Berikut dikopikan hasil penelitian tentang intervensi pendidikan kesehatan untuk menumbuhkan kesadaran pasien asma dalam menjalani terapi obat agar tujuan terapi tercapai. Artikel diambil dari jurnal imunologi alergi asia pasifik.
NEJM baru saja menerbitkan artikel review tentang perkembangan penatalaksanaan pasien asma. artikel lengkapnya sbb”
A Patient with Asthma Seeks Medical Advice in 1828, 1928, and 2012″
People have suffered from asthma for millennia.1 Although the clinical presentation of asthma has probably changed little, there are many more people who now bear its consequences than there were 200 years ago. As a result of an intense interest in the condition, our understanding of its pathobiology, how to diagnose it, and — most important — how to treat it has evolved dramatically over the past two centuries. To illustrate this change, we provide three fictional reports of consultations performed for essentially the same patient, who has what we in 2012 would refer to as asthma. (A timeline of the major advances in the treatment of asthma from 1812 through 2012 is available with the full text of this article at NEJM.org.)
The first report is from 1828, the year that the New England Journal of Medicine and Surgery and Collateral Branches of Science joined with the Medical Intelligencer to form the Boston Medical and Surgical Journal. The second is from 1928 when the title of the publication was changed to the New England Journal of Medicine, and the third report is from the present.
The three accounts reflect the way in which care was delivered at the time. The first account is in the voice of a general practitioner who was contacted for consultation about a woman with intermittent episodes of dyspnea. The second is in the voice of a generalist who works in a private practice and has an interest in asthma; the patient has been referred to this physician by her own general physician. The third account is in the voice of a sub-subspecialty physician whose practice is limited to the care of patients with asthma. The contemporary patient identified this physician as a specialist in asthma through an Internet search and is consulting him for a second opinion about the appropriateness of her asthma care. She brings to the consultation a detailed history that she wrote, as well as notes from her primary care physician and an allergist.
Our three views of this medical consultation for a patient with asthma are not meant to provide a history of asthma but rather to offer a set of snapshots of the care that the same patient might have received had she sought medical advice in these distinct epochs. There are many diagnostic and therapeutic techniques that we do not mention; this does not mean that they are not important; it simply means that their use does not fit the time frame of our fictitious consultations. Finally, since this article is meant to contribute to the celebration of the Journal‘s 200th anniversary, we have largely, but not exclusively, used literature from the Journal; our apologies to others who claim primacy.
Office Note on Mrs. A. Smith
I attended at the home of a woman aged 35 years who had just moved with her family to Boston. Her household includes herself and her husband of 17 years, four children, a cook, two maids, a stable boy, and a footman. She sent for me with a complaint of repeated shortness of breath.
The History of Her Illness
When a fit of dyspnea occurs, the patient hears a musical noise in her chest, and she must labor to draw and expel a full breath. When she is stricken, it is her custom to stop all her activities and to inhale the steam coming from the spout of a kettle that her cook keeps always at the ready. With such treatment, she usually recovers within one or two days. Once or twice a year she has a severe fit, which may last for a week, and she is confined to her sick bed.
She has suffered such fits of laborious breathing since her childhood. They occur at any time of the year but are more common in the spring, when the trees bloom, and in the late summer than at other times. In the winter she reports that it is common for her to be so stricken when she walks from the harbor to her home, a distance of nearly a mile along a path that ascends steeply. This difficulty of respiration has become such a frequent occurrence that she now routinely calls for her coach even for very short journeys outside her home. During each of her periods of confinement for childbearing, the fits were far less numerous and severe in character, but within a few months after she had given birth, they returned.
Often, even when she is not suffering from laborious breathing, she will arise in the dark of the night and stand at the open window, gasping for air. By the time that dawn arrives she has usually regained control of her breathing and returns to sleep.
Her difficulty of respiration is accompanied by itchy eyes and a runny nose. She has a cough with these fits, but she does not produce phlegm. She does not have hemoptysis. No one among her family or close acquaintances has died from consumption. Her weight has been stable, and when she is not suffering from laborious breathing, her strength is good. She has not had rheumatic fever.
Her mother, now deceased, also suffered from difficulty of respiration; her father did not. Of her four children, ages 14, 12, 9, and 7, her two eldest, both boys, have suffered from the same symptoms, although her oldest son has not had a fit of laborious breathing for more than a year.
Observation of her breathing on the occasion of my consultation revealed nothing far out of the ordinary. Her speech was full and normal. The movements of her chest were full. I could palpate nothing abnormal in her heart motion. There was no swelling of her liver or her legs. I used a newly acquired stethoscope to examine her chest. Although the patient could not hear the musical sounds that have been termed “wheezes,” I was able to hear them.
The patient clearly suffers from an asthma; she may also have what has been described as “hay fever” in the spring and fall.2 I believe her fits of laborious breathing are similar to the asthmatic fits that Sir John Floyer suffered from and described in his “Treatise of the Asthma.”3 He describes this type of asthma as follows: “[T]he expiration is very slow and leisurely and wheezing, and the asthmatic can neither cough, sneeze, spit nor speak freely; and in the asthmatic fit, the muscular fibres of the bronchia and vesiculae of the lungs are contracted, and that produces the wheezing noise which is most often observable in expiration.” I have no concern that she suffers from consumption or from conditions of the heart that may lead to dropsy.
I think that she may benefit from smoking the leaf of Datura stramonium, also known as the thorn-apple plant. Many asthma sufferers have tried this remedy, and it seems to provide relief from a fit, even though it will not prevent a recurrence. Several years ago, Dr. Bree reported in the New England Journal of Medicine and Surgery that such smoking had a deleterious effect on a number of patients suffering from difficulty of respiration.4 However, in my experience, patients such as this woman will derive benefit from such treatment in that it shortens the duration of their indisposition from an asthmatic fit. I recommended this treatment to my patient, and she tells me that she has benefited from it.
Comment: In the early 1800s, there were many “asthmas,” since this was the term for any episodic shortness of breath. The physician needed to be sure that the primary cause was not tuberculosis or cardiac disease (e.g., mitral stenosis); both were very common at the time. Once a diagnosis of asthma (as we know it now) was established, the number of effective treatments was quite limited; inhalation of smoke from burning Datura stramonium was probably the best. This agent had anticholinergic properties and was the forerunner of the currently used antimuscarinic agents, such as ipratropium and tiotropium.5 There were numerous other treatments, such as inhalation of the fumes of hydrocyanic acid6 or inflation of the lungs with a bellows.7 Fortunately, such treatments and many others that produced no benefit and probably caused harm are no longer used.
Letter Regarding Mrs. A. Smith
Dear Dr. Jones,
Thank you for referring your patient, Mrs. A. Smith, for evaluation concerning a possible diagnosis of asthma. I found the patient’s history, as recounted in your office notes, to be complete and accurate.
The critical feature of her case is that Mrs. Smith, age 35, has been having “asthma attacks” since her early childhood. Her attacks are characterized by the relatively sudden onset of dyspnea; they are more frequent in the spring and fall, when they are often preceded by symptoms of rhino-conjunctivitis. If untreated, an attack will last for a few days, but if she is treated with a subcutaneous injection of adrenaline, as you have administered at your office, she often has relief from acute symptoms, and the attack may or may not recur. Recently, her attacks have been more frequent, and she does not feel that her breathing is improved to the point where she can carry out her responsibilities as a wife and mother.
