Hyperlipidemia refers to a range of genetic and acquired disorders that lead to elevated levels of lipids in the body, such as cholesterol, chylomicrons, lipoproteins, LDL, VLDL, apolipoproteins, and HDL. A diagnosis is made when LDL, total cholesterol, lipoprotein levels, or triglyceride levels are higher than the 90th percentile or when HDL levels are lower than the 10th percentile compared to the general population.
Numerous studies have consistently shown that high LDL cholesterol levels increase the risk of vascular disease and atherosclerotic plaques, while high levels of HDL cholesterol help regulate cholesterol levels and reduce the risk of atherosclerotic vascular disease.
The target LDL cholesterol goal for each patient depends on their cardiovascular risk, and treatment should be individualized accordingly. Lowering LDL cholesterol is critical for the primary prevention of atherosclerotic cardiovascular disease, as epidemiological evidence demonstrates a continuous positive association between LDL cholesterol levels, cardiovascular events, and patient mortality.
Epidemiology
Hyperlipidemia is a progressive and chronic disease that requires dietary and lifestyle modifications and lipid-lowering medications for many individuals. The number of individuals diagnosed with hyperlipidemia is increasing rapidly, with over three million adults affected in the United States and Europe. The incidence of hyperlipidemia is particularly high in patients who develop premature coronary artery disease, occurring in males before the age of 55 to 60 years and females before the age of 65 years.
In this group, the prevalence of hyperlipidemia is approximately 75-85%, whereas it is approximately 40-48% in a control population of similar age without premature coronary artery disease. Despite the increased incidence of elevated LDL levels, studies suggest that less than 35% of patients with hyperlipidemia effectively manage their condition.
Countries with lower obesity rates and lower consumption of saturated fats generally have lower coronary artery disease and hyperlipidemia rates than the United States and Europe. Furthermore, non-genetic pediatric hyperlipidemia may develop in children under the age of two who are underweight or obese.
Anatomy
Pathophysiology
Hyperlipidemia is an accumulation of fats or lipids in the blood caused by various factors, including endothelial damage, inflammation, hypertension, smoking, and immune factors. Atherosclerosis, the hardening and narrowing of arteries due to the deposition of fatty substances, may not show symptoms until the plaque build-up reaches 70-80% of the vessel’s diameter. The process of atherosclerosis begins with the loss of nitric oxide in the endothelium, leading to inflammation and lipid accumulation in the inner layer of the vessel wall.
This leads to the formation of foam cells as macrophages engulf lipids. Cholesterol build-up in foam cells can cause mitochondrial dysfunction, apoptosis, and necrosis of surrounding tissues, which smooth muscle cells then enclose to produce a fibrotic plaque that prevents lipid clearance. Tissue factor and increased platelet activity initiate coagulation, increasing the chances of plaque rupture and thrombosis, leading to chronic plaque build-up and rapid luminal obstruction.
Hyperlipidemia patients usually have a polygenic inheritance and can be influenced by factors such as central obesity, saturated fat intake, and cholesterol content in their diet. High levels of apo B-100 lipoproteins in plasma can also lead to atherosclerotic disease, even without other risk factors. Genetic and environmental factors contribute to an individual’s risk of developing hyperlipidemia and cardiovascular disease.
Etiology
Hyperlipidemia can be classified into primary (familial) or secondary (acquired). Primary hyperlipidemia is caused by genetic disorders inherited from birth, while secondary hyperlipidemia is typically caused by factors such as an unhealthy diet, medications, hypothyroidism, uncontrolled diabetes, and poor lifestyle habits. Family history is important in identifying underlying disturbances in lipoprotein metabolism, as they are often hereditary.
In some cases, patients with a history of premature coronary artery disease may have an underling hereditary disorder. Polygenic inheritance patterns are common in most patients with hyperlipidemia, with secondary factors like cholesterol content in diet, saturated fat intake, and central obesity playing a major role in its manifestation.
Cholesterol, a circulating fatty substance, is a major contributor to the atherogenic process, with 300 to 700 mg per day originating from excessive dietary fat intake and 800 to 1200 mg per day from the endogenous synthesis in the liver.
