Talk:Thrombophilia

History

http://bloodjournal.hematologylibrary.org/cgi/content/full/112/1/19 JFW | T@lk 21:00, 10 July 2008 (UTC)

No point

Uncomplicated VTE is no indication for thrombophilia testing. In the MEGA study, those who were tested were no less likely to have a recurrence: PMID 1854099. JFW | T@lk 19:56, 26 August 2008 (UTC)

PMID is wrong, but it was a primary study anyway. JFW | T@lk 00:20, 21 February 2011 (UTC)

Causes

I took a clue from WhatamIdoing (talk · contribs), who on the assessment page suggested that the list of causes probably had too many bullet points. I have started to prosaify the content, basing myself on the current references and adding a load more.

This has prompted the realisation that we are probably not discussing the specific acquired scenarios in sufficient detail. For instance, antiphospholid syndrome is (according to the Lancet review) regarded as a strong indication for long-term anticoagulation. I also need to append the relevant epidemiological data to the "epidemiology" section. JFW | T@lk 10:10, 25 February 2011 (UTC)

More genetics!

doi:10.1111/j.1538-7836.2009.03394.x is a review from two Dutch kings of genetic thrombophilia (Rosendaal and Reitsma). It is fairly short but discusses the utility of genome-wide association studies and the fact that most genetic thrombophilias confer at most a moderate risk of VTE. JFW | T@lk 12:52, 27 February 2011 (UTC)

Smoking

Kumar4 is used as a source to support the claim that cigarette smoking is linked with venous thromboembolism. It turns out that it very difficult to find a good corrobative secondary source for this claim. doi:10.1002/ajh.21059 is a primary research study, which in turn cites PMID 9039882 (Nurses' Health Study, 1997). The topic has not been reviewed independently from OCP use. I am removing it until we can support this with better sources, and I remain open to suggestions. JFW | T@lk 14:18, 27 February 2011 (UTC)

Obesity

This is little question that obesity, apart from by mechanical reasons, also has its associated thrombophilia; this is presumed to be due to PAI-1 hypersecretion by fat cells. PMID 19700047 is a review on the topic, but I can't access it currently. It should probably be included. JFW | T@lk 14:25, 27 February 2011 (UTC)

GA Review

This review is transcluded from Talk:Thrombophilia/GA1. The edit link for this section can be used to add comments to the review.

Reviewer: WhatamIdoing (talk) 04:40, 18 March 2011 (UTC)

Checklist

GA review – see WP:WIAGA for criteria

1. Is it reasonably well written?

   A. Prose quality:

   B. MoS compliance for lead, layout, words to watch, fiction, and lists:

2. Is it factually accurate and verifiable?

   A. References to sources:

   B. Citation of reliable sources where necessary:

   C. No original research:

3. Is it broad in its coverage?

   A. Major aspects:

   B. Focused:

4. Is it neutral?

   Fair representation without bias:

5. Is it stable?

   No edit wars, etc:

6. Does it contain images to illustrate the topic?

   A. Images are copyright tagged, and non-free images have fair use rationales:

   B. Images are provided where possible and appropriate, with suitable captions:

7. Overall:

   Pass or Fail:

Initial comments

These are mostly content questions that occurred to me while I was reading:

1. What's the relationship to superficial venous thromboses? Are DVTs even possible in the arms? (Aren't all the veins in the arm more or less superficial?) Is Paget-Schroetter syndrome the only form of VTs in arms? Is it properly thrombophilia? (It sounds more 'mechanical' than 'problem with consistency of the blood' to me.)
2. Under ==Congenital==: Are the "type II defects" part of a general classification of congenital defects, or specific to this? Are all rare forms more severe?
3. Under ==Acquired==: I don't understand HIT. You take away all the platelets, and then you somehow have blood clots?
4. Under ==Treatment==: I thought that ==Acquired== named four kinds that require "particular" treatment, but the first sentence says there is no specific treatment. The phrase "Apart from the abovementioned forms of thrombophilia..." isn't working for me. Which forms? All of them?
5. Under ==Prognosis==: Is it worth adding something about the prognosis from a thrombotic event, e.g., if a clinically significant clot forms, what's the short-term mortality rate? I suppose that someone who had this condition would like to know about any overall effects on lifespan. (Excellent job contextualizing the risks.)
6. Should we address the risk of overdiagnosis (e.g., finding tiny PEs on CT scans for other purposes)?
7. If you've had a DVT/something similar, how likely is it that you have thrombophilia?

