scholarly journals Cytomegalovirus Induced Thrombocytopenia with No Platelets in an Immunocompetent Young Male

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4904-4904
Author(s):  
Sujatha Baddam ◽  
Jose Cavo ◽  
Jorge Diaz Castro
Keyword(s):  
Platelet Count ◽  
Viral Load ◽  
Immune Globulin ◽  
Influenza A ◽  
Conflicts Of Interest ◽  
Fatal Outcome ◽  
Laboratory Data ◽  
High Dose ◽  
Severe Epistaxis ◽  
Immunocompetent Adults

Introduction Immune thrombocytopenic purpura (ITP) is a common cause of acquired thrombocytopenia in an otherwise asymptomatic adult. It is generally believed to be caused by auto- antibodies against platelet antigens that destroy platelets peripherally and autoreactive cytotoxic T cells, as well as humoral and cellular autoimmunity directed at megakaryocytes, causing impaired platelet production. Cytomegalovirus (CMV) is a known cause of cause of morbidity and mortality in patients with immunosuppressed states, whereas in immunocompetent patients, it commonly manifest as asymptomatic or mononucleosis like syndrome. We are presenting a case of CMV induced thrombocytopenia with severe epistaxis and platelet count of 0 x10 9 in an otherwise healthy immunocompetent male who failed to improve after standard treatments with high dose steroids and intra venous immune globulin (IVIG). Case Description A 36-year-old Caucasian male without any past medical history presented to emergency room (ER) with flu like symptoms for five days associated with subjective fevers, anorexia, nausea, cough and weight loss of 15 lb. in two weeks. He also reported possible tick bite while working in the yard two days prior to admission. No dizziness, vomiting, diarrhea or any bleeding were reported. Denied any smoking, alcohol use or any illicit drug use. No significant family history was reported. On evaluation he was afebrile, normotensive with normal heart rate and respiratory rate. Physical examination was unremarkable. Initial laboratory data revealed hemoglobin of 11.2, platelet count 4 x109, white cell count of 13,100 with 4.5% atypical lymphocytes, aspartate aminotransferase of 41, alanine aminotransferase of 49, and creatinine of 1.4. He tested positive for Influenza A, CMV Immune globulin (Ig)M and IgG antibody. Serological tests for tick panel including anaplasma, babesia, Lyme disease and ehrlichia were negative. Epstein-Barr virus (EBV) antibody, parvo virus antibody, hepatitis screen, HIV screen, auto antibodies including anti-nuclear antibody and anti-double stranded DNA were negative. Coombs test was negative. Further work up includes ADAMTS13 activity was normal. No laboratory evidence of ADAMTS13 deficiency. After excluding all other causes, diagnosis of ITP was made. He was started on Tamiflu for Influenza A and high dose intra venous (IV) methyl prednisone for ITP. After platelet transfusion and two days of IV steroids platelet count improved 43 x 109 and he was discharged home with prolonged prednisone taper. Five days later, he presented to ER with severe epistaxis. Laboratory data revealed platelet count of 0 x109. Serum CMV-DNA was determined by PCR showed viral load of 8,790 copies/ml. Ultrasound abdomen showed mild splenomegaly. He received three doses of IVIG (1g/kg). Platelet count failed to improve after administration of IVIG. Bone marrow biopsy revealed hyper cellular marrow with trilineage hematopoiesis with no increase in CD 34 blasts. Per infectious disease and hematology recommendations, he was started on valganciclovir (900 mg PO BID). One month later, platelet count improved to 150 x 109 and CMV viral load dropped to 413 with subsequent resolution of patient's symptoms. Discussion Secondary ITP is an acquired thrombocytopenia caused by autoantibodies against platelets. Many patients with ITP are asymptomatic. For those who do have symptoms, initial presentations of ITP are petechiae, purpura and epistaxis, with a more severe progression to intracranial hemorrhage or gastrointestinal bleeding leading to a fatal outcome, if treatment is not started on a promptly manner. CMV induced thrombocytopenia in immunocompetent adults seems to be rare. we are presenting a case of CMV induced ITP which failed to improve after standard treatment with high dose steroids and IVIG but responded to anti-viral therapy with valganciclovir. In conclusion, it may be worthwhile to test for CMV infection in patients presenting with ITP. Further research is needed in order to establish treatment guidelines for CMV induced ITP in immunocompetent adults. Disclosures No relevant conflicts of interest to declare.