Her mother carried a diagnosis of asthma, as do two of her children. She is currently not using any medications.
Her physical examination, at a time when she was not having acute asthmatic symptoms, showed normal body temperature, blood pressure, and pulse. She had no rashes. Her nasal passages were closely examined and showed inflammation and edema but no polyps. Her respirations were 24 and slightly labored. She had diminished tactile fremitus. Expiratory wheezing of modest profusion was audible in all lung fields. Her cardiac examination was normal. There was no clubbing, cyanosis, or edema.
I examined the radiograph of the chest that she brought with her, which was taken within the last month. It showed hyperinflation of the lungs, but there were no abnormal shadows; there were no findings that would suggest tuberculosis. Her cardiac silhouette did not show any abnormalities.
A blood smear was made, showing 14 per cent eosinophils; in a normal person this is most often less than 5 per cent. A sputum sample was also examined, and all the polymorphonuclear leukocytes observed were eosinophils. Specialized skin testing was performed. She had positive reactions to extracts of ragweed and horse dander.
Your diagnosis of asthma is correct. The episodes are characteristic, and there is no other likely cause suggested by her medical history or the physical examination and laboratory findings. In fact, the presence of eosinophils in the blood and sputum makes the diagnosis virtually certain. The positive skin tests make this case one of extrinsic asthma. Hypersensitivity to proteins is the likely physiological basis of asthma, although the exact mechanisms leading to sensitization are not clear.
Treatment is difficult. Your use of adrenaline injections for acute attacks is appropriate8; there is reason to believe that treatment with oral ephedrine may also help with her asthmatic episodes.9 The relief is of longer duration than with injected adrenaline and the patient can administer it herself. Ephedrine is not a substitute for injections of adrenaline when the patient is in extremis.
The critical factor in treatment is removing the patient from exposure to the proteins to which she is sensitive. Her positive skin test to ragweed pollen extract is in agreement with the clinical history of worsening disease in the autumn. However, there may be proteins to which she is allergic that were not included in our skin test panel. In my experience, removing a protein from a patient’s exposure is very hard to accomplish. One strategy, which I am loath to suggest unless there is no other hope, is a move to a climate where there are fewer proteins in the air to which the patient would be exposed.10
Comment: By 1928, the differential diagnosis of asthma was well established, and diagnostic techniques were available that made it possible to be reasonably certain that patients did not have heart disease or pneumonia when they were labeled as asthmatic.11 Physicians of the time often used the term “asthma” to refer to episodic dyspnea, but qualifiers such as “cardiac” were used. By 1928, eosinophils in the blood and sputum were known to be characteristic of asthma.12 Skin tests for allergies had been developed and were used clinically to help clinicians identify specific offending environmental proteins. The issues that plague us today — allergies to multiple allergens and difficulty in interpreting skin tests — were of concern to physicians in 1928.
There was not much available in the way of treatment. Ephedrine, an orally active sympathomimetic agent, had been discovered in China9 and used in asthma treatment, but other than allergen removal and adrenaline injections, there was little to offer patients with asthma beyond advising them to smoke “asthma cigarettes” (made from the leaves of D. stramonium [Figure 1Figure 1Asthma Cigarettes.]). Theophylline was available but was used as a diuretic; its value in the treatment of asthma had not yet been discovered. Aerosol inhalation therapy had not been widely adopted by 1928, but by the 1940s an inhaled formulation of epinephrine was marketed for asthma treatment (Figure 2Figure 2Personal Inhaler.).
E-Mail Message to Ms. Smith
Dear Ms. Smith,
Thank you for asking me to provide you with a direct personal consultation concerning your asthma and your asthma care. I will summarize the salient facts from the detailed written history and physician’s note you kindly provided.
As pointed out in your written history, you have had asthma since childhood. Among your earliest recollections is receiving injection treatments and later inhalation treatments for asthma in an emergency room. In your early teenage years you started treatment with inhaled Vanceril (beclomethasone), two puffs twice a day; 10 years ago, you switched to inhaled Qvar (beclomethasone driven by a hydrofluoroalkane [an ozone-layer–friendly] propellant), and Singulair (montelukast) was added to your regimen. Over the past 10 years, you have tried two different “combination inhalers,” containing both inhaled glucocorticoids and long-acting β2-agonists — namely, Advair (fluticasone propionate and salmeterol) and Symbicort (budesonide and formoterol fumarate dehydrate). These medications did not improve your symptoms or lung function as compared with inhaled beclomethasone alone, and you switched backed to Qvar.
Even with this regimen, however, your asthma symptoms are still present and bothersome. For example, two to three times a month you are awakened from your sleep between 3 a.m. and 4 a.m. by shortness of breath and cough; you can hear yourself wheeze. If you use your rescue albuterol inhaler, you are usually able to get back to sleep by 5 a.m.
Two years ago, skin tests were performed, and your total IgE level was measured. Your only positive skin tests were for house-dust mites and ragweed. Your total IgE level was 75 IU per milliliter. The allergist who did the testing suggested that you add a nonsedating antihistamine, such as loratadine, to your treatment during the times of year when you are most susceptible to symptoms; the loratadine was of some small help in controlling your runny nose, but there was no change in your asthma symptoms. Your allergist also referred you to a gastroenterologist, who performed 24-hour esophageal pH monitoring and found no abnormalities.
In the past decade, you have required treatment with oral prednisone on three occasions; the last instance was in 2009. Each of these exacerbations occurred during your allergy season. You have a peak-flow meter, which you use occasionally. Your best reading is 500 liters per minute; on most days, your peak-flow values are between 350 and 400 liters per minute.
You work in an office. You live with your husband and two children in a single-family home heated and air-conditioned with forced air. You have taken extensive measures to remove allergens from your home, including having the air ducts cleaned and tested for allergens. You have no pets. You have never smoked, and the same is true for your husband and your children. Smoking has not been allowed in your workplace for more than a decade. Your mother had asthma.
Your current medications are Qvar, 80 μg per puff, two puffs twice a day; Singulair, 10 mg per day, taken at night; and one multivitamin per day.
You would like a single consultation and confidential second opinion as to how your asthma has been managed and how to improve your asthma control.
On physical examination today, you looked well. Your weight was 135 lb [61.2 kg]. Your blood pressure was 110/75 mm Hg, and your pulse was 77 beats per minute according to the pulse oximeter, which also indicated that your hemoglobin saturation while you were breathing ambient air was 95%. Your physical examination was largely normal. No abnormalities were noted in your eyes, nose, or ears. Your chest examination was normal except for the presence of scattered expiratory wheezes, which were heard best during rapid, shallow breathing. There were no abnormalities in your extremities. Your neurologic examination was normal as well. Lung-function testing was performed in our laboratory; the results are attached to this letter (Figure 3Figure 3Spirometric Results for Ms. Smith.).
I think that the diagnosis of asthma is well established. You have a long history of asthma and have had salutary symptomatic responses to asthma treatments, your lung-function tests still show reversibility of airway obstruction of more than 15% with albuterol, and no other competing diagnosis has emerged over many years. The major issue now is to determine whether there are additional treatments that could help suppress your asthmatic symptoms without increasing the treatment burden.
