By L. Amul. Sterling College, Vermont. 2019.
Plasmablastic lymphoma: a new subcategory of HIV-related NHL baycip 500mg with amex. Successful reduced-intensity conditioning allogeneic HSCT for HIV-related primary effusion lymphoma trusted baycip 500 mg. Primary effusion lymphoma cell lines harbouring human herpesvirus type-8 best 500mg baycip. HHV-8-positive body-cavity-based lymphoma: a novel lymphoma entity. Progressive multifocal leukoencephalopathy following rituximab therapy in HIV negative patients: a report of 57 cases from the Research on Adverse Drug Event and Reports (RADAR) project. HIV-associated plasmablastic lymphoma: lessons learned from 112 published cases. Rituximab in combination with chemotherapy versus chemotherapy alone in HIV-asso- ciated non-Hodgkin lymphoma: a pooled analysis of 15 prospective studies. Human immunodeficiency virus-associated plasmablastic lymphoma: poor prognosis in the era of highly active antiretroviral therapy. Bortezomib in combination with infusional dose-adjusted EPOCH for the treatment of plasmablastic lymphoma. KSHV-positive solid lymphomas represent an extra-cavitary variant of primary effusion lymphoma. Survival of non-Hodgkin lymphoma patients with and without HIV infection in the era of combined antiretroviral therapy. Plasmablastic lymphoma in HIV+ patients: an expanding spectrum. Excessive neurotoxicity with ABVD when combined with protease inhibitor- based antiretroviral therapy in the treatment of AIDS-related Hodgkin lymphoma. Detrimental clinical interaction between ritonavir-boosted protease inhibitors and vinblastine in HIV-infected patients with Hodgkin’s lymphoma. Incidence and risk factors of HIV-related non-Hodgkin’s lymphoma in the era of combi- nation antiretroviral therapy: a European multicohort study. Potential hazard drug-drug interaction between boosted protease inhibitors and vinblastine in HIV patients with Hodgkin’s lymphoma. Intensive sequential chemotherapy with hematopoietic growth factor support for non-Hodgkin lymphoma in patients infected with the human immunodeficiency virus. The role of tumor histogenesis, FDG-PET, and short course EPOCH with dose-dense rituximab (SC-EPOCH-RR) in HIV-associated diffuse large B-cell lymphoma. Low-intensity therapy in adults with Burkitt’s lymphoma. Causes of death in HIV-infected patients from the Cologne-Bonn cohort. Epeldegui M, Breen EC, Hung YP, Boscardin WJ, Detels R, Martínez-Maza O. Elevated expression of activation induced cytidine deaminase in peripheral blood mononuclear cells precedes AIDS-NHL diagnosis. Incidence, predictors and significance of severe toxicity in patients with human immunodeficiency virus-associated Hodgkin lymphoma. Distinct subsets of primary effusion lymphoma can be identified based on their cellular gene expression profile and viral association. Safety and activity of a new intensive short-term chemoim- munotherapy in HIV-positive patients with Burkitt lymphoma. Changing patterns of cancer incidence in the early- and late-HAART periods: the Swiss HIV Cohort Study. Molecular histogenesis of plasmablastic lymphoma of the oral cavity. Characteristics of non-Hodgkin lymphoma arising in HIV-infected patients with suppressed HIV replication. Gibson TM, Morton LM, Shiels MS, Clarke CA, Engels EA. Risk of non-Hodgkin lymphoma subtypes in HIV- infected people during the HAART era: a population-based study. B-cell stimulation and prolonged immune deficiency are risk factors for non- Hodgkin’s lymphoma in people with AIDS. Allogeneic hematopoietic cell transplantation in human immunodefi- ciency virus-positive patients with hematologic disorders: a report from the center for international blood and marrow transplant research. Hocqueloux L, Agbalika F, Oksenhendler E, Molina JM. Long-term remission of an AIDS-related primary effusion lymphoma with antiviral therapy. No evidence for an early excess incidence of progressive mul- tifocal leukencephalopathy in HIV-infected patients treated with rituximab. Hodgkin lymphoma is as common as non-Hodgkin lymphoma in HIV- positive patients with sustained viral suppression