Aplastic anemia in the elderly
Introduction
Introduction to aplastic anemia in the elderly Aplastic anemia (referred to as aplastic anemia) is a group of bone marrow stem cells and hematopoietic microenvironment damage caused by chemical, physical, biological factors and unexplained causes, so that the red pulp centripetal atrophy, replaced by fat marrow, blood in the whole blood cell reduction . There are no malignant cells in the bone marrow and no reticular fibrosis. basic knowledge Sickness ratio: 0.05% Susceptible people: the elderly Mode of infection: non-infectious Complications: heart failure pulmonary edema
Cause
The cause of aplastic anemia in the elderly
Drugs (25%):
Drugs are the most common cause of illness, and there are two types of drug aplastic anemia:
1 is related to the dose, which is a toxic effect of the drug. When it reaches a certain dose, it will cause bone marrow suppression, which is generally reversible. For example, various anti-tumor drugs, cell cycle-specific drugs such as cytarabine and methotrexate mainly play a role in More mature pluripotent stem cells that are easy to divide, so when the whole blood cell is reduced, the bone marrow still retains a certain amount of pluripotent stem cells, and the aplastic anemia can be recovered after stopping the drug; the busulfan and nitrosourea not only act on the proliferative cycle. Stem cells, and also act on non-proliferative stem cells, so often lead to long-term bone marrow suppression difficult to recover, in addition, inorganic arsenic, estrogen, phenytoin, phenothiazine, thiouracil and chloramphenicol can also cause dose-related Myelosuppression.
2 and the dose has little relationship, only individual patients with hematopoietic disorders, multi-drug allergic reactions, often lead to persistent aplastic anemia, a wide variety of such drugs, common with chlorinated (mycin), organic arsenic, mipalin , trimethyl ketone, phenylbutazone, gold preparation, aminopyrine, piroxicam (inflammatory pain), sulfonamide, thiamphenicol, carbimazole (methamperin), methimazole (tazodazole), Chloramperil, etc., the most common drug aplastic anemia is caused by chloramphenicol. According to domestic investigation, the risk of aplastic anemia in patients taking chloramphenicol within three months is 33 times that of the control group, and there is a dose-response. Relationship, chloramphenicol can occur in the above two types of drug aplastic anemia, the chemical structure of chlorinated mycin contains a nitrobenzene ring, and its bone marrow toxicity is related to nitroso-chloramphenicol, which inhibits Mitochondrial DNA polymerase in bone marrow cells leads to a decrease in DNA and protein synthesis, and also inhibits the synthesis of heme. There are vacuoles and iron granules in the red cytoplasm. This inhibition is reversible once the drug stops. Use, the blood is restored, chloramphenicol can also cause the agent Lesser allergic reactions, causing myelosuppression to occur more than weeks or months after taking chloramphenicol, can also occur suddenly during the treatment, such effects are often irreversible, in vitro studies found chloramphenicol and thiamphenicol It can inhibit the growth of CFU-E and CFU-C, so it is likely to cause aplastic anemia by toxic effects on stem cells.
Chemical poisons (20%):
The relationship between benzene and its derivatives and aplastic anemia has been confirmed by many experimental research institutes. Benzene enters the human body and is easily fixed in fat-rich tissues. When chronic benzene poisoning, benzene is mainly fixed in the bone marrow. The bone marrow toxicity of benzene is its metabolite (benzene). Related to diphenols and catechols, phenols are protoplasmic toxicants, which can directly inhibit nuclear division. Since the reform and opening up, township enterprises have risen. Due to inattention to labor protection, the incidence of benzene poisoning has increased, and benzene poisoning has increased. Aplastic anemia can be chronic or acute, and the latter is mostly.
Ionizing radiation (10%):
X-rays, gamma rays or neutrons can directly damage hematopoietic stem cells and the bone marrow microenvironment through or into cells, and long-term super-allowed radiation exposure (such as radioactive source accidents) can cause aplastic anemia.
