Acne vulgaris (AV) is a common skin disease that usually presents in adolescence and can persist into adulthood. Some cases may start in adulthood, especially in women. Acne vulgaris remains a challenge to treat successfully, both in teenagers and adults. Unrealistic expectations that therapy will rapidly clear and sustain clearance of AV completely can lead to incomplete adherence or complete cessation of treatment.^1-4 Local tolerability reactions also may decrease adherence to topical medications. Suboptimal adherence to medications for AV is one of the major reasons for treatment failure.⁵ Acne vulgaris can strongly influence psychological well-being and self-esteem.⁶ In general, severe AV causes more psychological distress, but the adverse emotional impact of AV can be independent of its severity.⁷

An effective relationship between the patient and his/her physician and staff is believed to be important in setting realistic expectations, optimizing adherence, and achieving a positive therapeutic outcome. One component related to setting reasonable expectations is the discussion about when the patient may begin to visibly perceive that the treatment regimen is working. This article evaluates the time course of a clinically meaningful response using pivotal trial data with clindamycin phosphate 1.2%–benzoyl peroxide 3.75% (clindamycin-BP 3.75%) gel for treatment of AV.

Are data available that evaluate the time course of a clinically relevant response to treatment of AV?

Unfortunately, data on what might be perceived as a clinically meaningful improvement in AV and how long it might take to achieve this treatment effect are limited. A meta-analysis of more than 4000 patients with moderate to severe AV suggested that a 10% to 20% difference in acne lesion counts from baseline as compared to a subsequent designated time point was clinically relevant.⁸ A review of 24 comparative studies of patients with mild to moderate AV used a primary outcome parameter of a 25% reduction in mean inflammatory lesion count to evaluate time to onset of action (TOA) to achieve a clinically meaningful benefit.⁹ This outcome was based on a previously identified threshold of clinical relevance and the authors’ clinical experience in a patient population with milder AV. In this same analysis, a difference of greater than 4 days between the active group and the vehicle group was considered to be relevant to the patient.⁹

A faster onset of visible improvement as perceived by the patient should be more desirable and is likely to improve treatment adherence, as long as it is not counterbalanced by an increase in adverse events.

What is meant by TOA?

Time to onset of action refers to the duration required to achieve a 25% mean lesion count reduction from baseline, which is believed to correlate with the time point at which many patients would be able to perceive visible improvement when viewing their full face. Therefore, TOA represents an attempt to correlate data that is quantitative (based on lesion count reduction) with what is likely to be the average time that a patient may qualitatively observe an initial visible improvement in their AV. This concept may be useful as a tool when communicating with AV patients but should not be used in a way that will overpromise and underdeliver; rather, it is a guide for discussion with the patient and with a parent or guardian when applicable.

Consistent with the comparative AV study analysis that evaluated TOA, a linear course of lesion reductions between the provided time intervals was assumed. In this linear model, the TOA was calculated using the 2 extracted lesion count values between which the 25% lesion reduction was achieved as well as their corresponding given time points.⁹ Differences between the results in the active and vehicle study arms were calculated for a number of determinants.

How was pivotal trial data with clindamycin-BP 3.75% gel used to assess TOA?

A total of 498 patients with moderate to severe AV were randomized (1:1) to receive clindamycin-BP 3.75% gel or vehicle in a multicenter, double-blind, controlled, 12-week, 2-arm study.¹⁰ Before randomization, patients were stratified by acne severity based on a static Evaluator’s Global Severity Score (EGSS) ranging from 0 (clear) to 5 (very severe). Specifically, moderate AV (EGSS of 3) was described as predominantly noninflammatory lesions with evidence of multiple inflammatory lesions; several to many comedones, papules, and pustules; and no more than 1 small nodulocystic lesion. Severe AV (EGSS of 4) was characterized by inflammatory lesions; numerous comedones, papules, and pustules; and possibly a few nodulocystic lesions.¹⁰

Male and female patients aged 12 to 40 years with moderate to severe AV—defined as 20 to 40 inflammatory lesions (papules, pustules, nodules), 20 to 100 noninflammatory lesions (comedones), and no more than 2 nodules—were included in the study. Standard washout periods were required for patients using prior prescription and over-the-counter acne treatments.¹⁰

Efficacy evaluations included inflammatory and noninflammatory lesion counts and EGSS at screening, baseline, and during treatment (weeks 4, 8, and 12).¹⁰ Primary efficacy end points included absolute change in mean inflammatory and noninflammatory lesion counts and the proportion of patients who achieved at least a 2-grade reduction in EGSS from baseline to week 12 (treatment success at end of study). Secondary efficacy end points included mean percentage change from baseline to week 12 in inflammatory and noninflammatory lesion counts and the proportion of patients who considered themselves clear or almost clear at week 12.¹⁰

After 12 weeks of daily treatment, inflammatory and noninflammatory lesion counts decreased by a mean of 60.4% and 51.8%, respectively, with clindamycin-BP 3.75% gel compared to 31.3% and 27.6%, respectively, with vehicle (both P<.001). At weeks 4, 8, and 12, the difference in inflammatory and noninflammatory lesion counts for the active treatment was 17.4%, 24.8%, and 29.1%, respectively, and 8.1%, 19.8%, and 24.2%, respectively, for vehicle.¹⁰

Treatment success (at least a 2-grade improvement in EGSS) was achieved by 9.1% of patients using clindamycin-BP 3.75% gel compared to 4.6% using vehicle by week 4. Additionally, 6.3% of patients considered their AV as clear or almost clear compared to 3.5% with vehicle at week 2 (Figure 1).¹⁰

This analysis represents the first attempt to evaluate and report TOA results with clindamycin-BP 3.75% gel. Time to onset of action for inflammatory lesions treated with clindamycin-BP 3.75% gel was calculated as 2.5 weeks versus 6.2 weeks for vehicle (Figure 2A). Time to onset of action for noninflammatory lesions was 3.7 weeks with clindamycin-BP 3.75% gel versus 8.6 weeks with vehicle (Figure 2B). The difference in TOA between the active and vehicle study groups was 3.7 weeks and 4.9 weeks, respectively. In addition, among actively treated patients, TOA was shorter in females (2.1 weeks) than in males (2.6 weeks) and in moderate AV (2.5 weeks) compared to severe AV (3.0 weeks).

Comment

Differences in lesion counts between clindamycin-BP 3.75% gel and vehicle suggest a clinically relevant benefit in favor of active treatment with both inflammatory and noninflammatory lesions. Nearly twice as many patients were rated as treatment successes using EGSS by week 4 or clear or almost clear as early as week 2 compared to the vehicle group.¹⁰ However, these data are suggested as an overall guide but do not provide adequate guidance on when visible improvement may start to be evident in a given patient.

The analysis reported here shows a TOA of 2.5 weeks with clindamycin-BP 3.75% gel for inflammatory lesions, approximately 4 weeks faster than with the vehicle. In most cases, a reduction in inflammatory lesions is more likely to have a greater impact on patient perception of TOA. Unless a patient is aware or focused enough to actively distinguish visibly between inflammatory and noninflammatory (comedonal) AV lesions, their eye is more likely to be drawn initially to reduction in inflammatory lesions, which are erythematous and more visible at a greater viewing distance. Although noninflammatory AV lesions usually require closer inspection to visualize them (especially closed comedones), they are often slower to respond to treatment. Analysis of the pivotal trial data reports a longer TOA with clindamycin-BP 3.75% gel for noninflammatory lesions (3.7 weeks) versus inflammatory lesions (2.5 weeks).

As expected, TOA was shorter in patients with moderate AV than severe AV (2.5 weeks vs 3.0 weeks). Time to onset of action also was shorter in females overall. It is unclear why we see gender differences in acne studies. A number of reasons have been suggested, including differences in AV pathophysiology and/or treatment adherence.^11,12 Greater efficacy of clindamycin-BP 3.75% gel in females compared with males has already been reported, and better overall efficacy leading to a shorter TOA has been noted by others.¹³

There are limitations with this analysis. First, it is not possible to assess the contributions from each of the monads to the efficacy of clindamycin-BP 3.75% gel or TOA. Also, the data extraction method used assumes a linear progression model during the provided time points and was used to provide some comparison with calculations for other combination products.⁹ Although no strong deviations from the linear model are likely, calculations of TOA using other methodologies may give different results. The definition of a clinically meaningful benefit, defined here as a 25% reduction in the mean lesion count, has been used as a guide, but it has not been validated in clinical practice. It also is important to recognize that the initial visible perception of improvement of AV is likely to differ based on interpatient variability; that is, how different individuals perceive improvement. It also may be affected by differences in baseline severity of AV among different patients. Additionally, the TOA reflects an average duration of time, so it should not be described to patients as a suggestion of when they will definitely see visible improvement in their AV.

Conclusion

Unrealistic expectations of acne therapy or poor tolerability can lead to low adherence and poor clinical outcomes.^1-4 The data on TOA reported here suggests that a clinically meaningful benefit with clindamycin-BP 3.75% gel may be seen in some patients within 2 to 3 weeks and maybe sooner in females or those with milder disease; however, longer durations may be required in some patients. This information can help clinicians and their staff in providing reasonable expectations and stress the importance of encouraging patients about the need to adhere to treatment.

