SARIDON 20CPR

SARIDON COMPRESITION

active ingredients

One tablet contains: 250 mg paracetamol, propifenazone 150 mg, caffeine 25 mg. For the full list of excipients, see paragraph 6.1.

Excellent

Cellulose microgranular, povidone, corn starch, ipromellosa, talc, magnesium stearate, silica precipitate.

Therapeutic indications

Syntomatic treatment of acute painful states (headache; toothache; neuralgies; menstrual pains) and fever states.

Contraindications

- Hypersensitivity to active ingredients, to other substances closely related to chemical and/or any of the excipients. - History of gastrointestinal hemorrhage or perforation related to previous active treatments or history of hemorrhage/recurring peptic ulcer (two or more separate episodes of proven ulceration or bleeding). - Hemopaths such as granulocytopenia and intermittent porphyries. - Paracetamol-based products are contraindicated in patients with manifest insufficiency of glucose-6-phosphate dehydrogenase and those with severe haemolytic anemia. - Severe liver failure (Child-Pugh >9). - Severe kidney failure - severe heart failure. - For caffeine, the product should not be given to children under 12 years of age. - Pregnancy and nursing.

Population

Adults: 1-2 tablets, up to 4 tablets in 24 hours, with a plentiful sip of water. Do not exceed the recommended doses: especially older patients should comply with the above minimum dosages. Intake of oral analgesic preparations must take place on a full stomach. Do not take for more than 3 consecutive days without consulting your doctor.

Conservation

Do not store at temperature above 30°C

Warnings

Do not take for more than 3 consecutive days without consulting your doctor. High or prolonged doses of the product may result in a high-risk hepatopathy and even severe blood pressure alterations. During the administration of therapeutic doses of paracetamol an increase in serum aminotransferase (ALT) may occur. Moderate intake of alcohol in conjunction with taking paracetamol may increase the risk of liver toxicity. Carefully administer in subjects with kidney or liver failure (Child-Pugh Gastrointestinal Risks The use of Saridon must be avoided in conjunction with NSAIDs, including selective COX-2 inhibitors. Senior patients have an increase in the frequency of adverse reactions to NSAIDs, especially for gastrointestinal bleeding and perforations, which may be fatal (see paragraph 4.2). Gastrointestinal hemorrhage, ulceration and drilling: during treatment with all NSAIDs, at any time, with or without warning symptoms or previous history of serious gastrointestinal events, gastrointestinal hemorrhage, ulceration and perforation, which may be fatal. In the elderly and patients with ulcer history, especially if complicated by hemorrhage or perforation (see paragraph 4.3), the risk of gastrointestinal hemorrhage, ulceration or perforation is higher with higher doses of NSAID. These patients must begin treatment with the lowest dose available. Concurrent use of protective agents (misoprostol or protonic pump inhibitors) must be taken into account for these patients and also for patients taking low doses of acetylsalicylic acid or other drugs that may increase the risk of gastrointestinal events (see below and paragraph 4.5). Patients with history of gastrointestinal toxicity, especially elderly, must report any unusual gastrointestinal symptoms (especially gastrointestinal hemorrhage) in particular in the early stages of treatment. Caute should be lent in patients taking concomitant medications that could increase the risk of ulceration or hemorrhage, such as oral corticosteroids, anticoagulants such as warfarin, selective serotonin reuptake inhibitors or anti-aggregating agents such as acetyl acid (see paragraph 4.5). When bleeding or gastrointestinal ulceration occurs in patients taking Saridon, treatment must be suspended. NSAIDs should be given with caution in patients with a history of gastrointestinal disease ( ulcerative colitis, Crohn's disease) since such conditions can be exacerbated (see paragraph 4.8). The use of Saridon must be carefully monitored by a doctor in case of gastric or duodenal ulcers. Cardiovascular and cerebrovascular effects Clinical studies and epidemiological data suggest that the use of some NSAIDs (especially high doses and long-term treatments) may be associated with a modest increase in the risk of arterial thrombotic events (e.g. myocardial infarction or stroke). Cautela is required before starting treatment in patients with positive anamnesis for hypertension and/or heart failure, as retention of fluid, hypertension and edema was found in association with NSAIDs. It is recommended caution if the paracetamol is administered in conjunction with flucloxacillin due to increased risk of metabolic acidosis with high anionic gap (HAGMA), in particular in patients with severe renal impairment, sepsis, malnutrition and other sources of glutathione deficiency (e.g. chronic alcoholism), as well as in those using the daily maximum doses of paracetamine. Careful monitoring is recommended, including the measurement of 5-oxoproline urinary.

