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Aspen

3016 Lake Drive, Citywest Business Campus, Dublin 24, Ireland
Telephone: 003531 630 8400
Medical Information Direct Line: 0080000404142 - Freephone
Medical Information e-mail: aspenmedinfo@professionalinformation.co.uk


Summary of Product Characteristics last updated on medicines.ie: 14/11/2017
SPC Septrin Forte 160mg/800mg Tablets


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1. NAME OF THE MEDICINAL PRODUCT

Septrin Forte 160 mg/800 mg Tablets


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2. QUALITATIVE AND QUANTITATIVE COMPOSITION

Each tablet contains 160 mg trimethoprim and 800 mg sulfamethoxazole.

For the full list of excipients, see section 6.1.


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3. PHARMACEUTICAL FORM

Tablet

White, biconvex, elongated tablets, scored along the shorter axis and coded S3 on one side.

The scoreline is only to facilitate breaking for ease of swallowing and not to divide into equal doses.


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4. CLINICAL PARTICULARS

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4.1 Therapeutic indications

Co-trimoxazole should only be used where, in the judgement of the physician, the benefit of treatment outweighs any possible risks, and where there is good reason to prefer the combination to a single antimicrobial agent.

Urinary tract infections: For simple urinary tract infections, trimethoprim alone or another single antimicrobial agent is the preferred treatment. Since trimethoprim is also as efficacious as co-trimoxazole for the prophylaxis of recurrent urinary tract infections, co-trimoxazole is not indicated for prophylactic use.

Respiratory tract infections: Co-trimoxazole may be used as second line therapy in chronic obstructive airways disease or other respiratory tract infections, including acute otitis media where sensitivity has been demonstrated or is highly probable. (Septrin is not indicated for prophylactic or prolonged administration in otitis media).

Treatment and prevention of Pneumocystis carinii pneumonia (see 4.2 Posology and Method of Administration and 4.8 Undesirable Effects).

Co-trimoxazole may be used in the management of other serious conditions such as nocardiasis, toxoplasmosis and brucellosis.

(See Section 5.1, Pharmacodynamic properties for further information).


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4.2 Posology and method of administration

Adults and Children over 12 years of age: One tablet every 12 hours.

Pneumocystis carinii pneumonitis: The dosage required for the treatment of Pneumocystis carinni pneumomtis is generally higher than that recommended for other conditions. A dosage of 20 mg trimethoprim/kg bodyweight/day plus 100 mg sulfamethoxazole/kg bodyweight/day, given in equally divided doses every six hours for 14 days is suggested.

For this reason, treatment should be undertaken only if facilities for regular monitoring of plasma concentrations of the sulfamethoxazole component are available.

Elderly: If there is renal impairment in the elderly patients then the dosage recommendations given for patients with renal impairment apply. Since elderly patients are more susceptible to blood dyscrasias and adverse reactions in general, caution is recommended when treating these patients.

Patients with impaired renal function:

Creatinine Clearance (ml/min)

Recommended Dosage

> 30

Usual dosage

15 to 30

Half the standard dosage

<15

Not recommended


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4.3 Contraindications

Septrin should not be given to patients with a history of hypersensitivity to sulphonamides, trimethoprim or co- trimoxazole or any excipients of the presentations.

Contra-indication in patients with severe renal insufficiency where repeated measurements monitoring of plasma drug concentration cannot be performed.

Use in patients with severe impairment of liver function. Use in patients with existent or severe blood dyscrasias.

Use in patients with glucose-6-phosphate dehydrogenase deficiency.

Septrin should not be given to premature babies nor to full-term infants during the first 6 weeks of life.


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4.4 Special warnings and precautions for use

Life threatening adverse reaction

Fatalities, although very rare, have occurred due to severe reactions including Stevens-Johnson syndrome, toxic epidermal necrolysis, fulminant hepatic necrosis, agranulocytosis, aplastic anaemia, other blood dyscrasias and hypersensitivity of the respiratory tract.

Life-threatening cutaneous reactions Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) have been reported with the use of Septrin. Patients should be advised of the signs and symptoms and monitored closely for skin reactions. The highest risk for occurrence of SJS or TEN is within the first weeks of treatment. If symptoms or signs of SJS or TEN (e.g. progressive skin rash often with blisters or mucosal lesions) are present, Septrin treatment should be discontinued (see section 4.8).

