Mechanism of Anemia in Zieveʼs Syndrome*

Haemolytic Anaemia in Alcohol Abuse

“…The relative importance of alcohol per se and the liver injury in causing haemolysis is unknown. Although all the patients described by other authors (2,9,26) as well as those in the present report displayed some evidence of liver disease, there is no correlation between the severity of liver affection and the degree of haemolysis.…”

“…In 1958 Zieve (26) described the syndrome that came to bear his name, comprising haemolytic anaemia, hyperlipidaemia and jaundice, in individuals with moderate alcoholic liver disease and no evidence of splenic hyperactivity. Subsequently, a number of reports confirming the existence of this syndrome in its complete (2,9,10) or "partial" (17) form have appeared in the literature, although others (4) have been reluctant to recognize its existence. Extracorpuscular (2) as well as intracorpuscular (9) mechanisms have been proposed to explain the haemolysis seen in this postulated syndrome.…”

Hyperbilirubinaemia and haemolytic anaemia in acute alcoholic hepatitis: there's oil in them thar veins

“…The ‘triggering factor’ could be markedly elevated haemolysins in the plasma23 such as lysolecithin3 and lysocephalin, or an extracorpuscular factor23 that increases erythrocyte destruction of host RBCs and transfused compatible donor cells during an acute illness. In vitro incubation of remission stage erythrocytes with plasma preserved from the acute illness did not hasten erythrocyte destruction, suggesting that the inciting factor does not circulate in plasma but instead may work synergistically with an additional intracellular defect.…”

Alcoholic Dyshaematopoiesis: Morphological Features of Alcohol-Induced Bone Marrow Damage in Biopsy Sections Compared with Aspiration Smears

“…The erythropoietic hyperplasia and megalo blastic changes seem to be due to several factors [1,3,[6][7][8][9][10], low-degree haemolysis being one of them. This hae molysis can be attributed to alcohol-induced hyperlipaemia leading to a destabilization of the red cell mem brane [3,[11][12][13][14], which also leads to the formation of erythrocytic inclusions with a high content of (3-glucuronidase. As previously explained, the (3-glucuronidase is thought to originate from an extraerythrocytic source and to enter erythrocytes at the sites of membrane damage [15][16][17], Similar mechanisms could produce the siderotic granules found in erythrocytes and erythroid precursors in 73% of our cases.…”