Thrombophilia linked to increased risk of recurren

[mother bear]

http://www.hearingreview.com/reuters_article.asp?id=20090218clin023.html

"Fifty-two women received thromboprophylaxis with low-dose acetylsalicylic acid (n = 33), low-molecular-weight heparin (n = 15), or both (n = 4), starting no later than the end of the first trimester," Dr. Facchinetti and colleagues report. "The rate of recurrence of preeclampsia in thrombophilic women receiving such pharmacologic intervention was 40% (11/29 cases), no different from that observed in thrombophilic women not receiving thromboprophylaxis (17/31 cases, 55%)."

Am J Obstet Gynecol 2009;200:46-48

I was looking for research on the effectiveness of prophylactic lovenox on reducing the risk of recurrence of pe for thrombophilic women, and I was having a hard time finding any, but this is what I came up with. I suspect that the finding of no significance has a lot to do with the lack of power, and if they had included more women in their study (not that I would wish it on anyone), the results might have been significant, but maybe not. Could somebody include a link to the actual study? I'm interested in their definition of "thrombophilia". Some studies deliberately disinclude mthfr from their definition of "thrombophilia", and some don't, so I'd like to check.

[caryn]

They've been looking at this a lot lately; while the argument for anti-clotting therapy is plausible, the evidence for it is getting weaker with time.

http://www.ncbi.nlm.nih.gov/pubmed/18845284

Sixty women (34.9%) showed the presence of a thrombophilic defect. They had a higher risk for the recurrence of preeclampsia (odds ratio [OR], 2.5; 95% confidence interval [CI], 1.2-5.1), compared to patients without thrombophilia. Similar findings were observed considering only heritable thrombophilia. Thrombophilic patients were at increased risk for the occurrence of very early preterm delivery (< 32 weeks; OR, 11.6; 95% CI, 3.4-43.2).

It's interesting to see the difference between the abstract and the popular press. :-) The only claim the abstract makes in the conclusion is that thrombophilia testing is useful for preconception counselling and pregnancy management!

http://www.ncbi.nlm.nih.gov/pubmed/19114274

Pregnancy outcomes are often good in asymptomatic women with thrombophilias in the absence of treatment. Treatment of these women during pregnancy should be considered investigational.

http://www.ncbi.nlm.nih.gov/pubmed/19070828

Thrombophilia was present in 14% of patients and 21% of control subjects (adjusted logistic regression odds ratio, 0.6; 95% confidence interval, 0.3-1.3). Placental underperfusion was present in 63% of patients vs 46% of control subjects (P < .001) and was more frequent in women with folate levels in the lowest quartile (P = .04), but was not associated with thrombophilia.

[mother bear]

What it sounds like to me, is that there is a smallish subset of women who would benefit from prophylactic anti-clotting agents, because they tend to develop blood clots in their placentas (which then leads to hypoxia of fetus, etcetera), but that they have not yet figured out what subset of women that actually is, and that genetic testing doesn't quite cut it in terms of selection, although recurrent miscarriages tends be a better indicator of benefit from prophylactic anti-clotting agents than genetics alone. But it's complicated, because not all women do the placenta blood clot thing, and not all women start with the blood clotted placenta but rather may develop it later on in the cascade. I've heard they're doing trials using LMWH as a treatment for poor placental profusion instead of just prophylaxis, with some early reported success, but even this is complicated by all those other variables. Interesting about the folate levels, though...

[caryn]

Exactly, which is why they're leaning in the direction of phenotypic research. Those of us with a particular subset of risk factors may well have a different trigger to the cascade than those of us with a different subset of risk factors, and maybe you need MTHFR plus an autoimmune disease to get a particularly nasty result...

The researchers know this is the stumbling block, so hopefully we'll start to get some newer data on this. At the NICHD conference in September 2006 there was quite a bit of discussion about phenotypic study populations.

[mother bear]

Like, for example, what if in one hypothetical case, a woman went skiing in mid-2nd trimester (gee, don't know anyone who would do that, I say while rolling my eyes upwards), and while walking across the icy parking lot, slipped and fell on the ice on her side, causing minor placental abruption due to trauma, not genetics. Thinking everything was fine, she went about her life, but the hypoxic cascade had started, and 9 weeks later, she delivers early due to fetal indicators. Figuring out whether the fall and trauma was the cause, or whether it was a shallowly implanted placenta from the start due to underlying genetics, isn't as easy to figure out as it sounds, and the prophylaxis (if any) might be completely different between the two triggers. In the trauma case, being on blood thinners might actually make things worse.

I don't wanna do lovenox again! (I say in my whinyest little toddler voice). I just wanted to know for a more up to date picture of risk vs. benefits that was not based solely upon pain and expense, so I could discuss such things sometime sooner rather than later with my OB who is generally clueless about the latest research. It's my health, ya know.