Tips for Coping With IBS Symptoms

By Robert Shmuts, MD, Gastroenterologist—Virtua Gastroenterology

If you’ve recently been diagnosed with irritable bowel syndrome (IBS), then you’re probably coping with chronic abdominal discomfort or pain, bloating, and changes in bowel habits. Depending on what type of IBS you have, you may experience constipation, diarrhea, or both. These symptoms can cause physical and psychological discomfort.

If you think you may have IBS but haven’t been diagnosed, make sure your healthcare provider checks to see if you have celiac disease, exocrine pancreatic insufficiency, carbohydrate malabsorption or other diseases that can cause similar symptoms. If you’re over 45 and experience a sudden change in bowel symptoms, be sure to be screened for colon cancer. IBS most often starts in the teens or early adulthood, not after 50.

Once you’ve been diagnosed with IBS, it’s important to find a management plan that works for you. This likely will involve trial and error at first and changes along the way.  

With IBS, your bowel is extra-sensitive to stimuli. Ordinary things like eating and having gas can trigger symptoms. Identifying what triggers your abnormal bowel function can help prevent or minimize your symptoms. You may want to keep a record of what foods, events and activities trigger your symptoms.

If your symptoms are mild, you may be able to manage your IBS through diet and lifestyle changes. These can include avoiding foods that trigger your symptoms, exercising regularly, drinking a lot of fluids, and getting enough sleep. If your symptoms are more severe, your health care provider may suggest medications.

Here are some options to help you manage your IBS:  

Dietary changes

Avoid high-fat meals. If you have IBS with diarrhea (IBS-D), it’s important to limit fats. Most people have an urge to have a bowel movement about 60 minutes after a meal, but for a person with IBS-D, that reaction can occur more quickly and more strongly, and the reaction is related to the amount of fat in the meal. High-fat meals can cause vigorous colon contractions, triggering cramping, and diarrhea in people with IBS-D.

Try eliminating certain foods. The role of food in triggering IBS symptoms is not completely understood, but some people report more severe symptoms after eating certain foods. Your diet should be individualized for you. If you experience bloating, you may want to try limiting foods likely to cause gas, such as carbonated beverages, raw fruits and cruciferous vegetables including broccoli, Brussels sprouts, cabbage, and cauliflower. For some people, a low-fat, higher-fiber diet may help, while others feel better with a high-protein, low-carbohydrate diet. The American College of Gastroenterology suggests that low-FODMAP diets show promise in relieving symptoms. A FODMAP diet is low in fat, high in protein and low in fermentable carbohydrates such as fructose and lactose, called FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols). FODMAPs are found in some grains, vegetables, fruits and dairy products. You can experiment with a strict low-FODMAP diet. If it helps, you can work with a dietitian to gradually add back foods one at a time and see which ones bother you. A strict FODMAP diet isn’t intended to be a permanent eating plan.

Consume dietary fiber. Dietary fiber may provide relief from symptoms, particularly by easing constipation. Whole-grain breads and cereals, beans, fruits and vegetables are good fiber sources. If dietary fiber causes uncomfortable bloating or isn’t working, talk to your health care provider about fiber supplements or other medications. Only about one in six people experience improvements from increased dietary fiber, so don’t get frustrated if it doesn’t help.

Take pre- or probiotics. Some research indicates pre- and probiotics can help IBS symptoms by affecting bacteria in the gut. You can get these in many forms, ranging from live-culture yogurt, such as Activia, to capsules and powders. Start with a cup or two of yogurt a day and see if your symptoms respond. If more is needed, try over-the-counter capsules or packets that you can sprinkle on food. These supplements are available in grocery stores, pharmacies, health food stores and online. Talk to your health care provider about what form and dosage may be right for you.

Medications

Fiber supplements. Over-the-counter fiber supplements taken with fluids can provide fiber and help ease constipation or diarrhea, but studies on their effectiveness in treating IBS are inconclusive. For some people, they may cause discomfort, rather than relief. Talk to your health care provider about what may work best for you.

Laxatives. If supplements don’t help, your provider may recommend a laxative for IBS with constipation (IBS-C). There are many types, including osmotic laxatives such as magnesium hydroxide (Milk of Magnesia) and polyethylene glycol (Miralax). Cathartic laxatives (Dulcolax), which usually contain senna or bisacodyl, work by irritating the inside of the colon. They aren’t recommended for long-term use because they stop working after a while.

Anti-diarrheal medications. If you have IBS-D, you may try over-the-counter medications, such as loperamide (Imodium) to help control diarrhea. You also may benefit from bile acid binders, such as cholestyramine (Prevalite), colestipol (Colestid) or colesevelam (Welchol). These can cause bloating.

