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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Learning about ezetimibe.📜📜📜

Ezetimibe was the first drug to inhibit cholesterol absorption in the gut. It can be combined with statins to enhance the ability to lower cholesterol levels. It is widely used clinically. The following will introduce the relevant knowledge about ezetimibe.

1. The mechanism of ezetimibe.

Ezetimibe is converted to ezetimibe-glucuronide in the intestinal tract. Ezetimibe-glucuronide acts at the brush border of intestinal epithelial cells. It inhibits the activity of the sterol carrier transporter NPC1L1, thereby reducing intestinal absorption of cholesterol.

Dosage: Once a day, 10mg ezetimibe each time. Ezetimibe can be taken any time of the day. It can also be taken on an empty stomach or with food.

2. The enterohepatic circulation of ezetimibe.

First, ezetimibe is converted to ezetimibe-glucuronide in the intestine. It then travels from the portal vein to the liver and from the liver to the bile. Finally it goes back into the intestines. Enterohepatic circulation maintains ezetimibe-glucuronide in the brush border of intestinal epithelial cells. It can inhibit the intestinal absorption of cholesterol. In addition, enterohepatic circulation can also slow the elimination of ezetimibe-glucuronide. Its half-life is 22 hours.

3. The lipid-lowering intensity of ezetimibe.

Cholesterol in the human body can be divided into endogenous synthesis by the body and exogenous absorption in the diet. About 2/3 of cholesterol is synthesized endogenously and 1/3 of cholesterol is absorbed exogenously. 

Ezetimibe alone can reduce low-density lipoprotein cholesterol (LDL-C) by about 20%. 

	Total cholesterol (TC)	Low-density lipoprotein cholesterol (LDL-C)	High-density lipoprotein cholesterol (HDL-C)	Triglycerides (TG)
Ezetimibe	13%↓	18%↓	8%↓	1%↑
Pravastatin	17%↓	25%↓	8%↓	7%↑
Simvastatin	26%↓	36%↓	17%↓	7%↑
Atorvastatin	32%↓	44%↓	25%↓	4%↑

From the above table, it can be seen that statins have stronger lipid-lowering intensity than ezetimibe. Therefore, ezetimibe is often used in combination with statins to further reduce LDL-C.

	Lipid-lowering treatment plan	Reduced levels of LDL-C
Monotherapy	Ezetimibe	20%
	Moderate-intensity statins (eg, simvastatin, pravastatin)	30%
	High-intensity statins (eg, atorvastatin, rosuvastatin)	50%
	PCSK9 inhibitors (eg, evolocumab, alirocumab)	60%
Combination therapy	High-intensity statin + Ezetimibe	65%
	High-intensity statin + PCSK9 inhibitor	75%
	High-intensity statin + PCSK9 inhibitors + Ezetimibe	85%

4. Adverse reactions.

Because ezetimibe is not metabolized by CYP450 enzymes, it is less likely to have drug interactions. Ezetimibe was well tolerated and safe. Its adverse effects are mild and mostly transient. Its main adverse reactions are gastrointestinal discomfort and headache. In addition, side effects such as muscle pain and increased transaminases can occur when it is used in combination with statins.

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Repeated damage to cells can cause cancer, so do muscle cells?💪💪💪

Chronic injury and inflammation are major risk factors for cancer. Carcinogenic factors such as eating hot food, drinking hot tea, smoking, and air pollution are all due to their repeated damage to human tissues. But why does repeated tissue damage lead to cancer? Although the mechanism of this carcinogenesis is complex, one of the more easily understood reasons is that the repair of damaged tissue requires cell division. Every time a cell divides, a gene may mutate. Repeated tissue damage increases the number of cell divisions, which increases the probability of mutation into an oncogene. At this time, fitness enthusiasts may think that muscle fibers are constantly damaged and repaired during muscle exercise. Will it also increase the risk of cancer?

Does muscle building increase the chance of a genetic mutation?

Its answer is of course not. Muscle building does not increase your risk of cancer. The main reason is that with or without exercise, muscle tissue rarely develops tumors. Lung cancer, breast cancer, liver cancer, etc. are all common, but muscle cancer is rare. It is because the muscle tissue rarely develops tumors. Although this does not mean that muscle tissue is completely tumor-free, for example, rhabdomyosarcoma is a tumor with muscle tissue characteristics. However, it is not caused by muscle building. Rhabdomyosarcoma is a common childhood tumor. Congenital or early developmental genetic mutations are its main cause. Adults over the age of 30 generally do not have rhabdomyosarcoma. 