Viral infection (10%):
The relationship between viral hepatitis and aplastic anemia has been more certain, called viral hepatitis-related aplastic anemia, which is one of the most serious complications of viral hepatitis, with an incidence of less than 1.0%, accounting for 3.2% of patients with aplastic anemia. The type of hepatitis for aplastic anemia has not yet been confirmed, about 80% of which is caused by non-A, non-B hepatitis, may be hepatitis C, and the rest is caused by hepatitis B. There are two types of hepatitis-related aplastic anemia: acute type majority The onset is acute, the interval between hepatitis and aplastic anemia is about 10 weeks, hepatitis is in the recovery period, but the aplastic anemia is serious, the survival time is short, and the age of onset is light, mostly on the basis of non-A, non-B hepatitis; Chronic type is a minority, mostly on the basis of chronic hepatitis B, the disease is mild, the period of hepatitis and aplastic anemia is long, and the survival period is also long. The pathogenesis is still unclear. The hepatitis virus has a direct inhibitory effect on hematopoietic stem cells. Can cause chromosomal aberrations, and can be caused by virus-mediated autoimmune abnormalities, viral infection can still destroy the bone marrow microcirculation.
Immunity factor (10%):
Aplastic anemia can be secondary to thymoma, systemic lupus erythematosus and rheumatoid arthritis, and antibodies to suppress hematopoietic stem cells can be found in the serum of patients.
Genetic factors (10%):
Fanconi anemia is an autosomal recessive hereditary disease. It is familial. Anemia is found in 5 to 10 years old. Most cases are accompanied by congenital malformations, especially the skeletal system, such as short or missing thumb, multi-finger, shortened tibia. Short stature, small head, small eye cracks, strabismus, deafness, renal malformation and cardiovascular malformations, skin pigmentation is also very common, the disease HbF is often increased, the incidence of chromosomal abnormalities is high, DNA repair mechanisms are defective, so malignant tumors In particular, the incidence of leukemia increased significantly, and 10% of the children had a history of close relatives.
7. Paroxysmal nocturnal hemoglobinuria
(PNH) PNH and aplastic anemia are closely related, 20% to 30% PNH may be associated with aplastic anemia, and 15% aplastic anemia may have dominant PNH, both of which are hematopoietic stem cell diseases, clearly changing from aplastic anemia to PNH And the performance of aplastic anemia is not obvious; or clearly changed from PNH to aplastic anemia, and PNH performance is not obvious; or PNH with aplastic anemia and aplastic anemia with PNH red blood cells, can be called aplastic anemia - PNH syndrome.
8. Other factors
Rare cases report that aplastic anemia is gestational during pregnancy, remission after childbirth or abortion, and recurrence at the second pregnancy, but most scholars believe that it may be coincidence. In addition, aplastic anemia can be secondary to chronic renal failure, severe Thyroid or anterior (gland) pituitary dysfunction.
Pathogenesis
The main lesions of aplastic anemia include hematopoietic dysfunction, abnormal hemostatic mechanism and decreased immune function.
Hematopoietic dysfunction
(1) Hematopoietic tissue lesions:
1 reduction of myeloid hyperplasia: the total amount of red pulp in the whole body is reduced. According to Hashimoto's opinion, the red pulp cavity of the whole body is full of red pulp when the person is born. With the increase of age, the red pulp is concentrically fat, to middle age. The upper marrow of the red pulp is from the upper third of the tibia to the upper third of the tibia, and the lower limb to the upper third of the femur. The long tubular bone of the disease is completely changed into the fat marrow and is waxy yellow oily. In severe cases, the flat bone also becomes the fat marrow. Some are scattered in the fat marrow in some hematopoietic foci.
Some people think that there is a normal or hyperplasia of myeloproliferation, but this is not found in autopsy materials. The so-called "proliferative sputum" aplastic anemia may be due to the illusion caused by the extraction of cells from the proliferative foci during bone marrow puncture. 52Fe, 99mTc and 111In-C13 for bone marrow scanning also confirmed that the total amount of hematopoietic marrow was reduced. We observed that the bone marrow granules showed a decrease in hematopoietic tissue, increased adipocytes, interstitial edema, and decreased capillary cells in the capillary arteries. It was found that the stromal cells under the electron microscope also showed atrophic lesions. In addition, the trabecular bone was reduced under the light microscope, and the osteoblasts and osteoclasts were reduced. Therefore, the aplastic anemia was not only atrophy of the bone marrow hematopoietic tissue, but also the bone marrow stroma and cortical bone were atrophied. It is a disease in which the hematopoietic tissue and its surrounding bones are all atrophied.
