Composition:
Application:
Utilisé dans le traitement:
Examiné médicalement par Fedorchenko Olga Valeryevna, Pharmacie Dernière mise à jour le 25.03.2022
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Trandor est indiqué pour:
- Soulagement de la douleur légère à modérée chez l'adulte
- Soulagement des signes et symptômes de la polyarthrite rhumatoïde
- Soulagement des signes et symptômes de l'arthrose
Instructions générales de dosage
Considérez attentivement les avantages et les risques potentiels de Trandor et d'autres options de traitement avant de décider d'utiliser Trandor. Utilisez la dose efficace la plus faible pour la durée la plus courte compatible avec les objectifs de traitement individuels du patient Utilisez la posologie efficace la plus faible pour la durée la plus courte compatible avec les objectifs de traitement individuels du patient.
Trandor peut être administré avec des repas ou avec du lait. Bien que la quantité totale absorbée ne soit pas affectée, les taux sanguins maximaux sont retardés et diminués.
Les patients atteints de polyarthrite rhumatoïde semblent généralement nécessiter des doses de Trandor plus importantes que ceux souffrant d'arthrose. La plus petite dose qui donne un contrôle acceptable doit être utilisée.
Bien que des améliorations puissent être observées en quelques jours chez de nombreux patients, 2 à 3 semaines supplémentaires peuvent être nécessaires pour évaluer tous les avantages du traitement.
Analgésie
Pour le traitement de la douleur légère à modérée, la posologie recommandée est de 200 mg administrés par voie orale toutes les 4 à 6 heures, au besoin.
Arthrite rhumatoïde et arthrose
Pour le soulagement des signes et symptômes de la polyarthrite rhumatoïde ou de l'arthrose, la dose recommandée est de 400 à 600 mg administrée par voie orale, 3 ou 4 fois par jour. La dose doit être adaptée aux besoins du patient et peut être augmentée ou diminuée en fonction de la gravité des symptômes. Des ajustements posologiques peuvent être effectués après le début du traitement médicamenteux ou lors des exacerbations de la maladie. La posologie quotidienne totale ne doit pas dépasser 3 200 mg.
Trandor est contre-indiqué chez les patients suivants:
- Hypersensibilité connue (par ex., réactions anaphylactiques et réactions cutanées graves) au fénoprofène ou à tout composant du produit médicamenteux
- Antécédents d'asthme, d'urticaire ou d'autres réactions de type allergique après la prise d'aspirine ou d'autres AINS. Des réactions anaphylactiques sévères, parfois mortelles, aux AINS ont été rapportées chez ces patients
- Dans le cadre de la chirurgie de pontage aortocoronarien (CABG)
WARNINGS
Included as part of the PRECAUTIONS section.
PRECAUTIONS
Cardiovascular Thrombotic Events
Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, including myocardial infarction (MI) and stroke, which can be fatal. Based on available data, it is unclear that the risk for CV thrombotic events is similar for all NSAIDs. The relative increase in serious CV thrombotic events over baseline conferred by NSAID use appears to be similar in those with and without known CV disease or risk factors for CV disease. However, patients with known CV disease or risk factors had a higher absolute incidence of excess serious CV thrombotic events, due to their increased baseline rate. Some observational studies found that this increased risk of serious CV thrombotic events began as early as the first weeks of treatment. The increase in CV thrombotic risk has been observed most consistently at higher doses.
To minimize the potential risk for an adverse CV event in NSAID-treated patients, use the lowest effective dose for the shortest duration possible. Physicians and patients should remain alert for the development of such events, throughout the entire treatment course, even in the absence of previous CV symptoms. Patients should be informed about the symptoms of serious CV events and the steps to take if they occur.
There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID, such as fenoprofen, increases the risk of serious gastrointestinal (GI) events.
Status Post Coronary Artery Bypass Graft (CABG) Surgery
Two large, controlled clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10–14 days following CABG surgery found an increased incidence of myocardial infarction and stroke. NSAIDs are contraindicated in the setting of CABG.
Post-MI Patients
Observational studies conducted in the Danish National Registry have demonstrated that patients treated with NSAIDs in the post-MI period were at increased risk of reinfarction, CV-related death, and all-cause mortality beginning in the first week of treatment. In this same cohort, the incidence of death in the first year post-MI was 20 per 100 person years in NSAID-treated patients compared to 12 per 100 person years in non-NSAID exposed patients. Although the absolute rate of death declined somewhat after the first year post-MI, the increased relative risk of death in NSAID users persisted over at least the next four years of follow-up.
