THE STATE OF HEMATOLOGICAL PARAMETERS IN APLASTIC ANEMIA

Annotasiya

To analyze laboratory changes in peripheral blood and myelogram in adult patients with aplastic anemia.

Manba turi: Konferentsiyalar
Yildan beri qamrab olingan yillar 2022
inLibrary
Google Scholar
Chiqarish:
35-38
48

Кўчирилди

Кўчирилганлиги хақида маълумот йук.
Ulashish
Akhmedova, Z. ., Matkarimova, D. ., & Boboev , K. . (2025). THE STATE OF HEMATOLOGICAL PARAMETERS IN APLASTIC ANEMIA. Наука и инновации в системе образования, 4(2), 35–38. Retrieved from https://www.inlibrary.uz/index.php/sies/article/view/66368
Crossref
Сrossref
Scopus
Scopus

Annotasiya

To analyze laboratory changes in peripheral blood and myelogram in adult patients with aplastic anemia.


background image

SCIENCE AND INNOVATION IN THE

EDUCATION SYSTEM

International scientific-online conference

35

THE STATE OF HEMATOLOGICAL PARAMETERS IN APLASTIC

ANEMIA

Akhmedova Zukhra Bakhtiyarovna

basic doctoral student

RSSPMCH, number: +99894 726 87 88.

Matkarimova Dilfuza Saburova

Professor of the Department of Hematology, Transfusiology and Laboratory

Science of TMA, number: +99897 412 91 18.

Boboev Kodirjon Tukhtabaevich

Head of the Department of Molecular Medicine and Cellular Technologies of the

RSSPMCH, number: +99890 319 39 57.

Republican specialized scientific

practical medical center of Hematology

Tashkent medical academy

https://doi.org/10.5281/zenodo.14858046

Summary

Purpose of the study.

To analyze laboratory changes in peripheral blood

and myelogram in adult patients with aplastic anemia.

Methods.

The material for clinical and laboratory studies in the work were

patients with AA (n=86) who sought diagnostic help and subsequent inpatient
examination at the republican specialized Scientific and Practical Medical Center
of Hematology (RSNPMCG, Tashkent) from 2019 to 2023. Patients with AA
ranged in age from 18 to 79 years, while the median age was 40.8±1.8 years. The
diagnosis was made taking into account clinical and laboratory data.

The research methods included laboratory examination (general blood test

(UAC) and myelogram) and statistical methods of processing the results using
the PC application package "OpenEpi 2009, Version 2.3".

Conclusions.

Despite the severity of form A, UAC is characterized by a

decrease in hemoglobin concentration, the number of erythrocytes, platelets,
and leukocytes due to neutropenia, lymphocytosis, and acceleration of ESR. The
myelogram shows a decrease in the cellularity of the red bone marrow, three-
stage cytopenia and replacement of the red brain with a fatty brain.

Key words:

UAC, myelogram, three-stage cytopenia, fatty brain.

Introduction.

AA is a rare type of bone marrow insufficiency syndrome

(BCM), which is characterized by severe pancytopenia and bone marrow
hypoplasia of varying severity [1,2,4]. Acquired AA, also called idiopathic AA,
accounts for the majority (∽70%) of all newly diagnosed cases [5,7,10].

The diagnosis of aplastic anemia should be suspected in any patient

presenting with pancytopenia. Aplastic anemia is a diagnosis of exclusion [3].


background image

SCIENCE AND INNOVATION IN THE

EDUCATION SYSTEM

International scientific-online conference

36

The severity of AA was assessed in accordance with the parameters of the

blood test and the results of the bone marrow examination. Severe AA (SAA)
was defined as a BM cell count of < 25% or 25-50% with < 30% residual
hematopoietic cells and at least two of the following: (I) absolute neutrophil
count < 0.5 × 109/l, (II) platelets < 20 × 109/L and (III) the number of
reticulocytes < 20 × 10 9 /l . Patients with AA who did not meet the SAA criteria
were classified as non-severe AA (NSAA). The result of the treatment was based
on previous literature [6,8,9].

Purpose of the study.

To analyze laboratory changes in peripheral blood

and myelogram in adult patients with aplastic anemia.

Methods.

The material for clinical and laboratory studies in the work

were patients with AA (n=86) who sought diagnostic help and subsequent
inpatient examination at the republican specialized Scientific and Practical
Medical Center of Hematology (RSNPMCG, Tashkent) from 2019 to 2023.
Patients with AA ranged in age from 18 to 79 years, while the median age was
40.8±1.8 years. The diagnosis was made taking into account clinical and
laboratory data.

