Endometriosis linked to higher CHD risk

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Endometriosis linked to higher CHD risk

Endometriosis is associated with a significantly increased risk of coronary heart disease, at least in part because of one of its principal treatments – hysterectomy/oophorectomy, according to a new analysis of the Nurses’ Health Study II.

In what the researchers described as the first large prospective study to examine this possible association, the link between endometriosis and coronary heart disease (CHD) was mediated by patient age.

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Women with endometriosis had a higher incidence of CHD than those without the gynecologic disorder until they reached their late 50s; after that, the two populations had similar CHD rates, wrote Fan Mu, Sc.D., of the department of epidemiology, Harvard T. H. Chan School of Public Health in Boston, and her associates (Circ Cardiovasc Qual Outcomes. 2016 Mar 29. doi: 10.1161/circoutcomes.115.002224).

“This association may have important clinical and public health implications among women in their early 40s to early 50s,” the researchers wrote. “It is possible that the observed increased risk associated with surgical menopause from hysterectomy/oophorectomy among women with endometriosis started to diminish with age partially because nearly every woman had reached menopause by the age of 55 years.”

The researchers chose to study this topic because endometriosis has been linked to chronic systemic inflammation, oxidative stress, and adverse lipid profiles, factors that also play key roles in the pathogenesis of atherosclerotic CHD. They assessed the incidence of myocardial infarction, angina, and the combined outcome of coronary artery bypass graft (CABG)/angioplasty/stenting using data from the Nurses’ Health Study II, a prospective cohort study involving 116,430 women, aged 25-42 years at baseline in 1989, who were followed for approximately 20 years.

A total of 5,296 of the study participants had laparoscopically confirmed endometriosis at baseline, and another 6,607 developed the disorder during follow-up. There were 1,438 incident cases of CHD during follow-up.

Compared with women who didn’t have endometriosis, those who did showed increased relative risks for myocardial infarction (1.63), angiographically confirmed angina (2.07), CABG/angioplasty/stent (1.49), and combined CHD (1.73). The results remained statistically significant after the researchers adjusted for potential confounders.

About 42% of this association was statistically accounted for by the greater frequency of hysterectomy/oophorectomy among women who had endometriosis and the earlier age of these surgeries among women with endometriosis. Women who underwent the surgery had an absolute incidence of CHD of 139 per 100,000 person-years, compared with an incidence of 60 per 100,000 person-years among the women who didn’t have hysterectomy/oophorectomy.

“Physicians need to consider the potential long-term impact that the surgeries may cause and weigh the risks and benefits of the treatment in dialogue with patients, particularly with respect to endometriosis where pain recurrence risk remains,” the researchers wrote. “Although oophorectomy confers obvious prevention for ovarian cancer, with which endometriosis has been associated, CHD is the leading cause of mortality and morbidity in women in the United States and United Kingdom.”

The study was supported by the National Institutes of Health. The researchers reported having no relevant financial disclosures.

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Endometriosis is associated with a significantly increased risk of coronary heart disease, at least in part because of one of its principal treatments – hysterectomy/oophorectomy, according to a new analysis of the Nurses’ Health Study II.

In what the researchers described as the first large prospective study to examine this possible association, the link between endometriosis and coronary heart disease (CHD) was mediated by patient age.

©designer491/Thinkstock

Women with endometriosis had a higher incidence of CHD than those without the gynecologic disorder until they reached their late 50s; after that, the two populations had similar CHD rates, wrote Fan Mu, Sc.D., of the department of epidemiology, Harvard T. H. Chan School of Public Health in Boston, and her associates (Circ Cardiovasc Qual Outcomes. 2016 Mar 29. doi: 10.1161/circoutcomes.115.002224).

“This association may have important clinical and public health implications among women in their early 40s to early 50s,” the researchers wrote. “It is possible that the observed increased risk associated with surgical menopause from hysterectomy/oophorectomy among women with endometriosis started to diminish with age partially because nearly every woman had reached menopause by the age of 55 years.”

The researchers chose to study this topic because endometriosis has been linked to chronic systemic inflammation, oxidative stress, and adverse lipid profiles, factors that also play key roles in the pathogenesis of atherosclerotic CHD. They assessed the incidence of myocardial infarction, angina, and the combined outcome of coronary artery bypass graft (CABG)/angioplasty/stenting using data from the Nurses’ Health Study II, a prospective cohort study involving 116,430 women, aged 25-42 years at baseline in 1989, who were followed for approximately 20 years.

A total of 5,296 of the study participants had laparoscopically confirmed endometriosis at baseline, and another 6,607 developed the disorder during follow-up. There were 1,438 incident cases of CHD during follow-up.

Compared with women who didn’t have endometriosis, those who did showed increased relative risks for myocardial infarction (1.63), angiographically confirmed angina (2.07), CABG/angioplasty/stent (1.49), and combined CHD (1.73). The results remained statistically significant after the researchers adjusted for potential confounders.

About 42% of this association was statistically accounted for by the greater frequency of hysterectomy/oophorectomy among women who had endometriosis and the earlier age of these surgeries among women with endometriosis. Women who underwent the surgery had an absolute incidence of CHD of 139 per 100,000 person-years, compared with an incidence of 60 per 100,000 person-years among the women who didn’t have hysterectomy/oophorectomy.

“Physicians need to consider the potential long-term impact that the surgeries may cause and weigh the risks and benefits of the treatment in dialogue with patients, particularly with respect to endometriosis where pain recurrence risk remains,” the researchers wrote. “Although oophorectomy confers obvious prevention for ovarian cancer, with which endometriosis has been associated, CHD is the leading cause of mortality and morbidity in women in the United States and United Kingdom.”

The study was supported by the National Institutes of Health. The researchers reported having no relevant financial disclosures.

Endometriosis is associated with a significantly increased risk of coronary heart disease, at least in part because of one of its principal treatments – hysterectomy/oophorectomy, according to a new analysis of the Nurses’ Health Study II.

In what the researchers described as the first large prospective study to examine this possible association, the link between endometriosis and coronary heart disease (CHD) was mediated by patient age.

©designer491/Thinkstock

Women with endometriosis had a higher incidence of CHD than those without the gynecologic disorder until they reached their late 50s; after that, the two populations had similar CHD rates, wrote Fan Mu, Sc.D., of the department of epidemiology, Harvard T. H. Chan School of Public Health in Boston, and her associates (Circ Cardiovasc Qual Outcomes. 2016 Mar 29. doi: 10.1161/circoutcomes.115.002224).

“This association may have important clinical and public health implications among women in their early 40s to early 50s,” the researchers wrote. “It is possible that the observed increased risk associated with surgical menopause from hysterectomy/oophorectomy among women with endometriosis started to diminish with age partially because nearly every woman had reached menopause by the age of 55 years.”

The researchers chose to study this topic because endometriosis has been linked to chronic systemic inflammation, oxidative stress, and adverse lipid profiles, factors that also play key roles in the pathogenesis of atherosclerotic CHD. They assessed the incidence of myocardial infarction, angina, and the combined outcome of coronary artery bypass graft (CABG)/angioplasty/stenting using data from the Nurses’ Health Study II, a prospective cohort study involving 116,430 women, aged 25-42 years at baseline in 1989, who were followed for approximately 20 years.

A total of 5,296 of the study participants had laparoscopically confirmed endometriosis at baseline, and another 6,607 developed the disorder during follow-up. There were 1,438 incident cases of CHD during follow-up.

Compared with women who didn’t have endometriosis, those who did showed increased relative risks for myocardial infarction (1.63), angiographically confirmed angina (2.07), CABG/angioplasty/stent (1.49), and combined CHD (1.73). The results remained statistically significant after the researchers adjusted for potential confounders.

