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| {{Infobox_Disease |
| | __NOTOC__ |
| Name = {{PAGENAME}} |
| | '''For patient information click [[Idiopathic thrombocytopenic purpura (patient information)|here]]''' |
| Image = |
| | {{ITP}} |
| Caption = |
| | {{CMG}}; {{AE}} {{KS}} |
| DiseasesDB = 6673 |
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| ICD10 = {{ICD10|D|69|3|d|65}} |
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| ICD9 = {{ICD9|287.31}} |
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| ICDO = |
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| OMIM = 188030 |
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| MedlinePlus = |
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| eMedicineSubj = emerg |
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| eMedicineTopic = 282 |
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| MeshID = D016553 |
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| }} | |
| {{SI}} | |
| {{CMG}} | |
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| {{Editor Help}} | | {{SK}} ITP; Werlhof disease; essential thrombocytopenia; haemogenia; haemogenic syndrome; haemorrhagic purpura; morbus haemorrhagicus maculosus; morbus maculosis haemorrhagicus; morbus maculosus werlhofii; peliosis werlhofi; primary splenic thrombocytopenia; primary thrombocytopenia; primary thrombocytopenic purpura; purpura haemorrhagica; purpura thrombocytopenica; purpura werlhofii; splenic thrombocytopenic purpura; thrombocytolytic purpura |
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| ==Overview==
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| '''Idiopathic thrombocytopenic purpura''' (ITP) is the condition of having a low [[platelet]] count ([[thrombocytopenia]]) of no known cause ([[idiopathic]]). As most causes appear to be related to [[antibody|antibodies]] against platelets, it is also known as '''immune thrombocytopenic purpura'''. Although most cases are [[asymptomatic]], very low platelet counts can lead to a [[bleeding diathesis]] and [[purpura]].
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| ==Synonyms==
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| ITP knows many synonyms, but idiopathic or immunological thrombocytopenic purpura are the most common names. There's also an [[eponym]], [[Paul Gottlieb Werlhof|Werlhof]]'s disease,<ref>{{WhoNamedIt|synd|3349}}</ref> but this is used infrequently.
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| Other synonyms include: essential thrombocytopenia, haemogenia, haemogenic syndrome, haemorrhagic purpura, idiopathic thrombopenic purpura, morbus haemorrhagicus maculosus, morbus maculosis haemorrhagicus, morbus maculosus werlhofii, peliosis werlhofi, primary splenic thrombocytopenia, primary thrombocytopenia, primary thrombocytopenic purpura, purpura haemorrhagica, purpura thrombocytopenica, purpura werlhofii, splenic thrombocytopenic purpura, thrombocytolytic purpura.
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| ==Signs and symptoms==
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| The incidence of ITP is 50–100 new cases per million per year, with children accounting for half of that amount.
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| More than 70% of the cases in children end up in remission within 6 months whether treated or not.<ref name="pmid15494875">{{cite journal |author=Watts RG |title=Idiopathic thrombocytopenic purpura: a 10-year natural history study at the children's hospital of alabama |journal=Clinical pediatrics |volume=43 |issue=8 |pages=691-702 |year=2004 |pmid=15494875 |doi=}}</ref><ref name="pmid17460024">{{cite journal |author=Treutiger I, Rajantie J, Zeller B, Henter JI, Elinder G, Rosthøj S |title=Does treatment of newly diagnosed idiopathic thrombocytopenic purpura reduce morbidity? |journal=Arch. Dis. Child. |volume=92 |issue=8 |pages=704-7 |year=2007 |pmid=17460024 |doi=10.1136/adc.2006.098442}}</ref><ref name="pmid17352309">{{cite journal |author=Ou CY, Hsieh KS, Chiou YH, Chang YH, Ger LP |title=A comparative study of initial use of intravenous immunoglobulin and prednisolone treatments in childhood idiopathic thrombocytopenic purpur |journal=Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi |volume=47 |issue=5 |pages=226-31 |year=2006 |pmid=17352309 |doi=}}</ref> Moreover, a third of the remaining chronic cases remitted during the follow-up observation, and another third ended up with only mild thrombocytopenia (>50,000 platelets per μL).