2 lymphoid tissue including the spleen, lymph nodes are atrophy.
(2) Ineffective erythropoiesis and ineffective heme synthesis: Although chronic aplastic anemia has a site of compensatory hyperplasia, this site may have ineffective erythropoiesis, which is due to an increase in plasma iron turnover rate and a decrease in blood red iron utilization. Excretion of fecal gallbladder increased and the survival time of red blood cells was normal or near normal. The erythroid hyperplasia of the bone marrow and the reticulocytes in the blood decreased. In addition, the blood of the medical institute found that excretion of fecal porphyrin increased, and fecal porphyrin excretion increased. Biliary is the product of heme destruction. Fecal porphyrin is a by-product of heme synthesis. This indicates that the synthesis and destruction of hemoglobin increases during aplastic anemia. As the total amount of red blood cells in the body decreases, the protoporphyrin of red blood cells increases. The iron particles contained therein increased, and it was speculated that there was ineffective heme synthesis in the red blood cells.
(3) Study of iron metabolism: In most patients, iron storage increased, plasma iron content increased significantly, unsaturated iron binding capacity decreased significantly, and total iron binding capacity decreased in some patients. Extracellular fertile iron content in bone marrow increased in iron in bone marrow. The positive rate of granulocytes and the number of iron particles in young red blood cells were significantly increased, and there may be mature red blood cells containing iron particles (not found in normal bone marrow); autopsy materials showed that the iron content of organs was also significantly higher than other diseases; The iron kinetics study of 59Fe found that the plasma radioactive iron elimination time (T1/2) was prolonged, the bone marrow iron incorporation decreased and the liver and spleen iron incorporation increased, and the utilization rate of mature red blood cells in the blood circulation decreased, indicating that the iron utilization was poor, and the patient's serum was also The increase in copper and the decrease in copper in red blood cells indicate barriers to the utilization of copper by bone marrow.
(4) Others: autopsy adrenal cortical atrophy, clinical determination of urinary 17-keto and -keto alcohol excretion increased, but after ACTH load these adrenal cortex hormone metabolites could not increase correspondingly, indicating that the adrenal cortex increased, but the reserve The ability to reduce, the patient's plasma and blood cells cAMP content decreased, autopsy male patients with testicular atrophy, serum testosterone decreased, estradiol increased, which is more detrimental to hematopoiesis.
2. The abnormal part of hemostasis mechanism prolonged the clotting time, the thromboplastin production disorder, the heparin anticoagulant substance appeared in the blood of a few patients, the protein C antigen content and antithrombin III activity increased, and the platelet quality was abnormal.
3. The immune function reduces the granulocyte decrease in patients, and the alkaline phosphatase positive rate and positive index increase, which may be related to cell senescence. The absolute value of lymphocytes decreases, T and B cells decrease, T8 increases, and T4/T8 decreases. Even inversion, serum total protein and albumin levels are lower than normal, acute IgA is decreased, and lymphokines are also changed. Serum IL2, IL2 receptor, -interferon and tumor necrosis factor are increased (all of these have bone marrow hematopoiesis) Inhibition), indicating that lymphocytes are activated, due to increased Tac antigen-positive lymphocytes, in addition to natural killer cells (NK cells), the reasons for these changes indicate that the immune function of patients with red blood cells (C3B receptor rosette yield decreased The immune compound has a normal rosette rate, indicating that the patient's humoral and cellular immune functions are abnormal.
Prevention
Elderly aplastic anemia prevention
Primary prevention
Before the onset of senile aplastic anemia, the pathogenic factors are eliminated or reduced as much as possible to prevent the occurrence of aplastic anemia.
details as follows:
(1) With the rapid development of China's medical and health care work and atomic energy industry, the number of people engaged in radioactive work is increasing. It has been confirmed that chronic external exposure can cause aplastic anemia, so those engaged in radiation work should strengthen protective measures to avoid chronic external exposure. The occurrence of the resulting aplastic anemia will be prevented.
