Diclofenac Potassium

×

Overview

What is Diclofenac Potassium?

Diclofenac potassium is a benzeneacetic acid derivative. Diclofenac potassium is available as immediate-release tablets of 50 mg (light brown) for oral administration. The chemical name is 2-[(2,6-dichlorophenyl)amino] benzeneacetic acid, monopotassium salt. The molecular weight is 334.25. Its molecular formula is C14H10Cl2NKO2, and it has the following structural formula:

What does Diclofenac Potassium look like?

What are the available doses of Diclofenac Potassium?

Sorry No records found.

What should I talk to my health care provider before I take Diclofenac Potassium?

Sorry No records found

How should I use Diclofenac Potassium?

Carefully consider the potential benefits and risks of diclofenac potassium immediate-release tablets and other treatment options before deciding to use diclofenac potassium immediate-release tablets. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see WARNINGS).

Diclofenac potassium immediate-release tablets are indicated:

Carefully consider the potential benefits and risks of diclofenac potassium immediate-release tablets and other treatment options before deciding to use diclofenac potassium immediate-release tablets. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see WARNINGS).

After observing the response to initial therapy with diclofenac potassium immediate-release tablets, the dose and frequency should be adjusted to suit an individual patient’s needs.

For treatment of pain or primary dysmenorrhea the recommended dosage is 50 mg t.i.d. With experience, physicians may find that in some patients an initial dose of 100 mg of diclofenac potassium immediate-release tablets, followed by 50-mg doses, will provide better relief.

For the relief of osteoarthritis the recommended dosage is 100-150 mg/day in divided doses, 50 mg b.i.d. or t.i.d.

For the relief of rheumatoid arthritis the recommended dosage is 150-200 mg/day in divided doses, 50 mg t.i.d. or q.i.d.

Different formulations of diclofenac, like diclofenac sodium enteric-coated tablets, diclofenac sodium extended-release tablets or diclofenac potassium immediate-release tablets are not necessarily bioequivalent even if the milligram strength is the same.

What interacts with Diclofenac Potassium?

Sorry No Records found

What are the warnings of Diclofenac Potassium?

Sorry No Records found

What are the precautions of Diclofenac Potassium?

Sorry No Records found

What are the side effects of Diclofenac Potassium?

Sorry No records found

What should I look out for while using Diclofenac Potassium?

Diclofenac potassium immediate-release tablets are contraindicated in patients with known hypersensitivity to diclofenac. Diclofenac potassium immediate-release tablets should not be given to patients who have experienced asthma, urticaria, or allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see WARNINGS, Anaphylactoid Reactions, and PRECAUTIONS, Preexisting Asthma).

Diclofenac potassium immediate-release tablets are contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see WARNINGS).

Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal. All NSAIDs, both COX-2 selective and nonselective, may have a similar risk. Patients with known CV disease or risk factors for CV disease may be at greater risk. To minimize the potential risk for an adverse CV event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible. Physicians and patients should remain alert for the development of such events, even in the absence of previous CV symptoms. Patients should be informed about the signs and/or symptoms of serious CV events and the steps to take if they occur.

There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID does increase the risk of serious GI events (see GI WARNINGS).

Two large, controlled, clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10-14 days following CABG surgery found an increased incidence of myocardial infarction and stroke (see CONTRAINDICATIONS).

NSAIDs, including diclofenac potassium immediate-release tablets, can lead to onset of new hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events. Patients taking thiazides or loop diuretics may have impaired response to these therapies when taking NSAIDs. NSAIDs, including diclofenac potassium immediate-release tablets, should be used with caution in patients with hypertension. Blood pressure (BP) should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Fluid retention and edema have been observed in some patients taking NSAIDs. Diclofenac potassium immediate-release tablets should be used with caution in patients with fluid retention or heart failure.

NSAIDs, including diclofenac potassium immediate-release tablets, can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients, who develop a serious upper GI adverse event on NSAID therapy, is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occur in approximately 1% of patients treated for 3-6 months, and in about 2-4% of patients treated for one year. These trends continue with longer duration of use, increasing the likelihood of developing a serious GI event at some time during the course of therapy. However, even short-term therapy is not without risk.

