Mypaid 200mg / 250mg Capsules

MYPAID is indicated in adults and children over 12 years for the relief of headache from musculoskeletal origin, fever, muscular, menstrual and dental pain.

Posology
Adults and children over 12 years: Two capsules every four hours, but not more than six capsules in twenty-four hours. Capsules are to be taken with food or after meals with sufficient water. Consult your doctor if no relief is obtained with the recommended dosage. Use the lowest effective dose for the shortest possible duration of treatment. DO NOT EXCEED THE RECOMMENDED DOSE
Paediatric population
Not recommended for use in children under twelve years of age.
Method of administration:
Oral administration only.

• hypersensitivity to ibuprofen, paracetamol or to any of the excipients listed in section 6.1
• patients with uncontrolled asthma or bronchospasm,
• bleeding disorders,
• cardiovascular disease,
• heart failure,
• history of gastrointestinal perforation, ulceration, or bleeding (PUBs) related to previous NSAIDs, including MYPAID. The risk of gastrointestinal perforation, ulceration or bleeding (PUBs) is higher with increasing doses of MYPAID in patients with a history of ulcers, and the elderly. When gastrointestinal bleeding or ulceration occurs in patients receiving MYPAID, treatment with MYPAID should be stopped.
• renal failure,
• severe liver function impairment.
• patients receiving coumarin anticoagulants.
• pregnant or breastfeeding women: do not use NSAIDs in women around 30 weeks gestation and later in pregnancy due to the risks of oligohydramnios / foetal renal dysfunction and premature closure of the foetal ductus arteriosus.
• patients who have previously shown hypersensitivity reactions (e.g. asthma, rhinitis, angioedema, or urticaria) in response to aspirin or other non-steroidal anti-inflammatory medicines.
• nasal polyps associated with aspirin-induced bronchospasm.

• Dosages in excess of those recommended may cause severe liver damage.
• Consult a doctor if no relief is obtained from the recommended dosage.
• Do not use for more than ten days without consulting a doctor.
• MYPAID should be given with care to the elderly. Patients with congestive heart failure, cirrhosis, diuretic-induced volume depletion, or renal insufficiency require local synthesis of vasodilating prostaglandins to maintain renal perfusion and therefore these patients are at greater risk of developing renal dysfunction due to NSAID-induced inhibition of renal prostaglandin synthesis.
• MYPAID should be discontinued in patients who experience blurred or diminished vision or changes in colour vision.
• Patients with collagen disease may be at increased risk of developing aseptic meningitis.
• Caution is required in patients with a history of hypertension as fluid retention and oedema have been reported in association with MYPAID therapy. In view of the MYPAIDu2019s inherent potential to cause fluid retention, heart failure may be precipitated in some compromised patients.
• This product contains paracetamol which may be fatal in overdose. In the event of overdosage or suspected overdose and notwithstanding the fact that the person may be asymptomatic, the nearest doctor, hospital or Poison Centre must be contacted immediately.
• Caution should be advised in patients receiving concomitant medications which could increase the risk of ulceration or bleeding, such as oral corticosteroids, selective serotonin-reuptake inhibitors or anti-platelet medicines such as aspirin (see section 4.5).
• MYPAID should be given with caution to patients with a history of gastrointestinal disease (e.g. ulcerative colitis, Crohnu2019s disease, hiatus hernia, gastro-oesophageal reflux disease, angiodysplasia) as the condition may be exacerbated.
• Serious skin reactions, some of them fatal, including exfoliative dermatitis, Stevens-Johnson syndrome (SJS), and toxic epidermal necrolysis have been reported. MYPAID should be discontinued at the first appearance of skin rash, mucosal lesions, or any other sign of hypersensitivity.
• Foetal Toxicity: Limit use of NSAIDs, including MYPAID, between 20 to 30 weeks of pregnancy due to the risk of oligohydramnios/foetal renal dysfunction. Avoid use of MYPAID in women around 30 weeks gestation and later in pregnancy due to the risks of oligohydramnios/foetal renal dysfunction and premature closure of the foetal ductus arteriosus. If NSAIDs treatment is prescribed between 20 weeks and 30 weeks gestation, limit MYPAID use to the lowest effective dose and shortest duration possible. Consider ultrasound monitoring of amniotic fluid if MYPAID treatment extends beyond 48 hours. Discontinue MYPAID if oligohydramnios occurs and follow up according to clinical practice.
• The antipyretic, analgesic and anti-inflammatory action of ibuprofen may mask symptoms of the occurrence or worsening of infection. This has been observed in bacterial community acquired pneumonia and bacterial complications to varicella. When MYPAID is administered for fever or pain relief in relation to infection, monitoring of infection is advised. In non-hospital settings, the patient should consult a doctor if symptoms persist or worsen.
• Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) has been reported in patients taking NSAIDs such as MYPAID. Some of these events have been fatal or life-threatening. DRESS typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling. Other clinical manifestations may include hepatitis, nephritis, haematological abnormalities, myocarditis, or myositis. Sometimes symptoms of DRESS may resemble an acute viral infection. Eosinophilia is often present. Because this disorder is variable in its presentation, other organ systems not noted here may be involved. It is important to note that early manifestations of hypersensitivity, such as fever or lymphadenopathy, may be present even though rash is not evident. If such signs or symptoms are present, discontinue MYPAID and evaluate the patient immediately.
• Severe cutaneous adverse reactions (SCARs) such as toxic epidermal necrolysis (TEN), Stevens-Johnson syndrome (SJS), acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS)/ Drug-induced hypersensitivity syndrome (DIHS) and fixed drug Eruptions (FDE) have been reported in patients treated with paracetamol containing medicines. If a patient develops SCAR, treatment with MYPAID must immediately be discontinued and appropriate treatment instituted (see Section 4.8).
• Severe hypokalaemia and renal tubular acidosis have been reported due to prolonged use of ibuprofen at higher than recommended doses. Ibuprofen induced renal tubular acidosis should be considered in patients with unexplained hypokalaemia and metabolic acidosis associated with non-steroidal anti-inflammatory medicine (NSAID) usage.
• This medicine contains less than 1 mmol sodium (23mg) per dosage unit, that is to say essentially u2018sodium-freeu2019.