You and your physicians have done an excellent job of managing your asthma. The treatments you are using now are well established and known to be effective. There are three treatments that could be added to your regimen, but it is difficult to be certain that they would be effective. First, oral theophylline could be added to your regimen. Although you cannot recall having received treatment with theophylline, given your age and asthma history, it is likely that you were treated with this agent as a child. This therapy could be of value, but it is necessary to monitor blood levels of the drug to obtain an optimum response, and some patients find testing to be burdensome. There is a small chance that theophylline could make your asthma worse by relaxing the muscle that separates your stomach from your esophagus; if this occurred, the treatment would be stopped.
Second, Singulair could be replaced with Zyflo CR (zileuton, controlled release). The active ingredient in Singulair is montelukast, which blocks the action of the cysteinyl leukotrienes at the CysLT1 receptor, whereas zileuton prevents the synthesis of both cysteinyl leukotrienes and dihydroxy leukotrienes. There are theoretical reasons to believe that controlled-release zileuton would yield a clinical benefit, but there are no compelling data to support this approach. Monitoring of liver function is required during initiation of treatment with zileuton.
Third, Xolair (omalizumab) could be added to your regimen. This anti-IgE monoclonal antibody is given once a month by injection. There is clearly an allergic component of your disease; your total IgE level is elevated, but it is not so high as to preclude the use of omalizumab.
As we discussed, I think your primary care physician has done an excellent job in designing your asthma treatment. You should discuss our consultation with her and decide what is in your best interest.
Comment: There have been three major changes in our understanding of asthma between 1928 and 2012. First, spirometry, which had been invented in the 1840s,13 was refined by adding time to volume output, and between the late 1940s and early 1950s, measurements made from forced exhalations were used in the diagnosis and treatment of asthma.14 Other lung-function tests were developed and used, and the relationships between clinical physiology and symptoms were delineated.15 Second, glucocorticoids were identified as an effective and useful asthma treatment. They were first used systemically in the early 1950s16 and were subsequently made available in inhaled form17,18,; these agents remain the standard of care today. Third, our understanding of the immunobiology of asthma progressed beyond the view that the essential mechanism was an immediate hypersensitivity reaction.19,20, Unfortunately, these advances in understanding the cell biology of asthma have not yet been translated into new therapies, although new therapies have been derived from our improved understanding of immediate hypersensitivity responses — notably, the use of leukotriene modifiers21 and anti-IgE antibodies.22
Our patient is current in her medical knowledge and is using medical information widely available on the Internet to help in the management of her chronic condition. The consultant used measures of lung function to quantify her physiological deficit. The consultant also measured the patient’s IgE level, which was consistent with allergic asthma, and provided the information needed for anti-IgE treatment, should the patient elect this approach. The patient has used all the standard asthma therapies but has residual symptoms. The consultant outlines other asthma treatments that the patient could try, highlighting the need to try different treatments to see whether one or another will work. Sadly, we still do not have a way to predict a given patient’s response to therapy.
These three case histories illustrate that asthma as a disease has not changed for two centuries. We have made real progress in identifying patients with asthma and in understanding its biologic basis and its treatment. Progress has also been made in diagnostic testing, which has been refined to measure lung function with great accuracy and repeatability. In addition, we can measure the lung’s responsiveness to triggering agents and thereby obtain objective indications of disease activity, in addition to the patient’s history. We have come to realize that allergic responses often substantially contribute to both chronic persistent asthma and acute exacerbations of asthma symptoms, although this association may have been overemphasized. The current focus is on immune responses in affected patients; we believe that airway inflammation plays a critical role in asthma, but the precise nature of that inflammation remains a mystery. The knowledge that asthma runs in families has become the basis for very sophisticated studies of the genetics of asthma, but not much of its heritability can be explained by all the genes identified to date. In spite of all the progress achieved over the past two centuries, we still do not understand the fundamental causes of asthma. Hence, we do not have therapies that address the underlying mechanisms; we have no cure for asthma. The medications at hand provide relief of symptoms and improve lung function and airway responsiveness, but they do not prevent exacerbations or progression of disease, and the most desirable accomplishment, the primary prevention of asthma, is a vision that has not yet become a reality.
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.
From the Division of Pneumology–Allergology, University Children’s Hospital, Munich, Germany (E.M.); and the Pulmonary Division, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston (J.M.D.).
Address reprint requests to Dr. von Mutius at Pneumologie and Allergologie, Dr. von Haunersches Kinderspital, Lindwurmstr. 4, D-80337 Munich, Germany.
NEJM telah melaporkan hasil uji klinik vaksin antimalaria. Berita selengkapnya sebagai berikut:
A Field Trial to Assess a Blood-Stage Malaria Vaccine
Mahamadou A. Thera, M.D., M.P.H., Ogobara K. Doumbo, M.D., Ph.D., Drissa Coulibaly, M.D., Matthew B. Laurens, M.D., M.P.H., Amed Ouattara, Pharm.D., Abdoulaye K. Kone, M.D., Ando B. Guindo, M.D., Karim Traore, M.D., Idrissa Traore, M.D., Bourema Kouriba, Pharm.D., Ph.D., Dapa A. Diallo, M.D., Issa Diarra, Pharm.D., Modibo Daou, Pharm.D., Amagana Dolo, Pharm.D., Ph.D., Youssouf Tolo, Pharm.D., Mahamadou S. Sissoko, M.D., M.S.P.H., Amadou Niangaly, Pharm.D., Mady Sissoko, Pharm.D., Shannon Takala-Harrison, Ph.D., Kirsten E. Lyke, M.D., Yukun Wu, Ph.D., William C. Blackwelder, Ph.D., Olivier Godeaux, M.D., Johan Vekemans, M.D., Ph.D., Marie-Claude Dubois, M.Sc., W. Ripley Ballou, M.D., Joe Cohen, Ph.D., Darby Thompson, M.S., Tina Dube, Ph.D., Lorraine Soisson, Ph.D., Carter L. Diggs, M.D., Ph.D., Brent House, Ph.D., David E. Lanar, Ph.D., Sheetij Dutta, Ph.D., D. Gray Heppner, Jr., M.D., and Christopher V. Plowe, M.D., M.P.H.
N Engl J Med 2011; 365:1004-1013September 15, 2011
Blood-stage malaria vaccines are intended to prevent clinical disease. The malaria vaccine FMP2.1/AS02A, a recombinant protein based on apical membrane antigen 1 (AMA1) from the 3D7 strain of Plasmodium falciparum, has previously been shown to have immunogenicity and acceptable safety in Malian adults and children.
Full Text of Background…
In a double-blind, randomized trial, we immunized 400 Malian children with either the malaria vaccine or a control (rabies) vaccine and followed them for 6 months. The primary end point was clinical malaria, defined as fever and at least 2500 parasites per cubic millimeter of blood. A secondary end point was clinical malaria caused by parasites with the AMA1 DNA sequence found in the vaccine strain.