Why do muscles rarely get cancer?

Long-term muscle building can lead to repeated muscle growth and injury, but why do muscles rarely get cancer? Because of the special structure of skeletal muscle, it has its own anti-cancer function. 

The structure of muscle.

As it can be seen from the above figure, a skeletal muscle cell is also called a muscle fiber. It has two main features:

1. Most cells in the human body generally have only one nucleus. However, a myofibroblast will have many nuclei. It belongs to multinucleated cells.
2. Muscle cells, which are multinucleated cells, do not divide and proliferate by themselves. They do not go from one muscle fiber directly to two muscle fibers.

So how does muscle training make muscles stronger without splitting muscle fibers? This makes muscles stronger both by making the muscle cells bigger and by fusing more muscle cells. Muscles tend to get bigger because each muscle fiber cell gets bigger, not because there are more of them. Myofibroblasts use nutrients in the body to synthesize more protein when stimulated by exercise. It makes muscle cells larger, but does not proliferate. 

Muscle building

How do muscles repair after muscle damage?

Muscle stem cells are responsible for muscle repair. Although myofibroblasts cannot divide and proliferate, muscle stem cells can. Muscle stem cells usually only attach to the surface of muscle fibers and do not proliferate. Muscle stem cells are activated if the muscle is growing or repairing damage. They divide and proliferate to create new muscle cells. Most stem cell divisions produce new cells that fuse with old myofibroblasts and repair damaged muscle fibers. The rest retain the properties of muscle stem cells and attach to the surface of muscle fibers.

Muscle Repair.

Why doesn't the division and proliferation of muscle stem cells increase cancer risk?

One of the main reasons is that most muscle stem cells fuse into muscle fibers after they divide and proliferate. When these stem cells fuse into muscle fibers, they lose their ability to divide and proliferate. They do not accumulate mutations. Although a single muscle stem cell division may lead to cancer-causing mutations, one mutation is not enough to generate cancer cells. Adults generally need to accumulate multiple mutations to form cancer cells. And in many cases, specific mutation types and sequences are required to cause cancer. The process is also relatively long. And when a muscle stem cell has an oncogene mutation, it is quickly fused into the muscle fiber. Even if the muscle is damaged by the next exercise, it will not divide and grow again. Normally, it does not accumulate into cancer cells and cause cancer. This biological feature is the anticancer function of skeletal muscle. In addition, a number of studies have shown that regular muscle training does not increase cancer risk but significantly reduces cancer incidence.

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Drinking water like this is bad for your body.😖😖😖

Many people know that drinking more water is good for the body. Many people know that drinking more water is good for the body. However, drinking water indiscriminately can be harmful to the body's organs and the damage is not immediately reflected. It can cause long-term damage to your body without even noticing it. Therefore, here are some bad drinking habits, so that you can change your drinking habits in time.

Too cold water is bad for the stomach and intestines.

With summer approaching, many people like to drink cold water. Drinking it can refresh you when you are sleepy, and it can cool down quickly after exercising. This is very refreshing. However, if a person suddenly drinks too cold water, the smooth muscles of the stomach and intestines will spasm, and the blood vessels will suddenly contract. It may cause stomach and intestinal dysfunction, indigestion, constipation and other problems. Especially during or after exercise, these problems are more likely to be caused. 

When a person is exercising, the functions of various organs in the human body will be adjusted due to the exercise. The functions of exercise-related tissues and organs such as the heart, lungs and muscles will be enhanced. Organs involved in metabolism or energy storage, such as the gastrointestinal tract, are also weakened. The rate of gastric emptying is also reduced. In addition, a person's body temperature rises during and after exercise. At this time, if you drink too much or drink too cold water quickly, it will not only easily cause gastrointestinal disorders, but also cause water retention in the stomach. It can cause nausea, stomach pain, bloating, indigestion and constipation.

Drinking water too fast is bad for the heart.

The heart pumps blood throughout the body through the contraction of the myocardium, and returns the blood to the heart through the relaxation of the myocardium. However, as people age, the function of the heart also declines. After the function of the heart declines, its ability to withstand sudden stimuli will also decrease. Even small stimuli, such as drinking water quickly, can damage the heart due to the increased burden. Especially with a lot of people who are thirsty after a bath, they drink water instantly and quickly. It is very dangerous. Heart rate generally rises right after taking a shower. If you drink water quickly at this time, too much water will enter the blood vessels. This water can make the heart more burdened. People with poor heart function, patients with cardiovascular disease and the elderly may experience symptoms such as palpitation and sweating.

