Can Testosterone Induce Blood Clots and Thrombosis? Interview with Dr Charles Glueck

In my work collecting information for ExcelMale.com, I review abstracts daily on latest studies related to testosterone, men's health, nutrition, and more. I am always looking for studies that stand out and are no just repetitions of what we have seen before. Contrarian data to what I assume we know is what motivates me to read. In particular, I am looking for negative data and results in studies using testosterone. I have been using this hormone since 1993 to save my life and its quality and have not had any side effects. However, I know everyone is different and some people may have genetic or other variations that may make them susceptible to at least one side effect.

Good read:

What to do if you have a blood clot



The first time I read a paper than mentioned thrombosis risk in people on testosterone replacement (read abstract at the end of this article), my goal is to get in contact with the author. Dr Charles Glueck was kind to reply for my request for an interview to help me educate physicians and patients. He is a graduate from Harvard and Western Reserve Universities and has over 35 years of medical practice and have produced over 600 publications. He is currently the Medical Director of the Jewish Hospital Cholesterol Center. To say that he has credentials is an understatement.



I am impressed by his willingness to help anyone who may be concerned about this issue (he provides contact information below)

Here is the short interview:

Dr Glueck, Thank you so much for agreeing to educate my readers about your research.

Can you give give us a brief background of why you were interested in looking into thrombophilia and thrombosis in people on testosterone replacement therapy? Can you explain those terms to us?

Dr Glueck: As physicians who deal with deep venous thrombosis (DVT) and pulmonary embolus (PE), as well as blood clots in the eyes (central retinal vein and central retinal artery thrombosis), and ischemic stroke, and arterial blood clots, we realized that many of our referrals had started exogenous conventional testosterone therapy before sustaining their blood clots. Because we were very experienced with the diagnosis of thrombophilia and hypofibrinolysis, we hypothesized that the exogenous testosterone was interacting with underlying coagulation disorders producing the blood clots. We have now proven this in multiple publications.

In your best estimate or opinion, what is the incidence of this problem in men on testosterone replacement?

Dr Glueck: The incidence of DVT-PE or other clots in men on T therapy is not known, but our best estimates are that about 1-2% of men taking T will develop blood clots related to underlying inherited clotting abnormalities or to acquired thrombophilia (the antiphospholipid antibody syndrome). These men who landed in the hospital with dangerous and potentially lethal blood clots in the deep veins of the legs or in the lungs developed these clots within three months of starting testosterone therapy. None of them knew previously that they had an inherited clotting disorder that put them at greater risk for developing clots, nor did their providers test them before putting them on testosterone therapy.

You suggest that "thrombophilia should be ruled out before administration of exogeneous testosterone". How can that be done and are the tests commercially available or research tools? You used these tests in your study: factor V Leiden heterozygosity, high factors VIII and XI, high homocysteine, low antithrombin III, the lupus anticoagulant, high anticardiolipin antibody lgG, and the hypofibrinolytic 4G4G mutation of the PAI-l gene. Should all be performed? Would these tests be reimbursed by insurance and, if not, what do you think the retail value would be?

Dr Glueck: The 4 tests we would do include Factor V Leiden, Prothrombin gene, Factor VIII and Factor XI, all routinely available commercially at Lab Corp and Quest (big national labs), and at almost all regional labs as well. In our experience these tests are routinely covered by insurance. If not covered, I would estimate that the cost would be expensive, $800.

You also suggest a link between high estradiol with thrombophilia. Can you explain this finding? Would anastrozole or other E2 inhibitor improve outcome if used with TRT?


Dr Glueck: We have data to show that when T is aromatized in the body to estradiol (E2), the high E2 may be the agent which directly interacts with the underlying thrombophilia to produce the clots. We do not have enough data to know whether Arimidex used to lower E2 would be protective, but we know that Arimidex alone is prothrombotic in all of the thrombophilias and hence, probably not a good idea.

