In the September 28, 2006 edition of DB's Medical Rants we find a great quote from Scapel entitled "Are all physicians equal?"
In one of the subsequent letters to Scapel we are correctly told that in the health care "market" prices are determined by a fairly small number of payers, e.g. CMS and the major insurers who follow CMS lead. In regard to physician's fees, there is -for the most part- price controls.Since insurers tend to duplicate CMS's fee structures we have in effect government price controls on physician fees.
(I realize there are a small minority of physicians who operate outside of this control system, for example some dermatologists who do mainly cosmetic work and the concierge practices)
I wrote about this issue before when I suggested an important addition to the medical school curriculum, namely a primer on basic real world economics.What happens when there are price controls is well recognized and repeatedly has been explained in great clarity by economists such as Thomas Sowell.Here are some of his comments on that subject.
Four things tend to happen when there are price controls:
1.Demand increases,there is increased use of the service or product (A recent example-see how long it takes to get in for a colonoscopy since Medicare began covering screening exams)
2.Supply decreases and shortages develop(with price controls in place, suppliers do not rush into that market and we are seeing that in the area of primary care, where fees are set the lowest, fewer medical graduates are opting for primary care specialties)
3.Quality decreases.(providers have little reason to try and differentiate themselves on the basis of quality because of 1 and 2 they have no need for new customers.They may try and make up for lower unit prices by increasing their volume of business, spending less time with each customer, etc.)
4.Black markets tend to develop.This apparently has not happened yet here but has in rigidly socialized countries.
To quote Sowell (from Applied Economics,Thinking Beyond Stage One,2004,Basic Books, p.93)
"All of these things have been found when the prices of medical care have been controlled-and all are particularly harmful in matters involving, pain ,disability and death".
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Friday, September 29, 2006
Tuesday, September 19, 2006
The DREAM study, Are we preventing or just delaying diabetes?
The results of the DREAM study have published in the NEJM (ramipril arm) and the Lancet ( rosiglitizone arm) . This trial will get a lot of press and in the eyes of cynical old docs like me a lot of spin. Fortunately, the eagle eyed and clear thinking world of medical bloging will have offer anti-spin or at the least an opinion a bit different from the pharm company's press releases ( see here and here ) and the repetition of some of it by main stream media .
DREAM was large randomized clinical trial involving patients with the label pre-diabetes ( impaired fasting glusoce and/or glucose intolerance) and the aim was to see if a TZD (thiazolidenedione) and/or an ace inhibitor would prevent the progression of pre diabetes to diabetes. The rosi group received daily rosiglitizone for 3 years plus education regarding diet and exercise and 11.6 % progressed to diabetes in 3 years versus 26% of the placebo group.In the rosi group 0.5% developed heart failure versus 0.1% in the placebo group.The ramipril trial was negative in the sense of no effect on the development of diabetes.
Here is how the study's authors framed things in the final paragraph of their discussion section-paraphrased- If you treat 1000 patients for three years with rosiglitizone, 144 cases of diabetes will be prevented and 5 will develop heart failure.
The problem I have with that is the use of the word "prevented". I take prevent to mean you will not develop a condition. In this situation I believe you are simply delaying what seems to be almost always the case in type 2 diabetes-and by extension pre-diabetes- progressive worsening of the glucose control. Here prevention seems to mean to "prevent" diabetes for three years. The data is just not sufficient to make the statement that diabetes has been prevented.To be able to say that you would need a really long follow up.
It is well known that TZDs can improve blood sugar control in diabetes and it is no surprise it could do the same in patients with early diabetes -or pre-diabetes-and it is also well known that they may cause fluid retention and heart failure. so I see nothing really new here except what I think is exaggerated talk about prevention.
The comments made after the Diabetes Prevention Trial( o.k., they called it prevention)were much more appropriately circumspect. That trial compared exercise plus diet, metformin and a control group all with glucose intolerance and over a 3 year period 29% of the control group , 22% of the metformin group and 14% of the exercise/diet group developed diabetes."We simply don't know how long beyond the 3 year period diabetes can be delayed " was the comment made by one of the study's authors. This is a study whose results I frequently discussed with overweight patient with borderline blood sugars in the hope of encouraging life style changes but I did not promise diabetes would be prevented.
DREAM was large randomized clinical trial involving patients with the label pre-diabetes ( impaired fasting glusoce and/or glucose intolerance) and the aim was to see if a TZD (thiazolidenedione) and/or an ace inhibitor would prevent the progression of pre diabetes to diabetes. The rosi group received daily rosiglitizone for 3 years plus education regarding diet and exercise and 11.6 % progressed to diabetes in 3 years versus 26% of the placebo group.In the rosi group 0.5% developed heart failure versus 0.1% in the placebo group.The ramipril trial was negative in the sense of no effect on the development of diabetes.
Here is how the study's authors framed things in the final paragraph of their discussion section-paraphrased- If you treat 1000 patients for three years with rosiglitizone, 144 cases of diabetes will be prevented and 5 will develop heart failure.
The problem I have with that is the use of the word "prevented". I take prevent to mean you will not develop a condition. In this situation I believe you are simply delaying what seems to be almost always the case in type 2 diabetes-and by extension pre-diabetes- progressive worsening of the glucose control. Here prevention seems to mean to "prevent" diabetes for three years. The data is just not sufficient to make the statement that diabetes has been prevented.To be able to say that you would need a really long follow up.
It is well known that TZDs can improve blood sugar control in diabetes and it is no surprise it could do the same in patients with early diabetes -or pre-diabetes-and it is also well known that they may cause fluid retention and heart failure. so I see nothing really new here except what I think is exaggerated talk about prevention.
The comments made after the Diabetes Prevention Trial( o.k., they called it prevention)were much more appropriately circumspect. That trial compared exercise plus diet, metformin and a control group all with glucose intolerance and over a 3 year period 29% of the control group , 22% of the metformin group and 14% of the exercise/diet group developed diabetes."We simply don't know how long beyond the 3 year period diabetes can be delayed " was the comment made by one of the study's authors. This is a study whose results I frequently discussed with overweight patient with borderline blood sugars in the hope of encouraging life style changes but I did not promise diabetes would be prevented.
Monday, September 18, 2006
NIH report on use of multi-vitamins-we just don't know
The September 5, 2006 issue of the Annals of Internal Medicine reports on a NIH Conference on the use of multivitamins/mineral supplements (MVMs) and chronic disease prevention.
Their conclusion:
...the present evidence is insufficient to recommend either for or against the use of MVMs by the American public to prevent chronic disease."
A major reason for the panel's inability to make a firm recommendation is the lack of randomized clinical trials.However, the panel interestingly also states that "multivitamin trials are unlikely to lead to generalizable knowledge".
This is because a distinction between the effects of the individual components is unlikely to be made for several reasons including 1)the placebo group is likely to take vitamins anyway, 2)a very large sample size would be required making funding and execution of the trial problematic and 3)results would be likely outdated as the composition of the commonly used MVMs tend to change. Further, there is reason to believe that some subgroups may benefit from a given component while another subgroup might be harmed.
So what are we hearing? We cannot say if MVMs should be taken by everyone to prevent chronic disease or cancer because of the lack of RCTs and it is unlikely that even if we could the related RCTs they probably would not answer the question anyway. Should we withhold judgment if there is no randomized trial directly addressing the issue? Are we unnecessarily limiting ourselves by punting every question if RCTs are not available? That does appear to be the modus operandi of the public health community and yet in that context there is justification for withholding judgment until the evidence is quite strong. To make policy decisions sound evidence is required. Individual physicians have to often make decisions with the data they have not the evidence they wished they had. Of course, physicians do not have to tell everyone what to do , just the patient on the other side of the desk.
Their conclusion:
...the present evidence is insufficient to recommend either for or against the use of MVMs by the American public to prevent chronic disease."
A major reason for the panel's inability to make a firm recommendation is the lack of randomized clinical trials.However, the panel interestingly also states that "multivitamin trials are unlikely to lead to generalizable knowledge".
