Brands of Diclofenac Potassium in Kenya
KNAC® , Universal Corporation Limited.
Brands of Diclofenac Sodium in Kenya:
Adiflam®, Leben Laboratories Pvt Ltd.
Dicloas®, Astra Lifecare
Diclogen Retard® , Agio
Diclofenac sodium®, Laborate
Diclofen suppositories for children® ,United Pharmaceuticals
Dinac Retard®, Universal corporation Limited.
Dynapar AQ PFS®, Troikaa
Elfenac® , Elys
Maxiclofenac TR®, Navana
Rheumac®, Lab & Allied
MODE OF ACTION
Diclofenac has analgesic, anti-inflammatory, and antipyretic properties.
The mechanism of action of diclofenac , like that of other NSAIDs, is not completely understood but involves inhibition of cyclooxygenase (COX-1 and COX-2).
- Rheumatoid arthritis
- Low back pain
- Migraine attacks
- Acute musculo-skeletal disorders and trauma such as periarthritis (especially frozen shoulder), tendinitis, tenosynovitis, bursitis, sprains, strains and dislocations; relief of pain in fractures
- Ankylosing spondylitis
- Acute gout
- Control of pain and inflammation in orthopaedic, dental and other minor surgery
- Pyrophosphate arthropathy and associated disorders
Hypersensitivity to the active substance or any of the excipients.
Active, gastric or intestinal ulcer, bleeding or perforation.
History of gastrointestinal bleeding or perforation, relating to previous NSAID therapy.
Active, or history of recurrent peptic ulcer / haemorrhage (two or more distinct episodes of proven ulceration or bleeding).
Last trimester of pregnancy .
Established congestive heart failure (NYHA II-IV), ischemic heart disease, peripheral arterial disease and/or cerebrovascular disease.
Like other non-steroidal anti-inflammatory drugs (NSAIDs), diclofenac is also contraindicated in patients in whom attacks of asthma, angioedema, urticaria or acute rhinitis are precipitated by ibuprofen, acetylsalicylic acid or other nonsteroidal anti-inflammatory drugs.
DICLOFENAC DRUG INTERACTIONS
Lithium: If used concomitantly, diclofenac may increase plasma concentrations of lithium. Monitoring of the serum lithium level is recommended.
Digoxin: If used concomitantly, diclofenac may raise plasma concentrations of digoxin. Monitoring of the serum digoxin level is recommended.
Diuretics and antihypertensive agents: Like other NSAIDs, concomitant use of diclofenac with diuretics and antihypertensive agents (e.g. beta-blockers, angiotensin converting enzyme (ACE) inhibitors may cause a decrease in their antihypertensive effect via inhibition of vasodilatory prostaglandin synthesis.
Drugs known to cause hyperkalemia: Concomitant treatment with potassium-sparing diuretics, ciclosporin, tacrolimus or trimethoprim may be associated with increased serum potassium levels, which should therefore be monitored frequently.
Anticoagulants and anti-platelet agents: Caution is recommended since concomitant administration could increase the risk of bleeding . Although clinical investigations do not appear to indicate that diclofenac has an influence on the effect of anticoagulants, there are reports of an increased risk of haemorrhage in patients receiving diclofenac and anticoagulant concomitantly. Therefore, to be certain that no change in anticoagulant dosage is required, close monitoring of such patients is required. As with other nonsteroidal anti-inflammatory agents, diclofenac in a high dose can reversibly inhibit platelet aggregation.
Other NSAIDs including cyclooxygenase-2 selective inhibitors and corticosteroids: Co-administration of diclofenac with other systemic NSAIDs or corticosteroids may increase the risk of gastrointestinal bleeding or ulceration. Avoid concomitant use of two or more NSAIDs .
Selective serotonin reuptake inhibitors (SSRIs): Concomitant administration of SSRI’s may increase the risk of gastrointestinal bleeding.
Antidiabetics: Clinical studies have shown that diclofenac can be given together with oral antidiabetic agents without influencing their clinical effect. However there have been isolated reports of hypoglycaemic and hyperglycaemic effects necessitating changes in the dosage of the antidiabetic agents during treatment with diclofenac. For this reason, monitoring of the blood glucose level is recommended as a precautionary measure during concomitant therapy.
