scholarly journals Clinicohematological Study of Thrombocytosis in Children

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Nathiya Subramaniam ◽  
Suneel Mundkur ◽  
Pushpa Kini ◽  
Nalini Bhaskaranand ◽  
Shrikiran Aroor

Introduction. Primary thrombocytosis is very rare in children; reactive thrombocytosis is frequently observed in children with infections, anemia, and many other causes. Aims and Objectives. To identify the etiology of thrombocytosis in children and to analyze platelet indices (MPV, PDW, and PCT) in children with thrombocytosis. Study Design. A prospective observational study. Material and Methods. A total of 1000 patients with thrombocytosis (platelet > 400×109/L) were studied over a period of 2 years. Platelet distribution width (PDW), mean platelet volume (MPV), and plateletcrit (PCT) were noted. Results. Of 1000 patients, 99.8% had secondary thrombocytosis and only two children had primary thrombocytosis (chronic myeloid leukemia and acute myelogenous leukemia, M7). The majority of the children belonged to the age group of 1month to 2 years (39.7%) and male to female ratio was 1.6 : 1. Infection with anemia (48.3%) was the most common cause of secondary thrombocytosis followed by iron deficiency alone (17.2%) and infection alone (16.2%). Respiratory infection (28.3%) was the predominant infectious cause observed. Thrombocytosis was commonly associated with IDA among all causes of anemia and severity of thrombocytosis increased with severity of anemia (P=0.021). With increasing platelet count, there was a decrease in MPV (<0.001). Platelet count and mean PDW among children with infection and anemia were significantly higher than those among children with infection alone and anemia alone. None were observed to have thromboembolic manifestations. Conclusions. Primary thrombocytosis is extremely rare in children than secondary thrombocytosis. Infections in association with anemia are most commonly associated with reactive thrombocytosis and severity of thrombocytosis increases with severity of anemia.

2020 ◽  
Vol 8 (A) ◽  
pp. 660-665
Author(s):  
Marwa Abdulnabi ◽  
Enass Abdul Kareem Dagher Al-Saadi

AIM: The aim of this study was to measure the prevalence of myeloproliferative disorders in a sample of Iraqi patients and to measure the changes in patients’ blood parameters. BACKGROUND: Myeloproliferative disorders are a group of neoplasms affecting the bone marrow progenitor cells characterized by excess cells with a risk of transforming to acute leukemia. There is a gap in knowledge about the prevalence of Iraqi population. Thus, we investigated the prevalence and distribution of different types of myeloproliferative disorders in a sample of Iraqi patients. MATERIALS AND METHODS: Cross-sectional study is done at the National Center of Hematology from November 2019 till March 2020 on 75 patients who were diagnosed by a specialist hematopathologist to have one subtype of myeloproliferative disorders (MPDs). Blood samples were taken from them and analyzed to get complete blood count, blood film, bone marrow aspirate, and biopsy that were analyzed for each patient. Blood samples were taken from them and analyzed in terms of blood indices, which include red blood cells, white blood cells, and platelets. RESULTS: The 75 patients were found to be comprising 35 chronic myelogenous leukemia (CML) patients (46.7%), myelofibrosis 22 patients (29.3%), essential thrombocythemia (ET) 9 patients (12%), and polycythemia vera (PV) 9 patients (12%). In terms of male/female ratios, they were as follows: Myeloproliferative neoplasms (MPNs) male-to-female ratio is 1.2, CML= 0.94, myelofibrosis= 2.14 and ET= 0.5 and PV male-to-female ratio is 2. CONCLUSIONS : MPN male-to-female ratio in Iraq, which is 1.2, CML is the most common subtype. Regarding myelofibrosis, in our study, the male-to-female ratio is 2.14, which is much higher other countries. This could be attributed to high exposure to benzene and toluene which are well known to be causative agents for myelofibrosis. Regarding ET or PV, the male-to-female ratios were compatible with other countries.


