How to use statins correctly?(Part 2: Statin therapy.)✅✅✅

Here is part 2. It is about how to use statins correctly.

What are statins and how should they be used?

There are 7 kinds of statins that are more commonly used in clinical practice. There are 7 kinds of statins that are more commonly used in clinical practice. The seven statins are atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin and simvastatin.

Their characteristics are as follows:

• Atorvastatin is a potent and long-acting statin. It can be taken at any time. It is mainly metabolized via the hepatic enzyme CYP3A4. Therefore, it has more interactions with other drugs, and it is necessary to pay attention to drug interactions when taking it in combination.
• Pitavastatin is a moderate-strength, long-acting statin. It can be taken at any time. Its dose is the smallest among statins. It is mainly excreted through feces. It has fewer interactions with other drugs. It has few side effects and it has minimal effect on blood sugar.
• Pravastatin is a moderate-strength statin. Since it is not metabolized by liver enzymes, it has fewer interactions with other drugs. It has few side effects and it has less effect on blood sugar. However, it has a shorter potency and needs to be taken at bedtime.
• Rosuvastatin is a potent and long-acting statin. It can be taken at any time. It is excreted mainly in the feces and partly in the kidneys. Since only a small amount is metabolized by the liver, it has fewer interactions with other drugs. Combination medication has higher safety.
• Simvastatin is metabolized by the liver enzyme CYP3A4. Many drugs are metabolized through this pathway, so it has more interactions with other drugs. The drug-drug interactions should be paid attention to in combination therapy. It also has a shorter duration of action. Therefore, it needs to be taken at bedtime for the best lipid-lowering effect.

The initial drug should be a moderate-intensity statin, and then the dose should be adjusted according to the patient's lipid-lowering efficacy and tolerance. If the patient's cholesterol level fails to reach the target, it should be combined with other lipid-lowering drugs. The lipid-lowering intensities and doses of statins are as follows:

• Low-intensity (daily dose lowers LDL-C < 30%): Fluvastatin 20-40mg, Lovastatin 20mg, Pitavastatin 1mg, Pravastatin 10-20mg, Simvastatin 10mg.
• Moderate-intensity (daily dose lowers LDL-C 30 to 50%): Atorvastatin 10-20mg, Fluvastatin 80mg, Lovastatin 40mg, Pitavastatin 2-4mg, Pravastatin 40-80mg, Rosuvastatin 5-10mg, Simvastatin 20-40mg.
• High intensity (daily dose lowers LDL-C ≥50%): Atorvastatin 40-80mg, Rosuvastatin 20mg.

The lipid-lowering treatment options.

The usual doses of statins are: atorvastatin 10-20mg, fluvastatin 80mg, pitavastatin 2-4mg or rosuvastatin 5-10mg. If blood lipids still do not reach the target after 3 to 4 weeks of treatment, 10 mg of ezetimibe daily is combined with treatment for 4 weeks.

If the blood lipids still do not reach the target after treatment, there are generally two options. The first option is to increase the dose of the statin. The advantage of this approach is lower cost but an increased risk of side effects (despite doubling the statin dose, the LDL-C reduction is only 6%). The second option is to use a combination of PCSK-9 inhibitors (eg, evolocumab). This regimen will be more effective, but more expensive. Higher-dose statin, ezetimibe and PCSK-9 inhibitor combined use of the three drugs will further enhance the cholesterol-lowering effect. However, it is necessary to strengthen the monitoring of adverse reactions in patients when combined.

However, in patients with homozygous familial hypercholesterolemia, their LDL-C is usually significantly elevated. Even if they are treated with the above-mentioned combination drugs, it is still difficult to have reasonable blood lipid control. Plasma exchange therapy every 1 to 2 weeks may be considered for this type of patient. If the patient's triglycerides are only borderline high (between 1.7 and 2.26 mmol/L), no medical treatment is required. These patients can control their blood lipids by controlling their diet, eating more vegetables, reducing calorie intake, increasing exercise, losing weight and not drinking alcohol.

Patients with moderately elevated triglycerides (between 2.26 and 5.6 mmol/L), especially those with comorbidities such as diabetes or ASCVD, may consider statin therapy. When patients have severely elevated triglycerides above 5.6 mmol/L, they are at high risk for acute pancreatitis. Therefore, they should immediately lower triglycerides to relatively safe levels with drugs such as fibrates, niacin extended-release.

Which patients need to take statins for lipid-lowering therapy?