<ref name="pmid15494875"/> ITP is usually chronic in adults<ref name="pmid11919310">{{cite journal |author=Cines DB, Blanchette VS |title=Immune thrombocytopenic purpura |journal=N. Engl. J. Med. |volume=346 |issue=13 |pages=995-1008 |year=2002 |pmid=11919310 |doi=10.1056/NEJMra010501}}</ref> and the probability of durable remission is 20–40%.<ref name="pmid17122451">{{cite journal |author=Stevens W, Koene H, Zwaginga JJ, Vreugdenhil G |title=Chronic idiopathic thrombocytopenic purpura: present strategy, guidelines and new insights |journal=The Netherlands journal of medicine |volume=64 |issue=10 |pages=356-63 |year=2006 |pmid=17122451 |doi=}}</ref> The male:female ratio in the adult group is 1:1.2–1.7 (for children it is 1:1) and the median age of adults at the diagnosis is 56–60.<ref name="pmid15941913">{{cite journal |author=Cines DB, Bussel JB |title=How I treat idiopathic thrombocytopenic purpura (ITP) |journal=Blood |volume=106 |issue=7 |pages=2244-51 |year=2005 |pmid=15941913 |doi=10.1182/blood-2004-12-4598}}</ref> Usually, ITP patients suffer from [[bruising]]; [[petechia]]e, [[nosebleed]]s and bleeding [[gums]] may occur if the platelet count is below 20,000,<ref name="pmid15660520">{{cite journal |author=Cines DB, McMillan R |title=Management of adult idiopathic thrombocytopenic purpura |journal=Annu. Rev. Med. |volume=56 |issue= |pages=425-42 |year=2005 |pmid=15660520 |doi=10.1146/annurev.med.56.082103.104644}}</ref> compared to a normal range of 150,000–400,000 per mm<sup>3</sup>.[[Subarachnoid hemorrhage|Subarachnoid]], [[intracerebral hemorrhage]] or other internal bleeding are very serious possible complications of this disease. Fortunately, these are unlikely in patients with the platelets count above 20,000.
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| Evan's syndrome can occur in ~1% of cases and is manifest by an autoimmune (Coombs +)hemolytic anemia with ITP.
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| The bone marrow biopsy in ITP can show increased (thought not always) megakaryocytes, bizarre giant platelets and platelet fragments. (Large platelets are often seen in the peripheral blood smear though this can be seen in other diseases.) When the spleen is removed it may show increased lymphatic nodularity. Platelet-associated antibody (IgG), which was the standard test of past years, is not now considered mandatory to diagnose ITP. Test for platelet antibody are not helpful as both their sensitivity and specificity are limited.
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| ==Pathogenesis==
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| In many cases, the cause is not actually [[idiopathic]] but [[autoimmune]],<ref>{{cite journal |author=Coopamah M, Garvey M, Freedman J, Semple J |title=Cellular immune mechanisms in autoimmune thrombocytopenic purpura: An update |journal=Transfus Med Rev |volume=17 |issue=1 |pages=69–80 |year=2003 |pmid=12522773}}</ref> with [[antibodies]] against platelets being detected in approximately 60% of patients. Most often these antibodies are against platelet membrane [[glycoprotein]]s IIb-IIIa or Ib-IX, and are of the [[IgG]] type. The famous [[Harrington–Hollingsworth Experiment]] established the immune [[pathogenesis]] of ITP.<ref name="pmid18046034">{{cite journal |author=Schwartz RS |title=Immune thrombocytopenic purpura--from agony to agonist |journal=N. Engl. J. Med. |volume=357 |issue=22 |pages=2299–301 |year=2007 |pmid=18046034 |doi=10.1056/NEJMe0707126}}</ref>
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| The cause of ITP is thought to be related to chronic infections such as HIV, hepatitis C and H. Pylori. The mechanism involved is thought to be MOLECULAR MIMICRY, that is, antibody is formed against the infection and this cross-reacts with platelets. Autoantibodies in ITP react with platelet IIb/IIIa glycoprotein, less commonly with GPIb/IX. Lymphocytes in the spleen make the antiplatelet antibody; this is why splenectomy works so well. There is a correlation between a platelet's short survival and high turnover rate and the subsequent excellent response to splenectomy.
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| The antibodies also appear to damage megakaryocytes, preventing them from releasing platelets. Autoantibody-mediated phagocytosis of platelets has long been thought to be the primary mechanism of the disease. Platelet kinetic studies show that platelet production is normal or reduced rather than increased in about two thirds of ITP patients. Also, autoantibodies from patients with ITP inhibit megakaryocyte growth in vitro. IgG from ITP-plasma inhibits megakaryocyte production.
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| Ultrastructural studies of the bone marrow in ITP show increased signs of megakaryocyte apoptosis and reduced platelet shedding.
