What it is
Dexketoprofen is the active enantiomer of ketoprofen: the half of the molecule that does the work. That is why it achieves the same effect with lower doses (25 mg) than its predecessor. It is an NSAID designed for acute pain, with notable analgesic efficacy and an acceptable profile in short courses.
In Spain it comes as tablets and as granules for oral solution; the latter is absorbed slightly faster. Its summary of product characteristics limits treatment to the period with symptoms: it is not an NSAID for long-term use.
Mechanism of action
Like the other non-selective NSAIDs:
- It inhibits COX-1 and COX-2, reducing prostaglandin synthesis
- By lowering inflammatory mediators, pain relief is greater in pain with inflammation
- Because it inhibits COX-1, it shares the gastric, kidney and cardiovascular risk of the family
At the counter
When to recommend it
- Acute musculoskeletal pain: sprains, bruises, acute low back pain
- Primary dysmenorrhoea
- Dental pain
- Mild to moderate acute pain in short courses
When not to
- Active inflammatory bowel disease (Crohn's disease, ulcerative colitis)
- Decompensated heart failure
- History of active peptic ulcer
- Moderate to severe kidney failure
Warnings
- Important Peptic ulcer: a risk similar to other NSAIDs. Use gastric protection when there are risk factors.
- Important Cardiovascular and cerebrovascular complications with long-term use, especially when there are risk factors.
- Caution Fluid retention: it can decompensate heart failure. Keep an eye on patients with heart disease.
- Caution Interactions with anticoagulants: it increases the risk of bleeding. Combine only if essential.
Pharmacokinetics
- Absorption
- Rapid oral absorption, with bioavailability around 90%. Onset of action at 30–45 minutes. The oral solution is absorbed slightly faster than the tablets.
- Distribution
- Widely distributed in tissues, especially inflamed areas. Plasma protein binding of 99%, which explains some interactions. It crosses the placenta.
- Metabolism
- Hepatic metabolism by glucuronidation. Unlike ketoprofen, it does not produce significant active metabolites.
- Elimination
- Renal elimination of conjugated metabolites. Half-life of 1–2 hours.
Dexketoprofen vs ibuprofen
| Aspect | Dexketoprofen | Ibuprofen |
|---|---|---|
| Analgesic potency | High | Moderate to high |
| Anti-inflammatory activity | High | High |
| Onset of action | Fast (30–45 min; slightly sooner as oral solution) | Moderate (45–60 min; sooner with lysine salts) |
| Gastrointestinal risk | Similar | Similar |
| Usual dose | 25 mg | 400 mg |
Dexketoprofen for acute pain in short courses. Ibuprofen has more experience of use, more presentations (including for children) and is cheaper.
Self-assessment
Three questions. When you check your answers you will see the explanation for each one.
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Dexketoprofen is the pharmacologically active enantiomer of ketoprofen, which allows lower doses (25 mg) with effects comparable to higher doses of ketoprofen.
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NSAIDs, dexketoprofen included, increase the risk of peptic ulcer. With a history of ulcer, it needs a medical assessment and probably gastric protection.
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Its summary of product characteristics limits treatment to the period with symptoms: it is for acute pain in short courses. For long-term pain the cause has to be assessed, and the cardiovascular and gastric risk of a continuous NSAID weighed up.
Training content. It does not replace the summary of product characteristics or clinical judgement.