Interactions with other medicines

• NSAIDs: use of two or more NSAIDs concomitantly could result in an increase in side effects.
• Anti-coagulants: MYPAID may enhance the effects of anti-coagulants such as warfarin.
• Anti-platelet medicines and selective serotonin reuptake inhibitors (SSRIs): increased risk of gastrointestinal bleeding.
• Aspirin: Concomitant administration of MYPAID and aspirin is not generally recommended due to the increased adverse effects.
• Antihypertensives or diuretics: MYPAID may reduce the antihypertensive effect of ACE inhibitors, beta-blockers and diuretics, and may cause natriuresis and hyperkalaemia. Diuretics can increase the risk of nephrotoxicity of NSAIDs.
• Alcohol, corticosteroids, clopidogrel, ticlopidine, bisphosphonates, oxpentifylline may increase the risk of gastrointestinal perforation, bleeding and ulceration (PUBs) (see section 4.4).
• Cardiac glycosides: MYPAID may exacerbate cardiac failure, reduce GFR and increase plasma glycoside levels.
• Lithium: MYPAID may increase the steady-state concentration of lithium.
• Methotrexate: MYPAID may increase and prolong the methotrexate plasma concentration and increase risk of methotrexate toxicity.
• Nephrotoxic medicines e.g. ciclosporin, tacrolimus may increase the risk of nephrotoxicity further.
• Quinolones antibiotics: Animal data indicate that NSAIDs can increase the risk of convulsions associated with quinolone antibiotics. Patients taking MYPAID and quinolones may have an increased risk of developing convulsions.
• Mifepristone: MYPAID should not be used for 8 to 12 days after mifepristone administration as NSAIDs can reduce the effect of mifepristone.
• Phenytoin: MYPAID may enhance the effects of phenytoin.
• Sulphonylurea antidiabetics: NSAIDs may enhance the effects of sulphonylurea antidiabetics.
• Bone marrow depressants: The leucopenic and/or thrombocytopenic effects of these medicines may be increased.
• Hepatotoxic medicines (zidovudine, co-trimoxazole, isoniazid, tuberculosis medicines): Hepatotoxic substances may increase the possibility of paracetamol accumulation and overdose. The risk of hepatotoxicity of paracetamol may be increased by medicines which induce liver microsomal enzymes such as anticonvulsants and alcohol.
• Metoclopramide and domperidone: Absorption of paracetamol may be accelerated.
• Cholestyramine: Absorption of paracetamol is reduced if given within one hour of cholestyramine.
• Probenecid: MYPAID excretion may be affected, and plasma concentrations altered.
• Medicines which decrease gastric emptying: paracetamol absorption is decreased by substances that decrease gastric emptying, e.g. propantheline, antidepressants with anticholinergic properties, and narcotic analgesics.
• Chloramphenicol: paracetamol may increase chloramphenicol plasma concentrations.
• Moclobemide: The effects of NSAIDs might be enhanced by use with moclobemide.

Interactions with laboratory tests
Diabetic patients may experience false results with blood glucose tests.

Pregnancy
MYPAID is not recommended for use by pregnant or breastfeeding women (see section 4.3). Use of NSAIDs, including MYPAID, can cause premature closure of the foetal ductus arteriosus and foetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, the use of MYPAID duration between 20 and 30 weeks of gestation should be limited and avoided at dose and around 30 weeks of gestation and later in pregnancy.
Fertility
The use of MYPAID may impair female fertility and is not recommended in women attempting to conceive. In women who have difficulties conceiving or who are undergoing investigation of infertility, withdrawal of MYPAID should be considered.

MYPAID may impair the ability to drive and use machinery. No studies on the effect of ability to drive or use machines have been performed. Undesirable effects such as dizziness, fatigue and visual disturbances are possible after taking NSAIDs. If affected, patients should not drive or operate machinery.

System Organ Class Frequency Undesirable effect
Infections and infestations Less frequent Aseptic meningitis (especially in patients with existing autoimmune disorders, such as systemic lupus erythematosus and mixed connective tissue disease) with symptoms of stiff neck, headache, nausea, vomiting, fever or disorientation (see section 4.4).
Blood and lymphatic system disorders Less frequent Blood disorders e.g., neutropenia, leucopoenia, pancytopenia, agranulocytosis, thrombocytopenia, haematopoietic disorders (anaemia, haemolytic anaemia, aplastic anaemia), bleeding episodes (e.g. epistaxis, menorrhagia).
Immune system disorders Less frequent Hypersensitivity reactions including skin rashes, urticaria and pruritus as well as asthmatic attacks. Severe hypersensitivity reactions where symptoms can include facial, tongue and larynx swelling, dyspnoea, tachycardia, hypotension up to life-threatening shock, serum sickness, lupus erythematosus syndrome, Henoch-Schu00f6nlein vasculitis, angioedema Unknown Drug-induced hypersensitivity syndrome (DIHS) [Hypersensitivity reactions characterised by urticaria, dyspnoea, and hypotension] (see Section 4.4).
Metabolic and nutrition disorders Less frequent Gynaecomastia, hypoglycaemic reaction Unknown Pyroglutamic aciduria (5-oxoprolinuria), high-anion gap metabolic acidosis, Hypokalaemia*
Psychiatric disorders Frequent Nervousness Less frequent depression, confusion, emotional lability, hallucinations, dream abnormalities.
Nervous system disorders Frequent dizziness, headache Less frequent paraesthesia, drowsiness, insomnia, somnolence, paradoxical stimulation, optic neuritis, psychomotor impairment, extrapyramidal effects, tremor, convulsions.
Eye disorders Less frequent Visual impairment, blurred vision, other ocular reactions.
Ear and labyrinth disorders Less frequent Tinnitus, vertigo.
Cardiac disorders Less frequent Oedema, cardiac failure, angina pectoris, cardiac dysrhythmias, palpitations.
Vascular disorders Less frequent hypertension.
Respiratory, thoracic and mediastinal disorder Less frequent Asthma, bronchospasm, dyspnoea, wheezing, thickened respiratory tract secretions.
Gastrointestinal disorders Frequent Dyspepsia, nausea, vomiting, diarrhoea, abdominal cramps and pain, bloating, constipation, ulcerative stomatitis, exacerbation of colitis, Crohn's disease (see section 4.4), gastritis, peptic ulceration, gastrointestinal bleeding and perforation with symptoms of melaena haematemesis sometimes fatal, particularly in the elderly. Less frequent pancreatitis, flatulence, decreased appetite.
Hepatobiliary disorders Less frequent Abnormalities of liver function tests, hepatic damage, particularly in long-term therapy, acute hepatitis, jaundice.
Skin and subcutaneous tissue disorders Less frequent Skin rash, pruritus, sensitivity reactions resulting in reversible skin rash usually erythematous or urticarial, but sometimes more serious and may be accompanied by fever and mucosal lesions), exfoliative dermatoses and bullous reaction including Stevens-Johnson syndrome and toxic epidermal necrolysis. Unknown Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS syndrome). Acute Generalised Exanthematous Pustulosis (AGEP), Fixed drug eruptions (FDE) (see Section 4.4)
Renal and urinary disorders Less frequent Impairment of renal function, nephrotic syndrome; interstitial nephritis that may be accompanied by acute renal insufficiency; renal tissue damage (papillary necrosis) with increased serum urea, haematuria, proteinuria, urinary retention, acute reversible renal failure, renal colic Unknown Renal tubular acidosis*
Post-marketing experience: The following side effects have been reported, and frequencies are unknown: Fixed drug eruptions (FDE) and drug-induced hypersensitivity syndrome (DIHS) (see Section 4.4). *Renal tubular acidosis and hypokalaemia have been reported in the post-marketing setting typically following prolonged use of the ibuprofen component at higher than recommended doses
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicine is important. It allows continued monitoring of the benefit/risk balance of the medicine. Healthcare providers are requested to report any suspected Adverse drug reactions to SAHPRA via the Med Safety APP (Medsafety X SAHPRA) and eReporting platform (who-umc.org) found on SAHPRA website. Adverse Drug Reactions may also be reported to Adcock Ingram Limited using the following email: [email protected]

