Nurofen Plus, film-coated tablets, 12 pcs.
Avoid simultaneous use of the drug with the following drugs:
Acetylsalicylic acid: with the exception of low doses of acetylsalicylic acid (no more than 75 mg/day) prescribed by a doctor, since combined use may increase the risk of side effects. When administered simultaneously, ibuprofen reduces the anti-inflammatory and antiplatelet effect of acetylsalicylic acid (an increase in the incidence of acute coronary insufficiency in patients receiving small doses of acetylsalicylic acid as an antiplatelet agent is possible after starting ibuprofen).
Other NSAIDs, in particular selective COX-2 inhibitors: the simultaneous use of two or more drugs from the NSAID group should be avoided due to a possible increased risk of side effects.
Prescribe with caution simultaneously with the following drugs
Anticoagulants: NSAIDs may enhance the effect of anticoagulants, in particular warfarin.
Antihypertensives (ACE inhibitors and angiotensin II antagonists) and diuretics: NSAIDs may reduce the effectiveness of drugs in these groups. In some patients with impaired renal function (for example, dehydrated patients or elderly patients with impaired renal function), co-administration of ACE inhibitors or angiotensin II antagonists and COX-inhibiting agents may lead to deterioration of renal function, including the development of acute renal failure (usually reversible). These interactions should be considered in patients taking coxibs concomitantly with ACE inhibitors or angiotensin II antagonists. In this regard, the combined use of the above drugs should be prescribed with caution, especially in elderly people.
Patients should be prevented from dehydration and consideration should be given to monitoring renal function upon initiation of this combination treatment and periodically thereafter. Diuretics and ACE inhibitors may increase the nephrotoxicity of NSAIDs.
GCS: increased risk of gastrointestinal ulcers and gastrointestinal bleeding.
Antiplatelet agents and SSRIs: increased risk of gastrointestinal bleeding.
Cardiac glycosides: simultaneous administration of NSAIDs and cardiac glycosides can lead to worsening heart failure, a decrease in GFR and an increase in the concentration of cardiac glycosides in the blood plasma.
Lithium preparations: there is evidence of the likelihood of an increase in the concentration of lithium in the blood plasma during the use of NSAIDs.
Methotrexate: there is evidence of the likelihood of an increase in the concentration of methotrexate in the blood plasma during the use of NSAIDs.
Cyclosporine: increased risk of nephrotoxicity when NSAIDs are administered concomitantly with cyclosporine.
Mifepristone: NSAIDs should be started no earlier than 8 to 12 days after taking mifepristone as NSAIDs may reduce the effectiveness of mifepristone.
Tacrolimus: When NSAIDs and tacrolimus are coadministered, the risk of nephrotoxicity may increase.
Zidovudine: Concomitant use of NSAIDs and zidovudine may result in increased hematotoxicity. There is evidence of an increased risk of hemarthrosis and hematomas in HIV-positive patients with hemophilia who received concomitant treatment with zidovudine and ibuprofen.
Quinolone antibiotics: In patients receiving concomitant treatment with NSAIDs and quinolone antibiotics, the risk of seizures may be increased.
Myelotoxic drugs: enhance the manifestations of hematotoxicity of the drug.
Caffeine enhances the analgesic effect.
MAO inhibitors: When using codeine in patients receiving therapy with MAO inhibitors or who have received it within the previous two weeks, CNS depression or worsening of the clinical picture may occur.
Moclobemide: risk of developing hypertensive crisis.
Hydroxyzine: Concomitant use of hydroxyzine (anxiolytic) and codeine can lead to increased analgesic effects, as well as greater CNS depression, increased sedative and antihypertensive effects.
CNS depressants (sedatives): The sedative effect of codeine is enhanced by substances that depress the central nervous system, such as alcohol, anesthetics, hypnotics, sedatives, tricyclic antidepressants and antipsychotic drugs and phenothiazines.