Anticholinergic and antispasmodic medications. These medications can reduce cramping. They may be used if you have diarrhea, but can worsen constipation and may cause difficulty urinating. They include hyoscyamine (Levsin) and dicyclomine (Bentyl). They should be used with caution if you have glaucoma.

Peppermint oil. Over-the-counter time-release capsules may ease cramping and spasms for people with IBS. As a side effect, they may also increase reflux.

Antidepressants. If you have pain or are depressed, talk to your health care provider about antidepressants. Your health care provider may suggest a selective serotonin reuptake inhibitor (SSRI), such as fluoxetine (Prozac, Sarafem) or paroxetine (Paxil), or a low-dose tricyclic antidepressant, such as imipramine (Tofranil) or nortriptyline (Pamelor). In addition, serotonin-norepinephrine reuptake inhibitors (SNRIs), such as Celexa, are shown to be extremely helpful in IBS patients who have an overlap of chronic neuropathic pain as well as depression and/or anxiety. Even if you’re not depressed, an antidepressant may help take the edge off your pain. All antidepressants can cause some side effects, so be sure and discuss with your health care provider.

Antibiotics. Your health care provider may prescribe antibiotics such as rifaximin (Xifaxan). More research is needed on treating IBS with antibiotics.

IBS-specific prescription medications.  Several medicines are approved specifically for IBS. These are usually prescribed only when lifestyle changes and other treatments have not been successful.

• Lubiprostone (Amitiza) is approved for women over age 18 who have IBS with severe constipation. It increases fluid secretion in the small intestine to relieve constipation. Side effects may include nausea, diarrhea, and abdominal pain.
• Alosetron (Lotronex and generic) is intended only for women with severe IBS who have diarrhea and haven’t responded to other medications. It is supposed to relax the colon and slow movement of waste through your bowel. It isn’t approved for men and has been linked to some side effects.
• Linaclotide (Linzess) is approved to treat IBS-C and chronic idiopathic constipation in women and men over age 18. It increases fluid secretion in the small intestine to relieve constipation. Side effects may include diarrhea.
• Eluxadoline (Viberzi) is used to treat IBS-D in men and women. It’s not approved for people who have had their gallbladder removed, those who have a history of pancreatic issues, or those who consume excessive alcohol on a daily basis. It’s important to discuss this medication with your physician to see if it’s right for you.

Lifestyle changes

Practice stress reduction. Physical, emotional, and environmental stress may make your symptoms worse. Stress-reduction and relaxation strategies can help relieve or prevent IBS symptoms. You can try anything from personal meditation, yoga, or tai chi to stress-management counseling or hypnosis. There are many apps available to guide relaxation and stress reduction.

Get to the root of the problem. If you have a history of abuse or trauma, getting care for the long-term psychiatric effects of that trauma may help your symptoms.

Is your gut health in check?

If stomach issues affect you often, it may be time to call 888-847-8823 to schedule an appointment with a Virtua gastroenterologist. 

For the latest digestive health information, sign up for Virtua’s digestive health newsletter.  

Updated October 28, 2021

Increased colonic bile acid exposure: a relevant factor for symptoms and treatment in IBS

Save citation to file

Format:

Summary (text)PubMedPMIDAbstract (text)CSV

Add to Collections

• Create a new collection
• Add to an existing collection

Name your collection:

Name must be less than 100 characters

Choose a collection:

Unable to load your collection due to an error
Please try again

Add to My Bibliography

• My Bibliography

Unable to load your delegates due to an error
Please try again

Your saved search

Name of saved search:

Search terms:

Test search terms

Email:

(change)

Which day?

The first SundayThe first MondayThe first TuesdayThe first WednesdayThe first ThursdayThe first FridayThe first SaturdayThe first dayThe first weekday

Which day?

SundayMondayTuesdayWednesdayThursdayFridaySaturday

Report format:

SummarySummary (text)AbstractAbstract (text)PubMed

Send at most:

1 item5 items10 items20 items50 items100 items200 items

Send even when there aren’t any new results

Optional text in email:

Create a file for external citation management software

Full text links

HighWire

Full text links

. 2015 Jan;64(1):84-92.

doi: 10.1136/gutjnl-2013-305965.

Epub 2014 Apr 12.

Antal Bajor 
¹
, Hans Törnblom 
²
, Mats Rudling 
³
, Kjell-Arne Ung 
⁴
, Magnus Simrén 
²

Affiliations

Affiliations

• ¹ Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
• ² Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden University of Gothenburg Centre for Person-Centred Care (GPCC), Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
• ³ Department of Medicine, Metabolism Unit, Center for Endocrinology, Metabolism, and Diabetes, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden Molecular Nutrition Unit, Department of Biosciences and Nutrition, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
• ⁴ Department of Internal Medicine, Medicine and R&D Unit, Skaraborgs Hospital, Skövde, Sweden.

