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Volume-39_Issue-1_May-2025
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STUDYING THE DIAGNOSIS OF PERIPHERAL BLOOD AND
BONE MARROW IN ANEMIA OF CHRONIC DISEASES.
Madrakhimova Nigora Shokir qizi
Master of the Department of Military Field Therapy,
Hematology and Diagnostics" of the Urgench
branch of the Tashkent Medical Academy
madraximovanigora19@gmail.com
Fazilova Sharifa Mirhamidovna
Associate professor, of the Department
of Military Field Therapy, Hematology
and Diagnostics"of the Urgench branch
of the Tashkent of the Medical
Academy Associate, PhD
Summary:
Thus, the detection of anemia in patients determines the need for
mandatory clarification of the causes of this pathological condition. Timely
verification of the etiology of anemia makes it possible to start adequate therapy
without delay, which determines its effectiveness and improves the quality of life of
people.
Key words:
chronic disease anemia
,
metabolism
,
transferrin
At present, researchers are paying special attention to a form of anemia - chronic
disease anemia (ACD). A characteristic feature of this anemia is impaired iron
metabolism - a combination of iron deficiency available for erythropoiesis (reduced
level of transferrin saturation with iron-TBAT) with sufficient iron supply in the
reticuloendothelial system [6, 8].
ACD is a secondary anemia that occurs against the background of various
infectious, inflammatory, autoimmune or tumor diseases lasting more than 1-2
months. This type of anemia is also called "chronic inflammation anemia" or
"cytokine-induced anemia." ACD ranks 2nd in prevalence after iron deficiency
anemia (IDA). For the first time, concomitant anemia in a chronic disease was
mentioned in 1842, when French researchers discovered a decrease in the mass of red
blood cells in patients infected with smallpox. Further observations of patients with
typhoid fever, tuberculosis, and syphilis allowed M. Wintrobe and G. Cartwright to
introduce the term "inflammatory anemia" in 1949 and in 1952 [11,15].
In the early 80s of the last century, E. Weinberg presented a theory that iron
serves as a necessary component for maintaining the vital functions of all living
organisms, including bacteria and tumor cells [5,7]. Based on this theory, we can
conclude that anemia of the inflammatory response is a natural defense mechanism
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aimed at limiting free iron (Fe3+) in the blood when it enters the div pathogens,
which is achieved by the rapid binding of iron to lactoferrin, as well as by its
deposition (ferritin). In inflammatory processes, the synthesis of ferritin and
lactoferrin increases, resulting in iron deficiency, which helps to reduce the growth of
pathogenic microorganisms. Hepcidin, which plays a fundamental role in the
pathogenesis of the development of ACD, is an acute-phase protein and blocks the
absorption of iron in the intestine and its release from the depot. ACD is often found
(8–33% of patients) against the background of chronic infectious, inflammatory, and
destructive lung diseases, such as chronic obstructive pulmonary disease (COPD),
bronchiectasis, abscess, pleural empyema, and tuberculosis [4,9]. According to a
number of studies, the prevalence of anemia among patients with COPD is 7.5–
33.0%. ACD often develops with diffuse connective tissue diseases (systemic lupus
erythematosus, scleroderma), rheumatoid arthritis, systemic vasculitis, sarcoidosis,
autoimmune bowel diseases (ulcerative colitis, Crohn's disease), liver diseases
(autoimmune hepatitis, cirrhosis of the liver) and thyroid gland (autoimmune
thyroiditis, hypothyroidism). Against the background of rheumatoid arthritis, ACD is
detected in 25–64% of cases. The main role in the development of anemia in
rheumatoid arthritis is played by changes in iron metabolism, inadequate production
of red blood cells by the bone marrow. This may be due to exposure to various pro-
inflammatory cytokines such as interferon-γ, interleukins, TNF-α. The main
mechanism for the development of ACD is immunoinflammatory. Increased
expression of pro-inflammatory cytokines is a key link in the pathogenesis of ACD.
Against the background of infectious diseases, tumor processes, and immune
conditions, T-cells and monocytes are activated, which produce cytokines such as
IFN-γ, TNF-α, IL-1, IL-6, IL-10 during the immune response [1,10,14]. The
pathogenetic effect of pro-inflammatory cytokines in ACD is diverse: impaired iron
metabolism, decreased erythropoietin formation, and inhibition of normal
erythropoiesis in the bone marrow. The pathogenesis of this phenomenon is not
entirely clear. Most likely, the cause is the overproduction of cytokines (IL-1), which
increase the ability of macrophages to absorb and destroy red blood cells. Due to
phagocytosis of red blood cells in tissue macrophages, there is an excessive
accumulation of iron in the form of hemosiderin and ferritin, which leads to a decrease
in the content of the trace element in the serum depot bodies, which is considered to
be the main feature of the AHZ. The clinical manifestations of ACD mainly depend
on the disease with which it is associated [12,13]. In most cases, the symptoms of the
underlying disease prevail over anemia, but sometimes the anemic syndrome may be
its first manifestation. Patients with anemia have clinical signs of hypoxia (weakness,
fatigue, general malaise, decreased concentration, shortness of breath with slight or
moderate exertion, palpitations, headache). in the presence of concomitant diseases,
the development of heart failure is possible. An important symptom of anemia is the
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Volume-39_Issue-1_May-2025
30
pallor of the skin, visible mucous membranes and nail beds. An objective examination
shows an increase in cardiac impulse and heart sounds, the appearance of a functional
systolic murmur on auscultation of the heart.
In most cases, ACD is normochromic and normocytic in nature with a low level
of reticulocytes. In ACD, the indicators of serum iron and transferrin saturation are
usually reduced or normal, and the level of ferritin in the blood serum is increased,
the OVSS is within the normal range, low EPO production, and inadequate severity
of anemia. In addition, in ACD, there is a more pronounced activation of the immune
system (increased levels of hepsidin, IL-6, IFN-γ/-α, TNF-α, sICAM-1, and
lactoferrin) [2,3].
Conclusion.
Thus, the detection of anemia in patients determines the need for
mandatory clarification of the causes of this pathological condition. Timely
verification of the etiology of anemia makes it possible to start adequate therapy
without delay, which determines its effectiveness and improves the quality of life of
people.
To date, markers of chronic disease anemia (ACD) in patients have not been
developed to assess the contribution of chronic disease to the progression of chronic
diseases and the development of its complications, which determines the need to
improve methods for early diagnosis and treatment of chronic diseases.
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