Avoid the use of Trandor in patients with a recent MI unless the benefits are expected to outweigh the risk of recurrent CV thrombotic events. If Trandor is used in patients with a recent MI, monitor patients for signs of cardiac ischemia.
Gastrointestinal Bleeding, Ulceration, And Perforation
NSAIDs, including Trandor, cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients who develop a serious upper GI adverse event on NSAID therapy is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occurred in approximately 1% of patients treated for 3-6 months, and in about 2%-4% of patients treated for one year. However, even short-term NSAID therapy is not without risk.
Risk Factors for GI Bleeding, Ulceration, And Perforation
Patients with a prior history of peptic ulcer disease and/or GI bleeding who used NSAIDs had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Other factors that increase the risk of GI bleeding in patients treated with NSAIDs include longer duration of NSAID therapy; concomitant use of oral corticosteroids, aspirin, anticoagulants, or selective serotonin reuptake inhibitors (SSRIs); smoking; use of alcohol; older age; and poor general health status. Most postmarketing reports of fatal GI events occurred in elderly or debilitated patients. Additionally, patients with advanced liver disease and/or coagulopathy are at increased risk for GI bleeding.
Strategies To Minimize The GI Risks In NSAID-treated Patients
- Use the lowest effective dosage for the shortest possible duration.
- Avoid administration of more than one NSAID at a time.
- Avoid use in patients at higher risk unless benefits are expected to outweigh theincreased risk of bleeding. For such patients, as well as those with active GIbleeding, consider alternate therapies other than NSAIDs.
- Remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy.
- If a serious GI adverse event is suspected, promptly initiate evaluation and treatment, and discontinue Trandor until a serious GI adverse event is ruled out.
- In the setting of concomitant use of low-dose aspirin for cardiac prophylaxis, monitor patients more closely for evidence of GI bleeding.
Hepatotoxicity
Elevations of ALT or AST (three or more times the upper limit of normal [ULN]) have been reported in approximately 1% of NSAID-treated patients in clinical trials. In addition, rare, sometimes fatal, cases of severe hepatic injury, including fulminant hepatitis, liver necrosis, and hepatic failure have been reported.
Elevations of ALT or AST (less than three times ULN) may occur in up to 15% of patients treated with NSAIDs including fenoprofen.
Inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, diarrhea, pruritus, jaundice, right upper quadrant tenderness, and “flu-like” symptoms). If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), discontinue Trandor immediately, and perform a clinical evaluation of the patient.
Hypertension
NSAIDs, including Trandor, can lead to new onset of hypertension or worsening of preexisting hypertension, either of which may contribute to the increased incidence of CV events. Patients taking angiotensin converting enzyme (ACE) inhibitors, thiazide diuretics, or loop diuretics may have impaired response to these therapies when taking NSAIDs.
Monitor blood pressure (BP) during the initiation of NSAID treatment and throughout the course of therapy.
Heart Failure And Edema
The Coxib and traditional NSAID Trialists' Collaboration meta-analysis of randomized controlled trials demonstrated an approximately two-fold increase in hospitalizations for heart failure in COX-2 selective-treated patients and nonselective NSAID-treated patients compared to placebo-treated patients. In a Danish National Registry study of patients with heart failure, NSAID use increased the risk of MI, hospitalization for heart failure, and death.
Additionally, fluid retention and edema have been observed in some patients treated with NSAIDs. Use of fenoprofen may blunt the CV effects of several therapeutic agents used to treat these medical conditions (e.g., diuretics, ACE inhibitors, or angiotensin receptor blockers [ARBs]).
Avoid the use of Trandor in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure. If Trandor is used in patients with severe heart failure, monitor patients for signs of worsening heart failure.
Renal Toxicity And Hyperkalemia
Renal Toxicity
Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury.
Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients, administration of an NSAID may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors or ARBs, and the elderly. Discontinuation of NSAID therapy is usually followed by recovery to the pretreatment state.
No information is available from controlled clinical studies regarding the use of Trandor in patients with advanced renal disease. The renal effects of Trandor may hasten the progression of renal dysfunction in patients with preexisting renal disease.
