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Fenofibrate and losartan
  1. S S Daskalopoulou1,
  2. D P Mikhailidis1,
  3. V G Athyros2,
  4. A A Papageorgiou2,
  5. M Elisaf3
  1. 1Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital, Royal Free and University College Medical School, London, UK
  2. 2Atherosclerosis Unit, 2nd Propedeutic Department of Internal Medicine, Aristotelian University, Hippocration Hospital, Thessaloniki, Greece
  3. 3Department of Internal Medicine, Medical School, University of Ioannina, Greece
  1. Correspondence to:
    D P Mikhailidis
    Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital, Royal Free and University College Medical School, Pond street, London NW3 2QG, UK;

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The leader by Professor Bardin1 makes an excellent point. We could benefit from the hypouricaemic action of drugs that are not licensed for this use (for example, losartan and fenofibrate).

Other drugs in common use may also have a uricosuric effect. For example, atorvastatin can reduce serum uric acid concentrations in patients with peripheral arterial disease or hyperlipidaemia.2–4 However, the mechanisms involved are not clear cut; we speculate that atorvastatin can increase renal blood flow and decrease serum creatinine levels.2–4 Thus, the Medical Research Council/British Heart Foundation Heart Protection Study (HPS) showed that simvastatin decreased the deterioration of the glomerular filtration rate (GFR) over a period of 4.6 years in high risk patients with (n = 5963) or without (n = 14 573) diabetes.5 This effect on GFR would almost certainly influence urate excretion. These statin mediated effects are relevant because, as Professor Bardin1 points out, patients with hyperuricaemia may also be dyslipidaemic.

Closer to the interests of rheumatologists are the non-steroidal anti-inflammatory drugs (NSAIDs). Some NSAIDs may exert a favourable effect on urate excretion. For example, diflunisal has been reported to have a uricosuric effect, although the inhibition of xanthine oxidase activity has also been proposed.6,7 Azapropazone (not used as a first line option) has been shown to lower serum urate levels.7,8 Indometacin may have uricosuric properties.7 Tiaprofenic acid is another NSAID with hypouricaemic effect.9

Aspirin has a bimodal effect on the renal handling of uric acid. High doses (>3 g/day) are uricosuric, while lower doses (1–2 g/day) cause urate retention.10 At the lowest dose (75 mg/day) aspirin caused a 15% decrease in urate excretion with a slight but significant increase in serum urate levels.10

The clinical significance of these “additional” uricosuric effects remains to be established. There is also a need to assess the value of using combinations of these drugs (for example, losartan and fenofibrate together with an NSAID with beneficial effects on urate excretion).

The search for NSAIDs that do not exert renal toxicity may well be worthwhile because of their widespread use. Acute attacks of gout are usually treated with high doses of NSAIDs. It could be useful to have NSAIDs with uricosuric properties as well as the analgesic and anti-inflammatory effect.