User login
Bone quality: A soft concept, hard to ignore
In the case of the antiresorptive drugs for treating osteoporosis, the bisphosphonates have been shown not only to improve bone density but also to reduce the risk of fractures. The clinical trials used dual-energy x-ray absorptiometry (DXA) measurements as a surrogate marker for fragility fractures, and the two correlated reasonably well. Thus, clinicians for the past 10-plus years have used DXA results to justify prescribing these drugs for patients (primarily women) with low T scores to prevent future fractures. There is no doubt that osteoporosis had previously been undertreated, and the projected number of patients with hip and spine fractures would overflow chronic-care beds. Yet there has been a sense that bisphosphonates are prescribed so often they may as well be “put in the water,” and that we are prophylactically treating many thousands of patients who are never going to suffer a fracture.
How can we better predict who will, with a given low T score, have a fracture of the hip or spine and who will not? Why do patients exposed to excess corticosteroids suffer strikingly more fractures than patients with identical T scores who were not exposed to steroids? Why do smoking and family history of fracture contribute to fracture risk in a way not accounted for by density measures alone?
Thus enters the intellectually pleasing concept of bone quality. However, bone quality is pragmatically as tough to measure as emotional stress. Yet we have learned to not minimize either of these when looking at hard outcomes. In this issue of the Journal, Dr. Angelo Licata discusses how clinicians can use the concept of bone quality in daily practice.
In the case of the antiresorptive drugs for treating osteoporosis, the bisphosphonates have been shown not only to improve bone density but also to reduce the risk of fractures. The clinical trials used dual-energy x-ray absorptiometry (DXA) measurements as a surrogate marker for fragility fractures, and the two correlated reasonably well. Thus, clinicians for the past 10-plus years have used DXA results to justify prescribing these drugs for patients (primarily women) with low T scores to prevent future fractures. There is no doubt that osteoporosis had previously been undertreated, and the projected number of patients with hip and spine fractures would overflow chronic-care beds. Yet there has been a sense that bisphosphonates are prescribed so often they may as well be “put in the water,” and that we are prophylactically treating many thousands of patients who are never going to suffer a fracture.
How can we better predict who will, with a given low T score, have a fracture of the hip or spine and who will not? Why do patients exposed to excess corticosteroids suffer strikingly more fractures than patients with identical T scores who were not exposed to steroids? Why do smoking and family history of fracture contribute to fracture risk in a way not accounted for by density measures alone?
Thus enters the intellectually pleasing concept of bone quality. However, bone quality is pragmatically as tough to measure as emotional stress. Yet we have learned to not minimize either of these when looking at hard outcomes. In this issue of the Journal, Dr. Angelo Licata discusses how clinicians can use the concept of bone quality in daily practice.
In the case of the antiresorptive drugs for treating osteoporosis, the bisphosphonates have been shown not only to improve bone density but also to reduce the risk of fractures. The clinical trials used dual-energy x-ray absorptiometry (DXA) measurements as a surrogate marker for fragility fractures, and the two correlated reasonably well. Thus, clinicians for the past 10-plus years have used DXA results to justify prescribing these drugs for patients (primarily women) with low T scores to prevent future fractures. There is no doubt that osteoporosis had previously been undertreated, and the projected number of patients with hip and spine fractures would overflow chronic-care beds. Yet there has been a sense that bisphosphonates are prescribed so often they may as well be “put in the water,” and that we are prophylactically treating many thousands of patients who are never going to suffer a fracture.
How can we better predict who will, with a given low T score, have a fracture of the hip or spine and who will not? Why do patients exposed to excess corticosteroids suffer strikingly more fractures than patients with identical T scores who were not exposed to steroids? Why do smoking and family history of fracture contribute to fracture risk in a way not accounted for by density measures alone?
Thus enters the intellectually pleasing concept of bone quality. However, bone quality is pragmatically as tough to measure as emotional stress. Yet we have learned to not minimize either of these when looking at hard outcomes. In this issue of the Journal, Dr. Angelo Licata discusses how clinicians can use the concept of bone quality in daily practice.
Enigmas of a mother’s heart
We tend to take successful gestation for granted. We understand the adverse fetal effects of environmental and genetic influences and infection, as well as the effects of diseases such as chronic kidney disease, diabetes, and pulmonary hypertension. But some disorders, such as preeclampsia and the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia), dramatically and uniquely affect the apparently healthy pregnant woman and thus require prompt recognition and treatment. Yet, despite their severity, their pathophysiology eludes our full understanding, and they tend to be underrepresented in our internal medicine curricula.
In this issue, Ramaraj and Sorrell discuss another enigma of maternal-fetal medicine, peripartum cardiomyopathy—a condition with significant heterogeneity in outcome and, likely, several triggers. But the variability of recurrence in subsequent pregnancy (even if cardiac function recovers from the first episode) argues that peripartum cardiomyopathy is not simply the effect of the cardiovascular stress of pregnancy on occult left ventricular dysfunction. This variability of recurrence also argues against a primary autoimmune mechanism, as does the observation that other autoimmune diseases often go into remission during pregnancy (but may flare postpartum). The higher incidence in African Americans and particularly in Haitians argues for some genetic contribution, and yet the variable rate of recurrence also challenges “bad genes” as the sole explanation.
Although the authors discuss diagnostic tests, peripartum cardiomyopathy still primarily requires astute clinical recognition with exclusion of other causes of acute heart failure. Thus, despite its low prevalence in the United States, this potentially fatal condition is worth reviewing. It is too tempting to attribute the early signs and symptoms of heart failure (dyspnea, edema, fatigue) to “just” the late stages of pregnancy.
We tend to take successful gestation for granted. We understand the adverse fetal effects of environmental and genetic influences and infection, as well as the effects of diseases such as chronic kidney disease, diabetes, and pulmonary hypertension. But some disorders, such as preeclampsia and the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia), dramatically and uniquely affect the apparently healthy pregnant woman and thus require prompt recognition and treatment. Yet, despite their severity, their pathophysiology eludes our full understanding, and they tend to be underrepresented in our internal medicine curricula.
In this issue, Ramaraj and Sorrell discuss another enigma of maternal-fetal medicine, peripartum cardiomyopathy—a condition with significant heterogeneity in outcome and, likely, several triggers. But the variability of recurrence in subsequent pregnancy (even if cardiac function recovers from the first episode) argues that peripartum cardiomyopathy is not simply the effect of the cardiovascular stress of pregnancy on occult left ventricular dysfunction. This variability of recurrence also argues against a primary autoimmune mechanism, as does the observation that other autoimmune diseases often go into remission during pregnancy (but may flare postpartum). The higher incidence in African Americans and particularly in Haitians argues for some genetic contribution, and yet the variable rate of recurrence also challenges “bad genes” as the sole explanation.
