Sulfadimethoxine 500 mg 10 tablets blister

Infectious-inflammatory diseases caused by sensitive microflora: tonsillitis, bronchitis, pneumonia, sinusitis, otitis media, dysentery, inflammatory diseases of the biliary and urinary tracts (uncomplicated), erysipelas, wound infection, trachoma.

Orally, once a day; on the first day - 1-2 g, then - 0.5-1 g/day. For children aged 3 to 12 years, on the first day - 25 mg/kg/day, then - 12.5 mg/kg/day. For children over 12 years, on the first day - 1 g, then - 0.5 g. Treatment course - 7-10 days.

1 tablet contains
active ingredient: sulfadimethoxine - 500 mg.
Excipients: calcium stearate, gelatin, potato starch.

Tablets of white or white with a creamy tint color, flat-cylindrical with a score and bevel.

Hypersensitivity, bone marrow suppression, renal/hepatic insufficiency, chronic heart failure, congenital glucose-6-phosphate dehydrogenase deficiency, porphyria, azotemia, pregnancy, lactation period, age under 3 years.

During therapy, abundant alkaline drinking is recommended, along with monitoring of blood and urine parameters.
It is not a first-line drug of choice.

Headache; dyspepsia; leukopenia; agranulocytosis; nausea; vomiting; allergic reactions; cholestatic hepatitis.

Symptoms: cases of overdose are unknown.
Treatment: gastric lavage, monitoring of vital functions, symptomatic therapy.

Reduces the effectiveness of bactericidal antibiotics that act only on dividing microorganisms (including penicillins, cephalosporins).
Procaine, benzocaine, and tetracaine reduce antibacterial activity.
Para-aminosalicylic acid and barbiturates enhance antimicrobial action.
Salicylates increase activity and toxicity.
Methotrexate and phenytoin increase the toxicity of sulfadimethoxine.
Non-steroidal anti-inflammatory drugs, thioacetazone, and chloramphenicol enhance toxic effects on blood (leukopenia, agranulocytosis).
Enhances the action of indirect anticoagulants, phenytoin, and sulfanilamides with hypoglycemic action; pyrazolone derivatives, indomethacin, and salicylates increase the free fraction of the drug in the blood.
Reduces the effectiveness of oral contraceptives.
Enhances the metabolism of cyclosporine.
Myelotoxic drugs enhance the manifestations of the hematotoxicity of the drug.

Antimicrobial bacteriostatic agent, long-acting sulfanilamide. The mechanism of action is based on competitive antagonism with para-aminobenzoic acid, inhibition of dihydropteroate synthase, and disruption of the synthesis of tetrahydrofolic acid, which is necessary for the synthesis of purines and pyrimidines. Active against gram-positive and gram-negative microorganisms: Staphylococcus spp., Streptococcus spp., including Streptococcus pneumoniae, Klebsiella pneumoniae, Escherichia coli, Shigella spp., Chlamydia trachomatis.

After oral administration, it is detected in the blood within 30 minutes, with a peak concentration period of 8-12 hours. Unlike other long-acting sulfonamides, it poorly penetrates the blood-brain barrier, resulting in low concentrations in cerebrospinal fluid. However, during inflammation of the meninges, the permeability of the blood-brain barrier sharply increases. Therapeutic concentrations in adults are observed with a dosage of 1-2 g on the first day and 0.5-1 g on subsequent days. The drug accumulates in the blood primarily due to a high degree of binding to blood proteins (90-99%). It is well distributed throughout organs and systems. It penetrates well into pleural fluid (60-90% of the concentration in blood) and the biliary system, where its concentrations are 1.5-4 times higher than in blood. Unlike other sulfonamides, the predominant metabolism occurs via microsomal glucuronidation, NADPH-dependent, and associated with cytochrome P450.

It is excreted slowly, primarily due to retention in the blood by plasma proteins and a high degree of reabsorption in the renal tubules (93-97.5%). In the blood, 5-15% of acetylated metabolites are present, in urine - 10-25% of acetyl derivatives and 75-90% of glucuronide of sulfadimethoxine; the latter is well soluble and does not provoke the development of crystalluria. The acetyl derivative is not reabsorbed and is completely excreted by the kidneys. Within 24 hours, 20-44% of the administered dose is excreted; within 48 hours, up to 56%; and within 96 hours, up to 83.3%.