(2) A considerable number of causes of aplastic anemia are drug-induced, and domestic and foreign investigations have suggested that chloramphenicol is the most dangerous factor causing drug-induced aplastic anemia, followed by benzene and Baotaisong in Japan. Since 1975, due to the notification of restrictions on chloramphenicol, the incidence and mortality of male aplastic anemia have decreased.
In order to prevent the occurrence of drug-induced aplastic anemia, the following points should be noted:
1 Strictly grasp the indications for medication, especially for chlorine (bio)mycin, which can be replaced by other drugs.
2 rigorous hematological observation of patients with damaged bone marrow hematopoietic drugs, bone marrow examination if necessary, once the white blood cells are found to have a downward trend, the presence of vacuoles in the cytoplasm of bone marrow young red blood cells should be stopped in time.
3 Promote the importance of medication under the guidance of a doctor.
4 It is recommended that some drugs, such as chlorinated bismuth, cannot be sold at the store.
(3) Exposure to pesticides 1605, 1059, etc. can also cause aplastic anemia. These pesticides are short-term for half a year, and long-term exposures are likely to cause aplastic anemia if the protection is not good. Therefore, the necessary protective measures must be taken to use pesticides. In-depth publicity and education on protection and health knowledge to prevent the occurrence of pesticide poisoning to reduce the incidence of aplastic anemia.
(4) There have been reports of aplastic anemia in the long-term consumption of excessive saccharin water, so it should be noted that saccharin should not be eaten in large quantities at will.
(5) Prevention of infection: Certain infectious diseases can be secondary to aplastic anemia. For example, in the case of viral infection, infectious hepatitis is the most common with aplastic anemia. It is often called hepatitis-related aplastic anemia. Such cases have been reported in foreign countries in the 1950s. After the 1960s, the number of cases is increasing. Non-A, non-B hepatitis can be complicated by aplastic anemia. Young men are more common. Most of them are in the recovery period of hepatitis. The prognosis is poor. Most of the causes of hepatitis-related aplastic anemia are due to hepatitis virus invading the bone marrow and bone marrow. Micro-environment damage, hindering stem cell proliferation and differentiation leading to aplastic anemia, in view of the infection can be secondary to aplastic anemia, so strengthen physical exercise, regular life, comfortable spirit, work combined with work and rest, appropriate nutrition can enhance physical fitness It can effectively prevent infections from occurring. Once infections are treated promptly and effectively, it is important to prevent the disease as soon as possible.
2. Secondary prevention
Screening for high-risk groups of senile aplastic anemia, in order to find asymptomatic pre-clinical aplastic anemia patients, to achieve early diagnosis, early treatment, improve patient survival rate, reduce mortality, regular blood test, necessary Bone marrow puncture and bone marrow biopsy were performed, and drug treatment was used to prevent recurrence and aggravation in the diseased population.
3. Three levels of prevention
Active systemic treatment of patients with clinical aplastic anemia to prevent complications to improve the quality of life of patients and prolong their survival.
4. Risk factors
(1) Chemical factors: The drugs and chemical substances that cause aplastic anemia include benzene, chlorine (bio)mycin, various anticancer drugs, and sulfa drugs.
(2) Physical factors: X-ray, radium, radionuclide, etc.
(3) Biological factors: viral hepatitis, various serious infections, burns, etc.
In the aplastic anemia caused by various physical and chemical factors, some pathogenic factors are related to their dose, that is, sufficient dose is accepted, and the general population can develop aplastic anemia; some pathogenic factors have little relationship with the dose, but are related to individual sensitivity. Although the dose is not large, but the incidence of individuals, Wintrobe reported the cause of the disease.
Complication
Elderly aplastic anemia complications Complications heart failure pulmonary edema
The disease is mainly complicated by intracerebral hemorrhage, heart failure, pulmonary edema and various serious infections.
Symptom
Symptoms of aplastic anemia in the elderly Common symptoms Whole blood cells reduce visceral hemorrhage aging Accelerate bleeding tendency Refractory anemia Proteinuria Intracranial hemorrhage Hematuria septica Visual impairment
Acute aplastic anemia
Acute onset, rapid progress, often with bleeding and infection fever as the first and main performance, the initial anemia is often not obvious, but as the disease progresses, there is progressive progress, almost all bleeding tendency, more than 60% have visceral bleeding, Mainly manifested in gastrointestinal bleeding, hematuria, fundus hemorrhage (often accompanied by visual impairment) and intracranial hemorrhage, skin, mucosal hemorrhage is extensive and serious, and difficult to control, almost fever in the course of the disease, with infection, often in the oropharynx Necrotic ulcers occur around the anus and anus, leading to sepsis, pneumonia is also common, infection and bleeding are causal, causing the disease to worsen and most die within 1 year.
