Yasmin Lawsuit

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Yasmin Lawsuit News (1/24/12): If you’ve had the potentially life-threatening complication of blood clots after taking Yasmin, please consider talking with a Yasmin Lawsuit lawyer. The FDA has released safety information concerning Yasmin and other birth controls containing drospirenone. This hormone has been linked to the formation of blood clots in several cases, leading women to pursue Yasmin Lawsuits. Best Legal Source is an experienced company that connects consumers of potentially dangerous drugs to attorneys. Pursue a Yasmin Lawsuit today by calling us at (800) 611-7080 or by completing the form to the right.

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Yasmin Lawsuit Info

Best Legal Source works only with attorneys who will take your Yasmin Lawsuit on a contingency basis. The consultation for a Yasmin Lawsuit is free, and you have nothing to lose. Call Best Legal Source to discuss your legal options regarding a Yasmin Lawsuit. Blood clots can lead to further complications including strokes, pulmonary embolism, deep vein thrombosis and heart attacks. A Yasmin Lawsuit might give you a possible avenue to pay for the medical expenses you’ve accumulated.

Yasmin Lawsuit and Yasmin Lawsuit lawyer are general terms used to describe the particular drug and legal action we are referring to. The members of the Best Legal Source team are not in business with the maker of Yasmin. In fact, our goal is to provide access to attorneys for clients seeking a Yasmin Lawsuit.

If you developed blood clots after taking this drug, you might consider talking to a Yasmin Lawsuit lawyer. Best Legal Source can help you find a qualified representative to file your Yasmin Lawsuit. Call us at (800) 611-7080 or contact us through the form above. Best Legal Source can arrange a consultation with Yasmin Lawsuit lawyers regarding Yasmin Lawsuits.

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Yasmin Lawsuit : Information from the FDA
Questions and Answers – Ongoing safety review of birth control pills containing drospirenone and a possible increased risk of blood clots

On May 31, 2011, the U.S. Food and Drug Administration (FDA) informed the public about new information that is being assessed as part of FDA’s ongoing safety review of birth control pills containing the progestin hormone drospirenone. Two recently published studies report that there is an increased risk of deep vein thrombosis (DVT) and pulmonary embolus associated with the use of birth control pills containing drospirenone compared to the risk associated with the use of birth control pills containing a different progestin hormone (levonorgestrel).1, 2

DVT is a rare condition in which blood clots form inside a vein, most commonly in the legs. A blood clot can break loose, move through the body to the lungs, and cause a serious, potentially fatal, problem called a pulmonary embolism (PE).3

The following questions and answers provide an overview of this potential safety issue.

Q1. What is drospirenone?

Q2. Which oral contraceptives contain drospirenone?

Q3. What is a deep vein thrombosis (DVT) and pulmonary embolus (PE)?

Q4. What is already known about combination birth control pills and the risk of venous thromboembolism (VTE)?

Q5. Why is FDA further reviewing the risk of venous thromboembolism (VTE) and birth control pills containing drospirenone?

Q6. How is FDA evaluating these conflicting study results regarding the risk of venous thromboembolism (VTE) in users of oral contraceptives containing drospirenone in order to decide if any regulatory action is needed?

Q7. What should women do if they are currently taking birth control pills containing drospirenone?

Q8. Are there women who should not take birth control pills, particularly those containing drospirenone?

Q9. Has FDA communicated to the public about this issue before?

Q10.What are European regulators doing about birth control pills containing drospirenone?

Q1. What is drospirenone?

A. Most birth control pills (combination oral contraceptives) combine a synthetic version of the female hormone progesterone (referred to as a progestin) with a synthetic version of the female hormone estrogen. Drospirenone is one of several different progestins that are used in birth control pills.

Q2. Which oral contraceptives contain drospirenone?

Birth control pills containing drospirenone include: Beyaz, Gianvi, Loryna, Ocella, Safyral, Syeda, Yasmin, Yaz, and Zarah.

Some birth control pills containing drospirenone are also approved to treat symptoms of premenstrual dysphoric disorder (PMDD), to treat moderate acne, and to raise folate levels, in women who choose to use an oral contraceptive for contraception.

Q3. What is a deep vein thrombosis (DVT) and pulmonary embolus (PE)?

