Polygenic Hypercholesterolemia is an elevated total cholesterol or LDL-C caused by multiple polymorphisms throughout the genomic region. While monogenic hypercholesterolemia, like FH, is characterized by mutations in specific genes such as LDLR, APOB or PCSK9, polygenic hypercholesterolemia is due to multiple common, low effect genes increasing cholesterol concentration.
Epidemiology
Currently, more than 100 million people in the United States have elevated LDL-C levels out of the population. Among them, only 50% sought any treatment, and even fewer of them, <35%, can achieve the target level of blood cholesterol, which puts them at a higher risk of ASCVD. Cohort evidence from different countries also supports that the prevalence of heterozygous familial hypercholesterolaemia may range up to 0.40 %. Familial hypercholesterolemia is diagnosed in less than one out of ten cases; Clinical familial hypercholesterolemia is likely to range from 20 to 30 % of patients with polygenic hypercholesterolemia.
Anatomy
Pathophysiology
Genetic Variants: Various common genetic variations (polymorphisms) affecting cholesterol metabolism also cause increased levels of LDL cholesterol.
These include genes that affect: The metabolism of lipoproteins (which includes variants in APOE, LDLR, PCSK9).
Cholesterol synthesis (particularly related to HMGCR).
HDL metabolism (e.g., CETP).
Each variation on its own has a small effect, but in combination they markedly raise LDL cholesterol.
Increased LDL-C Synthesis: Enhanced synthesis of cholesterol within the cholesterol biosynthesis pathway, particularly relating to changes in enzymatic activity targeting HMG-CoA reductase, the known goal of statin drugs.
Decreased LDL-C Clearance: Because of genetic variations in the LDLR gene or related pathways, the plasma clearance of LDL-containing particles declines, leading to a high LDL particle concentration.
Endothelial Dysfunction and Atherosclerosis: High levels of LDL-C are sustained as a cause of endothelial dysfunction; it has been linked with depositions of cholesterol on the walls of blood vessels. This is one of the ways by which the formation of atherosclerotic plaques is confirmed; later, cases of cardiovascular diseases including coronary artery diseases.
Etiology
Genetics: Several SNPs in genes known to regulate lipid metabolism, including LDLR (the LDL receptor), APOB (apolipoprotein B), and PCSK9 modify levels of cholesterol. These SNPs usually have additive effects.
Gene-Environment Interaction: Lifestyle, diet, or exercise may either aggravate or mitigate a predisposition to hypercholesterolemia.
Polygenic risk score: It is possible to make a polygenic risk score based on these SNPs. Thus, it helps serve as a predictive element for predisposing an individual to hypercholesterolemia.
No Apparent Dominant Mutation: While familial hypercholesterolemia is caused by a dominant mutation presenting with a high level of cholesterol, polygenic hypercholesterolemia is caused by minor increases in multiple genes.
Genetics
Prognostic Factors
Genetic Risk Score (GRS): Increasing the polygenic risk score which depends on the activity of multiple genetic markers is linked with increased cholesterol rates and ASCVD risk.
 LDL-C Levels: Studies have suggested that sustained hypercholesterolemia and particularly sustained hyper-LDL cholesterolemia is a massive prognostic factor.
Family History of Cardiovascular Disease: The family history correlate is defined by occurrences like a heart attack or a stroke that would have happened before age 55 in male or age 65 in female.
Age: Cholesterol is proved to be dangerous with increasing age because it causes cardiovascular complications during longtime inflammation.
Clinical History
Age Group:
Middle aged (Above 40+ years): The target group are middle-aged people with most of them being within the 40-60 years age group. Polygenic hypercholesterolemia becomes manifest in middle age and may be detected during the general clinical examination or screening of total cholesterol levels.
Older Adults (60+ years): Long-time polygenic hypercholesterolemia patients are likely to develop cardiovascular events such as a heart attack or stroke.
