Antilipemic Agents, HMG-CoA Reductase Inhibitors


Article Author:
Agam Bansal


Article Editor:
Manouchkathe Cassagnol


Editors In Chief:
Sisira Reddy
Joseph Nahas


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
8/14/2019 8:20:21 PM

Indications

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as "statins," are used adjunctively to diet and exercise to treat hypercholesterolemia by lowering total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) concentrations while increasing high-density lipoprotein cholesterol (HDL-C) concentrations. The approved FDA indications vary slightly between each statin but generally are indicated for the treatment and/or prevention of primary and secondary prevention clinical atherosclerotic cardiovascular disease (ASCVD) (e.g., myocardial infarction or stroke).  The choice of agent should have its basis on patient-specific characteristics, the pharmacokinetic profiles of each medication, and the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol[1]:

Primary prevention (age 40 to 75 years): In patients without clinically significant cardiovascular disease, statins in addition to heart-healthy lifestyle measures are indicated in the following conditions to reduce the risk of developing myocardial infarction, stroke or undergoing revascularization procedures.

  • LDL-C greater than 190 mg/dl: Initiate high-intensity statin therapy with an aim towards achieving over 50% reduction in LDL-C concentration. If LDL-C is greater than or equal to 100 mg/dL; add ezetimibe +/- PCSk-9 inhibitor 
  • LDL-C 70 to 189 mg/dL:
    • With diabetes: Initiate moderate-intensity statin with an aim towards achieving 30 to 49% reduction in LDL-C concentration. If multiple ASCVD risk factors, age 50 to 77 years; initiate high-intensity aim to achieve over 50% reduction in LDL-C concentration.
    • Without diabetes and 10-year ASCVD risk greater than 20% (high risk): Initiate high-intensity statin therapy with an aim towards achieving over 50% reduction in LDL-C concentration
    • Without diabetes and 10-year ASCVD risk greater than or equal to 7.5% to less than 20% (intermediate risk): With the evaluation of risk enhancers (e.g., family history, chronic kidney disease, metabolic syndrome, inflammatory disease, ethnicity factors, condition-specific to women, persistently elevated LDL-C greater than or equal to 60 mg/dL) and coronary artery calcium score if uncertain. Initiate moderate-intensity statin with an aim towards achieving 30 to 49% reduction in LDL-C concentration.
    • Without diabetes and 10-year ASCVD risk 5 to less than 7.5% (borderline risk):  Initiate lifestyle, select moderate intensity with the presence of risk enhancers (risk discussion indicated)
    • withOUT diabetes and 10-year ASCVD risk less than 5% (low risk): Initiate lifestyle and risk discussion 

Secondary prevention (age over 18 years): History of multiple major ASCVD events (recent acute coronary syndrome within the past 12 months, history of MI, history of ischemic stroke, symptomatic peripheral artery disease) or 1 major ASCVD event with multiple high-risk conditions (age greater than or equal to 65 years, heterozygous familial hypercholesterolemia, diabetes mellitus, hypertension, chronic kidney disease, current smoking, history of heart failure, history of PCI or CABG, persistently elevated LDL-C greater than or equal to 60 mg/dL).

  • Very high-risk ASCVD: Initiate maximally tolerated statin. If LDL-C greater than or equal to 70 mg/dL add ezetimibe +/- PCSk9 inhibitor (with LDL-C greater than or equal to 70 mg/dL and non-HDL-C higher than 100 mg/dL)
  • Stable ASCVD: Initiate high to moderate-intensity statin with the aim towards achieving LDL-C lowering as described above

Additionally, statins are useful in the management of the following dyslipidemias:

  • Familial hypercholesterolemia (type II a hyperlipoproteinemia), characterized by LDL receptor deficiency 
  • Familial combined hyperlipidemia (type II b hyperlipoproteinemia), characterized by decreased LDL receptor and increased apo B lipoprotein
  • Familial dysbetalipoproteinemia (type III hyperlipoproteinemia), characterized by abnormal function of apo E receptor that is necessary for the clearance of chylomicron remnants
  • Familial hypertriglyceridemia (type IV hyperlipoproteinemia), characterized by increased VLDL production 