Correct volume status in dehydrated or hypovolemic patients prior to initiating Trandor. Monitor renal function in patients with renal or hepatic impairment, heart failure, dehydration, or hypovolemia during use of Trandor. Avoid the use of Trandor in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function. If Trandor is used in patients with advanced renal disease, monitor patients for signs of worsening renal function.
Hyperkalemia
Increases in serum potassium concentration, including hyperkalemia, have been reported with use of NSAIDs, even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemichypoaldosteronism state.
Anaphylactic Reactions
Fenoprofen has been associated with anaphylactic reactions in patients with and without known hypersensitivity to fenoprofen and in patients with aspirin-sensitive asthma.
Seek emergency help if an anaphylactic reaction occurs.
Exacerbation Of Asthma Related To Aspirin Sensitivity
A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps; severe, potentially fatal bronchospasm; and/or intolerance to aspirin and other NSAIDs. Because cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, Trandor is contraindicated in patients with this form of aspirin sensitivity. When Trandor is used in patients with preexisting asthma (without known aspirin sensitivity), monitor patients for changes in the signs and symptoms of asthma.
Serious Skin Reactions
NSAIDs, including fenopropfen, can cause serious skin adverse reactions such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Inform patients about the signs and symptoms of serious skin reactions, and to discontinue the use of Trandor at the first appearance of skin rash or any other sign of hypersensitivity. Trandor is contraindicated in patients with previous serious skin reactions to NSAIDs.
Premature Closure Of Fetal Ductus Arteriosus
Fenoprofen may cause premature closure of the fetal ductus arteriosus. Avoid use of NSAIDs, including Trandor, in pregnant women starting at 30 weeks of gestation (third trimester).
Hematologic Toxicity
Anemia has occurred in NSAID-treated patients. This may be due to occult or gross blood loss, fluid retention, or an incompletely described effect on erythropoiesis. If a patient treated with Trandor has any signs or symptoms of anemia, monitor hemoglobin or hematocrit.
NSAIDs, including Trandor, may increase the risk of bleeding events. Co-morbid conditions such as coagulation disorders, concomitant use of warfarin, other anticoagulants, antiplatelet agents (e.g., aspirin), serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) may increase this risk. Monitor these patients for signs of bleeding.
Masking Of Inflammation And Fever
The pharmacological activity of Trandor in reducing inflammation, and possibly fever, may diminish the utility of diagnostic signs in detecting infections.
Laboratory Monitoring
Because serious GI bleeding, hepatotoxicity, and renal injury can occur without warning symptoms or signs, consider monitoring patients on long-term NSAID treatment with a CBC and a chemistry profile periodically.
Ocular Effects
Studies to date have not shown changes in the eyes attributable to the administration of Trandor. However, adverse ocular effects have been observed with other anti-inflammatory drugs. Eye examinations, therefore, should be performed if visual disturbances occur in patients taking Trandor.
Central Nervous System Effects
Caution should be exercised by patients whose activities require alertness if they experience CNS side effects while taking Trandor.
Impact On Hearing
Since the safety of Trandor has not been established in patients with impaired hearing, these patients should have periodic tests of auditory function during prolonged therapy with Trandor.
Patient Counseling Information
Advise the patient to read the FDA-approved patient labeling (Medication Guide) that accompanies each prescription dispensed. Inform patients, families, or their caregivers of the following information before initiating therapy with Trandor and periodically during the course of ongoing therapy.
Cardiovascular Thrombotic Events
Advise patients to be alert for the symptoms of cardiovascular thrombotic events, including chest pain, shortness of breath, weakness, or slurring of speech, and to report any of these symptoms to their health care provider immediately.
Gastrointestinal Bleeding, Ulceration, And Perforation
Advise patients to report symptoms of ulcerations and bleeding, including epigastric pain, dyspepsia, melena, and hematemesis to their health care provider. In the setting of concomitant use of low-dose aspirin for cardiac prophylaxis, inform patients of the increased risk for and the signs and symptoms of GI bleeding.
Hepatotoxicity
Inform patients of the warning signs and symptoms of hepatotoxicity (e.g., nausea, fatigue, lethargy, pruritus, diarrhea, jaundice, right upper quadrant tenderness, and “flu-like” symptoms). If these occur, instruct patients to stop Trandor and seek immediate medical therapy.
Heart Failure And Edema
Advise patients to be alert for the symptoms of congestive heart failure including shortness of breath, unexplained weight gain, or edema and to contact their healthcare provider if such symptoms occur.