and limited immune deficiency: a prospective cohort study. Successful autologous stem cell transplantation in a severely immuno- compromised patient with relapsed AIDS-related B-cell Lymphoma. AIDS-related B-cell lymphoma (ARL): correlation of prognosis with differentiation profiles assessed by immunophenotyping. Response to highly active antiretroviral therapy strongly predicts outcome in patients with AIDS-related lymphoma. AIDS-associated Burkitt or Burkitt-like lymphoma: short intensive poly- chemotherapy is feasible and effective. Long-term control of HIV by CCR5 Delta32/Delta32 stem-cell transplan- tation. Nonmyeloablative conditioning followed by transplantation of geneti- cally modified HLA-matched peripheral blood progenitor cells for hematologic malignancies in patients with AIDS. Rituximab does not improve clinical outcome in a randomized phase III trial of CHOP with or without rituximab in patients with HIV-associated non-Hodgkin’s lymphoma: AIDS-malig- nancies consortium trial 010. Low-dose compared with standard-dose m-BACOD chemotherapy for non- Hodgkin’s lymphoma associated with HIV infection. Non-Hodgkin lymphoma in HIV-infected patients in the era of HAART. Malignant Lymphomas 431 Krishnan A, Palmer JM, Zaia JA, Tsai NC, Alvarnas J, Forman SJ. HIV status does not affect the outcome of autol- ogous stem cell transplantation (ASCT) for non-Hodgkin lymphoma (NHL).
It is bounded above by subscapularis and teres minor and below by The acromioclavicular joint teres major discount baycip 500mg mastercard. The long head of triceps and the surgical neck of the • Type: atypical synovial joint 500 mg baycip free shipping. As for the sternoclavicular joint order baycip 500mg with visa, the the long head of triceps. The circumﬂex scapular artery passes articular surfaces are covered with ﬁbrocartilage and an articular disc from front to back through this space to gain access to the hangs into the joint from above. The pectoral and scapular regions 75 33 The axilla Pectoralis minor Pectoralis major Short head of biceps Trapezius Coracobrachialis Clavicle Subclavius Long head Lateral cord of biceps Axillary artery Clavipectoral (tendon) Medial cord fascia Axillary vein Axillary space Posterior cord Latissimus Pectoralis dorsi (tendon) minor Chest wall Pectoralis major Fascial floor of axilla Serratus anterior Subscapularis Fig. The posterior cord is hidden behind the axillary artery 76 Upper limb The major nerves and vessels supplying and draining the upper limb anastomosis. It compensates for compromised ﬂow that may occur due pass through the axilla. The principal arteries involved are the The axilla is a three-sided pyramid. Its apex is the small region suprascapular, from the third part of the subclavian artery, and the sub- between the 1st rib, the clavicle and the scapula through which the scapular, from the third part of the axillary artery with contributions major nerves and vessels pass. The walls of the axilla are composed as follows: • The axillary vein: is formed by the conﬂuence of the venae comit- • The anterior wall is made up from the pectoralis major and minor antes of the axillary artery and the basilic vein (p. It becomes the muscles and the clavipectoral fascia. The named tributar- • The posterior wall is made up of the subscapularis, teres major and ies of the axillary vein correspond to those of the axillary artery. Running downwards from above are the corachobrachialis and In breast cancer surgery the axillary lymph nodes are cleared rou- short head of biceps as well as the long head of biceps in the intertuber- tinely. During the dissection for this procedure one must clearly iden- cular sulcus. Injury to the thoracodorsal nerve results in paralysis The contents of the axilla (Figs 33. Injury to the long thoracic nerve causes paralysis of • The axillary artery: an important anastomosis exists between the serratus anterior resulting in weakened arm abduction. On clinical subclavian artery and third part of the axillary arteryathe scapular examination the latter injury results in winging of the scapula. The axilla 