These are largely article-writing issues:

1. I think the lead needs to more firmly differentiate between 'having a blood clot, regardless of the reason' and 'having a blood clot because of a problem with the consistency of the blood'. Can we say something like "The thrombophilias are a group of medical conditions that cause some, but not all, blood clots in veins"?
2. Under ==Signs and symptoms==: Pregnancy stuff might be more 'Risk factors' or Epidemiology than 'Signs and symptoms'. Isn't the stuff about Protein C deficiency really a congenital cause rather than a symptom?
3. Under ==Mechanism==: Probably each of the proteins should be wikilinked once in this section.

I haven't read any of the sources yet; I've only read the article. I don't expect to be able to get back to this in a serious way until at least Saturday, but ping my talk page if you want a quick response or need clarification. WhatamIdoing (talk) 04:56, 18 March 2011 (UTC)

Responses to content questions:

1. The sources said very little about superficial thromboses, and I am not sure if there is much data on a link with thrombophilia. DVTs of the arms are certainly possible (they are called UEDVT or "upper extremity DVT"), but the actual clot tends to be in the subclavian or axillary vein. Whether to use the term "Paget van Schroetter syndrome" for all UEDVT is a matter of nomenclature - when I corresponded with Frits Rosendaal about the subject some time back, he used the terms interchangeably.
2. I'm wondering if I'm overusing the Crowther/Kelton classification, which doesn't seem to have found wide acceptance. They don't seem to classify all forms of thrombophilia into their system. The classification is specific to thrombophilia. Not all rare thrombophilias are severe, as shown later.
3. HIT is fascinating. I wrote the article a few years ago. The number of platelets is diminished (although the number that remains is usually at a level where effective coagulation would be sustained), but the ones that remain are seriously pissed off (they are activated by the antibody reaction), leading to a profound prothrombotic state.
4. This depends on whether you regard PNH, HIT, IBD and nephrotic syndrome as "thrombophilias" in the narrow or the wide sense. The "Kumar4" source and many other sources bunch them together with the "pure" thrombophilias that do not have other repercussions. I'll continue to think of a way to phrase this in a brain-friendly way.
5. I was hoping to bypass the discussion of the prognosis of individual events, because this requires a lot of discussion. For instance, small peripheral pulmonary emboli have a great prognosis, while large pulmonary emboli can cause life-threatening haemodynamic instability; this would require discussion of all the pathophysiological mechanisms. The topic is potentially endless (e.g. the prognosis of other forms of thrombosis, the risk of pulmonary hypertension due to PE).
6. This is again something I would prefer to leave out, as it is more pertinent to the individual events. I do agree that the subject of overdiagnosis requires attention in the pulmonary embolism article (especially in pregnancy, as clearly discussed in doi:10.1016/S0140-6736(09)60996-X
7. I think we answer this question in a roundabout way. There are probably still undiscovered forms of thrombophilia, so all we can do is list the frequency at which the currently known forms are detected.

Article-writing issues:

1. In many cases, thrombophilia is not the cause but one of a number of contributory factors. If an overweight smoking man develops a DVT after a 4h flight, and is subsequently found to have the factor V Leiden mutation, was the thrombophilia the actual cause? Only in a small proportion of thromboses, a subsequently discovered thrombophilia can legitimately be regarded as the cause.
2. The "pregnancy stuff" was added to "signs and symptoms" because thrombophilic states cause these complications. Similarly, purpura fulminans is a symptom of protein C deficiency.
3. I was being cautious with overlinking, but I will add them back for completeness.