2. Chronic aplastic anemia
Slow onset, with anemia as the first and main performance; bleeding is limited to the skin mucosa, and not serious; can be complicated by infection, but often with respiratory tract, easy to control, if treated properly, perseverance, many patients can obtain long-term relief Even after recovery, but some patients have been unhealed for many years, even for a long period of 10 years, a few to late clinical manifestations of acute aplastic anemia, known as chronic aplastic anemia.
Examine
Examination of aplastic anemia in the elderly
Acute type
(1) Blood picture:
1 hemoglobin and red blood cells: positive color positive cell anemia, this type of hemoglobin can be as low as 10g / L, the highest can be 50g / L most of the 30g / L up and down, some patients with a large number of blood transfusions although hemoglobin increased, but the maintenance time is short And soon fell to a low level.
2 Reticulocytes: Reticulocytes are the values of young mature red blood cells in the surrounding blood, which can reflect the formation function of bone marrow red blood cells. They have important significance for the diagnosis of aplastic anemia and the observation of therapeutic response. This type of reticulocyte is the least. It is 0, up to about 1.4%, and most cases are below 1%.
3 white blood cells and classification: white blood cell count at least 0.7 × 109 / L or lower, up to (2 ~ 3) × 109 / L, most in (1 ~ 2) × 109 / L; the proportion of lymphocytes in the differential count is relatively significantly increased Most of the white blood cells are small lymphocytes, and the proportion of lymphocytes is more than 60%, and up to more than 90%.
4 platelets: at least 2 × 109 / L, most of them within 10 × 109 / L.
(2) Bone marrow: The red pulp has a wide range of lesions, and the multiple bone marrow images show the following changes:
1 hyperplasia reduced or severely reduced, granules, red blood cell line decreased, lymphocytes increased relatively (up to 80%); or active hyperplasia but mainly lymphocytes.
Mature granulocytes are most common in the 2 cell lines.
Among the nucleated red blood cells, the late red blood cells were the most common, and the morphology of mature red blood cells did not change significantly.
4 plasma cells, tissue basophils, reticular cells, etc. increased.
5 In addition to individual cases, bone marrow cannot find megakaryocytes.
2. Chronic type
(1) Hemoglobin and red blood cells; positive orthonormal cell anemia or large cell anemia, blood protein as low as 20% to 30%, up to 100g / L, more than 30 ~ 40g / L.
(2) Reticulocytes: 0.8% to 2.3%, up to 3% to 5%, most >1%.
(3) White blood cells and classification: The white blood cell count can be at least 1×109, up to 4×109/L, and most of them are (23)×109/L; the proportion of lymphocytes in the classification count is increased up to 60. %~70% or more.
(4) Platelets: at least 5 × 109 or less, up to 4 × 109 / L, and most (10 ~ 20) × 109 / L.
Bone marrow: bone marrow is focal hematopoiesis, some bone marrow hyperplasia (many oil drops when observed by the naked eye, after smear, there are many oil drops on the slide, not easy to dry) some bone marrow hyperplasia (proliferation active or obvious active), hyperplasia The bad part is similar to the acute type of bone marrow, but the general plasma cell tissue basophils and reticular cells are not like acute type, the hyperplasia is good, the granulocyte system is normal or lower than normal, the red blood cell line is increased, and the young cells are Mainly, mature red blood cells are mildly uneven in size, with a small amount of multiple erythrocytes, mild lymphocytes, and decreased megakaryocytes, which can be distinguished from bone marrow of other proliferative anemia (the number of megakaryocytes in various proliferative anemias) Aplastic anemia is more).
