas

H. Smith, PA-C, Texas

R. Trien, Texas

J. Anderson, ACNP, Utah

C. Mitchell, MD, Vermont

L. Lawson, Virginia

S. Glass, MD, Washington

J. Joy, MHA, Washington

D. Farmer, BS, DO, MS, West Virginia

D. Nunev, MD, West Virginia

The State of Hospital Medicine (SoHM) report is the most comprehensive survey of hospital medicine in the country and provides current data on hospitalist compensation and productivity and also covers practice demographics, staffing levels, staff growth, and compensation models.

“The SoHM report is an indispensable tool for hospital medicine group directors,” says Andrew White, MD, SFHM. “I really appreciate the breakdown by characteristics, such as region of the country, academic practice, pediatrics, family medicine, and the involvement of NP and PA providers. The SoHM represents an excellent value. It has a ton of information in an easy-to-read format.”

Don’t miss out on getting your copy when it becomes available. Order now and be notified directly when the report is released in September at www.hospitalmedicine.org/Survey.

The State of Hospital Medicine (SoHM) report is the most comprehensive survey of hospital medicine in the country and provides current data on hospitalist compensation and productivity and also covers practice demographics, staffing levels, staff growth, and compensation models.

“The SoHM report is an indispensable tool for hospital medicine group directors,” says Andrew White, MD, SFHM. “I really appreciate the breakdown by characteristics, such as region of the country, academic practice, pediatrics, family medicine, and the involvement of NP and PA providers. The SoHM represents an excellent value. It has a ton of information in an easy-to-read format.”

Don’t miss out on getting your copy when it becomes available. Order now and be notified directly when the report is released in September at www.hospitalmedicine.org/Survey.

The State of Hospital Medicine (SoHM) report is the most comprehensive survey of hospital medicine in the country and provides current data on hospitalist compensation and productivity and also covers practice demographics, staffing levels, staff growth, and compensation models.

“The SoHM report is an indispensable tool for hospital medicine group directors,” says Andrew White, MD, SFHM. “I really appreciate the breakdown by characteristics, such as region of the country, academic practice, pediatrics, family medicine, and the involvement of NP and PA providers. The SoHM represents an excellent value. It has a ton of information in an easy-to-read format.”

Don’t miss out on getting your copy when it becomes available. Order now and be notified directly when the report is released in September at www.hospitalmedicine.org/Survey.

Patient receiving chemotherapy

Photo by Rhoda Baer

The risk of death from acute myeloid leukemia (AML) may be influenced by where a patient lives, according to a study published in Cancer.

Three regions in North Carolina were found to be associated with a higher risk of death, when compared to the rest of the state.

Patients had a significantly higher risk of death if they lived in northeastern North Carolina (from Wilson to Roanoke Rapids), in a region around Greenville, and a region around Wake County, including Durham County.

The increased risk remained even when the researchers controlled for other factors.

“The geographic survival disparities we found could not be explained by other sociodemographic variables or proximity to experienced treating facilities,” said study author Ashley Freeman, MD, of the University of North Carolina (UNC) in Chapel Hill.

“This raises the possibility that more complex features of the local healthcare infrastructure, including provider referral and practice patterns, are affecting patient outcomes.”

To study death rates from AML across North Carolina, Dr Freeman and her colleagues analyzed data on 553 adults who were diagnosed with AML between 2003 and 2009 and received inpatient chemotherapy within 30 days of diagnosis.

The team used the UNC Lineberger Integrated Cancer Information and Surveillance System, a database that links insurance claims information to a state information database called the NC Cancer Registry.

The researchers assessed the risk of death in 9 regions defined by the North Carolina Area Health Education Centers (AHEC) Program, a program established in 1972 to address physician shortages and the uneven distribution of healthcare services in North Carolina.

“We looked at geographic disparities because we are trying to improve outcomes for all citizens in North Carolina, consistent with the mission of our cancer center,” said William A. Wood, MD, of UNC.

“We are also trying to find situations in which disparities shouldn’t exist but do for arbitrary reasons—such as where a patient happens to live—so that we can figure out how to improve equity across the state.”

The researchers determined that a region around Greensboro had the lowest risk of death for AML.

Compared to the Greensboro region, the risk of death was 4 times higher in an area of northeastern North Carolina that included Roanoke Rapids, Rocky Mount, and Wilson—the highest in the state.

Compared to the Greensboro region, the risk of death was more than 2 times greater in the eastern region of the state around Greenville, and it was nearly twice as high in the region around Wake County.

“There are areas of the state where there is an elevated mortality, and we need to better understand the factors that are driving that—whether they’re environmental, patient, or provider-related,” said Anne-Marie Meyer, PhD, of UNC.

Nearly half of patients in the study received their care at hospitals not affiliated with one of the state’s 3 National Cancer Institute (NCI) comprehensive cancer centers.

The researchers did not find a significant link between the risk of death and the distance from patients’ homes to their treating facility or the nearest NCI-designated center.

And there was no significant difference in the risk of death at 1 year between patients who received treatment at an NCI-designated cancer center and those who did not. However, patients with a more serious prognosis were more likely to be treated at an NCI-designated cancer center.

The researchers did identify regional differences in healthcare resources. “Area L,” which is the name for the region in northeastern North Carolina that spans from Wilson to Roanoke Rapids, for example, has some of the lowest proportion of general practitioner physicians and radiation oncologists, as well as the highest burden of disease.

However, it is not clear why the disparities continued even after the researchers controlled for regional factors like poverty and education. The team believes other factors could be involved, such as the providers’ experience with treating rare or complex diseases or how supportive care is delivered.

Although there was not a significant association between survival and treatment at an NCI-designated center, there may be other features of treatment facilities, such as patient volume and academic affiliation, that are important for patient outcomes.

The researchers said their next step is to identify those factors and develop programs to try to close the gaps.

“The message here is that acute myeloid leukemia is representative of diseases that are uncommon, involve high-complexity care, and have high risk for morbidity and mortality,” Dr Wood said.

“If we can figure out how to coordinate and improve delivery of effective interventions for this disease throughout the state of North Carolina, then we may be able to develop a model for improving outcomes in many other diseases throughout the state as well.”

Patient receiving chemotherapy

Photo by Rhoda Baer

The risk of death from acute myeloid leukemia (AML) may be influenced by where a patient lives, according to a study published in Cancer.

Three regions in North Carolina were found to be associated with a higher risk of death, when compared to the rest of the state.

Patients had a significantly higher risk of death if they lived in northeastern North Carolina (from Wilson to Roanoke Rapids), in a region around Greenville, and a region around Wake County, including Durham County.

The increased risk remained even when the researchers controlled for other factors.

“The geographic survival disparities we found could not be explained by other sociodemographic variables or proximity to experienced treating facilities,” said study author Ashley Freeman, MD, of the University of North Carolina (UNC) in Chapel Hill.

“This raises the possibility that more complex features of the local healthcare infrastructure, including provider referral and practice patterns, are affecting patient outcomes.”

To study death rates from AML across North Carolina, Dr Freeman and her colleagues analyzed data on 553 adults who were diagnosed with AML between 2003 and 2009 and received inpatient chemotherapy within 30 days of diagnosis.

The team used the UNC Lineberger Integrated Cancer Information and Surveillance System, a database that links insurance claims information to a state information database called the NC Cancer Registry.

The researchers assessed the risk of death in 9 regions defined by the North Carolina Area Health Education Centers (AHEC) Program, a program established in 1972 to address physician shortages and the uneven distribution of healthcare services in North Carolina.

“We looked at geographic disparities because we are trying to improve outcomes for all citizens in North Carolina, consistent with the mission of our cancer center,” said William A. Wood, MD, of UNC.

“We are also trying to find situations in which disparities shouldn’t exist but do for arbitrary reasons—such as where a patient happens to live—so that we can figure out how to improve equity across the state.”

The researchers determined that a region around Greensboro had the lowest risk of death for AML.

