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Immune thrombocytopenic purpura

immune thrombocytopenic purpura, immune thrombocytopenic purpura treatment
Immune thrombocytopenia1 ITP is a type of thrombocytopenic purpura defined as isolated low platelet count thrombocytopenia with normal bone marrow and the absence of other causes of thrombocytopenia It causes a characteristic purpuric rash and an increased tendency to bleed Two distinct clinical syndromes manifest as an acute condition in children and a chronic condition in adults The acute form often follows an infection and has a spontaneous resolution within two months Chronic immune thrombocytopenia persists longer than six months with a specific cause being unknown

ITP is an autoimmune disease with antibodies detectable against several platelet surface antigens

ITP is diagnosed by a low platelet count in a complete blood count a common blood test However, since the diagnosis depends on the exclusion of other causes of a low platelet count, additional investigations such as a bone marrow biopsy may be necessary in some cases

In mild cases, only careful observation may be required but very low counts or significant bleeding may prompt treatment with corticosteroids, intravenous immunoglobulin, anti-D immunoglobulin, or immunosuppressive drugs Refractory ITP not responsive to conventional treatment may require splenectomy, the surgical removal of the spleen Platelet transfusions may be used in severe bleeding together with a very low count Sometimes the body may compensate by making abnormally large platelets

Contents

  • 1 Signs and symptoms
  • 2 Pathogenesis
  • 3 Diagnosis
  • 4 Treatment
    • 41 Steroids
    • 42 Anti-D
    • 43 Steroid-sparing agents
    • 44 Intravenous immunoglobulin
    • 45 Thrombopoietin receptor agonists
    • 46 Surgery
    • 47 Platelet transfusion
    • 48 H pylori eradication
    • 49 Other agents
  • 5 Epidemiology
  • 6 Pregnancy
  • 7 History
  • 8 References
  • 9 External links

Signs and symptomsedit

Signs include the spontaneous formation of bruises purpura and petechiae tiny bruises, especially on the extremities, bleeding from the nostrils and/or gums, and menorrhagia excessive menstrual bleeding, any of which may occur if the platelet count is below 20,000 per μl2 A very low count <10,000 per μl may result in the spontaneous formation of hematomas blood masses in the mouth or on other mucous membranes Bleeding time from minor lacerations or abrasions is usually prolonged

Serious and possibly fatal complications due to extremely low counts <5,000 per μl include subarachnoid or intracerebral hemorrhage bleeding inside the skull or brain, lower gastrointestinal bleeding or other internal bleeding An ITP patient with an extremely low count is vulnerable to internal bleeding caused by blunt abdominal trauma, as might be experienced in a motor vehicle crash These complications are not likely when the platelet count is above 20,000 per μl

Pathogenesisedit

In approximately 60 percent of cases, antibodies against platelets can be detected3  Most often these antibodies are against platelet membrane glycoproteins IIb-IIIa or Ib-IX, and are of the immunoglobulin G IgG type The Harrington–Hollingsworth experiment, established the immune pathogenesis of ITP4

The coating of platelets with IgG renders them susceptible to opsonization and phagocytosis by splenic macrophages, as well by Kupffer cells in the liver  The IgG autoantibodies are also thought to damage megakaryocytes, the precursor cells to platelets, although this is believed to contribute only slightly to the decrease in platelet numbers  Recent research now indicates that impaired production of the glycoprotein hormone thrombopoietin, which is the stimulant for platelet production, may be a contributing factor to the reduction in circulating platelets  This observation has led to the development of a class of ITP-targeted drugs referred to as thrombopoietin receptor agonists

The stimulus for auto-antibody production in ITP is probably abnormal T cell activity567  Preliminary findings suggest that these T cells can be influenced by drugs that target B cells, such as rituximab8

Diagnosisedit

The diagnosis of ITP is a process of exclusion  First, it has to be determined that there are no blood abnormalities other than a low platelet count, and no physical signs other than bleeding  Then, secondary causes 5–10 percent of suspected ITP cases should be excluded  Such secondary causes include leukemia, medications eg, quinine, heparin, lupus erythematosus, cirrhosis, HIV, hepatitis C, congenital causes, antiphospholipid syndrome, von Willebrand factor deficiency, onyalai and others29  In approximately one percent of cases, autoimmune hemolytic anemia and ITP coexist, a condition referred to as Evans syndrome, a condition that points to CLL as a possible cause9