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| ITP has a strong association with immune thyroid disease.
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| Recent evidence suggests that the stimulus for autoantibody production in ITP is due to abnormal [[T helper cell]]s reacting with platelet antigens on the surface of antigen presenting cells.<ref>{{cite journal |author=Semple JW, Freedman J |title=Increased antiplatelet T helper lymphocyte reactivity in patients with autoimmune thrombocytopenia |journal=Blood |volume=78 |issue=10 |pages=2619-25 |year=1991 |pmid=1840468 |doi=}}</ref> This important finding suggests that therapies directed towards T cells may be effective in treating ITP.
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| | ==[[Idiopathic thrombocytopenic purpura overview|Overview]]== |
| | ==[[Idiopathic thrombocytopenic purpura historical perspective|Historical Perspective]]== |
| | ==[[Idiopathic thrombocytopenic purpura classification|Classification]]== |
| | ==[[Idiopathic thrombocytopenic purpura pathophysiology |Pathophysiology]]== |
| | ==[[Idiopathic thrombocytopenic purpura causes|Causes]]== |
| | ==[[Idiopathic thrombocytopenic purpura differential diagnosis|Differentiating Idiopathic Thrombocytopenic Purpura from other Diseases]]== |
| | ==[[Idiopathic thrombocytopenic purpura epidemiology and demographics|Epidemiology and Demographics]]== |
| | ==[[Idiopathic thrombocytopenic purpura risk factors|Risk Factors]]== |
| | ==[[Idiopathic thrombocytopenic purpura screening|Screening]]== |
| | ==[[Idiopathic thrombocytopenic purpura natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| ==Diagnosis== | | ==Diagnosis== |
| The diagnosis of ITP is a diagnosis of exclusion. First, one has to make sure that there are no other blood abnormalities except for low platelet count and no physical signs except for signs of bleeding. Then, the secondary causes (usually 5-10% of suspected ITP cases) should be excluded. Secondary causes could be [[leukemia]], medications (e.g. [[quinine]], [[heparin]]), [[lupus erythematosus]], [[cirrhosis]], [[HIV]], [[hepatitis]] C, congenital causes, [[antiphospholipid syndrome]], [[von Willebrand factor]] deficiency and others.<ref name="pmid15941913"/><ref name="pmid15660520"/>
| | [[Idiopathic thrombocytopenic purpura diagnostic study of choice|Diagnostic Study of Choice]] | [[Idiopathic thrombocytopenic purpura history and symptoms|History and Symptoms]] | [[Idiopathic thrombocytopenic purpura physical examination|Physical Examination]] | [[Idiopathic thrombocytopenic purpura laboratory findings|Laboratory Findings]] | [[Idiopathic thrombocytopenic purpura electrocardiogram|Electrocardiogram]] | [[Idiopathic thrombocytopenic purpura x ray|X Ray]] | [[Idiopathic thrombocytopenic purpura CT|CT]] | [[Idiopathic thrombocytopenic purpura MRI|MRI]] | [[Idiopathic thrombocytopenic purpura ultrasound|Ultrasound]] | [[Idiopathic thrombocytopenic purpura other imaging findings|Other Imaging Findings]] | [[Idiopathic thrombocytopenic purpura other diagnostic studies|Other Diagnostic Studies]] |
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| Despite the destruction of platelets by splenic macrophages, the spleen is normally not enlarged. In fact, an enlarged spleen should lead a clinician to investigate other possible causes for the thrombocytopenia.
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| Bleeding time is prolonged in ITP patients; however, the use of bleeding time in diagnosis is discouraged by the American Society of Hematology practice guidelines<ref name="pmid9036806">{{cite journal |author= |title=Diagnosis and treatment of idiopathic thrombocytopenic purpura: recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel |journal=Ann. Intern. Med. |volume=126 |issue=4 |pages=319-26 |year=1997 |pmid=9036806 |doi=}}</ref> as useless. For example the [[BMJ]] review of the basics of hematology states: "The bleeding time may or may not be prolonged in congenital or acquired platelet dysfunction, and therefore a normal bleeding time does not exclude these conditions."<ref name="pmid9081003">{{cite journal |author=Liesner RJ, Machin SJ |title=ABC of clinical haematology. Platelet disorders |journal=BMJ |volume=314 |issue=7083 |pages=809-12 |year=1997 |pmid=9081003 |doi=}}</ref>
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| A [[bone marrow examination]] may be performed on patients over the age of 60 and people who do not respond to treatment, or when the diagnosis is in doubt.<ref name="pmid15941913"/> The blood analysis for the antiplatelet antibodies is a matter of clinician's preference, as there is a disagreement whether the 80% specificity of this test is sufficient.<ref name="pmid15941913"/> In conditions associated with bone marrow failure (aplastic anemia) thrombopoietin (TPO)levels are high whereas in ITP thrombopoietin levels are low. Thus TPO could distinguish between decreased platelets due to bone marrow failure or increased due to their destruction. The bone marrow in ITP contains normal or high numbers of megakaryocytes but they may be small or immature (& may have been damaged by antibodies).