About 42% of this association was statistically accounted for by the greater frequency of hysterectomy/oophorectomy among women who had endometriosis and the earlier age of these surgeries among women with endometriosis. Women who underwent the surgery had an absolute incidence of CHD of 139 per 100,000 person-years, compared with an incidence of 60 per 100,000 person-years among the women who didn’t have hysterectomy/oophorectomy.

“Physicians need to consider the potential long-term impact that the surgeries may cause and weigh the risks and benefits of the treatment in dialogue with patients, particularly with respect to endometriosis where pain recurrence risk remains,” the researchers wrote. “Although oophorectomy confers obvious prevention for ovarian cancer, with which endometriosis has been associated, CHD is the leading cause of mortality and morbidity in women in the United States and United Kingdom.”

The study was supported by the National Institutes of Health. The researchers reported having no relevant financial disclosures.

References

References

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Endometriosis linked to higher CHD risk
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FROM CIRCULATION: CARDIOVASCULAR QUALITY AND OUTCOMES

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Key clinical point: Endometriosis is associated with a significantly increased risk of coronary heart disease.

Major finding: Women with endometriosis showed increased relative risks for MI (1.63), angiographically confirmed angina (2.07), CABG/angioplasty/stent (1.49), and combined CHD (1.73).

Data source: A secondary analysis of data from the Nurses’ Health Study II, a prospective cohort study involving 116,430 women followed for 20 years.

Disclosures: The study was supported by the National Institutes of Health. The researchers reported having no relevant financial disclosures.

Anxiety and depression: Easing the burden in COPD patients

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Anxiety and depression: Easing the burden in COPD patients

PRACTICE RECOMMENDATIONS

› Initiate both pharmacologic and psychological therapies for anxiety or depression coexisting with COPD to improve patient outcomes. B
› Consider buspirone as an alternative to benzodiazepines for anxiety coexistent with COPD. B
› Consider motivational interviewing as a behavioral approach to help patients who are ambivalent about or resistant to change. B

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B
Inconsistent or limited-quality patient-oriented evidence
C
Consensus, usual practice, opinion, disease-oriented evidence, case series

CASE A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.1 Family physicians, who are the primary caregivers for most patients with the disease,2 can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,5 reaching upwards of 55%.1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.1

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,5 perhaps owing in part to breathlessness and “air hunger.”10

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.11

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.11 Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.12 MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.11

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.6 Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,7 exhibit poorer physical and social functioning,13 and experience greater impairment of quality of life than patients with lung dysfunction alone.1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.11 Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.11

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.9 Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.9 Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.9 Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

 

 

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.6

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.15 Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.14

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.16 All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).16 Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.17 Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients5,14(TABLE18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior20 has been proposed as a standard of care in the treatment of COPD.21 A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.22 While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,22 patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.21

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.23 MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.23

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.21 Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.21 This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

 

 

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

  • Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.5,14
  • Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
  • Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.24
  • Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority5 or equivalence25 to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.26 However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; [email protected].

References

1. Yohannes AM, Willgoss TG, Baldwin RC, et al. Depression and anxiety in chronic heart failure and chronic obstructive pulmonary disease: prevalence, relevance, clinical implications and management principles. Int J Geriatr Psychiatry. 2010;25:1209-1221.

2. Punturieri A, Croxton TL, Weinmann G, et al. The changing face of COPD. Am Fam Physician. 2007;1:315-316.

3. Willgoss TG, Yohannes AM. Anxiety disorders in patients with COPD: a systematic review. Respir Care. 2013;58:858-866.

4. Porthirat C, Chaiwong W, Phetsuk N, et al. Major affective disorders in chronic obstructive pulmonary disease compared with other chronic respiratory diseases. Int J Chron Obstruct Pulmon Dis. 2015;10:1583-1590.

5. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. 2003; 65:963-970.

6. Singh G, Zhang W, Kuo YF, et al. Association of psychological disorders with 30-day readmission rates in patients with Chronic Obstructive Pulmonary Disease. Chest. 2015;Jul 23:[Epub ahead of print].

7. Vögele C, von Leupoldt A. Mental disorders in chronic obstructive pulmonary disease. Respir Med. 2008;102:764-773.

8. Aydin IO, Ulusahin A. Depression, anxiety comorbidity, and disability in tuberculosis and chronic obstructive pulmonary disease patients: applicability of GHQ-12. Gen Hosp Psychiatry. 2001;23:77-83.

9. Dalal AA, Shah M, Lunacsek O, et al. Clinical and economic burden of depression/anxiety in chronic obstructive pulmonary disease patients within a managed care population. COPD. 2011;8:293-299.

10. Janssen DJA, Wouters EFM, Spruit MA. Psychosocial consequences of living with breathlessness due to advanced disease. Curr Opin Support Palliat Care. 2015;9:232-237.

11. Atlantis E, Fahey P, Cochrane B, et al. Bidirectional associations between clinically relevant depression or anxiety and COPD. Chest. 2013;144:766-777.

12. Esser RW, Stoeckel MC, Kirsten A, et al. Structural brain changes in patients with chronic obstructive pulmonary disease. Chest. 2015;Jul 23:[Epub ahead of print].

13. Ng TP, Niti M, Tan WC, et al. Depressive symptoms and chronic obstructive pulmonary disease: effect on mortality, hospital readmission, symptom burden, functional status, and quality of life. Arch Intern Med. 2007;167:60-67.

14. Kim HF, Kunik ME, Molinari VA, et al. Functional impairment in COPD patients. Psychosomatics. 2000;41:465-471.

15. Cleland JA, Lee AJ, Hall S. Associations of depression and anxiety with gender, age, health-related quality of life and symptoms in primary care COPD patients. Fam Pract. 2007;24:217-223.

16. Kroenke K, Spitzer RL, Williams JB et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359.

17. Ajmera M, Sambamoorthi U, Metzger A, et al. Multimorbidity and COPD medication receipt among Medicaid beneficiaries with newly diagnosed COPD. Respir Care. 2015;60:1592-1602.

18. Medscape. Psychiatrics. Available at: http://reference.medscape.com/drugs/psychiatrics. Accessed March 1, 2016.

19. Physicians’ Desk Reference. Available at: http://www.pdr.net. Accessed March 1, 2016.

20. Kazdin AE. Behavior Modification in Applied Settings. Belmont, CA: Wadsworth/Thomson Learning; 2001.

21. Benzo R, Vickers K, Ernst D, et al. Development and feasibility of a self-management intervention for chronic obstructive pulmonary disease delivered with motivational interviewing strategies. J Cardiopulm Rehabil. 2013;33:113-123.

22. Zwerink M, Brusse-Keizer M, van der Valk PD, et al. Self management for patients with chronic obstructive pulmonary disease. Cochrane Database System Rev. 2014;(3):CD002990.

23. Miller WR, Rollnick S. Motivational Interviewing. 3rd ed. New York, NY: Guilford Press; 2013.

24. de Godoy DV, de Godoy RF. A randomized controlled trial of the effect of psychotherapy on anxiety and depression in chronic obstructive pulmonary disease. Arch Phys Med Rehabil. 2003;84:1154-1157.

25. Kunik ME, Veazey C, Cully JA, et al. COPD education and cognitive behavioral therapy group treatment for clinically significant symptoms of depression and anxiety in COPD patients: a randomized controlled trial. Psychol Med. 2008;38:385-396.

26. McDaniel SH, Fogarty CT. What primary care psychology has to offer the patient-centered medical home. Prof Psych Res Pract. 2009;40:483-492.

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Sydney Marsh, BA
Thomas P. Guck, PhD
Department of Family Medicine, Creighton University School of Medicine, Omaha, Neb
[email protected]

The authors reported no potential conflict of interest relevant to this article.

