Does atorvastatin cause dry mouth. Atorvastatin Side Effects: Understanding Dry Mouth and Other Oral Symptoms

06.07.202313.06.2023 by alexxlab

What are the potential side effects of atorvastatin on oral health. How common is dry mouth as a side effect of statin medications. What other oral symptoms may occur when taking atorvastatin. When should you consult a doctor about statin side effects.

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What is Atorvastatin and How Does it Work?

Atorvastatin belongs to a class of medications known as statins, which are widely prescribed to help lower cholesterol levels in the blood. Specifically, atorvastatin works by reducing the production of low-density lipoprotein (LDL) cholesterol, often referred to as “bad” cholesterol.

This medication is typically prescribed to individuals with high cholesterol levels who are at risk of developing cardiovascular diseases. By lowering LDL cholesterol, atorvastatin helps reduce the risk of heart attacks, strokes, and other cardiovascular events.

How Effective is Atorvastatin in Reducing Cardiovascular Risk?

Studies have shown that statins like atorvastatin can significantly reduce the risk of cardiovascular disease. On average, statin therapy induces a 26% reduction in the risk of cardiovascular events such as angina, stroke, and heart attacks. This substantial risk reduction has made statins a cornerstone in the management of hypercholesterolemia and cardiovascular disease prevention.

Common Side Effects of Atorvastatin

While atorvastatin is generally well-tolerated, like all medications, it can cause side effects in some individuals. Common side effects may include:

Muscle pain or weakness
Headache
Digestive issues (nausea, diarrhea, constipation)
Fatigue
Mild cognitive effects

It’s important to note that most people taking atorvastatin do not experience significant side effects, and the benefits of the medication often outweigh the potential risks for those with high cardiovascular risk.

Oral Side Effects of Atorvastatin: Dry Mouth and Beyond

While less commonly discussed, atorvastatin and other statins can sometimes cause oral side effects. These symptoms can be bothersome for some patients and may impact their quality of life.

Does Atorvastatin Cause Dry Mouth?

Yes, dry mouth (xerostomia) has been reported as a side effect of atorvastatin use. While not among the most common side effects, some patients do experience a sensation of dryness in their mouth while taking this medication.

Dry mouth can be more than just an inconvenience. It can lead to difficulties in speaking, chewing, and swallowing, and may increase the risk of dental problems such as tooth decay and gum disease if left unaddressed.

Other Oral Symptoms Associated with Atorvastatin

In addition to dry mouth, studies have identified several other oral symptoms that may occur in some individuals taking atorvastatin:

Itchiness in the mouth
Bitterness or altered taste
Cough (which may be related to throat irritation)

These symptoms, while not life-threatening, can be uncomfortable and may impact a patient’s adherence to their medication regimen if not properly addressed.

Research Findings on Atorvastatin and Oral Health

Several studies have investigated the relationship between statin use and oral health symptoms. One notable study published in BMC focused on patients aged 50-70 years who were receiving statin treatment for hypercholesterolemia.

What Did the Study Reveal About Oral Symptoms?

The study found that a significant percentage of participants reported oral symptoms during statin therapy. These symptoms included:

Dry mouth
Itchiness in the oral cavity
Bitterness in the mouth
Cough

Interestingly, the research team observed a marked improvement in these symptoms after temporarily interrupting statin treatment. This finding suggests a potential causal relationship between statin use and the reported oral side effects.

How Common Are These Oral Side Effects?

While the exact prevalence of oral side effects from atorvastatin use is not well-established, the studies indicate that they are not rare occurrences. However, it’s important to note that not all patients taking atorvastatin will experience these symptoms, and the severity can vary among those who do.

Managing Oral Side Effects of Atorvastatin

If you’re experiencing oral side effects while taking atorvastatin, there are several strategies you can employ to manage these symptoms:

How Can You Alleviate Dry Mouth?

Stay hydrated by drinking plenty of water throughout the day
Use sugar-free gum or lozenges to stimulate saliva production
Avoid caffeine and alcohol, which can worsen dry mouth
Use a humidifier, especially at night
Consider over-the-counter saliva substitutes

What Should You Do About Other Oral Symptoms?

For symptoms like itchiness, bitterness, or cough:

Maintain good oral hygiene to reduce irritation
Rinse your mouth with salt water to soothe irritation
Use throat lozenges to alleviate cough and irritation
Consider timing your medication to minimize taste disturbances

It’s crucial to consult your healthcare provider before making any changes to your medication regimen or if symptoms persist or worsen.

When to Consult Your Doctor About Statin Side Effects

While some side effects may be manageable at home, there are instances when you should seek medical advice:

What Are the Red Flags for Statin Side Effects?

