Thyroxine in Goiter, H. pylori Infection, and Gastritis
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《新英格兰医药杂志》
To the Editor: Centanni et al. (April 27 issue)1 describe conditions influencing the resorption of thyroxine and conclude that gastric acidity has a considerable effect on the bioavailability of iodothyronines. We do not share this opinion. In a recent crossover trial with healthy participants,2 we demonstrated that therapy with a high-dose proton-pump inhibitor (pantoprazole, 40 mg per day), resulting in elevated gastrin levels 1 week before the administration of thyroxine, did not influence absorption kinetics. The mechanisms of iodothyronine resorption are not fully understood, but malabsorption may be caused by numerous factors, including inflammatory diseases.3 In this context, it should be pointed out that all groups of patients studied by Centanni and colleagues and noted to have elevated gastric pH (those with atrophic gastritis, those with Helicobacter pylori infection, and those with gastroesophageal reflux) also had gastrointestinal inflammation. Therefore, we believe their study does not conclusively identify gastric acidity as a major determinant of thyroxine resorption.
Johannes W. Dietrich, M.D.
Bergmannsheil Hospitals
D-44789 Bochum, Germany
Bernhard O. Boehm, M.D.
Ulm Medical University Hospital
D-89081 Ulm, Germany
bernhard.boehm@uniklinik-ulm.de
References
Centanni M, Gargano L, Canettieri G, et al. Thyroxine in goiter, Helicobacter pylori infection, and chronic gastritis. N Engl J Med 2006;354:1787-1795.
Dietrich JW, Gieselbrecht K, Holl RW, Boehm BO. Absorption kinetics of levothyroxine is not altered by proton-pump inhibitor therapy. Horm Metab Res 2006;38:57-59.
Hays MT. Thyroid hormone and the gut. Endocr Res 1988;14:203-224.
To the Editor: We would like to see the results of basal and stimulated acid output for the patients in the study by Centanni et al. Without such information, their conclusion that absorption of thyroxine is dependent on gastric acid secretion seems questionable.
Kirstin M. Taylor, M.B., B.S.
Guy Sisson, M.B., B.S.
Adam W. Harris, M.D.
Kent and Sussex Hospital
Tunbridge Wells, Kent TN4 8AT, United Kingdom
kirstin.taylor@nhs.net
The authors reply: With regard to the comments by Dietrich and Boehm, our findings are not directly comparable with theirs.1 They examined the effect on acid inhibition of 40 mg of pantoprazole per day for 1 week in healthy euthyroid subjects. That model is quite different from one in which patients with thyroid disease received long-term treatment with omeprazole at a dose of 40 mg per day. Indeed, we are not surprised that Dietrich and colleagues did not observe any modification in thyroxine absorption after 7 days of treatment, since as we reported in our study, only after 6 months of omeprazole treatment was the dose of thyroxine increased to achieve low levels of serum thyrotropin. Furthermore, as Dietrich et al. stated in their article, thyroxine absorption in subjects with healthy thyroid glands may differ from that in patients with thyroid disease.1
Regarding the request of Taylor et al., basal acid output and pentagastrin-stimulated acid output were part of the diagnostic workup in patients with atrophic gastritis. In fact, these patients had a median basal acid output of 0 mEq per hour (range, 0 to 2.4) and a median pentagastrin-stimulated acid output of 0 mEq per hour (range, 0 to 10.5). These values indicated the presence of hypochlorhydria and achlorhydria, since both values were below our laboratory's normal ranges for basal acid output (median, 4.1 mEq per hour ) and pentagastrin-stimulated acid output (median, 31.1 mEq per hour ).2,3 Thus, we believe that these data support the hypothesis that reduced gastric acid secretion impairs effective absorption of thyroxine in patients with atrophic gastritis.
Bruno Annibale, M.D.
Marco Centanni, M.D.
Gianfranco Delle Fave, M.D.
University La Sapienza
00161 Rome, Italy
marco.centanni@uniroma1.it
References
Dietrich JW, Gieselbrecht K, Holl RW, Boehm BO. Absorption kinetics of levothyroxine is not altered by proton-pump inhibitor therapy. Horm Metab Res 2006;38:57-59.