In your opinion, should all men on TRT be on low dose aspirin?

Dr Glueck: Low dose aspirin would have no effect on the clotting events seen in men on T who have underlying thrombophilia and I would not recommend it.

Are you planning to do any further studies on this troubling issue?

Dr. Gluek: We are working hard to better understand this troubling issue. If any of your readers have had DVT-PE or other clots while taking exogenous T, or during hCG or clomid therapy to raise T, we would be glad to help them out with expert consultative advice free of charge. Have them contact us by email ([email protected]) or by phone (513-924-8250) fax (513-924-8273) and we will advise them on what blood samples to have drawn, and how to deal with their problem. All of their information will, of course, be entirely private and totally confidential. We will also be glad to work with their doctors in their local communities.

Thank you so much for your time and I will be contacting you in a few months to see if you have any updated data for us.


____________________________________________

ClincAppl Thromb Hemost. 2014 Jan;20(1):22-30. Epub 2013 Apr 23.


Testosterone, thrombophilia, and thrombosis.

Glueck CJ, Richardson-Royer C, Schultz R, Burger T, Labitue F, Riaz MK, Padda J, Bowe D, Goldenberg N, Wang P.


Abstract

We describe thrombosis, deep venous thrombosis (DVT) pulmonary embolism (PE; n = 9) and hip-knee osteonecrosis (n = 5) that developed after testosterone therapy (median 11 months) in 14 previously healthy patients (13 men and 1 woman; 13 Caucasian and 1 African American), with no antecedent thrombosis and previously undiagnosed thrombophilia-hypofibrinolysis. Of the 14 patients, 3 were found to be factor V Leiden heterozygotes, 3 had high factor VIII, 3 had plasminogen activator inhibitor 1 4G4G homozygosity, 2 had high factor XI, 2 had high homocysteine, 1 had low antithrombin III, 1 had the lupus anticoagulant, 1 had high anticardiolipin antibody Immunoglobulin G, and 1 had no clotting abnormalities. In 4 men with thrombophilia, DVT-PE recurred when testosterone was continued despite therapeutic international normalized ratio on warfarin. In 60 men on testosterone, 20 (33%) had high estradiol (E2 >42.6 pg/mL). When exogenous testosterone is aromatized to E2, and E2-induced thrombophilia is superimposed on thrombophilia-hypofibrinolysis, thrombosis occurs. The DVT-PE and osteonecrosis after starting testosterone are associated with previously undiagnosed thrombophilia-hypofibrinolysis. Thrombophilia should be ruled out before administration of exogenous testosterone.

Click here for part 2:

Article: Second Interview with Dr Charles Glueck About Testosterone and DVT

 

Marco - I am on 20mg. Started out on 15 twice a day. Now I would very much like to move to 15 for a few months and then down to 10mg.

Am I reading correctly that Dr. G only sees testosterone as an issue for those with a genetic factor that tilts towards clotting?

If one is dehydrated that alone can predispose an individual to high clotting risk. There is at least one study that shows that staying hydrated can cut the risk of a heart attack in half. In a nutshell low blood viscosity (thinner blood) is extremely protective for both arteries and veins.

One additional risk factor I may have the fact I have been low-carb for years. There are quite a few studies that show low-carb increase the blood viscosity where true wheat free vegetarians enjoy very low viscosity.
Short history - This June on Father's Day (Sunday) I was doing sprints on steps midday with the temperature around 90 degrees. On the sixth set I passed out briefly; probably because of not eating first and dehydration. I was at a resort hotel on the Gulf Coast so plenty of people responded. Within 10 or 15 minutes of that event I was fine and went home. Spent the next few days working and sitting for long hours, something I normally do. By Wednesday my left leg started swelling quickly and was painful. I also developed a mild cough which may have been about the time the pulmonary embolism happened. By Thursday I was in the hospital. I would never have known I had a pulmonary embolism if not for the CT in the hospital.

