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Loryna Class Action Lawsuit News – 2/16/2012: Loryna may be linked to serious negative side effects. If you took Loryna and believe you suffered negative side effects as a result, contact us today so that we can make arrangements for a free consultation with a law firm that is investigating cases related to the side effects of Loryna.

Loryna Class Action Lawsuit: An emerging concept of GP IIb/IIIa inhibition, based on evidence from two trials, is that these agents appear to be able to reduce the size of an evolving non-ST-elevation MI, and potentially prevent the development of myocardial ne­crosis. In the troponin substudy of PRISM-PLUS, patients randomized to tiro- fiban plus heparin and aspirin had a significantly lower peak troponin level as compared with patients who received heparin and aspirin alone. This observation was made among patients who had a negative CK-MB on admis­sion. In PURSUIT, using peak CK-MB as a measure of infarct size, it was observed that infarct size, either the index MI or a recurrent MI, was signifi­cantly smaller in patients treated with eptifibatide. Thus, when using these potent antiplatelet therapies early in the course of treatment, there appears to be an immediate reduction of the severity of the presenting illness, which is similar to the beneficial effect of chronic aspirin use in reducing the severity of the pre­senting acute coronary syndrome.

Thrombolytic therapy has dramatically reduced mortality following acute myo­cardial infarction. Its benefit is due to early achievement of infarct-related artery patency, which limits myocardial infarct size, decreases left ventricular dysfunc­tion, and improves survival. While thrombolytic therapy has proved to be a major advance in the treatment of patients with acute myocardial infarction, current regimens are limited by failure of initial reperfusion, inadequate perfusion with delayed flow (TIMI grade 2 flow), reocclusion, and reinfarction in sig­nificant percentages of patients. Because these problems are associated with increased subsequent mortality, and because platelets play a central role in failed reperfusion, reocclusion, and reinfarction, attention has turned to the promising glycoprotein IIb/IIIa inhibitors.

In the setting of ST-elevation MI, IIb/IIIa inhibition was first used following thrombolysis in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI)-8 trial using abciximab following tissue plasminogen activator (tPA). A consistent dose-dependent inhibition of platelet aggregation was observed and major bleeding was not increased. Eptifibatide was tested in the Integrilin to Manage Platelet Aggregation and Combat Acute Myocardial Infarction (IMPACT-AMI) trial. In addition to accelerated, full-dose tPA, aspirin, and heparin, patients were randomized to ep­tifibatide, at one of six doses, or placebo. The highest dose of eptifibatide ap­peared to improve the 90-min rate of TIMI grade 3 flow (66 vs. 39% for placebo; p = 0.006). More recently, a pilot study combined full-dose streptokinase (1.5 million U/h) and three doses of eptifibatide (180-^g/kg bolus and either 0.75-, 1.33-, or 2.0-^g/kg/min infusion for 24 h) or placebo. Adding the IIb/IIIa inhibitor led to a modest improvement in early complete reperfusion (TIMI grade flow 3 at 90 min) from 38% with placebo to approximately 50% with eptifibatide. The highest dose of eptifibatide was associated with increased bleeding and was discontinued. Further testing of eptifibatide is planned with reduced-dose thrombolytic agents.

The combination of a reduced-dose fibrinolytic agent and a GP IIb/IIIa inhibitor was tested in the TIMI-14 trial, using tPA, streptokinase, and reteplase; in SPEED (Strategies for Patency Enhancement in the Emergency Department) using rete- plase; and in INTRO-AMI and several ongoing trials. In the TIMI-14 trial dose-ranging phase, 681 patients with ST-segment- elevation MI meeting with standard eligibility criteria were randomized within 12 h of onset of chest pain to receive one of four reperfusion regimens (each with several dose levels): accelerated (full-dose) tPA alone (the control arm); reduced-dose tPA plus abciximab; reduced-dose streptokinase plus abciximab; or abciximab alone. All patients received aspirin and heparin, with the initial heparin dosage being 70-U/kg bolus and a 15-U/kg/h infusion in the tPA control arm, and 60-U/kg bolus and a 7-U/kg/h infusion in the abciximab groups.

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Loryna Class Action Lawsuit: Abciximab alone was associated with a rate of TIMI grade 3 flow at 90 min of 32% and patency rate of 48% (43). The combination of streptokinase and abciximab produced only slight improvement in 90-min TIMI grade 3 flow: 42% in the 0.5-MU group; 39% in the 0.75-MU group; and 47% in the 1.25-MU group. The 1.5-MU regimen plus abciximab was discontinued after four of six patients developed a major hemorrhage, one of whom had an ICH. Of the various dosing regimens of tPA tested, the best angiographic results were obtained using a 50-mg dose given as a 15-mg bolus and a 35-mg infusion over 60 min. The rate of TIMI grade 3 flow at 90 min was 77% compared with 62% for tPA alone (p = 0.02). Overall patency was achieved in 93% of patients with the combination of abciximab and half-dose tPA compared with 78% for full-dose tPA alone (p = 0.09). An even greater difference was observed at 60 min: accelerated tPA achieved only 43% TIMI grade 3 flow at 60 min compared with 72% for 50-mg tPA plus abciximab (p = 0.0009). Major hemorrhage was similar (approximately 6%) among the tPA plus abciximab and control groups. In-hospital mortality was low in all groups, ranging from 3 to 5%.

The Orbofiban in Patients with Unstable Coronary Syndromes (OPUS-TIMI)-16 trial tested the oral Il/IIIa inhibitor, orbofiban, in patients with acute coronary syndromes. This trial enrolled 10,288 patients at 888 hospitals in 28 countries. The inclusion criteria were onset of an acute coronary syndromes within 72 h, defined as an episode of rest ischemic pain lasting at least 5 min associated with either positive cardiac enzymes (i.e., an acute MI), ECG changes, or a prior his­tory of coronary or vascular disease. Exclusion criteria included renal insuffi­ciency (creatinine >1.6 mg/dL, increased high bleeding risk, or need for oral anticoagulation. All patients received 150 to 162 mg of ASA daily and were randomized, in double-blind fashion, to one of two doses of orbofiban or placebo. In one group, orbofiban was administered as 50 mg twice daily throughout the trial (50/ 50 group); in the other group, 50 mg was given twice daily for the first 30 days (the highest risk period), and was reduced to 30 mg twice daily for the remainder of the trial (50/30 group). Other treatments were at the discretion of the pa­tient’s physician. The primary endpoint was a composite of death, MI, recurrent ischemia leading to rehospitalization or urgent revascularization, or stroke. The planned sample size was 12,000 patients, but the trial was terminated early after an unexpected finding of increased mortality at 30 days in one of the orbofiban groups.

Mortality through 10 months was 3.7% for the placebo group versus 5.1% in the 50/30 group (p = 0.008) and 4.5% in the 50/50 group (p = 0.11). There were no differences in the primary composite endpoint at 10 months (22.9, 23.1, and 22.8%, for the placebo, 50/30, and 50/50 groups, respectively). Major or severe bleeding (but not intracranial hemorrhage) was higher with orbofiban; it occurred in 2.0, 3.7 (p = 0.0004), and 4.5% (p < 0.0001) of patients, respec­tively. Exploratory subgroup analyses did identify that patients who underwent percutaneous coronary intervention had a lower mortality and a significant reduc­tion in the composite endpoint (p = 0.001) with orbofiban. Two substudies from OPUS-TIMI-16 found that orbofiban led to increases in measures of platelet activation, notably P-selectin. These data are con­sistent with observations of other agents, which induced an apparent prothrom- botic effect, with increases in measures of platelet activation and increases in platelet aggregation when drug levels were low. Interestingly, in the TIMI-12 trial, no increase in P-selectin was observed with sibrafiban therapy. Active research is ongoing, but these initial studies suggest that there may be differences among the various oral IIb/IIIa inhibitors with regard to potential prothrombotic effects.

