Co-trimoxazole, 480 mg tablets

Drug formTablets

ATC categoryAntibacterials

ATC subcategorySulfanilamides for systematic use

Brand nameCo-trimoxazole

Generic nameCo-trimoxazole (Sulfamethoxazole / Trimethoprim)

Leaflet in Uzbek: Co-trimoxazole 480 mg tablets


Each tablet of Co-trimoxazole 480 mg contains:

active ingredients: sulfamethoxazole-400 mg, trimethoprim-80 mg;

excipients: microcrystalline cellulose, maize starch, sodium starch glycolate, magnesium stearate.

Pharmacological group and ATC code

Antibacterial; J01EE01.


Co-trimoxazole is defined as a mixture of 5 parts of sulfamethoxazole and 1 part of trimethoprim.

Trimethoprim is a diaminopyrimidine antibacterial that is used for the treatment of infections due to sensitive organisms, including gastro-enteritis and respiratory-tract infections, and in particular for the treatment and prophylaxis of urinary-tract infections.

Sulfamethoxazole is an intermediate-acting sulfonamide.

Mechanism of Action

Co-trimoxazole usually is bactericidal. sulfamethoxazole is bacteriostatic and trimethoprim usually is bactericidal. Co-trimoxazole acts by sequentially inhibiting enzymes of the folic acid pathway; sulfamethoxazole inhibits the formation of dihydrofolic acid from p-aminobenzoic acid and, by inhibiting dihydrofolate reductase, trimethoprim inhibits the formation of tetrahydrofolic acid from dihydrofolic acid. By inhibiting synthesis of tetrahydrofolic acid, the metabolically active form of folic acid, co-trimoxazole inhibits bacterial thymidine synthesis.

Sequential inhibition by co-trimoxazole of two steps in the folic acid pathway appears to be responsible for the antibacterial synergism of the trimethoprim-sulfamethoxazole combination. For most organisms, optimum synergistic antibacterial action occurs in vitro at a trimethoprim:sulfamethoxazole ratio of about 1:20, which is also the approximate peak serum concentration ratio of the 2 drugs achieved following oral or IV administration of co-trimoxazole. Synergistic activity also has been observed in vitro at trimethoprim:sulfamethoxazole ratios of 1:1–1:40.

Susceptibility of organisms to trimethoprim usually is more critical to the efficacy of co-trimoxazole than is susceptibility to sulfamethoxazole. Many organisms that are resistant to sulfamethoxazole but susceptible or only moderately susceptible to trimethoprim will show synergistic antibacterial response to co-trimoxazole. However, for Neisseria gonorrhoeae, susceptibility to sulfamethoxazole is required for antibacterial response to co-trimoxazole.

Antimicrobial Action

The actions and spectrum of activity of co-trimoxazole are essentially those of its components, sulfamethoxazole and trimethoprim.

Because they act at different points of the folate metabolic pathway a potent synergy exists between its components in vitro with an increase of up to about 10-fold in antibacterial activity, and a frequently bactericidal action where the components individually are generally bacteriostatic. The optimum effect against most organisms is seen at a ratio of 1 part trimethoprim to 20 of sulfamethoxazole; although co-trimoxazole is formulated as a 1 to 5 ratio, differences in the pharmacokinetics of the two drugs mean that the ratio of the peak concentrations is approximately 1:20. However, it is not clear that the optimum ratio is achieved at all sites and, given that both drugs are present in therapeutic concentrations, the contribution of synergy to the effects of co-trimoxazole in vivo is uncertain.

Resistance to co-trimoxazole develops more slowly in vitro than to either component alone. Resistance has increased, and although initially slow, a more rapid increase was seen in many countries during the 1980s, occurring in both Gram-positive and Gram-negative organisms. Resistance has occurred notably among Enterobacteriaceae. Resistant strains of Brucella melitensis, Haemophilus influenzae, streptococci, and Vibrio cholerae have been reported rarely. Although resistant organisms are usually resistant to both components of the mixture, strains resistant to either the sulfonamide or trimethoprim, and with a reduced sensitivity to co-trimoxazole, have been reported.


Trimethoprim is a dihydrofolate reductase inhibitor. It inhibits the conversion of bacterial dihydrofolic acid to tetrahydrofolic acid which is necessary for the synthesis of certain amino acids, purines, thymidine, and ultimately DNA. It acts in the same metabolic pathway as the sulfonamides. It exerts its selective action because of a far greater affinity for the bacterial than the mammalian enzyme. Trimethoprim may be bacteriostatic or bactericidal depending on growth conditions; pus, for example, may inhibit the action of trimethoprim because of the presence of thymine and thymidine.