This is because a distinction between the effects of the individual components is unlikely to be made for several reasons including 1)the placebo group is likely to take vitamins anyway, 2)a very large sample size would be required making funding and execution of the trial problematic and 3)results would be likely outdated as the composition of the commonly used MVMs tend to change. Further, there is reason to believe that some subgroups may benefit from a given component while another subgroup might be harmed.
So what are we hearing? We cannot say if MVMs should be taken by everyone to prevent chronic disease or cancer because of the lack of RCTs and it is unlikely that even if we could the related RCTs they probably would not answer the question anyway. Should we withhold judgment if there is no randomized trial directly addressing the issue? Are we unnecessarily limiting ourselves by punting every question if RCTs are not available? That does appear to be the modus operandi of the public health community and yet in that context there is justification for withholding judgment until the evidence is quite strong. To make policy decisions sound evidence is required. Individual physicians have to often make decisions with the data they have not the evidence they wished they had. Of course, physicians do not have to tell everyone what to do , just the patient on the other side of the desk.
Saturday, September 16, 2006
From the Annals of Internal Medicine:Oscar winners live longer-no,wait, maybe they don't
The September 2006 issue of the Annals of Internal Medicine published an article (Do Oscar Winners Live Longer than less Successful Peers? A reanalysis of the evidence.Sylvestre,Huszti,and Hanley.Annals Internal Medicine,vol.145, no. 5, p. 361) that contradicted an earlier Annals'article that claimed Oscar winners live longer than their fellow actors.The abstract is available online. Why does a respected medical journal bother itself with this issue anyway?
Subscription is required for the full text of the article and also for the important letter from two of the Annals editors, Steven Goodman, an epidemiologist whose work I have found very impressive and useful and Harold Sox the editor. The original paper was published 5 years ago and found-by one analysis-a 3.9 year increase in life expectancy in Oscar winners. Here the operative words appear to be "by one analysis". The results vary significantly based on the type of analysis used and the epidemiologists-statisticians are not in agreement on how to analyse the data.
The issue here, as explained by Goodman and Sox is "when to start the clock" in a situation wherein there is a sudden change in risk due some event. Such events could include starting a treatment and in that instance there would be considerable medical interest, certaintly more than Oscar winner' longevity. Starting the clock at the wrong time can trigger something called "the immortal time bias" ( also known as "time zero" problem) something I have posted about before in the context of COPD treatment.
One study demonstrated that inhaled corticosteroids (ICS) treatment increased survival in COPD but another analysis indicated that the survival advantage was not real but an example of the immortal time bias although the original authors denied that was the case. Just as in the Oscar winner longevity controversy there was disagreement if there was or was not a bias in the ICS data due to disagreements about the clock starting issue.
The Annals editorialists state their explanatory comments are published largely because "the analytic methods at issue apply to many health care research questions ."Apparently the statistical issue of how to handle the zero time issue is not settled as Goodman and Sox invite other members of the statistical fraternity to "take up the challenge of determining the most appropriate way to measure the effect of winning an Oscar and the statistical uncertainty around the results." Of course, their concern is not really with Oscar winners's longevity but with the application of these techniques to more therapeutically relevant medical studies.
How to analyze the evidence in evidence based medicine is still to a large degree a work in progress.
Subscription is required for the full text of the article and also for the important letter from two of the Annals editors, Steven Goodman, an epidemiologist whose work I have found very impressive and useful and Harold Sox the editor. The original paper was published 5 years ago and found-by one analysis-a 3.9 year increase in life expectancy in Oscar winners. Here the operative words appear to be "by one analysis". The results vary significantly based on the type of analysis used and the epidemiologists-statisticians are not in agreement on how to analyse the data.
The issue here, as explained by Goodman and Sox is "when to start the clock" in a situation wherein there is a sudden change in risk due some event. Such events could include starting a treatment and in that instance there would be considerable medical interest, certaintly more than Oscar winner' longevity. Starting the clock at the wrong time can trigger something called "the immortal time bias" ( also known as "time zero" problem) something I have posted about before in the context of COPD treatment.
One study demonstrated that inhaled corticosteroids (ICS) treatment increased survival in COPD but another analysis indicated that the survival advantage was not real but an example of the immortal time bias although the original authors denied that was the case. Just as in the Oscar winner longevity controversy there was disagreement if there was or was not a bias in the ICS data due to disagreements about the clock starting issue.
The Annals editorialists state their explanatory comments are published largely because "the analytic methods at issue apply to many health care research questions ."Apparently the statistical issue of how to handle the zero time issue is not settled as Goodman and Sox invite other members of the statistical fraternity to "take up the challenge of determining the most appropriate way to measure the effect of winning an Oscar and the statistical uncertainty around the results." Of course, their concern is not really with Oscar winners's longevity but with the application of these techniques to more therapeutically relevant medical studies.
How to analyze the evidence in evidence based medicine is still to a large degree a work in progress.
Thursday, September 14, 2006
No pens or mugs allowed from Big Pharma at Stanford
It has not gone unnoticed (whatever does) by the medical blogger world the irony or hypocrisy of Stanford's Medical School prohibiting the receipt of drug companies' pens and mugs (which are recognized to contain tiny and incredibly powerful mind-control devices) but continuing to allow faculty to be involved in numerous financial arrangements with drug and other medically related business entities. Free lunches and drug samples are also prohibited in their new policy but apparently faculty members can sit on boards of directors of drug and other medical businesses.
Multiple examples of the multiple conflicts of interests at Stanford was highlighted by Health Care Renewal 's Sept 14,2008 posting. No mention is made in the Stanford game plan to do away with the lucrative arrangements between faculty members Big Pharma and other medically related commercial enterprises. Standford's Dean Pizzo's video explaining the new policy can be found on their web site.
Multiple examples of the multiple conflicts of interests at Stanford was highlighted by Health Care Renewal 's Sept 14,2008 posting. No mention is made in the Stanford game plan to do away with the lucrative arrangements between faculty members Big Pharma and other medically related commercial enterprises. Standford's Dean Pizzo's video explaining the new policy can be found on their web site.
Sunday, September 10, 2006
FDA offers recipe for proper mixing of aspirin and ibuprofen
Aspirin is widely used to decrease the risk of heart attacks. It is an essential part of secondary prophylaxis and typically is recommended to persons who have not had a cardiac event but who have an increased risk of developing coronary artery disease. The American Heart Association recommends prophylactic aspirin for those who have a ten year heart attack risk of 10% or greater and the usually-much-more conservative U.S Preventive Services Task Force recommends aspirin for those who have a five year risk of 3 % or higher.
Ibuprofen is widely used for a variety of aches and pains and its use is prevalent in the same age group who usually qualify for aspirin prophylaxis. However, there is evidence that ibuprofen may interfere with the beneficial effect that aspirin has on blood platelets. It is thought that ibuprofen and perhaps other NSAIDs interfere with aspirin gaining access to the molecular site on which it acts to inhibit platelet aggregation which is the putative mechanism involving in aspirin's success in decreasing coronary events.( Ibuprofen and aspirin are thought to chemically link up to sites in close proximity so that ibuprofen's presence may "crowd out" aspirin)
The FDA has recently published a paper explaining what is known about the asa-ibuprofen interaction issue and what practically can be done to enjoy whatever cardioprotective effect aspirin has and still be able to take ibuprofen for various pains. It is well worth reading and perhaps having copies handy to give patients.
Basically the advice is this:
Wait at least 1/2 hour after taking immediate release aspirin before taking ibuprofen. Wait 8 hours after taking 400 mg. of ibuprofen before taking aspirin.
The above advice does not apply to the popular enteric coated aspirin (ECASA) whose absorption is slower and 1/2 hour may not be long enough for aspirin to complete its inhibition of cyclooxygenase.The FDA did not believe there was adequate evidence to make specific recommendations regarding other NSAIDs-other than a general cautionary note. However, one recent article provided some data indicating a similar problem with the combination of aspirin and naproxen.
