Descrizione Clinica
Anti-inflammatory Oki pain and fever 12cpr eff Oki
OKI DOLOGY AND FEBRUARY 25 MG COMPRESSE EFFERS
active ingredients
Each tablet contains the active ingredient ketoprofen 25 mg (such as ketoprofen salt of lysine 40 mg). Excipients with known effects: This medicine contains 147 mg of sorbitol per effervescent tablet. This medicine contains 321.9 mg of sodium per effervescent tablet, equivalent to approximately 16% of the maximum daily intake recommended by the WHO which corresponds to 2 g sodium for an adult. For the full list of excipients, see paragraph 6.1.Excellent
Mannitol (E421), Sodium Hydrogenocarbonate (E500), Citric Acid (E330), Orange Aroma, Sorbitol (E420), Sodium Carbonate (E500), Leucine, Sodium Saccarin (E954), Polysorbate 20 (E432), Simeticone, Nidra colloidal Silica (E551).Therapeutic indications
OKi pain and fever is recommended in the short-term symptomatic treatment of acute pain of mild to moderate intensity and/or fever. OKi pain and fever is indicated in adults aged 18 or older.Contraindications
The medicinal product should not be used in the following cases: • In patients with a history of hypersensitivity reactions such as bronchospasm, asthma attack, acute rhinitis, hives, rashes or other allergic reactions to ketoprofene or substances with similar mechanism of action (such as acetylsalicylic acid or other NSAIDs). Severe reactions have been observed in these patients and, on rare occasions, fatal reactions (see paragraph 4.8). • In patients with hypersensitivity to any of the excipients listed in paragraph 6.1. • During the third quarter of pregnancy (see paragraph 4.6). • In case of severe heart failure. • In patients with active or recurrent peptic ulcer or hemorrhage anamnesi, ulceration or gastrointestinal perforation.• Anamnesis of hemorrhage or gastrointestinal perforation resulting in a previous therapy with NSAIDs. • In patients with gastric ulcer or duodenal, chronic dyspepsia and gastritis • In patients with leukocytopenia or thrombocytopenia, hemorrhage in place or hemorrhagic diathesis in treatment with anticoagulants • In patients with severe kidney or liver failure, such as liver cirrhosis or severe hepatitis.Population
Population| Indication | Age range | Dose | Duration |
| Syntomatic pain relief and fever | Adults aged 18 or older | 1 tablet in repeated single dose 2-3 times a day, in need. * | You need to use the minimum effective dose for as little time as possible to relieve symptoms (see paragraph 4.4). |
Conservation
Store the medicine in the original packaging, to protect it from moisture and light.Warnings
Very rare cases of serious reactions, some of which fatal, including exfoliative dermatitis, Stevens-Johnson syndrome and toxic epidermal necrolysis, were reported in association with the use of NSAIDs (see paragraph 4.8). Patients seem to be at higher risk for these reactions in the early stages of therapy: the onset of the reaction occurs in most cases within the first month of treatment. The intake of ketoprofene salt of lysine must be suspended at the first signs of rash, lesions of the mucosa or any other sign of hypersensitivity. Concurrent use of OKi pain and fever with other NSAIDs, including selective cyclooxygenase-2 inhibitors, should be avoided. Undesirable effects can be minimized with the use of the minimum effective dose for the shortest time needed to control symptoms. Excessive use of NSAIDs can cause drug-induced headaches, it is recommended for patients to stop treatment. Patients should be warned of possible withdrawal symptoms, which may include a worsening of headaches that may last several days. Seniors: in the elderly increases the frequency of adverse reactions to the NSAIDs, especially hemorrhage and gastrointestinal perforation that could be fatal (see paragraph 4.2). Hemorrhage, gastrointestinal ulceration and drilling: hemorrhage, ulceration or gastrointestinal perforation, with also fatal outcome, have been reported for all NSAIDs at any time of treatment, with or without prodromic symptoms or even in the absence of previous cases of serious events charged to the gastrointestinal tract. Some epidemiological evidence suggests that ketoprofen could be associated with a high risk of severe gastrointestinal toxicity, compared to other NSAIDs, especially at high doses (see also paragraphs 4.2 and 4.3). The risk of bleeding, ulceration or perforation of the gastrointestinal tract is greater with the increase of the dosage of NSAIDs, in patients who have manifested cases of