The Evaluation of oral Xemilofiban in Controlling Thrombotic Events (EXCITE) trial studied xemilofiban in 7232 patients undergoing PCI with either stenting or balloon angioplasty without adjunctive intravenous IIb/IIIa inhibition. Patients were randomized in a double-blind fashion to receive one of two doses of xemilofiban or placebo: All the xemilofiban patients received a first 20-mg dose 30 to 90 min prior to PCI, followed by either 10 or 20 mg three times daily for 6 months. The primary endpoint—death, MI, or urgent revascularization at 6 months—occurred in 13.6% of patients in the placebo group, 14.1% of patients in the xemilofiban 10-mg group, and 12.6% of patients in the xemilofiban 20­mg group (p = NS) (78). There was a trend toward fewer periprocedural MIs over the first 48 h following PCI, but this benefit was not sustained at 30 days or 6 months. Mortality at 6 months was 1.0% for placebo, 1.6% for the 10­mg xemilofiban dose group, and 1.1% in the 20-mg dose group. Major bleed­ing was significantly more common in the xemilofiban-treated patients. Thus, xemilofiban did not significantly reduce cardiac events in this patient popu­lation.

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Loryna Class Action Lawsuit: The second Symphony trial was terminated prematurely at the time the results from the first Symphony trial were available (and not due to safety issues). It compared the combination of low-dose sibrafiban plus aspirin vs. high-dose si­brafiban (without aspirin) vs. aspirin alone in 6671 patients with stabilized acute coronary syndromes. With an average follow-up of 90 days, the primary endpoint, death, MI, or severe recurrent ischemia, was not different among the three groups: 10.5% in the high-dose sibrafiban group; 9.2% for low-dose sibrafiban plus aspi­rin vs. 9.3% for aspirin alone. In this trial (but not in the larger first Symphony trial), mortality was significantly higher with the high-dose sibrafiban group: 2.4 vs. 1.7% for the low-dose sibrafiban plus aspirin group vs. 1.3% for placebo. Recurrent MI followed a similar pattern: 6.9% for high-dose sibrafiban, 5.3% for the low-dose plus aspirin group, and 5.3% for aspirin. Major bleeding was more common with high-dose sibrafiban (4.6%), and higher still for the combination of low-dose sibrafiban plus aspirin (5.7%) vs. 4.0% for aspirin alone.

It is an exciting time for the practicing physician given the availability of this important new therapy that can significantly reduce death, MI, or refractory ischemia/urgent revascularization. The benefits apply to essentially all patients undergoing PCI, thereby becoming a new standard of care in this setting. For the huge number of patients with unstable angina and non-ST-elevation MI, IIb/ IIIa inhibition will significantly reduce recurrent ischemic events. The trials to date have targeted the higher risk unstable angina patients—those with ECG changes or positive cardiac enzymes, and thus these are the patients in clinical practice who should be targeted for early use of IIb/IIIa inhibitors.

Platelets are integrally involved in the thrombotic complications of atherosclero­sis. Their contribution to thrombosis complicating a ruptured atherosclerotic plaque is well established. Interference with platelet function, therefore, should help to prevent thrombotic occlusion of arteries affected by atherosclerosis. In­deed, numerous studies have demonstrated that antiplatelet agents decrease ad­verse cardiovascular events in patients with atherosclerosis. This chapter will focus on three such antiplatelet agents: aspirin, ticlopidine, and clopidogrel. It will include a brief review of platelet function followed by a discussion of the mechanisms of action of these antiplatelet drugs. Thereafter, clinical evidence supporting the notion that antiplatelet agents reduce adverse cardiovascular events in patients with atherosclerosis will be presented.

The three principal events in the formation of a platelet plug include platelet adhesion, activation, and aggregation. Platelets normally circulate in an inacti­vated state. Vascular injury and disruption of the endothelial lining initiates the process of platelet adhesion, in which platelets are deposited on the intimal surface of blood vessels. Among the most important substances to mediate platelet adhesion to the vascular surface is von Willebrand factor. It binds suben­dothelial collagen to the platelet glycoprotein Ib-IX-V receptor. Binding of plate­lets to the vascular surface prompts an intracellular signaling mechanism, includ­ing the metabolism of arachidonic acid to thromboxane A₂. In addition, the platelets release constituents of their alpha and dense granules such as p-selectin.

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Loryna Class Action Lawsuit: Aspirin inhibits arachidonic acid metabolism and prevents the formation of thromboxane A₂ by irreversibly inhibiting cyclooxygenase via acetylation of a serine moiety. Platelet inhibition occurs approximately 60 min following the oral ingestion of aspirin. The inhibitory effects of platelets last the life of a platelet, which is approximately 10 days. Hemostatic recovery following a single dose of aspirin occurs as new platelets are formed and enter the circulation. Both ticlopidine and clopidogrel are thienopyridines. These inhibit the function of platelet ADP receptors and thereby limit conformational changes in the glycoprotein IIb/IIIa receptor. Inhibition of platelet aggregation occurs ap­proximately 1 to 2 days following administration of these drugs, and 40 to 60% inhibition of ADP-induced aggregation is observed 3 to 5 days following inges­tion. Platelet function is restored approximately 3 to 4 days after discontinua­tion of ticlopidine or clopidogrel.

The beneficial effects of aspirin on cardiovascular outcome in patients with ath­erosclerosis is well established. The Antiplatelet Trialists’ Collaboration per­formed a metanalysis of over 73,000 patients with clinical manifestations of ath­erosclerosis such as acute myocardial infarction, prior myocardial infarction, or prior stroke or transient ischemic attack, in which patients were treated with either antiplatelet therapy or a control. The most widely studied antiplatelet drug was aspirin. Overall, antiplatelet therapy was associated with a 25% odds reduc­tion for the aggregate endpoint of stroke, myocardial infarction, or vascular death. The studies included in this metanalysis, as well as some more recent studies, highlight the efficacy of aspirin in reducing cardiovascular morbidity and mortality in patients with atherosclerosis. Some of the larger studies involving patients with coronary artery disease, cerebrovascular disease, or peripheral arte­rial disease are described below.

In the Antiplatelet Trialists’ Collaboration, antiplatelet therapy, primarily aspirin, was associated with a 29% odds reduction for stroke, myocardial, or vascular death among approximately 20,000 patients with acute myocardial infarction and a 25% odds reduction for these adverse events among approximately 20,000 pa­tients with prior myocardial infarction. The largest trial for acute myocardial infarction included in the Antiplatelet Trialists’ Collaboration was the Second International Study of Infarct Survival (ISIS-2), which randomized over 17,000 patients with acute myocardial infarction to aspirin, streptokinase, both, or neither. Compared to placebo, aspirin was associated with a 23% risk reduction for vascular death, a 50% reduction for nonfatal reinfarction, and a 46% reduction for nonfatal stroke 5 weeks after randomization. The combination of streptokinase and aspirin was more effective than either agent alone in reducing vascular death. The efficacy of aspirin in preventing coronary reocclusion follow­ing thrombolysis for acute myocardial infarction is supported by a metanalysis of 32 studies. Reocclusion occurred in 11% of 419 patients treated with aspirin versus 25% of 513 patients not treated with aspirin, and recurrent ischemic events occurred in 25% of 2977 patients treated with aspirin compared to 41% of 721 patients who were not treated with aspirin.