2020 ◽  
Vol 8 (1) ◽  
pp. 93-99
Author(s):  
Balaji Varaprasad Mallula ◽  
Jithender Reddy Chintala ◽  
Srinadh Boppanna ◽  
S. Annapurna

Background: Stroke is the second single most common cause of death in the world causing approximately 6.7 million deaths each year. It has a greater disability impact on an individual than any other chronic disease. The aim of the study is to review the value of CTA in detection and evaluation of non-traumatic cervicocerebral vascular disease (stroke). Subjects & Methods: A prospective observational study conducted in the Department of Radiodiagnosis, Kamineni Hospitals, L.B. Nagar, Hyderabad over 60 patients during April 2016 to May 2017. Results: Out of 60 patients, 35(58.3%) patients had ischemic stroke, 25(41.6%) had hemorrhagic stroke. Overall stroke was seen mostly in the age group of 61-70 (28.3%) years, with a Male to female ratio of 3:2. Conclusion: Hypertension was the most common risk factor associated with this disease, followed by diabetes. CTA helps in accurate diagnosis, risk stratification and planning management protocols.


2006 ◽  
Vol 203 (2) ◽  
pp. 371-381 ◽  
Author(s):  
Hanna S. Radomska ◽  
Daniela S. Bassères ◽  
Rui Zheng ◽  
Pu Zhang ◽  
Tajhal Dayaram ◽  
...  

Mutations constitutively activating FLT3 kinase are detected in ∼30% of acute myelogenous leukemia (AML) patients and affect downstream pathways such as extracellular signal–regulated kinase (ERK)1/2. We found that activation of FLT3 in human AML inhibits CCAAT/enhancer binding protein α (C/EBPα) function by ERK1/2-mediated phosphorylation, which may explain the differentiation block of leukemic blasts. In MV4;11 cells, pharmacological inhibition of either FLT3 or MEK1 leads to granulocytic differentiation. Differentiation of MV4;11 cells was also observed when C/EBPα mutated at serine 21 to alanine (S21A) was stably expressed. In contrast, there was no effect when serine 21 was mutated to aspartate (S21D), which mimics phosphorylation of C/EBPα. Thus, our results suggest that therapies targeting the MEK/ERK cascade or development of protein therapies based on transduction of constitutively active C/EBPα may prove effective in treatment of FLT3 mutant leukemias resistant to the FLT3 inhibitor therapies.


Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1233-1239 ◽  
Author(s):  
Joseph G. Jurcic ◽  
Steven M. Larson ◽  
George Sgouros ◽  
Michael R. McDevitt ◽  
Ronald D. Finn ◽  
...  

Unlike β particle–emitting isotopes, α emitters can selectively kill individual cancer cells with a single atomic decay. HuM195, a humanized anti-CD33 monoclonal antibody, specifically targets myeloid leukemia cells and has activity against minimal disease. When labeled with the β-emitters 131I and 90Y, HuM195 can eliminate large leukemic burdens in patients, but it produces prolonged myelosuppression requiring hematopoietic stem cell transplantation at high doses. To enhance the potency of native HuM195 yet avoid the nonspecific cytotoxicity of β-emitting constructs, the α-emitting isotope 213Bi was conjugated to HuM195. Eighteen patients with relapsed and refractory acute myelogenous leukemia or chronic myelomonocytic leukemia were treated with 10.36 to 37.0 MBq/kg 213Bi-HuM195. No significant extramedullary toxicity was seen. All 17 evaluable patients developed myelosuppression, with a median time to recovery of 22 days. Nearly all the 213Bi-HuM195 rapidly localized to and was retained in areas of leukemic involvement, including the bone marrow, liver, and spleen. Absorbed dose ratios between these sites and the whole body were 1000-fold greater than those seen with β-emitting constructs in this antigen system and patient population. Fourteen (93%) of 15 evaluable patients had reductions in circulating blasts, and 14 (78%) of 18 patients had reductions in the percentage of bone marrow blasts. This study demonstrates the safety, feasibility, and antileukemic effects of 213Bi-HuM195, and it is the first proof-of-concept for systemic targeted α particle immunotherapy in humans.


2013 ◽  
Vol 3 (5) ◽  
pp. 345-350
Author(s):  
S Shrestha ◽  
J Shrestha ◽  
CB Pun ◽  
T Pathak ◽  
S Bastola ◽  
...  

