Occult cancer in patients with deep-vein thrombosis [DVT].

[pjoshea13]

New study below [1].

It's a reminder that dysfunctional coagulation is an early event in cancer & after a DVT , a man should be screened for cancer - particularly PCa.

But for men with PCa who have not suffered a DVT, it is a warning that coagulation factors are nonetheless altered. In PCa, micro-clots are implicated in metastasis. Nattokinase can dissolve micro-clots, as well as reverse developing DVTs.

...

"From 182 patients with primary DVT, 30 (16.5%) presented occult cancer: Thirteen males and 17 females, with an average age of 61 years. In males, prostate cancer prevailed (6/13, 46%); meanwhile, in females, pelvic gynecologic cancers predominated (7/17, 41%)."

...

In a 2016 paper [2]:

"We assessed TED {thromboembolic disease} risk for 42,263 men with PCa who were receiving ADT compared with a matched cohort of 190,930 without PCa."

"... 11,242 men with PCa received anti-androgen monotherapy, 26,959 men received gonadotropin-releasing hormone (GnRH) agonists, 1,091 men received combined androgen blockade and 3,789 men underwent orchiectomy."

"... GnRH agonist users and surgically castrated men had a higher risk of TED than the comparison cohort" Risk factor of 1.67 and 1.61 respectively.

"Men on anti-androgen monotherapy had {half the} risk: HR for DVT ..."

"TED risk was highest among those who switched from anti-androgen to GnRH agonists" Risk factor of 2.55.

"This increased ... to 4.05 ... in year 2."

Lupron is a GnRH agonist.

It is fairly well-known that the old ADT treatment, diethylstilbestrol [DES], a synthetic estradiol, increased the risk for thromboembolic events, but it appears that castration therapy can also increase risk.

Nattokinase can accelerate the breakdown of the fibrin in growing clots.

-Patrick

[1] ncbi.nlm.nih.gov/pubmed/286...

J Res Med Sci. 2017 May 30;22:63. doi: 10.4103/jrms.JRMS_559_16. eCollection 2017.

Occult cancer in patients with deep-vein thrombosis in a general hospital at Mexico City: A pilot study.

Ramírez-Serrano Torres CO1, Román-Guzmán E2, Ortiz-Mendoza CM3.

Author information

Abstract

BACKGROUND:

We aimed to explore the frequency of occult cancer in patients with deep-vein thrombosis (DVT) at a general hospital in Mexico City.

MATERIALS AND METHODS:

From March 2012 to February 2015, all patients with primary DVT of lower extremities attended in the emergency department of our hospital were studied. Initially, all patients were evaluated with clinical history, physical examination, basic laboratories, abdominal ultrasound, chest X-ray, and duplex venous ultrasonography. In a case-by-case approach, if necessary, computed tomography, endoscopy, colonoscopy, and tumor markers were done.

RESULTS:

From 182 patients with primary DVT, 30 (16.5%) presented occult cancer: Thirteen males and 17 females, with an average age of 61 years. In males, prostate cancer prevailed (6/13, 46%); meanwhile, in females, pelvic gynecologic cancers predominated (7/17, 41%).

CONCLUSION:

Our results suggest that in Mexican patients with primary DVT, occult cancer is frequent.

KEYWORDS:

Cancer; Trousseau's syndrome; deep-vein thrombosis; thromboembolism/prevention and control; venous thrombosis/etiology

PMID: 28616050 PMCID: PMC5461588 DOI: 10.4103/jrms.JRMS_559_16

...

[2] ncbi.nlm.nih.gov/pubmed/264...

BJU Int. 2016 Sep;118(3):391-8. doi: 10.1111/bju.13360. Epub 2015 Nov 19.

Risk of thromboembolic disease in men with prostate cancer undergoing androgen deprivation therapy.

O'Farrell S1,2, Sandström K1, Garmo H1,3, Stattin P4, Holmberg L1,2,3,5, Adolfsson J6,7, Van Hemelrijck M1,2,8.

Author information

1

Division of Cancer Studies, Cancer Epidemiology Group, King's College London, London, UK.

2

NIHR Guy's and St Thomas' NHS Foundation Trust, King's College London's Comprehensive Biomedical Research Centre, London, UK.

3

Regional Cancer Centre, Uppsala Örebro, Uppsala, Sweden.

4

Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.

5

Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.

6

Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.

7

Swedish Council for Health Technology Assessment, Stockholm, Sweden.

8

Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.

Abstract

OBJECTIVES:

To investigate the risk of thromboembolic disease (TED) in men with prostate cancer (PCa) on androgen deprivation therapy (ADT), while accounting for known TED risk factors.