Acknowledgments

The author thanks Brian Bulley, MSc (Inergy Limited, Lindfield, West Sussex, United Kingdom), for publication support. Valeant Pharmaceuticals North America, LLC, funded Inergy’s activities pertaining to this analysis. The author did not receive funding or any form of compensation for authorship of this publication.

Acne vulgaris (AV) is a common skin disease that usually presents in adolescence and can persist into adulthood. Some cases may start in adulthood, especially in women. Acne vulgaris remains a challenge to treat successfully, both in teenagers and adults. Unrealistic expectations that therapy will rapidly clear and sustain clearance of AV completely can lead to incomplete adherence or complete cessation of treatment.^1-4 Local tolerability reactions also may decrease adherence to topical medications. Suboptimal adherence to medications for AV is one of the major reasons for treatment failure.⁵ Acne vulgaris can strongly influence psychological well-being and self-esteem.⁶ In general, severe AV causes more psychological distress, but the adverse emotional impact of AV can be independent of its severity.⁷

An effective relationship between the patient and his/her physician and staff is believed to be important in setting realistic expectations, optimizing adherence, and achieving a positive therapeutic outcome. One component related to setting reasonable expectations is the discussion about when the patient may begin to visibly perceive that the treatment regimen is working. This article evaluates the time course of a clinically meaningful response using pivotal trial data with clindamycin phosphate 1.2%–benzoyl peroxide 3.75% (clindamycin-BP 3.75%) gel for treatment of AV.

Are data available that evaluate the time course of a clinically relevant response to treatment of AV?

Unfortunately, data on what might be perceived as a clinically meaningful improvement in AV and how long it might take to achieve this treatment effect are limited. A meta-analysis of more than 4000 patients with moderate to severe AV suggested that a 10% to 20% difference in acne lesion counts from baseline as compared to a subsequent designated time point was clinically relevant.⁸ A review of 24 comparative studies of patients with mild to moderate AV used a primary outcome parameter of a 25% reduction in mean inflammatory lesion count to evaluate time to onset of action (TOA) to achieve a clinically meaningful benefit.⁹ This outcome was based on a previously identified threshold of clinical relevance and the authors’ clinical experience in a patient population with milder AV. In this same analysis, a difference of greater than 4 days between the active group and the vehicle group was considered to be relevant to the patient.⁹

A faster onset of visible improvement as perceived by the patient should be more desirable and is likely to improve treatment adherence, as long as it is not counterbalanced by an increase in adverse events.

What is meant by TOA?

Time to onset of action refers to the duration required to achieve a 25% mean lesion count reduction from baseline, which is believed to correlate with the time point at which many patients would be able to perceive visible improvement when viewing their full face. Therefore, TOA represents an attempt to correlate data that is quantitative (based on lesion count reduction) with what is likely to be the average time that a patient may qualitatively observe an initial visible improvement in their AV. This concept may be useful as a tool when communicating with AV patients but should not be used in a way that will overpromise and underdeliver; rather, it is a guide for discussion with the patient and with a parent or guardian when applicable.

Consistent with the comparative AV study analysis that evaluated TOA, a linear course of lesion reductions between the provided time intervals was assumed. In this linear model, the TOA was calculated using the 2 extracted lesion count values between which the 25% lesion reduction was achieved as well as their corresponding given time points.⁹ Differences between the results in the active and vehicle study arms were calculated for a number of determinants.

How was pivotal trial data with clindamycin-BP 3.75% gel used to assess TOA?

A total of 498 patients with moderate to severe AV were randomized (1:1) to receive clindamycin-BP 3.75% gel or vehicle in a multicenter, double-blind, controlled, 12-week, 2-arm study.¹⁰ Before randomization, patients were stratified by acne severity based on a static Evaluator’s Global Severity Score (EGSS) ranging from 0 (clear) to 5 (very severe). Specifically, moderate AV (EGSS of 3) was described as predominantly noninflammatory lesions with evidence of multiple inflammatory lesions; several to many comedones, papules, and pustules; and no more than 1 small nodulocystic lesion. Severe AV (EGSS of 4) was characterized by inflammatory lesions; numerous comedones, papules, and pustules; and possibly a few nodulocystic lesions.¹⁰

Male and female patients aged 12 to 40 years with moderate to severe AV—defined as 20 to 40 inflammatory lesions (papules, pustules, nodules), 20 to 100 noninflammatory lesions (comedones), and no more than 2 nodules—were included in the study. Standard washout periods were required for patients using prior prescription and over-the-counter acne treatments.¹⁰

Efficacy evaluations included inflammatory and noninflammatory lesion counts and EGSS at screening, baseline, and during treatment (weeks 4, 8, and 12).¹⁰ Primary efficacy end points included absolute change in mean inflammatory and noninflammatory lesion counts and the proportion of patients who achieved at least a 2-grade reduction in EGSS from baseline to week 12 (treatment success at end of study). Secondary efficacy end points included mean percentage change from baseline to week 12 in inflammatory and noninflammatory lesion counts and the proportion of patients who considered themselves clear or almost clear at week 12.¹⁰

After 12 weeks of daily treatment, inflammatory and noninflammatory lesion counts decreased by a mean of 60.4% and 51.8%, respectively, with clindamycin-BP 3.75% gel compared to 31.3% and 27.6%, respectively, with vehicle (both P<.001). At weeks 4, 8, and 12, the difference in inflammatory and noninflammatory lesion counts for the active treatment was 17.4%, 24.8%, and 29.1%, respectively, and 8.1%, 19.8%, and 24.2%, respectively, for vehicle.¹⁰

Treatment success (at least a 2-grade improvement in EGSS) was achieved by 9.1% of patients using clindamycin-BP 3.75% gel compared to 4.6% using vehicle by week 4. Additionally, 6.3% of patients considered their AV as clear or almost clear compared to 3.5% with vehicle at week 2 (Figure 1).¹⁰

This analysis represents the first attempt to evaluate and report TOA results with clindamycin-BP 3.75% gel. Time to onset of action for inflammatory lesions treated with clindamycin-BP 3.75% gel was calculated as 2.5 weeks versus 6.2 weeks for vehicle (Figure 2A). Time to onset of action for noninflammatory lesions was 3.7 weeks with clindamycin-BP 3.75% gel versus 8.6 weeks with vehicle (Figure 2B). The difference in TOA between the active and vehicle study groups was 3.7 weeks and 4.9 weeks, respectively. In addition, among actively treated patients, TOA was shorter in females (2.1 weeks) than in males (2.6 weeks) and in moderate AV (2.5 weeks) compared to severe AV (3.0 weeks).

Comment

Differences in lesion counts between clindamycin-BP 3.75% gel and vehicle suggest a clinically relevant benefit in favor of active treatment with both inflammatory and noninflammatory lesions. Nearly twice as many patients were rated as treatment successes using EGSS by week 4 or clear or almost clear as early as week 2 compared to the vehicle group.¹⁰ However, these data are suggested as an overall guide but do not provide adequate guidance on when visible improvement may start to be evident in a given patient.

The analysis reported here shows a TOA of 2.5 weeks with clindamycin-BP 3.75% gel for inflammatory lesions, approximately 4 weeks faster than with the vehicle. In most cases, a reduction in inflammatory lesions is more likely to have a greater impact on patient perception of TOA. Unless a patient is aware or focused enough to actively distinguish visibly between inflammatory and noninflammatory (comedonal) AV lesions, their eye is more likely to be drawn initially to reduction in inflammatory lesions, which are erythematous and more visible at a greater viewing distance. Although noninflammatory AV lesions usually require closer inspection to visualize them (especially closed comedones), they are often slower to respond to treatment. Analysis of the pivotal trial data reports a longer TOA with clindamycin-BP 3.75% gel for noninflammatory lesions (3.7 weeks) versus inflammatory lesions (2.5 weeks).

As expected, TOA was shorter in patients with moderate AV than severe AV (2.5 weeks vs 3.0 weeks). Time to onset of action also was shorter in females overall. It is unclear why we see gender differences in acne studies. A number of reasons have been suggested, including differences in AV pathophysiology and/or treatment adherence.^11,12 Greater efficacy of clindamycin-BP 3.75% gel in females compared with males has already been reported, and better overall efficacy leading to a shorter TOA has been noted by others.¹³

There are limitations with this analysis. First, it is not possible to assess the contributions from each of the monads to the efficacy of clindamycin-BP 3.75% gel or TOA. Also, the data extraction method used assumes a linear progression model during the provided time points and was used to provide some comparison with calculations for other combination products.⁹ Although no strong deviations from the linear model are likely, calculations of TOA using other methodologies may give different results. The definition of a clinically meaningful benefit, defined here as a 25% reduction in the mean lesion count, has been used as a guide, but it has not been validated in clinical practice. It also is important to recognize that the initial visible perception of improvement of AV is likely to differ based on interpatient variability; that is, how different individuals perceive improvement. It also may be affected by differences in baseline severity of AV among different patients. Additionally, the TOA reflects an average duration of time, so it should not be described to patients as a suggestion of when they will definitely see visible improvement in their AV.

