Talk:Immune thrombocytopenic purpura

This is not a medical advice forum

Wikipedia is not the place to look for help with idiopathic thrombocytopenic purpura or any other medical condition. This article has been written only to be a source of information, and posting questions such as seen below regarding ITP is inappropriate. Most of those who have edited this article are not medical professionals and therefore are not qualified to suggest anything related to treating ITP, other than to recommend you seek professional help. If you or a loved one has been diagnosed with ITP, you need to see a hematologist or similarly qualified medical professional for answers and recommended courses of treatment.

Some of the editors of this article have been diagnosed with ITP, putting them in a position to contribute some knowledge to this article. At least one of them is an elderly male patient who is chronic and refractory, and whose case, due to its rarity, has undergone extensive clinical analysis, as well as treatment. Since being diagnosed, this individual has engaged in extensive research about ITP and the efforts underway to develop treatments, both for personal benefit and to contribute more knowledge about ITP. He is, however, not a medical professional and will not answer questions regarding treatment courses or long-term prognosis.

A suggested resource on the Internet for ITP patients is the Platelet Disorder Support Association (http://www.pdsa.org). Be aware, however, that some PDSA netizens advocate the use of herbs, Chinese medicine and other non-scientific methods of treatment to attempt to "cure" ITP. There is currently no cure for chronic ITP, and no scientific evidence that any of these alternative methods will affect ITP in a positive way. In some cases, the use of such methods may interact in unpredictable ways with drugs being administered to treat ITP, possibly posing a health risk over and above ITP itself. Caveat emptor! — Preceding unsigned comment added by [[User:{{{1}}}|{{{1}}}]] ([[User talk:{{{1}}}|talk]] • [[Special:Contributions/{{{1}}}|contribs]])

We can only rely on published high-quality sources, not original research. JFW | T@lk 07:29, 8 July 2013 (UTC)

AIDS

Low platelet count is very common in people with aids, can we reference it ? http://www.thebody.com/Forums/AIDS/Cancer/Archive/chemo/Q16511.html

HIV is now mentioned. Andrew73 12:05, 16 October 2005 (UTC)

Units

I believe that the page has incorrect units for platelet count. They are usually given in microliters (uL), not milliliters (mL). Your counts used in examples would be correct for uL and you use mm^3 in a comment which is equivalent to uL.

So wait, is 10,000 per uL the same as 30,000 per cu/ml? --LycanFury09 16:51, 27 October 2006 (UTC)

I'm not sure what you mean by "cu/ml", but a uL (microlitre) and mm^3 (cubic millimetre) are the same. Thus 10,000 platelets/uL = 10,000 platelets/mm^3. -- Coneslayer 17:29, 27 October 2006 (UTC)

Pretty sure the units under "Treatment" section are wrong. The numbers 20/uL and 30/uL are used, but it should most likely be 20,000/uL and 30,000/uL, respectively. -- Dentropy (talk) 18:14, 20 September 2024 (UTC)

Antibodies

I believe the statement that says antibodies are detected in a minority of pts may be incorrect. In Robbin's Pathology, 7th ed. (p. 651) it states, "Antibodies reactive with these membrane glycoproteins can be demonstrated in the plasma as well as bound to the platelet surface (platelet-associated immunoglobulins) in approximately 80% of patients."--Jfurr1981 05:58, 13 October 2005 (UTC)

Perhaps the distinction refers to clinical use of platelet antibody assays. The performance of these tests needs some improvement before they can be routinely used. See also the recent Blood review article [1]. Andrew73 12:05, 16 October 2005 (UTC)

Platelet counts in the UK are given in much lower units which, I suspect, are those quoted elsewhere/1000. i.e a count of 10 is low, 150 is reasonable and 500 is high. Just referring to my individual case, I'm not a medic.

You're correct. In the UK they are expressed as billion per litre (10⁹/L). The normal range is usually 150-450. JFW | T@lk 21:24, 6 December 2005 (UTC)

After a splenectomy?

My father has had ITP and after a splenectomy and three years of cortison his hermatologist discovered the article in the British Journal of Hermatology (2002, 118, p. 584-588) which reported evidence about a relation between helicobacter bacteria and ITP (see reference in the article). My father got a 1 week treatment with antibiotics and recovered fully. This is now 5 years ago and he has never had any issues since. You might want to ask your hermatologist to review the articles (there are two quoted in the reference list) and test for helicobacter. The treatment would simply be antibiotics, so side effects are limited. —Preceding unsigned comment added by 88.71.91.196 (talk) 22:51, 19 March 2010 (UTC)

My wife has this disease, has had her spleen removed, and still suffers from it. The article implies that removing the spleen is the last step in treatment...I'm kind of curious as to why this didn't work. Does anyone have any insight? For the record, she is now taking azathioprine and seeing a hematologist every 3 months, though I'm not sure what they do there...she also tells me her condition is very rare.

This is when rituximab is tried. But don't ask a bunch of strangers here. JFW | T@lk 07:49, 16 November 2005 (UTC)

I thought this was exactly the type of place to seek knowledge from strangers. Was I mistaken? I'm not looking for medical advice or what treatment is offered (I know that), I'm just curious as to why removing the spleen, which this article says should cure the disease, did not. Oh, and I meant to sign that last one. Sorry. --UsaSatsui 07:03, 22 November 2005 (UTC)

I would recommend that you check out pdsa.org. I found the PDSA site when I was first diagnosed and it was an incredible help in my education of the condition. The discussion groups with other patients was an incredible support group. --garthoid 01:44, 21 March 2006 (UTC)

The article states that "Splenectomy is said to be successful in 60% of cases although it is less successful in older people"... the reason the spleen is taken out is that spleen is involved in breaking down platelets... as to why it didn't work well I can only assume the spleen turned out not to be the cause of the disorder... though don't take my word for it I'm only learning about it now. --someone87 05:24, 29 November 2007

I actually did have my spleen removed after two years of different treatments. My platelets were 3,000 when I was diagnosed. They did IVIG, steroids, chemo, winrho, pretty much everything. I even did have the H. pylori, and they treated me for that until it went away, but there was still no change in my platelet count. The IVIG and steroids worked but only for a week or so at a time. The chemo and winrho did nothing for me. Splenectomy was sort of a last attempt outside of experimental treatment. It worked for me, fortunately. My count was 1.7 million the morning after surgery, and it eventually evened out to a nice 400,000 or so. The doctors do not jump straight to splenectomy because it is often not necessary, as most cases are acute and last for less than a year. Also, obviously a splenectomy is a surgery, and there are serious risks to surgery. Another obvious disadvantage is that I don't have my spleen any more; and while my spleen was destroying my platelets, it also used to protect me from infection. Many people don't think that a spleen is an important organ, but a lack of one does add minor complications to my medical health. I have to take antibiotics a lot, and if I get a fever above 101 for more than two hours, I have to go to the hospital. I once had strep throat three times in two months, and I had to go get shots for that. Don't get me wrong though, I would much rather live without a spleen than live with ITP. If a splenectomy doesn't work however, the patient is now living with both - a serious and unfortunate situation. If someone doesn't respond to a splenectomy, it's because the spleen wasn't doing anything wrong to begin with. Something else in the body is destroying the platelets, or the platelets may not be being formed to begin with. Whatever the case, it is a serious problem. —Preceding unsigned comment added by Tafatula (talk • contribs) 23:34, 3 October 2009 (UTC)

Just for information, if the spleen isn't doing the killing off of platelets it's the liver doing it and it isn't a serious problem at all. It's just the way it is. There's a test you can have in the UK called an Indium Platelet Survival Study which shows where the platelets are being killed off. I had it done and it showed the liver was responsible so I knew not to have a splenectomy. Ann Tortoise (talk) 14:37, 22 November 2009 (UTC)

Again, I will reiterate. This is not a medical forum. Discussion such as above should be at places like pdsa.org, where often-erroneous advice is given (e.g., herbs will "cure" ITP).