scholarly journals Which Is the Best Mobilizing Regimen in POEMS Syndrome? a Retrospective Italian Study of Two Haematological Centres

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5692-5692
Author(s):  
Francesco Autore ◽  
Nicola Piccirillo ◽  
Andrea Nozza ◽  
Idanna Innocenti ◽  
Rossana Putzulu ◽  
...  
Keyword(s):  
Body Weight ◽  
Cell Count ◽  
Conflicts Of Interest ◽  
Conditioning Regimen ◽  
Laboratory Data ◽  
Case Series ◽  
Poems Syndrome ◽  
High Dose ◽  
Data Set ◽  
Hematopoietic Stem

Abstract Introduction. POEMS syndrome is a rare paraneoplastic condition associated to an underlying plasmacellular dyscrasia. The use of alkylating agents and autologous peripheral blood stem cell transplantation (aPBSCT) seem to be the best strategy. At present aPBSCT should be considered the first line therapy in young patients with POEMS, eligible for high-dose Melphalan (HD-Mel), in absence of organ dysfunction. The best protocol to collect PBSC in patients affected by POEMS remains to be defined, because of the disease rarity and the heterogeneity of published case series. We therefore decided to combine the case series of our two institutions to describe and compare results and outcomes in order to contribute to the definition of the best CD34+ cell mobilization strategy. Patients and methods. We collected clinical and laboratory data of patients affected by POEMS syndrome undergoing hematopoietic stem cells (HSC) mobilization for aPBSCT from 2003 to 2018. Data were organized in order to perform a statistical analysis using "GraphPad Prism" GraphPad Software Inc., (5755 Oberlin Drive, #110, San Diego, CA 92121, USA). The COBE Spectra continuous flow cell separator (Terumo BCT, Shinagawa, Tokyo) was used for leukapheresis. Results. Our data set consisted of 25 patients, of whom 11 were mobilized using cyclophosphamide (CY) 4 g/m2 followed by granulocyte colony-stimulating factor (G-CSF) 5 μg/kg and 14 patients were mobilized using G-CSF 10 μg/kg for 5 days. All patients submitted to mobilization underwent collection procedure. Three patients, because of low CD34+ cells after the administration of G-CSF alone, were submitted to plerixafor infusion achieving a median pre-apheresis CD34+cell count of 28 cells collecting a median of 4.5 CD34+cell/kg body weight. All patient underwent aPBSCT after HD-Mel conditioning regimen receiving an infusion of 4.7 CD34+cell/kg body weight (range 1.5-8.4) and achieved a successful engraftment. At present all the patients are alive and in remission. In order to compare mobilization schedule we performed a comparison analysis between 11 patients receiving chemotherapy as mobilizing regimen versus 14 patients receiving only G-CSF. Data analysis according to mobilization schedule was reported in Table 1. Analysing mobilization efficacy, chemo-mobilized patients achieved a higher pre-apheresis CD34+ cell count (57 vs 33 cells/µl, p<0.05). This result allowed a significantly shorter procedure (2.3 TBV vs 3 TBC, p<0001). Patients receiving only G-CSF showed a WBC count significantly higher than chemo-mobilized patients (40.000 vs 8.140, p<0.05). The incidence of poor mobilization was low (3 out of 25 patients, 12%) and not statistically different between the two mobilization schedules. Discussion. The collection of these data allowed us to achieve one of the major series published in literature and to perform a comparison between two different approaches. The data suggest that both schemes (CY plus G-CSF vs. G-CSF alone) were able to harvest a sufficient CD34+ cell dose. Disclosures No relevant conflicts of interest to declare.

scholarly journals Fatal outcome of human influenza A (H5N1) is associated with high viral load and hypercytokinemia