The research methods included laboratory examination (general blood test

(UAC) and myelogram) and statistical methods of processing the results using
the PC application package "OpenEpi 2009, Version 2.3".

Results.

In patients with AA, a decrease in hemoglobin concentration of

cytopenia (decrease in the number of erythrocytes, platelets and leukocytes),
absolute neutropenia, relative lymphocytosis and acceleration of ESR were
found in clinical blood analysis compared with healthy ones.

Analyzing the average values of the indicators of the general blood test in

the main group of patients with AA in comparison with the control, the changes
characteristic of the disease manifested by cytopenia were established. In
patients with AA, there was a significant decrease in hemoglobin by 2.5 times
(52.8±1.7 g/l versus 134.2±2.4 g/l; P<0.01) and erythrocytes by 2.0 times
(1.7±0.07 x 1012/l versus 3.4±0.5 x 1012/l; P<0.05).

At the same time, the median platelet count was statistically significantly

reduced by 21.1 times (13.6±3.0 x 1012/l versus 287.2±2.1 x 1012/l; P<0.001),
and leukocytes by 6.2 times (1.2±0.05 x 1012/l versus 7.4±1.2 x 1012/l;
P<0.001).

The above data show some of the main changes in the UAC characteristic of

AA. Meanwhile, the key factor in the UAC for confirming the diagnosis of AA was
a decrease in the absolute number of neutrophils among patients by 11.2 times


background image

SCIENCE AND INNOVATION IN THE

EDUCATION SYSTEM

International scientific-online conference

37

compared with the control (0.423±0.03 x 1012/l versus 4,743±0.25 x 1012/l;
P<0.001).

A 1.7-fold increase in the number of lymphocytic cells was also specific for

this pathology (61.0±1.1% vs. 35.5±1.4%; P<0.05), as well as a 7.2-fold increase
in the level of ESR (52.0±2.1 mm/h vs. 7.2±1.4 mm/h; P<0.001)

Thus, the laboratory signs of AA in the UAC were normocytic anemia, severe

cytopenia (erythro-, thrombo- and leukopenia), neutropenia, relative
lymphocytosis and accelerated ESR. Moreover, these signs differed in severity
depending on the severity of AA, respectively, having deeper disorders in severe
and superheavy forms, which were associated with the severity of clinical
manifestations in patients with AA.

The results of morphological and quantitative analysis of the bone marrow

showed a picture of small cells in the normoblastic type of hematopoiesis with a
content of 0.18±0.009% blast cells in the main AA group, which showed no
increase in their content.

Microscopy revealed fatty voids, as well as single areas containing reticular,

erythroid and lymphoid cells. The sum of erythroid elements was reduced to
6.4±0.2% of their minimum normal number by 2.3 times (14.5%; P<0.01), and
from the maximum by 4.1 times (26.5%; P<0.001). The number of lymphocytes,
which amounted to 24.3 ±0.4% of the maximum normal number, was increased
by 1.8 times (13.7%; P<0.05), and from the minimum allowable by 5.6 (4.3%;
P<0.001).

Meanwhile, the content of plasma cells, eosinophils, basophils and

monocytes were within the reference norms (see Table 3.13). While the number
of neutrophils and megakaryocytes (MCC) significantly decreased below the
permissible normal values by 2.0 (26.1-1.0% vs. 52.7%; P<0.05) and 2.5 times
(2.0±0.1 against 5; P<0.01), respectively.

Thus, the myelogram picture was characterized by bone marrow

hypocellularity, manifested by three-stage cytopenia, narrowing of granulocytic
and erythroid sprouts with normoblastic type of hematopoiesis, the presence of
voids and the replacement of the red brain with yellow. All these signs are key
characteristics of AA.

Conclusion.

In the UAC, all degrees of severity of AA are characterized by a

decrease in hemoglobin concentration, the number of erythrocytes, platelets,
and leukocytes due to neutropenia, lymphocytosis, and acceleration of ESR. The
myelogram shows a decrease in the cellularity of the red bone marrow, three-
stage cytopenia and replacement of the red brain with a fatty brain.


background image

SCIENCE AND INNOVATION IN THE

EDUCATION SYSTEM

International scientific-online conference

38

References:

1.