Several large trials have demonstrated the efficacy of aspirin in preventing myocardial infarction and death in patients with unstable angina. A Veterans Administration Cooperative study randomized 1256 men with unstable angina to aspirin or placebo for 12 weeks. The incidence of fatal or nonfatal myocardial infarction was reduced by 51% in the group treated with aspirin compared to the group treated with placebo. A Canadian multicenter trial randomized 555 patients with unstable angina to aspirin, sulfinpyrizone, both, or neither to 24 months of treatment. The incidence of fatal or nonfatal myocardial infarction was 8.6% in the groups receiving aspirin compared to 17% in the groups not receiving aspirin, resulting in a 51% risk reduction with aspirin. Theroux et al. compared the efficacy of aspirin, intravenous heparin, both, or neither in 479 patients with unstable angina. Approximately 6 days following randomization, myocardial infarction had occurred in 11.9% of patients who received neither aspirin nor heparin, in 3.3% who received any aspirin, in 0.8% of those who received only heparin, and in 1.6% of patients who received both aspirin and heparin. The Research Group on Instability in Coronary Artery Disease in Southeast Sweden (R.I.S.C.) randomized 796 men with unstable angina or non-Q-wave myocardial infarction to aspirin or placebo. After 1 year, myocardial infarction occurred in 21.4% of patients treated with placebo and in 11% of patients treated with aspirin. Thus, aspirin treatment reduced the risk of nonfatal or fatal myocardial infarction by 48%.

Our use of the term or terms Loryna Class Action Lawsuit 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.

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Loryna Class Action Lawsuit

Loryna Class Action News – 2/16/2012: If you were prescribed Loryna and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

Loryna Class Action: The findings from the observational studies that hormone users are at generally lower risk from coronary disease do not necessarily imply cause and effect. Women and their physicians decide on estrogen therapy. Often the health status of the woman will have an important influence on this decision and on the results of studies that examine these women. Thus, some have argued that hormone use is merely a marker rather than a cause of good health. Most of the observational studies reviewed here have provided some in­formation bearing on this critical point. The Nurses’ Health Study tried to evalu­ate whether increased medical care of women using postmenopausal hormones might be responsible for the benefit observed. In an analysis limited to women who reported regular physician visits (50% of the cohort), results were sim­ilar to those found in the larger population of all subjects: the relative risk for major coronary heart disease was 0.52 (95% CI, 0.37-0.74) for current hormone use.

Another approach is to examine the risk profile of estrogen users and non­users to determine whether the differences, if any, are sufficient to explain the large decrease in risk among estrogen users. Barrett-Connor observed that, in a cohort of postmenopausal women, those taking estrogens reported more in­tensive health-care behavior, including frequent screening tests such as blood cholesterol measurement and mammograms. An examination of determinants of estrogen therapy in 9704 women participating in a large, multicenter study of osteoporotic fractures found that hormone users tended to be better educated, less obese, and drank alcohol and participated in sports more often than nonusers. Similarly, in a prospective study of randomly selected premenopausal women, observed a better cardiovascular risk factor profile prior to hormone use among the women who subsequently took hormones at menopause than among women who did not.

For hormone users compared to nonusers and, after further adjustment for high blood pressure, history of angina, MI, or stroke, alcohol use, smoking, body mass index, and age at menopause, the relative risk was virtually the same (RR = 0.79; 95% CI, 0.71-0.88), implying an equivalent risk status for users and nonusers. In addition, to further examine this issue, the Nurses’ Health Study conducted an analysis limited to a subgroup of low-risk women (i.e., those with no diagnosis of hypertension, diabetes, or high serum cholesterol who were nonsmokers and had a Quetelet’s Index below 32 kg/m²). Even with such restrictions, the relative risk for coronary disease was almost 40% lower for current hormone users. In summary, to explain the overall benefit of hormone therapy as a result of con­founding by health status, one would have to presume unknown risk factors which are extremely strong predictors of CHD and very closely associated with estrogen use.

LMWHs, like UFH, bind a cofactor called antithrombin to produce their predominant anticoagulant effect. Binding is mediated through a unique pentasac­charide sequence of the mucopolysaccharide that increases by 1000-fold both the interaction between antithrombin and thrombin (factor II_a), and the interaction between antithrombin and factor Xa. However, a minimum chain length of 15 to 18 saccharides (corresponding to a molecular weight of > 5400 daltons) is required to inactivate thrombin. In contrast, inhibition of factor Xa can occur with short polysaccharide chains. Thus, one potentially important distinc­tion between UFH and LMWH, and among LMWHs themselves, is the varying ratio of factor Xa to factor IIa. The factor Xa:IIa activity for UFH is approxi­mately 1.2, while ratios for the various LMWH preparations vary from 2 to 4. Table 1 lists LMWHs in order of anti Xa:IIa ratio.

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Loryna Class Action: The ESSENCE study was a double-blind, placebo-controlled trial that ran­domly assigned 3171 patients with angina at rest or non-Q-wave myocardial in­farction to receive 2 to 8 days therapy with either 1 mg/kg of enoxaparin subcuta­neously twice daily or continuous intravenous UFH. At 14 days, the risk of death, myocardial infarction, or recurrent angina was significantly lower in the patients assigned to enoxaparin than in those assigned to UFH (16.6% vs. 19.8%; p = 0.019). At 30 days, the risk of this composite endpoint remained significantly lower in the enoxaparin group (19.8% vs. 23.3%; p = 0.016). The need for revas­cularization procedures at 30 days was also significantly less frequent in the pa­tients assigned to enoxaparin (27.1% vs. 32.2%; p = 0.001). The 30-day inci­dence of major bleeding complications was 6.5% in the enoxaparin group and 7.0% in the unfractionated-heparin group, but the incidence of bleeding overall was significantly higher in the enoxaparin group (18.4% vs. 14.2%; p = 0.001), primarily because of ecchymoses at injection sites. Thus, the ESSENCE trial indicates that enoxaparin plus aspirin is more effective than UFH plus aspirin in reducing the incidence of ischemic events in patients with unstable angina or non-Q-wave myocardial infarction in the early phase. This benefit was associated with an increase in minor, but not major, bleeding.

In TIMI-11B, 3910 patients with unstable angina or non-Q-wave MI were randomized to either intravenous UFH for 3 to 8 days followed by subcutaneous placebo injections, or enoxaparin during both the acute phase (initial 30-mg IV bolus followed by injections of 1.0 mg/kg every 12 h for 3 to 8 days) and outpa­tient phase (injections every 12 h for up to 43 days of 40 mg for patients weighing >65 kg and 60 mg for those weighing <65 kg). The primary endpoint (death, myocardial infarction, or urgent revascularization) occurred by 8 days in 14.5% of patients in the UFH group and 12.4% of patients in the enoxaparin group (OR 0.83 [0.69 to 1.00]; p = 0.048) and by 43 days in 19.7% of the UFH group and 17.3% of the enoxaparin group (OR 0.85 [0.72 to 1.00]; p = 0.048). During the first 72 h and also throughout the entire initial hospitalization, there was no differ­ence in the rate of major hemorrhage in the treatment groups. During the outpa­tient phase, major hemorrhage occurred in 1.5% of the group treated with placebo and 2.9% of the group treated with enoxaparin (p = 0.021). Consistent with the ESSENCE findings described above, the results of the TIMI-11B study demon­strate that enoxaparin is superior to UFH in reducing a composite of death and serious cardiac ischemic events during the acute management of patients present­ing with unstable angina, but does not cause a significant increase in the rate of major hemorrhage.