Conclusion

Unrealistic expectations of acne therapy or poor tolerability can lead to low adherence and poor clinical outcomes.^1-4 The data on TOA reported here suggests that a clinically meaningful benefit with clindamycin-BP 3.75% gel may be seen in some patients within 2 to 3 weeks and maybe sooner in females or those with milder disease; however, longer durations may be required in some patients. This information can help clinicians and their staff in providing reasonable expectations and stress the importance of encouraging patients about the need to adhere to treatment.

Acknowledgments

The author thanks Brian Bulley, MSc (Inergy Limited, Lindfield, West Sussex, United Kingdom), for publication support. Valeant Pharmaceuticals North America, LLC, funded Inergy’s activities pertaining to this analysis. The author did not receive funding or any form of compensation for authorship of this publication.

Acne vulgaris (AV) is a common skin disease that usually presents in adolescence and can persist into adulthood. Some cases may start in adulthood, especially in women. Acne vulgaris remains a challenge to treat successfully, both in teenagers and adults. Unrealistic expectations that therapy will rapidly clear and sustain clearance of AV completely can lead to incomplete adherence or complete cessation of treatment.^1-4 Local tolerability reactions also may decrease adherence to topical medications. Suboptimal adherence to medications for AV is one of the major reasons for treatment failure.⁵ Acne vulgaris can strongly influence psychological well-being and self-esteem.⁶ In general, severe AV causes more psychological distress, but the adverse emotional impact of AV can be independent of its severity.⁷

An effective relationship between the patient and his/her physician and staff is believed to be important in setting realistic expectations, optimizing adherence, and achieving a positive therapeutic outcome. One component related to setting reasonable expectations is the discussion about when the patient may begin to visibly perceive that the treatment regimen is working. This article evaluates the time course of a clinically meaningful response using pivotal trial data with clindamycin phosphate 1.2%–benzoyl peroxide 3.75% (clindamycin-BP 3.75%) gel for treatment of AV.

Are data available that evaluate the time course of a clinically relevant response to treatment of AV?

Unfortunately, data on what might be perceived as a clinically meaningful improvement in AV and how long it might take to achieve this treatment effect are limited. A meta-analysis of more than 4000 patients with moderate to severe AV suggested that a 10% to 20% difference in acne lesion counts from baseline as compared to a subsequent designated time point was clinically relevant.⁸ A review of 24 comparative studies of patients with mild to moderate AV used a primary outcome parameter of a 25% reduction in mean inflammatory lesion count to evaluate time to onset of action (TOA) to achieve a clinically meaningful benefit.⁹ This outcome was based on a previously identified threshold of clinical relevance and the authors’ clinical experience in a patient population with milder AV. In this same analysis, a difference of greater than 4 days between the active group and the vehicle group was considered to be relevant to the patient.⁹

A faster onset of visible improvement as perceived by the patient should be more desirable and is likely to improve treatment adherence, as long as it is not counterbalanced by an increase in adverse events.

What is meant by TOA?

Time to onset of action refers to the duration required to achieve a 25% mean lesion count reduction from baseline, which is believed to correlate with the time point at which many patients would be able to perceive visible improvement when viewing their full face. Therefore, TOA represents an attempt to correlate data that is quantitative (based on lesion count reduction) with what is likely to be the average time that a patient may qualitatively observe an initial visible improvement in their AV. This concept may be useful as a tool when communicating with AV patients but should not be used in a way that will overpromise and underdeliver; rather, it is a guide for discussion with the patient and with a parent or guardian when applicable.

Consistent with the comparative AV study analysis that evaluated TOA, a linear course of lesion reductions between the provided time intervals was assumed. In this linear model, the TOA was calculated using the 2 extracted lesion count values between which the 25% lesion reduction was achieved as well as their corresponding given time points.⁹ Differences between the results in the active and vehicle study arms were calculated for a number of determinants.

How was pivotal trial data with clindamycin-BP 3.75% gel used to assess TOA?

A total of 498 patients with moderate to severe AV were randomized (1:1) to receive clindamycin-BP 3.75% gel or vehicle in a multicenter, double-blind, controlled, 12-week, 2-arm study.¹⁰ Before randomization, patients were stratified by acne severity based on a static Evaluator’s Global Severity Score (EGSS) ranging from 0 (clear) to 5 (very severe). Specifically, moderate AV (EGSS of 3) was described as predominantly noninflammatory lesions with evidence of multiple inflammatory lesions; several to many comedones, papules, and pustules; and no more than 1 small nodulocystic lesion. Severe AV (EGSS of 4) was characterized by inflammatory lesions; numerous comedones, papules, and pustules; and possibly a few nodulocystic lesions.¹⁰

Male and female patients aged 12 to 40 years with moderate to severe AV—defined as 20 to 40 inflammatory lesions (papules, pustules, nodules), 20 to 100 noninflammatory lesions (comedones), and no more than 2 nodules—were included in the study. Standard washout periods were required for patients using prior prescription and over-the-counter acne treatments.¹⁰

Efficacy evaluations included inflammatory and noninflammatory lesion counts and EGSS at screening, baseline, and during treatment (weeks 4, 8, and 12).¹⁰ Primary efficacy end points included absolute change in mean inflammatory and noninflammatory lesion counts and the proportion of patients who achieved at least a 2-grade reduction in EGSS from baseline to week 12 (treatment success at end of study). Secondary efficacy end points included mean percentage change from baseline to week 12 in inflammatory and noninflammatory lesion counts and the proportion of patients who considered themselves clear or almost clear at week 12.¹⁰

After 12 weeks of daily treatment, inflammatory and noninflammatory lesion counts decreased by a mean of 60.4% and 51.8%, respectively, with clindamycin-BP 3.75% gel compared to 31.3% and 27.6%, respectively, with vehicle (both P<.001). At weeks 4, 8, and 12, the difference in inflammatory and noninflammatory lesion counts for the active treatment was 17.4%, 24.8%, and 29.1%, respectively, and 8.1%, 19.8%, and 24.2%, respectively, for vehicle.¹⁰

Treatment success (at least a 2-grade improvement in EGSS) was achieved by 9.1% of patients using clindamycin-BP 3.75% gel compared to 4.6% using vehicle by week 4. Additionally, 6.3% of patients considered their AV as clear or almost clear compared to 3.5% with vehicle at week 2 (Figure 1).¹⁰

This analysis represents the first attempt to evaluate and report TOA results with clindamycin-BP 3.75% gel. Time to onset of action for inflammatory lesions treated with clindamycin-BP 3.75% gel was calculated as 2.5 weeks versus 6.2 weeks for vehicle (Figure 2A). Time to onset of action for noninflammatory lesions was 3.7 weeks with clindamycin-BP 3.75% gel versus 8.6 weeks with vehicle (Figure 2B). The difference in TOA between the active and vehicle study groups was 3.7 weeks and 4.9 weeks, respectively. In addition, among actively treated patients, TOA was shorter in females (2.1 weeks) than in males (2.6 weeks) and in moderate AV (2.5 weeks) compared to severe AV (3.0 weeks).

Comment

Differences in lesion counts between clindamycin-BP 3.75% gel and vehicle suggest a clinically relevant benefit in favor of active treatment with both inflammatory and noninflammatory lesions. Nearly twice as many patients were rated as treatment successes using EGSS by week 4 or clear or almost clear as early as week 2 compared to the vehicle group.¹⁰ However, these data are suggested as an overall guide but do not provide adequate guidance on when visible improvement may start to be evident in a given patient.

The analysis reported here shows a TOA of 2.5 weeks with clindamycin-BP 3.75% gel for inflammatory lesions, approximately 4 weeks faster than with the vehicle. In most cases, a reduction in inflammatory lesions is more likely to have a greater impact on patient perception of TOA. Unless a patient is aware or focused enough to actively distinguish visibly between inflammatory and noninflammatory (comedonal) AV lesions, their eye is more likely to be drawn initially to reduction in inflammatory lesions, which are erythematous and more visible at a greater viewing distance. Although noninflammatory AV lesions usually require closer inspection to visualize them (especially closed comedones), they are often slower to respond to treatment. Analysis of the pivotal trial data reports a longer TOA with clindamycin-BP 3.75% gel for noninflammatory lesions (3.7 weeks) versus inflammatory lesions (2.5 weeks).