As for the the indium platelet survival study, its accuracy is far from certain. In my case, an IPSS suggested that the spleen was the point of destruction for platelets. I relapsed about 4 months after the splenectomy and almost bought the farm in the process (count was sub-1000 at one point). To this day, my hematologist is uncertain as to what is causing the loss of platelets. The count is being sustained with periodic injections of romiplostim.

Just for information, if the spleen isn't doing the killing off of platelets it's the liver doing it and it isn't a serious problem at all.

No problem at all—until your count goes into the toilet and you are rushed to the ER with a brain bleed. That's the sort of ignorant thinking (along with advice to use herbs or over-the-counter remedies) that can lead to major complications or death.

The article states that "Splenectomy is said to be successful in 60% of cases although it is less successful in older people"... the reason the spleen is taken out is that spleen is involved in breaking down platelets... as to why it didn't work well I can only assume the spleen turned out not to be the cause of the disorder... though don't take my word for it I'm only learning about it now.

Post-splenectomy ITP relapses occur more often in older folks because the spleen's role in clearing the blood of circulating pathogens (including platelets mistakenly targeted by the immune system) is lessened with age. In a younger person, the spleen is much more active. Folks my age (over 60) who are otherwise reasonably healthy can get along fine without a spleen in most cases.

Bigdumbdinosaur (talk) 23:04, 29 November 2009 (UTC)

I think I have a right to come back to this. I didn't say that having a low count wasn't serious, I said the fact that it's the liver killing off the platelets is no more serious than when the spleen does so. It's exactly the same in either case. The Survival Study gives more of an idea about the percentage chance of success, that's all it claims to do. For me the chance of success is very low so I won't risk it. I am not ignorant by the way. I've read everything there is to read about ITP and keep up with all the advances in treatment. I too am on romiplostim now with success. Ann Tortoise (talk) 17:32, 1 December 2009 (UTC)

Trigger mechanism

I had a severe, but acute, case of ITP. It started with huge blood blisters inside my cheeks and on my tongue, immediately after starting a sulfa-based antibiotic prescribed for a urinary infection. The hematologist dismissed that as a possible trigger, but I recently learned that sulfa-based drugs are known to trigger autoimmune responses, such as lupus. I say dismiss it at your peril. Nobody will ever put a sulfa drug in this body again. --Bob K 21:26, 4 February 2006 (UTC)

IVIg

The comments on IVIg seem to strongly state that this should only be used in extreme situations. This seems to contradict other reading I've done on the web where, for children at least, IVIg is a common treatment (it's what we are doing). Example quote "Intravenous immunoglobulin (IVIg) is used for life threatening cases". --141.212.111.116 18:07, 22 August 2006 (UTC)

It was used in my case. My platelet count was down to 6000 when I was finally diagnosed. The first of 5 or 6 IVIgs was started immediately, about 10 pm. And I believe I was given Prednisone. My count was up to 10000 by the next morning, and things proceeded smoothly after that until I was off the Prednisone 5 months later. That was 13 years ago.

Some of the IVIgs were administered as an outpatient, and that proved to be more expensive for my insurance company than staying in the hospital would have been, even with the extra cost of the especially sterile room I was in (designed for AIDS patients). The reason given was that the hospital is able to negotiate a much lower price for the IVIg. So if you are expecting to save money, keep that in mind.

Since my recovery was uneventful and complete, I would not dare to change a thing. But the IVIgs were very expensive and each one took such a big chunk out of my day, that I might as well have stayed in the hospital. I later learned that my insurance company thought it would be safer, from a secondary infection POV, to take my chances amongst the general population than the hospital population. However, they did not know that I had been transferred into an AIDS room.

--Bob K 22:45, 22 August 2006 (UTC)

I was diagnosed about three years ago with ITP and CVID. IVIG is a treatment option for both conditions and considered fairly safe. After several once a month treatments with IVIG, my platelet count stayed around 100,000. My insurance company decided that that was stable enough to stop IVIG treatments because of the cost. A couple months later I was in Atlanta and noticed bruising on my arms and legs. I went to a walk-in clinic and ask them to check my count. It was found that my count was below 6,000. I now receive IVIG once a month and Rituxan every three months. This keeps my count right at 150,000 which is the low end of normal. My hematologist feels that these treatments work for me and are safer than a spleen removal. I agree with him on this and reason that I can always change treatment but can't grow a new spleen. I would also caution that everyone reacts differently to any treatments. I would only use the advice on here as a guide not as absolutes. Snap1790 (talk) 22:32, 29 December 2012 (UTC)

This is not a discussion board to have detailed conversations about individual cases, including yourself. See WP:TALK. JFW | T@lk 23:31, 29 December 2012 (UTC)

Dapsone

Added a bit on Dapsone. It's really helping my child! Given the generally minor side effects, I'd encourage everyone with long-term ITP to consider it. One pill a day from home.... Hobit (talk) 05:26, 16 December 2007 (UTC)

• Thanks for those that got me to add references and those who correctly formated those references! Hobit (talk) 23:01, 1 January 2008 (UTC)

Score

doi:10.1111/j.1365-2141.2007.06635.x describes an 11-point score to assess severity of bleeding in ITP. JFW | T@lk 22:50, 23 June 2007 (UTC)

I.T.P with Erythema Nodosum

I'm not sure what this page is but I'm hoping it's one where I may get some urgently needed answers. I have had ITP for 2 years and now have been diagnosed with a disease called Erythema Nodosum. My doctor is very upset that he can't find what has caused it and how to treat it it. So far I am just getting sent home after short hospital stays with a load of pain meds. I may be the first known case of ITP with E N and it's not going away. Help! Anyone? 71.61.253.91 (talk) 06:11, 8 May 2008 (UTC)

• Not a doctor and this is the wrong forum for questions like this. That said, I'd certainly suspect some form of cancer. 68.40.58.255 (talk) 02:25, 12 June 2008 (UTC)

Thrombopoietin Receptor Agonists

I relocated the subsection on eltrombopag to the TRA section below romiplostim, since the two agents behave in similar fashion and because eltrombopag was FDA-approved in November, effectively removing it from the "novel agent" classification.

Bigdumbdinosaur (talk) 22:21, 18 December 2008 (UTC)

Platelet Transfusions

I modified the treatment subsection on platelet transfusions to remove the following:

An exception to this rule is when a patient is bleeding profusely, when transfusion of platelets can quickly form a platelet plug to stop bleeding. 

I couldn't find anything in the medical literature to support the above, and a discussion with the hematologist who is treating me for chronic ITP, contradicted the claim that a platelet transfusion will "quickly form a platelet plug."

Bigdumbdinosaur (talk) 07:03, 23 December 2008 (UTC)

Blood review

doi:10.1182/blood-2009-01-129155 is the latest review in Blood. Should probably be cited. JFW | T@lk 16:10, 19 July 2009 (UTC)

I had a read of the article but am not yet certain as to how to fit in a citation. The article does promote some new insight on occurrence rates and possible changes in gender balance, especially as a function of age, which may be of value. I guess it all depends on just how technical we want to get.

Bigdumbdinosaur (talk) 21:57, 25 August 2009 (UTC)

Latest information re ITP is in the International Consesus Report in Blood http://bloodjournal.hematologylibrary.org/cgi/content/full/115/2/168 which should maybe be used to update the information given here.

For example it says that it is now known that platelet production is impaired whereas here you say that on examination of the bone marrow an increase of megakaryocytes may be observed. This is now known not to be true.

