72 Agege Motor Road, Alakara, Mushin.
Tel: 01-81507361, 2663986, 234-8033018912, 08033054541
Wuhan Pharmaceutical Co. Ltd, No. 5, Gutian Road, Wuhan, China.
Dosage Form, Composition & NAFDAC Registration Number (NRN)
Injection (NRN: 04-5282): Each 3 mL contains Diclofenac sodium 75 mg, Benzyl alcohol 4% (Preservative), Sodium metabisulfite 0.35% (Antioxidant).
How to identify the Product: A clear, colourless liquid free from visible particles.
Pack size: 10 x 10's.
The exact mechanism of action is not entirely known, but the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is thought to be inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.
Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid. This is also the main side effect of diclofenac. Diclofenac has a low to moderate preference to block the COX2-isoenzyme (approximately 10-fold) and is said to have, therefore, a somewhat lower incidence of gastrointestinal complaints than noted with indomethacin and aspirin.
The action of one single dose is much longer (6 to 8 hr) than the very short half-life of the drug indicates. This could be partly because it persists for over 11 hours in synovial fluids.
Diclofenac may also be a unique member of the NSAIDs. Some evidence indicates it inhibits the lipoxygenase pathways, thus reducing formation of the leukotrienes (also pro-inflammatory autacoids). It also may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain its high potency - it is the most potent NSAID on a broad basis.
Diclofenac injection is suitable as initial therapy for inflammatory and degenerative rheumatic diseases as well as for the treatment of painful conditions due to inflammation of non-rheumatic origin.
- Contra-indications to Diclofenac or other NSAIDs and other ingredients in the formulation.
- History of gastric ulcer, liver and kidney problems related to NSAIDs.
Hepatic or renal failure. Serious interactions have been reported after the concomitant use of methotrexate and diclofenac.
Aspirin:When Diclofenac sodium extended-release is administered with aspirin, its protein binding is reduced. The clinical significance of this interaction is not known; however, as with other NSAIDs, concomitant administration of Diclofenac and aspirin is not generally recommended because of the potential of increased adverse effects.
Methotrexate: NSAIDs have been reported to competitively inhibit methotrexate accumulation in rabbit kidney slices. This may indicate that they could enhance the toxicity of methotrexate. Caution should be used when NSAIDs are administered concomitantly with methotrexate.
Cyclosporine: Diclofenac sodium extended-release, like other NSAIDs, may affect renal prostaglandins and increase the toxicity of certain drugs. Therefore, concomitant therapy with Diclofenac sodium extended-release may increase cyclosporine's nephrotoxicity. Caution should be used when Diclofenac sodium extended-release is administered concomitantly with cyclosporine.
ACE-inhibitors:Reports suggest that NSAIDs may diminish the antihypertensive effect of ACE inhibitors. This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE inhibitors.
Furosemide:Clinical studies, as well as post-marketing observations, have shown that Diclofenac sodium extended-release can reduce the natriuretic effect of furosemide and thiazides in some patients. This response has been attributed to inhibition of renal prostaglandin synthesis. During concomitant therapy with NSAIDs, the patient should be observed closely for signs of renal failure, as well as to assure diuretic efficacy.
Lithium:NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium clearance. The mean minimum lithium concentration increased 15% and the renal clearance was decreased by approximately 20%. These effects have been attributed to inhibition of renal prostaglandin synthesis by the NSAID. Thus, when NSAIDs and lithium are administered concurrently, subjects should be observed carefully for signs of lithium toxicity.
Warfarin:The effects of warfarin and NSAIDs on GI bleeding are synergistic, such that users of both drugs together have a risk of serious GI bleeding higher than users of either drug alone.
Nausea and diarrhoea, headache, tinnitus or dizziness. Peripheral oedema anad skin reactions, such as drug rash and eczema, have also been encoutered. CNS side effects such as tiredness, insomnia, nervousness, depression or irritability, have occured. Blurred vision and other ocular reactions.
Sensitivity reactions (e.g. bronchspasm, anaphylactic/anaphylactoid systemic reactions), elevated transaminase levels, jaundice, hepatitis, renal failure and nephrotic syndrome, may occur. Dyshaemopolesis (leucopenia, thrombo-cytopenia, aplastic anaemia) and erythema multiforme have been observed. Agranulo-cytosis and haemolytic anaemia have been observed. Abscesses and local necrosis have also occurred, particularly in elderly diabetics.
Dosage & Administration
Not intended for IV route of administration.
For adults, the dosage is generally one Acu-diclofenac injection daily, injected deep intragluteally into the upper outer quadrant.
By way of exception, in severe cases two injections separated by an interval of a few hours, can be given per day (one into each buttock). Acu-diclofenac injection should not be given for more than a few days.
Store below 25ºC. Protect from light.