Background: Immunophenotyping of acute leukemia is one of the most important clinical applications of fl ow cytometry. The aim of this study was to determine the immunophenotyping profi le of acute leukemia, by means of a fl ow cytometric method, using monoclonal antibodies all marked with a fl uorochrome, in four colour systems to assess their distribution according to type of leukemia (lymphoid B or T / myeloid). Materials and Methods: We retrospectively collected data of immunophenotyping from 52 acute leukemia patients at the department of pathology in B.P. Koirala Memorial Cancer Hospital from January 2010 to December 2011. Diagnosis was based on peripheral blood and bone marrow examination for morphology, cytochemistry and immunophenotypic studies. Results: Out of total 52 cases of acute leukemia diagnosed by fl ow cytometry over a two year period, there were 31 cases (59.6 %) of acute lymphoblastic leukemia, 20 cases (38.4 %) of acute myelogenous leukemia and one case (1.9 %) of bi-phenotypic acute leukemia. Leukemia was diagnosed among adults in 44.2 % whereas among children with age less than or equal to 15 years in 55.7 %. Thirty eight (73%) were male and 14 (27 %) were female with a male: female ratio of 2.7:1. For acute myelogenous leukemia, it was found that M0 (5.0 %), M1 (20%), M2 (60%), M3 (15%), M4 (5.0 %) were detected. CD13 and CD33 were the most useful markers in the diagnosis of acute myelogenous leukemia. The most common subtype was AML-M2. Of the 31 cases with acute lymphoblastic leukemia, 20 cases (64.5 %) were identifi ed as B-ALL and 11 cases (35.5%) as T-ALL. Aside from cytoplasmic CD3 (cCD3) and CD7 were the most sensitive antigens present in all cases of T-ALL. All cases of B-ALL showed expression of pan B-cell markers CD19 and CD22, but 15 (75 %) of 20 cases expressed CD10. Conclusion: Flow cytometric immunophenotyping was found to be especially useful in the correct identifi cation and diagnosis of acute myeloid or lymphoblastic leukemia and its subtypes. In combination with French-American-British (FAB) morphology and immunophenotyping, we were able to diagnose and classify all patients with acute leukemia in this study. Journal of Pathology of Nepal (2013) Vol. 3, No.1, Issue 5, 345-350 DOI: http://dx.doi.org/10.3126/jpn.v3i5.7856


2001 ◽  
Vol 19 (11) ◽  
pp. 2804-2811 ◽  
Author(s):  
R. A. Krance ◽  
C. A. Hurwitz ◽  
D. R. Head ◽  
S. C. Raimondi ◽  
F. G. Behm ◽  
...  

PURPOSE: To develop more effective chemotherapy regimens for childhood acute myelogenous leukemia (AML). PATIENTS AND METHODS: Between June 1991 and December 1996, we administered the nucleoside analog 2-chlorodeoxyadenosine (2-CDA) to 73 children with primary AML and 20 children with secondary AML or myelodysplastic syndrome (MDS). Patients received one or two 5-day courses of 2-CDA (8.9 mg/m2/d) given by continuous infusion. All patients then received one to three courses of daunomycin, cytarabine, and etoposide (DAV) remission induction therapy. RESULTS: Seventy-two patients with primary AML were assessable for response. Their rate of complete remission (CR) was 24% after one course of 2-CDA, 40% after two courses of 2-CDA, and 78% after DAV therapy. Of the 57 patients who entered CR, 11 subsequently underwent allogeneic bone marrow transplantation (BMT), and 40 underwent autologous BMT. Twenty-nine patients remain in continuous CR after BMT. Two patients remain in CR after chemotherapy only. The 5-year event-free survival (EFS) estimate was 40% (SE = 0.080%). Patients with French-American-British (FAB) M5 AML had a higher rate of CR after treatment with 2-CDA (45% after one course and 70.6% after two courses) than did others (P = .002). In contrast, no patient with FAB M7 AML (n = 10) entered CR after treatment with 2-CDA. Similarly, no patient with primary MDS (n = 6) responded to 2-CDA. Seven patients with secondary AML or MDS (n = 14) had a partial response to one course of 2-CDA. CONCLUSION: This agent was well tolerated, and its toxicity was acceptable. Future trials should examine the effectiveness of 2-CDA given in combination with other agents effective against AML.