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| The ITP in AIDS has a thrombocytopenia that is multifactorial involving both TPO and platelet problems. Mechanisms may involve portal hypertension that leads to splenomegaly causing platelet sequestration. Hepatits C (HCV) causes decreased TPO production leading to decreased platelet production. Steroids may be helpful but, with their taper, the count usually decreases again. Intravenous immunoglobulin's effect is transient. For ITP-HIV the primary treatment should be directed at HIV suppression with HAART. HIV patients whose platelet count fails to increase to > 50,000 with HAART can be treated with steroids. Splenectomy is safe and effective in ~80% of patients with refractory HIV-related thrombocytopenia and treated with interferon (IFN) may be effective in refractory cases of patients coinfected with HCV. A decrease in platelets in HIV can arise secondary to both HCV and hepatitis B (HBV).
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| Pregnant patients with ITP and platelet counts < 30,000 can be treated with intravenous immunoglobulin (IV-IgG) or steroids at the lowest dose possible to avoid hypertension, eclampsia and adrenal suppression of the fetus. ~10-30% of pregnant females with ITP have an infant with platelets <50,000, however, intracranial hemorrhage is rare. For these females administer prednisone during the last month of pregnancy to decrease the likelihood of thrombocytopenia in the fetus.
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| Mothers with ITP who have previously given birth to infants without thrombocytopenia tend not to be thrombocytopenic. The maternal platelet count doesn't correlate with fetal and females with a prior history of ITP with ITP in remission (eg after splenectomy) may still deliver severely thrombocytopenic infants. This likely occurs because asplenic patients in clinical remission may not necessarily be in immunologic remission and circulating platelet-reactive IgG may still be present in their plasma.
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| ==Treatment== | | ==Treatment== |
| | [[Idiopathic thrombocytopenic purpura medical therapy|Medical Therapy]] | [[Idiopathic thrombocytopenic purpura radiation|Radiation]] | [[Idiopathic thrombocytopenic purpura surgery|Surgery]] | [[Idiopathic thrombocytopenic purpura primary prevention|Primary Prevention]] | [[Idiopathic thrombocytopenic purpura secondary prevention|Secondary Prevention]] | [[Idiopathic thrombocytopenic purpura cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Idiopathic thrombocytopenic purpura future or investigational therapies|Future or Investigational Therapies]] |
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| Mechanism-based Approach to Treatment;
| | ==Case Studies== |
| 1) Inhibit phagocyte-mediated clearance of antibody-coated platelets.
| | [[Idiopathic thrombocytopenic purpura case study one|Case #1]] |
| Steroids
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| Splenectomy
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| Anti-D
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| IV-IgG
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| 2) Decreased autoantibody production
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| Rituximab
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| Steroids
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| Azathioprine & other immunosuppressants (eg cytoxan, cyclosporine, etc)
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| 3) Impair T & B cell interactions.
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| Steroids
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| Rituximab
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| 4) Enhance platelet production.
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| Thrombopoietic agents
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| IL-11
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| ===Observation===
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| Most children with ITP will recover even without specific treatment. Among adults ITP is typically a chronic disease. It is insidious in onset and, in some patients, refractory to treatment. 90% of childhood ITP cases are an acute, self-limited disease, developing several weeks after a viral illness, lasting for 4-6 weeks, then spontaneously remitting. The bleeding risk is low and treatment is reserved only for the most severely affected patients. Because spontaneous recovery is expected in children wit ITP some pediatric hematologists recommend supportive care only, no drugs. In less than 20% of children thrombocytopenia may persist for >6-12 months and even many of these kids can experience a spontaneous remission.
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| ===Steroids/IVIgG===
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| [[Platelet count]] below 20,000 is an indication for treatment; the patients with 20,000–50,000 platelets/μL are considered on a case by case basis, and there is generally no need to treat the patients with above 50,000 platelets/μL.<ref name="pmid15941913"/> Hospitalization is recommended in the cases of significant internal or mucocutaneous bleeding. The treatment begins with intravenous steroids (methylprednisolone or prednisone), [[intravenous immunoglobulin]] (IVIg) or their combination and sometimes platelet infusions in order to raise the count quickly. After the platelet count stabilized and in the less severe cases oral prednisone (1–2 mg/kg) is used. Most cases respond during the first week of treatment (RR ~70%). After several weeks of prednisone therapy, the dose is gradually reduced. However, 60–90% of patients relapse after the dose decreased below 0.25 mg/kg and stopped.<ref name="pmid15941913"/><ref name="pmid17122451"/> Pulsed high-dose dexamethasone shows (in untreated patients) a high RR of ~90% with a long-term RR of ~80% when several cycles of treatment are given. However long term high dose steroids have a myriad of toxicities and should be avoided if possible. | |
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| ===Splenectomy===
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| Splenectomy offers a 2nd line treatment for those who fail steroids. The criteria for surgery are severe thrombocytopenia (<10,000), high risk of bleeding or the requirement of frequent steroids/IVIgG/anti-D treatment to maintain an adequate platelet count. Of the ~15% of children with persistent thrombocytopenia bleeding symptoms are uncommon and splenectomy is rarely required. However splenectomy is an effective treatment option for children with severe / symptomatic thrombocytopenia with a CR of ~75%. Because of the risk for overwhelming sepsis after splenectomy it should be deferred until after 5 years of age. Remember to give immunizations before splenectomy and perioperative antibiotics. Response to IV-IgG often predicts a response to splenectomy (increasing the platelet count to >50,000 with IgG means a >90% RR to splenectomy).
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| ===Anti-D===
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| A relatively new strategy is treatment with [[Rho(D) Immune Globulin|anti-D]], an agent also used in mothers who have been sensitized to [[rhesus]] antigen by a Rh+ baby, but the patient must be Rh+.
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| IV anti-D (WinRhoSD) can also increase the platelet count especially at a higher dose of 75 mcg / kg. IV anti-D is effective in patients who are Rh-positive and non-splenectomized with a RR equal to 70%. Its toxicities include mild hemolysis, fever, chills, headache, nausea and vomiting.
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| ===Steroid-sparing agents===
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| Immunosuppresants like [[mycophenolic acid|mycophenolate mofetil]] and [[azathioprine]] are becoming more popular for their effectiveness. [[Rituximab]] has also been used successfully for some patients. <ref>Braendstrup P, Bjerrum OW, Nielsen OJ, Jensen BA, Clausen NT, Hansen PB, Andersen I, Schmidt K, Andersen TM, Peterslund NA, Birgens HS, Plesner T, Pedersen BB, Hasselbalch HC. ''Rituximab chimeric anti-CD20 monoclonal antibody treatment for adult refractory idiopathic thrombocytopenic purpura.'' Am J Hematol 2005;78:275-80. PMID 15795920.</ref><ref>
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| Patel V, Mihatov N, Cooper N, Stasi R,
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| Cunningham-Rundles S, Bussel JB,''Long-term responses seen with rituximab in patients with ITP'', Community Oncology Vol. 4 No. 2, February 2007:107 [http://www.communityoncology.net/journal/articles/0402107.pdf PDF]</ref> Rituximab is used in refractory ITP with success; circulating B-cells become undetectable after a single dose of Rituximab but recover after 3-6 months. Rituximab can be detected in the serum of patients 3-6 months after treatment. The duration of Rituximab correlates with the stability of hte platelet response. However, although the short-term CR = 46% the long-term CR is only 18%. The typical schedule is 375 mg / m2 qwk x4 wks. Rituximab (375 mg / m2 d7, 14, 21, 28) / Dexamethasone was compared to Dexamethasone alone (40 mg QD, d1 through 4, given in qmonthly cycles. Initial and sustained response rates were better with the combination therapy (reference; Zaja R et al ASH 2008).
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| Extreme cases (very rare, especially rare in children) may require [[vincristine]], a [[chemotherapy]] agent, to stop the immune system from destroying platelets. For the most part this and other agents such as cytoxan, cyclosporine and danazol have fallen into disuse.