• PMID:

  24727487

• DOI:

  10.1136/gutjnl-2013-305965

Antal Bajor et al.

Gut.

2015 Jan.

. 2015 Jan;64(1):84-92.

doi: 10.1136/gutjnl-2013-305965.

Epub 2014 Apr 12.

Authors

Antal Bajor 
¹
, Hans Törnblom 
²
, Mats Rudling 
³
, Kjell-Arne Ung 
⁴
, Magnus Simrén 
²

Affiliations

• ¹ Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
• ² Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden University of Gothenburg Centre for Person-Centred Care (GPCC), Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
• ³ Department of Medicine, Metabolism Unit, Center for Endocrinology, Metabolism, and Diabetes, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden Molecular Nutrition Unit, Department of Biosciences and Nutrition, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
• ⁴ Department of Internal Medicine, Medicine and R&D Unit, Skaraborgs Hospital, Skövde, Sweden.

• PMID:

  24727487

• DOI:

  10.1136/gutjnl-2013-305965

Abstract

Objective:

Bile acids may play a role in the pathogenesis of IBS. We investigated the potential effects of bile acids entering the colon and its role in the symptom pattern in IBS.

Design:

We measured 75Se-labelled homocholic acid-taurine (75SeHCAT) retention, and serum levels of 7α-hydroxy-4-cholesten-3-one (C4) and fibroblast growth factor (FGF) 19 in patients with IBS (n=141) and control subjects (75SeHCAT n=29; C4 and FGF19 n=435). In patients with IBS stool frequency and form, as well as GI symptom severity were registered, and in a proportion of patients colonic transit time and rectal sensitivity were measured (n=66). An 8-week open-label treatment with colestipol was offered to patients with 75SeHCAT <20%, and the effect of treatment was evaluated with IBS severity scoring system and adequate relief of IBS symptoms.

Results:

Compared with controls, patients with IBS had lower 75SeHCAT values (p=0. 005), higher C4c levels (C4 corrected for cholesterol) (p<0.001), but similar FGF19 levels. Abnormal 75SeHCAT retention (<10%) was seen in 18% of patients, whereas 23% had elevated C4c levels. Patients with IBS with 75SeHCAT retention <10% had more frequent stools, accelerated colonic transit time, rectal hyposensitivity, a higher body mass index, higher C4c and lower FGF19 levels. Colestipol treatment improved IBS symptoms (IBS severity scoring system 220±109 vs. 277±106; p<0.01), and 15/27 patients fulfilled criteria for treatment response (adequate relief ≥50% of weeks 5-8).

Conclusions:

Increased colonic bile acid exposure influences bowel habit and colonic transit time in patients with IBS. A high response rate to open label treatment with colestipol supports this, but placebo-controlled studies are warranted.

Keywords:

Bile Acid; Irritable Bowel Syndrome.

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Similar articles

• Bile Acid Deficiency in a Subgroup of Patients With Irritable Bowel Syndrome With Constipation Based on Biomarkers in Serum and Fecal Samples.

  Vijayvargiya P, Busciglio I, Burton D, Donato L, Lueke A, Camilleri M.

  Vijayvargiya P, et al.
  Clin Gastroenterol Hepatol. 2018 Apr;16(4):522-527. doi: 10.1016/j.cgh.2017.06.039. Epub 2017 Jun 27.
  Clin Gastroenterol Hepatol. 2018.

  PMID: 28666948
  Free PMC article.

• Role of bile acids in lymphocytic colitis.

  Ung KA, Kilander A, Willén R, Abrahamsson H.

  Ung KA, et al.
  Hepatogastroenterology. 2002 Mar-Apr;49(44):432-7.
  Hepatogastroenterology. 2002.

  PMID: 11995467

• [Postprandial serum bile acid level and 75SeHCAT retention in diagnosis of bile acid malabsorption syndrome. A comparative study].

  Balzer K, Breuer N, Quebe-Fehling E.

  Balzer K, et al.
  Med Klin (Munich). 1993 Feb 15;88 Suppl 1:23-8.
  Med Klin (Munich). 1993.

  PMID: 8464395

  German.

• Bile Acid diarrhea: prevalence, pathogenesis, and therapy.

  Camilleri M.

  Camilleri M.
  Gut Liver. 2015 May 23;9(3):332-9. doi: 10.5009/gnl14397.
  Gut Liver. 2015.

  PMID: 25918262
  Free PMC article.

  Review.

• Biomarkers as a diagnostic tool for irritable bowel syndrome: where are we?

  Camilleri M, Halawi H, Oduyebo I.

