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Original Article
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Volume 354:1787-1795 April 27, 2006 Number 17
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Thyroxine in Goiter, Helicobacter pylori Infection, and Chronic Gastritis
Marco Centanni, M.D., Lucilla Gargano, M.D., Gianluca Canettieri, M.D., Nicola Viceconti, M.D., Antonella Franchi, M.D., Gianfranco Delle Fave, M.D., and Bruno Annibale, M.D.

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ABSTRACT

Background Malabsorption of thyroxine has been described in patients treated with drugs that modify an acidic environment. We determined whether there is an increased need for thyroxine in patients with euthyroid multinodular goiter and impaired secretion of gastric acid.

Methods We assessed the dose of thyroxine required to obtain a low level of thyrotropin (0.05 to 0.20 mU per liter) in 248 patients with multinodular goiter. Of these 248 patients, 53 also had Helicobacter pylori–related gastritis and 60 had atrophic gastritis of the body of the stomach (31 with evidence of H. pylori infection and 29 without such evidence). The reference group comprised 135 patients with multinodular goiter and no gastric disorders. In addition, variation in the level of serum thyrotropin was prospectively studied in 11 patients treated with thyroxine before and after H. pylori infection and both before and during treatment with omeprazole in 10 patients treated with thyroxine who had gastroesophageal reflux.

Results The daily requirement of thyroxine was higher (by 22 to 34 percent) in patients with H. pylori–related gastritis, atrophic gastritis, or both conditions than in the reference group. In prospective studies, the occurrence of H. pylori infection in the 11 patients treated with thyroxine led to an increase in the level of serum thyrotropin (P=0.002), an effect that was nearly reversed on eradication of H. pylori infection. In a similar way, omeprazole treatment was associated with an increase in the level of serum thyrotropin in all 10 patients treated with thyroxine, an effect that was reversed by an increase in the thyroxine dose by 37 percent.

Conclusions Patients with impaired acid secretion require an increased dose of thyroxine, suggesting that normal gastric acid secretion is necessary for effective absorption of oral thyroxine.


Source Information

From the Endocrinology Unit, Department of Experimental Medicine and Pathology, University La Sapienza, Polo Pontino, Latina (M.C., L.G., G.C., N.V., A.F.); and the Department of Digestive and Liver Diseases, Sant'Andrea Hospital, University La Sapienza, Rome (G.D.F., B.A.) — both in Italy.

Address reprint requests to Dr. Centanni at the Department of Experimental Medicine and Pathology, Policlinico Umberto I, Viale Regina Elena 324, 00161 Rome, Italy, or at marco.centanni{at}uniroma1.it.

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Related Letters:

Thyroxine in Goiter, H. pylori Infection, and Gastritis
Dietrich J. W., Boehm B. O., Taylor K. M., Sisson G., Harris A. W., Annibale B., Centanni M., Fave G. D.
Extract | Full Text | PDF  
N Engl J Med 2006; 355:1177, Sep 14, 2006. Correspondence

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