Thanks for your comments so far, and I am looking forward to the rest. JFW | T@lk 01:00, 20 March 2011 (UTC)

In case someone is reading this later, I have read and agreed with all of the above responses. WhatamIdoing (talk) 21:26, 26 March 2011 (UTC)

Ref notes

Here are my current notes from reading the refs:

Lead

• In Ref 2, a quick sum of the numbers in Table 8 suggests a prevalence as high as 11%. I don't know if we'd want to rely on that.

Signs and symptoms

• Ref 2 also lists 'sudden death' as a sign
• Unable to find "Whether thrombophilia also increases the risk of arterial thrombosis (which is the underlying cause of heart attacks and strokes) is less well established" in Ref 2 (did I overlook it?). Ref 24 (Middeldorp in BJH) does cover it, though.
• Ref 8 technically unnecessary in this section, as Ref 2 includes "recurrent fetal loss"

Causes

• I'm not sure that "Various explanations exist for this link" is the best statement here. Perhaps something about multiple mechanisms being involved might be more faithful to the sources?

History

• The Hughes paper isn't an ideal source for the fact that the condition is named after Hughes.
• In general, the citations to the original papers seem unnecessary to me. (Keep them if you want; it doesn't matter to me.)

There's a {{dead link}} in Ref 4 (both the URL and the doi; it looks like they're rearranging their website).

I haven't yet read Refs 9–13. Of the others, I don't have:

• Ref 1 (Robbins textbook)
• Ref 3 (Kyrle in The Lancet, PMID 21131039)
• Ref 21 (Tchaikovski in Thromb Res, PMID 20163835)

Off hand, I'd say that there are no significant problems. I hope to get through the remaining five sources within the next 24–48 hours. (Please ping my talk page again if I don't get the notes posted!) WhatamIdoing (talk) 18:52, 25 March 2011 (UTC)

Here's the last few notes in the verification pass:

Signs and symptoms

• "Whether thrombophilia also increases the risk of arterial thrombosis (which is the underlying cause of heart attacks and strokes) is less well established"—Ref 9 (practice guideline, under "Coronary, cerebral and peripheral arterial thrombosis") seems to say that the association has been established, but is just too small (relative to other risk factors) to change the treatment.

Causes

• "...and familial dysfibrinogenemia (an abnormal fibrinogen)." I didn't find this mentioned in Ref 11 (Rosendaal in ASH)

Refs

• For ref 10 (in Annals), you might want to link to the (free) lay summary at http://www.annals.org/content/138/2/I-39.full

As you've indicated that you want to have the article in American English, I will make it that way in a few minutes. WhatamIdoing (talk) 20:40, 26 March 2011 (UTC)

Response to ref notes

I have bunched responses per section, mainly for my own convenience.

Lead:

• I have rephrased the sentence in question because I was not comfortable with a non-worldwide figure that I could not trace to Heit's paper on re-reading.

Signs and symptoms:

• I would imagine "cardiac arrest" and "sudden death" are technically synonymous. Even so, completely unheralded death is unusual; often, there have been symptoms of dyspnoea etc
• The mention of arterial thrombosis is in Table 3 of Heit's article; agree that Middeldorp and also de Moerloose address the question. Reading Middeldorp's conclusions, I'm wondering how Baglin et al can be so certain in view of the methodological issues
• Heit gives fairly little detail on the miscarriage issue, on which Rai/Regan is an authoritative subject (and the same source is needed elsewhere anyway)

Causes:

• Rephrased the line on the various explanations. In the end, one of the several mechanisms will probably turn out to be the predominant link.
• Dysfibrinogenaemia is in table 1 in Rosendaal2005
• Have added the lay summary

History:

• Will look for better source wrt Hughes syndrome
• I like the old citations from a historian's perspective - I don't think there are specific MEDMOS guidelines about them

Thanks for all the comments so far! JFW | T@lk 22:05, 26 March 2011 (UTC)

I'm not convinced that Hughes syndrome really requires a citation for GA standards. It's not exactly a controversial sort of statement. If you're absolutely determined to have one, a relatively weak source like the WhoNamedIt entry would be more than adequate.

