Myelodysplastic syndrome (MDS) refers to a group of hematologic disorders characterized by dysplastic hematopoiesis in the bone marrow, cytopenia (affecting one or more blood cell lineages) and morphological abnormalities in peripheral blood, as well as immune dysfunction, caused by damage to hematopoietic stem cells due to certain factors. The exact etiology of this disease remains unclear, but it may be associated with factors such as viral hepatitis, exposure to benzene, organophosphates, radiation, or the use of medications like chloramphenicol and dibazole. MDS is a clonal disorder of hematopoietic stem cells. The incidence of MDS in children is lower than in adults. The disease often progresses slowly, with a transformation rate to acute leukemia ranging from 15% to 64%, and the time to transformation varying from 1 month to 15 years. Some patients may die during the MDS phase due to bone marrow failure, complications such as bleeding or infection, or malignancy, while a small number may experience spontaneous recovery. Timely and appropriate diagnosis and treatment can reduce the rate of leukemic transformation.

bubble_chart Clinical Manifestations

1. The onset is slow, with anemia, varying degrees of bleeding, and fever. A small number of patients may only exhibit bleeding and fever without anemia. 2. Mild to moderate (Grade II) hepatosplenomegaly, with a few cases showing lymphadenopathy, bone pain, etc.

bubble_chart Diagnosis

1. Chronic onset of refractory anemia, bleeding, and fever. 2. Mild hepatosplenomegaly (grade II), possible lymphadenopathy. 3. Peripheral blood pancytopenia or

1. bicytopenia, with possible presence of macrocytic, dysmorphic, polychromatic stippled erythrocytes, as well as leukocyte nuclear left shift, right shift, nuclear畸形, binucleation, excessive or scanty cytoplasmic granules, vacuolation, etc. Giant or dysmorphic platelets and small megakaryocytes may be observed. 4. Bone marrow findings: (1) Erythroid hyperplasia (occasionally hypoplasia), megaloblastoid changes, binucleation, multinucleation, nuclear畸形, and increased immature forms. (2) Myeloid hyperplasia or hypoplasia, monocytoid changes, maturation arrest, nuclear-cytoplasmic asynchrony, binucleation,畸形, megaloblastoid changes, with myeloblasts + promyelocytes possibly accounting for 5–30%. (3) Megakaryocytes may be increased, normal, or decreased, with presence of small megakaryocytes, large single megakaryocytes, or binucleated forms, cytoplasmic granules that are enlarged or abnormally shaped, and reduced platelet production. 5. Bone marrow histochemical staining: Decreased peroxidase and alkaline phosphatase in neutrophils, decreased nonspecific esterase and acid phosphatase in monocytes, and increased sideroblasts.

bubble_chart Treatment Measures

Treatment

1. Supportive therapy: Blood transfusion (including component transfusion). 2. Symptomatic treatment. 3. Induction differentiation therapy. 4. Cytokine application. 5. Chinese medicine Chinese medicinals: Begonia.

bubble_chart Cure Criteria

1. Cure: (1) Clinical symptoms disappear, with no anemia, bleeding, or hepatosplenomegaly. (2) Blood picture and bone marrow morphology return to normal. 2. Improvement: (1) Symptoms improve, with only grade I anemia, no bleeding or grade I bleeding, and reduction in liver and spleen size. (2) Blood picture gradually approaches normal. (3) Bone marrow morphology shows a decrease in the proportion of blast cells + promyelocytes, with improvement in cellular morphological abnormalities. 3. No improvement: (1) No alleviation of clinical symptoms. (2) No progress in blood picture examination. (3) No reduction in blast cells + promyelocytes in bone marrow morphology, with persistent cellular morphological abnormalities.

[Expert Tip]

This disease lacks typical clinical manifestations, and the cause is unknown. If symptoms such as pale complexion, bleeding, fatigue, fever, or bone pain occur, seek medical attention promptly. Follow the doctor's advice for blood tests, and if necessary, undergo bone marrow examination and biopsy for timely diagnosis and treatment. If diagnosis and treatment are delayed, this disease may progress to leukemia. However, with proper and timely treatment, progression to leukemia may be prevented. Treatment for this condition is prolonged and often yields suboptimal results, so patience and cooperation with medical professionals are essential for the best outcome. To prevent this disease, avoid prolonged exposure to benzene and radiation, use medications like chloramphenicol and dibazole cautiously, and undergo regular blood tests if exposed to such substances.