Chlorothiazide
Sources réglementaires consultées
Indications approuvées
- Traitement adjuvant des œdèmes associés à l'insuffisance cardiaque congestive, à la cirrhose hépatique, aux traitements par corticostéroïdes ou œstrogènes et aux atteintes rénales, notamment le syndrome néphrotique, la glomérulonéphrite aiguë et l'insuffisance rénale chronique.
Contre-indications
Absolues
- Anurie.
- Hypersensibilité au chlorothiazide, à l'un des composants ou à d'autres médicaments dérivés des sulfamides.
Mises en garde cliniques
- Mise en garde majeure · Une atteinte rénale sévère peut entraîner une azotémie et une accumulation ; réévaluer et envisager l'arrêt si l'insuffisance rénale progresse. — DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
- Mise en garde majeure · Surveiller les déséquilibres hydroélectrolytiques, notamment l'hyponatrémie, l'alcalose hypochlorémique et l'hypokaliémie ; des variations mineures peuvent déclencher un coma hépatique en cas de cirrhose ou d'hépatopathie évolutive. — DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
- Les thiazidiques peuvent activer ou aggraver un lupus érythémateux systémique. — DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
Interactions médicamenteuses
- SévèreLithium
Mécanisme: La diminution de la clairance rénale du lithium augmente son exposition et sa toxicité.
Recommandation: Éviter généralement l'association ; si elle est indispensable, surveiller étroitement le lithium.
DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
- ModéréeCorticostéroïdes ou ACTH
Mécanisme: Ils majorent les pertes électrolytiques, en particulier l'hypokaliémie.
Recommandation: Surveiller le potassium et l'équilibre hydroélectrolytique.
DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
- ModéréeAnti-inflammatoires non stéroïdiens
Mécanisme: Ils peuvent réduire les effets diurétique, natriurétique et antihypertenseur.
Recommandation: Surveiller la réponse clinique et la fonction rénale.
DailyMed setid 377dc515-e381-4196-8bc7-b738606c57ac
- SévèreDigitaliques
Mécanisme: L'hypokaliémie induite par le chlorothiazide peut accroître la sensibilité myocardique à la toxicité digitalique et favoriser les arythmies.
Recommandation: Surveiller la kaliémie, l'ECG et les signes de toxicité digitalique ; corriger l'hypokaliémie.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=377dc515-e381-4196-8bc7-b738606c57ac
- ModéréeInsuline et antidiabétiques oraux
Mécanisme: Les thiazidiques peuvent modifier la tolérance au glucose et les besoins en traitement antidiabétique.
Recommandation: Surveiller la glycémie et ajuster l'antidiabétique si nécessaire.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=377dc515-e381-4196-8bc7-b738606c57ac
- ModéréeAlcool, barbituriques, narcotiques et autres antihypertenseurs
Mécanisme: Ils peuvent potentialiser l'hypotension orthostatique ou produire un effet antihypertenseur additif.
Recommandation: Surveiller la pression artérielle et ajuster les traitements concomitants selon la réponse clinique.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=377dc515-e381-4196-8bc7-b738606c57ac
- ModéréeBloqueurs neuromusculaires non dépolarisants tels que la tubocurarine
Mécanisme: Le chlorothiazide peut augmenter la réponse au bloqueur neuromusculaire.
Recommandation: Anticiper une réponse accrue et surveiller le bloc neuromusculaire.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=377dc515-e381-4196-8bc7-b738606c57ac
Effets indésirables
Communs (≥1%)
Faiblesse · Hypotension · Nausées · Vomissements · Diarrhée · Hyperuricémie · Hyperglycémie · Déséquilibre électrolytique
Rares mais graves
Pancréatite · Ictère cholestatique · Syndrome de Stevens-Johnson ou nécrolyse épidermique toxique · Insuffisance rénale ou néphrite interstitielle · Dyscrasies sanguines graves
Grossesse et allaitement
Les thiazidiques traversent le placenta ; n'utiliser pendant la grossesse qu'en cas de nécessité clairement établie. Le chlorothiazide peut provoquer un ictère et une thrombopénie chez le fœtus ou le nouveau-né. En raison du risque d'effets indésirables graves chez le nourrisson allaité, décider d'interrompre l'allaitement ou le médicament en tenant compte de l'importance du traitement pour la mère.
