scholarly journals Clinicopathological study of patients with pancytopenia

Author(s):  
Y. Srinivas ◽  
Mohammed Elyas

Background: Pancytopenia is due to bone marrow failure characterized by anemia, leukopenia, and thrombocytopenia. It a common hematological disorder. Low blood counts in the bone marrow failure disease result from deficient hematopoiesis. Marrow damage and dysfunction also may be secondary to infection, inflammation, or cancer. Pancytopenia has an extensive differential diagnosis and it can result from damage to bone marrow destruction of preformed blood cells peripherally with increased reticulocyte count. Aim of the study were to study the different etiological conditions and clinical features of pancytopenia in rural medical college.Methods: This study has been conducted in the department of general medicine in association with the pathology department and between March 2019 to February 2020, 45 patients were included in this study. males were 27 and females were 18. The age group is between 20 years and 60 years. 2 ml of anticoagulant blood send for HB% total count, platelet count, packed cell volume, and RBC indices.Results: The total no. of patients included in this study were 45 among these 45 patients, males were 27, and females were 18. The common age group is between 20 and 60 years and the common causes of aplastic anemia in our study are megaloblastic anemia.Conclusions: Pancytopenia is a common hematological problem in India. In our study megaloblastic anemia is the most common cause of pancytopenia females are affected during pregnancy. So, periodical clinically examined and investigations may reduce the incidence. of further research with a large sample size and meticulous investigations required to replicate the finding of the study.

Author(s):  
Tirumala Kanakadurga Sripati ◽  
S. Palaniandavan ◽  
. Govindarajan ◽  
J. Thanka

Thrombocytopenia is a physiological deficiency in platelet counting. Fragmented RBC can be a chronic   trigger   for a subclinical micro angiopathy that results in chronic consumption of platelets. The platelet is a small, lentiform, anucleated cell that play a vital role in hemostasis and are produced in the bone marrow from megakaryocytes. To evaluate different etiological factors of thrombocytopenia by the study of clinical profile and laboratory parameters in patients with thrombocytopenia carried out in Sree Balaji Medical College and Hospital, Chennai. After evaluating all cases of thrombocytopenia, it is concluded that infective causes are more common than non-infective causes. Infections like dengue, malaria and septicemia were the common causes of thrombocytopenia along with megaloblastic anemia. Whenever thrombocytopenia is detected, a further investigation has to be done for specific diagnosis in the most of the cases so that appropriate treatment can be given.


Author(s):  
Kevin B. Hoover

Chapter 74 discusses anemia conditions including sickle cell disease and thalassemia. Anemia is a condition of decreased oxygen delivery to organs caused by a deficit of functional red blood cells. It is a very common clinical condition and has a wide variety of causes. Of the common causes, the hemoglobinopathies have the most characteristic imaging findings. There are common imaging findings secondary to the compensatory increase in red blood cell and precursor number. Radiographs are a standard initial imaging study. MRI is the most sensitive imaging study for the sequelae of anemia. Iron deficiency anemia is treated with iron supplementation, aplastic anemia is treated by removal of the inciting agent, and painful crises of sickle cell are treated symptomatically.


Blood ◽  
1951 ◽  
Vol 6 (4) ◽  
pp. 344-349 ◽  
Author(s):  
EDWARD H. REISNER ◽  
ROY KORSON

Abstract 1. In 9 patients with various types of megaloblastic anemia responding to treatment with vitamin B12, folic acid or liver extract, no significant deviations from the normal amounts of total or polymerized DNA were observed in the nuclei of red blood cells in marrow smears. 2. During the maturation of megaloblasts in the bone marrow there is a gradual loss of nuclear DNA. 3. This pattern is quantitatively and qualitatively similar for normal marrow and for that of pernicious anemia in relapse and after treatment.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3765-3765
Author(s):  
Jose R. Borbolla Escoboza ◽  
Marcos E. Garza-Madrid ◽  
Luis Villela ◽  
Manuel A. Lopez-Hernandez ◽  
Jorge Vela-Ojeda