77 34 The shoulder (gleno-humeral) joint Coracoclavicular Coraco-acromial ligament ligament Subacromial bursa Long head Acromion of biceps Supraspinatus Subscapularis Subscapular Infraspinatus bursa Glenoid fossa Teres minor Capsular ligament Long head of triceps Fig. It is formed by the articulation of the humeral head with the shallow glenoid fossa of the scapula (see p. The Shoulder movements glenoid is slightly deepened by a ﬁbrocartilaginous rimathe glenoid The shoulder is a ‘ball and socket’ joint allowing a wide range of move- labrum. Both articular surfaces are covered with hyaline cartilage. Much of this range is attributed to the articulation of the shallow • The capsule: of the shoulder joint is lax permitting a wide range of glenoid with a rounded humeral head. It is attached medially to the margins of the glenoid and lat- of compromised stability of the joint. The capsule is signiﬁcantly strengthened • Flexion (0–90°): pectoralis major, coracobrachialis and deltoid by slips from the surrounding rotator cuff muscle tendons. The latter comprise: three gleno-humeral ligaments ior ﬁbres). The main • External (lateral) rotators (0–55°): infraspinatus, teres minor and stability of the shoulder is afforded by the rotator cuff. Each of these muscles can perform its own function anterior. Almost simultan- • Bursae: two large bursae are associated with the shoulder joint. The eously the scapula is rotated so that the glenoid faces upwards; this subscapular bursa separates the shoulder capsule from the tendon of action is produced by the lower ﬁbres of serratus anterior which are subscapularis which passes directly anterior to it. The subscapular inserted into the inferior angle of the scapula and by the trapezius which bursa communicates with the shoulder joint. The subacromial bursa pulls the lateral end of the spine of the scapula upwards and the medial separates the shoulder capsule from the coracoacromial ligament end downwards. The subacromial bursa does not communicate with the joint. The tendon of supraspinatus lies in the ﬂoor of the bursa. It surrounds the intracapsular tendon of biceps and extends dislocation as the head usually comes to lie anteriorly in the subcora- slightly beyond the transverse humeral ligament as a sheath. Sometimes the force of the injury is sufﬁcient to tear the the subscapular bursa anteriorly by protruding through the anterior wall glenoid labrum anteriorly thereby facilitating recurrence. The shoulder (gleno-humeral) joint 79 35 The arm Supraspinatus Suprascapular nerve Deltoid Pectoralis Infraspinatus major Teres minor Axillary nerve Biceps Brachial artery retracted on brachialis Deltoid (pulled back) Median nerve Brachioradialis Lateral head of triceps Tendon of biceps Long head Radial nerve Bicipital of triceps Lateral aponeurosis cutaneous nerve of Medial head of forearm triceps Fig. The thick black lines represent the deep fascia and the intermuscular septa 80 Upper limb When viewed in cross-section the arm consists of skin and subcutan- • The musculocutaneous nerve and branches (remember that, after pro- eous tissue in which the superﬁcial veins and sensory nerves course. Medial and lateral intermuscular septa the deep fascia in the mid-arm to become the lateral cutaneous nerve of arise from the supracondylar lines of the humerus and extend to the the forearm): see p. The anterior (ﬂexor) compartment contents include (Figs 35. The arm 81 36 The elbow joint and cubital fossa Attachment of capsular ligament Radial fossa Coronoid fossa Capitulum Lax part of capsule Trochlea Annular ligament Head of radius Tendon of biceps Coronoid process of ulna Radius Interosseous membrane Radial tuberosity Ulna Fig. It is crossed by the median cubital vein 82 Upper limb The elbow joint (Figs 36. At the elbow the humeral capitulum This is a pivot joint. It is formed by the articulation of the radial head articulates with the radial head, and the trochlea of the humerus with and the radial notch of the ulna. The superior radio-ulnar joint commun- the trochlear notch of the ulna. Fossae immediately above the trochlea icates with the elbow joint.