Although the authors discuss diagnostic tests, peripartum cardiomyopathy still primarily requires astute clinical recognition with exclusion of other causes of acute heart failure. Thus, despite its low prevalence in the United States, this potentially fatal condition is worth reviewing. It is too tempting to attribute the early signs and symptoms of heart failure (dyspnea, edema, fatigue) to “just” the late stages of pregnancy.
We tend to take successful gestation for granted. We understand the adverse fetal effects of environmental and genetic influences and infection, as well as the effects of diseases such as chronic kidney disease, diabetes, and pulmonary hypertension. But some disorders, such as preeclampsia and the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count associated with preeclampsia), dramatically and uniquely affect the apparently healthy pregnant woman and thus require prompt recognition and treatment. Yet, despite their severity, their pathophysiology eludes our full understanding, and they tend to be underrepresented in our internal medicine curricula.
In this issue, Ramaraj and Sorrell discuss another enigma of maternal-fetal medicine, peripartum cardiomyopathy—a condition with significant heterogeneity in outcome and, likely, several triggers. But the variability of recurrence in subsequent pregnancy (even if cardiac function recovers from the first episode) argues that peripartum cardiomyopathy is not simply the effect of the cardiovascular stress of pregnancy on occult left ventricular dysfunction. This variability of recurrence also argues against a primary autoimmune mechanism, as does the observation that other autoimmune diseases often go into remission during pregnancy (but may flare postpartum). The higher incidence in African Americans and particularly in Haitians argues for some genetic contribution, and yet the variable rate of recurrence also challenges “bad genes” as the sole explanation.
Although the authors discuss diagnostic tests, peripartum cardiomyopathy still primarily requires astute clinical recognition with exclusion of other causes of acute heart failure. Thus, despite its low prevalence in the United States, this potentially fatal condition is worth reviewing. It is too tempting to attribute the early signs and symptoms of heart failure (dyspnea, edema, fatigue) to “just” the late stages of pregnancy.
Spring brings changes to CCJM
First, we welcome our new deputy editor Dr. Timothy Gilligan. Tim, a medical oncologist with a journalism degree, takes over the reins from Dr. David Rolston, who left last year to become Associate Director of General Internal Medicine at Geisinger Medical Center in Danville, PA. David continues to provide input to the Journal as a member of our editorial board.
Also, the Journal joins an expanding movement in medical journalism by screening all submitted manuscripts with a new online service called CrossCheck to detect plagiarism—whether self-plagiarism or traditional plagiarism. In this way, we will do our part to uphold the integrity of the medical literature.
And as always, I urge you to continue to submit your ideas for articles, particularly ideas for 1-Minute Consults. We review and value all of your suggestions.
First, we welcome our new deputy editor Dr. Timothy Gilligan. Tim, a medical oncologist with a journalism degree, takes over the reins from Dr. David Rolston, who left last year to become Associate Director of General Internal Medicine at Geisinger Medical Center in Danville, PA. David continues to provide input to the Journal as a member of our editorial board.
Also, the Journal joins an expanding movement in medical journalism by screening all submitted manuscripts with a new online service called CrossCheck to detect plagiarism—whether self-plagiarism or traditional plagiarism. In this way, we will do our part to uphold the integrity of the medical literature.
And as always, I urge you to continue to submit your ideas for articles, particularly ideas for 1-Minute Consults. We review and value all of your suggestions.
First, we welcome our new deputy editor Dr. Timothy Gilligan. Tim, a medical oncologist with a journalism degree, takes over the reins from Dr. David Rolston, who left last year to become Associate Director of General Internal Medicine at Geisinger Medical Center in Danville, PA. David continues to provide input to the Journal as a member of our editorial board.
Also, the Journal joins an expanding movement in medical journalism by screening all submitted manuscripts with a new online service called CrossCheck to detect plagiarism—whether self-plagiarism or traditional plagiarism. In this way, we will do our part to uphold the integrity of the medical literature.
And as always, I urge you to continue to submit your ideas for articles, particularly ideas for 1-Minute Consults. We review and value all of your suggestions.
Identifying and classifying myocardial infarctions
But way back then, although the patient (and the physician) were often diaphoretic, the acute diagnosis was of limited significance to acute management. We rushed to put the patient to bed rest, started the lidocaine drip at the first sign of a few premature ventricular contractions, slapped on the oxygen prongs, got serial electrocardiograms to watch for conduction blocks—and a few forward thinkers began heparin drips.
As therapeutic options became more interventional, the need for rapid diagnostic tests and better biomarkers of prognosis became more critical. ST elevations took on new meaning, but the major diagnostic advance was the incorporation of cardiac troponin into our diagnostic algorithm.
In this issue of the Journal, Drs. Shaun Senter and Gary Francis discuss the power of these tests in the diagnosis of acute MI. They are not perfect tests. Acute pericarditis can still present diagnostic challenges, with sometimes confusing ECG findings, and almost a third of patients have elevated troponins (Bainey KR, Bhatt DL, Mayo Clin Proc 2009; 84:5–6; Imazio M, et al, J Am Coll Cardiol 2003; 42:2144–2148). Troponins may occasionally be elevated in acute severe heart failure and aortic dissection. In my practice, elevation of troponins may be difficult to interpret in the setting of chronic inflammatory muscle disease; it is not always easy to distinguish whether the leakage of these biomarkers is from injured regenerating skeletal muscle or from cardiac muscle.
When treating patients with a possible acute coronary syndrome, prompt diagnosis and intervention are often warranted, but the risks of using thrombolytic therapy inappropriately in the setting of pericarditis or an acute intracranial process with ECG changes are substantial.
Senter and Francis review for us the latest “precise definition” of acute myocardial infarction and provide a commentary on the utility of different diagnostic tests. They also highlight the value of using different diagnostic modalities to obtain the information we need for prognostication and treatment decisions.
But way back then, although the patient (and the physician) were often diaphoretic, the acute diagnosis was of limited significance to acute management. We rushed to put the patient to bed rest, started the lidocaine drip at the first sign of a few premature ventricular contractions, slapped on the oxygen prongs, got serial electrocardiograms to watch for conduction blocks—and a few forward thinkers began heparin drips.
As therapeutic options became more interventional, the need for rapid diagnostic tests and better biomarkers of prognosis became more critical. ST elevations took on new meaning, but the major diagnostic advance was the incorporation of cardiac troponin into our diagnostic algorithm.
