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Abstract Number: 139

Lack of Effect of Supplemental Vitamin C On Serum Urate in Patients with Gout

Lisa K. Stamp1, Christopher Frampton1, John L. O'Donnell2, Jill Drake3 and Peter T. Chapman4, 1Department of Medicine, University of Otago, Christchurch, Christchurch, New Zealand, 2Rheumatology Immunology & Allergy, Canterbury Health Laboratories, Christchurch, New Zealand, 3Rheumatology, Immunology and Allergy, Christchurch Hospital, Christchurch, New Zealand, 4Rheumatology, Immunology & Allergy, Christchurch Hospital, Christchurch, New Zealand

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: gout, uric acid and vitamins

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Session Information

Title: Metabolic and Crystal Arthropathies

Session Type: Abstract Submissions (ACR)

<>Background/Purpose:   The key to effective long-term management of gout is sustained reduction of serum urate (SU) <0.36mmol/L. It has been suggested that supplemental vitamin C reduces SU in healthy controls via its uricosuric effect. However, it is unclear whether the reduction in SU is of a similar magnitude in patients with gout (who have reduced urate excretion) or whether co-administration of allopurinol lessens the magnitude of SU reduction from vitamin C.  The aims of this study were to determine effects of modest dose supplemental vitamin C on SU in patients with gout both as monotherapy and in combination with allopurinol. Methods: Patients with gout and a SU >0.36mmol/L were recruited. 20 patients already receiving allopurinol were randomised to either increase the dose of allopurinol or commence vitamin C 500mg/d. 20 patients not receiving urate lowering therapy were randomised to either start allopurinol or vitamin C 500mg/d. Plasma ascorbate, creatinine, SU, urine urate and creatinine were measured at days 0 and week 8.

 

Results:   18/20 patients who received Vitamin C were male with a mean age of 61.2 years (39-86). 18/20 patients who did not receive vitamin C were male with mean age of 55.0years (27-78). There was no significant difference in baseline SU or eGFR between those who received vitamin C and those who did not (SU 0.50 ±0.11mmol/l vs. 0.50 ± 0.09mmol/l p=0.89; eGFR 65.5 ± 15.7 vs. 67.9 ± 20.7 p=0.67). 30% in the vitamin C group were receiving diuretics compared to 25% in the no vitamin C group (p=0.72).

 

In the 20 patients receiving supplemental vitamin C there was a significant increase between week 0 and week 8 in plasma ascorbate (34.2µmol/l; p<0.001). There was no significant change in plasma ascorbate in those who did not receive vitamin C. The reduction in SU was significantly less in those 20 patients receiving vitamin C compared to those who started or increased the dose of allopurinol (0.014mmol/l vs. 0.118mmol/l p<0.001) (Figure). Allowing for eGFR did not affect these results.

 

Since Vitamin C is uricosuric we assessed change in urinary urate excretion using the Simkin index. In those patients already receiving allopurinol, addition of Vitamin C or an increase in allopurinol dose had no effect. In contrast, in those patients starting allopurinol there was a significant reduction in the Simkin index compared to those starting vitamin C (-0.13 vs. 0.002 p<0.011).

 

Conclusion: In this study supplemental vitamin C at modest dose (500mg/d) for 8 weeks had no significant urate lowering effect in patients with gout despite increasing plasma ascorbate concentrations. These results differ from findings in hyperuricaemic healthy controls.  The uricosuric effect of modest dose vitamin C appears less in patients with gout both as monotherapy and in combination with allopurinol. Whether larger doses will be effective remains to be determined.

 

Figure: Effect of vitamin C and allopurinol on serum urate


Disclosure:

L. K. Stamp,
None;

C. Frampton,
None;

J. L. O’Donnell,
None;

J. Drake,
None;

P. T. Chapman,
None.

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