Abstract Aplastic anemia (AA) is a classic bone marrow failure syndrome simply defined as peripheral blood pancytopenia and a hypocelular bone marrow, yet the diagnosis must be made by excluding other causes of bone marrow failure. The incidence rate of AA reported by the International Aplastic Anemia and Agranulocytosis Study (IAAAS) in the 1980s was 2 cases per 1 million people. This disease is known to be caused by exposure to radiation, chemotherapy and some viral agents, yet most of the cases are idiopathic. Epstein Barr virus and non-A, non-B or non-C Hepatitis virus have classically been related to the development of some AA cases. Recently there have been some reports of AA following Parvovirus B19 (PvB19) infection. This virus, the only parvoviridae virus capable of infecting humans, attacks erythrocyte precursors attaching to the P antigen in their surface and requiring Beta1 integrin for viral entry. Although PvB19 seems to infect only erytroid precursors, it is widely recognized that the infection with this virus can cause not only anemia, but neutropenia and thrombocytopenia as well, producing aplastic crisis of varying intensity. A correlation has recently been found between PvB19 DNA in peripheral blood and AA in children. We pretend to corroborate this observation and include adult patients in order to improve our understanding of the relationship between PvB19 and AA. So far we have taken peripheral blood samples from 9 AA patients and 9 controls paired by age, sex and community; we plan to include 100 AA patients and their controls from several hospitals around Mexico. DNA was extracted using the PUREGENE DNA extraction kit (Gentra, Minneapolis MN). Nested PCR was performed using the sense primer (P1) 5-AATACACTGTGGTTTTATGGGCCG-3, antisense (P2) 5-CCATTGCTGGTTATAACCACAGGT-3 for the first round and the sense primer (P3) 5-AATGAAAACTTTCCATTTAATGATGTAG-3 and antisense primer (P4) 5-CTAAAATGGCTTTTGCAGCTTCTAC-3for the second round. A DNA sample from a patient with active infectious mononucleosis with positive IgG and IgM against PvB19 in serum was used as positive control. Two samples from the AA group (22%) and 1 from the control group (11%) have turned positive for PvB19 DNA. The reported incidence for the presence of this virusDNA in the peripheral blood of the population is 3%. We expect that, as the number of patients grows, the percentage of positive samples in the control group will decrease, while the percentage of positive samples in the AA group will rise or be sustained. Our partial results point towards a possible relationship between AA and the presence of PvB19 DNA in the peripheral blood cells. It is possible that this virus is one of many factors capable of precipitating the development of AA by limiting the bone marrows capacity to produce blood cells. We are in the process of gathering more samples to prove if a relationship really exists and, if so, future studies will likely shed light upon the mechanism by which PvB19 contributes to the development of AA and other marrow failure syndromes.


Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1489-1489
Author(s):  
Takamasa Katagiri ◽  
Zhirong Qi ◽  
Yu Kiyu ◽  
Naomi Sugimori ◽  
J. Luis Espinoza ◽  
...  

Abstract Abstract 1489 Poster Board I-512 The hematopoietic stem cell (HSC) differentiation pathway in humans remains largely unknown due to the lack of an appropriate in vivo assay allowing the growth of HSCs as well as of clonal markers that enable the tracing of their progenies. Small populations of blood cells deficient in glycosylphosphatidylinositol-anchored proteins (GPI-APs) such as CD55 and CD59 are detectable in approximately 50% of patients with aplastic anemia (AA) and 15% of patients with refractory anemia (RA) of myelodysplastic syndrome defined by the FAB classification. Such blood cells with the paroxysmal nocturnal hemoglobinuria (PNH) phenotype (PNH-type cells) are derived from single PIGA mutant HSCs and their fate depends on the proliferation and self-maintenance properties of the individual HSCs that undergo PIG-A mutation by chance (Blood 2008;112:2160, Br J Haematol 2009 in press) Analyses of the PNH-type cells from a large number of patients on the diversity of lineage combination may help clarify the HSC differentiation pathway in humans because PIG-A mutant HSCs in patients with bone marrow failure appear to reflect the kinetics of healthy HSCs. Therefore, different lineages of peripheral blood cells were examined including glycophorin A+ erythrocytes (E), CD11b+ granulocytes (G), CD33+ monocytes (M), CD3+ T cells (T), CD19+ B cells (B), and NKp46+ NK cells (Nk) from 527 patients with AA or RA for the presence of CD55−CD59− cells in E and G, and CD55−CD59−CD48− cells in M,T, B, Nk with high sensitivity flow cytometry. Two hundred and twenty-eight patients (43%) displayed 0.003% to 99.1% PNH-type cells in at least one lineage of cells. The lineage combination patterns of PNH-type cells in these patients included EGM in 71 patients (31%), EGMTBNk in 43 (19%), EG in 37 (16%), T alone 14 (6%), EGMBNk in 11 (5%), G alone in 10 (4%), GM in 10 (4%), EGMNk in 7 (3%), EGMT in 7 (3%), EGMB in 6 (3%), EM in 5 (2%), EGMTB in 3 (1%), EGNk in 1 (0.4%), EGMTNk in 1 (0.4%), GMTB in 1 (0.4%), and GT in 1 (0.4%) (Table). All patterns included G or M, except for 14 patients displaying PNH-type T cells alone. No patients showed TB or TBNk patterns suggestive of the presence of common lymphoid progenitor cells. Peripheral blood specimens from 123 patients of the 228 patients possessing PNH-type cells were examined again after 3 to 10 months and all patients showed the same combination patterns as those revealed by the first examination. PIG-A gene analyses using sorted PNH-type cells from 3 patients revealed the same mutation in G and Nk for 1 patient and in G and T for 2 patients. These findings indicate that human HSCs may take a similar differentiation pathway to that of murine HSCs, the ‘myeloid-based model’ that was recently proposed by Kawamoto et al. (Nature 2008; 10:452), though the cases with PNH-type T cells alone remain to be elucidated. Table. Lineages of cells containing PNH-type cells in patients with AA or RA. The number in the parenthesis denotes the proportion of patients showing each combination pattern in the total patients possessing PNH-type cells. (+ ; presence of PNH-type cells) Disclosures No relevant conflicts of interest to declare.