NSAIDs should be prescribed with extreme caution in those with a prior history of ulcer disease or gastrointestinal bleeding. Patients with a prior history of peptic ulcer disease and/or gastrointestinal bleeding who use NSAIDs have a greater than 10-fold increased risk for developing a GI bleed compared to patients with neither of these risk factors. Other factors that increase the risk for GI bleeding in patients treated with NSAIDs include concomitant use of oral corticosteroids or anticoagulants, longer duration of NSAID therapy, smoking, use of alcohol, older age, and poor general health status. Most spontaneous reports of fatal GI events are in elderly or debilitated patients and therefore special care should be taken in treating this population.

To minimize the potential risk for an adverse GI event in patients treated with an NSAID, the lowest effective dose should be used for the shortest possible duration. Patients and physicians should remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy and promptly initiate additional evaluation and treatment if a serious GI adverse event is suspected. This should include discontinuation of the NSAID until a serious GI adverse event is ruled out. For high risk patients, alternate therapies that do not involve NSAIDs should be considered.

Caution should be used when initiating treatment with diclofenac potassium immediate-release tablets in patients with considerable dehydration.

Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury. Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients, administration of a nonsteroidal anti-inflammatory drug may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors, and the elderly. Discontinuation of nonsteroidal anti-inflammatory drug therapy is usually followed by recovery to the pretreatment state.

No information is available from controlled clinical studies regarding the use of diclofenac potassium immediate-release tablets in patients with advanced renal disease. Therefore, treatment with diclofenac potassium immediate-release tablets is not recommended in these patients with advanced renal disease. If diclofenac potassium immediate-release tablets therapy must be initiated, close monitoring of the patient's renal function is advisable.

As with other NSAIDs, anaphylactoid reactions may occur in patients without known prior exposure to diclofenac potassium immediate-release tablets. Diclofenac potassium immediate-release tablets should not be given to patients with the aspirin triad. This symptom complex typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other NSAIDs. (See CONTRAINDICATIONS and PRECAUTIONS, Preexisting Asthma.) Emergency help should be sought in cases where an anaphylactoid reaction occurs.

NSAIDs, including diclofenac potassium immediate-release tablets, can cause serious skin adverse events such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity.

In late pregnancy, as with other NSAIDs, diclofenac potassium immediate-release tablets should be avoided because it may cause premature closure of the ductus arteriosus.

What might happen if I take too much Diclofenac Potassium?

Symptoms following acute NSAID overdoses are usually limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which are generally reversible with supportive care. Gastrointestinal bleeding can occur. Hypertension, acute renal failure, respiratory depression and coma may occur, but are rare. Anaphylactoid reactions have been reported with therapeutic ingestion of NSAIDs, and may occur following an overdose.

Patients should be managed by symptomatic and supportive care following an NSAID overdose. There are no specific antidotes. Emesis and/or activated charcoal (60 to 100 g in adults, 1 to 2 g/kg in children) and/or osmotic cathartic may be indicated in patients seen within 4 hours of ingestion with symptoms or following a large overdose (5 to 10 times the usual dose). Forced diuresis, alkalinization of urine, hemodialysis, or hemoperfusion may not be useful due to high protein binding.

How should I store and handle Diclofenac Potassium?

Store bottles of 1000 SINGULAIR 5-mg chewable tablets and 8000 SINGULAIR 10-mg film-coated tablets at 25°C (77°F), excursions permitted to 15-30°C (59-86°F) [see USP Controlled Room Temperature]. Protect from moisture and light. Store in original container. When product container is subdivided, repackage into a well-closed, light resistant container. Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03Diclofenac Potassium Tablets 50 mg are available for oral administration as light brown, round shaped, unscored, film coated tablets, imprinted “APO” on one side and “DP” over “50” on the other side. They are supplied as follows: Bottles of 100 NDC 60505-0135-0 Bottles of 1000 NDC 60505-0135-1 Store at 20°-25°C (68°-77° F) [see USP Controlled Room Temperature]. Dispense in a tight, light-resistant container [see USP]. Apotex Inc. Diclofenac Potassium Tablets 50 mg Manufactured by: Manufactured for: Apotex Inc. Apotex Corp. Toronto, Ontario Weston, Florida Canada, M9L 1T9 33326 Revised: January 2006 Rev. 03

×

Clinical Information

Chemical Structure

No Image found

Clinical Pharmacology

Diclofenac is a nonsteroidal anti-inflammatory drug (NSAID) that exhibits anti-inflammatory, analgesic, and antipyretic activities in animal models. The mechanism of action of diclofenac, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition.