Compared to the Greensboro region, the risk of death was 4 times higher in an area of northeastern North Carolina that included Roanoke Rapids, Rocky Mount, and Wilson—the highest in the state.

Compared to the Greensboro region, the risk of death was more than 2 times greater in the eastern region of the state around Greenville, and it was nearly twice as high in the region around Wake County.

“There are areas of the state where there is an elevated mortality, and we need to better understand the factors that are driving that—whether they’re environmental, patient, or provider-related,” said Anne-Marie Meyer, PhD, of UNC.

Nearly half of patients in the study received their care at hospitals not affiliated with one of the state’s 3 National Cancer Institute (NCI) comprehensive cancer centers.

The researchers did not find a significant link between the risk of death and the distance from patients’ homes to their treating facility or the nearest NCI-designated center.

And there was no significant difference in the risk of death at 1 year between patients who received treatment at an NCI-designated cancer center and those who did not. However, patients with a more serious prognosis were more likely to be treated at an NCI-designated cancer center.

The researchers did identify regional differences in healthcare resources. “Area L,” which is the name for the region in northeastern North Carolina that spans from Wilson to Roanoke Rapids, for example, has some of the lowest proportion of general practitioner physicians and radiation oncologists, as well as the highest burden of disease.

However, it is not clear why the disparities continued even after the researchers controlled for regional factors like poverty and education. The team believes other factors could be involved, such as the providers’ experience with treating rare or complex diseases or how supportive care is delivered.

Although there was not a significant association between survival and treatment at an NCI-designated center, there may be other features of treatment facilities, such as patient volume and academic affiliation, that are important for patient outcomes.

The researchers said their next step is to identify those factors and develop programs to try to close the gaps.

“The message here is that acute myeloid leukemia is representative of diseases that are uncommon, involve high-complexity care, and have high risk for morbidity and mortality,” Dr Wood said.

“If we can figure out how to coordinate and improve delivery of effective interventions for this disease throughout the state of North Carolina, then we may be able to develop a model for improving outcomes in many other diseases throughout the state as well.”

Patient receiving chemotherapy

Photo by Rhoda Baer

The risk of death from acute myeloid leukemia (AML) may be influenced by where a patient lives, according to a study published in Cancer.

Three regions in North Carolina were found to be associated with a higher risk of death, when compared to the rest of the state.

Patients had a significantly higher risk of death if they lived in northeastern North Carolina (from Wilson to Roanoke Rapids), in a region around Greenville, and a region around Wake County, including Durham County.

The increased risk remained even when the researchers controlled for other factors.

“The geographic survival disparities we found could not be explained by other sociodemographic variables or proximity to experienced treating facilities,” said study author Ashley Freeman, MD, of the University of North Carolina (UNC) in Chapel Hill.

“This raises the possibility that more complex features of the local healthcare infrastructure, including provider referral and practice patterns, are affecting patient outcomes.”

To study death rates from AML across North Carolina, Dr Freeman and her colleagues analyzed data on 553 adults who were diagnosed with AML between 2003 and 2009 and received inpatient chemotherapy within 30 days of diagnosis.

The team used the UNC Lineberger Integrated Cancer Information and Surveillance System, a database that links insurance claims information to a state information database called the NC Cancer Registry.

The researchers assessed the risk of death in 9 regions defined by the North Carolina Area Health Education Centers (AHEC) Program, a program established in 1972 to address physician shortages and the uneven distribution of healthcare services in North Carolina.

“We looked at geographic disparities because we are trying to improve outcomes for all citizens in North Carolina, consistent with the mission of our cancer center,” said William A. Wood, MD, of UNC.

“We are also trying to find situations in which disparities shouldn’t exist but do for arbitrary reasons—such as where a patient happens to live—so that we can figure out how to improve equity across the state.”

The researchers determined that a region around Greensboro had the lowest risk of death for AML.

Compared to the Greensboro region, the risk of death was 4 times higher in an area of northeastern North Carolina that included Roanoke Rapids, Rocky Mount, and Wilson—the highest in the state.

Compared to the Greensboro region, the risk of death was more than 2 times greater in the eastern region of the state around Greenville, and it was nearly twice as high in the region around Wake County.

“There are areas of the state where there is an elevated mortality, and we need to better understand the factors that are driving that—whether they’re environmental, patient, or provider-related,” said Anne-Marie Meyer, PhD, of UNC.

Nearly half of patients in the study received their care at hospitals not affiliated with one of the state’s 3 National Cancer Institute (NCI) comprehensive cancer centers.

The researchers did not find a significant link between the risk of death and the distance from patients’ homes to their treating facility or the nearest NCI-designated center.

And there was no significant difference in the risk of death at 1 year between patients who received treatment at an NCI-designated cancer center and those who did not. However, patients with a more serious prognosis were more likely to be treated at an NCI-designated cancer center.

The researchers did identify regional differences in healthcare resources. “Area L,” which is the name for the region in northeastern North Carolina that spans from Wilson to Roanoke Rapids, for example, has some of the lowest proportion of general practitioner physicians and radiation oncologists, as well as the highest burden of disease.

However, it is not clear why the disparities continued even after the researchers controlled for regional factors like poverty and education. The team believes other factors could be involved, such as the providers’ experience with treating rare or complex diseases or how supportive care is delivered.

Although there was not a significant association between survival and treatment at an NCI-designated center, there may be other features of treatment facilities, such as patient volume and academic affiliation, that are important for patient outcomes.

The researchers said their next step is to identify those factors and develop programs to try to close the gaps.

“The message here is that acute myeloid leukemia is representative of diseases that are uncommon, involve high-complexity care, and have high risk for morbidity and mortality,” Dr Wood said.

“If we can figure out how to coordinate and improve delivery of effective interventions for this disease throughout the state of North Carolina, then we may be able to develop a model for improving outcomes in many other diseases throughout the state as well.”

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for ibrutinib (Imbruvica), a Bruton’s tyrosine kinase inhibitor, as a potential treatment for chronic graft-versus-host-disease (cGVHD) in patients who have failed 1 or more lines of systemic therapy.

The FDA has also granted ibrutinib orphan drug designation for this indication.

The request for breakthrough therapy designation and orphan designation for ibrutinib in patients with cGVHD was based on preliminary data from a phase 1b/2 study of patients with steroid-dependent or refractory cGVHD.

Results from this trial were presented at the 2015 ASCO Annual Meeting (abstract 7024) and the 2016 EBMT meeting (abstract P124).

About ibrutinib

Ibrutinib is an oral, once-daily therapy that inhibits Bruton’s tyrosine kinase, a signaling molecule in the B-cell receptor signaling complex that plays an important role in the survival and spread of malignant B cells.

Ibrutinib is FDA-approved to treat patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL), including those with 17p deletion, patients with mantle cell lymphoma (MCL) who have received at least 1 prior therapy, and patients with Waldenström’s macroglobulinemia.

Accelerated approval was granted for the MCL indication based on overall response rate. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trials.

The FDA previously granted ibrutinib breakthrough designation for the treatment of relapsed or refractory MCL, Waldenström’s macroglobulinemia, and CLL/SLL patients with 17p deletion. The FDA also granted ibrutinib orphan designation for all 3 indications.

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

About breakthrough designation

The FDA’s breakthrough therapy designation is intended to expedite the development and review of new therapies for serious or life-threatening conditions.

To earn the designation, a treatment must show encouraging early clinical results demonstrating substantial improvement over available therapies with regard to a clinically significant endpoint, or it must fulfill an unmet need.

About orphan designation

The FDA grants orphan designation to drugs and biologics intended to treat, diagnose, or prevent diseases/disorders that affect fewer than 200,000 people in the US.

The designation provides incentives for sponsors to develop products for rare diseases. This may include tax credits toward the cost of clinical trials, prescription drug user fee waivers, and 7 years of market exclusivity if the drug is approved.

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for ibrutinib (Imbruvica), a Bruton’s tyrosine kinase inhibitor, as a potential treatment for chronic graft-versus-host-disease (cGVHD) in patients who have failed 1 or more lines of systemic therapy.

