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I would like to inquire is anyone knows if there is now in effect a class action suit for avandia ?

My mom would like to get in the suit if there is because we feel this is what caused my dad to die of a heart attack.

Any information you may have would help on this important issue!

2007-07-10 16:25:37 · 0 answers · asked by Anonymous in Politics & Government Law & Ethics

0 answers

There appears to be a number of sites sponsored by lawyers concerning Avandia. I know nothing about them. I included one below.

Just enter "avandia" and "class action" and do a search to get more of them.

2007-07-13 09:22:33 · answer #1 · answered by SPLATT 7 · 0 0

The active constituent of Avandia is rosiglitazone ,there are related active constituents to rosigliatazone like pioglitazone,

you can buy search for a brand name has pioglitazone ,by the way i cannot say a brand name foir you becasue it difefrs from country to another ,and i guiss you are amercan .i donot live in USA so i cannot recomend a certain brand name.

http://www.apotex.ca/En/ProfessionalAffairs/CEEssentials/Modules/diabetes/medications.asp#Med4


look at the information below,it has great benefit for you ,although it is long

Thiazolidinediones (Glitazones)

Nonproprietary Names
Pioglitazone, Rosiglitazone

Mechanism of Action
The glitazones are referred to as insulin sensitizers: they reduce hyperglycemia by improving insulin action, resulting in enhanced cellular uptake of glucose. Because glitazones decrease insulin resistance, serum insulin levels are reduced. In addition, hepatic glucose production is modestly reduced. (7)

The actual mechanism of action is complex. Glitazones activate a receptor (PPAR-gamma), primarily in the nucleus of fat cells, which regulates the transcription of genes involved in glucose and lipid metabolism. Glitazones therefore reduce serum free fatty acid levels, which are thought to cause 'lipotoxicity' resulting in insulin resistance, impairment of insulin secretion and increased hepatic glucose production. Preliminary evidence suggests that the glitazones may improve, or at least preserve, insulin secretory function. (7,8)

Glitazones have potentially beneficial effects on CV risk factors, including improvement of the lipid profile, modest reduction in blood pressure, increased fibrinolysis, improved endothelial function and reduction in microalbuminuria. However, whether these nonglycemic effects will translate into a reduction in CV events is unknown. (7,8)

The effects of the individual glitazones on the lipid profile appear to differ. Compared with rosiglitazone, pioglitazone causes greater increases in HDL-C, smaller increases in LDL-C, and greater decreases in triglycerides; the impact of these differences on CV disease risk is unknown. (8)

Clinical Use*
The glitazones are now considered first-line agents for use as monotherapy or in combination treatment of type 2 diabetes. The CDA Guidelines recommend that metformin is the drug of first choice, and that a glitazone should be considered either as an alternative to metformin, or for add-on therapy. The glitazones have been studied in combination with metformin, a sulfonylurea, a meglitinide or insulin. (8) As well, the glitazones have been studied as part of a three-drug combination along with metformin plus a sulfonylurea, (18) or metformin plus insulin. (3)

Effectiveness
The glitazones reduce A1c levels by 1-2%. (3,7,8) (The CDA Guidelines suggest that a decrease of 1.0-1.5% is more realistic.) (4) However, evidence suggests that a relatively high proportion (25-30%) of treatment-naïve patients fail to respond to initial glitazone monotherapy. (8) Non-responders are thought to have less insulin resistance, greater insulin deficiency, or both. (7) The onset of glucose-lowering effect may be evident 2-4 weeks after starting treatment; however, maximal improvement is not achieved for 6-12 weeks. (4,8)

Clinical Advantages
Advantages of the glitazones include:
Lack of hypoglycemia when used alone.
Suitable for use in renal insufficiency.
Convenient once-daily dosing.
They may improve/preserve pancreatic beta cell function, possibly delaying or preventing the deterioration of insulin secretion and glycemic control.
They may be proven to reduce macrovascular disease (trials are ongoing).
They may prevent or delay the development of type 2 diabetes; (10) however, current guidelines list only metformin and acarbose as options. (11)