Despite the destruction of platelets by splenic macrophages, the spleen is normally not enlarged  In fact, an enlarged spleen should lead to a search for other possible causes for the thrombocytopenia  Bleeding time is usually prolonged in ITP patients  However, the use of bleeding time in diagnosis is discouraged by the American Society of Hematology practice guidelines10 and a normal bleeding time does not exclude a platelet disorder11

Bone marrow examination may be performed on patients over the age of 60 and those who do not respond to treatment, or when the diagnosis is in doubt9  On examination of the marrow, an increase in the production of megakaryocytes may be observed and may help in establishing a diagnosis of ITP  An analysis for anti-platelet antibodies is a matter of clinician's preference, as there is disagreement on whether the 80 percent specificity of this test is sufficient to be clinically useful9

Treatmentedit

With rare exceptions, there is usually no need to treat based on platelet counts Many older recommendations suggested a certain platelet count threshold usually somewhere below 200/µl as an indication for hospitalization or treatment Current guidelines recommend treatment only in cases of significant bleeding Treatment recommendations sometimes differ for adult and pediatric ITP12

Steroidsedit

Initial treatment usually consists of the administration of corticosteroids, a group of medications that suppress the immune system The dose and mode of administration is determined by platelet count and whether there is active bleeding: in urgent situations, infusions of dexamethasone or methylprednisolone may be used, while oral prednisone or prednisolone may suffice in less severe cases Once the platelet count has improved, the dose of steroid is gradually reduced while the possibility of relapse is monitored 60–90 percent will experience a relapse during dose reduction or cessation913 Long-term steroids are avoided if possible because of potential side-effects that include osteoporosis, diabetes and cataracts14

Anti-Dedit

Another option, suitable for Rh-positive patients with functional spleens is intravenous administration of RhoD immune globulin Human; Anti-D The mechanism of action of anti-D is not fully understood However, following administration, anti-D-coated red blood cell complexes saturate Fcγ receptor sites on macrophages, resulting in preferential destruction of red blood cells RBCs, therefore sparing antibody-coated platelets There are two anti-D products indicated for use in patients with ITP: WinRho SDF and Rhophylac The most common adverse reactions are headache 15%, nausea/vomiting 12% chills <2% and fever 1%

Steroid-sparing agentsedit

There is increasing use of immunosuppressants such as mycophenolate mofetil and azathioprine because of their effectiveness In chronic refractory cases, where immune pathogenesis has been confirmed,15 the off-label use of the vinca alkaloid161718 and chemotherapy agent vincristine may be attempted1920 However, vincristine has significant side effects21 and its use in treating ITP must be approached with caution, especially in children

Intravenous immunoglobulinedit

Intravenous immunoglobulin IVIg may be infused in some cases in order to decrease the rate at which macrophages consume antibody-tagged platelets  However, while sometimes effective, it is costly and produces improvement that generally lasts less than a month  Nevertheless, in the case of an ITP patient already scheduled for surgery who has a dangerously low platelet count and has experienced a poor response to other treatments, IVIg can rapidly increase platelet counts, and can also help reduce the risk of major bleeding by transiently increasing platelet counts

Thrombopoietin receptor agonistsedit

Thrombopoietin receptor agonists are pharmaceutical agents that stimulate platelet production in the bone marrow In this, they differ from the previously discussed agents that act by attempting to curtail platelet destruction22 Two such products are currently available:

  • Romiplostim trade name Nplate is a thrombopoiesis stimulating Fc-peptide fusion protein peptibody that is administered by subcutaneous injection  Designated an orphan drug in 2003 under United States law, clinical trials demonstrated romiplostim to be effective in treating chronic ITP, especially in relapsed post-splenectomy patients2324 Romiplostim was approved by the United States Food and Drug Administration FDA for long-term treatment of adult chronic ITP on August 22, 200825
  • Eltrombopag trade name Promacta in the USA, Revolade in the EU is an orally-administered agent with an effect similar to that of romiplostim  It too has been demonstrated to increase platelet counts and decrease bleeding in a dose-dependent manner26  Developed by GlaxoSmithKline and also designated an orphan drug by the FDA, Promacta was approved by the FDA on November 20, 200827

Side effects of thrombopoietin receptor agonists include headache, joint or muscle pain, dizziness, nausea or vomiting, and an increased risk of blood clots22