  Camilleri M, et al.
  Expert Rev Gastroenterol Hepatol. 2017 Apr;11(4):303-316. doi: 10.1080/17474124.2017.1288096. Epub 2017 Feb 13.
  Expert Rev Gastroenterol Hepatol. 2017.

  PMID: 28128666

  Review.

See all similar articles

Cited by

• The neurobiology of irritable bowel syndrome.

  Mayer EA, Ryu HJ, Bhatt RR.

  Mayer EA, et al.
  Mol Psychiatry. 2023 Apr;28(4):1451-1465. doi: 10.1038/s41380-023-01972-w. Epub 2023 Feb 2.
  Mol Psychiatry. 2023.

  PMID: 36732586
  Free PMC article.

  Review.

• Current and Future Therapeutic Options for Irritable Bowel Syndrome with Diarrhea and Functional Diarrhea.

  Piovezani Ramos G, Camilleri M.

  Piovezani Ramos G, et al.
  Dig Dis Sci. 2023 May;68(5):1677-1690. doi: 10.1007/s10620-022-07700-8. Epub 2022 Nov 14.
  Dig Dis Sci. 2023.

  PMID: 36376576

  Review.

• Abnormal bile acid metabolism is an important feature of gut microbiota and fecal metabolites in patients with slow transit constipation.

  Fan Y, Xu C, Xie L, Wang Y, Zhu S, An J, Li Y, Tian Z, Yan Y, Yu S, Liu H, Jia B, Wang Y, Wang L, Yang L, Bian Y.

  Fan Y, et al.
  Front Cell Infect Microbiol. 2022 Jul 28;12:956528. doi: 10.3389/fcimb.2022.956528. eCollection 2022.
  Front Cell Infect Microbiol. 2022.

  PMID: 35967856
  Free PMC article.

• Functional bowel disorders with diarrhoea: Clinical guidelines of the United European Gastroenterology and European Society for Neurogastroenterology and Motility.

  Savarino E, Zingone F, Barberio B, Marasco G, Akyuz F, Akpinar H, Barboi O, Bodini G, Bor S, Chiarioni G, Cristian G, Corsetti M, Di Sabatino A, Dimitriu AM, Drug V, Dumitrascu DL, Ford AC, Hauser G, Nakov R, Patel N, Pohl D, Sfarti C, Serra J, Simrén M, Suciu A, Tack J, Toruner M, Walters J, Cremon C, Barbara G.

  Savarino E, et al.
  United European Gastroenterol J. 2022 Jul;10(6):556-584. doi: 10.1002/ueg2.12259. Epub 2022 Jun 13.
  United European Gastroenterol J. 2022.

  PMID: 35695704
  Free PMC article.

  Review.

• Pathophysiology and Clinical Management of Bile Acid Diarrhea.

  Marasco G, Cremon C, Barbaro MR, Falangone F, Montanari D, Capuani F, Mastel G, Stanghellini V, Barbara G.

  Marasco G, et al.
  J Clin Med. 2022 May 30;11(11):3102. doi: 10.3390/jcm11113102.
  J Clin Med. 2022.

  PMID: 35683489
  Free PMC article.

  Review.

See all “Cited by” articles

Publication types

MeSH terms

Substances

Full text links

HighWire

Cite

Format:

AMA

APA

MLA

NLM

Send To

Treatment of stable CAD | Association of Cardiovascular Surgeons of Russia Section “Cardiology and Imaging in Cardiac Surgery”

Treatment of stable coronary artery disease

improving the quality of life of the patient; in patients who have had myocardial infarction – to prevent left ventricular remodeling, which can lead to the development of heart failure.

Pharmacological treatment of stable CAD.

Antiplatelet therapy.

Atherosclerosis is a primary condition associated with diseases of the coronary arteries and cerebral vessels, the main causes of morbidity and mortality. The rupture of atherosclerotic plaques and the subsequent formation of a thrombus play a decisive role in the development of clinical syndromes. When a plaque ruptures, the highly thrombogenic lipid core comes into contact with circulating blood elements, in particular platelets, which leads to the launch of a complex process of their activation, adhesion and aggregation. These mechanisms are similar regardless of the location of the lesion and are currently considered as priority pathways for both the progression of the atherosclerotic process and the development of acute vascular disorders. Recognition of the central role of platelets in the formation of arterial thrombosis pathogenetically substantiates the use of antiplatelet agents for the treatment of cardiovascular diseases.

To date, there is a fairly impressive list of groups of drugs with antiplatelet activity, however, for the treatment of stable forms of coronary artery disease and as measures of primary and secondary prevention, aspirin – acetylsalicylic acid and clopidogrel are recommended.

