nitrofurantoin
Sources réglementaires consultées
Indications approuvées
- Cystite aiguë non compliquée due à des germes sensibles ; elle n’est pas indiquée dans la pyélonéphrite, l’infection urinaire haute, la bactériémie ou le sepsis.
Contre-indications
Absolues
- Hypersensibilité à la nitrofurantoïne ; porphyrie aiguë ; déficit en G6PD ; ClCr <45 ml/min sauf exception limitée de 30 à 44 ; 2 dernières semaines de grossesse ; âge inférieur à 3 mois.
Mises en garde cliniques
- Il peut provoquer des réactions pulmonaires aiguës, subaiguës ou chroniques, une hépatotoxicité sévère, une neuropathie périphérique et une hémolyse ; arrêter en cas de symptômes respiratoires, hépatiques, neurologiques ou hématologiques. — DailyMed, set_id 729f6bbb-ab64-4b65-979a-4ad7605c5947
Interactions médicamenteuses
- ModéréeTrisilicate de magnésium
Mécanisme: Il réduit l’absorption de la nitrofurantoïne.
Recommandation: Éviter l’administration simultanée.
DailyMed, set_id 729f6bbb-ab64-4b65-979a-4ad7605c5947
- SévèreProbénécide ou sulfinpyrazone
Mécanisme: Ils réduisent la sécrétion tubulaire, augmentent la toxicité et diminuent les concentrations urinaires.
Recommandation: Éviter l’association.
DailyMed, set_id 729f6bbb-ab64-4b65-979a-4ad7605c5947
- ModéréeQuinolones
Mécanisme: Un antagonisme antibactérien in vitro a été décrit ; sa pertinence clinique dépend du microorganisme et du contexte.
Recommandation: Éviter l’association sauf justification microbiologique et surveillance clinique.
DailyMed, set_id 729f6bbb-ab64-4b65-979a-4ad7605c5947
- SévèreInhibiteurs de l’anhydrase carbonique ou alcalinisants urinaires
Mécanisme: L’alcalinisation urinaire réduit l’activité antibactérienne de la nitrofurantoïne.
Recommandation: Éviter l’association pendant le traitement de l’infection urinaire.
DailyMed, set_id 729f6bbb-ab64-4b65-979a-4ad7605c5947
Effets indésirables
Communs (≥1%)
Nausées, céphalées, flatulences et diarrhée
Rares mais graves
Fibrose pulmonaire, hépatite fulminante, neuropathie irréversible et anémie hémolytique
Grossesse et allaitement
Elle est contre-indiquée pendant les 2 dernières semaines de grossesse. En dehors de cette période, utiliser uniquement si indiqué. Évaluer l’allaitement selon l’âge, le statut G6PD et l’état du nourrisson.
Bibliographie récente (PubMed)
Urinary tract infections (UTIs) are the most common infection among pregnant women and have been associated with maternal and foetal complications. Antimicrobial exposure during pregnancy is not without risk. International guidelines recommend a single screen-and-treat approach to asymptomatic bacteriuria (ASB); however, this approach has been questioned by recent studies. The aim of this narrative review was to assess the pathophysiology, current risk factors and management of UTI during pregnancy, its impact on pregnancy outcomes, and to develop recommendations on the best use of antimicrobials. PubMed, Cochrane database, and ClinicalTrials.gov. Owing to the physiological changes related to pregnancy, pregnant women are at higher risk of UTI. All types of UTIs combined have been estimated to affect approximately 2% to 15% of women. ASB affects 2% to 7% of pregnant women. Recent studies do not provide good-quality evidence for an association between ASB and acute pyelonephritis if ASB is untreated. There is low-to-moderate-quality evidence that treatment of ASB results in a reduction in the incidence of low birth weight and preterm birth, which justifies screening practices for ASB with only a single urine culture in the first trimester. If the clinician opts for treatment, a short course of β-lactams, nitrofurantoin, or fosfomycin should be favoured. Studies on cystitis during pregnancy are limited. Acute pyelonephritis has been shown to be associated with increased maternal complications and in some studies has also been associated with preterm delivery and low birth weight. Preferred antimicrobials for the management of pyelonephritis are amoxicillin combined with an aminoglycoside, third-generation cephalosporins, or carbapenems. Studies on recurrent UTIs during pregnancy are limited, making it difficult to draw conclusions regarding prophylactic measures. Further research is required to understand the true incidence of ASB-related complications and the benefit
Drug-induced autoimmune hepatitis (DIAIH) is a specific phenotype of drug-induced liver injury that may lead to the devastating outcome of acute liver failure requiring liver transplantation. Drugs implicated in DIAIH include antimicrobials such as nitrofurantoin and minocycline, non-steroidal anti-inflammatory drugs, statins as well as anti-tumor necrosis agents. The clinical features of drug-induced liver injury are indistinguishable from idiopathic autoimmune hepatitis (AIH) as both may have positive AIH-related autoantibodies, elevated immunoglobulin G, as well as similar histopathological findings. In patients who show no clinical improvement, or there is progressive liver injury despite cessation of the suspected drug, a liver biopsy should be considered, whereby the presence of advance fibrosis on histology favors the diagnosis of idiopathic AIH. Empirical treatment with corticosteroids may be required in patients with non-resolving liver injury. A typical clinical scenario supportive of DIAIH includes a history of drug exposure with spontaneous resolution of liver injury after drug withdrawal and the absence of relapse after rapid steroid taper. In this article we report two cases of DIAIH secondary to Sorafenib and Atorvastatin along with a review of currently available literature. Early identification and treatment often lead to a favorable outcome in DIAIH.
Drug-induced liver injury (DILI) can mimic almost all other liver disorders. A phenotype increasingly ascribed to drugs is autoimmune-like hepatitis (ALH). This article summarises the major topics discussed at a joint International Conference held between the Drug-Induced Liver Injury consortium and the International Autoimmune Hepatitis Group. DI-ALH is a liver injury with laboratory and/or histological features that may be indistinguishable from those of autoimmune hepatitis (AIH). Previous studies have revealed that patients with DI-ALH and those with idiopathic AIH have very similar clinical, biochemical, immunological and histological features. Differentiating DI-ALH from AIH is important as patients with DI-ALH rarely require long-term immunosuppression and the condition often resolves spontaneously after withdrawal of the implicated drug, whereas patients with AIH mostly require long-term immunosuppression. Therefore, revision of the diagnosis on long-term follow-up may be necessary in some cases. More than 40 different drugs including nitrofurantoin, methyldopa, hydralazine, minocycline, infliximab, herbal and dietary supplements (such as Khat and Tinospora cordifolia) have been implicated in DI-ALH. Understanding of DI-ALH is limited by the lack of specific markers of the disease that could allow for a precise diagnosis, while there is similarly no single feature which is diagnostic of AIH. We propose a management algorithm for patients with liver injury and an autoimmune phenotype. There is an urgent need to prospectively evaluate patients with DI-ALH systematically to enable definitive characterisation of this condition.