Abstract

Background: According to most clinical guidelines hypothyroidism should be excluded as a cause in the analysis of euvolemic hyponatremia. Although this axiom has been well established in clinical practice, relatively little evidence supports a relation between hypothyroidism and hyponatremia. The current study was conducted to prove an association between hypothyroidism and the occurrence of hyponatremia. In addition, we sought to determine the effect of L-thyroxine replacement therapy on plasma sodium levels. Methods: Data from 2009 to 2011 were retrospectively reviewed. The database included blood samples in which both thyroid function and plasma sodium were determined. Regression analysis and ANOVA were performed to reveal an association between hypothyroidism and hyponatremia. Results: Linear regression analysis of plasma sodium on plasma TSH revealed no relationship (R2 = 0.005). The corresponding gradient belonging to the regression line was ﹣0.427 mmol/log plasma TSH (p = 0.22). No significant relation between plasma sodium and TSH concentration could therefore be found. 32 hypothyroid patients who were treated with L-thyroxine, were identified. No clear change in plasma sodium could be discerned with regression analysis (0.707 mmol/L per year, p = 0.147). Conclusion: Hypothyroidism is not a common cause of hyponatremia. Screening for thyroid function does not seem warranted in the initial analysis of a hyponatremic patient.

Highlights

  • Most guidelines consider hypothyroidism to be a cause for hyponatremia [1]-[3]

  • Little epidemiological data supports the notion that hypothyroidism is an important cause of hyponatremia

  • Study population: A cohort was retrospectively defined by searching the database for blood samples that contained plasma TSH, as well as plasma sodium and free serum thyroxin concentration

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Summary

Introduction

Most guidelines consider hypothyroidism to be a cause for hyponatremia [1]-[3]. Proposed mechanisms for hypothyroidism induced hyponatremia include increase in vasopressin (ADH) release [4]-[7] and reduced renal glomerular filtration rate (GFR) [2] [8]-[17]. Whether the increased vasopressin levels are a direct effect of low plasma thyroxin levels or secondary to reduced cardiac output due to hypothyroidism, is unknown [2] [3] [15] [17]. None of the studies including adult subjects, investigated plasma sodium concentrations after supplementation of L-thyroxine. In addition we set out to investigate the effect of L-thyroxine replacement therapy on plasma sodium concentration in hypothyroid patients

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