Ibuprofen is widely used for a variety of aches and pains and its use is prevalent in the same age group who usually qualify for aspirin prophylaxis. However, there is evidence that ibuprofen may interfere with the beneficial effect that aspirin has on blood platelets. It is thought that ibuprofen and perhaps other NSAIDs interfere with aspirin gaining access to the molecular site on which it acts to inhibit platelet aggregation which is the putative mechanism involving in aspirin's success in decreasing coronary events.( Ibuprofen and aspirin are thought to chemically link up to sites in close proximity so that ibuprofen's presence may "crowd out" aspirin)
The FDA has recently published a paper explaining what is known about the asa-ibuprofen interaction issue and what practically can be done to enjoy whatever cardioprotective effect aspirin has and still be able to take ibuprofen for various pains. It is well worth reading and perhaps having copies handy to give patients.
Basically the advice is this:
Wait at least 1/2 hour after taking immediate release aspirin before taking ibuprofen. Wait 8 hours after taking 400 mg. of ibuprofen before taking aspirin.
The above advice does not apply to the popular enteric coated aspirin (ECASA) whose absorption is slower and 1/2 hour may not be long enough for aspirin to complete its inhibition of cyclooxygenase.The FDA did not believe there was adequate evidence to make specific recommendations regarding other NSAIDs-other than a general cautionary note. However, one recent article provided some data indicating a similar problem with the combination of aspirin and naproxen.
Friday, September 08, 2006
Should the single digital FOBT be abandoned?
For years physicians in the office setting have included a digital rectal exam and then tested stool captured by the gloved finger for occult blood.
A recent study published in the Annals of Internal Medicine compared the results of the single digital FOBT ( fecal occult blood test) with the take home FOBT kit which involves the patient testing 6 samples of stool at home presumably after following the dietary guidelines indicated in the literature found with the kit. 6 samples should be better than 1 in terms of sensitivity which is exactly what the researchers found in 2655 patients who also underwent screening colonoscopy.
The single FOBT test did badly, with a sensitivity of only 4.9% in detecting "advanced neoplasia" which was defined as tubular adenomas larger than 10 mm., adenomas with villous patterns, high grade dysplasia or invasive cancer. The six test kit did better with a sensitivity of 23.9%.
Specificities for the two tests were in the 90% plus range. The authors concluded that the single finger FOBT is a poor screening test and clearly it is not enough to do if the intent is screening for colon cancer or polyps. I would add that the six-sample method is certainly not a substitute for colonoscopy either.
A recent study published in the Annals of Internal Medicine compared the results of the single digital FOBT ( fecal occult blood test) with the take home FOBT kit which involves the patient testing 6 samples of stool at home presumably after following the dietary guidelines indicated in the literature found with the kit. 6 samples should be better than 1 in terms of sensitivity which is exactly what the researchers found in 2655 patients who also underwent screening colonoscopy.
The single FOBT test did badly, with a sensitivity of only 4.9% in detecting "advanced neoplasia" which was defined as tubular adenomas larger than 10 mm., adenomas with villous patterns, high grade dysplasia or invasive cancer. The six test kit did better with a sensitivity of 23.9%.
Specificities for the two tests were in the 90% plus range. The authors concluded that the single finger FOBT is a poor screening test and clearly it is not enough to do if the intent is screening for colon cancer or polyps. I would add that the six-sample method is certainly not a substitute for colonoscopy either.
Wednesday, September 06, 2006
More on Quality Improvement Organizations"-another study fails to clearly show they work
I have written before the Quality Improvement Organizations (QICs) .The Sept 5, issue of the Annals of Internal Medicine published another study that was unable to clearly demonstrate that their efforts to improve quality in fact improves quality. The accompanying editorial noted that although the study tended to show some rather small improvements in the group that received a quality improvement "intervention", other factors not adequately controlled for could also have been responsible study design and analysis left much to desire. The editorialist quotes a 2006 publication for the Institute of Medicine that noted of 33 recent studies investigating QICs efficacy 9 show positive results, 16 yielded ambiguous results and 8 either found no impact or a negative impact .
Allthough the QIC website proclaims the organization strives to "make sure patients get the right care at the right time" studies-including their own such as this one from the Annals- seem unable to unambiguously demonstrate that what they do improve quality and even when some indication of quality improves (and in the interest of fairness it should be noted that a number of indicators did show improvement) after intervention the studies are so poorly designed they cannot attribute the results to their efforts.
I can't decide if their statement "make sure patients get the right care at the right time" is born of extreme naivete or typical governmental bureaucratic hubris but I think that any physician who has been in practice for more than five minutes would never promise anything so grandiose and impossible to deliver.The QICs seem unable to do something much simpler,namely to show that their interventions actually do what they purport to do but do not loose faith, the authors promise us more and better designed studies.
Allthough the QIC website proclaims the organization strives to "make sure patients get the right care at the right time" studies-including their own such as this one from the Annals- seem unable to unambiguously demonstrate that what they do improve quality and even when some indication of quality improves (and in the interest of fairness it should be noted that a number of indicators did show improvement) after intervention the studies are so poorly designed they cannot attribute the results to their efforts.
I can't decide if their statement "make sure patients get the right care at the right time" is born of extreme naivete or typical governmental bureaucratic hubris but I think that any physician who has been in practice for more than five minutes would never promise anything so grandiose and impossible to deliver.The QICs seem unable to do something much simpler,namely to show that their interventions actually do what they purport to do but do not loose faith, the authors promise us more and better designed studies.
Tuesday, September 05, 2006
Trial underway to test use of steroids in severe pneumonia
In the August 14,2006 issue of Internal Medicine News we learn of reports that corticosteroids may reduce the morbidity and mortality of severe bacterial pneumonia.
Dr. Antoni Torres from the University of Barcelona apparently become interested in the potential value of steroids in this application from his observational study of 1,424 hospitalized patients in which one of the independent protective risk factors was COPD. This seems counterintuitive but he reasoned that perhaps it was the use of steroids (which is routine in exacerbations of COPD) that was protective.
The news article reported that a small RCT (46 patients) showed a reduction in mortality in the group receiving 200 mg of hydrocortisome IV followed by 7 days of a lower dose(Am J. Respir.Crit.Care.2005,171:242-8). I could not find that reference on PUBMED but here Dr. Torres discusses the issue.
Another larger RCT is currently in progress in Italy. Patients will be those with community acquired pneumonia who have a high mortality risk and a C-reactive-protein above 15. The thought here seems to be that in severe pneumonia -as flagged by the CRP value-there is an important element of systemic inflammatory response which might be mitigated by the steroids.
The value of steroids in sepsis has been difficult to ascertain as indicated in this 2004 Annals of Internal Medicine summary of a recent meta-analysis. I suspect the value of steroids may be a bit hard to sort out in pneumonia as well. RCTs in seriously ill patients who are heterogeneous in multiple aspects offer quite a challenge and finding the right dose-if there is one-may be difficult as suggested by the results of the sepsis treatment meta-analysis in which it appeared that "high-dose" was harmful and "low dose" helpful.
Dr. Antoni Torres from the University of Barcelona apparently become interested in the potential value of steroids in this application from his observational study of 1,424 hospitalized patients in which one of the independent protective risk factors was COPD. This seems counterintuitive but he reasoned that perhaps it was the use of steroids (which is routine in exacerbations of COPD) that was protective.
The news article reported that a small RCT (46 patients) showed a reduction in mortality in the group receiving 200 mg of hydrocortisome IV followed by 7 days of a lower dose(Am J. Respir.Crit.Care.2005,171:242-8). I could not find that reference on PUBMED but here Dr. Torres discusses the issue.
Another larger RCT is currently in progress in Italy. Patients will be those with community acquired pneumonia who have a high mortality risk and a C-reactive-protein above 15. The thought here seems to be that in severe pneumonia -as flagged by the CRP value-there is an important element of systemic inflammatory response which might be mitigated by the steroids.