It also says that ITP, which they now call Immune Thrombocytopenia, is always an immune-mediated disease. And so on. The report was written to replace both the American and British guidelines. It would be good for the page here to be updated as I know that many people rely on it for information.

Burnt Toast UK (talk) 18:39, 27 March 2010 (UTC)

I've read that report and believe you are reading more into it than warranted. For example, nowhere does it say ITP "is always an immune-mediated disease." It appears at this time that ITP is an autoimmune condition, but other causes have not been completely ruled out. I believe you may be misunderstanding the scope of the article's introductory section, in which forms of thrombocytopenia are discussed, ITP being one of them.

The general consensus of the paper's authors is that the "...traditional view of increased platelet destruction mediated by autoantibodies [has evolved to] to more complex mechanisms in which both impaired platelet production and T cell–mediated effects play a role." In other words, knowledge accumulation has resulted in more identifiable factors, in addition to autoimmune activity. For example, the T-cell role has been suspected for some time and is one the reasons the off-label use of rituximab as a treatment course is sometimes prescribed. The fact that rituximab therapy fails in many cases indicates that T-cells do not play a role in all patients. The primary pathogenesis is still autoimmune, but in a more complex way than previously thought.

"For example it says that it is now known that platelet production is impaired..." The article does not say anything of the sort. It merely lists subnormal platelet production as a possible contributing factor. Subnormal production alone is not characteristic of ITP (see http://en.wikipedia.org/wiki/Thrombocytopenia#Causes). In my case, for example, bone marrow aspiration indicated that platelet production was elevated, evidently a response to the ongoing destruction.

If you carefully read the Pathogenesis section of the ITP article, you will see The stimulus for auto-antibody production in ITP is probably abnormal T cell activity. Preliminary findings suggest that these T cells can be influenced by drugs that target B cells, such as rituximab. The article, as currently written, reflects present-day thinking on ITP.

Bigdumbdinosaur (talk) 19:56, 27 May 2010 (UTC)

Spontaneous intracerebral hemorrhage

Hobbit: (Undid revision 319329955 by 72.51.124.202 (talk) revert good faith edit. I think we need a source for that.)

It may have been a good faith edit but you were correct in reverting it. There's nothing obvious in the medical literature on ITP that indicates that a very low platelet count in itself will cause spontaneous bleeding. In every case I've read about, some sort of external influence was involved. That is to say, there doesn't seem to be any evidence that ITP per se predisposes one to spontaneous intracerebral hemorrhage. It (ITP) merely increases the susceptibility to intracerebral hemorrhage following head trauma.

• I know I've read something about spontaneous hemorrhaging. But I don't know where and my spotty memory says it was for below 3,000. But that may have been info from a doctor (I have a child with long-term ITP...) Hobit (talk) 03:24, 26 October 2009 (UTC)

I made my weekly hegira to the vampire clinic today for my weekly CBC and while there, queried the head vampire (the chief hematologist) about this. He said he was not aware of any instance where intracerebral hemorrhage started on its own as a consequence of ITP. In the cases which with he was familiar (including mine—I was admitted to the ER last December with a headache that proved to be a bit of intracerebral hemorrhage), the hemorrhaging started following a good bump to the head. At the time it happened to me my count was 6,000 and went as low as 2000 before it was reversed. Needless to say, I got a bit nervous about it.

Anyhow, I think that until we have documented evidence that ITP in itself can result in spontaneous intracerebral hemorrhage no such entry should be made in the article.—Bigdumbdinosaur (talk) 02:31, 27 October 2009 (UTC)

Not-so-notables

I removed two entries from the "notables" section: Justin Lindley, on who I couldn't find anything to indicate he is a real person, and Keeth Smart. In the latter's case, 1) he was an obscure Olympian, largely unknown outside of fencing circles; and 2) there are conflicting stories as to exactly what malady he developed while in Beijing during the 2008 Olympics.

As is well known in the medical literature, there is no true cure for ITP and little understanding of its exact cause. Based on the claims that Smart was allegedly cured of what ailed him in a matter of days—he went on to compete in fencing—it is extremely doubtful he had developed ITP. Most likely, the doctors' diagnosis was incorrect—not at all uncommon, since the diagnosis is a process of exclusion, not leaping to a conclusion.

A footnote to the Keeth Smart situation is that I placed dubious tags in his Wikipedia bio where his developing ITP was mentioned. It'll be interesting to see if anyone looks further into the matter. In any case, I don't think he qualifies as noteworthy, even if he does have ITP. I have it and I'm definitely not noteworthy by anyone's measure.

BigDumbDinosaur (talk) 05:31, 27 November 2009 (UTC)

Keeth Smart had something called onyalai. It says so on page 5 of the report written by the hospital he attended. But even they say it's a form of ITP which if you look it up you will see that it isn't. The report is in pdf format at http://www.nym.org/upload/document/Annual%20Report%2008-1.pdf Burnt Toast UK (talk) 18:04, 27 March 2010 (UTC)

I read up on onyalai and also asked my hematologist about it. He stated (he's an assistant professor of medicine at a well-known university in the USA) that onyalai differs from ITP in several ways, especially in the immune pathogensis and is mistakenly diagnosed as ITP due to the nearly identical symptoms. Here's some info I found that seems to support his opinion:

6.2 Onyalai, clinical aspects

The disease differs clinically, epidemiologically and immunologically from idiopathic thrombocytopenic purpura (ITP). The age of onset varies from 6 months to 70 years with a peak incidence between 11 and 20 years. It is an acute disease, characterised by the formation of haemorrhagic vesicles and blisters on the palatal and buccal mucous membranes, together with severe thrombocytopenia. Sometimes, haemorrhagic blebs do appear on the skin, including on the soles of the feet. The general condition tends to be good and there are no signs of a constitutional disorder. This acquired form of thrombocytopenic purpura can lead to haematuria and melena. Epistaxis, petechiae and ecchymoses are common, as are subconjunctival bleeding and menorrhagia. The median duration of bleeding is about 8 days, but recurrent bleeding episodes are common. About 80% of cases will have chronic thrombocytopenia with a risk of intermittent attacks of acute haemorrhage. Haemorrhage from ruptured bullae, epistaxis or gastrointestinal bleeding can be severe and may cause shock and even death.

The above, along with what my hematologist says, supports my conclusion that Keeth Smart was not an ITP patient.

Incidentally, there is no Wikipedia article for onyalai.

BigDumbDinosaur (talk) 04:44, 5 April 2010 (UTC)

I started an article on onyalai.

BigDumbDinosaur (talk) 20:14, 9 April 2010 (UTC)

Stacy Clark

Is she really notable? I haven't found much about her on-line and in checking with those who would be inclined to listen to her sort of music, I couldn't find anyone that knew about her. Bigdumbdinosaur (talk) 05:17, 10 September 2010 (UTC)

• • She's notable. How notable, I don't know.

Adding people

Hi folks, if you are going to add people to the list of folks with ITP, please source your addition or at least link to an article that mentions ITP.

Hobit (talk) 12:41, 22 September 2010 (UTC)

I'd rather we keep the trivia out of the article. The fact that Joe Blow or John Doe have ITP is not relevant. The article is about the disease, not folks who have it.

Bigdumbdinosaur (talk) 20:28, 15 October 2010 (UTC)

US centric?

I don't feel qualified to edit the article itself, but I think it paints too bleak a picture, it may be too US centric.

I have a 3yr old with chronic ITP in the UK. The initial measurements were between 3,000 and 12,000, which is not "generally an indication for treatment" here, let alone a reason for hospitalisation or a medical emergency (after the exclusion of other conditions). Over here, the treatment is decided based on the symptoms and not on the platelet count; they just monitor the situation with a blood test every few months (see also the treatment section in http://www.itpsupport.org.uk/childhooditp.htm)

The symptoms mentioned can recede over time, even if the platelet count stays low; the body apparrantly adapts. I also read in a medical article (sorry, can't find the link) that there is no simple linear relationship between the platelet count and blood clothing; the working theory being that "young" platelets are much more effective than "older" ones.