Diuretics and antihypertensive agents: The antihypertensive effects of diuretics and antihypertensive agents may be enhanced when used concomitantly with opioid pain relievers.
Antidiarrheals and motility suppressants: Concomitant use of codeine and antidiarrheals and motility suppressants, such as loperamide and kaolin, may increase the risk of severe constipation.
Antimuscarinics: Concomitant use of antimuscarinics or drugs with muscarinic effects, such as atropine and some antidepressants, may increase the risk of severe constipation, which in turn may lead to severe paralytic ileus and/or urinary retention.
Muscle relaxants: The respiratory depression effects caused by muscle relaxants may be additive to the major respiratory depression effects associated with opioid analgesics.
Quinidine: May inhibit the analgesic effect of codeine.
Mexiletine: Codeine may delay the absorption of mexiletine, and thereby reduce the antiarrhythmic effect of the latter.
Metoclopramide, cisapride and domperidone: Codeine may suppress the gastrointestinal effects of metoclopramide, cisapride and domperidone.
Cimetidine: Cimetidine inhibits the metabolism of opioid painkillers, resulting in increased plasma concentrations.
Naloxone: Naloxone inhibits the analgesic, CNS, and respiratory depressant effects of opioid pain medications.
Naltrexone also blocks the therapeutic effects of opioids.
Impact on laboratory test results: Opioid painkillers affect the results of a number of laboratory tests, including determination of plasma concentrations of amylase, lipase, bilirubin, alkaline phosphatase, LDH, ALT and AST.
Opioids may also interfere with examinations because they slow gastric emptying, and hepatobiliary imaging using disophenine, a technetium Tc 99m opioid, may cause contraction of the sphincter of Oddi and increased bile duct pressure.
Nurofen® Plus
When using Nurofen® Plus for 2-3 days, practically no side effects are observed. In case of long-term use, the following side effects may occur:
From the gastrointestinal tract:
Nausea, vomiting, heartburn, anorexia, pain and discomfort in the epigastrium, diarrhea, flatulence, possible erosive and ulcerative lesions of the gastrointestinal tract (in some cases complicated by perforation and bleeding), abdominal pain, irritation, dryness of the oral mucosa or pain in the mouth, ulceration of the gum mucosa, aphthous stomatitis, pancreatitis, constipation, hepatitis.
From the nervous system:
Headache, dizziness, insomnia, agitation, drowsiness, depression, confusion, hallucinations, aseptic meningitis (more often in patients with autoimmune diseases).
From the cardiovascular system:
Heart failure, increased blood pressure (BP), tachycardia.
From the urinary system:
Nephrotic syndrome (edema), acute renal failure, allergic nephritis, polyuria, cystitis.
From the hematopoietic organs:
Anemia (including hemolytic, aplastic), thrombocytopenia and thrombocytopenic purpura, agranulocytosis, leukopenia.
From the senses:
Hearing loss, ringing or tinnitus, reversible toxic optic neuritis, blurred vision or diplopia, dry and irritated eyes, swelling of the conjunctiva and eyelids (allergic origin), scotoma.
Allergic reactions:
Skin rash, itching, urticaria, Quincke's edema, anaphylactoid reactions, anaphylactic shock, fever, erythema multiforme exudative (including Stevens-Johnson syndrome), toxic epidermal necrolysis (Lyell's syndrome), eosinophilia, allergic rhinitis.
From the respiratory system:
Bronchospasm, shortness of breath, respiratory failure, suppression of the cough center.
Other: increased sweating.
With long-term use in large doses - ulceration of the mucous membrane of the gastrointestinal tract, bleeding (gastrointestinal, gingival, uterine, hemorrhoidal), visual impairment (impaired color vision, scotoma, amblyopia).
Regular use of codeine leads to the development of dependence, as well as agitation and irritability when the drug is discontinued.
If side effects occur, you should stop taking the drug and consult a doctor.