For a long time, aspirin (acetylsalicylic acid), which has proven its effectiveness in both primary and secondary prevention of vascular events, has dominated this issue. Absorbed in the stomach, it appears in the blood within 10 minutes, reaching a peak plasma concentration in 30-40 minutes.

According to the currently available
“Recommendations” VNOK “All patients
with stable angina pectoris in the absence of absolute contraindications

(gastrointestinal bleeding,
allergy to aspirin) are recommended
unlimited long-term use of aspirin in 9000 7 daily dose 75-100 mg . In patients with stable
angina pectoris, clopidogrel
at a daily dose of 75 mg may be an alternative to aspirin
in the presence of
contraindications to taking it.

Aspirin and clopidoger act on different but complementary pathways for platelet activation. Clopidogrel selectively blocks ADP-induced platelet aggregation and ADP-dependent increase in the concentration of other agonists, thus inhibiting the binding of fibrinogen and GP IIb/IIIa receptors.

Like aspirin, clopidogrel has a cumulative and long-term effect. The half-life of the metabolite SR 26334 is 8 hours. With regular, daily intake of clopidogrel, the degree of platelet inhibition increases, remaining even after discontinuation of the drug. The platelet response to ADP is restored slowly, in parallel with the formation of new cells.

Lipid-lowering therapy

Impaired lipid metabolism is one of the most important factors in the development of atherosclerosis and coronary artery disease. Correction of dyslipidemia is one of the main pathogenetically substantiated directions in the treatment of coronary artery disease.

Drugs that affect lipid metabolism include: statins, an inhibitor of absorption (absorption) of cholesterol in the intestine, fibrates, nicotinic acid (niacin), omega-3 polyunsaturated fatty acids.

Statins. Statins are structural inhibitors of the HMG-CoA enzyme, the main enzyme that regulates cholesterol biosynthesis in hepatocytes.

Clinical studies have shown that treatment with statins results in:
– A 30% reduction in all cardiovascular complications and overall mortality.
– Decrease in LDL cholesterol by 30-50%, triglycerides by 20%.
– Decreased apo-B and apo-E by 15-25%.

The therapeutic effect of statins may be associated with the stabilization of atherosclerotic plaques, a decrease in their predisposition to rupture, an improvement in endothelial function, a decrease in the tendency of coronary arteries to vasospasm, and suppression of inflammatory reactions. Statins have a positive effect on a number of indicators that determine the tendency to thrombosis: blood viscosity, platelet aggregation, fibrinogen concentration. In patients with coronary artery disease, statin therapy should be initiated regardless of total cholesterol and LDL cholesterol levels.

Statins are given at a dose of 20 to 80 mg/day as a single dose with evening meals. Due to the fact that the biosynthesis of cholesterol is carried out mainly during sleep, evening administration of the drug is more effective. The initial dose is increased every 4 weeks if the desired lipid level is not reached. The target level of lipid-lowering therapy is estimated by the level of LDL cholesterol and is 1.8 mmol / l or a decrease in LDL by 50% from the initial level.

When prescribing statins, it is necessary to initially take a blood test for lipid profile, AST, ALT, CPK. After 4 weeks of treatment, the tolerability and safety of treatment should be assessed (patient complaints, repeated blood tests for lipids, AST, ALT, CPK). When titrating the dose, one should focus on the tolerability and safety of treatment, and secondarily on the achievement of target lipid levels. To ensure the safety of treatment, biochemical monitoring is required monthly during the dose selection period (the first 3 months). During maintenance therapy, biochemical analyzes can be done once every 3-6 months.

Contraindications to the prescription of statins are active pathological processes in the liver, initially elevated levels of liver enzymes (more than 50% above normal values), individual intolerance to the drug, pregnancy and lactation.

Cholesterol intestinal absorption inhibitor. When prescribing the drug in the form of monotherapy at a minimum dose of 5 mg / day, the level of LDL cholesterol is reduced by 15.7%, and when prescribing the usual therapeutic dose of 10 mg / day, by 18.5%. The effect of ezetimibe on other lipid parameters is insignificant, triglyceride levels are reduced by 6-8%, and HDL-C levels are increased by 2-4%.

Fibrates. Fibric acid derivatives (fibrates) predominantly affect the metabolism of triglyceride-rich lipoprotein particles. Treatment with fibrates leads to a decrease in triglyceride levels by 20-50% from baseline and an increase in HDL-CL by 10-20%. Fibrates significantly reduce the degree of postprandial dyslipidemia. In comparative studies with statins, fenofibrate was superior in reducing triglycerides by up to 50% over initial doses of simvastatin, pravastatin, and atorvastatin (-12-25%).

Nicotinic acid in doses of 2-4 g/day has a lipodemic effect.