Diclofenac is 100% absorbed after oral administration compared to IV administration as measured by urine recovery. However, due to first-pass metabolism, only about 50% of the absorbed dose is systemically available. In some fasting volunteers, measurable plasma levels are observed within 10 minutes of dosing with diclofenac potassium immediate-release tablets. Peak plasma levels are achieved approximately 1 hour in fasting normal volunteers, with a range of .33 to 2 hours. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption and a reduction in peak plasma levels of approximately 30%.

The apparent volume of distribution (V/F) of diclofenac potassium is 1.3 L/kg.

Diclofenac is more than 99% bound to human serum proteins, primarily to albumin. Serum protein binding is constant over the concentration range (0.15-105 µg/mL) achieved with recommended doses.

Diclofenac diffuses into and out of the synovial fluid. Diffusion into the joint occurs when plasma levels are higher than those in the synovial fluid, after which the process reverses and synovial fluid levels are higher than plasma levels. It is not known whether diffusion into the joint plays a role in the effectiveness of diclofenac.

Five diclofenac metabolites have been identified in human plasma and urine. The metabolites include 4'-hydroxy-, 5-hydroxy-, 3'-hydroxy-, 4',5-dihydroxy- and 3'-hydroxy-4'-methoxy diclofenac. In patients with renal dysfunction, peak concentrations of metabolites 4'-hydroxy- and 5-hydroxy-diclofenac were approximately 50% and 4% of the parent compound after single oral dosing compared to 27% and 1% in normal healthy subjects. However, diclofenac metabolites undergo further glucuronidation and sulfation followed by biliary excretion.

One diclofenac metabolite 4’-hydroxy-diclofenac has very weak pharmacologic activity.

Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites.Little or no free unchanged diclofenac is excreted in the urine. Approximately 65% of the dose is excreted in the urine and approximately 35% in the bile as conjugates of unchanged diclofenac plus metabolites.Because renal elimination is not a significant pathway of elimination for unchanged diclofenac, dosing adjustment in patients with mild to moderate renal dysfunction is not necessary. The terminal half-life of unchanged diclofenac is approximately 2 hours.

The pharmacokinetics of diclofenac has not been investigated in pediatric patients.

Pharmacokinetics differences due to race have not been identified.

Hepatic metabolism accounts for almost 100% of diclofenac elimination, so patients with hepatic disease may require reduced doses of diclofenac potassium immediate-release tablets compared to patients with normal hepatic function.

Diclofenac pharmacokinetics has been investigated in subjects with renal insufficiency. No differences in the pharmacokinetics of diclofenac have been detected in studies of patients with renal impairment. In patients with renal impairment (inulin clearance 60-90, 30-60, and less than 30 mL/min; N=6 in each group), AUC values and elimination rate were comparable to those in healthy subjects.

Non-Clinical Toxicology

Diclofenac potassium immediate-release tablets are contraindicated in patients with known hypersensitivity to diclofenac. Diclofenac potassium immediate-release tablets should not be given to patients who have experienced asthma, urticaria, or allergic-type reactions after taking aspirin or other NSAIDs. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see WARNINGS, Anaphylactoid Reactions, and PRECAUTIONS, Preexisting Asthma).

Diclofenac potassium immediate-release tablets are contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see WARNINGS).

Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal. All NSAIDs, both COX-2 selective and nonselective, may have a similar risk. Patients with known CV disease or risk factors for CV disease may be at greater risk. To minimize the potential risk for an adverse CV event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible. Physicians and patients should remain alert for the development of such events, even in the absence of previous CV symptoms. Patients should be informed about the signs and/or symptoms of serious CV events and the steps to take if they occur.

There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID does increase the risk of serious GI events (see GI WARNINGS).