DanielZee (talk) 22:33, 25 March 2011 (UTC)

it paints too bleak a picture

No more so than articles for other chronic conditions. This article is encyclopedic in nature and has been extensively researched to produce a neutral point of view. Actually, at this point in time, the long-term prospects for ITP patients are better than they ever have been. New drugs have been developed to treat ITP (I'm living proof that one of them , romiplostim, works as advertised) and a much better understanding of ITP's behavior exists. I suspect things will continue to improve. Fifty or sixty years ago, the situation may have been somewhat bleak due to a very limited number of treatment options. That is no longer the case, and nowhere in the article is "too bleak a picture" presented. It simply states the facts.

I have a 3yr old with chronic ITP in the UK.

What makes you so sure your child's case is chronic? In the opinion of my hematologist (who is a recognized expert on ITP), your child is probably too young to justify such a conclusion at this time. Most childhood cases are acute and auto-remit, but may take some time to do so. You didn't indicate when your child was diagnosed. The timeline is an important factor in childhood cases. Now, should your child go another year without improvement s/he may well be a chronic case. Until that happens, it should be considered acute.

Also, a misdiagnosis is certainly within the realm of possibility—thrombocytopenia can result from factors not related to an immune pathogenesis. Time will tell the tale.

The initial measurements were between 3,000 and 12,000, which is not "generally an indication for treatment" here, let alone a reason for hospitalisation or a medical emergency (after the exclusion of other conditions). Over here, the treatment is decided based on the symptoms and not on the platelet count...

Standards of care vary from country to country and in countries with socialized healthcare, the standards may be lowered as a cost containment strategy. The standard of care mentioned in this article has been widely adopted, both in the USA and in other countries, and does err on the side of caution. Better to adopt a conservative approach than to have to plan a funeral due to taking the cheap route. I suspect your hematologist is working with a more relaxed standard that may reflect thinking that is not based solely on sound medical practices.

Also, ITP cases in very young children are not as critical as chronic cases in adults. The 3000 to 12,000 range you are quoting (I'm assuming you are using the UK scale, not the one used in the USA) is mild thrombocytopenia and is primarily a case of observation rather than treatment. You may be trying to compare apples to oranges.

As for determining whether or not to initiate treatment based upon visible symptoms rather than CBC results, that suggests an intentionally relaxed standard of care consistent with cost containment. An ITP patient can have a dangerously low count and not immediately present with any of the classic visible signs. Again, I speak from personal experience, as well as discussion I have had with medical personnel familiar with the malady.

The standard of treatment for juvenile cases is also not as stringent as for adult cases (which are invariably chronic). A child's immune system is far from fully developed and often self-corrects. This fact is evident in that none of the new treatments for ITP (romiplostim and eltrombopag) are targeted to anyone under the age of 18. I suspect your child will respond well to light doses of corticosteriods and will eventually remit. You child is only three, so please don't read too much into the situation just yet,

The symptoms mentioned can recede over time, even if the platelet count stays low; the body apparrantly adapts.

Adaptation is more likely in children, again because they are, by definition, immature. Adults cases are, with rare exceptions, chronic and the underlying causes more complex and more difficult to treat. In my case, the thrombocytopenia had consistently resisted treatment prior to being started on romiplostim. It is now suspected that my liver has ceased producing thrombopoietin, which is the exact opposite of what one would expect if adaptation were to occur.

I also read in a medical article (sorry, can't find the link) that there is no simple linear relationship between the platelet count and blood clothing; the working theory being that "young" platelets are much more effective than "older" ones.

There's no simple linear relationship to much of anything in human physiology, which is why it's such a devilishly difficult science to master. As for platelet age, that's a theory that has yet to bear fruit. Platelets don't last all that long (5 to 9 days is typical), so relative age may be less a factor than thought. Only time and research will tell.

...it may be too US centric.

In what way? Granted, the standard of care described is "US-centric" (actually North American-centric, as Canada follows the same general treatment guidelines). However, ITP knows no national boundaries. Hence the article is presenting information that is as relevant in Europe, Asia or Australia as it is in Canada and the USA.

Bigdumbdinosaur (talk) 06:11, 15 April 2011 (UTC)

Just to be clear in case anyone else reads this and gets the wrong idea, the scale for platelet counts is exactly the same in the UK as it is in the US. The only difference is maybe that instead of saying 3,000 we would shorten that to 3, although I know that they often do that in the US too. But the person above saying that 3,000 to 12,000 is a mild thrombocytopenia is totally wrong. Anything under about 20,000 is severe. 87.194.81.2 (talk) 09:39, 11 May 2011 (UTC)

I appreciate your in-depth response.

I can't really judge if the UK treatment strategy stems from cost containment (I am privately insured) or from an US inclination to over-medicate. As most 1st world countries have a 'socialised healthcare' system it would be hard to draw any conclusions from that alone. Reading between the lines of your response, you may be unintentionally mixing in your political views. As you are maintaining this article, I think you need to be more open to finding an explanation for international differences in treatment beyond a "lower standard of care". I think there is something to be said for not putting a 3-year old on steroids to "err on the side of caution".

My kid has had low platelet counts for a bit over 2.5 years, which is chronic in the UK definition. Obviously, I too speak from personal experience and discussions with medical personnel. DanielZee (talk) 11:45, 20 July 2011 (UTC)

The article at http://tulsapedsresidency.net/wards/hemeonc/ITP.doc (American, so presumably not affected by socialised healthcare cost cutting) confirms that for childhood chronic ITP, the ideal approach is "watchful waiting" when the "platelet count is >20 _or_ when minimal bleeding signs and symptoms allow for a normal lifestyle". He concludes that "Unfortunately, no randomized controlled studies have yet been conducted to determine which therapy, if any, is best for children with newly diagnosed or chronic ITP. The few randomized trials that have been performed have assessed platelet count as the only outcome measure. Future studies must consider bleeding signs and symptoms, side effects of therapy, cost of treatment, and quality of the patient's and parent's life, in addition to platelet count, to determine which therapy is best for each child. "

Your reference [9] does not provide a backup to the statement "A platelet count below 20,000 per μl is generally an indication for treatment", as the introduction clearly states it is an opinion of the writer. Further, the document discusses adults only. DanielZee (talk) 10:46, 21 July 2011 (UTC)

History

doi: 10.1111/j.1365-2141.2010.08562.x is a historical review that has just appeared. JFW | T@lk 16:52, 11 April 2011 (UTC)

Unfortunately, the article is not publicly accessible.

Bigdumbdinosaur (talk) 05:50, 15 April 2011 (UTC)

Idiopathic or Immune

I've just reverted two good-faith edits that changed the name in the lead from "Idiopathic thrombocytopenic purpura" to "Immune thrombocytopenic purpura". At a quick glance, it looks like there might be some support for the change, but "idiopathic" is used by most of the med sources in the infobox, and ICD-10 actually switched to "idiopatchic" from ICD-9's "immune", so I don't feel this should be done without some discussion. I'm just a WikiGnome here and have no medical knowledge of the condition whatsoever, so I lack any experience to say that either makes more sense in the context of the article. – RobinHood70 ^talk 16:35, 6 May 2011 (UTC)

There are lots of references to both "immune thrombocytopenic purpura" and "idiopathic thrombocytopenic purpura" and the terms are used basically interchangeably. UpToDate, a fantastic resource geared towards healthcare professionals with several articles written about ITP by hematologists, refers to the disease as "immune (idiopathic) thrombocytopenic purpura". Since the disease is caused by IgG autoantibodies, it is an "immune" disease, even though the underlying reason why these autoantibodies are produced is unknown (idiopathic). "immune" is probably a more descriptive term at this point, and treatments are immunosuppresants. Wawot1 (talk) 15:23, 7 May 2011 (UTC)

In that case, we can probably put it back to "immune", but we should cite something (UpToDate?) that indicates that that's the case. – RobinHood70 ^talk 20:29, 7 May 2011 (UTC)

I'm just a WikiGnome here and have no medical knowledge of the condition whatsoever, so I lack any experience to say that either makes more sense in the context of the article.

