Primary Pulmonary Hypertension
Until recently, only about one or two people per million had Primary Pulmonary Hypertension also known as pph , but the use of diet drugs drugs such as Pondimin (Fenfluramine-the first "Fen" in "Fen-Phen") and/or Redux (Dexfenfluramine) has created a new outbreak of this deadly condition. Because of the irresponsibly of pharmaceutical companies many people have been injured and diagnosed with PPH. Victims of Primary Pulmonary Hypertension may be entitled to large cash awards for their pain and suffering.
PPH causes some of the cell lining of the lung's blood vessels to weaken and allow leakage. The leaking of blood out of the vessels causes the muscles that surround the blood vessels to constrict. This continuous constriction increases the pressure within the blood vessels. Gradually over time, this chokes off the flow of blood between the heart and lungs. The cutoff of blood will cause causing dizziness, exhaustion, fainting and may lead to heart failure. Effective treatment can allow a PPH victim to survive more than 10 years after diagnosis.
What causes Primary Pulmonary Hypertension?
Scientists do not know what exactly causes Primary Pulmonary Hypertension. Some researchers believe the blood vessels are particularly sensitive to certain internal or external factors, and constrict, or narrow, when exposed to these factors. There may be a genetic factor, an immune system factor, or sensitivity to drugs or other chemicals.
Diet drugs present a possible cause
Recently, an association between some PPH cases and the serotonin-effecting appetite suppressants fenfluramine (Pondimin) and dexfenfluramine (Redux) has been established. A long term study in Europe showed that out of 95 cases, 30 had tacken one of these appetite suppressants: dexfenfluramine (Redux), fenfluramine (Pondimin), diethylpropion (Tenuate), clobenzorex, fenproporex, or phenmetrazine. Of the 30 cases, 18 had used them more than three months.
If you have take a Fen-phen, Redux or another related diet drug and have Primary Pulmonary Hypertension, our we will put you in contact with Primary Pulmonary Hypertension attorney best suited to your case.
Diagnosis of PPH: Cardiac Catheterization
A method of detecting PPH is using a catheter. A hollow, flexible tube for insertion into a body cavity, duct, or vessel. The tube extends into the heart to measure blood pressure. Unlike the echocardiogram, which is harmless and not risky, there is some risk associated with the catheterization. Exercising may have the effect of increasing the ability of a cardiac catheter to detect PPH.
Treatment may involve use of Flolan and Calcium Channel Blocking Drugs such as nifedipine - to improve the heart's ability to pump blood supplemental oxygen, Anticoagulants - decrease the tendency of the blood to clot and permit blood to flow more freely, Diuretics - decrease the amount of fluid in the body and reduce the amount of work the heart has to do drugs. Flolan is administered through a catheter that is surgically implanted. It only acts for 2-3 minutes and must be constantly infused with a small pump.
UT-15 is a man made form of prostacyclin that dilates the pulmonary blood vessels for 4-6 hours. UT-15 is not as potent as Flolan, but can be delivered under the skin rather than through a central I.V. line. Ut-15 is awaiting FDA approval, but a clinical trial is nearing completion (March 2001).
Lung and Heart Transplantation is an extreme measure for patients with serious end stage PH. Current survival rates are as high as 80% at 1 year following transplantation and 60% at 4 years.
A lung transplant is donated from a human who has been declared brain-dead but remains on life-support. Tissue matches must be made to assure the patient's best chance of fighting off rejection of the transplanted tissue. While the patient is deep asleep and pain-free (general anesthesia), an incision is made through the breast bone (sternum). Tubes are used to re-route the blood to a heart-lung bypass machine to keep the blood oxygenated and circulating during the surgery. The patient's lungs are removed and the donor lungs are stitched into place. Drainage tubes (chest tubes) are inserted to drain air, fluid, and blood out of the chest for several days to allow the lungs to fully re-expand. The body's immune system considers the transplanted organ as an invader (much like an infection) and fights it. To prevent rejection, organ transplant patients must take anti-rejection (immunosuppression) drugs (such as cyclosporine and corticosteroids) that reduce (suppress) the body's immune response and reduce the chance of rejection. These drugs also reduce the body's natural ability to fight off various infections.