In this issue of the Journal, Drs. Shaun Senter and Gary Francis discuss the power of these tests in the diagnosis of acute MI. They are not perfect tests. Acute pericarditis can still present diagnostic challenges, with sometimes confusing ECG findings, and almost a third of patients have elevated troponins (Bainey KR, Bhatt DL, Mayo Clin Proc 2009; 84:5–6; Imazio M, et al, J Am Coll Cardiol 2003; 42:2144–2148). Troponins may occasionally be elevated in acute severe heart failure and aortic dissection. In my practice, elevation of troponins may be difficult to interpret in the setting of chronic inflammatory muscle disease; it is not always easy to distinguish whether the leakage of these biomarkers is from injured regenerating skeletal muscle or from cardiac muscle.
When treating patients with a possible acute coronary syndrome, prompt diagnosis and intervention are often warranted, but the risks of using thrombolytic therapy inappropriately in the setting of pericarditis or an acute intracranial process with ECG changes are substantial.
Senter and Francis review for us the latest “precise definition” of acute myocardial infarction and provide a commentary on the utility of different diagnostic tests. They also highlight the value of using different diagnostic modalities to obtain the information we need for prognostication and treatment decisions.
But way back then, although the patient (and the physician) were often diaphoretic, the acute diagnosis was of limited significance to acute management. We rushed to put the patient to bed rest, started the lidocaine drip at the first sign of a few premature ventricular contractions, slapped on the oxygen prongs, got serial electrocardiograms to watch for conduction blocks—and a few forward thinkers began heparin drips.
As therapeutic options became more interventional, the need for rapid diagnostic tests and better biomarkers of prognosis became more critical. ST elevations took on new meaning, but the major diagnostic advance was the incorporation of cardiac troponin into our diagnostic algorithm.
In this issue of the Journal, Drs. Shaun Senter and Gary Francis discuss the power of these tests in the diagnosis of acute MI. They are not perfect tests. Acute pericarditis can still present diagnostic challenges, with sometimes confusing ECG findings, and almost a third of patients have elevated troponins (Bainey KR, Bhatt DL, Mayo Clin Proc 2009; 84:5–6; Imazio M, et al, J Am Coll Cardiol 2003; 42:2144–2148). Troponins may occasionally be elevated in acute severe heart failure and aortic dissection. In my practice, elevation of troponins may be difficult to interpret in the setting of chronic inflammatory muscle disease; it is not always easy to distinguish whether the leakage of these biomarkers is from injured regenerating skeletal muscle or from cardiac muscle.
When treating patients with a possible acute coronary syndrome, prompt diagnosis and intervention are often warranted, but the risks of using thrombolytic therapy inappropriately in the setting of pericarditis or an acute intracranial process with ECG changes are substantial.
Senter and Francis review for us the latest “precise definition” of acute myocardial infarction and provide a commentary on the utility of different diagnostic tests. They also highlight the value of using different diagnostic modalities to obtain the information we need for prognostication and treatment decisions.
The battle of the clot
In this issue of the Journal we review two special situations in which low-molecular-weight heparins have special advantages. Babu and Carman discuss patients with cancer and thromboembolic disease. These patients are particularly difficult to manage since they tend to have recurrent thrombosis, sometimes even while on anticoagulant therapy, and they tend to have more bleeding complications from warfarin therapy. Inanition, drug interactions, and organ dysfunction make warfarin titration problematic, and the possibility of vascular metastases is always a concern. Low-molecular-weight heparins —which, unlike warfarin, work primarily by antagonizing factor Xa activity—have proven to be as effective as warfarin in reversing the many hypercoagulable effects of malignancy, although it wasn’t obvious at first that they would be.
Gibson and Powrie review the issues we face when pregnant patients need anticoagulation. While drug interactions and organ dysfunction are rarely problems in this setting, warfarin is teratogenic and is therefore strongly contraindicated early in pregnancy, and its peripartum use has been associated with bleeding complications. Furthermore, unfractionated heparin is associated with the development of osteoporosis, and it requires frequent injections. The low-molecular-weight heparins thus have a definite niche in the management of pregnant women, but with a caveat: dosing of these agents by weight alone in this setting is fraught with the potential for underdosing. Catastrophic outcomes have been reported in pregnant patients with older mechanical cardiac valves who were switched from warfarin to low-molecular-weight heparin therapy. Plus, if the patient is to receive neuraxial regional anesthesia, low-molecular-weight heparins should be discontinued at least 12 hours before catheter placement if prophylactic doses have been given, or 24 hours if therapeutic doses have been given.
Low-molecular-weight heparins have greatly enhanced our ability to treat thromboembolic disease. But, as the authors of these two papers discuss, many management nuances still must be noted.
In this issue of the Journal we review two special situations in which low-molecular-weight heparins have special advantages. Babu and Carman discuss patients with cancer and thromboembolic disease. These patients are particularly difficult to manage since they tend to have recurrent thrombosis, sometimes even while on anticoagulant therapy, and they tend to have more bleeding complications from warfarin therapy. Inanition, drug interactions, and organ dysfunction make warfarin titration problematic, and the possibility of vascular metastases is always a concern. Low-molecular-weight heparins —which, unlike warfarin, work primarily by antagonizing factor Xa activity—have proven to be as effective as warfarin in reversing the many hypercoagulable effects of malignancy, although it wasn’t obvious at first that they would be.
Gibson and Powrie review the issues we face when pregnant patients need anticoagulation. While drug interactions and organ dysfunction are rarely problems in this setting, warfarin is teratogenic and is therefore strongly contraindicated early in pregnancy, and its peripartum use has been associated with bleeding complications. Furthermore, unfractionated heparin is associated with the development of osteoporosis, and it requires frequent injections. The low-molecular-weight heparins thus have a definite niche in the management of pregnant women, but with a caveat: dosing of these agents by weight alone in this setting is fraught with the potential for underdosing. Catastrophic outcomes have been reported in pregnant patients with older mechanical cardiac valves who were switched from warfarin to low-molecular-weight heparin therapy. Plus, if the patient is to receive neuraxial regional anesthesia, low-molecular-weight heparins should be discontinued at least 12 hours before catheter placement if prophylactic doses have been given, or 24 hours if therapeutic doses have been given.
Low-molecular-weight heparins have greatly enhanced our ability to treat thromboembolic disease. But, as the authors of these two papers discuss, many management nuances still must be noted.