The value of steroids in sepsis has been difficult to ascertain as indicated in this 2004 Annals of Internal Medicine summary of a recent meta-analysis. I suspect the value of steroids may be a bit hard to sort out in pneumonia as well. RCTs in seriously ill patients who are heterogeneous in multiple aspects offer quite a challenge and finding the right dose-if there is one-may be difficult as suggested by the results of the sepsis treatment meta-analysis in which it appeared that "high-dose" was harmful and "low dose" helpful.
Wednesday, August 30, 2006
Is interval training better for metabolic syndrome?
Physicians routinely recommend exercise for patients with the metabolic syndrome-typically walking.Exercise is a generally accepted strategy to loose weight and improve lipids and glucose tolerance.
Interval training (IT) has been popular with runners for years. The famous distance runner Emile Zatopek popularized it in the 1950's. IT involves alternating high speed or high intensity exercise periods with rest or low energy output periods, e.g. sprinting for 100 yards followed by jogging or walking for 100 yards.There is a "loading" period and a "recovery period".In the recovery period there is at least partial regeneration of adenosine triphosphate and creatine phosphate and decrease in lactate and hydrogen ions.IT is contrasted with constant loading exercise (CLE) or continuous exercise at more or less the same pace or energy output level. Muscle strength and endurance have been shown to increase with interval training while CLE mainly improves endurance.
Recently, Dr. Anna Tjonna and associates from Norway published the results of a small study that indicated that interval training was better than traditional exercise ( i.e prolonged exercise at a lower energy output aka continuous exercise) in terms of improvement in HDL cholesterol and blood sugar in patients with the metabolic syndrome. The IT group exercised at 90-95% of maximum heart rate for 4 minutes followed by a 3 minute rest. They did 4 sets three times a week. The comparison group exercised at 70% of max heart rate for 40 minutes three times a week.
There is a understandable reluctance to encourage sedentary, overweight middle and older aged patients to exercise at that high a level of exercise because of a perceived greater risk of cardiac events and the likelihood of greater musculo-skeletal injuries.We almost always tell patients to begin with a walking program and go from there. "Going from there" often involves someone jogging for a short distance and then walking and then jogging again, which is basically a mild form of interval training. But it is not clear how much exercise or what level of energy output is required to actually change the metabolic parameters of the metabolic syndrome.In fact, the literature on the effect of running on HDL is a bit murky as well. There is some evidence that a higher level of exercise is required to significantly elevate a low HDL than occurs with the usual middle aged metabolic syndrome patient as they try to
"get healthier" with a walking program.Patients with elevated triglycerides usually enjoy a greater increase in HDL with exercise as a result of the fall in triglyceride levels.
I am not going to send a 55 year old man with a BMI of 31 and metabolic syndrome over to the high school track to do wind sprints but the notion of interval training is getting more attention from exercise physiologists and rehab professionals. Deep water running (running in place with a flotation vest in a swimming pool) has been a technique to keep injured athletes fit while they heal and has been applied to older patients to increase their level of cardiovascular fitness and appears to be a relatively low injury risk type exercise.For example,deep water running seemed safe and effective in increasing fitness levels in older women in this study from Sweden. IT has been shown to be feasible and effective in increasing fitness in patients with chronic obstructive lung disease and has been shown to increase anaerobic capacity as well as aerobic in cardiac rehab patients while continuous type training only increased the later.
The single study quoted above is not going to change physicians' exercise prescriptions but maybe there is something metabolically desirable (perhaps a greater increase in the GLUT4 glucose transporter protein or something like that) about the interval training. If so and further data confirm the study from Norway,deep water running may become a way to "treat metabolic syndrome" by providing a safe way to do intervals. ( Disclosure: I became an avid advocate of aquatic exercising 2 years ago.While I was recovering from a subcortical trabecular fracture of the femur aqua-jogging kept me reasonably fit until I could go back to running and was good mental therapy for me and those around me who had to deal with someone who for the first time in 30 years was not running regularly.)
Interval training (IT) has been popular with runners for years. The famous distance runner Emile Zatopek popularized it in the 1950's. IT involves alternating high speed or high intensity exercise periods with rest or low energy output periods, e.g. sprinting for 100 yards followed by jogging or walking for 100 yards.There is a "loading" period and a "recovery period".In the recovery period there is at least partial regeneration of adenosine triphosphate and creatine phosphate and decrease in lactate and hydrogen ions.IT is contrasted with constant loading exercise (CLE) or continuous exercise at more or less the same pace or energy output level. Muscle strength and endurance have been shown to increase with interval training while CLE mainly improves endurance.
Recently, Dr. Anna Tjonna and associates from Norway published the results of a small study that indicated that interval training was better than traditional exercise ( i.e prolonged exercise at a lower energy output aka continuous exercise) in terms of improvement in HDL cholesterol and blood sugar in patients with the metabolic syndrome. The IT group exercised at 90-95% of maximum heart rate for 4 minutes followed by a 3 minute rest. They did 4 sets three times a week. The comparison group exercised at 70% of max heart rate for 40 minutes three times a week.
There is a understandable reluctance to encourage sedentary, overweight middle and older aged patients to exercise at that high a level of exercise because of a perceived greater risk of cardiac events and the likelihood of greater musculo-skeletal injuries.We almost always tell patients to begin with a walking program and go from there. "Going from there" often involves someone jogging for a short distance and then walking and then jogging again, which is basically a mild form of interval training. But it is not clear how much exercise or what level of energy output is required to actually change the metabolic parameters of the metabolic syndrome.In fact, the literature on the effect of running on HDL is a bit murky as well. There is some evidence that a higher level of exercise is required to significantly elevate a low HDL than occurs with the usual middle aged metabolic syndrome patient as they try to
"get healthier" with a walking program.Patients with elevated triglycerides usually enjoy a greater increase in HDL with exercise as a result of the fall in triglyceride levels.
I am not going to send a 55 year old man with a BMI of 31 and metabolic syndrome over to the high school track to do wind sprints but the notion of interval training is getting more attention from exercise physiologists and rehab professionals. Deep water running (running in place with a flotation vest in a swimming pool) has been a technique to keep injured athletes fit while they heal and has been applied to older patients to increase their level of cardiovascular fitness and appears to be a relatively low injury risk type exercise.For example,deep water running seemed safe and effective in increasing fitness levels in older women in this study from Sweden. IT has been shown to be feasible and effective in increasing fitness in patients with chronic obstructive lung disease and has been shown to increase anaerobic capacity as well as aerobic in cardiac rehab patients while continuous type training only increased the later.
The single study quoted above is not going to change physicians' exercise prescriptions but maybe there is something metabolically desirable (perhaps a greater increase in the GLUT4 glucose transporter protein or something like that) about the interval training. If so and further data confirm the study from Norway,deep water running may become a way to "treat metabolic syndrome" by providing a safe way to do intervals. ( Disclosure: I became an avid advocate of aquatic exercising 2 years ago.While I was recovering from a subcortical trabecular fracture of the femur aqua-jogging kept me reasonably fit until I could go back to running and was good mental therapy for me and those around me who had to deal with someone who for the first time in 30 years was not running regularly.)
Monday, August 28, 2006
Houston V.A. physicians examine P4P data and find evidence of gaming and treating the chart
The possibility that health care providers (HCP) might try to game the system and treat the chart when offered or forced to play the P4P game is well recognized and quite consistent with basic human nature.
Researchers from the Houston Veteran's Administration Hospital have published an article indicating that behavior of that type does in fact occur. Dr. Laura S. Peterson and her associates write in the August 15 2006 issue of the Annals of Internal Medicine.
They reviewed 16 articles and in 4 studies they found evidence of unintended effects-adverse selection and gaming or treating the chart to achieve financially rewarded goals. Importantly, for those of us who believe this entire P4P movement is motivated by a desire to save money, they found no evidence that these efforts are cost effective. Of course, lack of evidence does not necessarily mean evidence that they are not cost effective but the third party payers and CMS may at some point pull back if they are continue to be unable to show they there are cost savings to the payers. I hope so.
