Dexalgin 25 - instructions for use, doses, side effects, contraindications, price, where to buy

Dexalgin® 25 (Dexalgin® 25)

The following interactions are common to all NSAIDs.

Undesirable combinations

With other NSAIDs, including salicylates in high doses (more than 3 g/day):

simultaneous use of several NSAIDs due to the synergistic effect increases the risk of gastrointestinal bleeding and ulcers.

With anticoagulants

: Dexketoprofen, like other NSAIDs, may enhance the effect of anticoagulants such as warfarin due to high plasma protein binding, inhibition of platelet aggregation and damage to the gastrointestinal mucosa. If simultaneous use is necessary, careful monitoring of the patient's condition and regular monitoring of laboratory parameters is necessary.

With heparin:

with simultaneous use, the risk of bleeding increases (due to inhibition of platelet aggregation and damaging effects on the mucous membrane of the gastrointestinal tract). If simultaneous use is necessary, careful monitoring of the patient's condition and regular monitoring of laboratory parameters is necessary.

With glucocorticosteroids:

with simultaneous use, the risk of ulcerative lesions of the gastrointestinal tract and bleeding increases.

With lithium preparations:

NSAIDs increase the concentration of lithium in the blood plasma up to toxic levels, and therefore this indicator must be monitored when used simultaneously with dexketoprofen, changing the dosage, and also after discontinuation of NSAIDs.

With methotrexate in high doses (15 mg/week or more):

it is possible to increase the hematological toxicity of methotrexate due to a decrease in its renal clearance when used simultaneously with NSAIDs.

With hydantoins and sulfonamides:

their toxic effect may be enhanced.
Combinations

requiring caution
With diuretics, angiotensin-converting enzyme (ACE) inhibitors, aminoglycoside antibiotics, angiotensin II :

simultaneous use with NSAIDs is associated with a risk of developing acute renal failure in dehydrated patients (decreased glomerular filtration rate due to decreased synthesis of prostaglandins). When used concomitantly, NSAIDs may reduce the antihypertensive effect of some drugs. When using dexketoprofen and diuretics simultaneously, it is necessary to ensure that the patient has no signs of dehydration, and also monitor renal function at the beginning of simultaneous use.

With methotrexate in low doses (less than 15 mg/week):

it is possible to increase the hematological toxicity of methotrexate due to a decrease in its renal clearance during simultaneous use with NSAIDs. A blood cell count is necessary when coadministration is initiated. In the presence of even mild renal dysfunction, as well as in elderly people, careful medical supervision is necessary.

With pentoxifylline:

there may be an increased risk of bleeding. Close clinical monitoring and regular checking of bleeding time (blood clotting time) is necessary.

With zidovudine:

There is a risk of increased toxicity to red blood cells due to effects on reticulocytes, with the development of severe anemia one week after starting NSAID use. It is necessary to conduct a general blood test with counting the number of reticulocytes 1-2 weeks after starting NSAID therapy.

With oral hypoglycemic agents:

NSAIDs may enhance the hypoglycemic effect of sulfonylureas due to the displacement of sulfonylurea from sites of binding to plasma proteins.

Combinations

that
need to be taken into account
With
beta -blockers:
When used simultaneously with NSAIDs, the antihypertensive effect of beta-blockers may be reduced due to inhibition of prostaglandin synthesis.

With cyclosporine and tacrolimus:

NSAIDs may increase nephrotoxicity, which is mediated by the action of renal prostaglandins. During simultaneous use, it is necessary to monitor renal function.

With thrombolytics:

the risk of bleeding increases.

The risk of bleeding from the gastrointestinal tract increases when used simultaneously with serotonin reuptake inhibitors

(citalopram, fluoxetine, sertraline) and anticoagulants.

With probenecid:

it is possible to increase the concentration of NSAIDs in the blood plasma, which may be due to the inhibitory effect of probenecid on renal tubular secretion and/or conjugation with glucuronic acid; NSAID dose adjustment may be required.

With cardiac glycosides:

simultaneous use with NSAIDs may lead to an increase in the concentration of cardiac glycosides in the blood plasma.