Acknowledgments: We extend our appreciation to the clinical advisors listed below for their thoughtful advice and input during our research process generic baycip 500 mg without a prescription. Marshall Dahl baycip 500mg low cost, MD University of British Columbia Diane Elson cheap 500mg baycip fast delivery, MD University of Wisconsin, Madison Irl Hirsch, MD University of Washington John Newcomber, MD Washington University The investigators greatly appreciate the technical assistance provided by Judith Logan, MD, MS, our database manager, and Arkady Mak, MD, PhD, and Leah Williams-Morris, our manuscript editors. Diabetes Page 5 of 99 Final Report Drug Effectiveness Review Project INTRODUCTION Diabetes mellitus (diabetes) is a chronic and insidious disease affecting more than 20 million 1 Americans, approximately 7% of the population. Of those diagnosed, 90-95% have type 2 diabetes, while 5-10% have type 1 diabetes. Type 1 diabetes is characterized by autoimmune destruction of beta cells of the pancreas resulting in absolute insulin deficiency. Type 2 diabetes encompasses a heterogeneous group of disorders characterized by slow progressive loss of beta cell function and mass leading to variable degrees of insulin resistance, impaired insulin secretion, and increased hepatic glucose production. Among the counterregulatory hormones, higher glucagon levels relative to insulin also plays a significant role in the pathogenesis and management of type 2 diabetes, making optimal control difficult to maintain. The 2008 American Diabetes Association treatment guidelines recommend achieving and maintaining an A1c goal of <7% in nonpregnant patients with the caveat that less stringent goals may be appropriate for certain populations, all the while maintaining minimal hypoglycemia in 2 order to prevent micro- and perhaps macrovascular outcomes. Pharmacologic options for type 2 diabetes have primarily included sulfonylureas, biguanides, thiazolidinediones, meglitinides, alpha-glucosidase inhibitors, and insulin. Because of the progressive nature of diabetes, practitioners and patients experience challenges in reaching and sustaining American Diabetes Association goals. In fact, it is estimated that more than 50% of persons with type 2 diabetes will require more than one oral hypoglycemic agent after 3 years of diagnosis and approximately 70% will require combination oral therapy with or without 3 insulin 6 to 9 years from diagnosis. Within the last 1 to 2 years, three new antihyperglycemic agents have been approved: pramlintide, exenatide, and sitagliptin (Table 1). These agents offer mechanisms of glycemic control beyond that of “traditional” oral agents and insulin by targeting alternate gluco- regulatory receptors and hormones such as amylin, glucagon-like peptide-1 (GLP-1), glucose- dependent insulinotropic peptide (GIP), and dipeptidyl peptidase-4 (DPP-4). Amylin is a neuroendocrine hormone co-secreted with insulin from beta cells in response to elevated blood glucose concentrations and complements the actions of insulin. GLP-1 and GIP are secreted by L-and K-type cells in the intestinal tract in response to a combination of endocrine and neural signals initiated by the entry of food into the gut. Both endogenous GLP-1 and GIP are rapidly degraded by the proteolytic enzyme DPP-4. Diabetes Page 6 of 99 Final Report Drug Effectiveness Review Project Table1. Characteristics of pram lintide,exenatide,andsitagliptin Drug Drugclass Brandnam e (M anufacturer) F DA indications Contraindications Dose Approvaldate Dosage M ono-orcom bined Precautions adjustm ents Country How supplied therapy Pregnancycategory M onitoring Adjunctivetherapyin DM 1,DM 2,adults Decreaserapid- DM 1:Initiateat15m cg only,whouse orshort-acting subQ beforem ajor prandialinsulinand insulins, m eals(≥30g of faileddesired including fix ed- carbohydrate)and glucosecontrol m ix insulins titrateby15m cg every Contraindications: despiteoptim al (such as70/30) 3daysto30or60 Hypersensitivityto therapy(+/-SU by50% to m cg/m ealastolerated. Patientswho of the45or60m