Researchers from the Houston Veteran's Administration Hospital have published an article indicating that behavior of that type does in fact occur. Dr. Laura S. Peterson and her associates write in the August 15 2006 issue of the Annals of Internal Medicine.
They reviewed 16 articles and in 4 studies they found evidence of unintended effects-adverse selection and gaming or treating the chart to achieve financially rewarded goals. Importantly, for those of us who believe this entire P4P movement is motivated by a desire to save money, they found no evidence that these efforts are cost effective. Of course, lack of evidence does not necessarily mean evidence that they are not cost effective but the third party payers and CMS may at some point pull back if they are continue to be unable to show they there are cost savings to the payers. I hope so.
Sunday, August 27, 2006
heuristics and statistics-we need and use both in medicine
In spite of at least one terrible publication to the contrary-the criticism of which is reviewed here- there can be little doubt that experienced clinicians perform better than do novices. Experience and practice really no matter.During the five to ten years it seems to take for a recent medical graduate to become at least a low level expert basically no time is spent on courses on medical decision making.
Does the experienced clinician talk about or think about likelihood ratios or prior probabilities? Does he explicitly use equations to determine positive predictive values etc? Not the ones I have been associated with. What the experienced docs seem to deal in mainly are heuristics. These are rules of thumb,short cuts, and simple judgments that operate in many of the decisions that physicians make.
Dr. Pat Croskerry published an interesting article in the Canadian Journal anesthesiology ( vol. 52:6 p.r1) in which he discusses decision making. He does this from the viewpoint of anesthesiology but it has broad application to medical decision making in general.
His major point is that physicians make many decisions through the mechanisms of heuristics and while they often are effective there are cognitive impediments that limit their usefulness. We need to be aware of those mental tendencies so that we can compensate for them .One example, about which I have written earlier, is "premature closure"., i.e. making a diagnosis and then shutting out consideration that it could be incorrect even as evidence to the contrary accumulates. He mentions many other cognitive tendencies which he refers to as "cognitive dispositions to respond" (CDRs) rather then the earlier tendency to label them as biases or fallacies.Some have intriguing names such as "playing the odds", "Sutton's Slip" and "ego bias". I have not had time yet to research what those terms refer to but some of them may be the topic of a later posting.
His position is that doctors do not typically think in a formalized, statistical manner using formulas which dispassionately weigh the evidence and we should recognize that fact of life and learn about and make efforts to control the CDRs in order to better harness our use of heuristics.
Statistical analysis is an essential element in clinical research but many of the decisions we make in the heat of the clinical battles that take place every day rely on mental processes that seem to have little to do with statistics.
Does the experienced clinician talk about or think about likelihood ratios or prior probabilities? Does he explicitly use equations to determine positive predictive values etc? Not the ones I have been associated with. What the experienced docs seem to deal in mainly are heuristics. These are rules of thumb,short cuts, and simple judgments that operate in many of the decisions that physicians make.
Dr. Pat Croskerry published an interesting article in the Canadian Journal anesthesiology ( vol. 52:6 p.r1) in which he discusses decision making. He does this from the viewpoint of anesthesiology but it has broad application to medical decision making in general.
His major point is that physicians make many decisions through the mechanisms of heuristics and while they often are effective there are cognitive impediments that limit their usefulness. We need to be aware of those mental tendencies so that we can compensate for them .One example, about which I have written earlier, is "premature closure"., i.e. making a diagnosis and then shutting out consideration that it could be incorrect even as evidence to the contrary accumulates. He mentions many other cognitive tendencies which he refers to as "cognitive dispositions to respond" (CDRs) rather then the earlier tendency to label them as biases or fallacies.Some have intriguing names such as "playing the odds", "Sutton's Slip" and "ego bias". I have not had time yet to research what those terms refer to but some of them may be the topic of a later posting.
His position is that doctors do not typically think in a formalized, statistical manner using formulas which dispassionately weigh the evidence and we should recognize that fact of life and learn about and make efforts to control the CDRs in order to better harness our use of heuristics.
Statistical analysis is an essential element in clinical research but many of the decisions we make in the heat of the clinical battles that take place every day rely on mental processes that seem to have little to do with statistics.
Tuesday, August 22, 2006
The gabapentin story: "Medical education drives this market"
The quote "Medical education drives this market" is attributed to an author of a Parke -Davis business plan found in a legal exhibit in the proceedings of the United States vs Pfizer, and Parke-Davis. Public documents in this case were reviewed and analyzed by Dr. Michael A. Steinman and his colleagues at the San Francisco Veterans Affairs Medical Center in San Francisco and published in the August 15, 2006 issue of the Annals of Internal Medicine. Federal legal action had been taken against gabapentin manufacturer for promoting off-label uses of the drug.
After a physician or medical student or house officer reads this article she should never view certain "CME" activities in the same way.
An important part of the influence campaign of Parke-Davis (P-D)to promote off-label use of gabapentin was though "thought leaders". These physicians are influential physicians often identified by the affiliation with major academic centers. These department chairs, directors of academic training programs or divisions received payments ranging from $10,000 to about $150,000 between 1993 and 1997 in the forms of honoraria, research grants and educational grants. These folks were often the likely role models for house officers , fellows and medical students. This aspect of the multifaceted efforts of P-D to promote non-FDA approved use of gabapentin is the most troubling to me because of the role well respected physicians played. At some early point,a person could have been simply naive and was duped but at some point most had to be complicit at some level.
There are other aspects detailed by the authors including the use of "medical education" companies hired by P-D to ghost write articles and organize meetings, and supply various CME products which were basically advertisements for off-label use of gabapentin.
The full text version of the Annals article is not available until 6 months after publication on line but an excellent review of the article and commentary about both the article and the accompanying editorial can be found in two posts from August 18,2006 on Health Care Renewal.
In addition to outlining the various tactics (advisory boards, consultant meetings, speakers bureaus, programs funded through unrestricted educational grants), Dr Poses raises valid questions about the multiple corporate positions held by the Annals editorial writer as well an academic appointment and how difficult it would seem to be to fulfill the apparently conflicting fiduciary duties that those various roles demand.
The Annals article and Dr. Poses's posts should be part of medical students courses on evidence based medicine. They need to recognize the borders between research,education and promotion which the authors described as "porous". We can hope they will guard these borders better than some-perhaps too many-of their mentors have done. I am grateful to Dr. Steinman and his associates for their work in plowing through some 8000 pages of publicly available documents to give us a "game plan" for selling a drug to physicians. Hopefully this will be as helpful to physicians as giving the offensive play book to the defensive coordinator of a rival football team.
After a physician or medical student or house officer reads this article she should never view certain "CME" activities in the same way.
An important part of the influence campaign of Parke-Davis (P-D)to promote off-label use of gabapentin was though "thought leaders". These physicians are influential physicians often identified by the affiliation with major academic centers. These department chairs, directors of academic training programs or divisions received payments ranging from $10,000 to about $150,000 between 1993 and 1997 in the forms of honoraria, research grants and educational grants. These folks were often the likely role models for house officers , fellows and medical students. This aspect of the multifaceted efforts of P-D to promote non-FDA approved use of gabapentin is the most troubling to me because of the role well respected physicians played. At some early point,a person could have been simply naive and was duped but at some point most had to be complicit at some level.
There are other aspects detailed by the authors including the use of "medical education" companies hired by P-D to ghost write articles and organize meetings, and supply various CME products which were basically advertisements for off-label use of gabapentin.
The full text version of the Annals article is not available until 6 months after publication on line but an excellent review of the article and commentary about both the article and the accompanying editorial can be found in two posts from August 18,2006 on Health Care Renewal.