With mifepristone:

Due to the theoretical risk of changes in the effectiveness of mifepristone under the influence of prostaglandin synthesis inhibitors, NSAIDs should not be used earlier than 8-12 days after discontinuation of mifepristone.

With quinolones:

Data obtained from experimental studies in animals indicate a high risk of developing seizures when NSAIDs are used concomitantly with quinolones in high doses.

If necessary, simultaneous use of the drug Dexalgin

®
25 with the above medications, you should consult your doctor.

The inflammatory reaction is a general biological response of the body to the action of any damaging factors. In periodontics, the damaging effects are caused largely by plaque microbes. In turn, the inflammatory reaction itself, especially pronounced and prolonged, leads to profound morphological and functional disorders in tissues. Therefore, if removal of dental plaque does not provide the desired effect, it is necessary to use anti-inflammatory drugs in complex pathogenetic therapy.

In dental practice, drugs of both general and local action are widely used [3, 5]. There are groups of pharmacological agents that have a direct effect on one or more phases of the inflammatory response simultaneously. Such drugs are actually anti-inflammatory. Like antibacterial, anti-inflammatory drugs should be prescribed only reasonably, taking into account the peculiarities of the course of the inflammatory process in each individual case.

If the constant change in the antibiotic market is determined mainly by the development of microbial resistance, then the search for new anti-inflammatory drugs is largely due to their lack of effectiveness and/or side effects.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have an anti-inflammatory effect because they affect two phases of inflammation: exudative and proliferative. There are compelling reasons for their widespread use in the treatment of inflammatory periodontal lesions - gingivitis and periodontitis [1].

The mechanisms of the pathogenetic action of NSAIDs are that they, like hormonal drugs, stabilize cellular and intracellular membranes and suppress the synthesis of prostaglandins and small peptides (oligopeptides), which in turn are mediators of inflammation, pain and fever. This explains their not only anti-inflammatory, but also pronounced analgesic effect. In addition, NSAIDs reduce the level of free radicals in tissues and affect cells that are directly involved in inflammatory reactions. In particular, their effect on neutrophils increases the bactericidal effect of these cells. As a result, the destruction of pathogenic microorganisms is accelerated and the normalization of periodontal tissue occurs faster [6].

Due to the diversity of their chemical structure, a perfect classification of NSAIDs does not yet exist. There are many NSAIDs used in dentistry. Despite the diversity of the chemical structure of non-steroidal drugs, the main mechanism of action of most of them is the inhibition of the synthesis of prostaglandins, which take an active part in the formation and course of inflammatory reactions.

One of the leading positions in medical practice and in dentistry, in particular, over the last few decades has been occupied by the drug ketoprofen, a derivative of propionic acid. The drug is a racemic mixture of enantiomers. The mechanism of its action is associated with inhibition of the activity of cyclooxygenase, the main enzyme in the metabolism of arachidonic acid, which is a precursor of prostaglandins, which play a major role in the pathogenesis of inflammation, pain and fever.

However, numerous studies have shown that only the S(+) isomer inhibits cyclooxygenase isoenzymes. In humans, approximately 10% of R(-)-ketoprofen is converted to the S(+) isomer, although this amount varies significantly between individuals. To increase therapeutic efficacy, the S(+)-isomer was isolated from the racemic mixture and presented in the form of a water-soluble salt as a new NSAID - dexketoprofen trometamol. As a result, the resulting salt of dexketoprofen trometamol has improved physicochemical properties, avoids the development of undesirable metabolic effects, and has low toxicity [2, 4].

In 2008, a new generation NSAID, dexalgin, was registered in Russia. The drug is widely used both in trauma medicine and in the complex treatment of chronic diseases. The main active ingredient is dexketoprofen trometamol. The combination of dexketoprofen with trometamol promotes accelerated absorption of the active substance and a rapid effect. Compared to ketoprofen, the maximum concentration of dexketoprofen trometamol achieves higher results, and the analgesic effect occurs faster - 30 minutes after administration and lasts 4-6 hours.

The high inhibitory activity of dexalgin against cyclooxygenases determines its peripheral and central analgesic effects, while the high anti-inflammatory activity of the drug is combined with good tolerability. However, in each specific case the possibility of side effects and contraindications should be taken into account.