Annibale B, Marignani M, Azzoni C, et al. Atrophic body gastritis: distinct features associated with Helicobacter pylori infection. Helicobacter 1997;2:57-64.
Marignani M, Delle Fave G, Mecarocci S, et al. High prevalence of atrophic body gastritis in patients with unexplained microcytic and macrocytic anemia: a prospective screening study. Am J Gastroenterol 1999;94:766-772.
Johannes W. Dietrich, M.D.
Bergmannsheil Hospitals
D-44789 Bochum, Germany
Bernhard O. Boehm, M.D.
Ulm Medical University Hospital
D-89081 Ulm, Germany
bernhard.boehm@uniklinik-ulm.de
References
Centanni M, Gargano L, Canettieri G, et al. Thyroxine in goiter, Helicobacter pylori infection, and chronic gastritis. N Engl J Med 2006;354:1787-1795.
Dietrich JW, Gieselbrecht K, Holl RW, Boehm BO. Absorption kinetics of levothyroxine is not altered by proton-pump inhibitor therapy. Horm Metab Res 2006;38:57-59.
Hays MT. Thyroid hormone and the gut. Endocr Res 1988;14:203-224.
To the Editor: We would like to see the results of basal and stimulated acid output for the patients in the study by Centanni et al. Without such information, their conclusion that absorption of thyroxine is dependent on gastric acid secretion seems questionable.
Kirstin M. Taylor, M.B., B.S.
Guy Sisson, M.B., B.S.
Adam W. Harris, M.D.
Kent and Sussex Hospital
Tunbridge Wells, Kent TN4 8AT, United Kingdom
kirstin.taylor@nhs.net
The authors reply: With regard to the comments by Dietrich and Boehm, our findings are not directly comparable with theirs.1 They examined the effect on acid inhibition of 40 mg of pantoprazole per day for 1 week in healthy euthyroid subjects. That model is quite different from one in which patients with thyroid disease received long-term treatment with omeprazole at a dose of 40 mg per day. Indeed, we are not surprised that Dietrich and colleagues did not observe any modification in thyroxine absorption after 7 days of treatment, since as we reported in our study, only after 6 months of omeprazole treatment was the dose of thyroxine increased to achieve low levels of serum thyrotropin. Furthermore, as Dietrich et al. stated in their article, thyroxine absorption in subjects with healthy thyroid glands may differ from that in patients with thyroid disease.1
Regarding the request of Taylor et al., basal acid output and pentagastrin-stimulated acid output were part of the diagnostic workup in patients with atrophic gastritis. In fact, these patients had a median basal acid output of 0 mEq per hour (range, 0 to 2.4) and a median pentagastrin-stimulated acid output of 0 mEq per hour (range, 0 to 10.5). These values indicated the presence of hypochlorhydria and achlorhydria, since both values were below our laboratory's normal ranges for basal acid output (median, 4.1 mEq per hour ) and pentagastrin-stimulated acid output (median, 31.1 mEq per hour ).2,3 Thus, we believe that these data support the hypothesis that reduced gastric acid secretion impairs effective absorption of thyroxine in patients with atrophic gastritis.
Bruno Annibale, M.D.
Marco Centanni, M.D.
Gianfranco Delle Fave, M.D.
University La Sapienza
00161 Rome, Italy
marco.centanni@uniroma1.it
References
Dietrich JW, Gieselbrecht K, Holl RW, Boehm BO. Absorption kinetics of levothyroxine is not altered by proton-pump inhibitor therapy. Horm Metab Res 2006;38:57-59.
Annibale B, Marignani M, Azzoni C, et al. Atrophic body gastritis: distinct features associated with Helicobacter pylori infection. Helicobacter 1997;2:57-64.
Marignani M, Delle Fave G, Mecarocci S, et al. High prevalence of atrophic body gastritis in patients with unexplained microcytic and macrocytic anemia: a prospective screening study. Am J Gastroenterol 1999;94:766-772.