Clinical medicine profile
Aceclofenac gel
NSAID / analgesic–anti-inflammatory
- Route
- ORAL / TOPICAL / RECTAL / IM (agent-dependent)
- Schedule
- POM
- ATC
- Not assigned
- PPB status
- registered
Safety essentials
The information most likely to change a prescribing or dispensing decision.
Contraindications
- Active peptic ulcer / GI bleeding.
- Severe heart failure.
- NSAID-exacerbated respiratory disease (aspirin-sensitive asthma) for non-selective agents.
- Third trimester pregnancy (ductus arteriosus, oligohydramnios — class warning).
- Severe renal impairment for many agents.
- Hypersensitivity to NSAIDs.
Precautions
- Lowest effective dose, shortest duration.
- GI protection (PPI) if high risk.
- CV risk (MI/stroke) with many NSAIDs — caution in known CVD.
- Monitor renal function in elderly, diuretic/ACEI/ARB users (triple whammy).
- Avoid combining multiple NSAIDs.
Dosing matrix
Population and organ-function guidance, shown together for faster comparison.
Apply to the affected area 2-3 times daily. Rubbing or massaging should be usually avoided.
See label paediatric section if present; otherwise use paediatric formulary — do not extrapolate adult doses.
Haemodynamically mediated AKI risk — high alert in volume depletion and renin-angiotensin blockade.
- CrCl 0–120: Confirm renal dosing in product SmPC / primary label.
Rare idiosyncratic hepatitis; more concern with prolonged high doses/diclofenac in some datasets.
Use, effects & interactions
Indications
- Pain, inflammation and swelling cases of osteoarthritis, soft tissue, rheumatic disorders, sports, and accidental injuries.
- Clinical selection for Aceclofenac gel should follow culture results where relevant, Kenya STG/EML recommendations, and the current product SmPC.
- Class context: NSAID / analgesic–anti-inflammatory.
- Confirm site-specific dose, duration and monitoring before prescribing.
Adverse effects
- Dyspepsia, nausea, fluid retention, raised BP.
- Serious: peptic ulcer/bleed, AKI, heart failure exacerbation, severe skin reactions, bronchospasm, hepatitis (rare).
Drug interactions
Open multi-drug checker ↗- Risk-stratify GI and CV before prescribing.
- Prefer topical NSAIDs for local MSK pain when adequate.
- Review after short courses.
- Educate on black stools/haematemesis red flags.
Mechanism & disposition
Inhibitors of cyclo-oxygenase [COX-1 and COX-2] enzyme that catalyzes the conversion of arachidonic acid to PGH2.
Read complete mechanism
Inhibitors of cyclo-oxygenase [COX-1 and COX-2] enzyme that catalyzes the conversion of arachidonic acid to PGH2. NSAIDs inhibit cyclo-oxygenase (COX-1 and/or COX-2), reducing prostaglandin and thromboxane synthesis. This yields analgesic, antipyretic and anti-inflammatory effects. COX-1 inhibition drives many GI and platelet adverse effects; COX-2 selective agents spare some GI risk but retain CV warnings.
30–60 minutes
4–12 hours (agent-dependent)
ORAL / TOPICAL / RECTAL / IM (agent-dependent)
of metabolites. Half-lives vary widely (ibuprofen short; naproxen longer; oxicams long).
Pregnancy, lactation & diet
Avoid in third trimester. Earlier pregnancy: use only if needed; prefer paracetamol first-line.
Short-course ibuprofen generally acceptable; avoid chronic high-dose/long half-life agents when possible.
Brands & loaded prices
| Brand | Manufacturer | Pack | Observed price |
|---|---|---|---|
| No reviewed brand listings are linked yet. | |||
Sources & review state
Decision support only. Confirm patient-specific decisions against the current product SmPC, Kenya STG/EML, and professional judgement.