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis. Â
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle. Â
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor. Â
Acuity of presentation
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis.
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle.
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor.
Differential Diagnoses
Familial Hypercholesterolemia (FH)Â
Familial Combined HyperlipidemiaÂ
HypothyroidismÂ
Diabetes MellitusÂ
Liver DiseaseÂ
Nephrotic SyndromeÂ
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Exercise: Inform the patient about the type of physical activity they should opt for and instruct such patient to engage in moderate- intense aerobic activity for at least 150 mins in a week.
Statins: The first-line conventional treatment for low-density lipoprotein cholesterol are statins. Common examples include atorvastatin, rosuvastatin and simvastatin.
PCSK9 Inhibitors: Prescribed for those with extremely high LDL or those who cannot benefit adequately from the statins and ezetimibe combination.
Fibrates or Niacin: Sometimes contemplated in patients with certain lipid disorders, but not widely used.
Limit saturated fats and trans fats in processed foods, red meats, and full-fat dairy.
Physical Activity:
Regular exercises may improve HDL (good cholesterol) and reduce LDL (bad cholesterol).
Avoid Tobacco and Limit Alcohol: Smoking and Alcohol affects the ability to increase high density lipoprotein cholesterol and excessive alcohol raises cholesterol. It is better not to take alcohol, and it is advised to quit smoking.
Medication Adherence:
Individuals who use anti-cholesterol drugs such as statins, the level of compliance to reduce cholesterol levels is significant in such case.
Use of Bile acid sequestrants in treating polygenic hypercholesterolemia
It also works in combination with cholestyramine and is capable of binding bile acids, although most patients tolerate it better than cholestyramine.
Approved for use in reducing LDL cholesterol and may have beneficial effects in regulating the glycemia of patients with type 2 diabetes as well. This may be particularly beneficial in patients who cannot use statins.
Effectiveness of Antilipemic agents in treating polygenic hypercholesterolemia
Fenofibrate activates PPAR-α that increases the oxidation of fatty acids and decreases the level of triglycerides. It has the capacity to reduce the triglyceride level to some extent and enhance the HDL cholesterol.
Gemfibrozil
Like fenofibrate, gemfibrozil belongs to the subclass called PPAR-α activators; nevertheless, it is less potent than other drugs in the same group in terms of triglyceride level decrease. It also has a very favourable effect on triglyceride and modest effect on the aspect of the high-density lipoprotein cholesterol while it has less effect on the LDL cholesterol. Among them, gemfibrozil increases the risk of statin-induced myopathy if used together with the statins.
Use of PCSK9 Inhibitors in treating polygenic hypercholesterolemia
Evolocumab will work by blocking PCSK9 that leads to the degradation of LDL receptors. It will increase the availability of these receptors in the liver, thereby enhancing the clearance of LDL cholesterol from the blood.
Family History: Consider the family history of any disease associated with the heart and the history of cholesterol.
Lipid profile panel: Check the lipid profile panel for a better assessment of diagnosis.
Genetic Testing: However, if the level of suspicion for FH remains elevated, then genetic testing must be done.
Lifestyle Modifications:
Nutrition: Do not take processed foods or foods that contain high calories, saturated fats, sugar and salt.
Weight Management: It is significant to work on weight management methods in patients with overweight/ obesity to improve their cholesterol status.
Pharmacotherapy:
Statins: The initial pharmacologic intervention applied in managing low-density lipoprotein cholesterol.
Ezetimibe: May be used if statins are alone not sufficient.
PCSK9 Inhibitors: In situations where the LDL has risen to very high level or where the patient cannot be prescribed statin drugs for one reason or another.
Other Medications: In specific situations use bile acid sequestrants, niacin or fibrates according to the status of the patient.
Monitoring and Follow-up: Subsequently follow up the lipids periodically at each visit for 3-6 months in the first year of diagnose and every year after that for long term management.