Full Text of Methods…
The cumulative incidence of the primary end point was 48.4% in the malaria-vaccine group and 54.4% in the control group; efficacy against the primary end point was 17.4% (hazard ratio for the primary end point, 0.83; 95% confidence interval [CI], 0.63 to 1.09; P=0.18). Efficacy against the first and subsequent episodes of clinical malaria, as defined on the basis of various parasite-density thresholds, was approximately 20%. Efficacy against clinical malaria caused by parasites with AMA1 corresponding to that of the vaccine strain was 64.3% (hazard ratio, 0.36; 95% CI, 0.08 to 0.86; P=0.03). Local reactions and fever after vaccination were more frequent with the malaria vaccine.
Full Text of Results…
On the basis of the primary end point, the malaria vaccine did not provide significant protection against clinical malaria, but on the basis of secondary results, it may have strain-specific efficacy. If this finding is confirmed, AMA1 might be useful in a multicomponent malaria vaccine. (Funded by the National Institute of Allergy and Infectious Diseases and others; ClinicalTrials.gov number, NCT00460525.)
Non valvular atrial fibrilasis merupakan salah satu faktor risiko stroke iskemia dan embolisme pada pembuluh darah. Selama ini warfarin merupakan salah satu obat pilihan untuk pencegahan strok iskemia maupun pembentukan emboli pada pasien dengan fibrilasis termasuk pasien dengan nonvalvular atrial fibrilasis. Hasil Uji klinis untuk membandingkan kemanjuran rivaroxaban dengan warfarin pada nonvalvular atrial fibrilasis telah dilaporkan oleh NEJM.
Rivaroxaban versus Warfarin in Nonvalvular Atrial Fibrillation
Manesh R. Patel, M.D., Kenneth W. Mahaffey, M.D., Jyotsna Garg, M.S., Guohua Pan, Ph.D., Daniel E. Singer, M.D., Werner Hacke, M.D., Ph.D., Günter Breithardt, M.D., Jonathan L. Halperin, M.D., Graeme J. Hankey, M.D., Jonathan P. Piccini, M.D., Richard C. Becker, M.D., Christopher C. Nessel, M.D., John F. Paolini, M.D., Ph.D., Scott D. Berkowitz, M.D., Keith A.A. Fox, M.B., Ch.B., Robert M. Califf, M.D., and the ROCKET AF Steering Committee for the ROCKET AF Investigators
N Engl J Med 2011; 365:883-891September 8, 2011
- Citing Articles (1)
- Comments (3)
The use of warfarin reduces the rate of ischemic stroke in patients with atrial fibrillation but requires frequent monitoring and dose adjustment. Rivaroxaban, an oral factor Xa inhibitor, may provide more consistent and predictable anticoagulation than warfarin.
In a double-blind trial, we randomly assigned 14,264 patients with nonvalvular atrial fibrillation who were at increased risk for stroke to receive either rivaroxaban (at a daily dose of 20 mg) or dose-adjusted warfarin. The per-protocol, as-treated primary analysis was designed to determine whether rivaroxaban was noninferior to warfarin for the primary end point of stroke or systemic embolism.
In the primary analysis, the primary end point occurred in 188 patients in the rivaroxaban group (1.7% per year) and in 241 in the warfarin group (2.2% per year) (hazard ratio in the rivaroxaban group, 0.79; 95% confidence interval [CI], 0.66 to 0.96; P<0.001 for noninferiority). In the intention-to-treat analysis, the primary end point occurred in 269 patients in the rivaroxaban group (2.1% per year) and in 306 patients in the warfarin group (2.4% per year) (hazard ratio, 0.88; 95% CI, 0.74 to 1.03; P<0.001 for noninferiority; P=0.12 for superiority). Major and nonmajor clinically relevant bleeding occurred in 1475 patients in the rivaroxaban group (14.9% per year) and in 1449 in the warfarin group (14.5% per year) (hazard ratio, 1.03; 95% CI, 0.96 to 1.11; P=0.44), with significant reductions in intracranial hemorrhage (0.5% vs. 0.7%, P=0.02) and fatal bleeding (0.2% vs. 0.5%, P=0.003) in the rivaroxaban group.
In patients with atrial fibrillation, rivaroxaban was noninferior to warfarin for the prevention of stroke or systemic embolism. There was no significant between-group difference in the risk of major bleeding, although intracranial and fatal bleeding occurred less frequently in the rivaroxaban group. (Funded by Johnson & Johnson and Bayer; ROCKET AF ClinicalTrials.gov number, NCT00403767.)
Telah dilakukan penelitian untuk menilai kemanjuran antara operasi angioplasti dan pemasangan stanting dengan terapi obat pada pasien dengan stenosis arteri intracranial. NEJM edisi Minggu I septem ber 2011 telah melaporkan bahwa terapi obat pada pasien dengan stenosis arteri intracranial lebih menguntungkan jika dibandingkan dengan operasi angioplasti dan pemasangan stenting. Tidak dapat dipungkiri bahwa stenosis arteri intracranial merupakan faktor risiko utama kejadian stroke dan sering berakibat fatal. Makalah selengkapnya silakan baca di:
Stenting versus Aggressive Medical Therapy for Intracranial Arterial Stenosis
Marc I. Chimowitz, M.B., Ch.B., Michael J. Lynn, M.S., Colin P. Derdeyn, M.D., Tanya N. Turan, M.D., David Fiorella, M.D., Ph.D., Bethany F. Lane, R.N., L. Scott Janis, Ph.D., Helmi L. Lutsep, M.D., Stanley L. Barnwell, M.D., Ph.D., Michael F. Waters, M.D., Ph.D., Brian L. Hoh, M.D., J. Maurice Hourihane, M.D., Elad I. Levy, M.D., Andrei V. Alexandrov, M.D., Mark R. Harrigan, M.D., David Chiu, M.D., Richard P. Klucznik, M.D., Joni M. Clark, M.D., Cameron G. McDougall, M.D., Mark D. Johnson, M.D., G. Lee Pride, Jr., M.D., Michel T. Torbey, M.D., M.P.H., Osama O. Zaidat, M.D., Zoran Rumboldt, M.D., and Harry J. Cloft, M.D., Ph.D. for the SAMMPRIS Trial Investigators
September 7, 2011 (10.1056/NEJMoa1105335)
Comments open through September 21, 2011
Atherosclerotic intracranial arterial stenosis is an important cause of stroke that is increasingly being treated with percutaneous transluminal angioplasty and stenting (PTAS) to prevent recurrent stroke. However, PTAS has not been compared with medical management in a randomized trial.
We randomly assigned patients who had a recent transient ischemic attack or stroke attributed to stenosis of 70 to 99% of the diameter of a major intracranial artery to aggressive medical management alone or aggressive medical management plus PTAS with the use of the Wingspan stent system. The primary end point was stroke or death within 30 days after enrollment or after a revascularization procedure for the qualifying lesion during the follow-up period or stroke in the territory of the qualifying artery beyond 30 days.
Enrollment was stopped after 451 patients underwent randomization, because the 30-day rate of stroke or death was 14.7% in the PTAS group (nonfatal stroke, 12.5%; fatal stroke, 2.2%) and 5.8% in the medical-management group (nonfatal stroke, 5.3%; non–stroke-related death, 0.4%) (P=0.002). Beyond 30 days, stroke in the same territory occurred in 13 patients in each group. Currently, the mean duration of follow-up, which is ongoing, is 11.9 months. The probability of the occurrence of a primary end-point event over time differed significantly between the two treatment groups (P=0.009), with 1-year rates of the primary end point of 20.0% in the PTAS group and 12.2% in the medical-management group.