The high prevalence 'hidden' tables in some journals' online formats are the bane of citation reviewing. Thanks for pointing out what I missed. WhatamIdoing (talk) 23:00, 26 March 2011 (UTC)

Would you agree that the following reference is good enough to support the use of "Hughes syndrome"? (Yes, D'Cruz and Cuadrado work at the same department as Hughes...) Sanna G, D'Cruz D, Cuadrado MJ (2006). "Cerebral manifestations in the antiphospholipid (Hughes) syndrome". Rheum. Dis. Clin. North Am. 32 (3): 465–90. doi:10.1016/j.rdc.2006.05.010. PMID 16880079. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) JFW | T@lk 19:13, 28 March 2011 (UTC)

I agree. That journal/series is highly reputable, and "Hughes syndrome" does not seem to be a controversial eponym. -- Scray (talk) 21:32, 28 March 2011 (UTC)

Oh, sure. As I said above, I don't think this claim is either one of the four things absolutely required to have an inline citation according to the content policies or one of the five things required for GA, so an inline citation is IMO optional, strictly speaking. However, that one will do nicely, if you want to add it.

I expect to close this (as passed) tomorrow morning (~20 hours from now), assuming my last-minute checks don't turn up anything surprising. Scray, if you've got any objections, now's your chance to squawk. WhatamIdoing (talk) 21:52, 28 March 2011 (UTC)

No objections. Nice work, all! -- Scray (talk) 23:22, 28 March 2011 (UTC)

Kumar/Robbins

I'm comparing chapter 4 of the Robbins textbook (ref 1, "Kumar"), and seeing some differences from the article that seem important. I have already made some changes that were straightforward, but am getting into a bigger snag with the descriptions of HIT and PNH (described as rare, under acquired causes). Here is what Kumar says:

Among the acquired causes of thrombotic diathesis, the heparin-induced thrombocytopenia (HIT) syndrome and antiphospholipid antibody syndrome (previously called the lupus anticoagulant syndrome) deserve special mention.

• Seen in as many as 5% of the population, the HIT syndrome occurs when administration of unfractionated heparin (for therapeutic anticoagulation) induces autoantibodies to complexes of heparin and a platelet membrane protein (platelet factor 4) (Chapter 12). This antibody binds to similar complexes present on platelet and endothelial surfaces, resulting in platelet activation and endothelial cell injury, and a net prothrombotic state. The occurrence of HIT syndrome can be reduced by using low-molecular-weight heparin preparations that retain anticoagulant activity but do not interact with platelets; these preparations have the additional advantage of a prolonged serum half-life.
• Antiphospholipid antibody syndrome has protean manifestations, including recurrent thrombosis, repeated miscarriages, cardiac valve vegetations, and thrombocytopenia; it is associated with autoantibodies directed against anionic phospholipids (e.g., cardiolipin) or—more accurately—plasma protein antigens that are unveiled by binding to such phospholipids (e.g., prothrombin). In vivo these antibodies induce a hypercoagulable state, by inducing direct platelet activation or by interfering with endothelial cell production of PGI2. However, in vitro (in the absence of platelets and endothelium) the antibodies merely interfere with phospholipid complex assembly and thus inhibit coagulation (hence the designation lupus anticoagulant). Patients with antibodies to cardiolipins also have a false-positive serologic test for syphilis, because the antigen in the standard tests is embedded in cardiolipin.