cg dose, confirm eddiagnosis m eetanyof the hypoglycem ia. Pram lintide considered:Poor glucoseand subQ beforem ajor Precautions: Am ylinom im etic/am ylin com pliancewith A1c frequently. M arch 2005 self-bloodglucose m onitoring If nauseapersistsat Pregnancycategory: U S m onitoring,A1c data,historyof the120m cg dose,m ay C > 9%,recurrent hypoglycem ia, decreaseto60m cg. Diabetes Page 7 of 99 Final Report Drug Effectiveness Review Project Table1. Characteristics of pram lintide,exenatide,andsitagliptin Contraindications: Hypersensitivityto ex enatideoranyof its com ponents Precautions:N ota DM 2,adultsonly,in 5m cg BID subQ beforea substituteforinsulinin patientstaking m eal,canbeincreased insulin-requiring DecreaseSU m etform in,SU ,orTZD to10m cg BID subQ patients,type1 dosetoreduce with inadequate E x enatide befoream ealafter1 diabetes,diabetic riskof glycem ic control Incretin m onth. Suppliedas5 ketoacidosis,acute hypoglycem ia; Com binedtherapy m im etic/G L P-1 m cg 1. E x enatideim provesfasting andpostprandialglycem ic controlby suppressing elevatedglucagonlevelsfrom alpha-cellsof thepancreas,anddelaying gastric em ptying tim ewhileincreasing thesensationof satietybym im icking theactionsof G L P-1inthe gutandthrough stim ulationof G L P-1receptorslocatedinthecentralnervoussystem andvagus nerve. Decrease sitagliptindoseto Sitagliptin 50m g if CrCl30- Incretin Contraindications: 50m L /m inand M ono-orasadd-on Hypersensitivityto enhancer/DPP- decreasedoseto therapyinDM 2,adults sitagliptinorits 4enz ym e 25m g if CrCl<30 inhibitor 100m g oncedailywith only,inadequately com ponents m L /m in,oron orwithoutfood. Available m anagedondietand Precautions:Dose J anuvia dialysis. M echanism of action:Inhibitsthedegradationof endogenousG L P-1andglucose-dependent insulinotropic peptide(G IP),therebyprolonging theirhalf-livesandconcentrations. Itisunclear whethersitagliptinhasclinicallyrelevanteffectsonprolonging gastric em ptying tim eorreducing satiety. Abbreviations:AM P,adenosinem onophosphate;BID,twicedaily;CrCl,creatinineclearance;DM 1,type1diabetes; DM 2,type2diabetes;F DA,U S F oodandDrug Adm inistration;G L P-1,glucagon-likepeptide-1;SC,subcutaneous; SU ,sulfonylureas;TZDs,thiaz olidinediones. Diabetes Page 8 of 99 Final Report Drug Effectiveness Review Project Scope and Key Questions The purpose of this review was to compare the effectiveness and harms of newer diabetes medications for persons with diabetes mellitus. The key questions for this review were developed with input from experts in the fields of endocrinology and internal medicine. The Oregon Evidence-based Practice Center wrote preliminary key questions and identified the populations, interventions, outcomes of interest, and the eligibility criteria for studies. The key questions were reviewed and revised by representatives of organizations participating in the Drug Effectiveness Review Project. The participating organizations of the Drug Effectiveness Review Project were responsible for ensuring that the scope of the review reflected the populations, drugs, and outcome measures of interest to clinicians and patients in their constituencies. The participating organizations approved the following key questions to guide this review: Pramlintide: Key Questions 1. For children and adults with type 1 diabetes does pramlintide differ in efficacy, effectiveness, or harms in achieving glycemic control when added to prandial insulin compared with conventional insulin therapy? For children and adults with type 2 diabetes does pramlintide differ in efficacy, effectiveness, or harms in achieving glycemic control when added to prandial insulin compared with conventional insulin therapy with or without concurrent oral hypoglycemic agents? Are there subgroups of patients for which pramlintide is more or less suitable than other hypoglycemic agents? For children and adults with type 2 diabetes does exenatide differ in efficacy, effectiveness, or harms in achieving glycemic control compared with other hypoglycemic agents as monotherapy or combined therapy? For children and adults with