2006 ◽  
Vol 12 (10) ◽  
pp. 1203-1207 ◽  
Author(s):  
Menno D de Jong ◽  
Cameron P Simmons ◽  
Tran Tan Thanh ◽  
Vo Minh Hien ◽  
Gavin J D Smith ◽  
...  
Keyword(s):  
Viral Load ◽  
Influenza A ◽  
Fatal Outcome ◽  
High Viral Load ◽  
Human Influenza

scholarly journals A Case Report of Refractory Immune Thrombocytopenia (ITP) Following Reduced Intensity Conditioning (RIC) Hematopoietic Cell Transplantation (HCT) for Myelodysplastic Syndrome (MDS) Successfully Treated with Off-Label Use of Daratumumab

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 4976-4976 ◽  
Author(s):  
Yazan Migdady ◽  
Ridhi Gupta ◽  
Asiri Ediriwickrema ◽  
Francisco Socola ◽  
Sally Arai ◽  
...  
Keyword(s):  
Platelet Count ◽  
Case Report ◽  
Peripheral Blood ◽  
Hematopoietic Cell Transplantation ◽  
Plasma Cells ◽  
Conflicts Of Interest ◽  
High Dose ◽  
Severe Thrombocytopenia ◽  
Antibody Testing ◽  
Bone Marrow Biopsies

Abstract Background: A source of treatment refractoriness in immune cytopenias appears to be residual CD138/38 positive lymphocyte populations (Audia S et al, Blood 118:4394-400,2011; Mahevas M et al, J Clin Invest 123:432-442, 2013). Persistence of recipient's plasma cells can lead to prolonged refractory thrombocytopenia following RIC-HCT. (Fasano RM et al, Br J Haematol 166(3):425-34, 2014). Daratumumab was effective in the treatment of a child with refractory autoimmune hemolytic anemia after HCT (Tolbert et al, Blood 128:4819, 2016). Case Report: The patient is a 60-year-old man with intermediate-high risk MDS who underwent RIC-HCT with total lymphoid irradiation and antithymocyte globulin with peripheral blood graft from a fully matched unrelated male donor. The patient had mild thrombocytopenia prior to HCT consistent with MDS and had not received platelet transfusions. He had not received any prior therapy for MDS. Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine and mycophenolate mofetil. Cytomegalovirus (CMV) serologic testing for exposure was negative for the recipient and positive for the donor. Both the patient and the donor had evidence for prior exposure to Epstein-Barr virus (EBV). He achieved engraftment on day +12. His peripheral blood chimerism on day + 30 showed full donor origin (WB 98%,CD3 96%,CD15 95%, CD19 98%, CD56 95%) and has been maintained to date. Acute skin GVHD responded to corticosteroids. While on corticosteroid therapy, he developed an abrupt decline in platelet count from 156,000/mcl on day +152 to 9, 000/mcl on Day + 166 without evidence for recurrent or active GVHD. While this was initially attributed to simultaneous EBV and CMV reactivations, severe thrombocytopenia persisted after viral clearance. An extensive work up for other etiologies of thrombocytopenia was negative. Repeated bone marrow biopsies were normal, including adequate megakaryocytosis and no MDS recurrence. Platelet associated antibody testing and platelet antigen genotyping were not conclusive for autoimmune versus alloimmune etiology. Testing for platelet HLA antibodies showed calculated Panel Reactive Antibody of 31% and unsatisfactory corrected count increment after transfusion of HLA compatible platelets units. The patient experienced prolonged severe thrombocytopenia for over 26 weeks with platelet count less than 5000/mcl for 22 weeks and only above 10,000 /mcl on 6 occasions. Potentially responsible medications were discontinued serially, but testing for drug inducted ITP was not conducted. Therapy included high dose corticosteroids, high dose immune globulin, rituximab, plasma exchange, splenectomy, romiplostim 10 mcg/kg/week, eltrombopag 100 mg to 150 mg daily for over 24 weeks, and low dose danazol. Fostamatinib was not available. Prednisone dose was tapered over many weeks to 5 mg daily. The patient experienced recurrent life-threatening and vision-threatening bleeding. Cumulative transfusions following Day + 166 were 133 single donor platelet units and 42 red cell units. All products were from CMV negative donors. Eltrombopag and danazol were deemed ineffective and tapered to discontinuation. CD38 positive cells were present in spleen and marrow by immunohistochemistry. Daratumumab 1300 mg was infused weekly x 4. Four weeks after the last dose of daratumumab, his platelet count increased to 91,000/mcl. Platelet count normalized to 150,000/mcl in week 5 or HCT Day + 383. Hypogammaglobulinemia has been the only detectable toxicity. Testing to determine autoimmune versus alloimmune origin is ongoing. Conclusion: Clinical trials of daratumumab for the treatment of severe refractory ITP are indicated. Disclosures No relevant conflicts of interest to declare.

