itp Treatment & Management

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Immune Thrombocytopenic Purpura Treatment & Management
Author: Craig M Kessler, MD, MACP; Chief Editor: Emmanuel C Besa, MD more... Updated: Apr 8, 2013

Medical Care
The goal of medical care is to increase the platelet count to a safe level, permitting patients with immune thrombocytopenic purpura (ITP) to live normal lives while awaiting spontaneous or treatment-induced remission. ITP has no cure, and relapses may occur years after seemingly successful medical or surgical management.[7] Although the paradigm may be shifting somewhat with the expanding experience with thrombopoietin receptor analogs in chronic ITP, the long-term consequences associated with their use remain to be established and their delayed platelet count responses are not conducive to preventing or reversing the potential of acute bleeding complications in newly diagnosed ITP. Therefore, for now, corticosteroids (ie, oral prednisone, IV methylprednisolone) or high-dose dexamethasone[10, 11, 12] should remain the drugs of choice (DOCs) for the initial management of acute ITP. Treatment with corticosteroids may not only reduce the rate of platelet destruction but may also rapidly alter endothelial cell integrity to facilitate primary hemostasis and to reduce bleeding and bruising. Because corticosteroid administration may change marrow morphology performance of a bone marrow aspiration and biopsy should be considered to confirm the diagnosis of ITP if the clinical presentation, patient age, or other findings are atypical for acute ITP before the patient is treated with corticosteroids. IV immunoglobulin (IVIG) has been the drug of second choice (after corticosteroids) for many years.[13, 14] However, for Rh(D)-positive patients with immune thrombocytopenic purpura (ITP) and intact spleens, IV Rho immunoglobulin (RhIG) offers comparable efficacy, less toxicity, greater ease of administration, and a lower cost than IVIG.[15, 16] The limitation of using IV RhIG is the lack of efficacy in Rh(D)-negative or splenectomized patients. Also, IV RhIG induces immune hemolysis (immune hemolytic anemia) in Rh(D)-positive persons, which is the most common adverse effect, and should not be used when the hemoglobin concentration is less than 8 g/dL. Sporadic cases of massive intravascular hemolysis [17] disseminated intravascular coagulation (particularly in elderly individuals), and renal failure[18] have been reported. Most children with acute ITP do not require treatment, and thrombocytopenia resolves spontaneously.[8, 9] If bone marrow aspiration is unacceptable to parents and if the diagnosis of acute ITP is equivocal, IV RhIG is an effective treatment for ITP that avoids the problem of a misdiagnosis of acute leukemia because of steroid-related changes in the marrow.

In adults, the initial treatment for ITP is similar to that in children, except that additional precautions are required for persons with hypertension, peptic ulcers, recent aspirin ingestion, or other risk factors for increased bleeding. Aspirin inhibits platelet function by acetylating platelet cyclooxygenase, increasing the risk of bleeding because it adds a platelet functional defect to the quantitative defect already present from the severe thrombocytopenia. In addition, platelet dysfunction may be induced by the platelet antibody, which is potentiated by the superimposition of the aspirin-platelet defect. Because of this effect, aspirin is contraindicated in persons with ITP. Adults whose platelet counts are greater than (50 X 109 /L (>50 X 103 /µL) typically have minimal purpura, and the risk of a severe hemorrhage is low. They may be treated without a specific medication. Platelet transfusions may be required to control clinically significant bleeding but are not recommended for prophylaxis. Transfused platelets also have decreased circulation, and repeated platelet transfusions may lead to platelet alloimmunization. Pregnant women require special consideration for delivery.[19] If the platelet count is greater than 50 X 109 /L (>50 X 103 /µL), the risk of serious hemorrhage is low, but beginning oral prednisone a week before delivery is a reasonable precaution. If the platelet count is less than 50 X 109 /L (50 X 103 /µL) before delivery, treatment with oral prednisone and IVIG is recommended. The safety of thrombopoietin mimetics in pregnancy and breastfeeding has not been established. The standard dose of IV RhIG for ITP contains approximately 10-fold the concentration of anti-D that is in the standard antepartum dose of intramuscular RhIG for Rh immunoprophylaxis. Although the effects on an Rh(D)-positive fetus are unknown, avoiding the use of IV RhIG in this situation until safety data are available is advisable. Rarely, splenectomy may be required to manage acute hemorrhage.[20] For many years, the only treatment options after corticosteroids, IV RhIG, IVIG, and rituximab were cyclophosphamide, azathioprine, and danazol. Interventions with decreased certain efficacy and with conflicting reports in the literature include vinblastine, vincristine, ascorbic acid, colchicine, and interferon alfa.[45, 46, 47, 48, 49, 50] . In 2008, thrombopoietin receptor agonists became available for patients with chronic ITP. The limited clinical experiences with thrombopoietin mimetics are promising. In one prospective, randomized controlled study comparing romiplostin with the standard of care for the treatment of chronic ITP, romiplostim administration was associated with higher rates of platelet count responses, decreased need for splenectomy, fewer episodes of serious bleeding and blood transfusions, and decreased need for initiating additional medical treatments. Romiplostim therapy was also associated with improved quality of life.[51] The ultimate efficacy and safety of these new agents will not be fully evaluable until data on larger numbers of patients become available.

