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Aplastic Anemia

Q: A decrease in which cells leads to secondary immunodeficiency in aplastic anemia?

The development of secondary immunodeficiency and infectious complications in aplastic anemia is associated with a decrease in leukocytes, primarily neutrophils and granulocytes. Peripheral blood tests reveal leukopenia with profound neutropenia, as well as marked granulocytopenia (granulocyte levels drop below 2.0 × 10⁹/L). This cellular deficit predisposes patients to severe infections.

Q: What exogenous factors (chemical, physical, infectious) can cause acquired aplastic anemia?

Acquired aplastic anemia can be caused by the following exogenous factors: Physical factors — ionizing radiation, X-rays.Chemical factors and medications — benzene, cytostatics, immunosuppressants, sulfonamides, chloramphenicol, phenylbutazone, gold preparations, cimetidine, meprobamate, chlorpromazine.Infectious factors — hepatitis viruses, infectious mononucleosis virus, herpes viruses, tuberculosis.

Q: What hereditary (congenital) forms of aplastic anemia exist?

Hereditary (congenital) forms of aplastic anemia include the following variants: Fanconi anemia — a severe form frequently combined with skeletal anomalies or congenital heart defects.Estren-Dameshek anemia — familial hypoplastic anemia presenting as a severe form with pancytopenia.Diamond-Blackfan anemia — congenital pure red cell aplasia characterized by an isolated deficit of erythroid cells.

Q: What cellular composition changes are revealed by sternal puncture in patients with aplastic anemia?

Myelograms obtained from bone marrow aspiration in aplastic anemia patients reveal a sharp decrease in the number of all nucleated elements. A diagnostic hallmark is an overall decrease in bone marrow cellularity. Additionally, cytological specimens show a complete disappearance (absence) of megakaryocytes. In severe forms of the disease, these changes reflect the suppression of all hematopoietic lineages and the development of profound pancytopenia.

Q: What happens to the bone marrow in aplastic anemia?

There is a marked suppression of hematopoiesis. Trephine biopsy shows that active hematopoietic tissue is replaced by fat, with only isolated islands of myeloid cells remaining.

Q: What changes are found in the peripheral blood?

Profound pancytopenia develops. Erythrocytes are normocytic or macrocytic and normochromic, but a hallmark feature is the complete absence of reticulocytes.

Q: Which pathology clinically resembles aplastic anemia?

Myelophthisic anemia, which develops in granulomatous diseases, myelofibrosis, or replacement of the bone marrow by tumor metastases.

Anaemia aplastica

For medical students2 min readUpdated 2026-10-10

Study the key manifestations of Anaemia aplastica, a condition characterized by profound bone marrow suppression. You will learn about the development of pancytopenia, trephine biopsy findings, and essential differential diagnosis criteria.

PancytopeniaProfound reduction of all blood cell elements

Trephine biopsyReplacement of hematopoietic tissue with fat

ReticulocytesCompletely absent from the blood

SplenomegalyNot a feature of this pathology

Pathophysiological Process

The disease is based on marked suppression of hematopoiesis in the bone marrow. The primary issue is impaired proliferation and differentiation of hematopoietic stem cells. Due to the arrest of these processes, profound pancytopenia develops in the peripheral blood.

Clinical Manifestations

Patients experience severe clinical manifestations caused by blood cell deficits:

Severe hypoxemic syndrome due to red blood cell deficiency.
Hemorrhagic syndrome manifesting as an increased bleeding tendency.
Secondary immunodeficiency leading to frequent infectious complications.

It is important to remember that splenomegaly is not characteristic of this condition.

Laboratory and Morphological Findings

Key changes are identified through blood and bone marrow examination:

Bone marrow trephine biopsy: hematopoietic tissue is massively replaced by fat, with only small islands of myeloid tissue remaining.
Peripheral blood: erythrocytes remain normocytic or macrocytic and normochromic, but reticulocytes are completely absent.

Differential Diagnosis and Special Forms

The condition must be differentiated from several other states, including preleukemic conditions and myelodysplastic syndrome (MDS).

Special attention is drawn to myelophthisic anemia, which clinically resembles aplastic anemia. It occurs in the setting of myelofibrosis, granulomatous diseases, or tumor metastasis to the bone marrow.

Among the special forms, pure red cell aplasia is distinguished, which is more commonly diagnosed in adults and is frequently associated with a benign thymoma.

Mnemonic

Aplastic Anemia = A-plasia (no stem cell growth) + Fat instead of marrow + Zero reticulocytes + Spleen is not enlarged.

Frequently asked questions

A deficiency of which specific peripheral blood cells causes the development of hemorrhagic syndrome in aplastic anemia?

The development of hemorrhagic syndrome in aplastic anemia is associated with a peripheral blood platelet deficiency — thrombocytopenia. In severe aplastic anemia, platelet counts of 60–30 × 10⁹/L and hemorrhagic syndrome are described; a diagnostic criterion for aplastic anemia is also a platelet count < 100.0 × 10⁹/L. Bone marrow examination reveals an absence or disappearance of megakaryocytes.

A decrease in which cells leads to secondary immunodeficiency in aplastic anemia?

The development of secondary immunodeficiency and infectious complications in aplastic anemia is associated with a decrease in leukocytes, primarily neutrophils and granulocytes. Peripheral blood tests reveal leukopenia with profound neutropenia, as well as marked granulocytopenia (granulocyte levels drop below 2.0 × 10⁹/L). This cellular deficit predisposes patients to severe infections.

What exogenous factors (chemical, physical, infectious) can cause acquired aplastic anemia?

Acquired aplastic anemia can be caused by the following exogenous factors:

Physical factors — ionizing radiation, X-rays.
Chemical factors and medications — benzene, cytostatics, immunosuppressants, sulfonamides, chloramphenicol, phenylbutazone, gold preparations, cimetidine, meprobamate, chlorpromazine.
Infectious factors — hepatitis viruses, infectious mononucleosis virus, herpes viruses, tuberculosis.

What hereditary (congenital) forms of aplastic anemia exist?

Hereditary (congenital) forms of aplastic anemia include the following variants:

Fanconi anemia — a severe form frequently combined with skeletal anomalies or congenital heart defects.
Estren-Dameshek anemia — familial hypoplastic anemia presenting as a severe form with pancytopenia.
Diamond-Blackfan anemia — congenital pure red cell aplasia characterized by an isolated deficit of erythroid cells.

What cellular composition changes are revealed by sternal puncture in patients with aplastic anemia?