Aceclofenac

The main ingredient of this product is aceclofenac, its chemical name is: 2-[(2,6-dichlorophenyl)amino]phenylacetic acid carboxymethyl ester, its chemical structure is: Molecular formula: C16H13Cl2NO4 Molecular weight: 354.19

1. Avoid using with the following drugs: NSAIDs inhibit the secretion of methotrexate in the renal tubules and may have slight metabolic interactions, resulting in reduced clearance of methotrexate. Therefore, NSAIDs should always be avoided during high-dose methotrexate treatment. Certain NSAIDs can inhibit the elimination of lithium salts in the kidneys, resulting in increased serum lithium concentrations. Unless serum lithium levels can be measured regularly, lithium salts should be avoided in combination. NSAIDs inhibit platelet aggregation and damage the gastrointestinal mucosa, which can increase the activity of anticoagulants and increase the risk of gastrointestinal bleeding in patients using anticoagulants unless close monitoring can be performed. Aceclofenac should be avoided in combination with coumarin oral anticoagulants, ticlopidine, thrombolytic agents, and heparin. 2. The following combined medications require dose adjustment or attention: When using low-dose methotrexate, attention should also be paid to the possibility of drug interactions between NSAIDs and methotrexate, especially in patients with renal insufficiency. If NSAIDs and methotrexate are used simultaneously within 24 hours, caution should be exercised because the blood concentration of methotrexate may increase, leading to increased toxicity. When NSAIDs are used together with cyclosporine or taclidinium, the risk of renal toxicity increases due to reduced renal prostaglandin synthesis, so renal function should be closely monitored during combined treatment. Taking aspirin and other non-steroidal anti-inflammatory drugs at the same time will increase the incidence of adverse reactions. Be vigilant. Non-steroidal anti-inflammatory drugs can weaken the diuretic effect of furosemide (diuretic) and bufenoxic acid (budatanide, diuretic). The possible mechanism of action is to inhibit prostaglandin synthesis. They also reduce the antihypertensive effect of thiazide drugs (diuretics). Concomitant use with potassium-sparing diuretics will increase potassium levels, so blood potassium should be monitored. The simultaneous use of nonsteroidal anti-inflammatory drugs and ACE (angiotensin converting enzyme) inhibitors will increase the risk of acute renal failure in patients with dehydration. Although interactions with other antihypertensive drugs such as beta-receptor antagonists cannot be ruled out, the combined use of aceclofenac and bendroflumethiazide (diuretic antihypertensive drug) has not been found to affect its control of blood pressure. 3. Other possible interactions. There are reports on hypoglycemic and hyperglycemic effects, respectively. Aceclofenac may cause hypoglycemia, and the dose adjustment of hypoglycemic drugs should be considered when using it. No clinically significant differences in pharmacokinetics were observed after a single dose in patients with mild and moderate renal insufficiency. 4. Aceclofenac is mainly metabolized by cytochrome P4502G9, so there may be a risk of drug interactions with phenytoin sodium, digoxin, cimetidine, tolbutamide, phenylbutazone, amiodarone, imidazole and sulfaphenazole. 5. Like other NSAIDs, there is a risk of drug interaction with drugs that are eliminated through renal excretion, such as methotrexate and lithium salts. Aceclofenac is actually completely bound to plasma proteins, and will subsequently undergo a displacement effect with other highly protein-bound drugs, so attention must be paid.

The main ingredient of this product is aceclofenac.

1. Avoid co-administration with the following drugs: (1) NSAIDs inhibit the secretion of methotrexate in the renal tubules and may have slight metabolic interactions, resulting in reduced methotrexate clearance. Therefore, NSAIDs should always be avoided during high-dose methotrexate treatment. Some NSAIDs can inhibit the elimination of lithium salts in the kidneys, resulting in (2) increased serum lithium concentrations. Unless serum lithium levels can be measured regularly, co-administration with lithium salts should be avoided. NSAIDs inhibit platelet aggregation and damage the gastrointestinal mucosa, which can increase the activity of anticoagulants and increase the risk of gastrointestinal bleeding in patients using anticoagulants. Unless close monitoring can be performed, aceclofenac should be avoided in combination with coumarin oral anticoagulants, ticlopidine, thrombolytic agents and heparin. 2. The following combined medications require dose adjustment or precautions: (1) When using low-dose methotrexate, attention should also be paid to the possibility of drug interactions between NSAIDs and methotrexate, especially in patients with renal insufficiency. If (2) NSAIDs and methotrexate are used simultaneously within 24 hours, caution should be exercised because the blood concentration of methotrexate may increase, leading to increased toxicity. When NSAIDs are used together with cyclosporine or tacrolimus, the risk of renal toxicity increases due to reduced renal prostaglandin synthesis, so renal function should be closely monitored during combined treatment. (3) Concomitant use of aspirin and other nonsteroidal anti-inflammatory drugs will increase the incidence of side effects, so caution should be exercised. (4) Nonsteroidal anti-inflammatory drugs can weaken the diuretic effect of furosemide (diuretic) and bumetanide (diuretic), possibly through the inhibition of prostaglandin synthesis. They can also reduce the antihypertensive effect of thiazides (diuretics). Concomitant use with potassium-sparing diuretics will increase potassium levels, so blood potassium should be monitored. Concomitant use of nonsteroidal anti-inflammatory drugs and ACE (angiotensin-converting enzyme) inhibitors increases the risk of acute renal failure in patients with dehydration. Although interactions with other antihypertensive drugs, such as β-receptor antagonists, cannot be ruled out, the combined use of aceclofenac and bendroflumethiazide (diuretic antihypertensive drug) has not been found to affect its blood pressure control. 3. Aceclofenac is mainly metabolized by cytochrome P4502C9, so there may be a risk of drug interactions with phenytoin, digoxin, cimetidine, tolbutamide, phenylbutazone, amiodarone, miconazole and sulfaphenazole. Like other NSAID drugs, there is also a risk of drug interactions with drugs eliminated by renal excretion, such as methotrexate and lithium salts. Aceclofenac is actually completely bound to plasma proteins, and will then undergo a displacement effect with other high-protein-bound drugs, which must be noted. 4. Other possible interactions: There are reports on hypoglycemic and hyperglycemic effects, respectively. Aceclofenac may cause hypoglycemia, and the dose of hypoglycemic drugs should be adjusted when used. No clinically significant differences in pharmacokinetics were observed in patients with mild and moderate renal insufficiency after a single dose.