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Thomas P. Guck, PhD
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Thomas P. Guck, PhD
Department of Family Medicine, Creighton University School of Medicine, Omaha, Neb
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PRACTICE RECOMMENDATIONS

› Initiate both pharmacologic and psychological therapies for anxiety or depression coexisting with COPD to improve patient outcomes. B
› Consider buspirone as an alternative to benzodiazepines for anxiety coexistent with COPD. B
› Consider motivational interviewing as a behavioral approach to help patients who are ambivalent about or resistant to change. B

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B
Inconsistent or limited-quality patient-oriented evidence
C
Consensus, usual practice, opinion, disease-oriented evidence, case series

CASE A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.1 Family physicians, who are the primary caregivers for most patients with the disease,2 can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,5 reaching upwards of 55%.1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.1

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,5 perhaps owing in part to breathlessness and “air hunger.”10

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.11

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.11 Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.12 MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.11

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.6 Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,7 exhibit poorer physical and social functioning,13 and experience greater impairment of quality of life than patients with lung dysfunction alone.1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.11 Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.11

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.9 Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.9 Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.9 Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

 

 

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.6

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.15 Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.14

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.16 All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).16 Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.17 Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients5,14(TABLE18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior20 has been proposed as a standard of care in the treatment of COPD.21 A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.22 While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,22 patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.21

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.23 MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.23

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.21 Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.21 This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

 

 

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

  • Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.5,14
  • Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
  • Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.24
  • Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority5 or equivalence25 to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.26 However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; [email protected].

PRACTICE RECOMMENDATIONS

› Initiate both pharmacologic and psychological therapies for anxiety or depression coexisting with COPD to improve patient outcomes. B
› Consider buspirone as an alternative to benzodiazepines for anxiety coexistent with COPD. B
› Consider motivational interviewing as a behavioral approach to help patients who are ambivalent about or resistant to change. B

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B
Inconsistent or limited-quality patient-oriented evidence
C
Consensus, usual practice, opinion, disease-oriented evidence, case series

CASE A 66-year-old man you have seen many times for issues related to his chronic obstructive pulmonary disease (COPD) comes in to your clinic for a routine visit. He has been taking budesonide/formoterol twice a day for the last 3 years; however, he has not always been compliant with his medications and has been hospitalized within the last 6 months for disease exacerbations. Today, he says he has difficulty falling asleep and often becomes short of breath, even when physically inactive. His wife, who is accompanying him today, tells you he has become increasingly distant over the past few months and is not as engaged at family outings, which he attributes to labored breathing. They’re both concerned about this change and ask for advice.

Despite the increased awareness that generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common comorbidities of COPD, they remain underdiagnosed and undertreated in patients with COPD. The results are increased rates of symptom exacerbation and rehospitalization.1 Family physicians, who are the primary caregivers for most patients with the disease,2 can maximize patients’ quality of life by recognizing comorbid mental illness, motivating and engaging patients in their disease management, and initiating appropriate treatment.

Anxiety and depression in COPD: A 2-way street

Several studies have assessed the prevalence of psychological disorders in patients with COPD. Affective disorders, mainly GAD and MDD, are the ones most commonly associated with poor COPD prognoses.3,4 GAD is at least 3 times more prevalent in patients with COPD than in the general US population,5 reaching upwards of 55%.1,6 Prevalence of MDD is also high, affecting approximately 40% of patients with the disease.1

GAD and MDD are more prevalent as comorbidities of COPD than they are with other chronic diseases such as orthopedic conditions, pulmonary tuberculosis, hypertension and heart disease, stroke, diabetes, and cancer.5,7-9 Patients with COPD, more so than patients with other serious chronic diseases, report heightened edginess, anxiousness, tiredness, distractibility, and irritability,5 perhaps owing in part to breathlessness and “air hunger.”10

The connection between COPD and GAD or MDD is not unidirectional, with progression of lung disease exacerbating its psychological comorbidities. The interaction is reciprocal, as clarified by Atlantis, et al, in a 2013 systematic review and meta-analysis that assessed key variables in the development of COPD and GAD or MDD.11

COPD increases the risk of MDD, which is associated with increased tobacco consumption, poor adherence with COPD medications, and decreased physical activity.11 Compounding the problem of inactivity is the fact that COPD—particularly longstanding disease—can lead to volume reductions in the anterior cingulate cortex of patients, which correlates with a persistent fear of performing physical activity.12 MDD in the setting of COPD also complicates the already complex interplay between nicotine dependence and attempts at smoking cessation.11

GAD/MDD worsens COPD outcomes

Comorbid GAD and MDD increase demands on our health care system and decrease the quality of life for patients with COPD. Anxious or depressed patients have higher 30-day readmission rates and less frequent outpatient follow-up than COPD patients without these mental comorbidities.6 Patients with comorbidities tend to have a higher prevalence of systemic symptoms independent of COPD severity,7 exhibit poorer physical and social functioning,13 and experience greater impairment of quality of life than patients with lung dysfunction alone.1,14 Patients with GAD or MDD have a 43% increased risk of any adverse COPD outcome, which can include exacerbations, COPD-related diagnoses (eg, emphysema), new anxiety or depression events, and death.11 Specifically, the risk of a COPD exacerbation rises by 31% in patients with comorbid GAD or MDD, and risk of death in those with comorbid MDD increases by 83%.11

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease, instead of a psychological disorder.

GAD or MDD with COPD increases health care utilization and costs per patient when compared with patients who have COPD alone.9 Annual physician visits, emergency-room visits, and hospitalizations for any cause are higher in anxious or depressed COPD patients, and they have a 77% increased chance annually of a COPD-related hospitalization.9 Annual COPD-related health care costs for patients with GAD or MDD are significantly higher than the average COPD-related costs for patients without depression or anxiety, leading to significantly increased all-cause health care costs: $28,961 vs $22,512.9 Addressing and managing comorbid GAD or MDD in COPD patients could substantially reduce health care costs.

 

 

Be vigilant for anxiety, depression—even when COPD is mild

One reason comorbid GAD or MDD may be overlooked and underdiagnosed is that the symptoms can overlap those of COPD. In cases where suspicion of GAD or MDD is warranted, providers must keep separate the diagnostic inquiries for COPD and these comorbidities.6

Somatic symptoms of anxiety, such as hyperventilation, shortness of breath, and sweating, may easily be attributed to pulmonary disease instead of a psychological disorder. Differentiating the 2 processes becomes more difficult with patients younger than 60 years, as they are more likely to experience symptoms of GAD or MDD than older patients, regardless of COPD severity.15 Therefore, when assessing COPD patients, physicians need to be more vigilant for anxiety and depression, even in the mildest cases.14

Several methods exist for assessing anxiety and depression, including the Generalized Anxiety Disorder Screener 7 (GAD-7) and the Patient Health Questionnaire (PHQ) 2 or 9.16 All PHQ and GAD-7 screeners and translations are downloadable from www.phqscreeners.com/select-screener and permission is not required to reproduce, translate, display, or distribute them (FIGURE).16 Other anxiety and depression screening instruments are also available.

No one method has been shown to be most effective for rapid screening, and the physician’s comfort level or familiarity with a particular assessment tool may guide selection. One advantage of short screening instruments is that they can be incorporated into electronic health records for easy use across continuity visits. Although routine screening for these mental comorbidities takes slightly more time—especially in high-volume family practice clinics—it needs to become standard practice to protect patients’ quality of life.

Managing psychiatric conditions in COPD

Treatment for GAD and MDD in COPD is often suboptimal and may diminish a patient’s quality of life. In one study, COPD patients with a mental illness were 46% less likely than those with COPD alone to receive medications such as short- or long-acting bronchodilators and inhaled corticosteroids.17 Therapy for both the physiologic abnormalities and mental disturbances should be initiated promptly to maintain an acceptable state of health.