ulcer, in particular if complicated by hemorrhage or perforation (see paragraph 4.3), and in elderly patients. These patients should start treatment with the minimum dose available. Concurrent use of gastroprotectors (e.g. misoprostol or protonic pump inhibitors) should be considered for these patients and for patients taking low dose acetylsalicylic acid or other drugs that may increase the risk of gastrointestinal events (see below and paragraph 4.5). Patients who have manifested cases of gastrointestinal toxicity, especially if elderly, should be invited to report any unusual symptoms at the abdominal level (especially gastrointestinal hemorrhage), particularly in the early stages of treatment. Precaution is required in the treatment of patients taking concomitant medicines that could increase the risk of ulceration or hemorrhage, such as oral corticosteroids, anticoagulants such as warfarin, selective serotonin reuptake inhibitors or anti-aggregants such as acetyl acid (see paragraph 4.5). Interrupt treatment in case patients treated with ketoprofen salt of lisin manifest bleeding or gastrointestinal ulceration. NSAIDs should be administered with caution in patients with a gastrointestinal disease anamnesi ( ulcerative colitis, Crohn's disease), as these conditions may worsen (see paragraph 4.8). Patients should be monitored carefully, especially for the onset of gastrointestinal hemorrhage. Clinical studies and epidemiological data suggest that the use of some NSAIDs (especially at high doses and long-term treatments) may be associated with an increase in the risk of arterial thrombotic events (e.g. myocardial infarction or stroke). There is no sufficient data available to exclude a similar risk associated with ketoprofen. As with other NSAIDs, patients with uncontrolled hypertension, confirmed ischemic cardiomyopathy, peripheral arteriopathy and/or cerebrovascular disease can be treated with ketoprofen salt of lisina only after careful evaluation. Analogue considerations must be made before starting a long-term treatment in patients with risk factors for cardiovascular events (e.g. arterial hypertension, hyperlipidemia, diabetes mellitus, smoking). At the beginning of the treatment, kidney function must be carefully monitored in patients with heart failure, cirrhosis, nephrosic syndrome or probable hypovolemia, due to the increased risk of nephrotoxicity. This applies to patients treated with diuretics (see paragraph 4.5) and for patients with kidney impairment, especially if elderly. In such patients, the use of ketoprofen could cause a reduction in blood flow to the kidneys caused by the inhibition of prostaglandins and lead to kidney failure. Ketoprofen should be given with caution in patients with impairment of kidney function, bearing in mind that the compound is excreted through the kidneys. Like all NSAIDs, ketoprofen can increase values related to azotemia and sierica creatinine. Like other prostaglandin synthesis inhibitors, ketoprofen may be associated with adverse kidney events that cause glomerulonephritis, kidney papillar necrosis, nephrosic syndrome and acute kidney failure. In patients with abnormal values of liver function or anamnesi of liver disease, it is necessary to periodically evaluate the values of transaminers, especially during long-term treatment. Rare cases of jaundice and hepatitis were reported in association with the use of ketoprofen. Attention is required when the product is given to patients with liver porphyria, as it may trigger an attack. As with other NSAIDs, in the presence of an infection, it is necessary to remember that the anti-inflammatory, analgesic and antipyretic properties of ketoprofen could conceal the symptoms commonly associated with the progression of an infection, such as fever. In case of pregnancy, fertility or breastfeeding, see paragraph 4.6. Carefully administer patients with previous allergy manifestations. Patients with asthma associated with chronic or allergic rhinitis, chronic sinusitis and/or nasal polypoxes are more subject to allergies to acetyllic acid and/or NSAIDs than the rest of the population. The administration of ketoprofen salt of lysine could cause asthma attack or bronchospasm, shock and other allergic reactions in allergic to acetylicylic acid or NSAIDs (see paragraph 4.3). Stop the treatment in case of vision problems, as blurred vision. Masking the symptoms of underlying infections: OKi pain and fever 25 mg can mask the symptoms of infection, which may delay the start of proper treatment and