In that respect, I do have an "advantage." I have had chronic refractory ITP for some four years and having undergone a lot of clinical evaluation, as well as having been subjected to just about every on- and off-label treatment that exists (presently on romiplostim). Twice I have come perilously close to fatality due to sub-2000 counts. Needless to say, I have done a lot of research on ITP. I have discussed my situation in great detail with my hematologist and his associates, have attended several medical school lectures on the topic (one taught by my hematologist, who is an assistant professor of medicine at a well-known university), and have read numerous papers on the malady, spending hours pouring through medical texts learning terminology and all that stuff. All that activity doesn't make me a doctor, let alone an expert, but has given me a lot of insight into this strange thing my hematologist and I are fighting.

Just about every medical professional with whom I have had contact uses "idiopathic thrombocytopenic purpura" to describe the condition. I'm sure the term is mostly used because it is tradtional—it's been in use for nearly 100 years. Interestingly enough, none of these people call it a "disease." It's always a "condition."

Since the disease is caused by IgG autoantibodies, it is an "immune" disease, even though the underlying reason why these autoantibodies are produced is unknown (idiopathic).

Not quite the case. It is thought that IgG activity may be responsible for platelet destruction. There is little scientific consensus to support the notion that all ITP cases are being triggered by IgG activity.

I wasn't as precise as I should have been; I agree that not ALL cases of ITP are caused by IgG activity, but, to quote a 2010 review article by Cuker from the journal Hematology, (http://asheducationbook.hematologylibrary.org/cgi/content/full/2010/1/377), "Platelet life span is reduced as a consequence of antibody-mediated clearance by tissue macrophages in essentially all patients." Most frequently, IgG antibodies are to blame. Wawot1 (talk) 23:27, 15 May 2011 (UTC)

"immune" is probably a more descriptive term at this point, and treatments are immunosuppresants.

Also not entirely true. While the immune pathogenesis is ultimately demonstrated in many patients and early treatment is usually via immunosuppressants (e.g., prednisone, rituximab, etc.), immunosuppression is not a viable long-term treatment due to the cummulative (and sometimes fatal) side-effects of the pharmaceuticals involved, as well as the obvious problem of increased susceptibility to infection. The most recent treatments, romiplostim and eltrombopag, do not target the immune system at all.

Again, I should have been more precise. First line treatments are immunosuppressants and they are effective for many patients. You write that immunosuppressants predispose patients to infection; that's true, but that has nothing to do with the underlying etiology of the problem. You're right that thrombopoetin receptor antagonists (TRAs) such as romipolostim and eltrombopag do not suppress the immune system, but, according to the Cuker review "TRAs appear capable of overriding antibody-mediated platelet clearance in most patients." In other words, TRAs work in spite of antibody-mediated platelet destruction; the fact that they do work for some patients does NOT mean that these patients do not have antibody-mediated platelet destruction. Wawot1 (talk) 23:27, 15 May 2011 (UTC)

My opinion is that RobinHood's reverts were correct. "Idiopathic thrombocytopenic purpura" is not only the "traditional" name given to this problem, it does accurately describe the condition. Despite recent progress in treating ITP, the root cause is still elusive, a situation which the word "idiopathic" precisely describes. Ongoing research may eventually provide an answer but for now, it's mostly much educated conjecture.

This whole discussion is an argument about semantics, but I do think that in many (if not most) patients an immune process can be demonstrated. In this sense it is an immune thrombocytopenia - the underlying reason WHY this immune process is directed against self is often idiopathic, however. The Cuker review designates cases of ITP (which he calls IMMUNE thrombocytopenia, by the way) in which there is an identifiable cause as "secondary ITP" and cases that have no identifiable cause as "primary ITP". Wawot1 (talk) 23:27, 15 May 2011 (UTC)

I believe we should leave the intro section as it is now worded. That section also mentions the other terms in (more-or-less) historical order of use (Werlhof's disease excepted).

Incidentally, in my case the immune diagnosis was made early on but subsequently was proved to be only partially correct, It appears at this point in time, autoimmune activity is minimal, as I do not respond to immunosuppressants anymore. This situation, of course, presents me with a bit of a problem, in that traditional rescue therapy is not particularly effective.

Bigdumbdinosaur (talk) 06:29, 15 May 2011 (UTC)

The most up to date name for the disorder is 'Immune Thrombocytopenia'. The 'purpura' part has been dropped and by definition, if the aetiology is not immune related then it isn't ITP, although the exact immune process cannot yet be demonstrated in all cases. No drug works for everyone and many work less and less effectively in a patient each time it's used. Take rituximab for example which this article says is effective, it is actually only effective in about 40% of patients. 87.194.81.2 (talk) 23:22, 26 May 2011 (UTC)

The most up to date name for the disorder is 'Immune Thrombocytopenia'. The 'purpura' part has been dropped and by definition, if the aetiology is not immune related then it isn't ITP, although the exact immune process cannot yet be demonstrated in all cases.

Can you cite a reputable source to support such a sweeping statement? Or is this just another one of your opinions formed from selective reading at http://www.itpsupport.org.uk/ or the PDSA site?

Take rituximab for example which this article says is effective, it is actually only effective in about 40% of patients.

Here's a copy of the article subsection that mentions rituximab:

The off-label use of rituximab, a chimeric monoclonal antibody against the B cell surface antigen CD20, has been shown in preliminary studies to be an effective alternative to splenectomy in some patients (emphasis added). However, many patients experience significant side-effects, there is a small risk of fatality due to progressive multifocal leukoencephalopathy caused by a reactivated JC virus, and randomized controlled trials have yet to be conducted.

Exactly where does the above statement say "...is effective..." without qualification? You seem to have a problem with selective reading. Note the additional information about side-effects and lack of controlled studies. Also, exactly where did you get your 40 percent number? I'll bet I've read ten times as much medical literature about ITP as you have, and I can't recall anything quoting a percentage figure for successful treatment with rituximab.

I believe you are trying to push your point of view into this article, which is exactly contrary to Wikipedia policy. An encyclopedia is a compilation of facts, not uneducated opinions You should spend a little less time asserting "facts" that you can't support. Also, may I suggest you get a username and password instead of hiding behind an IP address?

Bigdumbdinosaur (talk) 04:57, 31 May 2011 (UTC)

Fatigue

It is not true that tiredness and fatigue is not a common symptom of ITP. Patients have known this for a long time and now the doctors are catching up. See the slides of a talk given at the recent ITP Convention. http://www.itpsupport.org.uk/conventionppt/showjulianewton2011.htm

As a general point, it is unfortunate that this Wiki likes to follow rather than to lead. So instead of immediately updating the information as new studies come out and new things are known about ITP, you wait until it's old news. Such a shame. 87.194.81.2 (talk) 23:09, 26 May 2011 (UTC)

It's an inherent problem of being an encyclopaedia...the entire purpose of the wiki is to follow and not to lead. Articles such as this are governed by guidelines such as MEDRS. It does create a bit of a disconnect when there's breaking information or when patient views and experiences are at odds with those of the establishment, but in some ways, it's understandable—like a news agency or any printed encyclopaedia, Wikipedia is here to report, not to advocate, and thus it generally has to follow the views of the medical establishment, though there can certainly be additional information outlining controversies and the like. – RobinHood70 ^talk 00:39, 27 May 2011 (UTC)

I don't agree. The purpose of an online encyclopaedia is to be up to date. That's the whole benefit of being online and not in paper format. 87.194.81.2 (talk) 09:54, 27 May 2011 (UTC)

That's the benefit compared to print, yes, but it still has to be up to date with information that, for the most part, can be found in reliable medical journals and similar high-quality sources. There are times that works to patients' detriment (believe me, I know...albeit not from ITP), but as is commonly said here, Wikipedia is about fact, not truth. Or to put it another way, it's not about what you know, it's about what you can prove. That's what the Wikipedia community has decided as a whole.