PNH is certainly rare, whereas quite a large proportion of the population (5%) may be at risk for HIT. Does our article reflect this? Still working through the rest of our article's cites of this source. -- Scray (talk) 02:02, 27 March 2011 (UTC)

I have reviewed all of the cites of Robbins/Kumar, and the second paragraph of Thrombophilia#Acquired is my only lingering concern. That paragraph is a mashup of very disparate conditions - from HIT (an iatrogenic complication of heparin therapy, fairly common and relatively easily recognized) to PNH (much less common and more difficult to diagnose, inciting cause not easily identified) and red cell dyscrasias. I think it needs to be reworked - at least to provide proper context for HIT and PNH, and a conceptual framework for combining them in this way, but I'm a late arrival here and am loath to change too much at this stage unless there's a clear consensus. -- Scray (talk) 02:16, 27 March 2011 (UTC)

This is the problem with using textbooks. I have no access to Kumar4 and personally have a preference for Harrison's. I'm not sure which editor added the content that was based on this source. Most of it was verifiable, and you will see that most assertions from Kumar4 are dually sourced to other sources.

I think our current mention of antiphospholipid syndrome is appropriately balanced and thoroughly sourced to the Lancet review. I don't think it needs much tweaking. With regards to HIT, I think that Kumar4 vastly overstates the risk. Keeling (and everything Theodore Warkentin has ever written) gives much lower figures, and of course it requires exposure to heparin.

I understand your concerns about the "acquired" paragraph. With regards to its inclusion criteria, I have tried to remain faithful to lists provided in Heit and Kumar (and Rosendaal2005, which contains a similar list). The only medical condition not traceable to that list is inflammatory bowel disease, which is not common but widely regarded as a prothrombotic state. If you have any idea on how to get this better, I am very much open to suggestions. JFW | T@lk 08:43, 27 March 2011 (UTC)

I share your preference for Harrison's, and have not been a student of Robbins. Overall, I agree that the article (Thrombophilia) is in great shape, and most statements sourced to Kumar were fine.

In your second paragraph above, you state that, "I think that Kumar4 vastly overstates the risk" of HIT. For this article, we just need to settle on statements and sources. It certainly varies by population and drug (sulfation of the UFH, in particular), but a recent review PMID 10073268 published in a high-quality journal summarized the literature in this way, "This 10-year retrospective summarizes how the understanding of HIT has changed over the past decade. In contrast to previous opinions, restated above, it is now evident that the risk for HIT-associated thrombosis is substantial, even >50% in certain patient populations (2)."^{(2) = PMID 7715641} The review goes on to say (in a section on "Frequency"):

Warkentin & Kelton reviewed 13 prospective studies of HIT (12), accepting a case as a probable episode of HIT only if thrombocytopenia began on day 5 or later of heparin treatment. Based on this criterion, approximately 3% of 1336 patients who received UFH in these studies may have had HIT. Even more important, 14 of these 1336 patients (1%) developed thrombosis in association with thrombocytopenia, i.e. HIT-associated thrombosis occurred in approximately 1 in 100 patients who received heparin for 5 days or more. Such a high frequency of clinically significant adverse events for a medication as commonly prescribed as heparin indicates that HIT is one of the most important adverse drug reactions physicians will encounter. Indeed, in one prospective study, HIT-associated thrombosis occurred in about 1 in every 40 patients who received UFH (2).

Differences in patient populations may influence the frequency of HIT antibody formation. Visentin and coworkers (31) found that 52% of patients receiving UFH for heart surgery developed IgG anti-heparin/PF4 antibodies. This high frequency could reflect wide fluctuations in PF4 release into the circulation of these patients, thus leading to the optimal ratio of heparin/PF4 that can trigger an immune response. In contrast, medical cardiac patients receiving UFH had a much lower frequency (2.5%) of anti-heparin/PF4 antibody formation in one study (32).

^{(12) = Bounameaux, H., ed. (1994). Low-molecular-weight heparins in prophylaxis and therapy of thromboembolic diseases. New York, N.Y: Marcel Dekker. pp. 75–127. ISBN 0-8247-9174-6.; (2) = PMID 7715641; (31) = PMID 8833886; (32) = PMID 9054645}

Clearly, HIT is a high-frequency complication of heparin treatment. All parties with an interest in thrombosis and anticoagulation should be cognizant. -- Scray (talk) 18:08, 27 March 2011 (UTC)