thus worsen the outcome of the infection. This was observed in bacterial pneumonia acquired in communities and bacterial complications of chickenpox. When OKi pain and fever 25 mg is administered for relief from fever or pain related to infection, it is recommended to monitor the infection. In non-hospital contexts, the patient should contact the doctor if symptoms persist or worsen. Warnings related to excipients: OKi pain and fever 25 mg effervescent tablets contains sorbitol; patients suffering from rare hereditary problems of fructose intolerance, glucose-galactose mal absorption or sucrasis-isomaltase deficiency should not take this medicine. This medicine contains 321.9 mg of sodium per effervescent tablet, equivalent to 16% of the maximum daily intake recommended by the WHO which corresponds to 2 g sodium for an adult. If symptoms persist or worsen or a new symptom occurs, the patient must consult a doctor.Interactions
Associations to avoid Alcol: alcohol consumed alone can cause irritation of the gastrointestinal tract, therefore, the intake of NSAIDs in conjunction with alcohol entails an increase in the risk of hemorrhage and gastrointestinal ulceration. Patients must be warned to avoid such an association. Antiagulants (such as heparin and warfarin): NSAIDs can enhance the effects of anticoagulants (see paragraph 4.4). If concurrent administration is necessary, patients must be monitored carefully due to increased hemorrhage risk. Ciclosporin: Concurrent administration of NSAIDs and cyclosporin leads to increased risk of nephrotoxicity. Dabigatran: Concurrent administration of NSAIDs and dabigatran entails a possible increase in the risk of hemorrhage.Erlotinib: Concurrent administration of NSAIDs and herlotinib involves an increase in the risk of hemorrhage. Litio: risk of increased plasma concentrations of lithium, which can reach toxic levels, due to a reduction of renal excretion of lithium. Where relevant, plasma levels of lithium must be monitored carefully and the appropriate dose during and after treatment with NSAIDs. Methotrexate, at doses greater than 15 mg/week: increased risk of haematological toxicity associated with methotrexate, particularly when administered at high doses (>15 mg/week), probably related to the displacement of methotrexate binding proteins and the reduction of renal clearance.Therefore, patients undergoing treatment with such medicinal products should consult a doctor before taking the product. Other (including selective cyclooxygenase-2 inhibitors) and high doses of salicylates (>3 g per day): increased risk of gastrointestinal ulceration and bleeding.Chinoloni: concurrent administration of NSAIDs and kinolones entails a possible increase in the risk of seizures.Venlafaxina: concomitant administration of NSAIDs and venlafaxine involves an increase in the risk of hemorrhage. Associations that require caution. Serotonin reuptake selective inhibitors and anti-aggregators (SSRI): increased risk of gastrointestinal hemorrhage (see paragraph 4.4). Antihypertensives, ACE inhibitors and antagonists of angiotensin II receptors: in patients with impairment of kidney function (e.g. dehydrated and elderly patients), concomitant administration of an ACE inhibitor or an antagonist of angiotensin II receptors and cyclooxygenase inhibitors may cause further deterioration of kidney function, including a potential acute kidney failure. Therefore, these associations must be administered with caution, especially in the elderly. Patients should be properly hydrated and renal function monitoring should be taken into consideration once the concomitant therapy has begun. NSAIDs can antagonize the effects of lowering arterial pressure of antihypertensive therapy. Baclofene: NSAIDs can reduce the excretion of baclofen (increasing the risk of toxicity). Heart glycosides: NSAIDs can increase the plasma concentration of heart glycosides, with possible exacerbation of heart failure and reduction of kidney function. Corticosteroids: increased risk of gastrointestinal ulceration or hemorrhage (see paragraph 4.4). Cumarisks: NSAIDs can intensify the anticoagulant effect of cumarinics. Fenitoine and sulfonamides: since ketoprofen has a strong connection with proteins, it may be necessary to reduce the dose of phenytoin or sulfonamides given during treatment. Diuretics: patients taking diuretics and among them, severely dehydrated ones, are more at risk of developing kidney failure depending on the reduction of kidney blood flow caused by the inhibition of