Thus, the high efficiency and good safety profile of dexalgin suggest its wider use not only in general medical practice, but also in periodontology, in particular, both at the stages of eliminating acute inflammation and in the postoperative period.

Dexalgin solution d/in 25 mg/ml 2 ml N5 (Berlin)

Dexalgin® should not be mixed in the same syringe with a solution of dopamine, promethazine, pentazocine, pethidine or hydroxyzine (a precipitate will form).

Dexalgin® can be mixed in one syringe with a solution of heparin, lidocaine, morphine and theophylline.

Dexalgin® - diluted solution for infusion should not be mixed with promethazine or pentazocine.

Dexalgin® - diluted solution for infusion is compatible with the following injection solutions: dopamine, heparin, hydroxyzine, lidocaine, morphine, pethidine and theophylline.

When storing Dexalgin® - diluted solutions for infusion in plastic containers or when using infusion systems made from ethyl vinyl acetate, cellulose propionate, low-density polyethylene or polyvinyl chloride, absorption of the active substance by the listed materials does not occur.

The following interactions are common to all NSAIDs.

Undesirable combinations

With other NSAIDs, including salicylates in high doses (more than 3 g/day):

simultaneous administration of several NSAIDs due to the synergistic effect increases the risk of gastrointestinal bleeding and ulcers.

With oral anticoagulants, heparin in doses exceeding prophylactic doses, and ticlopidine

: increased risk of bleeding due to inhibition of platelet aggregation and damage to the mucous membrane of the gastrointestinal tract.

With lithium preparations:

NSAIDs increase the level of lithium in the blood, up to toxic levels, and therefore this indicator must be monitored when prescribing, changing the dose and after discontinuation of NSAIDs.

With methotrexate in high doses (15 mg/week or more)

: increased hematological toxicity of methotrexate due to a decrease in its renal clearance during NSAID therapy.

With hydantoins and sulfonamide drugs:

the risk of increased toxic effects of these drugs.

Combinations requiring caution

With diuretics, angiotensin-converting enzyme inhibitors:

NSAID therapy is associated with a risk of acute renal failure in dehydrated patients (decreased glomerular filtration due to decreased prostaglandin synthesis). NSAIDs may reduce the hypotensive effect of some drugs. When coadministered with diuretics, ensure that the patient's fluid balance is adequate and monitor renal function before prescribing NSAIDs.

With methotrexate in low doses (less than 15 mg/week):

increased hematological toxicity of methotrexate due to a decrease in its renal clearance during NSAID therapy. It is necessary to conduct weekly blood cell counts during the first weeks of concomitant therapy. In the presence of even mild renal dysfunction, as well as in elderly people, careful medical supervision is necessary.

With pentoxifylline:

increased risk of bleeding. Intensive clinical monitoring and frequent checking of bleeding time (blood clotting time) is necessary.

With zidovudine

: Risk of increased toxicity to red blood cells due to effects on reticulocytes, with the development of severe anemia one week after administration of NSAIDs. It is necessary to count all blood cells and reticulocytes 1-2 weeks after starting NSAID therapy.

With sulfa drugs:

NSAIDs may enhance the hypoglycemic effect of sulfonylureas due to their displacement from sites of binding to plasma proteins.

With low molecular weight heparin preparations:

increased risk of bleeding.

Combinations to consider

With β-blockers:

NSAIDs may reduce the hypotensive effect of beta-blockers due to inhibition of prostaglandin synthesis.

With cyclosporine and tacrolimus:

NSAIDs may increase nephrotoxicity, which is mediated by the action of renal prostaglandins. During concomitant therapy, renal function should be monitored.

With thrombolytics

: increased risk of bleeding.

With probenecid:

Plasma concentrations of NSAIDs may increase, which may be due to an inhibitory effect on renal tubular secretion and/or conjugation with glucuronic acid, requiring NSAID dose adjustment.

With cardiac glycosides:

NSAIDs may lead to increased plasma concentrations of glycosides.

