Thyroxine in Goiter, Helicobacter pylori Infection, and Chronic Gastritis
Open accessAbstract
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.
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Increased gastric juice pH (>2) represents the leading cause of increased LT4 requirement in patients with all conditions of impaired gastric acidity.
“the increased gastric juice pH (>2) represents the leading cause of the increased LT4 requirement in patients with all conditions of impaired gastric acidity (47).”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
The Discussion (page unavailable) reports increased thyroxine requirements in the studied conditions of impaired gastric acid secretion, particularly atrophic gastritis and H. pylori infection. It does not establish a gastric-juice pH threshold of >2 or identify that threshold as the leading cause; it says the mechanism of impaired absorption is unknown. Its findings concern patients with multinodular goiter, not patients with every condition of impaired gastric acidity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn chronic atrophic gastritis, where acid-producing parietal cells are destroyed, LT4 need increased from 22 to 34%.
“First described in patients with chronic atrophic gastritis, where the acid-producing parietal cells are destroyed (LT4 need increased from 22 to 34%) (47)”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
The Daily Thyroxine Requirements section reports a 27% higher dose in patients with atrophic gastritis and 34% in those who also had H. pylori infection. The 22% increase applies to H. pylori-related gastritis, not atrophic gastritis, so the claimed 22–34% range misstates which groups produced those figures. The paper describes atrophic gastritis as involving low acid output and oxyntic atrophy, but does not explicitly say that parietal cells are destroyed. (LLM, conf=0.89)
Experimental — accuracy not yet measuredHelicobacter pylori treatment improves TSH levels and lowers the required dose of levothyroxine.
“In addition, there are studies that show improved levels of TSH upon Helicobacter pylori treatment that lower the required dose of levothyroxine (Centanni et al., 2006; Ribichini et al., 2017).”
From Thyroid disorders and gastrointestinal dysmotility: an old association (2024) · cites this paper as Centanni et al., 2006
The prospective-study passage reports that TSH fell after H. pylori eradication in 11 patients with multinodular goiter. It does not support the claimed reduction in levothyroxine dose: the median dose after eradication was slightly higher, 1.70 versus 1.56 μg/kg/day. (LLM, conf=0.92)
Experimental — accuracy not yet measuredEradication of H. pylori is associated with decreased TSH, and initiation of omeprazole with increased TSH.
“Furthermore, eradication of H. pylori infection and initiation of omeprazole were associated with decreased and increased TSH values, respectively.”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [153]
Daily LT4 requirement is up to 34% higher in patients with gastritis than in those without gastric disorders (2.05 vs 1.5 μg/kg/d).
“In another study, comparison of patients with gastritis, related either to H. pylori or atrophic gastritis, with a reference group without gastric disorders showed that the daily LT4 requirement was up to 34% higher in those with gastritis (2.05 vs. 1.5 l g/kg/d) (153).”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [153]
Helicobacter pylori infection and related gastritis represent the prototype of gastric juice alkalinization through bacterial urease activity and IL-1β and TNF-α production, and is also a frequent cause of increased need for LT4.
“Helicobacter pylori infection and related gastritis represent the prototype of gastric juice alkalinization through bacterial urease activity and IL-1β and TNF-α production (119), and is also a frequent cause of increased need for LT4 (47).”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
Patients with gastric disorders show a requirement for higher T4 doses.
“patients with gastric disorders show a requirement for higher T4 doses (47).”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
Patients with decreased gastric acid secretion due to proton pump inhibitor use may need higher LT4 doses to achieve target TSH levels.
“several studies have demonstrated that patients with decreased gastric acid secretion, owed to the use of proton pump inhibitors (PPIs), may need higher LT4 doses to achieve target TSH levels”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
Long-term PPI administration presents a heightened risk in patients with decreased gastric acid secretion who need higher LT4 doses.
“long-term PPI administration presenting a heightened risk in these cases (47, 78).”
From ETA guidelines for the use of levothyroxine sodium preparations in monotherapy to optimize the treatment of hypothyroidism (2025) · cites this paper as [47]
Altered T4 absorption owing to modified gastric physiology comes up as one of the critical reasons for increased thyroxine requirement.
“Among those, altered T4 absorption owing to modified gastric physiology comes up as one of the critical reasons (Centanni et al., 2006; Seng Yue et al., 2015).”
From Thyroid disorders and gastrointestinal dysmotility: an old association (2024) · cites this paper as Centanni et al., 2006
Patients with impaired stomach acid secretion require higher levothyroxine doses.