Last, the FRAXIS trial (29) randomized 3468 patients in a double-blind fashion to one of three treatment regimens: UFH (5000 IU bolus, followed by an infusion for 6 ± 2 days); nadroparin for 6 days (nadroparin 86 anti-Xa IU/kg IV bolus, followed by twice-daily subcutaneous injections for 6 ± 2 days); or nadroparin for 14 days (same dose as the prior group for 14 days). No statistically significant differences were observed among the three treatment regimens with respect to the primary outcome (cardiac death, myocardial infarction, refractory angina, or recurrence of unstable angina at day 14). The absolute differences between the groups in the incidence of the primary outcome were: -0.3% (p = 0.85) for the nadroparin 6-day group vs. the UFH group, and +1.9% (p = 0.24) for the nadro- parin 14-day group vs. the unfractionated heparin group. Furthermore, there were no significant intergroup differences regarding any of the secondary efficacy out­comes. However, there was an increased risk of major hemorrhage in the nadro­parin 14-day group compared with UFH (3.5% vs. 1.6%; p = 0.0035). Thus, similar to the FRISC-I trial findings with dalteparin, treatment with nadroparin for 6 days provides similar efficacy and safety to treatment with UFH for the same period. A prolonged regimen of nadroparin (14 days) does not provide any additional clinical benefit and is associated with an increase risk of major hemorrhage.

The use of LMWH as an adjunct to fibrinolytic therapy is actively under investi­gation (33-37). Preliminary results from the HART-II angiographic study (37) demonstrated slightly higher rates of infarct artery patency (80.1% vs. 75.1%; p = NS) and TIMI grade 3 flow rates (52.9% vs. 47.6%; p = NS) at 90 min among 200 patients receiving tPA and enoxaparin (30 mg IV bolus followed by 1 mg/ kg SQ twice daily for >72 h) compared to tPA and UFH. Clinical event rates were similar and reocclusion among patients with a patent artery at 90 min tended to be less frequent in those randomized to enoxaparin (5.9 vs. 9.8%; p = NS). In another angiographic study (36), dalteparin was compared with placebo in patients receiving streptokinase. TIMI grade 3 flow 20 to 28 h later tended to be higher in patients treated with dalteparin (68% vs. 51%; p = 0.10) and the number of ischemic episodes on continuous ECG monitoring was lower (16% vs. 38%; p = 0.04).

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Loryna Class Action: Direct thrombin inhibitors, as indicated by the class name, do not require anti­thrombin or another cofactor to inhibit the function of thrombin. Direct thrombin inhibitors inhibit all the major actions of thrombin, including thrombin-induced generation of fibrin, thrombin-induced platelet activation, as well as thrombin’s autocatalytic reaction. Potential advantages of direct thrombin inhibitors over heparin include: inhibition of clot-bound thrombin lack of inhi­bition by activated platelets; and stable anticoagulant response since no cofactor is required. The prototypic direct thrombin inhibitor is hirudin, a polypeptide consisting of 65 amino acids derived from the leech Hirudo medicinalis. Hirudin selec­tively binds thrombin in a 1:1 fashion at two locations: the carboxy terminus of hirudin binds to the substrate recognition site, the domain of thrombin that recognizes fibrinogen or the platelet and the amino terminus of hirudin binds to the catalytic site of thrombin. Hirudin does not inhibit factor Xa, IX, kallikrein, activated protein C, plasmin, tissue plasminogen activator, or other enzymes in the coagulation or fibrinolytic pathways. Although hirudin does not bind covalently to thrombin, the dissociation rate is extremely slow; thus, hirudin essentially irreversibly inhibits thrombin.

Lepirudin was compared to heparin in the OASIS-2 trial (56). While there were trends toward a reduction in cardiovascular death or MI at 72 h (2.0% vs. 2.6%; p = 0.04) and at 7 days (3.6% vs. 4.2%;p = 0.08), there was an attenuation of this benefit by day 35, in contrast to the sustained superiority of enoxaparin over UFH (30). Furthermore, major bleeding requiring transfusion was more fre­quent with lepirudin (1.2% vs. 0.7% for heparin; p = 0.01). The authors per­formed a metanalysis of all the hirudin trials and observed a modest 10% benefit favoring hirudin, although this was not statistically significant for patients with unstable angina/non-ST-elevation MI at 35 days. The Food and Drug Ad­ministration (FDA) recently reviewed the available clinical data and did not ap­prove hirudin for use in unstable angina/non-ST-elevation MI, citing the lack of sustained benefit and increased risk of bleeding.

In the HIT-3 trial, excess intracranial hemorrhage was observed with lepirudin (0.4 mg/kg bolus, 0.15 mg/kg/h infusion) compared to UFH (3.4% vs. 0%) among 302 patients receiving tPA. In the subsequent HIT-4 trial (71), involv­ing 1208 patients and using a lower dose of lepirudin (0.2 mg/kg bolus, 0.5 mg/ kg subcutaneously b.i.d.) in combination with streptokinase, TIMI flow grade 3 was observed in 40.7% in the lepirudin and in 33.5% in the heparin group (p = 0.16). No difference were seen between lepirudin and heparin in the rate of hemorrhagic stroke (0.2% vs. 0.3%), reinfarction (4.6% vs. 5.1%), or mortality (6.8% vs. 6.4%) at 30 days. Thus, intravenous lepirudin (as administered in HIT- 3) as an adjunct to tPA appears to be unsafe, and lower dose lepirudin in combina­tion with streptokinase does not significantly improve reperfusion or clinical out­comes.

Angiographic trials with other direct thrombin inhibitors in conjunction with fibrinolytic therapy have also been conducted. In a pilot study and the HERO trial, a trend toward improved early (90 to 120 min) TIMI grade 3 flow was observed with the higher dose of Hirulog as compared with heparin in patients receiving streptokinase. Testing with other agents found modest or no improvements compared with heparin. HERO-II, an international phase III trial of approximately 17,000 patients with ST-elevation MI treated with strep­tokinase, is randomizing patients to either Hirulog or UFH and should complete enrollment in the latter half of 2000.

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Loryna Class Action: Despite tremendous initial enthusiasm for the direct thrombin inhibitors, their current role in clinical practice is limited to use as an anticoagulant in patients with heparin allergy, or in the treatment of heparin-induced thrombocytopenia and thrombotic syndrome. Ongoing and future research, particularly as adjunctive therapy in patients receiving fibrinolysis or percutaneous coronary intervention, may identify other clinical situations in which these drugs could play a useful role. However, studies to date have identified a narrow therapeutic window, mar­ginal evidence of incremental, sustained efficacy over UFH, and the possibility of a ‘‘rebound’’ effect. These problems represent challenges to this class of anti­thrombotic drugs.

Because approximately 4 million patients each year are admitted to hospitals worldwide with unstable angina or acute myocardial infarction (MI), and nearly 1 million patients annually worldwide undergo percutaneous coronary intervention (PCI), physicians have focused a great deal of attention on developing new treat­ments for these acute coronary syndromes (ACS). The initiating event of these acute coronary syndromes is rupture of an atherosclerotic plaque followed by local thrombosis. Similar pathophysiology is present during PCI, which is essen­tially a ‘‘planned’’ plaque disruption.