Interactions

Drugs that slow gastric emptying (e.g. propantelin), can reduce the absorption rate of the paracetamol by delaying the therapeutic effect. Corticosteroids: increased risk of gastrointestinal ulceration or bleeding (see paragraph 4.4). Antiagulants: NSAIDs can increase the effects of anticoagulants, such as warfarin (see paragraph 4.4). Serotonin reuptake selective agents and inhibitors (SSRIs): increased risk of gastrointestinal hemorrhage (see paragraph 4.4). Diuretics, ACE inhibitors and antagonists of angiotensin II: NSAIDs can reduce the effect of diuretics and other antihypertensive drugs. In some patients with impaired kidney function (e.g. dehydrated patients or elderly patients with impaired kidney function) co-administration of an inhibitor ACE or an angiotensin II antagonist and agents inhibiting the cyclo-oxidase system may lead to further deterioration of kidney function, which includes a possible acute kidney failure, generally reversible. These interactions must be considered in patients taking Saridon in conjunction with ACE inhibitors or antagonists of angiotensin II. Therefore, the combination should be given with caution, especially in elderly patients. Patients should be properly hydrated and monitoring the kidney function should be taken into consideration after the start of the concomitant therapy. The product can interact with alcohol; in case of alcohol abuse the intake of paracetamol, even at low dosages, can cause liver damage. The product can interact with some hypoglycemics (acetoesamide, chlorpropamide, tolbutamide). The probenecid causes the reduction of paracetamol clearance of at least 2 times through the inhibition of its conjugation with glucuronic acid. In case of concomitant treatment with probenecid, a reduction in the dose of paracetamol should be considered. Metoclopramide and domperidone (metoclopramide accelerating gastric emptiness) can speed up the absorption rate of the paracetamol, while cholesteramine can slow its speed and absorption. Concurrent cloramfenicle administration can lead to an extension of the half-life of the paracetamol, with the risk of increasing its toxicity. It is not recommended to use the product if the patient is in treatment with other anti-inflammatory drugs. Use with extreme caution and under strict control during chronic treatment with drugs that can determine the induction of hepatic mono-oxygenases or in case of exposure to substances that may have such an effect (e.g. phenytoin, rifampin, cimetidine, antiepileptics such as glutetimide, phenobarbital, carbamazepine). Paracetamol administration may interfere with the determination of urine (by the method of phosphotungstic acid) and glycemia (by the method of glucose-oxidase-peroxidase). Concurrent use of paracetamol and AZT (zidovudine) increases the tendency to a reduction in the leukocytes count (neutropenia). The product, therefore, should not be taken in association with AZT (zidovudine) except on prescription. The simultaneous administration of NSAIDs or opioids leads to a mutual strengthening of the analgesic effect. Paracetamol can reduce the effectiveness of lamotrigine. Paracetamol (or its metabolites) interferes with enzymes involved in the synthesis of coagulation factors dependent on vitamin K. The interaction between paracetamol and warfarin or cumarinic derivatives can cause an increase in the normalized international relationship and an increase in the risk of bleeding. Patients in treatment with oral anticoagulants should not take paracetamol for long periods without medical control. The tropisetron and granisetron, antagonists of serotonin receptors 5-HT3, can completely inhibit the analgesic effect of paracetamol through pharmacodynamic interaction. Be careful when paracetamol is used in conjunction with flucloxacillin since concurrent intake was associated with metabolic acidosis with high anionic gap, especially in patients with risk factors (see paragraph 4.4).

Effects

The adverse reactions listed below derive from spontaneous signalling and there is therefore no organization for frequency categories. Pathologies of skin and subcutaneous tissue: Skin reactions of various types and severity have been reported, including rash, itching, urticaria, allergic edema and angioedema, generalized acute exantelosis, fixed erythema, multiform erythema, including bollose reactions Stevens-Johnson syndrome and toxic epidermal necrolysis (very rarely and with possible fatal outcome). Immune system disorders: Hypersensitivity reactions such as dispnea, sweating, nausea, hypotension, asthma, larynx edema, anaphylactoid reaction, anaphylactic reaction, anaphylactic shock have been reported. Emolinfopoietic system pathologies: Alterations of blood corpusculate elements count, such as thrombocytopenia, thrombocytopenic purple, leukopenia, anemia, agranulocytosis, pancitopenia. Diseases of the nervous system: Capogiri, drowsiness. Hepatobiliary diseases: Comprogation of liver, hepatitis, dose-dependent liver failure, potentially fatal liver necrosis (see paragraphs 4.4 and 4.9). Kidney and urinary pathologies: Acute renal insufficiency, interstitial nephritis, hematuria, anuria. Gastrointestinal diseases: The most commonly observed adverse events are gastrointestinal. Severe adverse events such as peptic ulcers, perforation or gastrointestinal hemorrhage (sometimes fatal, especially in the elderly can occur in association with the use of non-steroidal anti-inflammatory drugs (see paragraph 4.4). After administration of Saridon were reported: nausea, vomiting, diarrhea, flatulence, constipation, dyspepsia, abdominal pain, melena, hematemesis, ulcerative stomatitis, exacerbation of colitis and Crohn's disease (see paragraph 4.4). Less frequently gastritis were observed. Thoracic and median pathologies: Broncospasm and asthma, including asthmatic analgesic syndrome. In association with the treatment with the NSAIDs were reported edema, hypertension and heart failure. Clinical studies and epidemiological data suggest that the use of some NSAIDs (especially high doses and long-term treatments) may be associated with a modest increase in the risk of arterial thrombotic events (e.g. myocardial infarction or stroke) (see paragraph 4.4). Reporting of suspicious adverse reactions The reporting of suspicious adverse reactions that occur after the authorization of the medicinal product is important, as it allows continuous monitoring of the benefit/risk ratio of the medicinal product. Healthcare workers are required to report any suspected adverse reaction through the national reporting system, http://www.agenziafarmaco.gov.it/it/responsabili.