Spectrum of activity. Trimethoprim is active against a wide range of Gram-negative and Gram-positive aerobes, as well as some protozoa. The following species are usually susceptible.

Many Gram-positive cocci are sensitive, including Staphylococcus aureus, streptococci including Streptococcus pyogenes, Str. pneumoniae, and the viridans streptococci, and to a variable extent enterococci, although their sensitivity is reduced in the presence of folate.

Other sensitive Gram-positive organisms include strains of Listeria, Corynebacterium diphtheriae, and the Gram-positive bacilli.

Among the Gram-negative organisms, most of the Enterobacteriaceae are susceptible, or moderately so, including Citrobacter, Enterobacter, Escherichia coli, Hafnia, Klebsiella, Proteus mirabilis, Providencia, Salmonella, some Serratia, Shigella, and Yersinia. Legionella and Vibrio are also sensitive, and so are Haemophilus influenzae and H. ducreyi.

Anaerobic species are usually resistant, and so, to varying degrees are Brucella, Neisseria, and Nocardia. Mycobacterium tuberculosis is resistant although M. marinum may not be. Pseudomonas aeruginosa is resistant, and so are the Chlamydiaceae, Mycoplasma spp., and Rickettsia spp., as well as the spirochaetes.

Trimethoprim has some activity against Pneumocystis jirovecii and against some protozoa such as Naegleria, Plasmodium, and Toxoplasma.

Resistance. Resistance to trimethoprim may be due to several mechanisms. Clinical resistance is often due to plasmid-mediated dihydrofolate reductases that are resistant to trimethoprim: such genes may become incorporated into the chromosome via transposons. Resistance may also be due to overproduction of dihydrofolate reductase, changes in cell permeability, or bacterial mutants which are intrinsically resistant to trimethoprim because they depend on exogenous thymine and thymidine for growth. Despite fears of a rapid increase in resistance if trimethoprim was used alone there is little evidence that this has been any worse than in areas where it has been used in combination with sulfonamides. Nonetheless, trimethoprim resistance has been reported in many species, and very high frequencies of resistance have been seen in some developing countries, particularly among the Enterobacteriaceae.


Sulfamethoxazole and other sulfonamides have a similar structure to p-aminobenzoic acid and interfere with the synthesis of nucleic acids in sensitive micro-organisms by blocking the conversion of p-aminobenzoic acid to the coenzyme dihydrofolic acid, a reduced form of folic acid; in man, dihydrofolic acid is obtained from dietary folic acid so sulfonamides do not affect human cells. Their action is primarily bacteriostatic, although they may be bactericidal where concentrations of thymine are low in the surrounding medium. The sulfonamides have a broad spectrum of action, but the development of widespread resistance has greatly reduced their usefulness, and susceptibility often varies widely even among nominally sensitive pathogens.

Gram-positive cocci, particularly the Group A streptococci and some strains of Streptococcus pneumoniae, are usually sensitive and staphylococci also demonstrate sensitivity but to a lesser extent. Enterococci and many of the clostridia are more or less resistant, although strains of Clostridium perfringens are moderately susceptible. Among other Gram-positive organisms that have been reported to be sensitive are Bacillus anthracis and many strains of Nocardia, especially N. asteroides.

The Gram-negative cocci Neisseria meningitidis and N. gonorrhoeae were formerly extremely susceptible to sulfonamides, but many strains are now resistant. Susceptibility is often seen in Haemophilus influenzae although resistance in H. ducreyi is increasingly common. Susceptibility varies widely among the Enterobacteriaceae: strains of Escherichia coli, Klebsiella, Proteus, Salmonella, and Serratia are sometimes sensitive, but few strains of Shigella are now susceptible. Vibrio cholerae may be sensitive.

Other organisms that have been reported to be sensitive include Actinomyces spp., Brucella, Calymmatobacterium granulomatis, Legionella, and Yersinia pestis. Chlamydiaceae are sensitive, but not mycoplasmas, rickettsias, or spirochaetes, nor in general the mycobacteria. Pseudomonas aeruginosa is resistant, although sulfonamides may be effective against Burkholderia pseudomallei (Pseudomonas pseudomallei).