In addition to outlining the various tactics (advisory boards, consultant meetings, speakers bureaus, programs funded through unrestricted educational grants), Dr Poses raises valid questions about the multiple corporate positions held by the Annals editorial writer as well an academic appointment and how difficult it would seem to be to fulfill the apparently conflicting fiduciary duties that those various roles demand.
The Annals article and Dr. Poses's posts should be part of medical students courses on evidence based medicine. They need to recognize the borders between research,education and promotion which the authors described as "porous". We can hope they will guard these borders better than some-perhaps too many-of their mentors have done. I am grateful to Dr. Steinman and his associates for their work in plowing through some 8000 pages of publicly available documents to give us a "game plan" for selling a drug to physicians. Hopefully this will be as helpful to physicians as giving the offensive play book to the defensive coordinator of a rival football team.
Thursday, August 17, 2006
Yet another analysis of the ALLHAT trial
The idealized world of the medical student as he learns about randomized clinical trials (RCT) is one in which something like this is visualized. Let's do a RCT to find out which is the best way to treat hypertension and then we will have evidence based medicine directing our rational,quality filled medical care.. Well, the ALLHAT trial could be thought of as just such a undertaking so now we should know,right?
With trials of this scope and complexity a large amount of data is generated and rather than a simple black and white answer emerging there are often multiple conclusions all of which do not agree. Such is how this been with ALLHAT. The most recent analysis of this controversial BP trial is from Dr. Frans Leenen from the Ottawa heart Institute.
Here are some of his findings:
Calcium channel blockers(CCBs) were not associated with more coronary artery disease events but were blamed for more episodes of heart failure. Ace inhibitors (ACEi), on the other hand appeared to be more likely to cause stroke,gi bleeding, peripheral artery disease and angina and ( here is a surprise) angio-edema.
Rather than the simple "well that settles it" that was hoped for in ALLHAT, we have arguments and counter-arguments presented,editorials supporting the results and the BP recommendations (JNCVI) largely based on ALLHAT and editorials arguing that the trial was poorly designed and bears no resemblance to the way BP is really treated (i.e. did not compare realistic choices for BP meds) .
We have gone back and forth with CCBs as well. Are they harmful? Are they as good as any other BP treatment ( which is suggested by Leenen's article)? Not only do trial results seem to differ , various analyses in regard to the same trial differ.I doubt if the recent analysis by Leenen will settle much of anything.
With trials of this scope and complexity a large amount of data is generated and rather than a simple black and white answer emerging there are often multiple conclusions all of which do not agree. Such is how this been with ALLHAT. The most recent analysis of this controversial BP trial is from Dr. Frans Leenen from the Ottawa heart Institute.
Here are some of his findings:
Calcium channel blockers(CCBs) were not associated with more coronary artery disease events but were blamed for more episodes of heart failure. Ace inhibitors (ACEi), on the other hand appeared to be more likely to cause stroke,gi bleeding, peripheral artery disease and angina and ( here is a surprise) angio-edema.
Rather than the simple "well that settles it" that was hoped for in ALLHAT, we have arguments and counter-arguments presented,editorials supporting the results and the BP recommendations (JNCVI) largely based on ALLHAT and editorials arguing that the trial was poorly designed and bears no resemblance to the way BP is really treated (i.e. did not compare realistic choices for BP meds) .
We have gone back and forth with CCBs as well. Are they harmful? Are they as good as any other BP treatment ( which is suggested by Leenen's article)? Not only do trial results seem to differ , various analyses in regard to the same trial differ.I doubt if the recent analysis by Leenen will settle much of anything.
Monday, August 14, 2006
Osteopenia-A disease? when do you treat it with medications
Osteoporosis is defined as a decrease in bone mass with pathological changes in the microarchitecture of bone and tendency to fragility fractures. The operational definition is based on the bone mineral density (BMD) measurement and statistical definition is used with osteoporosis said to be present if the BMD is less then 2.5 standard deviations (T score) from the average 25 year old woman's value.For those readings between -1 and -2.5, the term osteopenia is used. By definition 16% of 35 year old women would be osteopenic.
40% of 65 year old women are osteopenic. Of those who should be offered medication? Currently the medications typically used are the bisphosphonates which have largely replaced estrogen which not too long ago was very popular as it was believed to not only mitigate the aging effects of estrogen decline butcould preserve heart health and lessen the risk of dementia.I considered this question because of a quite a number of women who I would see in the office had been placed on bisphosphonate medications by their gynecologist or family doctor or internist seemingly only because of a BMD score in the osteopenic range.
The Osteoporosis Foundation (NOF) and the American Association of Clinical Endocrinology (AACE) have different recommendations regarding the use of medications. NOF seems to recommend medications for those patients with osteopenia with no risk factors if the T score is below -2 and for those patients with T scores of less than -1.5 if they have one or more risk factors which include low body weight ( less than 127),history or family history of fragility fractures,smoking, estrogen lack or excessive alcohol use ,use of certain medications including steroids. AACE would recommends medication if the T score is less than 1.5 IF the patient has had fracture(s) or if the T score is less than -2.5.( This is the WHO definition of osteoporosis so-strictly speaking- AACE is recommending treatment for osteoporosis not osteopenia and recommends treatment for osteopenia only if there is a history of fractures.)
The consensus answer to the introductory questions is no, all persons said to be osteopenic on the basis of a bone density measurement do not need to receive medications. The opposite answer would seem to mean we should be treating those 16% of normal 25 year old women on the basis of their BMD score. Clinical judgment is required to sort out those patients with osteopenia and other risk factors and clinical features would might benefit from prescription medications.Of course with preventive medication use, you never really know if anything is prevented on not in the individual case only in the aggregate. It may make good sense to suggest a bisphosphonate in a 70 year old women who has one fragility fracture already and tends to be a bit unsteady even in the face on a mildly osteopenic BMD while a younger women with the same score who exercises regularly may not be as good a "candidate". As with all preventive treatments-if that is not an oxymoron-the decision should be one reached by the patient after discussion with the physician. and not a unilateral quasi-judicial decision.BMD is one of the factors to consider but not necessarily the determinative one.
A recent article in the Annals of Internal Medicine is referenced as a source for the statement that bisphosphonates are not longer recommended for osteopenic patients. This is misleading.The Annals article was a computer simulation with numerous assumptions (AKA- a cost effectiveness study) which concluded that therapy with bisphosphonates was not cost effective.But it was a close call and with decreases in drug prices the outcome would be turned around and drugs do have a way of becoming generic and cheaper with time.So folks should not take them now but wait until they are cheaper?As is generic with cost effectiveness articles the authors decide what costs too much not the person using the medications ( i.e. the patient).I realize that often the person using the medication is not the person or financial entity paying for the medications, which ,according to my cynical way of thinking,the reason we have cost effectiveness studies in medicine in the first place.In any event, I am not aware that NOF or AACE have made any changes in their recommendations
40% of 65 year old women are osteopenic. Of those who should be offered medication? Currently the medications typically used are the bisphosphonates which have largely replaced estrogen which not too long ago was very popular as it was believed to not only mitigate the aging effects of estrogen decline butcould preserve heart health and lessen the risk of dementia.I considered this question because of a quite a number of women who I would see in the office had been placed on bisphosphonate medications by their gynecologist or family doctor or internist seemingly only because of a BMD score in the osteopenic range.
The Osteoporosis Foundation (NOF) and the American Association of Clinical Endocrinology (AACE) have different recommendations regarding the use of medications. NOF seems to recommend medications for those patients with osteopenia with no risk factors if the T score is below -2 and for those patients with T scores of less than -1.5 if they have one or more risk factors which include low body weight ( less than 127),history or family history of fragility fractures,smoking, estrogen lack or excessive alcohol use ,use of certain medications including steroids. AACE would recommends medication if the T score is less than 1.5 IF the patient has had fracture(s) or if the T score is less than -2.5.( This is the WHO definition of osteoporosis so-strictly speaking- AACE is recommending treatment for osteoporosis not osteopenia and recommends treatment for osteopenia only if there is a history of fractures.)