In this issue of the Journal we review two special situations in which low-molecular-weight heparins have special advantages. Babu and Carman discuss patients with cancer and thromboembolic disease. These patients are particularly difficult to manage since they tend to have recurrent thrombosis, sometimes even while on anticoagulant therapy, and they tend to have more bleeding complications from warfarin therapy. Inanition, drug interactions, and organ dysfunction make warfarin titration problematic, and the possibility of vascular metastases is always a concern. Low-molecular-weight heparins —which, unlike warfarin, work primarily by antagonizing factor Xa activity—have proven to be as effective as warfarin in reversing the many hypercoagulable effects of malignancy, although it wasn’t obvious at first that they would be.
Gibson and Powrie review the issues we face when pregnant patients need anticoagulation. While drug interactions and organ dysfunction are rarely problems in this setting, warfarin is teratogenic and is therefore strongly contraindicated early in pregnancy, and its peripartum use has been associated with bleeding complications. Furthermore, unfractionated heparin is associated with the development of osteoporosis, and it requires frequent injections. The low-molecular-weight heparins thus have a definite niche in the management of pregnant women, but with a caveat: dosing of these agents by weight alone in this setting is fraught with the potential for underdosing. Catastrophic outcomes have been reported in pregnant patients with older mechanical cardiac valves who were switched from warfarin to low-molecular-weight heparin therapy. Plus, if the patient is to receive neuraxial regional anesthesia, low-molecular-weight heparins should be discontinued at least 12 hours before catheter placement if prophylactic doses have been given, or 24 hours if therapeutic doses have been given.
Low-molecular-weight heparins have greatly enhanced our ability to treat thromboembolic disease. But, as the authors of these two papers discuss, many management nuances still must be noted.
Surprises and reaffirmations in 2008 clinical trials
The ACCORD trial (Action to Control Cardiovascular Risk in Diabetes) investigated very aggressive glucose control in type 2 diabetes. To our surprise, it did not extend the findings of earlier landmark trials that had showed marked microvascular benefits with modestly aggressive glucose control. Instead, as discussed by Dr. Byron Hoogwerf in our October 2008 issue, the ACCORD trial found that more patients died who underwent the extremely aggressive glucose-control strategy.
Like the ACCORD trial, the JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) examined how far you can pharmacologically lower a causative factor—in this case, low-density lipoprotein cholesterol (LDL-C)—without causing adverse effects. In this month’s issue, Drs. Shishehbor and Hazen discuss the results of the JUPITER trial, in which “healthy” patients with LCL-C levels lower than 130 mg/dL and elevated high-sensitivity C-reactive protein (hs-CRP) levels were aggressively treated with rosuvastatin (Crestor). The median LDL-C level fell from 108 to 55 mg/dL, and the trial was stopped early when the number of predefined cardiovascular events was found to be 44% lower in the treated group than in the placebo group.
The efficacy result is not that surprising—there is probably no specific LDL-C number that should trigger a decision to treat. Furthermore, in JUPITER, unlike in ACCORD, there was no downside to the aggressive treatment that outweighed the benefits. The acute-phase reactant hs-CRP (or the company it kept, ie, metabolic syndrome) was a useful marker in identifying patients at risk of cardiovascular events, thus permitting the earlier-than-expected outcome differences. But the study does not resolve the question of whether hs-CRP is pathogenic in its own right.
So, as we begin 2009, we know that too much glucose is bad, but trying too hard to lower it in type 2 diabetes may be worse. We start the new year with a reaffirmation of the LDL-C hypothesis: LDL-C promotes cardiovascular morbidity, and starts to do so even when the person is apparently healthy. I am still not convinced that hs-CRP is an active player in the pathogenesis of atherogenesis, but that is a study for another year.
On behalf of the editorial staff of the Journal, I wish you all a happy, healthy, and most of all more peaceful 2009.
The ACCORD trial (Action to Control Cardiovascular Risk in Diabetes) investigated very aggressive glucose control in type 2 diabetes. To our surprise, it did not extend the findings of earlier landmark trials that had showed marked microvascular benefits with modestly aggressive glucose control. Instead, as discussed by Dr. Byron Hoogwerf in our October 2008 issue, the ACCORD trial found that more patients died who underwent the extremely aggressive glucose-control strategy.
Like the ACCORD trial, the JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) examined how far you can pharmacologically lower a causative factor—in this case, low-density lipoprotein cholesterol (LDL-C)—without causing adverse effects. In this month’s issue, Drs. Shishehbor and Hazen discuss the results of the JUPITER trial, in which “healthy” patients with LCL-C levels lower than 130 mg/dL and elevated high-sensitivity C-reactive protein (hs-CRP) levels were aggressively treated with rosuvastatin (Crestor). The median LDL-C level fell from 108 to 55 mg/dL, and the trial was stopped early when the number of predefined cardiovascular events was found to be 44% lower in the treated group than in the placebo group.
The efficacy result is not that surprising—there is probably no specific LDL-C number that should trigger a decision to treat. Furthermore, in JUPITER, unlike in ACCORD, there was no downside to the aggressive treatment that outweighed the benefits. The acute-phase reactant hs-CRP (or the company it kept, ie, metabolic syndrome) was a useful marker in identifying patients at risk of cardiovascular events, thus permitting the earlier-than-expected outcome differences. But the study does not resolve the question of whether hs-CRP is pathogenic in its own right.
So, as we begin 2009, we know that too much glucose is bad, but trying too hard to lower it in type 2 diabetes may be worse. We start the new year with a reaffirmation of the LDL-C hypothesis: LDL-C promotes cardiovascular morbidity, and starts to do so even when the person is apparently healthy. I am still not convinced that hs-CRP is an active player in the pathogenesis of atherogenesis, but that is a study for another year.
On behalf of the editorial staff of the Journal, I wish you all a happy, healthy, and most of all more peaceful 2009.
The ACCORD trial (Action to Control Cardiovascular Risk in Diabetes) investigated very aggressive glucose control in type 2 diabetes. To our surprise, it did not extend the findings of earlier landmark trials that had showed marked microvascular benefits with modestly aggressive glucose control. Instead, as discussed by Dr. Byron Hoogwerf in our October 2008 issue, the ACCORD trial found that more patients died who underwent the extremely aggressive glucose-control strategy.
Like the ACCORD trial, the JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin) examined how far you can pharmacologically lower a causative factor—in this case, low-density lipoprotein cholesterol (LDL-C)—without causing adverse effects. In this month’s issue, Drs. Shishehbor and Hazen discuss the results of the JUPITER trial, in which “healthy” patients with LCL-C levels lower than 130 mg/dL and elevated high-sensitivity C-reactive protein (hs-CRP) levels were aggressively treated with rosuvastatin (Crestor). The median LDL-C level fell from 108 to 55 mg/dL, and the trial was stopped early when the number of predefined cardiovascular events was found to be 44% lower in the treated group than in the placebo group.