The peptide and peptidomimetic inhibitors (e.g., tirofiban and eptifibatide) are competitive inhibitors of the IIb/IIIa receptor, with very rapid half-lives of dissociation from the IIb/IIIa receptor (10-20 s). Thus, the level of plate­let inhibition is directly related to the drug level in the blood. Since both inhibitors have short half-lives, when the drug infusion is stopped the antiplatelet activity reverses after a few hours, which is a potential benefit for avoiding bleed­ing complications. The third group of GP IIb/IIIa inhibitors are the oral agents. Within this group, there are also the two broad types of agents, those that are competitive inhibitors, and those that bind tightly to the receptor. The oral drugs are usually prodrugs, which are absorbed and then converted to active compounds in the blood. The oral agents all have longer half-lives, such that they can be given once, twice, or three times daily in order to achieve relatively steady levels of IIb/IIIa inhibition.

Abciximab was also found to be beneficial when started 24 h prior to a PCI in the c7E3 Fab Antiplatelet Therapy in Unstable Refractory Angina (CAPTURE) trial: death, MI, or urgent revascularization was reduced by abcix­imab from 15.9 to 11.3% (p = 0.012) (27). In the Evaluation of IIb/IIIa inhib­itor for Stenting (EPISTENT) trial (28), compared with stenting with only aspirin and heparin, the rate of death, MI, or urgent revascularization at 30 days was significantly reduced in both abciximab groups—from 10.8 to 5.3% for stent plus abciximab (p < 0.001) and 6.9% for balloon angioplasty with abciximab (p = 0.007) (28). Benefits were maintained at 6 month and 1 year, with a significant reduction in 1 year mortality in patients treated with stent plus abcix- imab compared with stent alone. In addition, a metanalysis of abciximab trials has shown that there is a significant reduction in mortality when GP IIb/ IIIa inhibition is used.

Our use of the term or terms Loryna Class Action News 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.

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Loryna Lawyer News: Please contact us today if you took Loryna and suffered unusual side effects or other injuries.

Loryna Lawsuit: Clinical evidence demonstrating anti-inflammatory and plaque-stabilizing effects of statin drugs has only recently become available. The first study to address whether patients with evidence of inflammation benefited from statin therapy was performed within the Cholesterol and Recurrent Events (CARE) trial, a secondary-prevention evaluation of pravastatin. Consistent with studies of primary prevention, participants in the CARE trial with elevated CRP levels were found to have higher risks of recurrent coronary events than those with lower levels of CRP. However, a clinically apparent interaction between statin therapy and inflammation was also observed in that the proportion of recurrent events prevented by pravastatin was 54% among those with inflammation com­pared with 25% among those without inflammation. Moreover, long-term therapy with pravastatin significantly reduced plasma levels of CRP in a manner that was not related to this agent’s effects on LDL cholesterol. In fact, in this hypothesis-generating study, there was no relationship between the change in CRP and the change in LDL cholesterol at the end of the 5-year follow-up period. Thus, these initial data provided clinical evidence that statin therapy may well have anti-inflammatory properties. While the mechanism of this effect is uncertain, the CARE data provide evidence for possible clinical relevance of laboratory observations demonstrating nonlipid effects of the HMG-CoA reductase inhibitors, such as modulation of immune function, antiproliferative effects on vascular smooth muscle, and antithrombotic properties, as well as morphological ef­fects.

Two major studies have now addressed the validity and clinical importance of these observations. The first, the Pravastatin Inflammation/CRP Evaluation (PRINCE) trial, was explicitly designed to address three questions. First, can the effects of pravastatin on CRP observed in the CARE trial be confirmed in a direct hypothesis-testing setting? Second, how quickly does any effect of pravastatin on CRP occur and are the effects of pravastatin on CRP truly inde­pendent of changes in LDLC? And third, are the effects of pravastatin on CRP observed in CARE (a secondary-prevention study) equally present in primary- prevention populations? In total, the PRINCE trial evaluated 2884 patients: 1182 in a secondary- prevention cohort who received pravastatin 40 mg daily, and 1702 in a primary- prevention cohort randomly allocated to either pravastatin 40 mg daily or placebo. Prior use of lipid-lowering therapy within the previous 6 months was not allowed, and those in the primary-prevention arm had to have LDL choles­terol levels greater than 130 mg/dL. Blood samples were collected at baseline.

As ensured by the randomization process, baseline levels of CRP (median 0.20 mg/dL), total cholesterol (231 mg/dL), LDL cholesterol (143 mg/dL), and HDL cholesterol (40 mg/dL) were virtually identical in the two primary- prevention arms of the PRINCE trial. In contrast, compared with those in the primary-prevention cohort, those with a prior history of cardiovascular disease who were enrolled in the secondary-prevention cohort of PRINCE had signifi­cantly increased CRP levels (median 0.26 mg/dL). As would be expected, those in the secondary-prevention cohort were also older and more likely to smoke or have diabetes, and the group had a higher proportion of aspirin users than the primary-prevention cohort. During the course of the study, highly significant re­ductions in total cholesterol, LDL cholesterol, and triglycerides were observed in the pravastatin groups, as was a clinically important increase in HDL choles­terol (all p values <0.001). No change was observed in any of these parameters among those allocated to placebo.

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Loryna Lawyer: The main analyses of PRINCE were the effects of statin therapy at both 12 and 24 weeks. In the primary-prevention cohort, pravastatin reduced median CRP levels by 16.9% compared with placebo at the end of the 24-week study period (p < 0.001). This effect was present at 12 weeks (median reduction in CRP with pravastatin 14.7%; p < 0.001). As shown in Figure 7, these effects were observed in all the PRINCE prespecified subgroups, including analyses stratified by age, smoking status, gender, obesity, and lipid levels. As had been hypothesized, virtually no association was observed between CRP and lipid levels either at the study beginning or during follow-up. In fact, in correlational analy­ses, less than 2% of the variance in the change in CRP could be explained by the change in any lipid parameter. Virtually identical effects were also seen in those in the secondary-prevention cohort of the study.

Several decades ago, homocystinuria, a rare pediatric condition, was noted to be associated with musculoskeletal abnormalities and the development of ven­ous thromboembolism and arterial disease in adolescence. The underlying metabolic defect for this condition was shown to be decreased enzymatic activ­ity of cystathionine beta-synthase. This deficiency was associated with in­creased levels of methionine and homocysteine and a decrease in blood levels of cysteine. Later investigations of a patient with elevated homocysteine levels and similar clinical findings, but with a low concentration of methionine in the plasma and evidence of abnormal vitamin B₁₂ metabolism, led to the conclusion that another defect could account for elevated homocysteine levels and vascular disease.

A large variety of factors have been associated with increased levels of homocys­teine, and only the key topics in healthy outpatients will be considered here. Fasting blood homocysteine concentrations are typically greater in the elderly compared with middle-aged adults, and higher in men than in women. Analyses of the Framingham Heart Study and the National Health and Nutrition Examination Survey data have shown that the prevalence of elevated homocyste­ine (>14 |j.mol/L) increases with age in both sexes, and plasma homocysteine levels are inversely correlated with vitamin intake. Vitamins Bj, B₂, B₆, B₁₂, folate, niacin, retinol, vitamin C, and vitamin E have all been studied, but the greatest interest has been shown for vitamins B₆, B₁₂, and folate, as these nutrients act as cofactors for several homocysteine metabolic pathways.