The best results in managing SJS and TEN come from early diagnosis and immediate discontinuation of any suspect drug. Early withdrawal is associated with a better prognosis. If the patient has developed SJS or TEN with the use of Septrin, Septrin must not be re-started in this patient at any time.

Elderly patients

Particular care is always advisable when treating elderly patients because, as a group, they are more susceptible to adverse reactions and more likely to suffer serious effects as a result particularly when complicating conditions exist, e.g. impaired kidney and/or liver function and/or concomitant use of other drugs.

Patients with renal impairment

For patients with known renal impairment special measures should be adopted (see section 4.2).

Urinary output

An adequate urinary output should be maintained at all times. Evidence of crystalluria in vivo is rare, although sulphonamide crystals have been noted in cooled urine from treated patients. In patients suffering from hypoalbuminaemia the risk may be increased.

Folate

Regular monthly blood counts are advisable when Septrin is given for long periods, or to folate deficient patients or to the elderly, since there exists a possibility of asymptomatic changes in haematological laboratory indices due to lack of available folate. Supplementation with folinic acid may be considered during treatment but this should be initiated with caution due to possible interference with antimicrobial efficacy (see section 4.5).

Patients with glucose-6-phosphate dehydrogenase deficiency

In glucose-6-phosphate dehydrogenase deficient (G-6-PD) patients, haemolysis may occur.

Patients with severe atopy or bronchial asthma

Septrin should be given with caution to patients with severe atopy or bronchial asthma.

Treatment of streptococcal pharyngitis due to Group A beta-haemolytic streptococci

Septrin should not be used in the treatment of streptococcal pharyngitis due to Group A β-haemolytic streptococci, eradication of these organisms from the oropharynx is less effective than with penicillin.

Phenylalanine metabolism

Trimethoprim has been noted to impair phenylalanine metabolism but this is of no significance in phenylketonuric patients on appropriate dietary restriction.

Patients with or at risk of porphyria

The administration of Septrin to patients known or suspected to be at risk of porphyria should be avoided. Both trimethoprim and sulphonamides (although not specially sulfamethoxazole) have been associated with clinical exacerbation of porphyria.

Patients with hyperkalaemia and hyponatraemia

Close monitoring of serum potassium and sodium is warranted in patients at risk of hyperkalaemia and hyponatraemia.

Patients with serious haematological disorders

Except under careful supervision Septrin should not be given to patients with serious haematological disorders (see section 4.8). Septrin has been given to patients receiving cytotoxic therapy with little or no additional effect on the bone marrow or peripheral blood.


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4.5 Interaction with other medicinal products and other forms of interaction

Diuretics (thiazides): in elderly patients concurrently receiving diuretics, mainly thiazides, there appears to be an increased risk of thrombocytopenia.

Pyrimethamine: occasional reports suggest that patients receiving pyrimethamine at doses in excess of 25mg weekly may develop megaloblastic anaemia should co-trimoxazole be prescribed concurrently.

Zidovudine: in some situations, concomitant treatment with zidovudine may increase the risk of haematological adverse reactions to co-trimoxazole. If concomitant treatment is necessary, consideration should be given to monitoring of haematological parameters.

Lamivudine: administration of trimethoprim/ sulfamethoxazole 160 mg/800 mg (co-trimoxazole) causes a 40% increase in lamivudine exposure because of the trimethoprim component. Lamivudine has no effect on the pharmacokinetics of trimethoprim or sulfamethoxazole.

Warfarin: co-trimoxazole has been shown to poteniate the anticoagulant activity of warfarin via stereo selective inhibition of its metabolism.

Sulfamethoxazole may displace warfarin from plasma-albumin protein-binding sites in vitro. Careful control of the anticoagulant therapy during treatment with Septrin is advisable.

Phenytoin: co-trimoxazole prolongs the half-life of phenytoin and if co-administered the prescriber should be alert for excessive phenytoin effects. Close monitoring of the patients conditions and serum phenytoin levels is advisable.

Interaction with sulphonylurea hypoglycaemic agents is uncommon but potentiation has been reported.