Sulfonamides have some activity against the protozoa Plasmodium falciparum and Toxoplasma gondii. They are also active against Pneumocystis jirovecii, but are ineffective against most fungi.

Sulfamethoxazole and other sulfonamides demonstrate synergy with the dihydrofolate reductase inhibitors pyrimethamine and trimethoprim which inhibit a later stage in folic acid synthesis.

The in-vitro antimicrobial activity of sulfamethoxazole is very dependent on both the culture medium and size of inoculum used.

Resistance. Acquired resistance to sulfonamides is common and widespread among formerly susceptible organisms, particularly Neisseria spp., Shigella and some other enterobacteria, staphylococci, and streptococci.

There appear to be several mechanisms of resistance including alteration of dihydropteroate synthetase, the enzyme inhibited by sulfonamides, to a less sensitive form, or an alteration in folate biosynthesis to an alternative pathway; increased production of p-aminobenzoic acid; or decreased uptake or enhanced metabolism of sulfonamides.

Resistance may result from chromosomal alteration, or may be plasmid-mediated and transferable, as in many resistant strains of enterobacteria. High-level resistance is usually permanent and irreversible. There is complete cross-resistance between the different sulfonamides.


When co-trimoxazole is administered by mouth, plasma concentrations of trimethoprim and sulfamethoxazole are generally around the optimal ratio of 1:20, although they may vary from 1:2 to 1:30 or more. The ratio of the two drugs is usually much lower in the tissues (often around 1:2 to 1:5) since trimethoprim, the more lipophilic drug, penetrates many tissues better than sulfamethoxazole and has a much larger volume of distribution. In urine the ratio may vary from 1:1 to 1:5 depending on the pH.


Trimethoprim is rapidly and almost completely absorbed from the gastrointestinal tract and peak concentrations in the circulation occur about 1 to 4 hours after an oral dose; peak plasma concentrations of about 1 microgram/mL have been reported after a single dose of 100 mg. About 45% is bound to plasma proteins. Trimethoprim is widely distributed to various tissues and fluids including kidneys, liver, lung and bronchial secretions, saliva, aqueous humour, prostatic tissue and fluid, and vaginal secretions; concentrations in many of these tissues are reported to be higher than serum concentrations but concentrations in the CSF are about one-quarter to one-half of those in serum. Trimethoprim readily crosses the placenta and it appears in breast milk. The half-life is about 8 to 10 hours in adults and somewhat less in children, but is prolonged in severe renal impairment and in neonates, whose renal function is immature.

Trimethoprim is excreted primarily by the kidneys through glomerular filtration and tubular secretion. About 10 to 20% of trimethoprim is metabolised in the liver and small amounts are excreted in the faeces via the bile, but most, about 40 to 60% of a dose, is excreted in urine, predominantly as unchanged drug, within 24 hours. Trimethoprim is removed from the blood by haemodialysis to some extent.


Sulfamethoxazole is readily absorbed from the gastrointestinal tract and peak plasma concentrations are reached after about 2 hours. Following a single 2-g dose by mouth, blood concentrations of up to 100 micrograms/mL are achieved. About 70% is bound to plasma proteins. The plasma half-life is about 6 to 12 hours; it is prolonged in patients with severe renal impairment.

Sulfamethoxazole, like most sulfonamides, diffuses freely throughout the body tissues and may be detected in the urine, saliva, sweat, and bile, in the cerebrospinal, peritoneal, ocular, and synovial fluids, and in pleural and other effusions. It crosses the placenta into the fetal circulation and low concentrations have been detected in breast milk.

Sulfamethoxazole undergoes conjugation mainly in the liver, chiefly to the inactive N4-acetyl derivative; this metabolite represents about 15% of the total amount of sulfamethoxazole in the blood. Metabolism is increased in patients with renal impairment and decreased in those with hepatic impairment. Elimination in the urine is dependent on pH. About 80 to 100% of a dose is excreted in the urine, of which about 60% is in the form of the acetyl derivative, with the remainder as unchanged drug and glucuronide.

Sulfamethoxazole is also oxidised to the hydroxylamine, a metabolite that has been implicated in adverse reactions to sulfonamides, although some doubt has been cast upon this hypothesis.