A. Deep vein thrombosis (DVT) is a rare but serious condition where a blood clot forms inside a vein. These blood clots usually form in the lower leg or thigh, but can break loose and travel to other areas of the body such as the lungs. If the clot travels to the lung, it is called a pulmonary embolism (PE), a potentially fatal condition where an artery in the lung becomes blocked.3 DVTs and PEs are also called venous thromboembolic events, or VTEs.

The symptoms of a DVT include the new onset of persistent leg pain, while those of a PE include severe chest pain, and sudden shortness of breath. Women experiencing these symptoms should contact a healthcare professional immediately because VTEs can be life-threatening.

Q4. What is already known about combination birth control pills and the risk of venous thromboembolism (VTE)?

A.VTE is already known to be a rare but serious potential side effect of taking any birth control pill containing a progestin and estrogen. The risk of VTE in users of birth control pills is low, although it is higher than the risk of VTE in women who do not take birth control pills. The risk of VTE in pregnant women (about 5 to 20 cases per 10,000 women) 4 is even higher than that in women who take birth control pills.

The drug labels for all combination birth control pills include warning information on the potential risk of VTE and describe additional factors that increase this risk. The risk of VTE associated with birth control pills increases as a woman gets older and is also higher in women who smoke. Usually the risk of VTE is highest during the first year after starting to use a combination birth control pill.

Q5. Why is FDA further reviewing the risk of venous thromboembolism (VTE) and birth control pills containing drospirenone?

A. FDA is aware of two newly published studies that evaluated the risk of VTE in women who use birth control pills that contain drospirenone.

The two recently published studies looked at whether there is a higher risk of blood clots in women taking birth control pills containing the progestin drospirenone when compared to similar women taking birth control pills containing a different progestin called levonorgestrel.1-2 These two new studies reported that there is a greater risk of VTE associated with birth control pills that contain drospirenone. This risk is reported to be up to 2 to 3 times greater than the risk of VTE associated with using levonorgestrel-containing pills.

Conflicting information already exists on this potential increased risk. Two previously published studies, which were conducted at the request of FDA or the European regulatory agencies after drug approval, did not report any difference in risk of VTEs between the drospirenone-containing product and products containing levonorgestrel or other progestins.5, 6 However, two publications in 2009 reported that the risk of VTEs is higher in women using a drospirenone-containing product than in women who use levonorgestrel-containing products. 7, 8 These four earlier studies are already described in the labeling for drospirenone-containing birth control pills.

FDA is currently evaluating all available information to assess fully the VTE risks of drospirenone-containing birth control pills. FDA will continue to communicate any new safety information to the public as it becomes available.

A. FDA is thoroughly reviewing the two recently published studies, which includes evaluating the strengths and weaknesses of the epidemiologic methods used in these two studies as compared to those used in the other published studies. FDA’s overall assessment of VTE risk for drospirenone contraceptives will be based on the strength of the scientific evidence from each of the studies. Data from an additional, large, FDA-funded, study on hormonal contraceptives is also being finalized and reviewed. This study includes over 800,000 US women and is designed to look at thrombotic and thromboembolic risks including VTE in a number of hormonal contraceptive products; results are expected later this summer.

Q7. What should women do if they are currently taking birth control pills containing drospirenone?

A. Women taking birth control pills containing drospirenone should continue taking their pills as directed unless told otherwise by their healthcare professional. Women should know how to recognize the symptoms of VTE and should contact their healthcare professional immediately if they experience persistent leg pain, severe chest pain, or sudden shortness of breath. Women should also discuss any questions or concerns about their use of combination birth control pills with their healthcare professional and report any side effects to the FDA MedWatch program using the “Contact Us’ information at the bottom of the page.

Q8. Are there women who should not take birth control pills, particularly those containing drospirenone?

A. Women with certain conditions or risk factors should not use any combination birth control pill. FDA recommends that women who are over age 35 and smoke should not take any type of combination birth control pill (including those containing drospirenone), due to an increased risk of serious cardiovascular events. The risk of VTE also increases with age and smoking. Women with a history of blood clots, heart attack, or stroke should not take combination birth control pills. Additionally, women who are pregnant or think they may be pregnant should not use combination birth control pills.