Mechanism of Action

Conversion of 3-hydroxy-3-methyl glutaryl-CoA (HMG-CoA) to mevalonate by HMG-CoA reductase in the hepatocytes is the first and rate-limiting step in cholesterol biosynthesis. Statins competitively inhibit HMG-CoA reductase enzyme. Statins bind to the active site of the enzyme and induce a conformational change in its structure, thus reducing its activity. Also, the binding affinity of statins for HMG-CoA reductase is 10000 times higher than the substrate (HMG-CoA), thus preventing the action of the enzyme and reducing the intracellular synthesis of cholesterol. Statins have a significant impact on lowering cholesterol since most of the circulating plasma cholesterol comes from the internal synthesis in hepatocytes rather than the diet.[2]

The reduced level of cholesterol in hepatocytes secondary to statin use activates the proteases that cleave membrane-bound sterol regulatory element-binding proteins (SREBP), which further migrate to the nucleus and binds sterol response elements. This binding results in increased transcription of the LDL receptor, which translocates to the liver cell membrane. The LDL and VLDL particles in plasma bind to the LDL receptors and endocytose in hepatocytes, where their cholesterol component gets processed into bile salts which are then excreted or recycled. This process increases the catabolism of LDL and VLDL cholesterol and results in further reduction of plasma cholesterol levels.[3]

Statins reduce the level of total cholesterol, LDL-C, VLDL-C, triglycerides, apo-B, and increase the level of HDL-C.

Apart from lowering lipid concentrations, statins also have cardiovascular protective effects (pleiotropic effects) which are primarily because of the inhibition of production of prenylated proteins (mainly farnesyl pyrophosphate and geranylgeranyl pyrophosphate) in the cholesterol biosynthetic pathway. Statins prevent cardiovascular disease progression via the following mechanisms[4][5][4]:

  • Plaque stabilization: Coronary artery plaque rupture predisposes to acute coronary syndrome. Statins maintain the integrity of the fibrous cap of atherosclerotic plaque, inhibit the proliferation of macrophages and decreases the expression of matrix metalloproteinases (MMP).
  • Reduces inflammation: Inflammation plays an essential role in atherosclerotic plaque rupture. Statins reduce the level of pro-inflammatory cytokines (TNF-a, IL-6, IL-8) and decrease the level of CRP.
  • Improve endothelial function: Statins increase eNOS activity within the endothelial cells resulting in vasodilation and thus improving myocardial blood flow.
  • Decreased thrombogenicity: Statins decrease the activity of platelets and reduce thromboxane A2 synthesis.

Administration

Since a majority of the cholesterol synthesis occurs at night in a fasting state, the recommendation is that statins with a shorter half-life (i.e., simvastatin, pravastatin, or fluvastatin) should be taken orally before bedtime to maximize its action[6]. Dosing with statins with a longer half-life such as atorvastatin, rosuvastatin, or pitavastatin can be in morning or evening, but individuals should take the medication around the same time every day. Lovastatin should be taken with morning or evening meals since its absorption increases with food.

Statins are classified based on their intensity as follows[7]:

  • Low-intensity statins: These include 20 to 40 mg fluvastatin, 20 mg lovastatin, 1 mg pitavastatin, 10-20 mg pravastatin, or 10 mg simvastatin. Low-intensity statins reduce LDL-C by less than 30%.
  • Moderate-intensity statins: These include 10 to 20 mg atorvastatin, 80 mg fluvastatin, 40 mg lovastatin, 2 to 4 mg pitavastatin, 40 to 80 mg pravastatin, 5 to 10 mg rosuvastatin, or 20 to 40 mg simvastatin. Moderate-intensity statins reduce LDL-C by 30 to 50%.
  • High-intensity statins: These include 40 to 80 mg atorvastatin or 20 to 40 mg rosuvastatin. High-intensity statins reduce LDL-C by greater than 50%.

Rosuvastatin is the most potent statin followed by atorvastatin. Statins also classify as lipophilic or hydrophilic. Lipophilic statins include simvastatin, lovastatin, and atorvastatin. Hydrophilic statins include pravastatin, fluvastatin, and rosuvastatin. Simvastatin 80 mg should not be a therapeutic choice in most patients.

Statins administration in specific patient population groups: 

Elderly patients: In individuals older than 75 years of age, who have a clinically significant ASCV, it is recommended to start them on moderate-intensity statins rather than high-intensity statins; this is because of increased side effects associated high-intensity statins, and reduction in the efficacy of metabolic pathways in elderly individuals. 