Rifampicin: concurrent use of rifampicin and Septrin results in a shortening of the plasma half-life of trimethoprim after a period of about one week. This is not thought to be of clinical significance.

Cyclosporin: reversible deterioration in renal function has been observed in patients treated with co-trimoxazole and cyclosporin following renal transplantation.

When trimethoprim is administered simultaneously with drugs that form cautions at physiological pH, and are also partly excreted by active renal secretion (e. g. procainamide, amantadine), there is the possibility of competitive inhibition of this process which may lead to an increase in plasma concentration of one or both of the drugs.

Digoxin: concomitant use of trimethoprim with digoxin has been shown to increase plasma digoxin levels in a proportion of elderly patients.

Hyperkalaemia: caution should be exercised in patients taking any other drugs that can cause hyperkalaemia.

Azathioprine: There are conflicting clinical reports of interactions, resulting in serious haematological abnormalities, between azathioprine and co-trimoxazole.

Methotrexate: co-trimoxazole may increase the free plasma levels of methotrexate.

If Septrin is considered appropriate therapy in patients receiving other anti-folate drugs such as methotrexate, a folate supplement should be considered (see section 4.4).

Repaglinide: trimethoprim may increase the exposure of repaglinide which may result in hypoglycaemia.

Folinic acid: folinic acid supplementation has been shown to interfere with the antimicrobial efficacy of trimethoprim-sulfamethoxazole. This has been observed in Pneumocystis jiroveci pneumonia prophylaxis and treatment.

Contraceptives: oral contraceptive failures have been reported with antibiotics. The mechanism of this effect has not been elucidated. Women on treatment with antibiotics should temporarily use a barrier method in addition to the oral contraceptive, or choose another method of contraception.

Laboratory tests interactions:

Trimethoprim interferes with assays for serum methotrexate when dihydrofolate reductase from Lactobacillus casei is used in the assay.

No interference occurs if methotrexate is measured by radio-immune assay.

Trimethoprim may interfere with the estimation of serum/plasma creatinine when alkaline picrate reaction is used. This may result in overestimation of serum/plasma creatinine of the order of 10%.

Functional inhibition of the renal tubular secretion of creatinine may produce a spurious fall in the estimated rate of creatinine clearance.


4.6 Fertility, pregnancy and lactation

Trimethoprim and sulfamethoxazole cross the placenta and their safety in human pregnancy has not been established. Trimethoprim is a folate antagonist and, in animal studies, both agents established have been shown to cause foetal abnormalities (see section 5.3, Preclinical safety Data). Case-control studies have shown that there may be an association between exposure to folate antagonists and birth defects in humans. Therefore co-trimoxazole should be avoided in pregnancy, particularly in the first trimester, unless the potential benefit to the mother outweighs the potential risk to the foetus; folate supplementation should be considered if co-trimoxazole is used in pregnancy.

Sulfamethoxazole competes with bilirubin for binding to plasma albumin. As significant maternally derived drug levels persist for several days in the newborn, there may be a risk of precipitating or exacerbating neonatal hyperbilrubinaemia, with an associated theoretical risk of kernicterus, when septrin is administered to the mother near the time of delivery. This theoretical risk is particularly relevant in infants at increased risk of hyperbilirubinaemia, such as those who are preterm and those with glucose-6-phosphate dehydrogenase deficiency.

Trimethoprim and sulfamethoxazole are excreted in breast milk. Administration of co trimoxazole should be avoided in late pregnancy and in lactating mothers where the mother or infant has, or is at particular risk of developing, hyperbilirubinaemia. Additionally, administration of co-trimoxazole should be avoided in infants younger than eight weeks in view of the predisposition of young infants to hyperbilirubinaemia.


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4.7 Effects on ability to drive and use machines

No specific studies have been performed.


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4.8 Undesirable effects

As Septrin contains trimethoprim and a sulphonamide the type and frequency of adverse reactions associated with such compounds are expected to be consistent with extensive historical experience.

Data from large published clinical trials were used to determine the frequency of very common to rare adverse events. Very rare adverse events were primarily determined from post-marketing experience data and therefore refer to reporting rate rather than a "true" frequency. In addition, adverse events may vary in their incidence depending on the indication.