BNP singkatan dari B type natriuretic peptide sering di sebut juga sebagai brain type natriuretic peptide. BNP merupakan peptida yang dihasilkan oleh tubuh kita, yaitu sel otot ventrikel jantung. Saat ini BNP menjadi penting oleh karena dapat menjadi indikator atau marker, dalam bahasa kito=petanda, yang akan mengarah pada adanya kelainan antara lain untuk kondisi yang mengarah kepada gagal jantung. Marker BNP ini lebih peka, artinya sebelum munculnya kelainan klinik, yaitu meskipun belum memunculkan keluhan ke arah gagal jantung, tetapi keberadaan BNP yang berlebihan telah menunjukkan kondisi jantung yang sedang kepayahan. Dengan memantau kadar BNP dapat memantau kebugaran jantung dan mengantisipasi akan terjadinya gagal jantung yang lebih berat. Cerita selengkapnya tentang BNP silakan baca artikel berikut:
BNP (B-TYPE NATRIURETIC PEPTIDE)
BNP (B-type natriuretic peptide) is a cardiac neurohormone secreted from cardiac ventricular myocyte in response to increased ventricular wall stretch or wall tension, increased ventricular volume or pressure. It is a potent vasodilator and it promotes diuresis. The half-live is short, about 18-22 minutes.
- Circulating BNP level increases in proportion to the severity of heart failure.
- Conditions that raise BNP level beside heart failure
- Age, sex (female), left ventricular hypertrophy, acute coronary syndrome, acute myocardial infarction, cardiac inflammation, arrhythmogenic RV with decrease ejection, primary pulmonary hypertension, worsening of corpulmonale with increased RV pressure and volume, acute pulmonary emboli, Kawasaki disease, advanced renal failure, cirrhosis, hyperaldosteronism, Cushing syndrome, and decreased clearance.
- Heart failure conditions that may have low BNP
- Flash pulmonary edema within 1 hour, acute chordal rupture, pulmonary congestion-edema from mitral stenosis, severe end stage heart failure, and heart failure in obese patients (BMI>30 kg/m2).
Potential usefulness are:
1. Diagnosis for HF
- Utilization of BNP level to help differentiate heart failure from other causes of dyspnea in ER or urgent care setting, using Point of Care measurement technique. BNP level over 100 pg/ml favors the diagnosis of heart failure. The range of BNP level in most heart failure patients is from a few hundreds to >1000 pg/ml. BNP should not be a stand alone test. Clinical judgment is always important, Elevated BNP are seen in other conditions (Table 1). Low BNP may be found in few acute heart failure conditions and in obese patients with heart failure.
Table 1. Common causes of BNP elevation in routine clinical practice
Renal failure (Cr >2) or on dialysis
Acute coronary syndrome
Pulmonary disease with right-side failure
Acute pulmonary embolism
Baseline left ventricular dysfunction
Utilization of BNP level as a diagnostic tool for heart failure with preserved systolic function. A heart failure patient with normal echocardiographic LV systolic function, abnormal diastolic filling abnormalities and elevated BNP should favor this diagnosis.
2. Follow up and Prognosis of heart failure
- During inpatient treatment of heart failure. Rising of the discharged BNP level from the admission level is a good predictor of poor prognosis and near future unfavorable outcome i.e… early readmission.
- During outpatient treatment followup, BNP guiding intensity of treatment may be useful.
- During acute MI, rising of BNP level few days after admission level indicates poorer prognosis
- Baseline BNP is necessary for comparison.
3. Treatment for acute decompensation
- Nesiritide (Natrecor) is a human recombinant BNP.
- Dosage: Intravenous 2 microgram/kg bolus, followed by infusion of 0.01 microgram/kg/min
- Duration: Up to 7 days (or more?).
- Action: Hemodynamic effect is observed in an hour or less. There is no tolerance for several days of infusion. Hemodynamic effect resolves by 2-4 hours after cessation of the infusion.
- Nesiritide promotes diuresis.
- Use appropriate dose of diuretic. Over diuresing may potentiate hypotension side effect.
- Side effects: Hypotension (more in cases taking ACEI), nausea, headache.
- Caution: Volume depletion, aortic stenosis, hypertrophic cardiomyopathy, cardiogenic shock.
- Usually does not require hemodynamic monitoring.
- Beware of drug incompatibility in the infusion process.
- May obtain proBNP but not BNP level during nesiritide infusion.
- In the responder cases, if the BNP level is checked 2 hours (BNP five halve life time) after stopping the infusion it should be lower than the preinfusion level.
4. Potential outpatient intermittent treatment in severe heart failure
(Waiting for FUSION 2 trial)
5. NT-proBNP (NT = N Terminal)
When cardiac myocyte Pro-BNP enter the circulation it split into BNP which is an active neurohormone and NT-proBNP which is inactive part but with longer half life. Level of NT-proBNP can be used for diagnosis, follow up and prognosis of heart failure the same way as BNP level. The physicians need to know whether the report are BNP or NT-proBNP since the level are significantly different and some laboratory may not label it correctly.
FDA memberikan layanan kusus tentang perkembangan terkini kejadian medication error. Kejadian medication error yang masih tinggi di masyarakat telah menjadi isue utama pada sistem layanan kesehatan dan menjadi keprihatinan para pengambil kebijakan bidang kesehatan di dunia. Gambaran global tentang layanan informasi medication error dari FDA adalah sebagai berikut:
- Medication Errors Reports and Articles
- Campaign to Eliminate Use of Error-Prone Abbreviations
- Name Differentiation Project
- Federal Regulations and Guidances
- How to Report a Medication Error
- Other Resources
- Drug Products Associated with Medication Errors
FDA receives medication error reports on marketed human drugs (including prescription drugs, generic drugs, and over-the-counter drugs) and nonvaccine biological products and devices. The National Coordinating Council for Medication Error Reporting and Prevention defines a medication error as “any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care professional, patient, or consumer. Such events may be related to professional practice, health care products, procedures, and systems, including prescribing; order communication; product labeling, packaging, and nomenclature; compounding; dispensing; distribution; administration; education; monitoring; and use.”
The American Hospital Association lists the following as some common types of medication errors:
- incomplete patient information (not knowing about patients’ allergies, other medicines they are taking, previous diagnoses, and lab results, for example);
- unavailable drug information (such as lack of up-to-date warnings);
- miscommunication of drug orders, which can involve poor handwriting, confusion between drugs with similar names, misuse of zeroes and decimal points, confusion of metric and other dosing units, and inappropriate abbreviations;
- lack of appropriate labeling as a drug is prepared and repackaged into smaller units; and
- environmental factors, such as lighting, heat, noise, and interruptions, that can distract health professionals from their medical tasks.
In 1992, the FDA began monitoring medication error reports that are forwarded to FDA from the United States Pharmacopeia (USP) and the Institute for Safe Medication Practices (ISMP). The Agency also reviews MedWatch reports for possible medication errors. Currently, medication errors are reported to the FDA as manufacturer reports (adverse events resulting in serious injury and for which a medication error may be a component), direct contact reports (MedWatch), or reports from USP or ISMP.