Omega-3 polyunsaturated fatty acids. A study in patients with coronary artery disease with a history of myocardial infarction showed that in the group of patients taking the drug, overall mortality was lower by 20%, cardiovascular mortality by 30%, and the frequency of sudden death was lower by 45%.

Beta-blockers

Beta-blockers (BABs) are effective antianginal drugs that improve symptoms, increase exercise tolerance, and reduce consumption of short-acting nitrates. They reduce the need for oxygen, reducing heart rate, blood pressure and myocardial contractility (negative chronotropic and negative inotropic effects). Perfusion of ischemic segments is improved by lengthening the diastole (i.e. the time of perfusion).

A meta-analysis of the effect of various β-blockers on mortality showed a significant reduction in mortality with long-term secondary prevention after myocardial infarction. BBs solve both problems in the treatment of stable coronary artery disease: they improve the prognosis (especially in patients with a history of myocardial infarction) and quality of life (due to the antianginal effect). In this regard, it is currently recommended to prescribe BAB to all patients with stable angina pectoris, if there are no contraindications to their use. If the patient did not tolerate MI, then it is possible to prescribe any drug of this group, however, preference should be given to cardioselective β-blockers due to fewer contraindications and side effects.

ACE inhibitors

To date, a sufficient amount of clinical and experimental data has been accumulated that significantly expanded the initial understanding of the mechanisms of action of ACE inhibitors. The beneficial effect of this class of drugs is associated with a decrease in the adverse effects of angiotensin II, potentiation of the positive effects of the bradykinin system. Drugs of this class contribute to the preservation of the structure and function of the left ventricle, prevent the development of fibrosis and hyperactivation of the sympathetic nervous system. They can improve endothelial function, neurohumoral balance, inhibit coronary artery remodeling, and stabilize the structure of atherosclerotic plaque.

Recommendations for pharmacotherapy that improves prognosis in patients with stable angina (ESC, 2006).
Class I
1. Aspirin 75 mg/day in all patients with no contraindications (active gastrointestinal bleeding, aspirin allergy or intolerance) (level of evidence A)
2. Statins in all patients with coronary heart disease (level evidence A)
3. ACE inhibitors in the presence of arterial hypertension, heart failure, left ventricular dysfunction, myocardial infarction with left ventricular dysfunction or diabetes mellitus (level of evidence A)
4. Oral beta-blockers in patients with a history of myocardial infarction or heart failure (level of evidence A)
Class II a
1. ACE inhibitors in all patients with angina and confirmed coronary heart disease (level of evidence B)
2. Clopidogrel as an alternative to aspirin in patients with stable angina who cannot take aspirin, e.g. due to allergy (level of evidence B)
with proven coronary heart disease (level of evidence B)
Class II b
1. Fibrates for low HDL or high triglycerides in patients with diabetes mellitus or metabolic syndrome (level of evidence B).

Drug therapy aimed at reducing the frequency of angina attacks (antanginal therapy)

Antianginal drugs – drugs that prevent angina attacks by preventing myocardial ischemia, significantly improve the well-being of patients and increase their exercise tolerance. Currently, there are three main groups of antianginal drugs: beta-blockers, nitrates and long-acting calcium antagonists. It is still not clear whether therapy with antianginal drugs affects the prognosis of life in patients with stable coronary artery disease. Several small studies have shown that the elimination of myocardial ischemia improves prognosis.

Guidelines for Antianginal Therapy in Patients with Stable Angina (ESC, 2006).
Class I
1. Short-acting nitroglycerin for angina relief and situational prophylaxis (patients should receive adequate instructions for the use of nitroglycerin) (level of evidence B).
2. Evaluate the effectiveness of beta1-blocker and titrate its dose to the maximum therapeutic; evaluate the appropriateness of using a long-acting drug (level of evidence A).
3. In case of poor tolerance or low efficacy of a beta-blocker, prescribe monotherapy with a calcium antagonist (level of evidence A), long-acting nitrate (level of evidence C).
4. If beta-blocker monotherapy is not effective enough, add a dihydropyridine calcium antagonist (level of evidence B).
Class II a
1. If a beta-blocker is poorly tolerated, prescribe the sinus node If channel inhibitor ivabradine (level of evidence B).
2. If monotherapy with a calcium antagonist or combination therapy with a calcium antagonist and a beta-adrenergic locator is ineffective, replace the calcium antagonist with long-acting nitrate. Avoid development of nitrate tolerance (level of evidence C).
Class II b
1. Metabolic agents (trimetazidine) may be used in addition to, or as an alternative to, conventional agents if not well tolerated (level of evidence B).

Buziashvili Yu.I. and co-authors “Clinical cardiology: diagnosis and treatment”, 2011. under the editorship of Bockeria L.A., Golukhova E.Z.