The following groups of people need oral statins for lipid-lowering therapy:

People with LDL-C>4.9mmol/L.

The patient has been diagnosed with ASCVD. In addition, patients with stable or unstable angina, acute coronary syndrome, peripheral vascular disease, coronary or other revascularization, myocardial infarction, transient ischemic attack, ischemic stroke, or confirmed coronary and Large and medium arteries such as the carotid artery have more than 50% stenosis.

Patients with diabetes or LDL-C (>3.4mmol/L) combined with hypertension.

Low HDL-C (<1.0mmol/L), obesity, smoking, hypertension of grade two or above and other three or more non-diabetic risk factors combined with hypertension.

Diabetic patients with LDL-C>1.8mmol/L or total cholesterol (TC)>3.1mmol/L and age>40 years old.

Some patients with carotid plaque.

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How to use statins correctly?(Part 1: Blood lipids and related diseases.)✅✅✅

Statins are effective and safe in lowering cholesterol and reversing plaque. Clinically they have become fundamental drugs for reducing the risk of cardiovascular disease and treating atherosclerosis. Due to the widespread use of statins, incorrect use of statins can cause adverse reactions in patients.

What are blood lipids?

Cholesterol in the human body is mainly present in the body in the form of cholesterol esters and free cholesterol. Although lipids are insoluble in water, lipids in plasma are mainly combined with apolipoproteins to form soluble lipoproteins, so that plasma is normally clear and transparent. Lipoproteins are classified into high density lipoprotein (HDL), intermediate density lipoprotein (IDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL) and chylomicrons (CM). In addition, there is a lipoprotein called lipoprotein a (LPa). Lipoproteins are the major transport form of blood lipids in the human body. Clinically, the level of LDL in the blood can be reflected by the level of low-density lipoprotein cholesterol (LDL-C). In addition, there are triglycerides in the blood, which are also commonly known as fats. Clinically, the two main indicators of concern are LDL-C and cholesterol. Because only cholesterol is the basis pathophysiology of atherosclerosis.

What is atherosclerotic cardiovascular disease?

Atherosclerotic cardiovascular disease (ASCVD) includes ischemic stroke, myocardial infarction (MI), stable and unstable angina, transient ischemic attack, and peripheral vascular disease (PAD).

What is the source of cholesterol in blood?

The main sources of cholesterol in the blood are synthesis in the body and dietary intake. The amount of synthesized in the body is about 2/3 (70%-80%) and the amount of dietary intake is about 1/3 (20%-30%). The main site of cholesterol synthesis in the body is the liver. However, cholesterol cannot enter the blood directly after being synthesized in the liver. It is excreted into the intestines through bile, and then absorbed by the intestines into the blood. This process is called enterohepatic circulation of cholesterol. Both the cholesterol synthesized by the liver and the cholesterol absorbed from the diet must be absorbed by the intestine before entering the blood. Therefore, the ability of the intestines to absorb cholesterol greatly affects the level of cholesterol in the body's blood. Clinically, ezetimibe has a lipid-lowering effect by inhibiting the absorption of cholesterol in the intestines. 

What are the causes of hyperlipidemia?

The causes of hyperlipidemia include the following:

1. Diet can cause hyperlipidemia. Long-term consumption of high-sugar, high-fat and high-energy foods or beverages can easily lead to hyperlipidemia. Lack of physical activity or excessive alcohol consumption can lead to dyslipidemia.
2. The disease causes hyperlipidemia. Some diseases may cause dyslipidemia, such as: thyroid disease, liver disease, pancreatitis, diabetes, obesity, gout, familial hypercholesterolemia, etc. Hypothyroidism can cause hyperlipidemia including cholesterol and triglyceridemia.
3. Drugs can also cause hyperlipidemia. Some drugs can also increase blood lipids, such as glucocorticoids, non-selective β-blockers, and diuretics, which can induce secondary dyslipidemia.

Who needs to be screened for blood lipids?

The following people need to be screened for blood lipids:

Men or women over the age of 40 (or postmenopausal women).

All patients with any of the following conditions, regardless of age, should be screened for lipids.

• Clinical evidence points to the presence of atherosclerotic cardiovascular disease.
• Diabetes.
• Hypertension.
• Hypertension in pregnancy.
• Chronic kidney disease (eGFR≤60ml/min 1.73m2).
• Abdominal aortic aneurysm.
• Chronic Obstructive Pulmonary Disease.
• Signs of dyslipidemia (eg, xanthomas, corneal arches).
• Inflammatory diseases (inflammatory bowel disease, psoriatic arthritis, systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis). 
• Family history of premature cardiovascular disease (age of onset in first-degree relatives: female < 65 years, male < 55 years).
• Obesity (BMI ≥ 30). 
• Still smoking. 