Surgeryedit

Splenectomy removal of the spleen may be considered in patients who are either unresponsive to steroid treatment, have frequent relapses, or cannot be tapered off steroids after a few months Platelets which have been bound by antibodies are taken up by macrophages in the spleen which have Fc receptors, and so removal of the spleen reduces platelet destruction  The procedure is potentially risky in ITP cases due to the increased possibility of significant bleeding during surgery  Durable remission following splenectomy is achieved in 60 to 65 percent of ITP cases, less so in older subjects28  The use of splenectomy to treat ITP has diminished since the development of steroid therapy and other pharmaceutical remedies

Platelet transfusionedit

Platelet transfusion alone is normally not recommended except in an emergency, and is usually unsuccessful in producing a long-term platelet count increase  This is because the underlying autoimmune mechanism that is destroying the patient's platelets will also destroy donor platelets, and so platelet transfusions are not considered a long-term treatment option

H pylori eradicationedit

In adults, particularly those living in areas with a high prevalence of Helicobacter pylori which normally inhabits the stomach wall and has been associated with peptic ulcers, identification and treatment of this infection has been shown to improve platelet counts in a third of patients In a fifth, the platelet count normalized completely; this response rate is similar to that found in treatment with rituximab, which is more expensive and less safe29 In children, this approach is not supported by evidence, except in high prevalence areas Urea breath testing and stool antigen testing perform better than serology-based tests; moreover, serology may be false-positive after treatment with IVIG30

Other agentsedit

  • Dapsone also called diphenylsulfone, DDS, or avlosulfon is an anti-infective sulfone drug  Dapsone may also be helpful in treating lupus, rheumatoid arthritis, and as a second-line treatment for ITP The mechanism by which dapsone assists in ITP is unclear but an increased platelet count is seen in 40–60 percent of recipients3132
  • The off-label use of rituximab, a chimeric monoclonal antibody against the B cell surface antigen CD20, may sometimes be an effective alternative to splenectomy However, significant side-effects can occur, and randomized controlled trials are inconclusive33

Epidemiologyedit

A normal platelet count is considered to be in the range of 150,000–450,000 per microlitre μl of blood for most healthy individuals  Hence one may be considered thrombocytopenic below that range, although the threshold for a diagnosis of ITP is not tied to any specific number

The incidence of ITP is estimated at 50–100 new cases per million per year, with children accounting for half of that amount  At least 70 percent of childhood cases will end up in remission within six months, even without treatment343536  Moreover, a third of the remaining chronic cases will usually remit during follow-up observation, and another third will end up with only mild thrombocytopenia defined as a platelet count above 50,00034 A number of immune related genes and polymorphisms have been identified as influencing predisposition to ITP, with FCGR3a-V158 allele and KIRDS2/DL2 increasing susceptibility and KIR2DS5 shown to be protective3738

ITP is usually chronic in adults39 and the probability of durable remission is 20–40 percent13  The male to female ratio in the adult group varies from 1:12 to 17 in most age ranges childhood cases are roughly equal for both genders and the median age of adults at the diagnosis is 56–609  The ratio between male and female adult cases tends to widen with age  In the United States, the adult chronic population is thought to be approximately 60,000—with women outnumbering men approximately 2 to 1, which has resulted in ITP being designated an orphan disease40

The mortality rate due to chronic ITP varies but tends to be higher relative to the general population for any age range  In a study conducted in Great Britain, it was noted that ITP causes an approximately 60 percent higher rate of mortality compared to gender- and age-matched subjects without ITP  This increased risk of death with ITP is largely concentrated in the middle-aged and elderly  Ninety-six percent of reported ITP-related deaths were individuals 45 years or older  No significant difference was noted in the rate of survival between males and females41

Pregnancyedit

Anti-platelet autoantibodies in a pregnant woman with ITP will attack the patient's own platelets and will also cross the placenta and react against fetal platelets Therefore, ITP is a significant cause of fetal and neonatal immune thrombocytopenia Approximately 10% of newborns affected by ITP will have platelet counts <50,000/uL and 1% to 2% will have a risk of intracerebral hemorrhage comparable to infants with neonatal alloimmune thrombocytopenia NAIT4243

No lab test can reliably predict if neonatal thrombocytopenia will occur The risk of neonatal thrombocytopenia is increased with:44

  • Mothers with a history of splenectomy for ITP
  • Mothers who had a previous infant affected with ITP
  • Gestational maternal platelet count less than 100,000/uL