3. Other inspections
Hematopoietic progenitor cell culture not only contributes to diagnosis, but also helps to detect the presence or absence of inhibitory lymphocytes or serum in the presence or absence of inhibitory factors, mature neutrophil alkaline phosphatase activity, serum lysozyme activity is reduced, anti- The amount of alkali hemoglobin is increased. In addition to the chromosomal aberrations of Fanconi anemia, the general aplastic disorder is normal. If there is a karyotypic abnormality, it often indicates the early stage of leukemia.
Bone marrow biopsy and radionuclide bone marrow scan: Because bone marrow smears are susceptible to peripheral blood dilution, sometimes 1 or 2 smears are difficult to correctly reflect hematopoiesis, and bone marrow biopsy is better than smearing Tablets can improve the correctness of diagnosis. Systemic bone marrow gamma photography of molybdenum sulfide or indium chloride can reflect the distribution of systemic functional bone marrow. The radioactive uptake of normal bone marrow in the case of aplastic anemia is low or even disappears, so it can indirectly reflect the reduction of hematopoietic tissue. Degree and location.
Diagnosis
Diagnosis and diagnosis of aplastic anemia in the elderly
Diagnostic criteria
The diagnostic criteria for aplastic anemia revised in the Fourth National Conference on Aplastic Indus in 1987 are as follows:
1. Complete blood cell reduction, reduced absolute value of reticulocytes.
2. Generally no splenomegaly.
3. Bone marrow examination shows that at least one part of the hyperplasia is reduced or severely reduced (such as hyperplasia, megakaryocytes should be significantly reduced, non-hematopoietic cells should be seen in the small bone marrow components, and those with conditions should be examined by bone marrow biopsy).
4. Can exclude other diseases that cause whole blood cell reduction, such as paroxysmal nocturnal hemoglobinuria, refractory anemia in myelodysplastic syndrome, stagnation of acute hematopoietic function, myelofibrosis, acute leukemia, malignant histiocytosis Wait.
5. General anti-anemia drug treatment is ineffective, acute type is also called severe aplastic anemia type I. If the chronic type of disease is worse, clinical, blood and bone marrow are the same as acute, called severe aplastic anemia.
Differential diagnosis
Aplastic anemia is characterized by a reduction in whole blood cells, and the diagnosis of aplastic anemia must be similar to the following diseases:
1. Paroxysmal nocturnal hemoglobinuria (PNH) Typical cases have hemoglobinuria, easy to identify aplastic anemia, atypical cases, no hemoglobinuria, clinically mainly chronic anemia, three blood cells in peripheral blood, bone marrow Can be proliferated and reduced, bone marrow can also be proliferated and reduced, it is easy to be mistaken for aplastic anemia, but PNH bleeding, infection is less and less light, reticulocytes are greater than normal, bone marrow hyperplasia is active, young red blood cells are more proliferative, containing iron yellow urea Rous can be positive, acidified serum hemolysis test (Ham) and venom factor hemolysis test (CoF) more positive, red blood cell micro-complement hemolytic susceptibility test (mCLST) can detect PNH red blood cells, N-ALP reduction, plasma and erythrocyte choline The esterase is significantly reduced.
2. Myelodysplastic syndrome (MDS) is difficult to distinguish from refractory anemia (RA) in MDS, because the main manifestation of RA is chronic progressive anemia, occasionally skin bleeding, blood shows whole blood cell reduction, reticulation Red blood cells sometimes do not increase or even decrease, these are easy to be confused with aplastic anemia, but RA is characterized by pathological hematopoiesis. Peripheral blood shows uneven red blood cell size, abnormal shape, occasionally huge red blood cells and nucleated red blood cells, mononuclear cells are increased, and immature grains are visible. Cells and giant platelets, bone marrow hyperplasia is more active, occasionally nucleus pulp development imbalance, visible nuclear abnormalities or excessive lobulation, many or increased megakaryocytes, occasionally lymphocyte-like small megakaryocytes, some cases showed nucleation The erythrocyte glycogen (PAS) is positive, the nucleated cells of the ring-shaped iron granules are increased, and the immunohistochemical examination may have small megakaryocytes. Further, according to the bone marrow biopsy, the immature early cell ectopic (ALIP) can be found, and the leukemia group can be found in the cell training. Cells (CFU-L), karyotypes can be abnormal, sister chromatid abnormalities (SCD positive), oncogenes and other tests to identify.