Thrombocytopenia and Human Immunodeficiency Virus in Children

PEDIATRICS ◽  
1988 ◽  
Vol 82 (6) ◽  
pp. 905-908
Author(s):  
Maadhava Ellaurie ◽  
Edward R. Burns ◽  
Larry J. Bernstein ◽  
Kiran Shah ◽  
Arye Rubinstein
Keyword(s):  
Human Immunodeficiency Virus ◽  
Platelet Count ◽  
Oral Prednisone ◽  
Fatal Outcome ◽  
Spontaneous Remission ◽  
High Dose ◽  
Sustained Remission ◽  
Platelet Counts ◽  
Immunodeficiency Virus ◽  
Clinically Significant

Thrombocytopenia occurs in 13% of children with symptomatic human immunodeficiency virus (HIV) infection. The clinical and laboratory course of 19 children infected with HIV with thrombocytopenia is described. Bone marrow aspirates showed normal to increased numbers of megakaryocytes. Levels of antiplatelet antibodies were increased in 80% of the children and circulating immune complexes were found in 74%. Clinically significant hemorrhage leading to anemia occurred in five patients, and CNS bleeding led to a fatal outcome in an additional three children. Spontaneous remission of thrombocytopenia occurred in three of the 19 subjects. High-dose IV γ globulin was effective in increasing the platelet counts of six of 15 patients (40%) but resulted in a sustained remission in only one subject. Oral prednisone was effective in increasing the platelet count of two thirds of those whose platelet counts could not be controlled by IV γ-globulin. Bleeding manifestations were eliminated in all patients whose platelet counts increased significantly. Of the 11 children whose counts increased either spontaneously or as a result of therapy, eight remain alive (72%). In contrast, all of the eight patients whose platelet counts did not improve have died. Thrombocytopenia in children with HIV disease is engendered by immune mechanisms and is a major cause of morbidity and mortality. High-dose IV γ-globulin and/or corticosteroids are temporarily effective in increasing the platelet count and reducing bleeding in about half of thrombocytopenic patients and are recommended for use. The ability to respond to therapy correlates with improved survival.

Comparison of Intravenous Immune Globulin and High Dose Anti-D Immune Globulin as Initial Therapy for Childhood Immune Thrombocytopenic Purpura.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3434-3434
Author(s):  
Ian Kane ◽  
Dominic Ragucci ◽  
Ibrahim Shatat ◽  
Ram Kalpatthi
Keyword(s):  
Platelet Count ◽  
Partial Response ◽  
Treatment Failure ◽  
Treatment Response ◽  
Immune Globulin ◽  
Intravenous Immune Globulin ◽  
High Dose ◽  
Severe Anemia ◽  
First Line ◽  
Thrombocytopenic Purpura