Because drospirenone, in contrast to other progestins used in combination oral contraceptives, has the potential to increase serum potassium levels, women with renal or adrenal disease should not use birth control pills containing drospirenone.

For additional labeling information on all combination birth control pills, visit Drugs@FDA.

Q9. Has FDA communicated to the public about this issue before?

A. FDA has included warning information about the risk of VTEs in the labels of all combination birth control products. FDA has also communicated previously about the potentially greater risk of VTE with drospirenone-containing birth control products. This prior communication can be found on the Agency’s website:

MedWatch Alert: April 2010

Q10. What are European regulators doing about birth control pills containing drospirenone?

A. The European Medicines Agency (EMA) has decided to update the product labeling for oral contraceptives containing drospirenone and ethinyl estradiol regarding the risk of venous thromboembolism after review of all available data, including the same newly published data FDA is reviewing. They have concluded that the risk of VTE for drospirenone-containing birth control pills is higher than that for levonorgestrel-containing pills, but that the risk of VTE with any birth control pill (including those with drospirenone) is very small and that there is no reason for women to stop taking drospirenone-containing birth control pills.

Because FDA’s review of these new data is still ongoing, we are issuing a Drug Safety Communication to alert patients and healthcare providers about this new information that is being assessed as part of our ongoing safety review. Labeling for these products currently describes the previously published studies, which provided conflicting results regarding whether the risk of VTE is higher for women who use birth control pills that contain drospirenone. Upon completion of our review, FDA will provide patients and healthcare providers with appropriate information about VTE risk, including a possible update to labeling, for drospirenone-containing birth control pills.

Yasmin Lawsuit

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Yasmin Lawsuit News – 2/1/2012:

You deserve to be compensated if you took Yasmin and suffered side effects that the public was not warned about. Contact us today and we will arrange a free consultation with a lawyer experienced in pharmaceutical and medical device ligation that can advise you of your legal rights.

Yasmin Lawsuit News: More information about your search

Yasmin Lawsuit: Endothelial cell dysfunction is marked by upregulation of intercellular adhesion molecules and production of chemokines that mediate increased adhesion and migration of monocyte-derived macrophages and T-lymphocytes. Intercellular adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and intercellular adhesion molecule 1 (ICAM-1) interact with integrins on the surface of leukocytes to facilitate movement of inflammatory cells into the subendothelial space. Concurrently, multiple chemoattrac- tant substances, including thrombin, connective tissue degradation products, oxidized LDL, and specific molecules secreted by endothelial and smooth muscle cells [monocyte chemotactic protein 1 (MCP-1), interleukin-8 (IL-8), and macrophage colony-stimulating factor (M-CSF)] enhance the recruitment of inflammatory cells to the site of injury. Directed by these mediators, a cellular inflammatory infiltrate is established within the arterial intima. With the uptake of LDL by subendothelial macrophages, they are transformed into the lipid-laden foam cells that characterize the fatty streak, the first recognizable progenitor of the advanced atherosclerotic lesion.

As they enter the arterial intima, arriving macrophages and T-lymphocytes generate inflammatory cytokines and growth factors that reinforce the influx of mononuclear leukocytes and the production of foam cells, and that initiates the migration and proliferation of vascular smooth muscle cells, which contribute to the maturation of the fatty streak into the intermediate atherosclerotic lesion. In particular, the elaboration of interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-a) augment the expression of adhesion molecules, as well as promote the oxidation and uptake of LDL. Simultaneously released mitogens, including platelet-derived growth factor, heparin-binding growth factor, and fibroblast growth factor, along with IL- 1 and IL-6, stimulate the proliferation of smooth muscle cells that lead to formation of an intermediate plaque composed of layers of monocytes and smooth muscle cells.