The consensus answer to the introductory questions is no, all persons said to be osteopenic on the basis of a bone density measurement do not need to receive medications. The opposite answer would seem to mean we should be treating those 16% of normal 25 year old women on the basis of their BMD score. Clinical judgment is required to sort out those patients with osteopenia and other risk factors and clinical features would might benefit from prescription medications.Of course with preventive medication use, you never really know if anything is prevented on not in the individual case only in the aggregate. It may make good sense to suggest a bisphosphonate in a 70 year old women who has one fragility fracture already and tends to be a bit unsteady even in the face on a mildly osteopenic BMD while a younger women with the same score who exercises regularly may not be as good a "candidate". As with all preventive treatments-if that is not an oxymoron-the decision should be one reached by the patient after discussion with the physician. and not a unilateral quasi-judicial decision.BMD is one of the factors to consider but not necessarily the determinative one.
A recent article in the Annals of Internal Medicine is referenced as a source for the statement that bisphosphonates are not longer recommended for osteopenic patients. This is misleading.The Annals article was a computer simulation with numerous assumptions (AKA- a cost effectiveness study) which concluded that therapy with bisphosphonates was not cost effective.But it was a close call and with decreases in drug prices the outcome would be turned around and drugs do have a way of becoming generic and cheaper with time.So folks should not take them now but wait until they are cheaper?As is generic with cost effectiveness articles the authors decide what costs too much not the person using the medications ( i.e. the patient).I realize that often the person using the medication is not the person or financial entity paying for the medications, which ,according to my cynical way of thinking,the reason we have cost effectiveness studies in medicine in the first place.In any event, I am not aware that NOF or AACE have made any changes in their recommendations
Friday, August 11, 2006
bacterial pharnygitis-not just beta-strep
Recent entries on DB's Medical Rants have called attention to a somewhat obscure cause of sore throat, namely a potentially very serious infection with a bacteria with the appropriately ominous name of Fusibacterium necrophorum. I will admit I was not aware of that issue.He discusses this infection in the important context of the "long tail" of diagnostic possibilities.
There is another, arguably a bit more common, cause of bacterial sore throat-infection with Arcanobacterium haemolyticum,formerly known as corynbacterium hemolyticum. This form of bacterial throat infection may be associated with a rash so that confusion with scarlet fever caused by beta-strep is possible. A CDC report indicates it may account for as many as 2.5 % of sore throat cases in young patients,occasionally cause a "membrane" on the throat as in diphtheria and may be penicillin resistant.
Clearly group A , beta-hemolytic streptococcal (GABHS) infection is the most common etiologic bacterial pathogen in pharyngitis but Arcanobacterium infection is easily missed. Not only is it similar to GABHS, a typical throat culture might miss A.Hemolyticum because the usual culture plate used for throat swabs may only show a small area of hemolysis after 24 hours with Arcanobacterium and the report would indicate only no beta strep present.
The e-Medicine article on Arcanobacterium infection suggests that the macrolide family of antibiotics are preferable to penicillin which is the traditional drug of choice for GABHS.
Neisseria gonorrhoeae and corynebacterium diphtheria have to mentioned as well although diphtheria is basically of historical interest only at least in the U.S. As time goes on,I'll bet we will add more bacterial pathogens to the recognized inhabitants of the long tail of etiologic agents of sore throat.
There is another, arguably a bit more common, cause of bacterial sore throat-infection with Arcanobacterium haemolyticum,formerly known as corynbacterium hemolyticum. This form of bacterial throat infection may be associated with a rash so that confusion with scarlet fever caused by beta-strep is possible. A CDC report indicates it may account for as many as 2.5 % of sore throat cases in young patients,occasionally cause a "membrane" on the throat as in diphtheria and may be penicillin resistant.
Clearly group A , beta-hemolytic streptococcal (GABHS) infection is the most common etiologic bacterial pathogen in pharyngitis but Arcanobacterium infection is easily missed. Not only is it similar to GABHS, a typical throat culture might miss A.Hemolyticum because the usual culture plate used for throat swabs may only show a small area of hemolysis after 24 hours with Arcanobacterium and the report would indicate only no beta strep present.
The e-Medicine article on Arcanobacterium infection suggests that the macrolide family of antibiotics are preferable to penicillin which is the traditional drug of choice for GABHS.
Neisseria gonorrhoeae and corynebacterium diphtheria have to mentioned as well although diphtheria is basically of historical interest only at least in the U.S. As time goes on,I'll bet we will add more bacterial pathogens to the recognized inhabitants of the long tail of etiologic agents of sore throat.
Monday, August 07, 2006
Practice,practice, practice-will current house officers have time to do that?
What do some cognitive scientists and the folks who teach you how to take a test (Stanley Kaplan et al) have in common? Answer- a belief in the power of practice and challenges just beyond one's level of competence.
The August 6, 2006 Issue of Scientific American has an interesting article by Phillip S. Ross entitled "The Expert Mind".
It discusses studies that have been done regarding master chess players ( who might be considered the Drosophila of the cognitive scientists) and how they approach and solve chess problems. Novices spend more time analyzing various possible moves than masters who quickly narrow the alternatives down apparently without consciously considering all of them.
Are the masters born or made? The author argues that they are made. The entire article should be read to review the evidence he presents.
"Effortful study" and Practice, Practice, practice with exposure to increasingly difficult problems is the key.What seems important is "challenges just beyond one's competence". To a medical student just beginning the clinical years, just about everything is beyond their competence.
It takes time. He quotes one cognitive scientist who believes it takes about ten years to become an expert.In the "old days" a internist who did specialty training did in fact about ten years total
training although some only took nine years.
Before Stanley Kaplan proved otherwise it was believed that the S.A.T. was an aptitude test. He showed one could be coached to improve one' s S.A.T.score and made a career of that. A key to that improvement was practice ( and of course, knowing what type of problems you would face and therefore be able to practice their solution)
I wonder if the current generation of internal medicine house officers will have enough time in their training to practice enough.With my generation's training (graduation in 1965) we had more time.Counting my two years of pulmonary fellowship, it was ten years from the year I entered medical school.Now someone can complete the IM program ( assuming no fellowship) in as little as 7 years from med school entry. In addition, there is less time per week with the current rules limiting time in the hospital and more material placed into the training requirements that takes away from doctor patient time ( e.g. quality training, cultural competency and my favorite "systems based practice").
One of my former partners in a large internal medicine clinic is convinced the level of clinical expertise in regard to general medicine problems is much greater in those docs who have had specialty training than those "general" internists who have had only 3 years post med school training and not just in their specialty but in general IM matters as well. Maybe the three year trainees need more practice.
The August 6, 2006 Issue of Scientific American has an interesting article by Phillip S. Ross entitled "The Expert Mind".
It discusses studies that have been done regarding master chess players ( who might be considered the Drosophila of the cognitive scientists) and how they approach and solve chess problems. Novices spend more time analyzing various possible moves than masters who quickly narrow the alternatives down apparently without consciously considering all of them.
Are the masters born or made? The author argues that they are made. The entire article should be read to review the evidence he presents.
"Effortful study" and Practice, Practice, practice with exposure to increasingly difficult problems is the key.What seems important is "challenges just beyond one's competence". To a medical student just beginning the clinical years, just about everything is beyond their competence.
It takes time. He quotes one cognitive scientist who believes it takes about ten years to become an expert.In the "old days" a internist who did specialty training did in fact about ten years total
training although some only took nine years.
Before Stanley Kaplan proved otherwise it was believed that the S.A.T. was an aptitude test. He showed one could be coached to improve one' s S.A.T.score and made a career of that. A key to that improvement was practice ( and of course, knowing what type of problems you would face and therefore be able to practice their solution)
I wonder if the current generation of internal medicine house officers will have enough time in their training to practice enough.With my generation's training (graduation in 1965) we had more time.Counting my two years of pulmonary fellowship, it was ten years from the year I entered medical school.Now someone can complete the IM program ( assuming no fellowship) in as little as 7 years from med school entry. In addition, there is less time per week with the current rules limiting time in the hospital and more material placed into the training requirements that takes away from doctor patient time ( e.g. quality training, cultural competency and my favorite "systems based practice").