Fenofibrate – description of the substance, pharmacology, use, contraindications, formula

Contents

• Structural formula

• Russian name

• English title

• Latin name

• chemical name

• Gross formula

• Pharmacological group of the substance Fenofibrate

• Nosological classification

• CAS code

• pharmachologic effect

• Characteristic

• Pharmacology

• The use of the substance Fenofibrate

• Contraindications

• Application restrictions

• Use during pregnancy and lactation

• Side effects of Fenofibrate

• Interaction

• Overdose

• Dosage and administration

• Precautionary measures

• Trade names with the active substance Fenofibrate

Structural formula

Russian name

Fenofibrate

English name

Fenofibrate

Latin name

Fenofibratum ( born Fenofibrati)

Chemical name

2-[4-(4-Chlorobenzoyl)phenoxy]-2-methylpropanoic acid 1-methylethyl ester

General formula

C ₂₀ H 9020 8 21 ClO ₄

Pharmacological group of the substance Fenofibrate

Fibrates

Nosological classification

List of ICD-10 codes

CAS code

49562-28-9

Pharmacological action

Pharmacological action –

antiplatelet , hypolipidemic , uricosuric .

Description

Lipid-lowering agent.

White, practically insoluble in water; soluble in acetone, ether, benzene, chloroform. Molecular weight 360.83.

Pharmacology

By activating PPARα receptors (peroxisome proliferator-activated alpha receptors), fenofibric acid (the active metabolite of fenofibrate) enhances lipolysis and plasma clearance of atherogenic high triglyceride lipoproteins by activating lipoprotein lipase and reducing the synthesis of apolipoprotein CIII. Activation of PPARα also leads to increased synthesis of apolipoproteins AI and AII.

The effects on lipoproteins described above lead to a decrease in the content of the LDL and VLDL fraction, which include apolipoprotein B, and an increase in the content of the HDL fraction, which include apolipoproteins AI and AII.

By correcting impaired VLDL synthesis and catabolism, fenofibrate increases LDL clearance and reduces the content of dense and small LDL particles, an increase in which is observed in patients with an atherogenic lipid phenotype (a common disorder in patients at risk of coronary artery disease).

In clinical studies, fenofibrate has been shown to reduce total cholesterol by 20-25% and triglycerides by 40-55% while increasing HDL-cholesterol by 10-30%. In patients with hypercholesterolemia, in whom LDL-cholesterol levels decreased by 20-35%, the use of fenofibrate led to a decrease in the ratios: “total cholesterol / HDL-cholesterol”, “LDL-cholesterol / HDL-cholesterol” and “Apo B / Apo AI ”, which are markers of atherogenic risk.

Given the effect on LDL-cholesterol and triglycerides, the use of fenofibrate is effective in patients with hypercholesterolemia, both accompanied and not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, incl. in type 2 diabetes mellitus. In addition, it reduces elevated plasma levels of fibrinogen and uric acid; with long-term therapy reduces extravascular cholesterol deposits.

After oral administration, fenofibrate is rapidly hydrolyzed by esterases. In plasma, only the main active metabolite of fenofibrate is found – fenofibric acid, T _max of which in plasma is reached within 2-3 hours. The binding of fenofibric acid to plasma proteins is about 99%, ss “> C _ss is achieved within 1 week Fenofibrate and fenofibric acid do not undergo oxidative metabolism with the participation of cytochrome P450. 1/2 “> T _1/2 fenofibric acid – approximately 20 hours. Excreted mainly by the kidneys (fenofibric acid and its glucuronide). Does not accumulate.

The clearance of fenofibric acid after a single dose of fenofibrate orally does not change depending on age and is 1.2 l/h in elderly patients (77–87 years), and 1.1 l/h in young patients.

In patients with severe renal insufficiency (Cl creatinine <30 ml / min), the exposure of fenofibric acid increases by 2.7 times and cumulation is observed with repeated administration. In case of impaired renal function of mild and moderate severity (Cl creatinine 30–80 ml / min), 1/2 "> T 9 increases0208 1/2 fenofibric acid.

Clinical studies compared two different formulations of fenofibrate, “micronized” and “non-micronized”. Comparison of blood samples from healthy volunteers after ingestion of these forms showed that 67 mg of the “micronized” form is bioequivalent to 100 mg of the “non-micronized” form.

Use of the substance Fenofibrate

Hyperlipidemia type IIa, IV and V types, as well as type IIb and III with insufficient dietary efficacy, elevated blood cholesterol levels during dynamic examination and / or the presence of concomitant risk factors.

Contraindications

Hypersensitivity, liver failure (including biliary cirrhosis), severe renal failure (Cl creatinine <30 ml / min), gallbladder disease, photosensitivity or phototoxicity with treatment with fibrates or ketoprofen in history, age up to 18 years (adequate and good controlled studies have not been conducted).