In the advanced stages of this progression, a resilient fibrous cap forms over the core of intra- and extracellular lipid, inflammatory monocytes, smooth muscle cells, and necrotic debris. This protective cap is composed of an extracellular matrix that derives its strength primarily from types I and III collagen as well as elastin synthesized by vascular smooth muscle cells. The dense fibrous matrix constitutes a barrier between the highly prothrombotic contents of the atheroma core and circulating platelets and coagulation proteins. Vascular smooth muscle cells maintain this barrier in the face of macrophage production of collagenases, elastases, and proteases that may cause areas of focal thinning or erosion. When these forces determining the integrity of the extracellular matrix become unbalanced toward compromise of the barrier, exposure of the atheroma core promotes arterial thrombosis. In some cases, the thrombus is nonocclusive and may, in the absence of symptoms, become organized and incorporated into the existing advanced atherosclerotic plaque. As such, repeated episodes of plaque disruption, mural thrombosis, and organization with layering of mural thrombi may contribute to progression of the atherosclerotic lesion. In contrast, when the forming thrombus leads to abrupt compromise of distal flow, acute tissue ischemia or infarction may result.

Until recently, it had appeared self-evident that (nonembolic) arterial thrombosis was the culmination of slow enlargement of the mature atherosclerotic lesion with progressive encroachment into the arterial lumen. This pathobiological construct supported the view that the risk of acute thrombosis was dominated by the severity of arterial stenosis. However, over the past decade, angiographic and pathological data obtained in the coronary arterial bed have challenged this construct. Angiography performed prior to or at the time of acute myocardial infarction has demonstrated that the infarct-related coronary atherosclerotic lesion is frequently not ‘‘critical’’ by standard angiographic criteria. Similarly, pathological examination of culprit lesions has demonstrated that the majority of acute coronary events occur with the formation of thrombus at the site of plaques obstructing <50% of the arterial lumen. Taken together with evidence for the importance of plaque disruption in the development of superimposed thrombus, such data have shifted focus from the degree of luminal stenosis to the morphological and histological characteristics of the atheromatous plaque that determine its propensity to rupture.

Vascular inflammation may also influence arterial vasomotor function through several possible mechanisms. Increased concentrations of thromboxane A2 and its metabolites produced in acute coronary syndromes mediate further platelet aggregation as well as arterial vasoconstriction. Leukocytes also produce en- dothelin-1, a potent modulator of vasoconstriction. In addition, certain inflammatory cytokines may increase vascular smooth muscle cell reactivity, as demonstrated in an animal model with IL-1. Finally, inflammatory infiltrates have been documented in the arterial adventitia with vascular nerve involvement and thus have been hypothesized to directly stimulate coronary vasospasm.

Yasmin Lawsuit News: News and Information from related Sources

Yasmin Lawsuit: In spite of continued advancements in the management of acute ischemic heart disease, morbidity and mortality due to atherosclerotic vascular disease continue to rise globally. Thus, the impetus for improving our strategies for the prevention and management of atherosclerosis has remained strong. In this regard, laboratory and experimental research describing key processes in the initiation, progression, and destabilization of the atheroma have pointed to novel directions for cardiovascular evaluation and management. In particular, recognition of the role of inflammation in atherothrombosis has directed attention to inflammatory mediators and indicators as potential targets for risk assessment and for treatment.

Epidemiological data have established a well-characterized set of vascular risk factors, including advanced age, tobacco use, obesity, diabetes, hypertension, and dyslipidemia. However, up to one-third of first coronary events occur among individuals without these traditional risk factors. Researchers have thus sought to identify inflammatory indicators that might add to these clinical factors for predicting myocardial infarction and stroke. Candidate markers have included several of the cytokines that promote the recruitment of monocytes in response to endothelial cell dysfunction; intercellular adhesion molecules that mediate the migration of activated monocytes into the subendothelial space; enzymes that might compromise the integrity of the protective fibrous cap, as well as the acute-phase proteins that are produced and released into the systemic circulation in response to inflammatory cytokines. As an amplified and readily quantified inflammatory signal, the prototypical acute- phase reactant C-reactive protein (CRP) has been a focus of clinical investigation to date.