Five days later I was discharged on Coumadin with an INR of 1.3 and self administered Lovenox. The doctor raised my Coumadin to 15mg at which point my INR jumped to 4.2. His nurse called and told me to get off Coumadin and Lovenox for the next 3 or 4 days. Within 24 hours I was in unbelievable pain.

Found a new doctor that let me start Xarelto. The pain was gone within 2 days.

 

Marco - I am on 20mg. Started out on 15 twice a day. Now I would very much like to move to 15 for a few months and then down to 10mg.

Am I reading correctly that Dr. G only sees testosterone as an issue for those with a genetic factor that tilts towards clotting?

If one is dehydrated that alone can predispose an individual to high clotting risk. There is at least one study that shows that staying hydrated can cut the risk of a heart attack in half. In a nutshell low blood viscosity (thinner blood) is extremely protective for both arteries and veins.

One additional risk factor I may have the fact I have been low-carb for years. There are quite a few studies that show low-carb increase the blood viscosity where true wheat free vegetarians enjoy very low viscosity.
Short history - This June on Father's Day (Sunday) I was doing sprints on steps midday with the temperature around 90 degrees. On the sixth set I passed out briefly; probably because of not eating first and dehydration. I was at a resort hotel on the Gulf Coast so plenty of people responded. Within 10 or 15 minutes of that event I was fine and went home. Spent the next few days working and sitting for long hours, something I normally do. By Wednesday my left leg started swelling quickly and was painful. I also developed a mild cough which may have been about the time the pulmonary embolism happened. By Thursday I was in the hospital. I would never have known I had a pulmonary embolism if not for the CT in the hospital.

Five days later I was discharged on Coumadin with an INR of 1.3 and self administered Lovenox. The doctor raised my Coumadin to 15mg at which point my INR jumped to 4.2. His nurse called and told me to get off Coumadin and Lovenox for the next 3 or 4 days. Within 24 hours I was in unbelievable pain.

Found a new doctor that let me start Xarelto. The pain was gone within 2 days.

My take was that Dr. G seems pretty staunch anti-TRT regardless, as is the case with most mainstream old school docs. That's not to say he isn't brilliant insofar as hematology and cardiology, but definitely from the old school of thinking. Myself, I would only be concerned if my clotting disorder were of genetic etiology and not caused by factors such as diet, meds (like too much thyroid hormone), and other environmental factors that are within a person's control.

Please post the studies that show that LC diets increase viscosity or hypercoagulation or is linked to hydration or lack thereof. But, then again, those are two different issues.

 

Here is the reverse of that search: https://www.google.com/?gws_rd=ssl#q=vegetarian+and+blood+viscosity+site:www.ncbi.nlm.nih.gov I'll dig up the low carb links ASAP

 

The Atkins diet is well known for causing a large decrease in weight initially which is mostly water related. I guess this could cause dehydration in some men. Dehydration increases blood viscosity. However, I doubt that low carb diets increase chances for blood clots.

 

What an interesting thread! I had a clot in 2006 (I was only 25 at the time) that travelled to the lungs and I was in ICU for 3 days... Cause was that I had a really bad flu and was lying in bed for about a week, not moving much and dehydrated.

After they fixed me up in the hospital I was put on Warfarin for about a year or so. No problems since. I am about to start TRT next week. Should I take the risk or just accept that I will have low energy for the rest of my life?

 

What an interesting thread! I had a clot in 2006 (I was only 25 at the time) that travelled to the lungs and I was in ICU for 3 days... Cause was that I had a really bad flu and was lying in bed for about a week, not moving much and dehydrated.

After they fixed me up in the hospital I was put on Warfarin for about a year or so. No problems since. I am about to start TRT next week. Should I take the risk or just accept that I will have low energy for the rest of my life?

In my experience, immobility can exacerbate an underlying clotting disorder, but rarely itself causes one as severe as you've mentioned. What you've mentioned sounds like a DVT that caused a PE (pulmonary embolism). To be on the safe side, I would do as many of the tests I listed upthread to make sure you don't have acquired or familial thrombophilia prior to starting TRT.

