Red Cell Metabolic and Membrane Features in Haemolytic Anaemia of Alcoholic Liver Disease (Zieve's Syndrome)

Abstract

Zieve's syndrome (ZS), which consists of transient haemolytic anaemia, jaundice, hyperlipoproteinaemia, and alcohol-induced liver disease, was studied in male patients during the acute (n = 20) and the remittent (n = 10) phase. Chronic alcoholics (n = 10) without haemolysis and healthy male persons (n = 10) served as controls. Erythrocytes were separated into old and young cells by means of density-layer centrifugation. Those fractions which contained older red cells disclosed a pyruvate-kinase instability which resulted in impaired metabolism. Changes in membrane lipid composition as indicated by increased cholesterol and polyunsaturated fatty acids (PUFA) were also detected in patients during the acute phase of ZS. Alcohol-induced red-cell vitamin-E deficiency with a decrease in PUFA levels may provoke an oxidation of reduced red-cell glutathione which in turn results in the enzyme instability. This study lends further support to the hypothesis that the putative role of the red-cell metabolic injury in the origin of haemolysis in ZS cannot be envisaged without introducing membrane-linked and extracellular cofactors.

Haemolytic Anaemia in Alcohol Abuse

“…Heck et al (10) have estimated the frequency of Zieve's syndrome in a general medical ward to be approximately one of I600 admissions. Interestingly, the large male preponderance regularly found in that and in other reports ( 2 , 9) is not confirmed in our study. Most of the studies on alcohol-induced haemolytic anaemia have been performed on regular, heavy drinkers or skid-row alcoholics with chronic liver disease.…”

“…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

“…This suggests that increased RBC lipids may thus be a more important association for haemolysis than increased plasma lipid 28. Another striking observation is a decrease in membrane-bound polyunsaturated fatty acids (PUFA) concentrations when correlated with the concurrently decreased serum and membrane tocopherol levels 29. Vitamin E is located primarily within the phospholipid bilayer of cell membranes and is particularly effective in preventing lipid peroxidation—a series of reactions involving the oxidative deterioration of PUFAs.…”

Alcohol and the blood.

“…The erythrocyte membrane is altered in composition,26 resulting in the development of spherocytes.27 Vitamin E deficiency may further contribute to instability of the red cell membrane. 28 The importance of alcohol as a direct haemopoietic toxin has been shown by Lindenbaum and Lieber,29 who studied the effects of high doses of alcohol given to former alcoholic patients. Adequate nutrition and vitamin intake was ensured.…”