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Diclofenac is one of the most commonly used pain relievers worldwide — as a tablet, gel, patch or syringe. It has a strong anti-inflammatory and analgesic effect, particularly for joint and muscle pain, osteoarthritis and rheumatic complaints.
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Diclofenac should be taken at the lowest effective dose for the shortest possible time. It is contraindicated in heart disease. This article does not replace medical advice.
Diclofenac is one of the most prescribed pain and rheumatism medicines worldwide – and at the same time the NSAID with the highest cardiovascular risk among the over-the-counter options. This is no small matter: the combination of wide availability and considerable cardiac risk makes diclofenac one of the pharmacologically most important topics for patient education in self-medication.
| Property | Details |
|---|---|
| Active substance | Diclofenac (as diclofenac sodium or potassium) |
| ATC code | M01AB05 |
| Drug class | Non-steroidal anti-inflammatory drug (NSAID) |
| Available forms | Tablets 25/50/75 mg, slow-release tablets 75/100 mg, gel 1–5%, patches, injection, suppositories, eye drops |
| Half-life | 1–2 hours (short!) |
| Onset of action | 30–60 min (oral), immediate (injection) |
| Bioavailability | approx. 50–60% |
| Maximum dose | 150 mg/day (oral) |
| Prescription status | Low doses over the counter (gel, low-dose); higher doses prescription only |
| Special feature | Highest cardiovascular risk of all OTC NSAIDs |
Diclofenac works – like all NSAIDs – by inhibiting the enzymes cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2). These enzymes produce prostaglandins, which play a central role in inflammation, pain, and fever. Blocking the enzymes reduces prostaglandin production and thereby inflammation and pain. So far the desired effect.
Here lies the pharmacological core of the problem. Diclofenac is more COX-2-selective than ibuprofen – it inhibits COX-2 more strongly relative to COX-1. That is actually a good property, because COX-2 is mainly responsible for inflammation. But COX-2 is also needed in the blood vessels: there it produces prostacyclin, a substance that widens blood vessels and prevents the platelets from clumping together.
When diclofenac inhibits the vascular COX-2, prostacyclin production falls. At the same time, thromboxane A2 – produced via COX-1 in the platelets – remains active. Thromboxane narrows blood vessels and promotes clot formation. The result is a shifted balance: more vasoconstriction, more tendency to thrombosis – and thus an increased risk of heart attack and stroke. This is exactly the mechanism that was also the problem with the coxibs (rofecoxib was withdrawn from the market in 2004 for this reason). Diclofenac is pharmacologically closer to the coxibs than to classic NSAIDs like ibuprofen.
In addition, all NSAIDs inhibit prostaglandin production in the kidneys. There, prostaglandins are important for regulating the kidney vessels and controlling blood pressure. Inhibiting them can raise blood pressure, worsen kidney function, and weaken the effect of blood-pressure-lowering medications – which is especially relevant for patients on ACE inhibitors or sartans.
Diclofenac is used for a broad spectrum of pain and inflammatory conditions. The most important basic rule: as low a dose as possible, for as short a time as needed. This is not an empty phrase – every extra day on diclofenac raises the cardiac risk. Record your intake in your digital medication plan, so that all treating doctors are informed.
| Indication | Oral dose | Duration | Alternative |
|---|---|---|---|
| Acute pain (teeth, head) | 50 mg 2–3×/day | Max. 3–5 days | Ibuprofen, paracetamol |
| Osteoarthritis | 75–150 mg/day in divided doses | Short-term! | Prefer topical gel |
| Rheumatoid arthritis | 100–150 mg/day | Under medical supervision | Possibly DMARDs instead of long-term NSAIDs |
| Back pain (acute) | 50–75 mg 2×/day | Max. 1–2 weeks | Gel + movement |
| Migraine | 50–100 mg (potassium salt) | Single dose for an attack | Triptans |
| Joint pain (local) | Gel 3–4×/day | Up to 3 weeks | Ibuprofen gel |
The cardiovascular risk of diclofenac is clinically documented and not to be underestimated. The most important study on it is the Coxib and traditional NSAID Trialists' Collaboration, a Lancet meta-analysis from 2013 that analysed data from 639 randomised studies with over 350,000 patients. The result: diclofenac increases the heart-attack risk by about 40% – a figure comparable to that of the coxibs. As a reminder: rofecoxib (Vioxx) was withdrawn from the market in 2004 because of the same risk. Danish healthcare data from 2018 confirm: diclofenac has a higher cardiovascular risk than ibuprofen, naproxen, and paracetamol.