Polygenic Hypercholesterolemia is an elevated total cholesterol or LDL-C caused by multiple polymorphisms throughout the genomic region. While monogenic hypercholesterolemia, like FH, is characterized by mutations in specific genes such as LDLR, APOB or PCSK9, polygenic hypercholesterolemia is due to multiple common, low effect genes increasing cholesterol concentration.
Currently, more than 100 million people in the United States have elevated LDL-C levels out of the population. Among them, only 50% sought any treatment, and even fewer of them, <35%, can achieve the target level of blood cholesterol, which puts them at a higher risk of ASCVD. Cohort evidence from different countries also supports that the prevalence of heterozygous familial hypercholesterolaemia may range up to 0.40 %. Familial hypercholesterolemia is diagnosed in less than one out of ten cases; Clinical familial hypercholesterolemia is likely to range from 20 to 30 % of patients with polygenic hypercholesterolemia.
Genetic Variants: Various common genetic variations (polymorphisms) affecting cholesterol metabolism also cause increased levels of LDL cholesterol.
These include genes that affect: The metabolism of lipoproteins (which includes variants in APOE, LDLR, PCSK9).
Cholesterol synthesis (particularly related to HMGCR).
HDL metabolism (e.g., CETP).
Each variation on its own has a small effect, but in combination they markedly raise LDL cholesterol.
Increased LDL-C Synthesis: Enhanced synthesis of cholesterol within the cholesterol biosynthesis pathway, particularly relating to changes in enzymatic activity targeting HMG-CoA reductase, the known goal of statin drugs.
Decreased LDL-C Clearance: Because of genetic variations in the LDLR gene or related pathways, the plasma clearance of LDL-containing particles declines, leading to a high LDL particle concentration.
Endothelial Dysfunction and Atherosclerosis: High levels of LDL-C are sustained as a cause of endothelial dysfunction; it has been linked with depositions of cholesterol on the walls of blood vessels. This is one of the ways by which the formation of atherosclerotic plaques is confirmed; later, cases of cardiovascular diseases including coronary artery diseases.
Genetics: Several SNPs in genes known to regulate lipid metabolism, including LDLR (the LDL receptor), APOB (apolipoprotein B), and PCSK9 modify levels of cholesterol. These SNPs usually have additive effects.
Gene-Environment Interaction: Lifestyle, diet, or exercise may either aggravate or mitigate a predisposition to hypercholesterolemia.
Polygenic risk score: It is possible to make a polygenic risk score based on these SNPs. Thus, it helps serve as a predictive element for predisposing an individual to hypercholesterolemia.
No Apparent Dominant Mutation: While familial hypercholesterolemia is caused by a dominant mutation presenting with a high level of cholesterol, polygenic hypercholesterolemia is caused by minor increases in multiple genes.
Genetic Risk Score (GRS): Increasing the polygenic risk score which depends on the activity of multiple genetic markers is linked with increased cholesterol rates and ASCVD risk.
 LDL-C Levels: Studies have suggested that sustained hypercholesterolemia and particularly sustained hyper-LDL cholesterolemia is a massive prognostic factor.
Family History of Cardiovascular Disease: The family history correlate is defined by occurrences like a heart attack or a stroke that would have happened before age 55 in male or age 65 in female.
Age: Cholesterol is proved to be dangerous with increasing age because it causes cardiovascular complications during longtime inflammation.
Age Group:
Middle aged (Above 40+ years): The target group are middle-aged people with most of them being within the 40-60 years age group. Polygenic hypercholesterolemia becomes manifest in middle age and may be detected during the general clinical examination or screening of total cholesterol levels.
Older Adults (60+ years): Long-time polygenic hypercholesterolemia patients are likely to develop cardiovascular events such as a heart attack or stroke.
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis.
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle.
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor.