type 2 diabetes, does exenatide differ in efficacy, effectiveness, or harms in achieving glycemic control when added to other hypoglycemic agents compared with conventional insulin therapy? Are there subgroups of patients for which exenatide is more or less suitable than other hypoglycemic agents? For children and adults with type 2 diabetes does sitagliptin differ in efficacy, effectiveness, or harms in achieving glycemic control compared with placebo? For children and adults with type 2 diabetes does sitagliptin differ in efficacy, effectiveness, or harms in achieving glycemic control as monotherapy compared with other hypoglycemic agents or when added as part of combined therapy? Are there subgroups of patients for which sitagliptin is more or less suitable than other hypoglycemic agents? When in October 2007 Pfizer announced that it would no longer provide the inhaled powder for use, the medication was removed from these key questions. According to Pfizer, the decision to remove Exubera was voluntary and was not based on safety or efficacy problems but on lack of demand for the drug.
The reason pravastatin had minimal effect on low- density lipoprotein was that patients were taking similar doses of a statin prior to their index event generic baycip 500mg free shipping. After an average of 2 years of follow-up (range 18 to 36 months) buy baycip 500mg fast delivery, fewer atorvastatin- treated patients had a major cardiovascular event (rates order baycip 500 mg free shipping, 22. Major events were defined as all-cause mortality, myocardial infarction, documented unstable angina requiring hospitalization, revascularization with either percutaneous transluminal coronary angioplasty or coronary artery bypass graft, and stroke. Looking at the individual components of the primary outcome, atorvastatin appeared to exhibit its greatest benefit in reducing recurrent Statins Page 36 of 128 Final Report Update 5 Drug Effectiveness Review Project unstable angina requiring hospitalization (rates, 3. There was a nonsignificant trend for all-cause mortality (rates, 2. The benefit of atorvastatin 80 mg on cardiovascular events was greater in a subgroup of patients with higher baseline low-density lipoprotein of ≥125 mg/dL and those without prior statin use. Among patients who had used statins, the 2-year event rates were 27. In contrast, among patients without prior statin use, event rates were lower for atorvastatin (20. Withdrawal rates due to any cause including adverse events were not significantly different between atorvastatin and pravastatin, but overall the rates were high at 2 years (30. No cases of rhabdomyolysis were reported in either group but more atorvastatin-treated patients observed elevations in alanine aminotransferase >3 times the upper limit of normal compared with pravastatin (69 patients [3. It is likely that the superior results of intensive therapy with atorvastatin were due to additional low-density lipoprotein-lowering. Pravastatin at any dose cannot achieve as much low-density lipoprotein reduction as atorvastatin 80 mg. PROVE-IT did not indicate whether atorvastatin would be better than other statins that reduce low-density lipoprotein to a similar degree. Patients who had previously taken a statin were eligible provided they had not been titrated to a dose higher than the equivalent of simvastatin 20 mg, and about 50% of those enrolled were taking simvastatin prior to randomization. The study was open-label with blinded endpoint classification. The median time since myocardial infarction was 21 to 22 months and 11% of patients were enrolled within 2 months of their myocardial infarction. There was no difference between treatment groups on the primary endpoint (coronary death, hospitalization for nonfatal acute myocardial infarction, or cardiac arrest with resuscitation). There was no difference in cardiovascular mortality or all-cause mortality, but a significant reduction in nonfatal myocardial infarction (hazard ratio, 0. Post-hoc analyses adjusting for age (<65 years compared with ≥65 years) and sex showed no significant