As expected, TOA was shorter in patients with moderate AV than severe AV (2.5 weeks vs 3.0 weeks). Time to onset of action also was shorter in females overall. It is unclear why we see gender differences in acne studies. A number of reasons have been suggested, including differences in AV pathophysiology and/or treatment adherence.^11,12 Greater efficacy of clindamycin-BP 3.75% gel in females compared with males has already been reported, and better overall efficacy leading to a shorter TOA has been noted by others.¹³

There are limitations with this analysis. First, it is not possible to assess the contributions from each of the monads to the efficacy of clindamycin-BP 3.75% gel or TOA. Also, the data extraction method used assumes a linear progression model during the provided time points and was used to provide some comparison with calculations for other combination products.⁹ Although no strong deviations from the linear model are likely, calculations of TOA using other methodologies may give different results. The definition of a clinically meaningful benefit, defined here as a 25% reduction in the mean lesion count, has been used as a guide, but it has not been validated in clinical practice. It also is important to recognize that the initial visible perception of improvement of AV is likely to differ based on interpatient variability; that is, how different individuals perceive improvement. It also may be affected by differences in baseline severity of AV among different patients. Additionally, the TOA reflects an average duration of time, so it should not be described to patients as a suggestion of when they will definitely see visible improvement in their AV.

Conclusion

Unrealistic expectations of acne therapy or poor tolerability can lead to low adherence and poor clinical outcomes.^1-4 The data on TOA reported here suggests that a clinically meaningful benefit with clindamycin-BP 3.75% gel may be seen in some patients within 2 to 3 weeks and maybe sooner in females or those with milder disease; however, longer durations may be required in some patients. This information can help clinicians and their staff in providing reasonable expectations and stress the importance of encouraging patients about the need to adhere to treatment.

Acknowledgments

The author thanks Brian Bulley, MSc (Inergy Limited, Lindfield, West Sussex, United Kingdom), for publication support. Valeant Pharmaceuticals North America, LLC, funded Inergy’s activities pertaining to this analysis. The author did not receive funding or any form of compensation for authorship of this publication.

Program Director

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Professor of Obstetrics and Gynecology
New York University School of Medicine
Director of Gynecological Ultrasound
Co-Director of Bone Densitometry
Department of Obstetrics and Gynecology
New York University Medical Center
New York, New York

Authors/Editors

Reni S. Butler, MD
Assistant Professor, Diagnostic Radiology
Yale University
New Haven, Connecticut

Bonnie N. Joe, MD, PhD, FSBI
Professor of Radiology and Biomedical Imaging
Chief, Breast Imaging
University of California, San Francisco
San Francisco, California

Bruce A. Porter, MD, FACR
Clinical Associate Professor
Department of Radiology
University of Washington School of Medicine
Seattle, Washington

Michael J. Ulissey, MD, FACR
Adjunct Professor of Radiology
University of Texas
Health Sciences Center
San Antonio, Texas
Breast Diagnostic Centers
Auburn and Federal Way, Washington

Conflict of Interest Disclosure

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Consultant: Cook OB/GYN, fees received
No Disclosures to Declare
Reni S. Butler, MD; Bonnie N. Joe, MD, PhD, FSBI;
Bruce A. Porter, MD, FACR; Michael J. Ulissey, MD, FACR;
Heidi M. Wilson, Course Director

Program Director

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Professor of Obstetrics and Gynecology
New York University School of Medicine
Director of Gynecological Ultrasound
Co-Director of Bone Densitometry
Department of Obstetrics and Gynecology
New York University Medical Center
New York, New York

Authors/Editors

Reni S. Butler, MD
Assistant Professor, Diagnostic Radiology
Yale University
New Haven, Connecticut

Bonnie N. Joe, MD, PhD, FSBI
Professor of Radiology and Biomedical Imaging
Chief, Breast Imaging
University of California, San Francisco
San Francisco, California

Bruce A. Porter, MD, FACR
Clinical Associate Professor
Department of Radiology
University of Washington School of Medicine
Seattle, Washington

Michael J. Ulissey, MD, FACR
Adjunct Professor of Radiology
University of Texas
Health Sciences Center
San Antonio, Texas
Breast Diagnostic Centers
Auburn and Federal Way, Washington

Conflict of Interest Disclosure

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Consultant: Cook OB/GYN, fees received
No Disclosures to Declare
Reni S. Butler, MD; Bonnie N. Joe, MD, PhD, FSBI;
Bruce A. Porter, MD, FACR; Michael J. Ulissey, MD, FACR;
Heidi M. Wilson, Course Director

Program Director

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Professor of Obstetrics and Gynecology
New York University School of Medicine
Director of Gynecological Ultrasound
Co-Director of Bone Densitometry
Department of Obstetrics and Gynecology
New York University Medical Center
New York, New York

Authors/Editors

Reni S. Butler, MD
Assistant Professor, Diagnostic Radiology
Yale University
New Haven, Connecticut

Bonnie N. Joe, MD, PhD, FSBI
Professor of Radiology and Biomedical Imaging
Chief, Breast Imaging
University of California, San Francisco
San Francisco, California

Bruce A. Porter, MD, FACR
Clinical Associate Professor
Department of Radiology
University of Washington School of Medicine
Seattle, Washington

Michael J. Ulissey, MD, FACR
Adjunct Professor of Radiology
University of Texas
Health Sciences Center
San Antonio, Texas
Breast Diagnostic Centers
Auburn and Federal Way, Washington

Conflict of Interest Disclosure

Steven R. Goldstein, MD, CCD, NCMP, FACOG
Consultant: Cook OB/GYN, fees received
No Disclosures to Declare
Reni S. Butler, MD; Bonnie N. Joe, MD, PhD, FSBI;
Bruce A. Porter, MD, FACR; Michael J. Ulissey, MD, FACR;
Heidi M. Wilson, Course Director

VANCOUVER—Ocrelizumab, a B-cell depleting humanized monoclonal antibody being developed by Hoffman–La Roche, consistently reduces relapses, disability progression, and new or enlarging lesions, compared with interferon beta-1a, in patients with relapsing-remitting multiple sclerosis (MS), according to two phase III trials reported at the 68th Annual Meeting of the American Academy of Neurology.

OPERA I and OPERA II

The identical trials, dubbed OPERA I and OPERA II, each included about 800 patients. Subjects were randomized one-to-one to 600 mg of IV ocrelizumab every 24 weeks or to 44 μg of subcutaneous interferon beta-1a three times weekly for 96 weeks. Patients had early disease, and a significant proportion was naive to MS treatments.

At 96 weeks, 47.9% and 47.5% of patients receiving ocrelizumab, respectively, had no evidence of disease activity (NEDA) versus 29.2% and 25.1% of patients receiving interferon. NEDA is a composite score defined as the absence of relapses, confirmed disability progression, and new or enlarging T2 or gadolinium-enhancing T1 lesions.

In both studies, relapses occurred in about 20% of patients receiving ocrelizumab versus about 35% of patients receiving interferon. About 10% of participants receiving ocrelizumab and about 15% of patients receiving interferon had clinical disease progression. Similarly, about 10% of patients receiving ocrelizumab developed new gadolinium-enhancing lesions, compared with about 35% of those receiving interferon. New or enlarging T2 lesions were found in about 40% of the ocrelizumab groups and in more than 60% of the interferon groups.

After week 24, 96% of patients receiving ocrelizumab, compared with between 60% and 70% of patients receiving interferon, were free of new or enlarging T2 lesions.

In short, ocrelizumab “resulted in greater achievement of NEDA versus [interferon] over 96 weeks, with elimination of new or enlarging T2 lesions in nearly all patients after week 24,” the researchers concluded.

Ocrelizumab Appears Safe

“These are very impressive numbers,” especially because ocrelizumab was compared with a standard treatment, said investigator Anthony Traboulsee, MD, a neurologist at the University of British Columbia in Vancouver, Canada. “There was a wonderful constancy of results” across the trials; “a very highly effective treatment is emerging for multiple sclerosis.” Many patients opted to stay on ocrelizumab at the end of the trials.

Roche plans to submit its approval package to the FDA in the first half of 2016. The FDA granted the biologic breakthrough, fast-track status for primary progressive MS based on the strength of an earlier phase III trial. At present, there are no MS agents indicated for primary progressive disease.

Patients in OPERA were 37 years old, on average, and two-thirds were women. The mean baseline score on the Extended Disability Status Scale was 2.77, and the mean time since diagnosis was about four years. Patients had had about 1.5 relapses in the first and second years before entering the studies.

An Alternative to Natalizumab?

The positive results and the increasing buzz about ocrelizumab in the MS community raise the question of how the treatment will fit into the MS armamentarium if it is approved. A review in Therapeutic Advances in Neurological Disorders addressed the issue in January, before the OPERA results were made public.

It’s unclear whether ocrelizumab will become the preferred option when patients have progression on first-line agents such as interferon and glatiramer acetate. Phase II data suggest that ocrelizumab’s “effect on clinical disease activity [seems] to be of the same magnitude, compared with that of fingolimod and natalizumab,” and that the treatment will likely be an alternative to natalizumab and alemtuzumab. “Ocrelizumab seems to have a more favorable risk–benefit profile, compared with natalizumab in [John Cunningham (JC)] virus antibody–positive patients, whereas natalizumab in JC virus antibody–negative patients appears safer. Hence, ocrelizumab could be an attractive option among second-line therapies in patients who are JC virus antibody–positive, whereas natalizumab, or, alternatively, oral fingolimod, would be the first choice among second-line therapies in JC virus antibody–negative patients,” said authors Per Soelberg Sorensen, MD, and Morten Blinkenberg, MD, PhD, both MS neurologists at the University of Copenhagen.