Low vitamin B₁₂ status can also account for elevated homocysteine levels, as this vitamin is a necessary cofactor in several homocysteine metabolic steps. Inadequate production of intrinsic factor in the stomach can result in a severe vitamin B₁₂ deficiency, with substantially elevated homocysteine concentrations, but this etiology is an infrequent cause of low vitamin B₁₂ status. Hypochlorhydria and achlorhydria are more common than inadequate intrinsic factor deficiency, especially in older individuals, and can lead to impaired absorption of vitamin B₁₂ because low pH is needed to dissociate B₁₂ from food.

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Loryna Lawyer: There are many genetic causes of elevated homocysteine levels. Enzymatic de­fects and variants have been associated with cystathionine beta-synthetase, meth­ylene tetrahydrofolate reductase (MTHFR), thermolabile and nonthermolabile variants, and methionine synthetase, to name a few. The MTHFR variant 677- C ^ T has gotten the most attention, as it is relatively common and affects 10 to 15% of North Americans and 5 to 25% of Europeans. This MTHFR variant has also been studied for associations with cardiovascular disease, and homo­zygosity has generally been associated with an increased occurrence of disease; however, several studies demonstrated no association between the MTHFR and vascular outcomes. A meta-analysis concluded that a modest association with increased risk for cardiovascular disease was present. The inconsistent asso­ciation between MTHFR variants and vascular disease may be partially explained by population dietary data. Persons homozygous for MTHFR 677-C ^ T and who had suboptimal folate status were especially likely to have elevated homo­cysteine levels.

Other studies have not always corroborated these results. In some instances, the associations with adverse outcomes were demonstrated for nutrient status, but not for homocysteine levels. For instance, higher homocysteine levels were not associated with greater risk in a MRFIT-nested case-control analysis (20); the ARIC study demonstrated higher folate and B₆ intake to be associated with lower CVD risk but associations with higher homocysteine were not significant (21); and the Nurses’ Health Study investigators found that higher folate and B₆ intake was associated with lower cardiovascular risk. Elevated homocysteine concentrations in the plasma may potentiate thrombin generation and may have relevance in the setting of acute coronary syndromes. A study of approximately 100 persons with acute coronary syndromes was found to have positive associa­tions with F1 + 2 and Factor Vila levels. It has been proposed that hyperho- mocysteinemia potentiates a procoagulant state that may adversely affect the en­dothelium and enhance tissue factor activity.

Large-scale interventional data that reduce homocysteine levels and dem­onstrate favorable effects on cardiovascular risk are lacking, but vitamin supple­ments are being included in a variety of ongoing studies and the results should be forthcoming. The minimal daily dose of folic acid that appears to have maximal efficacy to decrease plasma homocysteine is estimated as 0.4 ^g/day, with higher doses not generally being more effective. It is recommended that vitamin B₁₂ deficiency be ruled out prior to initiating folic acid therapy. Alterna­tively, persons on folic acid therapy can be supplemented with a dose of 400 to 1000 |J.g/day of vitamin B₁₂. The dose of vitamin B₆ recommended was 25 to 50 mg/day and there is little risk of developing complications such as sensory neuropathy at this supplement level.

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Loryna Lawyer: New factors associated with increased risk for coronary heart disease arouse great interest and enthusiasm, kindling the hope that we may enhance identification of individuals at risk for CHD. Important concerns are that such metabolic factors be biologically plausible, measurable, repeatable, strong, graded, and treatable (37-39). Measurement issues include accuracy and precision for the factor in the laboratory and evidence of low or modest variability in the clinical setting. If the laboratory or biological variability is very large, the utility of the measurement for predictive purposes is seriously reduced. Many years of experience and stan­dardization of measurements are available for some vascular risk factors, and less experience is available for homocysteine. New risk factors may provide clues to pathogenesis and in some instances may improve our ability to predict disease. The ability to predict new vascular disease events should be demonstrated after consideration of the core set of factors that are currently available, including age, sex, blood pressure, cholesterol or LDL cholesterol, HDL cholesterol, smoking, and diabetes mellitus. This criterion is often not met in new investigations and considerable experience and relatively large data sets and follow-up may be nec­essary to assure that new factors, such as homocysteine, prove useful in predicting vascular disease risk.

Elevated homocysteine levels may be accompanied by decreased blood levels and intake of folate, vitamin B₆, or vitamin B₁₂. These vitamins are important cofactors in the metabolism of homocysteine, and border­line deficiencies are relatively common, affecting approximately 30% of the el­derly participants in the Framingham Heart Study. Greater intake of these vitamins in the diet, with supplements in the form of multivitamins, or through fortification of foods, has led to less vitamin deficiency and a decrease in the prevalence of elevated homocysteine levels. Fortification of the food supply in the United States with folate was announced in early 1996 with a mandated enactment date of January 1, 1998. Analyses of homocysteine and folate levels before and after fortification have been undertaken in Framingham Heart Study participants and showed a dramatic decline in the prevalence of low folate levels, a reduction in the prevalence of elevated homocysteine from approximately 20 to 10%, and a modest decrease in mean homocysteine levels from approximately 10 to 9 |J.mol/L.

Lupus anticoagulants or nonspecific inhibitors interfere with the assembly of procoagulant complexes. In vitro, these antibodies are associated with the pro­longation of phospholipid-dependent blood-clotting times. Characteristically, clotting times return to normal with the addition of exogenous phospholipid. Lu­pus anticoagulants may demonstrate specificity for blood-clotting proteins, in particular prothrombin. However, the mechanism by which they promote throm­bosis is unknown. Lupus anticoagulants are likely associated with a high risk of first and recurrent thrombosis as well as recurrent pregnancy loss.

LAC are a heterogeneous group of autoantibodies, which prolong the clot­ting time in a variety of assays and may demonstrate specificity for beta- 2 glycoprotein-1. LAC do not prolong clotting times in assays in which phospholipid is present in excess. This suggests that LAC inhibit in vitro coagula­tion by interfering with the assembly of procoagulant complexes on phospholipid surfaces. This observation also forms the basis for the test for LAC—a prolonged clotting time, in a phospholipid-limited assay system, that normalizes with the addition of excess phospholipid confirms the presence of LAC. Anecdotal experi­ence suggests that lupus anticoagulants are much less common than anticardio- lipin antibodies, that they are infrequently transient, and that they are associated with a high risk of complications, although none of these observations has been adequately studied. Furthermore, laboratory assays for lupus anticoagulants.­

Our use of the term or terms Loryna Lawyer 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.

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Loryna Litigation News – 2/16/2012: If you were prescribed Loryna and have suffered negative side effects, please contact us today so that we can put you in touch with an attorney to advise you of your legal rights.

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.

Our use of the term or terms Loryna Litigation 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.

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Actos Lawsuit News 2/14/2012: Did you take Actos? Please contact us today if you took Actos 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.

Actos Lawsuit: The urinary bladder is a hollow, balloon-like organ located in the pelvis that collects and stores urine until it is ready to be excreted from the body. Urine is produced in the kidneys and is transported to the bladder through two tube-like structures called ureters. Pressure from the accumulation of urine in the urinary bladder forces the wall of the bladder to contract producing the urge to urinate. The urine is then excreted from the bladder via the urethra (a thin tube that carries urine from the bladder to the outside of the body).

A basic understanding of the terminology used by doctors to describe the various subtypes of bladder tumors is important in order to more fully appreciate the various approaches to treatment, the treatment options, and the prognosis (chances for recovery). Superficial bladder tumors are those that are localized (confined) to the transitional epithelium (urothelium) – the layer of epithelial cells that lines the inside of the bladder wall and is in direct contact with the urine – but have not spread to the deeper layers of the bladder. Additionally, bladder tumors that have invaded the lamina propria but have not invaded the muscularis propria can be considered as superficial. Invasive bladder cancer refers to a bladder tumor that is either invading the muscularis propria – the deeper layer of muscle cells that forms the wall of the bladder – or the perivesical fat located beyond the bladder muscle. This type of tumor is referred to as muscle-invasive bladder cancer. Muscle-invasive bladder cancer carries a higher risk of spreading beyond the bladder (metastases) and must be treated more aggressively than superficial bladder cancer. The term metastatic bladder cancer is used when the cancer cells have spread beyond the bladder to distant sites.