The FDA has also granted ibrutinib orphan drug designation for this indication.

The request for breakthrough therapy designation and orphan designation for ibrutinib in patients with cGVHD was based on preliminary data from a phase 1b/2 study of patients with steroid-dependent or refractory cGVHD.

Results from this trial were presented at the 2015 ASCO Annual Meeting (abstract 7024) and the 2016 EBMT meeting (abstract P124).

About ibrutinib

Ibrutinib is an oral, once-daily therapy that inhibits Bruton’s tyrosine kinase, a signaling molecule in the B-cell receptor signaling complex that plays an important role in the survival and spread of malignant B cells.

Ibrutinib is FDA-approved to treat patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL), including those with 17p deletion, patients with mantle cell lymphoma (MCL) who have received at least 1 prior therapy, and patients with Waldenström’s macroglobulinemia.

Accelerated approval was granted for the MCL indication based on overall response rate. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trials.

The FDA previously granted ibrutinib breakthrough designation for the treatment of relapsed or refractory MCL, Waldenström’s macroglobulinemia, and CLL/SLL patients with 17p deletion. The FDA also granted ibrutinib orphan designation for all 3 indications.

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

About breakthrough designation

The FDA’s breakthrough therapy designation is intended to expedite the development and review of new therapies for serious or life-threatening conditions.

To earn the designation, a treatment must show encouraging early clinical results demonstrating substantial improvement over available therapies with regard to a clinically significant endpoint, or it must fulfill an unmet need.

About orphan designation

The FDA grants orphan designation to drugs and biologics intended to treat, diagnose, or prevent diseases/disorders that affect fewer than 200,000 people in the US.

The designation provides incentives for sponsors to develop products for rare diseases. This may include tax credits toward the cost of clinical trials, prescription drug user fee waivers, and 7 years of market exclusivity if the drug is approved.

Ibrutinib (Imbruvica)

Photo courtesy of Janssen

The US Food and Drug Administration (FDA) has granted breakthrough therapy designation for ibrutinib (Imbruvica), a Bruton’s tyrosine kinase inhibitor, as a potential treatment for chronic graft-versus-host-disease (cGVHD) in patients who have failed 1 or more lines of systemic therapy.

The FDA has also granted ibrutinib orphan drug designation for this indication.

The request for breakthrough therapy designation and orphan designation for ibrutinib in patients with cGVHD was based on preliminary data from a phase 1b/2 study of patients with steroid-dependent or refractory cGVHD.

Results from this trial were presented at the 2015 ASCO Annual Meeting (abstract 7024) and the 2016 EBMT meeting (abstract P124).

About ibrutinib

Ibrutinib is an oral, once-daily therapy that inhibits Bruton’s tyrosine kinase, a signaling molecule in the B-cell receptor signaling complex that plays an important role in the survival and spread of malignant B cells.

Ibrutinib is FDA-approved to treat patients with chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL), including those with 17p deletion, patients with mantle cell lymphoma (MCL) who have received at least 1 prior therapy, and patients with Waldenström’s macroglobulinemia.

Accelerated approval was granted for the MCL indication based on overall response rate. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trials.

The FDA previously granted ibrutinib breakthrough designation for the treatment of relapsed or refractory MCL, Waldenström’s macroglobulinemia, and CLL/SLL patients with 17p deletion. The FDA also granted ibrutinib orphan designation for all 3 indications.

Ibrutinib is jointly developed and commercialized by Pharmacyclics LLC, an AbbVie company, and Janssen Biotech, Inc.

About breakthrough designation

The FDA’s breakthrough therapy designation is intended to expedite the development and review of new therapies for serious or life-threatening conditions.

To earn the designation, a treatment must show encouraging early clinical results demonstrating substantial improvement over available therapies with regard to a clinically significant endpoint, or it must fulfill an unmet need.

About orphan designation

The FDA grants orphan designation to drugs and biologics intended to treat, diagnose, or prevent diseases/disorders that affect fewer than 200,000 people in the US.

The designation provides incentives for sponsors to develop products for rare diseases. This may include tax credits toward the cost of clinical trials, prescription drug user fee waivers, and 7 years of market exclusivity if the drug is approved.

Micrograph showing DLBCL

The mTOR inhibitor everolimus may provide an additional benefit when combined with R-CHOP (rituximab,  cyclophosphamide, doxorubicin, vincristine, and prednisone) to treat patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL), according to researchers.

The combination was considered well-tolerated in a phase 1 trial, and 96% of patients responded to the treatment.

“There is an unmet need to develop new therapies based on R-CHOP to try to increase the cure rate for diffuse large B-cell lymphoma,” said Patrick Johnston, MD, PhD, of the Mayo Clinic in Rochester, Minnesota.

“This pilot study suggests that adding mTOR inhibitors to standard therapy could improve outcomes, though it needs to be validated in a larger clinical trial.”

Results from this study were published in The Lancet Haematology.

Patients and treatment

Dr Johnston and his colleagues conducted this study in 24 previously untreated DLBCL patients. Their median age was 58.5 (range, 49.5-71.5), and 58% were male. Most patients had stage IV disease (54%), followed by stage II (25%), and stage III (21%). Five patients (21%) had bulky disease.

The patients received standard R-CHOP-21 (rituximab at 375 mg/m², cyclophosphamide at 750 mg/m², doxorubicin at 50 mg/m², and vincristine at 1.4 mg/m²—all on day 1 of the 21-day cycle—as well as oral prednisone at 100 mg/m² each day on days 1–5 of the cycle) for 6 cycles, with scheduled pegfilgrastim at 6 mg on day 2 of each cycle.

They also received everolimus at 10 mg/day on 2 different schedules. Nine patients were enrolled initially—3 given everolimus on days 1–10 and 6 receiving it on days 1–14. As there were no dose-limiting toxicities in these patients, another 15 patients went on to receive everolimus on days 1–14.

Results

The median follow-up was 21.5 months. Twenty-three patients (96%) achieved an overall response and a complete metabolic response as assessed by PET. The remaining patient withdrew consent during cycle 1 and achieved a complete response with R-CHOP alone.

The 12-month event-free survival rate was 100%. Nine patients had sufficient follow-up and were event-free at 24 months. At last follow-up (March 30, 2016), no deaths or relapses had occurred.

The most common adverse events were hematologic, such as grade 4 neutropenia (75%) and grade 3 febrile neutropenia (21%).

Three patients experienced “significant” toxicity, according to the researchers. One patient had a treatment delay of 12 days due to grade 3 hypokalemia, which was considered possibly related to everolimus.

A second patient had grade 4 sepsis that was possibly related to treatment, and a third patient had a treatment delay of 10 days due to grade 3 infection that was possibly related to everolimus.

Ten patients (42%) had their dose of everolimus reduced, 2 patients permanently discontinued the drug after cycles 3 and 4, respectively, and 2 patients omitted everolimus for 1 and 2 cycles, respectively, then resumed everolimus for subsequent cycles.

“This study is the first to integrate a P13K-mTOR agent with standard R-CHOP,” Dr Johnston said.

“The encouraging outcome results and toxicity profile of this new regimen, along with the worldwide availability of everolimus, make it potentially applicable to the large population of DLBCL patients.”

Micrograph showing DLBCL

The mTOR inhibitor everolimus may provide an additional benefit when combined with R-CHOP (rituximab,  cyclophosphamide, doxorubicin, vincristine, and prednisone) to treat patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL), according to researchers.

The combination was considered well-tolerated in a phase 1 trial, and 96% of patients responded to the treatment.

“There is an unmet need to develop new therapies based on R-CHOP to try to increase the cure rate for diffuse large B-cell lymphoma,” said Patrick Johnston, MD, PhD, of the Mayo Clinic in Rochester, Minnesota.

“This pilot study suggests that adding mTOR inhibitors to standard therapy could improve outcomes, though it needs to be validated in a larger clinical trial.”

Results from this study were published in The Lancet Haematology.

