Colestipol
Sources réglementaires consultées
Indications approuvées
- Complément au régime pour réduire le cholestérol total et le LDL-C élevés dans l'hypercholestérolémie primaire lorsque la réponse au régime est insuffisante.
Contre-indications
Absolues
- Hypersensibilité à l'un des composants.
Mises en garde cliniques
- Mise en garde majeure · La constipation est l'effet principal et peut être sévère ; augmenter progressivement, accroître les liquides et les fibres, puis réduire ou arrêter si elle n'est pas contrôlée. Les hémorroïdes peuvent s'aggraver. — https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
- Mise en garde majeure · Les comprimés doivent être avalés entiers avec beaucoup de liquide ; une dysphagie et une obstruction œsophagienne transitoire ont rarement été rapportées. — https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
- Mise en garde majeure · Les triglycérides peuvent augmenter ; surveiller le profil lipidique et réduire, arrêter ou modifier le traitement en cas d'augmentation importante. — https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
- Mise en garde majeure · Il peut réduire l'absorption de l'acide folique et des vitamines A, D et K ; une carence en vitamine K peut provoquer une hypoprothrombinémie et une tendance hémorragique. Envisager une supplémentation et une surveillance selon le risque clinique. — https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
Interactions médicamenteuses
- ModéréeAutres médicaments oraux
Mécanisme: La résine peut fixer d'autres médicaments et retarder ou réduire leur absorption.
Recommandation: Les administrer au moins 1 heure avant ou 4 heures après le colestipol.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
- ModéréeDigoxine ou digitoxine
Mécanisme: La disponibilité peut être modifiée de façon imprévisible par liaison à la résine.
Recommandation: Surveiller lors de l'ajout ou de l'arrêt du colestipol et maintenir un large intervalle de prise.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=fa6c3e11-84e9-433d-aa74-7cd34336bbed
Effets indésirables
Communs (≥1%)
Constipation · Gêne abdominale · Ballonnements ou flatulences · Indigestion ou pyrosis · Diarrhée · Nausées ou vomissements
Rares mais graves
Obstruction œsophagienne transitoire · Ulcération peptique, cholécystite ou cholélithiase
Grossesse et allaitement
Une exposition systémique n'est pas attendue, mais les études adéquates manquent et la diminution de l'absorption des vitamines liposolubles peut être nocive ; évaluer le bénéfice et le risque pendant la grossesse. Utiliser avec prudence pendant l'allaitement, car la malabsorption vitaminique peut affecter le nourrisson.
Bibliographie récente (PubMed)
The aim of this paper is to raise awareness of MC as a clinically significant condition and to highlight its under-recognition, risk factors, diagnosis, management, and complications. This paper underlines the diagnostic and therapeutic challenges associated with the often nonspecific symptoms of MC. In order to create this article, we reviewed available articles found in the PubMed database and searched for articles using the Google Scholar platform. Microscopic colitis (MC) is a chronic inflammatory bowel disease, classified into three types: lymphocytic, collagenous, and unspecified. The average age of onset of MC is around 62-65 years and the disease is more common in women than men (nine times more common). The main symptom of MC is watery diarrhoea without blood, other symptoms include defecatory urgency, faecal incontinence, abdominal pain, nocturnal bowel movements, and weight loss. Once considered a rare disease, MC is now being diagnosed with increasing frequency, but diagnosis remains difficult. To date, a number of causative factors for MC have been identified, including smoking, alcohol consumption, medications (including NSAIDs, PPIs, SSRIs, and ICPIs), genetic factors, autoimmune diseases, bile acid malabsorption, obesity, appendicitis, and intestinal dysbiosis. It may be difficult to recognize and should be differentiated from inflammatory bowel diseases (Crohn's disease and ulcerative colitis), irritable bowel syndrome (IBS), coeliac disease, infectious bowel disease, and others. Diagnosis involves biopsy at colonoscopy and histopathological evaluation of the samples. Treatment consists of budesonide oral (the gold standard) or enema. Alternatives include bile acid sequestrants (cholestyramine, colesevelam, and colestipol), biologics (infliximab, adalimumab, and vedolizumab), thiopurines, methotrexate, and rarely, surgery.