If you want to add information to the article that says something about fatigue in ITP, try searching through pubmed.com for a review that talks about how it's now been found to be a common complaint among ITP patients, or anything along those lines. As I'm sure you can understand, we need more than just your word for it. :) – RobinHood70 ^talk 10:20, 27 May 2011 (UTC)

Okay, the 76.* IP has added patient literature as a reference from a relevant website. Since other reliable sources clearly state that fatigue is not associated with the disease, I've tried to balance the paragraph and present all sides. I know we're supposed to avoid phrases like "recent research", but I wasn't sure what else to do there given that it's both recent and primary, but also refutes the contention that fatigue isn't associated with the condition (which is acceptable as I understand MEDREV). If there are any concerns with the edit, please feel free to alter it accordingly and comment here if it's anything substantive, just to avoid any kind of edit warring. – RobinHood70 ^talk 02:30, 28 May 2011 (UTC)

———

It is not true that tiredness and fatigue is not a common symptom of ITP. Patients have known this for a long time and now the doctors are catching up. See the slides of a talk given at the recent ITP Convention. http://www.itpsupport.org.uk/conventionppt/showjulianewton2011.htm

Okay, Mr. 87.194.81.2, since you want to debate the fine points of encyclopedic information, let's debate. I'll address Julia Newton's presentation, which screams for contradiction, later on. Right now, I'll point out that statements such as "Patients have known this for a long time and now the doctors are catching up." are opinion. Just how do you know that "Patients have known this for a long time..."? Did you personally interview all of them? Can you point to an impartial source of information that can support such an assertion? Are you a medical professional who routinely screens ITP patients and asks about fatigue? Do you have ITP and thus know first hand what it is like?

You seem to have formed your opinions from unscientifically supported information gleaned from, among other places, the Platelet Disorder Support Association (PDSA) website. I do not consider PDSA to be a neutral source on ITP. While much of what they publish has previously been documented by the medical community in many other places, some of what they present as "fact" is not, or is distortion of fact. This is an organization with a slanted point of view whose membership seems to largely be women with some degree of hypochondria. By way of example, here is an except of "facts" from their "Coping with ITP" on-line pamphlet:

Q In addition to a low platelet count, I’m often tired. Is fatigue a normal part of the disease? Will anything improve this?

A Fatigue is a common experience for people with ITP. It may be caused by the disease or it could be a response to your medications or other treatments. Some patients report that changing to a healthy diet (especially adding dark, leafy greens) increases their energy level and reduces fatigue. Be sure to get adequate rest but be careful with using “sleep aids” because of possible side effects. Include as many activities in your life as you can that feed your soul and make you happy. Try to avoid draining, exhausting situations that will only sap your energy. Get plenty of exercise (check with your doctor for types of exercise appropriate for you). Breathe clean air and drink pure water.

Note the wording "common experience" and "may be caused by." That's not the same as a clinically-observed condition in which scientific methods and consensus establish a causal relationship between ITP and fatigue. The only part they got right was the ..."response to medications..." comment.

Comments such as "Try to avoid draining, exhausting situations..." and "Breathe clean air and drink pure water." in the context of ITP are absurd. "Draining, exhausting situations" are bound to get anyone tired, no matter how healthy. Exhortations to breath clean air and drink pure water are downright silly (no one would intentionally do otherwise), and may lead the naive to believe that foul air and brackish water cause ITP.

Also note some of the following wording:

Some patients report that changing to a healthy diet (especially adding dark, leafy greens) increases their energy level and reduces fatigue.

"Some patients report?" Sounds real scientific, eh? I'm an ITP patient and if I report that eating ice cream twice per day reduces fatigue, does that make it fact? Could it be these chronically tired women are simply suffering from a junk food diet, inadequate exercise and/or chronic weight issues having no relationship to ITP?

Incidentally, PDSA is the same "factual source" that has posted information to the effect that herbs and Chinese medicine can "cure" ITP—patently false. They are so "factual," in fact, I can't seem to find anyone with a medical degree and a specialty in hematology who considers them to be any kind of authority on ITP. Adding insult to injury, their pamphlet is out-of-date, to wit:

Q What are the main treatments available for ITP? What are the goals of treatment?

A The main treatments for ITP are medications (drugs), or splenectomy. The main drug treatments include corticosteroids (ex., prednisone), intravenous gamma globulin (IVIg), and anti-Rho(D) immune globulin (ex., WinRho SDF). Some additional drugs used to treat ITP may include azathioprine (Imuran), cyclophosphamide (Cytoxan), cyclosporine (Sandimmune), danazol (Danocrine), mycophenolate mofetil (ex. Cellcept), rituximab (ex., Rituxan), and vinca alkaloids (Vincristine). In some cases, surgery to remove the spleen (splenectomy) is recommended...

I find it odd that no mention is made of eltrombopag and romiplostim, both of which have been available since the latter part of 2008 and are the most promising drugs developed to date. Consider the paradox, Mr. 87.194.81.2. You expect Wikipedia to be instantly updated as soon as someone publishes something the deem to be fact, yet you didn't seem to notice that PDSA's pamphlet is, by definition, nearly three years out of date.

More PDSA bias in their pamphlet:

Q How can I find out about the latest developments in ITP treatment?

A Join the Platelet Disorder Support Association at pdsa.org

Right! Don't consult with an authority on the topic. Join our association and subscribe to our political points of view, as well as learn how to get rid of your ITP using totally non-scientific methods—which, by the way, could be dangerous in and of themselves. Also, please send us money so we can continue to publish our political message.

Getting back to the fatigue matter, medical authorities such as NIH, Mayo Clinic and my own hematologist, who is assistant professor of clinical medicine at a major university in the midwestern USA, as well as an author of several scientific papers on ITP, all state that ITP in itself does not cause fatigue, which is in sharp disagreement with what has been published by PDSA.ORG. Indeed, there is no clinical basis for such fatigue symptoms, as there is no known relationship between one's platelet count and one's general energy and alertness level. This isn't a case of "...doctors [not] catching up." This is the scientific method at work. Science is about careful and deliberate study and observation, not subscribing to crackpot theories.

It may well be that ITP patients are subject to secondary medical conditions that bring about fatigue—anemia is a possibility that has been cited. More likely, treatment is behind fatigue complaints. One of the possible side-effects of romiplostim is fatigue, a byproduct of induced anemia in some patients. Ironically, this same drug is also noted for causing insomnia. I suspect that almost all ITP patient reports of fatigue are the side-effects of the therapy(s) being administered to treat ITP. Also possible are psychological factors, such as anxiety or depression—what I refer to as the "Why me?" syndrome often exhibited by patients when saddled with a chronic condition.

...See the slides of a talk given at the recent ITP Convention. http://www.itpsupport.org.uk/conventionppt/showjulianewton2011.htm

This is a UK-based group with a non-neutral point of view, one that is constantly soliciting money, and one that is also dominated by women, as is the case with PDSA (not surprisingly, the talk was given by a woman). Again, while they do present information that is already widely known and accepted as fact, they deviate from fact in an apparent support of some sort of political agenda.