It is recommended that pregnant women with thrombocytopenia or a previous diagnosis of ITP should be tested for serum antiplatelet antibodies A woman with symptomatic thrombocytopenia and an identifiable antiplatelet antibody should be started on therapy for their ITP which may include steroids or IVIG Fetal blood analysis to determine the platelet count is not generally performed as ITP-induced thrombocytopenia in the fetus is generally less severe than NAIT Platelet transfusions may be performed in newborns, depending on the degree of thrombocytopenia It is recommended that neonates be followed with serial platelet counts for the first few days after birth,4244

Historyedit

After initial reports by the Portuguese physician Amato Lusitano in 1556 and Lazarus de la Rivière physician to the King of France in 1658, it was the German physician and poet Paul Gottlieb Werlhof who in 1735 wrote the most complete initial report of the purpura of ITP Platelets were unknown at the time45 The name "Werlhof's disease" was used more widely before the current descriptive name became more popular4546 Platelets were described in the early 19th century, and in the 1880s several investigators linked the purpura with abnormalities in the platelet count4547 The first report of a successful therapy for ITP was in 1916, when a young Polish medical student, Paul Kaznelson, described a female patient's response to a splenectomy45 Splenectomy remained a first-line remedy until the introduction of steroid therapy in the 1950s45

Referencesedit

  1. ^ Rodeghiero, F; Stasi, R; Gernsheimer, T; Michel, M; Provan, D; Arnold, DM; Bussel, JB; Cines, DB; Chong, BH; Cooper, N; Godeau, B; Lechner, K; Mazzucconi, MG; McMillan, R; Sanz, MA; Imbach, P; Blanchette, V; Kühne, T; Ruggeri, M; George, JN 12 March 2009 "Standardization of terminology, definitions and outcome criteria in immune thrombocytopenic purpura of adults and children: report from an international working group" Blood 113 11: 2386–93 PMID 19005182 doi:101182/blood-2008-07-162503 
  2. ^ a b Cines DB, McMillan R 2005 "Management of adult idiopathic thrombocytopenic purpura" Annu Rev Med 56: 425–42 PMID 15660520 doi:101146/annurevmed56082103104644 
  3. ^ Coopamah M, Garvey M, Freedman J, Semple J 2003 "Cellular immune mechanisms in autoimmune thrombocytopenic purpura: An update" Transfus Med Rev 17 1: 69–80 PMID 12522773 doi:101053/tmrv200350004 
  4. ^ Schwartz RS 2007 "Immune thrombocytopenic purpura—from agony to agonist" N Engl J Med 357 22: 2299–301 PMID 18046034 doi:101056/NEJMe0707126 
  5. ^ Semple JW, Freedman J 1991 "Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia" Blood 78 10: 2619–25 PMID 1840468 
  6. ^ Stasi R, Cooper N, Del Poeta G, et al August 2008 "Analysis of regulatory T-cell changes in patients with idiopathic thrombocytopenic purpura receiving B cell-depleting therapy with rituximab" Blood 112 4: 1147–50 PMID 18375792 doi:101182/blood-2007-12-129262 
  7. ^ Yu J, Heck S, Patel V, et al August 2008 "Defective circulating CD25 regulatory T cells in patients with chronic immune thrombocytopenic purpura" Blood 112 4: 1325–8 PMC 2515134  PMID 18420827 doi:101182/blood-2008-01-135335 
  8. ^ Godeau B, Porcher R, Fain O, et al August 2008 "Rituximab efficacy and safety in adult splenectomy candidates with chronic immune thrombocytopenic purpura: results of a prospective multicenter phase 2 study" Blood 112 4: 999–1004 PMID 18463354 doi:101182/blood-2008-01-131029 
  9. ^ a b c d e f Cines DB, Bussel JB 2005 "How I treat idiopathic thrombocytopenic purpura ITP" Blood 106 7: 2244–51 PMID 15941913 doi:101182/blood-2004-12-4598 