Other common causes of hypercholesterolemia or increased triglycerides include chronic renal failure, diabetes, nephrotic syndrome, sedentary lifestyle, hypothyroidism, and certain medications. Genetic dyslipidemias are rare but are responsible for about 60% of changes in blood lipid levels, often leading to cardiovascular diseases at an early age.
Genetics
Prognostic Factors
Hyperlipidemia is a manageable but life-long disease, and if left untreated, it can progress and lead to fatal vascular disease. Persistent high serum lipid levels during early adulthood increase the risk of coronary heart disease in a dose-dependent manner.
Adults with moderate or severe elevations in non-HDL cholesterol levels are at a higher risk of developing coronary heart disease and may benefit from aggressive medical treatment, such as high-intensity statin therapy, along with changes in diet and lifestyle.
10 mg orally every day in combination with diet and HMG-CoA reductase inhibitors
Dose Adjustments
Dosing Modifications Hepatic impairment
Adjusting the dose is not required in Mild (Child-Pugh class A)
Not recommended in case of Moderate to severe (Child-Pugh class B or C) Renal impairment
Monotherapy: Adjusting the dose is not required
Moderate to severe: Renal impairment is a Risk factors for statin-associated myopathy; use caution if simvastatin dose is more than 20 mg are being provided at the same time.
4 g orally every 1-2 times a day; progressively increase over more than 1-month intervals
Maintenance: 8-16 g daily Orally divided every 12 hours; should not exceed more than 24 g/day.
Overdose: Gastrointestinal obstruction is one of the symptoms; therapy is supportive.
Indicated for Hyperlipidemia
Tablet: Three tablets (i.e.,1.875 gm) orally two times a day or six tablets (i.e., 3.75 gm) orally every day
Oral suspension: Half packet (i.e., 1.875 gm) orally two times a day or one packet (i.e., 3.75 gm) orally every day
Diabetes Mellitus type-2
Tablet: Three tablets (i.e.,1.875 gm) orally two times a day or six tablets (i.e., 3.75 gm) orally every day
Oral suspension: Half packet (i.e., 1.875 gm) orally two times a day or one packet (i.e., 3.75 gm) orally every day
Note:
In patients who are with TG levels >500 mg/dl, it is contraindicated
For diabetic ketoacidosis or type -1 DM, it should not use
75 mg subcutaneous every two weeks or 300 mg subcutaneous every four weeks as a starting point.
If the patient is taking 300 mg every four weeks, evaluate LDL-C levels just before the next planned dose; in some patients, LDL-C levels may fluctuate between doses.
If the LDL-C response is unsatisfactory, the dose may be adjusted to 150 mg subcutaneous every two weeks.
Immediate release: 250 mg orally once a day; quantity or frequency modified every 4 to 7 days based on response and tolerance to initial therapeutic amount of 1.5 to 2 g orally divided every 6 to 8 hours.
Then modified every 2 to 4 weeks and maximum limit of 6 g/day should not be exceeded
Extended release: start with 500 mg/day orally at bedtime and modify the dosage every 4 weeks based on response and tolerance to the therapeutic dose of 1 to 2 g per day
Refrain from exceeding 1 to 2 g/day Dosing considerations
To reduce flushing, nonsteroidal anti-inflammatory drugs (NSAIDs) should be taken 30 to 60 minutes before dosing.
2 gm each day in divided doses orally
Dose Adjustments
In the case of renal impairment, when CrCl is <10ml/min, avoid the dosing
When CrCl ranges between 10-50ml/min, administer the dose every 12-18 hours
Hyperlipidemia refers to a range of genetic and acquired disorders that lead to elevated levels of lipids in the body, such as cholesterol, chylomicrons, lipoproteins, LDL, VLDL, apolipoproteins, and HDL. A diagnosis is made when LDL, total cholesterol, lipoprotein levels, or triglyceride levels are higher than the 90th percentile or when HDL levels are lower than the 10th percentile compared to the general population.
Numerous studies have consistently shown that high LDL cholesterol levels increase the risk of vascular disease and atherosclerotic plaques, while high levels of HDL cholesterol help regulate cholesterol levels and reduce the risk of atherosclerotic vascular disease.
The target LDL cholesterol goal for each patient depends on their cardiovascular risk, and treatment should be individualized accordingly. Lowering LDL cholesterol is critical for the primary prevention of atherosclerotic cardiovascular disease, as epidemiological evidence demonstrates a continuous positive association between LDL cholesterol levels, cardiovascular events, and patient mortality.
Hyperlipidemia is a progressive and chronic disease that requires dietary and lifestyle modifications and lipid-lowering medications for many individuals. The number of individuals diagnosed with hyperlipidemia is increasing rapidly, with over three million adults affected in the United States and Europe. The incidence of hyperlipidemia is particularly high in patients who develop premature coronary artery disease, occurring in males before the age of 55 to 60 years and females before the age of 65 years.
In this group, the prevalence of hyperlipidemia is approximately 75-85%, whereas it is approximately 40-48% in a control population of similar age without premature coronary artery disease. Despite the increased incidence of elevated LDL levels, studies suggest that less than 35% of patients with hyperlipidemia effectively manage their condition.
Countries with lower obesity rates and lower consumption of saturated fats generally have lower coronary artery disease and hyperlipidemia rates than the United States and Europe. Furthermore, non-genetic pediatric hyperlipidemia may develop in children under the age of two who are underweight or obese.
Hyperlipidemia is an accumulation of fats or lipids in the blood caused by various factors, including endothelial damage, inflammation, hypertension, smoking, and immune factors. Atherosclerosis, the hardening and narrowing of arteries due to the deposition of fatty substances, may not show symptoms until the plaque build-up reaches 70-80% of the vessel’s diameter. The process of atherosclerosis begins with the loss of nitric oxide in the endothelium, leading to inflammation and lipid accumulation in the inner layer of the vessel wall.
This leads to the formation of foam cells as macrophages engulf lipids. Cholesterol build-up in foam cells can cause mitochondrial dysfunction, apoptosis, and necrosis of surrounding tissues, which smooth muscle cells then enclose to produce a fibrotic plaque that prevents lipid clearance. Tissue factor and increased platelet activity initiate coagulation, increasing the chances of plaque rupture and thrombosis, leading to chronic plaque build-up and rapid luminal obstruction.
Hyperlipidemia patients usually have a polygenic inheritance and can be influenced by factors such as central obesity, saturated fat intake, and cholesterol content in their diet. High levels of apo B-100 lipoproteins in plasma can also lead to atherosclerotic disease, even without other risk factors. Genetic and environmental factors contribute to an individual’s risk of developing hyperlipidemia and cardiovascular disease.
Hyperlipidemia can be classified into primary (familial) or secondary (acquired). Primary hyperlipidemia is caused by genetic disorders inherited from birth, while secondary hyperlipidemia is typically caused by factors such as an unhealthy diet, medications, hypothyroidism, uncontrolled diabetes, and poor lifestyle habits. Family history is important in identifying underlying disturbances in lipoprotein metabolism, as they are often hereditary.
In some cases, patients with a history of premature coronary artery disease may have an underling hereditary disorder. Polygenic inheritance patterns are common in most patients with hyperlipidemia, with secondary factors like cholesterol content in diet, saturated fat intake, and central obesity playing a major role in its manifestation.
Cholesterol, a circulating fatty substance, is a major contributor to the atherogenic process, with 300 to 700 mg per day originating from excessive dietary fat intake and 800 to 1200 mg per day from the endogenous synthesis in the liver.
Other common causes of hypercholesterolemia or increased triglycerides include chronic renal failure, diabetes, nephrotic syndrome, sedentary lifestyle, hypothyroidism, and certain medications. Genetic dyslipidemias are rare but are responsible for about 60% of changes in blood lipid levels, often leading to cardiovascular diseases at an early age.
Hyperlipidemia is a manageable but life-long disease, and if left untreated, it can progress and lead to fatal vascular disease. Persistent high serum lipid levels during early adulthood increase the risk of coronary heart disease in a dose-dependent manner.
Adults with moderate or severe elevations in non-HDL cholesterol levels are at a higher risk of developing coronary heart disease and may benefit from aggressive medical treatment, such as high-intensity statin therapy, along with changes in diet and lifestyle.
10 mg orally every day in combination with diet and HMG-CoA reductase inhibitors
Dose Adjustments
Dosing Modifications Hepatic impairment
Adjusting the dose is not required in Mild (Child-Pugh class A)
Not recommended in case of Moderate to severe (Child-Pugh class B or C) Renal impairment
Monotherapy: Adjusting the dose is not required
Moderate to severe: Renal impairment is a Risk factors for statin-associated myopathy; use caution if simvastatin dose is more than 20 mg are being provided at the same time.
4 g orally every 1-2 times a day; progressively increase over more than 1-month intervals
Maintenance: 8-16 g daily Orally divided every 12 hours; should not exceed more than 24 g/day.
Overdose: Gastrointestinal obstruction is one of the symptoms; therapy is supportive.
Indicated for Hyperlipidemia
Tablet: Three tablets (i.e.,1.875 gm) orally two times a day or six tablets (i.e., 3.75 gm) orally every day
Oral suspension: Half packet (i.e., 1.875 gm) orally two times a day or one packet (i.e., 3.75 gm) orally every day
Diabetes Mellitus type-2
Tablet: Three tablets (i.e.,1.875 gm) orally two times a day or six tablets (i.e., 3.75 gm) orally every day
Oral suspension: Half packet (i.e., 1.875 gm) orally two times a day or one packet (i.e., 3.75 gm) orally every day
Note:
In patients who are with TG levels >500 mg/dl, it is contraindicated
For diabetic ketoacidosis or type -1 DM, it should not use
75 mg subcutaneous every two weeks or 300 mg subcutaneous every four weeks as a starting point.
If the patient is taking 300 mg every four weeks, evaluate LDL-C levels just before the next planned dose; in some patients, LDL-C levels may fluctuate between doses.
If the LDL-C response is unsatisfactory, the dose may be adjusted to 150 mg subcutaneous every two weeks.
Immediate release: 250 mg orally once a day; quantity or frequency modified every 4 to 7 days based on response and tolerance to initial therapeutic amount of 1.5 to 2 g orally divided every 6 to 8 hours.
Then modified every 2 to 4 weeks and maximum limit of 6 g/day should not be exceeded
Extended release: start with 500 mg/day orally at bedtime and modify the dosage every 4 weeks based on response and tolerance to the therapeutic dose of 1 to 2 g per day
Refrain from exceeding 1 to 2 g/day Dosing considerations
To reduce flushing, nonsteroidal anti-inflammatory drugs (NSAIDs) should be taken 30 to 60 minutes before dosing.
2 gm each day in divided doses orally
Dose Adjustments
In the case of renal impairment, when CrCl is <10ml/min, avoid the dosing
When CrCl ranges between 10-50ml/min, administer the dose every 12-18 hours
400 mg orally as a sustained-release tablet once daily
Take with food
https://www.ncbi.nlm.nih.gov/books/NBK559182/
medtigo
Hyperlipidemia
Updated :
August 30, 2023
Hyperlipidemia refers to a range of genetic and acquired disorders that lead to elevated levels of lipids in the body, such as cholesterol, chylomicrons, lipoproteins, LDL, VLDL, apolipoproteins, and HDL. A diagnosis is made when LDL, total cholesterol, lipoprotein levels, or triglyceride levels are higher than the 90th percentile or when HDL levels are lower than the 10th percentile compared to the general population.
Numerous studies have consistently shown that high LDL cholesterol levels increase the risk of vascular disease and atherosclerotic plaques, while high levels of HDL cholesterol help regulate cholesterol levels and reduce the risk of atherosclerotic vascular disease.
The target LDL cholesterol goal for each patient depends on their cardiovascular risk, and treatment should be individualized accordingly. Lowering LDL cholesterol is critical for the primary prevention of atherosclerotic cardiovascular disease, as epidemiological evidence demonstrates a continuous positive association between LDL cholesterol levels, cardiovascular events, and patient mortality.
Hyperlipidemia is a progressive and chronic disease that requires dietary and lifestyle modifications and lipid-lowering medications for many individuals. The number of individuals diagnosed with hyperlipidemia is increasing rapidly, with over three million adults affected in the United States and Europe. The incidence of hyperlipidemia is particularly high in patients who develop premature coronary artery disease, occurring in males before the age of 55 to 60 years and females before the age of 65 years.
In this group, the prevalence of hyperlipidemia is approximately 75-85%, whereas it is approximately 40-48% in a control population of similar age without premature coronary artery disease. Despite the increased incidence of elevated LDL levels, studies suggest that less than 35% of patients with hyperlipidemia effectively manage their condition.
Countries with lower obesity rates and lower consumption of saturated fats generally have lower coronary artery disease and hyperlipidemia rates than the United States and Europe. Furthermore, non-genetic pediatric hyperlipidemia may develop in children under the age of two who are underweight or obese.
Hyperlipidemia is an accumulation of fats or lipids in the blood caused by various factors, including endothelial damage, inflammation, hypertension, smoking, and immune factors. Atherosclerosis, the hardening and narrowing of arteries due to the deposition of fatty substances, may not show symptoms until the plaque build-up reaches 70-80% of the vessel’s diameter. The process of atherosclerosis begins with the loss of nitric oxide in the endothelium, leading to inflammation and lipid accumulation in the inner layer of the vessel wall.
This leads to the formation of foam cells as macrophages engulf lipids. Cholesterol build-up in foam cells can cause mitochondrial dysfunction, apoptosis, and necrosis of surrounding tissues, which smooth muscle cells then enclose to produce a fibrotic plaque that prevents lipid clearance. Tissue factor and increased platelet activity initiate coagulation, increasing the chances of plaque rupture and thrombosis, leading to chronic plaque build-up and rapid luminal obstruction.
Hyperlipidemia patients usually have a polygenic inheritance and can be influenced by factors such as central obesity, saturated fat intake, and cholesterol content in their diet. High levels of apo B-100 lipoproteins in plasma can also lead to atherosclerotic disease, even without other risk factors. Genetic and environmental factors contribute to an individual’s risk of developing hyperlipidemia and cardiovascular disease.
Hyperlipidemia can be classified into primary (familial) or secondary (acquired). Primary hyperlipidemia is caused by genetic disorders inherited from birth, while secondary hyperlipidemia is typically caused by factors such as an unhealthy diet, medications, hypothyroidism, uncontrolled diabetes, and poor lifestyle habits. Family history is important in identifying underlying disturbances in lipoprotein metabolism, as they are often hereditary.
In some cases, patients with a history of premature coronary artery disease may have an underling hereditary disorder. Polygenic inheritance patterns are common in most patients with hyperlipidemia, with secondary factors like cholesterol content in diet, saturated fat intake, and central obesity playing a major role in its manifestation.
Cholesterol, a circulating fatty substance, is a major contributor to the atherogenic process, with 300 to 700 mg per day originating from excessive dietary fat intake and 800 to 1200 mg per day from the endogenous synthesis in the liver.
Other common causes of hypercholesterolemia or increased triglycerides include chronic renal failure, diabetes, nephrotic syndrome, sedentary lifestyle, hypothyroidism, and certain medications. Genetic dyslipidemias are rare but are responsible for about 60% of changes in blood lipid levels, often leading to cardiovascular diseases at an early age.
Hyperlipidemia is a manageable but life-long disease, and if left untreated, it can progress and lead to fatal vascular disease. Persistent high serum lipid levels during early adulthood increase the risk of coronary heart disease in a dose-dependent manner.
Adults with moderate or severe elevations in non-HDL cholesterol levels are at a higher risk of developing coronary heart disease and may benefit from aggressive medical treatment, such as high-intensity statin therapy, along with changes in diet and lifestyle.
https://www.ncbi.nlm.nih.gov/books/NBK559182/
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