Drinking too little water is bad for your kidneys and bladder.

Drinking too little water can reduce urination. Decreased urination can cause the following:

Decreased urine output and increased urine concentration can saturate or supersaturate calcium phosphate, calcium oxalate, and uric acid in urine. They can precipitate as crystalline particles in the urine. These crystals continue to accumulate and eventually form kidney stones or bladder stones.

Decreased urination prevents bacteria from being excreted in time. It can easily cause acute cystitis, urinary tract infection, etc., especially in women. Because the female urethra is relatively short. External bacteria can easily pass through the infected urethra to the bladder.

If the weather is hot, people sweat more and drink too little water, which increases the risk of infection and urinary tract stones.

In addition, if you don't drink enough water for a long time, your body will be dehydrated. It also increases the risk of urinary system cancers.

Drinking too hot water is bad for the esophagus.

Many people drink some hot water to relieve discomfort when they feel uncomfortable. However, too hot water can actually harm our esophagus. The mucosal epithelial layer on the esophagus is very soft and thin. When hot water directly touches the mucosal epithelial layers, it is easy to burn them and cause breakage, ulceration, and bleeding. The mucosal epithelium generally repairs damaged tissue quickly. However, if the mucosal epithelium is often badly stimulated, it will easily appear some cells with abnormal functions and morphology due to frequent repair and proliferation, and then evolve into tumor cells. Although the maximum temperature that the mouth and esophagus can tolerate is 50 to 60 ^oC, the optimal temperature for food to be eaten by the human body is 10 to 40 ^oC. Therefore, food or water that is too hot should be ingested after it has cooled slightly. 

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What is the difference between the antiprotozoal drugs ornidazole, levornidazole and levornidazole disodium phosphate❓❓❓

Ornidazole is a third-generation nitroimidazole. It has an antagonistic effect on protozoa such as amoeba, trichomoniasis, and giardiasis. In addition, it also has a good anti-anaerobic effect. So, what is the difference between ornidazole, levornidazole and levornidazole disodium phosphate?

Antiprotozoal effect and anti-anaerobic bacteria effect.

For the treatment of anaerobic and protozoal infections, metronidazole, tinidazole, ornidazole, and levornidazole can be used. Secnidazole can only be used for the treatment of protozoal infections. Tinidazole and ornidazole are more resistant to anaerobic bacteria than metronidazole. These drugs have smaller molecular weight, better lipid solubility and poor water solubility. They can enter the placenta and cerebrospinal fluid.

Indications and dosage.

Ornidazole is a racemic compound. It is converted in the body to dexornidazole and levornidazole. Both of them have similar antiprotozoal and antianaerobic abilities. However, dexornidazole is more toxic than levornidazole. The half-lives of ornidazole and levornidazole are 12 to 14 hours and they have the same indications and dosages. The indications and dosage of ornidazole and levornidazole are as follows:

To treat anaerobic infections: 

• After dinner, take 1.5g orally, and take the medicine continuously for 1 to 3 days according to the condition.
• Take 0.5 to 1 g orally each time, once every 12 hours, and take the medicine continuously for 3 to 10 days according to the condition.
• The starting dose by intravenous infusion is 0.5 to 1 g every 12 hours for 5 to 10 days.

To treat trichomoniasis:

• After dinner, take 1.5g orally, and take the medicine continuously for 1 to 2 days according to the condition.

For the treatment of vaginal trichomoniasis, it is recommended that a single dose of metronidazole 2g or a single dose of tinidazole 2g is recommended.

Adverse reactions.

Common adverse reactions of nitroimidazoles are as follows:

• Oral gastrointestinal adverse reactions such as metallic taste, stomach pain, and nausea.
• Nervous system side effects such as numbness, spasms, tremors, dizziness, headache, and confusion in the limbs.

The incidence of gastrointestinal adverse reactions was similar between ornidazole and levornidazole. Taking ornidazole and levornidazole after meals can reduce gastrointestinal adverse effects. However, ornidazole has a higher incidence of neurological adverse effects than levornidazole. 