 

Kiwi81, please read the first post on this thread (page 1) to find Dr Glueck's email address. He can run tests for you before you start TRT.

 

Hi guys, ok. I will try and do those tests before I start TRT. Only problem is that I am in New Zealand and I don't think Dr Glueck can help me from the States? But I will email him anyway, to see if he has got any suggestions.

 

Freedman J, Glueck CJ, Prince M, Riaz R, Wang P. Testosterone, thrombophilia, thrombosis. Transl Res. http://www.sciencedirect.com/science/article/pii/S1931524414004678


We screened previously undiagnosed thrombophilia (V Leiden-prothrombin mutations, Factors VIII and XI, homocysteine, and antiphospholipid antibody [APL] syndrome) in 15 men and 2 women with venous thromboembolism (VTE) or osteonecrosis 7 months (median) after starting testosterone therapy (TT), gel (30-50 mg/d), intramuscular (100-400 mg/wk), or HCG (6000 IU/wk).


Thrombophilia was studied in 2 healthy control groups without thrombosis (97 normal controls, 31 subjects on TT) and in a third control group (n = 22) with VTE, not on TT.


Of the 17 cases, 76% had >/=1 thrombophilia vs 19% of 97 normal controls (P < 0.0001), vs 29% of 31 TT controls (P = 0.002).


Cases differed from normal controls by Factor V Leiden (12% vs 0%, P = 0.021), by high Factor VIII (>150%) (24% vs 7%, P = 0.058), by high homocysteine (29% vs 5%, P = 0.007), and from both normal and TT controls for APL syndrome (18% vs 2%, P = 0.023, vs 0%, P = 0.04).


Despite adequate anticoagulation with TT continued after the first deep venous thrombosis-pulmonary embolus (DVT-PE), 1 man sustained 3 DVT-PEs 5, 8, and 11 months later and a second man had 2 DVT-PEs 1 and 2 months later.


Of the 10 cases with serum T measured on TT, 6 (60%) had supranormal T (>800 ng/dL) and of 9 with estradiol measured on TT, 7 (78%) had supranormal levels (>42.6 pg/mL).


TT interacts with thrombophilia leading to thrombosis. TT continuation in thrombophilic men is contraindicated because of recurrent thrombi despite anticoagulation.



Screening for thrombophilia before starting TT should identify subjects at high risk for VTE with an adverse risk/benefit ratio for TT.

 

Freedman J, Glueck CJ, Prince M, Riaz R, Wang P. Testosterone, thrombophilia, thrombosis. Transl Res. http://www.sciencedirect.com/science/article/pii/S1931524414004678


We screened previously undiagnosed thrombophilia (V Leiden-prothrombin mutations, Factors VIII and XI, homocysteine, and antiphospholipid antibody [APL] syndrome) in 15 men and 2 women with venous thromboembolism (VTE) or osteonecrosis 7 months (median) after starting testosterone therapy (TT), gel (30-50 mg/d), intramuscular (100-400 mg/wk), or HCG (6000 IU/wk).


Thrombophilia was studied in 2 healthy control groups without thrombosis (97 normal controls, 31 subjects on TT) and in a third control group (n = 22) with VTE, not on TT.


Of the 17 cases, 76% had >/=1 thrombophilia vs 19% of 97 normal controls (P < 0.0001), vs 29% of 31 TT controls (P = 0.002).


Cases differed from normal controls by Factor V Leiden (12% vs 0%, P = 0.021), by high Factor VIII (>150%) (24% vs 7%, P = 0.058), by high homocysteine (29% vs 5%, P = 0.007), and from both normal and TT controls for APL syndrome (18% vs 2%, P = 0.023, vs 0%, P = 0.04).