“It needs to be emphasized that long-term data on the safety of ocrelizumab in the treatment of MS is warranted, and therefore postmarketing safety programs will be needed,” they said. The risk of PML with long-term use is unknown. “Another unsolved question is whether ocrelizumab therapy should be applied at fixed intervals, eg, every six months [as in OPERA], or if retreatment should be guided by the recovery of CD19-positive B cells.”

In any case, infusion reactions with ocrelizumab should be less common than with rituximab, another B-cell depleter used off-label for MS, because ocrelizumab is a more humanized antibody, they concluded.

—M. Alexander Otto

VANCOUVER—Ocrelizumab, a B-cell depleting humanized monoclonal antibody being developed by Hoffman–La Roche, consistently reduces relapses, disability progression, and new or enlarging lesions, compared with interferon beta-1a, in patients with relapsing-remitting multiple sclerosis (MS), according to two phase III trials reported at the 68th Annual Meeting of the American Academy of Neurology.

OPERA I and OPERA II

The identical trials, dubbed OPERA I and OPERA II, each included about 800 patients. Subjects were randomized one-to-one to 600 mg of IV ocrelizumab every 24 weeks or to 44 μg of subcutaneous interferon beta-1a three times weekly for 96 weeks. Patients had early disease, and a significant proportion was naive to MS treatments.

At 96 weeks, 47.9% and 47.5% of patients receiving ocrelizumab, respectively, had no evidence of disease activity (NEDA) versus 29.2% and 25.1% of patients receiving interferon. NEDA is a composite score defined as the absence of relapses, confirmed disability progression, and new or enlarging T2 or gadolinium-enhancing T1 lesions.

In both studies, relapses occurred in about 20% of patients receiving ocrelizumab versus about 35% of patients receiving interferon. About 10% of participants receiving ocrelizumab and about 15% of patients receiving interferon had clinical disease progression. Similarly, about 10% of patients receiving ocrelizumab developed new gadolinium-enhancing lesions, compared with about 35% of those receiving interferon. New or enlarging T2 lesions were found in about 40% of the ocrelizumab groups and in more than 60% of the interferon groups.

After week 24, 96% of patients receiving ocrelizumab, compared with between 60% and 70% of patients receiving interferon, were free of new or enlarging T2 lesions.

In short, ocrelizumab “resulted in greater achievement of NEDA versus [interferon] over 96 weeks, with elimination of new or enlarging T2 lesions in nearly all patients after week 24,” the researchers concluded.

Ocrelizumab Appears Safe

“These are very impressive numbers,” especially because ocrelizumab was compared with a standard treatment, said investigator Anthony Traboulsee, MD, a neurologist at the University of British Columbia in Vancouver, Canada. “There was a wonderful constancy of results” across the trials; “a very highly effective treatment is emerging for multiple sclerosis.” Many patients opted to stay on ocrelizumab at the end of the trials.

Roche plans to submit its approval package to the FDA in the first half of 2016. The FDA granted the biologic breakthrough, fast-track status for primary progressive MS based on the strength of an earlier phase III trial. At present, there are no MS agents indicated for primary progressive disease.

Patients in OPERA were 37 years old, on average, and two-thirds were women. The mean baseline score on the Extended Disability Status Scale was 2.77, and the mean time since diagnosis was about four years. Patients had had about 1.5 relapses in the first and second years before entering the studies.

An Alternative to Natalizumab?

The positive results and the increasing buzz about ocrelizumab in the MS community raise the question of how the treatment will fit into the MS armamentarium if it is approved. A review in Therapeutic Advances in Neurological Disorders addressed the issue in January, before the OPERA results were made public.

It’s unclear whether ocrelizumab will become the preferred option when patients have progression on first-line agents such as interferon and glatiramer acetate. Phase II data suggest that ocrelizumab’s “effect on clinical disease activity [seems] to be of the same magnitude, compared with that of fingolimod and natalizumab,” and that the treatment will likely be an alternative to natalizumab and alemtuzumab. “Ocrelizumab seems to have a more favorable risk–benefit profile, compared with natalizumab in [John Cunningham (JC)] virus antibody–positive patients, whereas natalizumab in JC virus antibody–negative patients appears safer. Hence, ocrelizumab could be an attractive option among second-line therapies in patients who are JC virus antibody–positive, whereas natalizumab, or, alternatively, oral fingolimod, would be the first choice among second-line therapies in JC virus antibody–negative patients,” said authors Per Soelberg Sorensen, MD, and Morten Blinkenberg, MD, PhD, both MS neurologists at the University of Copenhagen.

“It needs to be emphasized that long-term data on the safety of ocrelizumab in the treatment of MS is warranted, and therefore postmarketing safety programs will be needed,” they said. The risk of PML with long-term use is unknown. “Another unsolved question is whether ocrelizumab therapy should be applied at fixed intervals, eg, every six months [as in OPERA], or if retreatment should be guided by the recovery of CD19-positive B cells.”

In any case, infusion reactions with ocrelizumab should be less common than with rituximab, another B-cell depleter used off-label for MS, because ocrelizumab is a more humanized antibody, they concluded.

—M. Alexander Otto

VANCOUVER—Ocrelizumab, a B-cell depleting humanized monoclonal antibody being developed by Hoffman–La Roche, consistently reduces relapses, disability progression, and new or enlarging lesions, compared with interferon beta-1a, in patients with relapsing-remitting multiple sclerosis (MS), according to two phase III trials reported at the 68th Annual Meeting of the American Academy of Neurology.

OPERA I and OPERA II

The identical trials, dubbed OPERA I and OPERA II, each included about 800 patients. Subjects were randomized one-to-one to 600 mg of IV ocrelizumab every 24 weeks or to 44 μg of subcutaneous interferon beta-1a three times weekly for 96 weeks. Patients had early disease, and a significant proportion was naive to MS treatments.

At 96 weeks, 47.9% and 47.5% of patients receiving ocrelizumab, respectively, had no evidence of disease activity (NEDA) versus 29.2% and 25.1% of patients receiving interferon. NEDA is a composite score defined as the absence of relapses, confirmed disability progression, and new or enlarging T2 or gadolinium-enhancing T1 lesions.

In both studies, relapses occurred in about 20% of patients receiving ocrelizumab versus about 35% of patients receiving interferon. About 10% of participants receiving ocrelizumab and about 15% of patients receiving interferon had clinical disease progression. Similarly, about 10% of patients receiving ocrelizumab developed new gadolinium-enhancing lesions, compared with about 35% of those receiving interferon. New or enlarging T2 lesions were found in about 40% of the ocrelizumab groups and in more than 60% of the interferon groups.

After week 24, 96% of patients receiving ocrelizumab, compared with between 60% and 70% of patients receiving interferon, were free of new or enlarging T2 lesions.

In short, ocrelizumab “resulted in greater achievement of NEDA versus [interferon] over 96 weeks, with elimination of new or enlarging T2 lesions in nearly all patients after week 24,” the researchers concluded.

Ocrelizumab Appears Safe

“These are very impressive numbers,” especially because ocrelizumab was compared with a standard treatment, said investigator Anthony Traboulsee, MD, a neurologist at the University of British Columbia in Vancouver, Canada. “There was a wonderful constancy of results” across the trials; “a very highly effective treatment is emerging for multiple sclerosis.” Many patients opted to stay on ocrelizumab at the end of the trials.

Roche plans to submit its approval package to the FDA in the first half of 2016. The FDA granted the biologic breakthrough, fast-track status for primary progressive MS based on the strength of an earlier phase III trial. At present, there are no MS agents indicated for primary progressive disease.

Patients in OPERA were 37 years old, on average, and two-thirds were women. The mean baseline score on the Extended Disability Status Scale was 2.77, and the mean time since diagnosis was about four years. Patients had had about 1.5 relapses in the first and second years before entering the studies.

An Alternative to Natalizumab?

The positive results and the increasing buzz about ocrelizumab in the MS community raise the question of how the treatment will fit into the MS armamentarium if it is approved. A review in Therapeutic Advances in Neurological Disorders addressed the issue in January, before the OPERA results were made public.

It’s unclear whether ocrelizumab will become the preferred option when patients have progression on first-line agents such as interferon and glatiramer acetate. Phase II data suggest that ocrelizumab’s “effect on clinical disease activity [seems] to be of the same magnitude, compared with that of fingolimod and natalizumab,” and that the treatment will likely be an alternative to natalizumab and alemtuzumab. “Ocrelizumab seems to have a more favorable risk–benefit profile, compared with natalizumab in [John Cunningham (JC)] virus antibody–positive patients, whereas natalizumab in JC virus antibody–negative patients appears safer. Hence, ocrelizumab could be an attractive option among second-line therapies in patients who are JC virus antibody–positive, whereas natalizumab, or, alternatively, oral fingolimod, would be the first choice among second-line therapies in JC virus antibody–negative patients,” said authors Per Soelberg Sorensen, MD, and Morten Blinkenberg, MD, PhD, both MS neurologists at the University of Copenhagen.