The efficacy result is not that surprising—there is probably no specific LDL-C number that should trigger a decision to treat. Furthermore, in JUPITER, unlike in ACCORD, there was no downside to the aggressive treatment that outweighed the benefits. The acute-phase reactant hs-CRP (or the company it kept, ie, metabolic syndrome) was a useful marker in identifying patients at risk of cardiovascular events, thus permitting the earlier-than-expected outcome differences. But the study does not resolve the question of whether hs-CRP is pathogenic in its own right.
So, as we begin 2009, we know that too much glucose is bad, but trying too hard to lower it in type 2 diabetes may be worse. We start the new year with a reaffirmation of the LDL-C hypothesis: LDL-C promotes cardiovascular morbidity, and starts to do so even when the person is apparently healthy. I am still not convinced that hs-CRP is an active player in the pathogenesis of atherogenesis, but that is a study for another year.
On behalf of the editorial staff of the Journal, I wish you all a happy, healthy, and most of all more peaceful 2009.
Influenza: It’s right to bare arms
We were relatively spared in the last flu season, considering what might have been. The 2007–2008 vaccine, specifically formulated to stave off the strains predicted to predominate in North America last year, had lower-than-usual efficacy. Resistance to the oral antiviral oseltamivir (Tamiflu) became widespread, and the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) increased. MRSA is relevant to any discussion of influenza, since staphylococcal pneumonia was a lethal complication of influenza even before virulent MRSA emerged in the community. Nonetheless, the vaccination rate increased last year, fears of widespread bird-to-human spread of avian flu were not realized, and influenza-related death rates did not increase. And there are additional reasons for optimism in the upcoming years.
Vaccine for the coming flu season is readily available, and the targeted strains seem to be appropriate. Strategies to assure greater compliance with vaccination guidelines in the workplace, particularly in health care settings, continue to be implemented. If we should need it, there is a vaccine that is active against the H5N1 avian flu. Several studies have documented the safety and immunologic efficacy of the vaccine in therapeutically immunocompromised patients. Akin to using adjunctive corticosteroids when treating severe Pneumocystis jiroveci (formerly P carinii) pneumonia or bacterial meningitis, provocative preclinical studies found that down-modulating the inflammatory response to experimental influenza infection with cyclooxygenase-2-selective nonsteroidal anti-inflammatory drugs lessened lung injury and improved survival (Zheng BJ et al, Proc Natl Acad Sci U S A 2008; 105:8091–8096).
But the immediate realities are that the roof of my convertible will be up for the next 6 months, and that some of my patients will decline the flu shot, saying “I never get the flu,” or the “flu shot made me sick,” or “the flu shot gave my mother the flu.” As busy as we are in the office and hospital, it is worth spending extra time continuing to aggressively promote appropriate immunization to our patients, our staff, and ourselves.
We were relatively spared in the last flu season, considering what might have been. The 2007–2008 vaccine, specifically formulated to stave off the strains predicted to predominate in North America last year, had lower-than-usual efficacy. Resistance to the oral antiviral oseltamivir (Tamiflu) became widespread, and the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) increased. MRSA is relevant to any discussion of influenza, since staphylococcal pneumonia was a lethal complication of influenza even before virulent MRSA emerged in the community. Nonetheless, the vaccination rate increased last year, fears of widespread bird-to-human spread of avian flu were not realized, and influenza-related death rates did not increase. And there are additional reasons for optimism in the upcoming years.
Vaccine for the coming flu season is readily available, and the targeted strains seem to be appropriate. Strategies to assure greater compliance with vaccination guidelines in the workplace, particularly in health care settings, continue to be implemented. If we should need it, there is a vaccine that is active against the H5N1 avian flu. Several studies have documented the safety and immunologic efficacy of the vaccine in therapeutically immunocompromised patients. Akin to using adjunctive corticosteroids when treating severe Pneumocystis jiroveci (formerly P carinii) pneumonia or bacterial meningitis, provocative preclinical studies found that down-modulating the inflammatory response to experimental influenza infection with cyclooxygenase-2-selective nonsteroidal anti-inflammatory drugs lessened lung injury and improved survival (Zheng BJ et al, Proc Natl Acad Sci U S A 2008; 105:8091–8096).
But the immediate realities are that the roof of my convertible will be up for the next 6 months, and that some of my patients will decline the flu shot, saying “I never get the flu,” or the “flu shot made me sick,” or “the flu shot gave my mother the flu.” As busy as we are in the office and hospital, it is worth spending extra time continuing to aggressively promote appropriate immunization to our patients, our staff, and ourselves.
We were relatively spared in the last flu season, considering what might have been. The 2007–2008 vaccine, specifically formulated to stave off the strains predicted to predominate in North America last year, had lower-than-usual efficacy. Resistance to the oral antiviral oseltamivir (Tamiflu) became widespread, and the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) increased. MRSA is relevant to any discussion of influenza, since staphylococcal pneumonia was a lethal complication of influenza even before virulent MRSA emerged in the community. Nonetheless, the vaccination rate increased last year, fears of widespread bird-to-human spread of avian flu were not realized, and influenza-related death rates did not increase. And there are additional reasons for optimism in the upcoming years.
Vaccine for the coming flu season is readily available, and the targeted strains seem to be appropriate. Strategies to assure greater compliance with vaccination guidelines in the workplace, particularly in health care settings, continue to be implemented. If we should need it, there is a vaccine that is active against the H5N1 avian flu. Several studies have documented the safety and immunologic efficacy of the vaccine in therapeutically immunocompromised patients. Akin to using adjunctive corticosteroids when treating severe Pneumocystis jiroveci (formerly P carinii) pneumonia or bacterial meningitis, provocative preclinical studies found that down-modulating the inflammatory response to experimental influenza infection with cyclooxygenase-2-selective nonsteroidal anti-inflammatory drugs lessened lung injury and improved survival (Zheng BJ et al, Proc Natl Acad Sci U S A 2008; 105:8091–8096).
But the immediate realities are that the roof of my convertible will be up for the next 6 months, and that some of my patients will decline the flu shot, saying “I never get the flu,” or the “flu shot made me sick,” or “the flu shot gave my mother the flu.” As busy as we are in the office and hospital, it is worth spending extra time continuing to aggressively promote appropriate immunization to our patients, our staff, and ourselves.