MATERIALS AND METHODS:

We assessed TED risk for 42 263 men with PCa who were receiving ADT compared with a matched cohort of 190 930 without PCa. The associations between ADT and deep vein thrombosis (DVT) or pulmonary embolism (PE) were analysed using multivariate Cox proportional hazard regression models, while accounting for previous PCa-related surgeries and the following proxies for disease progression: transurethral resection of the prostate, palliative radiotherapy and nephrostomy.

RESULTS:

Between 1997 and 2013, 11 242 men with PCa received anti-androgen monotherapy, 26 959 men received gonadotropin-releasing hormone (GnRH) agonists, 1 091 men received combined androgen blockade and 3 789 men underwent orchiectomy. When accounting for previous surgeries and proxies of disease progression, GnRH agonist users and surgically castrated men had a higher risk of TED than the comparison cohort: hazard ratios (HRs) 1.67 (95% confidence interval [CI] 1.40-1.98) and 1.61 (95% CI 1.15-2.28), respectively. Men on anti-androgen monotherapy had a lower risk: HR for DVT 0.49 (95% CI 0.33-0.74). TED risk was highest among those who switched from anti-androgen to GnRH agonists: HR for PE 2.55 (95% CI 1.76-3.70). This increased from 2.52 (95% CI 1.54-4.12) in year 1, to 4.05 (95% CI 2.51-6.55) in year 2.

CONCLUSION:

The incidence of TED among men on ADT increased with the duration of therapy and the risk was highest for those who switched regimen, suggesting that disease progression as well as ADT contribute to the propagation of TED risk. Nonetheless, these findings support the hypothesis that only men with a relevant indication should receive systemic ADT.

© 2015 The Authors BJU International © 2015 BJU International Published by John Wiley & Sons Ltd.

KEYWORDS:

androgen deprivation therapy; disease severity; prostate cancer; thromboembolic disease

PMID: 26497726 DOI: 10.1111/bju.13360

[Indexed for MEDLINE]

[wagscure259]

Thank You Patrick For Another Execellent Post . After 2 years on ADT therapy I had an embolism in my R coronary artery in addition to a minor plaque formation . Can you comment on aspirin versus nattokinase or Plavix versus nattokinase .

[pjoshea13 in reply to wagscure259]

Aspirin & Plavix (clopidogrel) both inhibit the aggregation of platelets, which is the first stage of clot formation. We know that aspirin - even a low daily dose - is not without risk. I can't say how Plavix compares.

The second stage of clot formation involves fibrinogen, which forms fibrin - the bulk of the clot.

Clots can form fast. Plasmin in the blood will degrade fibrin, but very slowly. Plasmin cannot keep up with clots occuring due to dysfunctional coagulation. Nattokinase has a similar structure to plasmin, but works 4-5 (?) times faster.

Fibrinogen can be elevated in PCa. It represents clotting potential. Inflammation will increase levels. Nattokinase can lower fibrinogen while dissolving fibrin. It is not associated with side effects (that I am aware of.)

While it may be attractive to avoid unwanted clots (with Aspirin & Plavix), sometimes survival depends on rapid clotting. You don't wan't to bleed out on the way to the ER.

Using nattokinase is akin to putting a sump pump in a leaky basement. It doesn't stop the problem, but that is a good thing when one has a serious injury.

We are fortunate in having a blood test that gives a good indication that there is a clotting problem. D-dimer will be elevated when fibrin is being broken down by plasmin. The addition of nattokinase will speed up the breakdown. This will initially increase D-dimer, but it will ultimately fall to near zero. A maintenance dose will keep it there.

In the event of injury involving bleeding, simply stop taking nattokinase.

Even if using aspirin/Plavix, D-dimer should be monitored.

-Patrick

Arterial plaque can involve calcium, & vitamin K2 will prevent that & even reverse it.

Eliminating inflammation will help prevent non-calcium deposits. IMO

[BigRich in reply to pjoshea13]

Patrick,

The D-dimer score would be gotten from a blood test?

Rich

PS: I take 325 mg Aspirin for my A-Fib.

[pjoshea13 in reply to BigRich]

Rich - Yes, blood. It is a standard test for those going to the ER with chest pain.

If elevated they would do a scan of lungs. If the scan is negative, they don't investigate why D-dimer was elevated.

-Patrick

[Sisira]

Thank you for your post,

Sisira

[rococo]

Aftee2 taking high dose vit d3 a number of yrs. mh ct scan showed high levels arterial calcification. Than I stsrted taking vit k2 from natto 50 mg lowered vit d to get hydrox d blood test down from 100 to 70 ans 2yrs later arterial calcification less noted on scan. Rocco

[pjoshea13 in reply to rococo]

& with continued K2 use calcification might even be eradicated. K2 is quite an amazing solution - but how many doctors know?.

[rococo]

The doctors should know the biochemistry patrick. They just walk the line. One doc expressed his fear of the stigmata off a lowly herbalist placed on him. Rocco