Abstract Background: Intravenous immune globulin (IVIG) and anti-D immune globulin are common first line therapies for pediatric immune thrombocytopenic purpura (ITP). Recently, a prospective randomized study in childhood ITP showed that high dose anti-D immune globulin (75 mcg/kg) was superior to the standard dose (50 mcg/kg) and as effective as IVIG (Tarantino et al Journal of Pediatrics, 2006). Since then, high dose anti-D immune globulin is being increasingly used in children with ITP. However, anti-D immune globulin can be associated with hemolysis and other side effects, especially at higher doses. We review our experience with IVIG and high dose anti-D immune globulin as initial treatment of childhood ITP. Methods: We retrospectively reviewed the electronic medical records of children diagnosed with ITP between January 2003 and May 2008. We collected demographic data, complete blood counts, treatment details, adverse drug reactions (ADRs), and long-term outcome of these patients. Patients received either intravenous immune globulin (1 g/kg) or anti-D immune globulin (75 mcg/kg). All patients included received premedication with acetaminophen and diphenhydramine prior to either treatment. Response was defined by rise in platelet count after one dose or within 7 days of treatment; treatment failure = platelets<30,000/cmm, partial response= 30,000/cmm<platelets<50,000 response=”platelets” full=”” and=”” cmm,=””>50,000/cmm. Results: A total of 53 patients were included for analysis (Table 1). Both groups had similar treatment response and there was no statistical difference in their initial presentation (presence of wet purpura, baseline platelet count, and hemoglobin), length of hospital stay, need for additional treatments, or development of chronic ITP. However, patients who received anti-D immune globulin experienced a higher rate of ADRs, particularly chills and rigors. In addition, 2 patients in the anti-D immune globulin group developed severe anemia requiring medical intervention. One of these 2 patients had hemoglobinuria consistent with intravascular hemolysis. Also, patients with wet purpura had higher rates of treatment failure (32%) compared to those without wet purpura (6%), regardless of the treatment modality. Conclusions: Our study confirms that both IVIG and high dose anti-D immune globulin are effective first line therapies in childhood ITP. However, we observed increased ADRs in the high dose anti-D group in contrast to previously published reports. Further studies are needed to evaluate the safety of high dose anti-D immune globulin and determine the utility of using wet purpura to predict treatment failure. Table 1: Clinical and laboratory characteristics of study patients Parameters Anti-D 75 mcg/kg (n=24) IVIG 1mg/kg (n=29) P value </platelets<50,000> Males, Females 15, 9 13, 16 0.27 Initial platelet count (103/cmm) (25%, 75%) 6 (3, 11) 7 (3.5, 14.5) 0.41 Initial hemoglobin (g/dL) ± SD 12.0 ± 1.3 11.9 ± 1.7 0.78 Treatment Response
 Failure
 Partial response
 Full response
 Unable to determine 5 (21%)
 10 (42%)
 9 (38%)
 0 (0%) 4 (14%)
 9 (31%)
 15 (52%)
 1 (3%) 0.50 Hemoglobin decrease (g/dL) ± SD 2.23 ± 1.6 1.24 ± 0.8 0.01 Adverse drug reaction, total 14 (58%) 6 (21%) 0.01 Fever 4 (17%) 2 (7%) 0.25 Chills/rigors 9 (38%) 3 (10%) 0.02 Nausea/vomiting 5 (21%) 2 (7%) 0.14 Headache 1 (4%) 3 (10%) 0.38 Severe anemia requiring intervention 2 (8%) 0 (0%) 0.20

Cold Hemagglutinin Hemolysis and Hypercoagulable State Due to Mycoplasma Pneumoniae.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 5094-5094
Author(s):  
Gaurav Gulati ◽  
Anthony A Donato ◽  
Shuchi Gulati ◽  
Daniel A Forman
Keyword(s):  
Platelet Count ◽  
Hemolytic Anemia ◽  
Mycoplasma Pneumoniae ◽  
Skin Necrosis ◽  
Conflicts Of Interest ◽  
Anticardiolipin Antibody ◽  
The United States ◽  
Cold Agglutinin ◽  
High Dose ◽  
Superficial Skin