Nitroimidazoles can cause disulfiram-like reactions. They inhibit acetaldehyde dehydrogenase and prevent hepatic oxidative metabolism of acetaldehyde. It causes acetaldehyde to build up. Nitroimidazoles may also inhibit dopamine beta-hydroxylase activity and reduce dopamine metabolism. It increases dopamine levels in the brain leading to serotonin toxicity syndrome. Compared with other nitroimidazoles, ornidazole has less inhibitory effect on acetaldehyde dehydrogenase. However, it has also been reported that ornidazole can cause a disulfiram-like reaction. Therefore, it recommends that alcoholic beverages or medications should not be taken while taking ornidazole.

Difference between levornidazole and levornidazole phosphate disodium.

Levornidazole has poor water solubility. In order to enhance its water solubility, it is generally added with hydrochloric acid. This lowers the pH of the injection to 3.2 to 4.5. Injections with low pH are more likely to cause phlebitis.

The water solubility of levornidazole disodium phosphate will be higher than that of levornidazole. Its injectable dosage form has a pH of about 5.5. Some studies have pointed out that levornidazole phosphate disodium injection does not cause phlebitis.

When ornidazole and levornidazole are administered intravenously to patients, the injection should be diluted to a solution of ≤5 mg/ml. In addition, each intravenous infusion of 100ml of solution, the infusion time is not less than 30 minutes. Ornidazole and levornidazole injections should be stored in a shaded, airtight and cool place (temperature not exceeding 20°C).

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How to use eye drops correctly?👀

Nowadays, people often use electronic products such as mobile phones and computers. Watching the screen for a long time can easily cause eye discomfort. Whenever the eyes feel uncomfortable and dry, many people use eye drops to relieve the discomfort. However, not everyone knows the correct way to use eye drops and what to pay attention to when using them. The following will explain the correct use of eye drops.

1. Check the eye drops for any abnormality.

First of all, be sure to confirm whether the drug is an ophthalmic preparation. The pharmaceutical requirements for ophthalmic preparations are not the same as for general dosage forms. The resistance of the eyes is lower than that of the skin or the stomach. Ophthalmic preparations are used directly on the eyes, so their pharmaceutical requirements are much higher than those of general dosage forms. Medication in normal dosage form should not be used in the eyes. In addition, you should also check that the expiration date on the packaging has not expired when you use it. Not only eye drops, but all medicines should not be used after they have expired. All ophthalmic preparations should not continue to be used and should be thrown away if particles appear or if the color of the solution changes.

2. The correct procedure for eye drops.

You should wash your hands before applying eye drops or ointment. Then you can lie down or sit with your head thrown back. Use your index finger and thumb to gently pull the lower eyelid down to form a sac. Turn your eye upward so that your inferior fornix conjunctiva is fully exposed. Put the eye drops close to your eyelid. But do not touch the eyedrops on the eyelids, as this may contaminate the eyedrops. You dispense the eye drops as prescribed and close your eyes gently. Try not to blink immediately after instilling the eye drops. Gently press with one finger on the corner of the eye near the side of the nose for 1 to 2 minutes. If you don't do this, the eye drops may flow from the surface of the eye through the nasolacrimal duct into the nose and mouth. After 1 to 2 minutes you wipe off the excess eye drops with a clean tissue. 

When using eye ointment, squeeze a certain amount of eye ointment into the lower eyelid. Eye ointment should be squeezed into a thread. However, do not touch your eyelids or eyes when squeezing the ointment. Then close your eyes and roll them a few times. This allows the ointment to spread evenly.

3. How to store eye drops.

Eye drops bottles do not need to be wiped or rinsed after use, as this will contaminate the drops. Just screw the cap tightly and store it in a suitable environment. In addition, because the eye drops are sterile preparations, it is easy to breed bacteria after opening. Unless there are special regulations for eye drops, they should be used up within 1 month after opening. After opening, eye drops should be stored in a dry, cool place away from direct sunlight. Some eye drops will need to be refrigerated, but not frozen.

4. Precautions for combined use of eye drops.

Sometimes a patient may need to use several eye drops. However, these eye drops cannot be used together at the same time. Under normal circumstances, one eye drop is instilled first, and then another eye drop is applied 10 to 15 minutes later. If eye drops are used at the same time, the first eye drop is not fully absorbed and washed away by another eye drop. This can cause the first eye drop to be ineffective. 

In addition, in order to avoid eye drops that are too irritating to the eyes, it recommends that patients use less irritating eye drops first. For example, patients need to use levofloxacin eye drops and sodium hyaluronate eye drops in combination. It recommends that patients use sodium hyaluronate eye drops first, and then levofloxacin eye drops after 10 to 15 minutes. 