Severe muscle pain or weakness
Yellowing of the skin or eyes (jaundice)
Dark-colored urine
Unexplained fatigue or fever
Persistent oral symptoms that significantly impact quality of life

If you experience any of these symptoms, it’s important to contact your healthcare provider promptly. They may need to adjust your dosage, switch you to a different statin, or explore alternative treatments.

Balancing the Benefits and Risks of Atorvastatin

When considering the potential side effects of atorvastatin, it’s essential to weigh them against the significant cardiovascular benefits the medication provides. For many patients, the reduction in heart attack and stroke risk far outweighs the potential for side effects.

How Do Doctors Assess the Risk-Benefit Ratio?

Healthcare providers consider several factors when prescribing atorvastatin:

Individual cardiovascular risk
Baseline cholesterol levels
Presence of other risk factors
Potential for drug interactions
Patient’s overall health and medical history

This personalized approach helps ensure that the benefits of statin therapy outweigh the potential risks for each patient.

Alternative Approaches to Managing High Cholesterol

While statins like atorvastatin are highly effective in managing high cholesterol, they are not the only option available. For patients who experience significant side effects or prefer to explore other treatments, there are alternative approaches:

What Lifestyle Changes Can Help Lower Cholesterol?

Adopting a heart-healthy diet low in saturated fats
Increasing physical activity and exercise
Maintaining a healthy weight
Quitting smoking
Limiting alcohol consumption

Are There Other Medications for High Cholesterol?

Yes, there are several other classes of cholesterol-lowering medications, including:

Bile acid sequestrants
Cholesterol absorption inhibitors
PCSK9 inhibitors
Fibrates
Niacin

Each of these medications works differently and may be more suitable for certain patients depending on their specific health profile and cholesterol levels.

The Importance of Medication Adherence and Follow-up

Regardless of whether you experience side effects, it’s crucial to maintain open communication with your healthcare provider and adhere to your prescribed treatment plan.

Why is Consistent Statin Use Important?

Statins like atorvastatin are most effective when taken consistently over time. Stopping or intermittently using the medication can reduce its cholesterol-lowering effects and increase cardiovascular risk.

How Often Should You Have Follow-up Appointments?

Regular follow-up appointments are essential for monitoring both the effectiveness of the medication and any potential side effects. Typically, healthcare providers will recommend:

Initial follow-up within 4-12 weeks of starting therapy
Lipid panel tests every 3-12 months
Liver function tests as needed
Annual comprehensive health check-ups

These appointments allow for timely adjustments to your treatment plan if needed.

Future Directions in Cholesterol Management

As medical research continues to advance, new approaches to managing high cholesterol and reducing cardiovascular risk are emerging. These developments may offer additional options for patients who experience side effects from current treatments.

What New Therapies Are on the Horizon?

RNA interference therapies targeting cholesterol production
Novel PCSK9 inhibitors with less frequent dosing
Bempedoic acid, a new class of cholesterol-lowering drug
Combination therapies for enhanced efficacy

While these emerging treatments show promise, it’s important to note that they are still being studied and may not be widely available or suitable for all patients.

How Might Personalized Medicine Impact Cholesterol Treatment?

Advances in genetic testing and personalized medicine may allow for more tailored approaches to cholesterol management in the future. This could potentially help identify patients who are more likely to benefit from specific treatments or experience certain side effects, allowing for more precise and effective therapy.

Conclusion: Navigating Atorvastatin Treatment and Oral Health

Atorvastatin remains a crucial medication in the fight against high cholesterol and cardiovascular disease. While oral side effects like dry mouth can occur, they are generally manageable and often outweighed by the significant cardiovascular benefits of the medication.

If you’re taking atorvastatin and experiencing oral symptoms, it’s important to discuss these with your healthcare provider. They can help you manage side effects, explore alternative treatments if necessary, and ensure you’re receiving the most appropriate care for your individual needs.

Remember, maintaining open communication with your healthcare team, adhering to your prescribed treatment plan, and attending regular follow-up appointments are key to achieving the best possible outcomes in managing your cholesterol levels and overall cardiovascular health.

Statins side effects: A dry mouth, itchiness, bitterness or a cough could occur

Statins side effects: A dry mouth, itchiness, bitterness or a cough could occur | Express.co.uk

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STATINS are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood. Millions of people around the world take the drug, however, as with most things, the drug can cause a variety of side effects including these four mouth disorders.

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This Morning: Dr Chris reveals grapefruit can affect statins

Statins induce an average 26 percent reduction of the risk of cardiovascular disease (angina, stroke, ictus, etc.), but they are also related to severe adverse effects. One such side effect includes these mouth disorders.