Nurofen® plus (Nurofen plus)
Concomitant use of Nurofen Plus with acetylsalicylic acid and other NSAIDs is not recommended.
When administered simultaneously, ibuprofen reduces the anti-inflammatory and antiplatelet effect of acetylsalicylic acid (an increase in the incidence of acute coronary insufficiency may occur after starting ibuprofen in patients receiving small doses of acetylsalicylic acid as an antiplatelet agent).
When used simultaneously with anticoagulants and thrombolytic drugs (alteplase, streptokinase, urokinase), the risk of bleeding increases.
When used together with ibuprofen, cefamandole, cefoperazone, cefotetan, valproic acid, and plicamycin increase the incidence of hypoprothrombinemia.
When used together, cyclosporine and gold preparations enhance the effect of ibuprofen on prostaglandin synthesis in the kidneys, which leads to an increased nephrotoxic effect.
Ibuprofen increases the plasma concentration of cyclosporine and the likelihood of developing its hepatotoxic effects.
Drugs that block tubular secretion, when used simultaneously, reduce the excretion and increase the plasma concentration of ibuprofen.
When used together, inducers of microsomal oxidation (phenytoin, ethanol, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants) increase the production of hydroxylated active metabolites, increasing the risk of developing severe intoxications.
Inhibitors of microsomal oxidation reduce the risk of developing hepatotoxic effects of ibuprofen.
When used together, ibuprofen reduces the hypotensive activity of vasodilators, the natriuretic effect of furosemide and hydrochlorothiazide.
Ibuprofen reduces the effectiveness of uricosuric drugs and enhances the effect of indirect anticoagulants, antiplatelet agents, and fibrinolytics.
Increases the side effects of mineralocorticoids, corticosteroids, estrogens, ethanol.
When used together, it increases the hypoglycemic effect of oral antidiabetic agents (sulfonylurea derivatives) and insulin.
When taken simultaneously, antacids and cholestyramine reduce the absorption of ibuprofen.
When used together, ibuprofen increases the blood concentration of digoxin, lithium, and methotrexate.
Caffeine enhances the analgesic effect of ibuprofen.
Nurofen tablet 200 mg x20
Trade name: Nurofen International name: Ibuprofen
Release form: film-coated tablets 200 mg (blisters)
Ingredients: ibuprofen 200 mg
Pharmacological group: NSAID (non-steroidal anti-inflammatory drug)
Pharmacological group according to ATK: M01AE01 (Ibuprofen)
Pharmacological action: antiplatelet, antipyretic, NSAID, anti-inflammatory, analgesic,
Indications: Inflammatory and degenerative diseases of the musculoskeletal system: rheumatoid, juvenile chronic, psoriatic arthritis, osteochondrosis, neuralgic amyotrophy (Personage-Turner disease), arthritis with SLE (as part of complex therapy), gouty arthritis (in case of an acute attack of gout, fast-acting medications are preferred forms), ankylosing spondylitis (ankylosing spondylosis). Pain syndrome: myalgia, arthralgia, ossalgia, arthritis, sciatica, migraine, headache (including menstrual syndrome) and toothache, cancer, neuralgia, tendinitis, tendovaginitis, bursitis, neuralgic amyotrophy (Personage-Turner disease) , post-traumatic and postoperative pain syndrome, accompanied by inflammation. Algodismenorrhea, inflammatory process in the pelvis, incl. adnexitis, childbirth (as an analgesic and tocolytic agent). Feverish syndrome with “colds” and infectious diseases.