Overdosing

In case of overdose, contact a doctor or anti-veleni center immediately. Early medical intervention is important for both adults and children even if there are no obvious signs or symptoms. Acute toxicity The acute intoxication from paracetamol has been associated with hepatocellular toxicity, caused by the binding of paracetamol metabolites to liver cell proteins. At therapeutic doses these metabolites are related to glutathione and form non-toxic conjugates. In case of high overdose, the supply of SH-donatori liver (which promote the formation of glutathione) is exhausted, toxic metabolites accumulate and occurs necrosis of liver cells, resulting in liver failure which can lead progressively to liver coma. Acute kidney damage with acute tubular necrosis (see Intoxication Symptoms). The threshold of paracetamol overdose can be reduced in patients taking certain types of drugs or alcohol, or are seriously malnutrited. Chronic toxicity Chronic toxicity includes liver alterations of various types (see Intoxication Symptoms). Chronic toxicity data and paracetamol nephrotoxicity are controversial. It must be paid attention to the possible influence on the peripheral cell count. Symptoms of Intoxication The onset of acute poisoning by paracetamol is characterized by nausea, vomiting, abdominal pain, sweating and general malaise. The patient’s condition can improve after 24-48 hours, although symptoms may not disappear completely. For the presence of caffeine, always for high doses, hyperstimulation with excitement, insomnia, muscle tremor, nausea, vomiting, increased diuresis, tachycardia, extrasistolia. The size of the liver increases rapidly, transaminasis and bilirubin are high, protrombine time becomes pathological, urinary flow is reduced, a slight azotemia could develop. Hypokaliemia and metabolic acidosis can also be developed (including lactic acidosis) for acute and/or chronic overdose. Frequent clinical events after 3-5 days are jaundice, fever, liver, hemorrhagic diathesis, hypoglycemia, and liver damage. The liver damage can evolve in all stages of liver encephalopathy, brain edema and death. Acute kidney damage with acute tubular necrosis, strongly suggested by lumbar pain, hematuria and proteinuria in the absence of severe liver damage. Treatment of overdose Intensive medical therapy with close monitoring of vital signs, laboratory parameters and circulatory conditions. The gastric lavender is useful within the first 6 hours. Hemodialysis and hemoperfusion promote the elimination of the substance. It is recommended to control the plasma concentration of paracetamol. In case of suspected paracetamol poisoning, within 10 hours of ingestion, it is useful to administer groups-SH sources, which combine reactive metabolites and accelerate detoxification. N-acetylcysteine can have a certain protective effect up to 48 hours from ingestion.

Pregnancy Inhibition of prostaglandin synthesis can negatively affect pregnancy and/or embryo-fetal development. The results of epidemiological studies suggest an increased risk of abortion, heart malformation and gastroschisis after the use of an inhibitor of prostaglandin synthesis in the early stages of pregnancy. The absolute risk of heart failure increased from less than 1% to about 1.5%. It has been considered that the risk increases with dose and duration of therapy. In animals, the administration of prostaglandin synthesis inhibitors has shown to cause an increase in the loss of pre- and post-system and embryo-fetal mortality. In addition, an increase in the incidence of various malformations, including cardiovascular disease, was reported in the animals to which inhibitions of prostaglandin synthesis were given during the organogenetic period. During the third trimester of pregnancy, all prostaglandin synthesis inhibitors can expose the 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 and anti-aggregating effect that can occur even at very low doses; - inhibition of uterine contractions resulting in delay or extension of labor. We do not recommend the use of Saridon in case of alleged pregnancy. Nursing: The medicinal product is contraindicated in breastfeeding.

Source: Farmadati