If the patient needs to use eye ointment and eye drops at the same time, it recommends using eye drops in the morning and eye ointment at night before going to bed. After applying eye ointment, the ointment spreads into a film on the cornea. This can affect vision. It recommends using eye ointment at bedtime.

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Some dietary habits may cause liver cancer.👿👿👿

More and more attention is now paid to protecting the liver. Many people
know that staying up late and drinking alcohol can be harmful to the liver, but many people do not know that some eating habits are also harmful to the liver, even more damaging than staying up late. Here are some dietary habits that can damage the liver.

Eating this flavor is more damaging to the liver than staying up late.

Many people know that staying up late hurts the liver, but there is a taste that will make the liver more and more hurt. Eating this flavor for a long time is even worse than staying up late and that taste is sweet. Many people know that eating too many sweets can cause obesity, increase the risk of cardiovascular and cerebrovascular diseases and diabetes. However, eating too many sweets can actually damage the liver, and the damage of fructose is more serious. Fructose is one of these sugars. It is widely found in natural foods such as fruits and honey. Recent studies have identified excessive fructose intake as a risk factor for nonalcoholic fatty liver disease. The main risk factors for this type of fatty liver are obesity, insulin resistance, and excessive fructose intake. If the patient does not control the development of nonalcoholic fatty liver disease, it can develop into more serious diseases such as liver fibrosis, liver cirrhosis, liver cancer, and even lead to death.

But how does fructose damage the liver? This is because fructose is mainly metabolized by the liver. There are no rate-limiting enzymes during the process of hepatic metabolism of fructose. This results in the continuous production of intermediate products of fructose metabolism, which are then converted into fat and accumulated in the liver. Eventually, it develops into fatty liver and other metabolic diseases. In addition, the barrier function of the gut is also compromised by excessive fructose intake. This increases the enzymes in the liver to synthesize fat, causing the liver to accumulate more fat. Large amounts of fructose can also cause fatty denaturation of the liver. When these denatured fats combine with other risk factors, steatohepatitis can result. Fructose also doesn't make you feel full, like staying up late can cause drowsiness, and it won't cause discomfort like drinking too much alcohol. Therefore, many people do not feel that the fructose intake is excessive and the liver is continuously damaged unintentionally.

Does eating fruit also damage the liver?

As mentioned above, since fructose will damage the liver, and fruits also contain fructose, will eating fruit also damage the liver? In fact, only excessive intake of fructose can damage the liver. Therefore, it is safe and healthy to eat fruit within the normal range. 

Eat 200 to 350g of fruit per day.

Although fruits contain fructose, they also contain a lot of dietary fiber. Dietary fiber slows the rate at which fructose enters the bloodstream, making it less damaging to the liver. It is recommended to eat 200 to 350g of fruit per day.

Fruit should not be juiced.

Fruit juice is a high-sugar food. Although freshly squeezed juice still contains many minerals and vitamins, many people filter the juice after juicing. This removes substances rich in minerals and vitamins. The dietary fiber in the fruit is also removed. The absorption of fructose is accelerated. And after filtering out these nutrients, only a lot of fructose is left in the juice. For example, 500g of orange contains about 11g of fructose. Eating an orange directly not only does not consume too much fructose, but also absorbs nutrients such as vitamin C and fills the stomach. However, the orange juice drinks sold on the market generally contain about 20g of fructose in a 500ml bottle. Drinking fruit juice instead of eating fruit will not only consume more fructose, but also lack different nutrients and will not make you feel full.

Foods contain other sugars.

Processed foods such as packaged breads, snacks, biscuits, energy drinks, carbonated drinks, and seasonings all have high amounts of added sugar. Different added sugars such as fructose, glucose, and sucrose are added to these foods. When sucrose is digested, it will produce fructose and increase the burden on the liver. If you do not pay attention to the intake of sugar when eating, it is easy to lead to excessive intake of sugar. Therefore, in addition to paying attention to the intake of fructose, excessive intake of other sugars should also be avoided.

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Antihypertensive drug usage and common side effects.👀

What differences in characteristics, indications and adverse reactions of five commonly used antihypertensive drugs angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, β-blockers, dihydropyridine calcium channel blockers and thiazide diuretics?

Angiotensin-converting enzyme inhibitors.