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| [[Intravenous immunoglobulin]], while sometimes effective, is expensive and the improvement is temporary (generally lasting less than a month). However, in the case of a pre-splenectomy ITP patient with dangerously low platelet counts, and a poor response to other treatments, IVIgG treatment can increase platelet counts, making the splenectomy operation less dangerous. It is also commonly used as a long-term (though monthly) treatment. The administration of IV-IgG is safe for maternal and fetal platelet counts during pregnancy, delivery and in the neonatal period.
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| IV-IgG is administered at 400-1000 mg/kg/day over 1 to 5 days and gives a better RR than prednisone. The duration of action is only 2 to 4 weeks. Its toxicities are nausea, headache, chills and occasional vascular events (eg MI, CVA) in older patients. The possible mechanmism of action is a transient impairment of the reticulendothelial clearance or macrophage blockade, inhibition of complement binding to platelets and interference of immune complexes binding to platelets. IV-IgG and WinRho essentially are the same type of treatment.
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| ===Splenic Radiation===
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| Splenic radiation (RT) is usually given for steroid-resistant ITP. One to six weeks of 75-1370 cGy with or without concomittant post-RT steroids. Patients can respond for >1 year. It is a safe alternative for patients too old for splenectomy.
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| ===Platelet transfusion===
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| Platelet transfusion is not normally recommended and is usually unsuccessful in raising a patient's platelet count. This is because the underlying autoimmune mechanism that destroyed the patient's platelets to begin with will also destroy donor platelets. 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, a life-threatening hemorrhage. Intravenous immunoglobulin administration, with the platelet transfusion, may improve their survival.
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| ===Experimental/novel agents===
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| *AMG 531 (Romiplostum; Nplate) is an experimental treatment for stimulating platelet production. It is a thrombopoiesis stimulating Fc-peptide fusion protein (peptibody), a TPO peptide mimetic. Initial clinical trials show it to be effective in chronic ITP.<ref>{{cite journal |author=Bussel JB, Kuter DJ, George JN, ''et al'' |title=AMG 531, a thrombopoiesis-stimulating protein, for chronic ITP |journal=N. Engl. J. Med. |volume=355 |issue=16 |pages=1672–81 |year=2006 |pmid=17050891 |doi=10.1056/NEJMoa054626}}</ref>
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| *The novel agent [[eltrombopag]] has been demonstrated to increase platelet counts and decrease bleeding in a dose-dependent manner.<ref>{{cite journal|author=Bussel JB, Cheng G, Saleh MN, ''et al'' |year=2007|title=Eltrombopag for the treatment of chronic idiopathic thrombocytopenic purpura|journal=N. Engl. J. Med. |volume=357|pages=2237-2247|id=PMID 18046028}}</ref> It is NOT indicated for the treatment of thrombocytopenia due to any other cause other than ITP (eg NOT MDS). This is a therapeutic protein and therefore the patient may develop antibodies to it. Toxicities include bone marrow reticulin deposition.
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| *[[Dapsone]] (also called Diphenylsulfone, DDS, or Avlosulfon) is an anti-infective sulfone drug. In recent years Dapsone has also proved helpful in treating lupus, rheumatoid arthritis and as a second-line treatment for ITP. The exact mechanism by which Dapsone assists in ITP is unclear. However, limited studies report successful increases in platelet counts of around 40–50% of patients taking the drug. <ref name="pmid9163598">{{cite journal |author=Godeau B, Durand JM, Roudot-Thoraval F, ''et al'' |title=Dapsone for chronic autoimmune thrombocytopenic purpura: a report of 66 cases |journal=Br. J. Haematol. |volume=97 |issue=2 |pages=336–9 |year=1997 |pmid=9163598 |doi=}}</ref><ref>http://www.itppeople.com/dapsone.htm</ref>
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| ===H. pylori eradication===
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| Researchers in Japan (including Ryugo Sato, Oita University) and Italy (including Massimo Franchini, University of Verona) have found a possible connection between [[Helicobacter Pylori|H. Pylori]] ([[Helicobacter Pylori]]) infection and ITP. Some patients given antibiotic treatment to eradicate the bacterial infection have had their platelet count increase dramatically.
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| ==References==
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| {{Reflist|2}}
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| ==External links==
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| * {{cite web | url = http://www.itpsupport.org.uk/childhooditp.htm | title = Childhood ITP | accessdate = 2007-02-14 | publisher = ITP Support Association}}
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| * {{cite web | url = http://www.itppeople.com/warnings.htm | title = Drug Induced Thrombocytopenia | accessdate = 2007-02-14 | publisher = Platelet Disorder Support Association}}
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