Does tadalafil cause gout? This is a common concern for men prescribed this medication for erectile dysfunction or benign prostatic hyperplasia. Tadalafil, a phosphodiesterase type 5 (PDE5) inhibitor available in the UK as Cialis and generic formulations, is not known to trigger or worsen gout. There is no established clinical evidence linking tadalafil to elevated uric acid levels or gout attacks. If you experience joint pain whilst taking tadalafil, other factors such as diet, concurrent medications, or underlying health conditions are more likely responsible. This article examines the relationship between tadalafil and gout, clarifying the evidence and helping you understand when to seek medical advice.

What Is Tadalafil and How Does It Work?

Tadalafil is a prescription medication primarily used to treat erectile dysfunction (ED) and the urinary symptoms of benign prostatic hyperplasia (BPH). It belongs to a class of drugs called phosphodiesterase type 5 (PDE5) inhibitors, which also includes sildenafil and vardenafil. In the UK, tadalafil is available under brand names such as Cialis, as well as generic formulations.

The mechanism of action involves inhibiting the PDE5 enzyme, which is responsible for breaking down cyclic guanosine monophosphate (cGMP) in smooth muscle cells. By blocking this enzyme, tadalafil allows cGMP levels to remain elevated, promoting relaxation of smooth muscle in the penis, prostate and bladder. This increased blood flow facilitates erections in response to sexual stimulation and can also relieve lower urinary tract symptoms associated with BPH.

Tadalafil is notable for its long duration of action, with effects lasting up to 36 hours. It is typically taken as needed for ED (usually 10mg or 20mg doses) or as a daily treatment (2.5mg daily for ED only, or 5mg daily for ED or BPH). The medication is generally well-tolerated, though common side effects include headache, indigestion, back pain, muscle aches, flushing, and nasal congestion. These effects are usually mild and transient.

Tadalafil should not be used alongside nitrate medications (such as glyceryl trinitrate) or riociguat due to the risk of severe hypotension. Caution is needed with alpha-blockers (especially doxazosin), potent CYP3A4 inhibitors (e.g., ketoconazole, clarithromycin), and grapefruit juice. Patients with significant cardiovascular disease, recent stroke or heart attack, uncontrolled blood pressure, severe kidney or liver impairment, or history of non-arteritic anterior ischaemic optic neuropathy (NAION) should discuss their suitability for tadalafil with their GP or specialist before commencing treatment.

If you experience any side effects, you can report them through the Yellow Card Scheme at yellowcard.mhra.gov.uk.

Understanding Gout: Causes and Risk Factors

Gout is a form of inflammatory arthritis characterised by sudden, severe attacks of pain, swelling, redness, and tenderness in joints, most commonly affecting the base of the big toe. It results from the accumulation of uric acid crystals (monosodium urate) in joints and surrounding tissues. When uric acid levels in the blood become excessively high (a condition called hyperuricaemia), crystals can form and trigger an intense inflammatory response, although it's important to note that hyperuricaemia does not always lead to gout.

Uric acid is a waste product formed from the breakdown of purines—substances found naturally in the body and in certain foods such as red meat, seafood, and alcohol, particularly beer. Normally, uric acid dissolves in the blood and is excreted by the kidneys through urine. However, when the body produces too much uric acid or the kidneys excrete too little, levels can rise to problematic concentrations.

Key risk factors for developing gout include:

• Dietary factors: High intake of purine-rich foods, excessive alcohol consumption (especially beer and spirits), and sugar-sweetened beverages containing fructose

• Medical conditions: Obesity, hypertension, diabetes, metabolic syndrome, chronic kidney disease, and cardiovascular disease

• Medications: Diuretics (particularly thiazides), low-dose aspirin, and certain immunosuppressants

• Genetics: Family history of gout significantly increases risk

• Demographics: More common in men and postmenopausal women; prevalence increases with age

Gout affects approximately 2.5% of the UK population, with incidence rising due to increasing rates of obesity and associated metabolic conditions. Acute gout attacks can be extremely painful and debilitating, typically reaching peak intensity within 12–24 hours. Without appropriate management, gout can become chronic, leading to permanent joint damage and the formation of tophi (deposits of uric acid crystals under the skin).