Hematuria – Blood in the urine (hematuria) is often the first warning signal and the most common symptom of bladder cancer. It has been estimated that approximately 80% to 90% of patients with bladder cancer develop hematuria which is often painless. In some cases, sufficient numbers of red blood cells are present to turn the color of the urine to dark brown or red. This is known as gross hematuria and is easily recognized by the patient upon urinating. In other cases, insufficient numbers of red blood cells may be present in the urine to cause any evident changes in the color of the urine but red blood cells can be detected by examining the urine under a microscope. This type of hematuria is called microscopic hematuria and may also indicate the presence of bladder cancer. It is important to note that although hematuria is the most common symptom of bladder cancer.

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Actos Lawsuit: Cystoscopy is an important diagnostic tool that enables the physician to directly examine the urinary tract with an instrument called a cystoscope. During this procedure, which is usually performed by an urologist on an outpatient basis, the cystoscope – a long, flexible lighted tube – is inserted through the urethra (the tube that carries urine from the bladder to the outside of the body) and is advanced into the bladder. The cystoscope enables the doctor to view the bladder and urethra and look for any abnormalities including a tumor, infection, or obstruction. During this procedure, the physician may also remove a small piece of tissue from the bladder (biopsy) and submit the biopsy specimen to the pathology laboratory where it is examined under a microscope for the presence of cancer cells. If you have signs and symptoms suggestive of bladder cancer (hematuria and/or changes in bladder habits), your doctor will recommend a cystoscopy to rule out bladder cancer.

A small piece of bladder tissue (biopsy specim en) is obtained by the urologist during cystoscopy for microscopic evaluation. During the biopsy procedure, muscle tissue must be obtained as it is important to determine the extension of the tumor (how far the tumor has spread) since the treatment of superficial bladder cancer differs from muscle-invasive bladder cancer. The biopsy specimen will then be examined under a microscope by another doctor known as a pathologist.

In general, early diagnosis and treatment significantly improves the prognosis for patients with bladder cancer. A high level of suspicion of bladder cancer should be considered for any patient who presents with gross hematuria and known risk factors for the disease. Once the diagnosis is confirmed, patients are evaluated thoroughly to determine the stage (extent of spread) of the disease. The choice of treatment depends upon a variety of factors including the type of bladder cancer, stage of the disease, the presence of other underlying medical conditions, and the patient’s preferences.

Transurethral resection of the bladder tumor (TURBT) represents the primary treatment modality for superficial bladder cancer. During this procedure, which may be performed either under general or regional anesthesia, the tumor is removed using a cystoscope that is inserted into the bladder via the urethra. After surgical removal of the bladder tumor, any remaining cancer cells can be destroyed with either electrical current (fulguration) or with a high-energy laser.

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Actos Lawsuit: The term “intravesical therapy” refers to the instillation of a biological agent or a chemotherapy drug directly into the bladder in order to destroy any residual cancer cells. Intravesical therapy is a form of local drug therapy whereby the treatment is targeted directly at the site of the cancer (bladder) as opposed to systemic drug therapy where a drug is injected into a vein or is given orally and travels throughout the circulatory system in order to reach the target organ (e.g., bladder).

The most common type of intravesical therapy for superficial bladder cancer is immunotherapy with Bacillus Calmette-Guerin (BCG). BCG is a vaccine that is sometimes used to vaccinate people against tuberculosis. The rationale for using BCG for the treatment of superficial bladder cancer is to boost the body’s natural immune system to destroy the bladder cancer cells. It is thought that BCG induces regression of the bladder tumor through a non-specific inflammatory reaction at the tumor site. Intravesical therapy with BCG is a form of immunotherapy. Intravesical BCG immunotherapy is the treatment of choice for patients with carcinoma in situ (Stage Tis) where the bladder cancer is limited to the lamina propria of the bladder but has not invaded the surrounding tissue.

Patients who undergo a radical cystectomy for muscle-invasive bladder cancer also require urinary diversion reconstructive surgery to collect and eliminate urine. Urinary diversion, also known as urostomy, is the general term used to describe reconstructive surgical procedures that bypass the normal structures of the urinary system by creating a “diversion” or conduit for the passage of urine through an opening in the abdominal wall called a stoma.

Orthotopic continent diversion – In this type of continent diversion, a new bladder, called a neobladder, is created by the surgeon using a long segment of the small or large bowel that serves as a reservoir to collect and store the urine. One technique involves surgically connecting the neobladder to the urethra which enables the patient to void urine normally. This procedure may be more advantageous for younger patients who may not wish to wear a bag attached to the abdomen for collecting the urine.

Another potential side effect of radical cystectomy in men is nerve damage that results when the neurovascular bundles are not spared during surgery. Nerve damage often results in the loss of the ability to have an erection (erectile dysfunction). Younger men under age 60 have a greater likelihood of regaining erectile function following a radical cystectomy than men over age 60. Patients should discuss with their surgeon the advantages and disadvantages of using nerve-sparing procedures during radical cystectomy.

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Actos Lawsuit: In women, part of the vagina is also usually surgically removed during a radical cystectomy making sexual intercourse more difficult and painful. Intercourse may be made less painful by using lubricating gels, vaginal moisturizers, or vaginal dilators. Women who undergo radical cystectomy are, however, still capable of achieving sexual climax (orgasm). It is evident that radical cystectomy can have a significant impact on the sexual health of both men and women. Patients should talk openly with their doctor about the potential negative side-effects of radical cystectomy on their sexual well-being and discuss the options that may be available for resuming an active and pleasurable sexual relationship after surgery for bladder cancer.

Over the years, doctors have come to learn that radical cystectomy alone is not sufficient as the sole treatment modality for muscle-invasive bladder cancer because about 50% of patients develop recurrent distant metastasis after undergoing radical cystectomy. More recently, the role of systemic chemotherapy has become better defined in the management of patients with muscle-invasive bladder cancer. Systemic chem otherapy may be administered either before radical cystectomy in order to shrink the bladder tumor ( neoadjuvant chemotherapy) or it may be given following surgery to destroy any residual cancer cells remaining in the body (adjuvant chemotherapy).

An important study published in 2003 in the New England Journal of Medicine (Volume 349; pages 859-866) clearly demonstrated the benefits in terms of significantly prolonged survival among bladder cancer patients receiving neoadjuvant combination systemic chemotherapy with methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) as compared to the survival rate for patients treated with radical cystectomy alone. The median survival rate over an 11-year period of patients in this study who were treated with neoadjuvant M-VAC systemic chemotherapy followed by radical cystectomy was 77 months compared to only 46 months for patients treated with radical cystectomy alone. Based on the results of this study, the use of neoadjuvant combination chemotherapy has becom e much more prevalent for the treatment of muscle-invasive bladder cancer.

The data supporting the use of adjuvant chemotherapy for high-risk bladder cancer patients remains controversial. Nevertheless, it is generally accepted that patients with Stage T3 or T4 tumors and/or the presence of cancer in one or more lymph nodes at the time of surgery should receive 4-6 cycles of chemotherapy with either GC (gemcitabine) or M-VAC. Patients should discuss with their physicians the benefits and potential side effects of either neoadjuvant or adjuvant chemotherapy approaches.