3. Acute leukemia (AL), especially leukopenia and hypoplastic AL can be a chronic process, early liver, spleen, lymph nodes are not swollen, peripheral blood whole cells are reduced, bone marrow hyperplasia is reduced, easy to be confused with aplastic anemia, carefully observe the blood And many parts of the bone marrow, you can find the original grain, single, or primordial lymphocytes increased significantly, bone marrow biopsy also helps with the differential diagnosis of aplastic anemia.
4. Malignant histiocytosis (MH) is often accompanied by non-infectious hyperthermia, progressive failure, liver, spleen, lymphadenopathy, jaundice, hemorrhage, peripheral blood, complete blood cells, abnormal tissue cells, multi-site bone marrow examination Abnormal tissue cells can be found, often with phagocytosis, which can be distinguished from aplastic anemia.
5. Myelofibrosis (WF) Chronic cases often have splenomegaly, immature granulocytes and nucleated red blood cells can be seen in the peripheral blood, bone marrow puncture multiple dry pumping, bone marrow biopsy shows collagen fibers and or reticular fibers significantly hyperplasia.
6. Acute hematopoietic stagnation The so-called hematopoietic function usually refers mainly to the red blood cell system, and other systems can also be involved. This disease often occurs in patients with hemolytic anemia or normal bone marrow with infection and fever, such as hereditary spherocytosis. , sickle cell anemia, paroxysmal nocturnal hemoglobinuria, autoimmune hemolytic anemia, etc., so that peripheral blood three cells, especially red blood cells, suddenly drop, reticulocytes can be reduced to 0, bone marrow red blood cell system is reduced, so Similar to aplastic anemia, but the early stage of the disease, the bone marrow appears huge primitive red blood cells, its shape and structure are similar to the original red blood cells, and the histochemical reaction is also consistent with the original red blood cells, but its body is large, the disease is a self-limiting The disease can be naturally recovered after 7 to 10 days. Therefore, it is not difficult to distinguish from aplastic anemia by understanding the condition and related causes of the disease, and by controlling infection, supporting therapy and a good prognosis.
7. Renal anemia Anemia can occur in the late stage of chronic glomerulonephritis. As the disease progresses slowly, white blood cells and platelets are slightly reduced except for anemia. Sometimes, the patient's urine changes are not noticed, so it can be confused with the aplastic anemia. Anemia of kidney disease occurs in the late stage of nephritis. Patients have edema, nocturia, and severe renal damage. At this time, patients have protein, blood urea nitrogen increases, and other renal function tests are abnormal. These are helpful for aplastic anemia. the difference.
8. Simple red blood cell aplastic disorder Simple red blood cell aplasia and aplastic anemia have different pathogenesis. The former mainly affects erythroid hematopoietic progenitor cells, while the latter mainly affects pluripotent hematopoietic stem cells. Therefore, the former only manifests as a simple red system aplastic anemia, and the blood is often It is characterized by simple severe anemia, normal white blood cell and platelet count; bone marrow red system can be absent, while granulocyte system and megakaryocyte system are normal; the latter affects red, granulocyte and megakaryocyte cell lines, so the two are not difficult to distinguish.
9. Excessive consumption of red blood cells caused by hypersplenism due to hypersplenism, such as congestive splenomegaly (the most common cirrhosis), connective tissue disease (systemic lupus erythematosus, rheumatoid arthritis), lymphatic network Malignant tumors (malignant lymphoma), histiocytosis (hyperemia, le-blood disease) and primary spleen cytopenia; all have complete cytopenia, easy to be confused with aplastic anemia, such spleen is obvious Swelling, examination of the bone marrow can find abnormal cells, and some have obvious bone marrow hyperplasia, which is completely different from aplastic anemia.
10. Bone marrow metastasis in the bone marrow if metastases can lead to decreased hematopoietic function, blood can show complete blood cell reduction, similar to aplastic anemia, but this patient can be clinically characterized by severe bleeding and fever, blood smear can be nucleated Erythrocytes, reticulocytes, red blood cells, and immature granulocytes can also be found. Careful examination of bone marrow smears reveals clusters of metastatic tumor cells, sometimes accompanied by bone marrow necrosis, and some patients can show signs and symptoms of primary disease. These can be distinguished from aplastic anemia.
