Water balance in rheumatoid arthritis

C. van Heyningen

Department of Pathology, Southport District General Hospital, Southport, UK

Correspondence to: E-mail: charles.vanheyningen{at}southportandormskirk.nhs.uk

SIR, Kaushik and Binymin raise the interesting suggestion of a link between rheumatoid arthritis and the syndrome of inappropriate antidiuretic hormone (SIADH) [1]. The serum and urine osmolality results and urine sodium excretion do not, however, confirm the diagnosis of SIADH. Previous serum urea and creatinine concentrations and clinical features such as oedema, blood pressure and pulse are not described and liver function tests are not recorded.

The differential diagnosis includes the possibility of sick-cell syndrome [2] as part of a chronic inflammatory condition, hypervolaemic hyponatraemia secondary to chronic liver disease, or a reset osmostat [3]. The latter may have been induced by long-term diclofenac therapy. Non-steroidal anti-inflammatory drugs may potentiate the effect of antidiuretic hormone (ADH), leading to water retention [4]. This is mediated by a reduction in renal synthesis of prostaglandins, which normally antagonize the action of ADH.

These other mechanisms were not investigated by a water load test, hypertonic saline infusion test or plasma vasopressin estimations. Fluid restriction to one litre per day is only a weak therapy for SIADH and the ADH antagonist demeclocycline was not given a therapeutic trial.

My interpretation of the data presented for this case is that the findings suggest a probable drug effect, with diclofenac resetting the osmostat, and a possible acute-phase sick-cell syndrome with reduced ability of the cell membrane sodium pump to correct hyponatraemia. The gradual improvement in serum sodium with control of disease activity favours the latter mechanism, with a reduction in inflammation leading to the recovery of cell membrane sodium pump function.

In conclusion, I do not believe that this case report provides convincing evidence that inflammatory arthritis is another cause of SIADH.

The authors have declared no conflicts of interest.

References

  1. Kaushik VV, Binymin K. Is syndrome of inappropriate antidiuretic hormone secretion an extra-articular manifestation of rheumatoid arthritis? Rheumatology 2004;43:1589–90.[Free Full Text]
  2. Gill G, Leese G. Hyponatraemia: biochemical and clinical perspectives. Postgrad Med J 1998;74:516–23.[Abstract]
  3. Baylis, PH. The syndrome of inappropriate antidiuretic hormone secretion. Int J Biochem Cell Biol 2003;35:1995–9.
  4. Henrich WL. Nephrotoxicity of non-steroidal anti-inflammatory agents. Am J Kidney Dis 1983;2:478–84.[ISI][Medline]
Accepted 25 February 2005





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