Liver disease

Hematologic changes in acute liver disease will be discussed below. They are mainly represented by hemolytic or hypoplastic anemia.

Many years ago, Wintrobe (1936), studying the frequency of the various types of anemia in chronic liver disease, found signs of macrocytosis in 32,6% of patients normotsitoza - at 30,3%, the absence of anemia - a 22.7% and microcytic anemia - 14 , 4%.

Macrocytic anemia may be due to folic acid brand name viagra deficiency, associated with alcoholism, or even simultaneously existing pernicious anemia, but is usually not associated with deficiency of any vitamin, source macrocytes are bone marrow makronormoblasty. Macrocytes much more uniform in shape than similar cells in megaloblastic anemia similar severity. The volume of these macrocytes slightly increased compared to the norm, but they are thinner and have larger than normal red blood cells in diameter. Such cells are known as leptotsity [Binghan, 1961; Werre et al., 1970] and are of two types, one of which is mishenevidnymi cells. Mishenevidnost was influenced by serum factors - normal cells are introduced into the bloodstream of patients with circulating leptotsitami, capture an excess amount of cholesterol and acquire relevant leptotsitam properties, including resistance to salt solutions. Such changes are characteristic of severe hepatocellular lesions, in which certain cells take the form akantotsitov observed in a-b-lipoproteinemii. The presence of these cells poor prognosis, and those patients in whom they are found, usually die within 1-2 months.

Very often, especially if it is accompanied by chronic hepatitis or cirrhosis, anemia is moderate - hemoglobin levels rarely fall below 100 grams per liter. In such cases, the United neoslozh-normotsitarny and normochromic red blood cells.

If red blood cells in the peripheral blood normotsitarny or slightly megalocytic, the bone marrow hypoplasia exhibit the phenomenon, and erythroblasts become makronormoblasticheskimi [Nunally, Levine, 1961]. In makronormoblastov large nucleus, chromatin network more open and contains blocks or wedges of chromatin, rather than dense "blob" cores as the most recent normoblasts. There are giant metamyelocytes, but sometimes found the picture plazmotsitoza. Megaloblastic changes are observed only when the deficiency of folic acid.

Sometimes, as in the blood and bone marrow revealed changes characteristic of true iron deficiency. They arise due to blood loss, such as bleeding from esophageal varices, which may be complicated by hemorrhagic diathesis as a consequence of liver disease.

In anemia, concomitant liver disease, shortened life time of erythrocytes [Chaplin, Mollison, 1953; Cooksley et al., 1973]. Erythrocytes of these patients live less healthy and being transfused recipients; red blood cells of healthy individuals transfused to patients with liver disease, are short-lived. This demonstrates Viagra Is it possible Viagra will help you clearly the existence of intra-and extracellular hemolytic factor. The role of the spleen is unclear, and there is no direct correlation between the latter and the severity of hemolysis [Cooksley et al., 1973]. Splenectomy rarely improves the condition of patients and does not lead to an increase in red blood cell. It has been suggested that red blood cells are damaged during the passage through the liver [Dacie, 1967], but Cooksley et al. (1973) concluded that the passage of erythrocytes through the liver is not the primary cause of hemolysis and that this body is carried out only phagocytosis already altered cells. Kinetics of iron have shown that bone marrow is not able in the usual way to compensate for the increased destruction of red blood cells. Erythropoiesis is really growing, but not to such an extent as to prevent the development of moderate anemia. Evidence of ineffective erythropoiesis no [Kimber et al., 1965].

Lifespan of red blood cells can be reduced and in acute liver disease, but, except for the above-mentioned rare aplasia, any shortening of the red blood cell reliably compensated, so anemia is rare.

Sometimes severe hemolytic anemia may occur in patients with chronic liver disease at the time of exacerbations. One of these diseases, Tsive syndrome was first described in 1958 It occurs after a single dose of alcohol dose and is manifested in the form of severe hemolytic anemia following the hyperlipidemia and hypercholesterolemia. The syndrome is usually accompanied by weakness, vomiting, fever and pain in the epigastric region or in the lower chest. Severe hemolytic anemia may occur against the backdrop of attacks of acute viral hepatitis or developed after the Coombs-positive hemolytic anemia that accompanies chronic active hepatitis.

It should be remembered that drinking large amounts of alcohol can lead to megaloblastic or sideroblastic changes that will be imposed on the manifestations of anemia, a characteristic of chronic liver disease.

Moroccan Bath
University of Melbourne