prostaglandins. These patients must be rehydrated before starting concurrent administration and it is necessary to carefully monitor the kidney function (see paragraph 4.4) after the start of treatment. NSAIDs can reduce the effect of diuretics. Gemeprost: reduction of the effectiveness of gemeprost. Mortgage (continued): nSAIDs can intensify the effects of sulfaniluree through the smoothing of the bond to plasma proteins. Metotrexate at doses less than 15 mg/week: increase in hematological toxicity of metotrexate due to the reduction of its kidney clearance with the NSAIDs in general. In the first weeks of concurrent use, full weekly hemochromocytometric monitoring is required. Monitoring should be carried out more frequently in the presence of an alteration of renal functionality and older subjects. Mifepristone: theoretically, a reduction in the effectiveness of this contraceptive drug can be seen due to the antiprostaglandinic properties of the NSAIDs, including aspirin (acetylsalicylic acid). Limited evidence suggests that the concomitant use of NSAIDs on the day of administration of prostaglandins does not adversely affect the effects of mifepristone or prostaglandins on cervical maturation or uterine contractility and does not reduce the clinical effectiveness of the pharmacological interruption of pregnancy. Pentoxyphylline: increased risk of hemorrhage. It is necessary to increase the frequency of clinical checks and monitoring of bleeding time. Penicillamine: Concurrent administration of NSAIDs and penicillamines entails a possible increase in the risk of nephrotoxicity. Pemetrex: NSAIDs can reduce renal excretion of pemetrexed. Prasugrel: Concurrent administration of NSAIDs and prasugrel involves a possible increase in the risk of hemorrhage. Anti-platelet aggregates (ticlopidine and clopidogrel): increased risk of hemorrhage due to the inhibition of pyastrinic function and damage to gastrointestinal mucosa (see paragraph 4.4). If concurrent administration cannot be avoided, the patient must be monitored carefully. Probenecid: concurrent administration of probenecid can significantly reduce plasma clearance of ketoprofen and, consequently, plasma concentrations of ketoprofen could be increased. The interaction could be due to the inhibition of renal tubular secretion and glucuronoconjugation and requires the adjustment of the dose of ketoprofen. Tacrolimus: Concurrent administration of NSAIDs and tacrolimus leads to increased risk of nephrotoxicity. Zidovudina: the concomitant administration of NSAIDs and zidovudine causes an increase in the risk of hematological toxicity due to the effects of reticulocytes, resulting in severe anemia that arises a week after the start of treatment with NSAIDs. The hemochromocytometric framework and the reticle count must be monitored for one or two weeks from the start of treatment with the NSAID. Ritonavir: plasma concentrations of NSAIDs can be increased by ritonavir.Effects
Gastrointestinal: the most commonly observed adverse events are gastrointestinal. Peptic ulcers, perforation or gastrointestinal hemorrhage may occur, even fatal, especially in the elderly (see paragraph 4.4). After administration, nausea, vomiting, diarrhea, flatulence, constipation, dyspepsia, abdominal pain, melena, ematemesis, ulcerative stomatitis, exacerbation of colitis and Crohn's disease (see paragraph 4.4). Gastritis was detected with less frequency. In very rare cases, hypersensitivity can be manifested in the form of serious systemic reactions (laryngeal edema, glottis edema, dispnea, palpitations, Stevens-Johnson syndrome) until anaphylactic shock. In such cases immediate medical care is required.| Classification for systems and organs MedDRA | Very common (≥1/10) | Common (≥1/100, | Not common (≥1/1.000, | Rare (≥1/10.000, | Very rare ( | Frequency not known |
| Emolinfopoietic system pathologies | Hemorrhagic anemia | Trombocytopenia, agranulocytosis, medullary insufficiency and hypoplasia | ||||
| Immune system disorders | Anaphylactic reaction (including shock), hypersensitivity | |||||
| Psychiatric disorders | Noise altered | |||||
| Diseases of the nervous system | Cephalea, vertigo, drowsiness | Opinion | Convulsive crisis, disgeusia | |||
| Pathologies of the eye | Unused vision | |||||
| Ear and labyrinth pathologies | Tinnitus | |||||
| Heart disease | Heart failure | |||||
| Vascular diseases | Hypertension, vasodilation | |||||
| Respiratory, chest and mediastinic pathologies | Asthma | Broncospasm (especially in patients with acetylsalicylic acid and other NSAIDs), rhinitis | ||||