Surgical Care
In persons with acute immune thrombocytopenic purpura (ITP), splenectomy usually results in rapid, complete, and life-long clinical remission. In persons with chronic immune thrombocytopenic purpura (ITP), the results of splenectomy are typically less predictable than they are in patients with acute immune thrombocytopenic purpura (ITP). Platelet counts may not fully revert to normal values, and relapses are not uncommon after 5 years. Laparoscopic splenectomy is an interventional approach less invasive than traditional splenectomy and offers the promise of decreased postoperative morbidity and shorter recovery.[52, 53] However, the ultimate role for laparoscopic splenectomy in immune thrombocytopenic purpura (ITP) depends on long-term follow-up to determine whether this approach is as effective as conventional splenectomy for visual scrutiny of the abdominal cavity to identify accessory spleens. Splenectomy results in a lifelong increased risk of sepsis from infection by encapsulated bacteria[54, 55, 56] and Babesia.[57] In adults, this risk is estimated to be approximately 1%, with a fatal outcome in approximately 1 per 1500 patient-years. In children, the risk of bacterial sepsis after splenectomy is estimated to be 1-2%. Many pediatricians

recommend delaying splenectomy until children are aged 5 years. These estimates are presumably based on early data and may be inflated, given the increased alertness to the importance of early treatment, availability of more effective antibiotics, and availability of vaccines for prophylactic immunization against specific encapsulated bacteria. Before one concludes that medical management and splenectomy have failed and that treatment with alternative options is needed, perform an imaging study to ensure that the problem is not associated with an accessory spleen. Recent studies suggest that the initiation of thrombopoietin mimetics may be splenectomy sparing in a significant number of individuals with chronic ITP. In addition, splenectomy has also been associated in adults with an increased incidence of venous and arterial thrombosis,[58] an increase in deaths from cardiovascular disease by a factor of 2,[59] and an increased rate of pulmonary hypertension[60] . If elective splenectomy is planned for a child or an adult, initiate immunization with Haemophilus influenzae type b vaccine at least 14 days before surgery.[61] Immunize adults and children older than 2 years with polyvalent Streptococcus pneumoniae vaccine and quadrivalent meningococcal polysaccharide vaccine. Evaluate patients who have a relapse after having an initially satisfactory response to splenectomy for the possible presence of an accessory spleen.[62, 63] An accessory spleen is strongly indicated if Howell-Jolly bodies appeared on the peripheral smear after splenectomy but are no longer present. However, the continued presence of Howell-Jolly bodies does not exclude an accessory spleen. Imaging techniques using radionucleotide-labeled sulfur colloid, heat-damaged RBCs, or, preferably, autologous platelets provide more useful information than standard imaging with CT scanning or MRI.

Consultations
Selecting a treatment program for immune thrombocytopenic purpura (ITP) requires knowledge of current options and consultation with a hematologist. If 6 months of medical management fails to increase the platelet count to a safe range (about 30,000/µL), splenectomy becomes an option. Early consultation with a surgeon is useful for planning management.[64, 65] If the platelet count is less than 10 X 109 /L (< 10 X 103 /µL) or if the patient has other evidence of a clinically significant risk of serious hemorrhage, consult a radiologist to determine what noninterventional imaging procedures are available in case of emergency.

Contributor Information and Disclosures
Author Craig M Kessler, MD, MACP Professor, Department of Medicine and Pathology, Division of Hematology/Oncology, Georgetown University School of Medicine; Director, Clinical Coagulation Laboratory, Lombardi Comprehensive Cancer Center, Georgetown University Hospital Disclosure: NovoNordisk Honoraria Consulting; NovoNordisk Grant/research funds Other; Baxter-Immuno Honoraria Consulting; Octapharma Honoraria Speaking and teaching; Octapharma Grant/research funds None; Amgen Consulting fee Consulting; Bayer Review panel membership Coauthor(s) S Gerald Sandler, MD, FACP, FCAP Professor of Medicine and Pathology, Director, Transfusion Medicine, Department of Laboratory Medicine, Georgetown University Hospital S Gerald Sandler, MD, FACP, FCAP is a member of the following medical societies: American Association of Blood Banks, College of American Pathologists, and International Society of Blood Transfusions Disclosure: Nothing to disclose.

Specialty Editor Board Michael Paul Kosty, MD Associate Director, Associate Professor, Department of Internal Medicine, Divisions of Supportive Care Services and Hematology and Oncology, Ida M and Cecil H Green Cancer Center, Scripps Clinic Michael Paul Kosty, MD is a member of the following medical societies: American College of Physicians, American Society of Hematology, and Phi Beta Kappa Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Ronald A Sacher, MB, BCh, MD, FRCPC Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership Rajalaxmi McKenna, MD, FACP Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis Disclosure: Nothing to disclose. Chief Editor Emmanuel C Besa, MD Professor, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences Disclosure: Nothing to disclose. Additional Contributors The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author S Gerald Sandler, MD, FACP, FCAP, to the development and writing of this article. The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor Rumina Bhanji, MD to the development and writing of this article.

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