Abstract Abstract 5094 Introduction Mycoplasma pneumoniae is responsible for 7 to 20% of community-acquired pneumonia in the United States. Up to 25% of patients develop extra-pulmonary complications. Hemolytic anemia associated with multiple vascular thromboses is a rare but severe complication of Mycoplasma pneumoniae. We present a case of cold agglutinin-associated hemolysis and skin necrosis. Case Presentation An 81 year-old male on Coumadin for atrial fibrillation who recently returned from a cruise, developed non productive cough without fever and dyspnea. He was treated with a course of azithromycin. One week later he developed bruising and skin de-pigmentation of the tips of the pinnae and tip of the nose. On presentation to the emergency department, his physical exam was unremarkable except for these finding and mild rhonchi over his right posterior chest. Laboratory workup revealed a Hemoglobin of 13.5 g/ dL, leukocytosis of 23,700 c/mm3 and platelet count of 57,000 c/mm3. Moderate renal insufficiency was also present with a creatinine of 2.02. Evaluation of peripheral smear revealed mild Schistiocytosis with anisopoikilocytosis. Within 1 week, hemoglobin dropped to 7.4, platelet count reached a nadir of 16,000. Hemolytic parameters included LDH of 647 IU/L with haptoglobin of 26 mg/dL, and reticulocyte count of 1.3%. Total complement levels were severely depressed at 4 U/ml (normal: 30 to 75 U/ml), while there was a slight decrease in C4 complement levels and the C3 levels were normal. Immunoglobulin levels were within limits and cryofibrogen was negative. ANA, anticardiolipin antibody, myeloperoxidase and p ANCA levels showed normal titers. A bone marrow biopsy showed hypercellular marrow with erythroid hyperplasia. Urine Strep. pneumoniae antigen was negative. Cold agglutinin titers were done, which were negative. Due to our strong suspicion for mycoplasma-related cold agglutinin hemolysis, we repeated cold agglutinin titers which turned positive very slowly on prolonged standing. The patient was treated with high dose prednisone and received multiple sessions of plasmapheresis which improved his condition and platelet counts returned to baseline with LDH and haptoglobin levels trending back to normal. Discussion Our patient had a wide differential ranging from Coumadin induced skin necrosis, auricular perichondritis, frost bite, local infections, TTP/ HUS syndrome, and Wegner's granulomatosis. But the clinical presentation of superficial skin necrosis of peripheral skin along with the presence of low complement, recent chest infection, hemolytic anemia and thrombocytopenia with acute renal failure all contributed to our final diagnosis confirmed by the presence of slow reactive Coomb's direct anticoagulation test and supported by improvement with plasmapheresis and steroid therapy. The astute clinician should always remember mycoplasma infection in setting of acute onset hemolytic anemia and suspect it in recently treated chest and sinus infections. Disclosures No relevant conflicts of interest to declare.

scholarly journals Coinfection of Parvovirus B19 with Influenza A/H1N1 Causes Fulminant Myocarditis and Pneumonia. An Autopsy Case Report

Pathogens ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 958
Author(s):  
Domitille Callon ◽  
Fatma Berri ◽  
Anne-Laure Lebreil ◽  
Paul Fornès ◽  
Laurent Andreoletti
Keyword(s):  
Viral Load ◽  
Influenza A ◽  
Acute Myocarditis ◽  
Parvovirus B19 ◽  
Fatal Outcome ◽  
High Viral Load ◽  
Viral Reactivation ◽  
Fulminant Myocarditis ◽  
Viral Interactions ◽  
Influenza A H1n1

Parvovirus-B19 (PVB19) is a frequent causative agent of myocarditis. For unclear reasons, viral reactivation can cause acute myocarditis, a leading cause of sudden death in the young. Influenza A/H1N1(2009) virus (IAV/H1N1) is known for causing flu/pneumonia, but the heart is rarely involved. Co-infections of cardiotropic viruses are rarely reported and the mechanisms of viral interactions remain unknown. A 5-year old girl had a flu-like syndrome, when she suddenly presented with a respiratory distress and cardiac arrest. At autopsy, the lungs were found haemorrhagic. Lungs’ histology showed severe bronchiolitis, diffuse haemorrhagic necrosis, and mononuclear inflammation. In the heart, a moderate inflammation was found with no necrosis. IAV/H1N1 was detected in nasal and tracheal swabs, lungs, and the heart. The viral load was high in the lungs, but low in the heart. PVB19 was detected in the heart with a high viral load. Viral co-infection increases the risk of severe outcome but the mechanisms of interaction between viruses are poorly understood. In our case, viral loads suggested a reactivated PVB19-induced acute myocarditis during an IAV/H1N1 pneumonia. Viral interactions may involve an IAV/H1N1-induced cytokine storm, with a fulminant fatal outcome. Clinically, our case shows the importance of investigating inflammatory pathways as therapeutic targets.

