secondary sideroblastic anemia
Introduction
Introduction to secondary iron granulocyte anemia Secondary iron granulocyte anemia is secondary to certain drugs or chemical poisons (such as anticancer drugs, chlorin, alkylating agents and other anticancer drugs and lead, alcohol, etc.) and certain diseases (such as bone marrow After proliferative diseases and tumors, myeloproliferative disorders, and chronic syndromes of abnormal syndrome, the number of red blood cells, anemia, and iron in the circular iron particles is light. Once the drug is removed from the chemical poison or the primary disease is controlled, the symptoms can be eliminated by using vitamin B6. In addition, some diseases may also be associated with iron granulocyte anemia, such as hematopoietic diseases, malignant tumors, inflammatory diseases, hypothermia, etc., the mechanism is unknown. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: hemochromatosis diabetes digestive tract bleeding heart failure
Cause
Secondary iron granulocyte anemia
Hematopoietic system disease (30%):
Diseases that can cause this disease include hematopoietic diseases such as hemolytic anemia, pernicious anemia and other megaloblastic anemia, polycythemia vera, myelofibrosis, multiple myeloma, erythroleukemia, etc.; malignant tumors such as malignant lymphoma , prostate cancer, etc.; inflammatory diseases: rheumatoid arthritis, nodular polyarteritis and infection; other, such as hypothermia, mucinous edema, hyperthyroidism, uremia, erythropoietic and delayed porphyrin Sick and so on.
Drugs (20%):
These drugs are antagonists of PLP. Chloramphenicol, azathioprine, nitrogen mustard, and phenylpropionate inhibit RNA synthesis in bone marrow cells, and more importantly, inhibit mitochondrial proteins, including certain cytochromes and cytochromes. The synthesis of oxidase, the activity of iron chelatase and ALA synthase decreased with chloramphenicol, may be related to the damage of cytochrome in mitochondria, inhibit the conversion of pyridoxine to PLP, inhibit ALA dehydratase, heme synthesis Enzymes and inhibition of coproporphyrinogen III conversion to protoporphyrin III, so iron granulocyte anemia can occur in chronic lead poisoning, complete parenteral nutrition without copper supplementation can cause copper deficiency, at this time due to plasma copper blue Lack of protein (ferrous oxidase), leading to intestinal iron absorption and transport, from mononuclear macrophages and hepatocytes to plasma transferrin, while protoporphyrin, glycine and ALA production and heme synthase The activity is not reduced, and iron metabolism disorder occurs in the erythrocyte mitochondria. Due to the decrease of cytochrome oxidase, the reduction of ferric iron to divalent iron is reduced, and the reduction of ketone enzymes (such as cytochrome enzymes) in intestinal cells may also be He interferes with hematopoiesis and causes neutropenia.
Hazardous substances (20%):
Zinc can induce the production of intestinal protein metallothionein, which has the advantage of binding to copper, can prevent copper absorption and promote excretion, and is secondary to copper deficiency and cause disease.
In addition, some diseases may also be associated with iron blast cell anemia, such as hematopoietic diseases, malignant tumors, inflammatory diseases, hypothermia, etc., the mechanism is unknown.
Prevention
Secondary iron granulocyte anemia prevention
Actively treat the primary disease, avoid or reduce anti-tuberculosis and chloramphenicol drugs, and avoid exposure to harmful substances. Due to the drug, the general anemia can be corrected. If the blood is due to malignant tumors, the prognosis is poor.
Complication
Secondary iron granulocytic anemia complications Complications hemochromatosis diabetes digestive tract bleeding heart failure
Complications: may be due to massive deposition of iron combined with hemochromatosis, diabetes, cirrhosis, cardiomyopathy, etc.; can be caused by concurrent infection; can be complicated by bleeding in the digestive tract urinary tract; severe cases can be complicated by heart failure, liver dysfunction.
Symptom
Secondary iron granulocyte anemia symptoms common symptoms palpitations, gray liver dysfunction, hepatosplenomegaly, activity, shortness of breath
The main manifestation is that anemia caused by drugs can be quite serious, even requiring blood transfusion, but the symptoms are rapidly improved after stopping or (and) using pyridoxine, and anemia can be gradually reduced after chronic alcoholism stops drinking. Copper deficiency anemia Often more obvious, hemoglobin has decreased to 30 ~ 40g / L, and progressive exacerbation, iatrogenic long-term zinc supplementation can make the body zinc more than 2 to 3 times normal, resulting in obvious iron granule anemia, should cause doctors Be wary, after copper supplementation or zinc cessation, it can be gradually recovered. In rare cases, the disease occurs after using a certain drug, and the disease progresses after the suspicious drug is stopped. Some people think that the disease is caused by primary iron granulocyte anemia. Not drug-based.
Examine
Examination of secondary iron granulocyte anemia
1. Peripheral blood: The degree of anemia varies greatly. Most of the hemoglobin reduction is obvious. The characteristics of hypopigmentation anemia are obvious. The average red blood cell volume (MCV) is mostly reduced, a few are normal, and the individual is increased. The morphology of blood smear is often two-way. You can see two types of cells with normal and abnormal morphology. The red blood cells are obviously uneven in size; the abnormal shape, target shape, oval shape and erythrocyte increase, reticulocytes are normal, occasionally increased, white blood cells and platelets are normal, and red blood cells are infiltrated. Brittleness is obviously inconsistent, and can be increased or decreased.
2. Excessive proliferation of erythroid cells in the bone marrow: iron staining showed a significant increase in hemosiderin, iron granulocytes increased to 80% to 90%, and about 10% to 40% of ring-shaped iron granules were observed, the latter Most of them are middle and late erythrocytes. Iron granules can also be found in blood smears. Occasionally, giant erythrocytes are present, which may be accompanied by folic acid deficiency.
3. Most of the serum iron is increased, and the iron saturation is often significantly increased. The iron kinetics study usually shows that the plasma iron clearance rate is accelerated, which is 1/4 to 1/2 of normal; the iron utilization rate is reduced, about 1/5 of normal. One-third, liver biopsy showed iron deposition, and the liver of non-transfusion patients can have the same changes, often with asymptomatic small nodular cirrhosis, similar to liver lesions of hereditary hemochromatosis.
4. FEP in red blood cells decreased or at the lower limit of normal, FEC in erythrocytes was mostly normal, and in cases where pyridoxine treatment was ineffective, FEC was high and FEP was significantly reduced.
5. The survival time of red blood cells measured by 51Cr is normal or slightly shortened, and the average life span of red blood cells is 40 to 100 days.
6 Excretion of uric acid, uric acid (4,8-dihydroxyquinolinic acid) and/or canine quinolinic acid, indicating abnormal metabolism of tryptophan.
Diagnosis
Diagnosis and diagnosis of secondary iron granulocyte anemia
According to the characteristics of this disease, it is generally not difficult to make a diagnosis of iron granule anemia.
However, it needs to be differentiated from hereditary iron granulocyte anemia. Therefore, it must be considered based on detailed medical history and physical examination, except for hereditary iron blast anemia.