Patients and treatment

Dr Johnston and his colleagues conducted this study in 24 previously untreated DLBCL patients. Their median age was 58.5 (range, 49.5-71.5), and 58% were male. Most patients had stage IV disease (54%), followed by stage II (25%), and stage III (21%). Five patients (21%) had bulky disease.

The patients received standard R-CHOP-21 (rituximab at 375 mg/m², cyclophosphamide at 750 mg/m², doxorubicin at 50 mg/m², and vincristine at 1.4 mg/m²—all on day 1 of the 21-day cycle—as well as oral prednisone at 100 mg/m² each day on days 1–5 of the cycle) for 6 cycles, with scheduled pegfilgrastim at 6 mg on day 2 of each cycle.

They also received everolimus at 10 mg/day on 2 different schedules. Nine patients were enrolled initially—3 given everolimus on days 1–10 and 6 receiving it on days 1–14. As there were no dose-limiting toxicities in these patients, another 15 patients went on to receive everolimus on days 1–14.

Results

The median follow-up was 21.5 months. Twenty-three patients (96%) achieved an overall response and a complete metabolic response as assessed by PET. The remaining patient withdrew consent during cycle 1 and achieved a complete response with R-CHOP alone.

The 12-month event-free survival rate was 100%. Nine patients had sufficient follow-up and were event-free at 24 months. At last follow-up (March 30, 2016), no deaths or relapses had occurred.

The most common adverse events were hematologic, such as grade 4 neutropenia (75%) and grade 3 febrile neutropenia (21%).

Three patients experienced “significant” toxicity, according to the researchers. One patient had a treatment delay of 12 days due to grade 3 hypokalemia, which was considered possibly related to everolimus.

A second patient had grade 4 sepsis that was possibly related to treatment, and a third patient had a treatment delay of 10 days due to grade 3 infection that was possibly related to everolimus.

Ten patients (42%) had their dose of everolimus reduced, 2 patients permanently discontinued the drug after cycles 3 and 4, respectively, and 2 patients omitted everolimus for 1 and 2 cycles, respectively, then resumed everolimus for subsequent cycles.

“This study is the first to integrate a P13K-mTOR agent with standard R-CHOP,” Dr Johnston said.

“The encouraging outcome results and toxicity profile of this new regimen, along with the worldwide availability of everolimus, make it potentially applicable to the large population of DLBCL patients.”

Micrograph showing DLBCL

The mTOR inhibitor everolimus may provide an additional benefit when combined with R-CHOP (rituximab,  cyclophosphamide, doxorubicin, vincristine, and prednisone) to treat patients with newly diagnosed diffuse large B-cell lymphoma (DLBCL), according to researchers.

The combination was considered well-tolerated in a phase 1 trial, and 96% of patients responded to the treatment.

“There is an unmet need to develop new therapies based on R-CHOP to try to increase the cure rate for diffuse large B-cell lymphoma,” said Patrick Johnston, MD, PhD, of the Mayo Clinic in Rochester, Minnesota.

“This pilot study suggests that adding mTOR inhibitors to standard therapy could improve outcomes, though it needs to be validated in a larger clinical trial.”

Results from this study were published in The Lancet Haematology.

Patients and treatment

Dr Johnston and his colleagues conducted this study in 24 previously untreated DLBCL patients. Their median age was 58.5 (range, 49.5-71.5), and 58% were male. Most patients had stage IV disease (54%), followed by stage II (25%), and stage III (21%). Five patients (21%) had bulky disease.

The patients received standard R-CHOP-21 (rituximab at 375 mg/m², cyclophosphamide at 750 mg/m², doxorubicin at 50 mg/m², and vincristine at 1.4 mg/m²—all on day 1 of the 21-day cycle—as well as oral prednisone at 100 mg/m² each day on days 1–5 of the cycle) for 6 cycles, with scheduled pegfilgrastim at 6 mg on day 2 of each cycle.

They also received everolimus at 10 mg/day on 2 different schedules. Nine patients were enrolled initially—3 given everolimus on days 1–10 and 6 receiving it on days 1–14. As there were no dose-limiting toxicities in these patients, another 15 patients went on to receive everolimus on days 1–14.

Results

The median follow-up was 21.5 months. Twenty-three patients (96%) achieved an overall response and a complete metabolic response as assessed by PET. The remaining patient withdrew consent during cycle 1 and achieved a complete response with R-CHOP alone.

The 12-month event-free survival rate was 100%. Nine patients had sufficient follow-up and were event-free at 24 months. At last follow-up (March 30, 2016), no deaths or relapses had occurred.

The most common adverse events were hematologic, such as grade 4 neutropenia (75%) and grade 3 febrile neutropenia (21%).

Three patients experienced “significant” toxicity, according to the researchers. One patient had a treatment delay of 12 days due to grade 3 hypokalemia, which was considered possibly related to everolimus.

A second patient had grade 4 sepsis that was possibly related to treatment, and a third patient had a treatment delay of 10 days due to grade 3 infection that was possibly related to everolimus.

Ten patients (42%) had their dose of everolimus reduced, 2 patients permanently discontinued the drug after cycles 3 and 4, respectively, and 2 patients omitted everolimus for 1 and 2 cycles, respectively, then resumed everolimus for subsequent cycles.

“This study is the first to integrate a P13K-mTOR agent with standard R-CHOP,” Dr Johnston said.

“The encouraging outcome results and toxicity profile of this new regimen, along with the worldwide availability of everolimus, make it potentially applicable to the large population of DLBCL patients.”

THE CASE

A 35-year-old woman sought care for a fever and sore throat that she’d had for 4 days. She denied symptoms of cough, rhinorrhea, or sputum production.

The patient’s medical history included severe recurrent streptococcal pharyngitis as a child and teenager. At the age of 17, she developed a fever of 105° F with associated delirium, dysphagia, nausea, and vomiting, and missed several days of school. She also lost 82 pounds, developed oral thrush, and continued to feel fatigued for approximately a year. After her primary care physician noted a heart murmur on physical exam, she was sent for echocardiography and diagnosed with rheumatic fever secondary to streptococcal pharyngitis.

Eighteen years (and numerous streptococcal infections) later, the patient was at our facility and we were ordering a rapid antigen detection test (RADT) for her current illness. The throat specimen was positive for group A ß-hemolytic streptococcus (GAS). The patient’s 8-year-old daughter also had a sore throat, fever, and positive RADT; her symptoms resolved with oral amoxicillin for 10 days. The patient’s husband was also treated successfully with oral amoxicillin/clavulanate for 10 days for similar symptoms. The patient herself, however, was unsuccessfully treated with oral amoxicillin 500 mg twice daily for 7 days.

She was then given oral amoxicillin/clavulanate 875 mg twice daily for 14 days, but received no relief. Even after receiving clindamycin 600 mg twice daily for 10 days, she had minimal relief and remained positive for GAS on repeat RADT. It was at this point that tonsillectomy was considered as a possible treatment modality for her refractory GAS pharyngitis.

The patient consented to the procedure and underwent a tonsillectomy. She has remained asymptomatic for 2 years and there have been no reported outbreaks of GAS infection in her household.

DISCUSSION

Streptococcal pharyngitis is an infection of the oropharynx and/or nasopharynx that is caused by Streptococcus pyogenes (also known as GAS). It is one of the most frequent illnesses encountered by primary care physicians, and primarily occurs in children ages 5 to 15 years.^1,2 The signs and symptoms of GAS pharyngitis include an abrupt onset of a sore throat, tonsillar exudate, tender cervical adenopathy, and fever. (The classic presentation of GAS pharyngitis in a different patient can be seen in the FIGURE.)