Dosage regimen: Inside, after meals. Adults: for osteoarthritis, psoriatic arthritis and ankylosing spondylitis - 400-600 mg 3-4 times a day. For rheumatoid arthritis - 800 mg 3 times a day, for soft tissue injuries, sprains - 1.6-2.4 g / day in several doses. For algodismenorrhea - 400 mg 3-4 times a day, for moderate pain syndrome - 1.2 g / day. For children over 12 years of age, the initial dose is 150-300 mg 3 times a day, the maximum dose is 1 g, then 100 mg 3 times a day, for juvenile rheumatoid arthritis - 30-40 mg/kg/day in several doses. To reduce body temperature 39.2 degrees C and above - 10 mg/kg/day, below 39.2 degrees C - 5 mg/kg/day. Oral suspension - 5-10 mg/kg 3 times a day: children aged 6-12 months (only as prescribed by a doctor) - an average of 50 mg 3-4 times a day, 1-3 years - 100 mg 3 times per day, 4-6 years - 150 mg 3 times a day, 7-9 years - 200 mg 3 times a day, 10-12 years - 300 mg 3 times a day. For febrile syndrome after immunization - 50 mg, if necessary, after 6 hours, repeat administration at the same dose, maximum daily dose - 100 mg.
Contraindications: Hypersensitivity, erosive and ulcerative diseases of the gastrointestinal tract (including peptic ulcer of the stomach and duodenum in the acute stage, ulcerative colitis, peptic ulcer, Crohn's disease - nonspecific ulcerative colitis), "aspirin" asthma, blood clotting disorders (including hemophilia, prolongation of bleeding time, bleeding tendency, hemorrhagic diathesis), pregnancy, lactation.
Side effects: From the digestive system: NSAID gastropathy (nausea, vomiting, abdominal pain, heartburn, loss of appetite, diarrhea, flatulence, pain and discomfort in the epigastric region), ulceration of the gastrointestinal mucosa (in some cases complicated by perforation and bleeding) , irritation, dryness of the oral mucosa or pain in the mouth, ulceration of the gum mucosa, aphthous stomatitis, pancreatitis, constipation, hepatitis. From the respiratory system: shortness of breath, bronchospasm. From the senses: hearing loss, ringing or noise in the ears, reversible toxic optic neuritis, blurred vision or diplopia, dryness and irritation of the eyes, swelling of the conjunctiva and eyelids (allergic origin), scotoma. From the nervous system: headache, dizziness, insomnia, anxiety, nervousness and irritability, psychomotor agitation, drowsiness, depression, confusion, hallucinations, rarely - aseptic meningitis (more often in patients with autoimmune diseases). From the cardiovascular system: development or worsening of heart failure, tachycardia, increased blood pressure. From the urinary system: acute renal failure, allergic nephritis, nephrotic syndrome (edema), polyuria, cystitis. Allergic reactions: skin rash (usually erythematous, urticaria), skin itching, angioedema, anaphylactoid reactions, anaphylactic shock, bronchospasm, fever, erythema multiforme exudative (including Stevens-Johnson syndrome), toxic epidermal necrolysis (Lyell's syndrome) , eosinophilia, allergic rhinitis. From the hematopoietic organs: anemia (including hemolytic, aplastic), thrombocytopenia and thrombocytopenic purpura, agranulocytosis, leukopenia. Other: increased sweating. The risk of developing ulcerations of the gastrointestinal mucosa, bleeding (gastrointestinal, gingival, uterine, hemorrhoidal), visual impairment (impaired color vision, scotoma, amblyopia) increases with long-term use in large doses. Overdose. Symptoms: abdominal pain, nausea, vomiting, lethargy, drowsiness, depression, headache, tinnitus, metabolic acidosis, coma, acute renal failure, decreased blood pressure, bradycardia, tachycardia, atrial fibrillation, respiratory arrest. Treatment: gastric lavage (only within an hour after administration), activated charcoal, alkaline drinking, forced diuresis, symptomatic therapy (correction of CBS, blood pressure).
Pharmacodynamics: NSAIDs have analgesic, antipyretic and anti-inflammatory effects due to non-selective blockade of COX1 and COX2 and have an inhibitory effect on Pg synthesis. The analgesic effect is most pronounced for inflammatory pain. Like all NSAIDs, ibuprofen exhibits antiplatelet activity.