I've refactored paragraph 2 under acquired into two separate paragraphs; I hope others agree that it's an improvement. I've avoided direct reference to frequency, pending consensus here. -- Scray (talk) 18:20, 27 March 2011 (UTC)

At this point, I am satisfied that the article accurately reflects cited sources. -- Scray (talk) 18:29, 27 March 2011 (UTC)

Thanks for your comments and for your attention to the HIT/PNH paragraph. It does flow much better now and inter alia discusses the paradox that WhatamIdoing alluded to with regards to the nomenclature of HIT. Just to clarify: I do not dispute the importance of HIT and totally agree that it should be given the prominence we are giving it currently. At the same time, in absolute terms HIT-related thrombosis is rare compared to the other mechanisms. (COI I'm the main author of heparin-induced thrombocytopenia.) JFW | T@lk 20:09, 27 March 2011 (UTC)

Passed

I have decided that the article in its current form meets the Good article criteria. Congratulations to JFW and all the other editors who helped the article along the way. WhatamIdoing (talk) 16:43, 29 March 2011 (UTC)

Image

Unrelated to GA review: Do you think that File:Warfarintablets5-3-1.jpg (shown) might be a better choice for the likely audience than a chemical diagram? I believe it's famous for its color coding (which seems to vary by country). WhatamIdoing (talk) 18:54, 19 March 2011 (UTC)

I have no objection. JFW | T@lk 00:11, 20 March 2011 (UTC)

Article title

I was just wondering whether the title of this article has been discussed. I don't see such a discussion here on Talk; if it occurred elsewhere please point me. The term "thrombophilia" is unlikely to mean much to non-medical readers (except perhaps students of Latin). Harrison's textbook of medicine has a section, "Hypercoagulable state" under "Thrombotic disorders", which has no mention of "thrombophilia". Likewise, Robbins textbook (cited 7 times in this article) has zero occurrences of the term "thrombophilia". What is the basis for this title? Please don't assume I am resisting this usage: I actually like the term - its etymology makes great sense - but I would guess that there's a more encyclopedic rationale than that. In particular, the pattern I'm seeing in a lot of contexts suggests that "thrombophilia" is meant to apply to congenital (rather than acquired) hypercoagulability, in a manner that somewhat parallels "hemophilia". -- Scray (talk) 18:46, 27 March 2011 (UTC)

I've never really reflected on the nomenclature. I have the feeling that "thrombophilia" is more prevalent in the European literature, and indeed here in the UK clinicians order the "thrombophilia screens" on patients with thrombosis. Most sources I used for this article, though - on both sides of the Atlantic - use the term thrombophilia. Perhaps the concept "prothrombotic state" is somewhat broader than thrombophilia, but I have no evidence for this assertion. For instance, diabetic ketoacidosis should rightly be considered a prothrombotic state, but I would intuitively struggle to refer to this as a thrombophilia.

I've just run a couple of Googlefights, and "thrombophilia" wins hands down from "prothrombotic state" and "hypercoagulable state" (make sure you include the quotation marks). JFW | T@lk 20:21, 27 March 2011 (UTC)

FWIW, I also searched Pubmed for "thrombophilia"[ti] (1319 references), "hypercoagulable"[ti] (388 references), and "prothrombotic"[ti] (535 references). None of these metrics is authoritative, but I agree with the existing title ("Thrombophilia") even though use of the term is unfamiliar to me. Maybe the cornfield in which I work is too isolated. -- Scray (talk) 21:32, 27 March 2011 (UTC)

Surely, many texts use thrombophilia to refer specifically to the congenital or hereditary forms, but many generalize it to any prothrombotic/hypercoagulable state, and it's most appropriate to expand the scope of this article to the broadest sense, and it does so very well with the clear distinction between congenital and acquired causes. I agree hypercoagulability is more self-explanatory, but with the more common usage of thrombophilia, it seems to be appropriate enough. In short, I think the article title of Thrombophilia may remain, so no change needed. Mikael Häggström (talk) 09:57, 2 April 2011 (UTC)