Throat cultures are the gold standard for the diagnosis of GAS pharyngitis, but results take 24 to 48 hours, which can delay appropriate treatment. Therefore, the use of the RADT is often preferred clinically.¹ RADT is not recommended for children and adults who show clinical symptoms that are highly suggestive of a viral illness, such as cough, rhinorrhea, hoarseness, or oral ulcers. A negative RADT in children and adolescents necessitates a throat culture to confirm the diagnosis.²

The antibiotics of choice are either penicillin 50 mg/kg/d in 4 divided doses or amoxicillin 40 mg/kg/d in 3 divided doses (maximum for both is 2000 mg/d) for 10 days. Options for patients with penicillin allergies include clindamycin or clarithromycin for 10 days or azithromycin for 5 days.²

The Infectious Diseases Society of America (IDSA) does not recommend routine testing or empiric treatment of asymptomatic carriers. However, it does recommend treatment of GAS carriers in certain situations, such as when: ²

• the carrier has acute rheumatic fever
• there is a family or personal history of acute rheumatic fever
• there is a post-streptococcal glomerulonephritis outbreak
• a family has excessive anxiety about GAS infections
• a tonsillectomy is being considered.

When—and for whom—is tonsillectomy beneficial?

Tonsillectomy is a treatment option for patients with recurrent episodes of GAS pharyngitis. Indications include patients with 7 GAS infections in a year, 5 episodes in 2 years, or 3 episodes in 3 years.^3,4 In select patient populations, tonsillectomy has been shown to decrease missed work days and medical expenses caused by recurrent pharyngitis.^5,6

Alho et al demonstrated that adults with recurrent episodes of GAS pharyngitis benefit from tonsillectomy in terms of fewer repeat infections and more days without throat pain.⁷ A randomized controlled trial conducted by Koskenkorva et al found that the overall rates of pharyngitis, throat pain, rhinitis, and cough were significantly lower in adults who received a tonsillectomy vs those who did not.⁵ Still, whether tonsillectomy is worthwhile in adults is debatable; Burton et al found no evidence that tonsillectomy is effective for chronic or recurrent acute tonsillitis in adults.⁸

Our patient has not missed work or visited her primary care physician because of a GAS infection since her tonsillectomy.

Overall meta-analysis results indicate that tonsillectomy results in a 43% reduction in the incidence of pharyngitis in children between the ages of 4 and 16.^8,9 One study found that children without tonsillectomy were 3.1 times more likely to develop subsequent GAS pharyngitis than children who underwent tonsillectomy.⁹ Another study found that children who received tonsillectomy demonstrated a decrease in sore throat episodes by 1.2 episodes per year and a decrease in school absenteeism by 2.8 days per year.⁶ Tonsillectomy does carry a risk of intraoperative and postoperative bleeding in children and adults, which may make it a less desirable option for some patients.⁶

THE TAKEAWAY

Recurrent GAS pharyngitis poses a significant challenge for clinicians. When episodes recur, it may be prudent to treat asymptomatic carriers in the patient’s household. Tonsillectomy should be considered in refractory cases since recurrent GAS pharyngitis directly impacts the wellness and productivity of patients. Our patient certainly benefited from the surgery: She has not missed any work days or had to visit her primary care physician because of a GAS infection since her tonsillectomy.

THE CASE

A 35-year-old woman sought care for a fever and sore throat that she’d had for 4 days. She denied symptoms of cough, rhinorrhea, or sputum production.

The patient’s medical history included severe recurrent streptococcal pharyngitis as a child and teenager. At the age of 17, she developed a fever of 105° F with associated delirium, dysphagia, nausea, and vomiting, and missed several days of school. She also lost 82 pounds, developed oral thrush, and continued to feel fatigued for approximately a year. After her primary care physician noted a heart murmur on physical exam, she was sent for echocardiography and diagnosed with rheumatic fever secondary to streptococcal pharyngitis.

Eighteen years (and numerous streptococcal infections) later, the patient was at our facility and we were ordering a rapid antigen detection test (RADT) for her current illness. The throat specimen was positive for group A ß-hemolytic streptococcus (GAS). The patient’s 8-year-old daughter also had a sore throat, fever, and positive RADT; her symptoms resolved with oral amoxicillin for 10 days. The patient’s husband was also treated successfully with oral amoxicillin/clavulanate for 10 days for similar symptoms. The patient herself, however, was unsuccessfully treated with oral amoxicillin 500 mg twice daily for 7 days.

She was then given oral amoxicillin/clavulanate 875 mg twice daily for 14 days, but received no relief. Even after receiving clindamycin 600 mg twice daily for 10 days, she had minimal relief and remained positive for GAS on repeat RADT. It was at this point that tonsillectomy was considered as a possible treatment modality for her refractory GAS pharyngitis.

The patient consented to the procedure and underwent a tonsillectomy. She has remained asymptomatic for 2 years and there have been no reported outbreaks of GAS infection in her household.

DISCUSSION

Streptococcal pharyngitis is an infection of the oropharynx and/or nasopharynx that is caused by Streptococcus pyogenes (also known as GAS). It is one of the most frequent illnesses encountered by primary care physicians, and primarily occurs in children ages 5 to 15 years.^1,2 The signs and symptoms of GAS pharyngitis include an abrupt onset of a sore throat, tonsillar exudate, tender cervical adenopathy, and fever. (The classic presentation of GAS pharyngitis in a different patient can be seen in the FIGURE.)

Throat cultures are the gold standard for the diagnosis of GAS pharyngitis, but results take 24 to 48 hours, which can delay appropriate treatment. Therefore, the use of the RADT is often preferred clinically.¹ RADT is not recommended for children and adults who show clinical symptoms that are highly suggestive of a viral illness, such as cough, rhinorrhea, hoarseness, or oral ulcers. A negative RADT in children and adolescents necessitates a throat culture to confirm the diagnosis.²

The antibiotics of choice are either penicillin 50 mg/kg/d in 4 divided doses or amoxicillin 40 mg/kg/d in 3 divided doses (maximum for both is 2000 mg/d) for 10 days. Options for patients with penicillin allergies include clindamycin or clarithromycin for 10 days or azithromycin for 5 days.²

The Infectious Diseases Society of America (IDSA) does not recommend routine testing or empiric treatment of asymptomatic carriers. However, it does recommend treatment of GAS carriers in certain situations, such as when: ²

• the carrier has acute rheumatic fever
• there is a family or personal history of acute rheumatic fever
• there is a post-streptococcal glomerulonephritis outbreak
• a family has excessive anxiety about GAS infections
• a tonsillectomy is being considered.

When—and for whom—is tonsillectomy beneficial?

Tonsillectomy is a treatment option for patients with recurrent episodes of GAS pharyngitis. Indications include patients with 7 GAS infections in a year, 5 episodes in 2 years, or 3 episodes in 3 years.^3,4 In select patient populations, tonsillectomy has been shown to decrease missed work days and medical expenses caused by recurrent pharyngitis.^5,6

Alho et al demonstrated that adults with recurrent episodes of GAS pharyngitis benefit from tonsillectomy in terms of fewer repeat infections and more days without throat pain.⁷ A randomized controlled trial conducted by Koskenkorva et al found that the overall rates of pharyngitis, throat pain, rhinitis, and cough were significantly lower in adults who received a tonsillectomy vs those who did not.⁵ Still, whether tonsillectomy is worthwhile in adults is debatable; Burton et al found no evidence that tonsillectomy is effective for chronic or recurrent acute tonsillitis in adults.⁸

Our patient has not missed work or visited her primary care physician because of a GAS infection since her tonsillectomy.

Overall meta-analysis results indicate that tonsillectomy results in a 43% reduction in the incidence of pharyngitis in children between the ages of 4 and 16.^8,9 One study found that children without tonsillectomy were 3.1 times more likely to develop subsequent GAS pharyngitis than children who underwent tonsillectomy.⁹ Another study found that children who received tonsillectomy demonstrated a decrease in sore throat episodes by 1.2 episodes per year and a decrease in school absenteeism by 2.8 days per year.⁶ Tonsillectomy does carry a risk of intraoperative and postoperative bleeding in children and adults, which may make it a less desirable option for some patients.⁶

THE TAKEAWAY

Recurrent GAS pharyngitis poses a significant challenge for clinicians. When episodes recur, it may be prudent to treat asymptomatic carriers in the patient’s household. Tonsillectomy should be considered in refractory cases since recurrent GAS pharyngitis directly impacts the wellness and productivity of patients. Our patient certainly benefited from the surgery: She has not missed any work days or had to visit her primary care physician because of a GAS infection since her tonsillectomy.