The hospital guy redux
You responded to the parts of Dr. Lansdale’s commentary that struck a personal chord. Almost all responders shared his frustration. Many wrote that the American payer system fails to appropriately reward internists and primary care providers and called for restructuring the Medicare and third-party payer systems. Some of you took umbrage at his contention that hospitals are not safe, and that health care delivery systems do not always place quality care above economic imperatives as new programs and “centers of excellence” are implemented. And some of you reacted to the issues of physician satisfaction and difficulties in providing quality care in hospitals regulated by multiple agencies that generate unfunded mandates, while the hospitals already require high numbers of patients in order to survive financially.
I recently did a stint as rheumatology consultant at my hospital, and Dr. Lansdale’s commentary was fresh in my mind. I noticed with satisfaction that the physicians and nurses were using foam antiseptic on their hands. I noted the new checks on verbal orders and a successful emphasis on preventing deep vein thrombosis and bedsores. But I also noted more patient hand-offs between house staff and faculty, and difficulty in finding doctors who actually knew the patient (or doctors that patients recognized as being responsible for their care).
The electronic medical record is legible and available from all over the hospital, and I could tell who signed the notes. But many notes were actually cut-and-pasted from earlier notes, and thus I couldn’t always be sure who actually had said what and when. Technology is not an immediate panacea for the problem of limited physician time!
The house staff “lab” in the hospital with its microscope was closed due to regulatory concerns; thus, there was no easy way to look at a freshly spun urine sample for evidence of glomerulonephritis. This turned out to be a detriment to effective patient care: urine samples sent to the regular laboratory (with the usual transportation delay) rarely if ever reveal cellular casts. But we found creative, if inefficient, ways to deal with this and other problems.
At the end of the day, I realized that I still enjoy my time in the hospital. Patients’ problems can be presented to house staff and students at the bedside and their diagnoses and therapies discussed in real time. Junior physicians can observe how senior physicians talk to patients and families, including the many ways we have learned to say “I don’t know,” and learn to appreciate the value of a well-directed physical examination. There is still a synergy and intellectual satisfaction in being one of a group of senior consultants discussing the care of a shared patient who has complex medical problems.
With rational and caring involvement, individual physicians can alter the trajectory of patient management and remain the primary patient advocates within a health care system that can’t always easily deliver the quality that everyone desires. Caring, patient-focused physicians must remain in charge of health care delivery, lest we pay attention only to the financial and regulatory problems.
Tom, I am older and even more cynical than I was when we roamed the hospital together every third night and never went home on our post-call day until the last laboratory result had been checked and the last transfusion had been given. We inefficiently examined every patient’s urine ourselves (even from those being admitted for cardiac catheterization), and we had to convince patients of the (apparent) need for the urgent 3 AM blood draw to evaluate their 100.5° fever before we prepped the area and drew the blood. We drew blood for sedimentation rates and checked rapid plasma reagins at every admission and checked for urinary light chains in everyone with an elevated creatinine level and anemia, “just to be sure.” We blindly placed Swan-Ganz catheters to monitor many hypotensive patients in the intensive care units, and we aspirated pleural effusions on the basis of our percussive examination. We talked to patients and accepted enormous individual responsibility for their care, but we were also frequently numbed by the overwhelming intensity of the training and the practice.
I am all too aware of the many forces that are eroding physician-patient relationships and that can corrupt patient care in the name of efficiency, financial necessity, marketing advantage, or regulatory compliance. Many of these forces I hope to help change. But I remain a hospital guy because I can still make a difference. I still feel honored that patients entrust their care to me as we attempt to navigate our evolving and, yes, sometimes treacherous medical system. Evading the crocodiles and fighting insurance companies are now in my job description.
In this issue we run two letters in response to Dr. Lansdale’s commentary. In December we will publish more letters, though due to space limitations some will be abridged. We plan to run full text of many of the letters online at www.ccjm.org in December.
You responded to the parts of Dr. Lansdale’s commentary that struck a personal chord. Almost all responders shared his frustration. Many wrote that the American payer system fails to appropriately reward internists and primary care providers and called for restructuring the Medicare and third-party payer systems. Some of you took umbrage at his contention that hospitals are not safe, and that health care delivery systems do not always place quality care above economic imperatives as new programs and “centers of excellence” are implemented. And some of you reacted to the issues of physician satisfaction and difficulties in providing quality care in hospitals regulated by multiple agencies that generate unfunded mandates, while the hospitals already require high numbers of patients in order to survive financially.
I recently did a stint as rheumatology consultant at my hospital, and Dr. Lansdale’s commentary was fresh in my mind. I noticed with satisfaction that the physicians and nurses were using foam antiseptic on their hands. I noted the new checks on verbal orders and a successful emphasis on preventing deep vein thrombosis and bedsores. But I also noted more patient hand-offs between house staff and faculty, and difficulty in finding doctors who actually knew the patient (or doctors that patients recognized as being responsible for their care).
The electronic medical record is legible and available from all over the hospital, and I could tell who signed the notes. But many notes were actually cut-and-pasted from earlier notes, and thus I couldn’t always be sure who actually had said what and when. Technology is not an immediate panacea for the problem of limited physician time!
The house staff “lab” in the hospital with its microscope was closed due to regulatory concerns; thus, there was no easy way to look at a freshly spun urine sample for evidence of glomerulonephritis. This turned out to be a detriment to effective patient care: urine samples sent to the regular laboratory (with the usual transportation delay) rarely if ever reveal cellular casts. But we found creative, if inefficient, ways to deal with this and other problems.
At the end of the day, I realized that I still enjoy my time in the hospital. Patients’ problems can be presented to house staff and students at the bedside and their diagnoses and therapies discussed in real time. Junior physicians can observe how senior physicians talk to patients and families, including the many ways we have learned to say “I don’t know,” and learn to appreciate the value of a well-directed physical examination. There is still a synergy and intellectual satisfaction in being one of a group of senior consultants discussing the care of a shared patient who has complex medical problems.
With rational and caring involvement, individual physicians can alter the trajectory of patient management and remain the primary patient advocates within a health care system that can’t always easily deliver the quality that everyone desires. Caring, patient-focused physicians must remain in charge of health care delivery, lest we pay attention only to the financial and regulatory problems.
