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Anemia caused by liver diseases

  Anemia caused by liver diseases refers to the anemia complication that occurs during the course of liver disease, which is common in most patients with chronic liver disease. Epidemiology: According to the statistical data of Peking Union Medical College Hospital, 22% of the total inpatients with anemia are caused by hyperplasia of the spleen due to severe hepatitis. While there are few reports on the proportion of patients with chronic liver disease complicated with anemia in China. Abroad, two groups of reports show that the proportion of patients with chronic liver disease complicated with anemia is 20% to 75%.

 

Table of Contents

What are the causes of anemia caused by liver diseases?
2. What complications can anemia caused by liver disease lead to
3. What are the typical symptoms of anemia caused by liver disease
4. How to prevent anemia caused by liver disease
5. What laboratory tests need to be done for anemia caused by liver disease
6. Diet taboo for patients with anemia caused by liver disease
7. Conventional methods for the treatment of anemia caused by liver disease in Western medicine

1. What are the causes of anemia caused by liver disease

  First, Etiology

  The most common anemia in liver disease is Laennec cirrhosis, biliary cirrhosis, hemochromatosis, post-hepatic cirrhosis, acute hepatitis, and hepatolenticular degeneration, which can also cause anemia in liver disease.

  Second, Pathogenesis

  The pathogenesis of anemia in liver disease has not been fully understood, but it has been proven to be related to the following factors:

  1. Deficiency of hematopoietic factors:The liver is an important organ of the body's metabolism and plays an important role in maintaining the normal physiological function of the blood system. Including:

  (1) Storage of hematopoietic raw materials: Folic acid, vitamin B12, iron preparations, and many proteins and lipids are stored and used in the liver.

  (2) Synthesis of coagulation factors: Coagulation factors I, II, V, VII, IX, X, XII, XIII, and so on are all synthesized in the liver.

  (3) Partial secretion of erythropoietin: The liver is the main site for the renal secretion of erythropoietin.

  Therefore, when the above functions are impaired in liver disease, it can cause folic acid and vitamin B12 deficiency leading to megaloblastic anemia; coagulation mechanism disorders causing bleeding, leading to iron deficiency anemia.

  2. Shortened erythrocyte lifespan:A shortened erythrocyte lifespan can be seen in liver diseases such as alcoholic liver disease, biliary cirrhosis, obstructive jaundice, infectious hepatitis, and so on. Even in the above diseases without anemia, a shortened erythrocyte lifespan may occur, and about 70% of liver disease patients have a shortened erythrocyte lifespan. The exact cause of the shortened erythrocyte lifespan in liver disease is still not fully understood. When patients and healthy people are cross-transfused, the lifespan of the patient's erythrocytes in the healthy body is significantly prolonged, and the lifespan of the healthy person's erythrocytes in the patient's body is also shortened. This suggests that the shortened erythrocyte lifespan is caused by extracellular hemolysins. Research has shown that the following factors are related to the shortened erythrocyte lifespan of patients:

  (1) Spleen enlargement: Congestive splenomegaly in liver disease can be accompanied by splenic hyperfunction, causing excessive destruction of erythrocytes in the spleen. The method of using 51Cr-labeled erythrocytes to test has proved that the lifespan of erythrocytes in patients with splenomegaly is significantly shorter than that in patients without splenomegaly. Foreign experiments have shown that in patients with myeloproliferative diseases, for every 1kg increase in the weight of spleen enlargement, the daily destruction of erythrocytes in the spleen increases by 1% of blood cell volume.

  (2) Abnormal erythrocyte metabolism: In patients with liver disease, the erythrocyte pentose phosphate pathway metabolism is low, resulting in reduced intracellular reduced glutathione production, easy oxidation of hemoglobin, and the formation of Heinz bodies, leading to the easy destruction of erythrocytes. The low pentose phosphate pathway metabolism may be related to the decrease of nicotinamide adenine dinucleotide phosphate (NADP) or other unknown reasons. In addition, patients often have hypophosphatemia, which leads to a decrease in intracellular ATP levels and reduced membrane deformability, which can cause hemolysis.

