Triglycerides are vital to various cells functions and determine the amount of reserve energy that our body can offer. Triglycerides come from food and are also produced by the body. High blood triglyceride or hypertriglyceridemia is a lipid disorder. High triglyceride levels are usually accompanied by high total blood cholesterol levels. Blood triglyceride levels are indicative of a person's susceptibility to various diseases such as hypertension, heart attack, cardiovascular disease and atherosclerosis. High levels of triglycerides increase the risk of diabetes and pancreatitis. Blood triglyceride levels of around 150 200 mg/dL are considered normal. While high triglyceride levels are those above 200 mg/dL, those having triglyceride levels greater than 499 mg/dL are at high risk. High triglyceride levels also put a person at increased risk of thrombosis.
Blood triglyceride levels are measured with a blood test after abstaining from food for 12 hours and alcohol for 72 hours before testing. Drugs such as fibrates are often prescribed to reduce elevated levels of triglycerides and cholesterol. Tips to lower triglyceride:
Too much of lipid and/or lipoproteins in the blood can lead to hyperlipoproteinemia. Hyperlipoproteinemia is also known as hyperlipemia or hyperlipidemia and is a metabolic disorder. This disease remains silent for years together; only when the person suffers any heart ailment does this condition come to light. Heredity and diet play a major role in the onset of this disease; hereditary blood fat disorders are the main cause for Hyperlipoproteinemia.
Other common conditions that can cause this condition are diabetes, liver and kidney disease, hypothyroidism, alcohol and cigarette smoking. Few medications like progesterone, beta blockers, etc also increase the fat level in the bloodstream. If left unattended or untreated hyperlipoproteinemia can lead to cardiovascular and cerebrovascular diseases. This condition is common in adults rather than in children and can occur both in men and women. Depending on the excessive chemical found in the blood stream, hyperlipoproteinemia can be classified into five types:
Type I – Elevation of triglycerides
Type II – Elevated cholesterol and in few cases elevated triglycerides
Type III – Elevated cholesterol and triglyceride levels with subsequent vascular diseases
Type IV – Elevated triglycerides alone but no risk of vascular diseases
Type V – Similar to type I
No specific symptoms are shown for hyperlipoproteinemia. In very rare cases when the fat level in the blood shoots up too high, fat gets deposited in the form of bumps in the skin and tendons, this is referred to as xanthomas. In few cases, the liver and spleen enlarge when the triglycerides level shoot up too high. This leads to Pancreatitis causing severe abdominal pain. The diagnosis of hyperlipoproteinemia can be made by measuring the triglycerides, total cholesterol, lipid profile, LDL and the HDL levels in the blood.
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.
Most common symptoms due to long-term history of chronic alcoholism include:
Vomiting after heavy drinking
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.
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.
Bibliography / Reference
Collection of Pages - Last revised Date: March 23, 2019