Tom, I am older and even more cynical than I was when we roamed the hospital together every third night and never went home on our post-call day until the last laboratory result had been checked and the last transfusion had been given. We inefficiently examined every patient’s urine ourselves (even from those being admitted for cardiac catheterization), and we had to convince patients of the (apparent) need for the urgent 3 AM blood draw to evaluate their 100.5° fever before we prepped the area and drew the blood. We drew blood for sedimentation rates and checked rapid plasma reagins at every admission and checked for urinary light chains in everyone with an elevated creatinine level and anemia, “just to be sure.” We blindly placed Swan-Ganz catheters to monitor many hypotensive patients in the intensive care units, and we aspirated pleural effusions on the basis of our percussive examination. We talked to patients and accepted enormous individual responsibility for their care, but we were also frequently numbed by the overwhelming intensity of the training and the practice.
I am all too aware of the many forces that are eroding physician-patient relationships and that can corrupt patient care in the name of efficiency, financial necessity, marketing advantage, or regulatory compliance. Many of these forces I hope to help change. But I remain a hospital guy because I can still make a difference. I still feel honored that patients entrust their care to me as we attempt to navigate our evolving and, yes, sometimes treacherous medical system. Evading the crocodiles and fighting insurance companies are now in my job description.
In this issue we run two letters in response to Dr. Lansdale’s commentary. In December we will publish more letters, though due to space limitations some will be abridged. We plan to run full text of many of the letters online at www.ccjm.org in December.
You responded to the parts of Dr. Lansdale’s commentary that struck a personal chord. Almost all responders shared his frustration. Many wrote that the American payer system fails to appropriately reward internists and primary care providers and called for restructuring the Medicare and third-party payer systems. Some of you took umbrage at his contention that hospitals are not safe, and that health care delivery systems do not always place quality care above economic imperatives as new programs and “centers of excellence” are implemented. And some of you reacted to the issues of physician satisfaction and difficulties in providing quality care in hospitals regulated by multiple agencies that generate unfunded mandates, while the hospitals already require high numbers of patients in order to survive financially.
I recently did a stint as rheumatology consultant at my hospital, and Dr. Lansdale’s commentary was fresh in my mind. I noticed with satisfaction that the physicians and nurses were using foam antiseptic on their hands. I noted the new checks on verbal orders and a successful emphasis on preventing deep vein thrombosis and bedsores. But I also noted more patient hand-offs between house staff and faculty, and difficulty in finding doctors who actually knew the patient (or doctors that patients recognized as being responsible for their care).
The electronic medical record is legible and available from all over the hospital, and I could tell who signed the notes. But many notes were actually cut-and-pasted from earlier notes, and thus I couldn’t always be sure who actually had said what and when. Technology is not an immediate panacea for the problem of limited physician time!
The house staff “lab” in the hospital with its microscope was closed due to regulatory concerns; thus, there was no easy way to look at a freshly spun urine sample for evidence of glomerulonephritis. This turned out to be a detriment to effective patient care: urine samples sent to the regular laboratory (with the usual transportation delay) rarely if ever reveal cellular casts. But we found creative, if inefficient, ways to deal with this and other problems.
At the end of the day, I realized that I still enjoy my time in the hospital. Patients’ problems can be presented to house staff and students at the bedside and their diagnoses and therapies discussed in real time. Junior physicians can observe how senior physicians talk to patients and families, including the many ways we have learned to say “I don’t know,” and learn to appreciate the value of a well-directed physical examination. There is still a synergy and intellectual satisfaction in being one of a group of senior consultants discussing the care of a shared patient who has complex medical problems.
With rational and caring involvement, individual physicians can alter the trajectory of patient management and remain the primary patient advocates within a health care system that can’t always easily deliver the quality that everyone desires. Caring, patient-focused physicians must remain in charge of health care delivery, lest we pay attention only to the financial and regulatory problems.
Tom, I am older and even more cynical than I was when we roamed the hospital together every third night and never went home on our post-call day until the last laboratory result had been checked and the last transfusion had been given. We inefficiently examined every patient’s urine ourselves (even from those being admitted for cardiac catheterization), and we had to convince patients of the (apparent) need for the urgent 3 AM blood draw to evaluate their 100.5° fever before we prepped the area and drew the blood. We drew blood for sedimentation rates and checked rapid plasma reagins at every admission and checked for urinary light chains in everyone with an elevated creatinine level and anemia, “just to be sure.” We blindly placed Swan-Ganz catheters to monitor many hypotensive patients in the intensive care units, and we aspirated pleural effusions on the basis of our percussive examination. We talked to patients and accepted enormous individual responsibility for their care, but we were also frequently numbed by the overwhelming intensity of the training and the practice.
I am all too aware of the many forces that are eroding physician-patient relationships and that can corrupt patient care in the name of efficiency, financial necessity, marketing advantage, or regulatory compliance. Many of these forces I hope to help change. But I remain a hospital guy because I can still make a difference. I still feel honored that patients entrust their care to me as we attempt to navigate our evolving and, yes, sometimes treacherous medical system. Evading the crocodiles and fighting insurance companies are now in my job description.
In this issue we run two letters in response to Dr. Lansdale’s commentary. In December we will publish more letters, though due to space limitations some will be abridged. We plan to run full text of many of the letters online at www.ccjm.org in December.
When a quick sound bite won’t do
The sound bites about these trials in the news have confused physicians and patients alike. But, as we have all experienced during this election year, to understand complex problems requires an in-depth analysis instead of a sound bite.
I was troubled by the results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial,2 in which more patients who were treated with an intense hemoglobin A1c-lowering strategy died (mostly of macrovascular events) than those treated with a standard strategy. Older data showing a beneficial effect of glucose-lowering on the microvascular complications of diabetes are solid. I did not understand the mechanistic basis of the ACCORD results, unless the very aggressive therapy caused many hypoglycemic events with catecholamine surges, resulting in stroke or myocardial infarction, or whether a problem with a specific drug arose more often in the intensive-treatment group. There has been similar dialogue surrounding intensity of glucose control in critically ill inpatients3; here, the data suggest that hypoglycemic episodes may limit other benefits of aggressive treatment in the intensive care unit, such as reduced infection rates.
Not to be ignored is that the patients in all arms of the ACCORD trial fared far better than historical diabetic controls. The meticulous attention to management of blood pressure and LDL-C that all patients in the ACCORD trial received paid off. (If only we could do as well in our practices!) But what do we do about the sugar?
This large, well-done, ongoing trial deserves a detailed analysis for those of us who need to translate the conclusions regarding glucose control to our patients. This month in the Journal, I have invited Byron Hoogwerf, a clinical diabetologist, former internal medicine program director, well-published clinical trialist, and ACCORD investigator, to provide this analysis.4 His discussion is more detailed than what we often print purposefully, and it is well worth reading. Some issues simply can’t be understood as a sound bite.
