Immune Thrombocytopenic Purpura Treatment Information

Idiopathic Thrombocytopenic Purpura (ITP), also known as self thrombocytopenic purpura. Idiopathic Thrombocytopenic Purpura (ITP) is a condition in which bleeding blood does not clot as it should. The platelets (thrombocytes) are colorless blood cells that stop by the loss of blood clumping together at the site of injury to a blood vessel and form plugs holes in the ship. People with idiopathic thrombocytopenic purpura, because of their low platelet count, tend to bleed and bruise more easily injured. Bleeding from the nose and bleeding gums are also common. In adults, women are affected approximately 3 times more frequently than Idiopathic Thrombocytopenic Purpura is often divided into two categories: acute and chronic. It occurs mainly in children, boys and girls, and is the most common type of ITP. Chronic ITP lasts more than six months and is more prevalent among adults. Chronic ITP affects women 2 to 3 times more often than men. ITP does not run in families. Treatment of ITP in adults is aimed at increasing the blood platelet count. Immunosuppresants like mycophenolate mofetil and azathioprine are becoming more popular for their effectiveness. Rituximab has also been used successfully for some patients. Extreme cases may require vincristine.A chemotherapy agent, to stop the immune system from destroying platelets. Steroids help prevent bleeding by decreasing the rate of platelet destruction. Intravenous gamma globulin (IVGG) is a protein that contains many antibodies and also slows the destruction of platelets. Other possible treatments may include the use of immunosuppressant drugs such as rituximab (Rituxan) the safest and most commonly used of this group cyclophosphamide (Cytoxan), azathioprine (Imuran) or vinca alkaloids (Vincasar, Velban). Avoid medications that contain aspirin, as they may interfere with the body ’s ability to control bleeding.Immune Thrombocytopenic Purpura Treatment and Prevention Tips 1. Steroids help prevent bleeding by decreasing the rate of platelet destruction. 2. High-dose gamma globulin (an immune factor) injections are helpful.3. Rituximab has also been used successfully treatment of this condition.4. Vincristine, a chemotherapy agent, to stop the immune system from destroying platelets.5. Teenage girls may need to take hormones therapy to stop their menstrual cycle. 6. Passing the blood over a protein A column , which filters antibodies out of the blood stream.

Biologic therapy has revolutionized our approach to the treatment of rheumatoid arthritis (RA). Less than 10 years ago, the best we could hope for was to “modify disease” or slow it down and also help with symptoms. Now the goal is to not only control symptoms, it is to get RA into complete remission. Biologics are protein-based medicines that are synthesized in a laboratory. They act like laser beams to target the immune abnormalities that are felt to cause RA.

First generation biologics such as etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira) are known as TNF-inhibitors and have done wonders for many patients. Second generation biologic such as rituximab (Rituxan) which acts against B cells and abatacept (Orencia) which works on T cells are both welcome additions to the arsenal of weapons available to combat RA.

Cimzia (certolizumab) is an investigational TNF-inhibitor. It differs from the current crop of TNF-inhibitors since it is “pegylated.” This means that a substance called polyethylene glycol has been attached to the molecule. This pegylation lengthens the half-life of the drug- meaning the drug stays in the system longer. Cimzia also has had a piece of protein removed from the molecule. The piece of protein that has been removed contained a small amount of mouse protein (yes… these drugs are often created using mouse proteins). By removing the piece of mouse protein, it is hoped that Cimzia will cause fewer adverse reactions.

A recent presentation on June 14, 2007 at the annual meeting of the European Congress of Rheumatology (EULAR) described data on Cimzia.

The team studied 2 dose regimens, which patients received subcutaneously as add-on therapy to methotrexate.

In a phase 3, multicenter, double-blind, placebo-controlled, parallel-group study, the investigators recruited 992 patients with RA who received either the study drug or placebo. The investigators wanted to know the rate at which people had a 20% improvement, as defined by the American College of Rheumatology criteria (ACR 20).

The patients, who had previously been treated for at least 6 months with methotrexate, were randomized to treatment with either pegylated certolizumab or placebo. Those on treatment received 3 400-mg doses every 2 weeks, followed by 200 or 400 mg doses of certolizumab pegol every 2 weeks. The patients continued methotrexate as usual. The investigators assessed the efficacy and safety parameters at 2-week intervals.

In an early analysis at 24 weeks, the investigators found that 581 patients completed the study: 259 of the 397 on 200 mg of the drug, 278 of the 394 on 400 mg, and 44 of the 201 on placebo. The ACR20 response rate was 59.2% in the 200 mg group, 61.2% in the 400 mg group, and 13.5% of those who received methotrexate and placebo. The proportion of patients who experienced a significant side effect was 74.0% in the 200 mg group, 76.1% in the 400 mg group, and 57.7% in the placebo group. The majority of adverse events were mild to moderate.

“Pegylated certolizumab adds significant benefit in reducing the signs and symptoms of RA in combination with methotrexate, compared to using methotrexate alone,” said lead investigator Edward C. Keystone, MD, professor of medicine at the University in Toronto, and director of the Rebecca MacDonald Centre for Arthritis and Autoimmune Disease, in Ontario.

Bottom line: Pegylated certolizumab works like a TNF blocker and appears to treat the signs and symptoms of RA. Whether it’s better than the TNF blockers that are currently available is still no known. It is better than placebo.