Commonly used drugs include benazepril, enalapril, perindopril, etc.

Pharmacological effects: Their antihypertensive effects are achieved by inhibiting angiotensin-converting enzyme resulting in the blocking of renin-angiotensin II production and preventing the degradation of kininase.

Strong indications: prevention of atrial fibrillation, cardiac insufficiency after myocardial infarction, heart failure, metabolic syndrome, proteinuria, microalbuminuria, diabetic nephropathy or non-diabetic nephropathy in patients with hypertension.

Dosage of the drug: 

• Benazepril: 5 to 40 mg once a day. It peaks in about 2 to 4 hours. Its half-life is 11 hours.
• Captopril: 12.5 to 75 mg 3 times a day. It peaks in about 1 to 1.5 hours. Its half-life is 2 hours.
• Enalapril: 5 to 40 mg once a day. It peaks in about 1 hour. Its half-life is 11 hours.
• Fosinopril: 10 to 40 mg once a day. It peaks in about 3 hours. Its half-life is 12 hours.
• Imidapril: 2.5 to 10 mg once daily. It peaks in about 2 hours. Its half-life is 8 hours.
• Lisinopril: 5 to 40 mg once a day. It peaks in about 6 to 8 hours. Its half-life is 12 hours.
• Perindopril: 4 to 8 mg once a day. It peaks in about 2 to 4 hours. Its half-life is 30 to 120 hours.
• Ramipril: 2.5 to 10 mg once a day. It peaks in about 1 hour. Its half-life is 13 to 17 hours.
• Trandolapril: 1 to 4 mg once daily. It peaks in about 1 hour. Its half-life is 16 to 24 hours.

Side effects: A dry cough is a common side effect of these drugs. About 30% of patients develop a persistent dry cough that usually worsens when lying down. Female patients are more likely to have a dry cough than male patients. If the patient cannot tolerate a dry cough, an angiotensin II receptor inhibitor can be used instead.

Angiotensin II receptor inhibitors.

Commonly used drugs include irbesartan, losartan, valsartan, etc.

Pharmacological effects: Their antihypertensive effect is through the inhibition of angiotensin II receptors.

Strong indications: Angiotensin II receptor inhibitors can be used in patients who cannot tolerate angiotensin-converting enzyme inhibitors.

Dosage of the drug: 

• Candesartan: 4 to 16 mg once daily. It takes 3 to 4 hours to peak. Its half-life is 9 hours.
• Irbesartan: 150 to 300 mg once a day. It takes 1 to 1.5 hours to peak. Its half-life is 11 to 15 hours.
• Losartan: 50 to 100 mg once a day. It takes 3 to 4 hours to peak. Its half-life is 6 to 9 hours.
• Olmesartan: 20 to 40 mg once a day. It takes 1 to 2 hours to peak. Its half-life is 13 hours.
• Telmisartan: 40 to 80 mg once a day. It takes 0.5 to 1 hour to peak. Its half-life is more than 20 hours.
• Valsartan: 80 to 160 mg once a day. It takes 2 hours to peak. Its half-life is 9 hours.

Side effects: Angiotensin II receptor inhibitors can cause back pain as a side effect. Studies have shown that the incidence of back pain caused by valsartan is about 1.6%, and the incidence of joint pain is 1.0%.

β-blockers.

Commonly used drugs include bisoprolol, metoprolol, etc.

Pharmacological effects: Their antihypertensive effect is exerted by slowing heart rate, inhibiting myocardial contractility, and inhibiting excessive activation of sympathetic nerve activity.

Strong indications: They are suitable for patients with hypertension complicated with chronic heart failure, coronary heart disease and tachyarrhythmia.

Dosage of the drug: 

• Arotinolol: 10 to 20 mg twice a day. It has a peak time of 2 hours and a half-life of 10 to 12 hours.
• Bisoprolol: 2.5 to 10 mg once daily. It has a peak time of 3 to 4 hours and a half-life of 10 to 12 hours.
• Carvedilol: 12.5 to 50 mg twice daily. It has a peak time of 1 hour and a half-life of 6 to 7 hours.
• Metoprolol tartrate: 50 to 100 mg twice daily. It has a peak time of 1 to 2 hours and a half-life of 3 to 4 hours.
• Metoprolol tartrate extended-release tablets: 47.5 to 190 mg once a day. It has a peak time of 3 to 7 hours and a half-life of 12 to 24 hours.