Blood cancer: Itchy skin is a sign

In a study published in BMC, the effects of statins on dental and oral health were investigated.

The study noted: “Patients, aged 50–70 years old, who had been previously diagnosed with hypercholesterolemia and were receiving statin treatment were referred to a dentist’s office.

“Anamnesis regarding their oral symptoms was obtained on their initial visit.

“Statin treatment was then discontinued, which was followed by various laboratory tests and repeat visits to the dentist at seven and 15 days after statin discontinuation.

“Results showed that a high percentage of oral symptoms included dry mouth, itchiness, bitterness, and cough during statin therapy.

“There was a marked improvement in their symptoms after temporary interruption of statin treatment.”

READ MORE: Covid symptoms: Signs in the feet to spot – from skin lesions to Guillain-Barre Syndrome

Statins side effects: The four symptoms found in the mouth (Image: Getty Images)

In another study published in the US National Library of Medicine National Institutes of Health, side effects of statins in the oral cavity were looked at.

The studies objective was to analyse the side effects of statins in the mouth cavity, and to analyse the symptoms after interruption of the treatment.

Symptoms pertaining to the oral cavity from statin use included dry mouth patients, itchiness, bitterness in the mouth and cough.

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Adverse side effects of statins in the oral cavity

. 2008 Feb 1;13(2):E98-101.

Montserrat Pascual Cruz¹, Eduardo Chimenos Küstner, José António García Vicente, Xavier Mezquiriz Ferrero, Eulalia Borrell Thio, José López López

Affiliations

Affiliation

¹ Médico estomatólogo, ABS (Area Básica de Salud) Sant Roc Badalona, Facultad de Medicina UAB, Spain. [email protected]

PMID:
18223537

Free article

Montserrat Pascual Cruz et al.

Med Oral Patol Oral Cir Bucal.

2008.

Free article

. 2008 Feb 1;13(2):E98-101.

Authors

Montserrat Pascual Cruz¹, Eduardo Chimenos Küstner, José António García Vicente, Xavier Mezquiriz Ferrero, Eulalia Borrell Thio, José López López

Affiliation

¹ Médico estomatólogo, ABS (Area Básica de Salud) Sant Roc Badalona, Facultad de Medicina UAB, Spain. [email protected]

PMID:
18223537

Abstract

Increased plasma levels of cholesterol are high risk factors of cardiovascular disease. Statins are drugs that inhibit cholesterol synthesis at both pancreatic and extrahepathic levels, being the treatment of choice for hypercholesterolemia.

Objective:

To analyze the side effects of statins in the mouth cavity, and to analyze the symptoms after interruption of the treatment.

Design:

Observational study, preliminary.

Material and methods:

Patients aged 50-70, diagnosed with hypercholesterolemia and undergoing treatment with statins, referred from their primary care physician to the dentist’s office. Anamnesis over oral symptoms was performed in the first visit. Statin treatment was discontinued, followed by lab tests and control visits seven and fifteen days later. We monitored the improvement and/or remission of oral symptoms. Statin treatment was resumed, sending out a report of the patient evolution to the PCP. Symptoms were registered in sheet specially designed for the study.

Exclusion criteria:

patient refusal, use of drugs for dry mouth treatment, Sjögren’s syndrome.

Results:

n=26 patients. Dry mouth patients: improvement in 17 out of 23 patients (88.5%). Itchiness: 6 out of 15 cases improved (57.7%). Bitterness: improvement in 13 out of 14 patients (53.8%). Cough: improvement in 11 out of 12 patients (46.1%).

Discussion:

A high percentage of oral symptoms are associated to treatment with statins. There is a marked improvement after temporary interruption of the treatment. Little is known regarding the side effects of oral treatment with statins. This preliminary study includes a relatively small number of patients. The design of experimental treatments will be required to establish a true correlation between statin treatment and oral symptoms.

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Rosuvastatin – the best choice for the prevention and treatment of atherosclerosis | Oganezova L.G.

Cardiovascular diseases (CVD) are the leading cause of death both in Russia and in other countries of the world. In our country, mortality from diseases of the circulatory system remains 2-3 times higher than in developed countries. The leading causes of death are coronary heart disease and cerebral stroke [1, 2]. The pathogenetic basis of these diseases in most cases are atherosclerotic lesions of the arterial wall.