“It needs to be emphasized that long-term data on the safety of ocrelizumab in the treatment of MS is warranted, and therefore postmarketing safety programs will be needed,” they said. The risk of PML with long-term use is unknown. “Another unsolved question is whether ocrelizumab therapy should be applied at fixed intervals, eg, every six months [as in OPERA], or if retreatment should be guided by the recovery of CD19-positive B cells.”

In any case, infusion reactions with ocrelizumab should be less common than with rituximab, another B-cell depleter used off-label for MS, because ocrelizumab is a more humanized antibody, they concluded.

—M. Alexander Otto

NEW ORLEANS – Premenopausal women with type 1 diabetes mellitus have a higher cardiovascular risk, compared with their diabetes-free counterparts. Among postmenopausal women, however, those with type 1 diabetes do not have a higher cardiovascular risk, compared with their peers who do not have diabetes, with the exception of those aged 54 and older.

Those are key findings from an analysis of women enrolled in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study.

Doug Brunk/Frontline Medical News

“In general [premenopausal] women have a better cardiovascular profile than do men, but we don’t see that same effect in diabetic women,” lead author Amena Keshawarz said in an interview in advance of the annual scientific sessions of the American Diabetes Association. “They lose some of that protection. We’re wondering if that has some sort of relationship with menopause, because once women undergo menopause they tend to lose that protective factor.”

Ms. Keshawarz, a doctoral student and research assistant at the University of Colorado Barbara Davis Center for Childhood Diabetes, Aurora, and her associates used carotid intima-media thickness (cIMT) and the presence of coronary artery calcification to measure the cardiovascular risk by menopausal status in 106 women with type 1 diabetes and 140 nondiabetic women who were enrolled in CACTI. The patients ranged in age from 33-74 years and the data were collected between January 2014 and May 2016. Multivariable linear and logistic regressions were used to examine the differences in cIMT and to estimate the odds ratio for coronary artery calcification (CAC). The models were run for the following ages separately: 42, 42, 48, 51, 54, and 57 years.

As a group, women with type 1 diabetes were younger than their counterparts without diabetes (a mean age of 51 vs. 55 years, respectively; P = .002), but menopause age did not differ by diabetes status. Ms. Keshawarz reported that women with type 1 diabetes had significantly higher age-adjusted odds of significant CAC and higher cIMT, compared with those in the nondiabetic group, but these relationships differed by age and menopause status. For example, among premenopausal women, type 1 diabetes increased the odds of CAC at all ages, and cIMT was higher in women with type 1 diabetes, compared with those in the nondiabetic group at age 45 years and older. Among postmenopausal women, type 1 diabetes was associated with only higher CAC at age 54 years and older and with higher cIMT at age 57 years.

“Type 1 diabetic women face unique problems in their health that are not just endocrinology-related,” Ms. Keshawarz said. “If they haven’t undergone menopause yet, that needs to be taken into account when you’re proposing interventions and lifestyle and behavioral changes, because there is an increased possibility that they’re going to be at higher risk of coronary artery calcification and thicker [coronary] artery walls.”

The study was supported by grants from the American Diabetes Association and the National Institutes of Health. Ms. Keshawarz reported having no financial disclosures.

[email protected]

NEW ORLEANS – Premenopausal women with type 1 diabetes mellitus have a higher cardiovascular risk, compared with their diabetes-free counterparts. Among postmenopausal women, however, those with type 1 diabetes do not have a higher cardiovascular risk, compared with their peers who do not have diabetes, with the exception of those aged 54 and older.

Those are key findings from an analysis of women enrolled in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study.

Doug Brunk/Frontline Medical News

“In general [premenopausal] women have a better cardiovascular profile than do men, but we don’t see that same effect in diabetic women,” lead author Amena Keshawarz said in an interview in advance of the annual scientific sessions of the American Diabetes Association. “They lose some of that protection. We’re wondering if that has some sort of relationship with menopause, because once women undergo menopause they tend to lose that protective factor.”

Ms. Keshawarz, a doctoral student and research assistant at the University of Colorado Barbara Davis Center for Childhood Diabetes, Aurora, and her associates used carotid intima-media thickness (cIMT) and the presence of coronary artery calcification to measure the cardiovascular risk by menopausal status in 106 women with type 1 diabetes and 140 nondiabetic women who were enrolled in CACTI. The patients ranged in age from 33-74 years and the data were collected between January 2014 and May 2016. Multivariable linear and logistic regressions were used to examine the differences in cIMT and to estimate the odds ratio for coronary artery calcification (CAC). The models were run for the following ages separately: 42, 42, 48, 51, 54, and 57 years.

As a group, women with type 1 diabetes were younger than their counterparts without diabetes (a mean age of 51 vs. 55 years, respectively; P = .002), but menopause age did not differ by diabetes status. Ms. Keshawarz reported that women with type 1 diabetes had significantly higher age-adjusted odds of significant CAC and higher cIMT, compared with those in the nondiabetic group, but these relationships differed by age and menopause status. For example, among premenopausal women, type 1 diabetes increased the odds of CAC at all ages, and cIMT was higher in women with type 1 diabetes, compared with those in the nondiabetic group at age 45 years and older. Among postmenopausal women, type 1 diabetes was associated with only higher CAC at age 54 years and older and with higher cIMT at age 57 years.

“Type 1 diabetic women face unique problems in their health that are not just endocrinology-related,” Ms. Keshawarz said. “If they haven’t undergone menopause yet, that needs to be taken into account when you’re proposing interventions and lifestyle and behavioral changes, because there is an increased possibility that they’re going to be at higher risk of coronary artery calcification and thicker [coronary] artery walls.”

The study was supported by grants from the American Diabetes Association and the National Institutes of Health. Ms. Keshawarz reported having no financial disclosures.

[email protected]

NEW ORLEANS – Premenopausal women with type 1 diabetes mellitus have a higher cardiovascular risk, compared with their diabetes-free counterparts. Among postmenopausal women, however, those with type 1 diabetes do not have a higher cardiovascular risk, compared with their peers who do not have diabetes, with the exception of those aged 54 and older.

Those are key findings from an analysis of women enrolled in the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study.

Doug Brunk/Frontline Medical News

“In general [premenopausal] women have a better cardiovascular profile than do men, but we don’t see that same effect in diabetic women,” lead author Amena Keshawarz said in an interview in advance of the annual scientific sessions of the American Diabetes Association. “They lose some of that protection. We’re wondering if that has some sort of relationship with menopause, because once women undergo menopause they tend to lose that protective factor.”

Ms. Keshawarz, a doctoral student and research assistant at the University of Colorado Barbara Davis Center for Childhood Diabetes, Aurora, and her associates used carotid intima-media thickness (cIMT) and the presence of coronary artery calcification to measure the cardiovascular risk by menopausal status in 106 women with type 1 diabetes and 140 nondiabetic women who were enrolled in CACTI. The patients ranged in age from 33-74 years and the data were collected between January 2014 and May 2016. Multivariable linear and logistic regressions were used to examine the differences in cIMT and to estimate the odds ratio for coronary artery calcification (CAC). The models were run for the following ages separately: 42, 42, 48, 51, 54, and 57 years.

As a group, women with type 1 diabetes were younger than their counterparts without diabetes (a mean age of 51 vs. 55 years, respectively; P = .002), but menopause age did not differ by diabetes status. Ms. Keshawarz reported that women with type 1 diabetes had significantly higher age-adjusted odds of significant CAC and higher cIMT, compared with those in the nondiabetic group, but these relationships differed by age and menopause status. For example, among premenopausal women, type 1 diabetes increased the odds of CAC at all ages, and cIMT was higher in women with type 1 diabetes, compared with those in the nondiabetic group at age 45 years and older. Among postmenopausal women, type 1 diabetes was associated with only higher CAC at age 54 years and older and with higher cIMT at age 57 years.

“Type 1 diabetic women face unique problems in their health that are not just endocrinology-related,” Ms. Keshawarz said. “If they haven’t undergone menopause yet, that needs to be taken into account when you’re proposing interventions and lifestyle and behavioral changes, because there is an increased possibility that they’re going to be at higher risk of coronary artery calcification and thicker [coronary] artery walls.”

The study was supported by grants from the American Diabetes Association and the National Institutes of Health. Ms. Keshawarz reported having no financial disclosures.

[email protected]

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

[email protected]

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

[email protected]

DENVER – Much of the rising prevalence of insomnia among U.S. and Canadian adults may be driven by the sharp reduction in the use of hormone replacement therapy following the 2002 report from the Women’s Health Initiative, Sheila N. Garland, PhD, said at the annual meeting of the Associated Professional Sleep Societies.

“In 2002 the Women’s Health Initiative came out with findings that hormone replacement therapy increased the risk of coronary heart disease, breast cancer, stroke, and pulmonary embolism [JAMA. 2002 Jul 17;288(3):321-33]. A lot of women on hormone replacement therapy up until 2002 stopped using it then. The increase in difficulty sleeping we found between 2002 and 2012 could perhaps represent an untreated menopausal symptom,” according to Dr. Garland, a psychologist at Memorial University of Newfoundland in St. John’s.