A Comparative Retrospective Survey of Reinduction Chemotherapy Regimens for Acute Myeloid Leukemia (AML) in First Relapse: A Single-Institution Experience

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4273-4273 ◽  
Author(s):  
Andrew Brunner ◽  
Hossein Sadrzadeh ◽  
Lillian Werner ◽  
Karen K. Ballen ◽  
Yi-Bin A. Chen ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Conflicts Of Interest ◽  
Laboratory Data ◽  
Categorical Variables ◽  
High Dose ◽  
Single Institution ◽  
Significant Difference ◽  
First Relapse ◽  
Acute Myeloid

Abstract Abstract 4273 Introduction: Relapsed acute myeloid leukemia (AML) carries a poor prognosis. Although most newly diagnosed patients with AML achieve a complete remission after initial induction (CR1) using standard chemotherapy regimens, relapse follows in the majority of cases. The optimal reinduction chemotherapy regimen for patients following relapse remains unknown, and there is little comparative data to guide selection between various available reinduction regimens. The current study is a single-institution retrospective review over a 10 year period, which seeks to compare rates of response, disease-free survival (DFS) and overall survival (OS) between different reinduction regimens among patients with AML in first relapse. Methods: We performed a retrospective chart review of patients with AML who relapsed following CR1, and who were treated with reinduction chemotherapy at our institution between January 1, 2000, and December 31, 2010. Our patients were categorized into four groups based upon the type of reinduction chemotherapy they received: MEC (mitoxantrone, etoposide, cytarabine) or similar etoposide-containing regimens, 7+3 (infusional cytarabine and anthracycline) or 7+3-based regimens, HiDAC (high-dose cytarabine)-based regimens, and “other” combinations (less frequently used regimens including cytarabine and topotecan; decitabine; gemtuzumab; mitoxantrone and etoposide). Patients were identified using medical billing diagnosis codes, and included if they were above age 18 at diagnosis, obtained CR1 but experienced subsequent relapse, and were treated during first relapse with reinduction with intent to achieve remission. Exclusion criteria included patients with acute promyelocytic leukemia, primary refractory disease, and patients who were given chemotherapy for persistent disease on a mid-treatment bone marrow biopsy. Information about date of diagnosis, treatment regimens, tumor cytopathology and histology, comorbidities at diagnosis, and presenting laboratory data were collected. Statistical analysis was performed using the Kaplan-Meier method, and log rank tests where appropriate, to analyze DFS and OS. Fisher’s exact test was used to assess the associations between categorical variables. Results: We identified 66 patients who were treated with reinduction chemotherapy for AML in first relapse; of these, 28 (42%) achieved CR2. The type of reinduction chemotherapy received was not associated with any difference in the rates of CR2 (p=0.19). Patients who achieved CR2 had a median DFS of 5.1 months. For all patients, including those who failed to achieve CR2, the median OS following reinduction was 4.9 months. There was no significant difference in OS between re-induction regimens (p=0.09). However, there was a statistically significant difference in median DFS depending on regimen (p=0.006). Patients who received 7+3-based regimens, and to a lesser degree MEC, had longer median DFS than HiDAC-based regimens (8.9, 3.4, and 2.0 months, respectively). Patients who received 7+3-based re-induction regimens had a longer duration of preceding CR1 (p=0.006). Longer duration of CR1 (≥7.4 months, the median in our data) was associated with higher rate of CR2 (61% vs 22%, p=0.03) and OS (8.9 vs 2.9 months, p=0.0006) compared to duration of CR1 <7.4 months. Patients who were given “other” regimens (including demethylating therapies) were on average older (62 years old compared to 50, 52, and 54 years old in other groups); however, they had CR2 rates and OS similar to patients receiving 7+3, MEC, or HiDAC-based regimens. Conclusion: According to this retrospective analysis, patients treated with MEC or 7+3-based reinduction chemotherapy regimens had improved DFS compared to patients given HiDAC-based regimens. However, as expected, patients treated with 7+3-based reinduction chemotherapy were also more likely to have experienced a longer duration of CR1. Longer CR1 (≥7.4 months) was associated with improved DFS and OS following reinduction chemotherapy. It remains unclear whether the improved DFS seen in those AML patients who received 7+3-based regimens is due to the type of chemotherapy, or if this is related to the characteristics of their underlying disease, as manifested by the longer duration of CR1 seen in this treatment group. Our data does suggest that MEC may be preferable to HiDAC-based regimens for patients with early relapse following CR1. Disclosures: No relevant conflicts of interest to declare.