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Actos Lawsuit: Although radical cystectomy is currently considered as the first-line treatment modality for muscle-invasive bladder cancer, some patients may be either unwilling or, due to other underlying medical conditions, may not be eligible to undergo this surgical procedure. What are the treatment options available to these patients?

In recent years, doctors have developed a combination of three treatment modalities (trimodality therapy or multimodality therapy) consisting of transurethral resection (TUR), radiation therapy, and systemic chemotherapy as a means of eradicating the bladder tumor while, at the same time, preserving the patient’s own bladder. The primary advantages of the trimodality therapy approach is that it enables the patient to keep their own bladder by avoiding the need for a radical cystectomy and, thereby, experience an improved quality of life after treatment for bladder cancer.

Although some studies have reported similar survival rates between trimodality therapy and radical cystectomy for patients with muscle-invasive bladder cancer, some experts have expressed the opinion that the risk of local recurrence of the cancer along with the risk of metastatic disease is higher for patients treated with the trimodality approach as compared to patients undergoing radical cystectomy. For these reasons, radical cystectomy is currently still considered as the standard of care for most patients with muscle-invasive bladder cancer, while trimodality therapy is usually reserved for a small subset of patients who are either unwilling or unable to undergo radical cystectomy or those who may wish to enroll in a clinical trial involving trimodality therapy.

Currently, combination systemic chemotherapy is considered as the first-line treatment for patients with metastatic (Stage IV) bladder cancer. The chemotherapeutic regimen that has been used most commonly since 1990 for metastatic bladder cancer is M-VAC (methotrexate, vinblastine, doxorubicin, cisplatin). The median survival rate for patients with metastatic bladder cancer who are treated with M-VAC is only about one-year, however, a small percentage of patients achieve longer survival.

Our use of the term or terms Actos Lawsuit 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.

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Instant Soup Lawsuit News – 2/8/2012: How deep is the burn? Burn depth is measured in terms of “de­grees”. To understand this measuring system, it is help­ful to understand something about the structure of normal skin (see Figure 6.4). The outermost layer is the epidermis, which is composed of living keratinocytes and melanocytes, the pigment cells that impart color to the skin. As old epidermal cells die off, new cells replace them. Under the epidermis is the thicker layer of skin, called the dermis, which is largely made of the protein col­lagen. Blood vessels, nerves, oil glands, hair follicles, and sweat glands are located in this layer. The cells that regenerate skin line the hair follicles and sweat glands. Thus, these “accessory struc­tures” are necessary for the skin to be able to “heal itself.”

A first-degree burn is superficial, involving injury only to the outermost layer of skin—the epidermis—and is like a sunburn. The skin becomes red, warm, swollen, and painful. The skin may even peel, but the damage to the skin heals within a few days, by a process called epithelialization. A first-degree burn is sometimes called an epidermal burn. Second-degree burns are caused by brief contact with fire and by scalds from liquids that are mostly water, such as tea and coffee. A second-degree burn involves a portion of the dermis as well as the epidermis—this is called a partial-thickness burn. It can range from superficial to deep partial thickness, depending on how many of the epidermal accessory structures are left in the remain­ing dermis. The skin is blistered, moist, discolored, and painful.

Third-degree burns destroy the full thickness of skin—all of the epidermis and all of the dermis—and are commonly caused by contact with flame or liquids with a high boiling point (fat, tar, molten metal). A third-degree burn appears dry, pale, and leathery. The skin will not grow back. Skin grafts must be performed to keep infection from entering the body through the burn. Full-thickness burned skin contracts and loses its ability to stretch. It becomes tight around the extremity, eventually restrict­ing the blood supply to the hand or foot or limiting chest expan­sion during breathing. Third-degree burns that encircle the arm or leg or chest require an escharotomy. An escharotomy, usually per­formed in the emergency room or upon admission to the medical unit or the burn unit, is an incision in the burn made through the skin to the underlying fat. Because third-degree burns destroy nerve endings, the burned skin is numb and anesthesia is generally not needed for this procedure, although some sedation or pain medication may be given.

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Instant Soup Lawsuit: Fourth-degree burns involve the tissues beneath the skin such as muscle and bone. This term is rarely used, because burns of this depth are rare. They are usually caused by high-voltage electricity or by sleeping close to a fire for a long time in an altered state of consciousness. The limb is often destroyed and amputation is nec­essary. There are no reliable scientific tests to judge the depth of the burn or the ability of the wound to heal without skin-grafting procedures. The medical team must inspect and feel the burn and estimate its depth. Generally speaking, second-degree burns blis­ter and hurt more than third degree burns (because some of the skin nerves are still alive), but this is not always true. Quite often, the burn wound “evolves” over several days, particularly in chil­dren, and the physician cannot be sure of the depth for quite a while.

For the first two or three days after the injury the patient will receive fluids to make up the huge body fluid losses that seep out from the burn (this procedure is called resuscitation). The patient may be fed intravenously and may receive mechanical assistance with breathing and circulation. The burn wound is cleaned by the staff once or twice a day and then dressed, usually with a medication designed to kill germs (a burn cream) and thick dressings. The treatment of the burn is painful, and the patient will receive pain medications to ease the pain. Management of pain is an essential concern of the medical team, the nursing team, and the rehabilitation team. Specialists are frequently called in to consult with the doctors directly in charge of the burn patient. These individuals are highly qualified in medical areas such as infection control or the treat­ment of the various specific organ systems that may fail as a result of the burn.

Some types of burns require additional specific treatment. Chemi­cal bums, for example, are caused by alkalis, acids, oxidants, or other agents that destroy tissue upon contact. Chemical burns need to be rinsed with water to remove all traces of the toxic material. This is best done immediately, and with shower water, but occasionally chemical wounds are also treated with specific antidotes such as calcium injections or applications of an ammo­nium gel (for hydrofluoric acid burns).

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Instant Soup Lawsuit: A person with a high-voltage electrical burn is treated differ­ently than someone with a flame injury. Electrical injury causes damage to tissues beneath the skin surface: the electrical current passes through the body, heating the bone and causing damage to muscles from the inside out. Blood vessels also become damaged, and delayed muscle death can occur from the lack of circulation over the days to weeks following the initial injury. This internal damage causes swelling that in turn could cause further muscle and nerve injury. To prevent this, early surgery is performed to release pressure on muscle and nerves caused by swollen deep tissues.

If things are going well in the first two or three days, the swelling will decrease, the patient’s state of consciousness will improve, blood pressure will stabilize, and, for a patient on the respirator, the oxygen concentration will be decreased. If all of the patient’s burns are second-degree burns and the body percentage involved is moderate, the patient is now usually mobilized and discharge planning may begin.

The oxygen content of the air the patient is receiving via respira­tor or face mask is one indication of the patient’s progress. Ask the physician or nurse what percent oxygen the patient is breathing. The oxygen content of air is 21 percent, so if the patient is receiving air with an oxygen content close to that—say, 30 to 35 percent oxygen—the patient is nearing the point where the breathing tube can be removed. If the patient’s lungs were badly injured by smoke inhalation, the degree of support given by the respirator will increase rather than decrease as time goes on. It is not a good sign if a patient’s oxygen content is increased from SO up to 60 percent, for example. The percent of inspired or breathed oxygen is referred to as the FI0₂ (ef-i-oh-two) in medical jargon.

Our use of the term or terms Instant Soup Lawsuit 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.

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