Despite adequate anticoagulation with TT continued after the first deep venous thrombosis-pulmonary embolus (DVT-PE), 1 man sustained 3 DVT-PEs 5, 8, and 11 months later and a second man had 2 DVT-PEs 1 and 2 months later.


Of the 10 cases with serum T measured on TT, 6 (60%) had supranormal T (>800 ng/dL) and of 9 with estradiol measured on TT, 7 (78%) had supranormal levels (>42.6 pg/mL).


TT interacts with thrombophilia leading to thrombosis. TT continuation in thrombophilic men is contraindicated because of recurrent thrombi despite anticoagulation.



Screening for thrombophilia before starting TT should identify subjects at high risk for VTE with an adverse risk/benefit ratio for TT.

Here we are a year + later and it's the same old negative news with Glueck. Would be nice if someone would fund a friggin' study showing different anticoagulants used during TRT that just might turn out to be an effective workaround for those with irreversible thrombophilia. There has to be a way to safely replace or increase total and free T in those with whatever degree of thrombophilia. Remaining hypogonadal because of this is simply not a satisfactory option. My thinking is that increasing endogenous T is the least risky and what needs to be focused on.

 

We should contact researchers about that

 

The human body has in-built mechanisms to prevent clotting. Ideally, we should focus on providing it with the raw material needed to prevent clots rather than looking at medication and 'new' strategies.

IMO, the best methods to prevent thrombosis are:

Therapeutic fasting: The human body wasn't designed to remain in a feasted state. Fasting allows the body to clear garbage. Here's an article on fasting that could be of interest to some of you (talks of blood clotting):

http://www.trackyourplaque.com/library/fl_06-023fuhrman.asp

Fasting is, without a doubt, the single best thing most people can do for their body and mind. The human body is truly magical in its recuperative and repair abilities (and fasting helps us get out of our body's way).

Daily exercise: Exercise has shown to repair blood vessels and improve their elasticity
(research shows that 1) improved endothelial function can reduce coagulation and 2) exercise dramatically improves endothelial function)

PLENTY of the right foods: If someone is susceptible to thrombosis, his diet must contain higher than average amounts of veggies and a moderate amount of fruits. (Phytochemicals have been shown to prevent clotting.)

Water: More for those who love their coffee, or stay in hot weather zones, or are generally stressed, etc.

If you are on anabolics such as Nandrolone, you need to take precaution as well. Long-term use damages blood vessels and leads to endothelial dysfunction and mitochondrial dysfunction (even in low doses).


Unless you are genetically predisposed to clotting, there is little reason to panic. The real challenge for most of us is to lead the lives we were designed to lead (fasting, sufficient and deep rest, lots of laughter, light and healthy eating, commune with nature, etc.) When we do the basics, the body does what its supposed to do -- clean up and prepare us for another day.

Unfortunately, the human mind wants cutting-edge research that promises instant and permanent cure. May be that will happen some day, but until that day, I'm going to stick to the basics and give my body what it needs.

 

The human body has in-built mechanisms to prevent clotting. Ideally, we should focus on providing it with the raw material needed to prevent clots rather than looking at medication and 'new' strategies.

IMO, the best methods to prevent thrombosis are:

Therapeutic fasting: The human body wasn't designed to remain in a feasted state. Fasting allows the body to clear garbage. Here's an article on fasting that could be of interest to some of you (talks of blood clotting):

http://www.trackyourplaque.com/library/fl_06-023fuhrman.asp

Fasting is, without a doubt, the single best thing most people can do for their body and mind. The human body is truly magical in its recuperative and repair abilities (and fasting helps us get out of our body's way).

Daily exercise: Exercise has shown to repair blood vessels and improve their elasticity
(research shows that 1) improved endothelial function can reduce coagulation and 2) exercise dramatically improves endothelial function)

PLENTY of the right foods: If someone is susceptible to thrombosis, his diet must contain higher than average amounts of veggies and a moderate amount of fruits. (Phytochemicals have been shown to prevent clotting.)