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis. Â
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle. Â
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor. Â
Familial Hypercholesterolemia (FH)Â
Familial Combined HyperlipidemiaÂ
HypothyroidismÂ
Diabetes MellitusÂ
Liver DiseaseÂ
Nephrotic SyndromeÂ
Exercise: Inform the patient about the type of physical activity they should opt for and instruct such patient to engage in moderate- intense aerobic activity for at least 150 mins in a week.
Statins: The first-line conventional treatment for low-density lipoprotein cholesterol are statins. Common examples include atorvastatin, rosuvastatin and simvastatin.
PCSK9 Inhibitors: Prescribed for those with extremely high LDL or those who cannot benefit adequately from the statins and ezetimibe combination.
Fibrates or Niacin: Sometimes contemplated in patients with certain lipid disorders, but not widely used.
Endocrinology, Metabolism
Diet:
Limit saturated fats and trans fats in processed foods, red meats, and full-fat dairy.
Physical Activity:
Regular exercises may improve HDL (good cholesterol) and reduce LDL (bad cholesterol).
Avoid Tobacco and Limit Alcohol: Smoking and Alcohol affects the ability to increase high density lipoprotein cholesterol and excessive alcohol raises cholesterol. It is better not to take alcohol, and it is advised to quit smoking.
Medication Adherence:
Individuals who use anti-cholesterol drugs such as statins, the level of compliance to reduce cholesterol levels is significant in such case.
It also works in combination with cholestyramine and is capable of binding bile acids, although most patients tolerate it better than cholestyramine.
Approved for use in reducing LDL cholesterol and may have beneficial effects in regulating the glycemia of patients with type 2 diabetes as well. This may be particularly beneficial in patients who cannot use statins.
Fenofibrate activates PPAR-α that increases the oxidation of fatty acids and decreases the level of triglycerides. It has the capacity to reduce the triglyceride level to some extent and enhance the HDL cholesterol.
Gemfibrozil
Like fenofibrate, gemfibrozil belongs to the subclass called PPAR-α activators; nevertheless, it is less potent than other drugs in the same group in terms of triglyceride level decrease. It also has a very favourable effect on triglyceride and modest effect on the aspect of the high-density lipoprotein cholesterol while it has less effect on the LDL cholesterol. Among them, gemfibrozil increases the risk of statin-induced myopathy if used together with the statins.
Evolocumab will work by blocking PCSK9 that leads to the degradation of LDL receptors. It will increase the availability of these receptors in the liver, thereby enhancing the clearance of LDL cholesterol from the blood.
Like evolocumab, alirocumab also inhibits PCSK9, leading to increased LDL receptor recycling and reduced LDL cholesterol levels.
Endocrinology, Metabolism
Diagnosis and Assessment:
Family History: Consider the family history of any disease associated with the heart and the history of cholesterol.
Lipid profile panel: Check the lipid profile panel for a better assessment of diagnosis.
Genetic Testing: However, if the level of suspicion for FH remains elevated, then genetic testing must be done.
Lifestyle Modifications:
Nutrition: Do not take processed foods or foods that contain high calories, saturated fats, sugar and salt.
Weight Management: It is significant to work on weight management methods in patients with overweight/ obesity to improve their cholesterol status.
Pharmacotherapy:
Statins: The initial pharmacologic intervention applied in managing low-density lipoprotein cholesterol.
Ezetimibe: May be used if statins are alone not sufficient.
PCSK9 Inhibitors: In situations where the LDL has risen to very high level or where the patient cannot be prescribed statin drugs for one reason or another.
Other Medications: In specific situations use bile acid sequestrants, niacin or fibrates according to the status of the patient.
Monitoring and Follow-up: Subsequently follow up the lipids periodically at each visit for 3-6 months in the first year of diagnose and every year after that for long term management.
Polygenic Hypercholesterolemia is an elevated total cholesterol or LDL-C caused by multiple polymorphisms throughout the genomic region. While monogenic hypercholesterolemia, like FH, is characterized by mutations in specific genes such as LDLR, APOB or PCSK9, polygenic hypercholesterolemia is due to multiple common, low effect genes increasing cholesterol concentration.