THE CASE

A 35-year-old woman sought care for a fever and sore throat that she’d had for 4 days. She denied symptoms of cough, rhinorrhea, or sputum production.

The patient’s medical history included severe recurrent streptococcal pharyngitis as a child and teenager. At the age of 17, she developed a fever of 105° F with associated delirium, dysphagia, nausea, and vomiting, and missed several days of school. She also lost 82 pounds, developed oral thrush, and continued to feel fatigued for approximately a year. After her primary care physician noted a heart murmur on physical exam, she was sent for echocardiography and diagnosed with rheumatic fever secondary to streptococcal pharyngitis.

Eighteen years (and numerous streptococcal infections) later, the patient was at our facility and we were ordering a rapid antigen detection test (RADT) for her current illness. The throat specimen was positive for group A ß-hemolytic streptococcus (GAS). The patient’s 8-year-old daughter also had a sore throat, fever, and positive RADT; her symptoms resolved with oral amoxicillin for 10 days. The patient’s husband was also treated successfully with oral amoxicillin/clavulanate for 10 days for similar symptoms. The patient herself, however, was unsuccessfully treated with oral amoxicillin 500 mg twice daily for 7 days.

She was then given oral amoxicillin/clavulanate 875 mg twice daily for 14 days, but received no relief. Even after receiving clindamycin 600 mg twice daily for 10 days, she had minimal relief and remained positive for GAS on repeat RADT. It was at this point that tonsillectomy was considered as a possible treatment modality for her refractory GAS pharyngitis.

The patient consented to the procedure and underwent a tonsillectomy. She has remained asymptomatic for 2 years and there have been no reported outbreaks of GAS infection in her household.

DISCUSSION

Streptococcal pharyngitis is an infection of the oropharynx and/or nasopharynx that is caused by Streptococcus pyogenes (also known as GAS). It is one of the most frequent illnesses encountered by primary care physicians, and primarily occurs in children ages 5 to 15 years.^1,2 The signs and symptoms of GAS pharyngitis include an abrupt onset of a sore throat, tonsillar exudate, tender cervical adenopathy, and fever. (The classic presentation of GAS pharyngitis in a different patient can be seen in the FIGURE.)

Throat cultures are the gold standard for the diagnosis of GAS pharyngitis, but results take 24 to 48 hours, which can delay appropriate treatment. Therefore, the use of the RADT is often preferred clinically.¹ RADT is not recommended for children and adults who show clinical symptoms that are highly suggestive of a viral illness, such as cough, rhinorrhea, hoarseness, or oral ulcers. A negative RADT in children and adolescents necessitates a throat culture to confirm the diagnosis.²

The antibiotics of choice are either penicillin 50 mg/kg/d in 4 divided doses or amoxicillin 40 mg/kg/d in 3 divided doses (maximum for both is 2000 mg/d) for 10 days. Options for patients with penicillin allergies include clindamycin or clarithromycin for 10 days or azithromycin for 5 days.²

The Infectious Diseases Society of America (IDSA) does not recommend routine testing or empiric treatment of asymptomatic carriers. However, it does recommend treatment of GAS carriers in certain situations, such as when: ²

• the carrier has acute rheumatic fever
• there is a family or personal history of acute rheumatic fever
• there is a post-streptococcal glomerulonephritis outbreak
• a family has excessive anxiety about GAS infections
• a tonsillectomy is being considered.

When—and for whom—is tonsillectomy beneficial?

Tonsillectomy is a treatment option for patients with recurrent episodes of GAS pharyngitis. Indications include patients with 7 GAS infections in a year, 5 episodes in 2 years, or 3 episodes in 3 years.^3,4 In select patient populations, tonsillectomy has been shown to decrease missed work days and medical expenses caused by recurrent pharyngitis.^5,6

Alho et al demonstrated that adults with recurrent episodes of GAS pharyngitis benefit from tonsillectomy in terms of fewer repeat infections and more days without throat pain.⁷ A randomized controlled trial conducted by Koskenkorva et al found that the overall rates of pharyngitis, throat pain, rhinitis, and cough were significantly lower in adults who received a tonsillectomy vs those who did not.⁵ Still, whether tonsillectomy is worthwhile in adults is debatable; Burton et al found no evidence that tonsillectomy is effective for chronic or recurrent acute tonsillitis in adults.⁸

Our patient has not missed work or visited her primary care physician because of a GAS infection since her tonsillectomy.

Overall meta-analysis results indicate that tonsillectomy results in a 43% reduction in the incidence of pharyngitis in children between the ages of 4 and 16.^8,9 One study found that children without tonsillectomy were 3.1 times more likely to develop subsequent GAS pharyngitis than children who underwent tonsillectomy.⁹ Another study found that children who received tonsillectomy demonstrated a decrease in sore throat episodes by 1.2 episodes per year and a decrease in school absenteeism by 2.8 days per year.⁶ Tonsillectomy does carry a risk of intraoperative and postoperative bleeding in children and adults, which may make it a less desirable option for some patients.⁶

THE TAKEAWAY

Recurrent GAS pharyngitis poses a significant challenge for clinicians. When episodes recur, it may be prudent to treat asymptomatic carriers in the patient’s household. Tonsillectomy should be considered in refractory cases since recurrent GAS pharyngitis directly impacts the wellness and productivity of patients. Our patient certainly benefited from the surgery: She has not missed any work days or had to visit her primary care physician because of a GAS infection since her tonsillectomy.

In 1996, 2 exposure incidents sparked a movement to better understand children’s environmental health. In both incidents, children were exposed to significant toxicants in unexpected ways. In one, the organophosphate insecticide methyl parathion was applied illegally in indoor settings.¹ In another, elemental mercury residue was detected in apartments converted from a fluorescent bulb facility.² These incidents, and others like them, alerted physicians and government agencies to the collective lack of training and experience in the field of pediatric environmental health.

To address the situation, the Agency for Toxic Substances and Disease Registry and the Environmental Protection Agency created the Pediatric Environmental Health Specialty Unit (PEHSU) program. The program, which is now jointly operated by the American College of Medical Toxicology and the American Academy of Pediatrics, maintains sites in 10 regions³ and seeks to enhance education and promote consultation and referral related to reproductive and children’s environmental health.

This past fall, PEHSU updated its Web site at www.pehsu.net, which provides information, training, and resources for health professionals and the general public. The Web site provides news, fact sheets, and online education regarding environment-related pediatric and reproductive health issues. It also provides a tool for finding a local expert in the PEHSU national network, should a family physician need to refer a patient for more extensive assistance.

We believe that family physicians will find the PEHSU program resources informative, educational, and relevant to their practice.

Carl R. Baum, MD, FAAP, FACMT, Medical Director
Dana Turner, MPH, CHES
Amanda Allen, MS
PEHSU Program
National Office—West
Phoenix, Ariz

References

1. Esteban E, Rubin C, Hill R, et al. Association between indoor residential contamination with methyl parathion and urinary para-nitrophenol. J Expo Anal Environ Epidemiol. 1996;6:375-387.

2. Centers for Disease Control and Prevention (CDC). Mercury exposure among residents of a building formerly used for industrial purposes—New Jersey, 1995. MMWR Morb Mortal Wkly Rep. 1996;45:422-424.

3. Wilborne-Davis P, Kirkland KH, Mulloy KB. A model for physician education and consultation in pediatric environmental health—the Pediatric Environmental Health Specialty Units (PEHSU) program. Pediatr Clin North Am. 2007;54:1-13.

In 1996, 2 exposure incidents sparked a movement to better understand children’s environmental health. In both incidents, children were exposed to significant toxicants in unexpected ways. In one, the organophosphate insecticide methyl parathion was applied illegally in indoor settings.¹ In another, elemental mercury residue was detected in apartments converted from a fluorescent bulb facility.² These incidents, and others like them, alerted physicians and government agencies to the collective lack of training and experience in the field of pediatric environmental health.