  10. ^ "Diagnosis and treatment of idiopathic thrombocytopenic purpura: recommendations of the American Society of Hematology The American Society of Hematology ITP Practice Guideline Panel" Ann Intern Med 126 4: 319–26 1997 PMID 9036806 doi:107326/0003-4819-126-4-199702150-00010 
  11. ^ Liesner RJ, Machin SJ 1997 "ABC of clinical haematology Platelet disorders" BMJ 314 7083: 809–12 PMC 2126215  PMID 9081003 doi:101136/bmj3147083809 
  12. ^ Neunert C, Lim W, Crowther M, Cohen A, Solberg L, Crowther MA April 2011 "The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia" PDF Blood 117 16: 4190–207 PMID 21325604 doi:101182/blood-2010-08-302984 
  13. ^ a b Stevens W, Koene H, Zwaginga JJ, Vreugdenhil G 2006 "Chronic idiopathic thrombocytopenic purpura: present strategy, guidelines and new insights" The Netherlands journal of medicine 64 10: 356–63 PMID 17122451 
  14. ^ Buchman, AL Oct 2001 "Side effects of corticosteroid therapy" J Clin Gastroenterol 33 4: 289–294 PMID 11588541 doi:101097/00004836-200110000-00006 
  15. ^ Psaila, Bethan; Bussel, James B 2008 "Refractory immune thrombocytopenic purpura: current strategies for investigation and management" British Journal of Haematology 143 1: 16–26 doi:101111/j1365-2141200807275x 
  16. ^ van der Heijden, Robert; Jacobs, Denise I;  Snoeijer, Wim;  Hallard, Didier;  Verpoorte, Robert 2004 "The Catharanthus alkaloids: Pharmacognosy and biotechnology" Current Medicinal Chemistry 11 5: 607–628 PMID 15032608 doi:102174/0929867043455846 
  17. ^ Raviña, Enrique 2011 "Vinca alkaloids" The evolution of drug discovery: From traditional medicines to modern drugs John Wiley & Sons pp 157–159 ISBN 9783527326693 
  18. ^ Cooper, Raymond; Deakin, Jeffrey John 2016 "Africa's gift to the world" Botanical Miracles: Chemistry of Plants That Changed the World CRC Press pp 46–51 ISBN 9781498704304 
  19. ^ Kuboyama, Takeshi; Yokoshima, Satoshi; Tokuyama, Hidetoshi; Fukuyama, Tohru 2004 "Stereocontrolled total synthesis of +-vincristine" Proceedings of the National Academy of Sciences of the United States of America 101 33: 11966–11970 doi:101073/pnas0401323101 
  20. ^ Keglevich, Péter; Hazai, Laszlo; Kalaus, György; Szántay, Csaba 2012 "Modifications on the basic skeletons of vinblastine and vincristine" Molecules 17: 5893–5914 PMID 22609781 doi:103390/molecules17055893 
  21. ^ Ishida, Yoji; Tomiyama, Yoshiaki, eds 2017 Autoimmune Thrombocytopenia Springer Nature ISBN 9789811041426 
  22. ^ a b "Idiopathic thrombocytopenic purpura: Treatments and Drugs" Mayo Clinic Retrieved October 16, 2012 
  23. ^ Bussel JB, Kuter DJ, George JN, et al 2006 "AMG 531, a thrombopoiesis-stimulating protein, for chronic ITP" N Engl J Med 355 16: 1672–81 PMID 17050891 doi:101056/NEJMoa054626 
  24. ^ Kuter, DJ; Rummel, M; Boccia, R; Macik, BG; Pabinger, I; Selleslag, D; Rodeghiero, F; Chong, BH; Wang, X; Berger, DP November 2010 "Romiplostim or standard of care in patients with immune thrombocytopenia" N Engl J Med 363 20: 1889–99 PMID 21067381 doi:101056/NEJMoa1002625 
  25. ^ http://wwwamgencom/media/prjspyear=2008
  26. ^ Bussel JB, Cheng G, Saleh MN, et al 2007 "Eltrombopag for the treatment of chronic idiopathic thrombocytopenic purpura" N Engl J Med Lp 357 22: 2237–2247 PMID 18046028 doi:101056/NEJMoa073275 
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  28. ^ See http://wwwitpsupportorguk/american/%205%20Splenectomy%20in%20ITPpdf, page 2
  29. ^ Stasi R, Sarpatwari A, Segal JB, Osborn J, Evangelista ML, Cooper N, Provan D, Newland A, Amadori S, Bussel JB 2009 "Effects of eradication of Helicobacter pylori infection in patients with immune thrombocytopenic purpura: a systematic review" Blood 113 6: 1231–40 PMID 18945961 doi:101182/blood-2008-07-167155 
  30. ^ Provan D, Stasi R, Newland AC, et al 2010 "International consensus report on the investigation and management of primary immune thrombocytopenia" Blood 115 2: 168–86 PMID 19846889 doi:101182/blood-2009-06-225565 