Malignancy

Isn't malignancy one of the major causes of hypercoagulable states (and yes, I too see this term used much more than thrombophilia, but I digress...)? If so, I don't see much discussion of it. Am I missing something? Yobol (talk) 04:20, 30 March 2011 (UTC)

Some sources don't classify malignancy as a "thrombophilia" sensu strictu, possibly because cancer leads to thrombosis by other mechanisms rather than just rheological ones. For instance, large-volume retroperitoneal deposits cause flow abnormalities in the inferior vena cava and increase thrombosis risk by that mechanism. I see no problem mentioning malignancy, but it would need to have a suitable source. Heit mentions "active cancer" in his list, and so does Rosendaal2005. I will therefore add a few lines. JFW | T@lk 04:25, 30 March 2011 (UTC)

Promoter region?

In regards to prothrombin G20210A I was skeptical that the promoter region was the right way to describe it, so I made this edit[1] because that is what was verified, but I was reverted.[2] So I looked up this[3] and this.[4] It's clear the 20210 refers to the position on the sense strand, where position 1 to 3 is ATG for the start codon. 20210 occurs in the 14th and last exon, but in the 3' untranslated region after the 14th exon is done coding. 20210 is also next to/near where the poly-A tail is attached on the pre-mRNA. This can't be part of the promoter region, as far as my knowledge is concerned. It was mentioned in the discussion of the 1996 publication that the polymorphism could contribute to RNA stability/translation efficiency. Biosthmors (talk) 19:58, 1 February 2012 (UTC)

I reverted the change only because 3' untranslated region redirects to Three prime untranslated region, and I hadn't given your distinction between 3'UTR and promotor a second thought. My apologies for missing that. I will make the required correction. JFW | T@lk 20:45, 1 February 2012 (UTC)

Ah. No problem. My apologies for not using a more detailed edit summary. And I put the research to good use over at the other article.[5] Thanks. Biosthmors (talk) 16:35, 3 February 2012 (UTC)

Resources

Although this article contains reasonable number of references, the reference below can be cited and resources can still be drawn from:

• Remkova, A (2006). "Diagnostic approach to hypercoagulable states" (PDF). Bratislavske lekarske listy. 107 (8): 292–5. PMID 17125064.
• Schafer, AI (1985 Jun). "The hypercoagulable states". Annals of internal medicine. 102 (6): 814–28. PMID 3158262. {{cite journal}}: Check date values in: |date= (help)

Diptanshu^Talk 08:24, 27 May 2013 (UTC)

I don't see how either of these sources would add anything to the current content. The first simply discusses everything we already cover and is from a low-impact journal in Eastern Europe. The second is 27 years old and would qualify as "historical interest" only. JFW | T@lk 17:33, 27 May 2013 (UTC)

Risk scoring

Currently, decisions about prolonged prophylaxis and risk of recurrence in people with confirmed thrombophilia are very non-evidence based, and I wonder if there is a risk of defensive practice. Two French groups have proposed a risk score (MARNI) - doi:10.1111/jth.12461 that needs validation and is therefore not ready for inclusion, but something that is likely to become a feature of risk assessment in the future. JFW | T@lk 16:35, 12 December 2013 (UTC)

There are about 4-5 scoring systems to quantify the risk for thrombosis. They will appear shortly in the article on Thrombosis prevention

Barbara (WVS) (talk) 14:21, 24 December 2016 (UTC)

Circulation

Review by Heit doi:10.1161/CIRCULATIONAHA.113.001943 JFW | T@lk 21:15, 14 January 2014 (UTC)

doi:10.1161/CIRCULATIONAHA.113.007664 - further review by Piazza. JFW | T@lk 19:09, 20 July 2014 (UTC)

NEJM

doi: 10.1056/NEJMra1700365 JFW | T@lk 11:41, 24 September 2017 (UTC)

Celiac Disease

CD seems to be a significant risk factor, see https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616811/ --2A02:560:4147:A600:D14C:5C05:3258:AA20 (talk) 10:58, 23 March 2019 (UTC)