HIRUDOTHERAPY THE HEALING ART ...
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Hirudin is the principal anticoagulant in leech saliva. It is a polypeptide, which has highly potent antiprotease activity with a strict specificity for thrombin. Hirudin is now produced by recombinant DNA technology and is administered to patients undergoing coronary angioplasty, for the treatment of deep venous thrombosis and as a substitute for heparin in patients developing heparin-induced thrombocytopenia.

Leeches are also used in the treatment of such disorders as inflammation and peripheral venous and arterial diseases. Patients suffering from deep venous thrombosis in the legs could develop post-phlebitic syndrome, a complication that occurs as a consequence of venous valve destruction. Leech therapy has been successfully used for the treatment of such conditions (for review see Eldor et al., 1996).


Deep venous  thrombosis (DVT)

 (DVT) and Pulmonary Embolism (PE) are manifestations of a single disease entity, namely, venous thromboembolism (VTE). The earliest known reference to peripheral venous disease is found on the Eber papyrus, which dates from 1550 BC and documents the potentially fatal hemorrhage that may ensue from surgery on varicose veins. In 1644, Schenk first observed venous thrombosis when he described an occlusion in the inferior vena cava. In 1846, Virchow recognized the association between venous thrombosis in the legs and PE.

DVT is the presence of coagulated blood, a thrombus, in one of the deep venous conduits that return blood to the heart. The clinical conundrum is that symptoms (pain and swelling) are often nonspecific or absent. However, if left untreated, the thrombus may become fragmented or dislodged and migrate to obstruct the arterial supply to the lung, causing potentially life-threatening PE.

See the images below.

 Venous thrombus. Pulmonary embolus.



DVT most commonly involves the deep veins of the leg or arm, often resulting in potentially life-threatening emboli to the lungs or debilitating valvular dysfunction and chronic leg swelling. Over the past 25 years, the pathophysiology of DVT has become much better understood, and considerable progress has been made in its diagnosis and treatment.

DVT is one of the most prevalent medical problems today, with an annual incidence of 80 cases per 100,000. Each year in the United States, more than 200,000 people develop venous thrombosis; of those, 50,000 cases are complicated by PE. Lower-extremity DVT is the most common venous thrombosis, with a prevalence of 1 case per 1000 population. In addition, it is the underlying source of 90% of acute PEs, which cause 25,000 deaths per year in the United States (National Center for Health Statistics [NCHS], 2006.

Conclusive diagnosis has historically required invasive and expensive venography, which is still considered the criterion standard. The diagnosis may also be obtained noninvasively by means of ultrasonographic examination.

Early recognition and appropriate treatment of DVT and its complications can save many lives.

 The goals of pharmacotherapy for DVT are to reduce morbidity, prevent postthrombotic syndrome (PTS), and prevent PE. The primary agents include anticoagulants and thrombolytics.

Other than the immediate threat of PE, the risk of long-term major disability from postthrombotic syndrome is high.

The opposite of the pharmacotherapy is HIRUDOTHERAPY. The goal of HIRUDOTHERAPY FOR DVT is TO REDUCE MORBIDITY by NATURAL, NON-INVASIVE, NO- MEDICATION INVOLVED, NO-SIDE EFFECTS, SAFE alternative healing    Preventive hirudotherapy purifies the blood and protects against a development of venous thrombosis; prevents post-thrombotic syndrome and prevents Pulmonary Embolism (PE). It detoxifies body by penetration of lymphatic chambers, blood stream and connective tissue.

 

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