How long is the interval between blood lipid tests?

People between the ages of 20 and 40 should have their blood lipids tested every 5 years.

Men over the age of 40 should have their blood lipids checked once a year.

Postmenopausal women should have their blood lipids checked once a year.

Patients with ASCVD or their high-risk groups should have blood lipids measured every 3 to 6 months. (High-risk groups refer to people with multiple ASCVD risk factors, such as diabetes, hypertension, familial hyperlipidemia, family history of premature cardiovascular disease, obesity, smoking, etc.)

Inpatients with ASCVD should be tested for blood lipids at the time of hospital admission.

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Vitamin B3 may slow the progression of Alzheimer's disease.👴👵

Indiana University School of Medicine (IUSM) researchers have found in
laboratory models that people's intake of vitamin B3 (niacin) can slow the progression of Alzheimer's disease. The findings of this study offer new possibilities for treating Alzheimer's disease. They recently published the results of the study in the journal Science Translational Medicine. They investigated how vitamin B3 alters the response of microglia to amyloid plaques in animal models of Alzheimer's disease. The researchers believe the results of this study could identify a potential new therapeutic target for Alzheimer's disease. In addition, it could adjust the treatment guidelines for Alzheimer's disease. This therapeutic strategy has great potential in clinical treatment.

What are the benefits of niacin?

Niacin is also known as vitamin B3. Niacin can be obtained mainly through specific diets. It can maintain the function of metabolism of the whole body. Clinically, it is also used as a cholesterol-lowering drug or nutritional supplement. It is one of the water-soluble B vitamins. It occurs naturally in some foods, and it is added to foods as a supplement. Niacin and niacinamide are the two most common forms of niacin found in foods and supplements. In addition, an amino acid called tryptophan is also converted into niacinamide by the body. Because niacin is a water-soluble vitamin, the body excretes excess niacin in the urine when ingested in excess. Niacin works in the body as a form of coenzyme. There are more than 400 enzymes in the human body that depend on niacin for various reactions. It also helps convert nutrients into energy in the body, produces fat and cholesterol, generates and repairs DNA, and acts as an antioxidant.

Niacin interacts with highly selected HCAR2 receptors in the brain. HCAR2 receptors are present in immune cells associated with amyloid plaques. The researchers say that when niacin activates the receptor, these immune cells are stimulated by it to have beneficial effects on Alzheimer's disease. 

The results of the study showed that niacin treatment reduced amyloid plaques in an animal model of Alzheimer's disease. It also improves cognition in animal models of Alzheimer's disease. These effects are all due to the HCAR2 receptor. The researchers also said that past epidemiological and niacin studies on Alzheimer's disease indicated that people with higher dietary intake of niacin had a lower risk of developing Alzheimer's disease. In clinical trials, niacin has also been used in the treatment of glioblastoma and Parkinson's disease.

What are the main food sources of niacin?

In general, few people develop niacin deficiency. Because it is present in the food of many animals and plants. These foods include pork, poultry, fish, beef, beef liver, beans, nuts, seeds, brown rice, grains, bread, bananas, and more.

For more detail, you can read this article.👇

Miguel Moutinho, Shweta S. Puntambekar, Andy P. Tsai, Israel Coronel, Peter B. Lin, Brad T. Casali, Pablo Martinez, Adrian L. Oblak, Cristian A. Lasagna-Reeves, Bruce T. Lamb, Gary E. Landreth. The niacin receptor HCAR2 modulates microglial response and limits disease progression in a mouse model of Alzheimer’s disease. Science Translational Medicine, 2022; 14 (637) DOI: 10.1126/scitranslmed.abl7634

https://www.hsph.harvard.edu/nutritionsource/niacin-vitamin-b3/

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What common drugs are contraindicated in patients with glucose-6-phosphate dehydrogenase deficiency?📝📝📝

In recent years, broad beans and their products have become a favorite
snack for many people. However, some children will experience physical discomfort such as fever, chills, headache, dizziness, fatigue, abdominal pain or vomiting after eating these foods, and even dark yellow urine or jaundice. If children have the above symptoms after eating broad beans and their products for the first time, they may have glucose-6-phosphate dehydrogenase deficiency. 