differences in treatment 118, 120 effects. More high-dose atorvastatin patients discontinued therapy due to adverse events than simvastatin-treated patients (9. No differences in the rate of myopathy or rhabdomyolysis. Several factors might help explain the discrepant results of PROVE-IT and IDEAL: (1) All subjects in PROVE-IT had recent acute coronary syndrome, whereas only 11% of those in IDEAL had myocardial infarction within 2 months of randomization. This Statins Page 37 of 128 Final Report Update 5 Drug Effectiveness Review Project (2) The definition of the primary endpoint differed in the 2 trials. In IDEAL, the reduction in low-density lipoprotein cholesterol with atorvastatin was slightly less than expected, and adherence in the atorvastatin group was not as good as in the 118 simvastatin group (89% compared with 95%). In a fair-quality, 1-year trial in patients with stable coronary artery disease, intensive atorvastatin (up to 80 mg, to a target of low-density lipoprotein cholesterol less than 80 mg/dL) was not more effective than a control group of diet plus low-dose lovastatin (5 mg if needed, to a target of low-density lipoprotein cholesterol less than 130 mg/dL) for reducing the number of ischemic episodes as measured on ambulatory electrocardiogram, patient-reported angina 119 frequency, and nitroglycerin consumption. There was a reduction in the number of ischemic episodes in both groups, but no difference between groups. There was no significant difference in major clinical events between groups after 1 year, but the number of events was small and the study was powered to detect a difference in ischemia, not clinical events. Placebo-controlled trials Many trials comparing a statin to placebo or, in a few instances, to non-pharmacologic treatments, reported health outcomes. These trials indicated which statins have been proven to reduce the risk of cardiovascular events in various patient populations. This group included 27 118, 121-134 placebo-controlled trials and 2 head-to-head trials: 22 studies in outpatients 81, 117, and 7 studies in inpatients with acute myocardial infarction or unstable angina. Enrollment was in excess of 4000 patients with an average follow-up period of 5 years. All of the trials were good or fair quality and were considered the best evidence for demonstrating a reduction in cardiovascular health outcomes with statins. These included studies of patients hospitalized with acute myocardial infarction or unstable angina. There was 1 head-to-head trial of intensive atorvastatin therapy compared with a standard dose of pravastatin. Six other trials compared a statin to placebo or usual care. In these trials, coronary heart disease events or cardiovascular morbidity and mortality was reported either as a secondary endpoint or incidentally (that is, even though it was not a predefined endpoint). In general, these studies had 148, 155 insufficient power to assess coronary heart disease events. Only 2 of these trials Statins Page 38 of 128 Final Report Update 5 Drug Effectiveness Review Project enrolled more than 500 patients. The others ranged from 151 to 460 included patients. As evidence regarding reduction in coronary heart disease events, these trials were fair or fair-to-poor in quality. Three additional trials with clinical outcomes did not fit the 65, 166, 167 criteria for the other categories. Studies with primary coronary heart disease endpoints The major trials are summarized briefly in Tables 9 (outpatient studies) and 11 (inpatient studies) below and in more detail in Evidence Table 2. Statins Page 39 of 128 Final Report Update 5 Drug Effectiveness Review Project Table 9. Outpatient and community-based placebo-controlled trials of statins with coronary heart disease endpoints Number needed to Risk status/ Reduction in treat to Average annual Baseline Study coronary events prevent a Trial event rate in LDL duration % LDL (relative risk coronary a b (Quality) placebo group (mg/dL) (years) reduction reduction) event Trials of atorvastatin 171, 172 ASCOT HTN plus CHD risk Atorvastatin factors/ 133 3.