- Kastelein JJ, Akdim F, Stroes ES, et alENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med. 2008; 358:1431–1443.
- Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008; 358:2545–2559.
- Soylemez Wiener R, Wiener DC, Larson RJ. Benefits and risks of tight glucose control in critically ill adults: a meta-analysis. JAMA. 2008; 300:933–944.
- Hoogwerf BF. A clinician and clinical trialist’s perspective: does intensive therapy of type 2 diabetes help or harm? Seeking accord on ACCORD. Cleve Clin J Med. 2008; 75:729–737.
The sound bites about these trials in the news have confused physicians and patients alike. But, as we have all experienced during this election year, to understand complex problems requires an in-depth analysis instead of a sound bite.
I was troubled by the results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial,2 in which more patients who were treated with an intense hemoglobin A1c-lowering strategy died (mostly of macrovascular events) than those treated with a standard strategy. Older data showing a beneficial effect of glucose-lowering on the microvascular complications of diabetes are solid. I did not understand the mechanistic basis of the ACCORD results, unless the very aggressive therapy caused many hypoglycemic events with catecholamine surges, resulting in stroke or myocardial infarction, or whether a problem with a specific drug arose more often in the intensive-treatment group. There has been similar dialogue surrounding intensity of glucose control in critically ill inpatients3; here, the data suggest that hypoglycemic episodes may limit other benefits of aggressive treatment in the intensive care unit, such as reduced infection rates.
Not to be ignored is that the patients in all arms of the ACCORD trial fared far better than historical diabetic controls. The meticulous attention to management of blood pressure and LDL-C that all patients in the ACCORD trial received paid off. (If only we could do as well in our practices!) But what do we do about the sugar?
This large, well-done, ongoing trial deserves a detailed analysis for those of us who need to translate the conclusions regarding glucose control to our patients. This month in the Journal, I have invited Byron Hoogwerf, a clinical diabetologist, former internal medicine program director, well-published clinical trialist, and ACCORD investigator, to provide this analysis.4 His discussion is more detailed than what we often print purposefully, and it is well worth reading. Some issues simply can’t be understood as a sound bite.
The sound bites about these trials in the news have confused physicians and patients alike. But, as we have all experienced during this election year, to understand complex problems requires an in-depth analysis instead of a sound bite.
I was troubled by the results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial,2 in which more patients who were treated with an intense hemoglobin A1c-lowering strategy died (mostly of macrovascular events) than those treated with a standard strategy. Older data showing a beneficial effect of glucose-lowering on the microvascular complications of diabetes are solid. I did not understand the mechanistic basis of the ACCORD results, unless the very aggressive therapy caused many hypoglycemic events with catecholamine surges, resulting in stroke or myocardial infarction, or whether a problem with a specific drug arose more often in the intensive-treatment group. There has been similar dialogue surrounding intensity of glucose control in critically ill inpatients3; here, the data suggest that hypoglycemic episodes may limit other benefits of aggressive treatment in the intensive care unit, such as reduced infection rates.
Not to be ignored is that the patients in all arms of the ACCORD trial fared far better than historical diabetic controls. The meticulous attention to management of blood pressure and LDL-C that all patients in the ACCORD trial received paid off. (If only we could do as well in our practices!) But what do we do about the sugar?
This large, well-done, ongoing trial deserves a detailed analysis for those of us who need to translate the conclusions regarding glucose control to our patients. This month in the Journal, I have invited Byron Hoogwerf, a clinical diabetologist, former internal medicine program director, well-published clinical trialist, and ACCORD investigator, to provide this analysis.4 His discussion is more detailed than what we often print purposefully, and it is well worth reading. Some issues simply can’t be understood as a sound bite.
- Kastelein JJ, Akdim F, Stroes ES, et alENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med. 2008; 358:1431–1443.
- Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008; 358:2545–2559.
- Soylemez Wiener R, Wiener DC, Larson RJ. Benefits and risks of tight glucose control in critically ill adults: a meta-analysis. JAMA. 2008; 300:933–944.
- Hoogwerf BF. A clinician and clinical trialist’s perspective: does intensive therapy of type 2 diabetes help or harm? Seeking accord on ACCORD. Cleve Clin J Med. 2008; 75:729–737.
- Kastelein JJ, Akdim F, Stroes ES, et alENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia. N Engl J Med. 2008; 358:1431–1443.
- Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008; 358:2545–2559.
- Soylemez Wiener R, Wiener DC, Larson RJ. Benefits and risks of tight glucose control in critically ill adults: a meta-analysis. JAMA. 2008; 300:933–944.
- Hoogwerf BF. A clinician and clinical trialist’s perspective: does intensive therapy of type 2 diabetes help or harm? Seeking accord on ACCORD. Cleve Clin J Med. 2008; 75:729–737.
And then there were none? An internist’s reflections
I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.
At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.
In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.
I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.
Send your comments to [email protected]. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.
I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.
At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.
In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.
I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.
Send your comments to [email protected]. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.
I observe with sadness the decreasing number of our brightest medical students entering into internal medicine careers and other “cognitive” subspecialties. Much effort has been spent on many fronts to understand and reverse this trend, with limited success.
At the other end of their careers, physicians seem to be looking for ways to retire earlier or to withdraw from their usual and customary practice of internal medicine. Hearing these senior physicians’ reasons for withdrawing from clinical practice evokes an even stronger response in me, especially when the physician is a really good one, a role model for the next generation of our internists currently in training.
In an essay in this issue, Dr. Thomas Lansdale, internist and former chairman of medicine at a community teaching hospital, eloquently expresses a common theme: medicine just isn’t that much fun anymore. We don’t generally run this type of article in the Journal. But Dr. Lansdale’s words reflect an undercurrent that is changing the landscape of American medicine. We would like to hear responses from our readers, but not to simply agree or disagree with Dr. Lansdale. Rather, we’d like to hear some solutions, which we hope to print in a future issue.
I have known Dr. Lansdale for over 20 years; we trained together as residents at the University of Pennsylvania. He was a year or so behind me, and over the years I have had the opportunity to follow his clinical career from afar and occasionally to discuss patient care and education issues. He was (and is) a thoughtful and extremely insightful internist, devoted and capable of delivering the highest quality of care to his patients. He has always approached medicine, his trainees, and his patients in a serious and respectful manner. His words should prompt some serious self-reflection.
Send your comments to [email protected]. Please note that sending your comments constitutes permission to publish them, and also that we cannot respond to or publish all submissions.