Renal impairment: atorvastatin, fluvastatin, pravastatin, or simvastatin are indicated in patients with chronic kidney disease since they do not undergo renal elimination, and hence, no dose adjustment is required.

Liver impairment: pravastatin and rosuvastatin can be used in patients with compensated liver disease since they are metabolized to a lesser extent by the liver in comparison to other statins. When initiating statins in patients with liver disease, patients must abstain from alcohol. The statins mentioned above should initiate at a low dose and liver enzymes, and LDL-C should be monitored within 1 to 3 months. If no significant change occurs in the level of aminotransferase, therapy does not achieve the LDL-C target, increase the dose of statins. Statins are contraindicated in patients with acute liver failure or decompensated cirrhosis.

Drug interactions

Increase in plasma concentration of statins result from the following:

CYP 3A4 inhibition: Statins that are metabolized by CYP450 3A4 include lovastatin, simvastatin, and atorvastatin.[8] If patients use these statins in combination with CYP 3A4 inhibitors, it causes an increase in plasma level of statins and increases the risk of dose-related adverse effects (including myopathy). Pravastatin, fluvastatin, rosuvastatin, and pitavastatin are the drugs of choice when patients are concurrently using drugs that interfere with CYP 3A4. Medications which increase the plasma levels of statins are:

  • Macrolide antibiotics: clarithromycin and azithromycin
  • Immunosuppressants: immunosuppressive agents, including cyclosporine, or tacrolimus, are CYP 3A4 inhibitors, and they also inhibit OATP1B1. All the statins are substrates of OATP1B1 transporter and thus using them along with immunosuppressive agents increases the plasma concentration of statins. Amongst the statins, pravastatin or fluvastatin are the recommended agents for use in combination with immunosuppressive agents.
  • Protease inhibitors: protease inhibitors interact with statins metabolized by CYP 3A4 and increase the risk of muscle toxicity. Fluvastatin or pravastatin is the statin of choice in patients taking protease inhibitors
  • Grapefruit juice
  • Azole antifungals: itraconazole, ketoconazole

Using statins in combination with gemfibrozil increases the risk of muscle toxicity, including rhabdomyolysis. Fenofibrate is preferred if there is a need to start statin-fibrate combination therapy. However, if gemfibrozil is the only available fibrate or fenofibrate is not tolerated, then gemfibrozil should be used in combination with low-dose atorvastatin, pitavastatin or rosuvastatin.

Calcium channel blockers: Using amlodipine, diltiazem or verapamil in combination with simvastatin and lovastatin, increases the risk of toxicity due to statins

A decrease in plasma concentration of statins result from the following:

  1. CYP 3A4 induction: When the statins that are metabolized by CYP 3A4 are co-administered with CYP 3A4 inducers (efavirenz, rifampin, phenytoin), it results in a decrease in plasma level of statins and decreases their effectiveness. 
  2. Bile acid sequestrants: The plasma concentration of statins decrease when used in combination with bile acid sequestrants such as colestipol
  3. Antacids: The plasma concentration of statins decrease when combined with antacids 

Adverse Effects

Adverse effects of statins include the following[9][10]

  1. Musculoskeletal: Myalgia is the most common side effect of statins, and 1 to 10% of individuals using statins have myalgias. Myositis is less common and characteristically presents by an increase in creatine kinase (CK). Rhabdomyolysis rarely occurs (0.1% individuals) but is the most serious side effect of statins and is associated with marked elevation in CK (10 times the upper limit of normal), acute renal failure secondary to myoglobinuria, electrolyte disturbances and hemodynamic instability. Statins cause musculoskeletal toxicity because they decrease the concentration of coenzyme Q10 (ubiquinone) and end products of the mevalonate pathway (farnesyl pyrophosphate, geranylgeranyl pyrophosphate), which are essential for skeletal muscle energy production. The symptoms usually occur within weeks to months of therapy initiation. Individuals experience relief, and serum CK normalizes within days to weeks of medication discontinuation. Amongst the statins, Pravastatin and fluvastatin have least muscle-related adverse effects. In patients who develop myopathy on statins other than pravastatin or fluvastatin, it is recommended to switch to these two statins once symptoms have resolved. In patients who develop muscle side effects on pravastatin or fluvastatin, decrease the dose of statins. 
  2. Hepatic dysfunction: Statins can cause an increase in the level of serum transaminases. If an individual develops serum transaminases three times the upper limit of normal, then reduce the dose of statin or change to a different statin (preferably pravastatin) or switch to a different class of lipid-lowering drugs. 
  3. Renal dysfunction: High-intensity statins can cause proteinuria and hematuria. Also, rhabdomyolysis secondary to statin use can lead to renal failure. Rosuvastatin and simvastatin are the statins which cause kidney injury. Atorvastatin, fluvastatin, or pravastatin are the indicated choices in patients with renal impairment.
  4. Diabetes mellitus: Individuals taking high-intensity statins have a slightly increased risk of developing diabetes. The proposed mechanism is that statins inhibit the biosynthesis of cholesterol, which is essential for the production of GLUT-1, which mediates glucose uptake into the cell.[11] This mechanism results in increased plasma levels of glucose.