© Karen Winton / iStockphoto.com

She presented an analysis of data from the Canadian Community Health Survey, a national once-per-decade survey, which included 34,118 adults aged 20-80 years and older in the 2002 version and 23,089 in 2012.

The key finding from the standpoint of sleep medicine, the prevalence of self-reported trouble sleeping, increased from 15.6% in 2002 to 17.1% in 2012. And this increase was concentrated in 40- to 59-year-old women, where the prevalence of insomnia or poor sleep rose from 19% to 24.3%, the highest of any age group. Rates remained flat over time in men and women aged 20-39 years and 60-80 years and older as well as in 40- to 59-year-old men.

The sleep-related question put to survey participants in face-to-face or telephone interviews was this: “How often do you have trouble going to sleep or staying asleep?” If they answered “most of the time” or “all of the time” they were classified as having poor sleep.

When Dr. Garland saw the survey results she immediately asked herself, “What is happening with Canadian women?” She came up with two theories. They are not mutually exclusive. One hinges on the dramatic drop off in the use of hormone replacement therapy in response to the Women’s Health Initiative report. The other theory is that the increasing prevalence of insomnia in middle-aged women is a manifestation of stress among the growing population of what has been called “the sandwich generation,” people who care for their aging parents while also supporting their own children. Those responsibilities most often fall upon the mother.

She noted that a similar rise in the prevalence of insomnia or trouble sleeping is occurring south of the border – in the United States – as documented in a Centers for Disease Control and Prevention analysis. The CDC investigators examined data on 30,970 adult participants in the 2002 National Health Interview Survey, 23,344 in the 2007 survey, and 34,509 in the 2012 survey. The prevalence of insomnia or trouble sleeping increased from 17.5% in 2002 to 19.2% in 2012. That absolute 1.7% increase pairs well with the 1.5% rise over the same time frame in the Canadian survey. The prevalence was higher in U.S. women than men in all three survey years (Sleep Med. 2015 Mar;16[3]:372-8).

Dr. Garland said the Canadian national survey contains data on self-perceived stress levels. She plans to analyze those results to learn if being a member of the sandwich generation is a significant contributor to poor sleep.

Regardless of the underlying mechanism, she continued, it’s clear from these large national surveys that middle-aged women are particularly vulnerable to poor sleep.

“Increased recognition is necessary. Prevention and intervention programs may be warranted, given the individual and societal consequences of poor sleep, including increased psychiatric and medical disorders, work absenteeism, and health care costs,” she said.

One audience member rose to congratulate Dr. Garland on her detective work. He commented that her notion that the rise in insomnia can be traced to fallout from the 2002 Women’s Health Initiative is consistent with his own clinical experience.

“The most common way women over age 40 present to our sleep center with insomnia is because they’re menopausal and not on hormone replacement therapy,” he said.

The Canadian Community Health Survey is sponsored by Statistics Canada. Dr. Garland reported having no financial conflicts of interest.

[email protected]

Struan H. Coleman, MD, PhD

Associate Editor for Practice Management/Economics

Dr. Coleman is a board-certified orthopedic surgeon specializing in hip preservation and sports medicine at the Hospital for Special Surgery in New York and the Vincera Institute in Philadelphia, and currently is the Head Team Physician for the New York Mets. He earned a medical degree from Columbia College of Physicians and Surgeons and holds a D.Phil in Microbiology from Oxford University in England. He completed his residency in Orthopedic Surgery and a fellowship in Sports Medicine at the Hospital for Special Surgery. Dr. Coleman focuses on the treatment of sports-related injuries of the hip, knee, and shoulder with a particular interest in hip arthroscopy and hip preservation. He has published multiple articles and book chapters, and holds numerous patents for technologies that are utilized by sports medicine physicians and surgeons.

Jack Farr II, MD

Associate Editor for Patellofemoral

Dr. Farr is a board-certified orthopedic surgeon and has a subspecialty practice in knee and cartilage restoration. He is affiliated with the OrthoIndy Hospital and Community Hospital South. He is also the Vice President of the Patellofemoral Foundation, is on the board for the International Cartilage Repair Society, holds a board position with the Cartilage Research Foundation, and holds a voluntary clinical full professorship in Orthopedic Surgery at the Indiana University Medical Center. Dr. Farr earned his medical degree from Indiana University, and completed his Orthopedic Surgery residency at Indiana University Medical Center. He was a design surgeon for a meniscal allograft transplant system and 2 knee patellofemoral osteotomy systems. He is also a member of the American Academy of Orthopaedic Surgeons (AAOS), the Arthroscopy Association of North America (AANA), and the European Society of Sports Traumatology, Knee Surgery and Arthroscopy (ESSKA).

Kenneth Montgomery, MD

Associate Editor for Professional Sports

Dr. Montgomery is an orthopedic surgeon who is fellowship-trained in sports medicine and hand and upper extremity surgery. He is currently practicing at Tri-County Orthopedics and Sports Medicine in Morristown, New Jersey. He is also the Head Team Physician and Medical Director for the New York Jets. He served as a team orthopedist with the New York Islanders from 1997-2009, and was formerly the section chief of Sports Medicine at ProHEALTH Care Associates in Lake Success, New York. Dr. Montgomery completed his residency in Orthopedic Surgery at the Hospital for Special Surgery, and completed a Sports Medicine fellowship at Lenox Hill Hospital. He also completed a Hand and Upper Extremity fellowship at Harvard. He is one of the founders for OrthoNations, a nonprofit organization that helps educate orthopedic surgeons in developing countries. He is also one of the founding surgeons for Cayenne Medical, a medical device company specializing in sports medicine implants.

Struan H. Coleman, MD, PhD

Associate Editor for Practice Management/Economics

Dr. Coleman is a board-certified orthopedic surgeon specializing in hip preservation and sports medicine at the Hospital for Special Surgery in New York and the Vincera Institute in Philadelphia, and currently is the Head Team Physician for the New York Mets. He earned a medical degree from Columbia College of Physicians and Surgeons and holds a D.Phil in Microbiology from Oxford University in England. He completed his residency in Orthopedic Surgery and a fellowship in Sports Medicine at the Hospital for Special Surgery. Dr. Coleman focuses on the treatment of sports-related injuries of the hip, knee, and shoulder with a particular interest in hip arthroscopy and hip preservation. He has published multiple articles and book chapters, and holds numerous patents for technologies that are utilized by sports medicine physicians and surgeons.

Jack Farr II, MD

Associate Editor for Patellofemoral

Dr. Farr is a board-certified orthopedic surgeon and has a subspecialty practice in knee and cartilage restoration. He is affiliated with the OrthoIndy Hospital and Community Hospital South. He is also the Vice President of the Patellofemoral Foundation, is on the board for the International Cartilage Repair Society, holds a board position with the Cartilage Research Foundation, and holds a voluntary clinical full professorship in Orthopedic Surgery at the Indiana University Medical Center. Dr. Farr earned his medical degree from Indiana University, and completed his Orthopedic Surgery residency at Indiana University Medical Center. He was a design surgeon for a meniscal allograft transplant system and 2 knee patellofemoral osteotomy systems. He is also a member of the American Academy of Orthopaedic Surgeons (AAOS), the Arthroscopy Association of North America (AANA), and the European Society of Sports Traumatology, Knee Surgery and Arthroscopy (ESSKA).

Kenneth Montgomery, MD

Associate Editor for Professional Sports

Dr. Montgomery is an orthopedic surgeon who is fellowship-trained in sports medicine and hand and upper extremity surgery. He is currently practicing at Tri-County Orthopedics and Sports Medicine in Morristown, New Jersey. He is also the Head Team Physician and Medical Director for the New York Jets. He served as a team orthopedist with the New York Islanders from 1997-2009, and was formerly the section chief of Sports Medicine at ProHEALTH Care Associates in Lake Success, New York. Dr. Montgomery completed his residency in Orthopedic Surgery at the Hospital for Special Surgery, and completed a Sports Medicine fellowship at Lenox Hill Hospital. He also completed a Hand and Upper Extremity fellowship at Harvard. He is one of the founders for OrthoNations, a nonprofit organization that helps educate orthopedic surgeons in developing countries. He is also one of the founding surgeons for Cayenne Medical, a medical device company specializing in sports medicine implants.

Struan H. Coleman, MD, PhD

Associate Editor for Practice Management/Economics

Dr. Coleman is a board-certified orthopedic surgeon specializing in hip preservation and sports medicine at the Hospital for Special Surgery in New York and the Vincera Institute in Philadelphia, and currently is the Head Team Physician for the New York Mets. He earned a medical degree from Columbia College of Physicians and Surgeons and holds a D.Phil in Microbiology from Oxford University in England. He completed his residency in Orthopedic Surgery and a fellowship in Sports Medicine at the Hospital for Special Surgery. Dr. Coleman focuses on the treatment of sports-related injuries of the hip, knee, and shoulder with a particular interest in hip arthroscopy and hip preservation. He has published multiple articles and book chapters, and holds numerous patents for technologies that are utilized by sports medicine physicians and surgeons.