Cross-sectional studies have evaluated the association between elevated levels of CRP and the presence and extent of atherosclerotic vascular disease. Elevated levels of CRP have been demonstrated among patients with acute myocardial ischemia and infarction, as well as among individuals with stable coronary heart disease (CHD). In a cross-sectional survey of 388 British men aged 50 to 69 recruited from general practice registers, Mendall and colleagues demonstrated a 1.5-fold increase in the prevalence of CHD for each doubling in the levels of hs-CRP (95% CI, 1.25-1.92). Nevertheless, such cross-sectional data cannot exclude the possibility of important confounding, nor do they establish a cause-and-effect relationship. For example, blood levels of hs-CRP have been found to increase with age, body-mass index, and tobacco use, as well as in response to myocardial tissue necrosis. In contrast, prospective studies can control for such confounders and have been important in exploring the independent prognostic information offered by inflammatory markers.

Stratification by use of HRT showed that women on no HRT had a distribution of baseline CRP similar to men. The association between elevated hs-CRP and HRT was present regardless of the form of HRT used and has been corroborated by data from at least two other studies. In the Postmenopausal Estrogen/Progestin Interventions Study (139), women allocated to treatment with conjugated equine estrogens had a significant increase in hs-CRP with a mean 85% increase relative to placebo sustained at 3 years (p = 0.0001). Among elderly women treated with unopposed estrogen in the Cardiovascular Health Study, a 59% higher mean hs-CRP level was observed compared to nonusers. It has been hypothesized (139) that these data give some mechanistic insight into a transient increase in thrombotic risk associated with initiation of HRT suggested by the higher rate of thrombotic events observed during the first year of active therapy in the Heart and Estrogen/Progestin Replacement Study (HERS). However, further investigation will be important to assess whether these observations supporting the possibility of proinflammatory effects of HRT are clinically relevant.

Yasmin Lawsuit News: Additional Information and Resources

Yasmin Lawsuit: Several other studies have supported the value of baseline hs-CRP determination for assessment of longer term risk in acute coronary syndromes. The FRISC (Fragmin during Instability in Coronary artery disease) study group followed 965 patients for 5 months after initial presentation with a non-ST elevation acute coronary syndrome and found that stratification by tertile of baseline hs- CRP concentration established a gradient of mortality risk (1.6% vs. 4.6% vs. 6.9%, p = 0.005) (149). Similarly, among 102 patients with unstable angina followed for 3 months, an hs-CRP level above 0.3 mg/dL (90th percentile of normal controls) at presentation remained an independent predictor of new MI after adjustment for ECG changes and cardiac troponin T.

Data from ongoing and future investigation will be necessary to clarify the role of hs-CRP for risk assessment among patients presenting with acute coronary syndromes. In particular, the optimal timing of measurement remains in question. In two studies that included serial measurement of hs-CRP among patients with severe unstable angina, determination of hs-CRP at discharge was a better discriminator of risk of future events than measurement at hospital admission. However, among patients with myocardial necrosis, it is anticipated that the inflammatory response to tissue injury might confound evidence of systemic inflammation prior to the onset of necrosis, and it remains uncertain as to whether this inflammatory response to MI offers prognostic information beyond other measures of infarct size. In one series of 188 patients treated with thrombolytic therapy, the peak serum CRP concentration was found to correlate with the risk of mortality at 6 months, whereas peak CK and CKMB did not. Similar to CK, CRP falls more rapidly and reaches lower peak concentrations in patients with a patent infarct-related artery after reperfusion therapy.

Several inflammatory cytokines, in addition to IL-6, have been found to correlate with myocardial ischemia (109) and increased risk of recurrent events among those with unstable (164) and stable coronary artery disease (167). For example, TNF-a levels measured in 272 individuals stable for at least 3 months post-MI were significantly higher among those who subsequently suffered a recurrent event compared with age- and gender-matched study participants free from recurrent coronary heart disease events (p = 0.02) (167). The risk of experiencing a recurrent cardiac event was 2.7-fold higher (p = 0.004) among individuals with TNF-a levels greater than the 95th percentile of the control.

A number of inflammatory indicators other than hs-CRP have been evaluated as potential markers of cardiovascular risk both among individuals presenting with acute ischemic events, as well as among those at risk for atherosclerosis. As the primary stimulant for CRP production, IL-6 levels correlate closely with hs-CRP in noncardiovascular conditions. In addition, IL-6 may participate more directly through a broad range of humoral and cellular immune effects, as well as procoagulant actions. Levels of IL-6 are elevated in stable and unstable ischemic heart disease. Among patients with unstable angina, increased levels of IL-6 appear to predict higher risk for early adverse outcomes. Further, baseline elevation of IL-6 has been associated with increased risk of all-cause mortality among high-functioning elderly men and women from the Iowa 65+ Rural Health Study.