Pharmacotherapy. Reluctance to give traditional psychiatric medications to COPD patients contributes to the under-treatment of mental comorbidities. While benzodiazepines are generally not recommended—especially in severe COPD cases due to their sedative effect on respiratory drive—alternatives such as buspirone, tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) have been shown to effectively reduce GAD, MDD, and dyspnea in these patients5,14(TABLE18,19).

Non-pharmacotherapy approaches. Having patients apply behavioral-modification principles to their own behavior20 has been proposed as a standard of care in the treatment of COPD.21 A recent systematic review found that self-management (behavior change) interventions in patients with COPD improved health-related quality of life, reduced hospital admissions, and helped alleviate dyspnea.22 While that review could not make clear recommendations regarding the most effective form and content of self-management in COPD,22 patient engagement and motivation in creating treatment goals are considered critical ingredients for effective self-management.21

Motivational Interviewing (MI) is an evidence-based behavioral approach designed for patients who are ambivalent about or resistant to change.23 MI works by supporting a patient’s autonomy and by activating his/her own internal motivation for change or adherence to treatment. In MI, the physician’s involvement with the patient relies on collaboration, evocation, and autonomy, rather than confrontation, education, and authority. MI involves exploration more than exhortation, and support rather than persuasion or argument. The overall goal of MI is to increase intrinsic motivation so that change arises from within and serves the patient’s goals and values.23

The risk of a COPD exacerbation rises by 31% in patients with comorbid anxiety or depression; risk of death in those with comorbid depression increases by 83%.

Benzo, et al, provide a very detailed description of a self-management process that includes MI.21 Their protocol proved to be feasible in severe COPD and helped increase patient engagement and commitment to self-management.21 This finding and similar evidence of MI’s effectiveness in a variety of other health conditions suggest that pharmacotherapy and cognitive-behavior therapy can be delivered in combination with an MI approach.

Self-management depends on a patient’s readiness to implement behavioral changes. Patients engaged in unhealthy behavior may be reluctant to change at a particular time, so the physician may focus efforts on such behaviors as self-monitoring or examining values that may lead to future behavior change.

For example, a patient may not want to stop smoking, but the physician’s willingness to ask about smoking in subsequent visits may catch the patient at a time when motivation has changed—eg, perhaps there is a new child in the home, prompting a recognition that smoking is now inconsistent with one’s values and can be resolved with smoking cessation. Awareness of an individual’s baseline behavior and readiness to change assists physicians and other health professionals in tailoring interventions for the most favorable outcome.

 

 

Several other non-pharmacologic methods to reduce symptoms of GAD and MDD in patients with COPD have been studied and supported by the literature.

  • Progressive muscle relaxation, stress management, biofeedback, and guided imagery have been shown to decrease symptoms of anxiety, dyspnea, and airway obstruction.5,14
  • Pulmonary rehabilitation programs including psychotherapy sessions have also relieved symptoms of GAD and MDD for patients with COPD.
  • Programs that include physiotherapy, physical exercise (arm and leg exercise, aerobic conditioning, flexibility training), patient education, and psychotherapy sessions have significantly lowered GAD and MDD scores when compared with similar rehabilitation programs not offering psychotherapy.24
  • Cognitive-behavioral therapy has been variably effective in treating comorbid GAD and MDD, with studies citing either superiority5 or equivalence25 to COPD education alone.

Increasingly, psychologists have been integrated into primary care with implementation of the Patient-Centered Medical Home.26 However, if primary care physicians do not have behavioral specialists available, they can contact the American Psychological Association, their state psychological association, or professional organizations, such as the Society of Behavioral Medicine, for referral to professionals trained in behavioral self-management skills.

Initiation of treatment, whether pharmacological or non-pharmacological, and emphasis on self-management of the disease can greatly improve patients' perceptions of their condition and overall quality of life.

CASE The patient screens positive for GAD and you give him a prescription for venlafaxine to begin immediately. Using an MI approach, you help the patient clarify that being more engaged with his family is important to him. Acknowledging that your recommendations are consistent with his values, the patient agrees to pursue pulmonary rehabilitation and, with the aid of a behavioral health specialist, learn self-management techniques for medication adherence and social reengagement.

CORRESPONDENCE
Ms. Sydney Marsh, 3009 S 35th Ave., Omaha, NE 68105; [email protected].

References

1. Yohannes AM, Willgoss TG, Baldwin RC, et al. Depression and anxiety in chronic heart failure and chronic obstructive pulmonary disease: prevalence, relevance, clinical implications and management principles. Int J Geriatr Psychiatry. 2010;25:1209-1221.

2. Punturieri A, Croxton TL, Weinmann G, et al. The changing face of COPD. Am Fam Physician. 2007;1:315-316.

3. Willgoss TG, Yohannes AM. Anxiety disorders in patients with COPD: a systematic review. Respir Care. 2013;58:858-866.

4. Porthirat C, Chaiwong W, Phetsuk N, et al. Major affective disorders in chronic obstructive pulmonary disease compared with other chronic respiratory diseases. Int J Chron Obstruct Pulmon Dis. 2015;10:1583-1590.

5. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. 2003; 65:963-970.

6. Singh G, Zhang W, Kuo YF, et al. Association of psychological disorders with 30-day readmission rates in patients with Chronic Obstructive Pulmonary Disease. Chest. 2015;Jul 23:[Epub ahead of print].

7. Vögele C, von Leupoldt A. Mental disorders in chronic obstructive pulmonary disease. Respir Med. 2008;102:764-773.

8. Aydin IO, Ulusahin A. Depression, anxiety comorbidity, and disability in tuberculosis and chronic obstructive pulmonary disease patients: applicability of GHQ-12. Gen Hosp Psychiatry. 2001;23:77-83.

9. Dalal AA, Shah M, Lunacsek O, et al. Clinical and economic burden of depression/anxiety in chronic obstructive pulmonary disease patients within a managed care population. COPD. 2011;8:293-299.

10. Janssen DJA, Wouters EFM, Spruit MA. Psychosocial consequences of living with breathlessness due to advanced disease. Curr Opin Support Palliat Care. 2015;9:232-237.

11. Atlantis E, Fahey P, Cochrane B, et al. Bidirectional associations between clinically relevant depression or anxiety and COPD. Chest. 2013;144:766-777.

12. Esser RW, Stoeckel MC, Kirsten A, et al. Structural brain changes in patients with chronic obstructive pulmonary disease. Chest. 2015;Jul 23:[Epub ahead of print].

13. Ng TP, Niti M, Tan WC, et al. Depressive symptoms and chronic obstructive pulmonary disease: effect on mortality, hospital readmission, symptom burden, functional status, and quality of life. Arch Intern Med. 2007;167:60-67.

14. Kim HF, Kunik ME, Molinari VA, et al. Functional impairment in COPD patients. Psychosomatics. 2000;41:465-471.

15. Cleland JA, Lee AJ, Hall S. Associations of depression and anxiety with gender, age, health-related quality of life and symptoms in primary care COPD patients. Fam Pract. 2007;24:217-223.

16. Kroenke K, Spitzer RL, Williams JB et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359.

17. Ajmera M, Sambamoorthi U, Metzger A, et al. Multimorbidity and COPD medication receipt among Medicaid beneficiaries with newly diagnosed COPD. Respir Care. 2015;60:1592-1602.

18. Medscape. Psychiatrics. Available at: http://reference.medscape.com/drugs/psychiatrics. Accessed March 1, 2016.

19. Physicians’ Desk Reference. Available at: http://www.pdr.net. Accessed March 1, 2016.

20. Kazdin AE. Behavior Modification in Applied Settings. Belmont, CA: Wadsworth/Thomson Learning; 2001.

21. Benzo R, Vickers K, Ernst D, et al. Development and feasibility of a self-management intervention for chronic obstructive pulmonary disease delivered with motivational interviewing strategies. J Cardiopulm Rehabil. 2013;33:113-123.

