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Author’s Response: Low Plasma Bicarbonate Level in Hyponatremia Related to Adrenocorticotropin Deficiency

Department of Internal Medicine, Research Unit for Study of Hydromineral Metabolism, Brussels, 1070 Belgium

Address correspondence to: Guy Decaux, M.D., Ph.D., Department of Internal Medicine, Research Unit for Study of Hydromineral Metabolism, 808 Route de Lennik, Brussels, 1070 Belgium. E-mail: guy.decaux{at}skynet.be.

To the editor:

We read with interest the comments made by Tooraj Zahedi (1) concerning our article (2) on the low TCO₂ levels observed in hyponatremia related to ACTH deficiency. Unfortunately, interpretation of the acid-base equilibrium in this situation is not simple. The mean arterial blood value reported (pH 7.42; PCO₂, 30 mm Hg; HCO₃^–, 20 mEq/liter; base excess, –3.4 mEq/liter) is compatible with a mixed acid-base disturbance (respiratory alkalosis and metabolic acidosis). As mentioned in the manuscript, some patients presented with lower pH values (7.36 and 7.38), and, in those patients, the metabolic acidosis related to the hypoaldosteronism was probably the main factor for the low TCO₂. In two other patients, the respiratory alkalosis was clearly the main factor (pH 7.47 and 7.52; despite hypoaldosteronism). In chronic severe hyponatremia with normal ACTH function, TCO₂ is normal, but blood gases show a mixed respiratory and metabolic alkalosis (3), the latter condition due to development of a hyponatremia-related hyperaldosteronism (3). This hyperaldosteronism need requires the presence of cortisone as a cofactor (4). As discussed in our manuscript (2), in hyponatremia due to ACTH deficiency, we did not observe a metabolic alkalosis as seen in classical syndrome of inappropriate antidiuretic hormone. When these patients normalized their serum Na by water restriction (or urea therapy), but without cortisone administration, we observed a normalization of TCO₂ (due to the correction of the respiratory alkalosis). The low TCO₂ observed in hyponatremia related to ACTH deficiency could reflect compensated respiratory alkalosis and/or metabolic acidosis due to hypoaldosteronism. The respiratory alkalosis does not seem to be always secondary to the metabolic acidosis.

Received July 1, 2004.

References

1. Zahedi T 2004 Low plasma bicarbonate level in hyponatremia related to adrenocorticotropin deficiency. J Clin Endocrinol Metab 89:5271 (Letter)[Free Full Text]
2. Decaux G, Musch W, Penninckx R, Soupart A 2003 Low plasma bicarbonate level in hyponatremia related to adrenocorticotropin deficiency. J Clin Endocrinol Metab 88:5255–5257[Abstract/Free Full Text]
3. Decaux G, Crenier L, Namias B, Gervy C, Soupart A 1994 Normal acid-base equilibrium in acute hyponatremia and mixed alkalosis in chronic hyponatremia induced by arginine vasopressin or 1-deamino-8D-arginine vasopressin. J Lab Clin Med 123:892–898[Medline]
4. Decaux G, Crenier L, Namias B, Gervy C, Soupart A 1994 Restoration by corticosteroids of the hyperaldosteronism in hyponatraemic rats with panhypopituitarism. Clin Sci (Lond) 87:435–439[Medline]

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				G. Decaux Author's Response: Low Plasma Bicarbonate Level in Hyponatremia Related to Adrenocorticotropin Deficiency J. Clin. Endocrinol. Metab., October 1, 2004; 89(10): 5271 - 5271. [Full Text] [PDF]

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