Long term full dose eliquis for dvt

I have a successful watchman and was taking 2.5mg Eliquis BID until I got a huge 2.5cm DVT.

I have been shooting my stomach BID with heparin (stopped eliquis) and today the clot has not reduced in size.

I saw a leading dvt specialist today that thinks I may have to take 5mg Eliquis BID in the future because this is my second DVT.

That’s disappointing. Especially after having a watchman.

I’m supposed to get various images and he wants a chest and armpit ultrasound and colonoscopy and other tests. Also a body tumor test. And three others I need to translate



Edited 1 time(s). Last edit at 06/10/2024 04:01PM by susan.d.

Eliquis (apixaban) serum test levels, or anti-Xa levels, are measured to determine drug levels and adjust doses to prevent excessive anticoagulant effects or inadequate therapy. Peak values for humans taking low doses of apixaban can be up to 150 ng/mL, while higher intensity therapy can reach around 300 ng/mL. However, therapeutic target ranges for apixaban have not been established in human or veterinary medicine.
Some reasons for obtaining anti-Xa levels include: New bleeding, Before a surgical procedure, and Before heparin or fibrinolytic therapy.

My scores are low. Surprise since my meds are hand inspected at the airports and doesn’t go through X-rays and are stored in a temperature controlled room. It gives me false security that 2.5mg (study says >150) is working.

[www.drugs.com]
10mg BID vs 5mg vs 2.5mg:

Treatment of DVT and PE
The recommended dose of ELIQUIS is 10 mg taken orally twice daily for the first 7 days of therapy. After 7 days, the recommended dose is 5 mg taken orally twice daily.

Reduction in the Risk of Recurrence of DVT and PE
The recommended dose of ELIQUIS is 2.5 mg taken orally twice daily after at least 6 months of treatment for DVT or PE [see Clinical Studies (14.3)].



Edited 1 time(s). Last edit at 06/10/2024 06:03PM by susan.d.

Not on afib or DVT specifically, but more on aging generally & thrombosis risk. This is from a post I'm copying from another group. Note, much of this research was done in mice. This may be the root cause of why points for age are added in the CHADS2VASC metric for afib stroke risk.

An age-progressive platelet differentiation path from hematopoietic stem cells causes exacerbated thrombosis.

With advanced age, platelets generated by a differentiation pathway that shortcuts the canonical progenitor cascade to directly make megakaryotic precursor cells from hematopoietic stem cells cause thrombocytosis and are more prone to thrombosis compared with canonically derived platelets

(JUNE 2024) [doi.org]

Platelet dysregulation is drastically increased with advanced age and contributes to making cardiovascular disorders the leading cause of death of elderly humans.

Here, we reveal a direct differentiation pathway from hematopoietic stem cells into platelets that is progressively propagated upon aging. Remarkably, the aging-enriched platelet path is decoupled from all other hematopoietic lineages, including erythropoiesis, and operates as an additional layer in parallel with canonical platelet production. This results in two molecularly and functionally distinct populations of megakaryocyte progenitors. The age-induced megakaryocyte progenitors have a profoundly enhanced capacity to engraft, expand, restore, and reconstitute platelets in situ and upon transplantation and produce an additional platelet population in old mice. The two pools of co-existing platelets cause age-related thrombocytosis and dramatically increased thrombosis in vivo. Strikingly, aging-enriched platelets are functionally hyper-reactive compared with the canonical platelet populations.

These findings reveal stem cell-based aging as a mechanism for platelet dysregulation and age-induced thrombosis.
•Aging leads to two parallel platelet specification paths from HSCs
•The shortcut platelet pathway is perpetuated by highly expansive MkPs
•Canonical MkPs are resilient to age-induced changes
•The aging-induced shortcut path causes thrombocytosis and platelet hyper-reactivity


This scientific study, published in the journal Cell in June 2024, sheds new light on how the aging process affects the production of platelets, the tiny blood cells that play a crucial role in blood clotting and wound healing. The researchers used a special strain of mice, called "FlkSwitch" mice, to track the development of blood cells from their earliest stages in the bone marrow to their mature forms in the bloodstream.

In young mice, the researchers found that platelets are produced through a well-established series of steps, starting with hematopoietic stem cells (HSCs) in the bone marrow. These HSCs give rise to intermediate cells called multipotent progenitors (MPPs), which then develop into megakaryocyte progenitors (MkPs) - the cells that directly produce platelets. Throughout this process, the cells express a fluorescent protein called GFP, which allows the researchers to easily track their development.

However, as the FlkSwitch mice aged, the researchers noticed a surprising change in platelet production. In addition to the normal GFP-expressing platelets, a new population of platelets emerged that expressed a different fluorescent protein, called Tomato (Tom). These Tom+ platelets increased in number as the mice got older, eventually making up about half of all platelets in the bloodstream of elderly mice.

By analyzing the bone marrow of the aged mice, the researchers discovered that the Tom+ platelets were being produced through a new, "shortcut" pathway that bypassed the usual intermediate stages of development. Instead of arising from GFP+ MPPs and MkPs, the Tom+ platelets were being produced directly by a subset of HSCs that had never expressed GFP.

This aging-induced shortcut pathway had several important consequences. First, the Tom+ MkPs were functionally enhanced compared to their GFP+ counterparts, meaning they were better at producing platelets both in the laboratory and when transplanted into new mice. Second, the Tom+ MkPs were able to respond more quickly and robustly when the mice were experimentally depleted of platelets, rapidly restoring platelet numbers to normal levels.

Most strikingly, the researchers found that the Tom+ platelets produced by the shortcut pathway were functionally distinct from the GFP+ platelets. In a series of experiments, they showed that the Tom+ platelets were "hyper-reactive" - they were more prone to activating and aggregating in response to stimuli, and they formed larger, more stable clots at sites of blood vessel injury.

This hyper-reactivity of the aging-induced Tom+ platelets may help explain why elderly individuals are at higher risk for thrombosis, the formation of blood clots that can lead to heart attacks, strokes, and other cardiovascular events. The researchers propose that the shortcut pathway for platelet production, and the hyper-reactive platelets it generates, may be a key driver of age-related thrombosis risk.

The discovery of this aging-induced shortcut pathway for platelet production is significant for several reasons. First, it challenges the conventional understanding of how blood cells develop, showing that the process is more flexible and adaptable than previously thought. Second, it identifies a specific population of cells - the Tom+ MkPs and platelets - that could potentially be targeted with drugs or other interventions to reduce thrombosis risk in elderly individuals.

In summary, this study identifies a previously unknown pathway for platelet production that emerges with aging, and shows that this pathway generates hyper-reactive platelets that may contribute to age-related thrombosis risk. By illuminating the complex interplay between aging, stem cell biology, and cardiovascular health, this research opens up new avenues for understanding and potentially intervening in the aging process.