Let's start with the second slide of Professor Newton's presentation. In it, she states that bleeding is the only recognized symptom (emphasis added), which is precisely what every medical professional with the weight of authority in ITP says. Other aspects of her study are questionable:

• The low population sampled, 654 total individuals. An estimated 60,000 adult ITP patients exist in the USA alone, and 3000-4000 are said to exist within the UK, the latter number probably low due to various problems with the UK's socialized healthcare system. What puzzles me is why such a tiny sample was taken from Oklahoma in the USA instead of from more populous states where more ITP patients would be available for screening. I suspect some statistical engineering was involved.
  • Careful there....Dr James N. George is a giant in hematology and platelet disorders (in fact, was invited to write an editorial in the New England Journal of Medicine in the same issue that the Romiplostim study was published - see http://www.nejm.org/doi/full/10.1056/NEJMe1009141) who happens to live and practice at the University of Oklahoma. The slideshow thanks Dr George - I suspect that he submitted data for the slide presentation.Wawot1 (talk) 02:18, 31 May 2011 (UTC)
    • I'm well aware of Dr. George's credentials and accomplishments, and didn't say anything that was critical of his work—I'm not sure why you brought it up. I'm suspicious of Julia Newton's statistical methods in using such a small sample of the USA ITP population. It may well be that she approached Dr. George for information because he is so well known and respected in the field. It would be interesting to know why Professor Newton apparently approached no one else in the USA for data. My point stands: the respondent population was too low and was too biased to the female side. It's almost like a rigged election. Bigdumbdinosaur (talk) 04:33, 31 May 2011 (UTC)
• No controlling group, that is, no group whose only complaint was fatigue. The lack of a controlling group means it's likely that most of the respondents are chronic complainers, and that they are tired and have ITP is a coincidence.
• Overwhelming female responding group (73 percent) all out of proportion to ITP gender ratios. Women are far more likely to express frequent fatigue complaints regardless of medical condition. I'm willing to bet that if I surveyed 477 women and asked about frequent fatigue, the majority would say they are constantly tired.
• 42 percent of the respondents had other medical conditions. Could it be that the other medical condition(s) have something to do with fatigue?
• No mention of general physical characteristics of surveyed ITP patients. Are these people obese? Are they sedentary? Do they work two jobs to support themselves and their families? Do they party all night and then get up to go to work? Do they smoke or do recreational drugs? Any or all of these could be factors that evidently were not considered.
• Attempt to relate somnolence to fatigue. The two are not necessarily related to each other. Although use of the Epworth Sleepiness Scale was cited in Ms. Newton's exposition (the Epworth scale is scientifically accepted), it's hardly proof that the respondent is in fact fatigued. One could be predisposed to somnolence but have lots of energy.
• Last but not least, nothing was mentioned about an empirical method to determine if a respondent was, in fact, fatigued. Just because someone says they are fatigued doesn't mean they are. Fatigue is as much a state of mind as it is a physical condition. A marathon runner will definitely be fatigued at the end but very much up because he ran his best-ever race.

It appears, based on what I've gleaned from Ms. Newton's presentation, that the study's conclusions are largely based upon the subjective statements of a small population of mostly women. Show me where the medical community at large has accepted her study as fact and I'll change my opinion.

As a general point, it is unfortunate that this Wiki likes to follow rather than to lead. So instead of immediately updating the information as new studies come out and new things are known about ITP, you wait until it's old news. Such a shame. 87.194.81.2 (talk) 23:09, 26 May 2011 (UTC)

Not all "new studies" are scientifically vetted, although they may be published. Such publication is usually with a goal of peer review and acceptance or rejection of the studies' findings. Knee-jerk reactions based upon one small study that has not been widely adopted by the scientific community are not part of good encyclopedic procedure.

I don't agree. The purpose of an online encyclopaedia is to be up to date. That's the whole benefit of being online and not in paper format. 87.194.81.2 (talk) 09:54, 27 May 2011 (UTC)'

Your disagreement with RobinHood70 doesn't mean your opinion is correct. You're confusing the medium with the message. Wikipedia is an encyclopedia, not a weekly entertainment rag. The fact that your are reading this on a computer screen rather than in a book doesn't change the definition of an encyclopedia. As RobinHood70 indicated, an encyclopedia is supposed to present facts, not conjecture. The sources that have been cited as "proof" that ITP causes fatigue are suspect.

If you want to add information to the article that says something about fatigue in ITP, try searching through pubmed.com for a review that talks about how it's now been found to be a common complaint among ITP patients, or anything along those lines.

The only reference I was able to find on PUBMED.COM pointed back to Julia Newton's small-scale study. One should not read too much into the study's presence on PUBMED.COM. PUBMED.COM does not take an official position on the validity of any conclusions reached in a study.

I'm going to give this some additional thought before editing Mr. 87.194.81.2's material. I'd rather we err on the side of scientific fact, not New-Age thinking that has not been fully vetted. Right now, telling people ITP makes them tired is tantamount to promulgating false information. There's not enough scientific research to support such a conclusion. If nothing else, pushing the fatigue angle may simply give the hypochondriacs something new about which to complain.

Bigdumbdinosaur (talk) 02:20, 30 May 2011 (UTC)

Google Scholar seems to show that it's been cited by one other study, which usually means it's not particularly notable, but there could be other reasons for that as well. I don't have access to the full text of the study, so I can't even tell what context they're citing it in.

In any event, I think I've done my bit, and I have enough debates with the Chronic Fatigue Syndrome cluster of articles that are far more relevant to me, so I'm going to back out of this one and let you guys hash it out. :) – RobinHood70 ^talk 03:02, 30 May 2011 (UTC)

As I said, there's simply not enough scientific data at this point to conclude that because some ITP patients complain of fatigue it's being caused by ITP. Using that logic, if people suffering from psoriasis also complain about constipation then psoriasis must trigger bowel stoppages and therefore patients should be administered a laxative as part of the overall therapy.

Bigdumbdinosaur (talk) 04:33, 31 May 2011 (UTC)

Just a few points to correct. I'm not American and didn't get my information from the PDSA leaflet. I have never seen the leaflet and wouldn't put much credence on patients' leaflets anyway as they are always dumbed down. The study by Julia Newton wwas commissioned by the UK ITP Support Association who funds a lot of research. It was a proper scientific study complete with controls. I do have a copy of the full study but am not at liberty to share it which is a bit frustrating. For the record and as you ask, I do have ITP and my doctors are experts in the field and have written many papers and are at the forefront of research. Sorry I signed up with a nym.. I am the previous 87.194.81.2. London49 (talk) 10:25, 1 June 2011 (UTC)

Consensus guideline

In 2010 the following international consensus guideline appeared: doi:10.1182/blood-2009-06-225565. We should regard this as the standard of care. JFW | T@lk 13:57, 9 October 2011 (UTC)

Reverting

Bigdumbdinosaur (talk · contribs) didn't like the recent changes, and reverted to a remote version (unclear which one) with the edit summary "reverted to original structure -- recent editing has diminished the readability of this article."