Jack Farr II, MD

Associate Editor for Patellofemoral

Dr. Farr is a board-certified orthopedic surgeon and has a subspecialty practice in knee and cartilage restoration. He is affiliated with the OrthoIndy Hospital and Community Hospital South. He is also the Vice President of the Patellofemoral Foundation, is on the board for the International Cartilage Repair Society, holds a board position with the Cartilage Research Foundation, and holds a voluntary clinical full professorship in Orthopedic Surgery at the Indiana University Medical Center. Dr. Farr earned his medical degree from Indiana University, and completed his Orthopedic Surgery residency at Indiana University Medical Center. He was a design surgeon for a meniscal allograft transplant system and 2 knee patellofemoral osteotomy systems. He is also a member of the American Academy of Orthopaedic Surgeons (AAOS), the Arthroscopy Association of North America (AANA), and the European Society of Sports Traumatology, Knee Surgery and Arthroscopy (ESSKA).

Kenneth Montgomery, MD

Associate Editor for Professional Sports

Dr. Montgomery is an orthopedic surgeon who is fellowship-trained in sports medicine and hand and upper extremity surgery. He is currently practicing at Tri-County Orthopedics and Sports Medicine in Morristown, New Jersey. He is also the Head Team Physician and Medical Director for the New York Jets. He served as a team orthopedist with the New York Islanders from 1997-2009, and was formerly the section chief of Sports Medicine at ProHEALTH Care Associates in Lake Success, New York. Dr. Montgomery completed his residency in Orthopedic Surgery at the Hospital for Special Surgery, and completed a Sports Medicine fellowship at Lenox Hill Hospital. He also completed a Hand and Upper Extremity fellowship at Harvard. He is one of the founders for OrthoNations, a nonprofit organization that helps educate orthopedic surgeons in developing countries. He is also one of the founding surgeons for Cayenne Medical, a medical device company specializing in sports medicine implants.

NEW ORLEANS – Patients with diabetes who failed to show up for diabetes education classes were slightly younger and less likely to be insured, compared with those who attended the classes. Forty-one percent of those who failed to show were covered by private insurance, and 63% were women.

Those are key findings from an analysis by researchers to investigate the patterns of population characteristics related nonadherence to diabetes education classes that patients are referred to.

“What it shows us is that when we’re trying to get people to come to diabetes education classes, we have to be in tune with the sociodemographic characteristics that present different barriers or obstacles,” Ashby Walker, PhD, said in an interview at the annual scientific sessions of the American Diabetes Association.

Dr. Walker, of the department of health outcomes and policy at the University of Florida, Gainesville, and her associates, including Kathryn Parker, RD, program manager for diabetes education at the UF Health Shands Hospital, Gainesville, conducted a manual chart review to examine the demographics of 257 “no-shows” who were referred to a diabetes education class at the university’s hospital between January 2015 and March 2015. Data of interest included age, gender, diagnosis, reasons for referral, referring department, socioeconomic status, and race/ethnicity. For comparison purposes, the researchers also examined a cohort of 339 patients who showed up for their diabetes education classes between August 2014 and January 2015.

More than two-thirds of the no-shows (69%) had type 2 diabetes, 63% were women, and the mean age was 50 years. More than half (57%) were publicly insured or uninsured, while 41% had private insurance and 3% were self-pay or had missing data for insurance type.

The fact that a higher proportion of the insured no-shows were women surprised the researchers. “If you think about women who are working full time, they often shoulder the tremendous responsibility of household labor, too,” Dr. Walker said. “So for them to take time out of very busy lives to take care of themselves might create a different obstacle than someone who’s very low income or low health literacy who has transportation as a barrier. The findings show us that we have to tailor those interventions appropriately for different audiences.”

Another surprise finding, she said, was the fact that males were underrepresented in both the “no show” cohort (37%) and among those who honored their referrals (32%). “While there are some studies that indicate women fare worse with diabetes than men, the underrepresentation of men warrants further attention,” Dr. Walker said. “It begs the question: Are providers referring men less?”

Shannon Taylor, a fellow researcher at the University of Florida, said that the study’s findings underscore the need for clinicians “to be attuned to the different things about social life that can impact how people self-care, whether it’s gender differences or differences in socioeconomic status.”

The researchers reported having no financial disclosures.

[email protected]

NEW ORLEANS – Patients with diabetes who failed to show up for diabetes education classes were slightly younger and less likely to be insured, compared with those who attended the classes. Forty-one percent of those who failed to show were covered by private insurance, and 63% were women.

Those are key findings from an analysis by researchers to investigate the patterns of population characteristics related nonadherence to diabetes education classes that patients are referred to.

“What it shows us is that when we’re trying to get people to come to diabetes education classes, we have to be in tune with the sociodemographic characteristics that present different barriers or obstacles,” Ashby Walker, PhD, said in an interview at the annual scientific sessions of the American Diabetes Association.

Dr. Walker, of the department of health outcomes and policy at the University of Florida, Gainesville, and her associates, including Kathryn Parker, RD, program manager for diabetes education at the UF Health Shands Hospital, Gainesville, conducted a manual chart review to examine the demographics of 257 “no-shows” who were referred to a diabetes education class at the university’s hospital between January 2015 and March 2015. Data of interest included age, gender, diagnosis, reasons for referral, referring department, socioeconomic status, and race/ethnicity. For comparison purposes, the researchers also examined a cohort of 339 patients who showed up for their diabetes education classes between August 2014 and January 2015.

More than two-thirds of the no-shows (69%) had type 2 diabetes, 63% were women, and the mean age was 50 years. More than half (57%) were publicly insured or uninsured, while 41% had private insurance and 3% were self-pay or had missing data for insurance type.

The fact that a higher proportion of the insured no-shows were women surprised the researchers. “If you think about women who are working full time, they often shoulder the tremendous responsibility of household labor, too,” Dr. Walker said. “So for them to take time out of very busy lives to take care of themselves might create a different obstacle than someone who’s very low income or low health literacy who has transportation as a barrier. The findings show us that we have to tailor those interventions appropriately for different audiences.”

Another surprise finding, she said, was the fact that males were underrepresented in both the “no show” cohort (37%) and among those who honored their referrals (32%). “While there are some studies that indicate women fare worse with diabetes than men, the underrepresentation of men warrants further attention,” Dr. Walker said. “It begs the question: Are providers referring men less?”

Shannon Taylor, a fellow researcher at the University of Florida, said that the study’s findings underscore the need for clinicians “to be attuned to the different things about social life that can impact how people self-care, whether it’s gender differences or differences in socioeconomic status.”

The researchers reported having no financial disclosures.

[email protected]

NEW ORLEANS – Patients with diabetes who failed to show up for diabetes education classes were slightly younger and less likely to be insured, compared with those who attended the classes. Forty-one percent of those who failed to show were covered by private insurance, and 63% were women.

Those are key findings from an analysis by researchers to investigate the patterns of population characteristics related nonadherence to diabetes education classes that patients are referred to.

“What it shows us is that when we’re trying to get people to come to diabetes education classes, we have to be in tune with the sociodemographic characteristics that present different barriers or obstacles,” Ashby Walker, PhD, said in an interview at the annual scientific sessions of the American Diabetes Association.

Dr. Walker, of the department of health outcomes and policy at the University of Florida, Gainesville, and her associates, including Kathryn Parker, RD, program manager for diabetes education at the UF Health Shands Hospital, Gainesville, conducted a manual chart review to examine the demographics of 257 “no-shows” who were referred to a diabetes education class at the university’s hospital between January 2015 and March 2015. Data of interest included age, gender, diagnosis, reasons for referral, referring department, socioeconomic status, and race/ethnicity. For comparison purposes, the researchers also examined a cohort of 339 patients who showed up for their diabetes education classes between August 2014 and January 2015.

More than two-thirds of the no-shows (69%) had type 2 diabetes, 63% were women, and the mean age was 50 years. More than half (57%) were publicly insured or uninsured, while 41% had private insurance and 3% were self-pay or had missing data for insurance type.

The fact that a higher proportion of the insured no-shows were women surprised the researchers. “If you think about women who are working full time, they often shoulder the tremendous responsibility of household labor, too,” Dr. Walker said. “So for them to take time out of very busy lives to take care of themselves might create a different obstacle than someone who’s very low income or low health literacy who has transportation as a barrier. The findings show us that we have to tailor those interventions appropriately for different audiences.”

Another surprise finding, she said, was the fact that males were underrepresented in both the “no show” cohort (37%) and among those who honored their referrals (32%). “While there are some studies that indicate women fare worse with diabetes than men, the underrepresentation of men warrants further attention,” Dr. Walker said. “It begs the question: Are providers referring men less?”

Shannon Taylor, a fellow researcher at the University of Florida, said that the study’s findings underscore the need for clinicians “to be attuned to the different things about social life that can impact how people self-care, whether it’s gender differences or differences in socioeconomic status.”

The researchers reported having no financial disclosures.

[email protected]