Two hundred forty-eight patients with multinodular goiter who were receiving treatment with thyroxine were studied. Fifty-three of the patients also had Helicobacter pylori-related gastritis and 60 had atrophic gastritis (31 with evidence of H. pylori infection and 29 without such evidence). The daily requirement of thyroxine to maintain a low TSH level (0.05-0.20 mU/L) was 22-34% higher in patients with H. pylori-related gastritis, atrophic gastritis, or both conditions, than in patients without those conditions. In prospective studies, the development of H. pylori infection in 11 patients treated with thyroxine led to an increase in the TSH level (p = 0.002), an effect that was nearly reversed after eradication of H. pylori. In a similar way, omeprazole treatment, which reduces gastric acid secretion, was associated with an increase in the TSH level in all 10 patients treated with thyroxine, an effect that was reversed by an increase in the thyroxine dose by 37%.

Comment: These findings suggest that gastric acid secretion is necessary for effective absorption of thyroxine. Patients who develop conditions that result in reduced acid secretion (such as H. pylori infection or atrophic gastritis) and patients who take antacids or acid-blocking drugs may require an increase in their thyroxine dose to maintain a euthyroid state. Conversely, an increase in gastric acidity (as would result from discontinuation of antacids or acid blocking drugs, from treatment of a hypochlorhydric patient with hydrochloric acid, and possibly from the eradication of H. pylori) may require a decrease in their thyroxine dose. Patients being treated with thyroxine should be monitored more closely during periods in which their gastric acidity is expected to change.

Centanni M, et al. Thyroxine in goiter, Helicobacter pylori infection, and chronic gastritis. N Engl J Med. 2006;354:1787-1795.