Rifaximin
Sources réglementaires consultées
Indications approuvées
- États-Unis : traitement de la diarrhée du voyageur causée par des souches non invasives d'Escherichia coli chez les patients âgés de 12 ans ou plus.
- États-Unis : réduction du risque de récidive d'encéphalopathie hépatique manifeste chez l'adulte.
- États-Unis : traitement du syndrome de l'intestin irritable avec diarrhée chez l'adulte.
Contre-indications
Absolues
- Hypersensibilité à la rifaximine, aux autres dérivés de la rifamycine ou aux excipients.
Mises en garde cliniques
- Mise en garde majeure · Ne pas utiliser pour une diarrhée du voyageur avec fièvre ou sang dans les selles ni causée par des agents pathogènes invasifs. Évoquer Clostridioides difficile si une diarrhée apparaît ou s'aggrave après le traitement. — DailyMed, Xifaxan, setid c5e8e2fd-7087-4b78-9181-cc259c0be2f1
- Mise en garde majeure · Des réactions d'hypersensibilité sévères, y compris des réactions cutanées graves, peuvent survenir ; arrêter en cas de suspicion. — AEMPS CIMA, Spiraxin, ficha técnica 62250, sección 4.4
Interactions médicamenteuses
- ModéréeCiclosporine et autres inhibiteurs de la P-gp
Mécanisme: L’inhibition de la P-gp peut augmenter l’exposition systémique à la rifaximine.
Recommandation: Utiliser avec prudence et surveiller une augmentation des effets de la rifaximine.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c5e8e2fd-7087-4b78-9181-cc259c0be2f1
- ModéréeWarfarine
Mécanisme: Des variations de l’INR ont été rapportées avec la rifaximine et la warfarine.
Recommandation: Surveiller l’INR et ajuster l’anticoagulant selon l’indication clinique.
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c5e8e2fd-7087-4b78-9181-cc259c0be2f1
Effets indésirables
Communs (≥1%)
Nausées · Douleur abdominale · Céphalée · Vertiges
Rares mais graves
Colite à Clostridioides difficile · Syndrome de Stevens-Johnson · Nécrolyse épidermique toxique
Grossesse et allaitement
Il n’existe pas de données adéquates chez la femme enceinte. On ignore si la rifaximine est excrétée dans le lait humain; évaluer le bénéfice maternel face au risque potentiel.
Bibliographie récente (PubMed)
Irritable bowel syndrome is one of the most common functional bowel disorders, and has a substantial impact on patients' daily lives, as well as a big economic impact on society. It is characterised by abdominal pain, bloating and abdominal distention and altered bowel movements, with a predominance of diarrhoea, constipation, or alternation of these signs, which cannot be explained by a structural or biochemical abnormality. Its aetiopathogenesis and pathophysiological mechanism are unknown. The disease affects 5%-10% of healthy individuals at any given time and, in most people, has a relapsing-remitting course. This article reviews some of the main and most current evidence on its epidemiology, risk factors, pathophysiology, clinical manifestations, diagnostic approach, and therapeutic options, both dietary, pharmacological and psychotherapeutic.
Malnutrition, defined as deficiency, excess, or imbalance of nutrients, is a common complication in patients with liver disease, especially those with cirrhosis. Malnutrition may present as an isolated micronutrient deficiency, such as zinc deficiency, and it commonly presents as frailty and/or sarcopenia in patients with advanced liver disease. Patients with cirrhosis and/or alcohol-associated hepatitis should be assessed for malnutrition because it adversely affects patient outcomes including mortality, as well as waitlist and posttransplant outcomes among liver transplant candidates. The prevalence of malnutrition varies based on the method of assessment and disease severity, being higher in those with advanced liver disease. Among stable outpatients with cirrhosis, counseling should be done to eat small frequent meals, a night-time snack between 7 PM and 10 PM, and 2 or more cups of coffee daily. In selected patients with metabolic dysfunction-associated steatohepatitis, vitamin E 800 IU/d should be provided. Among hospitalized patients with cirrhosis, nutritional supplementation preferably by enteral route should be implemented in those with poor oral intake of daily requirements of proteins and/or calories. Protein intake should not be restricted including patients with decompensated cirrhosis and hepatic encephalopathy. A vegetable source of protein seems to be better tolerated than an animal source of protein in patients with hepatic encephalopathy. Branched chain amino acids augment the efficacy of lactulose and rifaximin in the treatment of hepatic encephalopathy. Level of evidence and strength of recommendations were evaluated using the Grading of Recommendations, Assessment, Development, and Evaluations system. This guideline was developed under the auspices of the American College of Gastroenterology Practice Parameters Committee.
Hepatic encephalopathy (HE) is a prognostically relevant neuropsychiatric syndrome that occurs in the course of acute or chronic liver disease. Besides ascites and variceal bleeding, it is the most serious complication of decompensated liver cirrhosis. Ammonia and inflammation are major triggers for the appearance of HE, which in patients with liver cirrhosis involves pathophysiologically low-grade cerebral oedema with oxidative/nitrosative stress, inflammation and disturbances of oscillatory networks in the brain. Severity classification and diagnostic approaches regarding mild forms of HE are still a matter of debate. Current medical treatment predominantly involves lactulose and rifaximin following rigorous treatment of so-called known HE precipitating factors. New treatments based on an improved pathophysiological understanding are emerging.
Cirrhosis consists of 2 main stages: compensated and decompensated, the latter defined by the development/presence of ascites, variceal hemorrhage, and hepatic encephalopathy. The survival rate is entirely different, depending on the stage. Treatment with nonselective β-blockers prevents decompensation in patients with clinically significant portal hypertension, changing the previous paradigm based on the presence of varices. In patients with acute variceal hemorrhage at high risk of failure with standard treatment (defined as those with a Child-Pugh score of 10-13 or those with a Child-Pugh score of 8-9 with active bleeding at endoscopy), a pre-emptive transjugular intrahepatic portosystemic shunt (TIPS) improves the mortality rate and has become the standard of care in many centers. In patients with bleeding from gastrofundal varices, retrograde transvenous obliteration (in those with a gastrorenal shunt) and/or variceal cyanoacrylate injection have emerged as alternatives to TIPS. In patients with ascites, emerging evidence suggests that TIPS might be used earlier, before strict criteria for refractory ascites are met. Long-term albumin use is under assessment for improving the prognosis of patients with uncomplicated ascites and confirmatory studies are ongoing. Hepatorenal syndrome is the least common cause of acute kidney injury in cirrhosis, and first-line treatment is the combination of terlipressin and albumin. Hepatic encephalopathy has a profound impact on the quality of life of patients with cirrhosis. Lactulose and rifaximin are first- and second-line treatments for hepatic encephalopathy, respectively. Newer therapies such as L-ornithine L-aspartate and albumin require further assessment.
Hepatic encephalopathy, characterized by mental status changes and neuropsychiatric impairment, is associated with chronic liver disease as well as acute liver failure. In children, its clinical manifestations can be challenging to pinpoint. However, careful assessment for the development of hepatic encephalopathy is imperative when caring for these patients as progression of symptoms can indicate impending cerebral edema and systemic deterioration. Hepatic encephalopathy can present with hyperammonemia, but it is important to note that the degree of hyperammonemia is not indicative of severity of clinical manifestations. Newer forms of assessment are undergoing further research, and include imaging, EEG and neurobiomarkers. Mainstay of treatment currently includes management of underlying cause of liver disease, as well as reduction of hyperammonemia with either enteral medications such as lactulose and rifaximin, or even with extracorporeal liver support modalities.