  (3) Abnormal red blood cell membrane lipids: The red blood cell membrane is composed of a bilayer of lipids. The outer side of the membrane is mainly free cholesterol and two phospholipids, namely phosphatidylcholine and sphingomyelin. The inner side of the membrane is mainly phosphatidylserine and phosphatidylethanolamine. In patients with hepatitis, cirrhosis, and obstructive jaundice, the free cholesterol and phosphatidylcholine on the outer side of the red blood cell membrane are increased by 20% to 50% compared to normal, leading to an increase in the surface area of red blood cells and forming specific thin macrocytes and target cells, causing them to stay for too long in the sinusoids of the spleen and be easily engulfed and destroyed by mononuclear macrophages. In addition, the activity of sialidase in patients with bile duct obstruction increases, causing an increase in the secretion of sialic acid on the red blood cell surface, leading to a decrease in red blood cell vitality.

  (4) Acanthocyte hemolytic anemia: The cholesterol on the red blood cell membrane of patients is significantly increased, while the phosphatidylcholine does not increase correspondingly, leading to a decrease in the deformability of red blood cells. When passing through the spleen, the cell membrane is engulfed by mononuclear macrophages in pieces, causing the surface area of red blood cells to continuously decrease and finally become acanthocytes. The mechanism of red blood cell membrane lipid changes is known to be related to the following factors:

  ① The ratio of cholesterol to phospholipid in low-density lipoprotein in blood: The mature red blood cells themselves cannot synthesize lipids and need to rely on lipoproteins in plasma for renewal. Abnormal lipoproteins in plasma change the lipid components on the red blood cell membrane. However, why some patients do not have an abnormal mechanism of plasma lipoprotein is still unclear.

  ② Decreased activity of phosphatidylcholine-cholesterol acyltransferase in plasma.

  ③ Bile retention in plasma.

  ④ Other factors: Alcoholic liver disease patients often produce alcohol-induced vitamin E deficiency, leading to a decrease in various unsaturated fatty acids on the red blood cell membrane, causing membrane deformation and decreased resistance to oxidants. In addition, portal hypertension and splenomegaly may also be a partial cause of hemolysis in liver disease.

  3. Decreased bone marrow hematopoietic function:The plasma iron turnover rate, intracellular iron utilization rate, and intracellular iron turnover rate in most liver disease patients are normal or decreased, indicating a decrease in bone marrow hematopoietic function. However, there are also reports of increased cases, which may be related to whether the patient has complications. Alcoholic liver disease patients have a significantly suppressed red blood cell hematopoietic function. This is manifested by megaloblastic changes in the erythroblasts of the bone marrow, vacuoles in the cytoplasm of erythroblasts and granulocytes, and an increase in ring-shaped sideroblasts, indicating pathologic erythropoiesis. After giving up alcohol, the above phenomena disappear.

  4. Increased plasma volume:The majority of chronic liver disease patients are complicated with anemia, and their plasma volume is about 15% higher than that of normal people. For some anemic patients, the red blood cell volume does not decrease, so blood dilution is also one of the causes of anemia in liver disease.

  5. Hemorrhage:Hepatic cirrhosis complicated with hemorrhage is reported to be between 24% and 75% in different reports. The main bleeding site in alcoholic cirrhosis patients is the gastrointestinal tract, followed by hemorrhoids and uterine bleeding. Abnormal coagulation mechanism further aggravates hemorrhage. Hemorrhage is also one of the causes of anemia in liver disease patients.

2. What complications are easy to cause anemia caused by liver diseases

  The most common complication is hemolytic anemia and upper gastrointestinal bleeding.

  1. Hemolytic anemia:It refers to a type of anemia that occurs when the red blood cell destruction accelerates and the bone marrow hematopoietic function is insufficient to compensate for it. If the bone marrow can increase red blood cell production enough to compensate for the shortened survival period of red blood cells, anemia will not occur. This condition is called compensatory hemolytic disease.

  2. Upper gastrointestinal bleeding:Refers to bleeding caused by esophageal, gastric, duodenal, upper jejunum (about 50cm below the duodenal suspensory ligament), and lesions of the pancreatic duct and bile duct. The clinical manifestations are mainly vomiting blood and melena, which is a common surgical emergency.

3. What are the typical symptoms of anemia caused by liver diseases

  Due to the different etiology of liver diseases, the degree of anemia and clinical manifestations also vary accordingly, generally mild to moderate anemia, severe anemia is rare. For patients with liver cirrhosis without complications, anemia is mostly normocytic, normohemoglobin anemia. For a few patients with alcoholic liver cirrhosis and biliary cirrhosis, hemolytic anemia with spiculated red blood cells may suddenly occur a few months before death due to the rapid deterioration of liver function. However, if the liver function improves, hemolysis will spontaneously resolve. In patients with alcoholic liver disease, even with slight liver function damage, there may also be paroxysmal hemolytic anemia. This hemolytic anemia is usually mild to moderate and self-limiting, can recur, improve within 2-3 weeks after abstinence from alcohol, and can be induced again after drinking. If the patient also has jaundice and hyperlipidemia, it is called 'Zieve syndrome'.