To address the situation, the Agency for Toxic Substances and Disease Registry and the Environmental Protection Agency created the Pediatric Environmental Health Specialty Unit (PEHSU) program. The program, which is now jointly operated by the American College of Medical Toxicology and the American Academy of Pediatrics, maintains sites in 10 regions³ and seeks to enhance education and promote consultation and referral related to reproductive and children’s environmental health.

This past fall, PEHSU updated its Web site at www.pehsu.net, which provides information, training, and resources for health professionals and the general public. The Web site provides news, fact sheets, and online education regarding environment-related pediatric and reproductive health issues. It also provides a tool for finding a local expert in the PEHSU national network, should a family physician need to refer a patient for more extensive assistance.

We believe that family physicians will find the PEHSU program resources informative, educational, and relevant to their practice.

Carl R. Baum, MD, FAAP, FACMT, Medical Director
Dana Turner, MPH, CHES
Amanda Allen, MS
PEHSU Program
National Office—West
Phoenix, Ariz

References

1. Esteban E, Rubin C, Hill R, et al. Association between indoor residential contamination with methyl parathion and urinary para-nitrophenol. J Expo Anal Environ Epidemiol. 1996;6:375-387.

2. Centers for Disease Control and Prevention (CDC). Mercury exposure among residents of a building formerly used for industrial purposes—New Jersey, 1995. MMWR Morb Mortal Wkly Rep. 1996;45:422-424.

3. Wilborne-Davis P, Kirkland KH, Mulloy KB. A model for physician education and consultation in pediatric environmental health—the Pediatric Environmental Health Specialty Units (PEHSU) program. Pediatr Clin North Am. 2007;54:1-13.

In 1996, 2 exposure incidents sparked a movement to better understand children’s environmental health. In both incidents, children were exposed to significant toxicants in unexpected ways. In one, the organophosphate insecticide methyl parathion was applied illegally in indoor settings.¹ In another, elemental mercury residue was detected in apartments converted from a fluorescent bulb facility.² These incidents, and others like them, alerted physicians and government agencies to the collective lack of training and experience in the field of pediatric environmental health.

To address the situation, the Agency for Toxic Substances and Disease Registry and the Environmental Protection Agency created the Pediatric Environmental Health Specialty Unit (PEHSU) program. The program, which is now jointly operated by the American College of Medical Toxicology and the American Academy of Pediatrics, maintains sites in 10 regions³ and seeks to enhance education and promote consultation and referral related to reproductive and children’s environmental health.

This past fall, PEHSU updated its Web site at www.pehsu.net, which provides information, training, and resources for health professionals and the general public. The Web site provides news, fact sheets, and online education regarding environment-related pediatric and reproductive health issues. It also provides a tool for finding a local expert in the PEHSU national network, should a family physician need to refer a patient for more extensive assistance.

We believe that family physicians will find the PEHSU program resources informative, educational, and relevant to their practice.

Carl R. Baum, MD, FAAP, FACMT, Medical Director
Dana Turner, MPH, CHES
Amanda Allen, MS
PEHSU Program
National Office—West
Phoenix, Ariz

References

1. Esteban E, Rubin C, Hill R, et al. Association between indoor residential contamination with methyl parathion and urinary para-nitrophenol. J Expo Anal Environ Epidemiol. 1996;6:375-387.

2. Centers for Disease Control and Prevention (CDC). Mercury exposure among residents of a building formerly used for industrial purposes—New Jersey, 1995. MMWR Morb Mortal Wkly Rep. 1996;45:422-424.

3. Wilborne-Davis P, Kirkland KH, Mulloy KB. A model for physician education and consultation in pediatric environmental health—the Pediatric Environmental Health Specialty Units (PEHSU) program. Pediatr Clin North Am. 2007;54:1-13.

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

A 2-year-old boy with atopic dermatitis developed a flare of his eczema after having a bath with mint-scented soap. His mother treated the flare with over-the-counter topical hydrocortisone cream. Two to 3 days later, he developed grouped vesicles on the right side of his neck. Three days after that, he developed a painful generalized vesicular eruption all over his body.

The boy was admitted to a hospital for supportive care and empiric antibiotics, but was discharged when no bacterial infection was found. The patient’s mother was instructed to follow up with his primary care provider in the next 2 weeks.

Three days after his hospitalization, the eruption on the young boy’s body spread and he was uncomfortable. He was brought to our hospital’s pediatric clinic, where physicians examined him and decided to transfer him to the university hospital for further evaluation.

On exam, the boy was afebrile, but uncomfortable and irritable. Diffuse heme-crusted and punched-out erosions covered about 90% of his body (FIGURE). His mucous membranes were not involved. Underneath the heme-crusted erosions, there were lichenified pink plaques on the antecubital fossae, popliteal fossae, periocular face, and buttocks. The patient’s right dorsal foot had a small vesicle; all other vesicles on his body had crusted over.

The patient’s family indicated that the child had received the varicella vaccine without incident at 12 months of age. He had no history of travel, no contact with sick individuals, and no exposure to pets or other animals.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Eczema herpeticum

Eczema herpeticum (EH) was suspected based on the appearance of the lesions. A Tzanck smear came back positive for multinucleated giant cells and a herpes simplex virus (HSV) amplified probe came back positive for HSV-1—confirming the diagnosis.

EH—also known as Kaposi varicelliform eruption—is a superficial generalized viral infection (typically caused by HSV-1; HSV-2 is less common). The infection commonly occurs in patients with underlying atopic dermatitis, but may also occur in those with Darier disease, pemphigus, burns, and other conditions that disrupt the skin barrier. Other viruses, such as Coxsackie virus, can also cause EH. Eczema vaccinatum is a variant that may occur after smallpox vaccination.¹ EH occurs more often in infants and children than in adults,² and is a potentially life-threatening dermatologic emergency.

Eczema herpeticum occurs more often in infants and children than in adults, and is a potentially life-threatening emergency.

Who’s at risk? Patients with underlying chronic skin conditions such as eczema may have impaired cell-mediated immunity, making them more susceptible to a viral infection like EH.¹ In addition, treatment of underlying chronic skin conditions with immunosuppressive therapies often increases susceptibility to superimposed infection.¹ (In this case, the patient’s parents had treated an eczema flare with a topical hydrocortisone cream.) Lastly, increased risk may be associated with mutations in the gene encoding filaggrin.²

Areas affected. EH typically appears in areas of pre-existing dermatitis as monomorphic, discrete, 2- to 3-mm, punched-out, heme-crusted erosions with scalloped borders.² The erosions initially appear as vesicles or pustules, which may appear concurrently with the erosions. The erosions can coalesce to form larger lesions.³ Fever, malaise, and lymphadenopathy may also be present.^2,3

4 factors differentiate EH from other conditions

The differential for eczema herpeticum includes impetigo, bullous impetigo, shingles, chicken pox, scabies, pustular psoriasis, bullous pemphigoid, drug hypersensitivity reactions, and exacerbation of a primary dermatosis or skin condition.^1,4

EH may be differentiated from these by its location, its development in the setting of pre-existing dermatitis, its response to antiviral medications, and the results of laboratory testing. Because of the vast differential, physicians must maintain a high index of suspicion for EH, particularly when a patient with a pre-existing skin condition presents with acute onset cutaneous pain.³

Perform a Tzanck smear to diagnose the underlying infection

If EH is suspected, treatment must be initiated immediately.³ (In our patient’s case, he was started on intravenous acyclovir 10 mg/kg every 8 hours.)

Once treatment is underway, a Tzanck smear of the vesicle base can be performed at the patient’s bedside to narrow the cause of the infection to HSV or varicella zoster virus (VZV). Multinucleated giant keratinocytes (as in our patient’s case) are diagnostic for one of the herpes viruses; concurrent inflammatory cells are also to be expected in an inflammatory skin condition but by themselves are not diagnostic of herpes.