Most people over the age of 20 have atherosclerotic lesions of varying severity in the arterial wall. Arterial lesions that are not accompanied by thrombosis and do not significantly narrow the lumen of the vessel are considered relatively benign. On the contrary, well-developed, stable atherosclerotic plaques (ASP), which significantly narrow the lumen of the arteries, create an obstacle to blood flow and thereby worsen the blood supply to organs and tissues. However, if there is no risk of developing thrombosis, then such lesions do not pose a great danger to human life [3]. In contrast, unstable, ruptured ASPs are the most dangerous lesions due to the high risk of thrombosis, which can lead to clinical consequences such as acute coronary syndrome and cerebral stroke.
According to most clinical and pathological-anatomical studies, the main role in the formation of unstable ASP is not played by its size, i. e. the degree of stenosis, and the type of plaque – its composition and morphology. The main components of ASP are soft, lipid-containing atheromatous “slurry” and hard, collagen-rich sclerotic tissue [4]. The formation of an atheromatous nucleus in the process of atherogenesis occurs both due to the penetration into the plaques from the lumen of the vessel of plasma macromolecules – lipoproteins, fibrinogen and albumin, and lipids coming from the base of the plaque through the newly formed capillary vessels. The sclerotic component of ASB is relatively harmless in terms of the development of complications. The atheromatous component, which occupies a smaller volume, is much more dangerous, because. it softens the plaques, contributing to their rupture and contact of the atheromatous “slurry” with the blood [5]. Therefore, the so-called “soft”, lipid-rich ASBs are more dangerous, because. they are prone to rupture and thrombus formation [6].
There is no doubt that an elevated level of lipids in the blood is a key moment in the formation of atherosclerosis. At the same time, hyperlipidemia is one of the few major modifiable risk factors for CVD. This has been confirmed by a large number of epidemiological studies, including the Framingham study [7] and the INTERHEART study [8].
Correction of lipid metabolism disorders consists of such measures as diet therapy, lifestyle correction and the rejection of bad habits. As for drug therapy, statins have become the undoubted leader in this area, which have radically changed the situation in the prevention and treatment of atherosclerosis throughout the world. Early 1970s Japanese scientist A. Endo created the first statin, which is an inhibitor of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which inhibited the synthesis of cholesterol (CS) at an early stage of its formation. This drug, mevastatin, was isolated from the waste products of Penicillium citrinum. It did not find clinical use, but another statin developed in the same laboratory, pravastatin, was subsequently widely used. In 1987, lovastatin appeared on the pharmaceutical market, then new semi-synthetic and synthetic statins, which confidently took their place in the correction of lipid metabolism disorders.
The mechanism of action of statins is based on the similarity of their chemical structure and part of the HMG-Co-reductase enzyme. The statin molecule binds to the part of the coenzyme A receptor where this enzyme is attached. Another part of the statin molecule inhibits the conversion of hydromethylglutarate to mevalonate, an intermediate product in the synthesis of the cholesterol molecule. Thus, inhibition of the activity of HMG-CoA reductase leads to a series of successive reactions, as a result of which the intracellular content of cholesterol decreases, a compensatory increase in the activity of low-density lipoprotein (LDL) receptors occurs and, accordingly, the catabolism of low-density lipoprotein cholesterol (LDL-C) is accelerated. The lipid-lowering effect of statins is directly associated with a decrease in the level of total cholesterol due to LDL cholesterol. Depending on the dose, statins reduce the level of this lipoprotein by up to 55% (rosuvastatin 40 mg / day). The effect of statins in lowering LDL-C levels is dose-dependent. Statins can also reduce triglyceride (TG) levels by an average of 20-30%, depending on the baseline, which is associated with a decrease in LDL-C. The effect of statins on high-density lipoprotein (HDL) cholesterol levels is ambiguous [9]. It is important that statins mainly act in the liver, and the activity of HMG-CoA reductase is not completely suppressed. Thus, the synthesis of hormones, the precursor of which is cholesterol – corticosteroids and sex hormones, is not disturbed.
Multicenter randomized clinical trials (WOSCOPS, CARE/LIPID, CAPS, HPS) showed high efficacy of statins in reducing cardiac mortality and preventing the development of cardiovascular complications by 24–42%. It has also been demonstrated in clinical studies that statins slow down the progression and even cause regression of coronary atherosclerosis [10]. The above benefits of statins are characteristic of the entire group of drugs. One of the most prominent representatives of this class is rosuvastatin, which has established itself as an effective and safe agent for the prevention and treatment of atherosclerosis.
Rosuvastatin has been widely used in clinical practice since the beginning of this century and is a fully synthetic hydrophilic drug of the latest generation. The pharmacokinetics and pharmacodynamics of rosuvastatin favorably distinguish it from those of other statins. After taking the drug, its maximum concentration is noted after 5 hours. It has the longest half-life – up to 19 hours. About 88% of the drug binds reversibly to plasma proteins. It is worth noting the fact that the pharmacokinetic characteristics of rosuvastatin are not significantly affected by age, gender, the presence of moderately severe liver failure, the time of its administration and concomitant food intake. Rosuvastatin for 90% is excreted in the faeces, and 10% in the urine. Unlike other statins, rosuvastatin interacts minimally with enzymes of the cytochrome P450 system, and therefore the likelihood of its interaction with many drugs is low. Drug interaction was revealed only with the joint appointment of rosuvastatin and fluconazone, which is a powerful inhibitor of the 2C9 isoenzyme, resulting in a decrease in its activity by 10% and a slight increase in the concentration of rosuvastatin.