The following convention has been used for the classification of adverse events in terms of frequency:-

Very common ≥1/10,

Common ≥1/100 and <1/10,

Uncommon ≥1/1000 and <1/100,

Rare ≥1/10,000 and <1/1000,

Very rare <1/10,000.

Infections and infestations

Common:

Monilial overgrowth

Blood and lymphatic system disorders

Very rare:

Leucopenia, neutropenia, thrombocytopenia, agranulocytosis, megaloblastic anaemia, aplastic anaemia, haemolytic anaemia, methaemoglobinaemia, eosinophilia, purpura, haemolysis in certain susceptible G-6-PD deficient patients

Immune system disorders

Very rare:

Serum sickness, anaphylaxis, allergic myocarditis, angioedema, drug fever, allergic vasculitis resembling Henoch-Schoenlein purpura, periarteritis nodosa, systemic lupus erythematosus

Metabolism and nutrition disorders

Very common:

Hyperkalaemia

Very rare:

Hypoglycaemia, hyponatraemia, anorexia

Psychiatric disorders

Very rare:

Depression, hallucinations

Nervous system disorders

Common:

Headache

Very rare:

Aseptic meningitis, convulsions, peripheral neuritis, ataxia, vertigo, tinnitus, dizziness

Aseptic meningitis was rapidly reversible on withdrawal of the drug, but recurred in a number of cases on re-exposure to either Septrin or to trimethoprim alone.

Respiratory, thoracic and mediastinal disorders

Very rare:

Cough, shortness or breath, pulmonary infiltrates

Cough, shortness of breath and pulmonary infiltrates may be early indicators of respiratory hypersensitivity which, while very rare, has been fatal.

Gastrointestinal disorders

Common:

Nausea, diarrhoea

Uncommon:

Vomiting

Very rare:

Glossitis, stomatitis, pseudomembranous colitis, pancreatitis

Eye disorders

Very rare:

Uveitis

Hepatobiliary disorders

Very rare:

Cholestatic jaundice, hepatic necrosis Cholestatic jaundice and hepatic necrosis may be fatal.

Oral:

Very rare:

elevation of serum transaminases, elevation of bilirubin levels

Skin and subcutaneous tissue disorders

Common:

Skin rashes

Very rare:

Photosensitivity, exfoliative dermatitis, fixed drug eruption, erythema multiforme, Severe cutaneous adverse reactions (SCARs): Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) have been reported (see section 4.4).

Musculoskeletal and connective tissue disorders

Very rare:

Arthralgia, myalgia

Renal and urinary disorders

Very rare:

Impaired renal function (sometimes reported as renal failure), interstitial nephritis

Effects associated with Pneumocystis jiroveci (P.cairnii) pneumonitis (PJP) management

Very rare:

Severe hypersensitivity reactions, rash, fever, neutropenia, thrombocytopenia, raised liver enzymes, rhabdomyolysis

At the high dosages used for PJP management severe hypersensitivity reactions have been reported, necessitating cessation of therapy. If signs of bone marrow depression occur, the patient should be given calcium folinate supplementation (5-10 mg/day). Severe hypersensitivity reactions have been reported in PJP patients on re-exposure to trimethoprim-sulfamethoxazole, sometimes after a dosage interval of a few days. Rhabdomyolysis has been reported in HIV positive patients receiving Septrin for prophylaxis or treatment of PJP.

Oral:

Very rare:      Hyperkalaemia, hyponatraemia


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4.9 Overdose

Nausea, vomiting, dizziness and confusion are likely signs/symptoms of overdosage. Bone marrow depression has been reported in acute trimethoprim overdosage.

If vomiting has not occurred, induction of vomiting may be desirable.

Gastric lavage may be useful, though absorption from the gastrointestinal tract is normally very rapid and complete within approximately two hours. This may not be the case in gross overdosage. Dependent on the status of renal function, administration of fluids is recommended if urine output is low.

Both trimethoprim and active sulfamethoxazole are moderately dialysable by haemodialysis. Peritoneal dialysis is not effective.