We can argue about readability, but the structure of the article is not really negotiable. When restructuring it, I followed WP:MEDMOS. I have therefore changed it back, pending discussion. JFW | T@lk 20:12, 7 November 2011 (UTC)

Hobit (talk · contribs) asked me to clarify whether I had intentionally removed this edit by Yurk (talk · contribs) (diff). This edit stated that caution should be applied in the elderly, who may suffer thrombotic complications from IVIG. The source did not meet WP:MEDRS, and I am worried this made the article sound a bit like WP:HOWTO. If this caution is discussed in MEDRS-compatible sources, I am very happy to reconsider a rephrased form. JFW | T@lk 08:45, 8 November 2011 (UTC)

I think you have a mishmash of improvements and problems introduced. First, the caption you added on the figure would seem to be wrong. That's not large bruising, at least not in the common use of the word "bruise". Also the removal of International consensus report on the investigation and management of primary immune thrombocytopenia reference seems very troubling. Why would we remove the largest study on the issue? It would seem to be the current best. I don't mind adding others, but I don't see why this would be removed. Hobit (talk) 00:35, 9 November 2011 (UTC)

• I'll also prefer to see Yurk's edit's restored. I don't see how that's a "how to". Dosages and stuff, sure. But his stuff seems reasonable and useful. Hobit (talk) 00:36, 9 November 2011 (UTC)

I will revise the use of the term "large bruise".

Where did I remove the international consensus report on the investigation and management of primary immune thrombocytopenia? I believe this was a reference that I identified and added to the article!

Finally, I have explained that Yurk's edit was not based on WP:MEDRS-compatible sources. If an appropriate secondary source states exactly that (i.e. that IVIG should be used with caution in elderly people, in whom it might cause complications) I will happily reintroduce the claims. There is, however, a risk of WP:HOWTO - IVIG is already used with caution because of the risk of side-effects and the cost (it is a human blood product). JFW | T@lk 13:19, 9 November 2011 (UTC)

Sorry, I just noticed your response. I'll look at it again in the next day or two. Thanks for making the change to the caption. Hobit (talk) 19:36, 14 November 2011 (UTC)

Fatigue

The following was added:

“ Patients with primary immune thrombocytopenia (ITP) commonly describe symptoms of fatigue. The prevalence of fatigue among both UK (39%) and US (22%) patients was significantly greater than expected compared with normal subjects (P<0.0001 and P<0.0001 respectively). In univariate analysis of the combined cohorts, fatigue was associated with a platelet count <100000/μL, treatment with steroids, bleeding symptoms, presence of other medical conditions, daytime sleepiness, and orthostatic symptoms. Fatigue was not associated with age, gender, duration of ITP, or splenectomy status. Multivariate analysis of the combined cohorts was stratified for the presence or absence of bleeding symptoms. Among 107 patients with bleeding symptoms, fatigue was independently associated with a platelet count <100000/μL and female gender. Among 491 patients without bleeding symptoms, fatigue was independently associated with a platelet count <30000/μL, presence of other medical conditions, daytime sleepiness, and orthostatic symptoms. ”

This is a summary of doi:10.1111/j.1600-0609.2011.01587.x, which is a primary research study. Newton's group is known for its fatigue-related research, but we cannot base content on primary studies and at any rate this discussion is rather too detailed for a general purpose article that might be read not just by patients but also by people just wanting a general overview. I would not be surprised if this study would eventually be covered in secondary sources (e.g. reviews). See WP:MEDRS. JFW | T@lk 23:31, 29 December 2012 (UTC)

A review due to be published in BJH pulls together recent reseach on the subject. doi:10.1111/bjh.13385 JFW | T@lk 11:19, 31 March 2015 (UTC)

References

MMR

This was added:

“ The MMR vaccine has been associated with an estimated six-fold increase in the incidence of ITP among children aged 13-24 months old during the 6 weeks following vaccination. While there is a significantly increased risk of developing ITP within the 6 weeks following the MMR vaccine, the attributable risk is low (1 in 25,000) and ITP below the age of 6 years old is generally a mild disease, rarely having long-term consequences. There is ongoing research which seeks to identify genetic differences underlying the susceptibility to ITP following MMR or MMR and varicella (MMRV) vaccination. ”

These are two primary sources. VIral infections (which is what live virus immunisation is, of course) is often linked with thrombocytopenia. I think we should only include this if a solid secondary source can be presented. JFW | T@lk 22:38, 22 June 2013 (UTC)

There are countless sources that state the exact same thing. It is the MMR vaccine specifically that causes ITP, not other viral infections.

“ CONCLUSIONS:ITP is unlikely after early childhood vaccines other than MMR. Because of the small number of exposed cases and potential confounding, the possible association of ITP with hepatitis A, varicella, and tetanus-diphtheria-acellular pertussis vaccines in older children requires further investigation. ”

http://pediatrics.aappublications.org/content/early/2012/01/04/peds.2011-1111.full.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884189/

http://adc.bmj.com/content/84/3/227.full

http://www.itpsupport.org.uk/mmrupdate.htm

http://www.healio.com/pediatrics/vaccine-preventable-diseases/news/online/%7B34e8fbf8-da96-4889-af3e-2f28cdce0fc0%7D/mmr-vaccine-associated-with-heightened-risk-for-itp — Preceding unsigned comment added by 24.4.232.243 (talk • contribs)

Please follow my advice and supply a secondary source (e.g. review article, textbook chapter) that will make your edit stick. I don't dispute the facts, but we cannot build an encyclopedia on primary studies. JFW | T@lk 07:29, 8 July 2013 (UTC)

Could I recommend PMC 2661332 JFW | T@lk 07:32, 8 July 2013 (UTC)

Secondary source: Vaccines for measles, mumps and rubella in children http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD004407.pub3/full#CD004407-bbs2-0041 Review article finding methodology of original article acceptable, whilst many articles were rejected: Risk of immune thrombocytopenic purpura after measles-mumps-rubella immunization in children. https://www.ncbi.nlm.nih.gov/pubmed/18310189 — Preceding unsigned comment added by 2A02:C7F:8A4D:7500:10B0:65A1:2AD2:C2D9 (talk) 11:06, 14 May 2018 (UTC) "This vaccine causes 1 case of immune thrombocytopenia purpura per every 40,000 doses. CONCLUSION:Measles-mumps-rubella vaccine that is given in the second year of life is associated with an increased risk of immune thrombocytopenia purpura."2A02:C7F:8A4D:7500:10B0:65A1:2AD2:C2D9 (talk) 11:08, 14 May 2018 (UTC)

References

Review

doi:10.1111/j.1538-7836.2012.04876.x is a review in JTH that I missed. JFW | T@lk 21:49, 21 January 2014 (UTC)

Name

71.190.186.99 (talk · contribs) added that ITP is now called "primary immune thrombocytopenia", but didn't back this up with a reference. Almost every publication I have seen in recent time uses the current terminology, so I remain to be convinced. JFW | T@lk 21:49, 21 January 2014 (UTC)

Requested move 31 December 2015

The following is a closed discussion of a requested move. Please do not modify it. Subsequent comments should be made in a new section on the talk page. Editors desiring to contest the closing decision should consider a move review. No further edits should be made to this section.

The result of the move request was: moved. Unopposed for over a week. Jenks24 (talk) 04:44, 10 January 2016 (UTC)

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Idiopathic thrombocytopenic purpura → Immune thrombocytopenic purpura – Over time the name has been slowly changing. At the moment reliable sources are split (for example Mayo clinic uses Idiopathic [2], NIH uses Immune [3]). A web search seems split. However the journal Blood (journal) has moved to Immune [4], which I find convincing as I believe it's the most relevant research journal. Obviously this move is going to involve a fair bit of editing as we change the primary name. Hobit (talk) 16:17, 31 December 2015 (UTC)

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The above discussion is preserved as an archive of a requested move. Please do not modify it. Subsequent comments should be made in a new section on this talk page or in a move review. No further edits should be made to this section.

• The handful of changes needed were made to deal with the move. I easily could have missed something, so please take a look. Thanks, Hobit (talk) 18:45, 13 January 2016 (UTC)

State of the art

doi:10.1111/bjh.14515 JFW | T@lk 13:13, 14 March 2017 (UTC)

NEJM today: doi:10.1056/NEJMcp1810479 JFW | T@lk 22:51, 4 September 2019 (UTC)

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