In addition to the well-known lipid-lowering effect, statins, in particular rosuvastatin, have many pleiotropic effects [11]. One of the important effects is the inhibition of platelet aggregation, which leads to a change in the content of cholesterol in their membrane and a decrease in the content of isoprostanoids, which are markers of oxidative stress and strong platelet activators. Rosuvastatin suppresses the expression of plasminogen activator-1 inhibitor on the surface of smooth muscle cells and enhances the expression of tissue plasminogen activator on the surface of endothelial cells, and this effect is dose-dependent [12]. The antithrombotic effect of statins may also be associated with an increase in the expression of NO synthetase during their administration, and, as a result, a decrease in aggregation under the action of NO. Rosuvastatin also normalizes endothelial function.
When taking rosuvastatin, a clear anti-ischemic effect was revealed, which, apparently, is directly related to the restoration of the normal function of the arterial endothelium. The antiischemic effect is expressed in a decrease in angina attacks and signs of myocardial ischemia during exercise tests. In patients, the magnitude of ST segment depression is significantly reduced and the time to the onset of ischemia during a stress test increases. Also, rosuvastatin reduces the adhesion of leukocytes to the endothelium in response to the effects of pro-inflammatory mediators (platelet activating factor, leukotriene B4).
The effect of rosuvastatin on the expression of C-reactive protein (CRP) in human hepatocytes has also been studied. The results of the experiment indicate a direct inhibitory effect of rosuvastatin on IL-6-induced CRP expression in hepatoma cell culture and human hepatocytes. It is possible that statins reduce CRP levels by inhibiting its formation in the liver, and not due to systemic anti-inflammatory effects. This fact is very important, because it was found that the higher the level of CRP in the patient’s blood, the higher the frequency of complications of atherosclerosis and mortality from them. Also in the experiment it was shown that rosuvastatin reduces the level of pro-inflammatory cytokines, increases the concentration of IL-4 and reduces the formation of reactive oxygen species in circulating monocytes of hypertensive rats.
Another important positive moment while taking rosuvastatin is a decrease in myocardial hypertrophy of the left ventricle of the heart. It has been demonstrated that rosuvastatin reduces the development of angiotensin II-induced hypertrophy and fibrosis of cardiomyocytes, and also blocks various cellular signaling pathways involved in the development of myocardial hypertrophy [11].
Rosuvastatin has been well studied in clinical trials. The widespread introduction of this drug into clinical practice was significantly facilitated by the Galaxy program, which consisted of 18 multicenter randomized controlled trials devoted to the study of rosuvastatin. In the JUPITER study (JusTification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating RosuvasTatin), which was organized as a study on the primary prevention of atherosclerosis and its complications in 89Rosuvastatin demonstrated its indisputable effectiveness in 00 individuals with a low risk of atherosclerosis who had a normal level of cholesterol and an elevated level of CRP [13]. Participants in the study took rosuvastatin 20 mg/day or placebo. The study included men over 50 and women over 60. When included in the study, participants should not have clinical signs of atherosclerosis and the level of LDL cholesterol is less than 3.4 mmol/l, the level of triglycerides should not exceed 5. 6 mmol/l. At the same time, a potential participant in the study had to have an elevated CRP level of more than 2 mg / l. The primary endpoint in the study was the first major vascular event—nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, revascularization procedure, or death from a cardiovascular cause.
As a result, it was shown that in the placebo group, the incidence of adverse outcomes was slightly lower than expected and amounted to 1.3% per year. However, the outcome in the treatment group was better than expected. The frequency of adverse outcomes there was 0.77% per year (OR 0.56; 0.46–0.69; p<0.00001). The rate of risk reduction was so high that the study had to be stopped prematurely, and the median follow-up was 1.9 years (instead of the planned 3.5). There was a decrease in the frequency of each component of the primary endpoint and, importantly, the frequency of death from all causes, which in all cases was highly significant. While taking rosuvastatin, there was a pronounced decrease in LDL levels by 50%. The degree of reduction in the level of CRP was also quite high and amounted to 37%. An analysis of safety parameters demonstrated that, in general, the incidence of adverse effects did not differ between the treatment and control groups.
Also, the JUPITER study demonstrated new evidence of the antithrombotic effect of rosuvastatin in assessing the incidence of thromboembolic complications. In total, the study recorded 94 cases of symptomatic deep vein thrombosis and episodes of thromboembolism. At the same time, there were 34 such episodes in the rosuvastatin group, and 60 in the placebo group. The degree of reduction in the risk of thromboembolic complications was 43%, p=0.007.