Pharmacokinetics: Well absorbed from the gastrointestinal tract. Absorption is slightly reduced when taking the drug after meals. TCmax when taken on an empty stomach - 45 minutes, when taken after meals - 1.5-2.5 hours, in synovial fluid - 2-3 hours (where it creates higher concentrations than in plasma). 90% bound to plasma proteins. Subject to presystemic and postsystemic metabolism in the liver. After absorption, approximately 60% of the pharmacologically inactive R form of ibuprofen is slowly transformed into the active S form. The CYP2C9 isoenzyme takes part in the metabolism of the drug. It has two-phase elimination kinetics with T1/2 2-2.5 hours (for retard forms - up to 12 hours). It is excreted by the kidneys (no more than 1% unchanged) and, to a lesser extent, with bile.
Special instructions: During treatment, monitoring of the peripheral blood picture and the functional state of the liver and kidneys is necessary. When symptoms of gastropathy appear, careful monitoring is indicated, including esophagogastroduodenoscopy, a blood test to determine Hb, hematocrit, and a stool test for occult blood. To prevent the development of NSAID gastropathy, it is recommended to combine it with PgE drugs (misoprostol). If it is necessary to determine 17-ketosteroids, the drug should be discontinued 48 hours before the study. Patients should refrain from all activities that require increased attention, rapid mental and motor reactions. During the treatment period, ethanol intake is not recommended. Carefully. Cirrhosis of the liver with portal hypertension, hyperbilirubinemia, peptic ulcer of the stomach and duodenum (history), gastritis, enteritis, colitis, liver and/or renal failure, nephrotic syndrome, CHF, arterial hypertension, blood diseases of unknown etiology (leukopenia and anemia ), children's age (for tablet forms - up to 12 years, 6 months - for oral suspension). Children 6-12 months are prescribed only on the recommendation of a doctor.
Interaction: Inducers of microsomal oxidation (phenytoin, ethanol, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants) increase the production of hydroxylated active metabolites, increasing the risk of severe hepatotoxic reactions. Microsomal oxidation inhibitors reduce the risk of hepatotoxicity. Reduces the hypotensive activity of vasodilators (including BMCC and ACE inhibitors), natriuretic and diuretic activity - furosemide and hydrochlorothiazide. Reduces the effectiveness of uricosuric drugs, enhances the effect of indirect anticoagulants, antiplatelet agents, fibrinolytics (increasing the risk of hemorrhagic complications), ulcerogenic effect with bleeding of MCS and GCS, colchicine, estrogens, ethanol, enhances the effect of oral hypoglycemic drugs and insulin. Antacids and cholestyramine reduce the absorption of ibuprofen. Increases the blood concentration of digoxin, Li+ drugs and methotrexate. Caffeine enhances the analgesic effect. When administered simultaneously, ibuprofen reduces the anti-inflammatory and antiplatelet effects of ASA (an increase in the incidence of acute coronary insufficiency in patients receiving small doses of ASA as an antiplatelet agent is possible after starting ibuprofen). When prescribed with anticoagulant and thrombolytic drugs (alteplase, streptokinase, urokinase), the risk of bleeding simultaneously increases. Cefamandole, cefaperazone, cefotetan, valproic acid, plicamycin increase the incidence of hypoprothrombinemia. Myelotoxic drugs increase the manifestations of hematotoxicity of the drug. Cyclosporine and Au preparations enhance the effect of ibuprofen on Pg synthesis in the kidneys, which is manifested by increased nephrotoxicity. Ibuprofen increases the plasma concentration of cyclosporine and the likelihood of developing its hepatotoxic effects. Drugs that block tubular secretion reduce excretion and increase plasma concentrations of ibuprofen.
Dispensed from pharmacies: Dispensed by prescription.
Drug registration number: P No. 013012/01
Date of registration (re-registration) of the drug: December 29, 2006