“Several studies demonstrate the requirement of higher levothyroxine doses in patients with stomach acid secretion impairment (Centanni et al., 2006; Ribichini et al., 2017).”
From Thyroid disorders and gastrointestinal dysmotility: an old association (2024) · cites this paper as Centanni et al., 2006
Levothyroxine absorption can be limited by gastrointestinal diseases including Helicobacter pylori infection, inflammatory bowel disease, celiac disease, lactose intolerance, atrophic body gastritis, gastric bypass, biliary pancreatic diversion, and gastroparesis.
“Levothyroxine absorption can be limited by a number of diseases of the gastrointestinal (GI) tract, including: Helicobacter pylori infection, inflammatory bowel disease (IBD), celiac disease, lactose intolerance, atrophic body gastritis (ABG), gastric bypass, biliary pancreatic diversion, and gastroparesis, among others”
From Diagnosis and management of treatment-refractory hypothyroidism: an expert consensus report (2017) · cites this paper as [5]
There is a large body of evidence that PPIs are prominent interfering substances that raise TSH levels and/or LT4 dose requirement.
“There is a large body of evidence (from general practice patient databases, electronic medical record reviews, and clinical trials) to indicate that PPIs are prominent interfering substances that raise TSH levels and/or the LT4 dose requirement [ 63 , 72 , 73 ].”
From Factors influencing the levothyroxine dose in the hormone replacement therapy of primary hypothyroidism in adults (2022) · cites this paper as [73]
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References 36 · Cited by 329
Research works printed but not linked: 7
- Fish LH, Schwartz HL, Cavanaugh J, Steffes MW, Bantle JP, Oppenheimer JH. Replacement dosage, metabolism, and bio- availability of levothyroxine in the treat- ment of hypothyroidism. N Engl J Med 1987;316:764-70.
- Erra- tum, N Engl J Med 1994;331:1035.
- Hays MT, Nielsen KRK. Human thy- roxine absorption: age effects and meth- odological analyses. Thyroid 1994;4:55-64.
- McQuaid KR. Dyspepsia. In: Feldman M, Friedman LS, Sleisenger MH, eds. Slei- senger & Fordtran's gastrointestinal and liver disease: pathophysiology, diagnosis, management. 7th ed. Vol. 1. Philadelphia: Saunders, 2002:102-18. 13. 14. 15. 16. 17. 18. 19. 20.
- Capurso G, Martino G, Grossi C, An- nibale B, Delle Fave G. Hypersecretory du- odenal ulcer and Helicobacter pylori infec- tion: a four-year follow-up study. Dig Liver Dis 2000;32:119-24.
- Siraj ES, Gupta MK, Reddy SS. Raloxi- fene causing malabsorption of levothyrox- ine. Arch Intern Med 2003;163:1367-70.
- The New England Journal of Medicine Downloaded from nejm.org on October 11, 2016. For personal use only. No other uses without permission. Copyright © 2006 Massachusetts Medical Society. All rights reserved. mucosal atrophy but reduces hypergastrin- emia and its related effects on body ECL- cell hyperplasia. Aliment Pharmacol Ther 2000;14:625-34.
- Authors
- Centanni, M., Gargano, L., Canettieri, G., Viceconti, N., Franchi, A., Fave, G. D., & Annibale, B.
- Affiliations
- Sapienza University of Rome (IT)
- Azienda Ospedaliera Sant'Andrea (IT)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2006-04-27
- Volume
- 354
- Issue
- 17
- Pages
- 1787-1795
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2003713859
- Cited by
- 329
- References
- 36
- Citations by year
- 2026: 11 · 2025: 9 · 2024: 17 · 2023: 8 · 2022: 19 · 2021: 12 · 2020: 14 · 2019: 14 · 2018: 15 · 2017: 21 · 2016: 28 · 2015: 17 · 2014: 33 · 2013: 15 · 2012: 21
- FWCI
- 10.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Surgery › Helicobacter pylori-related gastroenterology studies
- Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
- Keywords
- thyroxine, multinodular goiter, Helicobacter pylori infection, atrophic gastritis, gastric acid secretion, thyroid-stimulating hormone, omeprazole, gastroesophageal reflux, Helicobacter pylori eradication
- MeSH terms
- Adult, Aged, Anti-Ulcer Agents, Chronic Disease, Gastric Acid, Gastritis, Goiter, Humans, Intestinal Absorption, Middle Aged, Omeprazole, Prospective Studies, Thyrotropin, Thyroxine, Helicobacter pylori, Helicobacter Infections
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