Two large, controlled, clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10-14 days following CABG surgery found an increased incidence of myocardial infarction and stroke (see CONTRAINDICATIONS).

NSAIDs, including diclofenac potassium immediate-release tablets, can lead to onset of new hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of CV events. Patients taking thiazides or loop diuretics may have impaired response to these therapies when taking NSAIDs. NSAIDs, including diclofenac potassium immediate-release tablets, should be used with caution in patients with hypertension. Blood pressure (BP) should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Fluid retention and edema have been observed in some patients taking NSAIDs. Diclofenac potassium immediate-release tablets should be used with caution in patients with fluid retention or heart failure.

NSAIDs, including diclofenac potassium immediate-release tablets, can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients, who develop a serious upper GI adverse event on NSAID therapy, is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occur in approximately 1% of patients treated for 3-6 months, and in about 2-4% of patients treated for one year. These trends continue with longer duration of use, increasing the likelihood of developing a serious GI event at some time during the course of therapy. However, even short-term therapy is not without risk.

NSAIDs should be prescribed with extreme caution in those with a prior history of ulcer disease or gastrointestinal bleeding. Patients with a prior history of peptic ulcer disease and/or gastrointestinal bleeding who use NSAIDs have a greater than 10-fold increased risk for developing a GI bleed compared to patients with neither of these risk factors. Other factors that increase the risk for GI bleeding in patients treated with NSAIDs include concomitant use of oral corticosteroids or anticoagulants, longer duration of NSAID therapy, smoking, use of alcohol, older age, and poor general health status. Most spontaneous reports of fatal GI events are in elderly or debilitated patients and therefore special care should be taken in treating this population.

To minimize the potential risk for an adverse GI event in patients treated with an NSAID, the lowest effective dose should be used for the shortest possible duration. Patients and physicians should remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy and promptly initiate additional evaluation and treatment if a serious GI adverse event is suspected. This should include discontinuation of the NSAID until a serious GI adverse event is ruled out. For high risk patients, alternate therapies that do not involve NSAIDs should be considered.

Caution should be used when initiating treatment with diclofenac potassium immediate-release tablets in patients with considerable dehydration.

Long-term administration of NSAIDs has resulted in renal papillary necrosis and other renal injury. Renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. In these patients, administration of a nonsteroidal anti-inflammatory drug may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics and ACE inhibitors, and the elderly. Discontinuation of nonsteroidal anti-inflammatory drug therapy is usually followed by recovery to the pretreatment state.

No information is available from controlled clinical studies regarding the use of diclofenac potassium immediate-release tablets in patients with advanced renal disease. Therefore, treatment with diclofenac potassium immediate-release tablets is not recommended in these patients with advanced renal disease. If diclofenac potassium immediate-release tablets therapy must be initiated, close monitoring of the patient's renal function is advisable.

As with other NSAIDs, anaphylactoid reactions may occur in patients without known prior exposure to diclofenac potassium immediate-release tablets. Diclofenac potassium immediate-release tablets should not be given to patients with the aspirin triad. This symptom complex typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other NSAIDs. (See CONTRAINDICATIONS and PRECAUTIONS, Preexisting Asthma.) Emergency help should be sought in cases where an anaphylactoid reaction occurs.

NSAIDs, including diclofenac potassium immediate-release tablets, can cause serious skin adverse events such as exfoliative dermatitis, Stevens-Johnson Syndrome (SJS), and toxic epidermal necrolysis (TEN), which can be fatal. These serious events may occur without warning. Patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity.

In late pregnancy, as with other NSAIDs, diclofenac potassium immediate-release tablets should be avoided because it may cause premature closure of the ductus arteriosus.

The rate and extent of perindopril absorption and elimination are not affected by concomitant diuretics. The bioavailability of perindoprilat was reduced by diuretics, however, and this was associated with a decrease in plasma ACE inhibition.

Diclofenac potassium immediate-release tablets cannot be expected to substitute for corticosteroids or to treat corticosteroid insufficiency. Abrupt discontinuation of corticosteroids may lead to disease exacerbation. Patients on prolonged corticosteroid therapy should have their therapy tapered slowly if a decision is made to discontinue corticosteroids.

