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Patients with multinodular goiter required a thyroxine dosage increase of 22%-34% if they had impaired secretion of stomach acids, results from a large controlled study demonstrated.
The finding suggests that "normal gastric acid secretion is important for the subsequent intestinal absorption of thyroxine," wrote the researchers, who were led by Dr. Marco Centanni of the department of experimental medicine and pathology at La Sapienza University, Rome.
"Although the clinical importance of these findings is fairly clear, the mechanism by which intestinal absorption of thyroxine is impaired in patients with hypochlorhydria is unknown. We may only speculate that oral thyroxine is administered as sodium salt that is less lipophilic than the native hormone, which enters target cells both through passive diffusion and in a carrier-mediated, inhibitable way. In this respect, achlorhydria due to atrophic gastritis, the production of ammonia, or both, which are characteristic of [Helicobacter] pylori infection, may alter the ionization status and the conformational characteristics of the thyroxine molecule and thus the efficiency of intestinal absorption of the hormone."
Dr. Centanni and his associates studied 248 patients with nontoxic multinodular goiter who were seen at a referral center for thyroid disease between 1999 and 2004. Of the 248 patients, 53 also had H. 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 remaining 135 patients had no gastric disorders and served as the reference group (N. Engl. J. Med. 2006;354:1787-95).
All patients received an initial thyroxine dosage of 50 [micro]g/day and were followed for at least 30 months. The researchers evaluated the thyroid-pituitary axis every 4 months and, if needed, increased the thyroxine dosage until a low serum thyrotropin level was achieved on at least two consecutive measurements. The serum ...