Blood ◽  
1992 ◽  
Vol 79 (9) ◽  
pp. 2246-2255 ◽  
Author(s):  
E Estey ◽  
PF Thall ◽  
H Kantarjian ◽  
S O'Brien ◽  
CA Koller ◽  
...  

Abstract We gave 56 patients with newly diagnosed acute myelogenous leukemia (AML) granulocyte-macrophage colony-stimulating factor (GM-CSF) 20 or 125 micrograms/m2 once daily subcutaneously before (for up to 8 days or until GM-CSF-related complications developed) and during, or only during (patients presenting with blast counts greater than 50,000 or other leukemia-related complications) ara-C (1.5 g/m2 daily x 4 by continuous infusion) and daunorubicin (45 mg/m2 daily x 3) chemotherapy. Because results seemed independent of GM-CSF schedule, we compared results in these 56 patients with results in 176 patients with newly diagnosed AML given the same dose and schedule of ara-C without GM-CSF (110 patients ara-C alone, 66 patients ara-C + amsacrine or mitoxantrone). Comparison involved fitting a logistic regression model predicting probability of complete remission (CR) and a Cox regression model to predict survival (most patients in all three studies were dead) with treatment included as a covariate in both analyses. After adjusting for other prognostically significant covariates [presence of an antecedent hematologic disorder, an Inv (16), t(8;21), or abnormalities of chromosomes 5 and/or 7, performance status, age, bilirubin], treatment with ara-C + daunorubicin + GM-CSF was predictive of both a lower CR rate and a lower survival probability. There were no treatment-covariate interactions, suggesting that the negative effect of this GM-CSF treatment regime was not an artifact of some imbalance in patient characteristics. The unadjusted Kaplan-Meier hazard rate of the ara-C + daunorubicin + GM-CSF group was not uniquely high during the initial 4 weeks after start of therapy, but was highest among the three treatment groups throughout weeks 5 to 16, suggesting that the negative effect of this treatment was not caused by acute toxicity. Patients who did not enter CR with this treatment tended to have persistent leukemia rather than prolonged marrow aplasia, suggesting that this treatment and, in particular, GM-CSF may increase resistance of myeloid leukemia cells to chemotherapy. To date, relapse rates are similar in all three groups (P = .43) (as are survival rates once patients are in CR) but much of the remission duration data is heavily censored, unlike the survival data. Our results suggest caution in the use of GM-CSF to sensitize myeloid leukemia cells to daunorubicin + ara- C chemotherapy.


Blood ◽  
1996 ◽  
Vol 88 (6) ◽  
pp. 2259-2266 ◽  
Author(s):  
J Fairman ◽  
RY Wang ◽  
H Liang ◽  
L Zhao ◽  
D Saltman ◽  
...  

Acquired partial and complete deletions of chromosome 5 (5q-, -5) are common cytogenetic anomalies associated with myelodysplasia (MDS) and acute myeloid leukemia (AML). A critical region of consistent loss at 5q31.1 (in > 90% of cases) has led us and others to postulate the presence of a key negative regulator(s) of leukemogenesis. Although the interstitial deletion limits vary among patients, del(5) (q13q33) and del(5)(q13q35) constitute major subsets. Furthermore, it is not rare to encounter deletions, translocations, or paracentric inversions involving 5q11 to 5q13, which indicates inactivation or disruption of important gene(s) at that locus. In this report, we have localized a novel locus at 5q13.1 to a 2.0-Mb interval between the anonymous markers D5S672 and GATA-P1804. This locus resided within the region of loss in 12 of 27 patients with anomalies of chromosome 5; one of these cases had apparent retention of both alleles of all the telomeric loci. Fluorescence in situ hybridization (FISH) studies demonstrate that the AML cell line ML3 is disrupted at 5q13.1 by a translocation involving chromosome 3, with apparent retention of the entire chromosome 5 sequence. Our results suggest that this novel proximal locus encodes a critical gene that may be deleted or disrupted in a subset of MDS/AML patients with chromosome 5 anomalies.


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