Rheumatic anemia

Introduction to rheumatic anemia Rheumatism is also known as connective tissue disease. The clinical manifestations are usually anemia. About half of the patients have mild or moderate anemia during the course of the disease. Most of them are chronic anemia, and a few are autoimmune hemolytic anemia (AIHA). basic knowledge The proportion of illness: 0.005% - 0.008% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia

Cause of rheumatism anemia

Red blood cell life is shortened (30%):

Rheumatoid arthritis (RA) shortens the life span of red blood cells from normal 100-120 days to 80-90 days. After normal red blood cells are lost to RA patients, their lifespan is slightly shortened, and when the patient's red blood cells are lost to normal people, then The survival time is normal. The results of the above cross-transfusion indicate that the shortening of red blood cell life is caused by factors other than red blood cells. Under the stimulation of chronic inflammation, the mononuclear macrophage system (MMS) proliferates and the activity is enhanced, which may lead to increased destruction of red blood cells and shortened life span. With Felty syndrome, if there is obvious splenomegaly, anemia may also be related to hypersplenism. It has been reported that patients with rheumatism such as long-term fever, especially those with high fever may affect the erythrocyte membrane matrix protein, making it less deformable. It is destroyed, but the above changes usually take place above 45 °C, so it is unlikely.

Erythropoiesis (30%):

Normal people have several times the ability to produce red blood cells. Therefore, when the lifespan of red blood cells is slightly shortened, anemia does not occur clinically, and in addition to shortening the life span of red blood cells in ACD, there is still insufficient red blood cell production.

(1) Iron metabolism abnormality: iron utilization disorder is the main pathological link of ACD, that is, there is abnormal iron metabolism. In ACD, the iron absorption of the gastrointestinal tract is reduced, the iron retention in MMS is increased, and the iron released to the bone marrow young red blood cells is reduced, and the plasma iron is Also reduced, causing iron deficiency, some people labeled the red blood cells labeled with radioactive iron (59Fe) into rabbits experimentally induced inflammation, found that 59Fe was quickly taken up by MMS, and stayed, and the time of release to plasma was significantly delayed compared with the normal control. It is confirmed that chronic inflammation can cause iron retention in MMS. The cause of iron abnormality from MMS release is unknown. In recent years, the role of interleukin-1 (IL-1) has been noted. IL-1 is produced by macrophages. The protein, which can be detected in inflammatory exudates of patients with rheumatism, has biological effects such as activation of T cells, B cells, and induction of body fever, neutropenia, and within a few hours after IL-1 is injected into the animal. Caused a decrease in plasma iron concentration. It has been suggested that IL-1 can increase the release of lactoferrin from specific particles by neutrophils. It has a high affinity for iron and can compete with transferrin for binding to plasma iron. The free iron is reduced, and the iron bound to lactoferrin is quickly taken up and stored by MMS without being released to the bone marrow erythrocytes, because the young red blood cells only have the transferrin receptor, and no lactoferrin receptor, IL-1 can also The liver produces apoferritin, an acute phase reaction that occurs along with inflammation. It also binds to plasma iron and stores it in MMS, but Bently et al. use a highly specific synthetic colloid. Tracer detection studies the iron dynamics of MMS, and no ACD patients were found to have iron-depleted MMS defects.

(2) Relative reduction of erythropoietin (EPO): IL-1 also inhibits the production of EPO. The EPO level and the degree of anemia in ACD patients are not parallel, and the decrease is much larger than the decrease of red blood cells. When ACD is also found, The cytokines released by inflammatory cells can reduce the ability of the patient's bone marrow to respond to EPO, but it has been reported that ACD patients have normal EPO levels in the blood, or the EPO response ability of the bone marrow is normal.

(3) Cellular immune disorder: It has been reported that the lymphocytes of RA patients are mixed with normal red blood cells, and the synthesis of hemoglobin by red blood cells is inhibited; if the lymphocytes are stimulated with antigen in advance, the inhibitory effect is more significant. On the contrary, anti-lymphocyte antibodies are added. Or adrenal cortex hormones, can eliminate hemoglobin synthesis disorders.