One of my former partners in a large internal medicine clinic is convinced the level of clinical expertise in regard to general medicine problems is much greater in those docs who have had specialty training than those "general" internists who have had only 3 years post med school training and not just in their specialty but in general IM matters as well. Maybe the three year trainees need more practice.
Wednesday, August 02, 2006
More on the LABA controversy-a thoughtful analysis from an allergist's perspective
Dr. Stuart Henochowicz, an allergist-internist blogger,recently posted some cogent comments about the use of LABAs in asthma including comments regarding the combo inhalers ( steroids and a LABA).
Asthma patients are often treated by allergists or pulmonary docs or sometimes both and as a pulmonary physician I welcome his thoughts regarding the recent flare up of the concern about the safety of the long acting beta-agonists (LABAs). This exacerbation of concern was triggered mainly by the publication of the poorly done SMART trial and what I believe to be a flawed and overblown meta-analysis in the Annals of Internal Medicine by Salpeter.
Some of his key points are:
LABAs should not be used in asthma without inhaled steroid coverage.
The combo inhalers are very helpful in asthma treatment.
There are data supporting the value of those combination products.
I believe his comments reflect what I sense to be a consensus among physicians who treat asthma on a regular basis, allergists and pulmonary docs. I continue to have concerns that the annals' meta-analysis might cause asthma patients to discontinue their long acting beta agonist-steroid combination inhalers with resultant exacerbation of their asthma.In fact, some medical bloggers have commented that has already happened.
Asthma patients are often treated by allergists or pulmonary docs or sometimes both and as a pulmonary physician I welcome his thoughts regarding the recent flare up of the concern about the safety of the long acting beta-agonists (LABAs). This exacerbation of concern was triggered mainly by the publication of the poorly done SMART trial and what I believe to be a flawed and overblown meta-analysis in the Annals of Internal Medicine by Salpeter.
Some of his key points are:
LABAs should not be used in asthma without inhaled steroid coverage.
The combo inhalers are very helpful in asthma treatment.
There are data supporting the value of those combination products.
I believe his comments reflect what I sense to be a consensus among physicians who treat asthma on a regular basis, allergists and pulmonary docs. I continue to have concerns that the annals' meta-analysis might cause asthma patients to discontinue their long acting beta agonist-steroid combination inhalers with resultant exacerbation of their asthma.In fact, some medical bloggers have commented that has already happened.
Real medicine's "ill structured problems" versus guideline's well structured ones
I have been thinking lately about the type of medical problems that physicians face. Mathematicians and cognitive scientists talk about well-structured problems and ill-structured problems.
It seems that much of the challenge of patient care falls under the heading of ill-structured problems (ISP). Well structured problems (WSP) are those for which there is a known algorithm.
ISPs have these characteristics:
1.inadequate information form the outset
2.lack of defining guidelines to evaluate the problem
3.mutability of the problem-things changes as you go alone
4.lack of assurance that the problem has been solved
These are complicated problems without a clear cut solution and for which there may not be one right answer. There is no back-of-the-answer to compare with your analysis.
A recent post by Aggravated docsurg gives some great examples of ISPs that a general surgeon faced.Internists have equally demanding cases as well in addition to the simpler, quasi-no brainers.
An ill -structured problem is , by definition, one for which there is no algorithm. Much of the formal education I received in college physics and chemistry and calculus involved the mastery of WSPs of the following type. If a rock drops into a well and the splash is heard 4 seconds later how deep is the well? Physicians do not seem to do much of that type of thinking in their offices.
The folks who paint medicine as mostly a series of WSPs solable by algorithms and auditable for quality and reimbursable of the basis of obedience to those guidelines are either ignorant of or choose to ignore the reality of just how complex and ill structured the issues are that physicians face.
Clinical decisions in these ISPs will require all the knowledge, expertise and judgment the physician can bring to bear factoring in the values and wishes of the patient to try and find the particular "clinical truth" for the circumstances at hand. The quality gurus have no generic algorithm for that process.
It seems that much of the challenge of patient care falls under the heading of ill-structured problems (ISP). Well structured problems (WSP) are those for which there is a known algorithm.
ISPs have these characteristics:
1.inadequate information form the outset
2.lack of defining guidelines to evaluate the problem
3.mutability of the problem-things changes as you go alone
4.lack of assurance that the problem has been solved
These are complicated problems without a clear cut solution and for which there may not be one right answer. There is no back-of-the-answer to compare with your analysis.
A recent post by Aggravated docsurg gives some great examples of ISPs that a general surgeon faced.Internists have equally demanding cases as well in addition to the simpler, quasi-no brainers.
An ill -structured problem is , by definition, one for which there is no algorithm. Much of the formal education I received in college physics and chemistry and calculus involved the mastery of WSPs of the following type. If a rock drops into a well and the splash is heard 4 seconds later how deep is the well? Physicians do not seem to do much of that type of thinking in their offices.
The folks who paint medicine as mostly a series of WSPs solable by algorithms and auditable for quality and reimbursable of the basis of obedience to those guidelines are either ignorant of or choose to ignore the reality of just how complex and ill structured the issues are that physicians face.
Clinical decisions in these ISPs will require all the knowledge, expertise and judgment the physician can bring to bear factoring in the values and wishes of the patient to try and find the particular "clinical truth" for the circumstances at hand. The quality gurus have no generic algorithm for that process.
Thursday, July 27, 2006
Why is testing saw palmetto's efficacy different from testing Reiki's
Robert G. Newton in his book "The Truth of Science" (Harvard University Press, Cambridge, Massachusetts, 1997) talks about the Criterion of Coherence.
Newton said that "the most important criterion for ascertaining the truth of a statement is its coherence with a network of assertions that are also regard as true."
In regard to the often made accusation of proponents of unorthodox ideas ( parapsychology,etc) that scientists are inappropriately dismissive of their ideas and are elitists or closed minded he says:
"Researchers justifiably refuse to listen to these claims,to examine them or refute them in detail,because they are incoherent with the rest of our scientific knowledge."
Reiki and distant healing and homeopathy-to name a few-fall outside the boundaries of the coherent web of scientific learning while the possibility that a given herb or root might have some active pharmacological effect and be beneficial does not.In regard to the later there are numerous examples while the former violate too many well accepted and established and coherent scientific principles to seriously expend research time, money and brain power to bother to refute them. Manipulation of an undetectable energy force that is capable of healing any and all diseases,the mastery of which has to be taught by a master should not have to be investigated by a dubious controlled clinical trial.So the difference between testing saw palmetto and Reiki is the difference between testing something that is considered possible in the wide web of scientific knowledge and testing something that is just absurd.
Newton said that "the most important criterion for ascertaining the truth of a statement is its coherence with a network of assertions that are also regard as true."
In regard to the often made accusation of proponents of unorthodox ideas ( parapsychology,etc) that scientists are inappropriately dismissive of their ideas and are elitists or closed minded he says:
"Researchers justifiably refuse to listen to these claims,to examine them or refute them in detail,because they are incoherent with the rest of our scientific knowledge."
Reiki and distant healing and homeopathy-to name a few-fall outside the boundaries of the coherent web of scientific learning while the possibility that a given herb or root might have some active pharmacological effect and be beneficial does not.In regard to the later there are numerous examples while the former violate too many well accepted and established and coherent scientific principles to seriously expend research time, money and brain power to bother to refute them. Manipulation of an undetectable energy force that is capable of healing any and all diseases,the mastery of which has to be taught by a master should not have to be investigated by a dubious controlled clinical trial.So the difference between testing saw palmetto and Reiki is the difference between testing something that is considered possible in the wide web of scientific knowledge and testing something that is just absurd.
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