Currently, more than 100 million people in the United States have elevated LDL-C levels out of the population. Among them, only 50% sought any treatment, and even fewer of them, <35%, can achieve the target level of blood cholesterol, which puts them at a higher risk of ASCVD. Cohort evidence from different countries also supports that the prevalence of heterozygous familial hypercholesterolaemia may range up to 0.40 %. Familial hypercholesterolemia is diagnosed in less than one out of ten cases; Clinical familial hypercholesterolemia is likely to range from 20 to 30 % of patients with polygenic hypercholesterolemia.
Genetic Variants: Various common genetic variations (polymorphisms) affecting cholesterol metabolism also cause increased levels of LDL cholesterol.
These include genes that affect: The metabolism of lipoproteins (which includes variants in APOE, LDLR, PCSK9).
Cholesterol synthesis (particularly related to HMGCR).
HDL metabolism (e.g., CETP).
Each variation on its own has a small effect, but in combination they markedly raise LDL cholesterol.
Increased LDL-C Synthesis: Enhanced synthesis of cholesterol within the cholesterol biosynthesis pathway, particularly relating to changes in enzymatic activity targeting HMG-CoA reductase, the known goal of statin drugs.
Decreased LDL-C Clearance: Because of genetic variations in the LDLR gene or related pathways, the plasma clearance of LDL-containing particles declines, leading to a high LDL particle concentration.
Endothelial Dysfunction and Atherosclerosis: High levels of LDL-C are sustained as a cause of endothelial dysfunction; it has been linked with depositions of cholesterol on the walls of blood vessels. This is one of the ways by which the formation of atherosclerotic plaques is confirmed; later, cases of cardiovascular diseases including coronary artery diseases.
Genetics: Several SNPs in genes known to regulate lipid metabolism, including LDLR (the LDL receptor), APOB (apolipoprotein B), and PCSK9 modify levels of cholesterol. These SNPs usually have additive effects.
Gene-Environment Interaction: Lifestyle, diet, or exercise may either aggravate or mitigate a predisposition to hypercholesterolemia.
Polygenic risk score: It is possible to make a polygenic risk score based on these SNPs. Thus, it helps serve as a predictive element for predisposing an individual to hypercholesterolemia.
No Apparent Dominant Mutation: While familial hypercholesterolemia is caused by a dominant mutation presenting with a high level of cholesterol, polygenic hypercholesterolemia is caused by minor increases in multiple genes.
Genetic Risk Score (GRS): Increasing the polygenic risk score which depends on the activity of multiple genetic markers is linked with increased cholesterol rates and ASCVD risk.
 LDL-C Levels: Studies have suggested that sustained hypercholesterolemia and particularly sustained hyper-LDL cholesterolemia is a massive prognostic factor.
Family History of Cardiovascular Disease: The family history correlate is defined by occurrences like a heart attack or a stroke that would have happened before age 55 in male or age 65 in female.
Age: Cholesterol is proved to be dangerous with increasing age because it causes cardiovascular complications during longtime inflammation.
Age Group:
Middle aged (Above 40+ years): The target group are middle-aged people with most of them being within the 40-60 years age group. Polygenic hypercholesterolemia becomes manifest in middle age and may be detected during the general clinical examination or screening of total cholesterol levels.
Older Adults (60+ years): Long-time polygenic hypercholesterolemia patients are likely to develop cardiovascular events such as a heart attack or stroke.
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis.
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle.
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor.
