Loryna Litigation: Two recent large trials have studied the efficacy and safety of aspirin in patients with acute ischemic strokes. The International Stroke Trial ran­domized 19,435 patients with acute ischemic stroke to unfractionated heparin, either 5,000 or 12,500 units twice daily, aspirin 300 mg daily, or both heparin and aspirin (11). Among the patients treated with aspirin, there were 2.8% recurrent ischemic strokes within 14 days, compared to 3.9% in the groups not receiving aspirin, and no excess of hemorrhagic strokes. There was a nonsignificant trend for decreased mortality in patients treated with aspirin compared to those not treated with aspirin at 14 days (9% vs. 9.4%). At 14 days, therefore, there was a significant reduction in death or any nonfatal recurrent stroke in the aspirin- treated group (11.3% vs. 12.4%). In patients treated with heparin, there were 2.9% recurrent ischemic strokes within 14 days compared to 3.8% in the groups not receiving heparin, but an increase in hemorrhagic strokes (1.2% vs. 0.4%). As a consequence, there was no significant difference in the incidence of nonfatal recurrent stroke or death between the heparin and nonheparin groups (11.7% vs. 12%, respectively).

Several trials have studied the efficacy of aspirin as primary prevention for myo­cardial infarction, stroke, and death, but the results have not been consistent. The Physicians’ Health Study compared aspirin to placebo in 22,071 male physicians over the age of 40 and followed them for 5 years. Myocardial infarction occurred in 139 persons assigned to aspirin and 239 assigned to placebo. Thus, aspirin was associated with a 44% reduction in the risk of myocardial infarction. Cardiovascular death occurred in 81 persons assigned to aspirin and 83 assigned to placebo. Thus, there was no significant reduction in total cardiovascular mor­tality. The reduction in the risk of myocardial infarction occurred only among men 50 years of age and older. There was a nonsignificant, slightly increased risk of stroke among those taking aspirin compared to those taking placebo. A separate study of 5139 healthy British male physicians compared aspirin to pla­cebo. Total mortality was slightly, but not significantly, less in the control group compared to the aspirin-treated group. There was no significant difference in the incidence of nonfatal myocardial infarction or stroke.

Another British trial, the Thrombosis Prevention Trial, evaluated the effect of low-dose aspirin (75 mg/day) as well as oral anticoagulation with warfarin (average INR = 1.47) in 5499 healthy men aged 45 to 69 years who were random­ized to warfarin, aspirin, both, or neither. The average International Normal­ized Ratio (INR) for those receiving warfarin was 1.47. Warfarin was associated with a 21% reduction in coronary death, fatal, and nonfatal myocardial infarction, and aspirin was associated with a 20% reduction in coronary death and myocar­dial infarction. The risk of hemorrhagic and fatal strokes was increased in the warfarin-treated patients. The principal effect of aspirin was primarily a 32% reduction in nonfatal myocardial infarction; aspirin did not reduce total cardiovas­cular mortality. The effect of aspirin as primary prevention was also evaluated in 87,678 U.S. registered nurses who had been participating in a prospective cohort study. Among women taking one to six aspirin per week, there was a significant, 32% relative risk reduction for myocardial infarction, a nonsignifi­cant, 11% relative risk reduction for cardiovascular death, and no decrease in the risk of stroke.

An analysis of 21 trials included in the Antiplatelet Trialists’ Collaboration found that the odds ratio among persons using aspirin for upper gastrointestinal bleeding was 1.7; for peptic ulcer, 1.3; and for all gastrointestinal bleeding, 1.5 to 2.0. The risk of cerebral hemorrhage is increased by aspirin. A recent metanal- ysis of 16 trials constituting 55,462 persons found that the absolute risk of hemor­rhagic stroke in groups treated with aspirin was 1.2 per thousand individuals accounting for a relative risk of 1.84. Hypersensitivity reactions to aspirin, including nasal congestion, urticaria, and bronchospasm may occur. The frequency of these adverse effects in patients with chronic urticaria is 23%, in patients with asthma is 4 to 19%, and in patients with nasal polyps is approxi­mately 23%.

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Loryna Litigation: The Studio della Ticlopidinia nell’Angina Instabile Groupe evaluated the efficacy of ticlopidine in 652 patients with unstable angina. Following treat­ment for 6 months, 7.3% of the patients receiving ticlopidine had a nonfatal myocardial infarction or vascular death compared to 13.6% of patients who did not receive ticlopidine, accounting for a 46.3% relative risk reduction. Several trials have evaluated the efficacy of ticlopidine in preventing throm­bosis or ischemic events subsequent to placement of an intracoronary stent. The Full Anticoagulation versus Aspirin and Ticlopidine (FANTASTIC) study ran­domized patients to aspirin and ticlopidine or to aspirin and conventional antico­agulation with heparin or oral anticoagulants. The primary endpoint of bleed­ing or peripheral vascular complications occurred in 13.5% of patients treated with aspirin and ticlopidine and 21% of patients treated with aspirin and anticoag­ulants. The overall incidence of stent occlusion was similar in each group; yet, acute stent occlusion occurred more frequently in the antiplatelet group (2.4 vs. 0.4%), whereas subacute stent occlusion within 1 week occurred more frequently in the anticoagulant group (3.5 vs. 0.4%).

The Multicenter Aspirin and Ticlopidine Trial after Intracoronary Stenting (MATTIS) study randomized 350 high-risk patients following stent implantation to aspirin and ticlopidine or to aspirin and oral anticoagulation. After 30 days, the primary cardiac endpoint of cardiovascular death, myocardial infarction, or repeated revascularization occurred in 5.6% of the aspirin and ticlopidine group compared to 11% of the aspirin and anticoagulant group, accounting for approximately 50% reduction in the risk of an adverse event with the former compared to the latter group. Schomig et al. randomized 257 patients undergoing placement of coronary artery stents to aspirin and ticlopidine, or to aspirin plus anticoagulation with heparin or phenprocoumon. The primary cardiac endpoint of cardiac death, nonfatal myocardial infarction, coronary artery bypass surgery, or repeat angio­plasty occurred in 1.6% of patients randomized to aspirin plus ticlopidine as compared to 6.2% of those randomized to aspirin plus anticoagulation, account­ing for a relative risk of 0.25 in those randomized to antiplatelet therapy alone. Moreover, hemorrhagic complications occurred in 6.5% of the anticoagulant ther­apy group, but in none of the antiplatelet therapy group.