Data demonstrating an association between elevated levels of vascular adhesion molecules and future cardiovascular events further strengthen this evidence for a connection between vascular inflammatory processes and the predictive capacity of inflammatory markers. In contrast to nonspecific markers of systemic inflammation, such as the acute-phase proteins, vascular adhesion molecules are integral to vascular endothelial activation and leukocyte migration, and thus point more directly to the fundamental role of inflammation in mediating cardiovascular risk.

Yasmin Lawsuit News: Information and News

Yasmin Lawsuit:

Nevertheless, the pathobiological mechanisms through which elevation of inflammatory markers relate both to increased risk of atherothrombosis, and to higher risk of poor outcomes with acute cardiovascular events remain uncertain. In the setting of acute coronary thrombosis, it is plausible that the increase in circulating markers of inflammation is a manifestation of the intensification of vascular inflammatory processes contributing directly to plaque destabilization. However, this possible explanation has not been conclusively established. For example, it has been proposed that repetitive episodes of ischemia and reperfusion may trigger an inflammatory response within the myocardium. Contradicting this hypothesis, Maseri and colleagues have shown that the acute-phase reactants do not rise with recurrent episodes of myocardial ischemia- reperfusion due to coronary vasospasm. Nor does activation of the coagulation cascade alone result in increased production of CRP.

If inflammatory markers such as hs-CRP are to become useful in clinical practice, there must be evidence that they add to the prognostic information offered by traditional cardiovascular risk factors. In the case of hs-CRP, baseline elevation of the inflammatory marker remains highly predictive of future events after adjustment for traditional risk factors including age, hypertension, diabetes, body mass, index, and smoking status. When used in conjunction with lipid measurements in the Women’s Health Study and Physicians Health Study, hs-CRP added to the predictive information offered by the total to high-density cholesterol ratio (TC:HDL). Moreover, in a prospective evaluation in healthy women that compared traditional (TC and TC : HDL) as well as several ‘‘novel’’ (lipoprotein(a), homocysteine, hs-CRP) markers of cardiovascular risk, the combination of hs-CRP and the TC : HDL ratio was found to be the strongest predictor of first myocardial infarction. On the basis of these data, high-sensitivity testing for CRP used in conjunction with the TC.

Aspirin, an agent with both antiplatelet and anti-inflammatory effects, was the first specific pharmacological therapy tested for CRP interaction. In the Physicians Health Study, participants were randomly assigned to low-dose aspirin (325 mg p.o. q.o.d.) or placebo with a 44% reduction in the risk of first MI associated with aspirin use (p < 0.001). However, in a nested case control analysis, stratification by quartiles of baseline hs-CRP revealed an increasing gradient of benefit with aspirin, such that those in the highest quartile of hs-CRP realized a 55.7% (p = 0.002) reduction in the risk of first MI compared with 13.9% (p = 0.77) among those in the lowest quartile of hs-CRP concentration. Similar differential effects of aspirin on clinical outcomes in the presence or absence of elevated CRP levels has recently been reported in the setting of unstable angina. Indeed, in this setting, the prognostic value of CRP was found to be quite limited once patients had been treated with aspirin. These data suggest that at least part of the benefit of aspirin may result from an interaction with underlying low-grade vascular inflammation. To date, however, data have been conflicting as to whether aspirin use reduces CRP levels. Whether other COX-1 and/or COX-2 inhibitors impact upon CRP levels is currently under investigation.

While data on aspirin are important pathophysiologically, the most provocative data regarding preventive medical therapy interacting with CRP involves the hy- droxymethylglutaryl coenzyme A reductase inhibitors, or ‘‘statins.’’ In this regard, experimental evidence has for some time supported the idea that, in addition to lowering LDL cholesterol, statins may have relevant anti-inflammatory and thus plaque-stabilizing effects. For example, statins have been shown to reduce macrophage content within atherosclerotic plaques, decrease neointimal inflammation, and suppress matrix metalloproteinase expression, all processes involved in the vulnerability of luminal plaque.