Laboratory and Bone Marrow Evaluation in Patients with Cancer

1998 ◽  
Vol 5 (2_suppl) ◽  
pp. 12-16 ◽  
Author(s):  
Lynn C. Moscinski
Keyword(s):  
Bone Marrow ◽  
Laboratory Findings ◽  
Patients With Cancer ◽  
Bone Marrow Evaluation ◽  
Bone Marrow Histopathology ◽  
Multiple Causes

Anemia in patients with cancer has multiple causes. Since establishing a diagnosis can be difficult, evaluation via laboratory findings and bone marrow histopathology is often necessary. Cytopenias can result either directly or indirectly from the malignancy, or they occasionally are the result of other causes, such as AIDS or infection.

scholarly journals Pancytopenia in a child with cystic fibrosis and severe copper deficiency: Insight from bone marrow evaluation

2021 ◽  
Author(s):  
Maggie D. Seblani ◽  
Susanna A. McColley ◽  
Shunyou Gong ◽  
Lee M. Bass ◽  
Sherif M. Badawy
Keyword(s):  
Cystic Fibrosis ◽  
Bone Marrow ◽  
Copper Deficiency ◽  
Bone Marrow Evaluation

scholarly journals Optimizing Response to Enasidenib with Dose Escalation: Case Series

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 3-5
Author(s):  
Amany R. Keruakous ◽  
Sarah A. Schmidt ◽  
Marcus T. Autry ◽  
Pragathi Balakrishna ◽  
Julia Ye ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dose Escalation ◽  
Karyotype Analysis ◽  
Standard Dose ◽  
Case Series ◽  
Bone Marrow Evaluation ◽  
Poor Risk ◽  
Daily Dose ◽  
Variant Frequency ◽  
Idh2 Mutation

Background: Isocitrate dehydrogenase enzymes catalyze the conversion of isocitrate to alpha-ketoglutarate. Mutated IDH enzymes generate the "oncometabolite" 2-hydroxyglutarate (2-HG), which inhibits TET2 function. IDH2 mutations have been reported in 9% to 19% of acute myeloid leukemia (AML) cases. Inhibition of the mutant IDH2 enzyme led to decreased 2-HG levels and induced myeloid differentiation in IDH2 mutant AML. Enasidenib, a small-molecule inhibitor of mutant IDH2, was approved in 2017, after a successful phase I/II trial showing an overall response rate (ORR) of 40.3% in relapsed/refractory (R/R) disease, with 19.3% of patients achieving complete remission (CR). A Phase III trial is currently ongoing. It targets the mutant IDH2 variants R140Q, R172S, and R172K; at an approved dose of 100 mg oral daily dose. At higher doses the drug was less tolerated, however, few subjects received dose modification at the 650 mg daily dose group; these events did not qualify as a dose-limiting toxicity (DLT). In this descriptive study, we are reporting a case series of R/R AML, with an IDH2 mutation, that are treated with escalated dose enasidenib. Method: This case series is based on retrospective observations of patients with R/R IDH2 mutant AML since January 2017, who are treated with enasidenib. We are reporting two cases treated with an escalated dose of 200 mg daily. We included patients with intermediate to poor-risk AML, who received at least one prior line of therapy, started on standard dose enasidenib (100 mg daily) for a minimum of 6 months and followed until disease relapse or death. We excluded patients who are primarily resistant to enasidenib (AML risk stratification and response evaluation by ELN-Leukemia NET. IDH2 mutations were identified by a local diagnostic laboratory that is regulated under CLIA through PCR which is validated to detect 10% or more mutant allele frequency. To quantify IDH2 variant frequency, confirmatory testing was performed via ARUP next-generation sequencing panel (NGS). Results: Here we report the descriptive outcomes of 2 cases from a single institution, who were treated with escalated dose enasidenib (200 mg oral daily) for R/R AML with an IDH2 mutation. The first case describes a 65-year-old female diagnosed with poor-risk AML in the setting of pancytopenia with bone marrow evaluation consistent with the background of erythroid and granulocytic dysplasia, with normal karyotype analysis. The patient has treated with induction chemotherapy and 2 cycles consolidation that was complicated with bacterial infections, prolonged hospitalization, and profound deconditioning led to stopping treatment. After 18 months of surveillance, repeat bone marrow evaluation for new-onset pancytopenia revealed relapsed AML with evidence of IDH2 mutation at codon 140, with a variant frequency of 36.9% by NGS. The case was started on enasidenib at 100 mg oral daily dose. After 6 months of therapy, the patient continued to be cytopenic, repeated bone marrow evaluation showed residual AML with IDH2 variant frequency of 27.6%. The decision was made to increase the enasidenib dose to 200 mg daily. With follow up for another 5 months on the escalated dose, the patient achieved hematologic complete response (hCR) with normalization of peripheral platelet count and ANC. [Figures 1-2] The patient maintained hCR for another 5 months on 200 mg enasidenib daily until she died from COVID-19 infection. The second case describes a 59-year-old female with poor-risk AML in the setting of leukocytosis, with bone marrow evaluation consistent with the background of megakaryocytic dysplasia and karyotype analysis positive for monosomy 7. The patient was treated with induction chemotherapy and failed to respond. Repeat bone marrow evaluation showed primary refractory disease with positive IDH2 mutation at codon 140 with a variant frequency of 40.7%. Treatment with 100 mg enasidenib was started. The patient maintained a partial response for 6 months, then peripheral blasts counts started to gradually increase. The decision was made to increase enasidenib dose to 200 mg daily, which improved peripheral blasts within one month of escalated dose therapy. [Figure 3] The patient maintained a response to therapy for another 3 months before she relapsed. Conclusion: Our limited data showed that initial response to standard dose enasidenib could potentially be optimized by dose escalation to 200 mg daily. Disclosures No relevant conflicts of interest to declare.