In other studies, SIELLAR (Statin Therapies for Elevated Lipid Levels compared Across doses to RosuvasТatin), MERCURY I, II (Measuring Effective Reductions in CholesТerol Using RosuvasТatin therapy) compared rosuvastatin with other statins in terms of lipid-lowering activity [14-16]. As a result, it was shown that rosuvastatin exceeds atorvastatin in its dose-equivalent activity by approximately 2 times, and simvastatin by 4 times.
Another extremely important step in the study of the effect of rosuvastatin in atherosclerosis was the receipt of the results of the ASTEROID study, which included 349 patients [17]. In this study, using the method of intravascular ultrasound of the coronary arteries, the volume of ASP was assessed during therapy with rosuvastatin at a maximum daily dose of 40 mg for 24 months. As a result, it was demonstrated that the level of LDL-C in patients taking rosuvastatin decreased by 53% and reached 1.6 mmol / l. By the end of the follow-up, a significant decrease in the volume of ASP in the studied segments of the coronary arteries was recorded in 78% of patients. Thus, the possibility of reversal of the atherosclerotic process in the coronary arteries was shown, provided long-term therapy with high doses of statins.
Another possible therapeutic target for the use of statins, in particular rosuvastatin, was to be the presence of heart failure, which was studied in the CORONA (Controlled Rosuvastatin in Multinational Trial in Heart Failure) study, which evaluated the effect of rosuvastatin therapy in patients with severe heart failure III-IV functional class according to NYHA, mainly of ischemic etiology [18]. The purpose of this study was to evaluate the effect of rosuvastatin at a dose of 10 mg/day on cardiovascular and overall mortality. More than 5,000 patients (mean age 73 years) received rosuvastatin 10 mg/day or placebo. The study lasted over 2 years. According to the results of the study, despite a pronounced lipid-lowering effect and a decrease in CRP levels, there were no significant differences in mortality in the active therapy and placebo groups. At the same time, good tolerance and safety of long-term use of rosuvastatin were noted. Thus, the results of the CORONA study did not confirm the assumption about the need to prescribe rosuvastatin in order to prevent adverse events in patients with severe heart failure of ischemic etiology.
In clinical practice, rosuvastatin is prescribed at a dose of 10-20 mg, the maximum daily dose is 40 mg. An important issue is the safety of statin treatment. Attention to safety in the use of statins was drawn when the drug cerivastatin was withdrawn from the market, the uncontrolled use of which led to a large number of fatal complications. The emergence of a new drug in this class, rosuvastatin, has revived the discussion about the advisability of registering a new drug when a significant number of statins already exist. That is why this drug has been carefully studied in terms of safety. As a result, the drug has been shown to be as safe as other statins when the dosage and prescribing guidelines are followed, and data continues to grow.
Thus, rosuvastatin is a highly effective and safe drug for the prevention and treatment of atherosclerosis, which is indicated for a large number of patients for long-term use. An important aspect that limits patient adherence to treatment is the economic component, which (especially in the Russian Federation) serves as a limitation, which primarily concerns the use of original drugs. Generic drugs help to successfully overcome this problem.
Thus, the drug Mertenil (Gedeon Richter) containing rosuvastatin is widely used on the Russian pharmaceutical market. The drug Mertenil is available to most patients and is in no way inferior to the original drug, which is confirmed by the results of a sufficient number of studies that have studied the use of Mertenil. One such work is the 40×40 open-label prospective pilot study, which aimed to evaluate the lipid-lowering efficacy, safety and tolerability of treatment with Mertenil fixed dose 40 mg in 40 patients with very high cardiovascular risk with dyslipidemia who did not achieve the target level of LDL-C< 1.8 mmol/l during statin therapy [19]. The initial level of LDL-C in patients was 3.6 mmol/l. As a result, it was shown that when switching patients from current statin therapy to treatment with Mertenil (40 mg / day) without dose titration, an additional reduction in LDL-C by 22.4% was achieved, resulting in a significant increase in the number of patients with a target level of LDL-C . The tolerability and safety of Mertenil were good, and the activity indicators of AST, ALT after 12 weeks. therapy did not differ significantly from baseline. Creatine kinase activity was increased only in two cases (in patients with initially elevated values). Side effects (heaviness in the right hypochondrium, bitterness in the mouth, diarrhea, joint pain) were noted in 6 out of 40 patients.
Another study evaluated the efficacy and safety of Mertenil (40 mg/day) in 78 patients with acute coronary syndrome (ACS) [20]. As a result, it was shown that on the 30th day from the start of treatment, a 59% decrease in the level of LDL-C compared with baseline values was achieved, while the treatment was well tolerated. Positive changes were found in different types of microcirculation and CRP levels in patients with ACS during treatment with Mertenil. 24-hour ECG monitoring revealed a decrease in the frequency of ischemia episodes and their duration. As for the study of lipid-lowering effects and tolerability of treatment with Mertenil in patients with ACS who had not previously received statins, in 211 patients with ACS who received Mertenil at a dose of 20 mg / day for 2 weeks, a good significant decrease in LDL-C by 46 was obtained. .3% [21].
Thus, according to the results of the studies, Mertenil has a high lipid-lowering efficacy, a good tolerability and safety profile, and is indicated for the treatment of a wide range of patients. The ease of use of Mertenil is also associated with the full range of dosages presented (5, 10, 20 and 40 mg). Mertenil is the optimal statin and combines all the necessary qualities for successful and long-term use in CVD.