The pharmacological activity of diclofenac in reducing fever and inflammation may diminish the utility of these diagnostic signs in detecting complications of presumed noninfectious, painful conditions.

Borderline elevations of one or more liver tests may occur in up to 15% of patients taking NSAIDs including diclofenac potassium immediate-release tablets. These laboratory abnormalities may progress, may remain unchanged, or may be transient with continued therapy. Based on this experience, in patients on chronic treatment with diclofenac potassium immediate-release tablets, periodic monitoring of transaminases is recommended (see PRECAUTIONS, Laboratory Tests). Notable elevations of ALT or AST (three or more times the upper limit of normal) have been reported in approximately 2%-4% of patients, including marked elevations (eight or more times the upper limit of normal) in about 1% of patients in clinical trials with diclofenac. In addition, rare cases of severe hepatic reactions, including jaundice and fatal fulminant hepatitis, liver necrosis and hepatic failure, some of them with fatal outcomes have been reported.

A patient with symptoms and/or signs suggesting liver dysfunction, or in whom an abnormal liver test has occurred, should be evaluated for evidence of the development of a more severe hepatic reaction while on therapy with diclofenac potassium immediate-release tablets. If clinical signs and symptoms consistent with liver disease develop, or if systemic manifestations occur (e.g., eosinophilia, rash, etc.), diclofenac potassium immediate-release tablets should be discontinued.

Anemia is sometimes seen in patients receiving NSAIDs, including diclofenac potassium immediate-release tablets. This may be due to fluid retention, GI loss, or an incompletely described effect upon erythropoiesis. Patients on long-term treatment with NSAIDs, including diclofenac potassium immediate-release tablets, should have their hemoglobin or hematocrit checked if they exhibit any signs or symptoms of anemia.

NSAIDs inhibit platelet aggregation and have been shown to prolong bleeding time in some patients. Unlike aspirin, their effect on platelet function is quantitatively less, of shorter duration, and reversible. Patients receiving diclofenac potassium immediate-release tablets who may be adversely affected by alterations in platelet function, such as those with coagulation disorders or patients receiving anticoagulants, should be carefully monitored.

Patients with asthma may have aspirin-sensitive asthma. The use of aspirin in patients with aspirin-sensitive asthma has been associated with severe bronchospasm which can be fatal. Since cross-reactivity, including bronchospasm, between aspirin and other nonsteroidal anti-inflammatory drugs has been reported in such aspirin-sensitive patients, diclofenac potassium immediate-release tablets should not be administered to patients with this form of aspirin sensitivity and should be used with caution in all patients with preexisting asthma.

In 718 patients treated for shorter periods, i.e., 2 weeks or less, with diclofenac potassium immediate-release tablets, adverse reactions were reported one-half to one-tenth as frequently as by patients treated for longer periods. In a 6-month, double-blind trial comparing diclofenac potassium immediate-release tablets (N=196) versus diclofenac sodium delayed-release tablets (N=197) versus ibuprofen (N=197), adverse reactions were similar in nature and frequency.

In patients taking diclofenac potassium immediate-release tablets or other NSAIDs, the most frequently reported adverse experiences occurring in approximately 1%-10% of patients are:

Gastrointestinal experiences including: abdominal pain, constipation, diarrhea, dyspepsia, flatulence, gross bleeding/perforation, heartburn, nausea, GI ulcers (gastric/duodenal) and vomiting.

Abnormal renal function, anemia, dizziness, edema, elevated liver enzymes, headaches, increased bleeding time, pruritus, rashes and tinnitus.

Additional adverse experiences reported occasionally include:

Body as a Whole:

Cardiovascular System:

Digestive System:

Hemic and Lymphatic System:

Metabolic and Nutritional:

Nervous System:

Respiratory System:

Skin and Appendages:

Special Senses:

Urogenital System:

Other adverse reactions, which occur rarely are:

Body as a Whole:

Cardiovascular System:

Digestive System:

Hemic and Lymphatic System:

Metabolic and Nutritional:

Nervous System:

Respiratory System:

Skin and Appendages:

Special Senses:

×

Reference

This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"

While we update our database periodically, we cannot guarantee it is always updated to the latest version.

×

Disclaimer: