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Kasabach-Merritt Syndrome Medication

  • Author: Alexandra C Cheerva, MD, MS; Chief Editor: Hassan M Yaish, MD  more...
 
Updated: May 24, 2016
 

Medication Summary

No single therapy has been proved most effective in patients with Kasabach-Merritt syndrome (KMS). Multiple treatments have been used in many infants. Treatments that are effective in some patients have no benefit for others. Many of these medications have serious adverse effects, especially in patients with thrombocytopenia and disseminated intravascular coagulation (DIC), and should be administered only by physicians with expertise in this area.

The medications listed below are among the most frequently used, though other medications in these and other categories may also have been used to treat KMS. Most of these medications are not approved by the US Food and Drug Administration (FDA) for treatment of KMS.

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Corticosteroids

Class Summary

Systemic corticosteroids are synthetic chemicals that stabilize blood vessels and reduce fibrinolysis. They have been successfully used to treat proliferative vascular lesions; treatment of KMS is usually not as successful. High-dose oral prednisone (2-4 mg/kg/day) can rapidly increase the platelet count.

Prednisone (Rayos)

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. It may increase the sensitivity of arterioles and precapillaries to vasoconstriction and may competitively inhibit other hormonal agents.

Prednisolone (Pediapred, Prelone, Orapred, Millipred)

 

Prednisolone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. It may increase the sensitivity of arterioles and precapillaries to vasoconstriction and may competitively inhibit other hormonal agents.

Triamcinolone (Amcort)

 

Triamcinolone is used for inflammation responsive to steroids. It decreases inflammation by suppressing migration of PMNs and reversing capillary permeability.

Methylprednisolone (Solu-Medrol, Depo-Medrol, A-Methapred)

 

Methylprednisolone is used for inflammation responsive to steroids. It decreases inflammation by suppressing migration of polymorphonuclear leukocyte (PMN) activity and reversing capillary permeability.

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Immunomodulators

Class Summary

Antiangiogenic agents are naturally produced proteins that have antiviral, antitumoral, and immunomodulatory actions. Interferon alfa, beta, and gamma may be administered topically, systemically, or intralesionally. Antiangiogenic agents have a direct antiproliferative effect against vascular tumors. Agents in development include thalidomide, vascular endothelial growth factor (VEGF), receptor inhibitors (SU 5416), and anti-VEGF antibodies.

Interferon alfa-2b (Intron A)

 

Interferon alfa-2b is a protein product manufactured by means of recombinant DNA technology. The mechanism of its antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.

Interferon alfa is a protein product manufactured by means of recombinant DNA technology. It appears to produce its antiangiogenic effect by down-regulating the expression of basic fibroblast growth factor (bFGF) in the rapidly proliferating vascular lesion. The proliferative phase of growth is characterized by high bFGF expression, which then falls during involution of the lesion.

Vascular proliferative lesions vary in response to treatment with interferon. Most patients have been treated with interferon alfa-2a; however, some lesions have been treated with good results with interferon alfa-2b. Their similar clinical and in vitro effects on angiogenesis suggest that the 2 agents may have similar efficacy in these vascular lesions. Not all lesions respond to interferon alfa therapy.

Pegylated interferon alfa-2a (Pegasys)

 

PEG-IFN alfa-2a consists of IFN alfa-2a attached to a 40-kd branched PEG molecule. PEG-IFN has sustained absorption, a slower rate of clearance, and a longer half-life than unmodified IFN, which permits more convenient once-weekly dosing and significantly improves quality of life for patients.

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Hemorheologic Agents

Class Summary

Blood viscosity−improving agents improve blood flow through hemangiomas and decrease microthrombus formation.

Pentoxifylline

 

Pentoxifylline may alter the rheology of red blood cells (RBCs), thereby reducing blood viscosity.

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Anticoagulants, Hematologic

Class Summary

Anticoagulants decrease microthrombus formation in hemangiomas.

Heparin

 

Heparin augments the activity of antithrombin III (ATIII) and prevents conversion of fibrinogen to fibrin. It does not actively lyse but inhibits further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis.

Enoxaparin (Lovenox)

 

Enoxaparin is a low-molecular-weight heparin (LMWH) produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). It binds to ATIII, enhancing its therapeutic effect. The heparin-ATIII complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). LMWH differs from UFH in that it has a higher ratio of antifactor Xa to antifactor IIa.

Enoxaparin does not actively lyse but is able to inhibit further thrombogenesis. It prevents reaccumulation of clot after spontaneous fibrinolysis. Advantages include intermittent dosing and a decreased requirement for monitoring. Heparin antifactor Xa levels may be obtained if necessary to establish adequate dosing.

Enoxaparin prevents deep vein thrombosis (DVT), which may lead to pulmonary embolism (PE) in surgical patients at risk for thromboembolic complications. It is used for prevention in hip replacement surgery, knee replacement surgery, or abdominal surgery in those at risk for thromboembolic complications, as well as in nonsurgical patients at risk for thromboembolic complications secondary to severely restricted mobility. It is used with warfarin to treat acute DVT with or without PE (inpatient) or acute DVT without PE (outpatient).

There is no use in checking the activated partial thromboplastin time (aPTT); the drug has a wide therapeutic window, and the aPTT does not correlate with the anticoagulant effect. The average duration of treatment is 7-14 days.

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Antiplatelet Drugs

Class Summary

Antiplatelet agents decrease microthrombus formation.

Ticlopidine

 

Ticlopidine

Ticlopidine is a second-line antiplatelet therapy for patients who cannot tolerate aspirin therapy or in whom aspirin therapy fails.

Dipyridamole (Persantine)

 

Dipyridamole is used to complement the usual warfarin therapy. It is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine (itself an inhibitor of platelet reactivity). In addition, dipyridamole may inhibit phosphodiesterase activity, leading to increased cyclic-3', 5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2. It may enhance the effects of aspirin.

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Antifibrinolytic Agents

Class Summary

Antifibrinolytic agents inhibit thrombus breakdown, thus interfering with DIC. They are often administered with cryoprecipitate in patients with KMS.

Aminocaproic acid (Amicar)

 

Aminocaproic acid is a lysine analogue that inhibits fibrinolysis through inhibition of plasminogen activator substances and, to a lesser degree, through antiplasmin activity. It is widely distributed, with a half-life of 1-2 hours. Peak effect occurs within 2 hours, and hepatic metabolism is minimal. Aminocaproic acid may be administered either orally or intravenously (IV).

Tranexamic acid (Cyklokapron, Lysteda)

 

Tranexamic acid is an alternative to aminocaproic acid; it inhibits fibrinolysis by displacing plasminogen from fibrin.

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Antineoplastic Agents

Class Summary

Antineoplastic agents inhibit tumor cell growth and proliferation. The standard dosage is 1-1.5 mg/m2 or 0.05-0.065 mg/kg once weekly.

Vincristine (Vincasar PFS)

 

The mechanism by which vincristine acts is uncertain; it may involve a decrease in reticuloendothelial cell function or an increase in platelet production. However, neither of these mechanisms fully explains this agent's effect in patients with thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS).

Cyclophosphamide

 

Cyclophosphamide is a cyclic polypeptide that suppresses some humoral activity. In high doses, affects B cells by inhibiting clonal expansion and suppression of production of immunoglobulins. With long-term low-dose therapy, affects T cell functions.

Chemically related to nitrogen mustards, cyclophosphamide is biotransformed by cytochrome P-450 in the liver to its active metabolite, 4-hydroxycyclophosphamide, which alkylates the target sites in susceptible cells in an all-or-none type reaction. As alkylating agents, active metabolites may act through cross-linking of DNA, which may interfere with growth of normal and neoplastic cells. In autoimmune diseases, the mechanism of action is thought to involve immunosuppression due to destruction of immune cells via DNA cross-linking.

Dactinomycin (Cosmegen)

 

Dactinomycin intercalates between guanine and cytosine base pairs, inhibiting protein synthesis and DNA and RNA synthesis. It is administered in a free-flowing vein or central catheter.

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Contributor Information and Disclosures
Author

Alexandra C Cheerva, MD, MS Associate Professor of Pediatrics, University of Louisville School of Medicine; Director of Pediatric Blood and Marrow Transplantation, Section of Pediatric Hematology and Oncology, Kosair Children's Hospital

Alexandra C Cheerva, MD, MS is a member of the following medical societies: American Society for Blood and Marrow Transplantation, Children's Oncology Group, American Society of Clinical Oncology, International Pediatric Transplant Association, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Ashok B Raj, MD Professor, Section of Pediatric Hematology and Oncology, Department of Pediatrics, Kosair Children's Hospital, University of Louisville School of Medicine

Ashok B Raj, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association, Children's Oncology Group

Disclosure: Nothing to disclose.

Salvatore Bertolone, MD Director, Division of Pediatric Hematology/Oncology, Kosair Children's Hospital; Professor, Department of Pediatrics, University of Louisville School of Medicine

Salvatore Bertolone, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Education, American Association of Blood Banks, American Cancer Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Kentucky Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Hassan M Yaish, MD Medical Director, Intermountain Hemophilia and Thrombophilia Treatment Center; Professor of Pediatrics, University of Utah School of Medicine; Director of Hematology, Pediatric Hematologist/Oncologist, Department of Pediatrics, Primary Children's Medical Center

Hassan M Yaish, MD is a member of the following medical societies: American Academy of Pediatrics, New York Academy of Sciences, American Medical Association, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Michigan State Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

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.

Gary D Crouch, MD Associate Professor, Program Director of Pediatric Hematology-Oncology Fellowship, Department of Pediatrics, Uniformed Services University of the Health Sciences

Gary D Crouch, MD is a member of the following medical societies: American Academy of Pediatrics and American Society of Hematology

Disclosure: Nothing to disclose. Guy B Faguet, MD Former Professor, Department of Medicine, Section of Hematology and Oncology, Medical College of Georgia

Guy B Faguet, MD is a member of the following medical societies: American Association of Immunologists, American Society of Hematology, International Society of Hematology, New York Academy of Sciences, Southern Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Linda K Hendricks, MD Assistant Professor, Department of Internal Medicine, Section of Hematology and Oncology, Mercer University School of Medicine

Linda K Hendricks, MD is a member of the following medical societies: American Society of Hematology

Disclosure: Nothing to disclose.

Gary R Jones, MD Associate Medical Director, Clinical Development, Berlex Laboratories

Gary R Jones, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Hematology/Oncology, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

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.

Bernice R Krafchik, MBChB, FRCPC Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto

Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.

Sejal Kuthiala, MD Staff Physician, Department of Internal Medicine, Medical College of Georgia

Sejal Kuthiala, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

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

Carlos Suarez, MD Associate Professor, Department of Pediatrics, Section of Pediatric Hematology and Oncology, University of Louisville School of Medicine

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

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Leg with a Kaposiform hemangioendothelioma, lesion associated with Kasabach-Merritt Syndrome.
Back of an arm showing the typical bruising associated with Kasabach-Merritt Syndrome.
 
 
 
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