Side effects: β-blockers slow down the heartbeat and pulse, and they vary widely from person to person. The patient's heart rate should be monitored. Control of blood pressure in patients with hypertension and coronary heart disease should also reduce their resting heart rate to 50 to 60 beats per minute. Sudden withdrawal of the drug can cause severe angina and even sudden death. Therefore, the dose must be gradually reduced under the guidance of a doctor when the drug is discontinued, and the discontinuation process will take at least 2 weeks.

Dihydropyridine calcium channel blockers.

Commonly used drugs include amlodipine, felodipine, nifedipine, etc.

Pharmacological effects: Their blood pressure-lowering effect is caused by blocking calcium channels on vascular smooth muscle cells to dilate blood vessels.

Strong indications: They are indicated for patients with isolated systolic hypertension or elderly hypertension with coronary or carotid atherosclerosis, stable angina and peripheral vascular disease.

Dosage of the drug: 

• Amlodipine: 2.5 to 10 mg once daily. It has a peak time of 6 to 12 hours and a half-life of 35 to 50 hours.
• Felodipine extended-release tablets: 5 to 10 mg once a day. It has a peak time of 2.5 to 5 hours and a half-life of 11 to 16 hours.
• Nifedipine controlled-release tablets: 30 to 60 mg once a day. Its peak time is 6 to 12 hours.
• Nitrendipine: 10 to 20 mg 1 to 2 times a day. It has a peak time of 1 to 2 hours and a half-life of 10 to 22 hours.

Side effects: Common side effects of dihydropyridine calcium channel blockers are ankle edema, gingival hyperplasia, and constipation. Ankle edema is dose-related. Elevating the patient's foot can reduce edema symptoms. In addition, combined with angiotensin-converting enzyme inhibitors or angiotensin II receptor inhibitors can reduce the symptoms of edema. To reduce the incidence of gingival hyperplasia, patients should maintain oral hygiene during medication.

Thiazide diuretics.

Commonly used drugs include hydrochlorothiazide, indapamide, etc.

Pharmacological effects: They lower blood pressure by increasing the excretion of sodium and urine to lower blood volume.

Strong indications: They are suitable for isolated systolic hypertension, salt-sensitive hypertension, elderly hypertension, refractory hypertension, etc.

Dosage of the drug: 

• Hydrochlorothiazide: 12.5 to 25 mg once daily. It has a peak time of 4 hours and a half-life of 9 to 10 hours.
• Indapamide: 1.25 to 2.5 mg once daily. It has a peak time of 1 to 2 hours and a half-life of 14 to 18 hours.

Side effects: Their common side effects are hypokalemia, hyperuricemia, and photosensitivity.

• Hypokalemia: Its clinical symptoms include weakness, fatigue, confusion, nausea, anorexia, etc. Hypokalemia can be relieved by reducing sodium intake.
• Hyperuricemia: Severe cases can cause gout in patients. If the patient's serum uric acid level is ≥480 μmol/L, it is recommended to use other antihypertensive drugs.
• Photosensitivity: Patients may develop a rash. Patients should avoid direct sunlight while taking thiazide diuretics.

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What are the treatments for Pseudomonas aeruginosa?💊💊💊

Pseudomonas aeruginosa is a non-fermenting gram-negative bacillus and is a common opportunistic pathogen. It is widely distributed in the daily environment. Its main source is domestic sewage. It can cause lung infections, bloodstream infections, skin infections (often in people with burns), among others. In addition, Pseudomonas aeruginosa often causes nosocomial infections in patients. Studies have pointed out that patients with low immunity, skin and mucous membrane damage (such as mechanical ventilation, tracheal intubation, indwelling central venous catheter, etc.), structural lung disease (such as cystic fibrosis, bronchiectasis, chronic obstructive pulmonary disease, etc.), as well as patients who are using broad-spectrum antibiotics and have been hospitalized for a long time have a higher risk of infection with Pseudomonas aeruginosa. In addition, in patients with cystic fibrosis, respiratory infections caused by Pseudomonas aeruginosa may develop into chronic infections that are more difficult to treat.

Commonly used drugs against Pseudomonas aeruginosa.