Other side effects reported with statins in various case reports/case series include:

  • Respiratory: shortness of breath, interstitial lung disease
  • Gastrointestinal: statin-induced pancreatitis
  • Neurological: peripheral neuropathy, insomnia, dizziness, reversible cognitive impairment
  • Reproductive: sexual dysfunction, gynecomastia, oligospermia
  • Psychiatric: irritability, aggression or behavioral changes
  • Autoimmune: lupus-like syndrome, myasthenia gravis
  • Ophthalmic: cataract
  • Urinary tract: urinary tract infection, hematuria, albuminuria

Contraindications

The contraindications of statins include the following:

  • Hypersensitivity to medication
  • Pregnancy: Statins are contraindicated in pregnancy (category X). Cholesterol and its substrates are imperative for fetal development. Since statins inhibit cholesterol synthesis, it causes damage to the fetus. Reports exist of congenital anomalies including anal atresia, tracheoesophageal fistula (VATER association) in women taking statins. If a patient becomes pregnant while taking statins, they should discontinue the medication immediately, and the patient should have counseling regarding the potential hazards.
  • Lactation: Statin contraindications also include breastfeeding mothers
  • Acute liver failure or decompensated cirrhosis

Monitoring

Monitor lipid profile, liver function tests, creatine kinase (CK) and thyroid function tests in individuals who start statin treatment:

  • Lipid profile: Perform lipid profile at baseline before initiating statins. The lipid panel should be repeated 2 months after starting the therapy. If the level of LDL-C reduction is less than expected in an individual adherent to medication, then increase the dose of statin or change to another potent statin medication and repeat lipid profile after 2 months. If the level of LDL-C is within the expected range, repeat the lipid profile every 6 to 12 months.
  • Liver function tests: Perform liver function tests at baseline before initiating statins. Routine monitoring of LFTs is not a recommendation. LFTs require rechecking when the patient develops symptoms of liver disease.
  • Creatine kinase (CK): CK levels may be obtained at baseline before initiating statins. Routine monitoring of CK is not a recommendation.
  • Thyroid function tests: Hypothyroidism can cause abnormal lipid profile and myopathy. It is recommended to obtain thyroid hormone levels before starting statin therapy.

Toxicity

The most common presentation of statin overdose is muscle toxicity. In case of severe muscle symptoms or rhabdomyolysis, statins therapy should stop immediately, and patients require symptomatic care. This care includes adequate fluid resuscitation, monitoring urine output, and correcting electrolyte imbalances, especially hyperkalemia. There is no antidote available for statin overdose. After the recovery from an overdose, patients should restart on low-dose statins.

Enhancing Healthcare Team Outcomes

Statins play an essential role in lowering the level of lipids and in the prevention of clinical ASCVD. It is vital for healthcare personnel to educate patients about the benefits of statins and the importance of medication adherence. Additionally, patients need education about the side effects of statins to help improve their adherence to medication.

Physicians (MDs, DOs, NPs, PAs) will prescribe these drugs, and decide both which agent as well as the dose based on the patient's lipid status. Nursing will often offer initial counseling to the patient as they start statin therapy, and can be the first-line on monitoring treatment success, medication compliance, and the presence of adverse medication effects.  Pharmacist involvement comes in the form of verifying the agent selected, checking the dose, and performing medication reconciliation, as well as counseling on optimal administration and monitoring for adverse events. In both cases, nurses and pharmacists should report any concerns they encounter to the rest of the healthcare team.

The medical personnel, including the physicians, specialists, nurse practitioner, specialty-trained nurses, and pharmacist, should all work collaboratively as an interprofessional team when administering statin therapy. [Level V] All parties must be aware of the drug interactions and take a proper medication history before initiating statins.