scholarly journals Alemtuzumab Plus Cyclosporine Treatment of the Autoimmune Hemolytic Anemia in an Adult Bowel Transplant

2014 ◽  
Vol 2014 ◽  
pp. 1-4
Author(s):  
A. Lauro ◽  
M. Stanzani ◽  
C. Finelli ◽  
C. Zanfi ◽  
M. C. Morelli ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Hemolytic Anemia ◽  
Bone Marrow Biopsy ◽  
Autoimmune Hemolytic Anemia ◽  
Leukocyte Count ◽  
Pure Red Cell Aplasia ◽  
Febrile Episode ◽  
High Dose ◽  
Laboratory Findings ◽  
Transfusion Requirements

An adult male underwent a bowel transplant for tufting enteropathy, receiving alemtuzumab, tacrolimus, and steroids as immunosuppressants. Five years later, he developed an autoimmune hemolytic anemia (AIHA), anti-IgG positive, with reduced reticulocyte count, leukopenia, and thrombocytopenia with antiplatelet antibodies. After an unsuccessful initial treatment with high dose steroids, reduction in tacrolimus dose, and intravenous immunoglobulin (IVIG), a bone marrow biopsy revealed absence of erythroid maturation with precursor hyperplasia. The patient was switched to sirolimus and received four doses of rituximab plus two courses of plasmapheresis, which decreased his transfusion requirements. After a febrile episode one month later, the AIHA relapsed with corresponding decreases in platelet and leukocyte count: cyclosporine A (CsA) was started with a second course of rituximab and IVIG without response, even though repeat bone marrow biopsy did not reveal morphology correlated to an acquired pure red cell aplasia (APRCA). Considering the similarity in his clinical and laboratory findings to APRCA, alemtuzumab was added (three doses over a week) with CsA followed by steroids. The patient was eventually discharged transfusion-independent, with increasing hemoglobin (Hb) levels and normal platelet and leukocyte count. One year later he is still disease-free with functioning graft.

Abstract 193: Hemophagocytic lymphohistiocytosis following kawasaki disease:Differential Diagnosis in IVIG Refractory Kawasaki Disease

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Hyun Ok Jun ◽  
Eun Kyung Cho ◽  
Jeong Jin Yu ◽  
So Yeon Kang ◽  
Chang Deok Seo ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Coronary Artery ◽  
Kawasaki Disease ◽  
Skin Rash ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Clinical Symptoms ◽  
Early Recognition ◽  
Cervical Lymphadenopathy ◽  
Inflammatory Disorder ◽  
Laboratory Findings