Co-trimoxazole is a mixture of the sulfonamide, sulfamethoxazole, and the diaminopyrimidine, trimethoprim, in the proportion of 5 parts of sulfamethoxazole to 1 part of trimethoprim. It has been used in a wide variety of infections due to susceptible organisms, particularly those of the urinary, respiratory, and gastrointestinal tracts, although the indications for its use are restricted in the UK. The current place of co-trimoxazole in therapy was reviewed by the UK Committee on Safety of Medicines in 1995. As a result they recommended that its use should be limited to: pneumocystis pneumonia, toxoplasmosis, and nocardiosis; urinary-tract infections and acute exacerbations of chronic bronchitis, but only when there is bacteriological evidence of sensitivity to co-trimoxazole and good reason to prefer it to a single antibacterial; and acute otitis media in children, but again only when there is good reason to prefer it.

Its other uses have included the treatment of acne, biliary-tract infections, brucellosis (generally in combination with other drugs), chancroid, Burkholderia cepacia (Pseudomonas cepacia) infections in cystic fibrosis, gonorrhoea, granuloma inguinale, listeriosis, melioidosis, mycetoma, otitis media, pertussis, typhoid and paratyphoid fever, and Whipple’s disease. It has also been used for the prophylaxis of infections in immunocompromised patients.

Dosage and Administration

Co-trimoxazole is usually given by mouth in an adult dose of 960 mg (trimethoprim 160 mg and sulfamethoxazole 800 mg) twice daily; in severe infections 2.88 g daily in 2 divided doses has been given. Lower doses are given for long-term treatment and in patients with renal impairment.

Doses of co-trimoxazole to be given twice daily to children are:

(as pediatric suspension) -from 6 weeks to 5 months of age, 120 mg; 6 months to 5 years, 240 mg;

(as tablets) – 6 to 12 years, 480 mg.

Alternatively, children may be given a dose of 24 mg/kg twice daily. Co-trimoxazole should not generally be given to infants below 6 weeks of age because of the risk of kernicterus from the sulfonamide component, although it may be used in infants from 4 weeks of age for the treatment or prophylaxis of pneumocystis pneumonia.

Higher doses of co-trimoxazole of up to 120 mg/kg daily given in 2 to 4 divided doses for 14 to 21 days are used in the treatment of pneumocystis pneumonia in adults and children over 4 weeks of age; serum concentrations should be monitored and folate supplementation possibly considered. For prophylaxis in adults with AIDS, the standard dose of co-trimoxazole (960 mg twice daily) may be given, but has been associated with a high incidence of adverse effects. Alternatively the following dose regimens may be used: 960 mg daily (7 days each week); 960 mg daily on alternate days (3 days each week); or 960 mg twice daily on alternate days (3 days each week). Children may be given standard doses for prophylaxis; doses are given on 3 consecutive days per week or for 7 days per week.



Overdosage with co-trimoxazole may produce symptoms of nausea, vomiting, diarrhea, mental depression, fever, confusion, facial swelling, headache, bone marrow depression, and slight elevations of serum aminotransferases (transaminases).


In acute overdosage with oral co-trimoxazole, the stomach should be emptied immediately by inducing emesis or by lavage. Supportive and symptomatic treatment should be initiated. Patients should be monitored with blood counts and other appropriate laboratory studies (e.g., serum electrolyte concentrations). Hemodialysis may remove only moderate amounts of the drug; peritoneal dialysis is not effective in enhancing the elimination of co-trimoxazole. Intramuscular injection of folic acid.

  • Hypersensitivity to the active substances, to sulfonamides or trimethoprim, or to any of the constituent excipients.
  • Severe hepatic failure or marked parenchymal liver disease.
  • Severe renal impairment (creatinine clearance)
  • Megaloblastic anemia due to folic acid deficiency.
  • Use in premature infants or neonates during the first 6 weeks of life, as this may increase the risk of kernicterus.
  • Use in the last trimester of pregnancy.
  • Hyperbilirubinemia.
  • Serious haematological disorders and porphyria.
Adverse effects
The main undesirable effects are skin reactions and mild gastrointestinal upsets, which occurred in approximately 5% of treatment periods. The following undesirable effects were reported (arranged by frequency and MedDRA system organ classes):

‘Very common’-(≥1/10), ‘common’-(≥1/100, <1/10), ‘uncommon’-(≥1/1000, <1/100), ‘rare’-(≥1/10,000, <1/1000), ‘very rare’-(<1/10,000).

Infections and infestations

Very rare: Fungal infections such as candidiasis.

Blood and lymphatic system

Rare: Leukopenia, granulocytopenia, thrombocytopenia.
Very rare: Agranulocytosis, anemia (megaloblastic, immunohemolytic,aplastic), methemoglobinemia, pancytopenia. Most of the observed hematological changes were mild, asymptomatic and reversible on discontinuing the product.