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Antilipemic Agents, HMG-CoA Reductase Inhibitors - Questions

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A 46-year old male presents for a regular health examination. His past medical history is significant for hypertension diagnosed four years ago, and diabetes mellitus diagnosed three years back. His family history is significant for stroke in his father. He is currently taking enalapril and metformin. His blood pressure is 130/76 mmHg, and pulse is 76/min. His labs are within normal limits. His ten-year ASCVD risk is 9%. The provider plans to start the patient on atorvastatin. Which of the following statements are correct about the medication?



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A 63-year old male presents to the physician for a regular health examination. His past medical history is significant for epilepsy and diabetes mellitus. His family history is significant for diabetes and myocardial infarction in his father. He is an alcoholic and has a 20-pack-year smoking history. His current medications include phenytoin and metformin. His blood pressure is 120/80 mmHg and pulse is 78/min. His labs reveal the following: random blood glucose of 130 mg/dl, total cholesterol 240 mg/dl, HDL 40 mg/dl, LDL 140 mg/dl, and triglycerides 400 mg/dl. The provider decides to start the patient on statin medication. Which of the following statements is true?



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A 50-year old male presents for a regular health examination. His past medical history is significant for hypertension and diabetes mellitus. He has a 20 pack-year smoking history. His father had myocardial infarction at the age of 56 years. He is currently taking enalapril and metformin. His lipid profile reveals the following: total cholesterol 315 mg/dl, LDL-C 228 mg/dl, HDL-C 69 mg/dl, and triglycerides 446 mg/dl. The provider starts the patient on an additional medication. What is the mechanism of action of the medication most likely used?



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A 63-year old male presents to the physician for a routine health examination. His past medical history is significant for hypertension diagnosed seven years ago, and diabetes mellitus diagnosed five years ago. He has a 20 pack-year smoking history. His family history is significant for myocardial infarction in his mother at the age of 53 years. Currently, he is on enalapril and metformin. His labs reveal the following: total cholesterol 220 mg/dl, HDL 50 mg/dl, LDL 150 mg/dl, triglycerides 150 mg/dl and random blood glucose 144 mg/dl. The attending physician decides to start the patient on 40 mg atorvastatin. This treatment is an example of which of the following?



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A 63-year old male presents for a regular health examination. His past medical history is significant for diabetes mellitus diagnosed three years ago. He has a 20-pack year smoking history. His father died of myocardial infarction. He is currently taking metformin for his diabetes. His blood pressure is 126/76 mmHg, and pulse is 78/min. His labs reveal the following: total cholesterol 243 mg/dl, HDL-C 36 mg/dl, LDL-C 170 mg/dl, triglycerides 201 mg/dl and random blood glucose of 130 mg/dl. The provider starts the patient on atorvastatin. The patient needs to be educated of which of the following side effects of atorvastatin?



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A 63-year old male presents for a regular health examination. His past medical history is significant for hypertension diagnosed 20 years ago. He has severe alcohol use disorder and has a 30 pack-year smoking history. His current medication includes enalapril. His blood pressure is 130/84 mm Hg and pulse is 80/min. His labs reveal the following: total cholesterol 315 mg/dl, LDL-C 228 mg/dl, HDL-C 69 mg/dl, and triglycerides 446 mg/dl. On which of the following medication should the patient be started?



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Which of the following antilipemic drug classes is FDA approved for the primary prevention of atherosclerotic cardiovascular disease?



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A 63-year old male presents for a regular health examination. His past medical history is significant for hypertension and hypothyroidism. He has a 20 pack-year smoking history. His father had myocardial infarction at the age of 56 years, and his mother had a stroke at age 50 years. He is currently taking enalapril and levothyroxine. With these medications, his blood pressure and thyroid function tests are within normal limits. His lipid profile reveals the following: total cholesterol 315 mg/dl, LDL-C 228 mg/dl, HDL-C 69 mg/dl, and triglycerides 446 mg/dl. The provider starts the patient on atorvastatin. Which of the following is an indication for starting a statin in this patient?



