Zieves syndrome is an acute metabolic condition that can occur during withdrawal from prolonged heavy alcohol use. It is defined by hemolytic anemia (with spur cells and acanthocytes), hyperlipoproteinaemia (excessive blood lipoprotein), jaundice (elevation of unconjugated bilirubin), and abdominal pain. The underlying cause is liver delipidization. This is distinct from alcoholic hepatitis which, however, may present simultaneously or develop later.Diagnosis of Zieves syndrome should be considered in patients with prolonged alcohol use (especially after an episode of binge drinking) with an elevation of unconjugated bilirubin and without obvious signs of gastrointestinal bleeding. Pathogenesis
The proposed mechanism of the characteristic haemolytic anaemia in Zieves syndrome is due to alteration of the red cell metabolism, namely pyruvate kinase instability leaving them susceptible to circulating hemolysin such as lysolecithin. Changes in membrane lipid compositions such as increased cholesterol and polyunsaturated fatty acid (PUFA) have been reported during the hemolytic phase. Diagnosis
The diagnosis is demonstrated by the triad of alcoholic hepatitis or cirrhosis, hemolytic anemia, and hyperlipidemia. Treatment
Definitive treatment for Zieves syndrome is alcohol cessation. Individuals with markedly elevated triglycerides, particularly with a history of pancreatitis or intracerebral hemorrhage, may require plasmapharesis to avoid complications associated with hypertriglyceridemia. History
Zieves syndrome was initially described in 1958. Dr. Leslie Zieve described patients with a combination of alcoholic liver disease, hemolytic anemia and hypertriglyceridemia. References


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The disease is common in farmers and those exposed to soil and animals, suggesting that the infection is acquired from these sources.Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective T-lymphocyte (particularly TH1 population) function may be an important predisposing factor for the disease. In particular, circulating cells which are CD11b (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested T. whipplei bacteria. Diagnosis
Common clinical signs and symptoms of Whipples disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints.Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipples disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing nonacid-fast, Gram-positive bacilli.