22. Zwerink M, Brusse-Keizer M, van der Valk PD, et al. Self management for patients with chronic obstructive pulmonary disease. Cochrane Database System Rev. 2014;(3):CD002990.

23. Miller WR, Rollnick S. Motivational Interviewing. 3rd ed. New York, NY: Guilford Press; 2013.

24. de Godoy DV, de Godoy RF. A randomized controlled trial of the effect of psychotherapy on anxiety and depression in chronic obstructive pulmonary disease. Arch Phys Med Rehabil. 2003;84:1154-1157.

25. Kunik ME, Veazey C, Cully JA, et al. COPD education and cognitive behavioral therapy group treatment for clinically significant symptoms of depression and anxiety in COPD patients: a randomized controlled trial. Psychol Med. 2008;38:385-396.

26. McDaniel SH, Fogarty CT. What primary care psychology has to offer the patient-centered medical home. Prof Psych Res Pract. 2009;40:483-492.

References

1. Yohannes AM, Willgoss TG, Baldwin RC, et al. Depression and anxiety in chronic heart failure and chronic obstructive pulmonary disease: prevalence, relevance, clinical implications and management principles. Int J Geriatr Psychiatry. 2010;25:1209-1221.

2. Punturieri A, Croxton TL, Weinmann G, et al. The changing face of COPD. Am Fam Physician. 2007;1:315-316.

3. Willgoss TG, Yohannes AM. Anxiety disorders in patients with COPD: a systematic review. Respir Care. 2013;58:858-866.

4. Porthirat C, Chaiwong W, Phetsuk N, et al. Major affective disorders in chronic obstructive pulmonary disease compared with other chronic respiratory diseases. Int J Chron Obstruct Pulmon Dis. 2015;10:1583-1590.

5. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. 2003; 65:963-970.

6. Singh G, Zhang W, Kuo YF, et al. Association of psychological disorders with 30-day readmission rates in patients with Chronic Obstructive Pulmonary Disease. Chest. 2015;Jul 23:[Epub ahead of print].

7. Vögele C, von Leupoldt A. Mental disorders in chronic obstructive pulmonary disease. Respir Med. 2008;102:764-773.

8. Aydin IO, Ulusahin A. Depression, anxiety comorbidity, and disability in tuberculosis and chronic obstructive pulmonary disease patients: applicability of GHQ-12. Gen Hosp Psychiatry. 2001;23:77-83.

9. Dalal AA, Shah M, Lunacsek O, et al. Clinical and economic burden of depression/anxiety in chronic obstructive pulmonary disease patients within a managed care population. COPD. 2011;8:293-299.

10. Janssen DJA, Wouters EFM, Spruit MA. Psychosocial consequences of living with breathlessness due to advanced disease. Curr Opin Support Palliat Care. 2015;9:232-237.

11. Atlantis E, Fahey P, Cochrane B, et al. Bidirectional associations between clinically relevant depression or anxiety and COPD. Chest. 2013;144:766-777.

12. Esser RW, Stoeckel MC, Kirsten A, et al. Structural brain changes in patients with chronic obstructive pulmonary disease. Chest. 2015;Jul 23:[Epub ahead of print].

13. Ng TP, Niti M, Tan WC, et al. Depressive symptoms and chronic obstructive pulmonary disease: effect on mortality, hospital readmission, symptom burden, functional status, and quality of life. Arch Intern Med. 2007;167:60-67.

14. Kim HF, Kunik ME, Molinari VA, et al. Functional impairment in COPD patients. Psychosomatics. 2000;41:465-471.

15. Cleland JA, Lee AJ, Hall S. Associations of depression and anxiety with gender, age, health-related quality of life and symptoms in primary care COPD patients. Fam Pract. 2007;24:217-223.

16. Kroenke K, Spitzer RL, Williams JB et al. The Patient Health Questionnaire Somatic, Anxiety, and Depressive Symptom Scales: a systematic review. Gen Hosp Psychiatry. 2010;32:345-359.

17. Ajmera M, Sambamoorthi U, Metzger A, et al. Multimorbidity and COPD medication receipt among Medicaid beneficiaries with newly diagnosed COPD. Respir Care. 2015;60:1592-1602.

18. Medscape. Psychiatrics. Available at: http://reference.medscape.com/drugs/psychiatrics. Accessed March 1, 2016.

19. Physicians’ Desk Reference. Available at: http://www.pdr.net. Accessed March 1, 2016.

20. Kazdin AE. Behavior Modification in Applied Settings. Belmont, CA: Wadsworth/Thomson Learning; 2001.

21. Benzo R, Vickers K, Ernst D, et al. Development and feasibility of a self-management intervention for chronic obstructive pulmonary disease delivered with motivational interviewing strategies. J Cardiopulm Rehabil. 2013;33:113-123.

22. Zwerink M, Brusse-Keizer M, van der Valk PD, et al. Self management for patients with chronic obstructive pulmonary disease. Cochrane Database System Rev. 2014;(3):CD002990.

23. Miller WR, Rollnick S. Motivational Interviewing. 3rd ed. New York, NY: Guilford Press; 2013.

24. de Godoy DV, de Godoy RF. A randomized controlled trial of the effect of psychotherapy on anxiety and depression in chronic obstructive pulmonary disease. Arch Phys Med Rehabil. 2003;84:1154-1157.

25. Kunik ME, Veazey C, Cully JA, et al. COPD education and cognitive behavioral therapy group treatment for clinically significant symptoms of depression and anxiety in COPD patients: a randomized controlled trial. Psychol Med. 2008;38:385-396.

26. McDaniel SH, Fogarty CT. What primary care psychology has to offer the patient-centered medical home. Prof Psych Res Pract. 2009;40:483-492.

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The Journal of Family Practice - 65(4)
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The Journal of Family Practice - 65(4)
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Anxiety and depression: Easing the burden in COPD patients
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Anxiety and depression: Easing the burden in COPD patients
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Biologics for Pediatric Psoriasis Patients?

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Biologics for Pediatric Psoriasis Patients?

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

Author and Disclosure Information

Dr. Weinberg is from the Icahn School of Medicine at Mount Sinai, New York, New York.

Dr. Weinberg is a speaker for Amgen Inc.

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Dr. Weinberg is from the Icahn School of Medicine at Mount Sinai, New York, New York.

Dr. Weinberg is a speaker for Amgen Inc.

Author and Disclosure Information

Dr. Weinberg is from the Icahn School of Medicine at Mount Sinai, New York, New York.

Dr. Weinberg is a speaker for Amgen Inc.

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

Biologic agents for the treatment of psoriasis are approved for patients 18 years and older. Although some biologics are approved for juvenile idiopathic arthritis, the lack of approved biologic therapies for children with psoriasis has been a major gap in our treatment of the disease. The incidence of moderate to severe psoriasis in the pediatric population is much lower than in adults, but there are still many patients younger than 18 years who would benefit from systemic therapies.

A recent press release indicates that the US Food and Drug Administration has accepted for review a supplemental biologics license application for the expanded use of etanercept to treat pediatric patients with chronic severe plaque psoriasis.

In February 2016 Paller et al (J Am Acad Dermatol. 2016;74:280.e3-287.e3) published data evaluating long-term safety and efficacy of etanercept in children and adolescents with moderate to severe plaque psoriasis. This 5-year, open-label extension study enrolled those patients aged 4 to 17 years who had participated in an initial 48-week parent study. End points included occurrence of adverse events (AEs) and serious AEs including infections as well as rates of 75% and 90% improvement in psoriasis area and severity index (PASI) score and clear or almost clear status on the static physician global assessment.