  31. ^ Godeau B, Durand JM, Roudot-Thoraval F, et al 1997 "Dapsone for chronic autoimmune thrombocytopenic purpura: a report of 66 cases" Br J Haematol 97 2: 336–9 PMID 9163598 doi:101046/j1365-21411997412687x 
  32. ^ Wozel G, Blasum C 2014 "Dapsone in dermatology and beyond" Arch Dermatol Res 306 2: 103–24 PMC 3927068  PMID 24310318 doi:101007/s00403-013-1409-7 CS1 maint: Uses authors parameter link
  33. ^ National Institute for Health and Care Excellence Immune idiopathic thrombocytopenic purpura: rituximab October 2014 1
  34. ^ a b Watts RG 2004 "Idiopathic thrombocytopenic purpura: a 10-year natural history study at the children's hospital of Alabama" Clinical pediatrics 43 8: 691–702 PMID 15494875 doi:101177/000992280404300802 
  35. ^ Treutiger I, Rajantie J, Zeller B, Henter JI, Elinder G, Rosthøj S 2007 "Does treatment of newly diagnosed idiopathic thrombocytopenic purpura reduce morbidity" Arch Dis Child 92 8: 704–7 PMC 2083887  PMID 17460024 doi:101136/adc2006098442 
  36. ^ Ou CY, Hsieh KS, Chiou YH, Chang YH, Ger LP 2006 "A comparative study of initial use of intravenous immunoglobulin and prednisolone treatments in childhood idiopathic thrombocytopenic purpur" Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi 47 5: 226–31 PMID 17352309 
  37. ^ Nourse, JP Jan 2012 "The KIR2DS2/DL2 genotype is associated with adult persistent/chronic and relapsed immune thrombocytopenia independently of FCGR3a-158 polymorphisms" Blood Coagul Fibrinolysis 23 1: 45–50 PMID 22024796 doi:101097/mbc0b013e32834d7ce3 
  38. ^ Seymour, LA Mar 2014 "The presence of KIR2DS5 confers protection against adult immune thrombocytopenia" Tissue Antigens 83 3: 154–60 PMID 24571473 doi:101111/tan12295 
  39. ^ Cines DB, Blanchette VS 2002 "Immune thrombocytopenic purpura" N Engl J Med 346 13: 995–1008 PMID 11919310 doi:101056/NEJMra010501 
  40. ^ "Amgen to Discuss Romiplostim BLA" drugscom March 12, 2008 Retrieved 2008-11-04 
  41. ^ Schoonen WM, Kucera G, Coalson J, et al April 2009 "Epidemiology of immune thrombocytopenic purpura in the General Practice Research Database" Br J Haematol 145 2: 235–44 PMID 19245432 doi:101111/j1365-2141200907615x 
  42. ^ a b Roback et al AABB Technical Manual, 16th Ed Bethesda, AABB Press, 2008
  43. ^ Webert KE, Mittal R, Sigouin C, Heddle NM, Kelton JG December 2003 "A retrospective 11-year analysis of obstetric patients with idiopathic thrombocytopenic purpura" Blood 102 13: 4306–11 PMID 12947011 doi:101182/blood-2002-10-3317 
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  45. ^ a b c d e Stasi R, Newland AC May 2011 "ITP: a historical perspective" Br J Haematol 153 4: 437–50 PMID 21466538 doi:101111/j1365-2141201008562x 
  46. ^ synd/3349 at Who Named It
  47. ^ Liebman HA 2008 "Immune thrombocytopenia ITP: an historical perspective" Hematology Am Soc Hematol Educ Program 2008 1: 205 PMID 19074083 doi:101182/asheducation-20081205 

External linksedit

  • The ITP Foundation - A nonprofit organization dedicated to helping children with Immune Thrombocytopenic Purpura
  • ITPeducationcom This educational curriculum is designed to provide evidence-based clinical information on the diagnosis and management of patients with ITP to hematologists, oncologists, and other health care professionals
  • Platelet Disorder Support Association A non-profit corporation to provide information, support, and encourage research about ITP and other platelet disorders
  • ITP Support Association A UK registered charity which aims to promote and improve the general welfare of patients, and the families of patients, with Immune Thrombocytopenic Purpura

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