What is glucose-6-phosphate dehydrogenase deficiency?

Glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency) is also called favism. Human red blood cell membranes have an enzyme called glucose-6-phosphate dehydrogenase (G6PD). It is involved in the process by which red blood cells metabolize glucose. In the process, it produces a substance that protects red blood cells from being damaged by oxides. If people eat oxidative foods or drugs in the absence of G6PD, red blood cells will be easily destroyed by them and acute hemolysis will occur. Since most patients developed acute hemolysis within 48 hours of eating fresh broad beans or their products, G6PD deficiency is also known as favism.

What are the clinical manifestations of glucose-6-phosphate dehydrogenase deficiency?

In patients with G6PD deficiency, the onset is generally acute. Its incubation period can range from 2 hours to 15 days, but is generally 1 to 2 days. 

1. Prodromal symptoms include fever, dizziness, abdominal pain, nausea, vomiting, fatigue, and general malaise, which generally last for 1 to 2 days.
2. The manifestations of acute intravascular hemolytic anemia include rapid onset of jaundice, pale complexion, and dark yellow urine. Some patients also develop spleen and liver enlargement.
3. Severely ill patients may experience convulsions, lethargy, coma, severe anemia, acute renal failure, shock, and systemic failure.

What are the main causes of Glucose-6-Phosphate Dehydrogenase Deficiency?

1. Eating broad beans and their products, contacting broad bean pollen.
2. Nursing mothers ate fava beans and their products, or were exposed to broad bean pollen.
3. Taking medicines (such as antipyretic analgesics, some antimalarial drugs, or sulfonamides, etc.).
4. Infections: Viral infections (eg, flu, typhoid, mumps, pneumonia, hepatitis, etc.).

G6PD deficiency is most common in children under 5 years of age, and is more common in men than women. It is an inherited blood disorder. Therefore, it cannot be cured, but it can be prevented.

Why does glucose-6-phosphate dehydrogenase deficiency occur mainly in children?

Some studies suggest that it may be due to poor digestion, abnormal intestinal permeability and the easy entry of broad bean protein into children's bodies. In addition, some studies have pointed out that with the growth of children's age, the enzymes, liver, spleen and various physiological functions will gradually improve. At the same time, the human body will neutralize broad beans and some oxidative substances, so it will inhibit the pathogenesis of G6PD deficiency. 

Moreover, people with G6PD deficiency generally stop eating broad beans or other oxidative substances after they develop it in childhood. As a result, the incidence of G6PD deficiency in young and old is reduced.

What foods and drugs are contraindicated in patients with Glucose-6-Phosphate Dehydrogenase Deficiency?

Food: Broad beans and their products. Broad bean products include soy sauce, bean paste and other condiments. In terms of oxidative capacity, fresh fava beans will be stronger than cooked fava beans. In patients with favism, fresh fava beans will almost certainly cause hemolysis. In addition, broad bean pollen will almost certainly cause severe hemolysis in patients. Therefore, they should avoid visiting fava bean fields during the fava bean harvest season.

Mothballs: Naphthalene contained in mothballs can also cause acute hemolysis in patients with favism. Therefore, mothballs are prohibited in the patient's wardrobe. Once the clothes come into contact with mothballs, they must be exposed to the sun before the patient can wear them.

Topical medicines: The external use of salicylic acid and some Chinese herbal oils should also be prohibited by patients.

Traditional Chinese medicines: Patients should avoid using traditional Chinese medicines such as pearl powder, Sichuan lotus, bezoar, winter plum blossom, honeysuckle, and their proprietary Chinese medicines.

Medicines: Patients with favism should avoid self-medication and inform their doctor when seeking medical treatment. Patients with favism should try to avoid the following drugs:

• Antidiabetic drugs: such as glimepiride, gliclazide, glyburide, glipizide, etc.
• Antipyretic analgesics: such as aminopyrine, aspirin, acetaminophen, etc.
• Antimicrobial drugs: chloramphenicol, streptomycin, ciprofloxacin, moxifloxacin, levofloxacin, furazolidone, chloroquine, primaquine, etc.
• Vitamins: such as vitamin C, vitamin K1, vitamin K3, vitamin K4.
• Others: isosorbide nitrate, hydroxychloroquine, sulfasalazine, etc.
• In addition, levodopa, dopamine, phenytoin, diphenhydramine, chlorpheniramine, colchicine, and doxorubicin also have a lower risk.

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