Bile acid sequestrants (BASs) are non-systemic therapeutic agents used for the management of hypercholesterolemia. They are generally safe and not associated with serious systemic adverse effects. Usually, BASs are cationic polymeric gels that have the ability to bind bile salts in the small intestine and eliminate them by excretion of the non-absorbable polymer-bile salt complex. This review gives a general presentation of bile acids and the characteristics and mechanisms of action of BASs. The chemical structures and methods of synthesis are shown for commercial BASs of first- (cholestyramine, colextran, and colestipol) and second-generation (colesevelam and colestilan) and potential BASs. The latter are based on either synthetic polymers such as poly((meth)acrylates/acrylamides), poly(alkylamines), poly(allylamines) and vinyl benzyl amino polymers or biopolymers, such as cellulose, dextran, pullulan, methylan, and poly(cyclodextrins). A separate section is dedicated to molecular imprinting polymers (MIPs) because of their great selectivity and affinity for the template molecules used in the imprinting technique. Focus is given to the understanding of the relationships between the chemical structure of these cross-linked polymers and their potential to bind bile salts. The synthetic pathways used in obtaining BASs and their in vitro and in vivo hypolipidemic activities are also introduced.
Bile acid sequestrants (BASs) have often been used for bile acid diarrhea (BAD) but carry a high risk of adverse events. New generations of BASs show promising results; however, their efficacy remains unclear. This systematic review and meta-analysis was conducted using PubMed, Cochrane, and Embase to assess randomized controlled trials (RCTs) published up to November 2023 to retrieve studies that measured the parameters before and after the administration of BASs. The outcomes assessed were cessation or improvement in diarrhea, fecal consistency, abdominal cramping, frequency of diarrhea, and adverse events. Risk ratios (RRs) and mean differences with 95% confidence intervals (CIs) were pooled using a random-effects model. Statistical analyses were conducted using RStudio version 4.1.2. The protocol was prospectively registered with PROSPERO (CRD42023445444). Seven RCTs with a total of 311 patients were included, of which 168 (54%) were randomized to BASs. Among BAS-treated patients, 101 (60.1%) received colesevelam, 40 (23.8%) received chenodeoxycholate, 18 (10.7%) received cholestyramine, and 9 (5.3%) received colestid. BASs were associated with a significant improvement in the cessation of diarrhea (RR 3.27; 95% CI 2.08 to 5.15; P ≤ .05) and liquid stool to normal fecal consistency (RR 2.69; 95% CI 1.56 to 4.65; P ≤ .05), as well as an increase in abdominal cramps (RR 5.27; 95% CI 1.21 to 22.93; P ≤ .05). There were no differences in urgency, adverse events, or nausea between groups. These findings indicate that BASs are effective in the treatment of BAD, as indicated by the improvement or cessation of diarrhea episodes.
Bile acid sequestrants have been reported to reduce serum thyroid hormone levels by binding T4 and T3 excreted into the intestinal lumen, preventing their reabsorption into the systemic circulation and interrupting the enterohepatic circulation of these hormones. This meta-analysis evaluates whether adjunctive bile acid sequestrants accelerate reductions in serum iodothyronine when added to standard hyperthyroidism therapy. A systematic review and meta-analysis were conducted and registered in PROSPERO (CRD42025643217). MEDLINE, Embase, Web of Science, and Cochrane databases were searched from March 1971 to September 2025 for randomized controlled trials (RCTs) assessing adult non-critically ill patients with hyperthyroidism treated with standard therapy (thionamides and beta-blocker) plus adjunctive bile acid sequestrants (cholestyramine or colestipol) versus standard therapy alone. Primary outcomes included a reduction in serum-free T4 and total T3. The secondary outcome was adverse effect frequency. Initial search yielded 705 results. After removal of duplicates and title/abstract screening, 17 full-text articles were reviewed, and five RCTs met the inclusion criteria, totaling 173 adult patients: 93 (53.75%) received adjunctive therapy, and 80 (46.25%) were controls. Causes for thyrotoxicosis included Graves' disease, toxic adenoma, and multinodular goiter. Doses ranged from cholestyramine 1 g twice a day to 4 g four times a day, and colestipol 20 g daily. At 2 weeks of treatment, bile acid sequestrants showed a non-significant reduction in serum total T3 (mean difference [MD] -0.44 nmol/L, 95% confidence interval [CI]: -1.2 to +0.32) and free T4 level (MD -0.55 ng/dL, CI: -1.15 to +0.04). At 4 weeks, there was a statistically significant reduction in total T3 (MD -1.59 nmol/L, CI: -2.90 to -0.27) and free T4 level (MD -1 ng/dL, CI: -1.74 to -0.25). Adjunctive bile acid sequestrants with standard hyperthyroidism therapy appear to enhance reductions in serum tota