Abdel Hi M. Z. et al. Platelet indices as a predictor in patients with aplastic

anemia and immune thrombocytopenic purpura: a retrospective case–control
study //The Egyptian Journal of Internal Medicine. – 2024. – Т. 36. – №. 1. – С.
92.
2.

Atta E. H. et al. Predictors of early mortality after rabbit antithymocyte

globulin as first-line treatment in severe aplastic anemia //Annals of
hematology. – 2017. – Т. 96. – С. 1907-1914.
3.

Bacigalupo A. How I treat acquired aplastic anemia //Blood, The Journal of

the American Society of Hematology. – 2017. – Т. 129. – №. 11. – С. 1428-1436.
4.

Clé D. V. et al. Rabbit antithymocyte globulin dose does not affect response

or survival as first-line therapy for acquired aplastic anemia: a multicenter
retrospective study //Annals of hematology. – 2018. – Т. 97. – С. 2039-2046.
5.

DeZern A. E., Churpek J. E. Approach to the diagnosis of aplastic anemia

//Blood Advances. – 2021. – Т. 5. – №. 12. – С. 2660-2671.
6.

Killick S. B. et al. Guidelines for the diagnosis and management of adult

aplastic anaemia //British journal of haematology. – 2016. – Т. 172. – №. 2.
7.

Maciejewski, J. P., Selleri, C., Sato, T., Anderson, S., & Young, N. S. (1996). A

severe and consistent deficit in marrow and circulating primitive hematopoietic
cells (long-term culture-initiating cells) in acquired aplastic anemia. Blood,
88(6), 1983–1991.
8.

Peffault de Latour R. et al. Eltrombopag added to immunosuppression in

severe aplastic anemia //New England Journal of Medicine. – 2022. – Т. 386. –
№. 1. – С. 11-23.
9.

Tembe-Fokunang E. et al. The Scope of Aplastic Anaemia: Etiology,

Pathophysiology, Pharmacotherapy and Pharmacoeconomic Impact in Clinical
Patient Management //International Journal of Research and Reports in
Hematology. – 2022. – Т. 5. – №. 2. – С. 197-214.
10.

Young, N. S., Calado, R. T., & Scheinberg, P. (2006). Current concepts in the

pathophysiology and treatment of aplastic anemia. Blood, 108(8), 2509–2519.

Bibliografik manbalar

Abdel Hi M. Z. et al. Platelet indices as a predictor in patients with aplastic anemia and immune thrombocytopenic purpura: a retrospective case–control study //The Egyptian Journal of Internal Medicine. – 2024. – Т. 36. – №. 1. – С. 92.

Atta E. H. et al. Predictors of early mortality after rabbit antithymocyte globulin as first-line treatment in severe aplastic anemia //Annals of hematology. – 2017. – Т. 96. – С. 1907-1914.

Bacigalupo A. How I treat acquired aplastic anemia //Blood, The Journal of the American Society of Hematology. – 2017. – Т. 129. – №. 11. – С. 1428-1436.

Clé D. V. et al. Rabbit antithymocyte globulin dose does not affect response or survival as first-line therapy for acquired aplastic anemia: a multicenter retrospective study //Annals of hematology. – 2018. – Т. 97. – С. 2039-2046.

DeZern A. E., Churpek J. E. Approach to the diagnosis of aplastic anemia //Blood Advances. – 2021. – Т. 5. – №. 12. – С. 2660-2671.

Killick S. B. et al. Guidelines for the diagnosis and management of adult aplastic anaemia //British journal of haematology. – 2016. – Т. 172. – №. 2.

Maciejewski, J. P., Selleri, C., Sato, T., Anderson, S., & Young, N. S. (1996). A severe and consistent deficit in marrow and circulating primitive hematopoietic cells (long-term culture-initiating cells) in acquired aplastic anemia. Blood, 88(6), 1983–1991.

Peffault de Latour R. et al. Eltrombopag added to immunosuppression in severe aplastic anemia //New England Journal of Medicine. – 2022. – Т. 386. – №. 1. – С. 11-23.

Tembe-Fokunang E. et al. The Scope of Aplastic Anaemia: Etiology, Pathophysiology, Pharmacotherapy and Pharmacoeconomic Impact in Clinical Patient Management //International Journal of Research and Reports in Hematology. – 2022. – Т. 5. – №. 2. – С. 197-214.

Young, N. S., Calado, R. T., & Scheinberg, P. (2006). Current concepts in the pathophysiology and treatment of aplastic anemia. Blood, 108(8), 2509–2519.