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9. Susekov A.V. Secondary prevention of atherosclerosis: 30 years of use of HMG-CoA reductase inhibitors // Cardiology. 2005. No. 5. S. 6–9.
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11. Zadionchenko V.S., Shakhrai N.B., Shekhyan G.G., Shchikota A.M., Yalymov A.A. Features of the pharmacological and clinical properties of rosuvastatin // BC. Clinical guidelines and algorithms for practicing physicians. 2011. Vol. 19. No. 12, pp. 772–779.
12. Bonetti P.O., Lerman L.O., Napoli C. Statin effects beyond lipid lowering-are they clinically relevant? // Eur Heart J. 2003. Vol. 24. R. 225-248.
13. Ridker P.M. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low–density lipoprotein cholesterol and elevated high–sensitivity C–reactive protein: rationale and design of the JUPITER trial // Circulation. 2003 Vol. 108. R. 2292-2297.
14. Jones P.H., Hunninghake D.B., Ferdinand K.C., Stein E.A., Gold A., Caplan R.J. et al. Effect of rosuvastatin versus atorvaststin, simvastatin and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins and lipid rations in patients with hypercholesterolemia: additional results from the STELLAR trial // Clinical Therapeutics. 2004 Vol. 26 (9). R. 1388–1399.
15. Stender S., Schuster H., Barter P., Watkins C., Kallend D., MERCURY Study Group. Comparison of rosuvastatin with atorvaststin, simvastatin and pravastatin in achieving cholesterol goals and improving plasma lipids in hypercholesterolaemic patients with or without the metabolic syndrome in the MERCURY I trial // Diabetes, Obesity & Metabolism. 2005 Vol. 7(4). R. 430–438.
16. Jones P.H., Davidson M.H., Stain E.A., Bays H.E., McKenney J.M., Miller E. et al. Comparison of the efficacy and safety of rosuvastatin versus atorvaststin, simvastatin and pravastatin across doses (STELLAR Trial) // American Journal of Cardiology. 2003 Vol. 92(2). R. 152–160.
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Atorvastatin Pharmasyntez

