Department of Rheumatology, Southport and Ormskirk Hospital NHS Trust, Southport, UK
Correspondence to: K. Binymin, Southport District General Hospital, Town Lane, Southport PR8 6PN UK. E-mail: kbinymin2001{at}yahoo.co.uk
We are grateful to Dr van Heyningen for his remarks and interesting comments regarding our letter, in which we highlight a possible causal relationship between rheumatoid arthritis and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) [1]. However, we are surprised by the arguments used to analyse the data given and the subsequent conclusions he has made. He claims The serum and urine osmolality results and urine sodium excretion do not however confirm the diagnosis of SIADH! Dr van Heyningen failed to outline why and how these biochemical data do not confirm a diagnosis of SAIDH. He also failed to cite any reference or other diagnostic criteria that support his claim. We reported the serum osmolality at 248 mmol/kg, urine osmolality at 334 mmol/kg and urine sodium excretion of 44 mmol/l, confirming the diagnosis of SIADH. The criteria laid down by Bartter and Schwartz (Table 1) [2] (referenced in our letter) for diagnosis of SIADH were fulfilled in our patient. The clinical and biochemical abnormalities reported in our case satisfied the five cardinal features of SIADH. At the time of her symptomatic hyponatraemia she excreted concentrated urine, which was inappropriate to her hypo-osmolar state. We stated that there were no other systemic disorders apart from rheumatoid arthritis. Relevant investigations done in an attempt to identify an alternative cause for hyponatraemia were outlined in detail in our letter. Because of manuscript constraints, we were not able to list all other less relevant tests and normal results. Thus, most of the conditions known to cause SIADH were effectively ruled out.
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Dr van Heyningen concluded that there is no convincing evidence that inflammatory arthritis is another cause of SIADH, and he chooses to ignore the striking correlation between the clinical course, Na level and CRP concentration, as presented in our letter. He admits, however, that the Na level recovery after the prolonged course of hyponatraemia is probably due to better control of underlying inflammation.
It should be pointed out that correction of chronic hyponatraemia is often an elective procedure, because there are no pernicious symptoms or adverse events related to this type of hyponatraemia. If the decision to initiate treatment is made, fluid restriction remains the mainstay of treatment. The fact that this patient did not receive anti-ADH treatmentas she remained asymptomatic after discharge from hospitalprovided an excellent opportunity to uncover and study the natural history of chronic SIADH in patients with inflammatory arthritis.
We believe that the inflammatory process secondary to rheumatoid arthritis was in great part responsible for initiating and propagating hyponatraemia in this instance. The proposed explanation for this was a possible chemokine-induced release of ADH. We were unable to identify another possible cause for SIADH, and Dr van Heyningen, in his comments, failed to provide a convincing alternative diagnosis.
References
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