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A 60-year old male presents with a chief complaint of intermittent leg pain. He says that the pain occurs when he walks a few blocks and is relieved by rest. His past medical history is significant for hypertension and diabetes mellitus. He has a 25 pack-year smoking history. His family history is significant for stroke in his father. He is currently taking clopidogrel and lisinopril. His blood pressure is 130/72 mmHg, and his pulse is 76/min. On examination, his left foot is shiny and devoid of hair. The ankle-brachial index is 0.77 on the left and 1.0 on the right leg. Lab results reveal blood glucose of 92 mg/dl, total cholesterol 155 mg/dl, LDL-C 93 mg/dl, HDL-C 58 mg/dl, and triglycerides 120 mg/dl. Aside from the supervised exercise program, the attending physician starts the patient on rosuvastatin. The treatment with statins in this condition is an example of which of the following?



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A 52-year old female presents to the physician office for a regular health examination. Her past medical history is significant for hypertension and diabetes. His family history is significant for diabetes and myocardial infarction in his father. He is an alcoholic and has a 20-pack-year smoking history. His current medications include enalapril and metformin. His blood pressure is 126/80 mm Hg, and the pulse is 78/min. His labs reveal the following: random blood glucose of 130 mg/dl, total cholesterol 240 mg/dl, HDL 40 mg/dl, LDL 140 mg/dl, and triglycerides 400 mg/dl. The physician decides to start the patient on atorvastatin. Which of the following laboratory parameters should be monitored while initiating statin therapy in this patient?



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A 59-year-old patient received a heart transplant and was started on an immunosuppressant agent. The patient was seen in the transplant clinic, and blood work revealed blood urea nitrogen of 37 and creatinine of 2.0. He also had elevated LDL and low HDL cholesterol levels. He was started on an HMG-CoA reductase inhibitor. What is the one complication this patient is now prone to develop?



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A 66-year old male presents to the office with a chief complaint of intermittent leg pain. He says that the pain occurs when he walks a few blocks and is relieved by rest. His past medical history is significant for hypertension diagnosed 20 years ago, and chronic kidney disease with baseline serum creatinine 2 mg/dl. He has a 30 pack-year smoking history. His family history is significant for stroke in his mother. He is currently taking clopidogrel and lisinopril. His blood pressure is 136/78 mm Hg, and his pulse is 78/min. On examination, his left foot is shiny and devoid of hair. The ankle-brachial index is 0.79 on the left and 1.02 on right leg. Lab results reveal blood glucose of 92 mg/dl, total cholesterol 155 mg/dl, LDL 93 mg/dl, HDL 58 mg/dl, triglycerides 120 mg/dl and serum creatinine 2.2 mg/dl. Which of the following medications is an appropriate option for therapy in this patient?



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A 65-year old presented with complaints of weakness in his shoulders and lower limbs since the past week. The weakness has progressed, and the patient has reduced mobility in his limbs. His past medical history was significant for myocardial infarction 10 years ago. Since then, he is on aspirin, clopidogrel, high-intensity rosuvastatin, and metoprolol. Two weeks back, the patient had fever and cough with yellow sputum. His chest X-ray showed an infiltrate in left lower lobe. He was started on clarithromycin for his condition. The examination reveals proximal myopathy with 3/5 power in shoulder abduction and hip flexion. His labs reveal Hb of 14 g/dl, total cholesterol 155 mg/dl, LDL-C 93 mg/dl, HDL-C 58 mg/dl, and triglycerides 120 mg/dl, serum creatinine 3.4 mg/dl and creatine kinase of 5000 U/L. Which of the following describes the etiology and treatment of the patient's condition?



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A 65-year-old male presents to the emergency department with complaints of nausea, weakness, and abdominal distension of two weeks duration. The abdominal distension has worsened over the past week. He has also developed swelling over his lower limbs in the past week. His past medical history is significant for coronary heart disease, alcohol use disorder, diabetes, and hypertension. His medications include metformin, atorvastatin, metoprolol, aspirin, clopidogrel, and amlodipine. His blood pressure is 130/80 mm Hg, and his pulse is 82/min. On examination, sclerae are icteric, there is bilateral pedal edema, and ascites and varices are present on abdominal examination. His labs reveal the following: serum albumin of 2.8 g/dl, serum bilirubin 2.4 mg/dl, AST 180 U/L, ALT 80 U/L, total cholesterol 220 mg/dl, LDL 140 mg/dl, HDL 50 mg/dl, and triglycerides 150 mg/dl. Abdominal ultrasound reveals nodular liver and hypoechoic nodules suggestive of cirrhosis. Which of his medications should be discontinued?



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Antilipemic Agents, HMG-CoA Reductase Inhibitors - References

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