Findings published in the New England Journal of Medicine have revealed that a higher dose of thyroxine may be required in patients with multinodular goiter and concomitant atrophic gastritis, chronic Helicobacter pylori infection, or both.
The researchers, headed by Marco Centanni, from the University La Sapienza in Rome, Italy, say that these data support the hypothesis that gastric acid secretion is necessary for the effective absorption of thyroxine.
Explaining the background to their study, the team writes that "intestinal absorption of thyroxine is a key determinant of the effectiveness of therapy and is influenced by several factors," including absorption kinetics.
They therefore add: "The concomitant presence of such gastric disorders with thyroid diseases may lead to uncertainty about the daily dose of thyroxine and, thus, to a continuous need for care and monitoring."
Centanni and co-workers aimed to determine the dose of thyroxine required to obtain a low level of thyrotropin, of 0.05 to 0.20 mU per liter, in 248 patients with multinodular goiter.
Of these patients, 53 had H. pylori-related gastritis. A further 60 of these individuals had atrophic gastritis of the stomach, of whom 31 had evidence of H. pylori infection, and 29 were free from the bacterium.
In the 135 control patients without multinodular goiter and gastric impairment, a median thyroxine daily dose of 100 μg was sufficient to obtain a low level of thyrotropin.
In contrast, a similar dose of thyroxine was insufficient to lower thyrotropin values in 52 of the 53 patients with H. pylori-related gastritis and all of those with atrophic gastritis.
Compared with the levels required for controls, the daily dose of thyroxine needed to be increased by between 22% and 34% in patients with H. pylori-related gastritis, atrophic gastritis, or both conditions, to achieve lowered thyrotropin levels.
"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," Centanni et al note.
They suggest that one possible mechanism is that achlorhydria, the absence of hydrochloric acid from the gastric juice, alters the ionization status or conformational characteristics of the thyroxine molecule in a way that inhibits its intestinal absorption.