Asymptomatic: Many patients may not even notice any symptoms, and depending on the cholesterol level, they only come to know their condition during a routine blood analysis. Â
Risk Factors: Indeed, the same condition is usually more noticeable in patients with other risk factors regarding heredity, being overweight or diabetic or another factor like a sedentary diet and lifestyle. Â
Clinical Manifestations: Even though hypercholesterolemia may not lead to acute symptoms, it can lead to atherosclerosis whose symptom is felt when the outcome of angina, heart attacks or stroke when management is poor. Â
Familial Hypercholesterolemia (FH)Â
Familial Combined HyperlipidemiaÂ
HypothyroidismÂ
Diabetes MellitusÂ
Liver DiseaseÂ
Nephrotic SyndromeÂ
Exercise: Inform the patient about the type of physical activity they should opt for and instruct such patient to engage in moderate- intense aerobic activity for at least 150 mins in a week.
Statins: The first-line conventional treatment for low-density lipoprotein cholesterol are statins. Common examples include atorvastatin, rosuvastatin and simvastatin.
PCSK9 Inhibitors: Prescribed for those with extremely high LDL or those who cannot benefit adequately from the statins and ezetimibe combination.
Fibrates or Niacin: Sometimes contemplated in patients with certain lipid disorders, but not widely used.
Endocrinology, Metabolism
Diet:
Limit saturated fats and trans fats in processed foods, red meats, and full-fat dairy.
Physical Activity:
Regular exercises may improve HDL (good cholesterol) and reduce LDL (bad cholesterol).
Avoid Tobacco and Limit Alcohol: Smoking and Alcohol affects the ability to increase high density lipoprotein cholesterol and excessive alcohol raises cholesterol. It is better not to take alcohol, and it is advised to quit smoking.
Medication Adherence:
Individuals who use anti-cholesterol drugs such as statins, the level of compliance to reduce cholesterol levels is significant in such case.
It also works in combination with cholestyramine and is capable of binding bile acids, although most patients tolerate it better than cholestyramine.
Approved for use in reducing LDL cholesterol and may have beneficial effects in regulating the glycemia of patients with type 2 diabetes as well. This may be particularly beneficial in patients who cannot use statins.
Fenofibrate activates PPAR-α that increases the oxidation of fatty acids and decreases the level of triglycerides. It has the capacity to reduce the triglyceride level to some extent and enhance the HDL cholesterol.
Gemfibrozil
Like fenofibrate, gemfibrozil belongs to the subclass called PPAR-α activators; nevertheless, it is less potent than other drugs in the same group in terms of triglyceride level decrease. It also has a very favourable effect on triglyceride and modest effect on the aspect of the high-density lipoprotein cholesterol while it has less effect on the LDL cholesterol. Among them, gemfibrozil increases the risk of statin-induced myopathy if used together with the statins.
Evolocumab will work by blocking PCSK9 that leads to the degradation of LDL receptors. It will increase the availability of these receptors in the liver, thereby enhancing the clearance of LDL cholesterol from the blood.
Like evolocumab, alirocumab also inhibits PCSK9, leading to increased LDL receptor recycling and reduced LDL cholesterol levels.
Endocrinology, Metabolism
Diagnosis and Assessment:
Family History: Consider the family history of any disease associated with the heart and the history of cholesterol.
Lipid profile panel: Check the lipid profile panel for a better assessment of diagnosis.
Genetic Testing: However, if the level of suspicion for FH remains elevated, then genetic testing must be done.
Lifestyle Modifications:
Nutrition: Do not take processed foods or foods that contain high calories, saturated fats, sugar and salt.
Weight Management: It is significant to work on weight management methods in patients with overweight/ obesity to improve their cholesterol status.
Pharmacotherapy:
Statins: The initial pharmacologic intervention applied in managing low-density lipoprotein cholesterol.
Ezetimibe: May be used if statins are alone not sufficient.
PCSK9 Inhibitors: In situations where the LDL has risen to very high level or where the patient cannot be prescribed statin drugs for one reason or another.
Other Medications: In specific situations use bile acid sequestrants, niacin or fibrates according to the status of the patient.
Monitoring and Follow-up: Subsequently follow up the lipids periodically at each visit for 3-6 months in the first year of diagnose and every year after that for long term management.
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