Of 182 patients enrolled, 181 received etanercept and 69 completed 264 weeks of treatment. Through week 264, 161 (89.0%) patients reported an AE, most commonly upper respiratory tract infection (37.6%), nasopharyngitis (26.0%), and headache (21.5%). Seven patients reported 8 Serious AEs (n=8) were reported in 7 patients, and only 1 case of cellulitis was considered treatment related. No cases of opportunistic infections or malignancy were reported. Rates of 75% improvement (∼60%–70%) and 90% improvement (∼30%–40%) in PASI score were maintained through week 264 as well as static physician global assessment status of clear or almost clear (∼40%–50%).

What’s the issue?

If approved, etanercept would be the first US Food and Drug Administration–approved systemic drug for pediatric psoriasis patients, which would open up options for many patients in need. Would you be willing to treat your pediatric psoriasis patients with a biologic?

We want to know your views! Tell us what you think.

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Guideline update shortens minimum DAPT duration in CAD

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Guideline update shortens minimum DAPT duration in CAD

New guidelines decrease the minimum duration of dual-antiplatelet therapy (DAPT) to as little as 3 months after drug-eluting stent placement in certain lower-risk patients with coronary artery disease.

The updated recommendations harmonize and replace six other guidelines, and apply to everolimus and zotarolimus stents, not Cypher or Taxus stents, said Dr. Eric R. Bates, who helped author the American College of Cardiology/American Heart Association Focused Update. “The emphasis is on balancing ischemic risk versus bleeding risk. The recommendations give clinicians guideline coverage to make personalized DAPT recommendations,” he said in an interview.

Dr. Eric Bates

The guidance reflects recent evidence that shorter duration (3-6 months) of DAPT, compared with the standard 12 months of therapy does not increase the risk of stent thrombosis and potentially lessens bleeding risk in select patients. Other studies of an additional 18 or 36 months of DAPT found a decrease in the risk of MI and stent thrombosis, at the cost of greater risk of bleeding. Thus, the updated guidelines call for “a thoughtful assessment of the benefit-risk ratio, integration of study data, and consideration of patient preference” when selecting duration of DAPT. “In general, shorter-duration DAPT can be considered for patients at lower ischemic risk with high bleeding risk, whereas longer-duration DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk,” the authors wrote, led by Dr. Glenn N. Levineof Baylor College of Medicine, Houston (J Am Coll Cardiol. 2016 Mar 29. doi: 10.1016/j.jacc.2016.03.512).

The recommendations define DAPT as combination therapy with aspirin and a P2Y12 receptor inhibitor – that is, clopidogrel, prasugrel, or ticagrelor. “When indicated, ticagrelor and prasugrel have a Class IIa preference over clopidogrel,” Dr. Bates said. The recommended daily dose of aspirin is 81 mg (range, 75-100 mg), which is usually continued indefinitely, regardless of how long patients receive dual therapy.

The shortened durations of dual-antiplatelet therapy include several scenarios. For elective percutaneous coronary intervention, the former Class I recommendation for 12 months of DAPT has been reduced to 6 months, with a Class IIb recommendation for either longer treatment or shorter (3-month) treatment, Dr. Bates, professor of medicine at the University of Michigan Health System in Ann Arbor, said. For patients with acute coronary syndrome, the guidelines retain the Class I recommendation for 12 months of DAPT, but also add a Class IIb recommendation for longer or shorter (6 months) DAPT.

The guidelines also include a new Class IIb recommendation for 12 months of DAPT started early after coronary artery bypass graft in patients with stable ischemic heart disease. This strategy “may be reasonable to improve vein graft patency” in these patients, the recommendations state.

The guidance clarifies previous recommendations on the timing of elective noncardiac surgery, and assigns Class IIb support for consideration of such surgeries starting 3 months after implantation of drug-eluting stents, if the risks of delaying surgery outweigh the expected risk of stent thrombosis when it is necessary to stop P2Y12 inhibitor therapy.

©Svisio/Thinkstock
Blood cells in the blood vessel

The recommendations now distinguish between B and C levels of evidence to increase granularity, according to Dr. Bates. The document updates recommendations on duration of DAPT across six previously published guidelines – the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention (PCI); the 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery; the 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease; the 2013ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction; the 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes, and the 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.

The extensive evidence review that informed guideline development was simultaneously reported by Dr. John Bittl at Munroe Regional Medical Center in Ocala, Fla., and his colleagues. The investigators synthesized evidence from 11 randomized controlled trials of more than 33,000 patients who received mainly newer generation stents. They also reviewed a randomized controlled trial of more than 21,000 patients with stable ischemic heart disease who were more than 1 year post-MI, and a post hoc analysis of a trial of more than 15,000 such patients.

These reviews uncovered “moderately strong evidence” that prolonged DAPT after implantation of newer generation drug-eluting stents “entails a trade-off between reductions in stent thrombosis and MI and increases in major hemorrhage,” Dr. Bittl and his colleagues wrote. Likewise, they found moderately strong evidence that prolonged DAPT helps prevent cardiovascular events at the cost of increased bleeding in patients whose coronary thrombotic risk stemmed from prior MI, not stent implantation. They found weak evidence of increased mortality in stent patients who received prolonged DAPT.

 

 

Dr. Bates reported consulting relationships with Merck and AstraZeneca. Eight other coauthors disclosed financial relationships with a number of pharmaceutical or device companies. Dr. Glenn Levine and seven coauthors disclosed no relationships with industry.

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New guidelines decrease the minimum duration of dual-antiplatelet therapy (DAPT) to as little as 3 months after drug-eluting stent placement in certain lower-risk patients with coronary artery disease.

The updated recommendations harmonize and replace six other guidelines, and apply to everolimus and zotarolimus stents, not Cypher or Taxus stents, said Dr. Eric R. Bates, who helped author the American College of Cardiology/American Heart Association Focused Update. “The emphasis is on balancing ischemic risk versus bleeding risk. The recommendations give clinicians guideline coverage to make personalized DAPT recommendations,” he said in an interview.

Dr. Eric Bates

The guidance reflects recent evidence that shorter duration (3-6 months) of DAPT, compared with the standard 12 months of therapy does not increase the risk of stent thrombosis and potentially lessens bleeding risk in select patients. Other studies of an additional 18 or 36 months of DAPT found a decrease in the risk of MI and stent thrombosis, at the cost of greater risk of bleeding. Thus, the updated guidelines call for “a thoughtful assessment of the benefit-risk ratio, integration of study data, and consideration of patient preference” when selecting duration of DAPT. “In general, shorter-duration DAPT can be considered for patients at lower ischemic risk with high bleeding risk, whereas longer-duration DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk,” the authors wrote, led by Dr. Glenn N. Levineof Baylor College of Medicine, Houston (J Am Coll Cardiol. 2016 Mar 29. doi: 10.1016/j.jacc.2016.03.512).

The recommendations define DAPT as combination therapy with aspirin and a P2Y12 receptor inhibitor – that is, clopidogrel, prasugrel, or ticagrelor. “When indicated, ticagrelor and prasugrel have a Class IIa preference over clopidogrel,” Dr. Bates said. The recommended daily dose of aspirin is 81 mg (range, 75-100 mg), which is usually continued indefinitely, regardless of how long patients receive dual therapy.

The shortened durations of dual-antiplatelet therapy include several scenarios. For elective percutaneous coronary intervention, the former Class I recommendation for 12 months of DAPT has been reduced to 6 months, with a Class IIb recommendation for either longer treatment or shorter (3-month) treatment, Dr. Bates, professor of medicine at the University of Michigan Health System in Ann Arbor, said. For patients with acute coronary syndrome, the guidelines retain the Class I recommendation for 12 months of DAPT, but also add a Class IIb recommendation for longer or shorter (6 months) DAPT.

The guidelines also include a new Class IIb recommendation for 12 months of DAPT started early after coronary artery bypass graft in patients with stable ischemic heart disease. This strategy “may be reasonable to improve vein graft patency” in these patients, the recommendations state.