Anaphylactic Reactions
Inform patients of the signs of an anaphylactic reaction (e.g., difficulty breathing, swelling of the face or throat). Instruct patients to seek immediate emergency help if these occur.
Serious Skin Reactions
Advise patients to stop Trandor immediately if they develop any type of rash and to contact their healthcare provider as soon as possible.
Female Fertility
Advise females of reproductive potential who desire pregnancy that NSAIDs, including Trandor, may be associated with a reversible delay in ovulation
Fetal Toxicity
Inform pregnant women to avoid use of Trandor and other NSAIDs starting at 30 weeks gestation because of the risk of the premature closing of the fetal ductus arteriosus.
Avoid Concomitant Use Of NSAIDs
Inform patients that the concomitant use of Trandor with other NSAIDs or salicylates (e.g., diflunisal, salsalate) is not recommended due to the increased risk of gastrointestinal toxicity, and little or no increase in efficacy. Alert patients that NSAIDs may be present in “over the counter” medications for treatment of colds, fever, or insomnia.
Use Of NSAIDS And Low-Dose Aspirin
Inform patients not to use low-dose aspirin concomitantly with Trandor until they talk to their healthcare provider.
Nonclinical Toxicology
Carcinogenesis, Mutagenesis, and Impairment of Fertility
Carcinogenesis
Long-term studies in animals to evaluate the carcinogenic potential of fenoprofen have not been conducted.
Mutagenesis
Studies to evaluate the genotoxic potential of fenoprofen have not been conducted.
Impairment of Fertility Female and Male rats were treated with 60 to 70 mg/kg/day or 120 to 150 mg/kg/day fenoprofen calcium via the diet (approximately
0.2 or 0.4 times the maximum human daily dose of 3200 mg/day based on body surface area comparison, respectively). Male rats were treated from 77 days prior to mating and during mating. Female rats were treated from 14 days prior to mating and through gestation. Pregnancy rates were slightly reduced in the low and high dose groups compared to controls. There was no adverse effect on implantations, resorptions, or live fetuses.
Use In Specific Populations
Pregnancy
Risk Summary
Use of NSAIDs, including Trandor, during the third trimester of pregnancy increases the risk of premature closure of the fetal ductus arteriosus. Avoid use of NSAIDs, including Trandor, in pregnant women starting at 30 weeks of gestation (third trimester).
There are no adequate and well-controlled studies of Trandor in pregnant women. Data from observational studies regarding potential embryofetal risks of NSAID use in women in the first or second trimesters of pregnancy are inconclusive. In the general U.S. population, all clinically recognized pregnancies, regardless of drug exposure, have a background rate of 2-4% for major malformations, and 15-20% for pregnancy loss.
In animal reproduction studies, embryo-fetal lethality and skeletal abnormalities were noted in offspring of pregnant rabbits following oral administration of fenoprofen during organogenesis at 0.6 times the maximum human daily dose of 3200 mg/day. However, there were no major malformations noted following oral administration of fenoprofen calcium to pregnant rats and rabbits during organogenesis at exposures up to 0.3 and 0.6 times the maximum human daily dose of 3200 mg/day.
Based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, administration of prostaglandin synthesis inhibitors such as fenoprofen, resulted in increased pre- and post-implantation loss.
Clinical Considerations
Labor or Delivery
There are no studies on the effects of Trandor during labor or delivery. In animal studies, NSAIDS, including fenoprofen, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth.
Data
Human Data
There are no adequate and well-controlled studies of Trandor in pregnant women. Data from observational studies regarding potential embryofetal risks of NSAID use in women in the first or second trimesters of pregnancy are inconclusive.
Animal data
Pregnant rats were treated with fenoprofen using oral doses of 50 or 100 mg/kg (0.15 times and 0.3 times the maximum human daily dose (MHDD) of 3200 mg/day based on body surface area comparison) during the period of organogenesis. No major malformations were noted and there was no evidence of maternal toxicity at these doses, however, the exposures were below the exposures that will occur in humans.
Pregnant rabbits were treated with fenoprofen using oral doses of 50 or 100 mg/kg (0.3 times and 0.6 times the MHDD of 3200 mg/day based on body surface area comparison) during the period of organogenesis. Maternal toxicity (mortality) was noted in the high dose animals. Although no major malformations were noted, there was an increased incidence of embryo-fetal lethality and skeletal abnormalities were present at 0.6 times the MHDD.