With mifepristone:

Due to the theoretical risk of changes in the effectiveness of mifepristone under the influence of prostaglandin synthesis inhibitors, NSAIDs should not be prescribed earlier than 8-12 days after discontinuation of mifepristone.

With ciprofloxacin:

Data obtained from experimental studies in animals indicate a high risk of convulsions when NSAIDs are prescribed during therapy with high doses of ciprofloxacin.

Dexalgin, 25 mg/ml, solution for intravenous and intramuscular administration, 2 ml, 10 pcs.

Dexalgin® should not be mixed in the same syringe with a solution of dopamine, promethazine, pentazocine, pethidine or hydroxyzine (a precipitate will form).

Dexalgin® can be mixed in one syringe with a solution of heparin, lidocaine, morphine and theophylline.

Dexalgin®, diluted solution for infusion, must not be mixed with promethazine or pentazocine.

Dexalgin®, diluted solution for infusion, is compatible with the following injection solutions: dopamine, heparin, hydroxyzine, lidocaine, morphine, pethidine and theophylline.

When diluted solutions for infusion of the drug Dexalgin® are stored in plastic containers or when using infusion systems made from ethyl vinyl acetate, cellulose propionate, LDPE or PVC, absorption of the active substance by the listed materials does not occur.

The following interactions are common to all NSAIDs.

Undesirable combinations

With other NSAIDs, including salicylates in high doses (more than 3 g/day):

simultaneous administration of several NSAIDs due to the synergistic effect increases the risk of gastrointestinal bleeding and ulcers.

With oral anticoagulants, heparin, in doses exceeding prophylactic ones, and ticlopidine:

increased risk of bleeding due to inhibition of platelet aggregation and damage to the gastrointestinal mucosa.

With lithium preparations:

NSAIDs increase the level of lithium in the blood, up to toxic levels, and therefore this indicator must be monitored when prescribing, changing the dose and after discontinuation of NSAIDs.

With methotrexate in high doses (15 mg/week or more):

increased hematological toxicity of methotrexate due to a decrease in its renal clearance during NSAID therapy.

With hydantoins and sulfonamide drugs:

the risk of increased toxic effects of these drugs.

Combinations requiring caution

With diuretics, ACE inhibitors:

NSAID therapy is associated with a risk of developing acute renal failure in dehydrated patients (decreased glomerular filtration due to reduced PG synthesis). NSAIDs may reduce the hypotensive effect of some drugs. When coadministered with diuretics, ensure that the patient's fluid balance is adequate and monitor renal function before prescribing NSAIDs.

With methotrexate in low doses (less than 15 mg/week):

With pentoxifylline:

increased risk of bleeding. Intensive clinical monitoring and frequent checking of bleeding time (blood clotting time) is necessary.

With zidovudine:

risk of increased toxicity to red blood cells due to effects on reticulocytes, with the development of severe anemia one week after the administration of NSAIDs. It is necessary to count all blood cells and reticulocytes 1–2 weeks after starting NSAID therapy.

With sulfa drugs:

NSAIDs may enhance the hypoglycemic effect of sulfonylureas due to their displacement from sites of binding to plasma proteins.

With low molecular weight heparin preparations:

increased risk of bleeding.

Combinations to consider

With β-blockers:

NSAIDs may reduce the hypotensive effect of β-blockers due to inhibition of PG synthesis.

With cyclosporine and tacrolimus:

NSAIDs may increase nephrotoxicity, which is mediated by the action of renal PGs. During concomitant therapy, renal function should be monitored.

With thrombolytics:

increased risk of bleeding.

With probenecid:

Plasma concentrations of NSAIDs may increase, which may be due to an inhibitory effect on renal tubular secretion and/or conjugation with glucuronic acid, requiring NSAID dose adjustment.

With cardiac glycosides:

NSAIDs may lead to increased plasma concentrations of glycosides.

With mifepristone:

Due to the theoretical risk of changes in the effectiveness of mifepristone under the influence of PG synthesis inhibitors, NSAIDs should not be prescribed earlier than 8–12 days after discontinuation of mifepristone.

With ciprofloxacin:

Data obtained from experimental studies in animals indicate a high risk of convulsions when NSAIDs are prescribed during therapy with high doses of ciprofloxacin.