| Gastrointestinal diseases | Dispepsia, nausea, abdominal pain, vomiting | Stipsi, diarrhea, flatulence and gastritis | Stomatitis, peptic ulcer | Exacerbation of colitis and Crohn's disease, hemorrhage and gastrointestinal perforation, mouth ulceration, melena, hematemesis, drilling and duodenal ulcer | ||
| Hepatobiliary diseases | Hepatitis | |||||
| Pathologies of skin and subcutaneous tissue | rash, itching | Reaction of photosensitivity, alopecia, hives, angioedema, bollose skin reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis, edema and hexantema | ||||
| Kidney and urinary pathologies | Acute renal insufficiency, piping-interstitial nephritis, nephritic syndrome | |||||
| Systemic pathologies and conditions for administration | Tiredness, edema | |||||
| Diagnostic examinations | Increased weight, increased transaminasis and high concentrations of serum bilirubin due to liver disorders | Abnormal kidney function test |
Overdosing
Synonyms Overdose cases were reported with doses of up to 2.5 g ketoprofen. In most cases, observed symptoms were limited to letargy, drowsiness, abdominal pain, nausea, vomiting, generally reversible with support therapies. Following strong overdose of ketoprofen, respiratory depression, coma or seizures occurred. In addition, gastrointestinal hemorrhage, hypotension, hypertension or acute kidney failure may occur, but these are rare events. Treatment measures There are no specific antidotes for overdosing ketoprofene salt of lysine. In case of suspect overdose, the recommended treatment consists of gastric lavender associated with the administration of a symptomatic and support treatment to compensate for dehydration, monitoring urinary excretion and correction of acidosis, if present. In case of kidney failure, hemodialysis may be useful for eliminating the medicinal product in circulation.Pregnancy
: The inhibition of prostaglandin synthesis can adversely affect pregnancy and/or embryo-fetal development. Results of epidemiological studies suggest an increase in the risk of abortion and heart and gastroschisis, after the use of an inhibitor of prostaglandin synthesis in the early stages of pregnancy. The absolute risk of cardiovascular malformations increased from less than 1%, up to about 1.5%. It is believed that the risk increases proportionally to the dose and duration of therapy. It has been shown that in animals the administration of an inhibitor of the synthesis of prostaglandine causes an increase of pre- and post-system losses and embryo-fetal lethal. In addition, there was an increase in the incidence of various malformations, including cardiovascular malformations, in animals which had been given an inhibitor of prostaglandin synthesis during the organogenetic period. In the first and second trimester of pregnancy, ketoprofen salt of lysine should not be administered, if not in cases strictly necessary. If ketoprofen salt is used by a woman during conception or during the first and second trimester of pregnancy, the dose must be kept as low as possible for the duration of treatment as short as possible. During the third trimester of pregnancy, all prostaglandin synthesis inhibitors can expose • fetus to: • cardiopulmonary toxicity (with premature closure of arterial duct and pulmonary hypertension); • kidney dysfunction, which can progress in kidney failure with oligo-idroamnios; • the mother and the newborn, at the end of pregnancy, to: • possible prolongation of bleeding time, an anti-aggregating effect that can occur even at very low doses; • inhibition of uterine contractions resulting in delay or extension of labor. The use of ketoprofen during labor can adversely affect the pulmonary hemodynamics of the fetus with serious consequences on breathing. As a result ketoprofene salt of lysine is contraindicated in the third trimester of pregnancy.Food
: There are no sufficient data on the excretion of ketoprofene in breast milk. Ketoprofene salt of lysine is not recommended in nursing women.Fertility
: The long-term use of some NSAIDs is associated with a reduction in female fertility, reversible with the interruption of treatment. The use of ketoprofen, as of any inhibitor drug of cyclooxygenase/prostaglandine synthesis, could compromise fertility and is not recommended in women seeking pregnancy. It must be considered the suspension of treatment with ketoprofen in women who have difficulty in conception or who are subject to infertility assessments.Source: Farmadati