Two large clinical trials evaluated the efficacy of ticlopidine in patients with symptomatic cerebrovascular disease. The Canadian American Ticlopidine Stud­ies (CATS) randomized 1072 with recent thromboembolic stroke to ticlopidine or placebo and followed them for an average of 24 months. The primary endpoint of stroke, myocardial infarction, or vascular death occurred in 15.3% per year of those treated with placebo and 10.8% per year of those treated with ticlopidine, accounting for a relative risk reduction with ticlopidine of 30.2%. There was no significant difference in the total mortality rate, which was 4.5% per year in those receiving placebo and 4.1% per year in those receiving ticlopidine. The Ticlopidine Aspirin Stroke Study (TASS) randomized 3069 patients with recent transient ischemic attack, amaurosis fugax, or minor stroke to aspirin or ticlopidine.

Several studies have examined the efficacy of ticlopidine in patients with periph­eral arterial disease. Balsano etal. studied 151 patients with intermittent claudica­tion who were randomized to treatment with ticlopidine or placebo. Improve­ment in pain-free and maximal walking distance was greater in the ticlopidine than in the placebo group. The Swedish Ticlopidine Multicenter Study (STIMS) assessed the effect of ticlopidine on cardiovascular events in 687 patients with intermittent claudication followed for a median duration of 5.6 years. The incidence of myocardial infarction, stroke, and transient ischemic attack was 29% in patients treated with placebo compared to 25% among those treated with ticlopidine, accounting for a risk reduction of 11.4% in favor of ticlopidine. Mortality was 26.1% in the placebo group and 18.5% in the ticlopi­dine group, accounting for a relative risk reduction of 29%. A recent metanalysis involving studies of patients with intermittent claudication found that mortality was significantly decreased by ticlopidine compared to placebo, with an odds ratio of 0.68.

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Loryna Litigation: Several additional trials that are assessing the efficacy of clopidogrel in preventing cardiovascular events are currently taking place. These include: the Clopidogrel Reduction of Events During Extending Observation (CREDO) trial in which patients undergoing percutaneous revascularization will receive clopido­grel with aspirin for 1 year versus clopidogrel plus aspirin for 1 month followed by aspirin for another 11 months and the Warfarin and Antiplatelet Therapy in Chronic Heart Failure (WATCH) trial in which patients with congestive heart failure will be randomized to warfarin (titrated to an INR of 2.5-3.0), clopidogrel 75 mg/day, or aspirin 160 mg/day, and followed for up to 5 years.

In the CAPRIE trial, bleeding occurred with comparable frequency in the patients receiving clopidogrel compared to aspirin (9.27% vs. 9.28%, respectively). In patients receiving clopidogrel, intracranial hemorrhage occurred in 0.35% and gastrointestinal hemorrhage in 1.99%, the latter being less frequent than in pa­tients receiving aspirin. In patients receiving clopidogrel, diarrhea occurred in 4.46% and rash occurred in 6.02%. Of patients receiving clopidogrel, neutro­penia (<1200/|J.L) was present in 0.1%, severe neutropenia (<450/|J.L) in 0.05%, thrombocytopenia (<100 X 10³/|J.L) in 0.26%, and severe thrombocytopenia (<80 X 10³/|J.L) in 0.19% of patients receiving clopidogrel. A recent report high­lighted the potential association of thrombotic thrombocytopenic purpura with clopidogrel (41). Eleven patients who had been treated with clopidogrel, 10 of whom had been treated for 14 days or less, were identified over a 2-year period by active surveillance of medical directors of blood banks, hematologists, and a surveillance overseen by pharmaceutical manufacturers. At the time of this report, the authors estimated that more than 3 million people had received clopidogrel. Idiopathic thrombotic thrombocytopenic purpura has been estimated to occur in approximately 3.7 per million.

Heart failure was the first major area in which ACE inhibitors have proven their undisputed role in improving clinical outcomes, indeed, survival. In the early 1980s, the ‘‘vasodilator era,’’ then pioneering acute studies revealed that favor­able hemodynamic improvements could be obtained by ACE inhibitors in patients with severe heart failure. The first demonstration of a survival benefit with the use of an ACE inhibitor in any cohort of patients can be attributed to the Cooperative North Scandinavian ENalapril SUrvival Study (CONSENSUS), which randomized patients with severe heart failure. In this trial, despite the use of digitalis, diuretics, and other vasodilators, the placebo mortality rate was exceedingly high, approaching 50% at 6 months. Those randomized to the active therapy (enalapril) had a pronounced reduction in the risk of death. Indeed, the combination of the high placebo event rate and the relative effectiveness of ther­apy led to conclusive results in a population of approximately 500 patients.

The Studies of Left Ventricular Dysfunction (SOLVD) greatly expanded the indications for ACE inhibitors as a consequence of their results in two parallel randomized trials collectively involving over 6000 patients. In the treatment arm, symptomatic heart failure patients with left ventricular dysfunction (ejection fraction <35%) of all etiologies were randomized to placebo or enalapril. Despite background therapy with digitalis or diuretics or both, the enalapril group experi­enced a 16% reduction in the risk of death and clear reductions in the need for rehospitalization for heart failure. The same screening procedures identified and randomized over 4000 patients who also had left ventricular dysfunction. However, the study investigators did not feel that these patients had sufficient symptoms to warrant therapy—the Prevention Arm. In this unique group, the randomization to enalapril showed a favorable trend for a reduction in fatal events with a clear reduction in the development of heart failure during the ap­proximately 4 years of follow-up. As a consequence of these and other smaller studies, ACE inhibitors had proven themselves as an essential, indeed, ‘‘corner­stone’’ therapy for the management of patients with heart failure. In some respects, the V-HeFT-II study put the icing on the cake for the use of ACE inhibi­tors in heart failure. It showed that, in a group of symptomatic heart failure pa­tients randomized to either the combination of hydralazine and nitrates (the first life-sustaining therapy for heart failure) versus enalapril, the ACE inhibitor re­sulted in superior survival even compared to a previously proven therapy for heart failure. Taken together, we now had clear evidence that the morbidity and mortality of heart failure could be effectively reduced by the use of an ACE inhibitor.

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Loryna Litigation: The rationale for the treatment of patients with myocardial infarction with an ACE inhibitor stems from the pioneering work of the late Dr. Janice Pfeffer, beginning when she was a fellow in the Braunwald laboratory. Experimental models of infarctions were readily utilized to determine whether infarct size could be favorably modified by pharmacological therapy. Pfeffer explored the relation­ship between infarct size and ventricular function and incorporated important lessons from her doctoral training in hypertension at Edward Frohlich’s labora­tory to determine the long-term consequences of abrupt loss of myocardium from coronary ligation. Indeed, she demonstrated in the animal model that the loss of myocytes should be viewed as the beginning of an insidious phase of progressive ventricular enlargement (remodeling), which is related both to the extent of the histological damage as well as to the duration of time from the infarct. In­deed, the enlargement itself is a central component in the progressive worsening of dysfunction. Ventricular remodeling could also involve the normal remaining myocardium, which, as a consequence of unfavorable geometry and wall stress, could suffer an abnormal hemodynamic burden.

