The mechanism of action of diclofenac sodium, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition. Thought to block activity of cyclooxygenase, thereby inhibiting inflammatory responses of vasodilation and swelling and blocking transmission of painful stimuli.
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
• Store below 30 C°
• Protect from light and freezing
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
Lofedic®
Suppository 50mg
Non-steroidal anti-inflammatory drug (NSAID)
Nonopioid analgesic, antiarthritic
category C
The mechanism of action of diclofenac sodium, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition. Thought to block activity of cyclooxygenase, thereby inhibiting inflammatory responses of vasodilation and swelling and blocking transmission of painful stimuli.
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
• Store below 30 C°
• Protect from light and freezing
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
Lofedic®
[view] =>Lofedic®
) ) [field_contraindications] => Array ( [0] => Array ( [value] => [format] => [safe] => [view] => ) ) [field_dosage_form] => Array ( [0] => Array ( [value] => Suppository 50mg [format] => 1 [safe] =>Suppository 50mg
[view] =>Suppository 50mg
) ) [field_drug_interactions] => Array ( [0] => Array ( [value] => Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding Antihypertensives, diuretics: decreased efficacy of these drugs Antineoplastics: increased risk of hematologic adverse reactions Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects Cyclosporine, probenecid: increased risk of diclofenac toxicity Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity Potassium-sparing diuretics: increased risk of hyperkalemia [format] => 1 [safe] =>Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Non-steroidal anti-inflammatory drug (NSAID)
[view] =>Non-steroidal anti-inflammatory drug (NSAID)
) ) [field_precautions] => Array ( [0] => Array ( [value] => • severe cardiovascular, renal, or hepatic disease; bleeding tendency • history of porphyria or asthma • concurrent anticoagulant use • elderly patients • pregnant or breastfeeding patients • children [format] => 1 [safe] =>• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
category C
[view] =>category C
) ) [field_references] => Array ( [0] => Array ( [value] => [format] => [safe] => [view] => ) ) [field_side_effects] => Array ( [0] => Array ( [value] => CNS: dizziness, drowsiness, headache CV: hypertension EENT: tinnitus GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure Hematologic: prolonged bleeding time Hepatic: hepatotoxicity Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation Other: allergic reactions (including edema), anaphylaxis [format] => 1 [safe] =>CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
• Store below 30 C°
• Protect from light and freezing
• Store below 30 C°
• Protect from light and freezing
Nonopioid analgesic, antiarthritic
[view] =>Nonopioid analgesic, antiarthritic
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[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>Lofedic®
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[#printed] => 1 ) [#title] => [#description] => [#children] =>Lofedic®
Suppository 50mg
[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>Suppository 50mg
) [#title] => [#description] => [#children] =>Suppository 50mg
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[#printed] => 1 ) [#title] => [#description] => [#children] =>Suppository 50mg
Non-steroidal anti-inflammatory drug (NSAID)
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Nonopioid analgesic, antiarthritic
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category C
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[#printed] => 1 ) [#title] => [#description] => [#children] =>category C
The mechanism of action of diclofenac sodium, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition. Thought to block activity of cyclooxygenase, thereby inhibiting inflammatory responses of vasodilation and swelling and blocking transmission of painful stimuli.
[#title] => [#description] => [#printed] => 1 ) [field_pharmacokinetics] => Array ( [#type_name] => product [#context] => full [#field_name] => field_pharmacokinetics [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 4 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_pharmacokinetics [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => Absorption 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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%. Distribution The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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. Metabolism 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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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. Excretion 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 [format] => 1 [safe] =>Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
• Store below 30 C°
• Protect from light and freezing
• Store below 30 C°
• Protect from light and freezing
• Store below 30 C°
• Protect from light and freezing
• Store below 30 C°
• Protect from light and freezing
• Store below 30 C°
• Protect from light and freezing
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
Lofedic®
Suppository 50mg
Non-steroidal anti-inflammatory drug (NSAID)
Nonopioid analgesic, antiarthritic
category C
The mechanism of action of diclofenac sodium, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition. Thought to block activity of cyclooxygenase, thereby inhibiting inflammatory responses of vasodilation and swelling and blocking transmission of painful stimuli.
Absorption
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. Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%.
Distribution
The apparent volume of distribution (V/F) of diclofenac sodium is 1.4 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.
Metabolism
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. The major diclofenac metabolite, 4'-hydroxy-diclofenac, has very weak pharmacologic activity. The formation of 4'-hydroxy- diclofenac is primarily mediated by CPY2C9. Both diclofenac and its oxidative metabolites undergo glucuronidation or sulfation followed by biliary excretion. Acylglucuronidation mediated by UGT2B7 and oxidation mediated by CPY2C8 may also play a role in diclofenac metabolism. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy- and 3'-hydroxy-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.
Excretion
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
• Analgesia; dysmenorrhea
• Rheumatoid arthritis
• Osteoarthritis
• Ankylosing spondylitis
• severe cardiovascular, renal, or hepatic disease; bleeding tendency
• history of porphyria or asthma
• concurrent anticoagulant use
• elderly patients
• pregnant or breastfeeding patients
• children
Anticoagulants, antiplatelet agents, cephalosporins, thrombolytics: increased risk of bleeding
Antihypertensives, diuretics: decreased efficacy of these drugs
Antineoplastics: increased risk of hematologic adverse reactions
Colchicine, corticosteroids, other NSAIDs: additive adverse GI effects
Cyclosporine, probenecid: increased risk of diclofenac toxicity
Digoxin, lithium, methotrexate, phenytoin, theophylline: increased levels of these drugs, greater risk of toxicity
Potassium-sparing diuretics: increased risk of hyperkalemia
CNS: dizziness, drowsiness, headache
CV: hypertension
EENT: tinnitus
GI: diarrhea, abdominal pain, dyspepsia, heartburn, peptic ulcer, GI bleeding, GI perforation
GU: dysuria, frequent urination, hematuria, proteinuria , nephritis, acute renal failure
Hematologic: prolonged bleeding time
Hepatic: hepatotoxicity
Skin: eczema, photosensitivity, rash, contact dermatitis, dry skin, exfoliation
Other: allergic reactions (including edema), anaphylaxis
• Store below 30 C°
• Protect from light and freezing
• Diclofenac Sodium Injection 75mg / 3ml : 5 ampoules/box
• Diclofenac Sodium suppository 50mg: 5 suppositories/box
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