Pregnant rats were treated from Gestation Day 14 through Post-Natal Day 20 with oral doses of fenoprofen of 6.25, 12.5, 25, 50, or 100 mg/kg (0.02, 0.04, 0.08, 0.15, or 0.3 times the MDD of 3200 mg/day based on body surface area comparison). All doses produced significant toxicity, including vaginal bleeding, prolonged parturition, increased stillbirths, and maternal deaths.
Lactation
Risk Summary
In a published study, after a dose of 600 mg every 6 hours for 4 days in postpartum mothers, breastmilk fenoprofen levels were reportedly 1.6% of those in maternal plasma. The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for Trandor and any potential adverse effects on the breastfed infant from the Trandor or from the underlying maternal condition.
Females And Males Of Reproductive Potential
Infertility
Females
Based on the mechanism of action, the use of prostaglandin-mediated NSAIDs, including Trandor, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. Published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandinmediated follicular rupture required for ovulation. Small studies in women treated with NSAIDs have also shown a reversible delay in ovulation. Consider withdrawal of NSAIDs, including Trandor, in women who have difficulties conceiving or who are undergoing investigation of infertility.
Pediatric Use
Safety and effectiveness in pediatric patients under the age of 18 have not been established.
Geriatric Use
Elderly patients, compared to younger patients, are at greater risk for NSAID-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. If the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects.
Les effets indésirables suivants sont discutés plus en détail dans d'autres sections de l'étiquetage:
- Événements thrombotiques cardiovasculaires
- Saignement gastro-intestinal, ulcération et perforation
- Hépatotoxicité
- Hypertension
- Insuffisance cardiaque et œdème
- Toxicité rénale et hyperkaliémie
- Réactions anaphylactiques
- Réactions graves de la peau
- Toxicité hématologique
Expérience des essais cliniques
Étant donné que les essais cliniques sont menés dans des conditions très variables, les taux d'effets indésirables observés dans les essais cliniques d'un médicament ne peuvent pas être directement comparés aux taux dans les essais cliniques d'un autre médicament et peuvent ne pas refléter les taux observés dans la pratique.
Au cours des études cliniques sur la polyarthrite rhumatoïde, l'arthrose ou la douleur légère à modérée et des études de pharmacocinétique, des plaintes ont été compilées à partir d'une liste de contrôle des effets indésirables potentiels, et les données suivantes ont émergé. Ceux-ci englobent des observations chez 6 786 patients, dont 188 observés pendant au moins 52 semaines. À titre de comparaison, des données sont également présentées à partir de plaintes reçues des 266 patients qui ont reçu un placebo dans ces mêmes essais. Au cours des études à court terme sur l'analgésie, l'incidence des effets indésirables a été nettement inférieure à celle observée dans les études à plus long terme.
Effets indésirables signalés chez> 1% des patients au cours des essais cliniques
Système digestif - Au cours des essais cliniques avec Trandor, les effets indésirables les plus courants étaient de nature gastro-intestinale et sont survenus chez 20,8% des patients recevant Trandor contre 16,9% des patients recevant un placebo. Par ordre décroissant de fréquence, ces réactions comprenaient une dyspepsie (10,3% Trandor vs. 2,3% placebo), nausées (7,7% contre. 7,1%), constipation (7% contre. 1,5%), vomissements (2,6% contre. 1,9%), douleurs abdominales (2% contre. 1,1%) et la diarrhée (1,8% contre. 4,1%). Le médicament a été arrêté en raison de réactions gastro-intestinales indésirables chez moins de 2% des patients au cours des études de pré-commercialisation.
Système nerveux - Les réactions neurologiques indésirables les plus fréquentes étaient des céphalées (8,7% contre. 7,5%) et somnolence (8,5% contre. 6,4%). Vertiges (6,5% contre. 5,6%), tremblements (2,2% contre. 0,4%), et confusion (1,4% contre. aucun) ont été notés moins fréquemment. Trandor a été arrêté chez moins de 0,5% des patients en raison de ces effets secondaires lors des études de pré-commercialisation.
Peau et appendices— Transpiration accrue (4,6% contre. 0,4%), prurit (4,2% contre. 0,8%) et téméraire (3,7% contre. 0,4%) ont été déclarés. Trandor a été arrêté chez environ 1% des patients en raison d'un effet indésirable lié à la peau lors des études de pré-commercialisation.
