Talk:Prothrombin G20210A

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Blood type and prothrombin

I think there is a mistake in this article. As it is now it states "Behind O-blood type,[1] prothrombin G20210A is one of the most common genetic risk factors,...."

I ready the article cited and it says that "The other 3 moderately strong genetic factors are associated with an increase, directly or indirectly, of the procoagulant potential of the blood: factor V Leiden, prothrombin G20201A, and blood group non-O.

To me this means that those with blood type A, B or AB would be risk factors for thrombosis, not people with type O. I am not an expert on this but I think it needs to be looked at.... — Preceding unsigned comment added by Bethalean (talkcontribs) 18:49, 24 September 2012 (UTC)[reply]

That's my fault. Thank you for catching my error. I meant to say non- I'll fix that right now. Biosthmors (talk) 19:34, 24 September 2012 (UTC)[reply]

Expert needed throughout

Please do a diff from before and after my work today.

The article contained a lead mention of 2-3x increased risks of thromboembolism without clarity regarding which specific genetic condition and which source population was being described (single heterozygous vs other; generally healthy American, vs Asian, vs. No/So European, etc.), and the 2-3x information, where it appeared in the main body, was not sourced. (The extent that frequency/prevalence information appears later, it is various, for various populations.) Discussion of frequency/prevalence demands statement of whether the risks refer to homozygous versus heterozygous presentations, discussion of the occurence of this mutation in conjunction with Factor V Leiden, etc., etc. In short, the lead was simply not accurate, as presented.

In addition, the lead was far too long and detailed, and so some material was moved up, and then a break was created, and a Background section placed, to hold further introductory material unnecessary in the lead.

As well, various edits were made to the "Risk factors" (?) section, where a new naming nomenclature suddenly appeared (resulting in my UC to LC edit), and where mention was made of studies being "conversant" (made no sense, so removed). It appears that this and other copyedit-needing portions were added by a one-time, non-native English speaking editor, Madsread, see Edit history.

In that section, and elsewhere, inline citations to Wikipedia were removed as violations of WP:VERIFY, and tags were added to poor or dead sources. Finally, after some equivocation, I removed a photograph of a pair of legs, one apparently intended to present as discoloured and swollen—eventually removing it (i) because this is not an article about DVTs, but about one genetic locus that is a risk factor for that and other thrombophilic disorders, and (ii) because Doppler ultrasound and D-dimer and other factor and phospholipide clinical tests are the standard for accurate diagnosis treatment design (not physical examination, so the image is misleading). If we can find a flow chart related to diagnosis, or create a table placing G20210A alongside factor V Leiden, etc., etc. (see review added to Further reading), these would be better than the "believe me it is a DVT that involved the FII G20210 mutation" photograph.

The call for Expert was added to check these edits, and for the further reasons appearing in the tag and in the edit summaries.

Le Prof 50.153.156.160 (talk) 23:41, 19 May 2016 (UTC)[reply]

The "2-3x" definitely needs context. I'm not even sure this test is even ordered for pathological cases as it doesn't seem to affect treatment. A test for Lupus, Leiden factor V, Proteins S and C, anemia are usually done after diagnoses of the clot and treatment is already underway. The additional tests reveal other conditions that may need treatment or alter the standard treatment (i.e. warfarin for life instead of 90 days until resolution). A venologist may look for mechanical defects in valves and things like an abnormal crossover that compresses the vein. There's no context in to how this genetic anomaly relates to the frequency of these other causes including clots that form as a result of common surgeries on things like knees. Many doctors won't even order a test if they can't describe what the output would do to their treatment plan or clinical diagnoses - it just creates FUD (my first example of the difference between being scientific and clinical was going to the doctor with symptoms of strep throat and family member that just got over it with antibiotics. She did about a 4 minute exam, no tests and diagnosed strep and ordered antibiotics. I asked if she needed test to rule out virus her very practical response was that she would discount a negative rapid strep test as a false negative based on symptoms and history and the full test wouldn't return in time and she wouldn't wait for that test to start antibiotics. The tests then became meaningless so none ordered. This genetic anomaly sounds a lot like a sciency rather than clinical test. What do hematologists do with the knowledge? That's missing from the article even though it's discussed as if it's clinically significant. --DHeyward (talk) 11:43, 21 May 2016 (UTC)[reply]