4. How to prevent anemia caused by liver diseases

  Mainly for liver disease treatment, avoid alcohol consumption, strengthen nutrition, and actively adopt liver-protecting treatment methods. For patients with massive upper gastrointestinal bleeding and splenomegaly, surgical treatment can be performed. Necessary hematopoietic substances should be supplemented, including folic acid, vitamin B, and iron preparations, and certain patients may obtain certain efficacy. Diet should not be monotonous, and it should be avoided to prepare unreasonably, especially not to have a long-term preference for certain foods. When eating iron-rich foods, they should not be used at the same time as vegetables such as amaranth, fresh bamboo shoots, and strong tea, which have high oxalic acid or tannic acid content. Avoid drinking high-concentration白酒, avoid drinking coffee and strong tea excessively, and avoid smoking.

 

5. What laboratory tests are needed for anemia caused by liver diseases

  1. Peripheral blood:It is normocytic and normochromic anemia, but it can also present as macrocytic anemia, platelet count is reduced, but generally not below 50×109/L, white blood cell count is generally normal, but the classification can show a decrease in lymphocyte ratio, a decrease or increase in neutrophils, and neutrophil chemotactic inhibitor can be measured in plasma. There may be a decrease in all blood cells, and when combined with hemorrhage, the reticulocyte count increases.

  2. Bone marrow morphology:Hyperplasia is normal or significantly active, erythroid hyperplasia is often significantly active, causing the granulocyte/erythrocyte ratio to decrease, and it is common to have 'macrocytes', which refers to young erythrocytes with increased volume and normal chromatin structure, but about 20% of patients may have increased megaloblasts in the bone marrow.

  3. According to the condition, clinical manifestations, and symptoms, X-ray, ultrasound, CT, liver function, and biochemical tests can be chosen to be performed.

6. Dietary recommendations for anemia patients with liver diseases

  一、贫血的早餐推荐食物

  1、蛋白食物:First, recommended foods for breakfast for anemia

  1. Protein foods:Iron-fortified milk powder, milk with sugar, yogurt, soy milk with sugar, egg custard, boiled eggs, marinated eggs, lean sauce meat slices, tofu skin, etc.

  2. Staple foods:

  Second, recommended foods for lunch and dinner for anemia1. Vegetables:

  2. Staple foods:Red bean porridge, vegetable and meat wontons, beef dumplings, shrimp meat small dumplings, red bean paste buns, sesame buns, mixed sugar buns (walnut kernel, peanut kernel, sesame, dried fruit, raisins, honey dates, melon strips, Beijing gao, osmanthus, sugar), small dumplings, sesame sauce twist, minced meat vegetable porridge, minced chicken porridge, meat floss rice, dumpling soup, yolk porridge, fish meat floss porridge, sesame sauce twist, small meat roll, vegetable and meat small dumplings, fish meat dumplings, two-millet kidney bean porridge, corn flour soybean porridge, minced meat soft rice, egg noodles, minced meat noodles, scallion oil shrimp noodles.

7. Conventional methods of Western medicine for treating anemia caused by liver diseases

  1. Treatment of anemia caused by liver diseases should focus on the treatment of the primary liver disease, such as removing or improving the cause of liver disease, and anemia is often corrected accordingly. Actively adopt liver-protecting treatment, improve liver function, and strengthen the nutrition of patients.

  2. Patients with liver cirrhosis complicated with gastrointestinal bleeding or hypersplenism may consider surgical treatment.

  3. For patients with concurrent hemolytic anemia,戒酒, using hypolipidemic drugs to improve the ratio of abnormal cholesterol and phosphatidylcholine in the blood, and controlling the progression of fatty liver may be effective. Supplement hematopoietic raw materials according to the type of hematopoietic raw materials lacking in the patient.

  4. For those with concurrent megaloblastic anemia, supplementation of folic acid and vitamin B12 can often achieve good therapeutic effects.

  5. For those with concurrent hemorrhage, iron supplements or blood transfusion can be supplemented.

 

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