Bibliographie récente (PubMed)
Diuretics constitute a large family of medications that increase urine flow and induce urinary sodium loss and are widely used for therapy of hypertension, congestive heart failure, and edematous states. Diuretics in current use (and the year of their approval for use in the United States) include chlorothiazide (1958), hydrochlorothiazide (1959), bendroflumethiazide (1959), spironolactone (1960), chlorthalidone (1960), methyclothiazide (1961), polythiazide (1961), triamterene (1964), furosemide (1966), ethacrynic acid (1967), metolazone (1973), bumetanide (1983), indapamide (1983), amiloride (1986), acetazolamide (1986), torsemide (1993), and eplerenone (2002). Diuretics are typically classified as thiazide diuretics (bendroflumethiazide, chlorothiazide, chlorthalidone, hydrochlorothiazide, indapamide, metolazone and polythiazide), loop diuretics (bumetanide, ethacrynic acid, furosemide, and torsemide), and potassium-sparing agents (amiloride, eplerenone, spironolactone, and triamterene). The carbonic anhydrase blockers acetazolamide (1986) and methazolamide (1959) are also diuretics, but are more commonly used for the therapy of glaucoma. Diuretics are some of the most frequently used medications in medicine and are usually well tolerated. Common side effects are those that are caused by the diuresis and mineral loss such as weakness, dizziness, electrolyte imbalance, low sodium and potassium. Diuretics have not been associated with an appreciable increased rate of serum aminotransferase elevations and have rarely been associated with clinically apparent liver injury. Isolated case reports of idiosyncratic hepatotoxicity due to diuretics have been published, but there have been virtually no case series on individual diuretics or even whole class of drugs. The case reports that have been published provide only a very general pattern of injury that has not provided a clear clinical signature or suggestion that hepatotoxicity is a class effect among the thiazides and
Heart failure is a common condition with considerable associated costs, morbidity, and mortality. Patients often present to hospital with dyspnea and edema. Inadequate inpatient decongestion is an important contributor to high readmission rates. There is little evidence concerning diuresis to guide clinicians in caring for patients with acute decompensated heart failure. Contemporary diuretic strategies have been defined by expert opinion and older landmark clinical trials. To present a narrative review of contemporary recommendations, along with their underlying evidence and pharmacologic rationale, for diuretic strategies in inpatients with acute decompensated heart failure. PubMed, OVID, and Embase databases were searched from inception to December 22, 2022, with the following search terms: heart failure, acute heart failure, decompensated heart failure, furosemide, bumetanide, ethacrynic acid, hydrochlorothiazide, indapamide, metolazone, chlorthalidone, spironolactone, eplerenone, and acetazolamide. Randomized controlled trials and systematic reviews involving at least 100 adult patients (> 18 years) were included. Trials involving torsemide, chlorothiazide, and tolvaptan were excluded. Early, aggressive administration of a loop diuretic has been associated with expedited symptom resolution, shorter length of stay, and possibly reduced mortality. Guidelines make recommendations about dose and frequency but do not recommend any particular loop diuretic over another; however, furosemide is most commonly used. Guidelines recommend that the initial furosemide dose (on admission) be 2-2.5 times the patient's home dose. A satisfactory diuretic response can be defined as spot urine sodium content greater than 50-70 mmol/L at 2 hours; urine output greater than 100-150 mL/h in the first 6 hours or 3-5 L in 24 hours; or a change in weight of 0.5-1.5 kg in 24 hours. If congestion persists after the maximization of loop diuretic therapy over the first 24-48 hours, an adjunc
Bronchopulmonary dysplasia (BPD), a respiratory complication associated with neonatal prematurity, presents opportunities for pharmacological intervention due to its contributing risk factors. Despite diuretics' controversial usage in BPD treatment and varying institutional practices, this review aims to consolidate evidence from clinical trials regarding diuretic use in BPD. We conducted a systematic review following PRISMA guidelines, searching EMBASE, Medline, Web of Science and CINAHL databases (PROSPERO 2022: CRD42022328292). Covidence facilitated screening and data extraction, followed by analysis and formatting in Microsoft Excel. Among 430 screened records, 13 were included for analysis. Three studies assessed spironolactone and chlorothiazide combinations, two studied spironolactone and hydrochlorothiazide, while eight examined furosemide. All studies evaluated drug effects on dynamic pulmonary compliance and pulmonary resistance, serving as comparative measures in our review. Diuretics' effectiveness in treating bronchopulmonary dysplasia remains uncertain. The limited number of identified randomised controlled trials (RCTs) hampers high-level evidence-based conclusions when applying the Population, Intervention, Comparison, Outcome (PICO) approach. Conducting large prospective studies of good quality could provide more definitive insights, but the rarity of outcomes and eligible patients poses challenges. Further research, primarily focusing on RCTs assessing diuretics' safety and efficacy in this population, is warranted.