| NSAID | Heart-attack risk (relative) | Stroke risk | GI bleeding |
|---|---|---|---|
| Diclofenac | ↑↑↑ (+40%) | ↑↑ | ↑↑ |
| Ibuprofen (>1200 mg/day) | ↑↑ (+30%) | ↑ | ↑↑ |
| Naproxen | ↔ (neutral) | ↔ | ↑↑↑ (highest GI risk!) |
| Paracetamol | ↔ (neutral) | ↔ | ↔ |
| Celecoxib (coxib) | ↑ | ↑ | ↓ (lower than traditional NSAIDs) |
Important for putting this in perspective: the 40% relative risk refers to chronic use. For a healthy 35-year-old who takes diclofenac once for three days for toothache, the absolute risk is extremely small. For a 68-year-old patient with high blood pressure who takes diclofenac over weeks for osteoarthritis pain, it is clinically relevant. The risk is therefore strongly context-dependent – and should always be assessed individually.
This is one of the clinically most important and at the same time least known interactions in pain medicine. Low-dose aspirin works by binding irreversibly to the COX-1 binding site in the platelets and blocking it permanently. Diclofenac (and ibuprofen) block the same binding site – but reversibly. If diclofenac is taken before aspirin, it occupies the binding site before aspirin can dock. Aspirin no longer finds a free spot and cannot exert its irreversible inhibition. Result: the cardioprotection of low-dose aspirin is cancelled. Anyone taking aspirin daily for heart prevention should therefore switch to paracetamol as a painkiller.
The triple whammy is one of the most dangerous combinations in general medicine – and at the same time one of the most common. The principle is the same as described in the candesartan article: an NSAID + an ACE inhibitor or sartan + a diuretic hit kidney function from three directions at once.
NSAIDs like diclofenac reduce prostaglandin production in the kidneys, which lessens blood flow to the kidney. ACE inhibitors like ramipril and sartans like candesartan widen the outflowing kidney vessels and thereby lower the filtration pressure. Diuretics like hydrochlorothiazide or furosemide lower the circulating blood volume. Together, these three effects can lead to acute kidney failure – especially with dehydration, heat, or in older patients.
How does this combination arise in everyday life? A typical patient takes ramipril plus a diuretic for high blood pressure. They get back pain and buy diclofenac over the counter at the pharmacy – without knowing that this puts a triple burden on their kidneys. At the same time, diclofenac weakens the effect of ramipril and candesartan: blood pressure rises, and the patient wonders why their blood-pressure tablets "no longer work". The brite interaction check detects this combination automatically.
Like all NSAIDs, diclofenac inhibits prostaglandin production in the stomach lining. There, prostaglandins are responsible for the mucus production that protects the stomach wall from the aggressive hydrochloric acid. Without this protection, the risk of stomach ulcers and gastrointestinal bleeding rises – even with a short duration of use. Black stool is a warning sign of gastrointestinal bleeding and always an emergency.
The gastrointestinal risk with diclofenac is lower than with naproxen but higher than with paracetamol. It can, however, be reduced considerably with accompanying stomach protection.
| Risk factor | Increased risk |
|---|---|
| Age > 65 years | 2–4-fold |
| Concurrent corticosteroid (prednisolone) | 4–5-fold |
| Concurrent SSRI (citalopram) | 12-fold! |
| Concurrent low-dose aspirin | 2–3-fold |
| History of stomach ulcer | 10-fold |
| Anticoagulants (Marcumar) | 6–10-fold |