Immune system disorders

Very rare: Allergic reactions such as fever, angioedema, anaphylactoid reactions and serum sickness, periarteritis nodosa, allergic myocarditis.

Metabolic and nutritional disorders

Very common: Increase in serum potassium level: High-dose TM asused in patients with Pneumocystis carinii pneumonia induces aprogressive but reversible increase in serum potassium concentration in a substantial proportion of patients. In patients with disorders of potassium metabolism or renal insufficiency or given drugs that induce hyperkalemia, TM can cause hyperkalemia very frequently (in up to over 60% of patients), even at the recommended doses. Close monitoring of serum potassium should be ensured inthese patients. Hyponatremia. Hypoglycemia in non-diabetic patients, usually occurring in the first few days of treatment. Patients with renal dysfunction, liver disease or malnutrition and those receiving high doses of TM-SMZ are at particular risk.

Psychiatric disorders

Very rare: Hallucinations. Delirium and psychosis, particularly in elderly patients.

Nervous system

Very rare: Neuropathy (including peripheral neuritis and paresthesia), uveitis. Aseptic meningitis or meningitis-like symptoms, ataxia, convulsions, vertigo, tinnitus.

Respiratory organs

Very rare: Pneumonitis with eosinophilic infiltration.

Gastrointestinal disorders

Common: Nausea (with or without vomiting). Rare: Stomatitis, glossitis, diarrhea.
Very rare: Pseudomembranous enterocolitis, acute pancreatitis inseverely ill patients.

Hepatobiliary system

Very rare: Elevated transaminases and bilirubin, hepatitis, cholestasis, hepatic necrosis, vanishing bile duct syndrome.


Common: Rashes. These side effects are generally mild and rapidly reversible after withdrawal of the drug. Like many other medicinal products that contain sulfonamides: Very rare: Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (Lyell’s syndrome), purpura, Henoch Schoenleinpurpura, photosensitivity.

Musculoskeletal system

Very rare: Arthralgia, myalgia, rhabdomyolysis.

Kidneys and urinary tract

Very rare: Renal impairment and failure, interstitial nephritis, oliguria, anuria, elevated blood urea nitrogen (BUN), elevated serum creatinine, crystalluria. Sulfonamides, including Co-trimoxazole, can increase diuresis, particularly in patients with cardiac edema.

Undesirable effects in HIV-infected patients

HIV-infected patients with frequent comorbidities and their treatments usually receive longer prophylaxis or treatment of Pneumocystis carinii (Pneumocystis jiroveci) pneumonia with higher doses of Co-trimoxazole. Apart from a small number of additional side effects, the side effect profile in these patients is similar to that in the non-HIVinfected general population. However, certain side effects occur more frequently (in about 65%) and are often more severe, necessitating interruption or cessation of Co-trimoxazole therapy in 20–25% of patients. The following undesirable effects, in particular, have been observed additionally or with greater frequency:

Blood and lymphatic system – very common: Mainly neutropenia, but also anemia, leukopenia, granulocytopenia and thrombocytopenia. very rare: Agranulocytosis.

Immune system disorders – very common: Fever, usually in association with skin rashe, very rare: allergic reactions such as angioedema, anaphylactoid reactions and serum sickness.

Metabolic and nutritional disorders -very common: hyperkalemia. Close monitoring of serum potassium should be ensured in these patients. uncommon: hyponatremia, hypoglycemia.

Psychiatric disorders – very rare: acute psychosis.

Nervous system – very rare: neuropathy (including peripheral neuritis and paresthesia), hallucinations, uveitis. Aseptic meningitis or meningitis-like symptoms, ataxia, convulsions, Parkinson-like resting tremor, sometimes combined with apathy, ankle clonus and broad-based gait. Vertigo, tinnitus.

Respiratory organs – very rare: Pneumonitis with eosinophilic infiltration.

Gastrointestinal disorders – very common: Anorexia, nausea with or without vomiting and diarrhea.rare: stomatitis, glossitis, very rare:pancreatitis.

Hepatobiliary system – common: liver enzyme/transaminase elevation, cholestatic jaundice., very rare: Sometimes severe hepatitis.

Skin – very common: maculopapular rash that eventually causes itching and is rapidly reversible after withdrawal of the drug, usually with pruritus.rare: photosensitivity,.very rare: erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (Lyell’s syndrome), Henoch-Schoenlein purpura.