Water: More for those who love their coffee, or stay in hot weather zones, or are generally stressed, etc.

If you are on anabolics such as Nandrolone, you need to take precaution as well. Long-term use damages blood vessels and leads to endothelial dysfunction and mitochondrial dysfunction (even in low doses).


Unless you are genetically predisposed to clotting, there is little reason to panic. The real challenge for most of us is to lead the lives we were designed to lead (fasting, sufficient and deep rest, lots of laughter, light and healthy eating, commune with nature, etc.) When we do the basics, the body does what its supposed to do -- clean up and prepare us for another day.

Unfortunately, the human mind wants cutting-edge research that promises instant and permanent cure. May be that will happen some day, but until that day, I'm going to stick to the basics and give my body what it needs.

I agree with all you state and practice everything you preach above, however, what we are talking about here are those with likely familial or acquired thrombophilia that are also hypogonadal. I have been on Xarelto for the last 9 mos. as a prophylaxis for DVT. I have elevated Factor VIII, although it is not always consistently elevated. Since it also an acute phase reactant, there is always the possibility that it stems from some type of unknown stressor or inflammation and is not familial. We just don't know yet. Since I've been dealing with other health issues for the last 6 mos., I haven't had a chance to look into this deeper, but will be. Until then, better safe than sorry. Also, have withheld TRT, but my last T levels weren't too bad anyway for a 55 year old (TT: 548 FT: 90), hardly hypogonadal. Oral DHEA, Testofen and Nettles seems to be keeping me in check in the meantime. If I could eliminate the need for an anticoagulant med, I would do it in a heartbeat, but I can't take that risk at this point. At least Xarelto has a less side effect profile than Warfarin and I haven't noticed any while on it. I am also on a low dose (10mg). Only risk is that there's no commercial antidote yet for Xarelto if you hemorrhage.

Underlying chronic infections can cause a hypercoagulable state also, but I have tested for all, and all I show are past exposures and also don't have any symptoms (I have tested for Lyme, HHV-6, EBV, CMV, Candida, etc.).

 

Hi Marco,

I agree that a genetically predisposed (familial) condition requires more than the basics. Most acquired conditions, however, can be 'cured' if the underlying issues are resolved (something I'm sure you're looking to).

Your T levels are pretty good considering your age and the health issues you've been having (for the last 6 months as per your post). Honestly, if you're feeling good, there's little reason to move forward with T. I'm actually envious of your T levels (considering that my T has always been below 350 and I'm 34 years old).

I'm researching Coagulation Disorders and should I find something interesting, I'll certainly post it here. Do keep us updated on your health, etc. -- there are some very bright people here who can offer help that...believe me...most competent doctors cannot.

Take care, Marco, and stay healthy.

 

Testosterone therapy, thrombophilia, and hospitalization for deep venous thrombosis-pulmonary embolus, an exploratory, hypothesis-generating study - Abstract


Our hypothesis was that testosterone therapy (TT) interacts with previously undiagnosed thrombophilia-hypofibrinolysis, leading to hospitalization for deep venous thrombosis (DVT)-pulmonary emboli (PE).

We determined the prevalence of DVT-PE associated with TT 147 men hospitalized in the last 12months for DVT-PE. Of the 147 men, 2 (1.4%) had TT before and at the time of their DVT-PE. Neither had risk factors for thrombosis. Neither smoked. Case #1 (intramuscular T 50mg/week) had 2 PE, 6 and 24months after starting TT. DVT-PE in case #2 (T gel 100mg/day) occurred 24months after starting T. Both men were found to have previously undiagnosed familial thrombophilia (protein S deficiency, homocysteinemia, high Factor VIII). In case #2, on 100mg T gel/day, serum estradiol was high, 51pg/ml (upper normal limit 42.6pg/ml). At least 1.4% of men hospitalized for DVT-PE were on TT and had previously undiagnosed thrombophilia, suggesting a thrombotic interaction between exogenous T and thrombophilia-hypofibrinolysis. Given the increasing use of TT, our preliminary findings should facilitate design of a much-needed, multi-center, prospective study of pro-thrombotic interactions between T therapy and thrombophilia for subsequent thrombotic events including DVT-PE.

