It is a condition in which triglyceride levels are elevated.
It is a fairly common disorder. It is often related to uncontrolled diabetes mellitus, obesity, and sedentary habits, which are more frequent in industrialized societies than in developing nations.
In epidemiological studies, hypertriglyceridemia is a risk factor for coronary artery disease.
Hyperlipoproteinemia is a metabolic disorder characterized by abnormally high concentrations of specific lipoprotein particles in the plasma.
Hyperlipidemia (i.e., elevated cholesterol or triglyceride levels in plasma or both) is present in all hyperlipoproteinemias.
The primary form includes chylomicronemia, hypercholesterolemia, dysbetalipoproteinemia, hypertriglyceridemia, mixed hyperlipoproteinemia, and combined hyperlipoproteinemia.
Other diseases, such as diabetes mellitus, pancreatitis, kidney disease, and hypothyroidism, cause the secondary form.
Hypertriglyceridemia is usually asymptomatic until triglycerides are more significant than 1000-2000 mg / dL.
Signs and symptoms may include the following:
- Pain in the middle epigastric, thoracic, or posterior regions; Nausea, vomiting.
- Respiratory: Dyspnea.
- Dermatológico: Xanthomas.
- Ophthalmologic: Corneal arch, xanthelasmas.
In the exam, the findings may be expected or may include the following:
- Sensitivity to palpation in the middle epigastric quadrant or upper right/left quadrant; hepatomegaly.
- Dermatological: Eruptive xanthomas in the back, buttocks, thorax, and proximal extremities; Palmar xanthomas in dysbetalipoproteinemia.
- Cardiovascular: Decrease in pulses.
- Ophthalmologic: Corneal arch.
- Neurological: Memory loss, dementia, and depression in the presence of chylomicronemia syndrome.
Causes of hypertriglyceridemia
Genetic causes: Abnormalities of the enzyme pathway for chylomicron metabolism are the best-character genetic causes of hypertriglyceridemia.
Lipoprotein lipase and apo C-II deficiency are caused by autosomal recessive homozygous genes present at conception.
Type I hyperlipoproteinemia is the best-characterized genetic cause of hypertriglyceridemia and is caused by a deficiency or defect in the enzyme lipoprotein lipase or its cofactor, apo C-II.
Lipoprotein lipase hydrolyses triglycerides in chylomicrons and very-low-density lipoproteins (VLDL), releasing free fatty acids.
The enzyme is found in the endothelial cells of capillaries and can be released into the plasma by heparin.
Lipoprotein lipase is essential for metabolizing chylomicrons and VLDL, transforming them into their respective remnants. Apo C-II, an apolipoprotein present in both chylomicrons and VLDL, acts as a cofactor in the action of lipoprotein lipase.
The previous route is affected by other genetic disorders, particularly type 1 or type 2 diabetes, because lipoprotein lipase requires insulin for complete activity.
The second cause of hyperlipidemia, “second stroke,” must be present to develop dysbetalipoproteinemia.
In addition, the patient may be taking medications, such as protease inhibitors or tricyclic antidepressants that exacerbate hyperlipidemia.
Two more recently described syndromes include mutations in ApoAV that lead to a truncated ApoAV devoid of a lipid-binding domain and a glycosylphosphatidylinositol-linked HDL 1 binding protein that causes reduced hydrolysis of chylomicrons.
The genetic predisposition for dysbetalipoproteinemia is present in approximately 1% of the population, but only 1-2% of people with apolipoprotein (apo) E-2 develop this condition.
More than 90% of patients with dysbetalipoproteinemia are homozygous for apo E-2. Sporadic forms are associated with other genetic mutations in the apo E gene or the complete absence of apo E.
Metabolic causes: Uncontrolled diabetes mellitus, both type 1 and type 2, is one of the most common causes of hypertriglyceridemia and is often severe in patients with ketosis.
Patients with diabetes mellitus type 1 are deficient in insulin, and lipoprotein lipase is mainly ineffective.
The control of diabetes mellitus in these patients will restore the function of lipoprotein lipase, reduce triglyceride levels, and restore management of diabetes mellitus.
Causes for medications: Medications that can cause hypertriglyceridemia include the following:
- Thiazide diuretics in high doses.
- Beta-adrenergic blockers in high doses, excluding those with intrinsic sympathomimetic activity.
- Oral estrogen replacement therapy without opposition.
- Oral contraceptives with high estrogen content.
- Antiretroviral treatment.
- Atypical antipsychotics.
Other causes: Excessive consumption of alcohol and diets high in carbohydrates (more than 60% of caloric intake) are frequent causes of hypertriglyceridemia.
Acute pancreatitis can cause substantial elevations of triglycerides by unknown mechanisms.
However, much more frequently, severe hypertriglyceridemia causes acute pancreatitis. In patients with acute pancreatitis and triglycerides above 1000 mg / dL, it is prudent not to assume that triglycerides cause pancreatitis.
Other causes, such as obstruction of the common bile duct and alcoholism, should be considered possible etiologies.
One study indicated that obesity and elevation of uric acid have a strong additive interaction that increases the risk of non-alcoholic fatty liver disease and hypertriglyceridemia.
The interaction was responsible for 27% and 26% of the risk of expanded hypertriglyceridemia in men and women.
Treatment of hypertriglyceridemia
Most importantly, therapeutic lifestyle changes, emphasizing a low-fat diet and physical activity, are recommended for all patients.
The goal is to reduce the consumption of saturated fats to less than 7% of total calories and cholesterol to less than 200 mg/day, increase physical activity levels and promote weight loss.
Physical activity has a well-proven role in reducing body fat and triglyceride levels.
Plasma lipid values should be monitored every six weeks in the context of clinical visits to evaluate the success of the intervention.
It may be necessary for a professional to obtain the services of a dietitian to provide personalized dietary advice, as well as consider recruiting the patient into a program that offers structured and monitored guidance for a therapeutic lifestyle change, as demonstrated to be successful.
A 3- to 6-month trial of lifestyle modification is recommended in patients with low and average cardiac risk (0 to 1 risk factors) before using medications.
However, patients with high cardiac risk should be started with medication and changes in lifestyle.