Musculoskeletal system -very rare: arthralgia, myalgia, rhabdomyolysis.

Kidneys and urinary tract– uncommon: renal impairment, azotemia, elevated serum creatinine, crystalluria, very rare: sulfonamides, including Co-trimoxazole, can increase diuresis, particularly in patients with cardiac edema.

Drug interactions


Trimethoprim may increase serum concentrations and potentiate the effect of a number of drugs, including phenytoin, digoxin, and procainamide. The effect may be due to competitive inhibition of renal excretion, decreased metabolism, or both. It has been suggested that trimethoprim may potentiate the effects of warfarin. Trimethoprim has been reported to reduce the renal excretion and increase blood concentrations of zidovudine, zalcitabine, and lamivudine. Trimethoprim and dapsone increase each other’s serum concentrations, whereas rifampicin may decrease trimethoprim concentrations.

An increased risk of nephrotoxicity has been reported with the use of trimethoprim or co-trimoxazole and ciclosporin. Intravenous use of trimethoprim and sulfonamides may reduce ciclosporin concentrations in blood. In patients given trimethoprim who were also receiving diuretics, hyponatraemia has been reported (an increased risk of thrombocytopenia has been seen in elderly patients given co-trimoxazole with diuretics, although it is unclear which component is responsible).

Use of trimethoprim with other depressants of bone marrow function may increase the likelihood of myelosuppression, and there may be a particular risk of megaloblastic anaemia if it is given with other folate inhibitors, such as pyrimethamine or methotrexate.

Severe hyperkalaemia has been noted in patients given trimethoprim (or co-trimoxazole) together with an ACE inhibitor.


The action of sulfonamides may be antagonised by p-aminobenzoic acid and compounds derived from it, particularly potassium aminobenzoate and the procaine group of local anaesthetics.

Sulfamethoxazole and other sulfonamides may potentiate the effects of some drugs, such as oral anticoagulants, methotrexate, and phenytoin; this may be due to displacement of the drug from plasma protein binding sites or to inhibition of metabolism. However, the clinical significance of these interactions appears to depend on the particular sulfonamide involved. The possibility of interactions with other highly protein-bound drugs, such as NSAIDs, should be considered.

High doses of sulfonamides have been reported to have a hypoglycaemic effect; the antidiabetic effect of the sulfonylurea compounds may be enhanced by sulfonamides. Some sulfonamides have been associated with a decrease in plasma-ciclosporin concentrations when used together. Isolated reports have described possible failures of hormonal contraceptives resulting in pregnancy in patients given sulfonamides. Plasma levels of dofetilide increased markedly by co-administration with Co-trimoxazole resulting in the increase dofetilide-induced QT prolongation and the risk of arrhythmias.

The use of compounds which render the urine acidic may increase the risk of crystalluria.


Co-trimoxazole should not be given to patients with a history of hypersensitivity to it or to the sulfonamides or trimethoprim. It should be discontinued at the first appearance of skin rash, or if blood disorders develop. It should be avoided in patients with severe hepatic impairment and used with caution in patients with lesser degrees of impairment. Caution should be exercised in the appointment of co-trimoxazole in patients with chronic alcoholism, and patients taking immunosuppressive drugs.

Like its components, co-trimoxazole should be used with caution in renal impairment, and dosage adjustment may be necessary; it should not be used in severe renal impairment without monitoring of plasma drug concentrations. An adequate fluid intake should be maintained to reduce the risk of crystalluria, but alkalinisation of the urine, although it increases urinary excretion of the sulfamethoxazole component, decreases urinary trimethoprim excretion. Regular blood counts and urinalyses and renal-function tests should be carried out in patients receiving prolonged treatment with co-trimoxazole. Elderly patients may be more susceptible to adverse effects. Folate supplementation may be necessary in patients predisposed to folate deficiency, such as elderly patients and when high doses of co-trimoxazole are given for a prolonged period. Use with caution in patients with bronchial asthma and dysfunction of the thyroid gland.

Pregnancy and breast feeding

Co-trimoxazole should be avoided during pregnancy and breast feeding.


White scored cylindrical tablets, the end surface of which are flat.


2 blister packets with 10 tablets in each the cardboard box.

Expiry date

3 years. Do not use after the expiration date.

Storage conditions

Store at a room temperature (15-250C), in a dry place, out of the reach of children. Protect from light.