If available in the laboratory, direct fluorescent antibody testing can differentiate between HSV and VZV. Alternatively, a nucleic acid amplified probe test may be used to provide a quick and specific result. The most specific test is a viral culture, but it lacks sensitivity and usually requires 2 to 5 daysfor results.² A bacterial skin swab and blood culture should also be considered to direct antibiotic therapy if superinfection has occurred.

Antivirals and antibiotics should be given until lesions heal

Patients with EH should be admitted to the hospital for at least 24 to 48 hours of intravenous acyclovir.⁴ Antivirals—oral or intravenous—should be given for 10 to 14 days or until all mucocutaneous lesions are healed. Recommended dosing for acyclovir is 15 mg/kg (up to 400 mg) by mouth 3 to 5 times per day or, if severe, 5 mg/kg (if ≥12 years of age) to 10 mg/kg (if <12 years of age) intravenously every 8 hours.² Patients should also receive a 3- to 6-month suppressive course of oral acyclovir, valacyclovir, or famciclovir.⁴

Intravenous antibiotics should also be considered, pending the results of bacterial skin swabs and a blood culture, as the skin of patients with atopic dermatitis is colonized with staphylococcus 90% of the time.⁴

Potential complications. Bacterial sepsis resulting from superinfection and disseminated HSV, although extremely rare, is the main cause of death associated with EH.³ One case in the literature described a 43-year-old woman with extensive EH superimposed on atopic dermatitis, disseminated HSV, and Pseudomonas aeruginosa septicemia. Despite treatment with intravenous acyclovir and antibiotics in a burn center intensive care unit, the patient experienced septic shock and disseminated intravascular coagulation with progression to multiorgan failure and death.³

Our patient’s antiviral regimen was transitioned to a 14-day course of oral acyclovir, which he completed. Topical steroids and an immunosuppressant (tacrolimus ointment) were applied concurrently. He was subsequently prescribed a 6-month suppressive course of acyclovir and was scheduled for follow-up at an outpatient dermatology clinic to discuss resuming therapy for atopic dermatitis.

CORRESPONDENCE
Sahand Rahnama-Moghadam, MD, 7323 Snowden Road #1205, San Antonio, TX 78240; [email protected].

SAN FRANCISCO – St. Jude Medical’s Durata and Riata ST Optim defibrillator leads performed comparably to Medtronic’s Sprint Quattro out to 7 years in a Veterans Affairs analysis of almost 18,000 patients in the VA National Cardiac Device Surveillance Program.

The “highly satisfactory electrical survival” of the Optim leads, at least until year 5, should be of some reassurance to cardiologists, especially since the findings come from the VA, not a device company, investigator Seema Pursnani, MD, said.

The investigators combined Durata and Riata ST Optim leads together in their analysis, since they are similar; both are 7 Fr leads with St. Jude’s silicone/polyurethane Optim coating. After a mean follow-up of 3.4 years in 4,091 Durata patients and 351 Riata ST Optim patients, there were 26 electrical lead failures, which translated to 0.17% failures per device-year.

The investigators compared those results with Medtronic’s Sprint Quattro, which “is sort of a gold standard. It’s been around for quite a long time, and people have confidence in it,” said Dr. Pursnani. After a mean follow-up of 3.8 years in 13,254 patients, there were 57 failures, translating to 0.11% failures per device-year.

Seven-year lead survival was 97.7% with St. Jude’s products, and 98.9% with Medtronic’s. Although the difference was not statistically significant, “we need a little more follow-up to see why the curves are diverging at years 6 and 7,” said Dr. Pursnani, a cardiologist at the San Francisco Veterans Affairs Medical Center when the study was done, but now with the Kaiser Permanente San Leandro (Calif.) Medical Center.

There’s been lingering concern about St. Jude leads ever since the recall of earlier versions of Riata – with silicone-only insulation – in 2011 because of lead abrasion and subsequent safety problems. Optim was developed to address the issue.

“One of the most common modes of lead failure that we saw” with all three leads “was a rise in the pace-sense conductor impedance from the baseline impedance. Sometimes, there is nonphysiologic noise that can also be a sign of early failure,” she said.

There was no industry funding for the work, and the investigators have no disclosures.

[email protected]

SAN FRANCISCO – St. Jude Medical’s Durata and Riata ST Optim defibrillator leads performed comparably to Medtronic’s Sprint Quattro out to 7 years in a Veterans Affairs analysis of almost 18,000 patients in the VA National Cardiac Device Surveillance Program.

The “highly satisfactory electrical survival” of the Optim leads, at least until year 5, should be of some reassurance to cardiologists, especially since the findings come from the VA, not a device company, investigator Seema Pursnani, MD, said.

The investigators combined Durata and Riata ST Optim leads together in their analysis, since they are similar; both are 7 Fr leads with St. Jude’s silicone/polyurethane Optim coating. After a mean follow-up of 3.4 years in 4,091 Durata patients and 351 Riata ST Optim patients, there were 26 electrical lead failures, which translated to 0.17% failures per device-year.

The investigators compared those results with Medtronic’s Sprint Quattro, which “is sort of a gold standard. It’s been around for quite a long time, and people have confidence in it,” said Dr. Pursnani. After a mean follow-up of 3.8 years in 13,254 patients, there were 57 failures, translating to 0.11% failures per device-year.

Seven-year lead survival was 97.7% with St. Jude’s products, and 98.9% with Medtronic’s. Although the difference was not statistically significant, “we need a little more follow-up to see why the curves are diverging at years 6 and 7,” said Dr. Pursnani, a cardiologist at the San Francisco Veterans Affairs Medical Center when the study was done, but now with the Kaiser Permanente San Leandro (Calif.) Medical Center.

There’s been lingering concern about St. Jude leads ever since the recall of earlier versions of Riata – with silicone-only insulation – in 2011 because of lead abrasion and subsequent safety problems. Optim was developed to address the issue.

“One of the most common modes of lead failure that we saw” with all three leads “was a rise in the pace-sense conductor impedance from the baseline impedance. Sometimes, there is nonphysiologic noise that can also be a sign of early failure,” she said.

There was no industry funding for the work, and the investigators have no disclosures.

[email protected]

SAN FRANCISCO – St. Jude Medical’s Durata and Riata ST Optim defibrillator leads performed comparably to Medtronic’s Sprint Quattro out to 7 years in a Veterans Affairs analysis of almost 18,000 patients in the VA National Cardiac Device Surveillance Program.

The “highly satisfactory electrical survival” of the Optim leads, at least until year 5, should be of some reassurance to cardiologists, especially since the findings come from the VA, not a device company, investigator Seema Pursnani, MD, said.

The investigators combined Durata and Riata ST Optim leads together in their analysis, since they are similar; both are 7 Fr leads with St. Jude’s silicone/polyurethane Optim coating. After a mean follow-up of 3.4 years in 4,091 Durata patients and 351 Riata ST Optim patients, there were 26 electrical lead failures, which translated to 0.17% failures per device-year.

The investigators compared those results with Medtronic’s Sprint Quattro, which “is sort of a gold standard. It’s been around for quite a long time, and people have confidence in it,” said Dr. Pursnani. After a mean follow-up of 3.8 years in 13,254 patients, there were 57 failures, translating to 0.11% failures per device-year.

Seven-year lead survival was 97.7% with St. Jude’s products, and 98.9% with Medtronic’s. Although the difference was not statistically significant, “we need a little more follow-up to see why the curves are diverging at years 6 and 7,” said Dr. Pursnani, a cardiologist at the San Francisco Veterans Affairs Medical Center when the study was done, but now with the Kaiser Permanente San Leandro (Calif.) Medical Center.

There’s been lingering concern about St. Jude leads ever since the recall of earlier versions of Riata – with silicone-only insulation – in 2011 because of lead abrasion and subsequent safety problems. Optim was developed to address the issue.

“One of the most common modes of lead failure that we saw” with all three leads “was a rise in the pace-sense conductor impedance from the baseline impedance. Sometimes, there is nonphysiologic noise that can also be a sign of early failure,” she said.

There was no industry funding for the work, and the investigators have no disclosures.

[email protected]