Introduction: Hemophagocytic lymphohistiocytosis(HLH) is a systemic inflammatory disorder characterized by uncontrolled histiocytic proliferation, hemophagocytosis and up-regulation of inflammatory cytokines. Thus, both HLH and Kawasaki disease(KD) are characterized by prolonged fever, and are diagnosed by a clinical and laboratory scoring system, concurrent manifestation of HLH and KD has been described in the literature. We describe two cases of children who diagnosed as KD initially, but after intravenous gamma globulin(IVIG) failed to produce clinical response, were found to have HLH. Case report: A 3-year-old boy who had previous KD history 5 months ago was admitted for 9day fever and skin rash. His symptoms were fulfilled KD criteria, and echocardiography showed dilated right coronary artery of 4.2mm. He was treated with 2 cycles of IVIG until fever subsided. However, 2 days later, he got fever again and cytopenia(Hb<9.0), hypertriglyceridemia, high level of ferritin was shown and had splenomegaly on physical examination. In the suspicion of HLH, bone marrow biopsy was done and revealed hemophagocytosis, consistent with HLH. A second case of 11-month-old boy admitted for 8-day fever with Kawasaki feature. Although, he showed incomplete feature(fever, skin rash, conjunctival injection, cervical lymphadenopathy), echocardiography showed dilated left main coronary artery(3.5mm) and treated with IVIG. However, 2days after IVIG administration, he was still pyrexial. The laboratory findings fulfilled 5 diagnostic criteria of HLH; bicytopenia(anemia, thrombocytopenia), hypofibrinogenemia, hyperferritinemia, hemophagocytosis in bone marrow, raised level of soluble IL-2 receptor. In both cases, the patients treated according to the HLH protocol 2004, and after that clinical symptoms and laboratory findings were improved. Several causes of febrile illness, EBV, CMV, rubella, parvo-viral infection, for example, were excluded. Comment: There is considerable overlap between the clinical syndromes of KD and HLH and early recognition and treatment of these two disease entity is imperative to avoid fatal outcomes in severe cases. Thus, these should both be considered and excluded in any child with unremitting fever and rash.

Bone Marrow Evaluation for Lymphoma

2011 ◽  
pp. 887-917 ◽  
Author(s):  
Beverly P. Nelson ◽  
LoAnn C. Peterson
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Evaluation

scholarly journals Chronic myelodysplastic syndrome (preleukemia) with the Philadelphia chromosome

Blood ◽  
1980 ◽  
Vol 56 (2) ◽  
pp. 262-264 ◽  
Author(s):  
DG Roth ◽  
CM Richman ◽  
JD Rowley
Keyword(s):  
Bone Marrow ◽  
Myelodysplastic Syndrome ◽  
Bone Marrow Cells ◽  
Philadelphia Chromosome ◽  
Laboratory Findings ◽  
Chronic Granulocytic Leukemia ◽  
Hematologic Disorder ◽  
Erythroid Hyperplasia ◽  
Granulocytic Colony

Abstract A patient with severe anemia, reticulocytopenia, and erythroid hyperplasia of the bone marrow developed fatal acute nonlymphocytic leukemia after 3 yr. A Philadelphia chromosome with the typical 9/22 translocation t(9q +;22q-) was identified by banding techniques in a small number of bone marrow cells throughout the preleukemic phase of the illness (14%--38% of metaphases) and during the acute transformation (50%). Granulocytic colony formation in vitro was abnormal in the preleukemic phase. The diagnosis of chronic granulocytic leukemia was excluded on the basis of clinical and laboratory findings. The identification of the Ph1 chromosome in this form of chronic myelodysplastic syndrome (preleukemia) provides a new example of a hematologic disorder predisposing to acute leukemia in which this chromosomal abnormality occurs.

scholarly journals Rare Variant of Lipid Storage Disorders

Blood ◽  
1970 ◽  
Vol 35 (4) ◽  
pp. 533-538 ◽  
Author(s):  
PARVIN SAIDI ◽  
SADEGH P. AZIZI ◽  
REYHANALLAH SARLATI ◽  
NASROLAH SAYAR
Keyword(s):  
Bone Marrow ◽  
Mental Retardation ◽  
Macular Degeneration ◽  
Rare Variant ◽  
Lipid Storage ◽  
Laboratory Findings ◽  
Storage Disorders ◽  
Morphologic Appearance

Abstract A 16-year-old boy with brownish pigmentation of the skin, bilateral pingueculae, macular degeneration, hepatosplenomegaly, suggested mental retardation, and abnormal histiocytes in the bone marrow and liver is presented. The morphologic appearance of the histiocytes is unique and specific, and so far only six similar cases have been reported in the literature. The contents of these histiocytes are thought to be phospholipids and glycolipids of sphingomyelin and cerebroside variety, respectively. The significance of the clinical and laboratory findings of these cases and the possible relationship to the lipid storage disorders are discussed.

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