The Division of Medication Errors and Technical Support includes a medication error prevention program staffed with pharmacists and support personnel. Among their many duties, program staff review medication error reports sent to the USP Medication Errors Reporting Program and MedWatch, evaluate causality, and analyze the data to provide feedback to others at FDA.
FDA and the Institute for Safe Medication Practices (ISMP) have launched a national education campaign to eliminate the use of ambiguous medical abbreviations that are frequently misinterpreted and lead to mistakes that result in patient harm. The campaign seeks to promote safe practices among those who communicate medical information.
As part of the campaign, FDA recommends that healthcare professionals consider ISMP’s List of Error-Prone Abbreviations, Symbols, and Dose Designations [external link] whenever medical information is communicated. In addition, FDA and ISMP have provided a toolkit of resource materials available at ISMP and FDA Campaign to Eliminate Use of Error-Prone Abbreviations. [external link]
- FDA proposes bar codes for drugs, blood; new adverse reaction reporting.
- FDA Public Meeting On Bar Code Labeling For Drugs. Remarks by Lester M. Crawford, Jr., D.V.M., Ph.D.
- Guidance for Hospitals, Nursing Homes, and Other Health Care Facilities – FDA Public Health Advisory. (Issued and Posted 4/5/2001). This guidance is intended to alert hospitals, nursing homes, and other health care facilities to the hazards of medical gas mix-ups.
Flyer on FDA Public Health Advisory: Medical Gas Mix-Ups Can Cause Death and Serious Injury(Posted 10/10/2001). This one-page, color flier is intended to alert people who handle medical gases about the hazards of mix-ups. Please feel free to copy and distribute this flier. Comments and suggestions are welcome.
Drug Topics FDA Safety Pages
FDA Patient Safety News. FDA Patient Safety News is a televised series for health care professionals, aimed at hospitals and other medical facilities across the country. It features information on new drugs, biologics, and devices, on FDA safety notifications and product recalls, and on ways to protect patients when using medical products.
Healthfinder: Medical Errors. Links to specific resources and organizations on medication errors.
Quality Interagency Committee (QuIC) Task Force. The QuIC Task Force was established in response to the final report of the President’s Advisory Commission on Consumer Protection and Quality in the Health Care Industry. In response to the Institute of Medicine’s report on medication errors, QuIC issued a report called Doing What Counts for Patient Safety: Federal Actions to Reduce Medical Errors and Their Impact
Medication Errors Information from FDA
- FDA Drug Safety Communication: Medication errors resulting from confusion between risperidone (Risperdal) and ropinirole (Requip)
- FDA Drug Safety Communication: Serious medication errors from intravenous administration of nimodipine oral capsules
- FDA Drug Safety Communication: Product Confusion with Maalox Total Relief and Maalox Liquid Products
- Edetate Disodium Mix-ups between Insulin and Heparin
- FDA Patient Safety News (PSN):
- Elan Pharmaceuticals issued a “Dear Healthcare Professional” October 6, 2003 reporting serious adverse events and deaths resulting from accidental overdose of high concentration morphine sulfate oral solutions. MedWatch Safety Information
- FDA and UCB Pharma advised healthcare professionals of the risk of dispensing errors between KEPPRA (levetiracetam), an antiepileptic, and KALETRA (lopinavir/ritonavir), an antiretroviral.
- FDA, Janssen Pharmaceutical Products, and Johnson & Johnson Pharmaceutical Research & Development notify healthcare professionals of reports of medication errors involving confusion between Reminyl and Amaryl (glimepiride). MedWatch Safety Information
- Medication errors associated with flomax and volmax
- Medication errors associated with zantac and zyrtec
Medication Safety Information from Drug Topics FDA Safety Page
- A look at delayed- vs. extended-release Rxs (PDF – 83KB)
- Drug errors associated with Maalox (PDF – 103KB)
- Bextra: Valdecoxib or bucindolol? (PDF – 86KB)
- Curbing med errors involving Anzemet, Bentyl (PDF – 58KB)
- Confusion between methylphenidate and methadone (PDF – 58KB)
- Drug errors associated with opium tincture and paregoric (PDF – 193KB)
- Drug errors involving Keppra and Kaletra (PDF – 201KB)
- Fatal medication errors associated with Temodar (PDF – 91KB)
- Kaopectate reformulation and upcoming label change (PDF – 194KB)
- Drug Topics: Misadministration of capsules for inhalation (PDF – 75KB)
- Transdermal patches: High risk for error? (PDF – 52KB)
Medication Safety Alerts from Institute for Safe Medication Practices
- Human Drug Information
- (888) 463-6332
- (301) 796-3400
Division of Drug Information (CDER)
Office of Communications
10001 New Hampshire Avenue
Hillandale Building, 4th Floor
Silver Spring, MD 20993
Page Last Updated: 06/17/2011
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Keberadaan dan peran dokter dalam layanan kesehatan di masyarakat sudah menjadi keniscayaan. Sejak jaman Yunan sampai jaman modern saat ini, peran dokter dalam sistem layanan kesehatan di masyarakat tidak sedikit. Dalam islam keberadaan dokter maupun profesi kesehatan lainnya agar terselenggara sistem layanan kesehatan yang efektif dan efisien serta mampu meningkatkan derajat kesehatan masyarakat termasuk dalam hukum fardu kifayah. Bagaimana seharusnya menjadi dokter yang sesuai tuntutan jaman tetapi juga sesuai tuntunan etika ternyata tidaklah mudah. Artikel berikut memberikan gambaran bagaimana seharusnya seorang dokter di jaman modern.
The Doctor’s Dilemma — What Is “Appropriate” Care?
Victor R. Fuchs, Ph.D.
Most physicians want to deliver “appropriate” care. Most want to practice “ethically.” But the transformation of a small-scale professional service into a technologically complex sector that consumes more than 17% of the nation’s gross domestic product makes it increasingly difficult to know what is “appropriate” and what is “ethical.” When escalating health care expenditures threaten the solvency of the federal government and the viability of the U.S. economy, physicians are forced to reexamine the choices they make in caring for patients.
In an effort to address this issue, physicians’ organizations representing more than half of all U.S. physicians have endorsed a “Physician Charter” that commits doctors to “medical professionalism in the new millennium.” The charter states three fundamental principles, the first of which is the “primacy of patient welfare.” It also sets out 10 “commitments,” one of which states that “while meeting the needs of individual patients, physicians are required to provide health care that is based on the wise and cost-effective management of limited clinical resources.” How can a commitment to cost-effective care be reconciled with a fundamental principle of primacy of patient welfare?
The dilemma arises for two main reasons. First, recent decades have witnessed a flood of new, expensive medical technologies (drugs, imaging devices, surgical procedures) that are of varying degrees of value to patients. A few are true breakthroughs, with strong favorable effects on mortality and morbidity. Others make a meager contribution, at best, to health outcomes. Moreover, technologies that may provide high value for carefully selected patients are often used indiscriminately for a much larger cohort of patients. Second, health insurance, private or public, has become so widespread that 90% of the country’s health care bill is paid by third parties, not by the patient receiving the service.