Written by:
Glueck CJ, Friedman J, Hafeez A, Hassan A, Wang P.
Jewish Hospital Cholesterol Center, Jewish Hospital of Cincinnati, United States; Internal Medicine Residency Program, Jewish Hospital of Cincinnati, United States. [email protected]
Reference: Med Hypotheses. 2015 Jan 21. pii: S0306-9877(15)00041-9.
doi: 10.1016/j.mehy.2015.01.020.

 

EFFECT OF TESTOSTERONE REPLACEMENT THERAPY ON INCIDENCE OF DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM

Rishi Sharma; Olurinde Oni; Rajat Barua; Mukut Sharma; Ram Sharma; Guoqing Chen; Kamal Gupta

J Am Coll Cardiol. 2015;65(10_S):. doi:10.1016/S0735-1097(15)61422-X


Background:

Testosterone Replacement Therapy (TRT) prescriptions have increased 400% in the last decade. Concern over the risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) with TRT has led the FDA to issue an alert. The association of TRT with DVT/PE is not clearly understood. The aim of this study was to examine the incidence of DVT/PE following TRT using a large patient database.

Methods:


We used Veteran Affairs Informatics and Computing Infrastructure (VINCI) database, to select a cohort of US veterans who were found to have low serum total testosterone levels (sTT) during 1999 - 2012. We compared the risk of incidence of DVT/PE between those who received TRT resulting in normalization of sTT and those who did not receive TRT. Those with prior history of DVT/PE were excluded. The risk adjusted and unadjusted approaches were used to adjust for the potential confounding effects. We also assessed various independent risk factors and their association with DVT/PE risk.

Results:

Of a total of 54000 patients with low sTT, 41121 received TRT (mean age = 63.9 yrs ± 11.4, mean follow-up = 5.9 yrs ± 3.2) while 12879 did not (mean age = 67.0 yrs ± 13.4, mean follow-up = 4.4 yrs ± 3.0). New cases of DVT/PE were identified in 259 patients in the TRT group vs. 59 in the non-TRT group. Table shows that there was no statistically significant increase in the incidence of DVT/PE following TRT therapy.



Conclusion:

In patients with low sTT , TRT did not result in a statistically significant increase in incidence of DVT/PE.

 

Nelson - thanks for staying on top of this. Those numbers are nothing to worry about for sure...

 

Here is a recap of my situation. Been on TRT since March of 2013. In May 2014, was hospitalized for diverticulitis. I developed a superficial venous thrombus on the first day out of the hospital. The doctor who prescribed my TRT is a local cardiologist. I use him as my primary and have no cardiac issues.

In Nov 2014, my doc prescribed 12.5 mg of Eliques twice a day to pass the clots (found in my right leg). We agreed to d/c trt until further notice. This past March, he rescanned my leg and the clots were gone.

I had had previously contacted Dr Grueck and did all the labs he requested. FYI, with my insurance, I don't pay anything for lab work at Quest. These were considered experimental and they sent me a bill for $689 which I'm disputing. Here is his diagnosis:

Have received the laboratory tests. You have an acquired thrombophilia called the Lupus anticoagulant. This almost never is associated with the disease Lupus, and unless you have arthritis, joint pain, sun sensitivity, and a facial rash, would not worry about that. It is now clear that the blood clot which you had was related to the interaction of the testosterone with the lupus anticoagulant. As long as the lupus anticoagulant is present, ANY EXOGENOUS TESTOSTERONE IS CONTRAINDCATED, due to a huge increase in the risk of blood clotting.