Adverse Effects*
Glitazone monotherapy is associated with a weight gain of about 2-4 kg, which increases to 3-6 kg when used in combination with insulin. (19)

Edema occurs in approximately 3-5% of patients receiving glitazone monotherapy. The incidence is higher during combination therapy with oral antihyperglycemic agents (6-8%), and much higher when given with insulin (13-16%). Peripheral edema (e.g., swelling of the lower extremities) is most common; however, in some patients, the fluid retention can precipitate or exacerbate heart failure, which on rare occasions has been accompanied by pulmonary edema. The incidence of glitazone-induced heart failure has been low (about 1%). (19)

Cautions*
Glitazones are contraindicated in patients with severe heart failure (NYHA class II, III, or IV) due to the potential for fluid retention, increased plasma volume and edema. The glitazones are not licensed in Canada for use with insulin, as this combination increases the risk of glitazone-induced edema and heart failure. (4)

The American Heart Association and the American Diabetes Association have published the following recommendations: (19)

Before prescribing glitazone treatment, ascertain whether the patient has cardiac disease.
Determine whether the patient is currently taking any medications associated with fluid retention (e.g., vasodilators, NSAIDs) or pedal edema (e.g., calcium channel blockers).
If CHF is present, or the patient has SOB, monitor closely during the first three months of glitazone therapy.
Instruct patients to report any of the following: weight gain > 3 kg, pedal edema, SOB or fatigue.
If the patient has one or more risk factors for CHF, consider prescribing a low dose initially (rosiglitazone 4 mg, pioglitazone 15 mg) with gradual dosage titration and monitoring for adverse effects.
Patients with NYHA class I or II CHF should initially be prescribed no more than 2 mg of rosiglitazone or 15 mg of pioglitazone, with gradual dosage titration and monitoring.


Glitazones are contraindicated in patients with serious hepatic impairment, based on the hepatotoxicity seen with troglitazone (the first glitazone in clinical use), which led to its withdrawal from the U.S. market. Pioglitazone and rosiglitazone do not share this hepatotoxic potential. The incidence of liver function test abnormalities with these agents is no greater than placebo, and less than that observed with other oral antihyperglycemic agents. As well, there have been no documented cases of hepatic injury with pioglitazone or rosiglitazone. (3,8) Nevertheless, monitoring of liver function tests is recommended. Treatment should not be initiated if ALT is > 2.5 times the upper limit of normal, and should be discontinued if ALT elevation is > 3 times the upper limit of normal and the elevation persists.

The glitazones are not recommended in pregnant or breastfeeding women. When used in infertile women with polycystic ovary syndrome, glitazone therapy may result in resumption of ovulation and place the patient at risk of pregnancy. These patients may need to consider contraception prior to treatment. (20)

Drug Interactions*
Pioglitazone is metabolized by CYP 2C8 and 3A4. Rosiglitazone is metabolized primarily by CYP 2C8, and to a lesser extent 2C9. Clinically significant drug interactions have yet to be reported. Theoretically, it is possible that the fibrate gemfibrozil, a potent inhibitor of 2C8, may reduce clearance of the glitazones. (21)

Dosing Considerations
The glitazones are administered once daily without regard to mealtimes. The total dose of rosiglitazone may be given as two divided doses. Dosage increases should be avoided until six weeks of therapy has elapsed, as the maximal glucose-lowering effect may not be evident until 6-12 weeks after starting treatment. (4)

Monitoring Parameters
The efficacy of glitazone therapy can be assessed in the short term by monitoring fasting glucose values. Liver function monitoring is recommended at baseline and every two months for the first year of therapy. Patients should be encouraged to report signs and symptoms of impending or worsening heart failure, such as swelling, shortness of breath, weakness, fatigue or unexplained weight gain. (3,8)

2007-07-17 06:25:34 · answer #2 · answered by Anonymous · 0 0

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