What is a conscientious physician to do? Some new cancer drugs cost thousands of dollars per month for a single patient. The bills for many surgical procedures run to five or even six figures. Noninvasive imaging devices can offer information to assist in diagnosis, at a cumulative cost in the billions of dollars. U.S. patients, on average, get almost three times as many magnetic resonance imaging scans as Canadian patients; there is no evidence that this large differential can be explained by national differences in the medical condition of patients or that it results in significant national differences in health outcomes. So what level of utilization deserves to be called “appropriate”?
If insurance were not widespread, many physicians would be reluctant to order an expensive intervention unless it offered a good chance of substantial benefit — that is, unless it was cost-effective. Indeed, without U.S.-style cost-insensitive insurance, many expensive diagnostic and therapeutic innovations would not be developed and brought to market.1 The insured patient, on the other hand, will usually want any and all care that might possibly be of net benefit, regardless of cost. The physician may recognize that the intervention under consideration is not cost-effective but may recommend it anyway, for a variety of reasons: to keep the goodwill of the patient, to protect against a malpractice suit, or in the belief that the “primacy of patient welfare” makes the denial of such care “inappropriate” and “unethical.”
The doctor’s dilemma is the nation’s problem. Some policy experts think that if patients had “more skin in the game” — that is, had less insurance — the problem would be solved. It would not. Even the most ardent advocates of deductibles and copayments acknowledge the need for an annual cap on patients’ payments, beyond which insurance takes over completely. There is no consensus on the right level for the cap, but it is generally recognized that the average U.S. household, with large debts and minimal financial assets, could not handle much more than $5,000. But the extreme skew in annual health care expenditures, with 5% of individuals accounting for 50% of spending in any given year, means that many health care decisions, and especially those involving big-ticket interventions, will be made by and for patients whose costs have exceeded the cap.
Another popular “solution” is to eliminate care that does more harm than good — that is, “unnecessary” care. Such elimination would be desirable, but the potential savings from this source are smaller than is usually claimed. It is true that after the fact, many interventions turn out to be useless or even harmful for some patients. But the heterogeneity of patient populations and uncertainty about the response of individual patients to an intervention means that it is often difficult or impossible to determine in advance which ones will prove to help particular patients and which will turn out to have been unnecessary.
There is no escaping the fact that many interventions are valuable for some patients even if, for the population as a whole, their cost is greater than their benefit. Under what circumstances are they likely to be ordered, and when are they likely to be withheld? The context within which the physician practices, his or her assumption about the behavior of other physicians, and the economic and health consequences of ordering all the care that might do some good versus practicing cost-effective medicine will affect the physician’s choice. If the physician is paid on a fee-for-service basis and the patient has open-ended insurance, the scales are tipped in favor of doing as much as possible and against limiting interventions to those that are cost-effective. In that setting, who would benefit from the resources that are saved by practicing cost-effective medicine is not obvious to the physician.
In contrast, if the physician is practicing in a setting that has accepted responsibility for the health of a defined population and the organization receives an annual fee per enrollee, the chances of the physician’s practicing cost-effective medicine are substantially increased, even though all patients are insured. The physician’s colleagues are practicing the same way, and the resources saved can be used for the benefit of the defined population, which includes the physician’s patient. In Canada, which has universal insurance, per capita spending on health care is only 55% of the U.S. level because there is a limited overall budget, and all physicians in the system recognize the need for prudence in making decisions about care.
In short, when physicians are collectively caring for a defined population within a fixed annual budget, it is easier for the individual physician to resolve the dilemma in favor of cost-effective medicine. That becomes “appropriate” care. And it is an ethical choice, as defined by philosopher Immanuel Kant, because if all physicians act the same way, all patients benefit.2
Disclosure forms provided by the author are available with the full text of this article at NEJM.org.
From Stanford University, Stanford, CA.
- Weisbrod B. The health care quadrilemma: an essay on technological change, insurance, quality of care, and cost containment. J Econ Lit 1991;29:523-552Web of Science
- Kant I. Critique of practical reason and other writings in moral philosophy. Beck LW, trans. Chicago: University of Chicago Press, 1949.
Era baru sistem administrasi kesehatan. Perkembangan IT/TI telah merasuki seluruh sendi kehidupan dan secara masife merubah cara hidup manusia termasuk pada cara bagaimana meningkatkan derajat kesehatan masyarakat. Salah satu bagian dari proses perubahan dalam layanan administrasi oleh adanya TI adalah layanan administrasi kesehatan. Laporan berikut menunjukkan adanya arus besar menuju perubahan yang mendasar pada sistem administrasi layanan kesehatan.
Electronic Health Records and Quality of Diabetes Care
Randall D. Cebul, M.D., Thomas E. Love, Ph.D., Anil K. Jain, M.D., and Christopher J. Hebert, M.D.
Incentives to increase adoption and meaningful use of electronic health records (EHRs) anticipate a quality-related financial return.1,2 However, empirical data showing either quality improvement or cost savings from EHR adoption are scarce. Available studies have shown few quality-related advantages of current EHR systems over traditional paper-based medical-record systems.1-5 Projected cost savings are mostly based on models with largely unsupported assumptions about adherence to and the effect of fully functional EHR systems.6,7 Data are particularly scarce on EHR adoption by “priority primary care providers” — health care professionals practicing in small groups and those serving vulnerable populations, as such providers are defined in the Health Information Technology for Economic and Clinical Health (HITECH) Act.8 EHR adoption by such providers is supported by the national network of Health Information Technology Regional Extension Centers.
Innovations in care delivery as specified in the Affordable Care Act, such as accountable care organizations and patient-centered medical homes (PCMHs), also provide incentives for using information most easily obtained through EHR systems.9,10 Data regarding the benefits of PCMHs have come largely from reports by EHR-based organizations,11-13 and these data support the posited links among EHR use, quality improvement, and cost savings. However, these reports did not compare EHR and paper-based systems.
Regional quality-improvement initiatives, such as those supported by the Robert Wood Johnson Foundation’s Aligning Forces for Quality (AF4Q) program,14 by Medicare and state Medicaid initiatives,15,16 and by multistakeholder collaboratives,17 provide an opportunity to evaluate the effectiveness of EHRs and refinements in national payment policy.15,18 In greater Cleveland, one of 16 AF4Q sites nationwide, diverse EHR-based and paper-based ambulatory practices publicly report on the quality and outcomes of care for patients with chronic medical conditions. Regional achievement of diabetes-related standards has been reported six times to date. The reported data come from practices with high concentrations of priority primary care providers and allow a comparison of quality standards for EHRs and paper records, after adjustment for important patient-level attributes. We examined the independent association of EHR use with achievement of quality standards for the care of patients with diabetes.
We analyzed data from a retrospective cohort of primary care practices of seven diverse health care organizations that publicly reported achievement of quality standards for adults with diabetes between July 2007 and June 2010. Data reported here include the most recent yearlong cross section (July 2009 through June 2010) as well as practice-level trends across three years of reports.