I sent the same lab results to my primary. He believed, based on these results, I was destined to clot and the trt did not contribute. He recommended I resume trt as my T was now 197.

i have never been depressed or in the dumps. I prefer being on trt but don't want to be at risk. I resumed trt at 25 mg eod subq. I am prescribed 200mg / weekly.

Thoughts?

 

Hey TPCD - I had DVT with multiple, bilateral pulmonary embolism in June of 2014. Even with a genetic clotting factor there are things it takes to provoke a clot. The main two are dehydration and sitting for more than 30 minutes without standing up. Engaging you leg muscles is what transports the blood back up the leg. Without motion you have pooling. Those are the big two. The following may be life saving on two home fronts.

Stop the clot from forming and in most cases you stop the fatal event. Harvard out of Boston has been working for several years now on stopping clots in both Veins and Arteries with Rutin. So while we focus on things that might avoid heart disease and DVTs wouldn't it be nice to avoid dying from them in the meantime?

The Harvard work will likely result in a patented drug but right now it's using a very natural, readily available nutrient - Rutin. Xarelto (a blood thinner) took this same path. It came from a natural ingredient found in nature and now is a patented drug with a host of safety issues.

http://news.harvard.edu/gazette/story/2012/05/flavonoid-compound-can-prevent-blood-clots/ There are many papers published by this group in PubMed including several in 2015. What's so exciting about this is Rutin appears to stop the clot from a level in the clotting cascade that catches both veins and arteries.

I never thought about how important this really is. If you can stop a clot from forming in the circulatory system (a thrombosis) you prevent almost fatal heart attacks and DVTs. Think about it.

I have dozens of links and have corresponded with several of the doctors involved in this study.
Don't underestimate the value of Rutin. I am personally taking 500mg 3 times a day with 500 to 1000mg of Vitamin C 3 times a day. Vitamin C increases the bioavailability of Rutin.

Stop the clot and you stop the train wreck - read the papers. Stay hydrated, don't sit for more that 30 minutes without a 30 second stand up and move session - and above all else, consider Rutin...

http://www.icpjonline.com/documents/Vol1Issue12/07.pdf
http://www.ncbi.nlm.nih.gov/pubmed/25104801
http://www.bidmc.org/News/In-Research/2013/April/Furie-Grant.aspx
http://www.ncbi.nlm.nih.gov/pubmed/24677236
http://www.ncbi.nlm.nih.gov/pubmed/23541171
http://www.jci.org/articles/view/61228
https://ash.confex.com/ash/2014/webprogram/Paper66272.html
http://www.thejaps.org.pk/docs/v-24-3/37.pdf
http://www.jci.org/articles/view/61228

 

Clot Risk Not Higher in Older Men Taking Testosterone


"Dr Ramasamy and his colleagues retrospectively reviewed the medical records of 217 hypogonadal men older than 65 years.Of the 153 men who received testosterone therapy, 53 were treated with injections, 47 were treated with gel, and 53 were treated with pellets, which are placed intramuscularly beneath the skin. The remaining 64 men did not receive testosterone therapy.

Median follow-up was similar in the treated and untreated groups (3.8 vs 3.5 years), and median age was 74 to 75 in the two groups.


There were fewer deaths in the treated than in the untreated group (1 vs 6; P = .003). In addition, there were more myocardial infarctions in the treated than in the untreated group (1 vs 0), more cerebrovascular accidents (2 vs 1), and more pulmonary embolisms (1 vs 0), but these differences were not significant.

"One of the limitations of the study is its small sample size," Dr Ramasamy acknowledged.

We can confidently say that the risk of thrombosis does not appear to be higher in men who are treated.

However, unlike in epidemiologic studies, "the biggest advantage of our study is that we actually saw these patients, we treated them, we know what their testosterone levels were, we managed them appropriately, and we followed them," he explained. Therefore, "despite the small sample size, the study lends a lot more validity to the argument that testosterone therapy does not appear to increase the development of thrombotic events."

http://www.medscape.com/viewarticle/844816#vp_2