Medications That Can Trigger or Worsen Gout

Several medications are recognised to increase the risk of gout or precipitate acute attacks by raising serum uric acid levels or affecting its excretion. Understanding these drug-related risks is essential for both patients and healthcare professionals when managing gout or assessing new symptoms.

Diuretics are among the most common culprits. Thiazide diuretics (such as bendroflumethiazide) and loop diuretics (like furosemide) reduce uric acid excretion by the kidneys, leading to hyperuricaemia. These medications are widely prescribed for hypertension and heart failure, creating a clinical dilemma as cardiovascular disease and gout often coexist. Low-dose aspirin (typically used for cardiovascular protection) can also impair uric acid excretion, though the benefits for heart disease prevention usually outweigh this risk. It's important not to stop these medications without consulting your doctor, as the cardiovascular benefits often outweigh the gout risk.

Other medications associated with increased gout risk include certain immunosuppressants (ciclosporin and tacrolimus), chemotherapy agents, and medications containing nicotinic acid (niacin). Additionally, drugs that cause rapid cell turnover can increase purine breakdown and subsequently raise uric acid levels.

Regarding tadalafil specifically, there is no established clinical evidence linking it to gout development or exacerbation. Tadalafil is not listed in the Summary of Product Characteristics or British National Formulary as affecting uric acid metabolism or excretion. The drug's mechanism of action—PDE5 inhibition—does not appear to interfere with purine metabolism or renal handling of uric acid.

If you are taking tadalafil and experience symptoms suggestive of gout, it is more likely related to other risk factors such as diet, comorbid conditions, or concurrent medications rather than the tadalafil itself. However, any new joint symptoms should be evaluated by your GP to establish the correct diagnosis and identify potential contributing factors. Your doctor can review your complete medication list and assess whether any drugs might be influencing uric acid levels.

When to Seek Medical Advice About Gout Symptoms

Recognising when to seek medical attention for suspected gout is crucial for prompt diagnosis, effective pain relief, and prevention of long-term complications. You should contact your GP or seek urgent medical advice if you experience:

• Sudden, severe joint pain, particularly if it develops rapidly over a few hours

• Intense swelling, redness, and warmth around a joint, most commonly the big toe, but also potentially affecting ankles, knees, fingers, wrists, or elbows

• Joint pain accompanied by fever or feeling generally unwell, as this may indicate septic arthritis (joint infection), which requires emergency hospital assessment

• Symptoms that significantly impair mobility or prevent you from bearing weight on the affected limb

For a first suspected gout attack, prompt assessment is recommended to confirm the diagnosis and initiate appropriate treatment within 12-24 hours of symptom onset. Acute gout should be treated promptly with anti-inflammatory medications such as NSAIDs (like naproxen), colchicine, or corticosteroids, depending on individual patient factors and contraindications.

If you have established gout and experience a flare despite being on preventative treatment (such as allopurinol), contact your GP to review your management plan. According to NICE guidance, urate-lowering therapy (ULT) should be offered if you have had two or more gout flares in 12 months, and should be considered after a first flare if you have tophi, chronic kidney disease (stage 3 or worse), urate kidney stones, or are taking diuretics.

Patients taking multiple medications, including tadalafil, should inform their doctor of their complete medication list during assessment. Whilst tadalafil itself does not cause gout, your GP will want to review all medications to identify any that might contribute to hyperuricaemia.

Long-term gout management involves lifestyle modifications (weight management, dietary changes, limiting alcohol), treating underlying conditions, and potentially starting urate-lowering therapy. Regular monitoring of serum uric acid levels helps ensure treatment effectiveness, with a target level below 360 micromol/L (or below 300 micromol/L in severe or tophaceous gout). When starting ULT, prophylactic medication (such as colchicine) is often prescribed to prevent flares during the initial months of treatment. Early intervention and appropriate management can prevent the progression to chronic tophaceous gout and preserve joint function.

Frequently Asked Questions