Phlebitis opinions?

[EpsteinBarr]

Hallo, first of all, I am sorry for my english, but believe me, I do as much as possible. I try to explain my problem and hopefully you can help me to find some answers to my problem. I am 36 years old. I train regularly. (I started from 15 till 20...then university, job, family...now I train regularly for app. 3 years again. 3 years ago I was diagnosed phlebothrombosis (deep vein thrombosis), the true is, that during this time I have not lived very healthy. This experience caused that after healing I have strated train again.

Months ago, during holiday the same problem started again (exactly after 3 years). This time it was superficial thrombophlebitis. All blood tests were done this time and they have found mutation in gene for Factor V, Leiden, homozygot type. I am using Fraxiparine already 25 days. I suppose that MD will push me to warfarine or clopidogrel for sime time. Means, first case was for sure not caused by AAS as I have not used them this time. The second cause could be bounded to AAS as boldenon and AAS generally cause polycythemia, raise hematocrit etc... This second case I observed after more than 3 months after last cycle.

I have opinions with 3 cycles. Sustanon, methan, boldenon, winstrol, tst propionate (of course, not together!!! just to inform you what I used). I started internet searching and I have found out that AAS generaly in therapeutic doses have thrombolytic effect and could improve the situation and they have anti-thrombic effects. But in supra doses (common cycle) the effect is inversed and AAS increases blood clotting ability (hypercoagulability). I planned next cycle, all "staff" is ready but of course I stopped this. The future is a big questions.

Does anybody have opinions with this to discuss all possible factors and future...?

[LewdTenant]

Thrombus aka blood clots are caused by 3 things 1)endothelial damage, 2)stasis 3)hypercoagualble state. This makes up Virchows Triad. This Thrombus (blood clot) may dislodge from its initial location and may travel to another location which defines embolism. this embolism may travel from the venous system in the legs (most common site) to the lungs and cause a Pulmonary Embolism. If that PE happens to be a saddle embolism you have a poor prognosis. Even small clots can cause infarcts. Venous thrombi do not travel to the brain as they are filtered by the longs unless there is some right to left shunting in the heart. superficial thrombophlebitis will not cause a PE while a superficial vein thrombus may cause a PE. An important distinction to note.

The highest risk patients for clots are those with previous history and clotting deficiencies which you have. You have 2 copies of the Factor V gene so are at even greater risk. Coumadin will protect you but there are so many drugs that ineract with coumadin levels and the nature of the drug that levels must be montiored on a regular basis. Patients on Coumadin can easily be walking around at subtherapuetic level without knowing. Coumadin being bound to albumin may have its levels also altered from the dramatic changes in protein intake from dietary changes and metabolic demands while using AAS. Steoid-albumin interactions can not be ignored as well. Do not think that coumadin will COMPLETELY protect you. These combined factors may make your coumadin levels go too high or too low too quickly.

You seem to know a lot about your condition. homozygote Factor V L def. + past DVT + AAS (polycythemia risk) + fluctuating Coumadin levels and interactionsare a bad mix. Your HRT doc should get a consultation from your hematologist, but there seems to be too much going on here.