The guidance clarifies previous recommendations on the timing of elective noncardiac surgery, and assigns Class IIb support for consideration of such surgeries starting 3 months after implantation of drug-eluting stents, if the risks of delaying surgery outweigh the expected risk of stent thrombosis when it is necessary to stop P2Y12 inhibitor therapy.

©Svisio/Thinkstock
Blood cells in the blood vessel

The recommendations now distinguish between B and C levels of evidence to increase granularity, according to Dr. Bates. The document updates recommendations on duration of DAPT across six previously published guidelines – the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention (PCI); the 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery; the 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease; the 2013ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction; the 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes, and the 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.

The extensive evidence review that informed guideline development was simultaneously reported by Dr. John Bittl at Munroe Regional Medical Center in Ocala, Fla., and his colleagues. The investigators synthesized evidence from 11 randomized controlled trials of more than 33,000 patients who received mainly newer generation stents. They also reviewed a randomized controlled trial of more than 21,000 patients with stable ischemic heart disease who were more than 1 year post-MI, and a post hoc analysis of a trial of more than 15,000 such patients.

These reviews uncovered “moderately strong evidence” that prolonged DAPT after implantation of newer generation drug-eluting stents “entails a trade-off between reductions in stent thrombosis and MI and increases in major hemorrhage,” Dr. Bittl and his colleagues wrote. Likewise, they found moderately strong evidence that prolonged DAPT helps prevent cardiovascular events at the cost of increased bleeding in patients whose coronary thrombotic risk stemmed from prior MI, not stent implantation. They found weak evidence of increased mortality in stent patients who received prolonged DAPT.

 

 

Dr. Bates reported consulting relationships with Merck and AstraZeneca. Eight other coauthors disclosed financial relationships with a number of pharmaceutical or device companies. Dr. Glenn Levine and seven coauthors disclosed no relationships with industry.

New guidelines decrease the minimum duration of dual-antiplatelet therapy (DAPT) to as little as 3 months after drug-eluting stent placement in certain lower-risk patients with coronary artery disease.

The updated recommendations harmonize and replace six other guidelines, and apply to everolimus and zotarolimus stents, not Cypher or Taxus stents, said Dr. Eric R. Bates, who helped author the American College of Cardiology/American Heart Association Focused Update. “The emphasis is on balancing ischemic risk versus bleeding risk. The recommendations give clinicians guideline coverage to make personalized DAPT recommendations,” he said in an interview.

Dr. Eric Bates

The guidance reflects recent evidence that shorter duration (3-6 months) of DAPT, compared with the standard 12 months of therapy does not increase the risk of stent thrombosis and potentially lessens bleeding risk in select patients. Other studies of an additional 18 or 36 months of DAPT found a decrease in the risk of MI and stent thrombosis, at the cost of greater risk of bleeding. Thus, the updated guidelines call for “a thoughtful assessment of the benefit-risk ratio, integration of study data, and consideration of patient preference” when selecting duration of DAPT. “In general, shorter-duration DAPT can be considered for patients at lower ischemic risk with high bleeding risk, whereas longer-duration DAPT may be reasonable for patients at higher ischemic risk with lower bleeding risk,” the authors wrote, led by Dr. Glenn N. Levineof Baylor College of Medicine, Houston (J Am Coll Cardiol. 2016 Mar 29. doi: 10.1016/j.jacc.2016.03.512).

The recommendations define DAPT as combination therapy with aspirin and a P2Y12 receptor inhibitor – that is, clopidogrel, prasugrel, or ticagrelor. “When indicated, ticagrelor and prasugrel have a Class IIa preference over clopidogrel,” Dr. Bates said. The recommended daily dose of aspirin is 81 mg (range, 75-100 mg), which is usually continued indefinitely, regardless of how long patients receive dual therapy.

The shortened durations of dual-antiplatelet therapy include several scenarios. For elective percutaneous coronary intervention, the former Class I recommendation for 12 months of DAPT has been reduced to 6 months, with a Class IIb recommendation for either longer treatment or shorter (3-month) treatment, Dr. Bates, professor of medicine at the University of Michigan Health System in Ann Arbor, said. For patients with acute coronary syndrome, the guidelines retain the Class I recommendation for 12 months of DAPT, but also add a Class IIb recommendation for longer or shorter (6 months) DAPT.

The guidelines also include a new Class IIb recommendation for 12 months of DAPT started early after coronary artery bypass graft in patients with stable ischemic heart disease. This strategy “may be reasonable to improve vein graft patency” in these patients, the recommendations state.

The guidance clarifies previous recommendations on the timing of elective noncardiac surgery, and assigns Class IIb support for consideration of such surgeries starting 3 months after implantation of drug-eluting stents, if the risks of delaying surgery outweigh the expected risk of stent thrombosis when it is necessary to stop P2Y12 inhibitor therapy.

©Svisio/Thinkstock
Blood cells in the blood vessel

The recommendations now distinguish between B and C levels of evidence to increase granularity, according to Dr. Bates. The document updates recommendations on duration of DAPT across six previously published guidelines – the 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention (PCI); the 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery; the 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease; the 2013ACC/AHA Guideline for the Management of ST-Elevation Myocardial Infarction; the 2014 ACC/AHA Guideline for Non-ST-Elevation Acute Coronary Syndromes, and the 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.

The extensive evidence review that informed guideline development was simultaneously reported by Dr. John Bittl at Munroe Regional Medical Center in Ocala, Fla., and his colleagues. The investigators synthesized evidence from 11 randomized controlled trials of more than 33,000 patients who received mainly newer generation stents. They also reviewed a randomized controlled trial of more than 21,000 patients with stable ischemic heart disease who were more than 1 year post-MI, and a post hoc analysis of a trial of more than 15,000 such patients.

These reviews uncovered “moderately strong evidence” that prolonged DAPT after implantation of newer generation drug-eluting stents “entails a trade-off between reductions in stent thrombosis and MI and increases in major hemorrhage,” Dr. Bittl and his colleagues wrote. Likewise, they found moderately strong evidence that prolonged DAPT helps prevent cardiovascular events at the cost of increased bleeding in patients whose coronary thrombotic risk stemmed from prior MI, not stent implantation. They found weak evidence of increased mortality in stent patients who received prolonged DAPT.

 

 

Dr. Bates reported consulting relationships with Merck and AstraZeneca. Eight other coauthors disclosed financial relationships with a number of pharmaceutical or device companies. Dr. Glenn Levine and seven coauthors disclosed no relationships with industry.

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FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

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Medical Students Receive Grants from Society of Hospital Medicine

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

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

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

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

    Mentor: Nilam Soni, MD

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

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

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

    Mentor: Ria Dancel, MD, FHM

    Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

    Project Site: University of North Carolina Children's Hospital

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

    Mentor: Nasim Afsar, MD, SFHM

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

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

  • Haverly Snyder, Medical College of Wisconsin

    Mentor: Kathlyn Fletcher, MD, FHM

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

    Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

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

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

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

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

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

    Mentor: Nilam Soni, MD

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

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

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

    Mentor: Ria Dancel, MD, FHM

    Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

    Project Site: University of North Carolina Children's Hospital

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

    Mentor: Nasim Afsar, MD, SFHM

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

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

  • Haverly Snyder, Medical College of Wisconsin

    Mentor: Kathlyn Fletcher, MD, FHM

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

    Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

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

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

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

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

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

    Mentor: Nilam Soni, MD

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

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

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

    Mentor: Ria Dancel, MD, FHM

    Project: Analysis and Optimization of the Inpatient Pediatric Discharge Process

    Project Site: University of North Carolina Children's Hospital

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

    Mentor: Nasim Afsar, MD, SFHM

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

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

  • Haverly Snyder, Medical College of Wisconsin

    Mentor: Kathlyn Fletcher, MD, FHM

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

    Project Site: Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin

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

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New gout drug under investigation has dual benefit

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

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

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

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

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

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

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

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

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

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

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

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

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Dr. Tuhina Neogi

Arhalofenate provided a reduction in gout attack risk and serum urate level that appears to be clinically meaningful, particularly for patients who cannot use colchicine or nonsteroidal anti-inflammatory drugs for flare prophylaxis. It could potentially be the first in a new urate-lowering, antiflare therapy (ULAFT) class of drug.