β-lactam antibiotics:

• Penicillin: Piperacillin 9 to 16g intravenously daily, divided into 3 to 4 times.
• Penicillin/β-lactamase inhibitor: Piperacillin/tazobactam 4.5g intravenously every 6 to 8 hours.
• Cephalosporins: Ceftazidime 2g intravenously every 8 hours. Cefoperazone 2g intravenously every 8 hours. Cefepime 2g intravenously every 8 to 12 hours.
• Third generation cephalosporins/β-lactamase inhibitor: Cefoperazone/sulbactam 3g intravenously every 8 hours.
• Monobactams: Aztreonam 2g intravenously every 6 to 8 hours.
• Carbapenems: Imipenem/cilastatin 0.5 g intravenously every 6 hours or 1 g intravenously every 6 to 8 hours. Meropenem is administered intravenously at 1 g every 6 to 8 hours.

Aminoglycosides:

• Gentamicin: The dose is 7mg/(kg x d).
• Tobramycin: The dose is 7mg/(kg x d).
• Amikacin: The dose is 15mg/(kg x d).

Quinolones:

• Ciprofloxacin: The dose is 0.4g every 8 to 12 hours.
• Levofloxacin: The dose is 0.5 to 0.75 g daily.

Other:

• Polymyxin B: The dose is 2.5 to 5 mg/(kg x d) by intravenous infusion, divided into 3 to 4 times.
• Polymyxin E: The dose is 2.5 to 5 mg/(kg x d) by intravenous infusion, divided into 3 to 4 times.
• Fosfomycin: The dose is 300mg/(kg x d) by intravenous infusion, divided into 2 to 3 times.

Among these anti-Pseudomonas aeruginosa drugs, aztreonam, aminoglycosides, polymyxin and fosfomycin generally need to be used in combination with other antibiotics, and are not used alone. Clinically, the course of treatment will be determined according to the patient's condition. If the patient's condition is stable within 3 days after taking the drug, the recommended treatment course is 8 days. If the patient's efficacy is poor after treatment, the course of treatment can be extended to 10 to 14 days.

The drug resistance mechanism of Pseudomonas aeruginosa and its recommended medication.

Pseudomonas aeruginosa develops drug resistance by expressing efflux pumps, forming biofilms, changing target sites and outer membrane proteins, and producing β-lactamases. Some studies have pointed out that the resistance rate of Pseudomonas aeruginosa to polymyxin and amikacin is low, but the resistance rate to carbapenem can be as high as 23%. Drug-resistant Pseudomonas aeruginosa can be divided into:

• Multi-drug resistance: Pseudomonas aeruginosa is not susceptible to 3 or more antibacterial drugs against Pseudomonas aeruginosa.
• Extensive drug resistance: generally refers to that Pseudomonas aeruginosa is not sensitive to other antibiotics and only sensitive to polymyxins.
• Pandrug resistant: Pseudomonas aeruginosa is not sensitive to existing antibiotics.

Dual therapy regimens for extensively drug-resistant Pseudomonas aeruginosa:

1. Combined use of two β-lactam antibiotics: Ceftazidime + Piperacillin/tazobactam, Aztreonam + Piperacillin/tazobactam, Ceftazidime + Aztreonam, Ceftazidime + Cefoperazone/sulbactam.
2. Ciprofloxacin-based: Combine a β-lactam antibiotic or aminoglycoside.
3. Polymyxin-based: Combine a β-lactam antibiotic, ciprofloxacin, fosfomycin or rifampicin.
4. Based on β-lactam antibiotics: combined with ciprofloxacin, aminoglycoside or fosfomycin.

Triple therapy for extensively drug-resistant Pseudomonas aeruginosa:

1. Polymyxin + β-lactams + Ciprofloxacin.
2. Polymyxin + β-lactams + Fosfomycin.
3. Polymyxin (intravenous) + Polymyxin (aerosol inhalation) + Carbapenems.
4. Aztreonam + Ceftazidime + Amikacin.

Due to the increased risk of side effects (eg, increased nephrotoxicity with polymyxin and aminoglycosides, immune-mediated thrombocytopenia with rifampicin and piperacillin), rational drug selection and monitoring The patient's drug response.

Inhaled antimicrobials are believed to be the mainstay of treatment for Pseudomonas aeruginosa-related lung infections.

The goal of treatment for pulmonary infections caused by Pseudomonas aeruginosa is to reduce bacterial counts in the respiratory tract and improve patient outcomes. Antibiotics for inhalation have the advantage of a dosage form that allows the drug to accumulate in the respiratory tract to increase local drug concentration. This is believed to significantly improve the patient's respiratory symptoms and improve the patient's quality of life. There are now many inhaled formulations of antibiotic drugs into the field of research.

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