(4) renal insufficiency: advanced rheumatism, especially systemic lupus erythematosus (SLE) is associated with chronic renal insufficiency, even uremia, when EPO levels are significantly reduced, EPO inhibitors are elevated, and hematopoietic tissue is responding to EPO Decreased, all lead to the reduction of erythroid progenitor cells (CFU-E, BFU-E) and anemia. In addition, plasma toxic substances increase when renal insufficiency affects the biochemical metabolism of erythrocyte membrane and erythrocyte glucose metabolism, respectively, making red blood cells antioxidant. Reduced ability and deformability, accelerated destruction, and finally, patients with renal insufficiency due to reduced feeding, often lack of varying levels of hematopoietic materials, including folic acid and vitamin B12 plus secondary hyperparathyroidism inhibition of bone marrow hematopoiesis, Can block the production of red blood cells.

Treatment-related anemia (30%):

A considerable number of patients with rheumatism have long-term application of adrenocortical hormone. If improperly applied, they may have peptic ulcer. Some of them may cause chronic small amount of bleeding or acute upper gastrointestinal bleeding, which may lead to anemia, cyclophosphamide, methotrexate. The use of immunosuppressants such as azathioprine is very common, and if used improperly, it can cause bone marrow suppression and anemia occurs.

Recently, tumor necrosis factor (TNF-) is also involved in the pathological process of ACD. It is found that TNF- can inhibit the production of EPO; reduce the formation of CFU-E and BFU-E clones in bone marrow culture system, and inflammatory pathology in rheumatism. During the process, TNF- can be produced, which affects erythroid hematopoiesis while aggravating inflammation. It is also reported that TNF can inhibit hematopoiesis by inducing stromal cells to produce TNF-.

The pathogenesis of anemia caused by rheumatism has not yet been fully elucidated, but it tends to be affected by multiple factors under the combined effects of multiple factors.

Rheumatoid anemia prevention

1. Strengthen exercise and enhance physical fitness. Regular participation in physical exercise, such as health gymnastics, practicing Qigong, Tai Chi, doing radio gymnastics, walking, etc., is of great benefit. Those who insist on physical exercise, the body is strong, the disease resistance is strong, and it is rarely sick. Its ability to resist wind, cold and dampness is much stronger than that of people who have not been physically trained.

2, to avoid the invasion of wind, cold and damp. To prevent cold, rain and damp, the joints should be kept warm, not wearing wet clothes, wet shoes, wet socks, etc. Summer heat, don't be greedy and exposed, drink cold drinks and so on. The autumn climate is dry, but the autumn wind is cool and the weather is getting cold. It is necessary to prevent the cold from invading. Winter winds are biting, and keeping warm is the most important thing.

Rheumatoid anemia complications Complications anemia

(1) Cellular immune disorder: It has been reported that the lymphocytes of RA patients are mixed with normal red blood cells, and the synthesis of hemoglobin by red blood cells is suppressed; if the lymphocytes are stimulated with antigen in advance, the inhibition effect is more remarkable. Conversely, the addition of anti-lymphocyte antibodies or adrenocortical hormones can eliminate heme synthesis disorders.

(2) renal insufficiency: advanced rheumatism, especially systemic lupus erythematosus (SLE) is associated with chronic renal insufficiency or even uremia. At this time, the EPO level decreased significantly, the EPO inhibitory factor increased, and the decrease in the reactivity of hematopoietic tissue to EPO resulted in a decrease in erythroid progenitor cells (CFU-E, BFU-E) and anemia. In addition, the increase of plasma toxic substances in renal insufficiency affects the biochemical metabolism of red blood cell membrane and red blood sugar metabolism, which reduces the antioxidant capacity and deformability of red blood cells and accelerates the destruction. Finally, patients with renal insufficiency due to reduced food intake, often have varying levels of hematopoietic materials, including folic acid and vitamin B12 plus secondary hyperparathyroidism inhibition of bone marrow hematopoiesis, can block the formation of red blood cells.