Pharmacotherapeutic group

hypolipidemic agent – HMG-CoA reductase inhibitor

International name

Atorvastatin

Dosage form

tablets

Instructions

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Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase, the key enzyme that converts 3-hydroxy-3-methylglutaryl-CoA to mevalonate, a precursor of steroids, including cholesterol. Synthetic lipid-lowering agent.

In patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemia, atorvastatin reduces plasma concentrations of total cholesterol (CHC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo-B), as well as cholesterol of very low density lipoproteins (VLDL-C) and triglycerides (TG), causes an increase in the concentration of high-density lipoprotein cholesterol (HDL-C).

Atorvastatin reduces the concentration of cholesterol and LDL-C in the blood plasma, inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and increasing the number of “liver” LDL receptors on the cell surface, which leads to increased uptake and catabolism of LDL-C.

Atorvastatin reduces the formation of LDL-C and the number of LDL particles, causes a pronounced and persistent increase in the activity of LDL-receptors in combination with favorable qualitative changes in LDL-particles, and also reduces the concentration of LDL-C in patients with therapy-resistant homozygous familial hypercholesterolemia other lipid-lowering agents.

Atorvastatin in doses from 10 mg to 80 mg reduces the concentration of cholesterol by 30-46%, LDL-C by 41-61%, apo-B by 34-50% and TG by 14-33%. The results of therapy are similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia, including patients with type 2 diabetes mellitus.

In patients with isolated hypertriglyceridemia, atorvastatin reduces the concentration of total cholesterol, LDL-C, VLDL-C, apo-B, TG and increases the concentration of HDL-C.

In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate-density lipoprotein cholesterol (LDL-C).

In patients with hyperlipoproteinemia type IIa and IIb according to the Fredrickson classification, the mean increase in HDL-C concentration during treatment with atorvastatin (10-80 mg) compared with baseline is 5.1-8.7% and is not dose dependent.

There is a significant dose-dependent decrease in the ratios: total cholesterol/HDL-C and LDL-C/HDL-C by 29–44% and 37–55%, respectively.

Atorvastatin at a dose of 80 mg significantly reduces the risk of ischemic complications and mortality by 16% after a 16-week course, and the risk of readmission for angina pectoris accompanied by signs of myocardial ischemia by 26% (study of reducing the severity of myocardial ischemia against the background of intensive lipid-lowering therapy (MIRACL)). In patients with different initial concentrations of LDL-C, atorvastatin causes a decrease in the risk of ischemic complications and mortality (in patients with non-Q wave myocardial infarction and unstable angina in men, women and in patients younger and older than 65 years).

The decrease in plasma LDL-C concentration correlates better with the dose of atorvastatin than with its concentration in blood plasma. The dose is selected taking into account the therapeutic effect (see section “Method of application and dose”).

The therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum after 4 weeks and persists throughout the entire period of therapy.

Prevention of cardiovascular complications

Atorvastatin at a dose of 10 mg reduces the relative risk of developing coronary complications (coronary heart disease (CHD) with a fatal outcome and non-fatal myocardial infarction (MI) by 36%, general cardiovascular complications by 29%, fatal and non-fatal stroke by 26% (study of atorvastatin in patients with hypertension and risk factors (ASCOTLLA)).

Diabetes mellitus

In patients with diabetes mellitus, atorvastatin therapy reduces the relative risk of developing major cardiovascular complications (fatal and non-fatal myocardial infarction, silent myocardial ischemia, death due to exacerbation of coronary artery disease, unstable angina pectoris, coronary artery bypass grafting, percutaneous transluminal coronary angioplasty , revascularization procedures, stroke) by 37%, myocardial infarction (fatal and non-fatal) by 42%, stroke (fatal and non-fatal) by 48% regardless of gender, patient age or baseline LDL-C concentration (atorvastatin study in type 2 diabetes mellitus (CARDS)).

Does atorvastatin cause dry mouth. Atorvastatin Side Effects: Understanding Dry Mouth and Other Oral Symptoms

What is Atorvastatin and How Does it Work?

How Effective is Atorvastatin in Reducing Cardiovascular Risk?

Common Side Effects of Atorvastatin

Oral Side Effects of Atorvastatin: Dry Mouth and Beyond

Does Atorvastatin Cause Dry Mouth?

Other Oral Symptoms Associated with Atorvastatin

Research Findings on Atorvastatin and Oral Health

What Did the Study Reveal About Oral Symptoms?

How Common Are These Oral Side Effects?

Managing Oral Side Effects of Atorvastatin

How Can You Alleviate Dry Mouth?

What Should You Do About Other Oral Symptoms?

When to Consult Your Doctor About Statin Side Effects

What Are the Red Flags for Statin Side Effects?

Balancing the Benefits and Risks of Atorvastatin

How Do Doctors Assess the Risk-Benefit Ratio?

Alternative Approaches to Managing High Cholesterol

What Lifestyle Changes Can Help Lower Cholesterol?

Are There Other Medications for High Cholesterol?

The Importance of Medication Adherence and Follow-up

Why is Consistent Statin Use Important?

How Often Should You Have Follow-up Appointments?

Future Directions in Cholesterol Management

What New Therapies Are on the Horizon?

How Might Personalized Medicine Impact Cholesterol Treatment?

Conclusion: Navigating Atorvastatin Treatment and Oral Health

Statins side effects: A dry mouth, itchiness, bitterness or a cough could occur

STATINS are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood. Millions of people around the world take the drug, however, as with most things, the drug can cause a variety of side effects including these four mouth disorders.

This Morning: Dr Chris reveals grapefruit can affect statins

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Adverse side effects of statins in the oral cavity

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Rosuvastatin – the best choice for the prevention and treatment of atherosclerosis | Oganezova L.G.

Atorvastatin Pharmasyntez

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