Expert: Danil Hammoudi.MD - 4/30/2004

Question
My 44 year old sister has Leiden factor V and has been treated with coumadin for the past 20 years, but now it is not working, and her hematologist currently has her on 15 mg of coumadin and 1 mil of innohep a day, and her blood is still as thick as mud.  Her pt's are 11 and her inr is .80, and has been this way for weeks in spite of them upping her meds, and now she is nauseous all the time.  They took 12 vials of blood recently, tested for bone cancer and a lot of other stuff, all negative.  She is diabetic, 2nd stage renal failure, and 2 years ago lost her left forearm from blood clots following cervical fusion surgery after her doctor took her off her coumadin for 15 days.  When her arm was amputated, her pt's and inr's were just a little above what they are now, so she is afraid of what might happen, and her hematologist seems stumped as to what is going on with her blood.  How long can she go on like this without being in danger of blood clots?  Is all that coumadin poisoning her?  Any suggestions?  Your help is appreciated.

Answer
her first way to complicate is first from her diabetes , then from her clotting
I cannot tell you for how long it will go that way and I do not think anyone can this is the mystery of the body.
Factor V Leiden is the most common hereditary blood coagulation disorder in the United States. It is present in 5% of the white population and 1.2% of the black population.

Factor V Leiden increases the risk of venous thrombosis 3- to 8-fold for heterozygous and 30- to 140-fold for homozygous individuals. Anticoagulation is the cornerstone of therapy for venous thromboembolism; the optimal duration of this therapy depends on the balance between the risk of recurrent thrombosis if anticoagulants are stopped and the risk of bleeding if patients remain on treatment.

Patients who are homozygous for factor V Leiden are at a moderate risk for recurrence. There is no convincing evidence that, independent of other clinical factors (surgery, pregnancy, etc.), the presence of factor V Leiden should influence the use of primary prophylaxis or the duration of anticoagulant therapy following an episode of thrombosis.

Most patients typically present with DVT of the legs, pulmonary embolism, or both. Less common manifestations are superficial venous thrombosis and thromboses in the cerebral, visceral, and axillary veins. In more than 50% of cases, venous thrombosis is provoked by surgery, immobilization, advanced age, pregnancy, or the use of oral contraceptives or hormone-replacement therapy. Comprehensive guidelines for primary or secondary prophylaxis in these persons have not, to my knowledge, been formulated. The literature suggests that administration of low-molecular-weight or unfractionated heparin in high-risk conditions (such as during surgery), an avoidance of oral hormone replacements and contraceptives, maintenance of normal homocysteine levels with the use of folic acid, and weight loss all encompass adequate prophylaxis

so if coumadin is not working I think substitution with heparin is needed
and the treatment of diabetes as much important as the coagulation.
hope this help a bit
thanks
dan