Sens spéciaux - Acouphènes (4,5% contre. 0,4%), vision floue (2,2% contre. aucun) et diminution de l'audition (1,6% contre. aucun) ont été signalés. Trandor a été arrêté chez moins de 0,5% des patients en raison d'effets indésirables liés aux sens spéciaux lors des études de pré-commercialisation.
Cardiovasculaire - Palpitations (2,5% contre. 0,4%). Trandor a été arrêté chez environ 0,5% des patients en raison de réactions cardiovasculaires indésirables lors des études de pré-commercialisation.
Divers - Nervosité (5,7% contre. 1,5%), asthénie (5,4% contre. 0,4%), œdème périphérique (5,0% contre. 0,4%), dyspnée (2,8% contre. aucun), fatigue (1,7% contre. 1,5%), infection des voies respiratoires supérieures (1,5% contre. 5,6%) et la nasopharyngite (1,2% contre. aucun).
Effets indésirables signalés chez <1% des patients au cours des essais cliniques
Système digestif—Gastrite, ulcère gastro-duodénal avec / sans perforation, hémorragie gastro-intestinale, anorexie, flatulence, bouche sèche et sang dans les selles. Augmentation de la phosphatase alcaline, de la LDH, de la SGOT, de l'ictère et de l'hépatite cholestatique, des ulcérations aphteuses de la muqueuse buccale, du goût métallique et de la pancréatite.
Cardiovasculaire—Fibrillation auriculaire, œdème pulmonaire, modifications électrocardiographiques et tachycardie supraventriculaire.
Tract génito-urinaire —Insuffisance rénale, dysurie, cystite, hématurie, oligurie, azotémie, anurie, néphrite interstitielle, néphrose et nécrose papillaire.
Hypersensibilité—Angioedème (œdème angioneurotique).
Hématologique—Purpura, ecchymose, hémorragie, thrombocytopénie, anémie hémolytique, anémie aplasique, agranulocytose et pancytopénie.
Système nerveux—Dépression, désorientation, convulsions et névralgie trijumeau.
Sens spéciaux—Langue brûlante, diplopie et névrite optique.
Peau et appendices—Dermatite exfoliatrice, nécrolyse épidermique toxique, syndrome de Stevens-Johnson et alopécie.
Divers—Anaphylaxie, urticaire, malaise, insomnie, tachycardie, changement de personnalité, lymphadénopathie, mastodynie et fièvre.
Les symptômes après des surdosages d'AINS aigus ont généralement été limités à la léthargie, à la somnolence, aux nausées, aux vomissements et aux douleurs épigastriques, qui ont été généralement réversibles avec des soins de soutien. Des saignements gastro-intestinaux se sont produits. L'hypertension, l'insuffisance rénale aiguë, la dépression respiratoire et le coma se sont produits, mais étaient rares.
Gérez les patients avec des soins symptomatiques et de soutien après une surdosage d'AINS. Il n'y a pas d'antidotes spécifiques. Considérez les vomissements et / ou le charbon activé (60 à 100 grammes chez l'adulte, 1 à 2 grammes par kg de poids corporel chez les patients pédiatriques) et / ou cathartique osmotique chez les patients symptomatiques observés dans les quatre heures suivant l'ingestion ou chez les patients présentant une surdose importante (5 à 10 fois la posologie recommandée). La diurèse forcée, l'alcalinisation de l'urine, l'hémodialyse ou l'hémoperfusion peuvent ne pas être utiles en raison d'une forte liaison protéique.
Pour plus d'informations sur le traitement des surdosages, contactez un centre anti-poison (1-800-222-1222).
Absorption
Dans des conditions de jeûne, le fénoprofène est rapidement absorbé et des taux plasmatiques maximaux de 50 mcg / L sont atteints dans les 2 heures suivant l'administration orale de doses de 600 mg. Une bonne proportionnalité de dose a été observée entre 200 et 600 mg chez des volontaires masculins à jeun.
Distribution
Le fénoprofène est fortement lié (99%) à l'albumine.
Élimination
Métabolisme
La demi-vie plasmatique est d'environ 3 heures.
Excrétion
Environ 90% d'une dose orale unique est éliminée dans les 24 heures sous forme de glucuronide de fénoprofène et de glucuronide de 4'-hydroxyfénoprofène, les principaux métabolites urinaires du fénoprofène.