Author(s):  
Benazeer Mansuri ◽  
Komal P. Thekdi

Background: Megaloblastic anemias are hematologic disorders in which abnormal DNA synthesis causes blood and bone marrow disorders. The cause of thrombocytopenia in megaloblastic anemia has been postulated as hypoproduction in some studies, whereas ineffective thrombopoeisis has been proposed in other. Objective was to study spectrum of clinic-hematological features in megaloblastic anemia and comparative bone marrow aspiration study of thrombocytopenia secondary to megaloblastic anemia, hypoproduction and hyper-destruction. This study was done to understand the various megakaryocytic alterations in hematological disorders presenting with thrombocytopenia due to different mechanisms.Methods: Total 85 cases of thrombocytopenia included in the study. Bone marrow finding in 33 cases of thrombocytopenia of megaloblastic etiology were compared with 34 cases of marrow proven hypo productive thrombocytopenia (aplastic anemia, acute leukemia) and 19 cases of hyper destructive thrombocytopenia (immune thrombocytopenia).Results: Most common age group presenting megaloblastic anemia is 11-20 year, with male to female ratio is1.2:1, most common complaint were generalized weakness and fever. In megaloblastic anemia 24.33%, 60% and 15.67% of the cases shows increase, decrease and normal megakaryocytes respectively. Dysplastic megakaryocytes were observed in 24.3%, 27% and 20.5% of the cases of megaloblastic anemia, acute leukaemia and immune thrombocytopenic purpura respectively.Conclusions: Both hypoproduction and ineffective thrombopoiesis are the underlying path mechanisms in megaloblastic thrombocytopenia as evidenced by the marrow findings. We hereby infer that megaloblastic thrombocytopenia is to be included as a separate category apart from hypo proliferative and hyper destructive groups. The presence of dysplastic megakaryocyte should not prompt an interpretation


Blood ◽  
1960 ◽  
Vol 15 (1) ◽  
pp. 1-29 ◽  
Author(s):  
RICHARD W. VILTER ◽  
THOMAS JARROLD ◽  
JOHN J. WILL ◽  
JOHN F. MUELLER ◽  
BEN I. FRIEDMAN ◽  
...  

Abstract 1. The hematologic syndrome called refractory anemia with hyperplastic bone marrow, aregenerative anemia, chronic bone marrow failure, pseudo-aplastic anemia, and many other terms, has been separated into five types on the basis of clinical and hematologic studies on 23 patients carried out over a period of 16 years. These groupings are probably highly artificial but are made to facilitate presentation and description. As more is learned of the chemistry of the bone marrow cells in patients with refractory anemia, a more satisfactory classification will be possible. 2. Type 1 is characterized by bizarre chromatin in the normoblasts, mast cell hyperplasia, hemosiderosis or hemochromatosis and a tendency for spontaneous remissions to occur. 3. Type 2 is at first typified by complete or almost complete erythroid aplasia. Hyperplasia of erythroid cells with maturation arrest and bizarre chromatin pattern may occur later, and finally spontaneous remission may appear with considerable frequency. Mast cell hyperplasia, thymoma and hemosiderosis have been noted. 4. Type 3, associated with exogenous toxins and the preleukemia state, is characterized by pancytopenia and a bizarre chromatin pattern in the normoblasts. Some of these patients may he classified as "DiGuglielmo syndrome." 5. Type 4 also is typified by pancytopenia and hyperplasia of bone marrow but with cells of normal appearance. These patients responded partially or completely when splenectomy was performed, and probably represent a variant of the "hypersplenism" syndrome. 6. Type 5 is refractory megaloblastic anemia with typical cytologic changes evident in all cell types similar to those found in pernicious anemia. 7. Hypotheses are proposed to explain these various types of anemia on the basis of abnormalities in the metabolism of nucleic acids, particularly DNA. Deficiencies of metabolites, inhibition of metabolic reactions by exogenous or endogenous toxins, or by immune mechanism in which DNA serves as haptene, are possible explanations.


2009 ◽  
Vol 147 (1) ◽  
pp. 102-112 ◽  
Author(s):  
Chiharu Sugimori ◽  
Kanako Mochizuki ◽  
Zhirong Qi ◽  
Naomi Sugimori ◽  
Ken Ishiyama ◽  
...  

2017 ◽  
Vol 20 (2) ◽  
pp. 172-175
Author(s):  
Lisa Sutton ◽  
Nkechi Mba

Vitamin B12 deficiency is a known cause of megaloblastic anemia and bone marrow failure. Bone marrow biopsies are not frequently performed as part of the diagnostic workup and can demonstrate morphologic features that overlap with myelodysplastic syndrome (MDS) and acute leukemia. We describe a case of a dysplastic bone marrow with increased bone marrow hematogones detected by flow cytometry in a child with vitamin B12 deficiency. Hematogones are normal B cell precursors, and hyperplasia has been described in a variety of often reactive conditions and also disease. Hematogones are not typically seen in MDS. The presence of hematogones may help differentiate the dysplastic changes seen in vitamin B12 deficiency from MDS.


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