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5. PHARMACOLOGICAL PROPERTIES

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5.1 Pharmacodynamic properties

Pharmacotherapeutic Group: ANTIBACTERIALS FOR SYSTEMIC USE – SULFONAMIDES AND TRIMETHOPRIM Combinations of sulphonamides and trimethoprim, incl. derivatives, ATC Code: J01EE0l

Mechanism of action

Sulfamethoxazole competitively inhibits the utilisation of para-aminobenzoic acid in the synthesis of dihydrofolate by the bacterial cell resulting in bacteriostasis. Trimethoprim reversibly inhibits bacterial dihydrofolate reductase (DHFR), an enzyme active in the folate metabolic pathway converting dihydrofolate to tetrahydrofolate. Depending on the conditions the effects may be bactericidal. Thus trimethoprim and sulfamethoxazole block two consecutive steps in the biosynthesis of purines and therefore nucleic acids essential to many bacteria. This action produces marked potentiation of activity in vitro between the two agents.

Trimethoprim binds to plasmodial DHFR but less tightly than to the bacterial enzyme. Its affinity for mammalian DHFR is some 50,000 times less for the corresponding bacterial enzyme.

Resistance

In vitro studies have shown that bacterial resistance can develop more slowly with both sulfamethoxazole and trimethoprim in combination that with either sulfamethoxazole or trimethoprim alone.

Resistance to sulfamethoxazole may occur by different mechanisms. Bacterial mutations cause an increase the concentration of PABA and thereby out-compete with sulfamethoxazole resulting in a reduction of the inhibitory effect on dihydropteroate synthetase enzyme. Another resistance mechanism is plasmid-mediated and results from production of an altered dihydropteroate synthetase enzyme, with reduced affinity for sulfamethoxazole compared to the wild-type enzyme.

Resistance to trimethoprim occurs through a plasmid-mediated mutation which results in production of an altered dihydrofolate reductase enzyme having a reduced affinity for trimethoprim compared to the wild-type enzyme.

Susceptibility testing breakpoints

Testing of trimethoprim sulfamethoxazole was performed using the common dilution series to assess the Minimum Inhibitory Concentration (MIC). The MIC breakpoints for resistance are those recommended by CLSI (Clinical and Laboratory Standards Institute – formerly the National Committee for Clinical Laboratory Standards (NCCLS) and EUCAST guidelines.

Pharmacodynamic effects

The majority of common pathogenic bacteria are sensitive in vitro to trimethoprim and sulfamethoxazole at concentrations well below those reached in blood, tissue fluids and urine after the administration of recommended doses. In common with other antimicrobial agents in vitro activity does not necessarily imply that clinical efficacy had been demonstrated. These organisms include:

Gram Negative:-

Brucella spp.

Citrobacter spp.

Escherichia coli (including ampicillin-resistant strains)

Haemophilus ducreyi

Haemophilus influenzae (including ampicillin-resistant strains)

Klebsiella/Enterobacter spp.

Legionella pneumophila

Morganella morganii (previously Proteus morganii)

Neisseria spp.

Proteus spp.

Providencia spp. (including previously Proteus rettgeri)

Certain Pseudomonas spp. except aeruginosa

Salmonella spp. including S. typhi and paratyphi.

Serratia marcescens.

Shingella spp.

Vibrio cholerae

Yersinia spp.

Gram positive:-

Listeria monocytogenes.

Nocardia spp.

Staohylococcus aureus.

Staphylococcus epidermidis and saprophyticus

Enterococcus faecalis.

Streptococcus pneumoni ae.

Streptococcus viridans.

Many strains of Bacteroides fragilis are sensitive. Some strains of Campylobacter fetus subsp. Jejuni and chlamydia are sensitive without evidence of synergy. Some varieties of non-tuberculous mycobacteria are sensitive to sulfamethoxazole but not trimethoprim. Mycoplasmas, Ureaplasma urealyticum, Mycobacterium tuberculosis and Treponema pallidum are insensitive.

Satisfactory sensitivity testing is achieved only with recommended media free from inhibitory substances especially thymidine and thymine.


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5.2 Pharmacokinetic properties

Absorption

After oral administration trimethoprim and sulfamethoxazole are rapidly and nearly completely absorbed. The presence of food does not appear to delay absorption. Peak levels in the blood occur between one and four hours after ingestion and the level attained is dose related. Effective levels persist in the blood for up to 24 hours after a therapeutic dose. Steady state levels in adults are reached after dosing for 2-3 days. Neither component has an appreciable effect in the concentrations achieved in the blood by the other.