The most likely symptoms of overdosage are nausea, vomiting, and tinnitus. Treatment is symptomatic and supportive. Prolonged use at higher than recommended doses may result in severe hypokalaemia and renal tubular acidosis. Symptoms may include reduced level of consciousness and generalised weakness (see section 4.4 and section 4.8). Prompt treatment is essential. In the event of an overdosage, consult a doctor immediately, or take the person to a hospital directly. A delay in starting treatment may mean that antidote is given too late to be effective. Evidence of liver damage is often delayed until after the time for effective treatment has lapsed. Susceptibility to paracetamol toxicity is increased in patients who have taken repeated high doses (greater than 5 -10 g/day) of paracetamol for several days, in chronic alcoholism, chronic liver disease, AIDS, malnutrition, and with the use of drugs that induce liver microsomal oxidation such as barbiturates, isoniazid, rifampicin, phenytoin and carbamazepine. Symptoms of paracetamol overdosage in the first 24 hours include pallor, nausea, vomiting, anorexia and possibly abdominal pain. Mild symptoms during the first two days of acute poisoning do not reflect the potential seriousness of the overdosage. Liver damage may become apparent 12 to 48 hours, or later after ingestion, initially by elevation of the serum transaminase and lactic dehydrogenase activity, increased serum bilirubin concentration and prolongation of the prothrombin time. Liver damage may lead to encephalopathy, coma and death. Acute renal failure with acute tubular necrosis may develop even in the absence of severe liver damage. Abnormalities of glucose metabolism and metabolic acidosis may occur. Cardiac arrhythmias have been reported. Treatment for paracetamol overdosage: N-acetylcysteine should be administered to all cases of suspected overdose as soon as possible preferably within eight hours of overdosage, although treatment up to 36 hours after ingestion may still be of benefit, especially if more than 150 mg/kg of paracetamol was taken. An initial dose of 150 mg/kg N-acetylcysteine in 200 ml given intravenously over 15 minutes, followed by an infusion of 50 mg/kg in 500 ml dextrose injection over the next four hours, and then 100 mg/kg in 1000 ml dextrose injection over the next sixteen hours. The volume of intravenous fluid should be modified for children. Although the oral formulation is not the treatment of choice, 140 mg/kg dissolved in water may be administered initially, followed by 70 mg/kg every four hours for seventeen doses. A plasma paracetamol level should be determined four hours after ingestion in all cases of suspected overdosage. Levels done before four hours, unless high, may be misleading. Patients at risk of liver damage, and hence requiring continued treatment with N-acetylcysteine, can be identified according to their 4-hour plasma paracetamol level. The plasma paracetamol level can be plotted against time since ingestion in the nomogram below. Reference: Martindale: The Complete Drug Reference. Those whose plasma paracetamol levels are above the u201cnormal treatment lineu201d, should continue N-acetylcysteine treatment with 100 mg/kg IV over 16 hours repeatedly until recovery. Patients with increased susceptibility to liver damage as identified above, should continue treatment if concentrations are above the u201chigh risk treatment lineu201d. Prothrombin index correlates best with survival. Monitor all patients with significant ingestions for at least ninety-six hours.