Zieve's Syndrome
A syndrome that is characterized by acute metabolic condition that can occur during prolonged alcohol abuse. It was described initially in 1958 by Dr Leslie Zieve for patients with a combination of alcoholic liver disease Hemolytic Anemia and Hypertriglyceridemia. Zieve's syndrome exhibits liver and blood abnormalities caused by heavy alcohol consumption.
This is a condition associated with chronic alcoholism, frequently encountered in hospitalized alcoholics who have suddenly stopped alcohol. The underlying cause is liver delipidization and hemolytic anemia. This is distinct from alcoholic hepatitis which may be present simultaneously or develop later. The syndrome is defined by excessive blood lipoprotein, jaundice and abdominal pain.
Symptoms
Most common symptoms due to long-term history of chronic alcoholism include:
Nausea
Vomiting after heavy drinking
Anorexia
Abdominal pain
Hepatomegaly, enlarged spleen, late cirrhosis
Skin and yellow sclera
Hemolytic Anemia, Hemoglobinuria (hemoglobin is excreted in urine) and Hemosiderin (insoluble form of storage iron complex) in urine.
Hepatic dysfunction, Jaundice, Hyperlipidemia and reversible hemolytic anemia after alcohol abuse are prominent symptoms.
Causes of Zieve's Syndrome
Zieve's syndrome is caused by alcoholism due to liver cell damage and various degrees of cholestasis thus causing cancer. Fatty liver production of free fatty acids into blood stream, increased triglycerides that causes hyperlipidemia and increased cholesterol and phospholipid deposition, and damaged red blood cells which become hard and brittle and blocked by splenic sinusoids. In addition, alcoholism induced pancreatitis and vitamin E deficiency is associated with hemolysis.
Diagnosis of Zieve's Syndrome
The diagnosis is based from objective information about alcoholism, and blood test for the abnormalities. It is based on history and the triple disease – jaundice, hemolytic anemia and hyperlipidaemia. For jaundice, moderate and direct bilirubin test is done. Hemolytic anemia is visible in hemoglobinuria and hemosiderin urine. There could be drop in hemoglobin, reticulocytes, bone marrow erythroblastic hyperplasia, and increased erythrocyte fragility and shortened life of red blood cells.
Hyperlipidemia is detected by increase in cholesterol, triglycerides and phospholipids. Diagnostic tests include hemoglobin, bone marrow examination, blood lipids including cholesterol, phospholipids, triglycerides, serum bilirubin, alkaline phosphatase, and liver function test and liver biopsy. Ultrasonography is done to reveal the syndrome. There could be rapid serum level rise after alcohol withdrawal in patients with denial of drinking.
Treatment
Temperance for two to three weeks is essential for symptoms to disappear. A diet high in sugar-protein, vitamins and hepatoprotective drug is necessary. In addition to jaundice, treatment for high blood cholesterol and hemolytic anemia are essential. Basic therapy includes bed rest, adequate food intake, hydration and vitamin supplementation. The patient usually recovers from the symptoms very quickly, but the disease can recur if alcohol abuse persists.
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Bibliography / Reference
Collection of Pages - Last revised Date: October 9, 2024