Presentation and Outcome of Idiopathic Thrombocytopenic Purpura in Children: A Single Institution Experience

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4683-4683
Author(s):  
Kari Bradham ◽  
Felicia L. Wilson ◽  
Hamayun Imran
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Idiopathic Thrombocytopenic Purpura ◽  
Conflicts Of Interest ◽  
Laboratory Data ◽  
Bone Marrow Examination ◽  
Published Data ◽  
Thrombocytopenic Purpura ◽  
Chronic Itp ◽  
Increased Risk

Abstract Abstract 4683 PURPOSE: To review the presenting features, response to treatment and outcome in children diagnosed with idiopathic thrombocytopenic purpura (ITP) at the University of South Alabama, Children’s and Women’s Hospital and Specialty Clinic. METHODS: Using ICD code 287.3, data were collected from the specialty clinic’s medical records and hospital database for children diagnosed with ITP between January 2005 and September 2010. Recurrent and chronic ITP were defined as thrombocytopenia recurring within or more than 6 months of diagnosis, respectively. Univariate and multivariate logistic regression analyses were performed to evaluate variables associated with chronic ITP. RESULTS: Eight four patients were identified (M,F 1:1) with an average age of 70 months at diagnosis. Mean platelet count at presentation was 14k. Oral or nasal mucosal bleeding occurred in 19(23%) patients but none experienced a serious hemorrhage. Thirty three (39%) patients had an associated illness prior to diagnosis of ITP. Treatment consisted of intravenous immunoglobulin (IVIG) in 38(45%), WinRho in 11(13%), IVIG or WinRho followed by the other in 20(24%), data not available 8(10%) and no therapy in 7 patients (8%). Average platelet count at discharge and within 2 weeks after IVIG and WinRho was 57k, 337k and 57k, 375 respectively. Forty three (51%) were acute, 17(20%) became recurrent, and 24(29%) became chronic ITP. Bone marrow examination was performed in 26(30%) patients upon subsequent relapse but the diagnosis remained unaltered in all cases. Rituximab therapy was provided to five and splenectomy was performed in 7 patients. Four patients failed both modalities, all of whom currently are IVIG dependant. Age <5year (OR 0.12, 95%CI 0.22, 0.67, p=0.01) was protective against development of chronic ITP while platelet count >20k at presentation (OR 6.50, 95%CI 1.35, 31.30, p=0.02) and race other than white (OR 36.63, 95%CI 4.61, 291.09, p=0.001) were found to be significantly associated with the development of chronic ITP. Gender, mean platelet volume, total white cell count, and absolute lymphocyte count had no significant association. CONCLUSION: Our study supports the published data that patients with an initial platelet count >20k, older age and non-white race have an increased risk of progression to chronic ITP. Other published variables had no significant association in our analyses. Response to IVIG and WinRho was no different in our patients while rituximab or splenectomy did not lead to a complete resolution in refractory cases. Since bone marrow examination did not alter the diagnosis in any patient, we suggest that routine performance of this procedure may be omitted when a diagnosis of ITP is consistent with clinical history, physical examination and laboratory data. Disclosures: No relevant conflicts of interest to declare.

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