However, the trial used of lower-than-recommended doses of the comparator drug allopurinol. If the allopurinol dose had been up-titrated from 300 mg to 400 mg per day, an even greater proportion of patients in this arm would have likely reached the serum urate target of less than 6 mg/dL.

Starting the patients at 100 mg allopurinol before titrating upward as current recommendations advise, instead of initiating treatment at 300 mg without flare prophylaxis, could have lowered the flare rate.

Dr. Hyon K. Choi

It would also have been useful to see the effect of the drug in patients with renal impairment (subjects with a creatinine clearance less than 60 mL/min were excluded from the study), as well as explore further the potential metabolic effects first seen when the agent was first investigated as an insulin sensitizer.

Dr. Tuhina Neogi is with the department of medicine at Boston University, and Dr. Hyon Choi is a professor of medicine in the division of rheumatology, allergy, and immunology at Massachusetts General Hospital and Harvard Medical School, both in Boston. Their comments are derived from an editorial accompanying Dr. Poiley and his colleagues’ report (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39687). No conflicts of interest were disclosed.

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Body

Dr. Tuhina Neogi

Arhalofenate provided a reduction in gout attack risk and serum urate level that appears to be clinically meaningful, particularly for patients who cannot use colchicine or nonsteroidal anti-inflammatory drugs for flare prophylaxis. It could potentially be the first in a new urate-lowering, antiflare therapy (ULAFT) class of drug.

However, the trial used of lower-than-recommended doses of the comparator drug allopurinol. If the allopurinol dose had been up-titrated from 300 mg to 400 mg per day, an even greater proportion of patients in this arm would have likely reached the serum urate target of less than 6 mg/dL.

Starting the patients at 100 mg allopurinol before titrating upward as current recommendations advise, instead of initiating treatment at 300 mg without flare prophylaxis, could have lowered the flare rate.

Dr. Hyon K. Choi

It would also have been useful to see the effect of the drug in patients with renal impairment (subjects with a creatinine clearance less than 60 mL/min were excluded from the study), as well as explore further the potential metabolic effects first seen when the agent was first investigated as an insulin sensitizer.

Dr. Tuhina Neogi is with the department of medicine at Boston University, and Dr. Hyon Choi is a professor of medicine in the division of rheumatology, allergy, and immunology at Massachusetts General Hospital and Harvard Medical School, both in Boston. Their comments are derived from an editorial accompanying Dr. Poiley and his colleagues’ report (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39687). No conflicts of interest were disclosed.

Body

Dr. Tuhina Neogi

Arhalofenate provided a reduction in gout attack risk and serum urate level that appears to be clinically meaningful, particularly for patients who cannot use colchicine or nonsteroidal anti-inflammatory drugs for flare prophylaxis. It could potentially be the first in a new urate-lowering, antiflare therapy (ULAFT) class of drug.

However, the trial used of lower-than-recommended doses of the comparator drug allopurinol. If the allopurinol dose had been up-titrated from 300 mg to 400 mg per day, an even greater proportion of patients in this arm would have likely reached the serum urate target of less than 6 mg/dL.

Starting the patients at 100 mg allopurinol before titrating upward as current recommendations advise, instead of initiating treatment at 300 mg without flare prophylaxis, could have lowered the flare rate.

Dr. Hyon K. Choi

It would also have been useful to see the effect of the drug in patients with renal impairment (subjects with a creatinine clearance less than 60 mL/min were excluded from the study), as well as explore further the potential metabolic effects first seen when the agent was first investigated as an insulin sensitizer.

Dr. Tuhina Neogi is with the department of medicine at Boston University, and Dr. Hyon Choi is a professor of medicine in the division of rheumatology, allergy, and immunology at Massachusetts General Hospital and Harvard Medical School, both in Boston. Their comments are derived from an editorial accompanying Dr. Poiley and his colleagues’ report (Arthritis Rheumatol. 2016 Mar 18. doi: 10.1002/art.39687). No conflicts of interest were disclosed.

Title
Promising results for first in class drug
Promising results for first in class drug

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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New gout drug under investigation has dual benefit
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Key clinical point: The investigational uricosuric drug arhalofenate significantly reduced the incidence of flares in gout patients and also modestly reduced serum uric acid.Major finding: Arhalofenate at an 800-mg daily dose significantly reduced gout flares over 12 weeks by 46% versus allopurinol at a dose of 300 mg daily (0.66 flares vs. 1.24; P = .0056).

Data source: A 12-week, phase IIb, double-blind, randomized, placebo- and active-drug controlled trial involving 239 gout patients.

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

Genetics, smoking, and inflammation on MRI predict progression in axial SpA

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Genetics, smoking, and inflammation on MRI predict progression in axial SpA

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

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

Dr. Maxime Dougados

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

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

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

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

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

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

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

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

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

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

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

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

Dr. Maxime Dougados

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

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

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

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

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

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

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

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

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

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

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

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

Dr. Maxime Dougados

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

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

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

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

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

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

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

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

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

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

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Key clinical point: The switch from nonradiographic to radiographic axSpA, made by about 5% of patients over the 2-year study period, was influenced by HLAB27 positivity, smoking status, and inflammatory sacroiliac joint lesions on MRI.

Major finding: Multivariate analysis showed smoking status (OR, 3.3; 95% CI, 1.0-11.5), HLAB27 positivity (OR, 12.6; 95% CI, 2.3-274), and the presence of inflammation at MRI in the sacroiliac joints (SIJ) at baseline (OR, 48.8; 95% CI, 9.3-904) predicted progression.

Data source: An analysis of 2-year data from 449 patients with recent-onset inflammatory back pain participating in the multicenter, longitudinal DESIR study.

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

Research Finds the Main Cause of Inferior Vena Cava Thrombosis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

 

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

 

 

 

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

 

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

 

 

 

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

 

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

 

 

 

 

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Did You Commit to ‘Fight the Resistance’ at HM16?

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Did You Commit to ‘Fight the Resistance’ at HM16?

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

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

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

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

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

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

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

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

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

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Jerome C. Siy, MD, SFHM Explores Hospital Medicine’s Global Reach

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Jerome C. Siy, MD, SFHM Explores Hospital Medicine’s Global Reach

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

Jerome C. Siy, MD, SFHM, CHIE

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

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

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

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

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

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

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

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

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

 

 

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

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

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

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

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

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

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

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

 

 

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

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

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


Brett Radler is SHM’s communications coordinator.

Issue
The Hospitalist - 2016(03)
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Editor’s note: As SHM celebrates the “Year of the Hospitalist,” we’re putting the spotlight on some of our most active members who are making substantial contributions to hospital medicine. You can get involved, too! Log on to www.hospitalmedicine.org/yoth for more information on how you can join the yearlong celebration and help SHM improve the care of hospitalized patients.

Jerome C. Siy, MD, SFHM, CHIE

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

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

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

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

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

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

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

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

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

 

 

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

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

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

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

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

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

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

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

 

 

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

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

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


Brett Radler is SHM’s communications coordinator.

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

Jerome C. Siy, MD, SFHM, CHIE

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

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

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

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

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

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

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

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

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

 

 

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

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

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

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

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

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

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

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

 

 

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

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

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


Brett Radler is SHM’s communications coordinator.

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Jerome C. Siy, MD, SFHM Explores Hospital Medicine’s Global Reach
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