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Malena is a 31 year old woman of Cambodian descent who was diagnosed with rheumatoid arthritis seven years ago. Most of her joints continued to ache despite taking prednisone for inflammation and methotrexate to suppress her immune system. Her primary care physician originally told her the cause of her disease was unknown. As an autoimmune disease, he explained, her immune system was attacking her own body’s tissues.

Six months before Malena came to see me, her medical doctor had told her that her disease was progressing and he needed to take more aggressive measures. She was scared because the prednisone was already weakening her bones and making her skin thinner, whereas the methotrexate made her more susceptible to infections buy viagra online. She fell sick with a debilitating cold every other month, leaving her incapable of going to work. Her colleagues no longer relied on her for important projects with strict deadlines. She had lost hope and was filled with fear.

I told her, “The body has an amazing ability to heal. Your immune system is part of who you are, and we need it to be strong enough to prevent you from becoming sick and missing work.” Besides desiring a successful career, she also wanted to contribute to society by volunteering at local charities and donating blood.

Malena and I worked together for two months to upgrade her diet, strengthen her immune system and decrease her antibodies. Once we saw that the autoimmune component was resolved, she visited her medical doctor who guided her off the methotrexate. Within another eight months, Malena no longer suffered from joint pain and lives completely medication free. She now leads a team of six coworkers, donates blood regularly and travels once a year to Cambodia to volunteer for an organization that sponsors orphans for formal education.

Allopathic medical doctors have few tools to restore optimal wellness, health and vitality. Unfortunately, they also confuse patients by diagnosing them with ‘incurable,’ ‘progressing’ or ‘idiopathic’ (no known cause) diseases. Telling Malena that her disease was ‘idiopathic’ implied that he did not know how to help her heal. By ‘incurable’, he meant that he could not help, and he might make her situation worse. That her disease was ‘progressing’ meant he had made it worse or neglected to improve her health.

As a child watching the film The Wizard of Oz, I believed the Wizard had the power to help Dorothy return home to Kansas. However, once we go behind the curtains and discover what is underneath the white coat, it is evident that the Wizard and Malena’s doctor are merely ordinary people, just like you and me. As a child, I loved to watch the greatest magic shows of all. Today, many people pay for these performances with their medical co-pays.

The therapeutic range for anti-factor Xa activity depends on the dosing interval. Anti-factor Xa monitoring is prudent when administering weight-based doses of LMWH to patients who weigh > 150 kg. It has been determined that UFH infusion is preferable to LMWH injection in patients with creatinine clearance of < 25 mL/min, until further data on therapeutic dosing of LMWHs in renal failure have been published. However, when administered in low doses prophylactically, LMWH is safe for therapy in patients with renal failure. Protamine may help to reverse bleeding related to Reproduction of this article is prohibited without written permission from the American College of Chest Physicians.  Xa activity depends

Correspondence to: Jack Hirsh, CM, MD, FCCP, Henderson Research Centre, 711 Concession St, Hamilton, ON L8V 1C3, Canada Pharmacy.

LWMH, although anti-factor Xa activity is not fully normalized by protamine. The synthetic pentasaccharide fondaparinux is a promising new antithrombotic agent for the prevention and treatment of venous thromboembolism.

Abbreviations: aPTT = activated partial thromboplastin time; AT = antithrombin; BMI = body mass index; CI = confidence interval; CrCl = creatinine clearance; DVT = deep-vein thrombosis; HC = heparin cofactor; HIT = heparin-induced thrombocytopenia; LMWH = low-molecular-weight heparin; MI = myocardial infarction; PF = platelet factor; RR = relative risk; rt-PA = recombinant tissue plasminogen activator; SC = subcutaneous; TBW = total body weight; UFH = unfractionated heparineparin, a heterogeneous mixture of branched aminoglycans, was discovered to have antithrombotic properties by McLean almost 90 years ago. Brinkhous and associates then demonstrated that heparin is an indirect anticoagulant, requiring a plasma cofactor.

This cofactor was subsequently named antithrombin (AT) III by Abildgaard in 1968 and now is referred to simply as AT. The main anticoagulant action of heparin is mediated by the heparin/AT interaction. The mechanism of this interaction was elucidated by Rosenberg and colleagues and Lindahl et al in the 1970s. Heparin binds to lysine sites on AT, producing a conformational change at the arginine reactive center, which converts AT from a slow, progressive thrombin inhibitor to a very rapid inhibitor. The arginine reactive center on the AT molecule binds covalently to the active center serine of thrombin and other coagulation enzymes, thereby irreversibly inhibiting their procoagulant activity. Heparin then dissociates from the ternary complex and is reutilized (Fig 1). Subsequently, it was discovered that heparin binds to AT through a unique glucosamine unit that is contained within a pentasaccharide sequence.

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