Distribution

Approximately 50% of trimethoprim in the plasma is protein bound.

Tissue levels of trimethoprim are generally higher than corresponding plasma levels, the lungs and kidneys showing especially high concentrations. Trimethoprim concentrations exceed those in plasma in the case of bile, prostatic fluid and tissue, salvia, sputum and vaginal secretions. Levels in the aqueous humour, breast milk, cerebrospinal; middle ear fluid synovial fluid and tissue (interstitial) fluid are adequate for antibacterial activity.

Trimethoprim passes into amniotic fluid and foetal tissue reaching concentrations approximately those of maternal serum.

Approximately 66% of sulfamethoxazole in the plasma is protein bound. The concentration of active sulfamethoxazole in amniotic fluid, aqueous humour, bile, cerebrospinal fluid, middle ear fluid, sputum, synovial fluid and tissue (interstitial) fluid is of the order of 20-50% of the plasma concentration.

Biotransformation

Renal excretion of intact SMX accounts for 15-30% of the dose. This drug is more extensively metabolised than TMP, via acetylation, oxidation or glucuronidation. Over a 72 hour period, approximately 85% of the dose can be accounted for in the urine as unchanged drug plus the major (N4-acetylated) metabolite.

Elimination

The half-life of trimethoprim in man is in the range 8.6 to 17 hours in the presence of normal renal function. There appears to be no significant difference in the elderly compared with young patients.

The principle route of excretion of trimethoprim is renal and approximately 50% of the dose is excreted in the urine within 24 hours as unchanged drug. Several metabolites have been identified in the urine. Urinary concentrations of trimethoprim vary widely.

The half-life of sulfamethoxazole in man is approximately 9-11 hours in the presence of normal renal function.

There is no change in the half-life of active sulfamethoxazole with a reduction in renal function but there is prolongation of the half-life of the major, acetylated metabolite when the creatinine clearance is below 25ml/minute. The principle route of excretion of sulfamethoxazole is renal; between 15% and 30% of the dose recovered in the urine is in the active form. In elderly patients there is a reduced renal clearance of sulfamethoxazole.

Special patient populations

Renal impairment

The elimination half-life of trimethoprim is increased by a factor of 1.5-3.0 when the creatinine clearance is less than 10 mL/minute. When the creatinine clearance falls below 30 mL/min the dosage of Septrin should be reduced (see section 4.2).

Hepatic impairment

Caution should be exercised when treating patients with severe hepatic impairment as there may be changes in the absorption and biotransformation of trimethoprim and sulfamethoxazole

Older patients

In older patients, a slight reduction in renal clearance of sulfamethoxazole but not trimethoprim has been observed.

Paediatric population

See special dosage regimen (see section 4.2).


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5.3 Preclinical safety data

Reproductive toxicology: At doses generally in excess of the recommended human therapeutic dose, trimethoprim and sulfamethoxazole have been reported to cause cleft palate and other foetal abnormalities in rats, finding typical of a folate antagonist.

Effects with trimethoprim were preventable by co-administration of dietary folate. In rabbits, folate loss was seen at doses of trimethoprim in excess of human therapeutic doses.


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6. PHARMACEUTICAL PARTICULARS

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6.1 List of excipient(s)

Sodium starch glycolate type A

Povidone K30

Docusate sodium

Magnesium stearate


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6.2 Incompatibilities

Not applicable.


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6.3 Shelf life

5 years.


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6.4 Special precautions for storage

Do not store above 25°C.

Store in the original package in order to protect from light.


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6.5 Nature and contents of container

PVC/aluminium foil blister packs.

Packs of 100 tablets.


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6.6 Special precautions for disposal and other handling

No special requirement.


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7. MARKETING AUTHORISATION HOLDER

Aspen Pharma Trading Limited

3016 Lake Drive,

Citywest Business Campus,

Dublin 24

Ireland


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8. MARKETING AUTHORISATION NUMBER(S)

PA 1691/010/002


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9. DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

Date of first authorization: 14 June 1977

Date of last renewal: 14 November 2005


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10. DATE OF REVISION OF THE TEXT

October 2017



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Active Ingredients

 
   Trimethoprim
   Sulfamethoxazole