KETOPROFEN (ketoprofen)

There are 6 contraindications. Absolute contraindication.

Contraindication List
Aspirin exacerbated respiratory disease
Cerebrovascular accident
History of roux-en-Y gastric bypass
Post-operative from CABG surgery
Pregnancy
Renal transplant

There are 16 severe contraindications. Adequate patient monitoring is recommended for safer drug use.

Severe List
Acute myocardial infarction
Chronic heart failure
Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min
Chronic kidney disease stage 5 (failure) GFr<15 ml/min
Gastrointestinal hemorrhage
Gastrointestinal ulcer
History of kidney donation
Increased risk of bleeding
Increased risk of bleeding due to coagulation disorder
Kidney disease with likely reduction in glomerular filtration rate (GFr)
Nephrectomy
Peptic ulcer
Severe hepatic disease
Systemic mastocytosis
Thrombotic disorder
Tobacco smoker

There are 2 moderate contraindications. Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.

Moderate List
Hypertension
Hypoalbuminemia

There are 77 severe adverse reactions.

More Frequent	Less Frequent
Body fluid retention Edema	Altered mental status Aphthous stomatitis Blurred vision Cystitis Depression Diplopia Mood changes Skin rash Tinnitus Visual changes

Rare/Very Rare

Abnormal hepatic function tests Abnormal vaginal bleeding Acute cognitive impairment Acute myocardial infarction Acute pancreatitis Agranulocytosis Allergic dermatitis Anaphylaxis Anemia Angioedema Bloody stools Bloody vomit Bronchospastic pulmonary disease Bullous dermatitis Cardiac arrhythmia Cerebrovascular accident Chest tightness Chronic heart failure Conjunctivitis Cramps DRESS syndrome Drug-induced hepatitis Dry eye Dyspnea Epistaxis Erythema Esophageal ulcer Exfoliative dermatitis Gastric ulcer Gastritis Gastrointestinal hemorrhage Gastrointestinal perforation Gastrointestinal ulcer Hallucinations Hematuria Hemolytic anemia Hemoptysis Hepatitis Hyperkalemia Hypertension Increased risk of bleeding due to coagulation disorder Interstitial nephritis Jaundice Kidney disease with reduction in glomerular filtration rate (GFr) Laryngeal edema Memory impairment Migraine Myalgia Nail disorders Nephrotic syndrome Nephrotoxicity Neutropenic disorder Ocular pain Peptic ulcer Peripheral neuropathy Polydipsia Pruritus of skin Renal failure Retinal hemorrhage Rhinitis Stevens-johnson syndrome Thrombocytopenic disorder Toxic epidermal necrolysis Urticaria Wheezing

There are 24 less severe adverse reactions.

More Frequent	Less Frequent
Acute abdominal pain Constipation Diarrhea Flatulence Gastric acid hypersecretory conditions Headache disorder Irritability Nausea Nervousness	Anorexia Dizziness Drowsy Fatigue Hyperhidrosis Insomnia Vomiting

Rare/Very Rare
Dysgeusia Hearing loss Mouth irritation Palpitations Skin photosensitivity Tachycardia Weight loss Xerostomia

Use of NSAIAs during pregnancy at about 30 weeks of gestation or later can cause premature closure of the fetal ductus arteriosus, and use at about 20 weeks of gestation or later has been associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, use of NSAIAs should be avoided in pregnant women at about 30 weeks of gestation or later; if NSAIA therapy is necessary between about 20 and 30 weeks of gestation, the lowest effective dosage and shortest possible duration of treatment should be used. Monitoring of amniotic fluid volume via ultrasound examination should be considered if the duration of NSAIA treatment exceeds 48 hours; if oligohydramnios occurs, the drug should be discontinued and follow-up instituted according to clinical practice.

Pregnant women should be advised to avoid use of NSAIAs beginning at 20 weeks' gestation unless otherwise advised by a clinician; they should be informed that NSAIAs should be avoided beginning at 30 weeks' gestation because of the risk of premature closure of the fetal ductus arteriosus and that monitoring for oligohydramnios may be necessary if NSAIA therapy is required for longer than 48 hours' duration between about 20 and 30 weeks of gestation. Known effects of NSAIAs on the human fetus during the third trimester of pregnancy include prenatal constriction of the ductus arteriosus, tricuspid incompetence, and pulmonary hypertension; nonclosure of the ductus arteriosus during the postnatal period (which may be resistant to medical management); and myocardial degenerative changes, platelet dysfunction with resultant bleeding, intracranial bleeding, renal dysfunction or renal failure, renal injury or dysgenesis potentially resulting in prolonged or permanent renal failure, oligohydramnios, GI bleeding or perforation, and increased risk of necrotizing enterocolitis. Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment has been observed, on average, following days to weeks of maternal NSAIA use, although oligohydramnios has been observed infrequently as early as 48 hours after initiation of NSAIA therapy.

Oligohydramnios is often, but not always, reversible (generally within 3-6 days) following discontinuance of NSAIA therapy. Complications of prolonged oligohydramnios may include limb contracture and delayed lung maturation. A limited number of case reports have described maternal NSAIA use and neonatal renal dysfunction, in some cases irreversible, without oligohydramnios.

Some cases of neonatal renal dysfunction have required treatment with invasive procedures such as exchange transfusion or dialysis. Deaths associated with neonatal renal failure have been reported. Methodologic limitations of these postmarketing studies and case reports include lack of a control group; limited information regarding dosage, duration, and timing of drug exposure; and concomitant use of other drugs.

These limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants, and the extent to which certain reported risks can be generalized to full-term infants is uncertain. Animal data indicate that prostaglandins have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization.

In animal studies, inhibitors of prostaglandin synthesis, such as ketoprofen, were associated with increased pre- and post-implantation losses. Prostaglandins also have an important role in fetal kidney development. In animal studies, inhibitors of prostaglandin synthesis impaired kidney development at clinically relevant doses.

In animal reproduction studies in mice and rats, no teratogenic or embryotoxic effects were observed at ketoprofen dosages up to approximately 0.2 times the maximum recommended human dosage of 185 mg/m2 daily. In rabbits, maternally toxic dosages were associated with embryotoxicity but not with teratogenicity.

The effects of ketoprofen on labor and delivery in humans currently are not known, but the drug has delayed parturition in rats when administered in doses of 6 mg/kg (about 0.2 times the maximum daily recommended human dosage based on body surface area) before the onset of labor.

It is not known whether ketoprofen is distributed into human milk; 4-5% of circulating plasma concentrations of the drug are distributed into the milk of lactating dogs. In rats, perinatal development was not adversely affected in nursing offspring whose mothers received ketoprofen doses of 9 mg/kg (approximately 0.3 times the maximum daily recommended human dosage based on body surface area). The manufacturers recommend that ketoprofen not be used in nursing women.

No enhanced Geriatric Use information available for this drug.