Restrictions on use

Hepatic and/or renal insufficiency, hypothyroidism, alcoholism, old age, history of hereditary muscle diseases, concomitant use of oral anticoagulants, HMG-CoA reductase inhibitors.

Use in pregnancy and lactation

In pregnancy possible if the expected effect of therapy outweighs the potential risk to the fetus.

FDA fetal category C.

Stop breastfeeding during treatment.

Side effects of the substance Fenofibrate

From the side of the nervous system and sensory organs: dizziness, headache, fatigue.

From the side of the cardiovascular system and blood (hematopoiesis, hemostasis): venous thromboembolism (pulmonary embolism, deep vein thrombosis), increased hemoglobin level, leukocytosis.

From the digestive tract: abdominal pain, nausea, vomiting, diarrhea, flatulence, pancreatitis, cholelithiasis, increased levels of hepatic transaminases and creatine phosphokinase, hepatitis.

From the genitourinary system: acute renal failure, sexual dysfunction.

Musculoskeletal side: myalgia, myositis, muscle spasm, muscle weakness, rhabdomyolysis.

Allergic reactions: skin rash, itching, urticaria.

Other: interstitial pneumonia, photosensitivity, alopecia, hypercreatinemia, increased plasma urea.

Interactions

Fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding, which is associated with the displacement of the anticoagulant from the binding sites with blood plasma proteins (with simultaneous use, care should be taken). At the beginning of treatment with fenofibrate, it is recommended to reduce the dose of the anticoagulant by approximately 1/3, followed by a gradual dose adjustment under the control of the INR level.

Simultaneous treatment with fenofibrate and cyclosporine may reduce renal function (it is necessary to monitor the state of renal function in such patients and stop fenofibrate in case of a serious change in laboratory parameters). When coadministering fenofibrate and potentially nephrotoxic agents, the risks and benefits should be carefully assessed and fenofibrate should be used at the lowest effective dose.

When taking fenofibrate concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of rhabdomyolysis, myopathy and acute renal failure is increased (combined use is not recommended). Bile acid sequestrants reduce the absorption of fenofibrate (fenofibrate should be taken 1 hour before or 4-6 hours after taking them).

In vitro studies”> in vitro showed that fenofibrate and fenofibric acid are not inhibitors of cytochrome P450 isoenzymes CYP3A4, CYP2D6, CYP2E1 and CYP1A2. At therapeutic concentrations, these compounds are weak inhibitors of CYP2C19 and CYP2A isoenzymes 6 and weak or moderate inhibitors of CYP2C9

Overdose

Overdose not reported

Treatment: If overdose is suspected, symptomatic and, if necessary, supportive treatment should be given No specific antidote known Hemodialysis is ineffective

Dosage and administration

Inside, 200-400 mg/day in 3 doses, micronized forms – 145-200 mg 1 time per day.

Precautions

Liver transaminases should be monitored every 3 months during the first year of therapy; with an increase in ALT by 2 times or more, the appearance of myalgia and muscle weakness, fenofibrate is canceled. In the first 3 months of treatment, it is recommended to determine the concentration of creatinine (in case of an increase in the concentration of creatinine by more than 50% above the upper limit of normal, treatment should be suspended).

Treatment should be carried out for a long time, in combination with a hypocholesterol diet and under medical supervision. The effectiveness of therapy should be assessed by the content of lipids (total cholesterol, LDL, triglycerides) in the blood serum. In the absence of a therapeutic effect after 3–6 months of treatment, the advisability of prescribing concomitant or alternative therapy should be considered.

In patients with hyperlipidemia who are taking estrogens or hormonal contraceptives containing estrogen, it is necessary to determine whether the hyperlipidemia is primary or secondary in nature, since an increase in lipid levels may be caused by estrogens.

The risk of rhabdomyolysis may be increased in patients with a predisposition to myopathy and/or rhabdomyolysis, including age over 70 years, history of hereditary muscle disease, impaired renal function, hypothyroidism, alcohol abuse.

Co-administration of fenofibrate and a statin is acceptable only if the patient has severe mixed dyslipidemia and high cardiovascular risk, no history of muscle disease and under conditions of careful monitoring aimed at identifying signs of developing toxic effects on muscle tissue.

Trade names with the active ingredient Fenofibrate

Reset filters

Lek. form
All lek. capsule forms sustained-release capsules substance-powder tablets, film-coated

Dosage
All dosages 145 mg 200 mg 250 mg No dosage

Manufacturer
All manufacturers Veropharm AO Canonpharma production ZAO Koprima S.L. Laboratories Fournier S.