Methotrexate: Diclofenac can inhibit the tubular renal clearance of methotrexate hereby increasing methotrexate levels. Caution is recommended when NSAIDs, including diclofenac, are administered less than 24 hours before treatment with methotrexate, since blood concentrations of methotrexate may rise and the toxicity of this substance be increase. Cases of serious toxicity have been reported when methotrexate and NSAIDs, including diclofenac are given within 24 hours of each other. This interaction is mediated through accumulation of methotrexate resulting from impairment of renal excretion in the presence of the NSAID.
Ciclosporin: Diclofenac, like other NSAIDs, may increase the nephrotoxicity of ciclosporin due to the effect on renal prostaglandins. Therefore, it should be given at doses lower than those that would be used in patients not receiving ciclosporin.
Tacrolimus: Possible increased risk of nephrotoxicity when NSAIDs are given with tacrolimus. This might be mediated through renal antiprostagladin effects of both NSAID and calcineurin inhibitor.
Quinolone antibacterials: Convulsions may occur due to an interaction between quinolones and NSAIDs. This may occur in patients with or without a previous history of epilepsy or convulsions. Therefore, caution should be exercised when considering the use of a quinolone in patients who are already receiving an NSAID.
Phenytoin: When using phenytoin concomitantly with diclofenac, monitoring of phenytoin plasma concentrations is recommended due to an expected increase in exposure to phenytoin.
Colestipol and cholestyramine: These agents can induce a delay or decrease in absorption of diclofenac. Therefore, it is recommended to administer diclofenac at least one hour before or 4 to 6 hours after administration of colestipol/ cholestyramine.
Cardiac glycosides: Concomitant use of cardiac glycosides and NSAIDs in patients may exacerbate cardiac failure, reduce GFR and increase plasma glycoside levels.
Mifepristone: NSAIDs should not be used for 8-12 days after mifepristone administration as NSAIDs can reduce the effect of mifepristone.
Potent CYP2C9 inhibitors: Caution is recommended when co-prescribing diclofenac with potent CYP2C9 inhibitors (such as voriconazole), which could result in a significant increase in peak plasma concentrations and exposure to diclofenac due to inhibition of diclofenac metabolism.
Zidovudine: Increased risk of haematological toxicity when NSAIDs are given with zidovudine. There is evidence of an increased risk of Hemarthrosis and haematoma in HIV(+) haemophiliacs receiving concurrent treatment with zidovudine and ibuprofen.
ADVERSE DRUG REACTIONS:
Cardiovascular Thrombotic Events
GI Bleeding, Ulceration and Perforation
Heart Failure and Edema
Renal Toxicity and Hyperkalemia
Serious Skin Reactions
Reporting of suspected adverse reactions:
The PPB Department of Pharmacovigilance was set up with a vision to develop, implement and continuously upgrade an appropriate system for detecting, reporting and monitoring adverse drug reactions (ADRs) and other relevant problems with medicines in Kenya. The department strives to ensure the safety and efficacy of pharmaceutical products in Kenya.
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals/ Patients are encouraged to report any suspected adverse reactions via Pharmacovigilance Yellow Form, firstname.lastname@example.org or clicking below button:
Diclofenac in Kenya
Diclofenac in Kenya
Diclofenac in Kenya
Clinical | Pharmacokinetic data
Pregnancy Category: C
Routes of Administration: By mouth, rectal, intramuscular, intravenous (renal- and gallstones), topical
Bioavailability: Not Available
Protein Binding: More than 99%
Metabolosim: Liver, oxidative, primarily by CYP2C9, also by CYP2C8, CYP3A4, as well as conjugative by glucuronidation (UGT2B7) and sulfation; no active metabolites exist
Onset of Action: Not Available
Elimination Half life: 1.2–2 hr (35% of the drug enters enterohepatic recirculation)
Excretion: 40% biliary 60% urine
Legal Status | Dosage forms & Strengths
Prescription only Medicine (POM) , ℞-only
Narcotic Drugs and Psychotropic Substances (Control ) Act Schedule:
This drug is not a controlled substance under Narcotic Drugs and Psychotropic Substances (Control ) Act
Dosage Forms | Strengths:
Tablets | Injectable | Topical Gel | Suppositories | Opthalmic formulation
|CompTox Dashboard (EPA)|
- Menasse, R., et al. “Pharmacological properties of diclofenac sodium and its metabolites.” Scandinavian Journal of Rheumatology 7.sup22 (1978): 5-16.
- Willis, J. V., et al. “The pharmacokinetics of diclofenac sodium following intravenous and oral administration.” European journal of clinical pharmacology 16.6 (1979): 405-410.