These observations of ventricular remodeling provided a new therapeutic target for a novel use of ACE inhibition—to attenuate time-dependent ventricular enlargement following infarction. The use of ACE inhibitors was a natural exten­sion of her work in hypertension, where these agents were particularly effective in preventing hypertrophy and left ventricular chamber enlargement. In the myocardial infarction model, long-term administration of an ACE inhibitor did indeed attenuate ventricular enlargement as treated animals had smaller left ven­tricular cavities and more preserved ventricular pump function. In a subse­quent study, a prolongation of survival was demonstrated with ACE inhibitor treatment.

These animal studies provided the rationale for initially small mechanistic studies, which confirmed both the process of progressive enlargement post-myo­cardial infarction and the attenuation of enlargement with the use of an ACE inhibitor. These mechanistic studies were soon followed by an extensive series of international multicenter randomized trials testing the hypothesis that administration of an ACE inhibitor to patients in the acute and chronic phases of myocardial infarction would lead to improved survival. The Survival and Ven­tricular Enlargement (SAVE) study, as suggested by the trial’s acronym, tested the hypothesis that attenuation of ventricular enlargement in high-risk patients post-myocardial infarction would lead to improved survival. The SAVE study demonstrated that the addition of captopril to a conventionally treated pa­tient who survived a myocardial infarction with an ejection fraction less than 40% without overt heart failure would lead not only to a reduction in the risk of death, but also to a reduced risk of developing heart failure and experiencing a recurrent myocardial infarction. A detailed quantitative echocardiographic study did confirm an attenuation in remodeling in the ACE inhibitor group and, more­over, these investigators were able to demonstrate linkage between progressive enlargement, risk of an adverse cardiovascular event, and the favorable benefit of the ACE inhibitor therapy.

The Acute Infarction Ramipril Efficacy (AIRE) study administered the ACE inhibitor ramipril to patients starting in the acute phase of the infarct and continuing long term. The AIRE investigators identified high-risk patients based on clinical signs or symptoms of pulmonary congestion or transient heart failure. The long-term administration of the ACE inhibitor resulted in a 26% reduction in the risk of death and comparable reductions in other nonfatal cardiovascular endpoints. The TRandolapril Cardiac Evaluation (TRACE) investigators employed echocardiographic assessment of wall motion to identify higher risk acute infarct patients. Here, again, the randomization to the ACE inhibitor resulted in an im­portant reduction in the risk of death. In the Survival of Myocardial In­farction Long-term Evaluation (SMILE), the ACE inhibitor zofenopril was ad­ministered to patients with anterior myocardial infarction who had not received thrombolytic therapy. This randomized trial demonstrated a reduction in risk of death or development of heart failure during only 6 weeks of therapy. The TRACE and AIRE investigators have extended their observations beyond the formal trial period and demonstrated that the survival benefits persisted.

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Loryna Settlement: An overview of this selective approach to the use of ACE inhibitors for higher risk myocardial infarction patients indicates that approximately 20 to 30 lives are saved in the first month of treatment and that, with continued therapy, approximately 60 to 80 lives are saved per 1000 patients treated. It is impor­tant to underscore that the benefits of the use of an ACE inhibitor in myocardial infarct patients could be considered as additive to conventional therapy with thrombolytics, beta-blockade, and even aspirin. Therefore, it is fair to conclude that use of an ACE inhibitor in these patient populations results in a new and complementary modality to reduce risk of death and other major cardiovascular events.

The only ‘‘fly in the ointment’’ in the field of ACE inhibitors and acute myocardial infarction was from the CONSENSUS II study, which showed a nega­tive trend when ACE inhibitor therapy was started intravenously in the first day of the infarct and then continued orally for the projected study duration of 6 months. With over 100,000 patients in randomized, placebo-controlled trials of different designs, agents and durations, the consensus of international experts strongly recommends the use of an ACE inhibitor starting early and continued long term for patients at higher risk. These authoritative guidelines do indi­cate that there are sufficient rationale and data for clinicians to adopt a more global approach for the use of ACE inhibitors in an even broader population.

Additional mechanisms to explain the ACE inhibitor influence on coronary events soon came from novel experimental studies that revealed an important interface between the renin-angiotensin system and the balance between throm­bolysis and thrombosis. An infusion of angiotensin-II raised plasminogen activa­tor inhibitor-1 (PAI-1), which would alter the fibrinolytic balance toward throm­bosis. The randomized use of ACE inhibitors in patients with acute myocardial infarction did indeed lower PAI-1 levels and, particularly, the balance of PAI-1 to intrinsic tPA. Augmented PAI-1 levels had been associated with greater risk of infarct and others had speculated that reduced PAI-1 may be an indication of restoration of endothelial function. In the TREND study, the long-term treatment with the ACE inhibitor quinipril led to a better restoration of coronary endothelial function. Along these lines, it has been postulated that lowering angiotensin-II with an ACE inhibitor would reduce superoxide anions, promote nitric oxide, and limit further vascular damage.

In the mid-to-late 1990s, three major trials were initiated to determine whether an ACE inhibitor would reduce atherosclerotic events. The Heart Out­comes Prevention Evaluation (HOPE) study selected patients for clinical evi­dence of vascular disease with prior myocardial infarction, stroke, peripheral vas­cular disease, or diabetes plus another risk factor and randomized to conventional therapy plus placebo or ramipril. Patients with heart failure or known depressed ejection fraction were excluded. The Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) study, specifically designed as a follow- up of SAVE, included patients with documented coronary disease and an ejection fraction over 40% randomized to conventional therapy plus either trandolapril or placebo. The EUropean trial on Reduction Of cardiac events with Perindo­pril in stable coronary Artery disease (EUROPA) randomized patients with coro­nary disease regardless of their ejection fraction to either perindopril or placebo.

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Loryna Settlement: HOPE was the first of these major studies to be completed. Randomization to ramipril resulted in a convincingly consistent 20% and greater reduction in ath­erosclerotic events, such as cardiovascular death, myocardial infarction, and stroke. The HOPE study results are based on a substantial number of clinical events and consistent findings were present in all predefined subgroups. Again, the small reduction in blood pressure with the ACE inhibitor in and of itself could not explain the magnitude of the clinical benefits in this patient population. Within the HOPE study, a mechanistic trial evaluating carotid arterial thickness as a surrogate marker of the atherosclerotic process did demonstrate a dose-dependent reduction in ca­rotid thickness with the use of an ACE inhibitor. Other important mechanistic observations such as the reduction in the development of diabetes and diabetic complications may provide additional key insights. Indeed, the hemoglobin A1C levels in the subpopulation evaluated was reduced by chronic therapy with the ACE inhibitor. The HOPE study expands both the patient population who will receive benefits from ACE inhibitor therapy as well as the potential mechanisms that can be evoked to explain these impressive beneficial actions.

With the obvious broad overlap in patients who would benefit from both of these agents, a negative interaction with the concomitant use of these two agents would have major public health implications. At the outset, it must be acknowledged that there is yet to be a two- by-two trial of aspirin and ACE inhibitors as there was of thrombolytics and aspirin in ISIS-2. Indeed, with the now established benefits of both of these agents, such a trial in which patients would have either of these life-saving thera­pies withheld would be deemed unethical. Decisions will have to be based on the experience of prior trials. Since most of the major aspirin trials were con­ducted prior to the knowledge of the survival benefit of ACE inhibitors, there are few data on concomitant use. On the other hand, there is extensive experience in the ACE inhibitor trials with patients on aspirin.

The initial hypothetical question of a possible interaction, whereby the con­comitant use of both drugs offsets the potential benefits of an ACE inhibitor, was proposed by Donald Hall and his colleagues. A mechanistic study of patients with severe heart failure and marked neurohormone activation observed that the vasodilating effect of enalapril was offset by the concomitant use of aspirin. Since one of the important actions of an ACE inhibitor, aside from reducing the production of angiotensin-II, is to impede the breakdown of bradykinin, which also enhances the production of prostaglandins, it was reasoned that an aspirin effect on inhibiting prostaglandin synthesis could offset some of the hemody­namic benefits of administering an ACE inhibitor. Indeed, their work on the he­modynamics of severe heart failure was confirmed by others. This is similar to the use of nonsteroidal anti-inflammatory agents that had long been known to exacerbate signs and symptoms of heart failure, impairing renal function, and even offsetting antihypertensive effects of a variety of therapeutic compounds. Hall provided mechanistic underpinning and focus for important questions regarding a potential for aspirin to offset some of the clinical benefits of ACE inhibitor use in patients with severe heart failure.

Subsequently, a subgroup analysis from the SOLVD studies did indicate that there was a trend for less of a survival benefit in patients randomized to the ACE inhibitor who were reported to be on aspirin at baseline. Proponents of an important negative interaction whereby aspirin offsets some of the benefits of an ACE inhibitor could also turn to the CONSENSUS-II acute myocardial infarction study to bolster these positions. Conversely, subgroup analyses from other large studies appear to refute these observations. With the proven benefits of both of these agents independently and the overlapping clinical profile of pa­tients that should be receiving these therapies simultaneously, this becomes a critical question to resolve.

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Loryna Settlement: In the short term, broad-inclusion analysis of 96,712 patients, aspirin was used at baseline in 86,884 (89.4%) and not in 10,228 patients (10.6%). Aspirin use was not randomized and, as it turns out, there was a marked disparity in risk profile with respect to use of aspirin. Patients who did not receive aspirin were less likely to receive thrombolytics or beta-blockers, were older, and were more likely to have had pulmonary congestion as is manifested by Killip Class 2 and 3. Not surprisingly, regardless of ACE inhibitor status, the non-aspirin-treated patients had more than twice the mortality rate (14.4 vs. 6.5%, no aspirin vs. aspirin) in these short-term studies. The test for heterogeneity between the reductions in risk of death produced by randomization to the ACE inhibitor in the presence or absence of aspirin use at baseline was not significantly different. This analysis is inclusive of CONSENSUS-II, which is frequently cited as an example of an aspirin-ACE interaction where no benefit of the ACE inhibitor was observed in the presence of aspirin.

Since we have not had (and are unlikely to have) a direct two-by-two test of these two proven agents, interpretation of the information from the existing studies must suffice to generate our clinical conclusions. Along these lines, it is fortunate that use of ACE inhibitors for reduction of cardiovascular events is an extremely well-studied area. Particularly so in patients with myocardial in­farction, with over 100,000 patients in randomized trials and the majority on aspirin, providing a good data set from which to draw these conclusions. Just as the antiplatelet trialists have formed a collaboration to collectively extract more data from their individual studies, so have the ACE inhibitor myocardial infarction investigators. Representatives from eight major trials have pooled their individual data to provide more precise point estimates and to particularly probe prospective subgroup analyses for both efficacy and safety. The ACE Inhibitor Myocardial Infarction Collaborative group prospectively determined that the broad-inclusion, short-term studies should be analyzed separately from the elec- tive-inclusion, long-term studies. Both of these systematic overviews (metanal- ysis) have been completed and recently published.

Symptomatic arterial occlusive disease generally occurs when the artery lumen is reduced to half normal. Atherosclerosis is by far the most common cause of peripheral arterial occlusive disease. Other etiologies must be considered in individuals who do not have risk factors for atherosclerosis or in those who have an unusual distribution of arterial occlusive disease. These etiologies include Ta­kayasu arteritis and giant cell arteritis. Both of these arteritides may result in stenosis of any extremity vessel, visceral vessels, or the aorta. Other forms of vasculitis also result in symptomatic arterial occlusive disease. Thromboangiitis obliterans should be suspected if the distal arteries of the upper and lower extrem­ities are involved, particularly in those who smoke cigarettes. Acute arterial occlusion occurs as a consequence of embolism or thrombosis in situ. Thrombosis can develop acutely in atherosclerotic arteries or it can occur in locations such as the renal arteries in the presence of antithrombin-III deficiency.

Symptomatic lower extremity atherosclerosis is reported in 3% of those individuals over age 50. In individuals greater than 70, over 25% have evi­dence of peripheral arterial occlusive disease by noninvasive testing. The preva­lence of peripheral arterial disease is threefold greater when determined by nonin­vasive testing for arterial stenosis rather than by questionnaires regarding symptoms, consistent with the observation that two-thirds of affected individuals are asymptomatic by traditional history. Yet, in a recent community screening program, these asymptomatic individuals had lower functional capacity than those without peripheral arterial disease, as well as an increased risk of cardiovas­cular death.

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Loryna Settlement: Noninvasive testing for lower extremity arterial occlusive disease provides objec­tive information that, together with the history and physical examination, is used to make decisions regarding further evaluation and treatment. These tests can be used for screening, for physiological assessment of hemodynamically signifi­cant stenosis, and to follow-up after revascularization procedures. The most sim­ple and widely used noninvasive test of extremity arterial occlusive disease is measurement of systolic pressure using a sphygmomanometric cuff and a Doppler device to detect arterial flow. Duplex scanning extends the capabilities of nonin­vasive testing by identifying anatomical and physiological information at the sites of arterial stenoses.

Three-dimensional arterial reconstruction using magnetic resonance im­aging (MRI) arteriography and spiral CT arteriography can provide non­invasive assessment of the distal aorta and iliac vessels, but presently with less clarity than is available with invasive arteriography. Contrast arteriography is necessary to completely evaluate the anatomical extent of disease in the distal aorta and lower extremity arteries. It is generally performed only in order to determine the optimal revascularization procedure because of its invasive nature and risk. The functional significance of the arterial occlusive disease can be confirmed by invasive pressure measurements proximal and distal to the stenosis, and can be determined before and after administration of a vasodilator.

The combination of B-mode ultrasound scanning and pulsed Doppler interrogation allows noninvasive assessment of the anatomy and hemodynamic abnormalities in the arterial segments from the distal aorta to the popliteal trifurcation. For exam­ple, soft plaque and thrombi may have similar acoustic properties to blood and, therefore, may not be detected by B-mode imaging, but they will result in a flow disturbance that can be detected by Doppler evaluation. Equipment for peripheral arterial testing includes a linear array transducer, operating at a gray-scale fre­quency of 4 to 10 MHz, and capable of providing frequencies above 3 MHz for Doppler signal analysis. Gray-scale imaging is used to examine the arteries and the presence of detectable atherosclerotic plaque or thrombus. The pulsed Doppler spectral analysis is used to document the presence of blood flow and to determine blood flow velocity. Normal Doppler waveforms in the lower extremity will be triphasic, with a peak velocity less than 120 cm/s. Color Doppler flow mapping allows for a rapid survey of the arteries in order to identify those sites where more labor-intensive and precise Doppler spectral analysis is needed. Still, full evaluation of the lower extremity arteries takes from 1 to 2 h.

Duplex examination can be combined with exercise testing to detect disproportionate velocity increases with exercise and therefore identify the le­sions responsible for a patient’s symptoms. The duplex scan is potentially supe­rior to angiography in the evaluation of iliac artery, and in determining the hemo­dynamic status of ostial lesions in the profunda and superficial femoral arteries. Peripheral artery bypass grafts can be followed serially with duplex ultrasonogra­phy. The first month after surgery and every 1 to 2 years following surgery are key times to identify early changes consistent with stenosis within the graft. The criteria for discrete stenosis in bypass grafts is similar to that in native ves­sels. In addition, a peak systolic velocity that is decreased to 45 cm/s indicates a dramatically increased likelihood of graft failure and provides a rationale for early intervention. In addition, duplex evaluation is likely to be similarly useful in the follow-up of peripheral arteries following percutaneous revascularization.

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More information on Actos Warning

Although the relationship between squamous cell carcinoma of bladder and schistosoma infection is well established, currently the trends of BC in endemic zones, as Egypt, are changing. In fact, data from the largest tertiary cancer hospital in Egypt, NCI Cairo, were analyzed to verify the incidence of squamous cell carci­noma in the area. Data from 1980 to 2005 were obtained and data from 2778cases were available for analyses. The authors demonstrated a statically significant asso­ciation between period of diagnoses and histopathological type. In this way, patients diagnosed in 2005 had a sixfold higher odds associated to transitional cell carcinoma compared to those patients diagnosed in 1980 (Felix et al. 2008). Bilharzias associa­tion dropped from 82.4% to 55.3% and there was a significant increase of transi­tional cell carcinoma from 16% to 65%, while squamous cell carcinoma was less frequent, from 76% to 28%. Intimately related to this, there was an increase in the median age of patients from 47 to 60 years. The decline in the frequency of BC is related to a decline in bilharzias egg positivity in the specimen and this suggests a better control of the endemic disease in rural population (Gouda et al. 2007).

Information from other sources on Actos Warning

Even though association between inflammation in schistosoma infection and squamous BC is well established, the role of inflammation due to other infections in the origin of BC, even transitional cell carcinoma, is less clear.Of the epidemiologic studies regarding urinary tract infection (UTIs) and BC, including transitional cell carcinoma, with one exception (Kjaer et al.1989), all the retrospective observational studies have demonstrated a positive association between BC and UTIs. Relative risk in these studies range between 1.4 and 16 for any history of urinary infection versus none, and similar associations have been found in men and women. To date no prospective study has been conducted to clearly establish the role of infection in bladder carcinogenesis.

Therefore, it could be possible that those positive associations result from detec­tion bias or differential recall between cases and controls. Prospective studies with large number of patients and controls are warranted to determine the role of inflam­mation in BC (Michaud 2007).

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http://www.seedol.com

In subsequent years, the hepatitis B virus was photographed under an electron microscope and was propagated in cell culture. Its genetic material was analyzed. A schematic diagram of hepatitis B virus. The hepatitis B virus is a member of the Hepad- naviridae family; other very similar viruses in this family cause liver disease in woodchucks, ground squirrels, and ducks. These animals have served as experimental models for research on hepatitis B.

The genetic material of hepatitis B virus is a circular strand of DNA. This circular DNA encodes four viral proteins, two of which are struc­tural proteins of the viral particle. It is important to be familiar with these proteins, especially the hepatitis B surface and core proteins, because detection of these proteins in the blood, or detection of antibodies against them, plays a critical role in diagnosis.

Hepatitis B core antigen (HBcAg) is a protein that forms the nude- ocapsid, or core, of the viral particle and is associated with the viral DNA. Hepatitis B core antigen is not readily detectable in the blood of infected individuals but can be seen in the liver cells. If the virus is rapidly replicating in the liver, a smaller form of the hepatitis B core antigen can be detected in the infected patient’s blood. This form is known as hepatitis Be antigen (HBeAg). Detection of HBeAg in the blood has important clinical significance in the diagnosis of more seri­ous and more highly contagious disease.

More information on Multaq

Acute infection with the hepatitis B virus can cause a wide range of initial conditions, from no symptoms to fulminant hepatic failure. In newborn babies, acute infection, usually transmitted from the mother at the time of delivery, generally does not cause clinical disease. In younger children, acute infection with hepatitis B virus also does not usually cause clinically apparent disease. In adults, most acutely infected individuals develop acute clinical hepatitis that varies in severity.

In most adult cases, acute infection with the hepatitis B virus causes moderate illness that spontaneously resolves, as in Case 1 above. Symp­toms of hepatitis typically occur within six to fifteen weeks after infec­tion. Symptoms include nausea, vomiting, fever, right upper quadrant abdominal pain, and jaundice. Blood ALT and AST activities are ele­vated roughly in proportion to the degree of acute inflammation and liver cell death. Elevations in blood bilirubin concentration and, in more severe cases, prolongation of PT may also occur. About 2 percent of acutely infected adults develop fulminant hepatic failure. This is what happened to the patient described in Case 2. Most of these individu­als either die or require emergency liver transplantation. The vast majority of acutely infected adults, as seen in Case 1, have spontaneous resolution of acute hepatitis. About 5 percent of individuals infected as adults go on to develop chronic hepatitis. B, as did the patient in Case 4.

Hepatitis B virus infection is the leading cause of chronic liver dis­ease in the world. Most chronically infected individuals are infected as infants or children. Chronic infection can cause various problems. Some chronically infected individuals are clinically classified as chronic carriers. Chronic carriers have no clinically apparent liver disease; how­ever, this may be an inaccurate term as some so-called chronic carri­ers exhibit evidence of hepatitis on liver biopsy. Other individuals chronically infected with hepatitis B virus have clinically apparent chronic hepatitis. Long-standing chronic hepatitis resuiting from hepatitis B can lead to cirrhosis. Long-standing hepatitis B infection is also a major risk factor for the development of hepatocellular carci­noma or primary liver cancer, which is the number one or two (along with lung cancer) cause of cancer death worldwide.

Information from other sources on Multaq

Chronic carriers are considered to be individuals persistently infected with the hepatitis B virus who do not have clinical evidence of hepatitis. The woman described in Case 3 is an example of a chronic carrier. Chronic carriers have detectable HBsAg in their blood but no signs or symptoms of hepatitis or liver disease. The diagnosis is often made during routine screening of pregnant women, as in Case 3, or of blood donors. Typically, blood ALT and AST activities are normal and there is no laboratory evidence of liver damage or dysfunction. The term chronic carrier derives from the fact that these individuals have laboratory evidence of hepatitis B virus infection but no clinical or lab­oratory evidence of liver disease. About 75 percent of chronic carriers will have no evidence of inflammation on liver biopsy and can truly be called carriers who do not have evidence of chronic hepatitis. About 25 percent of chronic carriers, however, are not really only carriers and will have evidence of inflammation on liver biopsy. These individuals have chronic hepatitis despite normal laboratory tests and no exhibi­tion of symptoms. Some so-called chronic carriers may even have cir­rhosis if liver biopsy is performed. Therefore, although almost universally used to describe patients chronically infected with hepati­tis B virus and no evidence of liver disease, chronic carrier may not technically be a correct description of all such patients. Furthermore, individuals who are defined as chronic carriers can sometimes develop clinically apparent hepatitis at a later time.

Chronic hepatitis that is clinically apparent, as in the patient described in Case 4, occurs in many individuals chronically infected with the hepatitis B virus. These individuals have detectable serum HBsAg. They may have symptoms of chronic hepatitis including fatigue, depression, loss of appetite, and other nonspecific complaints. Sometimes, the disease is clinically silent and the patient will not have symptoms. Blood tests will usually reveal elevated ALT and AST activ­ities. Sometimes, chronic hepatitis will be diagnosed only by liver biopsy in an individual who is diagnosed clinically as a chronic carrier. •*– Individuals with chronic hepatitis B infection, especially those with evidence of ongoing liver inflammation, are at risk of developing cir rhosis over time. Signs and symptoms of cirrhosis may not be appar­ent, and the diagnosis may be made only on liver biopsy. Case 4 describes such an example. Some patients with long-standing chronic hepatitis B may not even seek medical attention until they are suffer­ing from complications of cirrhosis

Our use of the term or terms Multaq is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

To keep up to date on Multaq visit our site often.

http://www.seedol.com

News – 3/1/2012: Did you take Pradaxa? Please contact us today if you took Pradaxa and later experienced harmful side effects. We will connect you with a lawyer that is experienced in complex litigation that may be able to help you recover monetary damages.

Pradaxa Lawsuit: Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes. Primary ICH occurs when small intracranial vessels are damaged by chronic hypertension (HTN) or cerebral amyloid angiopathy (CAA), and accounts for 78-88% of all ICH. The incidence of ICH worldwide ranges from 10 to 20 cases per 100 000 population and increases with age. Certain populations, in particular, the Japanese and those of Afro-Caribbean descent, have a heightened incidence of 50-55 per 100 000 that may reflect a higher prevalence of HTN and/or decreased access to healthcare. The incidence of hemorrhage increases exponentially with age and is higher in men than in women. Neurologic deficits from ICH reflect the location of the initial bleeding and associated edema. In addition, seizures, vomiting, headache, and diminished level of consciousness are common presenting symptoms. A depressed level of alertness on initial evaluation occurs infrequently in acute ischemic stroke (AIS) but is seen in approximately 50% of patients with ICH.

Pradaxa Lawsuit:Spontaneous, or non-traumatic, ICH has a much poorer outcome than AIS.¹ There is a 62% mortality rate by 1 year, and only about 20% of survivors are living independently by 6 months. About half of the deaths due to ICH over the first 30 days will occur within the first 2 days, largely from cerebral herniation. Later, mortality is more commonly due to medical complications, such as aspiration pneumonia or venous thromboembolism. By far the most important modifiable risk factor for spontaneous ICH is HTN. Primary hypertensive hemorrhage results from the rupture of small penetrating arteries originating in the anterior, middle (i.e., articulateness), and posterior cerebral (i.e., thalamostriate) arteries and the pons (i.e., paramedian perforators) (1.3). HTN causes vessel rupture at or near the bifurcation of affected vessels, where degeneration of components of the arterial wall (media and smooth muscle) are identified. The annual risk of recurrent hemorrhage is 2% without antihypertensive treatment.

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Pradaxa Lawsuit: By far the most important modifiable risk factor for spontaneous ICH is HTN. Primary hypertensive hemorrhage results from the rupture of small penetrating arteries originating in the anterior, middle (i.e., lenticulostriate), and posterior cerebral (i.e., thalamostriate) arteries and the pons (i.e., paramedian perforators). HTN causes vessel rupture at or near the bifurcation of affected vessels, where degeneration of components of the arterial wall (media and smooth muscle) are identified. The annual risk of recurrent hemorrhage is 2% without antihypertensive treatment. A hematoma incites local edema and neuronal damage in the adjacent brain parenchyma. This edema typically increases in size over an interval as long as 3 weeks following the initial bleeding, with the greatest growth rate over the first 2 days. Thrombin within the hematoma plays a central role in promoting perihematomal edema. Hemoglobin and its products, heme and iron, are potent mitochondrial toxins, thereby increasing cell death.

Pradaxa Lawsuit:Cerebral amyloid angiopathy. This multiloculated, lobar lesion seen on non-contrast head CT scan (A), started in the right frontoparietal region (left) and by the next day (right), developed extensive intraventricular involvement, subfalcine herniation with right-to-left shift, and a subarachnoid component. The hyperdense finding in the frontal horns is an intraventricular catheter (arrowhead). Macropathology: lobar hematoma, with adjacent edema (B). Note the midline mass effect on and compression of the adjacent lateral ventricle (arrows). Micropathology: amyloid angiopathy, demonstrated by deposits within the vessel wall of an acellular, eosinophilic material (hematoxylin and eosin (H&E) stain) (C, 40x; D, 100x; arrows). The amyloid material exhibits a fluorescent green birefringence under polarized light (thioflavin S stain, 100x) (E). Illicit drug use and coagulopathic disorder are associated with an increased risk of ICH. Over-the-counter stimulants, particularly if taken in excessive quantities, may predispose to ICH (case study 1). A large case-control study associated phenylpropanolamine use with ICH in young patients. Up to 70% of patients with primary ICH develop some measurable amount of lesion expansion over the initial few hours. Hematoma growth is an independent determinant of both mortality and functional outcome after ICH.

Pradaxa Lawsuit:Hemorrhage may dissect from the brain parenchyma into the adjacent ventricular space, carrying a poor prognosis, Hemorrhage may also be isolated to the intraventricular space, and lesions can expand substantially by rupturing into the ventricular system. Ventricular involvement may cause obstructive hydrocephalus and can result in long-term cognitive impairment.

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Pradaxa Lawsuit: Venous occlusive intracranial disease is associated with oral contraceptive use the immediate post-partum period, and a wide range of hypercoagulable medical conditions. Significant cerebral venous thrombosis involves one or more of the major venous sinuses and typically results in parenchymal hemorrhage. By definition, the territories of the ischemic and hemorrhagic lesions are in a venous, rather than arterial, distribution. Involvement of the deep venous system (case study 3) carries a much worse prognosis than if only the superficial sinuses and/or cortical veins (1.20) are involved. Magnetic resonance venography (MRV) is commonly used to identify major venous sinus occlusions.

Pradaxa Lawsuit:Significant clinical deterioration associated with PH is known as ‘symptomatic hemorrhage, an important outcome measure in acute stroke treatment. One common definition for symptomatic hemorrhage is a clinical deterioration of >4 points on the National Institutes of Health Stroke Scale (NIHSS) associated with hemorrhage seen on CT scan. Various predictors for symptomatic hemorrhage include hyperglycemia, concur­rent heparin use, the timing of successful recanalization, a history of diabetes and cardiac disease; leukoariosis, early signs of infarct on CT scans, and elevated pretreatment mean blood pressure. Neurosurgical evacuation typically is not a helpful treatment for symptomatic hemorrhage, because the lesion is frequently large and multifocal. Extra-ischemic hematomas are: located remotely from the initial ischemic stroke lesion; may be isolated or multifocal, with or without mass effect (1.17);²³ and associated with concurrent coagulopathy and previously occult vasculopathies, such as CAA, microhemorrhages, or hypertensive vasculopathy. In the NINDS (National Institute of Neurological Disorders and Stroke) trial of IV t-PA for AIS, the incidence of extra-ischemic cerebral hematomas was 1.3%.

Pradaxa Lawsuit:The single mandated indication for neurosurgical decompression is cerebellar hemorrhage. Early craniotomy, prior to brainstem compression, is critical. The best surgical candidates are patients with an initial GCS <14 and hematoma volume >40 ml, while those with higher GCS and smaller lesions are likely to have a good outcome with conservative, non-surgical management. Neurosurgical evacuation of clot in primary hemispheric ICH has had mixed results in randomized and non­randomized clinical trials. The leading study, I-STICH (International Surgical Trial in Intracerebral Haemorrhage), identified neutral outcomes for early evacuation. Nonetheless, a role for neurosurgical decompression to reduce clot size may exist in highly selected patients, particularly younger patients (e.g., <60 years old) who have cerebellar hemorrhage, treated with neurosurgery. Head CT scan shows a large, primary ICH based in the cerebellar vermis, causing effacement of the basal cisterns around the pons and early obstructive hydrocephalus, with markedly enlarged temporal horns (arrows) (A). The patient underwent emergent craniotomy over the next few hours, and subsequent CT scan the following day (B) shows recovery of basal cisterns, reduction in ventricular size, and a pocket of air in the left cerebellar hemisphere (arrowhead), with some edema in the left middle cerebellar peduncle. Note the craniotomy defect from the left suboccipital approach.

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Pradaxa Lawsuit: Various clinical trials, including SHEP (Systolic Hypertension in the Elderly Program)and PROGRESS (Perindopril Protection Against Recurrent Stroke Study), have documented the critical role of antihypertensive agents in both primary and secondary stroke prevention of ICH. The JNC-7 report (Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) provides an extensive overview of the role of HTN in stroke risk, specific drug classes, lifestyle modifications, and target blood pressures. In general, lower blood pressures are associated with a proportional reduction of recurrent stroke and stroke mortality.

Pradaxa Lawsuit:Less invasive surgical interventions, such as catheter-based clot aspiration or thrombolysis, are being studied. Intraventricular ICH may contribute to elevated intra­cranial pressure (ICP) by causing obstructive hydrocephalus. The amount of ventricular blood to cause hydrocephalus need not be great (1.22). In this setting, external drainage of cerebrospinal fluid via ventricular catheter may be indicated to reduce ICP.

Pradaxa Lawsuit:Commonly considered agents: beta-blockers (labetalol, esmo­lol), calcium channel blockers (nicardipine), angiotensin con­verting enzyme (ACE) inhibitors (enalapril), and hydralazine. Other agents such as nitroprusside are effective as second-line options but carry the risk of significant vasodilation. Mass effect causing significant elevation of ICP, with the risk for cerebral herniation syndromes, may be managed emergently with osmotic agents, such as mannitol and/or hypertonic saline, and hyperventilation. However, these approaches have never been formally studied in clinical trials. Seizures occur in 10% of patients with primary ICH, usually at onset or within the initial 24 hours, and reflect cortical involvement of the lesion. Anticonvulsant agents are empirically recommended for patients with significant hematomas in peripheral territories in the cerebral hemispheres. The appropriate duration of anticonvulsant use has not been established. For patients who are seizure- free, guidelines suggest discontinuation of the anti-epileptic drug after the first month post-hemorrhage. Neurointensivist management of ICH in an intensive care unit (ICU) setting may improve patient outcomes.

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Pradaxa Lawsuit: A 36-year-old patient with a known history of HTN and reportedly excessive use of a weight-loss agent and stimulant, xenedrine, presented with an evolving large, left subcortical ICH. Despite aggressive neurocritical care, with ICP monitoring, cerebrospinal fluid (CSF) drainage and hypertonic saline, the patient died from cerebral herniation 7 days into the hospitalization. A CT scan (CS 1.1) on hospital day 5 showed the mass effect on the midbrain (CS 1.1 A) and, with associated edema, upon the lateral ventricle). The small hemorrhage between the frontal horns (arrowhead) was caused by the catheter tip of an external ventricular drain.

Pradaxa Lawsuit: A healthy 45-year-old woman with no significant past medical history, except for use of oral contraceptives, presented with lethargy and obtundation. Uncertainty of the diagnosis at another hospital led to an emergent transfer to a regional Stroke Center. A deep venous sinus thrombosis was suspected based upon the diffuse subcortical venous congestion seen on MRI on the FLAIR sequence, there is heightened signal intensity in the left, greater than right, basal ganglia and thalami; and on T1-weighted image with gadolinium contrast, the periventricular veins are dilated. The patient rapidly deteriorated despite treatment with IV heparin. Cerebral angiography was undertaken with the plan to directly reopen the deep venous system. A lateral view of the venous circulation showed normal drainage and wide patency of the superficial venous system and dural sinus; however, it also showed stagnation, with no opacification, of essentially the entire deep venous system, including the internal cerebral veins, the vein of Galen, and the straight sinus.

Pradaxa Lawsuit: Attempts were made over 3 hours to try to re-establish flow in the deep venous system. Local thrombolytic infusion with 12 mg of t-PA, delivered directly into the proximal straight sinus, with an approach from the right transverse sinus, partially established an irregular channel with limited antegrade flow across this sinus; the sinus is shown on subtracted (left) and unsubtracted (right) views). Markers of the microcatheter are noted in the middle and distal straight sinus (arrowheads). An additional attempt was made with a 4-mm balloon angioplasty and, to demonstrate relation to the skull base, that was also unsuccessful. This lesion resulted in a central herniation syndrome. The patient progressed to brain death within 2 days.

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In subsequent years, the hepatitis B virus was photographed under an electron microscope and was propagated in cell culture. Its genetic material was analyzed. A schematic diagram of hepatitis B virus. The hepatitis B virus is a member of the Hepad- naviridae family; other very similar viruses in this family cause liver disease in woodchucks, ground squirrels, and ducks. These animals have served as experimental models for research on hepatitis B.

The genetic material of hepatitis B virus is a circular strand of DNA. This circular DNA encodes four viral proteins, two of which are struc­tural proteins of the viral particle. It is important to be familiar with these proteins, especially the hepatitis B surface and core proteins, because detection of these proteins in the blood, or detection of antibodies against them, plays a critical role in diagnosis.

Hepatitis B core antigen (HBcAg) is a protein that forms the nude- ocapsid, or core, of the viral particle and is associated with the viral DNA. Hepatitis B core antigen is not readily detectable in the blood of infected individuals but can be seen in the liver cells. If the virus is rapidly replicating in the liver, a smaller form of the hepatitis B core antigen can be detected in the infected patient’s blood. This form is known as hepatitis Be antigen (HBeAg). Detection of HBeAg in the blood has important clinical significance in the diagnosis of more seri­ous and more highly contagious disease.

More information on Multaq

Acute infection with the hepatitis B virus can cause a wide range of initial conditions, from no symptoms to fulminant hepatic failure. In newborn babies, acute infection, usually transmitted from the mother at the time of delivery, generally does not cause clinical disease. In younger children, acute infection with hepatitis B virus also does not usually cause clinically apparent disease. In adults, most acutely infected individuals develop acute clinical hepatitis that varies in severity.

In most adult cases, acute infection with the hepatitis B virus causes moderate illness that spontaneously resolves, as in Case 1 above. Symp­toms of hepatitis typically occur within six to fifteen weeks after infec­tion. Symptoms include nausea, vomiting, fever, right upper quadrant abdominal pain, and jaundice. Blood ALT and AST activities are ele­vated roughly in proportion to the degree of acute inflammation and liver cell death. Elevations in blood bilirubin concentration and, in more severe cases, prolongation of PT may also occur. About 2 percent of acutely infected adults develop fulminant hepatic failure. This is what happened to the patient described in Case 2. Most of these individu­als either die or require emergency liver transplantation. The vast majority of acutely infected adults, as seen in Case 1, have spontaneous resolution of acute hepatitis. About 5 percent of individuals infected as adults go on to develop chronic hepatitis. B, as did the patient in Case 4.

Hepatitis B virus infection is the leading cause of chronic liver dis­ease in the world. Most chronically infected individuals are infected as infants or children. Chronic infection can cause various problems. Some chronically infected individuals are clinically classified as chronic carriers. Chronic carriers have no clinically apparent liver disease; how­ever, this may be an inaccurate term as some so-called chronic carri­ers exhibit evidence of hepatitis on liver biopsy. Other individuals chronically infected with hepatitis B virus have clinically apparent chronic hepatitis. Long-standing chronic hepatitis resuiting from hepatitis B can lead to cirrhosis. Long-standing hepatitis B infection is also a major risk factor for the development of hepatocellular carci­noma or primary liver cancer, which is the number one or two (along with lung cancer) cause of cancer death worldwide.

Information from other sources on Multaq

Chronic carriers are considered to be individuals persistently infected with the hepatitis B virus who do not have clinical evidence of hepatitis. The woman described in Case 3 is an example of a chronic carrier. Chronic carriers have detectable HBsAg in their blood but no signs or symptoms of hepatitis or liver disease. The diagnosis is often made during routine screening of pregnant women, as in Case 3, or of blood donors. Typically, blood ALT and AST activities are normal and there is no laboratory evidence of liver damage or dysfunction. The term chronic carrier derives from the fact that these individuals have laboratory evidence of hepatitis B virus infection but no clinical or lab­oratory evidence of liver disease. About 75 percent of chronic carriers will have no evidence of inflammation on liver biopsy and can truly be called carriers who do not have evidence of chronic hepatitis. About 25 percent of chronic carriers, however, are not really only carriers and will have evidence of inflammation on liver biopsy. These individuals have chronic hepatitis despite normal laboratory tests and no exhibi­tion of symptoms. Some so-called chronic carriers may even have cir­rhosis if liver biopsy is performed. Therefore, although almost universally used to describe patients chronically infected with hepati­tis B virus and no evidence of liver disease, chronic carrier may not technically be a correct description of all such patients. Furthermore, individuals who are defined as chronic carriers can sometimes develop clinically apparent hepatitis at a later time.

Chronic hepatitis that is clinically apparent, as in the patient described in Case 4, occurs in many individuals chronically infected with the hepatitis B virus. These individuals have detectable serum HBsAg. They may have symptoms of chronic hepatitis including fatigue, depression, loss of appetite, and other nonspecific complaints. Sometimes, the disease is clinically silent and the patient will not have symptoms. Blood tests will usually reveal elevated ALT and AST activ­ities. Sometimes, chronic hepatitis will be diagnosed only by liver biopsy in an individual who is diagnosed clinically as a chronic carrier. •*– Individuals with chronic hepatitis B infection, especially those with evidence of ongoing liver inflammation, are at risk of developing cir rhosis over time. Signs and symptoms of cirrhosis may not be appar­ent, and the diagnosis may be made only on liver biopsy. Case 4 describes such an example. Some patients with long-standing chronic hepatitis B may not even seek medical attention until they are suffer­ing from complications of cirrhosis

Our use of the term or terms Multaq is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.

To keep up to date on Multaq visit our site often.

http://www.seedol.com