Symptoms of rheumatic anemia common symptoms fatigue, shortness of breath, shortness of breath

Because anemia is mild to moderate, and slowly occurs, most patients have less obvious symptoms. Only a few have fatigue, shortness of breath, palpitations, paleness, etc., generally no jaundice, more patients are affected by various symptoms of rheumatism. As a result, ACD itself has no characteristic positive signs.

Rheumatoid anemia check

1. Peripheral blood: Most hemoglobin is in the range of 80-100g/L, and the hematocrit is reduced to 30%~35%. It is mildly small cell hypochromic anemia or positive cell pigmented anemia, mean red blood cell volume (MCV), red The mean hemoglobin concentration (MCHC) was normal or slightly reduced.

2. Reticulocytes are normal or slightly reduced, sometimes mildly elevated.

3. Bone marrow: Most of the abnormalities were not observed. Iron staining showed normal or increased iron storage. The iron content in macrophages increased, but the iron red blood cells decreased. This is related to the decrease of iron release from MMS to young red blood cells.

4. Serum iron, total iron binding capacity and iron saturation were all decreased, while serum ferritin was normal or elevated, indicating that the free iron in the circulation was reduced and the total stored iron in the body was increased.

5. Iron kinetics detected an increase in 59Fe uptake by MMS, while 59Fe was shortened from blood disappearance and 59Fe incorporation in red blood cells was reduced.

According to the condition, clinical manifestations, symptoms, signs, X-ray, electrocardiogram, B-ultrasound, biochemical examination.

Diagnosis and diagnosis of rheumatic anemia

diagnosis

A history of rheumatism accompanied by anemia, combined with peripheral blood, bone marrow and iron staining, serum iron and ferritin, and excluding autoimmune hemolytic anemia (AIHA), iron deficiency and other types of anemia, can be diagnosed as rheumatic Anemia, in which serum iron is a necessary condition for rheumatic anemia, sometimes anemia can be used as the first symptom or manifestation of rheumatism, which often causes great difficulty in diagnosis. Therefore, clinicians must consider rheumatism in the differential diagnosis of anemia. The possibility of illness, especially for young and middle-aged women.

Differential diagnosis

1. Autoimmune hemolytic anemia: clinically, there are usually jaundice, splenomegaly; elevated blood bilirubin, mainly indirect bilirubin; peripheral blood reticulocyte is significantly increased; bone marrow erythroid hyperplasia, grain / The red ratio is inverted; the antiglobulin test is positive, and in most cases it is not difficult to distinguish it from ACD.

2. Iron deficiency anemia: serum iron and iron saturation are also decreased, but serum ferritin is decreased in parallel, bone marrow iron staining shows decreased intracellular and extracellular iron, and soluble transferrin receptor is elevated; generally no discrimination with ACD Difficulties, a few difficult to identify can be distinguished by the experimental treatment of iron.

3. Anemia caused by chronic infection: also belongs to the category of ACD, the existence of primary infectious diseases is the key to identification.

4. Renal anemia: The anemia caused by uremia in the late stage of nephropathy is normal or elevated in serum iron, and blood urea nitrogen and creatinine are significantly elevated to confirm the diagnosis.

5. Myeloid anemia: Mostly caused by extensive metastasis of malignant tumor bone marrow, serum iron is usually normal or elevated, peripheral blood appears young, young red blood cells, bone marrow smear or biopsy pathological section to find tumor cells can be diagnosed, primary The detection of tumor foci can make a final diagnosis.

Patients with anemia with anemia, such as white blood cells and thrombocytopenia, need to be differentiated from aplastic anemia (AA), myelodysplastic syndrome (MDS) and acute leukemia, typically from myeloproliferative hypoplasia, MDS bone marrow and blood There must be more than one type of pathological hematopoiesis. At least 30% of leukemia cells in the bone marrow of acute leukemia should be identified according to the above characteristics.

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