Setting and Subjects
The primary care practice partners of Better Health Greater Cleveland (hereafter referred to as Better Health) are responsible for the majority of medical care for people with chronic disease in Cuyahoga County, an urban area in northeastern Ohio with 1.3 million residents; the county includes Cleveland, one of the nation’s poorest large cities, and its affluent suburbs. Participating practices include 21 sites of large not-for-profit health care organizations, 1 of which serves many vulnerable (“safety net”) patients; 12 sites of a large safety-net public hospital system; 1 safety-net practice of a university hospital; and the safety-net practices of all 3 of the county’s federally qualified health centers. Since the program’s inception in 2007, reporting primary care providers have included physicians in general internal medicine, family practice, and medicine–pediatrics. In July 2009, nurse practitioners and other health care professionals with prescription-writing privileges were added to the list of reporting providers. Patients include all adults (18 to 75 years of age) with diabetes who made at least two visits to the same primary care practice during each yearlong measurement interval.
Care and Outcome Standards
Better Health’s Clinical Advisory Committee approved nine quality standards for diabetes, including four standards of care and five standards of intermediate outcomes. Care standards are reported by standard and as an all-or-none composite19; outcome standards are reported by standard and as a composite indicating achievement of at least four of the five standards. Care standards include receipt of a glycated hemoglobin value, testing for urinary microalbumin or prescription of an angiotensin-converting–enzyme inhibitor or an angiotensin-receptor blocker, an eye examination to screen for diabetic retinopathy, and administration of a pneumococcal vaccination. Intermediate-outcome standards include a glycated hemoglobin value below 8%, a blood pressure below 140/80 mm Hg, a low-density lipoprotein (LDL) cholesterol value below 100 mg per deciliter or documented prescription for a statin medication, a body-mass index (the weight in kilograms divided by the square of the height in meters) below 30, and nonsmoking status. All care and outcome standards pertain to the most recent result documented in the measurement interval, except pneumococcal vaccination (administration at any time is sufficient for meeting this standard).
Patient information was collected regarding several sociodemographic variables, including insurance type (Medicare, commercial, Medicaid, or uninsured), race or ethnic group (white, black, Hispanic, or other), age, sex, estimated household income, and educational level, all prespecified for our analyses. Insurance type is the primary insurance reported during the most recent doctor’s visit. Data on race or ethnic group were primarily obtained through self-report. Household income and educational level were estimated by linking each patient’s home address to Census 2000 summaries.
Data Collection and Study Oversight
Clinical practices or health care organizations submitted a unique study code for each patient and health care provider to Better Health’s Data Management Center. EHR-based organizations provided data on all eligible patients. Data from paper-based organizations were gathered by centrally trained chart abstractors for a random sample of patients selected by the Data Management Center. More than 95% of patients in the sample had charts available for review. Each site reviewed summary results for accuracy before publicly reporting data. The MetroHealth System’s Human Privacy Board approved data collection and submission protocols.
The collaborative supports three types of quality-improvement assistance. First, partner sites receive comparisons with other practices in their organization and regionwide for case mix, achievement of Better Health’s standards, and quality improvement. Practice directors can identify data regarding specific providers. Public reports highlight the top 10% of practice sites with respect to achievement of standards or improvement, by insurance category and overall. Second, Better Health sponsors semiannual daylong summits featuring national speakers and sharing of best practices in quality improvement and management of reported chronic conditions. Third, since mid-2009, all practices have had the opportunity to receive program-sponsored practice coaching. Coaching has principally focused on culture change, workflow redesign, and quality-improvement projects related to specific metrics.
Apixaban sebagai inhibitor faktor Xa diduga dapat mencegah serangan ulang jantung iskemia jika ditambahkan pada antiplatelet. Proyek penelitian APPRAISE yang melibatkan lebih dari 7000 relawan, bertujuan untuk mengetahui kemanjuran penambahan apixaban pada terapi standar antiplatelet untuk mencegah serangan ulang pada pasien dengan acute coronary syndroma. Hasil penelitian selengkapnya dapat dibaca di NEJM:
Apixaban with Antiplatelet Therapy after Acute Coronary Syndrome
John H. Alexander, M.D., M.H.S., Renato D. Lopes, M.D., Ph.D., Stefan James, M.D., Ph.D., Rakhi Kilaru, M.S., Yaohua He, M.D., Ph.D., Puneet Mohan, M.D., Ph.D., Deepak L. Bhatt, M.D., M.P.H., Shaun Goodman, M.D., Freek W. Verheugt, M.D., Ph.D., Marcus Flather, M.D., Kurt Huber, M.D., Danny Liaw, M.D., Ph.D., Steen E. Husted, M.D., Jose Lopez-Sendon, M.D., Raffaele De Caterina, M.D., Petr Jansky, M.D., Harald Darius, M.D., Dragos Vinereanu, M.D., Jan H. Cornel, M.D., Frank Cools, M.D., Dan Atar, M.D., Jose Luis Leiva-Pons, M.D., Matyas Keltai, M.D., Hisao Ogawa, M.D., Ph.D., Prem Pais, M.D., Alexander Parkhomenko, M.D., Witold Ruzyllo, M.D., Rafael Diaz, M.D., Harvey White, M.D., Mikhail Ruda, M.D., Margarida Geraldes, Ph.D., Jack Lawrence, M.D., Robert A. Harrington, M.D., and Lars Wallentin, M.D., Ph.D. for the APPRAISE-2 Investigators
N Engl J Med 2011; 365:699-708August 25, 2011
Apixaban, an oral, direct factor Xa inhibitor, may reduce the risk of recurrent ischemic events when added to antiplatelet therapy after an acute coronary syndrome.
We conducted a randomized, double-blind, placebo-controlled clinical trial comparing apixaban, at a dose of 5 mg twice daily, with placebo, in addition to standard antiplatelet therapy, in patients with a recent acute coronary syndrome and at least two additional risk factors for recurrent ischemic events.
The trial was terminated prematurely after recruitment of 7392 patients because of an increase in major bleeding events with apixaban in the absence of a counterbalancing reduction in recurrent ischemic events. With a median follow-up of 241 days, the primary outcome of cardiovascular death, myocardial infarction, or ischemic stroke occurred in 279 of the 3705 patients (7.5%) assigned to apixaban (13.2 events per 100 patient-years) and in 293 of the 3687 patients (7.9%) assigned to placebo (14.0 events per 100 patient-years) (hazard ratio with apixaban, 0.95; 95% confidence interval [CI], 0.80 to 1.11; P=0.51). The primary safety outcome of major bleeding according to the Thrombolysis in Myocardial Infarction (TIMI) definition occurred in 46 of the 3673 patients (1.3%) who received at least one dose of apixaban (2.4 events per 100 patient-years) and in 18 of the 3642 patients (0.5%) who received at least one dose of placebo (0.9 events per 100 patient-years) (hazard ratio with apixaban, 2.59; 95% CI, 1.50 to 4.46; P=0.001). A greater number of intracranial and fatal bleeding events occurred with apixaban than with placebo.
The addition of apixaban, at a dose of 5 mg twice daily, to antiplatelet therapy in high-risk patients after an acute coronary syndrome increased the number of major bleeding events without a significant reduction in recurrent ischemic events. (Funded by Bristol-Myers Squibb and Pfizer; APPRAISE-2 ClinicalTrials.gov number, NCT00831441.)